Priscilla S Medicine With Addon Final PDF

Priscilla’s Medicine
Table of Contents
SHORT CASES IN MEDICINE ............................................................................................................................................................ 5
MEDICINE = CARDIO SHORTS................................................................................................................................................................................ 5
MEDICINE = RESPI SHORTS ................................................................................................................................................................................... 9
MEDICINE = RENAL SHORTS ...............................................................................................................................................................................14
MEDICINE = ENDOCRINE SHORTS ......................................................................................................................................................................15
MEDICINE = HANDS SHORTS...............................................................................................................................................................................16
ENDOCRINE ........................................................................................................................................................................................ 17
MEDICINE (THYROID) = PHYSICAL EXAMINATION.........................................................................................................................................17
MEDICINE (THYROID) = INTRODUCTION .........................................................................................................................................................20
MEDICINE (THYROID) = THYROID LUMPS .......................................................................................................................................................23
MEDICINE (THYROID) = MANAGEMENT OF HYPERTHYROIDISM .................................................................................................................23
SURGERY (THYROID) = HYPERTHYROIDISM ....................................................................................................................................................26
MEDICINE (THYROID) = HYPOTHYROIDISM ....................................................................................................................................................30
SURGICAL (THYROID) = THYROID CARCINOMA ..............................................................................................................................................33
SURGICAL (THYROID) = THYROIDECTOMY ......................................................................................................................................................36
RHEUMATOLOGY ............................................................................................................................................................................. 38
MEDICINE (RHEUMATOLOGY) = RHEUMATOID ARTHRITIS SONG ...............................................................................................................38
MEDICINE (RHEUMATOLOGY) = GENERAL POINTS ABOUT ARTHRITIS .......................................................................................................39
MEDICINE (RHEUMATOLOGY) = SYSTEMIC LUPUS ERYTHEMATOSUS (SLE).............................................................................................40
MEDICINE (RHEUMATOLOGY) = GALS SCREEN ..............................................................................................................................................46
MEDICINE (RHEUMATOLOGY) = RHEUMATOID ARTHRITIS ..........................................................................................................................48
MEDICINE (RHEUMATOLOGY) = EXAMINATION OF RHEUMATOID HANDS .................................................................................................56
MEDICINE (RHEUMATOLOGY) = CASE STUDY .................................................................................................................................................59
MEDICINE (RHEUMATOLOGY) = CLERKING OF RHEUMATOID ARTHRITIS .................................................................................................62
MEDICINE (RHEUMATOLOGY) = SCLERODERMA LONG CASE .......................................................................................................................63
MEDICINE (RHEUMATOLOGY) = GOUT .............................................................................................................................................................66
MEDICINE (RHEUMATOLOGY) = GOUT HISTORY TAKING .............................................................................................................................68
MEDICINE (RHEUMATOLOGY) = CHRONIC TOPHACEOUS GOUT (SHORT CASE) .........................................................................................71
DIABETES ............................................................................................................................................................................................ 72
MEDICINE (DIABETES) = HISTORY TAKING .....................................................................................................................................................72
MEDICINE (DIABETES) = DIETARY ADVICE .....................................................................................................................................................74
MEDICINE (DIABETES) = COUNSELING A NEWLY DIAGNOSED DIABETIC ....................................................................................................75
MEDICINE (DIABETES) = DIABETES MANIFESTATIONS ................................................................................................................................76
MEDICINE (DIABETES) = DIABETES MELLITUS ..............................................................................................................................................77
MEDICINE (DIABETES) = HYPOGLYCEMIA .......................................................................................................................................................79
MEDICINE (DIABETES) = DIAGNOSIS OF DM ..................................................................................................................................................81
RENAL MEDICINE ............................................................................................................................................................................. 83
MEDICINE (RENAL) = NEPHROTIC SYNDROME HISTORY TAKING...............................................................................................................83
MEDICINE (RENAL) = NEPHROTIC SYNDROME ...............................................................................................................................................85
MEDICINE (RENAL) = SECONDARY HYPERTENSION ......................................................................................................................................89
MEDICINE (RENAL) = DIALYSIS MODALITIES ..................................................................................................................................................90
MEDICINE (RENAL) = RENAL TRANSPLANT (MAJOR RISKS) .......................................................................................................................92
MEDICINE (RENAL) = ADULT POLYCYSTIC KIDNEY DISEASE (APKD) ......................................................................................................92
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MEDICINE (RENAL) = URINARY TRACT INFECTION / PYELONEPHRITIS ....................................................................................................94
MEDICINE (RENAL) = ASSESSING VOLUME STATUS .......................................................................................................................................96
MEDICINE (RENAL) = FLUID AND ELECTROLYTES (ACID- BASE DISORDERS) ...........................................................................................98
MEDICINE (RENAL) = RESPIRATORY DISORDERS........................................................................................................................................ 102
MEDICINE (RENAL) = RENAL TUBULAR ACIDOSIS (RTA) ........................................................................................................................ 103
MEDICINE (RENAL) = POTASSIUM DISORDERS ............................................................................................................................................ 105
MEDICINE (RENAL) = HYPONATRAEMIA ...................................................................................................................................................... 108
MEDICINE (RENAL) = HYPERNATRAEMIA .................................................................................................................................................... 111
GASTROLOGY .................................................................................................................................................................................. 113
MEDICINE (GIT) = HISTORY TAKING: GIT (GENERAL) ............................................................................................................................. 113
MEDICINE (GIT) = PHYSICAL EXAMINATION: GIT ...................................................................................................................................... 115
MEDICINE (GIT) = ISSUES FOR DISCUSSION ................................................................................................................................................. 119
MEDICINE (GIT) = APPROACH TO ASCITES .................................................................................................................................................. 122
MEDICINE (GIT) = ASCITES............................................................................................................................................................................. 124
MEDICINE (GIT) = CHRONIC LIVER DISEASE AND LIVER CIRRHOSIS ........................................................................................................ 128
MEDICINE (GIT) = HEPATOMEGALY.............................................................................................................................................................. 132
MEDICINE (GIT) = JAUNDICE (HISTORY-TAKING) ....................................................................................................................................... 135
MEDICINE (GIT) = APPROACH TO JAUNDICE ............................................................................................................................................... 137
MEDICINE (GIT) = ACUTE HEPATITIS ........................................................................................................................................................... 143
MEDICINE (GIT) = VIRAL HEPATITIS ............................................................................................................................................................ 144
MEDICINE (GIT) = ALCOHOLIC LIVER DISEASE........................................................................................................................................... 152
MEDICINE (GIT) = AUTOIMMUNE HEPATITIS.............................................................................................................................................. 153
MEDICINE (GIT) = METABOLIC LIVER DISEASE .......................................................................................................................................... 154
MEDICINE (GIT) = WILSON’S DISEASE (HEPATOLENTICULAR DISORDER) ............................................................................................ 156
SURGERY (GIT) = OBSTRUCTIVE JAUNDICE .................................................................................................................................................. 158
MEDICINE (GIT) = LIVER FAILURE ................................................................................................................................................................ 163
MEDICINE (GIT) = PORTAL HYPERTENSION ................................................................................................................................................ 165
MEDICINE (GIT) = CHRONIC DIARRHEA ....................................................................................................................................................... 167
MEDICINE (GIT) = INFLAMMATORY BOWEL DISEASE ............................................................................................................................... 171
REPIRATORY MEDICINE ............................................................................................................................................................. 179
MEDICINE (RESPI) = HISTORY TAKING: RESPIRATORY SYSTEM (GENERAL) ........................................................................................ 179
MEDICINE (RESPI) = PHYSICAL EXAMINATION: RESPIRATORY SYSTEM ................................................................................................. 182
MEDICINE (RESPI) = HAEMOPTYSIS .............................................................................................................................................................. 188
MEDICINE (RESPI) = DYSPNOEA..................................................................................................................................................................... 189
MEDICINE (RESPI) = APPROACH TO CHEST PAIN AND DYSPNEA ............................................................................................................. 191
MEDICINE (RESPI) = PULMONARY FIBROSIS ................................................................................................................................................ 193
MEDICINE (RESPI) = COPD ............................................................................................................................................................................ 194
MEDICINE (RESPI) = BRONCHIECTASIS ......................................................................................................................................................... 199
MEDICINE (RESPI) = COR PULMONALE ......................................................................................................................................................... 203
MEDICINE (RESPI) = RESPIRATORY INFECTIONS: TUBERCULOSIS ........................................................................................................... 205
MEDICINE (RESPI) = PANCOAST TUMOUR-UPPER LOBE LUNG CA........................................................................................................... 211
MEDICINE (RESPI) = PLEURAL EFFUSION..................................................................................................................................................... 212
MEDICINE (RESPI) =PNEUMOTHORAX .......................................................................................................................................................... 216
MEDICINE (RESPI) = RESPIRATORY FAILURE .............................................................................................................................................. 220
MEDICINE (RESPI) = SYSTEMIC APPROACH TO CXR ................................................................................................................................... 222
MEDICINE (RESPI) = MEDIASTINAL MASSES ................................................................................................................................................ 223
CARDIO VASCULAR SYSTEM ...................................................................................................................................................... 224
MEDICINE (CVS) = HISTORY TAKING: CVS.................................................................................................................................................. 224
MEDICINE (CVS) = PHYSICAL EXAMINATION: CVS .................................................................................................................................... 227
MEDICINE (CVS) = ISSUES FOR DISCUSSION ................................................................................................................................................. 231
MEDICINE (CVS) = APPROACH TO CHEST PAIN ........................................................................................................................................... 236
MEDICINE (CVS) = HO ON CALL..................................................................................................................................................................... 240
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MEDICINE (CVS) = ISCHAEMIC HEART DISEASE (HISTORY) .................................................................................................................... 242
MEDICINE (CVS) = ANGINA PECTORIS .......................................................................................................................................................... 244
MEDICINE (CVS) = ISCHAEMIC HEART DISEASE (HISTORY) .................................................................................................................... 248
MEDICINE (CVS) = ACUTE CORONARY SYNDROME (ACS) ....................................................................................................................... 250
MEDICINE (CVS) = CONGESTIVE CARDIAC FAILURE (CCF) ...................................................................................................................... 257
MEDICINE (CVS) = PATHOPHYSIOLOGY OF DYSPNOEA .............................................................................................................................. 264
MEDICINE (CVS) = PROGNOSTIC FACTORS OF HYPERTENSION ............................................................................................................... 264
MEDICINE (CVS) = HYPERTENSION............................................................................................................................................................... 266
MEDICINE (CVS) = ANTI HYPERTENSIVE MEDICATION ............................................................................................................................. 273
MEDICINE (CVS) = GUIDELINES FOR SELECTING DRUG TREATMENT OF HYPERTENSION .................................................................... 277
MEDICINE (CVS) = LIPIDS ............................................................................................................................................................................... 278
MEDICINE (CVS) = MYOCARDITIS.................................................................................................................................................................. 282
MEDICINE (CVS) = CARDIOMYOPATHY ......................................................................................................................................................... 284
MEDICINE (CVS) = TAKAYASU ARTERITIS ................................................................................................................................................... 286
MEDICINE (CVS) = VALVULAR HEART DISEASE ........................................................................................................................................... 287
MEDICINE (CVS) = VALVULAR HEART DISEASE ........................................................................................................................................... 289
MEDICINE (CVS) = PROSTHETIC HEART VALVES......................................................................................................................................... 294
MEDICINE (CVS) = INFECTIVE ENDOCARTITIS ............................................................................................................................................ 296
PRISCILLA’S MEDICINE ADD-ON .............................................................................................................................................. 300
SURGERY (THYROID) = INVESTIGATIONS ...................................................................................................................................................... 300
SURGERY (THYROID) = SHORT CASES ........................................................................................................................................................... 302
SURGERY (THYROID) = CONGENITAL ANOMALIES....................................................................................................................................... 303
MEDICINE (RHEUMATOLOGY) = APPROACH TO THE RHEUMATOLOGICAL CASE ................................................................................... 304
MEDICINE (RHEUMATOLOGY) = DERMATOMYOSITIS AND POLYMYOSITIS ............................................................................................. 309
MEDICINE (RHEUMATOLOGY) = HISTORY-TAKING ..................................................................................................................................... 313
MEDICINE (RHEUMATOLOGY) = HAND ......................................................................................................................................................... 315
MEDICINE (RHEUMATOLOGY) = HANDS & WRISTS, SHOULDER, C-SPINE, HIP ....................................................................................... 329
MEDICINE (DIABETES) = DIABETIC KETOACIDOSIS (DKA) ...................................................................................................................... 332
MEDICINE (DIABETES) = HYPEROSMOLAR HYPERGLYCAEMIC NON-KETOTIC (HHNK) STATE .......................................................... 336
MEDICINE (DIABETES) = MANAGEMENT OF DIABETES MELLITUS .......................................................................................................... 338
MEDICINE (ENDOCRINE) = CUSHING’S SYNDROME ..................................................................................................................................... 349
MEDICINE (ENDOCRINE) = ACROMEGALY .................................................................................................................................................... 354
MEDICINE (ENDOCRINE) = ADDISON’S DISEASE (CHRONIC 10 ADRENAL INSUFFICIENCY) .................................................................. 358
MEDICINE (ENDOCRINE) = HYPO-PITUITARISM .......................................................................................................................................... 360
MEDICINE (ENDOCRINE) = GYNAECOMASTIA .............................................................................................................................................. 363
MEDICINE (RENAL) = ACUTE RENAL FAILURE ............................................................................................................................................ 364
MEDICINE (RENAL) = CHRONIC RENAL FAILURE ........................................................................................................................................ 368
MEDICINE (RENAL) = CRF WITH FLUID OVERLOAD ................................................................................................................................... 376
MEDICINE (RENAL) = BALLOTABLE KIDNEYS.............................................................................................................................................. 377
MEDICINE (RENAL) = TRANSPLANTED KIDNEY .......................................................................................................................................... 379
MEDICINE (RENAL) = APPROACH TO OLIGURIA ........................................................................................................................................... 383
MEDICINE (RENAL) = APPROACH TO PROTEINURIA ................................................................................................................................... 384
MEDICINE (RENAL) = HAEMATURIA.............................................................................................................................................................. 387
MEDICINE (RENAL) = GLOMERULONEPHRITIS ............................................................................................................................................ 390
MEDICINE (RENAL) = DGIM RENAL TRANSPLANT .................................................................................................................................... 396
MEDICINE (GIT) = HEPATOSPLENOMEGALY ................................................................................................................................................ 398
MEDICINE (RESPI) = GENERAL APPROACH TO A HISTORY OF SHORTNESS OF BREATH....................................................................... 399
MEDICINE (RESPI) = ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) .......................................................................................... 400
MEDICINE (RESPI) = SYSTEMIC APPROACH TO CXR ................................................................................................................................... 402
MEDICINE (RESPI) = LUNG CANCER .............................................................................................................................................................. 406
MEDICINE (RESPI) = INFECTIONS – TUBERCULOSIS ................................................................................................................................... 411
MEDICINE (RESPI) = PNEUMONIA .................................................................................................................................................................. 416
MEDICINE (RESPI) = ASTHMA ........................................................................................................................................................................ 421
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MEDICINE (RESPI) = PULMONARY EMBOLISM ............................................................................................................................................. 427
Acknowledgements
Written by:
Dr Priscilla Phoon & her team of original authors
Transcribed by:
YLLSOM Class of Medicine 2013
Special Thanks to the following people for helping with the add-on:
Ong Eng Hui
Chew Bao Li
Steffi Chan
Teo Yi Lyn
Lucy Davis
Grace Lum
Edited and formatted by:

James Lee (Class of 2013)
Last Updated:
20st Febuary 2011
4
Short Cases in Medicine
Medicine = Cardio shorts
Prosthetic heart valves

Mdm XXX is an elderly Chinese lady who appears to be alert, well, comfortable and orientated at rest. Her
vitals are as follows = HR 80/min, irregularly irregular. There is no RR delay, RF delay or collapsing pulse. RR is
16/min, not tachypneic or dyspnoeic. She does not appear to be in any respiratory distress and is pink on
room air. On general inspection, I note the presence of a mid-line sternotomy scar with no corresponding
saphenous vein harvest site. There are no signs of pallor, jaundice or cyanosis.
On examination of the peripheries, there are no stigmata of infective endocarditis such as clubbing, splinter
haemorrhages, Janeway lesions or Osler nodes. There is no extensive bruising seen over the arms. I looked
for but did not find any evidence of an enlarged goitre or thyroidectomy scar.
On examination of the praecordium, there was a metallic click audible to the unaided ear. A visible apical
impulse was seen in the 6th intercostal space 1cm lateral to the mid-clavicular line. The apex beat was
heaving in nature. There was no parasternal heave or thrills felt over the base of the heart. On auscultation,
the first heart sound was metallic and sharp in nature. The second heart sound was native. There were no
additional heart sounds. In addition, there was a grade 3/6 PSM heard loudest over the apex with radiation
to the axilla.
This was not associated with signs of right heart failure as the jugular venous pressure was not raised and
there was no peripheral oedema. Auscultation of the lung bases also did not reveal the presence of
inspiratory crepitations.
So in summary, Mdm XXX is an elderly chinese lady who has a prosthetic mitral valve replacement. I say this
because
(a) midline sternotomy scar with no corresponding saphenous vein harvest site
(b) metallic click audible to the unaided ear
(c) sharp and metallic first heart sound heard on auscultation
This is most likely due to severe mitral regurgitation

(a) atrial fibrillation
(b) displaced and heaving apex beat
(c) grade 3/6 PSM heard loudest over the apex with radiation to the axilla
This is not complicated by congestive cardiac failure, infective endocarditis, over-anticoagulation or valve
haemolysis
Mitral stenosis
Mdm XXX is an elderly chinese lady who appears to be alert, well, comfortable and orientated at rest. Her
vitals are as follows = HR 80/min, irregularly irregular. There is no RR delay, RF delay or collapsing pulse. RR is
room air. On general inspection, there are no signs of pallor, jaundice or cyanosis.
haemorrhages, Janeway lesions or Osler nodes. There is no extensive bruising seen over the arms. I looked
for but did not find any evidence of an enlarged goitre or thyroidectomy scar.
On examination of the praecordium, there were no surgical scars or chest wall deformities. The apex beat
was not displaced. It was in the 5th intercostal space in the mid-clavicular line and was tapping in nature.
There was no parasternal heave or thrills felt over the base of the heart. On auscultation, the first heart
5
sound was loud and there was an opening snap followed by a mid-diastolic murmur heard best over the
apex which was accentuated with the patient in the left lateral position. There was no PSM heard over the
tricuspid area or Graham-Steell murmur heard over the pulmonary area.
So in summary, Mdm XXX is an elderly chinese lady who has mitral stenosis. I say this because
(a) presence of atrial fibrillation
(b) tapping apex beat which is not displaced
(c) opening snap with a MDM heard best over the apex and accentuated by the patient lying in the left
lateral position
This is not complicated by pulmonary hypertension, congestive cardiac failure, infective endocarditis or
over-anticoagulation
# Request to examine = neurological system (pronator drift for hemiplegia)

peripheral pulses (occlusion by emboli)
Mitral regurgitation
vitals are as follows = HR 80/min, regular. There is no RR delay, RF delay or collapsing pulse. RR is 16/min, not
tachypneic or dyspnoeic. She does not appear to be in any respiratory distress and is pink on room air. On
general inspection, there are no signs of pallor, jaundice or cyanosis.
haemorrhages, Janeway lesions or Osler nodes.
On examination of the praecordium, there were no surgical scars or chest wall deformities. The apex beat
was displaced in the 6th intercostal space 1cm lateral to the mid-clavicular line and was heaving in nature.
There was no parasternal heave or thrills felt over the base of the heart. On auscultation, the first and
second heart sounds were heard. There was no 3rd heart sound. In addition, there was a grade 3/6 PSM
heard loudest over the apex with radiation to the axilla. There was no radiation to the carotids.
So in summary, Mdm XXX is an elderly chinese lady who has mitral regurgitation. I say this because
(a) displaced apex beat which is heaving in nature
(b) grade 3/6 PSM heard loudest over the apex with radiation to the axilla
This is not complicated by congestive cardiac failure or infective endocarditis
Aortic stenosis
vitals are as follows = HR 80/min, regular. There is no RR delay, RF delay or collapsing pulse. However, I note
that the pulse is of low-volume and slow-rising in nature. RR is 16/min, not tachypneic or dyspnoeic. She
does not appear to be in any respiratory distress and is pink on room air. On general inspection, there are
no signs of pallor, jaundice or cyanosis.
On examination of the praecordium, there were no surgical scars or chest wall deformities. The apex beat is
6
not displaced and is thrusting in nature. There was no parasternal heave or thrills felt over the base of the
heart. On auscultation, the first and second heart sounds were heard. There was no 4 th heart sound. In
addition, there was a grade 3/6 ESM heard loudest over the aortic area with radiation to the carotids
which was accentuated by forced expiration.
So in summary, Mdm XXX is an elderly chinese lady who has aortic stenosis. I say this because
(a) low-volume slow-rising pulse (‘anacrotic pulse’)
(b) apex beat is not displaced and is thrusting in nature
(c) grade 3/6 ESM heard loudest over the aortic area with radiation to the carotids and accentuated by
forced expiration
# Request = BP (narrow pulse pressure)
Aortic regurgitation
vitals are as follows = HR 80/min, regular. There is a collapsing pulse noted but no RR delay or RF delay. RR is
room air. On general inspection, there are no signs of pallor, jaundice or cyanosis.
On examination of the praecordium, there were no surgical scars or chest wall deformities. The apex beat is
displaced in the 6th intercostal 1cm lateral to the mid-clavicular line and is heaving in nature. There was no
parasternal heave or thrills felt over the base of the heart. On auscultation, the first and second heart
sounds were heard. There was no 3rd heart sound. In addition, there was a grade 2/6 EDM heard loudest
over the upper left sternal edge which was accentuated with forced expiration. There was no Austin-Flint
murmur detected.
So in summary, Mdm XXX is an elderly chinese lady who has aortic regurgitation. I say this because
(a) collapsing pulse
(b) displaced apex beat which is heaving in nature
(c) grade 2/6 EDM heard loudest over the upper left sternal edge and accentuated by forced expiration
# Request = BP (wide pulse pressure; Hill’s sign)

other features of AR
7
Tricuspid regurgitation
Mr XXX is a young chinese gentleman who appears to be alert, well, comfortable and orientated at rest. His
vitals are as follows = HR 80/min, regular. There is no RR delay, RF delay or collapsing pulse. RR is 16/min, not
tachypneic or dyspnoeic. He does not appear to be in any respiratory distress and is pink on room air. On
general inspection, there are no signs of pallor or cyanosis. However, he appears to be jaundiced.
haemorrhages, Janeway lesions or Osler nodes. I did not note the presence of needle tracks in the cubital
fossae.
On examination of the praecordium, there are no surgical scars or chest wall deformities. The apex beat is
not displaced and is normal in nature. There was a parasternal heave detected but no thrills were felt over
the base of the heart. On auscultation, the first and second heart sounds were heard. There was no loud
P2. In addition, there was a grade 3/6 PSM heard loudest over the lower left sternal edge which was
accentuated with forced inspiration. I did not hear a MDM which might be suggestive of mitral stenosis.
This is associated with signs of right heart failure as the jugular venous pressure was raised till the level of the
mid-neck with giant v waves seen. There was also bilateral lower limb pitting oedema till the level of the
knees. However, auscultation of the lung bases also did not reveal the presence of inspiratory crepitations.
So in summary, Mr XXX is a young chinese gentleman who has tricuspid regurgitation. I say this because
(a) jaundiced
(b) parasternal heave but with no other signs of pulmonary hypertension
(c) grade 3/6 PSM heard loudest over the lower left sternal edge and accentuated by forced inspiration
(d) signs of right heart failure with raised JVP, giant v waves and lower limb pitting oedema
This is not complicated by left heart failure or infective endocarditis
# Request = abdomen (pulsatile liver, hepatomegaly, splenomegaly)

respiratory system (COPD, bronchiectasis, pulmonary fibrosis)
8
Medicine = Respi shorts
Bronchiectasis
(after examination) I would like to complete my examination by requesting for the vitals, sputum mug as
well as to examine the patient for a raised JVP and splenomegaly.
Mdm XXX is a middle-aged chinese lady who appears to be alert at rest. Her vitals are as follows: HR 80/min
regular and not bounding. She appears to be in respiratory distress as evidenced by tachypnoea with a RR
of 24/min, on supplemental oxygen via nasal prongs at 2L/min, use of accessory muscles of respiration as
well as the presence of intercostal retractions. However, there is no cyanosis or terminal asterixis. I also note
the presence of intravenous antibiotics hanging by the drip-stand suggesting that there is an underlying
infective process going on. There is also no sputum mug or bronchodilators by the bedside. On general
inspection, she does not appear to be cachexic. There are no signs of pallor or jaundice.
On examination of the peripheries, I note digital clubbing. However, there are no signs of tar stains, wasting
of the intrinsic hand muscles or swelling and pain over the wrist joints. There are no signs suggestive of
Horner’s syndrome. There is no displacement of the trachea or apex beat.
On examination of the chest, there are no surgical scars or chest wall deformities. The main physical
findings on examination are coarse pan-inspiratory crepitations heard throughout the posterior chest which
do not clear with coughing. This is associated with decreased air-entry and chest expansion, resonant
percussion note and a normal vocal resonance.
(infective exacerbation) In addition, there are also signs suggestive of consolidation in the right lower third
of the posterior chest. I say this because there is decreased chest expansion, dullness to percussion,
decreased air-entry with bronchial breath sounds and increased vocal resonance.
There is no cervical lymphadenopathy or signs of pulmonary hypertension. There was no parasternal heave
or palpable P2 detected. I would have liked to examine the neck for a raised JVP but I note that the
patient does not have lower limb oedema.
So in summary, Mdm XXX has features suggestive of an infective exacerbation of bronchiectasis. I say this
because
(a) digital clubbing
(b) coarse pan-inspiratory crepitations that do not clear with coughing
She is currently in respiratory distress but her condition is not complicated by pulmonary hypertension or cor
pulmonale
My differentials are
(a) infective exacerbation of COPD  signs of hyperinflation, expiratory rhonchi, prolonged expiratory
phase
(b) pulmonary fibrosis  dry cough, steroid toxicity, fine end-inspiratory crepitations
Pleural effusion
(after examination) I would like to complete my examination by requesting for the vitals and sputum mug.
Mr XXX is an elderly chinese gentleman who appears to be alert at rest. His vitals are as follows: HR 80/min,
regular and not bounding, RR 16/min, not tachypneic or dyspnoeic. He does not appear to be in any
respiratory distress and is pink on room air. I do not note the presence of a sputum mug or bronchodilators
by the bedside. On general inspection, he does not appear to be cachexic. There are no signs of pallor,
jaundice or cyanosis.
On examination of the peripheries, there is no evidence of digital clubbing, tar stains, wasting of the intrinsic
hand muscles or pain and swelling over the wrist joints. There are no features suggestive of Horner’s
syndrome. There is also no displacement of the trachea or apex beat.
9
On examination of the chest, I did not note any surgical scars or chest wall deformities. The main physical
findings are that of a right-sided pleural effusion. I say this because there is decreased chest expansion over
the right lower third of the posterior chest associated with stony dull percussion, decreased breath sounds
as well as decreased vocal resonance. There was no cervical lymphadenopathy.
I looked for but did not find any underlying aetiology. In particular, there were no other abnormal chest
findings, hand deformities, characteristic malar rash or stigmata of chronic liver and renal disease. I would
have liked to examine the cardiovascular system in detail but I note that there is no lower limb oedema.
So in summary, Mr XXX is an elderly chinese gentleman who has a right-sided pleural effusion. I say this
because the right lower chest
(a) decreased chest expansion
(b) stony dull percussion note
(c) decreased air entry
(d) decreased vocal resonance
This is likely to be a small effusion as there is no mediastinal displacement. He is currently not in respiratory
distress
Pulmonary fibrosis
(after examination) I would like to complete my examination by requesting for the vitals and sputum mug
as well as to examine the patient for a raised JVP
Mdm XXX is a middle-aged chinese lady who appears to be alert at rest. Her vitals are as follows: HR
80/min, regular and not bounding. She appears to be in respiratory distress as evidenced by tachypnoea
with a RR of 24/min, on supplemental oxygen via nasal prongs at 2L/min, use of accessory muscles of
respiration as well as the presence of intercostal retractions. There is also evidence of central cyanosis.
However, there is no terminal asterixis. On general inspection, she does not appear to be cachexic. There
are no signs of pallor or jaundice.
On examination of the peripheries, I note the presence of digital clubbing. However, there are no tar stains,
wasting of the intrinsic hand muscles or tenderness and swelling over the wrist joints. There are also no signs
suggestive of Horner’s syndrome. The trachea and apex beat are not displaced.
findings are suggestive of bibasal pulmonary fibrosis. I say this because there is dullness to percussion over
the lung bases associated with decreased air-entry and fine end-inspiratory crepitations that do not clear
with coughing. Vocal resonance is normal. There is no cervical lymphadenopathy.
There is no evidence of pulmonary hypertension as there was no parsternal heave or palpable P2

detected. I would have liked to examine the patient for a raised JVP but I note that there is no lower limb
oedema.
So in summary, Mdm XXX is an elderly chinese lady who has bilateral lower lobe fibrosis. I say this because
of
(a) digital clubbing
(b) bibasal fine end-inspiratory crepitations which do not clear with coughing
She is currently in respiratory distress as evidenced by tachypnoea and central cyanosis. However, her
condition is not complicated by pulmonary hypertension or cor pulmonale.
(a) congestive cardiac failure with pulmonary oedema  no clubbing, evidence of fluid overload,
crepitations clear with coughing
(b) bronchiectasis  productive cough, coarse pan-inspiratory  expiratory crepitations
10
Chronic obstructive pulmonary disease
as well as to examine the patient for liver ptosis and raised JVP
regular and not bounding. He appears to be in respiratory distress as evidenced by tachypnoea with a RR
of 24/min, on supplemental oxygen via nasal prongs at 2L/min and use of accessory muscles of respiration.
However, he does not appear cyanosed nor is there terminal asterixis. I note the presence of intravenous
antibiotics hanging by the drip-stand suggesting that there is an underlying infective process going on.
However, there is no sputum mug or bronchodilators by the bedside. On general inspection, he does not
appear to be cachexic. There are no signs of pallor or jaundice.
On examination of the peripheries, there is no sign of digital clubbing, tar stains, wasting of the intrinsic
hand muscles or tenderness and swelling over the wrist joints. There are also no signs suggestive of Horner’s
syndrome. The trachea and apex beat are not displaced.
On examination of the chest, there are no surgical scars or chest wall deformities. However, there are signs
of hyperinflation as evidenced by
(a) barrel-shaped chest = increased antero-posterior diameter cg lateral diameter
(b) decreased chest expansion
(c) resonant percussion note
(d) loss of cardiac and liver dullness
(e) decreased air-entry associated with expiratory wheeze and prolonged expiratory phase
(f) decreased vocal resonance
There is no cervical lymphadenopathy or signs of pulmonary hypertension as there was no parasternal

heave and palpable P2 detected. I would have liked to examine the patient for a raised JVP and I note
that there is unlikely to be right heart failure as there is no lower limb oedema
So in summary, Mr XXX is an elderly chinese gentleman who has evidence suggestive of an infective
exacerbation of COPD. I say this because
(a) signs of hyperinflation
(b) decreased air-entry, expiratory wheeze and prolonged expiratory phase
He is currently in respiratory distress but his condition is not complicated by pulmonary hypertension or cor
pulmonale
(a) infective exacerbation of bronchial asthma
(b) infective exacerbation of bronchiectasis  clubbing, coarse-inspiratory crepitations
Consolidation
regular and not bounding, RR 16/min not tachypneic or dyspnoeic. He does not appear to be in any
respiratory distress and is pink on room air. There is an intravenous antibiotic hanging on the drip-stand
suggesting an underlying infective process. On general inspection, Mr XXX does not appear to be
cachexic. There are/are no signs of pallor, cyanosis or jaundice.
syndrome. The trachea and apex beat are not displaced.
findings are in the lower 1/3 of the right posterior chest which is suggestive of consolidation. I say this
11
because there is decreased chest expansion, dullness to percussion, decreased air-entry associated with
coarse pan-inspiratory crepitations, bronchial breathing as well as increased vocal resonance. There is no
cervical lymphadenopathy.
So in summary, Mr XXX is an elderly chinese gentleman who has evidence suggestive of consolidation in
the lower 1/3 of the right posterior chest. I say this because
(a) decreased chest expansion
(b) dullness to percussion
(c) decreased air-entry, coarse pan-inspiratory crepitations, bronchial breathing
(d) increased vocal resonance
He is currently not in respiratory distress.
Collapse
respiratory distress and is pink on room air. On general inspection, Mr XXX appears to be cachexic. There
are no signs of pallor, cyanosis or jaundice.
syndrome. There is tracheal deviation to the right with no mediastinal displacement.
findings are in the upper 1/3 of the right anterior chest suggestive of an upper lobe collapse. I say this
because of right tracheal deviation, flattening of the right chest wall, decreased chest expansion, dullness
to percussion, decreased air-entry as well as decreased vocal resonance. There is no cervical
lymphadenopathy.
So in summary, Mr XXX is an elderly chinese gentleman who has evidence suggestive of a right upper lobe
collapse. I say this because
(a) right tracheal deviation
(b) flattening of right chest wall
(c) decreased chest expansion
(d) dullness to percussion
(e) decreased air-entry and vocal resonance
He is currently not in respiratory distress.
# important to exclude malignancy

# Brock’s syndrome = collapse due to compression of right middle lobe bronchus by enlarged lymph node
12
Lung cancer
respiratory distress and is pink on room air. On general inspection, I note that he is cachexic. There are/are
no signs of pallor or jaundice.
On examination of the peripheries, I note the presence of digital clubbing as well as hypertrophic
pulmonary osteoarthropathy. However, there are no tar stains, wasting of the intrinsic hand muscles or
features suggestive of Horner’s syndrome.
findings are that of a collapse-consolidation over the right upper 1/3 of the posterior chest as well as a
right-sided pleural effusion involving the lower 2/3 of the posterior chest. I say this because
(a) collapse-consolidation
- tracheal deviation to the right
- dull percussion note
- decreased air-entry with no adventitious sounds
- increased vocal resonance
(b) pleural effusion
- decreased chest expansion over the right lower chest
- stony dull percussion note
- decreased air-entry with no adventitious sounds
- decreased vocal resonance
- likely to be moderate in size as the apex beat is slightly displaced in the 6 th intercostal space 1cm lateral
to the mid-clavicular line
In addition, multiple small enlarged cervical lymph nodes were found bilaterally ranging from 1-2 cm in
length. They were non-tender, firm, matted and relatively immobile.
So in summary, Mr XXX has multiple chest findings including a right upper lobe collapse-consolidation as
well as a right-sided pleural effusion. He most likely has a right lung malignancy. This is supported by the
findings of cachexia, pallor, clubbing, HPOA as well as cervical lymphadenopathy.
I would like to examine the patient for hepatomegaly, focal neurological deficits and to percuss the
vertebral column for tenderness.
13
Medicine = Renal shorts
Polycystic kidney disease

I would like to complete by doing a per-rectal examination and requesting for the patient’s vitals esp the
BP. In addition, I would like to examine the cardiovascular system for MVP and the neurological system for a
focal neurological deficit.
Mr XXX is a young Chinese gentleman who appears to be alert and comfortable. His vitals are as follows =
HR ____, RR ____. On examination, he has bilateral ballotable kidneys most likely due to adult polycystic
kidney disease and is in ESRF on haemodialysis.
(confirm findings) I say this because on examination of the abdomen, I note a distinct fullness over the left
and right flanks. On palpation, there were bilateral ovoid masses measuring ___ cm by ___ cm, non-tender
and firm. I was able to get above the masses and they did not move with respiration. No splenic notch was
felt. The masses were ballotable and a band of resonance was detected on percussion.
(aetiology) I looked for but did not find any hepatosplenomegaly. There was no apparent focal
neurological deficit as Mr XXX was able to move all 4 limbs. However, I would like to confirm this by doing a
detailed neurological examination. In addition, I did not note the presence of diabetic dermopathy.
(complications) Functionally, Mr XXX is in ESRF as evidenced by his sallow appearance and conjunctival
pallor. In addition, I also note the presence of an AVF in the left cubital fossa with a palpable thrill and signs
of recent cannulation. However, Mr XXX does not appear to be uraemic as there are no signs of bruising,
scratch marks or terminal asterixis. He is also not in fluid overload as there is no lower limb oedema, ascites
and he is able to lie flat in bed with no signs of respiratory distress.
(summary) In summary, Mr XXX is a young Chinese gentleman who most likely has adult polycystic kidney
disease. I say this because of the presence of bilateral ballotable kidneys. This is complicated by end-stage
renal failure and Mr XXX is currently being managed by haemodialysis. He is not in uraemia or fluid
overload.
Transplanted kidney
Mdm XXX is a (age)(race)(gender) who has a transplanted kidney and is on immunosuppressive therapy
I say this because she has a J-shaped scar in her left iliac fossa, overlying a rounded mass x cm by x cm
which is non tender and firm to touch. There is no hepatosplenomegaly or ascites noted
In addition, she also has evidence of immunosuppression with a characteristic rounded facies, central
obesity, violaceous abdominal striae, oral thrush, gum hypertrophy, bruising and thin skin
I looked for but was unable to find any signs suggestive of the aetiology of end stage renal failure such as
bilaterally enlarged ballotable kidneys and diabetic dermopathy
Functionally, I note that she has a left arteriovenous fistula with a palpable thrill. There are no signs of recent
cannulation which suggests that the graft is functioning well. This is supported by the fact that she does not
have any evidence of uraemia. She does not appear sallow and there are no signs of bruising, scratch
marks or asterixis. She is also not in fluid overload as she is able to lie flat in bed with no signs of respiratory
distress and there are no signs of ascites or lower limb oedema
14
Medicine = Endocrine shorts
Cushing’s syndrome
Mdm XXX is a middle-aged Chinese lady who appears to be alert and comfortable at rest. On general
inspection, I note that she has Cushingnoid features as evidenced by
(a) characteristic rounded facies with facial plethora, hirsutism and acne
(b) central deposition of adiposity with thick violaceous abdominal striae
(c) supraclavicular and dorsal fat pads
(d) skin atrophy, bruising, proximal myopathy
(e) cataracts
(f) oral thrush
During the examination, I looked for but did/did not find any evidence of
(a) deforming arthropathy  RA, SLE
(b) characteristic malar rash  SLE
(c) clubbing or tar stains  small cell lung ca
(d) expiratory rhonchi or fine end-inspiratory bibasal crepitations  asthma, COPD, IPF
(e) transplanted kidney/liver
There are no hypocount scars over the finger-tips or diabetic dermopathy which may suggest the presence
of DM as a complication. However, I would like to confirm this by performing a urine dipstick to look for
glycosuria. In addition, I would like to take the BP for hypertension.
To end off my examination

(a) visual field  bitemporal hemianopia (pituitary adenoma)
(b) fundoscopy  cataracts
diabetic/hypertensive retinopathy
papilloedema/optic atrophy (SOL in optic chiasm)
Thyrotoxicosis
I would like to complete my examination by requesting for the patient’s vitals, performing Pemberton’s sign
, checking for hyper-reflexia as well as performing a cardiovascular examination looking out for signs of
congestive cardiac failure.
Miss XXX is a young Chinese lady who appears to be alert and comfortable at rest. She does not appear to
be agitated or nervous. On general inspection, I note that she has a diffuse anterior neck swelling. This is
most likely the thyroid gland as it moves with swallowing but not with tongue protrusion. There are no
overlying skin changes, dilated veins or previous surgical scars.
On palpation, the thyroid gland measured 10cm by 5cm in dimensions. There was no increased warmth or
palpable thrill. It was non-tender, firm in consistency and had a smooth and regular surface. It was not
attached to overlying skin or underlying muscle. There was no cervical lymphadenopathy or displacement
of the carotids and trachea. Retrosternal extension is unlikely as the inferior border of the gland was well
felt. In addition, there was no dullness to percussion over the manubrium. There was an audible bruit heard
over both lobes on auscultation.
Miss XXX is likely to be in thyrotoxicosis. I say this because she is in sinus tachycardia with a HR of 120/min. In
addition, she has warm and sweaty palms, palmar erythema as well as fine tremors. I did not note the
presences of thyroid acropathy, proximal myopathy or pre-tibial myoxedema. Furthermore, Miss XXX has
also features of thyroid eye disease as evidenced by lid retraction, exophthalmos and lid lag. However,
there is no proptosis, chemosis, limitation in eye movement or lagophthalmos.
So in summary, Miss XXX is a young Chinese lady who most likely has Graves’ disease complicated by
thyroid eye disease and is currently in thyrotoxicosis.
15
Medicine = Hands shorts
Chronic tophaceous gout

This patient has chronic tophaceous gout with asymmetrical joint involvement. I say this because there are
multiple gouty tophi seen over the extensor surfaces of both hands involving the MCPJ, PIPJ and DIPJ. These
tophi vary in sizes = smallest being __cm and the largest ___cm. They are firm, immobile and non-tender.
Some tophi have ulcerated and are extruding a chalky-white substance onto the skin surface. There are no
gouty tophi seen over the olecranon bursae.
The disease is likely to be quiescent as the joints are non-tender. In addition, there is no joint swelling,
erythema or increased warmth.
Functionally, there is deforming arthropathy with asymmetrical joint involvement resulting in limited ROM in
the finger and wrist joints as well as muscle wasting. However, he/she is still able to hold a cup, write and
unbutton.
I looked for but there were no xanthelasma seen on the face. In addition, the patient does not appear
uraemic as there is no sallow appearance nor are there bruises or scratch marks on the arms. There is also
no arteriovenous fistula noted.
Request
(a) presence of gouty tophi = olecranon bursae, pinna of ear, prepatellar bursae, archilles tendon
(b) feet, ankle and knee for similar changes
(c) haematological malignancy = hepatosplenomegaly, generalised lymphadenopathy
(d) signs of alcoholism = duputyren’s contracture, parotidomegaly
Differentials
1. Tendon xanthomata
- yellow (not chalky)
- stuck to tendons (not joints)
- bursa not involved
- no active arthritis
2. Rheumatoid arthritis
16
Endocrine
Medicine (Thyroid) = Physical Examination
Start
1. Ask the patient to sit comfortably at the edge of the bed or on a chair.
2. Introduce yourself and explain purpose for examination.
Inspection
1. General appearance
 restless, edgy, nervous
 thin/large body habitus
2. Eyes
 Thyroid stare
 Exophthalmos (visible sclera below lower limbus)
 Lid retraction (upper limbus visible due to sympathetic overstimulation of lipopolysaccharide)
 Lid oedema (chemosis, conjunctivitis, exposure keratitis, tarsorraphy)
 Strabismus
3. Neck
 Goiter (diffuse/nodular)
 Overlying skin changes (erythema, tethering of skin)
 Dilated veins (suggests retrosternal extension with thoracic inlet obstruction)
 Previous surgical scar along skin creases
4. Ask patient to drink a sip of water but only swallow at your command
 If neck swelling rises (due to attachment to larynx) → thyroid, thyroglossal cyst
 If inferior border not visible → retrosternal extension
5. Ask the patient to open mouth and protrude tongue → thyroglossal cyst
Palpation
1. Ask the patient if there is pain → subacute thyroiditis malignant infiltration, haemorrhage into cyst
2. Move behind the patient and look over his head for proptosis
3. Begin palpation from behind with pulps of fingers over the gland. Slightly flew patient’s neck to relax SCM
4. Feel the isthmus (overlies thyroid cartilage) and then the lobes
 Size = WHO grading of goiter
Grade 0 Not palpable or visible

Grade 1 Palpable goitre (larger than terminal phalanges of
examiner’s thumb)
1A = detectable only on palpation
1B = palpable and visible with neck extended
Grade 2 Goitre visible with neck in normal position
Grade 3 Large goitre visible from a distance
 Surface = smooth and diffuse, nodular

 Consistency = soft, firm, hard
 Tenderness
 Warmth
 Palpable thrill
 Mobility = on swallowing/on turning the neck from side to side (tethering to underlying muscles)
17
5. Palpate for cervical lymphadenopathy (infiltration by carcinoma), carotid artery (displacement/absence →
infiltration by carcinoma)
6. Move to the front and assess for trachea deviation
Percussion
1. Percuss manubrium from one end to the other (dullness may indicate retrosternal extension)
Auscultation
1. Listen over each lobe for bruit (increased vascularity)
Hands and arms

1. Ask patient to fully extend his arms
 Palms down = fine tremors, onycholysis (Plummer’s nails → separation of nail from nail bed),
acropathy (clubbing)
 Palms up = palmar erythema, sweaty, warm
2. Take radial pulse of patient = tachycardia, AF
3. Proximal myopathy
4. Test biceps jerks for hyper-reflexia
Eyes
1. Look from side to assess proptosis again
2. Assess visual acuity
 Impaired EOM (opthalmoplegia) = IR → MR → SR → LR
 Diplopia
 Lid lag (descent of upper lid lags behind eyeball)
3. Ask patient to close eyes → lagophthalmos
4. Grading of eye signs
Grade 1 MR palsy
Grade 2 Lid retraction and Lid lag
Grade 3 Opthalmoplegia
Grade 4 Exophthalmos and Chemosis
Legs
1. Pretibial myxoedema
 Elevated symmetrical skin lesions
 Well-defined
 Red but not inflamed
 Swollen but not edematous
 Skin is shiny and has peau d orange appearance
Request
1. Pemberton’s sign (thoracic inlet obstruction → retrosternal extension)
 Instructions = ask patient to lift arms over the head and wait for 1 minute
 +ve sign = facial plethora, cyanosis, inspiratory stridor, non-pulsatile elevation of JVP (main
features), periorbital oedema, exophthalmos, conjunctival injection, retinal venous dilation, dilated
collateral vessels on the chest
2. Vitals = T: (subacute thyroiditis), BP (wide pulse pressure, collapsing pulse)
3. Chest = gynecomastia, CVS examination (signs of CCF)
4. Eye examination and referral
 Visual field defect
18
 Impaired visual acuity and colour vision
 Papilloedema, optic atrophy (optic nerve compression → do fundoscopy)
 Proptosis (quantified by Hertel’s exophthalmometer)
5. Associated AI disorders
 Vitiligo
 Conjunctival pallor → pernicious anemia
 Myasthenia gravis
 Glycosuria → T1DM
 Hyperpigmentation of palmar creases → Addison’s disease
6. History
 Thyroid symptoms
 Compressive symptoms (dysphagia, stridor)
 Drug history (iodine containing medications, RAI)
 Exposure to radiation
 Family history of goiter
19
Medicine (Thyroid) = Introduction
Anatomy
1. Consists of two lateral lobes connected by isthmus (latter lies below the cricoids cartilage)
2. Gland lies anterior to trachea
3. Lateral lobes related to oesophagus
4. Enclosed by pre-tracheal fascia therefore seen to rise with trachea and larynx during swallowing
5. Functions
 Thyroid follicular cells synthesize thyroid hormones (T3 and T4)
 Para follicular C cells synthesize calcitonin (promotes bone absorption of Ca2+, inhibits osteoclastic
action)
Embryology
1. Descends from foramen caecum (lies in the midline at the junction of the anterior 2/3 and posterior 1/3 of
the tongue) to normal position in the neck
2. Brings with it parathyroid glands on each side
3. Eventually rises at the level of the 2nd and 3rd tracheal rings
4. Failure to descend → ectopic thyroid tissue
Physiology
Regulation of thyroid hormone release

1. Hypothalamus secretes TRH (thyrotropin-releasing hormone)
2. TRH stimulates the production of TSH (thyroid stimulating hormone) from the anterior pituitary gland
3. TSH acts on the thyroid gland to increase production and release of T3 and T4
4. T3 + T4 exerts negative feedback on TSH production by acting on the pituitary gland
20
hypothalamus
TR
anterior pituitary gland H
TSH
thyroid gland
T3 + T4
peripheral tissues
Synthesis of thyroid hormones

1. Iodide trapping = active transport of plasma iodide into thyroid follicular cells
2. Iodide oxidation to iodine by thyroperoxidase
3. Organification = binding of iodine to thyrosine in thyroglobulin to form mono-iodothyrosine + di-
iodothyrosine
4. Coupling of iodothyrosine molecules to T3 + T4 (tri-iodothyronine + thyroxine)
5. Endocytosis of thyroglobulin
6. Release of T3 and T4 into systemic circulation
Metabolism
1. Inactivation (minor) = deamination, decarboxylation, conjugation with glucuronide/sulphate
2. Deiodination (major) = 1/3 of T4 converted to T3
 Inactivation by 5’ deiodinase to reverse T3
 Activation by 5’ deiodinase to T3
Thyroid hormones
1. Principle hormone secreted is T4
2. T3 + T4 highly bound to serum thyroid hormone-binding proteins (esp thyroxine-binding globulin)
 T4 (99.9%) vs T3 (99.5%) → less free T4 than T3
3. Free fraction is the active fraction
4. 80% of T3 is derived from peripheral deiodination of T4 (1/3 of T4)
5. T3 (T ½ = 1.5 days) is 4x more metabolically active than T4 ( T ½ = 9 days)
Thyroid hormone receptors

1. Found in liver, kidney, heart, muscle, and pituitary gland
2. Homologous with the receptors for steroid hormones and vitamins A + D
3. 10x greater affinity for T3 than T4
4. Sites
 cell membrane → increases cellular uptake of glucose and amino acids
 cytoplasm → stimulates Na/K ATPase in mitochondria therefore increases O2 consumption
 nucleus → increases DNA transcription, mRNA synthesis, protein and enzyme synthesis
21
Functions of T3 and T4
1. binds to nuclear thyroid hormone receptor → hormone receptor complex binds to thyroid hormone
response elements in target genes → regulate gene expression
2. metabolic effects =
 up regulate carbohydrate and lipid catabolism
 stimulate protein synthesis
 increase basal metabolic rate therefore increase heat production
3. critical for development and function of
 central nervous system
 skeletal muscle (growth)
 reproductive tissue
4. effects are potentiated by human growth hormone
22
Medicine (Thyroid) = Thyroid Lumps
Solitary Lumps
* Benign = Thyroid Cyst
Follicular/Toxic adenoma
Dominant nodule of multi-nodular goitre
* Malignant= papillary carcinoma

Follicular carcinoma
Medullary carcinoma
Anaplastic carcinoma
Multiple Lumps
* multinodular goitre
Diffuse enlargement
* Hyperthyroidism = Grave’s disease
* Euthyroid = diffuse non toxic goitre (endemic/physiologic)
* Hypothyroidism = Hashimoto’s thyroiditis
De Quervain’s thyroiditis
Epidemiology
* 5% of adults have palpable thyroid lumps
* but only 5% of these lumps are malignant
* females > males
* more likely to be neoplastic in = solitary nodule, younger patients (<40 years old), males, ‘cold’ nodules, history of
Head and neck radiation
Differential diagnosis
* cervical lymphadenopathy
*lipoma, sebaceous cyst, dermoid cyst
* plunging ranula
Medicine (Thyroid) = Management of hyperthyroidism

Treatment modalities
* Conservative
(a) Anti-thyroid agents
(b) Radioactive iodine
(c) Symptomatic control
(d) Protective eye measures
* Surgical
Anti-thyroid agents
* Classes
iodide trapping anions (per chlorate, thiocyanate)
oxidation thioamides (carbimazole, PTU)
Organification thioamides
iodides
coupling thioamides
Endocytosis
release iodides
lithium
23
Anions
* No longer in use
Thioamides
* MOA = interferes with oxidation, Organification and coupling (inhibit thyroid peroxidase enzyme)
* 2 main types
(a) Propylthiouracil (PTU) (also inhibits peripheral conversion of T4 to T3)
- Strong binding to plasma proteins  unlikely to cross placenta and enter breast-milk
- For use in pregnant and lactating mothers
(b) Carbimazole
- Partially metabolised in liver to active metabolite (methimazole  longer t1/2)
- crosses placenta and secreted in breast-milk
- preferred over PTU due to more convenient dosing (OM vs TDS)
* Indications = definitive treatment for thyrotoxicosis (1-2yrs)
Pre-operative treatment (shrink gland before surgery)
Awaiting effects of RAI
* S/E = agranulocytosis (1st sign is sore throat; Mx = stop meds, admit immediately, take blood
C/s, IV broad-spectrum antibiotics, barrier nursing)
Hypersensitivity reactions (pruritic MP rash, fever)
Cholestatic hepatitis
Arthralgia
* Advantages = reversible hypothyroidism
Can be used in children
* Disadvantages = high relapse rate once drug is withdrawn (60-80%)
Side-effects
Slow onset (requires 3-4 weeks to deplete pre-formed thyroid stores)
Iodides
* MOA = interferes with Organification and release of thyroid hormones
* Indications = pre-operative treatment for surgery (given for 10 days prior)
Treatment of thyroid storm
Prophylaxis against endemic goiter
* S/E = hypersensitivity reaction
Iodism from chronic overuse (bleeding disorders, conjunctivitis, drug fever, inflamed
Salivary glands, metallic taste, oral ulcers, rash)
* Advantages = decreases size and vascularity of gland
* Disadvantages = increases thyroid iodine stores (delays effectiveness of thioamide and RAI
Therapy
Severe exacerbation of thyrotoxicosis on drug withdrawal
Radioactive iodine (RAI)

* MOA = RAI emits both β and γ waves
β waves penetrates 0.5mm of thyroid tissue and destroys follicular cells
No damage to surrounding tissue
Radioactivity disappears after 2 months (cytotoxic effects peak at 4 months)
* Advantages = convenient (single oral dose)
Inexpensive
Usually results in permanent cure
* Disadvantages = takes 2-3 weeks to take effect (need to give anti-thyroid drugs in the interim)
Cannot be used in children (risk of genetic damage  cancer)
Hypothyroidism  require life-long L-thyroxine
Exacerbates pre-existing thyroid eye disease
Radiation induced thyroid dysfunction (hyperthyroid in 5%, hypothyroid in
24
30%)
Radiation induced cancer
* Indications
(a) Not fit for surgery
(b) failed pharmacological therapy
(c) Adverse effects from anti-thyroid drugs  agranulocytosis, hepatotoxicity
(d) Relapse after previous surgery
* Contraindications
(a) Children
(b) Patients who are pregnant or intending to get pregnant within the next 6 months
(c) Lactating mothers
(d) Iodine allergy
(e) Severe thyroid eye disease
* Process = render patient euthyroid with anti-thyroid drugs
Stop medications 4 days prior to administration and restart 4 days later
* Advice to give
- Stay at home for 2-3 weeks
- avoid public places
- avoid pregnant women and children for 1/52
- Exacerbation of symptoms within first 2 weeks (esp if not euthyroid before treatment)
- Stress on importance of regular f/u and the need to report hyper/hypo-thyroid symptoms
- need for lifelong L-thyroxine
- avoid pregnancy for the next 6 months
- Condition may relapse
* Efficacy = 10-30% become hypothyroid in the 1st year
5% per year thereafter
Symptomatic control
* Sinus tachycardia = β-blockers
* AF = digoxin, β-blockers (rate control)
Warfarin (prevent embolic complications)
Protective eye measures

* General measures = hypromellose eye drops (day)
Lubricating eye ointment (night)
Tinted glasses (protection from sun, wind, and FB)
Stop smoking
* Specific measures
(a) Exposure keratitis, corneal ulceration  lateral tarsorraphy
(b) Strabismus, diplopia  prism glasses, surgery
(c) Papilloedema, loss of visual acuity, visual field defect
# Urgent Rx with PO prednisolone 60mg OM
# Orbital radiation
# Plasmapheresis
# Orbital decompression by surgical removal of floor and medial orbital wall (if no improvement within 72-
96 hours)
Surgery
* Advantages = usually results in permanent cure
* Disadvantages = will require life-long L-thyroxine
Risks of surgery (refer)
* Prognosis of the end of 1 year = 80% euthyroid, 15% hypothyroid, and 5% relapse
25
Surgery (Thyroid) = Hyperthyroidism
Thyrotoxicosis
* Hyperthyroidism (biochemistry changes) VS thyrotoxicosis ( biochemical changes + clinical manifestations)
* Hyper metabolic state caused by elevated levels of free T3 and T4
(a) Excessive release of preformed thyroid hormones = thyroiditis
(b) Extra-thyroidal source = TSH-secreting tumours, hCG-producing tumours, struma ovari
(c) Hyper functioning thyroid gland ( primary hyperthyroidism) = Grave’s disease
Toxic MNG
Toxic adenoma
(d) Drugs= amiodarone, lithium, L-thyroxine
* Clinical features result from hyper metabolic state and sympathetic over activity
Clinical Symptoms
* goitre = duration, speed of growth, pain
* neurological = restless, nervous, irritability, inability to concentrate , tremors, insomnia
* eyes= difficulty closing eyes, double vision, pain
* autonomic over activity= heat intolerant, excessive sweating
* CVS = palpitations, CCF ( chest pain, dyspnoea, ankle oedema, fatigue )
* GIT = polyphagia, LOW, chronic diarrhoea
* GUT = oligomenorrhoea
* musculoskeletal = proximal myopathy ( difficulty hanging clothes or walking up stairs)
Periodic paralysis ( after exercise or eating)
Osteodystrophy ( osteomalacia, osteoporosis)
* aetiology = recent fever and URTI ( subacute thyroiditis )
Drug history
History of radiation to the head and neck
Family history
* complications = compression ( dysphagia, stridor (tracheal narrowed to 20-30%), cough, dyspnoea, hoarseness)
Metastasis( LOA, LOW, fatigue, fever, bone pain, chest pain, SOB, haemoptysis, abdominal pain
Jaundice, change in bowel habits)
* systemic review
* management before and during current admission
* has this happened before? Describe prior episodes
* past medical history = IDDM, pernicious anaemia, vitiligo, myasthenia gravis, Addison’s disease, history of head and
Neck radiation (if suspect cancer)
* family history of thyroid lesions
Clinical Signs
* General appearance = restless/edgy/nervous, thin body habitus
* Hands= fine tremors, warm, sweaty, acropachy ( clubbing), onycholysis (Plummer’s nails), palmar erythema
* Pulse = tachycardia, AF
* Arms = proximal myopathy, hyper-reflexia
* Thyroid eye disease = lid oedema, chemosis, conjunctivitis, exposure keratitis, tarsorraphy, thyroid stare, lid
Retraction, exophthalmos, proptosis, strabismus, diplopia, restricted EOM, lid lag,
Lagophthalmos, decreased visual acuity/colour vision, optic atrophy, papilloedema ( optic
Nerve compression )
* Goitre= diffuse/nodular, warmth, tender, consistency, overlying skin changes, mobility, bruit, thrill, retrosternal
Extension, previous thyroidectomy scar
* Local effects = enlarged lymph nodes, displacement of trachea and carotid artery
* Chest = gynecomastia
Systolic flow murmurs, displaced apex beat, S3,gallop rhythm, bibasal lung crepitations
* Legs= pretibial myxoedema
* Pemberton’s sign
Decompensation
* High output cardiac failure
* Thyroid storm * Fixed opthalmoplegia = usually painful
26
Grave’s Disease ( GD )
* definition = diffuse enlargement of thyroid gland due to TSH receptor-stimulating auto antibodies which frequently
Results in Hyperthyroidism
* Commonest cause of thyrotoxicosis in Singapore (>90%)
* affects 1.28% of the population
* pathogenesis= stimulating auto-antibodies against TSH-receptor
* clinical features = diffuse and smooth goitre
Occurs in young females ( 20-40 years old )
Strongly associated with HLA-DR3 inheritance
Associated with AI disorders ( IDDM, pernicious anaemia, vitiligo, Addison’s disease, myasthenia
Gravis)
* 5 indicators of toxicity
(a) Resting tachycardia
(b) Warm and sweaty palms
(c) Fine Tremors
(d) Hyper-reflexia
(e) Thyroid bruit
*features unique to GD : Grave’s opthalmoplegia, pretibial myxoedema, thyroid bruit
*Grave’s opthalmoplegia
- increased volume of retro-orbital connective tissues and extraocular muscles
- does not depend on thyroid status
- orbital fibroblasts aberrantly express TSH receptors  differentiate into adipocytes  secrete
Glycosaminoglycansfibrosis and swelling
-due to = marked infiltration of retro-orbital space by mononuclear cells
Inflammatory oedema and swelling of extra-ocular muscles
Accumulation of ECM components ( glycosaminoglycans, hyaluronic acid)
Increased adipocyte differentiation leading to fatty infiltration
-factors that increase risk = age, male gender, smoking , RAI ( steroids usually given to decrease risk)
* Little evidence to suggest increased frequency of thyroid cancer in GD
* Management = anti-thyroid drugs ( PTU, carbimazole)
Β-blockers ( block sympathetic effects on CVS )
RAI
Subtotal thyroidectomy
Protective eye measures
* Grave’s disease in pregnancy = TSH-receptor Ab crosses placenta fetal hyperthyroidism
Anti-thyroid agents crosses placenta  fetal hypothyroidism
Multi-nodular Goitre
* epidemiology = commonest cause of goitre in the UK
Usually in older women ( ≈ 60 years old)
* pathogenesis = occurs spontaneously or in long standing simple goitre
-reflects impaired synthesis of thyroid hormones
-results from repeated stimulation and involution of thyroid follicles
- low levels of thyroid hormonescompensatory rise in serum TSH levelshypertrophy and hyperplasia of
Follicular cellsdiffuse goitreinvolution of follicular epithelium if dietary iodine increases or demand for
Thyroid hormone decreases
-endemic goitre= due to iodine deficiency
-physiological goitre= occurs in puberty and pregnancy due to increased demands
* Clinical features
(a) usually euthyroid
(b) Hyperthyroidism/Thyrotoxicosis
- hyperactive focal nodule within long-standing goitre (Plummer syndrome)toxic MNG
- Permanent with no spontaneous remission. Therefore, anti-thyroid drugs not appropriate long-term Rx.
(c) mass effects
(d) malignant change < 5%
* Management
(a) anti-thyroid drugs ( not useful as relapse occurs after withdrawal; autonomous nodule not responsive to
Medications)
(b) RAI = lower risk of hypothyroidism
(c) Subtotal thyroidectomy = for compressive symptoms
27
* Comparison with GD
Grave’s Disease Toxic nodular Goitre

Younger patients Older individuals
Diffuse goitre Nodular enlargement
Eye signs common Eye signs uncommon
AF uncommon AF and CCF common (≈40%)
Autoimmune disorders common Autoimmune disorders uncommon
Toxic adenoma
* Epidemiology= usually in females > 40 yrs old
* Arises from follicular adenoma ( benign neoplasia derived from follicular epithelium)
- vast majority are non-functional
- small portion undergo toxic change to cause thyrotoxicosis
- rarely precursors of cancer
* Pathogenesis= activating somatic mutations in TSH receptor signalling pathway chronic cAMP pathway
Stimulation generates cells that acquire growth advantage
* Histopathology = discrete solitary mass, well circumscribed, encapsulated, no infiltrative margins, atrophy of
Remaining gland, cut surface brown and glistening ( due to colloid), uniform follicular growth,
No areas of necrosis or haemorrhage
* Clinical features = painless mass
Mild hyperthyroidism ( 50% have isolated elevation of T3 only)
* Management
(a) Anti-thyroid drugs ( not useful as relapse occurs after withdrawal)
(b) RAI = lower risk of hypothyroidism due to compensation of remaining thyroid gland
(c) surgery
Thyrotoxic Periodic Paralysis

* Epidemiology = usually in Asian males
Onset in 3rd- 4th decades
* associated with transient hypokalemia
-triggers = high carbohydrate intake ( insulin release intracellular shift of K + )
Exercise/trauma/infection/emotional stress ( adrenalin release)
- dextrose and β agonists may exacerbate hypokalemia
* Clinical features
- episodic limb weakness lasting 7-72 hours
- no weakness in between attacks
* Investigations
(a) U/E/Cr
(b) ECG = ST depression, flattened T waves, prominent U waves
* Management
- control thyrotoxicosis
- replace K= propanolol, spironolactone , K+ supplements
Thyroid Storm
* acute life threatening hyper metabolic state induced by excessive release of thyroid hormones in individuals with
Thyrotoxicosis
(a) Surgical = inadequately prepared thyrotoxic patient undergoing thyroid surgery
Non-thyroidal surgery in patients with undiagnosed thyrotoxicosis
(b) Medical
-sepsis ( most common precipitating cause)
-RAI
-sudden withdrawal of anti-thyroid drugs
-administration of iodinated contrast medicum
-infarction ( AMI,CVA)
-trauma
* Clinical features
- hyperpyrexia, diaphoresis, palpitations, tachyarrythmias, hypertension with wide pulse pressure, CCF, tremors,
28
delirium, agitation, frank psychosis, seizures, nausea, vomiting, diarrhoea, abdominal pain, jaundice
-complications: high-output cardiac failurehypotensive shock. Dehydration. Multi-organ dysfunction syndrome
* Burch-Wartofsky score
-scoring system = >25 (thyrotoxicosis possible)
= >45 ( thyroid storm probable)
-based on = temperature
CNS effects
Hepatogastrointestinal dysfunction
Tachycardia
Congestive Cardiac Failure
AF
History suggestive of thyrotoxicosis
* Investigations = FBC, U/E/Cr, LFT, TFT, ECG, CXR, septic work-up
* Management
-admit patient in HD or ICU
-urgent referral to endocrinologist
(a) PO PTU/ carbimazole or lithium carbonate ( if allergic to the former) = rapidly lowers T3 levels
(b) IV sodium iodide = blocks further release
Must be given at least 1 hr after PTU (or else will exacerbate thyrotoxicosis)
(c)Tachycardia= IV propranolol
(d)AF = IV digoxin
Cardioversion if unstable
Anti-coagulate if unstable
(e) IV dexamethasone = protect against shock, block peripheral conversion of T4 to T3
(f) CCF = digoxin, diuretics
(g)supportive therapy = oxygen supplementation
Monitor vitals
IV hydration ( hyperpyrexia, diaphoresis, vomiting, diarrhoea)
Tepid sponging, ice packs, anti-pyretics (do not give aspirininhibits binding of thyroid
hormones to
Binding proteins)
Sedation if patient restless (chlorpromazine)
Treat precipitating cause (antibiotics)
* should respond to above therapy within 24-48 hours
Compressive effects of goitre

Venous drainage
* facial congestion
*cyanosis
*plethora
*dilated veins in face and neck
Oesophagus
*dysphagia
Trachea
*stridor=positional in nature (on neck extensionpush goitre into thoracic inlet)
*may cause trachomalaciapost operative complication
Recurrent laryngeal nerve

*direct invasions
*lymphadenopathy
*hoarseness of voice
Carotids
*arteries usually resistant to tumour invasion
*drop attacks(rare)
29
Medicine (Thyroid) = Hypothyroidism
Aetiology
* Primary hypothyroidism
(a) congenital -> agenesis, dyshormonogenesis, ectopic thyroid
(b) interference with hormone synthesis
- iodine-deficiency
- anti-thyroid drugs (lithium, amiodarone, radiocontrast, KI-containing expectorants)
(c) infective -> de Quervain’s thyroiditis
(d) autoimmune -> Hashimoto’s thyroiditis, post-partum thyroiditis, Riedel’s thyroiditis
(e) post-surgical/radioactive iodine (RAI)
* Secondary hypothyroidism -> TSH deficiency
* Tertiary hypothyroidism -> TRH deficiency
Clinical features
* Cretinism = hypothyroidism in infancy or early childhood
- impaired development of skeletal system and CNS
- mental retardation, short stature, coarse facial features (wide-set eyes and protruding
tongue), umbilical hernia
* Myxoedema = hypothyroidism in adults > 40 yrs old
deposition of muco polysaccharides beneath the skin
History
# symptoms = mental sluggishness (poor cognition/dementia)
depression
fatigue
cold-intolerance
weight gain despite LOA, constipation
menorrhagia, infertility
ankle oedema
neck pain and swelling
# aetiology = drug history
fever and recent URTI
# past medical history = hyperthyroidism s/p thyroidectomy/RAI therapy
autoimmune disorders
# family history of thyroid and AI disorders
Physical Examination
# general impression = large body habitus
slow mental capacity
vitiligo, malar rash, conjunctival pallor, palmar crease pigmentation
# face = coarse facial features (preorbital oedema, thick nose and lips, macroglossia)
loss of outer 1/3 of eyebrows
dry skin and hair (‘peaches and cream’ complexion)
xanthelasma
hoarse voice (sounds like ‘jabba the hutt’)
# neck = previous thyroidectomy scar
goitre
# neurology = ankle reflexes with delayed relaxation, proximal myopathy, carpal tunnel
syndrome, cerebellar syndrome, myxoedema coma, myxoedema madness,
dementia, deafness to high tones (Trotter’s syndrome)
# CVS = bradycardia, hyperlipidemia, mild HTN (10%), CCF, pericardial effusion, IHD
# resp = pleural effusion
# abdomen = faecal masses
# lower limbs = non-pitting oedema
Format for examination

* general impression
- obese
- physically and mentally slow
30
- excessively clothed (cold intolerant)
* face
- coarse facial features (periorbital oedema, thick nose and lips, macroglossia)
- loss of outer 1/3 of eyebrows
- xanthelasma
- hoarse voice (sound like ‘jabba the hutt’)
* neck
- previous thyroidectomy scar
- goitre
* peripheries
- pulse -> bradycardia
- Tinel’s test -> carpal tunnel syndrome
- finger-nose test and dysdiadochokinesis -> cerebellar syndrome
- proximal myopathy
- ankle jerks -> delayed relaxation
- abdomen -> faecal masses
Investigations
Confirm diagnosis
* thyroid function test = low fT4, high TSH
* thyroid auto-Ab panel = TSH-receptor inhibitory Ab, anti-TG Ab, anti-TPO Ab, anti-microsomal Ab
* RAI = reduced radioisotope uptake
Complications
* FBC = anaemia secondary to menorrhagia
* fasting lipid panel = increased TC and TG
Associated AI disorders
* IDDM = fasting glucose, HbA1c
* pernicious anaemia = Hb, MCV, vitamin B12 levels, anti-IF Ab, anti-parietal cell Ab
* Addison’s disease = U/E/Cr (hypo Na+ and hyper K+)
Evidence of decompensation
* serous effusions = pleural, pericardial, joint
* carpal tunnel syndrome
* cerebellar syndrome
* bradycardia/heart failure
* dyslipidaemia
* depression/psychosis
Hashimoto’s thyroiditis
* autoimmune inflammation of the thyroid gland usually in middle aged women (45-65 yrs old)
* a/w other AI disorders IDDM, Addison’s disease, pernicious anaemia, SLE, MG, B-cell NHL
* clinical features = insidious onset of hypothyroidism a/w painless enlargement of thyroid gland
* Mx = L-thyroxine replacement
monitor for malignancy (lymphoma) -> do serial neck examinations
Post-partum thyroiditis
* autoimmune inflammation of the thyroid gland occurring 2-10 months post-partum
- associated with anti-thyroid peroxidise antibodies
- very similar to Hashimoto’s thyroiditis -> cannot be distinguished on pathology specimens
- current theory = underlying asymptomatic AI thyroiditis that flares post-partum due to fluctuations
of immune function
- clinical features = silent (no pain or swelling)
short period of hyperthyroid -> prolonged but self-limiting period of hypothyroid
Riedel’s thyroiditis
* extremely rare disease
* unknown aetiology (? Autoimmune)
* clinical features = slight enlargement of thyroid gland
woody hard and fixed mass (thyroid parenchyma replaced with fibrous tissue which
filtrates into surrounding neck structures)
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* may be mistaken for infiltrating neoplasm
* a/w retroperitoneal fibrosis, sclerosing cholangitis and fibrosing mediastinitis
De Quervain’s thyroiditis (subacute thyroiditis)

* epidemiology = 20-40 yr old females (much less frequent than Hashimoto’s thyroiditis)
* viral-induced thyroid inflammation -> coxsackie virus, mumps, adenovirus
* clinical features = neck pain radiating to jaw, throat, ears
aggravated by swallowing, coughing and movement
tender enlarged thyroid
fever, anorexia, fatigue, myalgia, preceding URTI
transient hyperthyroidism for 4-6 wks -> transient hypothyroidism for 4-6 wks
high ESR
recovery virtually complete within 4-6 months
* Mx= analgesia, steroids
Myxoedema coma
* severe form of hypothyroidism
(a) defective thermoregulation -> hypothermia
(b) altered mental status -> stupor, coma, seizures
(c) precipitating cause -> sepsis
infarction (AMI, CVA)
trauma
recent administration of sedative/tranquilizer
prolonged exposure to cold
(d) other features -> hypo-reflexia, bradycardia, hypoventilation, heart failure
* investigations = FBC, U/E/Cr, glucose, TFT, serum cortisol, ABG, ECG, CXR, septic work-up
* management
~ admit patient into HD or ICU
~ urgent referral to endocrinologist
(a) thyroid hormone replacement = PO liothyronine
(b) IV hydrocortisone
(c) hypothermia = warm blankets, warm room, warmed fluids
(d) hypoventilation = supplemental O2, monitor with serial ABGs, consider mechanical ventilation
(e) treat precipitating cause
L-thyroxine
* indications = lifelong replacement therapy for hypothyroidism
TSH suppression in thyroid cancers
* pharmacokinetics
- usual starting dose = 50-100 ug OM (25 ug OM if underlying IHD)
- T1/2 = 7 days
- initial doses must be low and increased gradually (adjustments every 3 wks according to clinical
response and TSH suppression)
* start low and go slow in elderly -> rapid replacement may precipitate angina and AMI
* Cx of over-treatment = osteoporosis
* Liothyronine (T3) therapy reserved for myxoedemic coma
32
Surgical (Thyroid) = Thyroid Carcinoma
Epidemiology
Females>Males
9th most common cancer in Singaporean females
Good Prognosis (10 year survival >90%)
Aetiology
Environmental = head and neck radiation (first 2 decades of life)
Iodine deficiency -> pre-existing endemic goitre
Genetic mutations
Clinical features suggestive of carcinoma
High index of suspicion:
 Family history of medullary thyroid carcinoma / MEN 2 syndrome
 Rapid tumour growth
 Very hard/ firm nodule
 Fixation of nodule to adjacent structures
 Vocal cord paralysis
 Regional LAD
 Distant metastasis
Moderate index of suspicion:

 Age< 15 or >45 years old
 Male
 History of head and neck irradiation
 Nodule <4cm in diameter / partially cystic
 Micro calcifications
 Symptoms of compression
Pathology
2 main groups:
 well differentiated (papillary, follicular, medullary) -> good prognosis
 poorly differentiated (anaplastic) -> poor prognosis
Papillary Carcinoma
 Most common type of thyroid carcinoma (75-85%)
 best prognosis out of the 4 subtypes esp in young and female
 occurs usually in young adults (30-50 yrs old)
 slow-growing multicentric tumour with late lymphatic spread
 history of head and neck irradiation linked to development
 pathology:
o Papillary cells with nuclear grooves
o Intranuclear inclusion bodies
o Psammomma bodies (keratin pearl with calcifications)
 Treatment:
o Total thyroidectomy
o L thyroxine replacement
o Radioactive iodine
 Why thyroidectomy preferred?
1. Multifocal disease
33
2. Possibly of using radioactive iodine = cannot be used if only hemithyroidectomy done due to uptake in
normal thyroid lobe
3. Use of TG as surveillance method to detect recurrent or metastatic disease
Follicular Carcinoma
 Makes up 10-20% of thyroid carcinomas
 Occurs in young and middle aged adults (40-60 yrs old)
 Linked to endemic goitres
 Tendency to metastasize early by homogenous route (liver, bones, lungs). Worse prognosis!
 Tx
o L thyroxine replacement
o Radioactive iodine
Medullary Carcinoma
 Makes up 5% of thyroid carcinomas
 Occurs in young and middle aged adults (40-60 yrs old)
 Arises from parafollicular c (neuroendocrine) cells -> secrete calcitonin
 80% arises spontaneously (in the elderly) -> unifocal; worse prognosis
20% may be familial and linked to MEN 2 syndrome (screen family members) -> multifocal; better prognosis)
# MEN 2 syndrome = medullary thyroid cancer, pheochromocytoma, primary hyperparathyroidism due to RET
proto-oncogene mutation
100% penetrance for MTV; 90% penetrance for PCC, 50% for primary hyperparathyroidism
 Metastasize by local extension, lymphatic and hematogenous routes
 Pathology = amyloid trauma
 Tx :
o Pheochromocytoma (urinary catecholamine) and parathyroid hormone (ipTH and Ca2+)
o Screen pre op
o Total thyroidectomy (resect pheochromocytoma first, remove all parafollicular cells -> junction of
middle and lower third of thyroid gland)
o Monitor calcitonin levels
Anaplastic Carcinoma
 Least common of the thyroid carcinomas (<5%)
 Occurs in the elderly (60-80 yrs old)
 Aggressive tumour with local extension and distant metastasis via lymphatic and hematogenous routes
 Very poor prognosis (average survival is 6-9 mths after diagnosis)
 Must be differentiated from lymphoma (better outcome)
 Tx:
o Debulking surgery
o Palliative radiotherapy and chemotherapy
Lymphoma
 Require biopsy to make diagnosis
 Tx : radiotherapy and chemotherapy
34
Clinical Features
History
 Lump in neck
 Mass pressure effects = dyspnea, stridor, cough (airway obstruction)
Dysphagia
Hoarseness
 Usually euthyroid (no symptoms of hyperthyroidism)
 History of head and eck irradiation
 Family history of thyroid cancer
 Metastasis = LOA, LOW, fatigue, malaise, fever
Bone pain
Abdominal pain, jaundice, change in bowel habits
Prolonged cough, hemoptysis, hoarseness (infiltration into recurrent laryngeal nerve)
Physical examination
 Lump in the neck = ill defined, solitary, hard, immobile, tender
o Usually spreads to the LNs in the tracheal-oesphageal groove (level 6)
o Can affect levels 2 (jugulo-digastric), 3 (mid-jugular), 4 (supraclavicular) as superior thyroid pedicle
drains in a cephalic direction
o Not commonly seen or palpable unless >1.5-2 cm in diameter
 Palpable deep cervical lymph nodes (10% of cancers)
 Palpable deep cervical lymph nodes (10% of cancers)
 + or – signs of hyperthyroidism
Management
 Total thyroidectomy -> remove both sides + paratracheal lymph nodes +- cervical lymph nodes
Recurrence and mortality increases by 2x if not done!
 RAI – ablate residual cells
Scan for metastasis in chest cavity and bone
 Monitor TSH/TG regularly -> increases with recurrence (should not have any thyroid tissue left)
o No thyroglobulin
o TSH 0.1ng/ml
 Monitor calcitonin levels if patient has medullary carcinoma
 L-thyroxine replacement for life -> suppress TSH release (remove stimulus for remaining tirrue)
No remaining T3 + T4 synthesis
 Lifelong follow up : Physical examination (cervical LAD, thyroid gland)
Thyroid Ultrasound
35
Surgical (Thyroid) = Thyroidectomy
Types:
1. Lobectomy
2. Subtotal thyroidectomy (GD)
3. Total thyroidectomy (MNG, carcinoma)
# Normal thyroid lobe is the size of distal phalanx of the thumb (4g) -> leave the equivalent behind
Indications for thyroid surgery
C – Cancer
C- Control
C – Compression (dyspnoea, stridor, cough, hoarseness, dysphagia)
C – Comesis
Pre-operative considerations
 Reduce thyroid activity -> clinically euthyroid
 ENT referral to check vocal cords (normal cord mobility; exclude compensated cord paralysis_
Operating Procedure
 Papillary lesion ->
o Hemithyroidectomy
o Frozen section
 Follicular lesion ->
o Hemithyroidectomy
o Trace paraffin histology results
o KIV total thyroidectomy on a separate occasion
Post operative complications

General
a) Risk of anesthesia = AMI, CVA
b) Pain
c) Wound infection
d) Other causes of post-op fever = pneumonia, UTI
Specific
Early:
a) Haemorrhage
 Can compress trachea very easily (limited space between strap muscles and trachea)
 Clinical features = dyspnea, stridor, shock
 Management = remove sutures immediately
b) Pneumothorax
c) Thyroid storm
d) Hypoparathyroidism
 Inadvertent removal or injury to the parathyroid glands during surgery
 Hypocalcemic tetany usually occurs POD 2-5
 Clinical features =
a) Circumoral parasthesiae
b) Tingling of extremities
c) Painful carpopedal spasms
d) Laryngospasm
36
e) Chvostek’s sign (tapping of facial nerve in front of external auditory meatus will
cause hemifacial spasm
f) Trousseau’s sign (carpopedal spasms induced by tourniquet around arm)
 Management: slow infusion of 10ml of 10% calcium gluconate (extravasations can cause
necrosis) and oral calcium intake
e) Recurrent laryngeal nerve damage
 Lies behind the thyroid gland in the groove between oesophageal and trachea
 Close to the inferior thyroid artery
 Damage to 1 nerve -> slight hoarseness (weak voice)
 Damage to 2 nerves -> almost complete loss of voice + severe airway narrowing
f) External branch of the superior laryngeal nerve damage
 Travels with the superior arterio-venous pedicle
 Damage affects high frequency speech and voice projection
Late
a) Hypothyroidism -> L thyroxine for life if total thyroidectomy
b) Recurrent hypothyroidism
c) Keloid scarring
37
Rheumatology
Medicine (Rheumatology) = Rheumatoid Arthritis Song
Mdm XXX is a middle aged Chinese lady who is alert and comfortable at rest. On general inspection, I note
that she appears to be Cushingoid as evidenced by the characteristic rounded facies (facial plethora, acne,
and hirsutism). In addition, she also has a pair of rheumatoid hands.
Pathology
I say this because there is bilateral symmetrical deforming polyarthropathy involving the small joints of
the hand namely the MCPJ and PIPJ and sparing the DIPJ. I note bilateral Z-thumb deformities, swan neck
deformities affecting joints and Boutonniere deformity affecting joints. There is ulnar deviation of the
fingers, radial deviation at the wrists, ulnar subluxation at the MCPJ and dorsal subluxation of the DRUJ
(distal radial-ulnar joint). There are no rheumatoid nodules seen over the extensor surfaces or over the
olecranon process. I note muscle wasting of the intrinsic muscles. There are no nail changes or psoriatic
plaques seen.
Stage
The disease is likely to be in a quiescent stage and there is no overlying erythema, joint
swelling/tenderness of increased warmth.
Complication of the disease

Her disease is complicated by disabling arthritis as Mdm XXX is unable to make a fist and there is severe
limitation of movements at the wrist and shoulder joints. Therefore I do not note the presence of a trigger
finger, dropped fingers or carpal tunnel syndrome.
Function
Functionally, Mdm XXX is only able to hold a cup with both hands. She is unable to button her shirt, grasp
a pen and write.
Summary and Request

So in summary, Mdm XXX has features of rheumatoid arthritis complicated by disabling arthropathy. The
disease is likely to be in a quiescent stage and there are signs of steroid use.
Examine the other joints = elbow, shoulder, TMJ, neck, hip, knee, feet.
Extra articular features =
 Eyes (scleritis, conjunctival pallor, episcleritis)
 LAD
 Lungs(pulmonary fibrosis, pleural effusion, nodules)
 CVS (MR, AR)
 Abdomen (splenomegaly, hepatomegaly)
38
Medicine (Rheumatology) = General points about arthritis
Definition
 Pain and swelling involving joint(S)
 Cf arthralgia = pain without joint swelling
5 cardinal signs of inflammation

 Warmth
 Pain
 Erythema
 Swelling
 Loss of function
Inflammatory vs mechanical arthritis
Features Inflammatory Non-inflammatory

Morning stiffness  1 hr <30mins
Aggravating factors Rest (unless in severe/ active cases) Movement
Relieving factors Movement Rest
Systemic complaints Present Absent
Response to steroids yes mo
Key Words
 Symmetrical versus asymmetrical
 Mono/oligo/poly-arthropathy
o Mono = 1 joint
o Oligo = <5 joints
o Poly = >5 joints and more
 Small versus large joint
 Axial versus peripheral
Mono and poly arthritis

Monoarthritis Polyarthritis
Septic arthritis Rheumatoid arthritis
Gout/pseudo gout Osteoarthritis
Trauma (haemarthrosis) Connective tissue like SLE
Seronegative spondyloarthritis Reactive arthritis
Osteoarthritis Gout/ pseudo gout
Monoarthritic presentation of a polyarticular
disease
39
Medicine (Rheumatology) = Systemic lupus erythematosus (SLE)
Epidemiology
 An autoimmune multi system disorder with a remitting and relapsing course
 Strong female preponderance (approx 9:1)
 Onset usually in 2nd or 3rd decade of life but may manifest at any stage
Pathogenesis
 Autoimmune disorder with the fundamental defect of failure to maintain self tolerance
Type 3 hypersensitivity = immune complex formation with deposition in target organs
 Involves a bewildering array of auto-antibodies
 Antinuclear antibodies (ANA)
Directed against several nuclear antigens (DNA, histones, non-histone proteins)
Senstive = positive in 95% of patients with SLE
Not specific = also positive in Sjogren’s, polymyositis/dermatomyositis, RA, autoimmune hepatitis
 Anti-Sm Ab
Specific for SLE. Virtually diagnostic
 Anti-phospholipid antibodies (lupus anticoagulant, anticardiolipin Ab)
Present in 40-50% of lupus patients
Phospholipids required for coagulation. Therefore, prolonged aPTT that fails to correct even after
addition of normal plasma
Prothrombotic state = venous thrombosis (DVT/PE)
Arterial thrombosis (AMI/CVA)
Recurrent spontaneous miscarriages
Livedo reticularis
 Predisposing factors
 Genetic/family history
 Non genetic factors: Drug lupus = isoniazid, procainamide, hydralazine, chlorpromazine,
minocycline
 Lung and skin involvement >renal and CNS involvement
 Remits once drug is stopped
 Anti-histone Ab are characteristic (anti-dsDNA is almost never detected)
UV light = damages DNA and promotes cell injury
 Mechanism of injury
 Visceral lesions mediated by immune complexes (type 3 hypersensitivity)
 Abs against RBC, WBC and platelets (type 2 hypersensitivity)
 Extremely variable course
 Extremely benign course even without treatment
 May progress to death rapidly within months
Clinical features
 Constitutional symptoms
 LOW
 LOA
 Fatigue/malaise
 Fever
40
 Skin
 Erythematous malar rash sparing nasolabial folds
 Photosensitivity
 Discoid rash
 Alopecia
 Nail-fold infarcts, telangiectasia
 Raynaud’s phenomenon (white-blue-red)
 Eyes
 Dry eyes (Sjogren’s syndrome)
 Red eyes (episcleritis, scleritis, anterior uveitis)
 Cotton wool exudates (retinal vasculitis)
 Mouth
 Oral ulcers
 Dry mouth (Sjogren’s syndrome)
 Joints
 Non-evasive arthritis involving at least 2 peripheral joints
 Consists of a non-specific mononuclear infiltration in synovial membrane
 Seen in 90% of patients
 Deforming arthropathy may occur due to capsular laxity (jaccoud’s arthropathy)
 CNS
 Psychosis
 CVS
 Vessels = acute necrotizing vasculitis affecting small arteries and arterioles
 Heart = pericarditis (serous effusion, fibrinous exudates)
Myocarditis
Libman-sacks endocarditis (non-bacterial, less common due to steroid use)
 Lungs
 Pleuritis = serous effusion, fibrinous exudates
 Pulmonary fibrosis
 Renal
 One of the most commonest cause of death
 Deposition of immune complexes within glomeruli -> evokes inflammatory response
 6 classes (WHO classification)
 Class I = normal LM, EM and FM (rare)
 Class II = Mesangial lupus nephritis
o 20%
o Mild clinical symptoms
o Immune complex deposition in mesangium with slight increase in mesangial matrix
and cellularity
 Class III = focal lupus nephritis
o 25%
o Mild microscopic haematuria and proteinuria
o Microscopic = proliferation of endothelial and mesangial cells
Less than 50% of glomeruli affected
 Class IV = diffuse proliferative lupus nephritis
o Most serious form and also the most common, 50%
o Haematuria, moderate to severe proteinuria, HPT and renal insufficiency
41
o Microscopic = proliferation of endothelial and mesangial cells affecting entire
glomerulus
Crescent formation
o Glomerular injury eventually gives rise to glomerulosclerosis
 Class V = membranous lupus nephritis
o 15%
o Severe proteinuria and nephritic syndrome
o Microscopic = widespread thickening of capillary wall
 Class VI = advanced sclerosing lupus nephritis
o > 90% of glomeruli sclerosed globally
 Hematological
 Anaemia = hemolytic, chronic disease
 Leucopenia (esp lymphopenia)
 Thrombocytopenia
 Anti phospholipid syndrome = venous and arterial thrombosis, recurrent spontaneous miscarriages
 Generalized lympadenopathy +/- splenomegaly
Diagnostic criteria
 At least 4 out of 11
1. Malar rash Fixed erythema malar eminences sparing nasolabial
folds
2. discoid rash Erythematous raised patches with keratotic scaling and

follicular plugging +/- atrophic scarring
3. Photosensitivity Unusual reaction to sunlight
4. Oral ulcers Oral or nasopharyngeal ulceration (usually painless)
5. Arthritis Non-erosive arthritis involving at least 2 peripheral

joints
6. Serositis Pleuritis or pericarditis
7. Renal disorders Persistent proteinuria >0.5g/day or cellular crisis
8. Neurological disorders Seizures or psychosis in the absence of any known

course
9. Hematological disorders Hemolytic anemia, Leucopenia, thrombocytopenia,

lymphopenia
10. Immunological disorders Anti-dsDNA Ab, anti-Sm Ab, anti-phospholipid Ab (lupus

anticoagulant, anticardiolipin Ab)
11. ANA
 Major causes of death = renal failure, intercurrent infections and diffuse CNS involvement
42
Laboratory findings
1. FBC
 NCNC anemia = anemia of chronic disease
Hemolytic anaemia -> reticulocyte count, hepatoglobin, LDH, direct Coomb’s test
 Leucopenia/lymphopenia
 Thrombocytopenia
2. ESR, CRP
 ESR = raised
 CRP = normal (consider infection if raised)
3. PT/PTT
 Prolonged aPTT in anti phospholipid syndrome
4. U/E/Cr
 Renal impairment
 Proceed to do urine dipstick, UFEME, urine c/s , urine phase contrast, 24 hr CCT/UTP, urine PCR, renal
biopsy
5. Autoimmune markers
 ANA = sensitive but not specific
 Anti-dsDNA = specific
 Anti-Sm = specific
 Anti-Rho and anti-La (complete heart block in neonate)
 anti phospholipid Ab (lupus anticoagulant, anticardiolipin Ab)
6. Monitor disease activity
 anti-dsDNA = high
 serum complement = low C3 and C4
High C3 degradation product
 ESR = high (do CRP to distinguish lupus flare from infection)
Management
General measures
 Avoid sunlight = carry umbrella, wear sun block
 Wear warm socks and gloves for Raynaud’s phenomenon
 Avoid drug provocation (penicillin, sulphonamides)
Pharmacotherapy
 No curative therapy
 Different modalities
(a) Joint symptoms = NSAIDs
(b) Skin symptoms/joint symptoms not controlled by NSAIDs = hydroxychloroquine (annual eye check for
maculopathy)
(c) Renal involvement = steroid and pulsed IV cyclophosphamide
(d) Severe episodes = high dose prednisolone, cytotoxics (azathioprine, cyclophosphamide, methotrexate)
(e) Chronic disease = low dose prednisolone
Prognosis
 poor prognostic factors
(a) Renal disease (esp class IV)
(b) Hypertension
(C) male
(d) Young age
43
(e) APLS
(f) High disease activity
 prognosis = 90% 5 year survival
80% 10 year survival
Pregnancy and SLE

 Avoid during active disease (esp with sig organ impairment) due to high risk of spontaneous miscarriage
and exacerbation of SLE
 Should wait until disease has been quiescent for at least six months before attempting pregnancy
 Management of patients with active lupus = corticosteroids, NSAIDs and hydroxychloroquine
 Cyclophosphamide and methotrexate are contraindicated
 Azathioprine can be used cautiously
 Patients with migraine headaches, Raynaud’s phenomenon, history of phlebitis or APL Ab should not be
treated with OCPs (increases risk of thrombosis)
History taking
1. Malar rash
2. Discoid rash
3. Photosensitivity
4. Alopecia, dry eyes and mouth, oral ulcers
5. Gangrene of fingers, Raynaud’s phenomenon
6. Chest pain, dyspnoea
7. Joint pain
8. Seizures
9. Change in urinary frequency and volume, haematuria, frothy urine, loin pain
10. Anaemia = pallor, chest pain, palpitation, fatigue, giddiness, dyspnoea, jaundice
Leukopenia = susceptibility to infections
Thrombocytopenia = gum bleeding, easy bruising, menorrhagia
APLS = history of recurrent spontaneous abortion, DVT/PE, AMI, CVA
11. Constitutional (fever, LOA, LOW, malaise)
Examination
“This patient most likely has SLE as evidenced by the butterfly rash affecting the nose bridge but sparing
the nasolabial folds.”
Proceed with the following:

General appearance
 Weight loss (due to chronic inflammation)
 Cushingnoid appearance (due to steroid therapy)
Hands
 Nails (splinter hemorrhages, nail-fold infarcts)
 Gangrene (vasculitis
 Palmar erythema
 Raynaud’s phenomenon (white-blue-red)
 Arthropathy
Arms
 Livedo reticularis (bluish purple streaks without discrete borders)
44
 Purpura (vasculitis or autoimmune thrombocytopenia)
 Proximal myopathy (due to disease or steroid use)
Face
 Conjunctiva pallor
 Mouth ulcers
 Alopecia
Chest
 CVS = pericardial rub
 Lungs = pleural rub, pleural effusion, pulmonary fibrosis
Abdomen
 Mild splenomegaly +/-hepatomegaly
Legs
 Vasculitic rash
 Lower limb pitting edema (due to lupus nephritis)
Request to look at:

1. Vitals = temperature and BP
2. Urine dipstick = proteinuria haematuria
45
Medicine (Rheumatology) = GALS screen
Gait, Arms, Legs, Spine => look at appearance and movement
History
1. Have you had any pain or stiffness in your muscles, joints or back?
 Cardinal symptoms of rheumatic disease
2. Can you dress yourself completely without any difficulty?
 ADL = assessing functional problem of UL
3. Can you walk up and down stairs without any difficulty?
 ADL = assessing functional problem of LL
Physical examination (examine patient wearing his underwear only)

1. Gait
 Ask patient to stand
 Ease of transfer from chair/ lying position to standing position
 Get patient to walk, turn around and walk back
 Symmetry and smoothness of movement (legs, arm swing, pelvic tilting)
 Normal stride length
 Ability to turn quickly
2. Spine
 Inspection (from the back and side)
 Start from the back
 Scoliosis
 Symmetry of paraspinal muscles and girdle muscles
 Symmetrical pelvic position and level iliac crests
 Inspect from the side
 Excessive thoracic kyphosis
 Loss/excessive lumbar lordosis
 Movement
 Squeeze midpoint of supraspinatus muscle -> hyperalgesic response of fibromyalgia
 Schober’s test = measure of lumbar excursion
 From front
 Lateral flexion of C-spine (Place your ear on your shoulder)
3. Arms
 Place arms behind head
 Measure of shoulder abduction and external rotation
 Observe movement at glenohumeral, acromioclavicular and sternoclavicular joints
 Place arms by the side with palms facing outwards
 Full elbow extension
 Normal girdle muscle bulk and symmetry
 Bend elbows at 90ᵒ and pronate/supinate
 Wrist flexion and extension
 Lift elbows up
 Subcutaneous nodules
 Movement
 Clench fists and test grip strength
46
 Fingers on thumb
 Measurement of fine movements
 Squeeze across MCP joints
 Early arthritis = pain and tenderness on squeezing before other abnormalities seen
4. Legs
 Inspection
 Leg
 Deformities
 Knee
 Bulk of quadriceps muscle
 Loss of parapatellar fossae
 Feet
 Callus formation = abnormal weight bearing
 Movement
 Fully flex knee and hip joint
 Place hand on knee joint to feel for crepitus
 Internally and externally rotate hip joint
 Squeeze across MTP joints
 Early arthritis = pain and tenderness on squeezing before other abnormalities seen
47
Medicine (Rheumatology) = Rheumatoid Arthritis
Overview
 Description
► Systemic chronic inflammatory disease affecting multiple tissues but principally attacking joints to produce a non- suppurative proliferating
synovitis that frequently progresses to destroy articular cartilage and underlying bones with resulting disabling arthritis.
 Epidemiology
► Very common = ∼ 1% (higher in smokers)
► Female > Males (3:1)
► Peak incidence = 4th/5th decades of life
 Pathogenesis
► Initiation by an arthritogenic antigen with subsequent autoimmune reaction in which T cells release cytokines and inflammatory mediators that
ultimately destroy the joint.
► Causative microbial triggers are unknown but suspects include EBV, Borrelia species, Mycoplasma species, retrovirus and mycobacterium.
Principles of Diagnosis
 History
► Arthritis
- Classically, swollen, painful, stiff hands and feet worse in the morning
- Chronic inflammatory joint disease with relapsing and remitting course
- Insidious onset with joint pain and early morning stiffness
- Symmetrical polyarthropathy = PIPJ, MCPJ, wrist, MTPJ and knees (spares distal DIPJ)
- Joints progressively enlarge → limited ROM and complete ankylosis (stiffness due to abnormal adhesion and rigidity of the bones of the joint)
► Constitutional symptoms
- LoA, LoW, fatigue, fever, rash
- Anemia → chest pain, SOB, giddiness, palpitations, fatigue
► Extra-articular involvement
- Skin = Raynaud’s phenomenon, rash
- Head and Neck = red eyes, dry eyes and mouth (Sjögren’s syndrome)
- Pulmonary and Cardiac = chest pain, SOB
- CNs = numbness, parasthesiae, weakness
► Atypical presentations
- Palindromic = acute recurrent, relapsing, remittent arthritis usually affecting 1 large joint for a few hours, with symptom-free intervals of days
– months between attacks. (‘Was I Saw!’ → wrist, ankle, shoulder, IPJ)
- Persistent monoarthritis
- Systemic = pericarditis, pleurisy, LoW, constitutional symptoms
- Acute onset of widespread arthritis
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 Extra-articular involvement
1. Eyes
 Sclera – episcleritis, scleritis, scleromalacia, scleromalacia perforans
 Conjunctiva – pallor, keratoconjunctivitis sicca (Sjögren’s syndrome)
 Lens – cataracts from steroid use
 Extra-Ocular Muscles – mononeuritis multiplex, myasthenia 2º penicillamine, EOM tendon synovitis
 Fundi – maculopathy from hydroxycholoroquine use
2. Head and Neck
 Mouth – ulcers from DMARD treatment, dry mouth and enlarged parotids (Sjögren’s)
 TMJ – crepitus
 Neck – tenderness, muscle spasm, limited ROM (atlanto axial sublux, basilar invagination by dens protrusion,
subcervical spine)
3. Respiratory system
 Upper airway – cricoarytenitis
 Pleura – pleural effusion, pleurisy
 Bronchioles – bronchiolitis obliterans and organizing pneumonia (BOOP)
 Parenchyma – lower lobe pulmonary fibrosis, penumonitis, rheumatoid nodules
 Infiltration – Caplan’s (rheumatoid nodules in periphery of lung fields a/w coal worker’s pneumoconiosis)
4. CVS
 Pericarditis
 Aortic/mitral regurgitation
5. Lympadenopathy
6. GIT
 Splenomegaly (5%)
 Felty’s syndrome (1%) = RA w/splenomegaly and hypersplenism →anemia, leukopenia, thrombocytopenia and leg ulcers (ameliorated by
splenectomy)
 Methotrexate use → hepatomegaly
7. Upper Limb
 Vasculitis = nail-fold infarcts, splinter hemorrhage, telangiectasia, Raynaud’s phenomenon
 Subcutaneous nodules (indicates seropositivity and more aggressive arthritis, found on flexor and myocardium)
 Entrapment neuropathy
8. Lower Limb
 Hip – limited ROM
 Knees – quadriceps wasting, synovial effusion, flexion contracture, genu valgus deformity, Baker’s cysts in popliteal fossae
 Lower Leg – leg ulcers, calf swelling (ruptured Baker’s cyst), peripheral neuropathy, mononeuritis multiplex
 Ankle – limited ROM, nodules on Achilles tendon
 Feet – foot drop (peroneal nerve entrapment), MTPJ (swelling, subluxation)
 Differentials
49
* Deforming symmetrical chronic polyarthropathy = RA
Psoriatic Arthritis
Chronic tophaceous gout
* Arthritis and nodules = RA
SLE
RHD
Amyloid arthropathy (usually a/w multiple myeloma)
 Investigations
FBC  NCNC anemia of chronic disease

 WCC ↓
 Platelets ↑
ESR & CRP  Raised (c/f SLE, only ESR raised)
Rh factor  Positive in 80%
 Also positive in Sjögren’s (100%), SLE (30%),
mixed CTD (30%) and systemic sclerosis
ANA  Positive in 30%
X-ray of joints  Soft tissue swelling
 Juxta-articular osteoporosis
 ↓ joint space
 Juxta-articular bony erosions
‐ ± subluxation
‐ ± complete carpal destruction
 Joint dislocation
C-spine X-ray (lateral, AP, flexion and extension)  Atlanto-axial subluxation (↑ pre-odontoid gap)
Synovial fluid analysis  Turbid
 ↓ viscosity
 Clots
Monitor drug therapy  FBC
 U/E/Cr
 LFT
 Urinalysis
 Diagnostic Criteria (revised American Rheumatism Association Criteria (≥4 out of 7)

50
Diagnosis of RA made when ≥4 criteria are met (93% sensitivity and 90% specificity)
 Morning stiffness >1 hours
 Arthritis of ≥3 joints Fluid-filled presence of soft tissue swelling in

the following: wrist, PIP, MCP, elbow, knee,
ankle, MTP
 Arthritis of hand joints Wrist, MCP, or PIP joints among the

≥6 weeks
symptomatic joints observe
 Arthritis is symmetrical Right and left joints involved for one or more of
the following: wrist, PIP, MCP, knee, MTP, elbow,
ankle
 Rheumatoid nodules Subcutaneous nodules in regions surrounding

joints, flexor/extensor surfaces, or bony
prominences, sacrum, Achilles, sclera
 Rheumatoid factor +ve
 Radiological changes Hand and wrist films
51
Complications
 Complications of disease
‐ Increased risk of IHD and lymphoma
‐ Ruptured tendons
‐ Joint destruction and resultant disability
‐ Cervical myelopathy
‐ Amyloidosis → proteinuria, nephritic syndrome and renal failure
 Side effects of therapy
‐ Dyspepsia, BGIT, asthma (NSAIDs)
‐ Renal impairment (NSAIDs, penicillamine)
‐ Proteinuria (gold salts, penicillamine)
‐ Anemia (NSAIDs)
‐ Bone marrow depression (DMARDs)
 5 causes of anemia in RA
1. Anemia of chronic disease
2. Iron deficiency anemia
 BGIT due to NSAIDs use
3. Megaloblastic anemia
 Increased cellular turnover (folate acid ‘deficiency’)
 Methotrexate use
 Pernicious anemia
4. Hypersplenism
 2º to Felty’s syndrome
5. Aplastic
 BM suppression due to gold and penicillamine use
Assessment of disease severity

 Symptoms
‐ Duration of morning stiffness
‐ Pain score
‐ Severity of fatigue
 P/E
‐ Number of swollen joints
‐ Number of tender joints
‐ Degree of swelling ± tenderness
‐ Extra-articular disease
 Lab values
‐ ↑ESR and CRP = active disease, infection, Amyloidosis, Sjögren’s disease
52
‐ Anemia
‐ Rh factor titres = correlates with likelihood that patient has extra-articular disease (not activity of arthritis)
‐ Inflammatory joint fluid = high polymorph count, low complement, fibrin
 Imaging
‐ Progressive bony erosions on serial X-ray films
‐ Low bone marrow density
Sjögren’s syndrome
‐ Connective tissue disorder a/w dry eyes(keratoconjunctivitis sicca) and dry mouth (xerostoma)
‐ May be a/w autoimmune thyroid disease, MG or autoimmune liver disease
‐ Ix = Schirmer filter paper test (crude measure of tear production; <5mm, N → at least 15mm after 5 mins)
‐ Tx = artificial tears, artificial saliva and NSAIDs
Principles of Management
 Treatment modalities
Symptomatic relief
Paracetamol Pain
NSAIDs Pain Give with PPI or H2-R blocker

- Aspirin, Ibuprofen CI = BGIT, PUD, Asthma S/E = BGIT, interstitial nephritis,
- COX 2 inhibitor(Arcoxia), if bronchoconstriction
elderly
DMARDS (mono or combination therapy)
- Start if persistent synovitis > 6 weeks
- Slow onset of action (may take weeks to months)
Hydroxychloroquine Mild disease S/E = maculopathy, rash, N/V/D, ototoxicity,
aggravates psoriasis
Sulphaslazine Moderate disease S/E = N/V/D, rash, BM depression, oral ulcers,

SJS
 Monitor LFT & FBC
Methotrexate 1st choice for severe CI = pregnancy, liver disease, G6PD deficiency
disease Do not take with alcohol!!
S/E = N/V/D, lower lobe pulmonary fibrosis,
-Better tolerated
53
transaminitis, ↑no. of rheumatoid nodules
 Give with folate to reduce GI S/E
 Monitor LFT
Lefluonomide Inhibits activated T Takes months to work
cells S/E = BM depression, proteinuria, rash,
hepatitis
 Monitor LFT, FBC, urinalysis
Corticosteroids Indications S/E = metabolic, cosmetic, cataracts,
osteoporosis
- vasculitis  Monitor BSL & BP
- severe disease Rebound disease common on stopping steroids
- exacerbations not
responding to other
drugs
Azathioprine, Cyclosporin A, Severe disease with AZP = BM depression, transaminitis, oncogenic
cyclophosphamide failure of other CSP = gingival hypertrophy, HPT, renal
therapies impairment
Anti-cytokine therapy
-suppress disease activity only during treatment → relapse on discontinuation
Infliximab (against TNF) Progressive RA after 2 S/E = N/V/D, rash, infection (TB reactivation),
Etanercept (against TNF receptor) DMARDs failure neutralizing antibodies
Surgery To improve function, relieve pain and prevent complications
- Synovectomy & decompression of wrist & tendon sheaths

- tendon repair and transfer
- Arthrodesis
- Osteotomy
- Joint replacement
Paramedical services Physiotherapy
Occupational therapy = adaptive aids, orthoses (eg wrist splints), ADL
training
Others Patient education and Support groups
54
*drugs causing cytopenias = warn patient to stop meds and consult doctor if sore throat develops.
 Clinical course
 Variable
- most have fluctuating disease with the greatest progression during the initial 4-5 years
 Most develop deforming and destructive arthritis after 15-20 years
 Life expectancy reduced by 3-7 years
 Poor prognostic factors
1. Female
2. Older age of onset (>60 YO)
3. Systemic features: LoW, extra-articular manifestations
4. Vasculitis
5. Early bone erosions
6. Rheumatoid nodules
7. Persistent disease activity > 12 months
8. Insidious onset
9. HLA-DR 4 linkage
10. Rh factor > 1 in 512
55
Medicine (Rheumatology) = Examination of rheumatoid hands
Approach to RA short case
 Introduce yourself
 Sit patient at edge of bed, remove accessories, roll up sleeves and place hands on pillow (watch action)
 General inspection – Cushingoid appearance
 Hands
1. LOOK
‐ Palms down
 Deformities = symmetrical polyarthropathy involving small joints of the hand (sparing DIPJ)
Z-deformity of thumb, Swan neck and Boutonniere deformity of fingers
Ulnar deviation of fingers
Volar subluxation of MCPJ
Radial deviation of wrist
Dorsal subluxation of ulna at carpal joint → prominent radial styloid process
 Swelling = Rheumatoid nodules over extensor surfaces (never on IPJ)
 Discoloration = Erythema (active disease)
 Wasting of intrinsic muscles (guttering)
 Nails = Telangiectasia, nail fold infarcts, splinter hemorrhages, nail bed pallor, longitudinal ridging, thickening, pitting, onycholysis (rule out
psoriasis)
‐ Palms up
 Wasting of thenar and hypothenar eminences
 Palmar erythema
 Carpal tunnel release scar (over distal palmar crease)
2. FEEL
‐ Increased warmth (run back of hand across patient’s dorsum)
‐ Wrist = Tenderness (suggestive of synovitis → active disease)
Joint effusion (soft and boggy → synovitis)
Synovial thickening
Piano key sign = springs back into position when pressed
‐ MCPJ = Tenderness
Joint effusion (bulge sign)
Subluxation
‐ PIPJ = Tenderness
Joint effusion
3. MOVE
56
‐ Clench fists tightly and release = trigger finger
‐ Place palms on pillow and lift fingers off = dropped finger (tendon rupture/slipped off into gutter)
‐ ‘push against wall’ position = finger drop (PIN palsy due to inflammation around wrist)
‐ Wrist flexion and extension = limited ROM
‐ Fold arms across chest = subcutaneous nodules over elbows, psoriatic skin plaques
4. NEUROLOGICAL
‐ Radial nerve = EPL, sensation over 1st dorsal web space
‐ Median nerve = FPL, FDP of index finger, APB sensation over lateral palm and 3½ fingers, Tinel’s sign (CTS)
‐ Ulnar nerve = FDP of little finger, finger abduction, sensation over medial palm and 1½ finger
5. FUNCTION
‐ Power grip
‐ Unbutton clothes
‐ Write
‐ Hold a cup of water
6. REQUEST
‐ Feet for similar changes
‐ TMJ for crepitus
‐ Neck for tenderness
‐ Eyes = Episcleritis, scleritis
‐ Lymphadenopathy
‐ Lungs = Pleural effusion, end-inspiratory fine crepitations (pulmonary fibrosis), nodules
‐ CVS = aortic regurgitation
‐ Request to look at temperature chart, offer to take BP and perform urine dipstick test
Format for presentation
a) Describe deformities
b) Disease activity → active or quiescent
c) Functional status
d) Request to examine
e) Diagnosis and differentials
57
58
Medicine (Rheumatology) = Case Study
Ang King Siang
72 Chinese Female
Has 1 son and 4 daughters, lives with eldest son and daughter with maid
Ambulates with quad stick
Background:
1) Seropositive erosive rheumatoid arthritis f/u Dr F CHia
Diagnosed in 7/2003
Manifestation: 45 years of bilateral symmetrical polyarthritis: Joint pain over bilateral wrist, MCPs,
PIPs with early morning stiffness > 1hour
- Bilateral deformities of writs, MCPs, fingers, left elbow and right shoulder with ulnar deviation
- Crepitus left knee with genus varus
Serology:
RF 98, ANA 1/320
DsDNA –ve
Markers of activity
ESR baseline ~ 30 (highest 99, lowest 17), CRP normal,
Anti-HCV and HbsAg –ve, albumin baseline 31, creatinin baseline 200
X- ray hands 12/2005: Ulnar deviation mainly in MCPs with carpal bone fusion and erosions
Treatment: No treatment btw 7/2003 till 10/2005 (burnt out RA) given glucosamine for OA knee
a) Prednisolone: 5mg om 10/2005: left knee effusion; max dose 10mg om. Current 7.5 mg om
b) Sulfasalazine: 500mg om till 11/2005: Pancytopenia (WBC 3.9 Hb 9.7 Plt 129)
Restarted 6/2/2007 at 500mg Om when left knee and ankle jts remained active in spite of IA TA.
Stopped since 20/2/07: AoCRF; also left knee inflammatory OA rather than RA flare
c) Hydroxychloroquine: 200mg om 12/2005 till 2/2006: blurred vision, feels unwell
d) IA triamcinalone 10/2005 and 12/2005 and 12/2006 left knee
Last admitted to RAI for left knee effusion 20/10/2007 – 23/10/2007 thought to be inflammatory OA
with a ddx of active RA: PNL 5mg om and 2.5mg on (7.5mg od) ; GWR imp was that of inflammatory
OA left knee, decision then to stop SSZ. Reduced PNL to 2.5mg bd Plans to refer ortho output.
Since discharge: Joints quiescent; remained on tailing dose of PNL until 30/10/07
TKR 18.10.07
Seen 30/10/07: Advised early RAI rv by Dr Sat (ortho)

Co Post TKR: 2 days after developed Left forefoot and ankle pain. Mid tarsal jts red, swollen, tender RA
flare. Increased PNL from 1mg bd to 2.5 mg bd with plans for DMARD if still active
3.11.07: With interval mild improvement of left foot pain and swelling. But reported right foot pain as
well. Ddx: ?Crystal arthropathy with worsening renal impairment (Cr 239-258) PNL increased
10mg/d x 1 week then 7.5mg/d; uric acid 573 -> 590 -> 632 umol/L
2) Hyperlipidemia
– On simvastatin 10mg on
- Last lipid panel 8/07: Chol 5.0 LDL 3.0 HDL 1.4 TG 1.4
3) Type 2 DM
- On tolbutamide 250 mg tds
59
- Last HbA1c (10.11.07) 5.9%
4) Hypertension
- On atenolol 75 mg om, hydrallazine 50mg tds, amlodipine 10mg om
5) Osteopenia
- Last BMD 22/2/07 NOF-1.6, L2-4 -0.5
- Currently on calcium acetate
6) Hyperuricaemia
- Uric acid 20/2/07 – 590
- Previous 573, 98/06
7) Hypothyroidism
- On thyroxine 50 mg om
Last TFT (27.9.07): L Ft4 14; TSH 1.36
8) OA knees
- Fusion arthroplasty right knee > 15 years ago in TTSH
- S/p Left TKR 18/10/07
9) Nephrotic syndrome with chronic renal failure

-24 UTP 5.5g/day in 03/04 but not biopsied due to increased bleeding time
- Last 24hr UTP 1.392g/day and CCT 16ml/min in 8/06
- 3/06 urine dipstick/ufeme: wbc 8 rbc 5 no casts, protein 2+
- ANA 1/640, dsDNA –ve, c3/4 normal, HbsAg and antiHCV –ve
- Last serum electrophoresis in 3/06: normal, no paraprotein
- Renal biopsy 11/8/06: nodular glomerulosclerosis with mesangial hypercellularity, global and
segmental sclerosis with arterial and arteriolar nephrosclerosis; immunofluorescence microscopy
does not suggest immune complex mediated glomerulonephritis, supported by EM report.
- On recormon 4000u/week and irbesartan 300mg bd
Current admission:
Admitted from clinic 11/12/07
c/o:
1) SOB with easy fatigability
2) Increased polydipsia and polyuria
3) Rigors x few days
No fever reported dysuria and freq
No chest pain
Family volunteered that pt felt unwell x 4 days
Slow drift: Hb 10-> 9.9 -> 8.5 -> 7.3
Admitted for anaemia and septic w/u
O/e:
TP 38
BP 90/60 (manual 108/60)
HR 86
Spo2 95% RA
Alert nontoxic
H: S1S2
L: Clear
A: Soft NT renal punch neg
60
DRE: No malena/bld on PR
Jts: Left forefoot still swollen since 30/10/07
Left knee slight swelling, left ankle increased warmth

Other jts: Quiet
Labs:
FBC: WBC 6.2 Hb 6.3 PLT 232 Retics 4.8%
CRP 30.3 ESR 91
Renal Panel: Na 139 k 5.3 (Lysed) Cr 390 Urea 25.3
Alb 23 LFT normal
CKMB/CK/Trop 1 normal
Fe 22 Fe sat 67% H Ferritin 512 Transferrin 1.3 L
Vit B12 Folate normal
TFT normal
Random Cortisol Normal response 241
Ufeme
Urine c/s
Bld c/s
Issues:
1) Anemia for investigation: Post op vs GIT loss
Hb 6.3 MCV 99 (mild macrocytosis since May 07)
Fe sat 67% H transferring 1.3 Ferritin 512
Folate/vit B12 normal
2 pints PCT
Post transfusion FBC: Hb (12/12)
2) Fever for investigation? Flare vs UTI

Cultured and covered with IV rocephin 1g om since 11.12.07
Tw 6.2 Poly 61.9 CRP 22 -> 30.3 ESR 102 -> 91
UFEME (12.12.07) wbc >225 rbc 91 EC 5. (CXR unremarkable)
Urine culture/blood culture pending
3) ARU with UTI (secondary to constipation/poor mobility)

CIC RU 300mls
IDC since 12/12/07
4) Recent TKR with residual effusion of left knee

KIV ortho referral for RV
5) Left foot swelling? RA flare vs crystal arthropathy

KIV us effusion too small for aspiration
PNL dose 7.5mg om maintained
6) AoCRF likely secondary to dehydration
Cr 390 ur 25.3 (baseline Cr 233 -250)
Fluid hydration
Renal panel 12/12/07
61
Medicine (Rheumatology) = Clerking of Rheumatoid arthritis
Name/age/race/gender/occupation
Past medical history
Drug allergy
Date of admission
Presenting complaint » RA
1. Duration of disease
2. First presentation: initial clinical picture
- Joint pain and swelling: which joints involved
Acute/sudden onset
Character of pain (increase with rest, decrease with movement)
- Joint stiffness (morning stiffness > 1 hour)
- Constitutional symptoms: LOA, LOW, fatigue, fever, anaemia
- Initial investigations: x-rays, rheumatoid factors
- Initial treatment
3. Articular involvement
- How has the disease progressed?
- What joints are affected currently?
- Current symptoms: joint pain and swelling
Present everyday or occur in attacks
Frequency of exacerbations and management
Joint stiffness
- Medications: NSAIDs (renal involvement; BGIT)
DMARDS
Anti-cytokine therapy (TB reactivation, increased susceptibility to infection)
 Any recent changes
 Compliance
 Effectiveness
 Side-effects
- Physiotherapy/occupational therapy= any splints
- Surgeries: tendon transfers
Joint stabilization/replacement
- Deformities and disabilities: ADL
Work
Social recreation
Housework
Home modifications
4. Constitutional symptoms: LOA, LOW, fever, fatigue, anaemia, rash
5. Extra-articular involvement
- Eyes: episcleritis (red eyes)
Dry eyes
- Dry mouth
- Cervical spondylosis: neck pain/stiffness, radicular pain and weakness
Cervical myelopathy: bladder/ bowel involvement
Gait disturbances
LL numbness/ weakness
- Lungs: recent lung function test
Pleuritic chest pain, SOB
- Skin: vasculitic rash
Raynaud’s phenomenon
6. Associated with other AI disorders

- IDDM
- Vitiligo
- Thyroid abnormalities
- Pernicious anaemia
- Addison’s disease
62
Medicine (Rheumatology) = Scleroderma Long Case
Chronic disorder characterized by diffuse skin and internal organ fibrosis

Women: men 3:1, symptoms usually appear between 20-40
3 forms:
1. Systemic sclerosis
2. Limited cutaneous scleroderma
3. Diffuse cutaneous scleroderma
CREST syndrome (limited form) – better prognosis
 Calcinosis → sub-cutaneous tissue
 Raynaud’s phenomenon
 Esophageal immobility
 Sclerodactyly
 Telangiectasia
History
Skin Other organs

 Raynaud’s (90%)  Polyarthralgia
 Edema  Proximal myopathy
 Thickened stretched skin  Fever
 Cutaneous ulcers  Dysphagia
 Pigmentation, depigmentation (vitiligo)  Lungs
o SOB (due to anemia)
Dx criteria – 1 major or 2 or more minor  Cardiac
 Major: scleroderma affecting MCP and MTP o Chest pain – pericarditis
 Minor: Sclerodactyly, digital tip pitting or loss of o RHF – edema
subst of digital finger pads, bibasal pulmonary  GI
fibrosis o Malabsorption
 Renal
o Decrease urine – CRF
o Frothy urine – proteinuria
Initial presentation
Investigations done – biopsy etc.
Treatment and Cx treatment
Cx disease
Physical Exam
General Cachexia
Bird like facies
Hands Raynaud’s
Oatcinosis, ulcers
Telangiectasia
Arthropathy
Contractures
Arms/Skin Thick tethered skin
Pigmentation
Vitiligo
Proximal myopathy
Head Alopecia
Eyes
 Anemia (chronic dz, folate and B12 def, Fe def from chronic esophagitis,
microangiopathic hemolytic anemia)
 Sjogren’s
Mouth
63
 Microstomia: open <3cm max
Chest Roman breastplate tight skin
Pericardial rub
Pulmonary HTN
Lungs Fibrosis
Effusion
Chest infections
Alveolar cell carcinoma
Other joints Arthropathy
Flexion deformities
Other BP, urine dipstick for proteinuria
Investigations
 To confirm diagnosis
 To look for complications
Bloods FBC Anaemia

U/E/Cr Renal failure
ANA Nearly always +ve
Anti-centromere Ab
Urine Dipstick Proteinuria
Urinalysis
Radio CXR Effusion, fibrosis, CA
2D echo RHF
Management
 Supportive, symptomatic
Pt education
Scleroderma itself Cytotoxics
 Early stages: cyclophosphamide, MTX
 Late stage: penicillamine
Raynaud’s Vasodilators – CA++ blockers, aspirin
Oesophageal symptoms Antacids
PPIs
HTN Antihypertensives
Steroids have NO role in scleroderma
64
Look and proceed
1. FACE
 Avian-like facies with pinched nose
 Skin = tight
Puckering around the mouth (perioral tethering)
Telangiectasia
 Mouth = Microstomia (can 3 fingers pass through?)
2. HANDS
 Sclerodactyly (double-pinch test)
 Vitiligo
 Finger pulp atrophy
 Digital resorption
 Nails = breaking (pseudo clubbing)
Atrophic
 Raynaud’s phenomenon with vasculitic ulcer
 Telangiectasia
3. ELBOWS
 Subcutaneous Calcinosis
4. PROXIMAL MYOPATHY
5. LUNGS
 Bibasal pulmonary fibrosis → pulmonary HPT → cor pulmonale
6. REQUEST
(1) BP
(2) Assess function of hands
(3) Dysphagia
Raynaud’s phenomenon
Dry eyes & mouth
Diagnosis
1. Systemic sclerosis
2. Limited cutaneous scleroderma (extremities + face)
3. Diffuse cutaneous scleroderma (extremities + face + trunk)
4. Overlap syndrome (PMS, DMS, SLE)
If patient is Cushingnoid = overlap syndrome FX with steroids

Steroids in TCM taken for arthralgia
Steroids for ILD, MAHA
65
Medicine (Rheumatology) = Gout
Introduction
 Mono/oligo-articular crystal arthropathy resulting from a disorder in purine metabolism leading to
hyperuricemia and urate crystal formation.
 Epidemiology: usually presents at 30-60 years old
Males affected more than females (9:1)
Affected females usually post-menopausal
 Pathophysiology
 Urate crystals deposited in minute clumps in connective tissues and remain inert for years
 Release of crystals into joints due to trauma or local injury and causing a flare (acute arthritis)
 Due to phagocytosis of urate crystals by WBCs, hence release of inflammatory mediators.
 Clinical manifestations
 Asymptomatic hyperuricemia (technically not gout)
 Acute gouty arthritis
 Chronic tophaceous gout
 Urate urolithiasis
 Urate nephropathy
Gout Pseudogout
Males > 30 years old Females > 60 years old
Smaller joints affected Larger joints affected
Acute severe pain Gradual moderate pain
Gouty tophi Chondrocalcinosis
Hyperuricaemia Normal levels or uric acid
Monosodium urate crystals = needle shaped - Calcium pyrophosphate dehydrate crystals
ve birefringent crystals = rhomboid-shaped weakly +ve direfringent
crystals (apple green)
Age, DM, acromegaly, haemochromatosis,
hypothyroidism, hyperparathyroidism
Natural History
3 classes of stages
(a) Acute gouty arthritis
 Intense inflammatory response (clinically identical to septic arthritis)
 Asymmetrical mono/oligo-articular involvement
 Pain, swelling, increased warmth, erythema, decreased ROM
 Lasts for around 1-2 weeks
 Commonly affects = 1st metatarsophalangeal joint (podagra)
Ankle and knee joints
Finger joints
Olecranon bursa
 Precipitating factors = trauma
Dietary indulgence (meat, fish, alcohol, legumes, tofu)
Starvation
Drugs (diuretics, aspirin, allopurinol)
(b) Interval gout
 Asymptomatic period upon resolution of acute attack lasting for a variable duration.
 Polyarticular flares = sequential (migratory) or cluster of adjacent joints
 Peri-articular involvement = tendons, bursae
 Bony erosions and deformities
66
(c) Chronic tophaceous gout
 After recurrent attacks of acute gout (~75% affected over 20 years)
 Clinical features
- Polyarticular = stiffness, chronic pain, deformity
- Gouty tophi =pinna of ear, olecranon bursa, prepatellar bursa, Archilles
Tendon, MTP of big toe can ulcerate and discharge chalky
Material
- Renal involvement = urate urolithiasis
Nephropathy
Aetiology
Primary Hyperuricaemia (95%) Secondary Hyperuricaemia (5%)

⬆ production of ⬇ excretion of uric ⬆ turnover of purine ⬇ renal clearance
purine acid of uric acid
 Idiopathic  Idiopathic  Malignancies  Renal disease
 Genetic enzyme - myeloproliferative  Drugs
defects disease - aspirin
- Lesch-Nyhan - lymphoproliferative - diuretics
syndrome (X- disease (frusemide,
linked  Chronic haemolytic thiazides)
recessive) anaemia
 Cytotoxic
- methotrexate
- cyclosporine A
67
Medicine (Rheumatology) = Gout History taking
Name/age/ethnicity/gender/occupation
Date of admission
Presenting complaint
Acute painful and swollen joints
- pain, warmth, erythema
- swelling
- disability
- neurological symptoms
- constitutional symptoms= fever, chills, rigors, malaise, LOA
Etiology
- vascular= use of long term steroids
- infective= history of recent joint inoculation (septic arthritis)
History of recent URTI/GE, arthritis and conjunctivitis (reactive arthritis)
History of dysuria, urethral discharge, sexual history (gonococcal infection)
- trauma (haemarthrosis)
- autoimmune = rashes and other joint involvement (RA,SLE)
- metabolic= history of gout and gouty tophi (gout)
Usual triggers+ trigger for current episode
- inflammatory= history of chronic bloody diarrhea (IBD)
- neoplasia
History of presenting complaint

- duration of gout
- presenting complaint then do investigation and management
- follow-up with whom
- usual joints involved
- frequency of attacks= precipitants, usual treatment, duration, asymptomatic between
attacks
- Management= dietary changes
Medications
Compliance
- Current symptoms= chronic pain and swelling
Stiffness
Instability
Deformity
Disability (affect patient’s life= ADL, social interaction and recreation)
Primary or secondary gout

- Haematological malignancy= pallor, chest pain, SOB, palpitations, giddiness, fatigue, easy
bruising epitaxis, gum bleeding, menorrhagia, haematuria, susceptibility to infections, LOA,
LOW, night sweats, fever, swellings
- Chronic haemolytic anaemia= history of thalassaemia
- History of renal failure
- Drug history= aspirin, diuretics, cytotoxics
Complications
- Joint deformities
- Loss of function
68
- Urate urolithiasis= loin to groin pain, renal colic, dysuria, haematuria, FUN, obstructive
symptoms, history of stones
- Urate nephropathy= decreased urine output, history of renal impairment

- Associated metabolic conditions= HPT, DM, HCL, IHD
Drug history
- Drug allergy
Social history
Family history
- Gout, DM, HPT, HCL, IHD
Differentials
- Septic arthritis (cellulitis, septic bursitis)
- Pseudo-gout (if elderly female)
- Haemarthrosis
- Rheumatoid arthritis (if oligoarticular involvement)
Investigations
Bloods
- FBC= increase WBC (infection, inflammation)
Highly increase WBC and blasts (haematological malignancy)
- PBF
- U/E/CR=renal function
- ESR, CRP
- Serum uric acid level= hyperuricemia
- Blood cultures (if septic)
- Associated metabolic conditions= fasting lipid panel, fasting glucose, HbA1c, ECG
Joint aspirate (diagnostic and therapeutic)
- Clinical chemistry= WBC count
- Gram-staining and microscopy
- Culture and sensitivity
- Polarized light microscopy
X-ray
- Acute gout= soft tissue swelling
- Chronic gout= punched out erosions adjacent to tophi
Interosseous tophi
Secondary OA changes
69
Management
Acute management
1. Colchicine
- Most efficacious if given within first 24 hours
- MOA= inhibits urate phagocytosis by WBC
- Side effects= diarrhea, nausea, vomiting, bone marrow suppression, renal impairment
- Dosing regimen= 1 g stat, 0.5g 2 hourly until a maximum of 4g or pain subsides.
2. Analgesic
- NSAIDS: give indomethacin (DO NOT GIVE ASPIRIN)
- Corticosteroids (oral/ IM/ intra-articular)
3. Joint aspiration
4. Joint immobilization
- Jones bandage
5. Rest in bed or at least 1 day after pain subsides
Chronic management (aim= serum urate <5 mg/dL)
1. Lifestyle modifications ( refer dietician)
- Weight loss
- Low purine diet: avoid beans, meats, seafood, legumes
- Avoid alcohol
2. Review medications
- Cytotoxics
- Aspirin
- Diuretics (frusemide, thiazides)
3. Medications ( should be covered with NSAIDs or colchicines)
(a) Allopurinol
- Indications: frequent major attacks ( >5x/year)
Radiological evidence of bony erosions (end-stage disease)
Urate urolithiasis
- MOA= competitive xanthine oxidase inhibitor
- Side effects: rash (5-10% risk of SJS esp within the 1st month), bone marrow suppression,
renal impairment
- Never start within 1 month of acute flare (to be avoided during acute attacks because might
exacerbate the flare)
- Can be used in patients with abnormal renal function
(b) Uricosuric agents (probenecid, sulfinpyrazole)
- S/E = gastrointestinal irritation (nausea, vomiting)
Aplastic anaemia
Nephritic syndrome
- can only be used if renal function normal → must encourage fluid intake (ensure urine
output > 2L/day)
(c) rasburicase
- MOA = urate oxidase enzyme that promotes conversion of uric acid into allantoin (inactive
metabolite and 10x more water-soluble)
- Does not occur in humans
- Indications = prevention and treatment of tumor lysis syndrome in patients receiving
chemotherapy for leukemia and lymphoma
- Very expensive!
4. Surgical intervention
- Indications = infection, deformity, pain, ulcerating tophi
70
Medicine (Rheumatology) = Chronic tophaceous gout (short case)
(Confirm findings) This patient has chronic tophaceous gout with asymmetrical joint involvement. I
say this because there are multiple gouty tophi seen over the extensor surfaces of both hands
involving the MCPJ, PIPJ and DIPJ. These tophi vary in sizes = smallest being __cm and the largest __cm.
they are firm, immobile and non-tender. Some tophi have ulcerated and are extruding a chalky-white
substance onto the skin surface. There are no gouty tophi seen over the olecranon bursae.
(Disease activity) The disease is likely to be quiescent as the joints are non-tender. In addition, there is
no joint swelling, erythema or increased warmth.
Functionally, there is deforming arthropathy with asymmetrical joint involvement resulting in limited
ROM in the finger and wrist joints. However, he/she is still able to hold a cup, write and unbutton.
(Aetiology) I looked for but there were no xanthelasma seen on the face. In addition, the patient does
not appear uraemic as he/she does not appear sallow nor are there bruises or scratch marks on the
arms. There is also no arteriovenous fistula noted.
Request
(a) presence of gouty tophi = olecranon bursae, pinna of ear, prepatellar bursae, archilles tendon
(b) feet, ankle and knee for similar changes
(c) haematological malignancy = hepatosplenomegaly, generalized lymphadenopathy
(d) signs of alcoholism = duputyren’s contracture, parotidomegaly
(e) vitals = temperature, HPT
(f) urine dipstick = glycosuria (DM)
Differentials
1. Tendon xanthomata
- yellow (not chalky)
- stuck to tendons (not joints)
- bursa not involved
- no active arthritis
2. Rheumatoid arthritis
71
Diabetes
Medicine (Diabetes) = History taking
Date of admission
- Uncontrolled DM
- Hypoglycemia
- DKA/HHS
- Unrelated problem

1. Initial diagnosis of DM
- Age of diagnosis
- Type 1/2 DM
- Presenting complaint = polyuria, polydipsia, polyphagia, LOW, fatigue
- Investigations = random BSL, 2 hr OGTT
2. Current management
- Follow up with whom? How often? Compliance?
- Lifestyle modification
(a) Diet = dietary restrictions, compliance, meals at home/outside, how many meals and snacks
(b) Exercise = frequency, intensity, type of exercise, compliance
- Medications
(a) OHGA = started immediately after diagnosis? Type and dosage, compliance, any recent changes
(b) Insulin = started when, indications for starting, type and dosage, injection site + rotation, who fills it,
who injects it (important if patient has retinopathy), compliance, recent changes
(c) Monitoring = home glucose monitoring + how often, whether it is recorded down, average reading,
do you know what to do when it is too high/low
3. Current control
- Recent HbA1C
- Symptoms of hyperglycemia
- Acute complications
(a) Hypoglycaemia = extreme hunger, giddiness, diaphoresis, tremors, palpitations, fits
(b) DKA/HHS = abdominal pain and vomiting, managed in GW/HD/ICU
4. Screening for complications
- Retinopathy = history of cataracts/eye problems/laser treatment, BOV, annual diabetic retinopathy
screening/ophthalmologist follow up
- Nephropathy = management of renal impairment, annual screening (24 hour UTP/CCT), frothy urine,
lower limb oedema, polyuria/oligouria
- Neuropathy = numbness/ parasthesiae, weakness, postural giddiness, nocturnal diarrhea, gastroparesis
(early satiety, nausea and vomiting), dysphagia, urinary retention i.e. overflow incontinence/UTI,
impotence
- IHD/AMI = history of IHD/AMI, chest pain, SOB, diaphoresis, nausea/vomiting, giddiness
- CVA = history of CVA
- PVD = history of abscess, ulcers, gangrene, amputations, cellulitis, poor wound healing, vascular
claudication, foot care education, annual foot screening at OPD
72
- HPT, HCL, CRF, IHD/AMI, CVA, cancer, gestational DM
- Previous hospitalization
- Previous surgeries
Drug history
- Drug allergies
- Current medications
Social history
- Smoking
- Alcohol
- Family set up
- Main caregiver
- Type of housing
- Lift landing
- Finances
- Functional status
Family history
73
Medicine (Diabetes) = Dietary advice
Fats= Saturated fats < 10% DCI
Saturated fats not equal to 1/3 total fat
Change to olive/canola oil
Avoid fried and oily food
Sugars= Avoid simple sugars e.g. cakes, pastries, soft drinks, biscuits
Digest very quickly, therefore, rapid rise in blood sugar
Rice eat < ½ bowl
Bread < 2 pieces
Salt= Cut down especially in hypertensive patients
- Reduce use of sauces
- Eat more soupy stuff (gravy contains salt)
- Reduce junk food and preserved and canned food
- Use natural spices instead e.g. pepper
Protein= 15 to 20% DCI

Reduce if nephropathy present
Eat more white meat e.g. fish, chicken instead of red meat e.g. beef, pork etc.
Vegetables= Eat 2 servings per meal
Boil and don’t stir fry
Fruits= Eat 2 servings per meal
Avoid drinking fruit juice because it does not contain fibre to delay glucose absorption (eat it
whole instead)
Don’t eat too much because it increase blood sugar levels
Carbohydrates= Eat complex carbohydrates e.g. oat, bran, brown bread, cereal because it takes longer
to digest and is higher in fibre
50-60% DCI
Don’t eat too much rice and noodles
Avoid refined carbohydrates
Key is to eat small but frequent meals (5-6x/day)
74
Medicine (Diabetes) = Counseling a newly diagnosed diabetic
Facts of DM:
- 9% of adult Singaporeans have DM
- 2 types: Type 1 (IDDM), Type 2 (NIDDM)
- Risk factors:
o Age>40
o Family history of DM
o Obesity
o Race
o Gestational DM
o History of HPT, IHD, polycystic ovary syndrome
o IGT
Pathogenesis
- Explain action of pancreas = secretes insulin that allows peripheral uptake of glucose
- Insulin=Hormone
- In a patient with DM: insufficient insulin or insulin resistance
- Therefore increased glucose left in blood= DM
- Chronic complications: Microvascular and macrovascular
i) Microvascular: retinopathy, nephropathy, neuropathy
ii) Macrovascular: IHD, CVD, PVD
- DM doesn’t kill but its complications do
Weight loss
- Decreases insulin resistance
- Measure patient’s height and weight and calculate BMI (Ideal<23)
- Advise on ideal weight
Diet
- Decrease blood sugar level and other risk factors (HPT, HCL)
- Explain food pyramid
Exercise
- Decreases insulin resistance
- At least 5x/week, 30 mins each time
- Should break out into light sweat
Medications
- Ask patient what types of medications they are on and when they take it
- Explore compliance
- If on insulin, demonstrate technique, get them to show you
Others
- Explain importance of annual screening
- Ask patient if there are any questions
75
Medicine (Diabetes) = Diabetes Manifestations
1. Urogenital manifestations of DM
 Kidneys :
- Nephrotic syndrome
- Renal failure
- Glomerulosclerosis (Kimmelstein-Wilson lesion)
- Chronic pyelonephritis
- Emphysematous pyelonephritis
- Renal papillary necrosis
- Type 4 RTA
- Contrast nephropathy
 Renal Vasculature = Renal Artery Stenosis

 Bladder:
- Neurogenic Bladder
- UTI
 Genital
- Vaginal candidiasis
- Impotence
- Retrograde ejaculation
2. Skin Manifestations of DM
a) Suggestive of DM
- Acanthosis Nigricans
- Vitiligo
- Hyperpigmentation over neck, cheek, back of hands (Addison’s Disease)
- Thick greasy skin (Acromegaly)
- Papery thin skin (Cushing’s)
- Bronzed skin (Haemochromatosis)
b) Exclusive to DM
- Granuloma annulare
- Dermopathy
- Necrobiosis Lipodica Diabeticorum
- Scleroderma Diabeticorum (Thickening and hardening of skin)
c) Complications of Disease
- Xanthelasma and eruptive xanthomata
- Carbuncles, folliculitis, gangrene, ulcers, cellulitis, necrotizing fasciitis
d) Complications of treatment
- Lipodystrophy
- Jaundice (Tolbutamide)
76
Medicine (Diabetes) = Diabetes Mellitus
Introduction
 Metabolic disorder characterized by persistent hyperglycaemia due to relative/absolute insulin
deficiency
 a/w long term sequelae resulting from damage to various organs
Epidemiology
 Prevalence (Singapore) = 8.2% (2004 NHS), 8th most common cause of death
- Prevalence increases sharply with age
 18-29 years: 0.5%
 40-49 years: 7.9%
 60-69 years: 28.7%
- Gender: Males (8.9%) > Females (7.6%)
- Ethnicity: Indians (15.3%) > Malays (11.0%) > Chinese (7.1%)
 A/w considerable mortality and morbidity from chronic complications
- 3-fold increase in mortality mostly due to cardiovascular disease
Classification
 Primary Diabetes
- Type 1 DM (IDDM): absolute insulin deficiency resulting from destruction of beta cells
 Type 1A: Immune mediated
 Type 1B: Idiopathic, not a/w AI disorders, more common locally
 Associated AI disorders: Graves’ Disease, Hashimoto’s thyroiditis, Addison’s disease, myasthenia
gravis, celiac disease, vitiligo, pernicious anaemia
- Type 2 DM (NIDDM): disorder of insulin secretion and action (relative insulin deficiency)
 May range from predominantly insulin resistance with relative insulin deficiency to
predominantly secretory defect with insulin resistance
 Preceded by a period of abnormal glucose homeostasis (IFG/IGT)
 Secondary Diabetes: Disease causing pancreatic islet cell damage
- Genetic defects: maturity onset diabetes of the young
- Genetic syndromes: DIDMOAD, Down, Turner’s, Klinefelter syndrome
- Exocrine pancreatic defects: Chronic pancreatitis, Ca pancreas, CF, haemochromatosis
- Endocrinopathies: Cushing’s syndrome, acromegaly, hyperthyroidism, PCOS, phaechromocytoma,
glucagonoma
- Drugs: glucocorticoids, thyroxine, diuretics, phenytoin, alpha-interferon
 Gestational Diabetes )GDM): insulin resistance related to metabolic changes in pregnancy, increased
insulin requirements leading to impaired glucose tolerance
Pathogenesis
 Type 1 DM
- Absolute insulin deficiency resulting from autoimmune destruction of islet beta cells
- Commonly develops in childhood, manifests at puberty and progresses with age. But can occur at any
age (even in 8th, 9th decade of life)
- AI markers: Islet cell Ab; glutamic acid decarboxylase Ab, insulin Ab,
Phases
(a) Prediabetes = autoAb as markers
(b) - honeymoon phase = spontaneous decrease in insulin requirement after starting treatment, may
last 3 to 6 months, exogenous insulin abates inflammatory process and allows remaining beta cells to
function
- Relapse phase = progressive increase in insulin requirements
- Permanent phase = complete destruction of beta cells
 Type 2 DM
- Most common form of DM
77
- Multi-factorial: genetic, environmental
 no evidence of AI defects
- Associated with metabolic X syndrome = obesity, hypertension, dyslipidaemia and DM
- 2 main metabolic defects = insulin resistance + beta cell dysfunction
Comparing type 1 vs type 2 DM
Type 1 DM Type 2 DM
Aetiology Absolute insulin deficiency 1. Insulin resistance
- Genetics: - Genetics
 HLA-genes  no HLA-linkage
 Twins = 30-70%  Twins = 60-80%
concordance concordance
- AI destruction - Environment: obesity
- Viral infection? 2. Beta cell dysfunction
Age of onset Juvenile (<20 years) Adult-onset (>40 years)
Weight Normal/LOW Obese
Lab results
- Plasma insulin Absent/Low High/Normal
-Plasma glucagon High (due to low/no Low
insulin)
-Anti-islet cell antibodies Yes No
Islet cell morphology Insulitis No insulitis
Marked atrophy and Focal atrophy and amyloid
fibrosis deposition
Complications Diabetic ketoacidosis Hyperglycaemic
Hypoglycaemia Hyperosmolar State
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Medicine (Diabetes) = Hypoglycemia
Definition:
1) Low blood sugar levels: < 3.0 mmol/L (venous blood)
2) Classical symptoms
3) Relieved upon correction of low blood glucose
Causes
Healthy patients Ill-looking patients
Medications/Drugs Sepsis; Shock
- Alcohol
- Salicylates
- Non-selective B-blockers=
attenuate adrenergic response
to stress
- Overdose with insulin/OHGAs
esp. long-acting sulphonylureas
Intense exercise: Unexpected/unusual Infection: Malaria, esp. with
quinine/quinidine (dose-dependent
increase in insulin secretion)
Insulinoma (MEN-1 associated) Starvation: Anorexia Nervosa
Missed/Delayed/Inadequate meals Liver failure
Gastroparesis Heart failure
Renal failure (impaired
gluconeogenesis and impaired
clearance of DM medications)
Endocrine: HPA-axis insufficiency
(in cortisol and GH insufficiency),
Insulin antibodies
Non-islet cell tumour: sarcoma,
mesothelioma
Congenital liver problems: Defects in
carbohydrate, amino acid, fatty acid
metabolism
Pathogenesis
- Brain requires constant supply of glucose to maintain function: uses alternative fuel (ketones)
- When hypothalamus senses the hypoglycaemia
1. Sympathetic nervous system activated @ ~3.0 mmol/L  Adrenaline  Autonomic S/S
2. Release of catabolic hormones: Glucagon, adrenaline released
Clinical features
- Wide spectrum of neurological manifestations
Neurogenic/ Autonomic activation - Sweating
(BSL=2.8-3.0 mmol/L) - Trembling
- Tachycardia
- Pallor
- Hunger
- Anxiety
Neuroglycopenia (BSL <2.5-2.8 Behavioural disturbances
mmol/L) - Irritable
- Aggression
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- Confused/AMS
- In coordination
- Seizures
- Focal neuro deficits
- Speech difficulty
Drowsy ( GCS)
Non-specific - Nausea
- Headache
- Tiredness
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Medicine (Diabetes) = Diagnosis of DM
Asymptomatic AND Random plasma glucose>11.1mmol/L Symptomatic AND RPG>11.1
OR Fasting plasma glucose>7.0 mmol/L mmol/L OR FPG>7.0mmol/L
Acute metabolic
decompensation
No Yes
Repeat
FPG
DM
FPG>7.0m
mol/L
No Yes
FPG
6.1-
<6.0mmol
6.9mmol/
/L >11.1
L
Normal FG OGTT
7.8-11.0
2hr post Impaired glucose tolerance

challenge
glucose
<7.8
Impaired Fasting Glycemia
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Impaired Glucose Tolerance
 12% prevalence in ages 18-69 (NHS 2004)
 High risk of developing DM
- Develop complications before onset of DM
 Metformin may help to retard progression
Screening of asymptomatic individual for DM

 Opportunity screening>40 yrs old (earlier if risk factors present)
 If normal: screen every 3 years
 IFG/IGT: Screen yearly
 Risk factors
 Metabolic syndrome=HPT, HCL, Overweight/obese
 Ischaemic Heart Disease
 PCOS
 First degree relative with DM
 Previous GDM
 Previous IFG/IGT
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Renal Medicine
Medicine (Renal) = Nephrotic Syndrome History Taking
Name/Age/Race/Gender/Occupation
Past Medical History
Date of admission
Presenting Complaint
1. Lower limb oedema
 When did it start?
 Bilateral/unilateral?
 Getting progressively worse?
 Worse in the evening? Better in the morning?
2. Associated with
 Abdominal distension? Can clothes still fit?
 Increase in weight?
 SOB? Exertional dyspnoea/Orthopnea/Paroxysmal nocturnal dyspnoea?
 Periorbital/Facial oedema? (esp so in the morning)
3. Aetiology
 Renal
o Frothy urine, oliguria, concentrated urine (signs of proteinuria)
o Haematuria (Nephritic syndrome)
o Fever, URTI symptoms (trigger, post infectious glomerulonephritis)
o Diarrhoea (IgA nephropathy)
o History of Hepatitis B/C infection
o Recent drug intake
o Joint pain, rashes (autoimmune)
o Polyuria, polydipsia, polyphagia, LOW (DM)
 CVS
o Chest pain, SOB, palpitations, giddiness/syncope, diaphoresis, nausea/vomiting
 GIT
o LOA, LOW, lethargy, jaundice, pruritus, easy bruisability (chronic liver disease)
o Mucoid/bloody stools, alternating constipation and diarrhoea (inflammatory bowel disease)
4. Complications
 Spontaneous bacterial peritonitis (fever, abdominal pain)
 Hypovolemia (abdominal pain, vomiting, dizziness)
5. Management prior and during admission

6. Is this the first time that this happened? Describe prior episodes.

1. When was nephrotic syndrome diagnosed?
 Presenting complaint
 Investigations done (renal ultrasound, renal biopsy)
 Cause of nephrotic syndrome (if biopsy was done  likely glomerulonephritis)
2. Management
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 Followed up with whom? Frequency of follow up? Compliance to follow up? Investigations done at
every follow up? Annual investigations?
 Medications?
o Steroids, cyclophosphamide, chlorambucil, levamisole, cyclosporine A
o Compliance with medications?
o Side effects: obesity, hypertension, cataracts, osteoporosis, increased susceptibility to infections,
cosmetic changes, gastritis, diabetes
 Fluid and dietary restrictions
o Fluids: as desired
o Diet: no refined sugars, no fat (if patient is on steroids), less protein
 Level of control
o Number of relapses? Number of hospitalisations?
o For each relapse  Presentation? Triggers? Treatment?
o When was the last episode?
 Monitoring
o How often?
o Records in nephrotic diary?
o Do you know what to do when proteinuria is found?
o Indications for admission?
3. Complications
 Hypovolemia (abdominal pain, vomiting, giddiness)
 Acute renal failure
 Thromboembolism
o Was any blood clot found?
o Treatment with heparin/warfarin only if symptomatic or immobile
 Increased susceptibility to infections
 Spontaneous bacterial peritonitis
o History of abdominal pain of fever treatment?
o Pneumococcal vaccinations?
o Prophylactic antibiotics?
 Hyperlipidemia
o On statins?

1. Other medical problems
2. Previous hospitalisations
3. Previous surgeries
Drug History
1. Drug allergies
Social History
1. Smoking
2. Alcohol drinking
3. Family set-up? Main caregiver?
4. Finances
5. Have to miss a lot of work?
Family History
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Medicine (Renal) = Nephrotic Syndrome
*in an oedematous patient  always test for proteinuria and investigate for nephrotic syndrome if
albustick >= 2+
Definition
1. Clinical entity
2. Characterized by classical triad
 Proteinuria (> 3g/1.73m3/day)
 Hypoalbuminemia (<30g/L)
 Oedema
3. Usually associated with hyperlipidemia and lipiduria
4. Hypertension, haematuria and azotemia are rare (characteristic of nephritic syndrome)
Aetiology
1. Primary glomerulonephritis (usually non-proliferative glomerulonephritis)
 Minimal change disease
 Focal segmental glomerulosclerosis
 Membranous glomerulonephritis
 Membranoproliferative glomerulonephritis
2. Secondary glomerulonephritis
 Vascular (Henoch-Schönlein Purpura)
 Infective (hepatitis B/C, malaria, HIV, post streptococcal)
 Drugs (captopril, TCM, NSAIDS, gold, penicillamine)
 Autoimmune (SLE)
 Metabolic (diabetes)
 Infiltrative (Amyloidosis)
 Neoplasia (multiple myeloma, lymphoma)
Causes
1. Children
 Minimal change disease (80%)
2. Adults
 Minimal change disease (30%)
 Focal global sclerosis (21%)
 Mesangial proliferative glomerulonephritis (25%)
 Membranous glomerulonephritis (12%)
 Focal segmental glomerulosclerosis
Pathogenesis
1. Derangement in glomerular capillary walls  proteinuria  hypoalbuminemia
2. Loss of oncotic pressure  generalised oedema
3. Drop in plasma volume  diminished glomerular filtration rate  compensatory rise in aldosterone 
promotes retention of salt and water by kidneys  further aggravates oedema
Clinical signs
1. Oedema (periorbital, facial, lower limb, genitalia, sacral)
2. Pleural effusion
3. Ascites
4. Xanthelasma
5. Leuchonychia
6. JVP and BP
85
Complications
1. Hypovolemia
 Presents with abdominal pain, vomiting and giddiness
 Pathogenesis: third space loss results in insufficient blood volume in vessels to maintain adequate
blood pressure leads to peripheral vasoconstriction and urinary Na+ retention
 Indicators: decreased urinary Na+, increased hematocrit/urea/creatinine
 Management: IV 20% albumin
2. Acute renal failure (as a result of hypovolemia)

3. Thromboembolism
 Occurs in 10-40% of patients
 Pathogenesis
o Urinary loss of anti-thrombin III
o Increased synthesis of clotting factors and fibrinogen
o Increased hematocrit and hence increased viscosity
 Presents as deep vein thrombosis, pulmonary embolism, renal vein thrombosis, saggital sinus
thrombosis
 Management: prophylactic warfarin/heparin if patient is immobile
Renal Vein Thrombosis

 More common in membranous glomerulonephritis than other forms (6-8%)
 Clinical features (usually asymptomatic): loin pain, hematuria, proteinuria, bllotable kidneys,
renal impairment
 35% have concomitant pulmonary embolism
 Diagnosed by Doppler ultrasound, renal angiography, spiral CT, MRI
 Treatment by anticoagulants with warfarin for 3-6months
4. Increased susceptibility to infections

 Pathogenesis
o Urinary loss of immunoglobulins
o T cell abnormalities
o Use of immunosuppresants
 Presents as peritonitis (causative agent is Streptococcus pneumonia), urinary tract infection,
septicaemia
 Management
o Pneumococcal vaccination
o Prophylactic penicillin
5. Hyperlipidemia
 Pathogenesis
o Lipoprotein synthesis triggered by hypoalbuminemia
o Abnormal transport of circulating lipid particles
o Impaired breakdown of lipoproteins
 Usually improves with resolution of nephrotic syndrome
 Increases the risk of ischemic heart disease and arthrosclerosis
 Management
o Statins (if prolonged)
6. Negative nitrogen balance

 Pathogenesis
o Proteinuria
86
o LOA
Investigations
1. Confirm diagnosis of nephrotic syndrome
 Urine dipstick
o Proteinuria
o Haematuria
o Glycosuria
 UFEME and urine cultures to rule out urinary tract infection as a cause of proteinuria
 Liver function test to check for hypoalbuminemia
 Fasting lipid panel to check for hyperlipidemia
2. Rule out other causes

 ECG, cardiac enzymes, beta natriuretic peptide, Chest X-ray to rule out congestive cardiac failure
 Urea/Electrolytes/Creatinine to rule out renal impairment and test for severity of hypovolemia
(increased urea and creatinine)
 Liver function test to rule out deranged liver function
3. Aetiology
 Full blood count
o Anaemia, lymphopenia, thrombocytopenia  SLE
o Increased hematocrit  Severe hypovolemia
 Erythrocyte sedimentation rate, C-reactive protein  Underlying inflammatory condition
 Anti-nuclear antibody (ANA), anti-dsDNA, C3, C4  SLE
 Anti Neutrophil Cytoplasmic Antibody (ANCA), anti-glomerular basement membrane (anti-GBM) 
vasculitis
 Fasting glucose, HbA1c  Diabetes
 Hepatitis B/C serology: if Hepatitis B/C is the cause of nephrotic syndrome, there is a need to know
before starting steroids in view of decompensation
 Anti-streptolysin O titres  Post-streptococcal glomerulonephritis
 Renal ultrasound: need to know anatomy before doing biopsy
 Renal biopsy
Indications for Renal Biopsy

 Atypical features: gross hematuria, hypertension, renal impairment, persistently low serum
complement, poorly selective proteinuria, proteinuria > 1g/day
 Family history of glomerulonephritis
 Steroid resistance
 Steroid dependantpatient with unacceptable steroid toxicity
Acute management
1. Fluid restriction to < 1L/day
2. Low salt and low protein diet
3. Place on I/O charting
4. Daily weights and albustick
5. Monitor vitals Q4hourly (inform if systolic BP is <100mmHg or Hr >100/min)
6. Symptomatic treatment
 IV Lasix (furosemide) and PO Span K (aim for 1kg loss/day) with/without spironolactone (K+ sparing
diuretic) and IV 20% albumin  symptomatic treatment for hypotension
 PO ACE inhibitors/ Angiotensin II receptor blockers (ARB)  proteinuria
 PO statins  hyperlipidemia
87
 Thromboembolic deterrent (TED) stockings, anticoagulants  prevent thromboembolic event
o Consider ambulatory problems/immobility
o Consider risk factors for deep vein thrombosis (DVT)
o Consider severe proteinuria with low albumin
Chronic management
1. Immunosuppression
2. PO furosemide with Span K and low salt diet only if oedematous
3. Monitoring at home with albustick and educate patient on how to escalate therapy and when to admit
4. Prevention of infections
 Pneumococcal vaccination
 Prophylactic antibiotics
 Prompt treatment of infections
 NO LIVE ATTENUATED VACCINES (especially if on steroids)
Immunosuppresants
Immunosuppressive therapy is used for minimal change disease
1. Corticosteroids
 High dose prednisolone (1mg/kg/day)
 80% remission rate achieved by 16 weeks
 Regime
o High dose prednisolone continued for 1 week after remission is achieved
o Taper dose over 6 months, and subsequently discontinue
o Can give alternate day prednisolone during tapering to minimise side effects
 Complications
o Cosmetic changes: moon-like facies, hirsutism, acne, central obesity, buffalo hump,
supraclavicular fat pads
o Metabolic: obesity, diabetes, hypertension
o Endocrine: menstrual irregularities, Addisonian crisis, osteoporosis
o Musculoskeletal: proximal myopathy, aseptic necrosis
o Posterior subcapsular cataracts
o Gastritis/Peptic ulcer disease (PUD)
o Increased catabolism: thin skin, easy bruising, abdominal striae
o Increased susceptibility to infections especially opportunistic ones
o Steroid psychosis
2. Alkylating agents
 Cyclosporine A, cyclophosphamide
o Indicated in frequently relapsing, steroid dependant nephrotic syndrome (clinically significant
cataracts, difficult hypertension, diabetes, and disabling emotional disorders due to cosmetics
appearance)
3. Mycophenolate mofetil
4. Tacrolimus
88
Medicine (Renal) = Secondary Hypertension
 Indications for screening
o Age of onset <40years old or >55 years old
o Severe or refractory hypertension
o Sudden rise in BP over a previously stable value
 Renal artery stenosis
o Most correctable cause of secondary hypertension
o Presentation
 Patients <30yo with no family history/risk factors
 Patients >55yo presenting with severe hypertension
 Refractory or resistant hypertension (compliant to full dosages of an appropriate 3-drug
regimen including a diuretic)
 Hypertensive emergency
 Acute elevation in plasma Cr after use of ACE-I or ARB
 Unilateral abdominal bruit
o Causes
 Atheroma (elderly male smokers)
 Fibromuscular dysplasia (young females)
o Management
 Balloon angioplasty
 Conn’s syndrome (primary hyperaldosteronism)
o Primary hyperaldosteronism
 Excess pdn of aldosterone independent of RAA system
 Conn’s syndrome (aldosterone-secreting adenoma)
 Primary adrenocortical hyperplasia
 Adrenal carcinoma (rare)
o Secondary hyperaldosteronism
 Decreased renal perfusion (RAS, coarctation of aorta)
 Pregnancy (estrogen-induced increase in rennin)
 Arterial hypovolemia and oedema
o Clinical presentation
 Suspect conn’s syndrome in hypertensive patients with
 Hypokalemia
 Refractory hypertension
 Severe hypertension before 40yo (esp in females)
o Investigations
 U/E/Cr = hypokalemia, hypernatremia
 Plasma rennin and aldosterone = raised aldosterone with low rennin levels
 CT A/P
o Management
 Conn’s syndrome = surgery with pre-op spironolactone
 Hyperplasia = spironolactone/amiloride
 Pheochromocytoma
o Composed of chromaffin cells found in adrenal medulla which synthesize and release
catecholamines
o Rule of 10s
 10% rise in association with several familial syndromes (MEN 2, NF 1, von Hippel-
Lindau syndrome)
 10% are extra-adrenal
 10% are bilateral
 10% are biologically malignant
o Clinical presentation
 Abrupt onset of hypertension  hypertensive emergency
 Symptoms
 Episodic headaches, palpitations, diaphoresis, postural giddiness
 May be precipitated by sneezing, stress and smoking, etc
 Physical examination
89
 May have no signs
 Medullary thyroid cancer
o Investigations
Medicine (Renal) = Dialysis modalities

 Start when serum Cr > 700-800 umol/L
 Deciding between PD and HD
o Check LVEF with 2DE
 >50%  HD
 <50%  PD
o Consider
 Psycho-social and financial issues
 Patient’s ability to comply
 Family set-up and presence of caregiver
 Survival and hospitalization rates for complications are comparable
Peritoneal Dialysis
 Types
o Continuous ambulatory PD (CAPD)
o Automated PD (APD) – fluid exchange performed by machine, usually 3 cycles per night
 Process
o Hypertonic lactate + glucose solution placed into peritoneum via Tenchkoff catheter (inflow
10min; outflow 20min)
o Results in hyper filtration across peritoneal membrane
o Since lactate can diffuse into blood stream  patients tested and classified into high and low
transporters of lactate
 High transporters need to remove dialysis fluid after 3 hrs
 Low transporters need to remove dialysis fluid after 4-5 hrs
o Lactate degradation products can cause sclerosis of peritoneal membrane  compromises
hyper filtration and diffusion
 Advantages
1. Simple, reliable and safe from a cardiovascular point of view (suitable for patients with low EF)
2. Convenient  greater freedom of mobility
3. Pain free
4. Removes large volume of fluids
5. Greater freedom of diet and fluid intake
6. Preserves residual renal function as BP fluctuates less (BP fluctuations during HD causes
repeated renal micro infarcts)
 Disadvantages
1. Patient motivation and treatment compliance required
2. Limited to patients <75kg
3. Body imagine problems  catheter sticking out of abdomen
 Ideal candidates
1. Elderly
2. Diabetics
a. IP insulin
b. Difficult venous access
c. Low EF
3. Stroke patients
a. Mobility problems
4. Paediatric patients
5. IHD patients
a. Low EF
b. Cannot tolerate BP variations
 Contraindications
1. Polycystic kidneys = less intra-peritoneal volume available
90
2. Multiple abdominal surgery = adhesions (anatomical distortions), peritoneal fibrosis (decreased
efficacy)
3. Colostomy/ileostomy
4. Abdominal wall hernias
 Other things to take note
1. EPO injections
2. Vitamin D and calcium supplements
3. Prepare AVF in case Tenchkoff catheter needs to be removed (backup dialysis modality).
Otherwise IJ catheter will be required in event of PD failure.
4. High protein diet = replace protein loss in dialysis
5. Potassium supplements = replace losses in dialysis
 Complications
1. PD peritonitis
 Main complication
 Results in significant morbidity, catheter loss and long-term failure of peritoneal
viability for further PD
 Empirical Rx with cefazolin and gentamicin for 2-3 weeks until culture results
return
 Gram +ve (S aureus and S epidermidis): usually can resume PD once peritonitis
resolves
 Gram =ve (E coli): usually due to fecal contaminants or diverticular disease. Catheter
removed and patient given IV antibioitics
2. Exit site infection
3. Catheter blockade or displacement
4. Protein and potassium losses
5. Abdominal wall hernias
6. Basal atelectasis
7. Pleural effusion
 Peritoneal-pleural fistula = ligation
 Foramen of Morgagni = pleurodesis
8. Hydrocele (patent tunica vaginalis)
9. Hyperglycemia and lactic acidosis (dialysate left too long)
Haemodialysis
 Advantages
o No protein or potassium losses
o Removes large volumes of fluid
o Regular supervision and nursing intervention
o Patient free of burden of caring for self (esp for patients with poor motivation)
 Disadvantages
o Bound to dialysis centre  difficulties travelling abroad
o Heparin use  increased risk of bleeding
o Increased CVS instability
o Requires vascular access  difficult venous access. Blockade, infection, thrombosis.
 AVF: longer lifespan (7-10 yrs). Fewer complications.
 AVG: use of synthetic tubes or saphenous vein. Shorter lifespan (2yrs).
o B2-microglobin Amyloidosis: may cause CTS, arthralgia and bony changes. Better removed via
hemofiltration.
91
Medicine (Renal) = Renal Transplant (Major Risks)
 General risks
o Risk of GA (<1%)
o Risk of death (<1%)
o Pain
o Bleeding (<1%)
o Wound infection (<1%)
o Damage to surrounding structures
 Specific risks
o Early
 Renal vein thrombosis (<5%)
 Ureter anastomotic leak (<5%)
 Acute graft rejection
 Blood-borne infections
o Late
 Immunosuppresants
 Risk of infection (esp 1st 6mths)
 Risk of cancer
 Specific side effects
 Chronic graft rejection & graft failure
 Require HD/PD again
Medicine (Renal) = Adult Polycystic Kidney Disease (APKD)

 Introduction
o Prevalence 1:1000
o Accounts for 6% of adult CRF
o Occurs at birth but manifests in later years (~40yo)
o AD inheritance with nearly 100% penetrance
 PKD 1 located on chr 16 (85%)
 Encodes for polycystin 1 protein  cell-cell and cell-matrix interaction
 PKD 2 located on chr 4 (15%)
 Encodes for polycystin 2 protein  Ca and Na membrane channel proteins
o Bilateral disease (unilateral cases likely multicystic renal dysplasia)
 Differentials for bilateral renal cysts
 Multiple simple cysts
 Infantile polycystic kidney disease
 Tuberous sclerosis (angiomyolipomas)
 Von Hippel-Lindau syndrome
 Renal manifestations
o Grossly enlarged kidneys (ballotable +/- palpable)
o Multiple expanding cysts with little intervening parenchyma
 Filled with clear, turbid or hemorrhagic fluid
 Present in both renal cortex and medulla
 Eventually lose tubular connections and become isolated from glomeruli  require
transepithelial transport of solutes and fluid for further expansion
o Decrease in renal concentrating ability  polyuria
o Altered endocrine function
 Increased rennin secretion (intrarenal ischaemia from distortion of renal architecture)
 HTN
 Increased erythropoietin secretion  better maintained hct in ESRF
o Complications
 UTI (commonest)  pyelonephritis
 Gross intermittent haematuria
 Renal calculi (urinary stasis secondary distortion of collecting system by cysts)
 Cyst rupture/infection
 Hemorrhage into cyst
 Hypertension
92
 Renal failure from UTI, renal calculi and HTN
 Clinical features
o Clinical symptoms
 Gross intermittent haematuria
 Dragging sensation in loins
 Flank pain
 Fluid overload
 Urinary tract infection = dysuria, haematuria, colicky loin-to-groin pain, FUN,
obstruction
 Uremic symptoms = anorexia, nausea, vomiting, fatigue, hematemesis, melena,
abdominal pain, pruritus, bruising, chest pain, SOB, encephalopathy
 Past medical history = SAH, berry aneurysm, MVP
 Family history = APKD, SAH, berry aneurysm, MVP
o Clinical signs
 Signs of ESRF = sallow appearance, conjunctival pallor, scratch marks, easy bruising,
distal brown arc nails, penguinculae, peripheral oedema
 Presence of AVF
 Enlarged ballotable kidneys (+/- transplanted kidneys)
 Abdomen = hepatomegaly, splenomegaly, hernia
 CVS = mitral valve prolapse, AR, TR, MR
 Neurology = surgical 3rd nerve palsy (berry aneurysm), craniotomy scar (previous SAH)
 BP = hypertension
 Urine dipstick = microscopic haematuria
o Associated conditions
 Cysts in liver, spleen, pancreas, lung, ovaries, testes, uterus, thyroid, bladder
 Neurological = intracranial berry aneurysms, SAH
 CVS = mitral valve prolapse, AR, TR, MR
 GIT = colonic diverticular disease with increased risk of perforation, anterior abdominal
wall hernia
 Investigations
o Blood
 FBC = Hb
 U/E/Cr = renal impairment
 Estimated GFR
o Urine
 UFEME
 Urine c/s
o Imaging
 Renal u/s = diagnostic criteria (usu not useful before 20yo)
 <30yo = presence of at least 2 renal cysts in either 1 or both kidneys
 30-59yo = presence of at least 2 renal cysts in each kidney
 >60yo = presence of at least 4 renal cysts in each kidney
 MRI/MRA brain = berry aneurysm
 Management
o Monitor U/E/Cr and BP
o Treat hypertension with ACE inhibitors or ARB
o Screen family members
o Genetic counseling
o Cr > 600  renal replacement therapy (PD, HD, kidney transplant)
o Cr > 800  start dialysis
 Prognosis
o Relatively stable and slow progression
o ESRF by age 50
o Causes of death
 ESRF  uremia
 AMI and CVA (coronary and hypertensive heart disease)
 SAH
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- Bladder neck obstruction
Medicine (Renal) = Urinary Tract Infection / o Urethral strictures, BPH/prostate ca,
Pyelonephritis bladder calculi, bladder tumour, bladder
neck stenosis, Neurogenic bladder,
Definitions posterior urethral valve, constipation, ca
- UTI = pure growth of >105 colony forming cervix/uterus, ca colon, retroperitoneal
units/ml OR 108 CFU/L fistuli
o Urethritis - Reflux uropathy
o Cystitis o Vesico-ureteric reflux (VUR), intra-renal
o Prostatitis reflux
o Pyelonephritis - Instrumentation
- Bacteriuria = presence of bacteria in urine o Urinary catheterization, flexible cystoscopy,
o Asymptomatic (covert)  only requires TURP
further investigation and treatment if - Immunosuppression
occurring in infants, pregnant women or o DM, AIDS, steroids
urinary tract abnormalities
o Symptomatic
Organisms
- Abacterial cystitis/urethral syndrome = UTI
- E. coli (>70%)
symptoms but no Bacteriuria (1/3 of women)
- Enterococcus
- Recurrent UTI = a further infection with a new
- Enterobacter
organism
- Proteus
- Relapse UTI = a further infection with the same
- Klebsiella
organism
- Pseudomonas
Differential Diagnoses
Symptoms
- Acute appendicitis
Cystitis - Frequency
- Diverticulitis
- Urgency
- Cholecystitis
- Nocturia
- Salpingitis
- Dysuria
- Perinephric abscess
- Haematuria
- Suprapubic pain
Typical Patient Profile - Cloudy and foul
- Women = prevalence increases with age smelling urine
- Men = uncommon (usually in 1st year of life or - Obstructive
>60 y/o, a/w BPH) symptoms
o Must always rule out urinary tract Acute Pyelonephritis - Fever a/w chills and
abnormalities - Almost always a/w rigors
lower UTI - Renal colic
Classification (ascending) - Vomiting and
Upper UTI Lower UTI - Haematogenous diarrhoea
- Pyelonephritis - Urethritis route less common - Symptoms of lower
- Cystitis UTI
- Prostatitis - Acute renal failure 
oliguria
Uncomplicated Complicated - Sepsis
- Normal renal tract - Male patients Prostatitis - Flu-like symptoms
- Normal renal function - Abnormal urinary - Lower back ache
- Normal host defenses tract - Enlarged & tender
- Impaired renal prostate
function - Few urinary
- Impaired host symptoms
defenses Signs
- Virulent organisms - Fever
- Signs of dehydration
Risk Factors - Abdominal tenderness/guarding
- Female - Positive renal punch
- Sexual intercourse - Renal mass
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o Hydronephrosis, renal abscess Prostatitis trimethoprim (check G6PD
- Bladder distension status)
- Enlarged and tender prostate - Change as required when urine
o Prostatitis c/s results return
- Usually treat for 28 days
Complications - If severe: IV cephalosporin +
- Perinephric abscess gentamicin
- Pyonephrosis Advice - Drink > 2L water per day
- Necrotizing papillitis in pyelonephritis  ARF - Urinate frequently
- Urosepsis - Double void if reflux present
- Wipe from front to back after
Investigations micturition
Urine - Post-coital voiding
- Urine Leukocytes, nitrites, proteinuria, Prevention - Abx prophylaxis for recurrent
dipstick haematuria UTI: trimethoprim,
- UFEME WBC, RBC, casts nitrofurantoin
- Urine c/s - Cranberry juice (inhibits
adherence of E. coli to bladder
cells)
Bloods
- FBC WBC and differential count
- ESR and Inflammatory markers
CRP Sterile Pyuria
- U/E/Cr Renal impairment a) Renal TB
- Blood c/s If patient is septic b) Inadequately treated UTI
c) Calculi
d) Prostatitis
Imaging e) Bladder tumour
- KUB Radio-opaque stones f) Interstitial nephritis
- CT KUB Highly suspicious of stones g) Appendicitis
- Renal U/S Hydronephrosis
- IVU Physiological/anatomical upper Urinary Catheters and Lifespan
tract abnormalities
a) Foley’s = 2 weeks
Radiolucent stones b) Silicon-coated = 4-6 weeks
Renal function
c) Silicon = 3 months
- Flexible Lower urinary tract abnormalities
cystoscopy
- MCU Reflux uropathy
- DMSA Renal scarring and differential
- MAG-3 renal function (recurring UTI)
Management
Lower UTI - Empirical Abx: trimethoprim
(check G6PD status),
amoxicillin, nitrofurantoin
- Change as required when urine
c/s results return
Acute - Empirical Abx: broad-

pyelonephritis spectrum
cephalosporin, ciprofloxacin
- Change as required when urine
c/s results return
Acute - Empirical Abx: ciprofloxacin,
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Medicine (Renal) = Assessing volume status
1. Cx of hypovolemia:
- Cerebral hypoxia
- ARF
- AMI
- Hemorrhagic enteropathy
- Liver failure (fatty change, haemorrhagic necrosis, impaired lactate metabolism)
2. Cx of hypervolaemia
- Pulmonary oedema
- Pleural effusion
- AMI/CCF
- Hypertension
3. Physiology
2/3 intracellular
(40%)
2/3 water 1/3 extracellular 2/3 interstitial (13%)
(60%) (20%)
Body  1/3 intravascular (7%)
1/3 solids
(40%)
When determing volume status of patient, assess ECF compartment
4. Clinical signs of dehydration (mild, moderate, severe)

a. Mental state – alert, confused, drowsy, stupor, coma
b. Temperature – normal or raised
c. HR – normal or tachycardic
d. RR – normal or Kussmaul’s (acidosis in severe dehydration)
e. BP - postural hypotension with tachycardia (change in >15mmHg SBP, >10mmHg DBP, >15
bpm increase in HR). Standing BP not necessary if patient already hypotensive while supine
f. Capillary refill – normal is <2sec
g. Eyes - may be sunken
h. Mucous membranes – normal, dry, parched (look for absence of pooling of saliva at the area of
the frenulum)
i. JVP – flat vein (may only fill in the Trendelenberg position – while supine, body tilted such that
the feet are higher than the head))
j. Skin turgor – normal, reduced
k. Urine output – normal, oliguria, anuria
l. Heart, lungs, liver, legs normal
m. Lab results – increase in urea > increase in creatinine
5. Clinical signs of hypervolaemia

a. Mental state, uncomfortable, distressed, anxious
b. Temperature – normal
c. HR – normal, tachycardic (increases forward flow to relieve pulmonary venous congestion)
d. RR – normal, tachypneic (pleural effusion, pleural oedema)
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e. BP – normal, hypertensive
f. Capillary refill – normal
g. Eyes – normal
h. Mucous membranes – normal
i. JVP – normal, raised (>3cm)
j. Skin turgor – normal, increased (taut, non-pliable)
k. Heart – S3 best heard in left lateral position
l. Lungs – bibasal inspiratory crepitations, wheeze
m. Liver – enlarged, tender
n. Legs – normal, oedema
o. Urine output – normal
p. Lab results – dilutional effects
6. Replacement fluids
a. Crystalloids – normal saline (limited to extracellular space), Ringer’s lactate, Hartmann’s
solution
b. Colloids – albumin, gelafundin
i. Stays within intravascular space
ii. Indications: for volume expansion in acute blood loss, hypoalbuminaemic states eg.
cirrhosis (causes intravascular depletion and interstitial fluid excess)
c. Blood
7. Dextrose
a. Distributes within both intracellular and extra cellular spaces
b. Once dextrose is metabolised, infusion is essentially free water  may cause cell lysis
c. D5 consists of 50g of dextrose dissolved in 1L of water, has an osmolality of 252mosm/L
d. Can be used when treating hypoglycaemia or when keeping IV access patent in patients with
intravascular volume excess (quickly leaves intravascular space)
e. Dextrose/saline – maintenance IV fluid for patients who cannot accomplish normal oral intake
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Medicine (Renal) = Fluid and electrolytes (Acid- base disorders)
*acidosis = right shift of oxygen dissociation curve, poor pulmonary uploading, also a/w hyperkalemia
*alkalosis = left shift of oxygen dissociation curve, poor tissue unloading, also a/w hypokalemia and
hypocalcemia free ionic calcium decreases due to increased binding to serum albumin
Confirming the ABG

*[H+] = 24 x pCO2/ [HCO3]
* to convert pH to [H+]
- pH 7.4 = 40nmol/L
- increase/decrease of 0.1 unit = 40 multiply/divide by 0.8
*if calculated value differ by > 10% = error
Normal values
1. pH = 7.40 (7.35-7.40)
2. HCO3 = 24mmol/L (22-32)
3. PCO2 = 40mmHg (35-40)
Acid base disorders

(a) Simple
1. Metabolic acidosis (HAGMA, NAGMA)
2. Metabolic alkalosis
3. Respiratory acidosis
4. Respiratory alkalosis
(b) Mixed acid/base
1. Respiratory/metabolic combinations
- But never respiratory acidosis with respiratory alkalosis
2. Complex acid/base
- Metabolic acidosis, metabolic alkalosis and respiratory acidosis
pH pCO2 HCO3
Metabolic acidosis decrease decrease decrease
Metabolic alkalosis increase increase Increase
Respiratory acidosis decrease increase Increase
Respiratory alkalosis increase decrease decrease
Approaching acid base disorders

Step 1: alkalosis or acidosis
 pH (normal 7.35 – 7.45)
(a) high = alkalosis
(b) low = acidosis
(c) normal = look at pCO2 and HCO3 (compensated pH)
 even if pH appears normal
[HCO3] < 20 pCO2 < 35 Metabolic acidosis + respiratory alkalosis
[HCO3] > 24 pCO2 > 45 Metabolic alkalosis + respiratory acidosis
[HCO3] and pCO2 normal AG > 11 HAGMA + metabolic alkalosis
[HCO3] and pCO2 normal AG normal NAGMA + metabolic alkalosis
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Step 2: Respiratory or Metabolic?
 HCO3 decrease
(a) Common (esp < 12 mmol/L) = metabolic acidosis
(b) Uncommon = respiratory alkalosis + metabolic compensation
 pCO2 increase
(a) common = respiratory acidosis
(b) uncommon = metabolic alkalosis + respiratory compensation
Step 3: Mixed or Pure?

 Any compensation?
(a) In acute disorders, compensation may not have set in
 Adequate compensation?
(a) Simple compensation
Primary Initial Compensatory Expected compensation

disorder change response
Metabolic Decrease Decrease pCO2 Δ pCO2 = 1.2 x Δ [HCO3]
acidosis HCO3
Metabolic Increase Increase pCO2 Δ pCO2 = 0.6 x Δ [HCO3]
alkalosis HCO3
Respiratory Increase Increase HCO3 Acute = HCO3 increase by 1mmol/L for every
acidosis pCO2 10mmHg increase in pCO2
Chronic = HCO3 increase by 3.5mmol/L for every
10 mmHg increase in pCO2
Respiratory Decrease Decrease HCO3 Acute = HCO3 decrease by 2mmol/L for every
alkalosis pCO2 10mmHg decrease in pCO2
Chronic = HCO3 decrease by 5mmol/L for every
10 mmHg decrease in pCO2
Metabolic acidosis
 Primary cause = low HCO3
- Respiratory compensation = hyperventilation
 Calculate anion gap = (Na + K) – (Cl + HCO3)
- Normal = 12-17 mmol/L
- High anionic gap nearly always a/w metabolic acidosis
(a) HAGMA (95%)

1. Ketoacidosis = Diabetic ketoacidosis
Starvation (esp paediatric patients with GE)
Alcohol-induced
2. Renal failure = ARF,CRF
3. Lactic acidosis = Failure to excrete lactate (liver failure, biguanides)
Hypoxia (Cardiac  heart failure, AMI
Respiratory  bilateral pneumothorax
Blood  haemoglobinopathy
4. Poisoning (PEEMS)= paraldehyde, ethanol, ethylene glycol, methanol, salicylates
(b) NAGMA (5%)
1. Diarrhea
2. Carbonic anhydrase inhibitor ingestion
3. Renal tubular acidosis
4. Ureteral diversion
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 Calculate osmolar gap = serum osmolality – calculated osmolality (2Na + urea + glucose)
- Normal serum osmolality = 285-295 mOsm/kg
- Normal osmolar gap = 15 (10-20 mOsm/kg)
- Hyperosmolality but no osmolar gap = hypernatremia, hyperglycemia, uraemia
- Hyperosmolality with osmolar gap = small molecular weight molecules present in large
quantities that are not of the usual electrolytes
 Complications
1. Circulatory collapse = Decreased cardiac response to catecholamines
Depressed myocardial contractility
Venous constriction  redistribution of blood into central circulation,
therefore heart failure
2. Circulatory insufficiency  tissue hypoxia  lactic acidosis
3. Increase in pulmonary vascular resistance
4. Hyperkalemia
 Management
(a) Treat reversible causes
(b) IV 8.4% NaHCO3 infusion
- Indications = pH < 7.20 or HCO3 < 12mmol/L
- Usually correct only half the deficit
- Do not correct too quickly = Paradoxical intracellular acidosis
Hyperosmolar injury from NaHCO3
Secondary respiratory alkalosis
(c) Monitor ABG, serum K, serum Ca
(d) Severe acidosis = dialysis
Indications for dialysis
1. Hyperkalemia
2. Severe metabolic acidosis
3. Severe uraemia (encephalopathy and pericarditis)
4. Severe uncontrolled hypertension from severe fluid overload not responding to
diuretics
5. Severe pulmonary oedema
6. Poisoning (methanol, ethylene glycol, severe salicylates)
Metabolic alkalosis
 Primary cause = high HCO3
- Respiratory compensation = hypoventilation
 Causes
1. Excess alkali intake = acute alkali administration, excessive acetate in TPN, exchange transfusion
(from breakdown of citrate)
2. ECF contraction = vomiting, diarrhea, diuretic therapy (K depletion)
3. Mineralocorticoid excess (Cushing’s syndrome, primary hyperaldosteronism)
 Mechanisms = Acid loss (GIT, renal)
Acid shift (intracellular shift of H in hypokalemia)
Increased HCO3 intake (massive blood transfusion causing breakdown of
citration)
Contraction alkalosis (loss of HCO3 poor and Cl rich ECF)
 Complications
1. CNS = mental confusion, obtundation, seizures, parasthesia, cramps
2. Hypokalemia
3. Cardiac arrhythmias
 Management
(a) Identify reversible causes
(b) Saline responsive alkalosis (vomiting, diarrhea, diuretics) = NaCl infusion and KCl replacement
(c) Saline resistant alkalosis (Conn’s, Cushing’s) = treat underlying causes
(d) Severe alkalosis = arginine HCl, NH4Cl, acetazolamides (NAGMA)
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Respiratory acidosis
 Primary cause = hypoventilation
- Metabolic compensation = decreased renal excretion of HCO3
 Causes
1. Drugs = sedatives, opiates, anaesthetic agents
2. CNS depression = brainstem stroke
3. Neuromuscular disorder = GBS, myasthenia gravis, polio
4. Thoracic cage limitation = kyphoscoliosis, flail chest
5. Restricted lung expansion = pneumothorax, pleural effusion, hemothorax, diaphragmatic paralysis
6. Pulmonary disease = pneumonia, ARDS, pulmonary oedema, pulmonary fibrosis, COPD
Respiratory alkalosis
 Primary cause = hyperventilation
- Metabolic compensation = increased renal excretion of HCO3
 Causes
1. Drugs = salicylates, catecholamines, L-thyroxine
2. CNS stimulation = SAH, meningitis, stroke, encephalopathy
3. Psychogenic = hysteria, anxiety
4. Pulmonary disease = pneumonitis, asthma, pulmonary embolism, FB
5. Excessive mechanical stimulation
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Medicine (Renal) = Respiratory Disorders
Check for appropriate HCO3- compensation
Respiratory Acidosis Respiratory Alkalosis

4. Liver disease
1. CNS depression 4. Impaired lung expansion 1. Anxiety
5. Pulmonary disease
2. Neuromuscular disorder 5. Pulmonary disease 2. Drugs
6. Excessive mechanical
3. Thoracic cage limitation 6. Drugs 3. CNS stimulation
ventilation
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Medicine (Renal) = Renal Tubular Acidosis (RTA)
 Introduction
o Condition of systemic acidosis caused by renal tubular dysfunction
o 2 types of RTA
 1: Hypokalaemic hypochloraemic metabolic acidosis
 2: Hyperkalaemic hyperchloremic metabolic acidosis
o Renal function usually normal
 Type 1 (Distal RTA)
o Primary abnormality
 Failure of H+ excretion by distal tubule (defective H+ ATPase)
 Therefore…
 Failure of Na+ reabsorption
 Aldosterone release
o Biochemical results
 K+ , HCO3- , Cl- 
 Normal anion gap
 (Alkaline urine that cannot acidify following acid load)
o Causes
 Primary (AD,AR)
 Secondary
 Pyelonephritis, obstructive uropathy, lithium)
o Clinical features
 Growth failure
 Nephrocalcinosis
 Renal stones
 Osteomalacia
o Management
 HCO3- and K+ supplements
 Type 2 (Proximal RTA)
 Failure of proximal tubule in HCO3- reabsorption (Slow H+/NA+ pump)
o More severe than Type 1 RTA
 K+ , HCO3- , CL- 
 (Alkaline urine that can acidify following acid load)
o Causes
 Primary (AD, sporadic)
 Secondary
 Familial syndromes (Failure of glucose, PO43- and amino acid reabsorption)
o Clinical features
 Growth failure
 Rickets
 Polyuria, polydypsia, dehydration
 No renal calcification
o Management
 HCO3- and K+ supplements
 Type 4
 Aldosterone deficiency/resistance
  Failure of NA+ reabsorption and K+/H+ excretion
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 K+ , HCO3- , CL- 
 (Acidic urine)
o Causes
 Adrenal disorders (Addison’s disease, CAH), R A renal 
 Hyporeninaemic hypoaldosteronism (interstitial nephritis) R A renal
 Pseudohypoaldosteronism R A
o Clinical features
 Primary renal disease
 Adrenal disease
o Management
 HCO3- supplements
 K+ reduction (Eg. Furosemide, thiazides)
 Flucortisone
Comparison of Major Types of RTA

Type 1 Type 2 Type 4
Hyperchloraemic Yes Yes Yes
acidosis
Minimum Urine >5.5 <5.5 (but usually >5.5 before the acidosis <5.5
pH becomes established)
Plasma Low-normal Low-normal High
potassium
Renal stones Yes No No
Defect Reduced H+ excretion Impaired HCO3 reabsorption in proximal Impaired cation
in distal tubule tubule exchange in distal
tubule
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Medicine (Renal) = Potassium Disorders
Physiology
 K+ is the major intracellular cation
 Na+/K+ ATPase involved in regulating K+ balance -> stimulated by insulin and B-adrenergic agonsits
 Renal handling
1. ~90% of filtered K+ reabsorbed actively in the proximal tubule and thick ascending limb
2. actively secreted by distal nephron if GFR reduced -> avoid hyperkalemia
-mediated by aldosterone
 ECF H+ and K+ tend to vary together

o Compete with each other in exchange with Na+ across cell membranes and distal tubule of kidney
 Inhibition of RAA axis will tend to hyperkalemia
1. ACE inhibitors
2. NSAIDs (blocks prostaglandin-mediated rennin release)
3. B-Blockers
4. K+ sparing diuretics = spironolactone, amiloride
Hyperkalaemia
1. Definition = K+ > 5.0 mmol/L (3.5 – 5.0)
2. Causes
Increased K+ Intake  K+ containing medications = Span K

 High-potassium foods
Cellular death  Haemolysis
 Rhabdomyolysis
 Burns
 Catabolic states = fasting
Shift of intracellular K+ into ECF  Acidosis
 Hypoxia
 Insulin deficiency = DKA, non-compliant DM patient
 B-Blockers
 Digoxin toxicity
Impaired renal K+ excretion  Reduced GFR
o ARF
o CRF
o Obstructive uropathy
o Reduced renal perfusion = shock, dehydration
 Impaired tubular excretion of K_
o Reduced aldosterone synthesis
 Adrenal Gland disorders = Addison’s disease
Primary hypoaldosteronism
 Others
1. Reduced rennin synthesis
2. ACE inhibitors
3. NSAIDs
4. B-Blockers
o Tubular resistance to aldosterone
 Drugs = Spironolactone , amiloride
 Renal tubular acidosis
 Transplanted kidneys
 Amyloidosis
Spurious  Haemolysis of sample
 Incorrect blood sample handling = delay in reaching lab -> ATP depletion
use of blood tubes with EDTA
sequence of filling blood tubes
 Increased cellular elements = erythrocytosis, thrombocytosis, leucocytosis.
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3. Grading of severity
a. Mild = K+ <6.0 mmol/L
ECG can be normal or show tall tented T waves
b. Moderate = K+ = 6.0 -7.0mmol/L
ECG shows tall tented T waves
c. Severe = K+ >7.0mmol/L
 Clinical presentation = parasthesia (tingling around lips/fingers)
muscular weakness (flaccid paralysis, loss of tendon jerks)
abdominal distension, paralytic ileus
cardiac arrythmias -> sudden death
 ECG changes = tall tented T waves
increased PR interval
widening of QRS complex
ventricular tachycardia/fibrillation
4. Management
a. Resuscitate the patient = ABC
b. Create IV access
c. Place on continuous ECG monitoring
d. Treat reversible causes = hypovolemia, acidosis (do ABG)
e. 4-step management
i. Stabilize membrane potential = IV 10ml 10% calcium gluconate over 10 mins
 Immediate onset and effects last for 1 hr
 Cardio-protective function (does not reduce serum K+)
 IV calcium to be used only = ECG evidence of severe K+
o Severe hyper K+
o Significant neuromuscular weakness
 Use with absolute caution in patients on digoxin -> severe digitalis toxicity
 Ensure IV line is working -> extravasation of calcium into subcutaneous tissue can cause
necrosis
ii. Shift ECF K+ into ICF
1. IV bolus 40ml 50%D + 10units soluble insulin over 10min (6U to renal failure patients)
2. IV 0.5mg Salbutamol in 5%D over 10 min
neubulized salbutamol: N/S = 1:3 over 10mins
 Risk of tachycardia
iii. Remove K+ from the body
1. Resonium A (15 – 30g PO; 30g rectal enema)
2. haemodialysis
iv. Prevent further K+ increase
1. Medications review and advice
2. Dietary review and advice
f. Treat concomitant metabolic acidosis with 8.4% NaHCO3
5. HO on call
a. Check with sample is not haemolysed
b. Ask for patient’s vitals and symptoms (i.e. chest pain, SOB, palpitations, parasthaesiae, weakness)
c. Past medical history = ESRF
d. Order ECG if K+>5.5 mmol/L and place on contunous ECG mentoring if K+>6.0 mmol/L
e. Orders
i. K+ > 5.0 mmol/L = PO Resonium 15g stat or 30g fleet enema
ii. K+ > 5.5 mmol/L = as above
IV 10ml 10% calcium gluconate over 10mins
IV 40ml D50% + IV 10U soluble insulin
iii. K+ > 6.0 mmol/L = as above
nebulised salbutamol:N/S = 1:3 over 10 mins
iv. If fluid overloaded as well = IV Frusemide
urgent dialysis (if recalcitrant to treatment)
f. Recheck if K+ 2 hrs later
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Hypokalemia
1. Definition = K= < 3.5 mmol/L

 Urgent treatment required if K+ <2.5 mmol/L
 Hypokalemia exacerbates digoxin toxicity
 Usually occurs with hypocalcaemia and hyomagnesaemia
2. Causes
Reduced K+ intake  Inadequate dietary intake

 IV K+ free fluids
Intracellular shift of  Alkalosis
K+  Insulin = insulinoma, exogenous administraion
 Salbutamol
 Adrenaline
GIT losses  Vomiting
 Diarrhoea
 Pyloric stenosis
 Villous adenoma
 Intestinal fistua
 Sequestraion of fluid in bowel (ileus, IO)
Renal losses  Renal tubular acidosis
 Drugs = loop diuretics, thiazides
 Excess aldosterone =
o primary aldosteronism (conn’s sydrome, bilateral adrenal hyperplasia)
o secondary aldosteronism (RAS, coarctation of aorta, hypovolaemia)
 excess mineralocorticoid = Cushing’s syndrome
3. Clinical presentations
 Muscle weakness
 Hypokalemic periodic paralysis (intermittent weakness lasting up to 72hrs)
 Reduced intestinal motility -> paralytic ileus
 Cardiac effects
o Ventricular arrythmias
o Asystole
o Potentiation of digitalis toxicity
 ECG
o Flattened T waves
o Prominent U waves
o Prolonged PR interval
o Severe (ST depression, T wave inversion)
4. Management
 Absolute indications for treatment
1. Digoxin therapy
2. DKA treatment
3. Respiratory muscle weakness
4. Severe hypokalaemia (<2.5mmol/L)
5. HO on call
1. Check that sample not spurious, i.e. not taken distal to drip site
2. Check patient’s vitals, PMHx, current medications = stop diuretics, insulin and salbutomol
3. Order ECG if K+ < 3.0mmol/L and place on continuous ECG monitoring if K+ < 2.5 mmol/L
4. Orders
 K+ < 3.5 mmol/L
o Oral Span K+ 0.6 – 1.2g OM
o Mist KCL 10ml TDS
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 K+ < 2.5 mmol/L or K+ < 3.0 mmol/L with digoxin/AMI/IHD = IV KCl replacement
o Check that patient is not oliguiric
o Calculate K+ deficit = 0.6 X BW X (4 - __)
o 1 cycle = 10mmol of 7.45% KCl solution in 100ml water given over 1 hr increases K+ by 0.1 unit
o IV K+ = maximum 20 mmol/hr, maximum 20 mmol/pint, never given as IV bolus
5. recheck K+ 2 hrs post-replacement
Medicine (Renal) = Hyponatraemia

1. Definition
- Na+ < 135 mmol/L
- Pathophysiology = water gain and/or Na+ loss
2. Algorithm
Hyponatraemia
Spurious Non-Spurious
*Taken just distal
to drip site Step 1: Serum osmolality
(280 – 295 mosm/kg)
Low Normal/High
True Pseudohyponatraemia
hyponatraemia *Causes = ↑ lipids, ↑
Step 2: Urine osmolality proteins, ↑ glucose
*True Na+ =
<100mosm >300mosm
Fluid overload
Hypovolaemi Euvolaemia
Step 3: Urinary Na+ a
Step 3: Urinary Na+ Step 3: Urinary Na+
<20 mmol/L >20 mmol/L

1. Cardiac failure 1. Renal failure
Non-endocrine Endocrine
2. Nephrotic syndrome 1. Drugs 1. SIADH
3. Liver cirrhosis 2. 1° polydipsia 2. Hypothyroidism
4. Protein-losing enteropathy 3. Addisons’ disease
Extra renal loss Renal loss
1. Excess
GIT Skin diuretics
1. Vomiting 1. Burns 2. Tubulopathy
2. Diarrhea 2. Excessive
3. Intestinal sweating
fistula 3. Exudative skin
disease
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3. Clinical Features
- Defined as:
a) Absolute ↓ in serum osmolality
b) Rate of development of hyponatraemia
c) Volume status
- Hypervolaemia = oedema
o ± associated features of CCF, liver disease, renal disease
- Euvolaemia = drug history
o ± associated features of Addison’s disease, hypothyroidism
- Hypovolaemia = dehydration
- Hyponatraemia = neurological, due to cerebral oedema (headache, lethargy, weakness, altered mental state,
restlessness, fits, coma)
4. Management
- Usually replacement of Na+ if Na+ <125mmol/L
- Hypovolaemia
o Cannot correct > 10mmol/day
 ∴ Na+ deficit = (140 – Na+) x 0.6 x body weight
o Usually, do not add in daily requirements ∵ of risk of over-correcting

o [Na+] in replacement fluids
 0.9% N/S = 154 mmol/L
 0.45% N/S = 77 mmol/L
 0.23% N/S = 38.5 mmol/L
 (3% N/S = 514 mmol/L)
o Example = 60kg male, [Na+] = 130 mmol/L
Na+ deficit = 10 x 0.6 x 60 = 360 mmol/L
Volume of 0.9% N/S = 360/154 = 2.34L over 24 hours
o Correct too quickly  central pontine myelinosis
* If hyponatraemia develops slowly = brain adapted to ↓ing serum osmolality, ∴ sudden rise will cause shrinking
of brain cells which is potentially fatal
o Correct too quickly  APO
- Euvolaemia
o Fluid restriction
o Investigations: CXR, TFT, random cortisol (8am), synacthen test
- Hypervolaemia
o Fluid restriction
o Hypertonic saline with frusemide = limit treatment-induced CCF expansion
5. SIADH
- No history of diuretic history
- Absence of oedema/hypovolaemia
- Aetiology
a) Malignancy
 Small cell lung cancer
 Pancreatic cancer
 Duodenal cancer
b) CNS
 Meningitis
 CVA
 Subarachnoid haemorrhage
 Trauma
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c) Chest
 TB
 Pneumonia
 Abscess
 Aspergillosis
d) Metabolic
 Porphyria
e) Drugs
 Narcotics
 Chlorpropamide (OHGA)
 Anti-depressants (amitriptyline)
 Neuroleptics (haloperidol, fluphenazine, chlorpromazine)
- Management
o Fluid restriction
o Treat underlying cause
o Chronic symptomatic SIADH = demecleocycline/lithium (induces nephrogenic diuresis)
- In psychiatric patients = always think of drug-induced SIADH
- Exclusion criteria
o Normal renal/fluid/adrenal/thyroid function
- Inclusion criteria
o Plasma = ↓ Na+, ↓ osmolality
o Urine = ↑ Na+, ↑ osmolality
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Medicine (Renal) = Hypernatraemia
1. Definition
- Na+ > 145 mmol/L
- Usually treat when [Na+] > 150 mmol/L
2. Algorithm
Hypernatraemia
Input Disorder Urine Osm < Serum Output disorder

Osm Urine Osm > Serum
Osm
Impaired ADH
Inc. Salt intake Dec. H20 intake Excess H20 loss
regulation
1. Impaired thirst mech. Renal Extrarenal

2. Limited access to H20 1. Osmotic dieresis 1. Excess
Drugs Endocrine -DKA sweating
1. Excess 1. Conns -Urea 2.Burns
saline 2.Cushings -Mannitol
Water Deprivation Test
2.Drugs TPN
with high
Na content
3. NaHCO3
after
Pituitary DI Nephrogenic DI
cardiac
(desmopressin increases urine (desmopressin does not increases
arrest
Osm) urine Osm)
Hereditary Acquired
1. Head Injury Hereditary Acquired
1. DIDMOAD Syndrome
2. Pituitary 1. Hypokalaemia
surgery 2. Hypercalcaemia
3. CNS Infection 3. Obstructive uropathy
4. Idiopathic 4. Nephrotoxic drugs
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3. Physiology
- Increased serum osmolality cause a reflex increase in thirst and ADH secretion
- ∴ hypernatraemia is rare unless thirst mechanism is abnormal or there is limited access to water
4. Clinical Features
- Hypernatraemia: confusion, coma, seizures, weakness
- Dehydration
- Diabetes insipidus: polyuria, polydipsia, increased thirst
5. Management
- Free H20 deficit = [ (serum Na – 140) x 0.6 x BW] / 140
- (Serum Na – Fluid Na) / [(0.6 x BW) + 1] = 1 L of fluid will correct Na by ___ mmol/L
- Fluids:
o D5% = 0 mmol/L Na+
o 0.9% N/S = 154 mmol/L
o 0.45% N/S = 77 mmol/L
o 0.23% N/S = 38.5 mmol/L
- Total fluids = water deficit + maintenance
- Correct ½ the deficit over 24 h and the remainder over the next 1-2 days
- Eg 60/C/Female
[Na] = 160mmol/L
BW = 60kg
Free H20 deficit = (160-140)/140 x 0.6 x 60 = 5.1L
If D5% given : (160 – 0)/ [ (0.6 x 60) +1 ] = 4.3 1 L of D5% will decrease Na by 4.3 mmol/L
If 0.9% N/S given : (160-154)/ [(0.6 x 60)+1] = 0.16 1L of 0.9% NS will decrease Na by 0.16 mmol/L
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Gastrology
Medicine (GIT) = History Taking: GIT (General)
Date of admission
1. GI symptoms
a. Nausea + vomiting
 Describe vomitus = nature (liquid, digested/undigested food)
colour (yellow bilious liquid, coffee-ground, blood)
 Projectile  pyloric stenosis, raised ICP
 Timing = >1h after meal (GOO, gastroparesis)
early morning (pregnancy, raised ICP)
b. LOA + LOW  malignancy, depression
 How much weight was lost?
 Duration
c. Dysphagia
 Onset
 Frequency (intermittent suggests oesophageal spasm)
 Solids or liquids?
 Progressively getting worse (suggests ca, stricture, achalasia)
 Painful on swallowing (odynophagia)
 Able to initiate swallowing? (inability suggests neurological disease)
 Regurgitation (fluid regurgitation highly suggests neurological disease)
d. Heartburn + acid regurgitations (symptoms of GERD)
 Precipitants = foods
 Aggravating factors = lying supine, bending, alcohol, change in posture
 Relieving factors = antacids
e. Abdominal pain
 Onset, frequency, duration
 Sudden/gradual onset
 What were you doing at onset?
 Constant/intermittent
 Site and radiation
 Character (sharp, dull, crampy, colicky)
 Severity
 Precipitating factor(s) (food, lying down, alcohol)
 Aggravating factor(s) (movement in peritonitis)
 Relieving factor(s) (sitting up and leaning forwards, antacids/vomiting in GERD/PUD, defecation in
colonic disorders)
f. Constipation
Diarrhoea = frequency (usually > 3x/day)
consistency of stools (watery)
fever (infection)
mucous (IBD, IBS, solitary rectal ulcer, villous adenoma)
blood (colorectal ca, IBD)
travel and contact history)
g. GI bleeding  haematemesis, malaena, haematochezia
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 If present  other sites of bleeding (bleeding dyscrasia, coagulopathy from CLD)
 If present  chest pain, SOB, palpitations, giddiness, fatigue (symptoms of anaemia)
h. Fatigue (anaemia, chronic diseases)
i. Jaundice  obstructive jaundice (pale stools, steatorrhoea, tea-coloured urine, pruritus, easy-bruising,
previous history of right-sided colicky abdominal pain)
 Steatorrhoea = >7g of fat in a 24-hour stool collection. Stools are pale, fatty, extremely smelly, float in
the toilet bowl and difficult to flush away
j. Abdominal distension + ankle oedema
k. Easy bruising + pruritus
2. Aetiology (r/o differentials)
3. Complications
4. Systemic review
5. Management prior to and after admission
6. Details of previous similar episodes

- Presenting complaint
- Investigations
- Diagnosis
- Medications
- Surgeries

1. DM, HTN, ↑ lipids, IHD, CVA, cancer, PUD
3. Previous surgeries (can cause liver damage from anaesthesia, hypoxia or direct damage to bile ducts)
Drug History
1. Any known drug allergies
2. Long-term medications
- Types and indications for use (esp. NSAIDs, aspirin, warfarin)
- Dose, frequency of dosing
- Compliance with use
- Side-effects
3. TCM use
Social History
1. Smoking
2. Alcohol drinking
3. Family set-up (main caregiver, health of family members, finances)
4. Lift-landing
5. Functional status (ADL/iADL)
Family History
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Medicine (GIT) = Physical examination: GIT
Start
1. Examine patient on the right side of his bed
2. Introduce yourself and explain purpose
3. Lie the patien flat on bed with his head on a single pillow (relax abdominal muscles)
4. Achieve adequate exposure = nipple line to mid thigh
General appearance
1. Mental state (hepatic encephalopathy) = alert, drowsy, confused, stupor
2. Comfortable/ in distress
3. Cachexia = failure of GIT to absorb food normally, intra-abdominal malignancy
4. Obesity = fatty liver (non-alcoholic steatohepatitits)
5. Skin colour and pigmentation =
a. Haemochromatosis (due to haemosiderin stimulating melanocytes)
b. Addison’s disease (‘sunkissed pigementation of nipples, palmar creases, pressure areas and mouth)
6. Hydration
7. Abdomen: surgical scars, distension ± eversion of umbilicus, visible masses/ pulsations, moves well with
respiration, distended veins
Hands and arms

1. Measure pulse rate
2. Inspect nails:
a. Clubbing (cirrhosis, IBD, celiac disease)
b. Leuconychia (hypoalbuminaemia)
c. Cyanosis
d. Pallor
3. Inspect palms
a. Palmar crease pallor (anemia)
b. Palmar crease pigmentation (Addison’s disease)
c. Palmar erythema (CLD – hyper estrogenism)
d. Dupuytren’s contracture (visible and palpable thickening and contraction of palmar fascia causing
permanent flexion, esp of ring finger; sign of alcoholism)
4. Inspect arms
a. Bruising (CLD → ↓ clotting factors production; obstructive jaundice → reduced absorption of vit K)
b. Petechiae (hypersplenism 20 portal hypertension; BM depression 20 chronic alcoholism, DIVC in
severe liver disease)
c. Scratch marks (puritus 20 obstructive jaundice)
d. Spider naevi (hyperestrogenism 20 CLD → more than 5 is abnormal)
Face
1. Eyes: conjunctiva pallor, jaundice
2. Preorbital: xanthelasma (yellowish plaques in subcutaneous tisues; hypercholesterolaemia; cholestatsis;
primary billary cirrhosis)
3. Mouth:
a. Breath (fetor hepaticus is rather sweet smelling; due to methymercaptans derived from methionine
which is not demthylated by diseased liver)
b. Freckle-like spots on buccal mucosa (Peutz Jeghers syndrome)
4. Tongue
a. Central cyanosis
b. Glossitis (smooth appearance due to papillae atrophy due to nutritional deficiencies e.g. iron, folate,
vitamin B12, ; common in alcoholics)
c. Geographical tongue (slowly changing red rings and lines, painless; comes and goes; may be a sign
of riboflavin (vit B2 ) deficiency)
d. Leucoplakia (white mucosal thickening; premalignant 5s = sore teeth (poor dental hygiene), smoking,
spirits, sepsis, syphilis)
e. Macroglossia (cretinism, Down syndrome, acromegaly)
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5. Lips
a. Capillary haemorrhages (hereditary haemorrhagic telangiectasia or Rendu-Osler-Weber syndrome)
b. Perioral freckle-like spots (Peutz-Jeghers syndrome)
c. Angular stomatitis (iron-deficiency anaemia; Plummer-Vinson syndrome)
Neck
1. Palpate left supraclavicular fossa for enlarge lymph node (Virchow’s node – indicating advanced intra-
abdominal malignancy)
Chest
1. Check for gynaecomastia (palpate area around nipple) and spider naevi
Abdomen
1. Kneel down at the right side of the bed and position yourself so that you are at eye level with abdomen and
watch for asymmetrical movement
2. Ask patient to point to site of pain (if any)
3. Determine direction of flow in distended veins (empty a distended vein below the umbilicus by flattening it
out and occluding it at both ends, release lower finger, empty vein again, release upper finger; if the flow of
blood is downwards, the cause is portal hypertension; if the flow of blood is upwards, the cause is due to
obstruction of IVC)
4. Begin superficial (? Soft/ guarding/ tender) and deep (organs and masses) palpation. Use the pulps of
fingers (flex metacarpophalangeal joints and distal interphalangeal joints) and palpate systematicall (work
all the way up from one side to the other and always begin from the non-tender area). Look at face during
palpation for signs of pain
a. Guarding = may result from tenderness, anxiety, peritonitis
b. Rigidity (wash board rigidity) = peritonitis
c. Rebound tenderness = peritonitis
5. If there is a mass, describe it interms of : size, shape, surface, tender, mobility, consistency, pulsatile
a. Try to get below it (if it is a pelvic mass, cannot get below it)
b. Bimanually palpate if (if cannont, then mass is located more anterior)
6. Examine specific organs: liver, spleen, kidneys
Liver
1. Place lelft hand on right costal margin and right hand at a similar angle to the ribs
2. Start in the right iliac fossa
3. Palpate deeply during inspiration and move fingers upwards during expieration (will feel liver edge moving
towards fingers during inspiration)
a. Normal causes of palpable liver: ptosis 20 hyperinflation (asthma, emphysema),
supradiaphragmatic collection)
4. Percuss intercostals spaces downwards until dullness occurs – upper limit of liver dullness
5. Lower limit is where you feel the liver edge/ percuss upwards until dullness occurs
6. Describe liver in terms of size, (hepatomegaly – measure liver span and length below right costal margin),
surface (smooth.nodular), pulsatile, tender, consistency, edge
Gallbladder
1. If biliary obsturtion/ acute cholecystitis suspected, examining hand should be oriented perpendicular to
costal margin and feel from medial to lateral
2. Do Murphy’s sign: ask patient to take a deep breath and press finger at angle between costal margin and
border of rectal sheath. If inspiration is arrested, there is a positive sign (suspect cholecystitis)
Spleen
1. Place left hand on left costal margin and begin palpation from right iliac fossa
a. Enlarged spleen descends obliquely across the mideline (must enlarge by 2x for it to be palpate)
b. Can also feel enlarged para-aortic lymph nodes and abdominal aortic aneurysm)
2. Palpate deeply during inspiration and move fingers obliquely upwards during expiration
3. Percuss over lowest intercostals space in left anterior axillary line and spleen (both areas should be
resonant)
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Ascites
1. Place left middle finger on umbilicus and start persussing to the other end (should be resonant out to the
flanks); dullness in the flanks means that there is at least 2L of ascitic fluid
2. If there is dullness before the flanks, ask patient to lie on right lateral position and wait for 30-60s for fluid
equilibration. Percuss form site of dullness back towards midline. If site of dullness becomes resonant in
this position, there is ascites. Percuss for new position of dullness (fluid level in this position)
3. Further test for ascites: ask patient to place right hand vertically in midline of abdomen, then place your
hand on left abdomen and flick fingers on right abdomen (can feel fluid thrill if there is ascites)
4. In this position, palpate for spleen
5. Check for sacral edema and scars (bone marrow biopsy → ? myeloproliferative disease)
Kidneys
1. Bimanual palpation; place left hand under patient and right hand on the abdomen and push left hand
upwards twice during inspiration (do 2 time on each side)
a. If kidney enlarge, the righ hand will feel something hitting it
b. Enlarged kidney bulges forwards; perinephric abscess bulges backwards; transplanted kidneys
palpable in either iliac fossa
Ausculatation
1. Listen for bowel sounds (tinkling and hyper active = IO; absent over 3min period = paralytic ileus)
2. Listen for renal bruits
3. Hepatic arterial bruit = alcoholic hepatitis, HCC, liver mets
4. Abdominal venous hum = portal hypertension
Groin
1. Palpate for enlarge inguinal lymph nodes
2. Ask patient to cough to detect inguinal hernias
3. Inspect for testicular atrophy (CLD)
Legs
1. Look for bruising, scratch marks and edema (press thumb against the back of malleolus, look at patient’s
face for pain)
2. Inspect toe nails for clubbing, cyanosis, pallor, leukonychia
End
1. Sit the patient up
a. Hepatic asterixis for 15s (hepatic encephalopathy)
b. Cervical lymphadenopathy
c. Parotid/ submandibular gland enlargement)
2. Tell the examiners that you would like to complete the examination by doing a PR exam, taking blood
pressure and temperature. If patient has hepatomegaly, should examine JVP. If ascites/ pedal edema
present, check for pleural effusion
3. Thank patient for his help and dress him up properly
Template for presentation

On general inspection, the patient appears to be alert, comfortable, orientated and well at rest. There are no
signs of respiratory distress and the patient does not appear to be in any pain. The vital signs are stable (HR =...,
RR= ..., afebrile)
Examination of the peripheries did not show any signs of jaundice, pallor cyanosis, dehydration or stigmata of
chronic liver disease such as clubbing, leuconychia, palmar erythema, spider naevi, gynaecomastia etc.
Inspection of the abdomen did not reveal any surgical scars, abdominal distension, distended vein or any
visible masses or pulsations. The abdomen was symmetrical and moved well with respiration. On superficial
palplation, the abdomen was soft and non-tender with no guarding or rigidity of abdominal wall muscles. The
liver was found to be enlarged at 3cm below the right costal margin with a liver span of 16 cm as measured in
117
the mid-clavicular line. The surface of the liver was smooth with no nodules felt. It was non pulsatile and no
bruits were heard over the liver. The spleen and the kidneys were non-palpable. No ascites was detected. Bowel
sounds were normal and no renal bruits were heard.
Inguinal lympadenopathy and cough impulses suggestive of inguinal hernia were not detected in the groin.
Lower limb and sacral edema were absent. There was no hepatic flap.
In summary, the patient has features of _________ as evidenced by _________
118
Medicine (GIT) = Issues for discussion
1. Signs of chronic liver disease
a. Hands = clubbing, leuconychia, palmar erythema, asterixis, bruising, petechiae
b. Face= jaundice, fetor hepaticus
c. Chest = spider naevi, gyanecomastia, loss of axillary hair, wasting of pectoral muscles
d. Abdomen = portal hypertension (ascites, caput medusa, splenomegaly), sacral edema
e. Groin = testicular atrophy
f. Legs= edema
2. Peutz-Jeghers syndrome
a. Autosomal dominant condition
b. Features
i. Freckle like spots (discrete brown-black lesions) around the mouth, buccal mucosa, fingers,
toes
ii. Harmatomas of the small bowel(50%) and colon(30%) →can present with bleeding +
interssusception, increased incidence of GI adenocarcinoma
3. Rendu-Osler-Weber syndrome
a. Autosomal dominant condition
b. Multiple small tenlangiectasiae present on lips, tongue, and skin
c. GI features = chronic blood loss, torrential bleeding, liver AV malformation
4. Hepatic flap
a. Refers to jerky, irregular flexion-extension movement at the wrist and MCP joints often
accompanied by lateral movements of the fingers
b. Mechanism = interference with the inflow of joint position sense information to hte reticular
formation in brainstem resulting in rhythmical lapses of postural muscle tone
c. Characteristics = usually bilateral, absent at rest, brought by sustanined posture, not synchronous
on each side, absent when coma suepervenes
d. Characteristic but not diagnostic of liver failure (can also occur in cardiac, respiratory, and renal
failure; also in metabolic encephalopathy – hypoglycaemia, hypokalemia, hypomagnesaemia,
barbiturate intoxication)
5. Spider naevi
a. Consist of a central arteriole form which radiate numerous small vessels
b. Usual distribution is the area drained by SVC→ found on the arms, neck and chest wall
c. Pressure applied with a pointed object to the central arteriole causes blanching of the whole lesion
with rapid refilling from the centre to the periphery on release of pressure
d. Differentials:
i. Campbell de Morgan spots (flat/ slightly elevated red circular lesions which occur on the
abdomen or chest wall; do not blanch on pressure)
ii. Venours stars (due to elevated venous pressure; found overlying main tributary to a large
vein; occur on dorsum of feet, legs, back and lower chest; not obliterated by pressure; blood
flow from periphery to centre of lesion)
iii. Hereditary haemorrhagic telangiectasia
6. Troisier’s sign = presence of a large left supraclavicular lymph node with gastric carcinoma
7. Causes of abdominal distention (6Fs)
a. Fat = umbilicus buried in fat

b. Fluid = shifting dullness, fluid thrill, eversion of umbilicus, tense abdominal wall and flanks
c. Faeces = mass in the left lower quadreant, indentable, non-tender
d. Flatus
e. Fetus = umbilicus pushed upwards
f. Filthy big tumour
119
8. Sister Joseph nodule = metastatic tumor deposit in the umbilicus (antatomical region where the peritoneum
is closest to the skin)
9. Cullen’s sign = blue black discolouration of umbilicus (extensive haemoperitoneum, acute pancreatitis)
10. Liver
a. Normal liver span = <13 cm as measure in the mid-clavicular line
b. Pulsatile liver = tricuspid regurgitation, HCC
c. Tender liver = hepatitis, rapid liver enlargement, hepatic abscess, cholangitis
11. Gallbladder
a. Courvosier’s law= if the gallbladder is enlarged and the patient is jaundiced, unlikely to be
gallstones; gallbladder with stones is usually chronically fibrosed (small)
Gallbladder enlargement
With jaundice
1. Carcinoma of head of pancreas
2. Carcinoma of ampulla of Vater
3. Gallstones in CBD
4. Carcinoma of the gallbladder
Without jaundice
1. Mucocele/ empyema of gallbladder
2. Carcinoma of the gallbladder
3. Acute cholecysitits
12. Splenomegaly
Causes of splenomegaly
Vascular Portal hypertension
Infective Viral hepatitis , EBV, CMV
Bacterial (SBE)
Protozoal (malaria, kala-azar)
Trauma Haematoma
Autoimmune SLE
RA (felty’s syndrome)
Metabolic Storage disorders (Gaucher, Neimann-Pick, glycogen storage, lipid storage)
Infiltrative Amyloidosis
Sarcodosis
Neoplastic CML (invasive)
Myelofibrosis (massive)
Lymphoma
Lymphoproliferative disorders
Polycythemia ruba vera (massive)
Haematological Chronic haemolytic anemia, (spherocytosis, G6PD deficiency, thalassaemia)
13. Causes of hepatosplenomegaly

a. Chronic liver disease with portal hypertension
b. Infective = acute viral hepatitis, infectious mononucleosis, CMV, malaria
c. Autoimmune = SLE, RA
d. Metabolic = storage disorders
e. Infiltrative= amyloidosis, sarcoidosis
f. Neoplastic =myeloproliferative disorders, lymphoma, lymphoproliferative disorders
g. Haematological = Chronic haemolytic anemia, (spherocytosis, G6PD deficiency, thalassaemia)
14. Distinguishing features between a large left kidney and splenomegaly

a. Spleen descends inferomedially on inspiration while kidney descends downwards
b. Palpable splenic notch
120
c. Dull percussion note over spleen but resonant over kidney due to gas filled fowel loops
d. Kidney is ballotable but not the spleen
e. Cannot get above the spleen (can get above the kidney)
f. Friction rub may be heard over the spleen but never over the kidney (too posterior)
15. Succession splash

a. May be present in gastric outlet obstruction
b. Procedure
i. Explain to patien what is going to happen
ii. Grasp one iliac crest with each hand
iii. Place stethoscope close to epigastrium
iv. Shake patient from side to side
c. Ensure that the patient has not ingeted any fluids just prior to examination (at least 3 horus before)
16. Anterior abdominal wall masses

 Ask pateitn to fold arms across the upper chest and sit halfway up
o Intraabominal mass will disappear/ decrease in size
o Anterior abdominal mass will become more prominent/ remain unchanged
 Lipoma
 Sebaceous cyst
 Dermal fibroma
 Malignant deposits = melanoma, carcinoma
 Epigastric hernia
 Umbilical hernia
 Incisional hernia
 Rectus sheath divarication/ haematoma
17. Per-rectal examination

a. Explain to the patient the purpose of the examination and the procedure
b. Relax the patient and lie him on the left lateral side with the legs drawn up
c. Put on gloves and always use lubrication
d. Approach the rectum from the inferior aspect
 INSPECT THE PERIANAL AREA

o Skin tags,
o Protruding polyps
o Haemorrhoids
o Anal fissures (most often seen at 6 & 12 o’clock; often accompanined by sentinel tags)
 ASSESS ANAL WINK (anocutaneous reflex) = contraction of the anus on stroking the perianal region
 INSERT INDEX FINGER
o Assess anal tone: tight → anal stenosis ; loose → lower spinal lesion
o Ask patient to squeeze your finger
o Rectal masses
o Prostate enlargement
o Local tenderness e.g. retrocaecal appendix
 ON WITHDRWAL
o Fresh PR bleed or melena
121
Medicine (GIT) = Approach to ascites
Ascites is the effusion and accumulation of serous fluid in the abdominal cavity.
Symptoms and Differential Diagnoses of Ascites
1. Causes of a distended abdomen:
 Fat, faeces, fluid, flatus, fetus, filthy big tumour
2. Causes of ascites
 Chronic Liver Disease/ Cirrhosis (Commonest Cause)
 Chronic alcoholism
 Viral hepatitis
 Cardiac Failure
 Chronic Renal Failure
 Nephrogenic ascites secondary to dialysis
 Nephrotic syndrome
 Enlarged Lymph Nodes
 Primary and Metastatic
 Intra abdominal mass
 Malignancy : Primary and Metastatic
 Others :
 Tuberculosis
 SLE
 Pancreatitis
 Constrictive pericarditis
History
1. Past medical history : To identify the system responsible for the ascites
Any past medical history of any disorder like coronary artery disease, hypertension, alcohol abuse. Is
the patient on any drug that can cause cardiac, hepatic or renal disease? Does the patient have renal
failure or go for dialysis. If suspicious, a history of HIV and TB should be obtained.
2. Ascites: Alcohol history, Hepatitis B status, any intra-abdominal masses and their associated symptoms.
3. Past medical history : Hepatitis Vaccinations, any recent drugs used
4. Any associated early satiety and shortness of breath
General Appearance
 Does the patient have any stigmata of chronic liver disease?
 Is the patient on oxygen?
 Does the appear to be in any respiratory disease?
Vital Signs
 Any tachycardia
 Respiratory rate for tachypnea
 Blood pressure measurement for hypertension
CVS Examination
 Checking for raised JVP will provide great yield here as it would indicate heart failure
 Other signs to pick up will include displaced apex beat, gallop rhythm, bibasal crepitations and any
possible aetiology for heart failure like valvular heart disease
Abdominal Examination
122
 Ask for site of most intense pain first. Palpate for presence or organomegaly. The live in alcoholic
cirrhosis is unlikely to be enlarged. However, other stigmata of chronic liver disease can be sought for
like caput medusae.
 Percuss for ascites and shifting dullness
 Palpate for any suspicious intra abdominal masses
 Palpate for hepatosplenomegaly in portal hypertension
Lower Limbs
 Check for presence of pitting edema
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Medicine (GIT) = Ascites
Introduction
 Pathological accumulation of fluid in the peritoneal cavity = clinically detectable when > 500mls
 Pathogenesis
 Under filling theory = inappropriate fluid sequestration within splancnic vascular bed secondary
to portal hypertension > decreased intravascular volume > kidneys retain more Na+ and water by
activating RAA system
 Overflow theory = primary renal retention of Na+ and water
 Complications
a) Peritonitis
b) Dyspnea secondary to splinting of diaphragm
c) Pre-renal failure secondary to intravascular volume depletion
d) Early satiety
Aetiology
Transudate vs Exudate
Transudative Exudative
Cardiovascular Infection
 Congestive cardiac failure  TB peritonitis
 Right heart failure
 Constrictive pericarditis
 IVC obstruction
 Portal/hepatic vein obstruction
Renal Inflammation
 Acute renal failure  Pancreatitis
 Chronic renal failure
 End stage renal failure
 Nephritic syndrome
GI Intra-abdominal malignancy
 Chronic liver disease  Pancreatic/gastric/colonic ca
 Malnutrition  Ovarian ca
 Protein-losing enteropathy  Metastasis to liver
 Metastasis to peritonium
Generalised vs Localised
Generalised Localised
Cardiovascular Vascular
 Congestive cardiac failure  Portal HPT
 Right heart failure a) IVC obstruction
 Constrictive pericarditis b) Budd-chiari syndrome
c) veno-occlusive disease
d) Liver cirrhosis
e) Portal/splenic vein obstruction
Renal Infection
 Acute renal failure  TB peritonitis
 Chronic renal failure
 End stage renal failure
 Nephritic syndrome
GI Inflammation
 Chronic liver disease  Pancreatitis
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 Malnutrition
 Protein-losing enteropathy
Intra-abdominal malignancy
 Pancreatic/gastric/colonic ca
 Ovarian ca
 Metastasis to liver
 Metastasis to peritonium
History
Drug allergy
Date of admission
Symptoms
1. Abdominal distension
 duration
 acute/gradual
 quantity = how many inches? , weight gain
 associated with LL edema, SOB (exertional, orthopnea, PND), faciel edema
 fever and abdominal pain and diarrhea > SBP
Aetiology
1. CVS
 History of heart disease
 Chest pain, sob, diaphoresis
2. Renal
 Urine output (oliguria, appears concentrated)
 Hematuria and frothy urine
3. GIT
 Chronic bloody diarrhea
 LOA, LOW
 History of liver disease – jaundice, easy bruising, pruritis changes in uring and stool, fatigue
4. Infection
 History of TB
5. Inflammation
 Acute epigasttric pain radiating to the back
6. Malignancy
 LOA, LOW, fever, fatigue, abdominal pain, jaundice, recent changes in bowel habits,
haematochezia, melena, irregular menstrual bleeding
Underlying etiology for liver cirrhosis

Triggers for present episode
1. BGIT
2. Sepsis
3. Recent drug intake
4. Recent surgery/trauma
Complications (usually of CLD and cirrhosis)

1. Bleeding varices = hematemesis, haematochezia, melena
2. Encephalopathy = lethargy, drowsiness, confusion, personality changes
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Systemic review
Management prior and during admission
Has this happened before? Describe prior experiences
Differentials
 Fat
 Fetus
 Flatus
 Faeces
 Fluid
 Filthy big tumour
Investigations
ECG, Cardiac enzymes, CXR = CCF
Urine
 Urine dipstick = proteinuria, hematuria
 UFEME
 Urine phase contrast microscopy
 Urine PCR or 24hr UTP
Bloods
 FBC = WBC ↑ (SBP), HCT (hypovolemia)
 U/E/Cr = renal impairment
 LFT = liver impairment, albumin
 ESR, CRP
Imaging
 U/S Hepatobiliary system (HBS)
 CTAP
Microbiology
 Abdominal paracentesis
 Both diagnostic and therapeutic
 Clinical parameters
 Appearance (straw coloured; turbid = pyogenic, TB; bloody = malignant, TB; chylous =
pancreatitis)
 Clinical chemistry (cell count and differential; protein; albumin; glucose; amylase)
 Gram stain, microscopy, c/s, AFB smear, TB c/s
 Fluid cytology
 Serum-ascitic albumin gradient = serum albumin – ascitic albumin
 Correlates directly with portal pressure
 Transudate = gradient > 1.2 g/dl
 Excudate = gradient < 1.2 g/dl
 May be associated with a right pleural effusion via trans-diaphragmmatic lymphatics =
subpulmonic effusion
- Management = fluid restriction, strict I/O charting, vitals monitoring, IV albumin 20% with
diuretics
Management
Non-pharmacological
 Fluid restriction (1 L/day)
 Low salt diet
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 Strict I/O charing and daily weights
 Monitor vitals 4hourly – inform doctor if SBP < 100mmHg or HR > 100 bpm
Pharmacological
 IV diuretic therapy = frusemide spironolactone
 Albumin 20% only if patient is hypotensive – to bring back fluid from 3rd space
Watch out for

a) Hypokalemia
 diuretic therapy
 abdominal paracentensis ( >2-3 L a day may cause hypovolemia and hypohalemia)
 may also precipitate hepactic encephalopathy
b) dehydration
 over vigorous dieresis
 negative fluid balance not more than 1L a day
Diuretic-resistant ascites
 therapeutic abdominal paracentesis with IV albumin 20%
 TIPPS
 Liver transplant
Approach to ascites
 Abdominal masses
 Epigastric mass (gastric ca)
 RIF mass (ovarian ca, cecal ca)
 LIF mass (desceding colonic ca, sigmoid ca)
 If patient is jaundiced
a) Signs of CLD – liver cirrhosis Cx portal HPT
b) Minimal signs of CLD + smooth tender hepatomegaly = budd-chiari syndrome
+ craggy liver = intra-abdominal malignancy with liver/peritoneal mets
 Feel for supraclavicular LAD
 If patient is not jaundiced and no signs of CLD
a) Leuconychia – nephritic syndrome
b) Raised JVP – constrictive pericarditis or right heart failure
 If all negative
a) TB peritonitis = chest examination
b) Carcinomatosis peritoneii = paracentesis + FNAC to see malignant cells
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Medicine (GIT) = Chronic liver disease and Liver cirrhosis
Chronic liver disease
 Liver disease persisting >6 months based on LFT and histology
Liver cirrhosis
Strict criteria
a. Diffuse fibrosis
o Occurs in portal tracts, central veins and space of Disse
o Inflammation stimulates stellate cells in space of Disse  transforms into myofibroblasts
o Extension of fibrosis from space of Disse to other parts of lobule causes sinusoids to separate
from hepatocytes
o Venulization = sinusoids converted from fenestrated endothelial channels with free exchange of
solutes to high pressures and fast-flowing channels without such exchange
o Shunting of blood directly from portan vein to central vein = no detoxification of metabolites
hepatocytes derived of nutrients
b. Nodule formation = consisting of regenerating hepatocytes
c. Disruption of tissue architecture = bridging fibrosis and shunt formation
Results in subdivision of liver into nodules of regenerating hepatocytes surrounded by scar tissue
Aetiology
 Vascular
o Tricuspid regurgitation/right heart failure (cardiac cirrhosis)
o Veno-occlusive disease
o Budd Chiari syndrome
 Infective
o Hep B and C infection
 Toxin
o Chronic alcoholism
o Drugs (methotrexate, amiodarone)
o alfatoxin
 Autoimmune
o Autoimmune hepatitis
o Primary biliary cirrhosis
o Primary sclerosing cholangitis
o Secondary biliary cirrhosis (RPC or chronic CBD stones)
 Metabolic
o Wilson’s disease
o Secondary haemochromatosis (DO NOT mention HH as gene not found locally)
o Alpha1 antitrypsin deficiency
 Cryptogenic
History
Aetiology
 Vascular
o History of heart failure
 Infective
o Personal history of Hep B/C infection
o History of Hep B vaccination
o Maternal history of Hep B infection
o History of blood transfusion, IVDA, CSW contact, tattooing
 Toxin
o History of chronic alcoholism
o History of cytotoxic drug ingestion
 Autoimmune
o History of rash, joint pain and swelling
 Metabolic
128
o Family history of liver disease
Complications
 Hypoalbuminaemia
o Lover limb edema
o Abdominal distension +abdominal pain/fever (SBP)
 Bilirubin
o Jaundice
o pruritus
 Coagulopathy
o Easy bruisability
o Petechiae  may present like ITP
o Mucocutaneous bleeding
o menorrhagia
 Bleeding varices - Haematemesis, haematochezia, melena
 Encephalopathy - lethargy drowiness, confusion, sleep-wake inversion, personality change
 Hepatorenal syndrome - oligouria
 HCC
o LOA, LOW, fever, fatigue
o Regular f/u done? Annual U/S and AFP?
 CLD = jaundice, clubbing, leuconychia, palmar erythema, bruising, scratch marks, fetor hepaticus, spider
naevi, gynaecomastia, loss of axillary hair, testicular atrophy, lower limb edema
 Portal HPT = dilated veins, ascites, splenomegaly
 Encephalopathy = terminal asterixis
 HCC = hard and craggy hepatomegaly
 Alcoholism = duputyren’s contracture, parotid enlargement
 Hep B/C infection = tattoos, IV needle marks
Investigations
Aims
 Confirm diagnosis
 Look for underlying aetiology
 Assess severity
 Look for complications
Bloods
 FBC
o Hb decrease, WBC decrease, pII decrease (hypersplenism)
o WBC increase (SBP)
o Hb decrease (folate/iron-deficiency anemia)
o MCV decrease (alcoholism)
 LFT
o Bilirubin increase
o AST>ALT (alcoholic liver disease)
o GGT increase (alcohol liver disease)
o ALP increase (biliary obstruction)
o Albumin (marker of synthetic function; malnutrition)
 PT/PTT = prolonged PT (marker of synthetic function)
 U/E/Cr = hepatorenal syndrome
 Hepatitis serology
 Autoimmune screen
 Tumor markers = AFP
Imaging
129
 U/S HBS
o Development of HCC
o Biliary obbstruction
Liver biopsy/ERCP
Assessing severity
Child’s Pugh score
 Originally used to predict peri-operative morality
 Now used for
o Evaluating prognosis of liver cirrhosis
o Management (determine treatment required, necessity of liver transplant)
Measure 1 point 2 points 3 points

Albumin >35 28-35 <28
Bilirubin <34 34-50 >50
Coagulopathy (PT) 1-4s 4-6s >6s
Distension (ascites) None Mild Severe
Encephalopathy none Grade 1-2 Grade 3-5
Points Class Life expectancy Peri-operative

mortality
5-6 A 15-20 yrs 10%
7-9 B Candidate for 30%
transplant
10-15 C 1-3months 82%
Management
Ascites/Lower limb edema
 Fluid restriction
 Low-salt diet
 Strict I/O charting and daily weights
 IV diuretics = Furosemide +/- spironolactone
 Abdominal paracentensis (intermittent peritoneal taps)
o Therapeutic = relieves SOB
o Diagnostic = rule out peritonitis
 Peritoneovenous shunt
Spontaneous bacterial peritonitis

 Usually caused by S pneumoniae
 Investigations = abdominal paracentesis
 Empirical Abx = IV rocephine 1g OM
 Prophylactic Abx = PO Ciprofloxacin 250mg BD X 3/12
Portal HPT
 Results in = varices, ascites and spleomegaly
 Varices
o Portal gastropathy (watermelon stomach = strips of dark red and light red)
o Esophageal varices
o Caput medusae
o Haemorrhoids
 Management
o Propanolol 20mg BD
o TIPPS (does nt reduce mortality)
o OGD with banding/sclerotherapy
Bleeding varices  refer Surgery

130
Hepatic encephalopathy
 Identify triggers and treat
o Increase protein/urea load = excess dietary protein, constipation, BGIT, uraemia
o Infective = sepsis, HDV infection
o Drug-induced = alcohol binge, anti-depressants, narcotics, sedatives
o Trauma = surgery, porto systemic shunts, paracentensis (>3-5L will result in hypoK)
o Metabolic = hypokalemia
o Neoplastic = HCC
 Low-protein diet
 Constipation = fleet enema STAT, lactulose
 Neomycin = decreases bacterial decomposition of urea into ammonia
Malnutrition
 Vitamin D and calcium supplements
 IM vit K injections
Pruritus
 Ursodeoxycholic acid
Hepatic decompensation
 Jaundice
 Hepatic flap
 Coagulopathy
 Ascites
 Lower limb edema
131
Medicine (GIT) = Hepatomegaly
Causes of hepatomegaly
Right heart failure
Constructive pericarditis
Vascular IVC obstruction
Budd-Chiari syndrome (malignancy = myeloproliferative (PRV) and intra abdominal
(HCC, RCC); PNH, IBD, OCP, SLE/APLS)
Bacterial (Salmonella, Shigella)
Infective Viral (hepatitis, CMV, EBV)
Protozoal (malaria, amoebiasis)
Trauma Haematoma
Primary biliary cirrhosis
Primary sclerosing cholangitis
Autoimmune
SLE
RA
Fatty liver (alcohol, DM, obesity, pregnancy, Cushing syndrome, hyperthyroidism,
IBD, steroids, methotexate)
Metabolic
Storage disorders (type 4 glycogen storage disease, Wilson’s disease, cystic fibrosis,
haemochromatosis, 1-antitrypsin deficiency)
Amyloidosis
Infiltrative
Sarcoidosis
Primary (HCC, hepatic adenoma, hepatoblastoma, hemangioma)
Neoplastic
Secondary (metastasis)
Lymphoma (Hodgkin’s, non-Hodgkin’s)
Lymphoproliferative disease
Haematological
Myeloproliferative disease
Chronic haemolytic anaemia (spherocytosis, G6PD deficiency, thalessemia)
Common causes
 Moderate-large liver
a) Malignancy
b) Fatty liver (esp alcoholic liver disease)
c) Myeloproliferative disease
d) Right heart failure
 Hard and knobbly liver
a) Malignancy
b) Macronodular cirrhosis
c) Cystic  APKD, hydatid
d) Granulomatous/gummatous syphilis
e) Amyloidosis
# glass eye + hard knobbly liver = 1° ocular melanoma with liver metastasis
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Chronic Liver disease
Area Sign Aetiology to consider

Head and neck Xanthelesma Primary biliary cirrhosis
(females)  Must always consider in a middle-aged lady
with splenomegaly and minimal signs of CLD
Slate-grey Haemochromatosis
(males)
Parotidomegaly Alcoholic liver disease
 Liver is typically big even if cirrhotic
Raised JVP Right heart failure
Constrictive pericarditis
Kayser- Wilson’s disease
fleischer rings
Limb Duputyren’s Alcoholic liver disease
contracture  Liver is typically big even if cirrhotic
Chorea Wilson’s disease
Tattoo Post-viral (likely Hepatitis B)
Pyoderma Ulcerative colitis
gangrenosum
Lungs Lower zone 1-antitrypsin deficiency
emphysema
-thalessemia major
Short stature
Hyperpigmented
Overall
Thalessemic facies (frontal bossing, flat nosebridge,
maxillary hyperplasia)
Looks younger for age
Pituitary haemosiderosis Hypopigmented areolae
Loss of axillary hair
JVP v wave
Cardiac haemosiderosis Pulsatile liver
Lower limb edema
Hypocount marks on fingers
Pancreatic haemosiderosis
Diabetic dermopathy
Intervention Splenectomy
Request Gonadal examination
Specific conditions
Haemochromatosis
Request to examine for:
a) Arthropathy pseudogout
b) CCFcardiomyopathy
c) Testicular atrophy  pituitary involvement
d) Glycosuria with urine dipstick  DM
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Wilson’s Disease
Area Sign Interpretation
Overall Short stature Rickets secondary to
proximal RTA
Eyes Ptosis Penicillamine-induced MG
Pallor and jaundice Coomb’s negative
haemolytic anaemia
Kayser-Fleischer rings Copper deposits in
Descemet’s membrane of
cornea predominantly at 12
and 6 o’clock positions. Can
also occur in PBC and
cryptogenic cirrhosis. Look
out for sunflower cataract
as well
Face Malar Rash Penicillamine-induced
lupus
Upper limb Small hand joint arthritis Penicillamine-induced
lupus
Tremor/chorea Extrapyramidal syndrome
Lower limb Swollen knees Pseudogout
Request urinalysis for glycosuria (proximal RTA)
Chronic UC
CLD + pyoderma gangrenosum = chronic UC and
a) Cirrhosis
b) Chronic active hepatitis
c) Primary sclerosing cholangitis
d) Cholangiocarcinoma
e) Metastatic colorectal cancer
Request to examine
a) Joints sacroilitis, ankylosing spondylitis, peripheral large joint arthritis
b) Skin  erythema nodosum, pyoderma gangrenosum
c) Mouth  aphthous ulcers
d) Ocular  uveitis, iritis, episcleritis
Template for presentation (a)

“In summary, this patient has hepatomegaly likely secondary to chronic liver disease. I say this because
a) Evidence of stigmata of CLD found on peripheral examination
b) Presence of hepatomegaly measuring ___cm along the mid clavicular line and of ___consistency
The aetiology is likely to be secondary to Hep B virus (high local endemicity) or alcohol (duputyren’s
contracture, parotidomegaly). This is/is not complicated by portal hypertension and hypoalbuminemia.”
Template for presentation (b)

“In summary this patient has hepatosplenomegaly likely secondary to liver cirrhosis complicated by portal
hypertension. I say this because of
a) Evidence of stigmata of CLD found on peripheral examination
b) Presence of hepatomegaly measuring __cm along the mid-clavicular line and of ___consistency
c) Presence of splenomegaly measuring __cm
d) Features suggestive of portal HPT
This is/is not complicated by hypoalbuminaemia or hepatic encephalopathy”
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Medicine (GIT) = Jaundice (history-taking)
Name/age/ethnicity/gender
Occupation
Date of admission
1. Jaundice
- Duration
- Onset=acute or gradual
- Skin and eyes affected?
- Progression – getting better, worsening, fluctuating (periampullary ca, gallstones)
2. Obstructive
- Tea-coloured urine
- Acholic stools
- Steatorrhoea
- Pruritus
- Bleeding tendencies (gum bleeding, easy bruising)
3. Abdominal pain (epigastric/RHC pain) = obstructive/hepatic jaundice
4. Fever (a/w chills and rigors)
5. LOA, LOW, malaise
6. Nausea/vomiting
7. Changes in bowel habit (?CRC with liver mets)
8. Melena/PR bleeding (necrosis of periampullary ca? CRC with liver mets, portal HPT)
9. Abdominal distension and lower limb oedema
Aetiology
1. Pre-hepatic = symptoms of anaemia (pallor, chest pain, SOB, giddiness, palpitations)
History of G6PD deficiency and thalassaemia
History of recent blood transfusion
2. Hepatic
#infective
- Travel history
- Contact history
- Recent shellfish/seafood ingestion
- History of Hep B/C infection
- Maternal history/family history of Hep B/C
- Sexual history
- History of blood transfusion/tattoo-ing/IVDA
#drugs
- Alcoholism/recent alcoholic binge
- Recent drug/TCM intake
#autoimmune
- Rash, joint pain and swelling
#neoplasia
- Evidence of mets  chest pain, SOB, bone pain
- If primary: change in bowel habits, melena, tenesmus, haemoptysis
3. Post-hepatic
- History of gallstones
- History of epigastric pain radiating to the back (pancreatic ca)
- History of biliary surgery/instrumentation
Complications
1. Liver failure (acute/chronic)
- Coagulopathy
135
- Oedema = abdominal distension, ankle oedema
- Encephalopathy – confusion, drowsy, personality changes
2. Hepatorenal syndrome
- Decrease in urine output
Has this happened before?

1. CCF
2. Valve replacement mechanical haemolysis
3. DM, HPT, HCL, AMI, IHD, CVA, cancer, asthma
4. Previous hospitalizations and surgeries
Drug history
1. Any drug allergies
Social history
1. Smoker
2. Alcoholic drinker
3. Family set-up
4. Main caregiver
5. Finances
6. Type of housing
7. Lift-landing
8. Functional status
Family history
1. Gallstones
2. Cancers CRC, HCC
136
Medicine (GIT) = Approach to Jaundice
Definitions
 Jaundice=yellowish skin discolouration due to excess bilirubin in the blood (>35umol/L)
 Icterus=yellowish sclera discolouration
 Cholestasis=systemic retention of bilirubin, bile salts and cholesterol due to impaired biliary excretion
(hepatic dysfunction; intra/extra-hepatic biliary obstruction)
Other conditions that may mimic jaundice
 Hypercarotenaemia – absence of yellow scleral and mucosal discolouration, normal urine colour,
presence of yellow-brown pigmentation of carotenoid pigment in palms, soles and nasolabial folds.
 Chronic renal failure – sallow
 Haemochromatosis (hereditary or transfusion-related)
 Haemosiderosis
Features suggestive of jaundice
- involvement of skin and sclera,
- discolouration of urine and faeces
- pruritus
- epigastric/RHC tenderness (liver enlargement  stretching of Glisson’s capsule; inflammation of
biliary tree)
Bilirubin
 end-product of heme degradation heme
–  biliverdin 
Heme
bilirubin Biliverdin
 Formed outside the liver in cells of mononuclear
oxygenase phagocyte system
reductase
 Bound to serum albumin
 Hepatic processing
(a) Carrier-mediated uptake at sinusoidal membrane
(b) Conjugation with glucuronic acid to form bilirubin glucuronide
(c) Excreted in bile
 Most bilirubin glucuronide are deconjugated by gut bacteria to colourless urobilinogens
 Urobilinogens and remaining bilirubin glucuronides are largely excreted in the faeces
 ~20% of urobilinogens are reabsorbed in the ileum and colon and returned to the liver to be re-
excreted into bile (enterohepatic circulation)
 Small amount escaping this enterohepatic circulation is excreted in urine
Causes of hyperbilirubinaemia
(a) Over-production of bilirubin  haemolytic (pre-hepatic) jaundice
(b) Impaired hepatocyte uptake, conjugation or excretion of bilirubin hepatocellular (hepatic) jaundice
(c) Obstruction of bile outflow  obstructive (post-hepatic) jaundice
Pathophysiological classification
Predominantly unconjugated hyperbilirubinaemia
- Unconjugated bilirubin tightly complexed to serum albumin insoluble in water not excreted in
urine
- Unbound albumin-free portion highly toxic  deposited in brainkernicterus
- High affinity for basal ganglia choreoathetotic CP
 Over production of bilirubin
- Haemolytic anaemia
o enzyme defects (G6PD deficiency, pyruvate kinase deficiency)
o Membrane defects (spherocytosis, elliptocytosis)
o Hb synthesis defects (thalassemia, sickle cell anaemia)
o Blood group and Rh incompatibility
o Immune-mediated (drug-induced, SLE, idiopathic)
 Impaired hepatocyte uptake
- Drugs (interfere with membranous carrier systems) = rifampicin
- Gilbert syndrome (decreased uridine diphosphate-glucuronosyltransferase)
137
o Mild heterogeneous condition affecting 6% of the population
o Usually detected during recurrent illness or fasting
o No clinical consequences
 Impaired hepatocyte conjugation
- Gilbert syndrome (decreased uridine diphosphate-glucuronosyltransferase)
- Crigler-Najjar syndrome s I/II (lack or deficiency of uridine diphosphate-glucuronosyltransferase)
o Type 1 more fatal than Type 2 (former is unresponsive to phenobarbitone and requires
liver transplant)
o Causes kernicterus with neurological damage
- Hepatocellular disease
o Vascular (CCF, right heart failure, hypotension, Budd-Chiari syndrome)
o Infected (viral hepatitis, EMV, CMV, HSV, dengue, leptospirosis)
o Toxin (alcohol binge, drugs – paracetamol OD, anti-TB, statins, anti-epileptics, OC, TCM)
o Autoimmune (SLE, idiopathic)
o Metabolic (fatty liver, Wilson’s disease, haemochromatosis, α1-antitrypsin deficiency)
o Infiltrative (sarcoidosis, amyloidosis)
o Neoplasia (HCC, liver mets, leukaemia, lymphoma, myeloproliferative disorders,
myelodysplasia)
Predominantly conjugated hyperbilirubinaemia
- Designated when >15% of an elevated serum bilirubin is conjugated
- Conjugated bilirubin is water-soluble, non-toxic, loosely bound to serum albumin and is excreted in
urine
- Typically associated with cholestasis
 Impaired intra-hepatic excretion of bilirubin
- Dubin-Johnson syndrome
o Defect in the transport protein responsible for excretion of bilirubin glucuronides
o Darkly-pigmented liver
- Rotor’s syndrome
o Variant of DJS
o Liver is non-pigmented
- Hepatocellular disease (refer above + TPN)
 Intra-hepatic biliary obstruction
- Primary biliary cirrhosis
- Primary sclerosing cholangitis
o Recurrent pyogenic cholangitis – recurrent febrile episodes of jaundice
o Vicious cycle of intra-hepatic biliary ductal stonesscarringstrictures
- Cholangiocarcinoma
 Extra-hepatic biliary obstruction
- Gallstones in the CBD
- Liver abscess (amoebic, TB, meliodosis, enteric gram –ve bacilli)
- Ca head of pancreas
- Periampullary ca (cholangiocarcinoma, Ca ampulla of Vater, Ca duodenum)
- Biliary strictures
- Secondary biliary cirrhosis
- Lymphadenopathy at porta hepatis
Clinical features
Pre-hepatic jaundice
Onset Acute
Precipitating factor Usually present
1st episode Usually not the first time
Urine and stools Dark urine and stools
Anaemia Usually present, +/- splenomegaly
Progression Usually self-limiting and gradually improves once
precipitating factor is removed
Hepatic jaundice
138
Onset Viralgradual with prodromal symptoms
Drug/alcohol-inducedacute
Pain Dull and usually insignificant
Usually due to stretching of Glisson’s capsule
Fever May occur with viral hepatitis
Low-grade and non-specific
Urine and stools Dark urine and stools
Progression Usually self-limiting (die or get better)
Post-hepatic jaundice
Onset Gallstoneacute
Pain Gallstonebiliary colic (tenderness)
Ca pancreasepigastric pain radiating to the back
Hepatomegaly (Stretching of Glisson’s capsule)congestion
of intra-hepatic biliary spaces
Fever Characteristic of cholangitis (Charcot’s triad – feverRHC
painjaundice)
Spiking with chills and rigors
Urine and stools Dark urine
Acholic stools steatorrhoea
Progression Progressive and relentless
Fluctuating
- periampullary ca (necrosis of tumour may relieve
obstruction)
- Gallstones
Benign (Sx jaundice) Malignant (Sx jaundice)
Onset Gallstoneacute Usually gradual
Constitutional symptoms Usually absent LOA, LOW, fatigue, fever
Pain Acute and colicky Painless jaundice
Ca pancreasepigastric pain radiating to
back
Courvoisier’s sign: non-tender palpable gall bladder is unlikely to be caused
by gallstones, as enlargement of gall bladder is likely in Ca pancreas, not in
gallstones (- too acute).
Cholangitis More Less
- Charcot’s triad -regurgitation of small bowel -relentless tumour growth eventually leads
- Raynaud’s contents up biliary tree to complete obstruction
pentad ->90% will have infected bile -No regurgitation of small bowel contents to
cause infection
2-hit phenomenon Usually obstructs biliary tree Obstructs both biliary and pancreatic
only ductssteatorrhoea and LOW
Endocrine insufficiency Absent Worsens existing DM
Newly diagnosed DM
Migratory thrombophlebitis Usually absent Suggests Ca pancreas (esp body and tail)
Progression Self-limiting if gallstone Relentless and progressive
passes Fluctuatingperiampullary ca
Complications
1. Acute jaundice Acute liver failure
- Coagulopathy
- Ascites/LL oedema
- Encephalopathy=forgetfulness, confusion, drowsiness
- Hepatorenal syndrome – renal failure due to liver impairment
o Oliguria/anuria (urine becomes lesser and more concentrated(
o Liver unable to detoxify blood either due to porto-systemic shunting or impaired
hepatocyte function
 High levels of circulating endotoxins
139
 Formation and deposition of immune complexes in the glomeruli
glomerular/tubular dysfunction
- Hypoglycaemia
2. HBS sepsis
3. Malabsorption (protein, fat, vitamins A/D/E/K)
- Protein malnutritionascites, LL oedema pleural effusion
- Hypoglycaemia
- Fat malnutritionsteatorrhoea, LOW, easy bruising
4. Coagulopathy
- Mechanisms
o DIVC (HBS sepsis)
o Lack of production of coagulation factors (liver impairment)
o Lack of absorption of vitamin K (obstructive jaundice, ca pancreas)
- Clinical features
o BGIT (haematemesis, melena, haematochezia)
o Easy bruising
o ICH
o BGUT (haematuria, menorrhagia)
- Management
o correct by giving vit K if PT>3 above upper limit of normal
o Correct within 48 hrscholestasis
o Remains prolonged hepatocellular insufficiency
5. Portal hypertension
- Secondary to long-standing biliary obstructionbiliary cirrhosis
- Pathogenesis
o Accumulation of bile pigments within hepatocytes (foamy degeneration)
o Dilated bile canaliculi with green-brown plugs of bile
o Dilatation and proliferation of bile ductules (secondary to bile stasis and back pressure)
o Ruptured canaliculi leading to extravasation of bile into sinusoids
o Inflammationoedema + neutrophilic infiltrateportal tract fibrosis and cirrhosis
- Cx-ascites, splenomegaly, dilated veins (gastro-oesophageal varices, caput medusa, haemorrhoids),
portal hypertensive gastropathy: mucosal changes.
Investigations
Blood:
1. FBC
- WCC (leucocytosis in infections; leucopoenia in biliary cirrhosis and hypersplenism)
- Hb (anaemia if there is haemolysis, bleeding or underlying malignancy)reticulocyte count
- Haptoglobin assay
- PBF
2. U/E/Cr
- Renal impairment (hepatorenal syndrome)
- Serum glucose (hypoglycaemia)
3. LFT
(a) Establish if it is a predominantly unconjugated/conjugated hyperbilirubinaemia
(b) Hepatocyte integrity AST, ALT, LDH
(c) Biliary obstructionALP, GGT
(d) Synthetic function
- albumin, PT/PTT
- ALT>AST in viral hepatitis
- AST>ALT in alcoholic hepatitis
- Raised ALP/GGT in obstructive jaundice
- GGT specific for alcoholic hepatitis
4. PT/PTT
- Measure of liver function (PT affected as factors 5&7 have the shortest t1/2)
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- Check for coagulopathy
5. Serum ammonia = measure of liver function
6. Hepatitis screen
- Anti-HAV Ig M, anti-HAV Ig G
- HBsAg, HBeA (active replication), anti-HBc Ig M, anti-HBc Ig G
- Anti-HCV, HCV RNA
7. Autoimmune markers (anti-ds DNA, ANA, anti-mitochondrial Ab, anti-Sm Ab, ESR, CRP)
8. Tumour markers = α-fetoprotein, CA 19.9, CA 125, CEA
Imaging:
1. AXR
- Gallstones
- Pneumobilia (cholecystenteric fistula, cholangitis with gas-producing organism)
2. U/S HBS
- Dilated intra-hepatic ducts (obstruction)
- Gallstones in gallbladder
- Liver cirrhosis and masses
- Ascites
3. CT AP
- Gallstones in gallbladder or biliary tree
- Liver and pancreatic masses
- Level of biliary obstruction
- Double-duct sign (dilatation of both CBD and pancreatic duct  periampullary ca)
- LAD at porta hepatitis
- Ascites
4. CXR
- Lung primary or mets
5. ERCP (endoscopic retrograde cholangiopancreatography)
- If gallstones, lower CBD or pancreatic head pathology suspected
- Diagnostic
o Direct visualisation
o Obtain samples for histology/cytology (periampullary region, pancreatic fluid and bile)
- Therapeutic
o Remove gallstones
o Sphincterotomy
- Stenting of stricture at lower end
o Contraindications
o Gastrectomy (ECRP poses high risk of perforation as stomach is disconnected from
duodenum)
- Complications
o Traumatic pancreatitis
o Pancreatic/biliary sepsis
6. PTC
- If there is dilatation of intra-hepatic ducts or unsuccessful ERCP
- Diagnostic
o Direct visualisation
- Therapeutic
o Insert catheter for drainage
- Contraindications
o Coagulopathy
o Ascites (unable to tamponade liver puncture)
o HBS sepsis
7. MRCP
- If patient has contraindications to ERCP/PTC
8. Liver biopsy
- US/CT-guided core liver biopsy
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- Determine hepatic causes of jaundice/grade liver tumour
Decompensated liver cirrhosis
 BGIT
 Constipation
 Sepsis
 Drug-inducedalcohol, steroids
 Hep D infection
 HCC
Post-operative jaundice
(Usually occurs in first 3 post-operative weeks)
 Resorption
o Haematoma
o Haemoperitoneum
o Haemolysis of transfused RBCs (shorter t1/2)
o G6PD deficiency
 Impaired hepatocellular function
o Halogenated anaesthetics
o Sepsis
o Hepatic ischaemia 2° perioperative hypotension
 Extra-hepatic biliary obstruction
o Biliary stones
o Injury to biliary tree
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Medicine (GIT) = Acute Hepatitis
Aetiology
 Vascular: Ischemia
 Infective: Viral (hepatitis viruses, CMV, EBV, HSV, dengue)
Bacterial (salmonella, shigella)
Parasitic (malaria)
 Drug induced: Alcohol, paracetamol, TCM, anti-TB drugs (e.g. isonazid, rifampicin, pyrazinamide),
anti-convulsants (e.g. sodium valporate), satins
 Autoimmune: Autoimmune hepatitis
 Metabolic: Wilson’s disease
 Infiltrative:
 Neoplastic: Massive malignant infiltration
ALT-AST reversal
 Most liver diseases are characterized by greater ALT elevations than AST elevations
 Exception where AST: ALT ≥ 2
o Alcohol
o Drug induced
o Infections (e.g. salmonella, dengue)
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Medicine (GIT) = Viral Hepatitis
Introduction
 Viral hepatitis is caused by viruses that cause inflammation to the liver
Spectrum of clinical manifestations

 Asymptomatic/ subclinical infection = serologic evidence
 Acute hepatitis: symptoms are common to all viruses
 Carrier state = asymptomatic individual but harbouring replicating virus
 Chronic hepatitis → liver cirrhosis
Systemic viral infections
 Infectious mononucleosis (EBV)
 CMV
 Yellow fever
 Dengue fever
 Rubella
 Haantan virus
Immunological responses
 Normal → acute hepatitis
 Less adequate → chronic hepatitis
 Inadequate → asymptomatic
 Hyper → fulminant hepatitis
Acute hepatitis
4 phases
1. Incubation period
 Peak infectivity = last asymptomatic days of incubation period to early days of acute symptoms
2. Symptomatic pre-icteral phase
 Usually precedes development of jaundice by a few days to 2 weeks
 Non-specific prodromal illness : headache, myalgia, arthralgia, nausea and anorexia
 Vomitting, diarrhea, RHC pain
 May have dark urine and pale stools
 May have physical signs:
i. Liver is often tender but only minimally enlarged
ii. Occasionally, mild splenomegaly and cervical lymphadenopathy (more frequent in children
or EBV infx)
3. Symptomatic icteric phase
 Mainly conjugated hyperbilirubinaemia
 Common in actue HAV infection; absent in 50% of acute HBV infection; uncommon in acute HCV
 Jaundice may be mild and the diagnosis may be suspected only after finding abnormal liver blood
tests in the setting of non-specific symptoms. Symptoms rarely last longer than 3-6 weeks
4. Convalescence
Chronic hepatitis
 Symptomatic, biochemical or serological evidence of continuing hepatic disease > 6months with
histological evidence of inflammation and necrosis
Aetiology
o Infective = viral hepatitis (HBV, HCV)
o Drugs = chronic alcoholism, isonazid, methotrexate, methyldopa, nitrofurantoin
o Autoimmune = autoimmune hepatitis (may be associate with primary biliary cirrhosis and primary
sclerosing cholangitis)
o Metabolic = Wilson’s disease, haemochromatosis, α1 –antitrypsin deficiency
Clinical course unpredictable

144
o Spontaneous remission
o Indolent disease without progression
o Rapidly progressive disease → cirrhosis
Causes of death
o Liver cirrhosis
o Liver failure
o Haematemesis
o Hepatocellular carcinoma
Hepatitis A virus
 Epidemiology= usually found in developing world → substandard hygiene & sanitation;
prevelance of seropositivity increases with age
 Caused by picornavirus (ssRNA), 1 serotpe
 Mode of transmission=
o faecal oral route
o food & water borne (e.g. eating partially cooked cockles & oysters/ contaminated food & water)
o person-person (e.g. sexual oral-anal)
 Incubation period = 4-6 weeks
o HAV appears in faeces before clinical symptoms (usually 2-3 weeks before jaundice & 1 week after
onset of jaundice)
 Clinical presentation
o Asymptomatic (most) = subclinical & milder than HBV infection
o Acute hepatitis= usually bengn and self limiting
o Worse if superimposed on chronic hepatitis
o Does not cause chronic hepatitis or carrier state
 Complications: Fulminant hepatitis (rare)
 Serological picture:
o Transient viraemia → blood borne transmission rare
o IgM with acute infection → fecal shedding ends as IgM increases
o IgG for long term immunity
Prevention
 Avoid eating contaminated food or drinks
 Boiling 5 mins
 Immunization
o Passive immunization with Ig G
 IgG collected from blood of persons who have been exposed to the hepatitis A
 This method of immunization is getting obsolete because of the short supply of immune
globulin and the potential risk of transmission of other infection through blood products
o HAV vaccine
 Inactivated virus
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 Given in 2 doses, with the second dose being given 6 - 12 months later. Immunity after
vaccine lasts for 10 - 20 years. Protection against hepatitis A begins 4 weeks after
vaccination
People at risk of HAV
 Persons travelling to or working in countries that have high or intermediate rates of hepatitis A
 Persons who work with hepatitis A virus infected primates or with hepatitis A virus in a
research laboratory should be vaccinated.
 Persons with chronic liver disease eg. chronic hepatitis B carriers as these patients have been reported to
have a higher mortality.
Hepatitis B virus
 Epidemiology: endemic in Africa and Asia;
Microbiology
 Belongs to the Hepadnavirus family
 Has 3 well characterized antigens:
o HBsAg (surface) → stimulates anti-HBs
o HBcAg (core) → stimulates anti-HBc
o HBeAg (core associated) → stimulates anti-HBe
 Dane particle = infectious spherical HBsAg particle containing HBcAg core
 HBeAg arises from the same gene as HBcAg
o c gene has 2 initiation codons= precore and core region
o translation intitated at precore region = HBeAg → signal peptide that facilitates secretion (can be
used as surrogate marker for presence of HBcAG)
o translation initiated at core region = HBcAg → no signal peptide →not secreted into serum
 Nucleocapsid
o circular partially ds DNA
o DNA polymerase with reverse transcriptase activity
o HBcAg → remains in hepatocytes for complete assembly of virions, only detected in liver biopsy
samples
 Incubation period = 3-4months

 Pathogenesis
o Cell-mediated mechanisms = destruction of hepatocytes with viral/ modified surface antigens
o Humoral-mediated mechanisms = GN/ vasculitis from circulating immune complex
 Mode of transmission
o Vertical transmission
o Sexual transmission
o Parententral transmission: blood transfusion, organ transplant, needle-stick injury, IV drug abuser
 Clinical presentation:
o Asymptomatic disease (90%)
o Acute hepatitis
 Fulminant hepatitis rare
o Carrier status (10-15%)
o Chronic hepatitis (5%)
o Liver cirrhosis (3%)
o HCC (1%)
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Serology
1) Acute infection with recovery

 HBsAg= appears before onset of symptoms, peaks and declines rapidly, undetectable at 3-6months
 HBeAg= appears just after HbsAg, indicates active replication (infectiousness)
i. anti-HBe appears after disappearance of HBeAg (indicates waning infection)
 anti-HBc= IgM appears just prior to the onset of infection (indicates acute infection); replaced by
IgG
i. does not protect against re-infection
ii. serves as a surrogate marker for natural HBV infection
 anti-HBs IgG= appears after acute disease is over
2) Acute infection with progression to chronic disease

 Carrier state = presence of HBsAg > 6 months
 Chronic replication of HBV virions = persistent HBsAg, ±HBeAg and HBV DNA
 Chronic sequel: cirrhosis & HCC
 High risk of becoming a carrier:
i. Age at time of infection
 Perinatal: 85-95%
147
 Infants: 40-50%
 Children: 30-40%
 Adults: 5-10%
ii. Sex – male: female 3:1
iii. Ethnicity – Chinese> Malays> Indians; related to prevalence of female carriers and periantal
infx
iv. Impaired immune responses – transplants, drugs
Markers of past infectivity

 Anti-HBs IgG
 Anti-HBc IgG
 Anti- HBe
HBV mutants
 Pre-core mutant: variant C gene fails to produce HBeAg (–ve HBeAg viraemia); still infections because of
HBcAG
o HBV DNA necessary to detect presence of disease activity
 S mutants: mutation at ‘a’ epitope (HBsAg –ve viraemia) → vaccine not effective; low frequency in
Singapore
Treatment
 Anti-virals: lamivudine, adefovir
 Interferon-α
 Vaccination
Hepatitis C virus
 Caused by Flavivirus, ssRNA
 Transmission: blood-borne, sexual intercourse
 Incubation period: 6-12 weeks
o Mainly asymptomatic
o Acute hepatitis = general milder than HBV; no effective immunity
o Chronic hepatitis = hallmark of HCV infection
 60-80% develop chronic hepatitis
 20% go on to develop liver cirrhosis
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Acute infection with recovery
 HCV RNA detectable for 1-3 weeks
during active infection,
 HCV RNA frequently persists
despite neutralizing antibodies (Abs
present in 50-70% of acute
infection; 30-50% have anti-HCV
Abs after 3-6 weeks)
Chronic infection
 Persistence of HCV RNA despite
neutralising Ab
 Episodic elevations of HCV RNA
and transminases
Treatment
 Ribavirin and IFNα combination therapy → partial efficacy
 No vaccine available; difficult to cover agains the 6 major genotypes
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Hepatitis D virus
 Defective ssRNA virus → requires HBsAg coat to infect cells
 HBV serves as helper virus
Clinical presentation
1. Super infection: chronic HBV carrier exposed to HDV → severe hepatitis
2. Co-infection: exposed to HBV & HDV at the same time
a. HBV must become established first to provide HBsAg required for HDV virion production
b. Chronic hepatitis rare
c. Higher rates of fulminant hepatitis (3-4%)
Serology
 HDV RNA appears just before and during early acute symptomatic infection
 IgM anti-HDV = recent HDV exposure
 To differentiate co-infectin and super infection = correlate with HBV markers
Hepatitis E virus
 Calicivirus, ssRNA
 4 genotypes, endemic in India and the Middle East
 Transmission: faecal-oral, water borne
 Incubation period= 4-6 weeks
 Acute hepatitis
o Usually self-limiting and benign
o Abs are non-protective
 No chronic state or chronic hepatitis
 High rate of fulminant hepatitis in pregnant women (25% fatal); foetal mortality also high
 No vaccines
Serology
 HEV RNA and HEV virions present in stool and liver before onset of symptoms
 IgM anti-HEV present with rising transaminase → IgG
Hepatitis Screen
 HAV=
o Anti- HAV IgM (acute)
o Anti- HAV IgG (previous infection)
 HBV=
o HBsAG, HBeAG, anti-HBc, IgM (acute)
o Anti-HBs IgG, anti-HBe, anti-HBc IgG (previous infection)
 HCV=
o Anti-HCV IgM (acute)
o Anti-HCV IgG (previous infection)
 CMV = anti-CMV IgM
 EBV = anti EBV IgM
 HSV = anti-HSV IgM, HSV PCR (if patient presents with acute liver failure)
150
HAV HBV HCV HDV HEV HGV
Agent Icosohedral capsid, Enveloped dsDNA Enveloped ssRNA Enveloped ssRNA Unenveloped ssRNA ssRNA
ssRNA Calicivirus
Picornavirus Hepadnavirus Flavivirus Flavivirus
Transmission Faecal-oral Parenteral, close Parenteral, close Parenteral, close Waterborne Parenteral
contact, vertical contact contact
Incubation period 2 – 6 weeks 4 – 26 weeks 2 – 26 weeks 4 – 7 weeks 2 – 8 weeks Unknown
(superinfection)
Carrier state None 0.1 – 1% of blood 0.2 – 1% of blood 1 – 10% of drug Unknown / none 1 – 2% of blood
donors; 90 – 95% of donors; <1% are addicts, donors
those infected at healthy carriers haemophiliacs
birth (vertical
transmission); 1 –
10% infected as
adults (esp. If
immune-
compromised)
Chronic hepatitis None 5 – 10% of acute >60%; half then <5% if co-infection None None
infections (adults); progress to cirrhosis with HBV; 80% upon
90% in infected super infection with
neonates HBV
Fulminant hepatitis 0.1 – 0.4% <1% Rare 3 – 4% in co- 0.3 – 3% Unknown
infection 20% in pregnant
females
Hepatocellular Ca No Yes Yes No increase above Unknown, but None
HBV unlikely
Vaccine available Yes Yes No No No No
Others Acute hepatitis Fulminant hepatitis At present, not
(symptomatic, almost never occurs considered
asymptomatic) with HCV pathogenic
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Medicine (GIT) = Alcoholic Liver Disease
*clinical spectrum*
1) fatty change/hepatic steatosis
 Clinical features – asymptomatic, mild increase in serum bilirubin & ALP
 Pathology – soft, greasy hepatomegaly
Fat accumulation within hepatocytes
(micro macro-vesicular)
 Seen within days of ingestion on U/S
 Initially reversible
2) acute alcoholic hepatitis

 Clinical features – fever, RHC pain, jaundice
 RHC pain may result from – alcoholic gastritis, pancreatitis or srteching of Glisson’s capsule
 Spectrum may range from self-limiting episode to fulminant hepatitis
 Potentially reversible
3) alcoholic cirrhosis (10-15% of alcoholics)

 Clinical features – features of Chronic Liver Disease and portal HTN
 Irreversible and potentially fatal
 Micronodular cirrhosis
*physical findings of alcoholism*

 Duputyren’s contracture
 Dilated cardiomyopathy – displaced apex beat, signs of CCF
 Cerebellar signs
 Parotidomegaly
 Proximal myopathy
 Peripheral neuropathy
 Dementia
 Wernicke’s encephalopathy – classic triad of:
1) encephalopathy (confusion, loss of short-term memory)
2) ataxia
3) ophthalmoplegia (nystagmus, gaze palsies)
 Korsakoff’s psychosis/syndrome –
1) anterograde amnesia
2) retrograde amnesia
3) confabulation (invented memories which are then taken as true due to gaps in memory sometimes
associated with blackouts)
4) meagre content in conversation
5) apathy
6) lack of insight
152
*investigations*
 FBC – raised MCV
 LFT – raised ALP, GGT, AST > ALT, raised conjugated bilirubin, decreased albumin
 PT/PTT
 Hepatitis serology
 U/S liver
*causes of death*
 BGIT – haematemesis
 Hepatic encephalopathy
 Hepatorenal syndrome
 Sepsis
 HCC
Medicine (GIT) = Autoimmune Hepatitis
*2 main forms distinguished by type of circulating antibody:

 Type 1 – ANA, anti-SMA (smooth muscle actin) Ab, increased frequency of HLA B8 and
HLA DRw3
 Type 2 – anti-LKM1 (liver kidney microsomal 1) Ab
*epidemiology
 females > males (3:1)
 Premenopausal females
*clinical presentation
 acute hepatitis with autoimmune symptoms (fatigue, arthralgia, myalgia)
 chronic hepatitis
 incidental finding with signs of chronic liver disease
*associated with autoimmune disorders – RA, thyroditis, scleroderma, IBD, pernicious anaemia, IDDM,
AIHA, PSC
*investigations
 FBC – decreased Hb, decreased WBC, decreased platelets (w/ hypersplenism)
 LFT – raised AST
 Hyperglobulinaemia – raised IgG
 Autoimmune screen – ANA, anti-SMA Ab, anti- LKM1 Ab
 Hepatitis serology – negative
 Liver biopsy – mononuclear infiltrates of portal and peri-portal areas,
piecemeal necrosis  fibrosis  cirrhosis
*treatment
(a) immunosuppression – prednisolone, azathioprine (steroid-sparer)
(b) liver transplant
*prognosis – if untreated severe disease:
 40% die within 6 months,
 40% of survivors develop cirrhosis
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Medicine (GIT) = Metabolic Liver Disease
1) Non-alcoholic fatty liver and steatohepatitis

*non-alcoholic fatty liver disease (NAFL)*
 Characterized by increased serum transaminases and hepatic steatosis in the ABSENCE
of heavy alcohol consumption
 Associated with: DM, obesity, pregnancy, methotrexate, steroids, Cushing’s syndrome,
hyperthyroidism
*non-alcoholic steatohepatitis (NASH)*

 Characterized by hepatic steatosis and inflammation in the ABSENCE of heavy alcohol
comsumption
 Pathology: hepatocytes containing fat vacuoles
varying amounts of fibrosis
+/- inflammatory infiltrates
2) Haemochromatosis
*excessive iron accumulation with subsequent deposition in various organs esp. liver and pancreas
*primary haemochromatosis (hereditary haemochromatosis)*
 Autosomal recessive inheritance
 Males > females (6:1)
 Females diagnosed later (menstruation offers protection)
 Pathogenesis: unregulated intestinal Fe absorption  excess Fe  direct toxicity via free radical
formation/lipid peroxidation/Fe-DNA interactions
 Usually presents at around 20-30yrs old
Skin pigmentation – slate-grey appearance

Anterior pituitary gland – adolescent (delayed puberty, hypogonadism)
adult (appears young for age, amenorrhea, impotence/loss of
libido, testicular atrophy)
Pituitary failure – hypopituitarism
Liver – hepatomegaly  cirrhosis  HCC
Pancreas – DM
Heart – cardiomyopathy, arrhythmia
Musculoskeletal – pseudogout
*secondary haemochromatosis*
 Repeated blood transfusions – Thalassemia major, aplastic anaemia, sickle cell disease, myelodysplastic
syndrome, leukaemia, lymphomas
 Increased Fe intake – Fe-dextran injections
*investigations*
 Iron studies – high transferring saturation? High ferritin levels?
 U/S liver – HCC is the commonest cause of death (200x greater risk of getting HCC)
 Liver biopsy (diagnostic) – measure liver stores
 Genetic testing
*management*
 Early venesection – beneficial especially in those who have not developed DM/cirrhosis
154
prolongs life and reverses tissue damage
prevents progression of hepatic disease
3. a1-Antitrypsin deficiency
*autosomal dominant disorder
*pathogenesis – abnormally low levels of a1-antitrypsin (protease inhibitor)
*clinical features
 childhood and adult cirrhosis  HCC
 COPD
*diagnosis: liver biopsy  PAS +ve cytoplasmic globules in periportal hepatocytes

*management: liver transplant, quit smoking
155
Medicine (GIT) = Wilson’s disease (Hepatolenticular Disorder)
*History*
 Hx of consanguinity  Wilson’s disease has an autosomal recessive inheritance
 Considered in any patient younger than 40yrs with unexplained disorder of CNS, hepatitis, chronic
active hepatitis, haemolytic anaemia, unexplained cirrhosis, or has a relative with Wilson’s disease
*Physical Examination*
 Kayser-Fleischer rings: greenish yellow to golden brown pigmentation at the limbus of the cornea due
to deposition of copper in Descemet’s membrane
 Proceed to look for:
o Jaundice
o Sunflower cataracts
o Hepatomegaly
o Signs of liver failure
o Neurological manifestations: tremor, chorea, mask-like
facies
*Presentation*
 Hepatic – 50% of patients (usually presents in 2nd
decade/children)
1) Acute hepatitis – self limited
2) Parenchymal liver disease (chronic hepatitis) – may follow acute hepatitis or develop
insidiously without prior disease
Indistinguishable from chronic active hepatitis and cirrhosis
3) Cirrhosis – may develop insidiously after a lapse of decades
4) Fulminant hepatitis – generally fatal, characterized by progressive jaundice, ascites,
encephalopathy
 Neuropsychiatric – always accompanied by Kayser-Fleischer rings(usually the presenting complaint in

adults)
1) Acute
-bradykinesia
-behavioural change
-involuntary movements
-liver involvement common
-if untreated  death in 2yrs
2) Chronic
-marked proximal ‘wing-beating’ tremor
-dysarthria, dystonia and rigidity
-choreoathetoid movement
-psychosis, behavioural disorders and
dementia
-if untreated  death in 10yrs
156
*Discussion*
 Inheritance
o Autosomal recessive; chromosome 13
o A/w family history of consanguinity
 Pathophysiology
o Excessive absorption of Cu from the small intestine with decreased excretion by liver
o Increased tissue deposition esp in brain, cornea, liver and kindey Fanconi’s Syndrome
(glycosuria)
o Cavitation and neuronal loss occurs within the putamen and globus pallidus (basal ganglia)
 Biochemical changes
o Decreased serum ceruloplasmin
o Serum Cu concentration might be high, low or normal
o Increased urinary Cu excretion
o Increased liver Cu content
 Diagnosis
o Kayser-Fleischer rings + serum ceruloplasmin levels < 20mg/l
o Serum ceruloplasmin level < 200mg/l + Cu concentration in liver biopsy sample > 250 µg/g
o MRI (T2) shows thalamic and putaminal hyperintensity
 Clinical stages
o Stage I: asymptomatic accumulation of Cu in liver
o Stage II: asymptomatic or manifests with haemolytic anaemia or liver failure
o Stage III: Cu accumulates in brain
o Stage IV: progressive neurological disease
 Treatment
o Low Cu diet
o Chelating agent, eg. penicillamine.
-side effects: anaphylaxis, skin rash, bone marrow suppression and glomerulonephritis 
alternate treatment: trientine.
-penicillamine has anti-pyridoxine effect, thus pyridoxine given together
o Zinc sulphate: chelates with Cu in gut  slow maintenance treatment

-must not be given with penicillamine or trientine which can chelate zinc and render treatment
ineffective
o Adequate treatment compatible with normal life expectancy

o Genetic screening for rest of the family
o Liver transplant
157
Surgery (GIT) = Obstructive jaundice
A. Intrahepatic biliary obstruction
*Primary biliary obstruction*
*epidemiology:
 Predominantly affects middle-aged women (~50yrs old)
*pathology
 chronic granulomatous inflammation that destroys interlobular bile ducts  fibrosis  liver cirrhosis
 fatigue
 pruritus (main presenting complaint, may precede jaundice by mths/years)
 occasionally jaundice, RHC pain, diarrhoea/steatorrhea
*complications:
 Osteopenia/osteoporosis (due to malabsorption of fat-soluble Vitamin D)
 Coagulopathy (due to malabsorption of fat-soluble Vitamin K)
 Liver cirrhosis  portal HTN  HCC (relative risk=20)
 Increased risk of cancer overall
*clinical signs:
 Stigmata of chronic liver disease: palmar erythema, leukonychia, bruising, scratch marks, spider naevi,
gynaecomastia
 Digital clubbing
 Xanthelasma and xanthomata (over joints, skin folds and trauma sites)
 Signs of portal HTN: dilated veins, hepatosplenomegaly (early stages), ascites
 Request to examine for: proximal muscle weakness (osteomalacia)
peripheral neuropathy
*associated with autoimmune/connective tissue disorders:

 RA
 Systemic sclerosis
 Hashimoto’s thyroiditis
 Sjogren’s syndrome
*investigations:
 LFT
 PT/PTT
 Fasting lipid panel (should see raised TC levels)
 Anti-mitochondrial Ab
 U/S hepatobiliary system
 Liver biopsy
*management
 Nutrition: reduce fat intake, oral calcium, low-fat milk, vitamins A/D/K supplements , mid chain TG
supplements
 Ursodeoxycholic acid (bile salt therapy): partial replacement of water-soluble bile acids may reduce
pruritus and damage to hepatocytes already affected by autoimmune processes
 Pruritus (retention of bile acids with cholestasis: increase in concentration and up-regulation of
endogenous opioid receptors: 1st line  cholestyramine, 2nd line  ursodeoxycholic acid, rifampicin, 3rd
line  naloxone, propofol
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 Immunosuppressants (corticosteroids, cyclosporine A, azathioprine, tacrolimus, methotrexate)
*prognosis
 Survival < 2 yrs without liver transplant
*Primary sclerosing cholangitis*

*disorder of unknown aetiology characterized by inflammation, fibrosis and strictures of intra- and
extra-hepatic bile ducts
*epidemiology
 Males > females
 20-50yrs old
 L.O.A, L.O.W, fatigue
 Insidious development of jaundice and pruritus
 Intermittent RHC pain
*associated with IBD and HIV infection

*complications
 Chronic biliary obstruction  secondary biliary cirrhosis  liver cirrhosis  chronic liver disease and
portal HTN
 Bacterial cholangitis
 Cholangiocarcinoma (20-30%)
*investigations
 LFT
 PT/PTT
 Autoimmune screen (AMA –ve; ANA and ANCA may be +ve)
 ERCP
 Liver biopsy (fibrous obliterative cholangitis w/ onion skin appearance)
*management
 Conservative (corticosteroids, cholestyramine)
 Surgical (endoscopic stenting, t-tube drainage, liver transplant
*Recurrent pyogenic cholangitis (oriental cholangiohepatitis)*
*vicious cycle of:

 recurrent intrahepatic biliary ductal stone formation  obstruction  cholangitis  strictures
*epidemiology
 Found almost exclusively in S.E.A.
 No gender predilection
 Peak incidence in 3rd and 4th decades of life
 Recurrent bouts of cholangitis
 Pancreatitis
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*complications
 Cholangitis  liver abscess  HBS sepsis
 Pancreatitis
 Biliary obstruction  liver cirrhosis  portal HTN
 Increased risk for cholangiocarcinoma
*investigations
 U/S HBS
 CT A/P
 ERCP/MRCP
*management
 Treatment of acute cholangitis
o Take blood cultures  start on IV empirical broad-spectrum antibiotics  definitive antibiotics
once results available
o Biliary drainage – open vs. percutaneous
 Prevention of long-term complications
o General approach:
- removal of stones with regular surveillance (ERCP, percutaneous, surgery, laser)
- surgical resection of affected hepatobiliary segment with biliary-enteric anastomosis
*Cholangiocarcinoma*
* arises from epithelial cells of the intrahepatic and extrahepatic bile ducts
 Histological subtypes: adenocarcinoma (95%)
squamous cell carcinoma (5%)
*classification
 Intrahepatic (10%)
o Least common
 Extrahepatic (90%)
o Peri-hilar (65%)  confluence to upper border of pancreas
o Distal (25%)  upper border of pancreas to ampulla of Vater
^peri-hilar cholangiocarcinoma:
 Most common
 Also called Klatskin tumours (occur at bifurcation of right and left hepatic ducts)
 Bismuth classification: Type 1 (below the confluence)
Type 2 (reaching the confluence)
Type 3 (occluding common hepatic duct and either right/left hepatic duct)
Type 4 (multicentric)
 Diagnosis usually made in the 7th decade
 Males > females
 Usually presents late  metastatic at time of presentation
 Insidious onset of jaundice, pruritus, RHC pain
 May present with cholangitis
*associations
 Inflammatory conditions (ulcerative colitis, primary sclerosing cholangitis, RPC)
 Fibropolycystic liver conditions (choledochal cyst, Caroli’s disease)
 Parasitic infections (oriental liver fluke, chronic typhoid carrier state)
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 Toxin exposure (thorotrast)
*management
 Curative surgery (rarely possible)  wide resection and reconstruction of biliary tree
o Indications:
 inrahepatic tumour confined to 1 lobe of liver
 Extrahepatic tumour
 Patient fit for surgery
o Contraindications:
 bilateral/multifocal intrahepatic disease
 Invasion of portal vein/hepatic artery
 Nodal involvement
 Distant metastasis
 Palliation
o Stenting
o Surgical bypass – cholecystojejunostomy, choledochojejunostomy
 Adjuvant therapy
o Radiotherapy
o Chemotherapy
*dismal prognosis: 15% 5yr survival rate

B. Extrahepatic biliary obstruction
*Biliary strictures*
*aetiology
 Others (5%): impacted gallstone
 Post-traumatic (95%):
o Causes:
 Surgical
 Blunt abdominal trauma
o Classification:
 Early vs. late
 Early: due to technical problems
 Late: due to vascular insufficiency and problems with healing and fibrosis
 Anastomotic vs. non-anastomotic
 Anastomotic
o Due to post-operative oedema and inflammation
o Management: endoscopic balloon dilatation and stenting
o Require life-long surveillance as high recurrence rate
 Non-anastomotic
o Due to vascular insufficiency or recurrence of underlying disease
o More difficult to treat:
-endoscopic balloon dilatation with sphincterectomy and stenting
-surgery (choledochoduodenostomy, choledochojejunostomy, end-to-
end bile duct anastomosis)
*clinical presentation: intermittent cholangitis
*investigations: PTC/ERCP (depends on level of narrowing)
*complications
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 Cholangitis  liver abscess  HBS sepsis
 Secondary biliary cirrhosis  liver cirrhosis  portal HTN
*Periampullary carcinoma*
*includes: cholangiocarcinoma (involving distal common bile duct)
ampulla of Vater tumour
duodenal adenocarcinoma
*clinical presentation (presents early)

 Obstructive jaundice (intermittent/fluctuating as tumour necrosis periodically re-establishes duct
patency)
 Melaena (as tumour sloughs into duodenum)
 Palpable gallbladder
*metastasis more common than primary tumours
*management: Whipple’s operation
*better prognosis than Ca pancreas

 At time of diagnosis: if 80% are localized and small  resectable for cure
 50% 5 yr survival rates
*Mirizzi syndrome*
*rare cause of obstructive jaundice
*due to lodgement of gallstone in cystic duct/Hartmann pouch causing extrinsic compression of
common bile duct
*aetiology
 Acute/chronic inflammation causing constriction of gallbladder which fuses with and causes secondary
stenosis of common bile duct
 Cholecystocholedochal fistula secondary to direct pressure necrosis of adjacent duct walls
*classification
 Type 1: no fistula present
 Types 2-4: fistula present (depending on size of defect w.r.t. diameter of common bile duct)
*investigations
 U/S HBS
 CT A/P
 ERCP/PTC
*management: surgical (cholecystectomy and closure around T-tube)
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Medicine (GIT) = Liver Failure
Introduction
- Most severe clinical consequence of liver disease
- Large hepatic reserve 80-90 % of hepatocytes destroyed before liver failure sets in
- Pathogenesis
a) Sudden massive hepatic destruction (‘Fulminant hepatitis’)
o Progression of hepatic insufficiency to hepatic encephalopathy within 2-3 weeks
o Subfulminant hepatitis= less rapid course within 3 months
b) End point of progressive hepatic damage
o Usually tipped into decompensation by = sepsis, BGIT, heart failure
- Management
o MARS (membrane adsorbent recirculating system)
o Liver transplant (if not  70-90% mortality)
Aetiology
Fulminant Hepatitis
- Vascular = Ischemia (shock, hypoxia)
- Infective = Hep B > Hep A, HSV
- Drugs = Paracetamol, anti- TB drugs, MAOIs, Carbon Tetrachloride,
Halothane, TCM, Anti- cummisants
- Toxin = Amanita Phalloides (mushroom)
- Metabolic = Wilson’s Disease
- Neoplastic = Massive malignant infiltration (leukaemia)
- Idiopathic
Progressive Hepatic Damage (similar aetiology for cirrhosis)
Hepatic dysfunction without overt necrosis = Hepatocytes viable but unable to
perform normal metabolic function
- Reye syndrome
- Tetracycline toxicity
- Acute fatty liver of pregnancy
Clinical features
Hepatic dysfunction
- Jaundice
- Fetor hepaticus
- Hypoalbuminaemia  lower limb pitting oedema, ascites, pleural effusion
- Hypoglycaemia
- Hyperammonaemia  hepatic encephalopathy
- Hyperoestrogenaemia  palmar erythema, spider naevi, gynaecomastia,
testicular atrophy, loss of axillary hair
Portal hypertension
- Ascites
- Splenomegaly
- Porto-systemic shunts haemorrhoids, caput medusae, gastro-oesophageal varices
Complications
- Coagulopathy (inadequate synthesis of clotting factors2,7,9,10 or DIVC)
- Hepatic encephalopathy
- Hepato-renal syndrome
- Multiple organ failure = cardiovascular collapse, ARDS
- Sepsis
- Fluid electrolyte and acid base disturbances
Hepatic Encephalopathy
- Life threatening disorder of neurotransmission in CNS and NM system
- Reversible if underlying liver condition corrected
- Pathogenesis = Hepatocellular insufficiency leading to decrease in
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detoxification of ammonia
Intra-hepatic shunting (venulization)
Extra-hepatic collaterals that bypass liver and enter into
systemic circulation
- Results in elevated blood ammonia levels Neuronal function impaired
Generalised brain oedema
- Triggers
a) Excess protein/urea load = excess dietary protein, constipation, BGIT,
uraemia
b) Infective = sepsis, HDV infection
c) Drug-induced = alcohol binge, sedatives, narcotics, anti-depressants
d) Trauma = surgery, paracentesis (>3-5 L), porto-systemic shunts
(non-selective)
e) Metabolic = hypokalaemia
f) Neoplastic = HCC
- West Haven Classification
o Stage 0
 Minimal hepatic encephalopathy lack of detectable changes
o Stage 1
 Mild confusion
 Decreased attention span
 Disordered sleep (hypersomnia, insomnia or sleep-wake inversion)
o Stage 2
 Lethargy
 Moderate confusion
 Disorientation
 Personality changes and disinhibition
 ASTERIXIS present
o Stage 3
 Drowsy but arousable
 Marked confusion
 Disorientated to TTP
o Stage 4
 Comatose
 ASTERIXIS absent
- Clinical features
a) Impaired consciousness
b) Limb rigidity and hyper- reflexia
c) Asterixis
d) Seizures
e) EEG changes
- Management
o Treat precipitating cause
o Restrict protein intake
o Ensure adequate bowel movement (fleet enema)
o Liver transplant
Hepato-renal syndrome
- Life-threatening renal failure in patients with severe CLD  no intrinsic renal causes
- Renal function improves with correlation of underlying liver failure
- Pathogenesis = imbalance between systemic vasodilation and renal vascular vasoconstriction results in
decreased renal perfusion pressure  decreased GFR
- Clinical features
o Oliguria
o Rising BUN and creatinine
o Concentrating ability of kidney maintained= hyperosmolar urine; low urinary NA
- Poor prognosis median survival 2 weeks (rapid onset form) to 6 months (insidious-onset form)
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Medicine (GIT) = Portal Hypertension
Introduction
- Increased pressure within portal system such that there is increased resistance to portal blood
floe
- Defined as portal pressure > 5-10 mmHG OR
portal pressure gradient ≥ 12mmHg (pressure difference between
portal and hepatic veins)
- Anatomy of portal system
1) Portal vein drains from = small and large intestines
stomach
spleen
pancreas
gallbladder
2) Superior mesenteric vein + splenic vein unite behind neck of pancreas = portal vein
3) Divides into 2 lobar veins = right branch drains cystic vein
left branch drains umbilical and paraumbilical
veins
4) Coronary vein runs along lesser curvature of stomach = receives distal
oesophageal veins
Aetiology
Pre-hepatic
- Portal vein
o Extrinsic compression = malignancy, LAD
o Thrombosis =malignancy , peritoneal sepsis, pancreatitis
- Splenic vein
o Thrombosis
o Shunting of excessive blood secondary to massive splenomegaly
Intra-hepatic
- Liver cirrhosis
Post-hepatic
- Hepatic vein obstruction (Budd –Chiari Syndrome)
- Veno-occlusive disease
- IVC obstruction
- Right heart failure
- Constrictive pericarditis
Clinical features
- Porto- systemic venous shunts
o Develops wherever systemic and portal circulations share capillary beds
o Principle sites
 Portal gastropathy (watermelon stomach =strips of dark red and light red)
 Cardio- oesophageal junction  oesophageal varices
 Falciform ligament of liver (periumbilical veins)  caput medusae
 Rectum  haemorrhoids
 Retroperitoneum
- Ascites
o may be complicated by peritonitis
- Splenomegaly
o may be complicated by hypersplenism
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- Encephalopathy
Budd- Chiari Symdrome

- Obstruction of ≥ 2 major veins
- Pathogenesis
a) Idiopathic fibrosis of hepatic veins
b) Thrombosis = PRV, OCP
c) Tumour invasion = HCC, RCC
Veno-occlusive disease
- Aetiology
a) Toxic alkaloids (‘brush tea’ from Africa)
b) Cytotoxic drugs
- Results in toxic endothelial injury to hepatic vein  thrombosis and fibrosis
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Medicine (GIT) = Chronic Diarrhea
Introduction
Diarrhea= incr frequency of stool evacuation or change in stool consistency

= passage of >200g of stools a day
Classification
a. secretory (faecal osmotic gap < 50mOsm)
b. osmotic (faecal osmotic gap > 50mOsm)
Chronic Diarrhea= diarrhea of duration of 4 weeks or more

a. bloody
b. steatorrhea
c. non-bloody, non-steatorrhoeic
Bloody
5 typical causes
a. radiation
b. ischaemic colitis (self-limiting)
c. IBD
d. TB
e. enteroinvasive infection
Steatorrhea
-defined as >7g of fat in a 24-hr stool sample for 3 days

-stools are characteristically foul-smelling, pale, tend to float on water & difficult to flush.\
-due to fat malabsorption or maldigestion (uaually associated with malnutrition)
Aetiology
1. Pancreatic disease (e.g. chronic pancreatitis, pancreatic ca)

2. Small bowel disease (e.g. topical sprue, celiac disease, crohn’s disease)
3. Bile salt deficiency ( e.g. cholestatic liver disease)
4. Post-gastrectomy syndromes (e.g. bacterial overgrowth)
Complications
1. LOW (due to fat malabsorption)

2. night-blindness (vitamin A deficiency)
3. osteomalacia, osteoporosis (vitamin D deficiency)
4. coagulopathy (vitamin K deficiency)
Investigations
1. Bloods
-LFT (biliary obstruction)
-autoimmune screen (ANA, anti-SMA, anti-LKM1 Ab, IgG, IgM)
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-amylase (pancreatic disease)
2.Stool studies
-stool fat
-stool elastase/chromotrypsin (pancreatic disease)
3. Imaging
-AXR (pancreatic calcifications)
-CT A/P (ca pancreas)
-U/S HBS or ERCP (biliary obstruction)
Treatment
1. fat restriction
2. supplementation of pancreastic enqyme extracts
3. medium-chain triglycerides
4. treat cause (e.g antibiotics for bacterial overgrowth, steroids for CD)
Non-bloody, Non-steatorrhoeic
Aetiology
1. Infective
-giardiasis
- HIV
2. Drug-induced
-laxative abuse
-pseudomembranous colitis due to use of broad spectrum atibiotics e.g. clindacysin,cephalosporins &
ampicillin
-rarely antacids, anti-hypertensives, diuretics, chemotherapeutic agents
3. Metabolic
- DM with autonomic neuropathy (causing nocturnal diarrhea)
-thyrotoxicosis
-lactose intolerance
4. Irritable Bowel Syndrome

-common functional disorder affecting 20% of the population, & F>M
-diagnosis of exclusion made clinically based on Rome III Criteria
-Rome III Criteria = the presence of abdominal pain or discomfort for at least 3 days/month in the last 3
months along with ≥2 of the following:
a. improvement with defecation
b. onset (of each episode of discomfort) associated with a change in frequency of defecation or
c. change in consistency of stool.
-management
a. reassurance
b. incr dietary fibre
c. anti-spasmodic agents
d. antii-depressants
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History
Drug allergy
PMH
Symptoms
1. Diarrhea
-duration
-baseline & current frequency
- onset (acute/ gradual/ congenital)
- description of stools ( volume, presence of blood, watery or bloody, floating, foul-smelling or hard to
flush)
2. Mucoid stools
3. Urgency (any incontinence?)
4. Abdominal pain (ask SOCRATES, relieved on defecation?)
Aetiology
1.infective
-fever,abdominal pain, LOW
-recent travel & contact hx
-sexual orientation & CSW contact
2. drug-induced
-laxative abuse
-antibiotic usage
-drug hx (recent & current)
3. metabolic
- hx of diabetes, gastroparesis, postural hypotension, urinary retention, impotence,numbness/peripheral
neuropathy
-polyphagia, LOW, insomnia, irritability, heat intolerance, swetating, palpitaitons, beck swelling, personal &
family hx of thyroid disease
4.lactose-intolerance
-recent change in diet
Complications
-dehydration
-electrolyte imbalance
Systemic Review
Management prior to & during admission
1. General inspection
-general condition (goiter, thyroid eye disease)
-vitals
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-hydration status
2. Peripheries
-eyes (thyroid eye disease)
-abdomen (tenderness, guarding, distension)
-PR examination (anal tone)
- LL (diabetic dermopathy)
Investigations
1.FBC
-WBC & differential count (chronic infx)
-incr HCl (in dehydration)
2. U/E/Cr
-incr urea > incr Cr (in dehydration)
-electrolyte abnormalities
3.LFT
-albumin (protein-losing enteropathy)
4.TFT
-thyrotoxicosis
5.BSL & HbA1c
-DM
6.Stool studies
-stool OB
-stool pH (<5.6 indicated carbohydrate intolerance)
-gram staining
-microscopy for ova, cysts & leukocytes
-culture/ sensitivity
-C. difficile toxin
7.AXR
-spurious diarrhea form fecal loading
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Medicine (GIT) = Inflammatory Bowel Disease
Epidemiology
-young adults or middle age
-no gender predilection
-uncommon in asia (more common in Indians locally)
Aetiology
1.Genetic
-mutaton in NOD2 gene increases risk of crohn’s disease
-evident in Jews & Caucasians
-higer rates in monozygotic twine & first-degree relatives
-assoc. with SLE,Hashimoto’s thyroidiits & ankylosing spondylitis
2.Immunological
-profound derangement of mucosal immunity (T cells being the main driving force) where there is
abnormal host immunoreactivity, hence failure of downregulation
3. Environmental
-gut microbes likely provide antigenic trigger to dysregulated immune system
Pathogenesis
-inflammation is final common pathway
-activation of inflammatory cells (neutrophils & mononuclear cells), leading to non-specific tissue damage
a. mucosal destruction (loss of mucosal epithelial barrier & absorptive function
b. activation of crypt epithelial cell secretion
- resulting in characteristic intermittent bloody diarrhea
Pathology
Ulcerative Colitis
-diffuse inflammatory disease affecting colonic mucosa from rectum to caecum (rectum is always involved ,
while ileal involvement is present in backwash ileitis)
- course of disease
a. relapsing & remitting (70%)
b. continuous (10%)
c. single episode (10%)
d. fulminant episode requiring surgery (10%)
-typically presents in young adults with intermittent chronic bloody diarrhea assoc. with
a.fever
b.malaise
c.LOW
-triggers
a.stress
b.intercurrent infections
c.GE
d.antibiotics
e.NSAIDS
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-patterns of disease (according to site of colonic involvement)
Proctitis -PR bleeding/mucous duscharge

-tenesmus/urgency
- frequent stools of small volume OR constipation with pellety stools
Proctosigmoiditis -bloody diarrhea with mucous
-constitutional symptoms (e.g. fever, malaise, abdominal pain)
Pancolitis -bloody diarrea with mucous
-constitutional symptoms (e.g. fever, malaise, abdominal pain, LOA, LOW)
-physical findings (tachycardia, peritoneal inflammation)
-complications
a.primary sclerosing cholangitis (4%), hence incr risk of cholangiocarcinoma
b.incr risk of colorectal carcinoma, risk incr with duration & extent of disease (overall RR=8% ; for pancolitis
there is a 3% risk @ 15 yrs, 5% risk @ 20yrs & 9% risk @ 25 yrs)
* do yearly colonoscopy & biopsy ( @ every 10 cm of colon & @ raised/ulcerated areas) in pancolitis or 8
or more years duration
c.toxic megacolon (transverse colon diameter >6cm on AXR)
Crohn’s Disease
-recurrent inflammation that can affect any level of the GIT (but usually involves terminal ileum & colon)
-characterised by
a.sharply-demarcated transmural involvement of the bowel
b.skip lesions
c.non-caseating granulomas
d.fissuring with fistulae formation
-variable presentations of acute pain, diarrhea, LOW, malabsorption, I/O, appendicitis
-2 patterns of disease
Ileal disease -abdominal pain (subacute I/O)

-diarrhea (watery, non-bloody, non-mucoid
-LOW= LOA (aggravation of pain by food intake)+ malabsorption
Crohn’s colitis -bloody diarrhea with mucous
-constitutional symptoms (e.g. LOA,LOW,malaise)
-perianal disease
-rectal sparing
-vomiting with jejunal strictures
-severe anal ulcers
-complications
a.fistulae formation (entero-enteris,entero-vesical, entero-vaginal)
b.strictures (hence I/O)
c.lower BGIT
d.malignant change (lower risk than UC)
e.perianal disease (leading to perforation, acscess formation & peritonitis)
f. malabsorption syndromes (protein, Fe, vit B12)
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Differences between UC & CD
UC CD
1.Gross pathology
a. location Isolated to large bowel Any part of GIT
-small bowel + colon (50%)
-small bowel (30%)
-colon (20%)
b. skip lesions Absent Present (cobblestone mucosa)
c.stricture formation Absent Present
d.toxic megacolon Present Absent
e.fistula/sinus formation Absent Present
f.pseudopolyps Present Absent
2.Microscopic Pathology
a. inflammation Mucosa & submucosa Transmural
b.non-caseating granulomas Absent Present
c.ulceration Superficial Deep,linear serpentine
d.fibrosis Less more
e.glands Gland destruction, crypt abscess Intact glands
3.Clinical
a. bloody diarrhea Very common Uncommon
b.abdominal pain Pre-defecation urgency Post-prandial
c.palpable mass Uncommon Frequent (RIF)
d.perianal disease Less common More common
e.fat/vitamin malabsorption Absent Present (in small-bowel involvement)
f.malignant change Greater Lesser
e.recurrence after surgery Rare Common
Complications of IBD
Extraintestinal
Urinary calculi (esp oxalate in CD)
Liver (fatty liver, cirrhosis,PSC)
Cholelithiasis
Epithelium (oral aphthous ulcers
Retardation of growth & sexual maturation
Arthralgia (arthritis, AS, sacroilitis)
Trombosis (DVT, portal/mesenteric vein thrombosis)
Iatrogenic (steroids, blood transfustion, surgery)
Vitamin deficiencies
Eyes (uveitis,epicleritis,iridocyclitis,conjunctivitis)
Intestinal
Cancer
Obstruction (rare in UD, unless due to CRC. Common in CD)
Leakage (perforation)
Iron deficiency due to hemorrhage
Toxic megacolon (more in UC)
Inanition (severe wasting due to malabsorption & LOA)
Strictures, fistulas (enter-enteric, entero-vesical,entero-vaginal), perianal disease (CD)
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History-taking
Drug allergy
Symptoms
1. Bloody diarrhea
- Duration = chronic if persists more than/equals to 4 weeks
- Baseline and current frequency
- Acute/gradual/congenital onset
- Describe stools = watery
volume of stools
float, foul smelling, hard to flush away (differentiate from steatorrhoea)

color of blood (proximal colon dark red; distal colon bright red)
blood mixed with stools or on top of stools
staining of toilet paper
colour of stools (rule of melena)
- Anal pain and pre-defecation straining = rule out haemorrhoids
- Estimate blood loss = pallor, exertional chest pain and dyspnoea, non-vertiginous
giddiness, fatigue
2. Presence of mucous in stools
3. Urgency
- Faecal incontinence
4. Abdominal pain
- Ask about pain characteristics
- Relieved with defecation
Aetiology
 Infective = fever, abdominal pain, LOW
recent travel and contact history
history of TB
history of antibiotics usage (use of broad spectrum antibiotics = clindamycin,
ampicillin, cephalosporin)
 Trauma = history of radiation
 Autoimmune = oral ulcers, joint pain, back pain, unilateral red and painful eye
 Neoplastic = LOW, LOA, fever, fatigue, nausea/vomiting, abdominal pain, abdominal
distension, recent changes in bowel habit, preceding constipation, jaundice
Complications
 Dehydration = decreased urine output
 Protein losing enteropathy = LL oedema
Systemic Review
174
1. History of IBD
- Duration of disease
- Presenting complaint investigations management
- Currently on follow-up? Compliance
- Current medications = types
recent changes
compliance
side effects
- Control of symptoms = frequency of bloody diarrhea
frequency of exacerbations requiring admission
blood transfusion required
usual precipitating factors
- Triggers for present relapse = stress
intercurrent infections/GE
antibiotics/NSAIDs use
non-compliance to medications
- Complications= red eyes, oral ulcers, back pain, joint pain
toxic megacolon perforation
history of CRC on regular colonoscopy
liver problems (obstructive jaundice)
Drug history
Social history
Smoking
Alcohol drinking
Family set-up and main care-giver
Sexual orientation and contact = HIV can present as diarrhea
Type of housing
Lift-landing
Financial status
Functional level
How has illness affected your life?
Family history
General inspection
 General condition = in pain and distress
toxic-looking
pallor
cachexia
 Cushingnoid features
 Patient’s vitals
 Hydration status
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Peripheries
 Hands = digital clubbing, palmar crease pallor
 Eyes = conjunctival pallor, episcleritis, iritis, conjunctivitis
 Oral cavity = angular stomatitis, oral ulcers
 Abdomen = tenderness, guarding, peritoneal irritation, distended (toxic megacolon),
abdominal mass (thickened bowel loops/intra-abdominal abscess), rectal mass
on PR (CRC)
 Perianal disease = sentinel tags, fistulae, fissures, abscess
 Lower limbs = ankle oedema (protein-losing enteropathy), erythema nodosum, pyoderma
gangrenosum
Differentials
 Inflammatory bowel disease = ulcerative colitis
 Coorectal cnacer
 Infective colitis = amoebiasis, TB
 Radiation colitis/proctitis
 Ischaemic colitis
 Antibiotic-associated colitis (pseudomembranous colitis casued by C. difficile)
Investigations
Blood
 FBC = low Hb (anemia a/w iron deficiency)
WBC and differential count (chronic enteric infection)
Low platelet (bleeding diasthesis)
Elevated hct (dehydration)
 U/E/Cr = elevated urea > elevated creatinine (dehydration, BGIT)
Electrolyte abnormalities (hypokalaemia and metabolic acidosis)
 LFT = Albumin (LOW, LOA, protein-losing enteropathy)
Elevated conjugated bilirubin + ALP + GGT (primary sclerosing cholangitis a/w IBD)
 PT/PTT = BLEEDING DIASTHESIS
 GXM
 ESR and CRP = raised in acute UC
 Blood c/s (especially in febrile patients with known colitis/CD)
Stools
 Stool studies = gram-staining, culture /sensitivity
Microscopy for ova, cysts and leukocytes
C. difficile toxin
Imaging
 AXR = colitis (toxic megacolon, mucosal oedema aka ‘thumb-printing’, perforation)
 Colonoscopy and biopsy
- UC = confluent lesions most severe in rectum and distal colon
No strictures
- CD = skip lesions, apthoid ulcers and strictures, rectal sparing, perianal disease
- NSAID = microscopic colitis (scope may look normal but still biopsy)
 Barium study/Barium enema/Barium meal (if colonoscopy cannot be done)
- UC = shortened colon, loss of haustrations, lead pipe appearance, featureless colon
- CD = strictures (string-sign), skip lesions, cobble stoning of mucous, deep fissured
ulcerations, fistula, loss of haustrations
176
Management
 Acute exacerbation
(a) Stabilize patient’s vitals esp circulation
- Set 2 large-bore IV cannulas
- Take bloods for investigations esp GXM
- Fluid resuscitation if in shock = crystalloids colloids PCT
(b) Keep NBM and maintain on IV hydration. Start I/O charting
(c) IV empirical antibiotics if febrile = Ciprofloxacin or Metronidazole (cover against E. coli)
(d) IV high-dose hydrocortisone x 5/7
If refractory IV cyclosporine (much faster onset than azathioprine)
(e) Monitor vitals q4hrly = inform doctor is SBP <100mmHg or HR>100/min
Place on stool charting
 Surgery if not responsive to conservative treatment after 3-5 days

(a) Fulminant colitis = monitor for fever, tachycardia and signs of peritonitis
monitor stool frequencies and volumes
regular AXR for toxic megacolon/perforationurgent colectomy
(b) Perianal disease (fissures, fistula, abscess) = antibiotic cover
surgery
 Long-term management
(a) Pharmacotherapy
1. 5 ASA (5-aminosalicyclic acid)
- prototype = sulfasalazine (5 ASA + sulfapyridine)
- MOA = blocks arachidonic acid metabolism to prostaglandins and leukotrienes
- Routes of administration = oral
suppository (proctitis covers 10-15cm from anal verge)
enema (proctosigmoiditis)
- Topical = very effective for distal disease (up to splenic flexure)
better than steroids
oral = effective for pancolitis
- S/E = nausea, vomiting, headache, rashes, haemolytic anaemia, agranulocytosis
2. Steroids (oral prednisolone, hydrocortisone foam)

- Best drugs to remit acute disease
- May cause Hep B flare
 Chronic Hep B = immunity ineffective ineradicating Hep B, thus, exist in equilibrium
 Immune suppression = HBV DNA +++
 Once immune suppression removed = Hep B immunity recovers and causes a flare (T-cells
destroy hepatocytes
3. Immunosuppressants (azathioprine, methotrexate, cyclosporine, anti-TNF)

- Indications = steroid-dependent
Steroid toxicity
- Anti-TNF may reactivate pTB, thus, do CXR and mantoux test
4. Oral antibiotics for perianal disease (CD)
Introduction of remission
Mild disease  Oral 5 ASA
 5 ASA/steroid enema
Moderate disease  Oral prednisolone 40mg OM
Severe disease  IV hydrocortisone x 5/7
177
Maintain remission
Ulcerative colitis or Sulphasalazine (usu  Proven benefit in colitis = not for
Crohn’s colitis 2g) small bowel CD
 Decreases relapse risk from 60%
to 15%
Crohn’s ileal disease  Steroids
 Immunosuppressants
(b) Nutritional therapy

- Small bowel strictures (CD) = avoid nuts, raw fruits and vegetables
- Constipation = increase dietary fibre and fluid intake
- Malnutrition (esp in CD ileal disease) = refer dietician, diet supplements
(c) Surgery
- Indications = impaired quality of life
failure of conservative treatment
fulminant colitis/toxic megacolon (UC)

CRC/severe dysplasia
- UC = aiming for CURE (curative)
 Pan-proctocolectomy with ileostomy
 Proctocolectomy with ileal-anal anastomosis  may cause pouchitis (recurrent in
ileal pouch)
- CD = generally reserved for complications (fistulae, I/O, perforation, abscess, BGIT)
 At least 50% recurrence within 5 years
 Complications of ileal resection = <100cm (watery diarrhea due to impaired bile salt
absorption; cholestyramine)
>100cm (steatorrhoea due to bile salt deficiency;
Tx: fat restriction, medium-chain triglycerides)
 Perianal disease = I & D for abscess, stricture, plasty, fistulectomy
 Large bowel disease = pan-proctocolectomy with ileostomy (pouch not
recommended due to risk of recurrence)
Prognosis
 Life expectancy same as general population
178
Repiratory Medicine
Medicine (Respi) = History Taking: Respiratory System (General)
Date of admission
1. Respiratory symptoms
(a) Fever = when did it happen
acute/gradual onset
T max? associated with chills and rigours?
symptoms of raised ICP = vomiting, headache, photophobia, neck stiffness
pattern (constant, swinging, spiking)
relieved with anti-pyretics?
progressively better or getting worse?
Management before coming into hospital
(b) Cough = productive/dry
colour of sputum? amount? Smell?
haemoptysis (exclude haematemesis and trauma)
character (barking/brassy/hollow)?
- Barking = epiglottitis
- Brassy = tracheal compression by tumor
- Hollow = recurrent laryngeal nerve palsy (vocal cords are unable to close
completelybovine cough)
worse in the night/early morning or same throughout the day

does cough wake you up from sleep? Wake others up?
- Recent onset = acute bronchitis, pneumonia

- Chronic nocturnal cough and a/w wheezing = asthma, heart failure
- Irritating dry cough = GERD, ACE-inhibitors
- Large amount of purulent sputum = bronchiectasis, lobar pneumonia
- Foul-smelling dark coloured sputum = lung abscess with anaerobic organisms
- Pink and frothy = pulmonary oedema
(c) URTI symptoms = rhinorrhoea, blocked nose, sore throat

(d) Hoarseness (laryngitis, vocal cord tumour, recurrent laryngeal nerve palsy)
(e) Noisy breathing = inspiration (stridor)
expiration (wheeze)
(f) Chest pain = onset, frequency, duration
sudden/gradual onset
what were you doing at onset?
progressively worsening or getting better
site and radiation
character of pain
severity of pain
precipitating, aggravating and relieving factors
(g) Dyspnoea = onset, frequency, duration
179
progressively worsening or getting better
severity (must rest for how long)
precipitating, aggravating and relieving factors
effort tolerance (walking on level ground, climbing up stairs)
- a/w wheeze = asthma, heart failure, COPD

- chronic progression = pulmonary fibrosis, COPD
- acute onset = pneumonia, pneumonitis
- diurnal variation = asthma
- very rapid onset and a/w sharp chest pain = pneumothorax
(h) night sweats = ask about LOA, LOW, fatigue
2. Contact and travel history
3. Aetiology
4. Complications
5. Systemic review
6. Current management in hospital
7. Has this happened before? What happened? Investigations done? Management?

1. DM, HPT, HCL, IHD, CVA, cancer, asthma, TB
2. If suspect asthmaallergic rhinitis, allergic conjunctivitis, eczema, food allergy, drug allergy
3. Previous hospitalizations
4. Previous surgeries
Drug history
1. Any known drug allergy
- If yeswhat kind of drug? Drug reaction (angioedema, anaphylaxis, urticaria)
- For what medical conditions
- Type, length of use
- Dosage, frequency of dosing
- Side-effects
- Respiratory drugs = steroids, bronchodilators

- OCP = pulmonary embolism
- Amiodarone = pulmonary fibrosis
- Cytotoxics (methotrexate, cyclophosphamide) = interstitial lung disease
- NSAIDs/B-blockers = bronchospasm
- ACE inhibitors = dry cough
3. TCM use
180
Social history
1. Smoking (20 cigarettes/day for 1 year = 1 pack year)
2. Alcohol
3. Occupational history = exposure to dust/animals
duration of exposure
use of protective devices
do other workers have similar symptoms?

Improvement over the weekends or off-days?
4. Family set-up = main caregiver, health of family members, fiancés
5. Lift-landing
Family history
1. Asthma, AR, allergic conjunctivitis, food allergy
2. Bronchial carcinoma
3. TB
181
Medicine (Respi) = Physical Examination: Respiratory System
Start
1. Examine the patient on the right side of his bed
2. Introduce yourself, and explain to patient what you are about to do to and the purpose, note hoarseness
of voice (sore throat/RLN involvement)
3. Position the patient at 45°
4. Achieve adequate exposure by removing shirt
Inspection: Look at the patient’s general appearance

- Toxic looking/well
- Mental status: alert, orientated, drowsy, coma (narcosis in CO2 Retention)
- Respiratory distress: resting posture (hunched forward with arms used to support), breathing
through pursed lips, tachypnoea, dyspnoea, receiving supplemental oxygen, cyanosis,
wheeze/stridor, use of accessory muscles of respiration (sternocleidomastoids, platysma, strap
muscles, tracheal tug), suprasternal/intercostal/subcostal retractions, inability to speak in full
sentences
- Character of cough= chesty (chronic bronchitis, bronchiectasis, pneumonia)
dry (asthma, Ca bronchus, LVF, ACE inhibitors)
bovine (lack of the usual explosive beginning vocal cord paralysis)
- Chest for scars like thoracotomy scar which may indicate lobectomy and pneumonectomy ,
deformities*, radiotherapy changes (erythema and thickening of irradiated area), asymmetry in
chest movement, paradoxical inward motion of the abdomen during inspiration (diaphragmatic
paralysis, severe flattening of diaphragm in hyperinflation)
*pigeon-chest (Pectus carinatum) = outward bowing of the sternum and costal cartilages, occurring
in rickets, chronic childhood respiratory disease, right ventricular hypertrophy
*funnel chest (Pectus excavatum) = localized depression of the lower end of sternum occurring in
marfan’s (MVP)
*Harrison’s sulcus: linear depression of the lower ribs just above the costal margins at the site of
attachment of the diaphragm (severe childhood asthma/rickets)
- IV lines, nebulizer, sputum mug on table
- Respiratory rate
Hands
1. Take radial pulse for 15s (rate rhythm)
- Tachycardia=fever, hypoxia, treatment with β2-agonist
- Pulsus paradoxus: severe asthma, tension pneumothorax
- Bounding pulse= CO2 retention
2. Check hands for
- Clubbing (lung ca, bronchiectasis, empyema, lung abscess, pulmonary fibrosis, cystic fibrosis)
- Cyanosis
- Pallor of nail beds and palmar creases in anaemia
- Tar stains (cigarette smoking, tar is colourless)
- Guttering of small muscles of the hands
- Weakness of finger abduction-lung Ca involving the lower trunk of brachial plexus
- Palpate wrist for tenderness- Hypertrophic pulmonary osteoarthropathy
- Flapping tremor-patients to stretch out arms, dorsiflex wrists and spread out fingers  CO2
retention
Face
1. Eyes- partial ptosis, papillary constriction, loss of sweating (horner’s syndrome with apical lung ca)
182
2. Sinuses= palpate frontal and maxillary sinuses (tender=sinusitis)
3. Lips and tongues= central cyanosis
4. Oral cavity (teeth, gums, tonsils, pharynx)= URTI, lung abscess, pneumonia
Neck
1. Palpate for tracheal tug-signs of respiratory distress
2. Palpate for tracheal deviation (warn patient first)- deviated to same side in upper lobe collapse and
fibrosis, pushed to the other side in pleural effusion and tension pneumothorax
Chest
2. Palpate
- Apex beat (displaced in middle lobe or lower lobe pathologies)
- Parasternal heave of RVH
- Palpable p2 of pulmonary hypertension
- Symmetry of chest expansion and if it is reduced bilaterally. (place hands parallel to ribs with
thumbs meeting in midline and measure the distance moved during inspiration at least 5 cm)
3. Tell examiners that you would want to do tactile fremitus but acknowledge the fact that it is only useful
in cases of large pleural effusion or consolidations
- Place palms on either side of the chest while patient says 99, increased in consolidation, decreased
in pleural effusion
4. Percuss = apices, clavicles, anterior intercostal spaces and axillae
- Loss of cardiac and liver dullness 2° to hyperinflation in asthma/COPD/emphysema and
pneumothorax
- Dull: consolidation and collapse
- Stony dull: pleural effusion
5. Ascultate the apices (bell), anterior intercostal spaces, axillae
- Determine air entry and if expiratory phase is prolonged
- Breath sounds: Vesicular (2/3
inspiration, 1/3 expiration with inspiration louder and with gap)
Bronchial (1/2 inspiration, 1/3 expiration, expiration louder, and hollow and blowing and with
audible gap in between, heard over areas of lung consolidation and just above a pleural effusion.
- Adventitious sounds like rhonchi, crepitations, pleural rubs
6. Vocal resonance= ask patient to say 99 and listen with stethoscope
- muffled in normal lung (low pitched components heard with booming quality, high pitched
components are attenuated
-increased in consolidation (clearly audible, aegophony with bleating quality; whispering pectoriloquy-
whispered speech is distinctly heard
- decreased in pleural effusion
Sitting up
1. Get patient to sit up, hug a pillow and fold hands across chest
2. Inspect chest for shape and symmetry: check for increased AP diameter and barrel shaped chest in
hyperinflation in diseases like severe chronic asthma, and COPD
3. Kyphoscoliosis
4. Anklysing spondylosis
5. Examine back for scars, radiotherapy changes, asymmetry of chest expansion
6. Measure chest expansion
7. Tactile fremitus (usually not done)
8. Percussion
9. Auscultation and vocal resonance
10. Check submental, cervical and supraclavicular LNs
183
Legs
1. Check lower limbs for oedema and cyanosis of Cor pulmonale
End
1. Request for sputum mug, blood pressure and temperature chart
2. Look for pulmonary HPT (Palpable p2, Parasternal heave, loud p2)
3. RHF (Raised JVP, hepatomegaly, sacral oedema
4. Lung metastasis (hepatomegaly, lymphadenopathy)
Thank the patient for his help, help him button his shirt
Issues for discussion

1. Examination of the chest
- Ask patient to hug a pillow and fold hands across, inspect the finger nails for clubbing, cyanosis and
pallor
- Check for tracheal deviation
- Inspection chest expansion, tactile fremitus, percussion, auscultation, vocal resonance
- Flapping tremor
- Submental, cervical, supraclavicular and maxillary lymphadenopathy
2. Surface markings of the lungs
3. Signs of CO2 retention-bounding pulse, flapping tremours, AMS (confused, drowsy and obtunded),
retinal venous dilatation, papilloedema
4. Cyanosis
- Indicates significant ventilation-perfusion mismatch
- Becomes evident when [deoxygenated Hb] >5g/100ml of capillary blood of SaO2 < 90%
- Central cyanosis is a relatively late sign of hypoxemia
- Does not occur until even greater levels of arterial desaturation in patients with anaemia.
5. Hypertrophic Pulmonary Osteoarthropathy (HPOA): periosteal inflammation at the distal ends of long
bones, wrists, ankles, metacarpals and metatarsal bones, swelling and tenderness over affected areas,
usually occurring with clubbing
- Primary lung ca
- Pleural mesothelioma
6. Wheeze
- Continuous musical sounds
- May be heard during expiration or inspiration or both
- Due to continuous oscillations of opposing airway walls implying significant airway narrowing
- Tends to be louder on expiration as air ways normally dilate during inspiration and are narrower
during expiration
- Inspiratory wheeze implies severe airway narrowing
- Pitch varies (determined by velocity of the air jet) : Chronic obstruction like in COPD (low pitched),
acute obstruction in asthma (high pitched)
- Fixed bronchial obstruction like Lung Ca= localized, monophonic and does not clear with coughing
(ask patient to cough and listen again)
7. Crepitations
- Interrupted non musical sounds
- Loss of stability of peripheral airways that collapse on expiration
- Timing important:
Early Inspiratory crepitations  disease of the small airways
Late/pan Inspiratory crepitations  disease of the alveoli
- Quality:
Fine crepitations pulmonary fibrosis
184
Medium crepitations  LVF and pulmonary edema, pneumonia
Coarse crepitations: bronchiectasis (retained secretion): Gurgling quality that changes with
coughing
8. Pemberton’s sign
- Ask patient to lift the arms over the head and wait for 1 minute
- +ve: facial plethora, cyanosis, Inspiratory stridor, non pulsatile elevation of JVP, periorbital edema,
exophthalmos, conjunctiva injection, retinal venous dilation, dilated collated veins on chest, dilated
neck veins
- Occurs in SVC obstruction 2° retrosternal thyroid goitre, supraclavicular LAD, lung Ca
Disorder Mediastinal Chest wall Percussion Breath sounds Adventitious

displacement movement note sounds
Consolidation None Reduced dull Bronchial with Moderate/coarse

over increased VR Inspiratory
affected crepitations
area
Collapse Ipsilateral shift Reduced dull Absent or reduced, Absent
over VR resonance
affected varies
area,
flattening of
the chest
wall
Pleural Apex beat Reduced Stony dull Absent/reduced Absent
effusion displaced to the over over fluid,
opposite side affected bronchial at the
(tracheal area upper border with
deviation is decreased vocal
massive) resonance
Pneumothorax Tracheal Reduced Hyperresonant Absent/reduced Absent unless
deviation to the over with loss of subcutaneous
opposite side if affected cardiac and liver emphysema
tension area dullness
pneumothorax
Asthma None Reduced Normal/hyper Reduced with Expiratory
bilaterally Resonant prolonged rhonchi
expiratory phase
Pulmonary Tracheal Reduced Normal/dull Normal Fine Inspiratory
fibrosis deviation to bilaterally crepitations
affected side if
apical lesion
10. Emphysema (COPD)

 Definition = pathological increase in the size of the air spaces distal to the terminal bronchioles
 Clinical signs
a) Respiratory distress = dyspnoea, tachypnoea, pursed lip breathing = increases PEEP (keeps
airways open at the end of expiration; minimises air trapping), use of accessory muscles of
respiration, indrawing of intercostal muscles
b) ‘pink’ puffers = acyanotic
c) Hyperinflation = barrel-shaped chest (increased AP diameter), reduced expansion
symmetrically, loss of cardiac and liver dullness, liver ptosis, hyper-resonant percussion note,
decreased air entry, absent wheeze
11. Chronic bronchitis (COPD)

185
 Definition = daily production of sputum for 3 months a year for at least 2 consecutive years
 Clinical signs
a) Productive and chesty cough
b) ‘blue’ bloaters = cyanotic
c) Hyperinflation = barrel-shaped chest (increased AP diameter), reduced expansion
symmetrically, loss of cardiac and liver dullness, liver ptosis, hyper-resonant percussion note,
decreased air entry, end-expiratory wheeze, early inspiratory crepitations
d) Right ventricular failure = raised JVP, peripheral oedema, hepatomegaly
12. Pulmonary fibrosis

 Causes
a) Upper lobe (SCHART) = S (silicosis, sarcodosis)
C (coal workers’ pneumoconiosis)
H (histiocytosis)
A (ankylosing spondylitis, allergic bronchopulmonary
aspergillosis)
T (TB)
b) Lower lobe (RASCO) = R (RA)
A (asbestosis)
S (scleroderma, SLE)
C (cryptogenic fibrosing alveolitis)
O (other drugs eg bleomycin, nitrofuratoin, hydralazine,
methotrexate, amiodarone)
 Clinical signs
a) Respiratory distress = dyspnoea, cyanosis
b) Clubbing
c) Slightly reduced chest expansion
d) Fine late-inspiratory crepitations/pan-inspiratory creps
e) Signs of associated CTD = RA, SLE, Sjogren’s syndrome, scleroderma, polymyositis,
dermatomyositis
13. Lung ca (many patients have no signs)

 Respiratory signs
a) Haemoptysis
b) Cachexia
c) Clubbing a/w HPOA
d) Lung collapse/ pneumonia/ pleural effusion
e) Fixed inspiratory wheeze
f) Supraclavicular/ axillary LAD
g) Mediastinal compression = SVCO (+ve Pemberton’s sign)
Tracheal compression (stridor, respiratory distress)
Horner’s syndrome
RLN involvement (hoarseness)
 Metastasis
a) Tender ribs
b) Hepatomegaly
c) Brain
d) Bone
14. CXR signs

 Pleural effusion = upper margin of the effusion is curved (‘meniscus’ sign)
 Pneumothorax = increased translucency due to absence of vascular shadows
 Hydropneumothorax = air-fluid level (fluid no longer forms a meniscus at its upper margin)
 Emphysema = diaphragm projects >6 anterior ribs or >9 posterior ribs, almost horizontal ribs, low
and flattened hemidiaphragms, thin and slender mediastinum, increased translucency with loss of
vascular shadows
186
Presentation
Mr ___(name)___ is a pleasant-looking ___(age/race/gender)___ who appears to be alert, well, comfortable and
orientated at rest. His vitals are stable with a HR of ______, regularly regular and not bounding in nature, RR of
______ and currently afebrile. He does not appear to be in any respiratory distress: he is pink on room air and is
not on any supplemental oxygen. He also does not appear cachexic. There were no signs of cyanosis, pallor,
jaundice or dehydration.
On examination of the peripheries, there were no signs of clubbing or wasting of the small muscles of the hand.
There were no tar stains or flapping tremor seen. Tracheal tug and deviation were absent.
On inspection of the chest, I did not observe any surgical scars or chest wall deformities. Chest wall movement
was equal bilaterally. There was no displacement of the apex beat or signs of pulmonary hypertension. Chest
movement was adequate on deep inspiration and equal on both sides. Percussion note was normal. On
auscultation, normal vesicular breath sounds were heard with no adventitious sounds. Vocal resonance was
normal.
No lymphadenopathy was found. There was no peripheral oedema which could indicate right heart failure. I
would like to end my examination by requesting for the sputum mug as well as the temperature and BP charts.
187
Medicine (Respi) = Haemoptysis
1. Definition
 Expectoration of blood >200 mls over 24h
 Results in death by asphyxiation (rather than exsanguination)  80% mortality
 Haemoptysis = blood is coughed out, frothy, alkaline, bright red, no food particles
2. Aetiology
Respiratory V = pulmonary embolism, Wegener’s granulomatosis, Goodpasture’s syndrome, AVM
I = bronchitis, pneumonia, TB (ask for contact/travel hx, sexual hx, h/o HIV or AIDS, h/o DM,
steroids use), bronchiectasis, lung abscess
T = mucosal trauma after vigorous coughing
A
M
I
N = lung cancer
CVS Severe mitral stenosis
Acute left ventricular failure  APO
Bleeding diatheses
3. Investigations
Bloods
a) FBC
b) U/E/Cr
c) PT/PTT
d) GXM
e) ABG
f) Cardiac enzymes
g) D-dimer for pulmonary embolism
ECG
 PE = sinus tachycardia, S1Q3T3, right axis deviation, right BBB, p pulmonale, S1S2S3
Imaging
a) CXR = lung abscess, bronchiectasis, consolidation, TB, lung ca, APO
b) CT thorax = locate site of bleeding
c) Bronchial/ pulmonary artery angiogram = locates site of bleeding, allows for embolisation
d) Bronchoscopy = locate site of bleeding, allows for endobronchial tamponade
Specific
a) PE  spiral C/T, V/Q scan
b) Wegener’s granulomatosis  ESR, CRP, ANCA
c) Goodpasture’s syndrome  anti-GBM antibodies
d) Chest infection  sputum gram-staining, c/s
4. Management
 Airway = head tilt and chin lift (if bleeding profusely  left lateral position)
Breathing = ensure that patient is breathing spontaneously, give supplemental oxygen, obtain
saturation and monitor SpO2
Circulation = obtain ECG (r/o PE), HR, BP, large bore IV access  fluid resuscitate if in shock, obtain
bloods for investigation
 Monitor in MICU/HD
 Monitor vitals closely
 Correct coagulopathy
 Definitive management
 Bronchial artery embolisation
 Surgery = lobectom
188
CCF
Medicine (Respi) = Dyspnoea
Mitral/aortic valve disease
Dyspnoea = subjective feeling of discomfort a/w breathing Cardiomyopathy
Pericardial effusion/constrictive pericarditis
Respiratory Airway Neuromuscular Guillain-Barre syndrome
Asthma Myasthenia gravis
COPD (chronic bronchitis, emphysema) Others Anemia
Bronchiectasis Hyperventilation
Foreign body obstruction Acidosis
Cystic fibrosis
Laryngeal/pharyngeal tumor History taking
Bilateral vocal cord palsy
Tracheal obstruction/stenosis Name/age/ethnicity/gender/occupation
Tracheomalacia/ laryngomalacia Date of admission
Parenchyma Presenting complaint

Pneumonia/TB 1. Dyspnoea
Pneumothorax  Mode of onset (“what were you doing?”)
Pulmonary fibrosis  Frequency
Pulmonary oedema  Duration
Lung ca  Acute/gradual onset
Respiratory distress syndrome  Progressively worsening/getting better
Allergic alveolitis  Severity = able to speak in sentences, phrases or words/ activities
Sarcoidosis affected (NYHA class)
 Triggers = exertion (quantify effort tolerance), rest
Circulation  Aggravating factors
Pulmonary embolism  Relieving factors = bronchodilators, rest
Pulmonary AV malformation  a/w orthopnoea and PND
Pulmonary arteritis
2. aetiology
Chest wall and pleura  CVS = chest pain, nausea/vomiting, diaphoresis, palpitations,
Pleural effusion giddiness, syncope, ankle oedema, fatigue, intermittent
Rib fracture claudication
Ankylosing spondylitis  RT = fever, cough (+haemoptysis), recent URTI, hoarseness, noisy
Kyphoscoliosis breathing, chest pain, night sweats, LOA, LOW, malaise, history of
CVS Angina
Acute coronary syndrome (unstable angina, AMI)
189
trauma/FB aspiration, history of immobility/recent travel/major Main caregiver
surgery/OCP/HRT/LL swelling Type of housing/lift landing
 Neuromuscular = generalised weakness and numbness Finances
 Others = anemia (pallor, chest pain, SOB, giddiness, palpitations, Functional status
fatigue, PR bleeding, menorrhagia), hyperventilation (specific
situations, numbness/tingling/cramps in extremities) Family history
TB, lung ca, asthma, DM, HPT, HCL, AMI/IHD
3. Systemic review
 Recent changes in urinary/bowel habits Investigations
1. ECG and cardiac enzymes = ACS, PE
4. Management prior and during admission 2. FBC = Hb (anemia), WBC (leucocytosis in infections)
3. U/E/Cr = electrolyte disturbances in acidosis/alkalosis
5. Has this happened before? Describe? Investigations? Management? 4. ABG =acidosis/alkalosis, types 1 or 2 resp failure
5. CXR = hyperinflation, rib fracture, pneumothorax, consolidation,
Past medical history pleural effusion, mass, cardiomegaly, CCF
Asthma, COPD, TB, ca 6. D-dimer = if PE suspected
HPT, HCL, DM, AMI/IHD 7. β-natriuretic peptide = if CCF suspected
Previous hospitalisations and surgeries
Management
Drug history 1. Secure patient airway = head tilt chin lift, finger sweep, exclude upper
Any known drug allergy airway obstruction esp if stridor present, give supplemental oxygen
Current medications (COPD/smoker  O2 28% by Venturi mask), place on pulse oximetry
Recent drugs = beta blockers, NSAIDs, aspirin, thyroxine 2. Ensure pt is breathing spontaneously = auscultate lungs
Social history 3. Haemodynamically stable = look for signs of shock, HR/RR/BP, set
Smoker (significant smoking history of >10 pack years) large bore IV access, obtain bloods for investigations
Alcohol 4. Resuscitate pt if necessary
Occupational history 5. Obtain history and physical examination once pt is stable
Family set up
190
Medicine (Respi) = Approach to Chest Pain and Dyspnea
CVS causes Angina

Acute Coronary Syndromes (unstable angina, AMI)
Valvular disease
cardiomyopathy
Respiratory Airway
Asthma
COPD
Bronchiectasis
Parenchyma
Pneumonia
Pneumothorax
Lung cancer
Circulation
Pulmonary embolism
Chest wall and pleura

Pleural effusion
Rib fracture
Others Anemia
History
Name/age/race/gender/occupation/drug allergy
Date of admission
1. Chest pain
 Mode of onset
 Frequency
 Duration
 Triggers (exertion, palpitations, anxietyCVS, food GIT etc)
 Constant/intermittent
 Increasing in frequency/severity
 Site and radiation
 Character
 Pain score/severity
 Aggravating factors (coughing, deep inspiration, movement respi, sitting up and leaning forward
CVS, lying down, alcohol GIT)
 Relieving factors (GTN, rest CVS, bronchodilatorsrespi)
2. Dyspnea
 Mode of onset
 Frequency
 Duration
 Acute/gradual onset
 Progressively worsening/getting better
 Severity (able to speak in full sentences, phrases or words?)
 Triggers (exertion, rest. Quantify the effort tolerance!)
 Aggravating factors
 Relieving factors (bronchodilators, rest)
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 Orthopnea or Paroxysmal nocturnal dyspnea
3. Etiology
 CVS= nausea/vomiting, diaphoresis, palpitations, giddiness, syncope, ankle edema, fatigue,
intermittent claudications
 Respiratory tract= fever, cough, hemoptysis, recent URTI, hoarseness, noisy breathing, chest pain,
night sweats, LOA, LOW, malaise, history of trauma, history of immobility, recent travel, major
surgery, OCP/HRT
 GIT= epigastric pain, nausea/vomiting, reflux symptoms, dysphagia
 Others= anemia (pallor, chest pain, SOB, giddiness, palpitations, fatigue, PR bleed, menorrhagia)
4. Systemic changes= recent changes in urinary/bowel habits

5. Management prior and during to admission
6. Has this happened before? Describe? Investigations? Management?

Asthma, COPD, TB, cancer
HTN, HL, DM, AMI/IHD
GERD, PUD
Previous hospitalisation and surgeries
Drug history
Drug allergies
Current medications
Recent drugs = B-blockers, NSAIDs, aspirin, thyroxine
Social history
Smoker (significant smoking history more than 10 pack years)
Alcohol, occupational history, family set up, main caregiver, type of housing, lift landing, finances, functional status
Family history
TB, lung cancer, asthma, DM, HTN, HL, AMI/IHD
Investigations
1.ECG and cardiac enzymes= angina, ACS, pulmonary embolism
2.FBC (low Hb anemia, high WBC leukocytosis during infection)
3.U/E/Cr electrolyte disturbances
4.ABG alkalosis/acidosis, type 1 or 2 respiratory failure
5. CXR hyperinflation, rib fracture, pneumothorax, consolidation, pleural effusion, mass, cardiomegaly, CCF
6. D-dimer if PE is suspected
Management
Secure airway patency give supplementary O2 (COPD/smoker O2 28% by venturi mask). Start pulse oximetry
Ensure patient is breathing spontaneously= auscultate lungs
Haemodynamically stable= look for signs of shock, HR/RR/BP, ECG monitoring, set large bore IV access, obtain
bloods for investigation
Resuscitate patient if necessary
Obtain history and perform physical examination once patient is stable
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Medicine (Respi) = Pulmonary Fibrosis
Clinical features
Symptoms
 Progressive exertional dyspnea
 Chronic dry cough
 Right heart failure (ankle edema, ascites)
Etiology
 History of RA (joint pain, swelling, deformity)
 History of SLE (rash)
 Occupational history
 Drug history
 History of Ankylosing Spondylitis (back pain)
 History of Allergic Broncho-Pulmonary Aspergillosis (history of chronic asthma not responding to
treatment)
 History of radiotherapy in the thorax
 History of TB infection (chronic cough, hemoptysis, fever, LOW, night sweats, contact and travel
history)
Signs
 Digital clubbing
 Central cyanosis
 Bilateral basal fine crepitations
 Tachypnea
 Hands rheumatoid arthritis, systemic sclerosis
 Face malar rash (SLE), heliotrope rash (dermatomyositis), bird like facies (systemic sclerosis)
 Pulmonary hypertension (parasternal heave, loud and palpable P2)
 Cor pulmonale (raised JVP, peripheral edema)
Investigations
 Bloods (ESR, CRP, anti-dsDNA, anti-ANA, rheumatoid factor, ABG)
 Imaging (CXR, lung function tests restrictive lung disease pattern FEV decreased and FEV1/FVC
normal, high resolution CT thorax)
 Others (bronchoalveolar lavage, lung biopsy)
Management
 Corticosteroids (monitor with symptoms, CXR, lung function tests, consider
cyclophosamide/azathioprine in non-responders)
 Single lung transplant
Complications
 Type 2 respiratory failure
 Cor pulmonale
 Increased risk of bronchogenic carcinoma
 Secondary polycythemia
Differential diagnosis
 Bronchiectasis
 Pulmonary edema (CCF)
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Medicine (Respi) = COPD
Definition: Progressive and irreversible airway obstruction( 7th leading cause of death locally)
Chronic Bronchitis= persistent cough and sputum production for at least 3 consecutive months each year for at
least 2 consecutive years. (Clinical diagnosis)
Emphysema= irreversible dilation of air spaces distal to terminal bronchioles due to destruction of alveolar
walls in the absence of fibrosis (histological diagnosis)
Aetiology
1) Genes- alpha1 antitrypsin deficiency
2) Environment: Occupation- dust, coal, farming
Pollution
3) Smoking(significant if >10 pack years)
Clinical features
History:
1) Current symptoms: dyspnoea, chest tightness, wheezing, increased cough and sputum, change in
sputum colour, fever, LOA, malaise
2) Travel and contact history
3) History of previous episodes: presentation, investigations, management
4) Current management: bronchodilators, long term oxygen therapy, lung surgery
5) Current control: frequency of symptoms, frequency of SAB use, frequency of exacerbations requiring
hospitalisations
6) Baseline status: effort tolerance, ankle edema, LOW( probably due to increased TNF production a/w
chronic hypoxia)
7) Past Medical Hx: pTB, atopies (food allergy, drug allergy, asthma, AR, eczema, allergic conjunctivitis)
8) Social Hx: Smoking (significant if> 10 pack years)
Physical Examination:
Peripheries
1) Signs of respiratory distress: tachypnoea, dyspnoea, use of accessory muscles, pursed lip breathing,
tracheal tug, suprasternal/intercostals/subcostal retractions, paradoxical breathing NB: patients with
emphysema are more breathless (pink puffers)
2) Peripheral and Central cyanosis (in chronic bronchitis-> blue bloaters)
3) Palmar erythema (secondary to polycythemia)
4) Signs of CO2 retention: altered mental state, bounding pulse, asterixis, papilloedema
5) Nicotine/ tar stained fingers
Chest examination
1) Inspect for barrel chest, signs of hyperinflation
2) Chest expansion: decreased
3) Percussion: resonant/ hyperresonant, loss of liver and cardiac dullness
4) Auscultaion: decreased air entry, prolonged expiratory phase, expiratory rhonchi, inspiratory creps,
(chr bronchitis-> mucous plugging; absent in emphysema)
5) Vocal resonance: decreased
Complications
1) Abdominal examination: liver ptosis
2) Signs of cor pulmonale: raised JVP, parasternal heave, loud and palpable P2, hepatomegaly, peripheral
edema
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Complications
Chronic Bronchitis Emphysema
Type 2 respiratory failure: low paco2 due to v/q Type 1 respiratory failure: low po2 and low/normal
mismatch from mucous plugging. paco2
Short term: increased paco2 stimulates respiration

Long term: insensitive to high paco2 levels, hence
depend on hypoxic drive
polycythemia Pneumothorax from ruptured bullae
Pulmonary hypertension-> cor pulmonale Pulmonary hypertension-> cor pulmonale
Respiratory infections Respiratory infections
Obliterative bronchitis(due to mucous plugging) Increased incidence of PUD& liver cirrhosis (may be
linked to alpha1 anititrypsin deficiency)
Bronchogenic Carcinoma (sq metaplasia)
Differentials:
1) Bronchial asthma
2) Bronchiectasis
3) Obliterative bronchiolitis
4) CCF
Investigations
Bloods:
1) FBC: Hb for polycythemia, WCC
2) U/E/Cr: electrolyte imbalances
3) Blood cultures (if pt is septic)
4) ABG (FEV1 < 40% predicted, spo2 <92%, signs of respiratory failure)
5) Alpha1 antitrypsin assay (esp if pt has never smoked and has emphysema)
Sputum: (not recommended)

1) Gram staining
2) Culture for sensitivity
Imaging:
1) ECG: right heart strain (cor pulmonale)= R ventricular hypertrophy (R>S in lead V2), P pulmonale (tall p
wave)
2) CT/ HRCT thorax
3) CXR:
a) hyperinflation-> more than 6 ant ribs/ more than 9 post ribs seen above right hemidiaphragm in
mid clavicular line, horizontal ribs, flattened hemidiaphragm, thin and slender mediastinum, decreased
vascular markings.
b) consolidation
c) Pneumothorax
d)Bullae
Lung Function Test:

1) Spirometry:
a) obstruction= FEV1/FVC< 70%
b) severity ( look at FEV1 % predicted)
c)degree of reversibility with bronchodilators (200ml + change in FEV1 or FEV1/FVC > 12%)
d) others: increased TLC, FRC, RV
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Classification of Severity
Global Initiative for Chronic Obstructive Lung Disease(GOLD) Staging:
Stage/Severity FEV1/FVC FEV1 Treatment
I=mild <70% ≥ 80% Short acting bronchodilators:
1)SABA(salbutamol,fenoterol,terbutaline)
2)SAC(ipratropium bromide)
3)Combivent (SABA+SAC)
II=moderate <70% 50-80% Long acting bronchodilators:

1)LABA (formoterol, salmeterol)
2)LAC (tiotropium)
III=severe <70% 30-50% 1) SAB (sympathomimetic)
2) LAB + ICS (prophylactic):
a)seretide= salmeterol +fluticasone
b)symbicort=budesonide+formoterol
IV= very severe <70% <30% or <50%+resp failure 1) LAB + ICS

2) Theophylline
3) Pulmonary rehabilitation
4) Long term oxygen therapy
Management
Acute Exacerbations:
1) Supplemental O2
a) Controlled oxygen therapy=ventimask (start from Fio2 28% and monitor before escalating, ensure
paco2 does not increase)
b) Keep spo2 >92% (Aim 90-95%)
2) Nebulised salbutamol + Ipratropium bromide + N/S (1:2:1) for symptomatic relief
- use air driven nebuliser (less o2)
3) Assisted ventilation
a) Aim is to rest respiratory muscles and restore gas exchange
b) Types
-Non invasive ventilation(BiPAP-> Bilevel positive airway pressure; CPAP)
 Advantages=reduced mortality, need for intubation and length of hospitalisation
 Contraindications= facial trauma, drowsy patient
 Indicated in the presence if all the following depite 2-3 nebulisations:
 Tachypnea(>25 breaths/min)
 pH <7.35
 PaCO2 >45mmHg
-Endotracheal intubation
 Indications:
 If NIV fails
 pH<7.25
 respiratory arrest
 somnolence
 severe hemodynamic instability
c) Cut offs=
-pH< 7.35 (consider NIV)
-pH<7.30 (must use NIV)
-pH<7.25 (consider intubation)
-pH<7.20 (must intubate)
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4) Steroid Therapy= oral prednisolone (0.5mg/kg/day), IV hydrocortisone (100mg q6hrly)
-only useful in acute exacerbations
-does not influence course of chronic bronchitis
5) IV antibiotics
a) Indications: worsening dyspnoea, cough and increased sputum volume+ purulence
b) should cover against S.pneumoniae, H influenzae, and M catarrhalis (if recurrent->
Pseudomonas)
c) Start with amoxicillin, if no response proceed with augmentin + Klacid
d) Possible agents: rocephine, cipro, ceftazidine
6) Chest physiotherapy: if atlectasis/ sputum >25ml

7) Additional medications to consider
a) Mucolytics
b) Promethazine/ dihydrocodeine (relieves sense of breathlessness)
Chronic Management:
NB: The ONLY 2 things that improve mortality= smoking cessation and LTOT
1) Non pharmacological
a) All stages:
- Smoking cessation= reduce sputum production and bronchospasm. Can use bupropion
SR, nicotine gum, nicotine inhaler and nicotine patch
- Pneumococcal (ever 5 years) and Influenza vaccinations
- Refer to dietician if malnourished a/w decreased respiratory muscular function and
increased mortality
- Encourage ambulation and weight reduction
- Chest physiotherapy
- Patient education
b) Moderate-Severe COPD:
- Pulmonary rehabilitation:
 Consists of nutritional therapy, pulmonary exercises and chest physio
 Does not improve survival but improves quality of life
c) Long term oxygen therapy
- Indications: clinically stable COPD with pao2 < 55mmhg; COPD cx by polycythemia/
pulmonary htn/ cor pulmonale with pa02 < 60mmhg/ terminally ill patients with pao2
<55mmhg
- Regimen=continuous O2 for at least 15 hrs/day
- Advavntages=symptomatic relief, improve QoL and prognosis
- Disadvantages= expensive(oxygen concentrator), explosive (cannot smoke at home,
cannot put in kitchen, dangerous)
- Reassess every 3 months with ABG-> expensive
d) Treat depression
e) Discuss end of life issues
2) Pharmacological
a) Mucolytics
b) Bronchodilators
- MOA= relax bronchial smooth muscles and relieve bronchospasm
- Does not improve mortality or influence decline in lung function
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Inhaled SABA -Examples=salbutamil,terbutaline,fenoterol
-Fastest onset ~15 min (DOA 4-5 hours)
-May be ued up to max of 4-6times/day
-S/E: tremors,palpitations,hypokalemia
Inhaled SAAC -Example=ipratropium bromide (atrovent)

-MOA=blocks Ach-M3 receptors (attenutates vagal tone)
-equivalent if not more potent than SABA
-not taken PRN due to relatively slow onset
-taken on a 4-6 hrly basis
-adv: poor systemic absorption, no tachyptaxis
-S/E: dry mouth
Combination of SABA -example=combivent

and SAAC -adv: greater and sustained improvemtns in FEV1 than with either drug alone
Inhaled LABA -examples= samleterol, formoterol, bambuterol

-onset of action: salmeterol= 10-20min,
Formoterol=1-3min
-long DOA of ~ 12hrs
-used in patients with mod-severe COPD and freq exacerbations OR when symptoms are not
well controlled with SABA alone
Inhaled LAAC -example=tiotropium

-Long DOA of ~ 24hrs
Oral theophylline -MOA=bronchodilation, stimulates ventilation, anti-imflammatory

-used in patients who are non-compliant OR unable to use inhaled therapy OR symptom control
not achieved with bronchodilator therapy
-S/E: narrow therapeutic index, cardiac arrhythmias, GI intolerance, headaches, seizures
c) Inhaled Corticosteroids:
- Examples=beclomethasone, budesonide, fluticasone
- Recommended for patients with FEV1 <50% predicted value and experience freq
exacerbations
- Only a modest effect on lung function in COPD as compared to asthma
d) Combination of ICS and LABA
- Examples=seretide (salbutamol+ fluticasone) , symbicort (budesonide + formoterol)
3) Surgical
a) Indications: recurrent pneumothorax (from emphysema), isolated bullous disease
b) Types:
- Bullectomy
- Insertion of endobronchial valves
- Lung volume reduction surgery (thoracoscopic resection of 20-30% of poorly
functioning lung tissie in each lung -> reduce thoracic volume)
- Lung transplant (only if patient is <65y/o and has no serious co-morbidity)
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Medicine (Respi) = Bronchiectasis
Definition
- Chronic necrotizing infection of the bronchi and bronchioles leading to permanent dilatation due to destruction
of muscles and elastic supporting tissue.
- Main organisms= H. influenzae, S. pneumoniae, S. aureus, P.aeruginosa
- Not a primary disease
- More common in females
Predisposing conditions
- Congenital
(a) Cystic fibrosis= viscid secretions tend to block passages (mucoviscidosis); also decrease clearance
(b) Hypogammaglobulinaemia= decrease in all types of antibodies; hence increased susceptibility to recurrent
bacterial infections
(c) Kartagener’s syndrome (often in relatively young patients, look for left cholecystectomy/appendidectomy
scar) =
1. Ask for history of subfertility, sinusitis +/- otitis media, dextrocardia/ situs inversus, urinalysis for
amyloidosis
2. Autosomal recessive triad of situs inversus (50% have situs inversus totalis), chronic sinusitis and
bronchiectasis
3. Pathogenesis: immotile cilia  decreased mucociliary clearance infections
4. may occur in young people but never present at birth  sinuses not formed yet
- Acquired
(a) Bronchial obstruction
- tumour
- lymphadenopathy
- foreign body
- TB granuloma
(b) Post infective
- In children= measles, pertussis, bronchiolitis
- In adults= influenza, TB, S. aureus, Klebsiella, mixed infections
(c) Allergic bronchopulmonary aspergillosis (ABPA) = type 3 (complex-mediated) hypersensitivity affecting
mainly proximal bronchi; to suspect in pt with chronic asthma resistant to therapy and productive cough
investigations: eosinophilia, high IgE levels, aspergillus in sputum c/s, skin prick test
- Idiopathic (up to 50%)
Pathogenesis
- Obstruction or chronic persistent infection (either one may come first)
Chronic cough
Persistent necrotizing Wall damage and fibrosis due to Bronchial

inflammation inflammation dilation
Obstruction Air is resorbed (atelectasis)
- Bronchial dilation due to 3 causes=

(a) destruction of elastic tissues
(b) contraction of fibrous tissues exerts traction on bronchi
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(c) chronic cough leads to rise in bronchial pressure
- Localised bronchiectasis= mechanical obstruction, childhood bronchopulmonary infection
- Generalised bronchiectasis= inherited/ acquired impairment in host defences
Morphology
Macroscopic features
- cystic, smooth, glistening honeycomb appearance of cut surface of lung
- bronchi= grossly dilated up to 4 times the usual diameter , can be traced to pleural surface (normally can
only trace till 2-3 cm from pleura), thick fibrous walls, most severe distally
- obliteration of intervening lung parenchyma
- affects bilateral lower lobes
Microscopic features
- intense acute and chronic inflammatory exudates within bronchial and bronchiolar walls
- capillary congestion, interstitial oedema and hemorrhage
- +/- squamous metaplasia
- Hyperplasia of goblet cells  increased mucous secretion
- Destruction of elastic tissue
- Fibrosis
Reid’s classification
(a) cylindrical= uniformly dilated bronchi that end abruptly instead of tapering
(b) varicose = dilated bronchi with irregular bulging contours that end in bullae
(c) cystic =most severe form where dilated bronchi end in cystic pus- filled cavities
Clinical features
History
- Current symptoms= severe persistent cough with copious purulent sputum, haemoptysis, fever, dyspnoea,
pleuritic chest pain, wheeze, precipitated by URTI
- Aetiology = fever, LOA, LOW, night sweats, history of TB, travel and contact history, history of chronic cough
and purulent sputum since childhood (CF, Kartagener’s syndrome)
- Management of current episode= chest physiotherapy, antibiotics, bronchodilators
- History of prior episodes = treatment given, investigation conducted (CT chest, bronchoscopy)
- Past medical history = hypogammaglobulinaemia, COPD, asthma, allergies
- Drug history
- Social history = chronic smoker
- Family history
- fever, clubbing, central/ peripheral cyanosis
- coarse pan- inspiratory/ late inspiratory crepitations that does not clear with coughing
- rhonchi (mucous plugging/asthma/COPD/ABPA)
- sputum mug (voluminous, purulent, foul-smelling, blood- stained, layering of sputum)
- severe disease= cor pulmonale (raised JVP, parasternal heave, palpable and loud P2, peripheral oedema),
amyloidosis (splenomegaly)
- Presentation of findings:
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“In summary, this patient most likely has an infective exacerbation of bronchiectasis. I say
this because:
(a) presence of IV antibiotics
(b) bilateral coarse pan-inspiratory crepitations that does not clear with coughing
(c) digital clubbing
The patient is currenly not in any respiratory distress and his condition is not complicated
by pulmonary hypertension or cor pulmonale. “
Request to examine:
(a) anterior chest
(b) temperature chart
(c) sputum mug
(d) raised JVP for cor pulmonale
(e) splenomegaly 20 amyloidosis
Differentials:
1. Pulmonary fibrosis- distinguishing features
Pulmonary fibrosis Bronchiectasis
Dry cough Productive cough
Fine end-inspiratory creps Coarse pan-inspiratory +/- expiratory
creps
Steroid toxicity Splenomegaly
2. Infective exacerbation of COPD

*look for signs of hyperinflation, expiratory mucus, with prolonged expiratory phase
Complications
- Haemoptysis
- Pneumonia
- Pleurisy
- Pleural effusion
- Pneumothorax
- Lung abscess
- Empyema
- Bacteremia cerebral abscesses and meningitis
- Extensive lung destruction  Pulmonary hypertension and cor pulmonale
- Amyloidosis
Investigations
- Bloods= FBC, ESR, CRP, blood c/s, ABG
- Sputum = gram stain, c/s, AFB stain, TB c/s
- CXR = cystic shadows, thickened bronchial walls (tramline and ring shadows), air fluid levels
- High resolution CT (HRCT) thorax= assess extent and distribution of disease; slices are 1-2 mm thick CF
standard CT (10mm)
- Bronchoscopy = locate site of haemoptysis and exclude obstruction; largely superceded by HRCT
- Spirometry = obstructive picture
Management
Acute
- Give supplementary 02
- If rhonchi present  nebulized salbutamol
- Start IV antibiotics
- Chest physiotherapy = aid sputum expectoration and mucous drainage
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- Massive haemoptysis  bronchial artery embolisation
Chronic
-Smoking cessation
- Pneumococcal and influenza vaccination
- Bronchodilator therapy
- Chest physiotherapy
- Long term 02 therapy
Surgery
- Indication= localized disease which has failed medical therapy
- Options= lobectomy
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Medicine (Respi) = Cor Pulmonale
Pulmonary hypertension
- Primary pulmonary hypertension (much less than 5%)
- Most common in females (20-30 years old)
- Marked by fatigue, exertional dyspnoea and chest pain
- Pathogenesis = pulmonary endothelial dysfunction Decreased prostacyclin and NO
Vasoconstriction
- Secondary pulmonary hypertension

- More common cause
Cor pulmonale
- right heart failure cause by chornic pulmonary hypertension due to disorders in the lung, chest wall or
pulmonary circulation
- Aetiology:
Lung diseases Chronic severe asthma
COPD
Bronchiectasis
Pulmonary fibrosis
Lung resection
Pulmonary circulation Recurrent pulmonary embolisms
Pulmonary vasculitis
Primary pulmonary hypertension
Acute respiratory distress syndrome
Chest wall disorders Neuromuscular Myasthenia gravis
Poliomyelitis
Motor neurone disease
Duchenne muscular dystrophy
Chest wall Kyphoscoliosis
Obesity
Hypoventilation Obstructive sleep apnoea
Cerebrovascular accident
Clinical features
Symptoms
- exertional dyspnoea
- chronic productive cough
- ankle oedema
- Abdominal distension
Signs
- respiratory distress= Tachypnoea
Central cyanosis
- tar stains on fingers
- pulmonary hypertension = parasternal heave,
Loud and palpable P2
Pulmonary and tricuspid regurgitation
- cor pulmonale= as above plus raised JVP (prominent a and v waves)
Hepatomegaly (pulsatile liver in TR)
Ascites
Ankle oedema
- Aetiology = COPD (hyperinflation, expiratory wheeze, prolonged expiratory phase, inspiratory crepitations),
pulmonary fibrosis (bibasal fine end- inspiratory crepitations)
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Complications
(a) right heart failure
(b) respiratory failure
(c) secondary polycythaemia
Investigations
Bloods
- FBC= raised Hb and hematocrit (hct)
- ABG= hypoxia +/- hypercapnia
ECG
- p pulmonale (relatively narrow P wave with increased amplitude indicating R atrial dilation), RAD, RBBB, RVH+/- strain
CXR
- enlarged right atrium and ventricle
- prominent pulmonary arteries
Management
(a) treat underlying cause
(b) treat respiratory failure
- Give supplementary 02 cautiously if Pa02 < 60 mmHg
- Start at Fi02 = 24% and monitor with ABG 30 mins later
- Escalate oxygen if PaC02 remains stable
- If PaC02 increases  give doxapram (a respiratory stimulant)
- Consider assisted ventilation
(c) treat cardiac failure
- fluid restriction
- diuretics
(d) venesection if hct >55%
(e) heart- lung transplant in young patients
Prognosis
Very poor (50% mortality within 5 yrs)
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Medicine (Respi) = Respiratory Infections: Tuberculosis
Epidemiology
 Communicable disease
 Causes 6% of deaths worldwide, making it the most common cause of death from a single infectious
agent (WHO)
 Developing countries
 Incidence is increasing in developed countries as well, due to increasing prevalence of AIDS (most
important risk factor for development of TB) and migration
 Common in poverty stricken, overcrowded areas, malnutrition
 Common in those with chronic illnesses eg DM, chronic lung disease, elderly or immunocompromised
(AIDS)
 Notifiable disease
Aetiology
 Mycobacterium tuberculosis (M. bovis from unpasteurised cows’ milk is rare)
 Transmission: direct person-to-person transmission via airborne droplets from an active case (latent
disease is not transmissible unless it reactivates in times of immunosuppression). Significant exposure
of 6-8 hours in a confined space.
 Pathogenesis:
o Mycobacterium enter macrophages -> inhibit microbicidal activity -> uncontrolled proliferation
of mycobacterium -> bacteremia and seeding of multiple sites
o Recruitment of monocytes whch differentiate into epithelioid histiocytes that characterise the
granulomatous response
o Also results in delayed type tissue hypersensitivity
Pathology
Primary Tuberculosis
 Develops in previously unsensitised individuals.
 Usually asymptomatic
 Elderly persons may lose their sensitivity to MTB and hence develop primary TB more than once
 Source of organism is exogenous
 Bacilli deposit near the pleura proliferate in macrophages -> form tubercles with caseous necrosis
(Ghon focus)
 Bacili drain to the regional LN which also undergo caseous necrosis (Ghon complex = parenchymal
lesion + nodal involvement)
 Effective cell-mediated immune (CMI) response develops 2-6 weeks after infection
 Failure to develop CMI results in progressive destruction of the lung -> progressive primary TB
Complications
 Foci of scarring may harbour viable bacilli for years, and thus be the nidus of reactivation in times of
immunosuppression.
 Progressive primary tuberculosis: disease develops without interruption in immunocompromised
individuals eg. AIDS patients with CD4+ counts <200/mm3
o Inability to mount immunological reaction to contain the primary focus
o Absence of characteristic caseating granulomas (non-reactive TB)
o Miliary TB: multiple tubercles evenly distributed throughout the lung
Latent TB
 Stage in between primary and reactivation TB
Secondary TB (reactivation TB)
 Arises in previously sensistised host, from reactivation of dormant bacilli when host resistance is low
(only 5% of those with primary disease develop secondary TB)
 Classically localised to the apex of one or both upper lobs (may be due to high oxygen tension)
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 Due to hypersensitivity, bacilli excite a prompt and marked tissue response that tends to wall off the
focus (hence the regional LN are less prominently involved in early secondary TB compared to in early
primary TB)
 Cavitation occurs, erosion and dissemination along the airways -> sputum positive, person can spread
the disease.
Complications
 Progressive pulmonary tuberculosis: apical lesion enlarges, erodes into surrounding tissue
o Erosion into bronchus creates a ragged irregular cavity
o Erosion of blood vessels leads to hemoptysis
o Dissemination by blood or lymphatics
 Miliary pulmonary disease
 Pleural involvement: effusions, tuberculous empyema or obliterative fibrous pleuritis
 Lymphadenitis: the most common form of extrapulmonary TB
o Typically occurs in the cervical region (“scrofula”)
 Endobronchial, endotracheal and laryngeal TB
 Intestinal tuberculosis
 Pott disease: TB abcesses in the vertebrae (may spread along tissue planes to form “cold abscesses”
which present as a pelvic lump)
 Systemic military tuberculosis
o Hematogenous spread to other organs esp liver, bone marrow, spleen, meninges, adrenals,
kidneys -> fatal without treatment
Clinical features
Pulmonary TB
 Symptoms
o Fever, persistent cough, hemoptysis, pleural pain, spontaneous pneumothorax, non-resolving
pneumothorax, lethargy, LOW, night sweats
 Signs
o Crepitations, signs of consolidation, +/- signs of fibrosis, +/- signs of pneumothorax, +/- signs of
effusion
Miliary TB
 Persistent cough, SOB, crepitations, tachycardia, anaemia, hepatosplenomegaly, choroidal tubercles on
opthalmoscopy, fever, LOW, night sweats, lymphadenopathy
Extrapulmonary TB
 GI (intestine or peritoneum)
o Diarrhoea, malabsorption, I/O, ascites
o Management: Peritoneal fluid for AFB
 Pericardium
o Pericardial effusion or tamponade, constructive pericarditis due to post-infectious fibrosis
o Management: Requires steroids to reduce need for pericardiectomy
 GU
o Haematuria, frequency, dysuria, sterile pyuria, salpingitis, tubal abscess, epididymal TB-
swelling/sinus formation
o Management: 3 early morning urine for AFB, renal U/S, IVU
 CNS
o Headache, meningism, altered mental state, vomiting, neurological deficits
o Management: CSF for AFB – fibrin web, mononuclear cells, cell count 10-1000, decreased
glucose, normal or increased protein
 Lymph node
o Usually cervical lymph node, swelling and sinus formation
 Bone/Joint
o Vertebral collapse, pyrathrosis, osteomyelitis, cold abscess formation, bone marrow: anaemia,
thrombocytopenia
o Management: X-ray, MRi to determine extent of involvement, culture biopsies
 Others
o Adrenal gland destruction -> Addison’s disease
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o Skin: lupus vulgaris, erythema nodosum
o Eyes: Phlyctenular keratoconjunctivitis, iritis, choroiditis
 Symptoms of compression by lymph nodes eg. Monophonic wheeze, bronchiectasis, lung collapse
 Symptoms of affected organ systems eg. Headaches and seizures for TB meningitis, paraplegia for Pott
disease
 Risk factors: contact/travel history, crowded living conditions, HIV/immunocompromise, malnutrition,
alcoholism, steroid therapy, DM, previous TB
Investigations
 CXR
o Cavitation in the apices of the lung
o Calcification
o Reticulonodular shadowing (for military TB)
o Fibrosis (“scarring”) with traction
o Enlargement of hilar and mediastinal lymph nodes
o Cavity with aspergilloma: air crescent sign
(CXR does not give indication of the activity of the disease; it is not diagnostic)
 FBC
 LFT
 CRP
 Sputum AFB smear: MTB binds to Ziehl-Neelson stain and resists decolorisation (acd fast)
o Positive AFB smear makes a presumptive diagnosis of TB in a high risk patient, although a
positive stained smear is not specific for M. Tuberculosis
o 50% of AFB positive locals have MOTT (Mycobacteria other than TB)
o Most AFB positive foreign workers have MTB
o If the patient is not able to produce sputum, sputum induction with nebulized, hypertonic 3%
saline in a negative pressure isolation room is an alternative before more invasive procedures
(bronchoscopy)
 Sputum culture is the gold standard (culture on Lowenstein Jensen media requires 12 weeks; PCR can
provide faster results) *only culture can provide info on drug sensitivity
 Early morning gastric aspiration: most useful in young children where sputum is more difficult to
obtain, and is best performed following at least nine hours of fasting
 Nucleic acid amplification tests (NAAT), can provide rapid diagnostic information to the clinician,
generally within 24 to 72 hours
 Tuberculin skin test: TB antigen is injected intradermally and the cell mediated response at 48-72 hours
is recorded. A positive test indicates that the patient has immunity (ie, previously exposed or
vaccinated). A strong positive test suggests active disease. False negatives occur in immunosuppression
eg. Miliary TB, AIDS
 In HIV patients, atypical features include sputum smear negative for AFB; false negative tuberculin test
cos of tuberculin anergy, lack of granulomas in tissues
Management
 Notify CDC, refer to TBCU
 Contact tracing
o Household contacts of sputum smear positive PTs
o 2/3 step contact tracing
 Week 0: Do Mantoux, read at day 2-4
 If >15mm, means seroconvert – give prophylaxis
 If <15mm, repeat Mantoux
 Week 2: Do Mantoux
 If increase of week 0’s test by >10mm, means that first Mantoux reactivated
previously exposed immune system, now pt is displaying competent immune
response – don’t need prophylaxis
 If <10mm, do third Mantoux
 Week 12: Do Mantoux
207
 If increase >10mm of week 0, means pt has seroconverted. Pt has LTBI, give
prophylaxis
 If increase <10mm, no need prophylaxis
 Advise HIV testing
 Isolation whie infectious
 Ishihara colour vision testing before initiating therapy with ethambutol
 Give anti-TB drugs (directly observed therapy to improve compliance) + monitor liver function
 Monitor CXR weekly during treatment, monthly sputum AFB smear and cultures till two consecutive
negative cultures
 Most persons diagnosed with TB are begun on specific treatment before the diagnosis is confirmed by
the laboratory.
TB drugs
 Aims of therapy
o Successful treatment requires more than one drug to which the organisms are susceptible
o Sufficient dose
o Sufficient duration
o Compliance -> DOT (polyclinic DOT) – directly observed therapy
 TB drugs
o First line:
 Isoniazid (H): 15mg/kg PO 3x/week
 RIfampicin (R): 600-900mg PO 3x/week
 Pyrazinamide (Z): 2.5g PO 3x/week
 Ethambutol (E): 30mg/kg PO 3x/week
 Streptomycin (S): 0.75-1g/day IM
 Amikacin
 Kanamycin
o Pyridoxine is given to reduce peripheral neuropathy induced by isoniazid
o Pyrazinamide is given for the first 2 months to kill intracellular bacilli
o 6 month treatment
o Titrate according to body weight
o Initial drug regimen is based on knowledge of the likely drug susceptibility
o Four drugs are used in the initial phase of treatment when the total duration of treatment is 6
months, because of the high incidence of isoniazid-resistant organisms in most communities
o Usually RHZ or RHEZ for 2/12 followed by RH for 4/12
 Drug resistant TB
o Initial drug regimens need to be modified in areas with a known high prevalence of MDR-TB
o Development of drug resistance after initial drug sensitivity (secondary drug resistance) occurs
in patients who do not comply with treatment regimens, occurs mainly in HIV patients
o Nosocomial transmission significant
o Use 4 drugs, treat for 2 years
o Follow up for 1 year after eradication
o Second line drugs: Ofloxacin, Ciprofloxacin, Cycloserine, Ethionamide, Azithromycin
 Drug side effects
o Rifampicin
 Induces liver enzymes -> caution in drugs and OCP
 Stop if liver enzymes are more than 3x elevated
 Orange tears, sweat, sputum, urine
o Isoniazid
 Peripheral neuropathy
 Skin rash
 Hepatitis -> stop drug
o Pyrazinamide
 Precipitates gout
 Liver toxicity
o Ethambutol
208
 Dose related optic retrobulbar neuritis, presents with colour blindness, central scotoma,
reduction in visual acquity
o Streptomycin
 Irreversible damage to the vestibular nerve
 Allergic reactions are more common
TB and HIV
 TB in an HIV patient is an AIDS defining condition
 4 drugs are used instead of the usual 3
 Adverse reactions are common and the prognosis is poor
 Multiple drug resistance occurs in 6%
 M. avium intracellulare is another mycobacterium that can cause pulmonary infection in AIDS patients
 Negative Mantoux test
 Positive reactivation of TB
 Atypical presentation
 Negative smears for AFB
 Atypical CXR
 Extrapulmonary and disseminated disease common
 Increased toxicity from anti-TB and anti-RV therapy
 Immune reconstituition inflammatory response = anti-RV therapy reconstitutes CD4 count and immune
function. Therefore paradoxical worsening of TB symptoms
 Absence of caseating granulomas
Prevention
 BCG vaccination: live attenuated vaccine -> only protects against childhoos military and CNS TB. Repeat
vaccination in adolescence not found to affect outcome/ risk of TB, and is no longer indicated
 Contact tracing: CXR, Mantoux test
 Chemoprophylaxis for contacts and for HIV patients
o Isoniazid 200mg/day PO for 9 month/ rifampicin 4 months if Mantoux positive as descrbed
Mantoux test
 Used to identify patients with latent TB (useful for screening)
 Positive tuberculin test indicates infection with M. tuberculosis; it does not diagnose active disease
 Intradermal injecion of 0.1 ml of PPD (type 4 hypersensitivity reaction)
 Interpreted 48-72 hours after intradermal administration = wheal and flare reaction
 Transverse diameter of wheal should be measured and recorded in millimetres
 False negatives: newly diagnosed TB, HIV, TB meningitis, malnourished, immunosuppressed,
lymphoma, sarcoidosis, military TB
 Children who have received the BCG vaccine generally demonstrate PPD skin test reactions of 3-19mm
several months after vaccination. Most of these reactions wane significantly with time. Responses
indicative of a new infection include: >10mm induration in persons less than 35 years of age or >15mm
induration in >35 years old.
209
10 mm or
< 5mm of 5 to 9mm of
more of
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induration
Patient is All others All others

Is known to No risk factors for Risk factors for
a child,
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adolesce
suspected of low demographic high demographic risk
nt,
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with induration induration Initiate
infectious TB treatment of
or has a chest latent
radiograph tuberculosis
suggestive of Initiate infection
Initiate previous TB No therapy treatment of
treatment of latent
latent tuberculosis
tuberculosis infection
infection
Initiate
treatment of
latent
tuberculosis
infection
Pulmonary TB
 Sputum culture after 2 months of antibiotic treatment
o Decrease if positive
o Increase: continuation phase to 7months (therefore total treatment 9 months)
 Unable to tolerate pyrazinamde
o 2 months of RHE
o 7 months of RH
 Patient taken out of isolation once sputum culture negative
Extrapulmonary TB (10%)
 6-9 months regimens
 12 months = military TB, bone/ joint TB, TB meningitis
 Adjunctive treatment
o Corticosteroids = TB pericarditis/ meningitis
o Surgery = constructive pericarditis, spinal cord compression
210
Medicine (Respi) = Pancoast tumour-Upper lobe lung CA
General inspection
- Cachexia
-Radiotherapy marks
-SVCO=Unilateral UL edema, facial plethora
Peripheries
-Digital clubbing and Hypertrophic pulmonary osteoarthropathy
-Tar stains
-Horner’s syndrome= Partial ptosis, constricted pupil, facial anhydrosis, enopthalmos
-Compression of brachial plexus=weakness of finger abduction, wasting of intrinsic hand muscles, numbness
over T1 dermatome
-Cervical lymphadenopathy
Lung
-Trachea deviation
Away=pushed by mass
Towards=Collapse
-Consolidation= Decreased air entry, inspiratory creps, increased vocal resonance, dull percussion in
supraclavicular fossa, upper 1/3 of chest
1. Differential diagnosis
-upper lobe consolidation and lymph nodes a) Neoplastic Lymphoma, b)
Infective-TB, pneumonia, lung abscess, aspergillosis, hydrated cyst
-Upper lobe collapse -> consolidation

a)Luminal- Foreign body, tumour, mucous lung
b) Mural= Structure (TB, sarcoidosis, iatrogenic)
= Vasculitis (Wegener’s granulomatosis)
c) Extrinsic- Lymphadenopathy, medialstinal masses, aortic aneurysm
2. Request to examine- Vitals, sputum mug, posterior chest-pleural effusion, pemberton’s sign, abdomen-
hepatomegaly, vertebreal column-mets, paraneoplastic syndromes->Pigmentation of palmar creases,
gynacomastia, cerebellar syndrome, peripheral neuropathy
211
Medicine (Respi) = Pleural Effusion
Definition
*Excessive accumulation of fluid in the pleural space
-Detectable on CXR when fluid > 300ml
-Detectable clinically when fluid > 500ml
*5 major types= Exudate, transudate, empyema, haemothorax, chylothorax
Pathogenesis
Transudate
*Increased hydrostatic pressure
(a) Cardiac = Congestive cardiac failure, Constrictive pericarditis
(b) Renal = ARF, CRF, ESRF, nephritic syndrome
* Decreased oncotic pressure

 Malnutrition
 Protein-losing enteropathy
 Chronic liver disease
 Nephrotic syndrome
*Lymphatic obstruction
 Tumour compression
 Post-radiotherapy
 SVCO
*others
 Hypothyroidism
 Meig’s syndrome = Benign ovarian fibroma a/w right-sided pleural effusion
Exudate
*Increased vascular permeability
 Inflammation due to RA, SLE, pulmonary embolism, pancreatitis
 Infections like pneumonia, TB, Bronchiatasis
 Malignancy = Lung primaries or mets, mesothelioma lymphoma
 Drugs= Ergotamine, carbegeline, bromocriptine, methotraxate, nitrofurantoin, amiodarone
Clinical features
History
-asymptomatic
-pleuritic Chest pain
-Dyspnea
-Fever, LOA, LOW, Night sweats, cough, haemoptysis
Physical exam
-Usually would be asked to examine the back
-Trachea deviation away from side of effusion
-Decreased chest movement/expansion
-Stony dullness
-decreased/absent breath sounds -> Bronchial breath sounds may be heard above the effusion
-Decreased vocal resonance-> Aegophony may be heard above the effusion
-Aetiology
212
Transudate (usually bilateral) Exudate (usually unilateral)
Cardiac failure Malignancy
-raised JVP -Radiotherapy marks
-Displaced apex beat(heaving) -Mastectomy
-S3 heart sound -cachexia
-Gallop rhythm -clubbing
-nicotine stains
-HPOA
-Cervical lymphadenopathy
Chronic liver disease Inflammation
-Stigmata of Chronic Liver Disease -Rheumatoid hands(RA)
-Malar Rash(SLE)
Renal Failure Infective
-Stigmata of ESRF -Toxic looking, sputum mug, IV antibiotics
-Vascular access
Investigations
1. Erect CXR(PA and lateral)
-Findings on PA CXR =Blunting of the costophrenic angles, meniscus sign
-Findings on Lateral CXR =Obliteration of posterior costophrenic angle then hemidiaphragm
-If column of fluid visible and 5cm in height from posterior costophrenic angle of contralateral lung  Lateral
decubitus view not required
-Subpulmonic effusion  Raised hemidiaphragm
-Loculated pleural effusion Accumulation of fluid between major/minor fissures or along lateral chest wall
(With obtuse angles of interface)
*may be mistaken for tumour
*Invx = U/S
2. Lateral decubitus CXR

-indications = Very small pleural effusions, alternative is U/S
-Findings =Layering of pleural effusion
Layering of free fluid> 10mm before blind thoracocentesis may be attempted safely
3. Pleural tap
-Both diagnostic and therapeutic
-Procedure= Infiltrate skin, periostuem of rib and pariatal pleural with 1% lignocaine
Insert needle into 1-2 intercostal space below level of dull percussion note
-dry tap=absence of fluid, incorrect needle placement, inappropriately short needle
-Investigations
(a) Clinical chemistry
 Protein, albumin, LDH, Glucose, cholesterol
 Empyema =pH (taken in a ABG tube and sent in ice)
 Pancreatitis, malignancy, oesophageal rupture = Amylase
 Autoimmune =Rh factor, ANA
(b) Gram staining

(c) culture and sensitivity
(D) fluid cytology
-send blood simultaneously for protein, albumin, LDH and glucose
213
4. Aetiology
 CT thorax=useful for visualizing underlying lung parenchyma obscured on CXR by large pleural effusions
 Video assisted thoracoscopy(VAT)
-Indications=Unknown etiology, lung malignancy, mesothelioma, pleural malignancy, TB
 Closed pleural biopsy(CT or US guided)
-Indications=malignancy, TB pleurisy, pleural tap inconclusive
Transudate vs Exudate
Parameter Transudate Exudate

Gross appearance Straw coloured – clear Yellow – turbid
Bloody (trauma, malignancy, TB, PE)
Cytology Normal High WBC
* Neutrophils → infection, PE
* Lymphocytes → TB, malignancy
* Eosinophils → presence of air/blood
Malignant cells
Microorganisms
Clinical chemistry Protein <30g/L Protein >30g/L
Light’s criteria (any 1 criteria met)
* Used to prove exudate
* Pleural:serum protein ratio >0.5
* Pleural:serum LDH ratio >0.6
* pleural LDH >2/3 upper limit of serum LDH
Serum-effusion albumin gradient >1.2 Serum-effusion albumin gradient <1.2
Low glucose
* Infection
* Malignancy
Low pH (<7.2 = indication for drainage)
* Empyema
High amylase
* Pancreatitis
* Malignancy
* Oesophageal rupture
High cholesterol
* Malignancy
* Chylothorax
Immunology Negative Postive for Rh factor and ANA
214
Management
* Important to distinguish transudate from exudates
- transudate = treat underlying cause
- exudate = investigate aetiology and treat
* General measures
- Ensure close monitoring of vital signs
- supplemental O2
- large-bore IV excess and GXM (if haemothorax suspected)
- antibiotics for parapneumonic effusion and empyema
* Principles of treatment
1. Removing pleural fluid
- Indications for urgent drainage of parapneumonic effusions = frank pus
Pleural fluid pH <7.2
Loculated effusions
Positive bacterial cultures
- Complications = pneumothorax, haemothorax, re-expansion pulmonary oedema
(a) Thoracocentesis (pleural tap) = alleviate dyspnoea in symptomatic effusions
Prevent ongoing inflammation and fibrosis in exudative effusions
~ ensure that platelet count, PT/PTT are satisfactory
(b) Chest tube insertion
2. Prevention of recurrence → pleurodesis (tetracycline, bleomycin or talc)
- Indications = recurrent effusions (malignant effusions); >2x
* Surgical
- indications = persistent effusions
Increasing pleural thickness (on ultrasound)
Monitoring
* Monitor
(a) patient’s vitals
(b) amount of fluid drained
(c) quality of fluid drained
(d) air-leak (bubbling through water seal)
* Repeat CXR when drainage <100ml/day = evaluate if effusion has been fully drained
Causes of dullness at lung bases

* Pleural effusion (stony dullness)
* Consolidation
* Collapse
* Raised hemidiaphragm (usually 2° to phrenic nerve injury; usually the only clue is a supraclavicular scar)
* Lobectomy
* Pleural thickening
215
Medicine (Respi) =Pneumothorax
Definition
 Pneumothorax = air in pleural space
 Haemothorax = blood in pleural space
 Chylothorax = lymph in pleural space
 Empyema = pus in pleural space
Aetiology
 Spontaneous
(i) Primary
- No underlying lung disease
- Usually due to connective tissue defect in pleural wall → bleb formation and rupture
- a/w Marfan’s syndrome and Ehlers-Danlos syndrome (↓ collagen)
- Epidemiology = young tall and thin males (alveoli at lung apices subjected to greater
distending pressure cf to those at lung bases → more likely to develop sub-pleural blebs)
(ii) Secondary
- Due to underlying lung disease = COPD, asthma, TB, CF, lung cancer, bronchiectasis
 Traumatic
Types of pneumothorax
 Open
- Open communication between airways and pleural space (broncho-pleural fistula) →
persistant air-leak
 Closed
- No communication
- Air is reabsorbed at a rate of 1.25% of the total radiographic hemithoracic volume per
day
 Tension
- Valvular mechanism develops such that air is sucked into the pleural space during
inspiration but not expelled
- Results in = mediastinal shift, tracheal deviation
Increasing respiratory and cardiac embarrassment
Clinical features
History
- Asymptomatic
- Acute pleuritic chest pain
- Sudden onset/rapidly progressing dyspnoea
- Triggers = trauma, IJ (internal jugular) line insertions, recent H&N surgery
- Underlying lung disease – asthma, COPD, TB, CF, lung cancer
- Previous episodes of pneumothorax
- History of Marfan’s or Ehlers-Danlos syndrome
- Vital signs = tachycardia, tachypnoea, hypotension, pulsus paradoxus (inspiration: ↑ VR
(systemic venous return causing ↑ lung pooling) ∴ ↓ systolic BP → missing radial pulses;
seen in tension PTX)
- Signs of respiratory distress
- Decreased chest expansion, hyper-resonant percussion note, decreased breath sounds
- Subcutaneous emphysema
- Tracheal and mediastinal deviation if tension PTX
Investigations
 Erect CXR
- Radiological findings
(a) Ipsilateral lung edge seen parallel to chest wall
216
(b) No lung markings in pleural space
(c) Contralateral mediastinal and tracheal shift if tension PTX
(d) Deep sulcus sign = costophrenic angle is significantly lower than that on
contralateral side
(e) Contralateral lungs gets entire cardiac output and vascular markings become
more prominent
From:
http://www.meddean.luc.edu/lumen/MedEd/Radio/curriculum/Mechanisms/Atelecta
sis1.htm
- Assess rotation → obscure PTX and mimic mediastinal shift
- Side of PTX
(i) Small = apex-cupola distance < 3cm,
Visceral-parietal pleural separation < 2cm (BTS)
(ii) Large = apex-cupola distance ≥ 3cm,
Visceral-parietal pleural separation ≥ 2cm
- Evidence of underlying lung disease e.g. bullae, hyperinflation
 ABG
Management
 Supportive
- Supplementary O2 = 100% oxygen by NRM → creates concentration gradient → N2 diffusion
from PTX into alveoli → decreases size
 Tension pneumothorax
- Immediate needle decompression in the 2nd intercostals space along mid-clavicular line (14
gauge needle)
- Followed by chest tube insertion
 Primary spontaneous pneumothorax
- Small = observe at EMD → repeat CXR
Discharge if no progression of PTX
F/u CXR within 2 days
Observe at 2-weekly intervals until air is reabsorbed
- Large / unstable = chest tube inserted at EMD
Admit and observe
217
(i) Simple Aspiration
- Infiltrate with lignocaine
- Push 16 F gauge cannula into pleural space
- Connect cannula to three way tap and 50ml syringe
- Aspirate up to 2.5 L of air slowly → stop if there is resistance or patient coughs excessively
- Repeat expiratory CXR film
(ii) Chest tube insertion

- Open technique
- Position the patient = place arm above head
Lean forward on table
- Done under sterile technique
- Clean and drape
- Infiltrate with LA
- Incision made XXX (Suggestion: in the ‘safe triangle’ bordered by the) major muscle, mid-
axillary line and upper border of 5th rib (avoid neuromuscular bundle running along ingerior
border of rib)
- Blunt dissection with curved forceps
- Enter pleural cavity and check for adhesions/lung/diaphragm
- Place chest drain between jaws of curved forceps and insert into thorax → direct upwards
and backwards towards suprasternal notch
- Connect to underwater seal
# acts as one-way valve = air comes out but cannot re-enter pleural cavity
# always keep below level of patient
# continuous bubbling = persistent air-leak (lung laceration)
# do not clamp tube → tension pneumothorax
- Secure tube with purse-string suture
- Examine chest and look at parameters
- Order CXR to verify position = PA and lateral views to ensure chest tube is not in SC plane
(iii) Surgical pleurodesis

- Indications = persistent PTX on day 5
Recurrent PTX ( > 2x)
- Apical bullae = bullectomy
(iv) Chemical pleurodesis

- Done when surgery is contraindicated
- Avoided in patients with cystic fibrosis → difficult lung Tx in future
- Less effective (80-90%) than surgical pleurodesis (95-100%)
- Only done when lung has fully re-expanded so that pleural surfaces are apposed
- Injected into pleural cavity via chest tube
Complications of chest tube insertion

- Subcutaneous emphysema (chest tube not inserted deep enough)
- Tube blockade = kinked
Blocked by debris and lung tissue
- Pain
- Haemothorax (laceration of vessels)
- Lung laceration (adhesions not taken down)
- Diaphragmatic laceration (stomach/colon injury)
- Re-expansion pulmonary oedema
# occurs when pleural effusion or PTX is drained too fast
# correlates with size, speed of drainage and duration of PTX/effusion
# can be avoided by limiting effusion drains to 1.5L/day by clamping the tube (PTX drains cannot be limited)
218
Collapse > 72 hours Sudden re-expansion
Decreased Sudden inflow of blood, increased Alveolar distension

surfactant capillary pressure squeezes capillaries
Increased capillary leak Pulmonary oedema
Practical points
1) Indications for chest tube insertion
(a) Pneumothorax = large, tension, traumatic, failed aspiration
(b) Haemothorax
(c) Symptomatic pleural effusion
(d) Rib fractures and mechanically ventilated patients
Contraindications = bleeding diathesis
2) Apply suction if lung fails to re-expand after chest tube insertion

3) Haemopneumothorax (flat meniscus on CXR) → additional chest tubes required to drain blood and clots →
second chest tube should be directed inferiorly and posteriorly to diaphragm
4) Things to check for during ward rounds
- Patency of chest tube = air bubble should oscillate with respiration/coughing
- Amount and type of drainage = continuous bubbling indicates open air leak
- Drains < 100ml/day → order repeat CXR to check for resolution
5) Indications for chest tube removal
- Chest tube stops draining for at least 6 hours (after 4-6 hours of clamping)
- CXR shows resolution of PTX
6) Steps in chest tube removal
i) Requires 2 people
ii) Discontinue suction
iii) +/- clamping of chest tube (controversial)
iv) Cut anchoring sutures
v) Tell patient to breath in or out deeply and hold his breath
vi) Pull out tube and simultaneously secure purse string
vii) STO 10 days
219
Medicine (Respi) = Respiratory Failure
1. Definition
a. It occurs mainly when gas exchange is inadequate – resulting in hypoxia
b. Defined as PaO2 < 8kPa – subdivided into 2 typees according to PaO2 levels
2. Type 1 respiratory failure
a. Defined as hypoxia (PaO2 < 8kPa) with a normal/low PaCo2
b. Caused primarily by V/Q mismatch
i. Pneumonia
ii. Pulmonary oedema
iii. ARDS
iv. Pulmonary embolism
v. Asthma
vi. Emphysema
3. Type 2 respiratory failure
a. Defined as hypoxia (PaO2 < 8kPa) with hypercapnia (PaCO2 > 6kPa)
b. Caused by alveolar hypoventilation -> respiratory acidosis
i. Drugs – opiates, sedatives, anaesthetic agents
ii. CNS depression – brainstem stroke
iii. Thoracic cage limitation – kyphoscoliosis, flail chest
iv. Neuromuscular disorders – GBS, Myasthenia gravis, Polio
v. Restricted lung expansion – pneumothorax, pleural effusion, hemothorax, diaphragmatic
paralysis
4. Clinical features
a. Hypoxia = cyanosis, dyspnoea, restlessness/agitation, confusion
i. Long standing
1. Polycysthaemia
2. Pulmonary hypertension
3. Cor Pulmonalae
b. Hypercapnia = headache, drowsy, confusion, stupor, bounding pulse, flapping tremor, galilloedema,
peri – pleural vasodilatation, dilated retinal veins
5. Investigations
a. FBC = WCC (infection)
b. CRP
c. D-Dimer
d. ABG
e. Cardiac Enzymes
f. ECG = pulmonary embolism
g. CXR
h. Sputum & Blood Cultures
6. Management
a. Type 1 respiratory failure
i. Treat underlying cause
ii. O2 Via facemask (35-60%)
iii. Assisted ventilation (NIPPV = non – invasive +ve pressure ventilation) if PaO2 < 8kPa
despite PaO2 = 60%
b. Type 2 respiratory failure
i. Treat underlying cause
ii. Controlled O2 Therapy = start at PaO2 24%
1. Respiratory center may be relatively insensitive to Co2
a. Respiration driven by hypoxia – cant give O2 so quickly as a result
iii. Recheck ABG 20mins later
1. if PaCo2 remains steady/decrease = Increase PaO2 to 28%
2. if PaCo2 increase = respiratory stimulant (doxapram) + assisted ventilation (NIPPV)
iv. if all else fails = intubate & reventilate
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Medicine (Respi) = systemic approach to CXR
1. Name, date and projection
a. Check that it is the correct patient
b. Check the left/right marker to prevent missing dextrocardia (apex on the right and stomach bubble on
the left)
c. AP and supine films are second-best of PA films
i. AP -> heart appears enlarged (cannot comment accurately on heart size)
ii. Supine -> distension of posterior vessels = lung fields appear plethoric
1. Heart appears enlarged
“This is the erect AP/PA chest x-ray of Mr/Mdm __________ taken on the _______.”
2. Rotation, penetration, degree of inspiration
a. Rotation = medial ends of clavicles should be equidistant from the midline spinous processes
i. If one clavicle is nearer than the other -> lung on that side will appear whiter
b. Penetration = vertebral bodies should only just be visible through the cardiac shadow
i. Too clearly visible = over-penetration
ii. Cannot see at all -> under-penetration
c. Inspiration = 6th anterior rib should cut the midpoint of the right hemidiaphragm in the midclavicular
line
i. Poorly inspired film -> heart appears enlarged, basal shadowing, trachea deviated to the right
“The quality of the film is good = with no rotation, good penetration and taken on full inspiration.”
3. Mediastinum
a. Trachea = should lie in the mid-line
i. Comment on the presence of ETT
ii. Pushed away by large pleural effusion, pneumothorax, mediastinal mass or tumour
iii. Pushed by lung collapse or fibrosis
b. Thin and slender mediastinum = COPD
4. Hilum
a. Characteristics = mostly formed by the pulmonary arteries with the upper lobe veins superimposed +
left hilum slightly higher than right
b. Hilar enlargement = lymphadenopathy, large pulmonary artery
5. Heart
a. Characteristics
i. Straddles mid-line with 1/3 to the right and 2/3 to the left
ii. Right heart border formed by right atrium; left heart border by left ventricle
iii. Transthoracic diameter -> widest diameter above the costophrenic angles
iv. Cardiac diameter -> draw a vertical line from the trachea to the heart (assuming no deviation)
1. Sum of the 2 greatest lengths from the vertical line to both heart borders
b. Cardiomegaly = cardiothoracic diameter >50%
6. Diaphram
a. Characteristics = right hemidiaphragm should be higher than the left (due to liver)
b. Loss of costophrenic angle with meniscus = pleural effusion
c. Loss of diaphragmatic outline = lower lobe consolidation
d. Low and flat hemidiaphragms = COPD
e. Air below the diaphragm = free peritoneal gas (likely perforation)
7. Lung fields
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a. Division
i. Apices – lie above the level of the clavicles
ii. Upper zone – include the apices to the level of the 2nd costal cartilage
iii. Middle zone – lie between 2nd and 4th costal cartilage
iv. Lower zone – lie between 4th and 6th costal cartilage
b. Loss of cardiac silhouette – middle lobe consolidation
c. Increased translucency – hyperinflation
8. Bone and soft tissue
a. Rib fractures
b. Bone metastasis
c. Subcutaneous emphysema
Medicine (Respi) = Mediastinal masses

- Anterior superior mediastinum
o Retrosternal goitre
o Teratoma
o Bronchogenic carcinoma
o Aortic dissection/aneurysm
- Middle mediastinum
o Hilar lymphadenopathy
o Lymphoma
- Posterior mediastinum
o Neurogenic tumour
o Aneurysm
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Cardio Vascular System
Medicine (CVS) = History Taking: CVS
Date of admission
1. Cardiovascular symptoms
(a) Chest pain
 Onset, frequency, duration
 Sudden/gradual onset
 What were you doing at onset
 Progressively better/worse
 Site and radiation of pain
 Character of pain
 Severity
 Precipitating (none, exertion, palpitations, emotions -> cardiac symptoms)
(food, alcohol, lying down - > reflux symptoms)
 Aggravating (inspiration, coughing, movement of shoulders)
 Relieving factors (rest, GTN, antacids)
 Effort tolerance (level ground and climbing up stairs) -> significantly different from last time?
New York Heart Association (NYHA) Classification

Class 1 = asymptomatic
Class 2 = angina/dyspnoea during ordinary activity
Class 3 = angina/dyspnoea during less than ordinary activity
Class 4 = Angina/dyspnoea at rest
(b) Dyspnoea (rest/exertional/orthopnoea/paroxysmal nocturnal dyspnoea)

 Onset, frequency, duration
 What were you doing at onset
 Progressively better/worse
 Severity
 Precipitating (none, exertion, palpitations)
 Aggravating
 Relieving factors (rest, GTN)
 Effort tolerance (level ground and climbing up stairs) -> significantly different from last time?
 Require how many pillows to prop up at night?
(c) Palpitations
 Sudden/gradual onset
 Can you tap out the rhythm? (slow/fast, regular/irregular)
 Duration
 Sudden/gradual offset
 Precipitating/aggravating/relieving factors
 Associated with chest pain, dyspnoea, giddiness or syncope
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 Any learned manoeuvres (valsalva, carotid massage, coughing, swallowing cold water/ice cubes)
- Cardiac arrhythmias = instantaneous onset and offset

- Sinus tachycardia = gradual onset and offset
- Atrial fibrillation = irregularly irregular rhythm
- Ventricular tachycardia = rapid palpitations followed by syncope
(d) Ankle oedema

 Unilateral/bilateral
 Until what level
 Other areas affected (face/abdomen)?
 Worse at the end of the day?
 Better in the morning?
 Are you on CCB?
 How much weight gain?
(e) Symptoms of acute MI = diaphoresis, nausea, vomiting, giddiness/syncope
(f) Syncope (reflect either cardiac or CNS events)

 confirm that there is really LOC
 prodromal symptoms = chest pain, dyspnoea, palpitations
 r/o CNS causes (aura, headache, dysarthria, limb weakness)
 during the episode = signs of fits (limb jerking, uprolling eyes, apnoea, clenching of teeth, tongue biting,
foaming at mouth, urinary/faecal incontinence)
 recovery = rapid (likely cardiac)
 prolonged and a/w post-ictal drowsiness
(g) fatigue (reduced cardiac output and poor blood supply to skeletal muscles)
(h) intermittent claudication (PVD with poor blood supply to affected muscles)
 areas affected
 claudication distance
 must rest for how long
2. Aetiology
(a) Trauma = musculoskeletal injury
(b) Fever and productive cough = pneumonia causing pleurisy
(c) Preceding URTI = viral mycarditis/pericarditis
(d) Nausea, vomiting, epigastric pain, acid regurgitation, dysphagia = GERD
(e) Triggers = anaemia (PR bleeding), sepsis, hyperthyroidism
3. Systemic review
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4. Management prior and in hospital

(a) When
(b) What happened
(c) Similar circumstances and character of pain
(d) Investigations done = ECG, treadmill ECG, coronary angiogram
(e) Management = meals, PTCA (Percutaneous transluminal coronary angioplasty), CABG
1. DM, HPT, HCL, AMI, CVA, cancer
3. Previous surgeries = PTCA, CABG
Drug History
1. Any known drug allergy
- CNS = ACE inhibitors, B-Blockers, CCB, diuretics, GTN
- Other types of medications (indications for use)
- Dose, frequency of dosing
- Side-effects
3. Use of TCM
Social History
1. Smoking
2. Alcohol drinking
3. Family set-up (main caregiver, health of family members, finances)
4. Lift-landing
Family history
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Medicine (CVS) = Physical Examination: CVS
Start
1. Examine the patient on the right hand side of the bed
2. Introduce yourself and explain purpose (shake hands)
3. Position the patient at 45 degrees with adequate exposure
Inspection from the foot of the bed

1. General appearance
 Mental state = alert, orientated, confused, drowsy
 Comfortable/in pain
 Respiratory distress = supplemental oxygen, use of accessory muscles,
suprasternal/intercostals/subcostal retractions, dyspnoea, tachypnoea
 Malar flush (MS, low cardiac output) = peripheral cyanosis on cheeks
 Jaundice
 Giant v waves (TR)
 Surgical scars on chest
 Median sternotomy -> CABG, valve replacement
 Lateral thoracotomy -> mitral valvotomy
 Pacemaker/cardioverter – defibrillator box (under the right of left pectoral muscles)
 Chest wall deformities (pectus excavatum in marfan’s syndrome)
2. Respiratory rate (15s)
Hands
1. Pulse rate: hold patient’s hand with your right hand and take pulse with your left hand (15s)
 Rate, rhythm, volume, character
 Irregularly irregular = atrial fibrillation, multiple ectopic beats
 Regularly irregular = second-degree heart block, ventricular bigemini
 Regular = normal rhythm, sinus arrhythmia (increases with inspiration, decreases w expiration)
2. Radio-radial delay (aortic arch aneurysm, aortic dissection)
 Radio-femoral delay (coarcation of the aorta)
3. Collapsing pulse: ask if there is shoulder pain, lift up patient’s hand and feel an increase in volume (AR)
4. Check fingers for:
 Cyanosis (R->L shunt)
 Clubbing (IE)
 Splinter haemorrhages in nail beds (IE, Vasculitis)
 Tendon xanthomata (familial hypercholesterolaemia)
 Osler’s nodes (IE) = red raised tender nodules on finger pulps, thenar and hypothenar eminences
 Janeway lesions (IE) = non-tender erythematous maculopapular lesions containing bacteria
Head
1. Check eyes:
 Look down and pull up upper eyelid – jaundice (mechanical haemolysis by prosthetic valve; congestive
cardiac failure; hepatic congestion)
 Look up and pull down lower eyelid – pallor (anaemia)/spinter haemorrhages (IE)
 Xanthelasma (hyperlipidaemia)
2. Check mouth: lips and tongue – central cyanosis; teeth, gums, pharynx – IE
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Neck
1. Check for raised jugular venous pressure
 >3cm above sterna angle is abnormal
 Abdominojugular reflex: compress the abdomen over the liver to see if there is an increase in JVP
 +ve if rise in JVP persists throughout 15s compression
 Reflects RVF (inability to eject the increased venous return)
Chest
Palpation
1. Palpate for the apex beat (feel with the whole hand and localise with 1 finger). If cannot find on the left side,
check the R side for dextrocardia
 position: displacement in cardiomegaly/LVH
 character
 heaving = pressure loaded e.g. HPT,AS -> forceful, sustained, not displaced
 trusting = volume loaded e.g. MR, AR -> forceful, not sustained, displaced downwards and laterally
tapping (MS)
 double impulse (HOCM)
 if apex beat is non palpable: thick chest wall, emphysema, pericardial effusion, dextrocardia (palpable to
the right of the sternum)
2. Parasternal heave for RVH (place hand vertically over sternum for 3-5s – PS, pulmonary hypertension
3. Palpable tap of P2 over pulmonary area -> pulmonary hypertension
4. Thrills for palpable murmurs (place hand horizontally over base of heart) – systolic/diastolic
Auscultation
-If patient is hairy, use bell instead of diaphragm
-Bell is good for low pitched sounds and should be applied gently to the skin (if not -> becomes a
diaphragm)
- Diaphragm filters out low-pitched sounds and makes higher-pitched murmurs easier to detect
1. Auscultate mitral area first (left 5th intercostals space)
- Palpate carotid pulse to identify S1,S2
- PSM for MR -> radiates to axilla
- Get the patient to lie on the left lateral position: palpate for the apex beat (tapping in MS); Use bell to listen
for MDM of MS
2. Auscultate left sterna edge for PSM (VSD,TR) or EDM (AR)
3. Auscultate pulmonary (left 2nd intercostals space) and aortic (right 2nd intercostals space) areas
- Manoeuvres
a. Full inspiration for right sided murmurs (PS, PR)
b. Full expiration for left sided murmurs (AS, AR)
c. Inspiration -> -ve intra-thoracic pressure increases venous return to the heart; increased blood flow
through the right side of the heart
d. Expiration -> +ve intra-thoracic pressure increases outflow from the heart; increased blood flow
through the left side of the heart
- Valsalva manoeuvre for systolic murmurs -> decreases preload (squatting has opposite effects)
a. Accentuates -> MVP (apex), HOCM (LLSE)
b. Softens -> MR, AS
- Sit up in full expiration and auscultate -> LLSE for EDM (AR); aortic area for ESM (AS)
- Sit up in full inspiration and auscultate -> pulmonary area for ESM (PS) and EDM (PR)
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4. Ask the patient to hold his breath and auscultate the neck for carotid bruits and radiation of AS
- Radiation = same intensity as the original murmur
- Transmitted = lower intensity than the original murmur
5. Auscultate lungs
- Decreased air entry
- Crepitations
- Stony-dull percussion
6. Check sacral oedema
Murmurs Timing, area, pitch, loudness, effect of dynamic manoeuvres

Aortic High-pitched early-diastolic murmur
regurgitation Loudest with patient sitting up and in full expiration
Collapsing pulse
Aortic Harsh ejection systolic murmur radiating to carotids

stenosis Loudest in patient sitting up and in full expiration
Slow rising pulse  carotids
Mitral Loud S1
stenosis Low-pitched mid-diastolic murmur
Mitral Soft/ absent S1

regurgitation Pansystolic murmur maximal at apex beat radiating to mid-axillary line
Tricuspid Pansystolic murmur maximal over left sternal edge

regurgitation Large v waves
Pulsatile liver
In general:
 Low-pitched murmurs indicate turbulent flow under low pressure
 High-pitched murmurs indicate high velocity flow
Non-valvular murmurs
Pericardial Superficial scratching sound not confined to systole or diastole
fiction rub Caused by movement of inflamed pericardial surfaces
Can vary with posture and respiration (louder when patient is sitting up and in full
expiration)
Heard in pericarditis
Continuous Present throughout systole and diastole (permanent pressure gradient)
murmurs Communication existing between both parts of the circulation
Heard in PDA, AVF, ruptured sinus of Valsalva into right atrium/ventricle
Aortopulmonary connection (congenital, Blalock shunt)
Abdomen
- Lie the patient flat
1. Palpate liver: hepatomegaly (CCF); pulsatile (TR -> ask patient to hold his breath in full inspiration for 3-5s and
time with carotids)
2. Renal bruits
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Legs
1. Pedal oedema (look at patient’s face when doing it
2. Check R/L dorsalis pedis
3. Check for cyanosis and clubbing of toes
4. Thickening of Achilles tendon (hyperlipidaemia)
End
1. Tell examiners that you would like to complete the examination by checking for hepatomegaly, chest (pleural
effusions and crepitations), blood pressure, temperature, fundoscopy (roth’s spots in IE = retinal infarcts) and
urinalysis (haematuria in IE)
2. Thank patient for his help and help him button up shirt
3. Shake his hand before you go
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Medicine (CVS) = Issues for discussion
Clubbing
CVS Infective endocarditis

Grading
Congenital cyanotic heart disease
Grade 1 = fluctuance at nail bed
Respiratory Suppurative conditions (empyema,
bronchiectasis, abscess) Grade 2 = loss of nail bed angle
Lung carcinoma Grade 3 = Increased curvature of nail
Idiopathic pulmonary fibrosis (drumstick)
Cystic fibrosis Grade 4: HPOA (Hypertrophic
GIT Inflammatory bowel disease (eg. Pulmonary Osteoarthropathy)
Crohn’s)
Celiac disease
Biliary cirrhosis
Others Thyrotoxicosis (acropachy)
Idiopathic
Examination
- Inspect fingernails from the side to determine loss of angle between nail bed and finger
- Compress nail bed and rock it from side to side (increased sponginess of proximal nail bed)
- Hold nails of both hands together facing each other (clubbing present if no gap is seen)
Pulses
- Radial pulse -> assess rate and rhythm
- Brachial/carotid pulse -> assess character and volume
Bounding pulse = CO2 retention, sepsis

Small volume pulse = AS, pericardial effusion
Slow-rising (anacrotic) pulse [slow rise and fall] = AS (carotids)
Collapsing (water-hammer) pulse [rapid rise and fall] = AR, large AV malformations, PDA, ruptured sinus
of valsalva
Jerky pulses = HOCM
Pulsus alternans (alternating strong and weak beats) = LVF (AS, cardiomyopathy)
Pulsus paradoxus = severe asthma, pericardial constriction (pericardial effusion, constrictive
pericarditis), cardiac tamponade, tension pneumothorax;
Weak pulse that may disappear on inspiration; normal reduction in SBP with inspiration
is exaggerated (>10mmHg); gives rise to sinus arrhythmia if HR increases to
compensate
Number of mmHG between initial appearance of korokoff’s sounds in expiration and
their apperarance throughout the respiratory cycle
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Blood pressure
Pulse pressure
- Defined as the difference between SBP and DBP
- Narrow = AS; wide = AR
Postural hypertension
- Defined as a drop in SBP>20mmHg and DBP>10mmHg on standing
Korotkoff sounds
Korotkoff 1 = pressure at which a sound is first heard over the artery (SBP)
Korotkoff 2 = sound increases in intensity
Korotkoff 3 = sound decreases in intensity
Korotkoff 4 = sound becomes muffled
Korotkoff 5 = pressure at which sound disappears (DBP)
Jugular venous pressure

- IJV acts as a manometer of right atrial pressure = height + waveform
Characteristics
a. Visible but not palpable
b. Obliterated by finger pressure on vein
c. Varies with changes in respiration and posture (flatters with inspiration)
d. Double pulse for every arterial pulse
e. Rises transiently following pressure on the abdomen/liver
Measuring height
Procedure = Observe the patient at 45 degrees with his head turned slightly to the left
Right IJV lies medial to the clavicular head of the SCM
Measure the vertical height of the pulse above the sterna angle (raised JVP >3cm)
Recognising waveform
A wave = atrial systole

C wave = bulging of tricuspid valve into right atrium during ventricular isovolumic systole
X descent = ventricular systole leading to fall in atrial pressure
V wave = atrial filling against a closed tricuspid valve
Y descent = opening of tricuspid valve
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a. Raised JVP with abnormal waveform = fluid overload, RHF
b. Raised JVP with absent pulsation = SVCO
c. Raised JVP on inspiration (kussmaul’s sign) = constrictive pericarditis, cardiac tamponade, right ventricular
infarction (best elicited with patient sitting up at 90 degrees) – normally would flatten instead
d. Large a wave = pulmonary hypertension, pulmonary stenosis
e. Cannon a wave (right atrial systole against a closed tricuspid valve) = complete heart block, atrial flutter
ventricular arrhythmias/ectopics
f. Absent a wave = atrial fibrillation
g. Large systolic v wave = tricuspid regurgitation
Heart sounds
S1 Closure of mitral and tricuspid valves

S2 Closure of aortic and pulmonary valves
 P2 is loud in pulmonary hypertension
 Splitting of S2
o Due to closure of pulmonary valve later than that of the aortic valve (lower pressures
in the former)
o May be physiological  wider splitting during inspiration due to increased venous
return
o Best heard in LLSE and pulmonary area
S3 Pathological over 30 years of age
Occurs in a dilated left ventricle with rapid ventricular filling (MR, VSD)/ poor LV function (post-MI)
S4 Always abnormal; usually presents in people > 45 years old
Respresents atrial contraction against a stiff ventricle eg. hypertension, AS
Gallop 3rd/4th heart sound occurring with a sinus tachycardia (HR > 120bpm)
rhythm S3 gallop sounds like ‘ken-tucky’
S4 gallop sounds like ‘tenne-ssee’
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Cardiac murmurs
ESM (Ejection systolic PSM (Pan-systolic EDM (Early- MDM (Mid-

murmur) murmur) diastolic murmur) diastolic
murmur)
Waveform/ Crescendo-decrescendo Uniform murmur High-pitched and Low-pitched and
Character murmur with S2 heard which merges with S2 easily missed (listen rumbling with an
for ‘absence of opening snap after
silence’ in early S2
diastole
Occurs  Turbulent flow A ventricle leaks to a Organic (AR, PR) Impaired flow
when through the lower pressure during ventricular
aortic/pulmonary chamber/ vessel filling
valve orifices
 Or greatly increased
flow through the
heart
Causes  Innocent murmur  Organic (MR, TR, Graham-Steell Organic (MS, TS)
(esp in children) VSD, MVP) murmur = mitral
 High-output states *MVP  late systolic stenosis 
(anemia, pregnancy) murmur ± mid-systolic pulmonary
 Organic (AS, PS, click, accentuated by hypertension 
HOCM) valsalva manoeuvre pulmonary
regurgitation
Grading intensity of murmurs

- Commonly used for systolic murmurs
- Poor guide to the severity of the lesion (length of the murmur is impt)
Grade 1 = very soft, heard only after listening for a while

Grade 2 = soft but detectable immediately
Grade 3 = clearly audible with no palpable thrill
Grade 4 = clearly audible with palpable thrill
Grade 5 = audible with stethoscope only partially touching the chest
Grade 6 = audible without a stethoscope
LL oedema
Bilateral, pitting Cardiac (CCF, constrictive pericarditis)

GIT (liver cirrhosis, malnutrition, protein-losing enteropathy)
Renal (nephrotic syndrome, ESRF)
Unilateral, pitting DVT
Compression of large veins by tumour/LAD
Bilateral, non- Hypothyroidism
pitting Lymphoedema (infection, malignant, congenital)
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Presentation
Mr (name), a pleasant looking age/gender/race appears to be alert, well, comfortable and orientated at
rest. His vital signs are stable: HR is ___, regularly regular, RR is ___ and he is currently afebrile. He does
not appear to be in any respiratory distress and is pink on room air. He does not appear cachexic. On
inspection, there are no signs of cyanosis, jaundice, pallor, dehydration or peripheral oedema.
On examination of the peripheries, there was no clubbing observed or stigmata of infective endocarditis
such as splinter haemorrhages, osler nodes or janeway lesions. There was no radio-radio or radio-
femoral delays. Collapsing pulse was absent.
On inspection of the praecordium, there were no signs of surgical scars or chest wall deformities. The
apex beat was not displaced = it was in the left 5th intercostals space. There was no parasternal heave or
thrills were felt over the pulmonary or aortic areas.Palpable P2 was not felt. On auscultation, normal
S1S2 was heard. Loud P1 was not heard. There were no additional heart sounds or murmurs detected. No
bruit was heard over the carotids
There was no evidence of right heart failure = JVP was not raised and there was no sacral or pedal
oedema. Air-entry was good on auscultation of the lung bases. Normal vesicular breath sounds were
heard and there was no inspiratory crepitation sor wheeze detected.
I would like to end my examination by requesting for the temperature and BP charts.
235
Medicine (CVS) = Approach to chest pain
Cardiovascular Angina (stable, unstable, variant)

AMI
Pericarditis/Myocarditis
Aortic dissection
Pulmonary embolism
Respiratory Pneumonia with pleurisy
Pneumothorax
Chest wall Rib fractures
Thoracic herpes zoster
Muscular strain
Costochondritis (Tietze’s syndrome)
Gastrointestinal GERD
Oesophageal spasm
Oesophageal rupture
1. Angina
a. Usually a central dull ache in the retrosternal area
b. May radiate to the jaw or left arm
c. Characteristically occurs with exertion and relieved by rest or nitrates
d. GTN is not specific as it can also relieve esophageal spasm
2. Myocardial infarction
a. Often comes on at rest
b. Pain is more severe and lasts longer (>30mins)
c. Associated with dyspnoea, sweating, nausea, giddiness
3. Pleuritic pain
a. Made worse by inspiration, coughing and movement of shoulders
b. Due to pleurisy (pneumonia) or pericarditis
c. Often relieved by sitting up and leaning forward
4. Musculoskeletal
a. Sharp pain localised to a small area of the chest wall
b. Associated with respiration, coughing or movement of shoulders
5. Dissecting aneurysm
a. Shearing pain greatest at onset
b. Radiates to back (distal to left subclavian artery)
c. Think of this if patient presents with chest pain suggestive of AMI but with neurological symptoms as
well
6. Massive pulmonary embolism
a. Pain of very sudden onset
b. Associated with collapse, dyspnoea, cyanosis
7. Spontaneous pneumothorax
a. Sharp and localised pain
b. Associated with severe dyspnoea
8. Oesophageal spasm
a. Rare and difficult to distinguish from angina
b. Precipirated by food, alcohol and lying down
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c. Associated with dysphagia
d. Relieved by GTN (but time to relief is not as quick as for angina)
9. GERD
a. Burning sensation radiating to the neck
b. Associated with dysphagia and acid regurgitation
c. Precipitated by food, alcohl and lying down
d. Relieved by antacids
10. Oesophageal rupture
a. Chest pain followed by violent vomiting
b. Usually no haematemesis
c. CXR shows pneumomediastinum
6 life threatening causes of chest pain

1. AMI = cardiogenic shock, fatal dysrhythmias
2. Unstable angina (carries similar short-term prognosis as AMI)
3. Aortic dissection = cardiac tamponade, aortic rupture, acute aortic insufficiency, AMI, damage to other
organ systems
4. Pulmonary embolism = hypoxia, hypotension, acute cor pulmonale
5. Tension pneumothorax = hypoxia, hypotension (+ve intra-thoracic pressure)
6. Oesophageal rupture
History taking
Date of admission
1. Cardiovascular symptoms
Triggers = Anaemia,
a. Chest pain, sob, palpitations, ankle oedema, nausea, vomiting
Sepsis, Hyperthyroidism
b. Diaphoresis, giddiness, syncope, fatigue, intermittent claudication
2. Management prior to hospitalisation
3. Aetiology
a. History of trauma (muscular strain, rib #, oesophageal rupture)
b. Fever, URTI, productive cough (viral myocarditis, pneumonia)
c. Nausea, vomiting, epigastric pain, acid regurgitation, dysphagia (GERD)
4. Systemic review
5. Current management in hospital
Past medical history (identify risk factors)

Drug history
Social history (identify risk factors)
Family history (identify risk factors)
Features of cardiac pain

Character = dull, crushing pain/pressure (clenched fist over sternum -> Levine sign positive)
*if sharp -> likely pleurisy or pericarditis
Duration = >30mins usually indicates AMI
Site = diffuse
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*if well localised -> unlikely to be cardiac cause
Radiation = shoulder, either/both arms or neck/jaw
*can be epigastric pain as well
Precipitants = exercise, palpitations, emotion, food
*if brought on by food, lying flat, hot drinks, alcohol -> oesophageal spasm
Relieving factors = within mins by rest or GTN -> angina
GTN relieves oesophageal spasm more slowly
Antacids -> Gerd
Sitting up and leaning forward -> pericarditis
Aggravating factors = inspiration, coughing, movement of shoulders -> pleuritic
Features of non-cardiac chest pain
a. Sharp or stabbing in nature
b. Lasts <30s
c. Pleuritic component
d. No history of angina/AMI
e. Pain reproducible by palpating chest wall
1. Vitals
- Heart rate
a. tachycardia (tachydysrhythmia -> AF; sinus tachycardia -> pain; SVT; VT)
b. Bradycardia (AV nodal ischaemia 2o AMI, B-Blockers, CCB)
- BP
a. Usually normal
b. Hypertension – must treat if a/w AD(aortic dissection) or AMI
c. Hypotension – AMI, massive PE, tension pneumothorax, AD resulting in cardiac tamponade
d. Wide pulse pressure – proximal AD -> aortic insufficiency
e. Pulsus paradoxus – pericardial effusion/cardiac tamponade 2o AD, constrictive pericarditis, TP
- RR
a. Tachypnoea – usually a/w chest pain
- SpO2
2. Body habitus = tall, thin, patient with long limbs and arachnodactaly – AD
3. CVS examination
- Radio-radio delay/radio-femoral delay = AD
- Diminised femoral pulses = AD
- Unequal carotid pulses = AD
- Raised JVP = RVF 20 AMI, RVF 20 PE, tension pneumothorax (TP)
- Right ventricular heave = RVF 20 PE
- Left ventricular heave = CHF
- Displaced apex beat = TP
- Loud P2 = acute cor pulmonale 20 massive PE
- S3, gallop rhythm = CHF
- PSM = MR 2ndary to papillary muscle ischaemia/infarction (mitral valve prolapsed)
238
- AR = proximal AD
- Pericardial rub = pericarditis
- Peripheral oedema = CHF, RVF, DVT
4. Chest examination
- Tender costal cartilage, erythema, swelling = costochondritis
- Localised rib pain = rib #
- Deviation of trachea = TP
- Unequal chest expansion = TP
- Hyper-resonant percussion note = TP
- Decreased air-entry = pneumonia, TP
- Bronchial breathing = pneumonia
- Crepitations = CHF 2ndary to AMI, pneumonia
- Pleural rub = PE, pneumonia
- Pleural effusion = PE< pneumonia
5. Abdominal examination
- Guarding and rebound = perforated ulcer
- Epigastric tenderness = PUD
- Generalised abdominal pain = mesenteric infarction from AD
6. CNS
- Hemiplegia = AD involving carotid artery
7. Skin
- Herpes zoster = unilateral maculopapular rash/vesicles in dermatomal pattern
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Medicine (CVS) = HO on call
# questions to ask over phone
1. Is the patient stable (obtain vitals)
2. What is the patient currently admitted for? Diagnosis?
3. Past medical history
- Any history of angina or AMI? If yes is the pain similar?
- How bad is the pain?
- Any recent ECG or cardiac enzymes done?
#orders to be given over the phone
1. ECG stat
2. O2 by facemask or nasal prongs (2L/min)
- Keep SpO2 > 95%
3. S/L GTN 0.3-0.6mg every 5 mins (keep SBP >90mmHg; CI = hypotension)
#investigations to order
1. 4 blood tubes = FBC, GXM, U/E/Cr, PT/PTT
2. Cardiac enzymes (CK, CKMB, troponin-T) and bedside trop-T
3. ABG
4. ECG = normal ECG does not rule out angina or AMI
- NSTEMI/STEMI
- Inferior MI = do right sided leads to exclude RV MI
- PE (sinus tachycardia, S1Q3T3, RAD, RBBB, RVH, cor-pulmonale)
- AD (normal, LVH from longstanding HTN, electrical alternans from pericardial effusion)
- Pericarditis (ST elevation in all leads, low voltages)
5. 2D echocardiogram is helpful to confirm AMI if ECG changes are equivocal
- Assess LV function
- Exclude mechanical complications (VSD, MR)
- Screen for AD
6. CXR
- Pulmonary oedema – upper lobe diversion, pulmonary congestion
- Cardiomegaly
- Widened mediastinum and prominent aortic knuckle (AD)
- Peripheral PE
- Pneumothorax
- Pneumonia
- Rib #
- Pneumomediastinum (osesophageal rupture)
Specific management
1. AMI (MONA)
- CRIB
- Supplemental O2 (keep SpO2 >95%)
- Aspirin 300mg stat followed by 100mg OM (CI = asthma, BGIT, anaemia)
#give Ticlid 250mg OM if aspirin cannot be given (S/E = myelosuppression)
- S/L GTN stat and ISDN 10mg TDS (CI = hypotension, tachycardia; relative CI = inferior MI with possible RV
involvement)
- Atenolol 100mg OM (CI = asthma, COPD, complete heart block, severe heart failure)
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- Captopril 12.5mg BD if anterior AMI 9CI = CRF, bilateral renal artery stenosis)
Major AMI = IV morphine 5mg + maxolon
IV atenolol 5mg over 5 mins
IV ISDN 2-10mg/hr
Urgent cardio r/v if good premorbid status (PTCA, fibrinolytics)
- General measure = input/output chart
Fluid restriction (<1L/Day)
Soft diet/diabetic diet/low-salt diet
Stool softener (senna 2 tablets ON)
2. Angina
- CRIB
- Supplemental O2 (keep SpO2 >95%)
- S/L GTN stat
- Serial ECGs and cardiac enzymes (q8h x 3)
- Review precipitating cause, adjust anti-anginal medications, assessment by ICU/CCU staff if angina
occurred at rest or 1st episode of angina
3. Aortic dissection
- Arrange for CT thorax or TEE
- Trans-thoracic echocardiogram if neither can be arranged within the next house
#detect dilated aortic root, aortic regurgitation, pericardial effusion
- Refer cardio-thorax = confirm diagnosis with MRI or aortography
4. Pericarditis
- Non-urgent echocardiogram = pericardial effusion, haemodynamic compromise
- PO Idomethacin 25-50mg TDS/aspirin 650mg q4hrs
a. CI = samter’s syndrome (aspirin sensitivity, asthma, nasal polyps), BGIT, on anti-coagulation
b. Used with caution = CHF – sodium retaining properties
CRF – inhibit renal prostaglandins which maintain perfusion in those with pre-renal
conditions
5. Pneumothorax
- Order erect inspiratory and expiratory chest films
- Chest-tube insertion
- Tension pneumothorax = immediate needle decompression, chest-tube insertion
6. GERD
- Antacids = magnesium-containing ones cause diarrhoea; aluminium-containing ones cause constipation
- Elevation of head of bed
- Avoid night time snack
- H2 – receptor blocker
- PPI
- OGD KIV biopsy if PUD suspected
7. Costochondritis
- NSAID e.g. naproxen
8. Herpes zoster
- Unilateral chest pain in dermatomal distribution may precede typical skin lesions by 2-3 days
(maculopapular rash that rapidly evolves into vesicular lesions)
- Neuritis = narcotic analgesia, amltrityline HCL, steroids
- Antivirals (acyclovir) may reduce severity and duration
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Medicine (CVS) = Ischaemic Heart Disease (History)
Date of admission
Symptoms
1. Chest pain
- Mode of onset
- Duration
- Frequency
- Sudden/gradual onset
- Constant/intermittent
- Progressively worse/better
- Site and radiation
- Character
- Pain score and severity
- Triggers
 CVS -> exertion (quantify), cold exposure, emotion, palpitations, rest
 GIT -> food
- Aggravating factors
 RT -> deep inspiration, coughing, moving of shoulders
 GIT -> alcohol, lying down
- Relieving factors
 CVS -> rest, GTN
 GIT -> antacids, food
2. Dyspnoea
- Mode of onset
- Duration
- Frequency
- Sudden/gradual onset
- Progressively worse/better
- Severity
- Triggers = exertion (quantify and ?decrease in ET), emotion, rest
- Reliving factors = rest
- a/w orthopnoea and PND
3. Nausea vomiting
- Diaphoresis (excessive sweating)
- Palpitations, giddiness, syncope (loss of consciousness)
- Ankle oedema
- Intermittent claudication
Aetiology
1. Triggers
- Anaemia = chest pain, SOB, giddiness, palpitations, fatigue, pallor, BGIT, menorrhagia, gross haematuria
- Sepsis = fever
- Hyperthyroidism = goitre, fidgety, insomnia, increase in appetite, LOW, diarrhoea
242
2. History of recent trauma = pneumothorax, rib #
3. Fever, URTI, productive cough = viral myocarditis/pericarditis, pneumonia with pleurisy
4. Nausea, vomiting, heartburn, acidbrash, waterbrash, epigastric pain, dysphagia = GERD
Complications
Systemic review
Management prior and during hospitalisation

 Describe prior episodes
 Changes in character of pain
 Investigations done = ECG, stress ECG, coronary angiogram
 PTCA/CABG done

 IHD/AMI, DM, HTN, HCL, CVA
 Prior hospitalisations and surgeries
Drug History
 Drug allergies
 Current medications
Social history
 Smoking
 Alcohol
 Diet
 Physical activity
 Family set-up
 Main caregiver
 Finances
 Lift-landing
 Functional status
Family history
 IHD/AMI, DM, HTN, HCL, CVA
243
Medicine (CVS) = Angina Pectoris
Pathogenesis
- Imbalance between myocardial oxygen supply and demand
Oxygen supply Oxygen Demand

Duration of diastole Heart rate
Coronary perfusion pressure Blood pressure
(aorta DBP – coronary sinus DBP)
Coronary vasomotor tone Myocardial contractility
Oxygenation Left ventricular hypertrophy
- Causes
 Reduced coronary blood flow = atheroma, thrombosis, embolus, vasospasm, arteritis
 Decreased oxygenation = anaemia, CO poisoning, V/Q mismatch
 Increased myocardial demand = ventricular hypertrophy, HOCM, thyrotoxicosis
- Accumulation of metabolites from ischaemic muscles -> stimulate cardiac sympathetic nerves -> pain
(patients with cardiac transplants who develop CAD do not feel angina as heart is denervated)
Types of angina
1. Typical angina = Central crushing chest pain
Triggered by stress (emotional, exertion)
Relieved by rest
2. Decubitus angina (severe coronary disease) = on lying down
3. Nocturnal angina (critical coronary disease) = vivid dreams at night
4. Prinzemetal/variant angina = rest angina triggered by coronary vasospasm
Higher frequency in women
5. Unstable angina = angina of recent onset, at rest or change in character/worsening symptoms (frequency)
Pathology
- Stable angina = ischemia due to fixed atheromatous stenosis of 1 or more coronary arteries
- Prinzemetal angina = ischaemia due to coronary vasospasm
- Unstable angina = ischaemia due to plaque rupture with superimposed thrombosis (dynamic
obstruction)
Risk factors
Modifiable Non-modifiable
Smoking Gender (men)
- Risk of Ami same as non-smokers
after 2 years
- Risk of angina same as non smokers
after 10 years
Alcohol Ethnicity (Indians)
Obesity Age (older)
Physical inactivity Family history of IHD/AMI
Hypertension Personal history of IHD/AMI
Hyperlipidaemia Homocysteinaemia
Diabetes mellitus
244
Clinical Presentation
History
1. Chest pain
- Location = central substernal chest pain
- Character = crushing
- Radiation = left jaw and arm
- Duration = 5-10mins (AMI -> 30mins)
- Triggers = exertion, cold exposure, emotional stress, palpitations
- Relieved = rest, GTN
- ? recent changes in character of pain
2. Exertional dyspnoea (due to elevated end-diastolic pressure 2ndary to ischaemia
- Not a/w orthopnoea and PND
- ? decrease in effort tolerance
3. Intermittent claudication
4. No symptoms of nausea, vomiting, diaphoresis, giddiness/syncope, ankle oedema, fatigue
5. Triggers = anaemia -> recent BGIT/menorrhagia/gross haematuria
Recent illness/sepsis
Hyperthyroidism -> palpitations, fidgety, insomnia, increased appetite, LOW, diarrhoea
6. Risk factors
- Hypertension
- Hyperlipidaemia
- Obesity
- Smoking
- Alcohol
- Sedentary lifestyle
- Family history = 1st degree relatives (women <65 years old; men<55 years old)
- Personal history
1. General inspection = obese
Signs of thyrotoxicosis (goitre, thyroid eye disease)
2. Peripheries = anaemia, tar stains, xanthoma, xanthelesma, carotid bruit
3. CVS = cardiomegaly, valvular heart disease, cardiomyopathy
4. Lower limbs = signs of PVD
Investigations
Immediate
1. ECG
- Normal
- Previous AMI (pathological Q waves, LBBB)
- Ischemia (T wave invesion, ST segment depression)
- Left ventricular hypertrophy
2. Cardiac enzymes = not raised in stable angina
3. CXR = cardiomegaly
4. Underlying conditions
- FBC = Hb (anaemia); WBC (leucocytosis)
- TFT = hyperthyroidism
Later
1. Stress test
- Exercise ECG = planar/down-sloping ST segment depression indicative of ischemia
- Dobutamine
245
- Nuclear medicine
- MRI
2. 2D-echocardiogram
- Left ventricular ejection fraction
- Valvular heart disease
3. MIBI perfusion scan
4. MUGA functional scan (multiple gated acquisition scan)
5. Coronary angiogram (delineate exact coronary anatomy in patients going for revascularisation)
Management
Acute
1. Stabilise patient if necessary
- Ensure patent airway
- Ensure spontaneous breathing -> Give supplemental O2
Place on SpO2 monitoring (keep SpO2 >95%)
- Ensure good circulation -> Obtain vitals
Obtain ECG
Place on continuous ECG monitoring if necessary
2. S/L GTN
- MOA = relieves coronary vasospasm & pulmonary congestion; vasodilation
- Absolute contraindications = hypotension; tachycardia (SBP<90mmHg)
3. B-Blockers
- 1st line therapy (not GTN)
4. Aspirin
- MOA = anti-platelet
- Contraindications = anaemia; BGIT; Asthma
#other anti-platelets (e.g. clopidogrel, ticolpidine, Gp2b/3a inhibitors) given only when patient is going
for interventional procedures
5. ACE inhibitors
6. CCB (if pain is not relieved by above measures)
Long term
1. Patient education
2. Control risk factors
- Lifestyle modifications = quit smoking, drink less alcohol, exercise regularly, lose weight, healthy diet
- Hypertension
- Hyperlipidemia
- Diabetes
3. Medical Treatment
- Symptomatic relief = S/L GTN
- Prophylaxis
 Anti-platelet therapy = aspirin 75-150mg OM/Clopidogrel 75mg OM
 Anti-anginal therapy
 B blockers = atenolol 50-100mg *drug of choice in previous AMI)
 LA nitrates = ISMN (vasodilatation, relaxes coronary arteries)
 CCB = amoldipine (vasodilatation, relaxes coronary arteries, decreases contractility, slows
HR
 ACE inhibitors
4. Surgical treatment
- Percutaneous trans-luminal coronary angioplasty (PTCA)
 Ideal for a single and discrete lesion
246
 Use of balloon dilatation to relieve arterial obstruction (KIV stent placement ot prevent
re0obstruction)
 # stent coated with sirolimus -> prevents proliferation of endothelial fibroblasts -> reduces risk of
stenosis
 Effective symptomatic treatment for chronic stable angina
 No evidene that it improves survival
 Acute CX = occlusion of target vessel/side branch by thrombus or loose intimal flap -> ischemia
 Long term CX = re-stenosis
- Coronary artery bypass graft (CABG)
 Ideal for patients not suitable for PTCA or severe triple vessel disease
 Use of alternative arteries to bypass proximal stenosis
#left internal mammary artery (LAD) aka internal thoracic artery
Right internal mammary artery (RCA) aka internal thoracic artery
Reversed segments of saphenous veins
- Operative mortality = 1.5%
247
Medicine (CVS) = Ischaemic Heart Disease (History)
Date of admission
Symptoms
1. Chest pain
 Mode of onset
 Duration
 Frequency
 Sudden/gradual onset
 Constant/intermittent
 Progressively worse/better
 Site and radiation
 Character
 Pain score and severity
 Triggers = CVS  exertion (quantify), cold exposure, emotion, palpitation, rest
GIT  food
 Aggravating factors = RT  deep inspiration, coughing, movement of shoulders
GIT  alcohol, lying down
2. Dyspnoea
 Mode of onset
 Duration
 Frequency
 Sudden/gradual onset
 Progressively worse/better
 Severity
 Triggers = exertion (quantify and ?decrease in ET), emotion, rest
 Relieving factors = rest
 a/w orthopnoea and PND
3. Nausea/vomiting
Diaphoresis
Palpitations, giddiness, syncope
Ankle oedema
Intermittent claudication
Aetiology
1. Triggers
(a) Anaemia = chest pain, SOB, giddiness, palpitations, fatigue, pallor, BGIT, menorrhagia, gross haematuria
(b) Sepsis = fever
(c) Hyperthyroidism = goitre, fidgety, insomnia, increase in appetite, LOW, diarrhoea
2. History of recent trauma = pneumothorax, rib #
3. Fever, URTI, productive cough = viral myocarditis/pericariditis, pneumonia with pleurisy
4. Nausea, vomiting, heartburn, acid brash, water brash, epigastric pain, dysphagia = GERD
Complications
Systemic review
248
Management prior and during hospitalization

-describe prior episodes
-changes in character of pain
-investigations done = ECG, stress ECG, coronary angiogram

-PTCA/CABG done

-IHD/AMI, DM, HTN, HCL, CVA
-prior hospitalizations and surgeries
Drug history
-drug allergies
-current medications
Social history
-smoking
-alcohol
-diet
-physical activity
-family set-up
-main caregiver
-finances
-lift-landing
-functional status
Family history
-IHD/AMI, DM, HTN, HCL, CVA
249
Medicine (CVS) = Acute Coronary Syndrome (ACS)
Acute coronary syndrome

 consists of
(a) unstable angina
(b) NSTEMI
(c) STEMI
Pathology
 Unstable angina = ischemia due to plaque rupture with superimposed thrombosisDynamic obstruction, no
myocardial damage
 Myocardial infarction = myocardial necrosis caused by acute occlusion of a coronary artery by plaque rupture
and superimposed thrombosis
 NSTEMI = subendocardial infarct
 STEMI = transmural infarct
Vascular territory of STEMI

Anterior = V1 – V4 Right coronary artery (RCA) supplies right ventricle, inferior and posterior heart
Septal = V3 – V4 Left anterior descending artery (LAD) supplies anterior + septum
Lateral = V5 – V6 Left circumflex artery (LCA) supplies left atrium and left ventricle
Inferior = II, III, AVF
WHO criteria of AMI

 Chest pain > 10 mins
 ECG changes = new BBB
ST elevation of > 2mm in 2 or more contiguous leads
Posterior AMI (ST depression in lead V1+V2)
 Rise in cardiac enzymes
Clinical Presentation
History
1. Chest pain
-location = central substernal chest pain
-character = crushing
-radiation = left jaw and arm
-duration = prolonged (>30 mins)
-triggers = exertion, cold exposure, emotional stress, palpitations
# DM and elderly patients can present atypically  epigastric pain
Painless AMI
2. Dyspnoea (due to heart failure or elevated end-diastolic pressure)
3. Nausea, vomiting
Diaphoresis
Giddiness, syncope
Ankle oedema
4. Triggers = anaemia  recent BGIT/menorrhagia/gross haematuria
Recent illness/sepsis
Hyperthyroidism  palpitations, fidgety, insomnia, increased appetite, LOW, diarrhoea
5. Risk factors
- Hypertension
- Hyperlipidaemia
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- Obesity
- Smoking
- Alcohol
- Sedentary lifestyle
- Family history = 1st degree relatives (women < 65 yrs old; men < 55 yrs old)
- Personal history
1. General inspection = dyspnoeic and tachypnoeic
sweating
2. Cardiogenic shock = altered mental state
Hypotensive
Thin and thready pulse
Pale, cool and clammy extremities
Reduced capillary refill time
Reduced urine output
3. Hands = tar staining, peripheral cyanosis
4. Face = xanthelesma, central cyanosis
5. Neck = raised JVP
6. Praecordium = cardiomegaly
Additional heart sounds (S3, gallop rhythm)
Systolic murmurs (new onset VSD, MR)
7. Lungs = bibasal inspiratory crepitations
8. Abdomen = tender hepatomegaly
9. Lower limbs = bilateral ankle pitting oedema
PR = BGIT
Management
Acute
1. Stabilize patient
- Ensure patent airway
- Ensure spontaneous breathing  Give supplemental O2; place on SpO2 monitoring (keep SpO2 > 95%)
- Ensure good circulation  Obtain vitals (HR, BP, RR); Obtain ECG; place on continuous ECG monitoring if
necessary; create venous access and take bloods for investigations
- Resuscitate if patient is in cardiogenic shock (papillary muscle dysfunction/rupture, septal rupture, cardiac
tamponade)
# call cardiologist and CT surgeon
# start inotropic support = IV dobutamine/dopamine 5-20 g/kg/min
# catheterize patient to monitor urine output
2. IV morphine for pain relief
- Give with IV maxolon (anti-emetic)
3. Nitrates
- S/L GTN = relieve coronary vasospasm
- IV GTN = for ongoing chest pain, HTN and pulmonary congestion
Absolute CI: Hypotension (SBP <90mmHg), tachycardia
Relative CI: Inferior AMI with possible RV involvement
4. Aspirin 300mg stat followed by 100mg OM (can also give clopidogrel, ticlopidine, LMWH)
- Anti-platelet effect starts 1hr after ingestion
- Decreases mortality and re-infarction rate
- CI: asthma, anaemia, BGIT
5. -blocker  atenolol 100mg OM
251
Carvedilol ( -blocker of choice for large infarcts)
- Reduces HR, BP and contractility
- To be given only if patient is euvolemic
- CI: asthma, COPY, complete heart block, severe heart failure, urinary retention, bradycardia
6. ACE inhibitors  captopril 12.5mg BD
- Given in suspected STEMIs
- CI: hypotension, CRF, bilateral RAS
7. CCB  amlodipine
- If pain is not relieved with above measures
Specific measures
1. STEMI
- Consider myocardial salvage therapy in those presenting <12 hrs from onset
(a) Thrombolysis = tPA or streptokinase
(b) Percutaneous transluminal coronary angioplasty
# preferred reperfusion strategy if performed promptly (door-to-ballon time < 90 mins)
# indications = anterior MI, inferior MI with RV involvement, cardiogenic shock in patients < 75yo
Thrombolysis PTCA
Advantages  Rapid administration  Better clinical efficacy
 Widely available # superior vessel patency
 Convenient # reduced re-occlusion rates
 Does not require expertise  Less haemorrhagic risk
 Early definition of coronary
anatomy
# allows tailored therapy
# more efficient risk stratification
Disadvantages  Patency ceiling = vessel patency  Delay limits efficacy

restored in only 60 – 85%  Less widely available
 Less clinical efficacy  Requires expertise
# optimal reperfusion not
achieved in > 50% of patients
# higher rates of re-occlusion
 Haemorrhagic risk
Algorithm for thrombolytic therapy

Selection Criteria
 Typical chest pain of AMI

 ST elevation of at least 1mm in at least 2 inferior ECG leads (II, III,
aVF) OR
ST elevation of at least 2mm in at least 2 contiguous anterior leads
 Less than 12 hours from onset of chest pain
 Less than 75 yo
Fulfilled criteria
252
Contraindications
Do not administer thrombolytics if the answer to any of the
following is yes
 Suspected AD
 Previous CVA
 Known intracranial neoplasm
 Recent head trauma
 Other intracranial pathology
 Severe hypertension (BP>180/110)
 Hypotension (SBP<90)
 Acute peptic ulcer
 Acute internal bleeding
 Recent internal bleeding (<1 month ago)
 Recent major surgery (<1 month ago)
 Current use of anticoagulants
 Known bleeding diasthesis
 Prolonged CPR (>5 mins)
 Previous administration of thrombolytics
 Pregnancy
 Diabetic retinopathy
 LBBB on ECG
No contraindications
Streptokinase Recombinant tPA

 Most commonly used  < 50 yo
 Cost-effective  Anterior AMI
 Therapy of choice when risk of
intracranial haemorrhage is high
e.g. elderly patients
Risks of thrombolytics therapy

 Intracranial bleeding (1%) = age > 65, weight < 70kg, hypertension, use of tPA
 Streptokinase allergy (5%) = patients treated for the first time (esp those with recent strep
infection)
 Anaphylaxis (0.2%)
 Hypotension during IV streptokinase infusion (15%) = corrected by decreasing rate of
infusion and volume expansion
2. NSTEMI
(a) LMWH
-superior to UF heparin = no need to monitor PTT, greater bioavailability, less risk of bleeding
-can also use Gb2b/3a inhibitors = proven benefit in high-risk NSTEMI +UAP as well as PTCA for STEMI
(b) PTCA
-indications = high-risk patients (persistent ST-depression and/or raised trop-T)
253
General measures
1. Monitored in CCU for at least 2 days
-short term complications of AMI = arrhythmias, CCF, cardiogenic shock, pericarditis
-monitor vitals q4rly
-I/O chart
-fluid restriction < 1L/day
-low-salt diet
-stool softener
Investigations
Immediate
1. ECG
-a single ECG cannot rule out AMI
Serial ECGs can rule out STEMI but not NSTEMI
-unstable angina = normal, ST depression, T wave inversion
NSTEMI = ST depression, T wave inversion
STEMI = ST elevation of >2mm in 2 or more contiguous leads
New-onset BBB
Posterior AMI (ST depression in leads V1+V2)
-do right-sided ECG in inferior AMI to exclude concomitant RV infarct (GTN is contraindicated)
2. Cardiac enzymes (serial CE q8hrly)

- 1st set of CE can miss up to 40-60% of AMI
- 2nd set of CE can pick up 98% of AMI
(a) Myoglobin = detected within 1-2 hrs, peak at 6-9hrs, normalized by 24-36hrs
-earliest marker to rise in AMI
Useful in ruling out AMI early (raised in nearly all AMIs at 6hrs)
Disadvantages = not specific for cardiac muscle (skeletal muscle injury, NM disorders, renal failure, IM
injections, strenuous exercise, post-coronary bypass surgery
(b) Creatine kinase (CK-MB)= detected within 4-6hrs, peak at 18-24hrs, normalized by 48-72 hrs
-serological gold standard of AMI
-disadvantages = not specific for cardiac muscle, false positive values in CRF patients (renal failure),
narrow diagnostic window, failure of total CK to rise to abnormal values in all AMI
-relative % index = CKMB/total CK x 100% (≥ 5% suggestive of AMI)
(c) Troponin T = detected within 4-6hrs, peak within 12-120 hrs, normalized by 10-14 days
-useful for late presenting AMI
-Prognostic indicator in unstable angina
-Specific for cardiac muscle
-false positive values in CRF and dialysis patients
(d) Troponin I = detected within 4-6 hrs, peak at 12-36 hrs, normalized by 7-9 days
-the most cardiac-specific marker
-no false positive values in renal failure patients
-prognostic indicator in unstable angina
-not very widely available
3. CXR
-cardiomegaly
254
-acute pulmonary oedema
-upper lobe diversion
-congestive cardiac failure
-Kerley B lines
4. FBC = Hb (anaemia can ppt AMI)
WBC (infection/sepsis can ppt AMI)
U/E/Cr
PT/PTT = esp if patient needs to go for interventional procedures later
GXM
5. 2D-echocardiogram = LV ejection fraction
Complications of AMI (VSD, MR)
Later
1. Stress test = identify presence of residual ischemia
- ECG
- Dobutamine
- Nuclear medicine
- MRI
2. MIBI perfusion scan
3. MUGA functional scan (multiple gated acquisition scan)
4. Coronary angiogram (delineate exact coronary anatomy in patients going for revascularization)
Long-term management
2. Control risk factors
- Lifestyle modifications = quit smoking, drink less alcohol, exercise regularly, lose weight, healthy diet
-hypertension
-hyperlipidemia
-diabetes
3. Medical treatment
-symptomatic relief = S/L GTN
-prophylaxis
(a) anti-platelet therapy = aspirin 75-150mg OM
Clopidogrel 75mg OM
Ticlopidine
Gp 2b/3a inhibitors
(c) Anti-anginal therapy
# β-blockers = atenolol 50-100mg (drug of choice in previous AMIs)
# LA nitrates = ISMN (vasodilatation, relaxes coronary arteries)
# CCB = amlodipine (vasodilatation, relaxes coronary arteries, decreases contractility, slows HR)
4. Surgical treatment (choice depends on technical difficulty, patient’s condition)
(a) Percutaneous trans-luminal coronary angioplasty (PTCA)
-ideal for a single and discrete lesion
-use of ballon dilatation to relieve arterial obstruction (KIV stent placement to prevent re-obstruction) #
stent coated with sirolimus  prevents proliferation of endothelial fibroblasts  reduces risk of stenosis
-effective symptomatic treatment for chronic stable angina
-no evidence that it improves survival
-acute Cx = occlusion of target vessel/side branch by thrombus or loose intimal flapischaemia
Long-term Cx = re-stenosis
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(b) Coronary artery bypass graft (CABG)
-ideal for patients not suitable for PTCA or severe triple vessel disease
-use of alternative arteries to bypass proximal stenosis
# left internal mammary artery (LAD)
Right internal mammary artery (RCA)
Reversed segments of saphenous veins
-operative mortality = 1.5%
Complications
Early
 Arrhythmia
-most common complication due to formation of re-entry circuits at junction of necrotic and viable
myocardium
-sudden death, VF, AF, heart block, bradycardias
 Contractile dysfunction
-CCF
-LVH with pulmonary oedema
-cardiogenic shock
-papillary muscle dysfunction  valvular regurgitation
 Extension of infarct
 Rupture
-rupture of papillary muscle (D3)  severe MR
-rupture of septum  VSD
-free wall rupture (D10)  haemopericardium  cardiac tamponade
 Pericarditis (D3)
-onset of different pain = position, worse on inspiration
-pericardial rub and pericardial effusion may be present
-Dressier’s syndrome (post-MI syndrome) = persistent fever, pericarditis, pleurisy
# Mx = wait and see
High-dose aspirin, NSAIDs, steroids
 Mural thrombus  embolus
Late
 Ventricular aneurysm
-due to bulging of non-contractile fibrous myocardium during systole
 Recurrent AMI
Prognosis
 Prognostic indicators = age of patient, extent of infarct, residual LV function
 50% mortality within 24 hrs of onset (25% die before arriving at the hospital)
 40% mortality within the 1st month
 1st year survival rate = 80%
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Medicine (CVS) = Congestive Cardiac Failure (CCF)
Definition
 Structural or functional heart disorder that prevents adequate cardiac output for tissue perfusion OR only at an
elevated filling pressure
 Acute heart failure = present de novo acute decompensation of chronic heart failure
Epidemiology
 Accounts for 4.5% of all hospital admissions and 2.5% of overall mortality in the elderly
 Common condition = lifetime incidence is 20%
 No gender predilection
 Main risk factors
 coronary artery disease (DM, HCL, obesity, smoking)
 hypertension
 valvular heart disease
 cardiomyopathy
other risk factors = previous AMI, arrhythmias, family history
 poor prognosis = many die suddenly due to malignant ventricular arrhythmias or AMI
Pathophysiology
 arises from either systolic or diastolic dysfunction
(a) Systolic
- Reduced systolic dysfunction leads to 4 compensatory mechanisms
1. Increase pre-load by activating RAAS. # Starling’s law = cardiac output depends on preload (EDV),
afterload (arterial resistance) & myocardial contractility
2. Increase pre-load by ADH release
3. Sympathetic activation by releasing catecholamines
4. Local changes = ventricular hypertrophy (pressure load), ventricular hypertrophy and dilatation
(volume load)
(b) Diastolic
- Ischaemia  muscle fibrosis  decreased relaxation/elastic recoil or ventricle  elevated LV end-diastolic
pressure  decreased stroke volume
- Classically caused by hypertension and HOCM
- Normal LV ejection fraction
 causes of pulmonary and peripheral oedema
(a) high arterial pressures
(b) impaired renal perfusion  secondary aldosteronism  salt and water retention
- CCF causes increased venous pressure which transmits to renal venous system
- Decreased pressure gradient between renal arterial and venous system results in decreased renal
perfusion
Aetiology
 Pump failure
(a) Heart muscle = coronary artery disease (ischaemiafibrosis), cardiomyopathy, myocarditis
(b) Restricted filling = constrictive pericarditis, cardiac tamponade, restrictive cardiomyopathy
(c) Inadequate heart rate = negative inotropic drugs (anti-arrhythmics, β-blockers), arrhythmias (fast AF,
heart block), post-AMI
 Excessive preload
(a) Fluid overload
(b) Regurgitant valvular heart diease = MR, AR
 Excessive afterload
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(c) Right-sided
 LV failure (most common cause)
 Cor pulmonale
 Pulmonary stenosis
 Pulmonary embolism
(d) Left-sided
 Hypertension
 Aortic/mitral stenosis
 High-output states
(a) Severe anaemia
(b) Thyrotoxicosis
(c) Large AV shunts
(d) Pregnancy
Left-sided HF  Decreased LV output

 Increased LA or pulmonary venous pressure
 Acute ↑ = APO
 Gradual ↑ = reflex pulmonary vasoconstriction  pulmonary HPT
Right-sided HF  Decreased RV output
Biventricular  Causes = dilated CMP, IHD
HF
High-output HF
Systolic dysfn  Impaired myocardial contraction
 May be associated with diastolic dysfunction
 More likely in younger patients, history of MI, displaced apex beat, S3
gallop, cardiomegaly on CXR
Diastolic dystn  Defective diastolic filling due to decreased LV complianceimpaired LV
filling
Elevated left atrial and pulmonary venous pressures
 Causes = LVH due to HPT or IHD or HOCM
 Findings = LVH, dilated left atrium, normal ejection fraction
 More likely in older patients, history of HPT, thrusting apex beat, S4 gallop,
LVH on ECG
Drug allergy
Date of admission

Symptoms
 Left-heart failure
(a) Dyspnoea = duration, triggers (exertional or at rest), effort tolerance, severity (NYHA classification),
aggravating and relieving factors, associated with orthopnoea and PND
(b) Chest pain, nausea/vomiting, diaphoresis, giddiness  recent AMI
(c) Palpitations (fast AF can trigger CCF) = giddiness and syncope
(d) Fatigue
 Right-heart failure = ankle oedema, abdominal distension, facial oedema, RHC pain (tender hepatomegaly 
cardiac cirrhosis  nutmeg liver)
 Hypoperfusion = giddiness, confusion, oliguria
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Aetiology
 Recent AMI
 Sepsis = fever, RTI (productive cough), UTI (FUN, dysuria, haematuria)
 Anaemia = PR bleeding
 Non-compliance with fluid and salt restrictions
 Non-compliance with medications
Compliance
Systemic review
Management of current episode

 When was CCF first diagnosed?
- Presenting complaint
- Investigations done = ECG, treadmill ECG, 2DE, nuclear scans (MIBI/MUGA)
- Current management = follow-up with whom? Compliance? Medications (type, dosage, recent changes,
compliance), fluid and dietary restrictions (compliance)
- Level of control = number of relapses? Treatment

 DM, HPT, HCL, IHD, AMI, CVA
 Valvular heart disease
 Previous admissions and surgeries
Drug history
Social history
 Smoking
 Alcohol
 Family set-up
 Main caregiver
 Lift-landing
 Type of housing
 Financial status
 Functional level
Family history
 Vitals = HR, RR, BP, T, SpO2
 General condition = mental state, anasarca, respiratory distress (tachypnoea, dyspnoea, use of accessory
muscles of respiration, pursed lip breathing, intercostals/subcostal retractions, cyanosis), midline sternotomy
scar with saphenous vein harvest site (previous CABG)
 Peripheries = pulse (tachycardia, AF, weak and thready), cold and clammy skin, prolonged capillary refill time,
conjunctival pallor
 Signs of fluid overload = facial oedema, raised JVP, pleural effusion/pulmonary oedema, tender hepatomegaly,
ascites, sacral oedema, bilateral lower limb pitting oedema
 Praecordium = displaced and heaving apex beat, S3/4 heart sound, gallop rhythm, heart murmurs (valvular
heart disease)
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Differentials
1. Pulmonary embolism
2. Fluid overload = renal (nephrotic syndrome, ESRF), GIT (liver cirrhosis, protein-losing enteropathy, IBD)
3. Cor pulmonale
4. COPD
Investigations
Heart failure is principally a clinical diagnosis!
Bloods
 Cardiac enzymes = AMI
 FBC = Hb (anaemia), WBC (sepsis)
 U/E/Cr = hypokalaemia from RAAS activation and K+-losing diuretics, hyponatraemia (fluid overload), renal
impairment from hypoperfusion
 LFT = hepatic congestion, cardiac cirrhosis
 Serum NT-pro-BNP
- Peptide hormone secreted by ventricular myocytes  play key role in volume homeostasis
- Plasma concentration reflects ventricular pressure  raised in heart failure
- Actions = increases GFR, decreases renal sodium reabsorption
- High negative predictive value = useful in excluding diagnosis of heart failure in patients with dyspnoea/
fluid retention
 ABG (if SpO2 < 92%)
 Blood c/s if in sepsis
Imaging
 ECG
- MI(old infarcts  pathological Q waves; new infarcts  ST hyperacute changes)
- Arrhythmias (AF, heart block)
- LVH
- Goldberg’s triad for dilated CMP (poor R progression, small limb voltages, large chest voltages)
- Electrical alternans (cardiac tamponade, pericardial effusion)
 CXR
- Cardiomegaly, upper lobe diversion, peri-hilar bat’s wing shadow (alveolar oedema), Kerley B lines
(interstitial oedema), pleural effusion, pneumonia
 2D-echo
- Assess cardiac morphology
- Global and regional function
- Identify causes of heart failure (myocardial, vascular or pericardial origin)
 Identify underlying ischaemia and myocardial viability  revascularization
(a) 2D-echo = treadmill, dobutamine
(b) Radionuclide studies = MIBI (perfusion), MUGA (multiple gated acquisition scan)  functional
(c) MRI = useful for quantifying myocardial necrosis, perfusion and function; usually indicated in cardiac
masses, complex congenital heart disease or pericardial disease
(d) CT = calcifications (coronary artery, pericardium)
(e) Coronary angiogram and cardiac catheterization = indicated in patients with angina, history or MI or at
high risk for coronary artery disease.
Acute management
Acute decompensation of chronic heart failure
 Stabilize patient’s vitals
(a) Secure airway if unconscious
(b) Ensure that patient is breathing spontaneously
- Place on continuous pulse oximetry monitoring
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- Sit in upright position with legs hanging down to reduce venous return
- Give supplemental O2 via non-rebreather mask  non-invasive positive pressure ventilation
(BiPAP/CPAP)
- IPPV if patient is in respiratory distress and acute heart failure-induced respiratory muscle fatigue
(c) Obtain patient’s vitals = HR, RR BP, T
- Place on continuous ECG monitoring
- Examine for signs of shock = altered mental state, cold clammy peripheries, weak thread pulse,
prolonged capillary refill time, reduced urine output
- Set IV cannula = take bloods for investigation
- CXR, ABG
 Specific measures
(a) Diuretics = IV Lasix (40-80 mg bolus; onset in 20 mins; lasts for 6 hrs)
- Catheterize patient
- Monitor vitals and urine output to avoid volume contraction
- Achieve negative balance of 1-2L/day
(b) ACE inhibitors = captopril
- Monitor for hypotension (esp postural), hyperkalaemia and worsening renal function
(c) Nitrates = IV GTN (lower LV EDVrelieve symptoms of pulmonary congestion)
- IV nitroglycerine/nitroprusside
- Contraindicated in inferior/right ventricular infarct or hypotension (SBP must be >90mmHg)
- Continuous BP monitoring needed
(d) Digoxin if hypotensive
(e) - Complete rest in bed
- Fluid restriction (<1L/day)
- Low-salt diet (<2g/day)
- Strict I/O charting and daily weights
- Monitor vitals q4hrly (inform doctor if SBP < 100mgHg or HR > 100/min)
Acute pulmonary oedema

# pathophysiology = sympathetic overdrive leading to elevated LV EDV volume and pressure  No volume
overload per se  treatment is with vasodilators
# end point of Rx = resolution of sympathetic overdrive = PR, BP, restoration of warm dry extremities
# features of impending respiratory failure = altered mental state
- fatigue of respiratory muscles
- progressive desaturation (SpO2<92%, PaO2 <50 mmHg, PaCO2 > 50 mmHg)
- signs of shock (weak thread pulse, cold clammy peripheries, prolonged capillary refill time)
 stabilize patient’s vitals
(a) secure airway  intubate if in impending respiratory failure
(b) ensure that patient is breathing spontaneously
- place on continuous pulse oximetry monitoring
- sit in upright position with legs hanging down to reduce venous return
- Give supplemental O2 via non-rebreather mask  non-invasive positive pressure ventilation
(BiPAP/CPAP)
(c) obtain patient’s vitals = HR, RR, BP, T
- Place on continuous ECG monitoring
- Examine for signs of shock = altered mental state, cold clammy peripheries, weak thread pulse,
prolonged capillary refill time, reduced urine output
- Set IV cannula = take bloods for investigation
- CXR, ABG
 specific measures
(a) Diuretics = IV Lasix (40-80 mg bolus; onset in 20 mins; lasts for 6 hrs)
- Catheterize patient
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- Monitor vitals and urine output to avoid volume contraction
- Achieve negative balance of 1-2L/day
(b) ACE inhibitors = captopril
- Monitor for hypotension (esp postural), hyperkalaemia and worsening renal function
(c) Nitrates = IV GTN (lower LV EDVrelieve symptoms of pulmonary congestion)
- IV nitroglycerine/nitroprusside
- Contraindicated in inferior/right ventricular infarct or hypotension (SBP must be >90mmHg)
- Continuous BP monitoring needed
(d) Digoxin if hypotensive
(e) Admit = CCU  Acute coronary syndrome, intubated
HD  CPAP
General ward  the rest
(f) Order complete rest in bed
- Fluid restriction (<1L/day)
- Low-salt diet (<2g/day)
- Strict I/O charting and daily weights
- Monitor vitals q4hrly (inform doctor if SBP < 100mgHg or HR > 100/min)
Long-term management
Conservative
 Control risk factors = HPT, HCL, DM
- Obesity (weight loss, exercise, healthy diet)
- Stop smoking and drinking alcohol
 Fluid restriction only if oedematous
 Salt restriction (<2g/day)
 Influenze immunisation
 Monitoring = daily weights (avoid > 2kg/wk), symptoms and signs
Medical (started if EF < 40%)

(a) First-line therapy
1. Diuretics
- Mechanism of action = reduce preload BUT may cause hypovolaemia
- Agents = frusemide (Lasix)
spironolactone (indications = patients with NYHA class 3/4) hypokalaemia, predisposition to
arrhythmias, concurrent digoxin therapy
2. ACE inhibitors
- Mechanism of action = reduce afterload by preventing RAA axis and sympathetic activation
- Agents = captopril, enalapril, lisinopril
- Advantages = survival benefit
- S/E = first-dose hypotension, dry cough, maculopapular rash, fetotoxic, nephrotoxic,
hyperkalaemia, neutropenia
- Contraindications = bilateral renal artery stenosis
3. Β-blockers
- Mechanism of action = reduce sympathetic stimulation to increase EF
- Agents = carvedilol, metoprolol, bisoprolol
- Advantages = survival benefit when taken together with ACE inhibitors
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(b) Second-line therapy
1. ARB
- Mechanism of action = reduce afterload by preventing RAA axis and sympathetic activation
- Indications = patients cannot tolerate dry cough
- Agents = losartan
- Advantages = no dry cough
2. Vasodilators
- Mechanism of action = nitrates reduce preload, arterial dilators (hydralazine) reduce afterload
- Agents = nitrates (ISMN, ISDM), hydralazine
- Usually given together
- S/E = hypotension
3. Digoxin
- Mechanism of action = controls ventricular heart rate and small positive inotropic effect
- Indications = symptomatic patients despite ACE inhibitors + diuretics + β-blockers
Patients with NYHA class 3/4
AF
- No survival benefit
- Advantages = improves symptoms, reduces hospitalizations
(c) Adjuvant therapy

1. Anti-coagulants to prevent thromboembolism
- Indications = all heart failure patients with AF (target INR = 2.0-3.0)
- Selective patients with LV EF < 35%
Further management
 Qn = Will patient benefit from revascularization (PTCA/CABG)?
Complications
Hypokalaemia  K+-losing diuretics
 Hyperaldosteronism (due to RAAS activation)
 Impaired aldosterone metabolism due to hepatic
congestion
Hyponatraemia  Diuretics
 ADH secretion
 Failure of cell membrane ion pump due to ischaemia
Impaired liver  Hepatic venous congestion
function  Ischaemic hepatitis
Thromboembolism  Low cardiac output
 Immobility
 Arrhythmias and AF
 Intracardiac thrombus due to MS or LV aneurysms
Arrhythmias  Electrolyte changes
 Structural heart disease
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Medicine (CVS) = Pathophysiology of dyspnoea
1. Cardiac dyspnoea
- Typically chronic and occurs with exertion
- Failure of left ventricular output to rise with exercise acute rise in left-ventricular EDV  raised
pulmonary venous pressure  interstitial oedema  reduced lung compliance
2. Orthopnoea
- Definition = dyspnoea that develops when a patient is supine
- Supine = increased venous return to the right side of the heart and to the lungs
Left ventricular failure  rise in left ventricular EDV  raised pulmonary venous pressure 
interstitial oedema  reduced lung compliance
- Upright = redistribution of interstitial oedema  lower lung zones become worse and upper zones
better allows for overall blood oxygenation
3. Paroxysmal nocturnal dyspnoea

- Definition = severe dyspnoea that wakes the patient from sleep causing him/her to gasp for breath
- Sudden failure of left ventricular output  acute rise in pulmonary venous and capillary pressures
 interstitial oedema  reduced lung compliance
- May be precipitated by resorption of peripheral oedema at night when supine
4. Presence of orthopnoea or PND is more suggestive of cardiac failure than lung disease
Medicine (CVS) = Prognostic Factors of Hypertension
B. Decisions about management of patients with hypertension should not be made based on their BP levels alone,
but also on the presence of other risk factors, target organ damage, concomitant disease such as diabetes and
cardiovascular or renal disease, as well as other aspects of the patient’s individual and medical circumstances.
Factors influencing prognosis

Risk Factors for Cardiovascular Disease
 Levels of systolic and diastolic BP (Grades 1-2)  Total cholesterol > 6.2 mmol/L (240 mg/dL)
 Age (Men > 55 yrs; Women > 65 yrs)  Reduced HDL-C < 1.0 mmol/L (40mg/dL)
 Smoking  Raised LDL-C > 4.1 mmol/L (160 mg/dL)
 Family history of premature CVD (Men < 55 years;  Diabetes mellitus
Women < 65 years)  Obesity (BMI > 30 kg/m2) (BMI > *27.5 kg/m2)
* commensurate Asian BMI cut-point for action
Target Organ Damage (TOD)/Associated Clinical Condition (ACC)
Cerebrovascular disease Renal disease

 Ischaemic stroke  Microalbuminuria (microalbumin-creatinine
 Cerebral hemorrhage ratio > 30 mg/g) or Proteinuria (>0.5 g/24hrs)
 Transient ischaemic attack  Renal impairment [plasma creatinine
Heart disease concentration > 132 mmol/L(>1.5mg/dl)]
 LVH (ECG, 2DE or CXR)  Diabetic nephropathy
 Myocardial infarction Retinopathy
 Angina pectoris  Generalized or focal narrowing of the retinal
264
 Coronary revascularization arteries
 Congestive heart failure  Haemorrhages or exudates
Vascular disease  Papilloedema
 Dissecting aneurysm Atherosclerosis
 Symptomatic arterial disease / PVD  Ultrasound or radiological evidence of
atherosclerotic plaque (carotid, iliac, femoral
and peripheral arteries, aorta)
Risk assessment
Besides the level of BP, it is also important to assess the overall cardiovascular risk of a patient prior to definitive
therapy in order to optimize risk-benefit ratio. Adding the numbers of traditional, documented risk factors in a
person is one such way. The use of well tested and accepted risk tables, charts or formulae to estimate a patient’s
absolute risk is encouraged. In individuals such as those with known or established coronary heart disease (CHD),
atherosclerotic disease, diabetes mellitus, familial hypercholesterolemia or malignant hypertension, the overall
cardiovascular risk assessment may not be necessary as the risk is already high and treatment should be started as
soon as the diagnosis of hypertension is confirmed.
Risk stratification and treatment plan

BP Category Risk Group A Risk Group B Risk Group C
(No risk factors) (1-2 risk factors) (>3 risk factors or
Diabetes Mellitus or
TOD/ACC)
Systolic BP 130- LM LM LM + Rx
139mmHg/ Diastolic
BP 80-89mmHg
Systolic BP 140- LM + Rx* LM + Rx LM + Rx
159mmHg/ Diastolic
BP 90-99mmHg
Systolic BP >160 LM + Rx LM + Rx LM + Rx
mmHg/ Diastolic BP
>100 mmHg
*if BP control inadequate with LM alone

TOD = Target organ disease ACC = Associated Clinical Condition
LM = Lifestyle modification Rx = Drug therapy
Low risk Moderate risk High risk
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Medicine (CVS) = Hypertension
Definitions
 Hypertension = 3 or more elevated BP readings taken on 3 or more different settings separated by at least 2
hrs
JNC (Joint national committee) Classification
Category Systolic BP (mmHg) Diastolic BP (mmHg)

Normal BP <130 <80
High Normal 130-139 80-89
Stage 1 HPT 140-159 90-99
Stage 2 HPT >160 >100
Isolated systolic HPT >140 <90
 Hypertensive crisis
o Hypertensive emergency
 Life-threatening and severe hypertension (diastolic BP ~ 120-130 mmHg) associated with
acute progressive end-organ damage
 Characterized by accelerated microvascular damage with fibrinoid necrosis in vessel walls of
small arteries and arterioles resulting in intravascular thrombosis
 Clinical features
# CVS = Hypertensive left ventricular failure (APO)
Acute aortic dissection
Acute myocardial infarction
# CNS = Stroke } needs to be differentiated as BP lowering is contraindicated to stroke
Hypertensive encephalopathy
# Renal = acute renal failure
#eyes = papilloedema
# eclampsia
 Requires prompt BP reduction (ICU setting)
o Hypertensive urgency
 Severe hypertension without acute end-organ damage
 Hypertensive retinopathy
 Chronic renal failure
 Pre-ecampsia
 Accelerated hypertension = grade 3 hypertensive retinopathy
 Malignant hypertension = grade 4 hypertensive retinopathy
 BP should be reduced within 24 hrs (outpatient basis)
 Patients with accelerated/malignant hypertension should be admitted
266
Epidemiology
 Local prevalence rate = 24.9% (Singapore NHS 2004)
 Males > females
 Chinese > Indians > malays
Aetiology
Primary Hypertension
 Accounts for 95% of the cases
 No underlying cause found
 Possible aetiology
o Increased sympathetic neural activity with enchances beta-adrenergic responsiveness
o Increased angiotensin II activity and excess mineralcorticoids
o Genetic factors = strong family history, ethnicity
o Environmental influences = obesity, smoking, excessive alcohol consumption, lack of physical
exercise, diet
Secondary hypertension
 Accounts for 5% of the cases
 Must investigate for the following causes in a young hypertensive patient (<40 years old)
Renal = Renal impairment (glomerulonephritis, diabetic nephropathy, analgesic nephropathy, chronic

pyelonephritis, APKD, obstructive uropathy, reflux uropathy)
Renal Artery stenosis (atheroma, fibromuscular dysplasia)
Endocrine = Cushing’s syndrome

Conn’s syndrome
Phenochromocytoma
Acromegaly
Thyroid disorders (primary hypothyroidism, thyrotoxicosis)
Toxaemia of pregnancy (pre-eclampsia, eclampsia)
Drugs (OCP, steroids, cocaine, amphetamines)
Neurogenic = Raised ICP

Obstructive sleep apnoea
Aortic = Coactation of aorta

Atherosclerosis
Labile = Pschogenic
Stress-related
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Complications
 Cardiovascular
‐ Heart failure
‐ Ischaemic heart disease/coronary artery disease
‐ AMI
‐ Cardiac arrhythmias
‐ Peripheral vascular disease
 CNS
‐ CVA
‐ TIA
‐ SAH
‐ Hypertensive encephalopathy
 Renal
‐ Chronic renal failure -> hypertensive nephrosclerosis -> ESRF
# can directly cause renal failure eand accelerate disease progression
 Eyes
‐ Blindness
 Hypertensive crisis
History
Drug allergy
Symptoms
 Cardiovascular = chest pain (radiating to the back), SOB, palpitations, ankle oedema, intermittent claudication,
fatigue, giddiness, nausea/vomiting, diaphoresis
 CNS = headache, nausea/vomiting, giddiness, blurring of vision, focal neurological deficits, seizures
 Renal = haematuria, oliguria/polyuria
 Eye = decreased visual acuity
Aetiology
 Renal
‐ Haematuria, proteinuria, polyuria/nocturia, flank pain, ankle oedema
‐ History of renal impairment
‐ GN = vascular (childhood rash on legs)
Infective (Hep B, Hep C, HIV)
Toxin (recent drug intake)
Autoimmune (rash, joint pain and swelling, SLE)
Metabolic (DM)
‐ History of DM
‐ History of long-term analgesia
‐ History of urinary stones causing obstruction
‐ History of APKD
‐ History of reflux disease (recurrent UTI)
‐ History of kidney infection
‐ History of renal artery stenosis
 Endocrine
‐ Conn’s = muscle weakness (hypokalaemic periodic paralysis)
‐ Cushing’s = weight gain around abdomen and face
‐ Pheochromocytoma = episodic headaches, palpitations, diaphoresis, postural giddiness
‐ Hypothyroidism = neck swelling, constipation, weight gain, fatigue, oligomenorrhoea, cold intolerant
‐ Thyrotoxicosis = neck swelling, diarrhea, polyphagia, LOW, palpitations, irritable, insomnia,
amenorrhoea, diaphoresis, heat intolerant
‐ Toxaemia of pregnancy = Last menstrual period
Symptoms of pregnancy
‐ Recent ingestion of OCP and steroids
 Neurogenic
‐ OSA = snoring, daytime somnolence
 Aortic
‐ History of coarctation of aorta
 Labile
‐ Stressed recently
Systemic review
Has this happened before

 Duration of hypertension
 Initial presentation, investigations and management
 Follow-up with whom
‐ Frequency of follow-ups
‐ Compliance with follow-ups
‐ Annual investigations
‐ Level of control
‐ Home-monitoring system in place
 Conservative = weight loss, exercise, diet, compliance
 Medical therapy = types of drugs, dosages, side effects, recent changes, compliance
 Complications
‐ CVS = History of angina or AMI
Chest pain, Sob, palpitations
‐ Peripheral vascular disease = intermittent claudication, poor wound healing, pain, parasthesiae
‐ CNS = history of TIA/CVA/SAH
Headache, nausea/vomiting, BOV, focal neurological deficits
‐ Renal = history of CRF/ESRF
‐ Eyes = poor visual acuity, frequent DRP screening?
‐ Hypertensive emergency = history of such episodes
Presenting complaint, investigations and management

DM, HCL, IHD/CAD, AMI, CVA
Pre-eclampsia or eclampsia
Drug history
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Social history
Smoking
Alcohol consumption
Occupation -> stressful
Diet
Physical activity
Family history
Blood Pressure
 Procedure
- Refrain from smoking or ingesting caffeine 30 mins preceding BP measurement
- Ensure that patient is well-rested and not anxious -> white coat hypertension
- Use appropriate cuff = bladder within cuff should encircle at least 80% of arm
- Place sphygmomanometer at heart leavel
- Measure BP in both arms at first visit -> Coarcation of aorta
Aortic dissection
Patent ductus arteriosus
Thoracic outlet syndrome
- Take 2 or more readings separated by 2 mins and obtain average measurement (obtain more
readings if differ by >5mmHg)
 Take BP in both standing and supine positions for elderly and DM
- Increase DBP on standing = Primary HTN
- Decrease DBP on standing = secondary HTN
Postural hypotension 2ndary to anti-hypertensive medications
General inspection
 Sallow appearance, AV fitula/tenchkoff catheter, bruises and scratch marks = ESRF
 Round-like facies, central obesity, violaceous abdominal striae = cushing’s syndrome
 Prognathism, frontal bossing, large hands and feet = acromegaly
 Café au lait spots = NF-1 (renal artery stenossis, pheochromocytoma, coarctation of aorta)
Peripheries
 Pulse
 Radio-radio delay and radio-femoral delay = coarctation of aorta
CVS examination
 Raised JVP
 Displaced apex beat – LV hypertrophy
 Mitral regurgitation
 S4 heart sound
 Bibasal inspiratory crepitations
 Peripheral oedema
 Carotid bruit
Abdomen
 Bilateral ballotable kidneys = APKD
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 Adrenal mass = cushings
 Renal bruit = renal artery stenosis
Lower limb
 Neurological examination = deep tendon reflexes, focal neurological deficits
 Evidence of peripheral vascular disease = trophic skin changes, temperature gradient, capillary refill time,
pulses
Fundoscopy
Grade 1 = silver wiring of arteries (sclerosed vessel wall reduces transparency -> central light streak appears
broader)
Grade 2 = arteriovenous nipping
Grade 3 = flame-shaped haemorrhages
Soft exudates (cotton wool spots due to ischaemia)
Hard exudates (lipid residues from leaky vessels)
Grade 4 = papilloedema
Hypertensive crisis
History
 Mental state
 Takes BP on both arms
 CVS = heart failure, AR
 CNS = focal neurological deficits, confusion, coma, seizures
 Eyes = fundoscopy
Investigations
Bloods
 FBC
 U/E/Cr
 Cardiac enzymes
Urine
 Urine dipstick
Imaging
 ECG
 CXR
 CT head = hypertensive encephalopathy, stroke, SAH
 2D-scho/CT thorax = ? New onset AR (aortic dissection)
Causes
 Poor control of pre-existing hypertension = not detected
Inadequate treatment
Non-compliance with medications
 Secondary causes of hypertension
Management
 Stabilize patient’s vitals
o Secure airway if patient unconscious
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o Ensure patient is breathing spontaneously -> give supplymental O2, monitor pulse oximetry
o Obtain patient’s vitals (HR, RR, BP, SpO2)
o Obtain Ecg and place on continuous ECG monitoring
o Set IV canula -> take blood for investigation
 2 most urgent indications for immediate BP reduction = Hypertensive encephalopathy
Aortic dissection
 Hypertensive emergency
Target
 Lower MAP by 20-25% or DBP to no less than 100-110 mmHg within a few hours
 Aim for 160/100 mmHg over the next 2-6 hrs
Sodium  First line treatment

nitroprusside  Contraindicated in pre-delivery eclampsia (use hydralazine instead)
 S/E = cyanide/thiocynate toxicity -> lactic acidosis, AMS
 Monitor patient closely if used
Labetalol  Indications = failure of nitroprusside

IHD (decreased HR & O2 demand)
Aortic dissection (decreased systolic ejection force & sheer
stress)
 Cortraindications = asthma, COPD, CCF, bradycardia, heart block
Esmolol  Indications
o Use with nitroprusside for thoracic aortic dissection
o Used with phentolamine (alpha – blocker) for pheochromocytoma
crisis
Nitroglycerine  Indications = Hypertension complicating unstable angina
Disposition
 Admid ICU/CCU
 Hypertensive urgency
Target
 Lower DBP to 100mmHg over 24-48hrs
Oral Felodipine
PO Captopril
Disposition
 If BP improves in monitored area -> discharge with review in next 1-2 days
 If BP does not improve -> admit
 Malignant/accelerated hypertension -> admit
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Medicine (CVS) = Anti Hypertensive medication
1) Classes of anti-hypertensives
a) Ace inhibitors/angiotensin 2 receptor blockers (ARB)
b) B-Blockers
c) Calcium channel blockers
d) Diuretics
2) All drugs drop BP equally (SBP decrease 10-15mmHg)

a) Choice of drug not dependent on MOA but on clinical factors
b) Able to treat ~40% hypertensives successfully
3) Ace Inhibitors
a) Rennin – angiotensin – aldosterone axis
Angiotensinogen
Renin
Angiotensin I
ACE (angiotensin – converting enzyme
Angiotensin II
Aldosterone Vasoconstriction
Ace also inactivates bradykinin (causes vasodilation/dry cough) -> vasoconstriction

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b) Prototypes c) Advantages
i) Enalopril i) No dry cough of ACE inhibitors
- Pro-drug that is converted by de-esterification to ii) Renoprotective
elanoprilat (only IV use) iii) More selective than ACE inhibitors for angiotensin effects
ii) Captopril iv) More complete inhibition of angiotensin effects of ACE
- Competitive ACE inhibitor inhibitors
- Short T1/2 : TDS dosage
c) Side effects 5) B Blockers
i) Dry cough a) Mechanism of action = blocks B-adrenergic actions
ii) First – dose hypotension i) Negative inotropic and chronotropic effects
iii) Hyperkalemia & metabolic acidosis - Decrease Hr (decrease Av and SA conduction velocity)
iv) Macular rash - Decrease contractility – decrease cardiac output
v) Neutropenia - Vasodilatation
vi) Fetotoxicity - Increase diastolic time – increase coronary perfusion
vii) Nephropathy ii) Inhibits B mediated rennin release
- Reduces glomerular filtration pressure b) Contraindications
- Precipitates ARF in patients with impaired renal function i) Asthma/COPD
or RAS ii) Severe bradycardia
- Contraindicated if Cr > 300mmol/L iii) Complete heart block
- Check u/e/cr before and 1-2 weeks after starting Rx iv) Peripheral vascular disease
d) Advantages v) Diabetes
i) Very effective especially when given with diuretics c) Drug-drug interactions
ii) Renoprotective = prevents/reduces proteinuria i) Avoid verapamil and diltiazam = excessive negative inotropic
Stabilies renal function effect
iii) Extremely useful in Tx of heart failure ii) Effects decreased in presence of NSAIDS = reduced
iv) Greater fall in Bp in high rennin states production of prostaglandins (vasodilators)
iii) Metabolized by liver = increased concentrations if given with
4) Angiotensin 2 Receptor blockers cimetidine
a) Mechanism of action = competitive inhibition of angiotensin 2 d) Side effects
receptors – G protein linked i) CVS = bradycardia, hypotension, syncope
i) Lorsartan ii) CNS = giddiness, irritable, hearing and visual disturbances,
ii) Irbesartan confusion - usually with chronic treatment
b) Side effects iii) GIT = nausea, vomiting, abdominal pain, constipation,
i) Hyperkalemia and metabolic acidosis diarrhea
ii) Nephropathy iv) DM = hypoglycemia, mask positive signs of hypoglycaemia
iii) Fetoxicity v) Asthma = bronchoconstriction
vi) Withdrawal syndrome after discontinuation of prolonged use iv) K+ sparing late distal tubules = aldosterone antagonists –
- Tachycardia spironolactone
- Angina
- Hypertension b) Carbonic anhydrase inhibitors
- AMI i) Acetazolamide (diamox)
ii) Proximal tubule = iso-osmotic reabsorption of water
6) Calcium channel blockers Secretion of H+ and organic anions
a) Classification Reabsorption of Na+
i) Dihydropyridine iii) MOA = inhibits carbonic anhydrase which catalyses
- Amlodipine (norvasc) dehydration of carbonic acid (H2Co3)
- Nifedipine (adalat) - Affects Na+/H+ exchanger
ii) Non-Dihydropyridine - Inhibits Na/Hco3 reabsorption
- Verapamil iv) Weak diuretic – limited clinical utility due to compensation
- Diltiazam by Na/Cl cotransporter
b) Mechanism of action v) Side-effects = hypokalemia
i) Arteriodilatation = reduces afterlaod Metabolic acidosis
ii) Decreases contractility CNS toxicity
iii) Negative inotropic/chronotropic effects (except amlodipine vi) Indications = glaucoma
& nifedipine) Epileptic seizures
c) Contraindications Acute mountain sickness
i) Heart failure
ii) Prolonged QT syndrome c) Loop diuretics
iii) Heart block i) Example = frusemide (lasix)
d) Side effects ii) Ascending limb of LOH = active NaCl reabsorption/water
i) Fluid retention impermeable
ii) Constipation iii) Most potent diuretic
iii) Vasodilatation = dizziness, flushing, headache iv) Mechanism of action = inhibits Na/K/2Cl cotransporter
Induces prostaglandin synthesis
7) Diuretics v) Side effects
a) Sites of action - Hyponatremia
i) Proximal tubule = carbonic anhydrase inhibitors - Hypokalemia
ii) Thick ascending limb = loop diuretics (frusemide) – inhibits - Hypochloremia
Na/K/2CL - Hypomagnesmia
iii) Distal tubule = thiazides – inhibits Na/Cl cotransporter - Calciuria – no hypocalcemia as Ca is absorbed in PCT
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- Metabolic alkalosis ii) Short T1/2 = 10 mins
- Auditory and vestibular toxicity Bioactive metabolite (canrerone) has longer T1/2 = 15 hrs
- Venodilatation and hypovolaemia iii) Side effects
- Hyperglycemia - Hyperkalaemia
- Hyperuricaemia - Metabolic acidosis
- Hyperlipidemia - Anti-androgenic effects = gynacomastia/testicular
vi) Indications atrophy/menstrual disorders/hirstrusim
- CCF iv) Mild diuretic used together with other diuretics
- Oedema f) Osmolar diuretics
- Acute hyperkalemia and hypercalcemia i) Examples = mannitol, urea
d) Thiazides ii) Characteristics = small inert molecules that are filterable &
i) Example = hydrochlorothiazide non diffusible
ii) Distal tubule = active NaCl reabsorption/impermeable to Poor oral absorption
water Not metabolized
iii) Mechanism of action = inhibits NaCl cotransporter Excreted unchanged
Reduces peripheral resistance with Given IV
chronic use iii) Mechanism of action
iv) Side effects = hypo Na, hypo K, hypo Cl, hypo Mg - Act in segments that are freely permeable to H20 = PCT,
Reduced urinary Ca2+ descending limb
Metabolic alkalosis - Increases urine volume
Photodermatitis - Increases urine flow rate
Venodilatation and hypovolemia - Decreases contact time between fluid and tubular
Hyperglycemia, hyperuricaemia, epithelium
hyperlipidaemia - Decreases Na+ reabsorption
e) Aldosterone antagonists (K+ sparing) iv) Side effects
i) Examples - Dehydration and hyper Na+ (inadequate hydration;
- Spironolactone excessive use)
- Amilonide - ECF volume expansion & Hypo Na+ (may cause Heart
Mechanism of action = decreases synthesis of aldosterone Failure)
sensitive proteins – involved in Na+/K+ ATPase & apical Na+ v) Indications
channels - Increased ICP
*aldosterone = Stimulates Na+/H+ exchange - Cerebral oedema
Stimulates K+ excretion - Increased IOP
Acts on cytosolic and membrane
receptors
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Medicine (CVS) = Guidelines for selecting drug treatment of hypertension
Concomitqant conditions Recommended drugs Contraindicated drugs

Heart failure Diuretics Calcium channel blockers
ACE inhibitors
Angiotensin II receptor blockers
Angina Beta – blockers
Calcium channel blockers
Post Myocardial infarction Beta-blockers
ACE inhibitors
Isolated systolic Hypertension Diuretic
ACE inhibitors
Diabetes Mellitus with Proteinuria ACE inhibitors
(micro or Macroalbuminuria) Angiotensin II receptor Blockers
Diabetes Mellitus ACE inhibitors Beta Blockers
Angiotensin II receptor blockers Diuretics
Post Stroke Diuretics
ACE inhibitors
Asthma & Chronic Obstructive Beta Blockers
Pulmonary Disease
Heart Block Beta blockers
Gout Diuretics
Bilateral Renal Artery Stenosis ACE inhibitors
Peripheral Vascular Disease B Blockers
Pregnancy ACE inhibitors
Medicine (CVS) = Lipids
1. Reference Ranges
Patients w/o preexisting cardiac risk Patients with preexisting cardiac risk
LDL <3.4 mmol/L LDL < 2.6 mmol/L
HDL > 1.0 mmol/L HDL > 1.0 mmol/L
Total <5.2 mmol/L Total < 4.1 mmol/L
2. Lipid Disorders plays a major role in pathogenesis of CHD

- Hypercholesterolaemia Highest In
 Clinically relevant risk of CHD begins with min TC = Malays > Chinese > Indians
3.9 mmol/L Males > Females
 Escalates sharply when TC > 5.2 mmol/L
 Most impt is LDL – C
- HDL – C
 Powerful protective effect
 Low HDL – C independent risk factor for CHD
 Decrease HDL – C = Obesity/Smoking/sedentary lifestyle
 Increased HDL – C = exercise/alcohol intake
- Triglyceride
 Association with CHD not as well proven
3. Classification
Hypercholesterolaemia Increased LDL Increased Cholesterol

(Familial, Polygenic)
Mixed Dyslipedemia Increased LDL, VLDL Increased cholesterol & TG
(Familial, polygenic
Hypertriglyceridaemia Increased VLDL Increased TG
(TG > 4.5 mmol/L)
Severe Hypertriglyceridaemia Chylomicrons Increased TG
(TG > 10mmol/L)
*main CX = acute pancreatitis
*types of pipopriteins = Chylomicrons (transport dietary lipids to liver)

VLDL (transport TG from liver to tissues)
LDL (transport cholesterol from liver to tissues)
4. Secondary Dyslipidaemia
Diabetes mellitus Increased TG

Decreased HDL- C
Chronic renal failure Increased TG
Nephrotic syndrome Increased Total Cholesterol
Hypothyroidism Increased Total Cholesterol
Alcohol abuse Increased TG
Pregnancy Increased TG
Cholestasis Increased Total cholesterol
Drugs (diuretics, B-blockers, OCP, Steroids Increased TG
May increased Total Cholesterol
Decreased HDL - C
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5. Lipid Measurements
- TC and HDL – C can be measured at any time of the day
- TG must be obtained after 10-12hrs of fasting
- Direct measurements = TC, HDL –C, TG
- Indirect measurements = LDL – C
Friedwald Formula
LDL – C = TC – [HDL – C + (TG/2.2)]
*formula cannot be used if TG > 4.5 mmol/L
6. Risk stratification
- Catagories
 Low-risk = 10 year CHD risk < 10%
 Moderate – risk = 10 year CHD risk 10-20%
 High risk = 10 year CHD risk > 20%
Algorithm
Step 1 = identify individuals in high risk category

 Established CHD
 CHD-like equivalents
(a) DM
(b) CVS
(c) PVD
(d) AAA
Step 2 = input number of risk factors

0 – 1 = Low risk
> 2 = calculate 10 year CHD risk score
Step 3 = > 2 risk factors

Estimate 10 year CHD risk score and re-stratify patients into low/moderate/high risk
7. Management
- Lifestyle changes
 Stop smoking
 Reduce weight
 Exercise regularly
 Dietary restrictions = reduce alcohol consumption if TG raised
(may encourage alcohol if HDL – C low)
- Medical therapy
 Recommend drug therapy
Hypercholesterolaemia Statin, ezetimibe

Mix dyslipidaemia Statin + fibrate/nicotinic acid
Hypertriglyceridaemia Fibrate =/nicotinic acid
Severe hypertriglyceridaemia Fibrate/nicotinic acid + omega 3 fish oils
Isolated low HDL – C Fibrate/nicotinic acid
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 Pregnant = treatment only indicated in patients with severe hyper TG
Intensive dietary therapy = omega 3 fish oils
Statins (HMG Co-A Reductase inhibitors)

- Mechanism of action = lowers TC and LDL – C
- Most potent lipid lowering drug (decrease TC by 31-40 %)
 5mg rosvastatin = 10 mg atorvastatin = 20mg simvastatin = 40mg lovastatin = 80mg finvastatin
Side effects
- Transaminitis ( increase AST/ALT)
 Check LFT before and 2-3/12 after starting statin therapy -> annually
 Stop when AST/ALT > 3x upper limit of normal
 Restart at lower dose when liver function returns to baseline
- Myopathy and rhabdomyolysis
 Both likely to occur with high dosages of statins
#prescribe with caution in elderly, impaired renal function & when statin is combined with
fibrates/nicotinic acid
 Maybe due to depletion of mevalonate
 Stop when serum CK > 5x-10x upper limit of normal associated with muscle pain
 Severe rhabdomyolysis may precipitate ARF -> fatal
- Others = headache, nausea, vomiting, diarrhea, rash
#preferably given in evenings -> coincide with cholesterol biosynthesis
# Contraindications = pregnancy/lactating females
Children < 12 years old
Ezetimibe
- Mechanism of action = selectively inhibits intestinal absorption of cholesterol and related plant steroids
Bile acid binding resins

- E.g. cholestyramine
- Mechanism of action = binds bile acids and increases excretion
Increases cholesterol conversion to bild acids
Offset by increased intrahepatic cholesterol synthesis & up-regulation of LDL
receptors
# effect enhanced if given with statins
- Effective in lowering LDL – C & TC by 15-20%
#If combined with statins = 50%
- Only drugs that eliminate cholesterol from the body
- Infrequently used due to side-effects
 GIT = nausea, vomiting, constipation, steatorrhoea , sand like taste
Fibrates
- E.g. fenofibrate, gemfibrozil
- Mechanism of action = lowers VLDL and TG
Increases HDL – C
- Side effects
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 Transaminitis
 Myopathy
 Gasllstone disease
- Usually started when TG > 4.5 mmol/L
- Gemfibrozil should never be combined with a statin***
- Principles of combination therapy
 Start the 2nd drug at a lower dosage & increase gradually until goal level achieved

 Avoid high doses of statins
 Monitor LFT & serum CK before and 6-8 weeks after initiation of therapy
 Advise patient to report to doctors if got muscle pain/tenderness/weakness
Nicotinic acid/Niacin
- Mechanism of action = lowers TC & TG
Increases HDL – C
- Side effects = intense cutaneous flush & pruritus over face & upper body
Nausea, vomiting, diarrhea, dyspepsia
Transaminitis
Hyperuricaemia Avoid in these
Hyperglycaemia patients
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Medicine (CVS) = Myocarditis
Aetiology
 Infections
o Viruses = coxsackieviruses A & B, adenoviruses, influenza, HIV, CMV
o Bacteria = diphtheria, meningococcus, Lyme disease, clamydia, rickettsia
o Fungi = candida
o Protozoa = Trypanosomiasis, toxoplasmosis
o Helminthes = trichinosis
 Immune-mediated reactions
o Post viral
o Post streptococcal
o SLE
o Drug hypersensitivity reaction = methyldopa, sulfonamides, doxorubicin
o Cardiac allograft rejection
 Unknown
o Sarcoidosis – non caseating granulomas
o Amyloidosis – amyloid protein depositions
Pathology
Gross morphology
 Acute onset -> heart usually of normal size (esp if patients die soon after onset)
 Chronic onset -> dilated chambers
 Flabby and pale myocardium with small areas of haemorrhage -> mottled appearance
 Endocardium and valves unaffected
Clinical features
History
 Range from asymptomatic to severe CHF
 Fatigue, dyspnea, chest pain, palpitations
 Signs of heart failure
 Tachycardia
 Soft S1
 S4 gallop
Investigations
 ECG = ST segment elevation/depression, T wave inversion, atrial arrhythmias, transient AV block
 Serology
 Endomyocardial biopsy
Management
 Treat underlying cause
 Supportive measures
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Outcomes/complications
 Outcomes = usually recover without sequelae
Some may develop intractable chronic CCF
 Complications = arrhythmias, dilated CMP, sudden death
283
Medicine (CVS) = Cardiomyopathy
Dilated cardiomyopathy
 Epidemiology = may present at any age (usually between 20-60 years old)
Most common form of CMP (90%)
 Inheritance = usually sporadic but some are familial
 Aetiology
- Post-viral myocarditis
- Alcoholism
- Toxins = cobalt, doxorubicin
- Peripartum CMP
- Genetic mutations involving cytoskeletal proteins
 Pathology
- Progressive cardiac hypertrophy and dilatation of all chambers
- Results in contractile dysfunction -> ineffective contraction (EF < 25%)
- Substantial dilatation and poor contractile function -> mural thrombus formation -> emboli
 Clinical presentation
- CCF
- Ventricular arrhythmias
- Thromboembolism
 Management
- CCF = diuretics, ACE inhibitors, nitrates, digoxin if hypotensive, anticoagulation
- Heart transplant
Hypertrophic obstructive cardiomyopathy (HOCM)

 Epidemiology = may present at any age
 Inheritance = 50% autosomal dominant; 50% sporadic
 Pathology
- Asymmetrical septal hypertrophy characterized by
a) Myocardial hypertrophy = thick, muscular
b) Increased myocardial contractility = powerful hyperkinetic contractions which rapidly expel
blood from left ventricle BUT ineffective as amount of blood in ventricle is greatly reduced
c) Decreased elastic recoil (stiff ) = impaired diastolic filling
 Clinical presentation
- Asymptomatic
- Symptomatic (usually in young adults)
a) Angina
b) Exertional dyspnoea
c) Exertional syncope cardiac arrhythmia (e.g. ventricular arrhythmia, WPW syndrome) ->
sudden death
d) Infective endocarditis
e) CCF
 Management
- Arrhythmias = B-blockers, CCB, amiodarone
- CCF = diuretics, ACE inhibitors, nitrates, digoxin if hypotensive
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Anticoagulation
Implantable cardio-defebrillator, biventricular cardiac resynchronizing therapy
- Septal myomectomy
Restrictive cardiomyopathy
 Epidemiology = least common
 Pathology
- Primary decrease in ventricular compliance -> impaired diastolic filling
 Aetiology
a) Idiopathic
b) Infiltrative = amyloidosis, sarcoidosis, scleroderma
c) Radiation-induced fibrosis
d) Endomyocardial fibroelastosis
e) Endomyocardial fibrosis
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Medicine (CVS) = Takayasu Arteritis
Definition
 Granulomatous vasculitis of medium and large arteries
o May result in fibrous thickening of aortic arch -> obliterate origins of distal branches
o Absence of pulses in upper extremities
 Unknown aetiology (? Immune mechanisms)
Clinical features
Demographics Asian females

40-45 years old
Symptoms Early = non specific (fatigue, weight loss, fever)
Vascular symptoms = markedly lower BP and weaker pulses in upper extremities
compared to lower extremities with coldness or numbness of
fingers
Ocular disturbances = visual defects, retinal hemorrhages, total blindness
Neurological deficits
Complications Involvement of root of aorta -> aortic regurgitation
Narrowing of coronary ostia -> AMI
Involvement of distal aorta -> intermittent claudication
Involvement of pulmonary arteries -> pulmonary hypertension
Renal artery narrowing -> RAS
Course Variable = may be slow or rapidly progressing
Management
 Symptomatic treatment
 Treat complications
Large vessels
Small vessel
 Takayasu’s arteritis
 Henoch–Schönlein purpura
 Giant cell arteritis
 Wegener’s granulomatosis
Medium vessels  Infective endocarditis
 Polyarteritis nodosa  Cryoglobulinaemia
 Kawasaki’s disease
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Medicine (CVS) = Valvular heart disease
Murmur Location of max Diagnosis Signs

intensity
Mid diastolic Apex (heard with Mitral General:
-low-pitched bell) stenosis - Mitral facies (malar flush → purple cheeks)
-rumbling - Bruising (from warfarin anticoagulation)
Pulse:
- Small volume, slow-rising (anacrotic)
- Atrial fibrillation
Auscultation:
- MDM accentuated when patient turned to left lateral position/ exercise (↑flow)
- Loud S1 (occurs when leaflets are mobile, slammed shut during ventricular
systole)
- Opening snap (opening of stenosed mitral valve, indicates pliable leaflets)
- Loud P2 (if pulmonary HPT present)
- Graham-Steell murmur (EDM; MS → pulmonary HPT → PR)
- Functional TR
Lungs – bibasal crepitations (pulmonary congestion)
BP – narrowed pulse pressure
Signs of RV failure – raised JVP, hepatomegaly, ascites, peripheral edema
Ejection Aortic area Aortic Pulse:
systolic Radiation to carotids stenosis - Small volume, slow-rising (anacrotic)
- Crescendo- (ddx: HOCM) Apex beat:
decrescendo - heaving, not displaced
- Palpable thrill over aortic area
Auscultation:
- ESM accentuated with patient sitting up in full experiation
- Usu a/w loud S2
Lungs – bibasal crepitations
BP – narrowed pulse pressure
Aortic area Aortic Pulse – normal
No radiation to sclerosis Auscultation: normal S2
carotids Innocent
Pulmonary area Pulmonary Auscultation:
stenosis - ESM accentuated with patient sitting up in full inspiration (pulmonary stenosis)
ASD - Fixed wide splitting of S2 (ASD)
Innocent
Apex Innocent
Aortic
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sclerosis
Pansystolic Apex Mitral Pulse: normal, tachycardia, AF
regurgitation Apex beat: thrusting, displaced; palpable thrill over apex
Auscultation: PSM radiates to the axilla; S1 and S2 cannot be heard
Lungs: bibasal crepitations (LV failure)
LLSE Tricuspid General:
regurgitation - Jaundiced
- Raised JVP with giant V waves
Apex beat: not displaced, right parasternal heave

Auscultation:
- PSM accentuated with patient sitting up in full inspiration
- MDM of mitral stenosis
Signs of RV failure: pulsatile hpatomegaly, ascites, peripheral edema

VSD Mild VSD: displaced apex beat (LVH)
Moderately severe VSD: palpable thrill
Severe VSD – parasternal heave (RVH)
Early diastolic Usually middle/ Aortic General:
upper LSE regurgitation - Marfanoid features
- Rheumatoid hands
- Spinal deformity (ankylosing spondylitits)
- Argylll-Roberston pupil (syphilis)
- Head nodding (de Musset’s sing)
- Nail bed capillary pulsation (Quinke’s sign)
- Visible carotid pulsation (Corrigan’s sign → due to wide pulse pressure)
Pulse: collapsing pulse (waterhammer pulse)

Apex beat: thrusting, displaced
Auscultation:
- EDM accentuated with patient sitting up in full expiration; ‘absent of diastole’
- Austin-Flint murmur (MDM over apex w/o opening snap; indicator of severity;
vibration of anterior mitral cusp in regurgitant jet)
Lungs: bibasal crepitations (LV failure)
BP: wide pulse pressure
Others:
- Traube’s sign (systolic pistol-shots over fermoral artery)
- Durozlez’s sign (to and fro murmur when femorals are compressed by
stethoscope)
- Mueller’s sign (uvular pulsation in time with HR)
- Hill’s sign (SBP in LL > UL ; indicator of severity)
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Medicine (CVS) = Valvular heart disease
Valvular heart disease

 May be acquired or congenital
 Complications:
o Major haemodynamic burden → left/right heart failure
o Susceptibility to infection
Stenosis = failure to open completely ∴forward flow prevented

o Almost always due to cusps
o Imposes a pressure load
Regurgitation = failure to close completely ∴ allows reverse flow

o Usually involves cusps, valve ring, chordate tendinea and papillary muscle
o Imposes a volume load
Mitral stenosis
 Aetiology:
o Congenital: congenital parachute valve (rare)
o Acquired: rheumatic heart disease, calcification of mitral annulus & leaflets, CTD (e.g. RA, SLE) ,
malignant carcinoid
 History:
o Asymptomatic
o May be symptomatic during pregnancy esp 2nd trimester → significant increase in blood volume
and raised pulmonary pressures; improves in 3rd trimester as blood volume decreases
o Dyspnoea = exertional, orthopnoea, PND (pulmonary congestion)
o Chest pain (pulmonary hypertension)
o Palpitations (atrial fibrillation)
o Fatigue (low cardiac output)
o Haemoptysis (pulmonary congestion, pulmonary embolism)
o Cough (pulmonary congestion)
o Features of right heart failure = peripheral edema (LL swelling, abdominal distension)
 ‘Fish-mouth’ deformity (mitral valve orifice narrowed to slit-like channel)

o Normal cross-sectional area is 4-6cm2 (turbulent flow occurs when area is <2cm2)
 Severity of stenosis :
o Distance between opening snap and S2 (narrower→ more severe)
o Duration of diastolic murmur (longer MDM → more severe)
o Pulmonary HPT
o Right heart failure
 Investigations:
o ECG → atrial fibrillation, p mitrale (broad bifid wave)
o CXR → cardiomegaly, pulmonary congestion, pulmonary oedema (Kerley B lines → horizontal lines
in costophrenic angels)
o 2D-echocardiography → severity (thickened immobile cusps, reduced valve area, reduced rate of
diastolic filling of LV)
o Cardiac catheterization → assessment of coexisting coronary artery disease and mitral
regurgitation
 Complications:
o Elevated LA pressure → LA dilation → atrial fibrillation → mural thrombosis → systemic emboli
o Pulmonary congestion → pulmonary hypertension → pulmonary edema → right heart hypertrophy
& failure
o Infective endocarditis
o Tricuspid regurgitation
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 Management :
o Asymptomatic:
 Anticoagulants (warfarin)
 Antibiotic prophylaxis against IE before surgery and invasive procedures (amoxicillin)
o AF:
 Rate control (digoxin, beta-blockers, CCB)
 Warfarin
o Mild
 Diuretics (reduce LA pressure)
o Moderate- severe pulmonary HPT
 Percutaneous mitral balloon valvuloplasty
 Mitral valvotomy (open/closed)
 Valve replacement
*if AF present look out for

 Stroke (pronator drift if no obvious hemiplegia)
 Over-coagulation
 r/o goiter (check for neck swelling & thyroidectomy scar)
# Ortner’s syndrome = hoarseness due to left RLN palsy a/w enlarged left atrium
Mitral regurgitation
 Aetiology (MITRAL):
M – mitral valve prolapse
I – infective endocarditis
T – tensor apparatus dysfunction ( papillary muscle rupture/ dysfunction in AMI, ruptured chordate teandinea)
R – rheumatic heart disease
A – autoimmune (CTD: e.g. RA, SLE, ankylosing spondylitis, Marfan’s syndrome)
L – Large heart (cardiomyopathy – dilated, restrictive & hypertrophic; aortic regurgitation)
 History:
o Asymptomatic
o Dyspnoea (pulmonary venous congestion)
o Palpitations (AF, increased stroke volume)
o Fatigue (reduced cardiac output)
o Edema, ascities (right heart failure)
o History of AMI
 Investigations:
a) ECG → LVH, atrial fibrillation
b) CXR → cardiomegaly, pulmonary congestion, pulmonary edema
c) 2D-echocardiography → severity & etiology
d) Cardiac catheterization → dilated LV/ LA, mitral regurgitation, pulmonary HPT, coexisting coronary
heart disease
 Complications:
o Left ventricular hypertrophy → LA dilation → Atrial fibrillation * MR can cause CCF
o Left heart failure → pulmonary edema → pulmonary hypertension CCF can cause MR
 Management:
o Asymptomatic = antibiotics prophylaxis before surgeries (amoxicillin). Follow up 6 monthly with
2DE
o AF = rate control, anticoagulant
o Heart failure = diuretics, inotropes
o Surgery: if moderate symptoms persist despite medical therapy and ejection fraction (EF) is adequate
 Valve repair or replacement if LV EF <55% or LV end systolic diameter more than 45mm
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Aortic stenosis
 Aetiology:
o Rheumatic heart disease
o Infective endocarditis Features indicating severity:
o Degenerative calcification  Small volume an slow rising pulse
o Calcification of congential bicuspid valve (narrowed pulse pressure)
 History:  Heaving apex beat, systolic thrill
o Asymptomatic  Soft S2 with narrow/ reverse split
o Syncope during or immediately after exercise  Long ESM
o Fatigue (due to reduced cardiac output)  S4, left heart failure
o Dyspnoea = exertional, orthopnoea, PND  Narrow pulse pressure
o Extertional angina
o CVA
 Differential: HOCM
 Investivgations:
a) ECG → LVH
b) CXR → cardiomegaly
Post-stenotic dilatation of the ascending aorta
Calfcification of the aortic valve
c) 2D-echocardiograpy → severity, etiology
a. Grading = mild (valve area >1.5cm2)
Moderate (1.0 cm2 < valve area < 1.5cm2)
Severe (valve area <1.0cm2)
d) Cardiac catheterization → raised right heart pressures
 Complications:
a) Left ventricular hypertrophy and failure → pulmonary edema
b) Infective endocarditis
c) Syncope (due to electro-mechanical dissociation/ cardiac arrhythmia/ marked peripheral vaso dilation
w/o concmitnat increase in CO)
d) Angina
e) CVA (due to embolisation from disintergrated vavle apparatus)
f) Sudden death (due to conduction abnormality: ventricular arrhythmia, heart block)
g) Microangiopathic haemolytic anemia
h) Associated with angiodysplasia of the colon → PR bleeding
 Management:
a) Asymptomatic = antibiotic prophylaxis (amoxicillin)
b) Symptomatic = balloon valvuloplasty or
valve replacement (indicated if valvular gradient > 50mmHg or valve area less than
0.8cm2)
# Gallavardin phenomenon = high-frequency components of ESM radiating to apex
Aortic regurgitation
 Aetiology:
o Intrinsic valvular disease= Congential bicuspid valve
Infective endocarditis
Rheumatic heart disease
Rheumatoid arthritis
o Aortic root disease= calcific AS (degenerative aortic dilation)
Aortic dissection
Syphilis
Seronegtive spondylosis (ankylosing spondyloarthritis, psoriasis, Reiter’s
syndrome)
Marfan syndrome
 History:
o Asymptomatic
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o Dysponea = exertion, orthopnoea, PND
o Exertional angina (less cf AS)
o Palpiataions
 Features indicating increased severity: Detect isolated AR:
o Wide pulse pressure  Eyes (Argyll-Robertson pupils)
o Collapsing pulseECG  Hands (stigmata of IE)
o Signs of LVF Deviated apex beat  Back
o Soft S2
o Long EDM Request BP:
o Austin Flint murmur (MDM with no opening snap)  Wide pulse pressure
o Presence of S3  Severe HPT → functional AR
o Hill’s sign (higher SMP in leg than in arm)  UL & LL discrepancy
 Investigations
a) ECG → LVH
b) CXR → cardiomegaly (chronic regurgitation: dilated LV, dilated ascending aorta), pulmonary edema
c) 2D ecoocardiograpy → severity, aetiology
d) Cardiac catheterization → severity, anatomy of arotic root, LV function, CAD
 Management:
o Treatment of underlying conditions (e.g. endocarditis or syphilis)
o Asymptomatic = Antibiotic prophylaxis (amoxicillin)
Long term vasodilator therapy (e.g. nifedicine or ACEi) to control SBP
o Symptomatic = valve replacement (if LVEF <55% or LV end systolic diamension >55mm)
Tricuspid regurgitation
 Aetiology:
o Primary:
 Rheumatic heart disease
 Infective endocarditis: assoc with IV drug abusers; check for needle marks & damaged veins
 Congenital – Ebstein anomaly
 Carcinoid heart disease
o Secondary:
 Cardiomegaly (producing ‘functional TR’)
 Cor pulmonale due mitral valve diseases or lung pathology (COPD, bronchiectasis,
fibrosis)
 Cardiomyopathy associated with MR
 AMI with papillary muscle infarct; IHD
 Usually a/w mild mitral stenosis
 History:
o IV drug abuser
o Right heart failure = peripheral edema (LL swelling, abdominal distention)
o h/o COPD
 Complications:
a) Right heart hypertrophy & failure → peripheral edema + raised JVP ± pulsatile liver
b) Infective endocartitis
 Management
a) If cause is due to RV dilation → correct cause of RV overload (e.g. diuretics + vasodilators in CCF)
b) Surgery: valve repir/ valve replacement
Mixed mitral valve lesion (MR, MS)

 Aetiology:
o Rheumatic heart disease (common)
o Calcific degeneration
o If a scar is present, it may be a dysfunctional mitral valve repair or replacement
 Clinical features:
PSM + MDM at apex. Possiblities are:
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o MR + MS
o Severe Mr with functional MS. No opening snap is heard in this case
If there is concurrent MR and MS, determine which is predominant by the clinical signs:
Clinical signs MR predominant MS predominant

Apex Deviated, thrusting Not deviated, tapping
S1 Soft Loud
S3 Present Absent
 If hard to differentiate clinically → cardiac catheterization
Mixed aortic valve lesion

 Aetiology:
o Rheumatic heart disease
o Congenital bicuspid valve
 Clinical features:
o ± Pulsus bisferiens ( 2 strong systolic peaks separated by a midsystolic dip)
o 1 Lesion usually predominates over the other ∴ resembles that of the pure dominant lesion
Clinical signs AS predominant AR predominant

Pulse Small volume Large volume (bounding)
Apex beat Not deviated, heaving Deviated, thrusting
Pulse pressure Decreased Increased (wide)
Rheumatic fever
1. Jones criteria for the diagnosis of rheumatic fever
≥ 2 major criteria: OR 1 major + 2 minor criteria:

Carditis Fever
Arthritis (migratory polyarthritis) Arthralgia
Subcutaneous nodules Previous rheumatic fever
Erythema marginatum Raised ESR or CRP
Syndnham’s chorea Leukocytosis
First degree AV block
AND
Evidence of preceding streptococcal infx:
 Recent scarlet fever
 Raised antistreptolysin O or other
streptococcal antibody titre
 Positive throat culture of group A
2. Pathophysiology strep
 Due to pharyngeal infection with Group A beta-haemolytic streptococci (S. pyogenes) which triggers
rheumatic fever 2-4 weeks later
 Results in molecular mimicry: Ab to carbohydrate cell wall of streptococcus cross reacts with heart valve
tissues
 Also causes acute glomerulonephritis (1-2 weeks later)
3. Epidemiology
 Peak incidence = 5 – 15 years old
 2% of the population
4. Valves affected: (60% with carditis develop chronic RHD)
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 Mitral – 70%  Incompetent lesions develop during
 Aortic – 40% attack
 Tricuspid – 10%  Stenotic lesions occur years later
 Pulmonary – 2%
5. Investigations
 Evidence of systemic illness (non-specific)
o FBC for leukocytosis, raised ESR and CRP
 Evidence of preceding streptococcal infection (specific)
o Throat swab culture: group A beta haemolytic streptococci
o ASOT: rising titres or levels of >200 U (adults) or >300U (children)
 Evidence of carditis
o CXR: cardiomegaly; pulmonary congestion
o ECG: first- and rarely second-degree AV block; features of pericarditis; T-wave inversion; reduction
in QRS voltage
o Echocardiography: cardiac dilation and valve abnormalities
6. Management
 Single does benzyl penicillin 1.2million U i.m. OR oral phenoxymethylpenicillin 250mg 6 hourly for 10 days
o If penicillin allergic give erythromycin or cephalosporin
 Carditis: symptomatic treatment for CCF + aspirin
 Arthritis:
o Analgesia (aspirin/ NSAIDs)
o Immobilization in severe cases
 Chorea: haloperidol/ diazepam
 Secondary antibiotic prophylaxis for dental or other surgery
Medicine (CVS) = Prosthetic heart valves
General guidelines
 Mitral valve prostheses:
o Metallic S1 with opening snap
o Normal S2
o Systolic murmur (normal → does not indicate valve malfunction)
 Aortic valve prostheses:
o Metallic S2
o Normal S1
 Mitral & aortic valves prostheses:
o Metallic S1 and S2
o Systolic murmur (normal → does not indicate valve malfunction)
o If EDM heard → aortic valve malfunction
Types of prosthetic valves

 Mechanical:
o Types:
 Ball and cage device (Starr-Edwards valve) – can hear ball valve hitting the cage in systole
and diastole and the whossing sound of blood around the ball valve
 Tilting disc (Bjork-Shiley valve) or bileaflet valve (St Jude) – will hear metallic click of valves
shutting and should not hear any murmur
o Advantages:
 More durable (can last 20-30 years)
 Lower rate of re-operation cf porcine prostheses
o Disadvantage: requires lifelong anticoagulation
 Bioprosthetic
o Types: porcine or bovine
o Advantage:
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No need for chronic anticoagulation unless AF (anti-coagulation usually only for 3 months

post replacement)
 ∴ safe in elderly and women of childbearing age
o Disadvantages:
 Less durable (requires replacement within 7-10 years)
 Higher rate of re-operation cf prosthetic prostheses
 Calcification
o Suitable patients:
 Unable to anti-coagulate
 Not expected to live more than 7-10 years
 Elderly patients (slower rate of degeneration)
 Homografts
o Cadaveric aortic or pulmonary valve
o First choice treatment in a young patient requiring aortic valve replacement
o Advantage = more resistant to re-infection therefore useful in replacing infected valves
Complications
1. Thromboemoblism (esp with mechanical valves → req anticoagulation; INR usu kept at 2.5-3.5)
2. Valvular dysfunction (esp with bioprosthetic valves)
a. Leaking
b. Dehiscence
c. Fracture
d. Stiffening/ calcification → stenosis
e. Perforation → regurgitation
3. Haemolysis (esp with mechanical valves)
a. Haemolytic jaundice
b. Anemia
4. Infective endocarditis (involves suture line and adjacent perivalvular tissue)
a. Systemic emboli
b. Valvular destruction/ regurgitation/ obstruction
5. Complications of anti-coagulation
a. BGIT → anemia
b. Intra-cranial bleed → stroke
Causes of anemia
1. Bleeding from anticoagulation
2. Haemolysis with the mechanical valves
3. Bacterial endocarditis
“I say this is a prosthetic heart valve because of”
(a) Audible metallic click
(b) Midline sternotomy scar
(c) Metallic S1/S2 on auscultation
 Displaced apex beat & MVR = MR

 Undisplaced apex beat & MVR
OR MS
 AF & MVR (look for goitre or thyroidectomy)
Important things to mention

(a) Is the metallic heart sound sharp? Valve thrombosis
(b) Are there regurgitation murmurs? Valve leakage
(c) Is there jaundice & pallor? Valve haemolysis
(d) Signs of IE?
(e) Bruises over venepuncture sites? overcoagulation
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Medicine (CVS) = Infective Endocartitis
Definition
 Microbial infection of cardiac valves or endocardium resulting in the formation of adherent bulky mass of
thrombotic debris and organisms (vegetations)
 Usually affects left-sided valves (turbulent flow)
o 25-30% mitral valve
o 25-30% arotic valve
o 10% mitral and aortic valves
o 10% tricuspid valve
o 10% prosthetic valve
o 10% congential heart disease
Classification
Acute:
 High virulence organisms (e.g. S. aureus)
 Can infect structurally normal valves
 Rapidly progressive infection
 Little host reaction
Subacute:
 Lower virulence organisms
o Α-hemolytic streptococci (viridians)
o HACEK organisms
 Haemophilus aphrophilus
 Actinobacilus actinomycetemcomitans
 Cardiobacterium hominis
 Eikenella corrodens
 Kingella kingae
 Infects structurally abnormal valves
 Slowly progressive infection
 Greater host reaction
o Inflammation
o Granulation tissue
Predisposing factors
 Native valve
o Underlying abnormality = rheumatic heart disease, VSD, PDA, coarctation of the aorta
o Normal valve = IVDA (usu right sided endocarditis affecting tricuspid valve; S. aureus, streptococci,
gram –ve rods, fungi)
 Prosthetic valves = S. epidermidis (coagulase negative staphylococci)
Pathogenesis
 Derangement of blood flow due to underlying cardiac abnormalities
 Increased trauma to endocardial surfaces
 Formation of sterile platelet-fibrin deposits
 Seeding b blood-borne organisms during episodes of bacteraemia
o IVDA
o Dental or surgical procedures (e.g. urinary catheterization, cystoscopy, IV cannulation)
o Occult sources (e.g. brushing teeth)
o Clumping of gacteria due to agglutinating antibodies
Complications
 Valvular destruction, regurgitation or obstruction
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 CCF
 Extension of infection into adjacent myocardium → ring abscess → conduction disturbances
 Embolism → brain, kidneys, lungs, spleen, bowel
 Entrapment of infected emboli in walls of blood vessels → mycotic aneurysms
 Metastatic seeding of distal organs → cerebral abscess
 Glomerulonephritis (deposition of immune complexes and subsequent complement activation)
Clinical features
History
 Non-specific symptoms = fever a/w chills & rigors, malaise, symptoms of anemia, LOW, LOW
 Heart failure = dyspnoea, LL swelling, abdominal distension
 Symptoms suggesting embolism= to large vessels (e.g. brain, lungs) or small vessels (e.g. kidney with
haemturia or loin pain)
 Risk factors = IVDA, childhood RHD, cardiac abnormalities (ostium primum ASD, VSD, TOF), prosthetic
valve replacement
 Precipitating factors = recent dental/surgical procedures (time between procedure and diagnosis may be
up to 3 months)
 ? history of other major disease, esp those assoc with immune suppression (e.g. renal transplantation or
steroid use)
 Drug history= ?antibiotic allergies, use of antibiotics for prophylaxis
 How diagnosis was made (if known case) – including number of blood cultures, use of transthracic or
transoesophageal echocardiography (TOE)
 Management since admission to hospital, including the names of antibiotics used, the duration of treatment
and whether possibility of valve replacement has been discussed
1. Examine peripheral stigmata of endocarditis
 Hands:
o Clubbing (late sign)
o Splinter haemorrhages in nail beds
o Osler’s nodes on the finger pulp (always painful and palpable; prob an embolic phenomenon and
are rare)
o Janeway lesions (non-tender erythematous maculopapular lesions containing bacteria on the palms
or pulps; rare)
 Eyes:
o Roth spots in the fundus (retinal infarcts)
o Conjunctival petechiae
 Abdomen:
o Splenomegaly (late sign)
 Urine analysis: for haematuria and proteinuria
 Neurological signs of embolic disease
2. Examine heart to assess for predisposing cardiac lesions

 Acquired :
o Prosthetic valve (mechanical)
o MR, MS
o AS, AR
o Prosthetic valve (tissue
o Repaired mitral valve
o Mitral valve prolapsed with MR
 Congential
o Bicuspid aortic valve
o PDA
o VSD
o Coarctation of the aorta
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3. Examine for sings of cardiac failure. Look for signs of a prosthetic valve and for scars that may present from
previous valvotomy or repair operations
4. Look for source of infection and take patient’s temperature
# ostium secunndum ASD almost always never have IE
Investigations
1. 3-6 blood cultures over 24 hours at least 1 hour apart(98% of culture positive cases will give positive
results in the first 3 bottles)
2. FBC, ESR, CRP= NCNC anemia, neutrophilia, raised ESR, raised CRP.
a. ESR may remain elevated for months even after treatment has been successful but CRP levels falls
quite quickly→ useful in assessing the effectiveness of treatment
3. Urine dipstick= microscopic haematuria
4. ECG= atrial fibrillation in the elderly; conduction defects may occur but are not specific
5. Chest xray= cardiomegaly, pulmonary edema
6. Echocardiography= vegetations (negative study does not rule out IE as vegetations must be larger than
2mm to be detected)
Diagnostic criteria
Pathological criteria
1. Positive microbial culture = vegetation, embolus, intra-cardiac abscess
2. Histological confirmation = vegetation, intra-cardiac abscess
Diagnosis usually a clinical one. The Duke’s criteria is often used

Duke’s criteria (Clinical criteria)
1. Major
 Typical organisms in 2 separate blood cultures
 Evidence of endocardial involvement: 2D-echo showing mobile intra-cardiac mass on a valve or in path
of a regurgitant jet or an abscess or new valvular regurgitation
2. Minor
 Predisposing cardiac condition or IVDA
 Fever >380C
 Vascular phenomena or stigmata= major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,
intracranial hemorrhage, conjuncitval haemorrhages and Janeway lesions
 Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots and rheumatoid factor
 Serological or acute phase abnormalities
 2D echo results abnormal but not meeting major criteria
Diagnosis: 2 major OR 1 major + 3minor OR 5 minor
Management
 IV antibiotics: benzylpenicillin (for S. viridians) and gentamicin (for enterococcus) + cloxacillin (for S.
aureus)
 Follow progress by looking at temperature chart, serological results and haemoglobin values
 Indications for surgery:
o Resistant organisms (e.g. fungi)
o Valvular dysfunction causing moderate-to-severe cardiac failure
o Persistent positive blood cultures despite treatment
o Invasive paravalvular infection causing conduction disturbances or
o Paravalvular abscess or fistula
o Recurrent major embolic phenomena
Prognosis
 30% mortality with staphylococci
 14% mortalitiy with enteric gram –ve rods
 >70% with endogenous infection survive
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 50% with prosthetic valve survive
 IVDA good prognosis
Libman-Sacks endocarditis
 Sterile vegetations in patients with SLE or anti-phospholipid syndrome
 Not along lines of valve clousure
 Uncommon due to steroid therapy for SLE
 Usually a post-mortem finding
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6. Radioisotope scan
Only done in hyperthyroid patients
Priscilla’s Medicine Add-on Procedure:
Radioactive iodine (131I) injected intravenously
Surgery (Thyroid) = Investigations Thyroid gland scanned with a detector to map out areas of
1. Serum fT4 high or low uptake
‘hot’ nodule hyper-functioning area; almost never malignant (<5%)
2. Serum TSH
Decreased in hyperthyroidism; increased in hypothyroidism ‘cold’ nodule non-functioning area; 20% are malignant
If TSH low and T4 normal  request for T3 levels (T3
thyrotoxicosis)
neutral same as remaining thyroid gland
3. Serum thyroglobulin
Used to monitor recurrence of carcinoma
Detect factitious hyperthyroidism (self-medication = T4 + diffuse uptake Graves’ disease
TSH + T3 +  thyroglobulin)
4. Thyroid autoantibodies multiple ‘hot’ MNG

Thyroid-receptor autoantibodies (stimulating  Graves’ nodules
disease; inhibitory  Hashimoto’s thyroiditis)
Anti-thyroglobulin (TG) antibodies increased uptake by toxic adenoma
Anti-thyroperoxidase (TPO) antibodies adenoma with
Anti-microsomal antibodies  positive in 50% of patients
decreased uptake by
with Hashimoto’s thyroditis
remaining tissues
5. Thyroid ultrasound
Single or multiple Patient with ‘hot’ or ‘cold’ nodule can still be euthyroid
Consistency (cystic, mixed, solid)
Measurements of mass 7. FNAC (fine-needle aspiration cytology) and biopsy
Margins (irregular or well-defined) Single most important test!
Microcalcifications (indicative of psamomma bodies in Advantages of FNAC:
papillary thyroid CA) Simple (can be done in the clinic setting)
Chick the contralateral lobe for similar lesions Rapid results
Extra-thyroidal extension into surrounding structures Accurate (sensitivity > 90%)
Cervical lymph nodal involvment Diagnostic (best test to detect thyroid CA)
Therapeutic (cyst aspiration)
Disadvantages of FNAC:
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Cannot make distinction between follicular adenoma and normal TSH + hormone-binding problems = pregnancy,
carcinoma (need to see encapsulating capsule, therefore open abnormal T4 increased thyroid-binding proteins,
biopsy needed) amiodarone
(inappropriately high may affect T3 and T4 levels but fT4/fT3 levels
8. Others T4) remain normal  TSH normal
Isolated TSH a) subclinical hyperthyroidism
ECG Hypothyroidism (bradycardia, small complexes suppression b) recovery from overt hyperthyroidism
in all leads) c) 1st-trimester pregnancy
Hyperthyroidism (sinus tachycardia, atrial d) drugs (dopamine, glucocorticoids,
fibrillation) somatostatin)
Isolated TSH a) subclinical hypothyroidism
CT If patient suspected of having retrosternal goitre elevation b) recovery from overt hypothyroidism
Staging of thyroid cancer c) drugs (amiodarone, lithium)
Do not use iodinated contrast agents → risk of
inducing hyperthyroidism
MRI staging of thyroid cancer
PET useful for patients on f/u with raised TG but no

focus of detectable clinical disease
Interpretation of tests
 TSH +  T4 TSH-secreting tumour
thyroid hormone resistance
 TSH +  T4 primary hypothyroidism
 TSH + normal T4 subclinical hypothyroidism
TSH +  T3/T4 primary hyperthyroidism

 TSH + normal T4 subclinical hyperthyroidism
T3 thyrotoxicosis
 TSH +  T3/T4 pituitary disease (pituitary tumours, post-
pituitary surgery, post-NPC radiation)
sick euthyroidism (in systemic illness;
typically for ‘everything to be low’)
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Surgery (Thyroid) = Short Cases
Diffuse goitre
Mdm XXX is a middle-aged chinese lady who appears to be alert and comfortable at rest. She does not
appear restless. On general inspection, I note a diffusely enlarged goitre measuring __cm x __ cm in size
which moves with swallowing but not with tongue protrusion. It is non-tender, smooth, firm and not fixed
to the overlying skin or underlying muscles. There is no evidence of retrosternal extension, increased
vascularity or cervical lymphadenopathy. There is also no tracheal deviation or involvement of the carotid
arteries.
Mdm XXX is clinically euthyroid and there are no signs of thyroid eye disease.
So in summary, Mdm XXX has a diffuse goitre and is clinically euthyroid.
Multinodular goitre
appear restless. On general inspection, I note an asymmetrically enlarged goitre which moves with
swallowing but not with tongue protrusion. On palpation, the thyroid gland is nodular with the right lobe
larger than the left lobe. It is non-tender, firm and not fixed to the overlying skin or underlying muscles.
There is no evidence of retrosternal extension, increased vascularity or cervical lymphadenopathy. There
is also no tracheal deviation or involvement of the carotid arteries.
So in summary, Mdm XXX has a multinodular goitre and is clinically euthyroid.
Graves’ disease
Mdm XXX is a middle-aged chinese lady who is thin and restless on examination. On general inspection, I
note a diffusely enlarged goitre measuring __cm x __cm in size which moves with swallowing but not with
tongue protrusion. It is non-tender, smooth, firm and not fixed to the overlying skin and underlying
muscles. This is associated with signs of increased vascularity such as prominent dilated veins, increased
warmth, palpable thrill and bruit. There is no tracheal deviation or displacement of the carotid arteries. No
cervical lymphadenopathy was detected.
Mdm XXX is clinically hyperthyroid. I say this because she has fine tremors associated with sweaty and
warm palms. In addition, she is also in sinus tachycardia. However, there is no thyroid acropathy,
onycholysis, proximal myopathy, hyperreflexia or pretibial myxoedema. There are also no features
suggestive of thyroid eye disease.
So in summary, Mdm XXX most likely has Graves’ disease and is clinically hyperthyroid.
Thyroid nodule
appear restless. On general inspection, I note a hemispherical swelling in the anterior triangle of the neck
which moves with swallowing but not with tongue protrusion. This is likely to arise from the thyroid
gland. On palpation, the nodule is non-tender, firm and not fixed to the overlying skin or underlying
muscles. There is no evidence of cervical lymphadenopathy.
So in summary, Mdm XXX has a thyroid nodule and is clinically euthyroid.
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Surgery (Thyroid) = Congenital anomalies
Lingual thyroid
 thyroid gland fails to descend patient presents with a lump at the foramen caecum
 asymptomatic OR interferes with speech and swallowing
Thyroglossal cyst
 usually occurs in young adults
 presents as a fluctuant swelling in the midline of the neck
 remnant tract left behind by the thyroid gland as it descends
from the foramen caecum to its position in front of the trachea
 tract usually reabsorbs → results in thyroglossal cyst or fistula
formation if it persists
 characteristics = moves on swallowing (attachment to larynx
by pretracheal fascia)
moves upwards when tongue protrudes out
(attachment to hyoid bone)
 Tx = Sistrunk’s operation (cyst, thyroglossal tract, body of hyoid
bone)
 Cx = infection  abscess formation
thyroglossal fistula
- presents as a discharging area in the midline
- follows rupture or inadequate excision of a thyroglossal
cyst  recurrent inflammation  fistula intermittently
discharges mucous
- Tx = fistulectomy
malignant change is rare
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Medicine (Rheumatology) = Approach to the Rheumatological Case
GALS Screen
.
Appearance Movement
Gait
Arms
Legs
Spine
 History
1. Pain / Stiffness in muscle / joints / back
- Cardinal symptoms of rheumatic disease
2. Ability to wash and dress completely without difficulty
- ADL: Assessing functional problem of UL
3. Ability to get up and down stairs easily and ability to squat
- ADL: Assessing functional problem of LL
 Physical Examination
 Gait
1. Ask patient to stand
 Ease of transfer from chair / lying position to standing position
2. Get patient to walk and turn around
 Smoothness and symmetry of leg
 Pelvis and arm movement
 Normal stride length
 Ability to turn quickly
 Without pain
 Spine
1. Inspection (from back and from sides)
 Start from back
 Abnormal scoliosis curvature of spine
 Symmetry of paraspinal muscles and girdle muscles
 Symmetrical pelvic position, level iliac crests
 Inspect from sides
 Normal curvature in the neck and thoracic spine
 Normal lumbar lordosis
 Symmetry of paraspinal muscles
 From front
 Lateral cervical flexion ('Place your ear on your shoulder’)
 Hyperalgesic response of fibronyalgia (Squeeze over midpoint of supraspinatus
muscle)  If tender proceed to other sites, e.g. below medial epicondyle
2. Movement
 Put finger at spine along 2 lumbar vertebrae and ask patient to 'Bend forward and touch
toes'
 Finger to floor distance less than 15cm, lumbar expansion >6cm
 Arms
1. Inspection
 Arm:
 From front: Normal girdle muscle bulk and symmetry
 From back: Normal acromioclavicular sternoclavicular and glenohumeral joints; Full
elbow extension
 Examine dorsal surface. Squeeze at carpal region
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 No swelling, deformity
 Turn over to palmar surface.
 Supination movement (Arms and elbow)
 Palmar surface.
 Redness over palms in inflammatory arthritis, swelling, deformity
 Squeeze acoss MCP joint
 Early arthritis: pain and tenderness on squeezing before other abnormalities seen
2. Movement
 Make a fist. Spread out.
 Detection of power grip
 Pinch in pincer manner
 Impt for fine movements
 Spread elbows straight out
 Test shoulders. Put arms behind head and elbows back.
 Putting elbows back test full degree of external rotation
 Legs
1. Inspection
 Leg
 From front: No knee, forefooting or mid foot abnormalities
 Knee: Bulk of quadriceps muscle, normal concavities on each side of the patella (
concavities lost with effusion at knee joints)
 Feet
 Pay special attention to soles of feet. Deformity  change pressure points 
thickening of skin
2. Movement
 Bend leg up and twist
 Internal rotation first to go in hip disease
 Hand on knee joint feels for crepitus
 Look at knees and feel across lateral border
 Back of hand sensitive to temperature changes
 Squeeze across MTP joints
 Early arthritis: pain and tenderness on squeezing before other abnormalities seen
History
History of Presenting Complaint
 Pain
Aspect Differential
Distribution and Joint Acute monoarthritis
Involvement Septic arthritis, traumatic, gout/pseudogout, haemarthrosis
 N.B. arthralgia = presence of Chronic monoarthritis
joint pain wout swelling; Chronic infection e.g. TB, sero-ve spondyloarthritis,
arthritis = pain + swelling pigmented villonodular synovitis
Acute / chronic Acute polyarthritis
Getting better / worse Infection, onset of chronic polyarthritis
Chronic polyarthritis
RA, sero-ve spondyloarthritis, OA, gout, pseudogout, CTD e.g.
SLE, infection
Effect of exercise or rest  RA – symptoms worse aft rest
 OA – symptoms worse aft exercise
Sequence of onset of joint  RA/OA – symmetrical
involvement  Sero-ve spondyloarthritis – asymmetrical
 Approach to specific symptoms

 Back Pain – Where, Onset, Aggravation
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Type Subset Characteristics
Mechanical Well localised
Aggravated by mvt, coughing, straining
Spinal cord lesion Pain in dermatomal distribution
Non-mechanical Osteoporosis Progressive and unremitting pain
Osteomalacia
Malignancy
 Metastasis
 Leukaemia
 Myeloma
 Limb Pain – Where, Onset, Aggravation
Type Subset Characteristics
MSK Polymyositis Aching pain in muscles ard region a/w weakness
Polymyalgia Older pts, pain with stiffness
rheumatica
Bone dz e.g. OM,
osteomalacia,
osteoporosis
Tenosynovitis
Vascular Arterial occlusion Acute. Severe pain of sudden onset
PVD Chronic. Calf pain on exercise relieved by rest
Nervous system Entrapment and
neuropathy
 Morning Stiffness
 Classically in RA and other inflammatory arthropathies
 Deformity
 Instability
 Described as “giving way” or “coming out”
 Due to dislocation or muscle weakness / ligamentous problems
 Change in sensation
 Functional capacity
 Systemic symptoms
 Fatigue
 Wt loss
 Ulcers
 Dry eyes & mouth
 Stiffness
 Fever
 Treatment history + SEs
 H/o trauma or surgery
 H/o recent infection inc hepatitis, streptococcal pharyngitis, rubella, dysentery, gonorrhoea, TB
Social History
Family History
 General Principles
 Impt in assessing pt’s functional disability and gaining clues about diagnosis
 Can get pt to transfer to side of bed / sit out in chair / expose and in doing so observe for
functional ability
 Look, feel, move, measure, compare with opposite side
- Look
 Compare left VS right
 Inspect front, back, sides
 Skin: look for erythema, scars, rashes
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 Joint/bone: swelling, deformity, subluxation
 Muscle: wasting
- Feel
 Warmth
 Tenderness (say “please let me know if this is uncomfortable for you”): Grade I – pt c/o
pain, Grade II – pt c/o pain and winces, Grade III – pt c/o pain, winces and withdraws,
Grade IV – pt does not allow palpation
 Synovitis (soft and boggy swelling)
- Move
 Passive movement
 Active movement
 Stability – tested by attempting to move joint gently in abnormal directions
 Crepitus
 Examination of individual joints
Examine this patient’s hands
 Introduction - Nails
 Sit the pt over the side of the bed and  Psoriatic changes – pitting,
place hands on the pillow with palms ridging, onycholysis,
down hyperkeratosis, discolouration
 General Inspection  Feel and Move
- Cushingoid - Wrist  MCPJ  PIPJ  DIPJ
- Weight  Synovitis, effusiuon, ROM,
- Iritis, scleritis etc Crepitus
- Obvious other joint disease - Dorsi/Palmarflex
 Look - Radial/Ulnar deviation
- Dorsal  palmar - Palmar tendon crepitus
- Wrist - CTS tests
 Skin  Joints/Bone  Muscle - Active mvt
- MCPJ - Wrist ext / flex
 Ulnar deviation (= deviation of - Thumb ext / abd / add / opp
phalanges at MCPJ towards - Fist (intrinsics)
medial (ulnar) side of hand), volar  Hand Function
(anterior) subluxation - Grip strength
- PIPJ, DIPJ - Key grip
 Swan neck (hyperextension at - Opposition strength
PIPJ and FFD at DIPJ), - Practical ability
boutonniere (FFD at PIPJ and  Others
extension at DIPJ), Z deformity - Elbow
(hyperextension of IPJ and FF and  Subcutaneous nodules
subluxation of MCPJ)  Psoriatic rash
 DIPJ – Heberden’s nodes  Other joints
 PIPJ – Bouchard’s nodes  Signs of systemic diseases
Examine this patient’s feet

 Introduction - Subtalar joint
 Sit the pt over the side of the bed  Inversion and eversion
 General Inspection - Squeeze MTPJ
 Look  Tenderness  inflammation e.g.
- Skin: swelling, scars RA
- Bone/joints
 Deformity – hallux valgus,
clawing, crowding - Press upwards from sole of foot just
- Muscle proximal to the MTPJ of 3rd and 4th
- Nails toes
 Psoriatic changes  Pain  Morton’s metatarsalgia
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- Transverse and longitudinal arch - Feel and move each individual IPJ
 Psoriatic changes – pitting,  Pain in first MTPJ  acute gout
ridging, onycholysis,  IPJs typically affected in sero-ve
hyperkeratosis, discolouration aspondyloarthopathies
 Feel & Move - Palpate Achilles tendon for
- Ankle rheumatoid nodules
 Swelling around lateral and - Simmond’s test for Achilles tendon
medial malleoli rupture
- Talar joint - Tenderness at inferior aspect of heel
 Dorsi and plantar flex  Plantar fasciitis
.
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o Gottron’s sign – Erythematous, violaceous smooth or scaly
Medicine (Rheumatology) = Dermatomyositis and Polymyositis patches over the dorsal IPJ, MCPJ, elbows, knees, medial
Definition malleoli
 A number of conditions in which muscles become damaged by a non- o Erythema spares the phalanges (cf SLE – phalanges involved,
suppurative lymphocytic inflammatory process knuckles spared)
 Polymyositis – inflammation of muscles, Dermatomyositis – skin + o Erythematous rash may be present on the neck and upper
muscles chest (often in the shape of a V), shoulders (shawl sign),
Etiology and Pathophysiology elbows, knees, malleoli
 Polymyositis – CD8 cell-mediated muscle necrosis, found in adults o Cuticlies may be irregular, thickened, distorted
 Dermatomyositis – B-cell and CD4 immune complex-mediated o Lateral and palmar areas of the fingers – rough and cracked
perifascicular vasculitis with irregular “dirty” horizontal lines, resembling those in a
mechanic’s hands
HISTORY  Neurological examination of the UL/ LL
 Adult form usually occurs after the 40 yo o Main findings are in the power testing
 Progressive symmetrical weakness of proximal muscles evolving over  Proximal muscle weaknes and tenderness of muscles
weeks/ mths (muscle wasting absent/ minimal)
o Difficulty in getting up from low chair/ squatting position  Weakness of neck flexors in 2/3 of cases
o Difficulty in climbing stairs  Intact/ absent deep tendon reflexes
o Lifting and running  Requests
o Inability to raise head (lift head off pillow) o If the patient > 40yo, tell the examiner that you would like to
o Inability to get up from bed look for an underlying neoplasm
 Dysphagia (due to weakness of the muscles of the pharynx)  Summary
 Dysphonia o Depends on the stem
 Muscle pain and tenderness o If asked to examine UL or LL , say that this is a ___ yo ___ who
 Raynaud’s phenomenon has a pattern of proximal myopathy on neurological
 Rash worsened by sunlight (photosensitivity) examination of the UL or LL, with weakness of shoulder
abduction/ adduction/ of power grade __. There is also muscle
PHYSICAL EXAMINATION (stem – usu examine this patients UL/ LL) tenderness etc.
 General inspection o In addition I also noticed cutaneous features suggestive of
o Cushingoid features? dermatomyositis as evidenced by the presence of _____.
 Skin o Functionally he/ she is able/unable to stand from the
o Heliotrope rash or purplish-blue rash around the eyes, back of squatting position/ get up from lying positon/ unable to
hands swallow (NG tube) etc etc.
o Dilated capillary loops at the base of fingernails
o Gottron’s papules – pink, violaceous, flat-topped papules
overlying the dorsal surfaces of the IPJ
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CUTANEOUS MANIFESTATIONS
Heliotrope rash Periungual telangiectasia

SYSTEMIC MANIFESTATIONS AND COMPLICATIONS
Gottron’s sign on knuckles/ elbows
FIGURE 3. Shawl sign. FIGURE 4. Mechanic's hand.

Poikilodermatous macules Fissured, scaly, hyperkeratotic
appear in a "shawl" distribution and hyperpigmented hands are
over the shoulder, arms and suggestive of manual labor.
Gottron’s papules upper back.
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INVESTIGATIONS  Resistant cases – methotrexate, azathioprine, cyclophosphamide,
 Confirm diagnosis cyclosporine, high-dose IVIg
o Serum CK – elevated. Levels mirrors disease activity  Malignancy surveillance (regular f/u)
 Also  in DMD, drugs (statins, chloroquine, o Detailed history and physical (breast, pelvic, rectal exam)
colchicines, px on chronic haemodialysis) o CXR, abdominal and pelvic u/s, FOBT, Pap smear,
o EMG – myopathic changes (spontaneous fibrillation, salvos of mammogram
repetitive potentials, short duration of polyphasic potentials of  Those with underlying neoplasm may remit after treatment of the tumour
low amplitude)
o Muscle biopsy – necross and phagocytoss of muscle fibres,
interstitial and perivascular infiltration of inflammatory cells. Classification of polymyositis-dermatomyositis (Bohan)
o Myositis specific auto-antibodies - the aminoacyl–transfer RNA Group I Primary idiopathic polymyositis
(tRNA) synthetases (anti-Jo-1), the nuclear Mi-2 protein, and Group II Primary idiopathic dermatomyositis
components of the signal recognition particle (SRP). Group III Dermatomyositis (or polymyositis) a/w neoplasia
o CXR Group IV Childhood dermatomyositis (or polymyositis) a/w vasculitis
o Serum aldolase, LDH, ALT, AST, FBC, ANA/ENA, U/E/Cr Group V Polymyositis (or dermatomyositis) with associated collagen
o Urinalysis, urine myoglobin vascular dz
DIAGNOSTIC CRITERIA FOR DERMATOMYOSITIS/ POLYMYOSITIS Classification of Dermatomyositis and Polymyositis

Criteria Description
1. Progressive symmetric prox Typical involvement of shoulders
muscle weakness and hips
2. Elevated muscle enzymes  CK, aldolase, LDH, AST, ALT
3. EMG changes Short polyphasic motor units, high
freq repetitive discharge,
insertional irritability
4. muscle biopsy Segmental fibre necrosi, basophilic
regeneration, perivascular
inflammation and atrophy
5. typical rash of dermatomyositis Required for dx of dermatomyositis
 definite poly/dermatomyositis if 4 criteria fulfilled Overlap syndrome
 probable if fulfil 3 criteria  Dermatomyositis overlaps with systemic sclerosis and mixed connective
 possible if fulfill 2 criteria tissue dz
o Signs
TREATMENT  Sclerotic thickening of dermis
 Steroids – most patients respond  Contractures
o Prednisolone is first line drug  Oesophageal hypomotility
 Microangiopathy
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 Calcium deposits
Prognosis
 Dermato/polymyositis a/w malignancy
o  risk of malignancy if age > 50, DMY> PMY, normal CK,
refractory disease
o 2.4-6.5 fold  risk of underlying malignancy usu in internal
organs
DIFFERENTIAL DIAGNOSES of Dermatomyositis
Conditions associated with myositis

 Sarcoid myositis
 Focal nodular myositis
 Infectious polymyositis (Lyme disease, toxoplasma)
 Inclusion body myositis
 Eosinophilic myositis
Differential dx of proximal myopathy

 Endocrine – thyroid disorders, Cushing
 Drugs – TCM, steroids
 Infections
 Toxins – botox, NMBAs
 Autoimmune – polymyositis, dermatomyositis, SLE
 Electrolytes – hypo/ hyperkalaemic
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- triggers = movement (OA), rest (inflammatory arthritis)
Medicine (Rheumatology) = History-taking - relieving factors = movement (inflammatory arthritis), rest (OA)
name/age/ethnicity/gender/occupation 4. Instability (sense of joint giving way)

date of admission - a/w locking of the knee?
Presenting complaint 5. Deformity

Symptoms - kyphosis
“Priscilla says stupid individuals don’t do NS”
6. Disability
1. Pain - functional status = ability to dress, write, bath, transfer, feed
- mode of onset - require walking aids/splints
- frequency - ability to stand, walk , run and climb stairs
- duration - impact on social and recreational activities
- acute/sudden onset - mobility within home
- constant/intermittent - mobility outside home
- progressively worsening/improving
- site and radiation 7. Neurological symptoms
- character - numbness
- pain score and severity - parasthesiae
- triggers = movement (OA), rest (inflammatory arthritis) - weakness
- aggravating factors = movement (OA)
- relieving = analgesia, rest (OA), movement (inflammatory arthritis) Aetiology
Vascular = bleeding disorder, easy bruisability
2. Swelling Infective = fever, chills, rigors
- acute/gradual onset dysuria, urethral discharge, red eyes, recent URTI/GE (reactive
- history of trauma arthritis)
- frequency prolonged cough, haemoptysis, night sweats, LOA, LOW, malaise
- duration Trauma = history of trauma
- site Autoimmune = other joint involvement (see systemic review)
- associated with pain, redness and increased warmth Metabolic = h/o gouty attacks (gout)
- progressively worsening/improving Neoplasia = LOA, LOW, malaise, changes in urinary/bowel habit
3. Stiffness Complications (depends on underlying aetiology)

- duration of early morning stiffness = > 1hr (inflammatory arthritis), < 30
mins (OA) Systemic review
- site constitutional = LOA, LOW, fever, fatigue
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anaemia = chest pain, SOB, palpitations, giddiness, fatigue smoker
RA = dry eyes, dry mouth, chest pain, SOB, numbness, parasthesiae, weakness alcoholic drinker
SLE = alopecia, headache, sudden weakness/numbness, photosensitivity, occupation
malar rash, oral ulcers, chest pain, SOB, changes in urine output, haematuria, family set-up and main caregiver
frothy urine, increased susceptibility to infection, petechiae, easy bruising financial status
Sero-ve spondyloarthritis = red and dry eyes, dry mouth, back pain, alternating type of housing and lift-landing
constipation and diarrhoea, bloody and mucoid stools,
recurrent abdominal pain Family history
Behcet’s disease = oral and genital ulcers SLE, RA, gout, TB
DM, HPT, HCL, IHD/AMI, CVA, cancer

Describe initial presentation = symptoms, investigations, aetiology,
management
How has disease progressed over the years?
Regular follow-up = with whom? how often? compliance? yearly
investigations? what did specialist say at last visit?
Medications = what kind? compliance? side-effects? recent changes?
Non-pharmacological management = diet, PT/OT, intra-articular steroid
injections,
splinting, surgery
Complications of disease and management
Level of control = frequency of attacks? well in-between attacks? triggers?
management each time? number of admissions?
Current symptoms

DM, HPT, HCL, IHD/AMI, CVA, cancer, gout, TB, RA, SLE, AS, asthma
number of hospitalizations and surgeries
Drug history
any known drug allergies
current medications
steroids, aspirin, NSAIDs, warfarin
Social history
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Medicine (Rheumatology) = Hand
Permission (& presence of Pain)
Position Sitting
Exposure Exposed elbows
Examination
The hand is a complex instrument with intricate function. There are 14 joints in the hand excluding the carpus.
The carpus itself is a complex articulation which comprises eight bones linked by ligaments which provide
three degrees of motion. The approach to examination of the hand is thus different and must be preceded by a
hand screen. The hand screen is still based on the basic principles of an orthopaedic examination, namely look,
feel and move.
Look
Skin
Swellings - ganglions and other lumps
Scars - surgical (esp carpal tunnel)
Bones & Joints

Deformities - rheumatoid hand
Alignment
Effusion - wrist joint effusion
Muscles & Tendons

Atrophy - thenar, hypothenar, dorsal interossei
Discontinuity
Nerves
Attitude - ulnar claw, median benediction
sign, wrist & finger drop
Vessels Venous
Arterial - atrophic skin changes
Lymphatic
Feel
Skin
Temperature - red, dry skin
Characterise swellings
Bones & Joints

(Ligaments) Bony outline
Tenderness - 1st extensor compartment, anatomical snuffbox
Effusion
Muscles & Tendons

Subluxation
Tenderness - along flexor sheath
Nerve
Thickening - ulnar at elbow
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Gross sensation
Vessel
Pulse - capillary refill
Pitting edema
Move
PROM & AROM

Flexion/ extension
Abduction/ adduction
Rotation
Special tests
Stability
Anterior/ posterior
Lateral
Impingement - Finkelstein’s
Fixed deformity
Neurovascular assessment
Pulses - radial & ulnar
Peripheral nerve
Motor - *see special tests for nerve
Sensory
Reflexes
Functional assessment
prehension
316
Hand Screen
1. Palms up
1 3
Zones
1. thenar- wasting, crease
scar
2. fingers- attitude
3. hypothenar- wasting
4. wrist- scars
2
2. Finger flexion
Zones
1. joint ROM
2. trigger
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3. Dorsum up
3
Zones
1. 1st web &
intermetacarpal
spaces- wasting
1 2. fingers-
arthropathy
3. wrist dorsum-
ganglion
4. Ulnar border of forearm and elbow
Zones
1. subcutaneous border
of ulna and elbow-
rheumatoid nodules
318
Nerve screen
Median nerve
Ulnar nerve
Radial nerve
319
Vessel screen
Pulses
Cap refill
320
Allen’s test- hand
321
Allen’s test- finger
322
Nerve examination
Once a neuropathy has been identified, one must determine the level and the severity. Nerves have
essentially two functions, sensory and motor. As such, deficits from both these areas must be actively
sought.
Median
Look
1. wasting of the thenar eminence
Feel
2. light touch (median three and half fingers vs thenar eminence)
Move
3. Test for the FPL and FDP to index with ‘O’sign
4. Test the power of the APB
Provocative tests
5. Tinel’s test
6. Phalen’s test
Ulnar
Look
1. ulnar claw
2. wasting of hypothenar eminence
Feel
3. light touch (ulnar one and a half vs dorsal ulnar aspect of hand)
Move
4. FDP to little finger
5. Abductor digiti minimi
6. Finger crossing (palmar interossei)
7. Froment’s test
Provocative tests
8. Tinel’s at the elbow
9. elbow flexion test
Radial
Look
1. wrist and finger drop
2. wasting of triceps and forearm extensor compartment
Feel
3. light touch (1st dorsal web space)
Move
4. elbow extension
5. extension of the wrist
6. EPL
Provocative
7. Tinel’s at the spiral groove
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Wrist
Position Sitting
Exposure Elbows on the table, exposed
Examination
Look
Skin
Swellings - ganglions (volar and dorsal)
Scars - volar and dorsal
Bones & Joints

Deformities - dinner fork deformity
Alignment
Effusion - wrist swelling
Muscles & Tendons

Atrophy
Discontinuity
Nerves
Attitude
Vessels Venous
Arterial
Lymphatic
Feel
Skin
Temperature - radiocarpal joint
Characterise swellings
Bones & Joints

(Ligaments) Bony outline
Tenderness -radiocarpal joint line
-anatomical snuffbox
Effusion
Muscles & Tendons

Subluxation
Tenderness - FCR, FCU,
- 1st extensor compartment, ECU
Nerve
Thickening
Gross sensation
324
Vessel
Pulse
Pitting edema
Move
PROM & AROM

Flexion/ extension
Ulnar/ radial deviation
Supination/ pronation
Special tests
Stability
Impingement - Finkelstein’s
Fixed deformity
Neurovascular assessment
Pulses - radial & ulnar
Peripheral nerve
Motor
Sensory
Reflexes
Functional assessment
Grip strength
325
Wrist
Position Sitting
Exposure wrist on the table with elbows exposed
Examination
Look
1. Look for discrete and diffuse swellings over the dorsal and volar surfaces.
2. Look scars over the dorsal and volar surfaces.
3. Look dinner fork deformity.
Feel
4. Feel temperature of radiocarpal joint.

5. Feel for tenderness over the anatomical snuffbox.
*change position to elbows on the table with wrists off the table in neutral.
6. Feel for tenderness over radiocarpal joint line

7. Feel for tenderness over FCR, FCU and 1st extensor compartment, ECU
Move
8. Assess for passive extension/flexion, ulnar/radial deviation and pronation/supination.
Special tests
9. Finkelstein’s test
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Wrist
Permission (& presence of pain) sitting Wrist on table and

elbows exposed
Examination
1. swellings-
discrete and
diffuse
2. scars
Look
3. dinner fork deformity
4. temperature-
radiocarpal joint
Feel 5. Bony tenderness –

anatomical snuffbox
*Position change- wrist lifted off the table supported by elbow
327
Wrist
6. radiocarpal joint
tenderness
Feel
7. tenderness- FCR,
FCU, ECU, 1st extensor
comprtment
8. ROM- extension/flexion,
Move ulnar/radial deviation,
pronation/supination
Special test 9. Finkelstein’s test
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Medicine (Rheumatology) = hands & wrists, shoulder, C-spine, Hip
RA hands & wrists
Pathology
Synovitis of proximal joints & tendon sheaths
Bone and tendon erosions
Joint instability & tendon rupture  deformity, loss of function
Clinical features
Bilateral symmetrical involvement of the wrist and proximal joints of the hands
Patient c/o progressive pain, stiffness, swelling, deformity & disability (bathing, dressing, holding a
pen/utensils, cup, combing hair)
O/E
Hands
Ulnar deviation of the fingers
Subluxation/dislocation at the MCPJ
z-deformity of the thumb
swan-neck deformity (hyper-extension at PIPJ; flexion at DIPJ)
o inbalance of extensor vs flexor action
Boutonniere deformity (flexion at PIPJ; hyperextension at DIPJ)
o Mixture of central slip of extensor tendor & separation of lateral slips
Dinger-drop (extensor tendon rupture or subluxation into gutters)
Wrists
Swelling of DIPJ
Radial deviation
Piano-key sign (laxity/instability of DIPJ)
Volar subluxation with prominent ulnar styloid process
Look
Characteristic features in hands & wrists
Muscle wasting
Feel
Swelling, increased warmth
Piano-key sign
Move
Hand examination (ROM)
Assess function (grip strength, pinch gripm dressing, holding a cup, writing)
Examine
Knees for genu valgus
Elbow for rheumatoid nodules
C-spine (atlanto-axial subluxation, basilar invagination by dens protrusion, sub-cervical spine)
X-rays
Early stages
Soft-tissue swelling
Periarticular osteoporosis
Later
Narrowing of joint space + periarticular erosions
Last stage
Joint deformity & dislocation
Zig-zag deformity (ulnar deviation of fingers & radial deviation of wrist)
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Management
1. Central synovitis 2. Prevent deformity
NSAIDs Splintage
Low-dose corticosteroids Tendon repairs/transfers
2nd-line drugs Joint stabilization
H&L injections  synovectomy Physiotherapy
Physiotherapy
3. Reconstruction 4. Rehabilitation
Arthrodesis Physiotherapy
Arthroplasty Occupational therapy
Osteotomy
RA shoulder
Acromioclavicular joint, shoulder joint and various synovial pouches around the shoulder are
frequently involved in RA
Chronic synovitis  rupture of rotator cuff muscles, progressive joint erosion
RA C-spine
Severely affected in 30% of patients with RA
Types of lesions
1. Atlanto-axial subluxation
Erosion of atlantoaxial joints & transverse ligament
2. Basilar invagination by dens protrustion

Erosion of atlanto-occipital articulations
3. Subcervical spine
4. Erosion of facet joints  subluxation
Clinical features
Middle-aged/elderly female with RA
c/o neck pain & stiffness
decreased ROM
signs & symptoms of nerve root tension: UL numbness, parasthesiae & weakness
cervical myelopathy (cord compression)
cervical spondylosis
X-rays
1. AP
2. Lateral
3. Flexion & extension news  reveal subluxation/cervical instability
Treatment
Serious complications are uncommon!
Cervical collar (pain relief)
Spinal fusion (persistant & severe pain; a/w neurological deficits)
RA Hip
Hip joint is frequently affected in RA
Hallmark: progressive bone destruction bilaterally
Osteophyte formation (unless 2 OA)
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Clinical features
Rheumatoid disease affecting many joints
Insidious onset of pain in the groin
Limp
Difficulty getting out of chair
Marked muscle wasting of buttock & thigh
Limb is held in fixed flexion and external rotation
Movements are restricted & painful
Treatment
1. Conservative
If disease has not caused bone/articular erosion
General treatment to arrest progression of RA can slow down hip deterioration
Once bone/cartilage has been eroded, treatment can stop joint destruction
2. Surgical
Total hip replacement
Even in younger patients (polyarthritis has already limited activity that implants will not be
unduly stressed even after op)
X-ray
Early Stages Later Stages
osteoporosis (loss of radiological density; Erosion of femoral head & acetabulum
rarefaction) Gross bone destruction
Loss of joint space Can resemble TB arthritis
Bilateral involvement
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Medicine (Diabetes) = Diabetic Ketoacidosis (DKA)
Introduction
 Caused by absolute/relative decrease in insulin levels in the presence of excessive catabolic hormones
(eg. Glucagon)
 More common in Type 1 DM
 Diagnostic criteria
i. Hyperglycemia = BSL>14mmol/L
ii. Metabolic Acidosis = arterial pH <7.3
HCO3- <15 mmol/L
iii. Ketonemia/Ketonuria = [total ketones] > 5 mmol/L
Or urine ketone <3
Aetiology
 Idiopathic (40%)
 Infections = UTI, URTI, skin
 Intercurrent illness
 Insulin errors
 Infarction = AMI, CVA
Pathogenesis
 Insulin deficiency
i. Absolute lack  newly diagnosed Type 1 DM
ii. Relative lack in known Type 1 DM  reduced insulin dose or maintain normal dose during
intercurrent illness
iii. Relative lack in Type 2 DM 00> insulin resistance overwhelms -cell reserves
 High plasma glucose  osmotic diuresis  Na+ & H2O loss  dehydration (4-6 L)
 Hypovolemia
 Hypotension
 Hypoperfusion
 Shock
Clinical Features
SYMPTOMS
 Hyperglycemia = polyuria, polydipsia, LOW
 GIT = nausea, vomiting, abdominal pain
 Dehydration = postural giddiness, weakness
 Metabolic acidosis = AMS (drowsiness, lethargy, confused, stuporous, seizures)
 Underlying aetiology = infection (fever and localizing symptoms)
Infarction (chest pain, SOB, nausea/vomiting, diaphoresis, palpitations,
giddiness/syncope, focal neurological deficits)
Insulin errors (compliance, no increase in dosage during illness)
SIGNS
 Level of consciousness
 Vital signs = HR, BP, RR (Kussmaul’s breathing), temperature
 Dehydration
 respiratory exam
 CVS exam
 Neurological exam
Complications
DKA
 Fluid, electrolyte and acid-base disturbances
 Congestive cardiac failure
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 Thromboembolism (2° dehydration, occur on D3)  DVT, PE, AMI, CVA, DIVC
From treatment
 Cerebral edema
 Aetiology = over-rapid correction of fluids
Use of hypotonic saline
Rapid correction of hyperglycemia
 Clinical presentation = early  irritable, stuporous, drop in GCS
Late  raised ICP
 Usually occurs 6-12 hours after DKA Rx
 Mx = elevate head of bed
Intubate and hyperventilate
IV mannitol
 Hypoglycemia
 Hypokalemia (serum K<3 : arrhythmia, death)
 Hypophosphatemia
Management
The principles of treatment can be divided into 5 main areas – the ‘diabetic pentathlon’ –
1) Water and Na replacement
2) K+ replacement
3) Correction of acid-base imbalances
4) Insulin administration
5) Prevention of treatment complications
 Supportive measures
1. Assess patient vitals and resuscitate when necessary
2. A = ensure airway patent
B = ensure spontaneous breathing
Oxygen supplementation
Monitor SpO2
C = obtain ECG and place on continuous monitoring
Create 2 large-bore IV cannula
Obtain bloods for investigation
Fluid resuscitation if in shock (ensure good cardiac function first)
NGT if N/V, unconscious
3. Monitor
(a) strict I/O charting = catheterise if necessary
(b) urine dipstick
(c) BSL
(d) Vital parameters
4. Investigations
(a) Confirm diagnosis = plasma glucose
Urinary and serum ketones
ABG (metabolic acidosis)
(b) Assess severity = U/E/Cr (dehydration, electrolye abnormalities, glucose, Ca/Mg/PO4)
(c) Underlying etiology = ECG, cardiac enzymes (AMI)
CXR (pneumonia)
FBC (leukocytosis, raised Hct)
Blood c/s if septic
UFEME and urine c/s (UTI)
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 Specific measures
1. IV volume replacement
 1st hour = 0.9% N/S @ 5-20ml/kg/hr (change to colloids if still hypotensive)
Aim to correct estimated water loss (4-6L) within 24 hours
 2nd-4th hrs = 0.45% N/S @ 10-20ml/kg/hr
 Monitor urine output hourly
 Check U/E/Cr every 2-4hrs till stable
 Beware of over-rapid correction (esp in elderly, CCF) = serum osmolality not to ↓ >3
mOsm/kg/hr (may ppt cerebral edema)
2. Restoration of electrolye balances

 K+ replacement (low intracellular stores as acidosis increases extracellular
concentrations)
o ensure urine output first
o serum K+ < 3.3 mmol/L = 20-40 mEq KCL/hr
o serum K+ 3.3-4.9 mmol/L = 10-20 mEq KCL/hr
o serum K+ > 5mmol/L = check serum K+ every 2 hours
3. restoration of acid-base balance
 NaHCO3- only if arterial pH <7
4. Insulin administration
 bolus dose of IV soluble insulin 0.15U/kg
 continuous low-dose insulin infusion of 0.1 U/kg/hr
o adjust infusion rate to obtain drop in BSL of 3-4 mmol/L/hr
o monitor BSL hourly
 BSL<14mmol/L
o Do not stop insulin infusion (goal is not to achieve euglycemia, but to clear
acidosis)
o Halve infusion dose to 0.05 U/kg/hr
o Add D5% in IV fluids  maintain BSL @ 8-12 mmol/L
o Maintain insulin infusion till acidosis clears
 Convert to subcut insulin when
o Prerequisites = ketones  1 +
Patient able to eat
o total sc insulin = 2/3 total IV dose
o stop IV insulin infusion 30min after SC insulin
5. treat possible complications
 thromboembolism = subcut LMW heparin until mobile
6. treat precipitating factors
 sepsis  Abx
 AMI  MONA
Comparison of DKA and HHNK
DKA HHNK
Plasma glucose > 14 mmol/L >33mmol/L
Na + <135 (pseudohypoNa+) 135-145
K+ Normal/↑ Normal
Urea Increased Very Increased
Creatinine Increased Very Increased
Osmolality (mOsm/kg) 300-320 >330
pH < 7.3 > 7.3
HCO3 <15 >15
Ketonuria ++++ + or ++
Fluid loss 4-6 L 6-10L
Mortality risk Increased Markedly Increased
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IV insulin sliding scale
<8 8-12 12-14 14-16 16-18 >18

Off 1 U/hr 2U/hr 3U/hr 4U/hr 5U/hr
SC insulin sliding scale
<4 4-8 8-12 12-16 16-20 >20

Call Dr Off 4U 6U 8U Call Dr
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Medicine (Diabetes) = Hyperosmolar hyperglycaemic non-ketotic (HHNK) state
Diagnostic criteria
 BSl > 33 mmol/L
 Serum total osmolality >330mOsm/kg H20
 Absence of ketonuria/ketonemia (due to presence of insulin in type 2 DM)
o Arteria pH > 7.3
o HCO3- > 15 mmol/L
Salient points
 Longer disease course = days (vs hrs in DKA)
 More severe dehydration = fluid loss (6-10L)
 Greater K+ loss
 Patients are more sensitive to insulin  less insulin required
 a/w higher mortality
Causes
 Infection
 Intercurrent illness
 Infarction
 Insulin errors
 Dehydration = impaired thirst (elderly, immobility), excess diuretics, extensive burns
Clinical features
Commonly occurs in elderly patients with type 2 DM
SYMPTOMS
 Hyperglycaemia = polyuria, polydipsia, increased thirst, LOW
 Dehydration = postural giddiness, weakness
 Altered mental state
 Underlying aetiology
o Infection (fever and localizing symptoms)
o Infarction (chest pain, SOB, nausea/vomiting, diaphoresis, palpitations, giddiness/syncope,
focal neurological deficits)
o Insulin errors (compliance, no increase in dosage during illness)
SIGNS
 Level of consciousness
 Vital signs = HR, BP, RR, temperature
 Dehydration
 Sits of infection = skin, lungs
 CVS exam
 Neurological exam
Complications
HHNK
 Fluid and electrolyte disturbances
 Congestive cardiac failure
 Thromboembolism (secondary dehydration, occurs on D3)  DVT, PE, AMI, CVA
From treatment
 Cerebral oedema
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o Aetiology = over-rapid correction of fluids, use of hypotonic saline, rapid correction of
hyperglycaemia
o Clinical presentation = early  irritable, stuporous, drop in GCS, late  raised ICP
o Usually occurs 6-12 hours after Rc
o Mx = elevate head of bed, intubate and hyperventilate, IV mannitol
 Hypoglycaemia
 Hypokalemia
 Hypophosphataemia
Management
Supportive measures
 Assess patient’s vitals and resuscitate when necessary
o A = ensure airway patent
o B = ensure spontaneous breathing, oxygen supplementation, monitor SpO2
o C = obtain ECG and place on continuous monitoring, create 2 large-bore IV cannula, obtain
bloods for investigation, fluid resuscitation if in shock (ensure good cardiac function first)
 Monitor
o Strict I/O charting = catheterize if necessary
o BSL
o Vital parameters
 Investigations
o Confirm diagnosis = plasma glucose, serum osmolality, urinary and serum ketones, ABG
o Assess severity = U/E/Cr (dehydration, electrolyte abnormalities, glucose)
o Underlying aetiology =
 ECG, cardiac enzymes (AMI)
 CXR (pneumonia)
 FBC (leukocytosis, raised hct)
 Blood c/s if septic
 UFEME and uring c/s (UTI)
Specific measures
1. IV volume replacement  more important of DKA due to greater fluid loss
 Ensure good cardiac function
 Rapid bolus of 2L N/S fast (1 pint over 30 mins)  1 pint q4hrly
 Monitor urine output
 Check U/E/Cr every 2-4 hrs till stable
 Beware of over-rapid correction (esp in elderly, CCF) = serum osmolality not to ↓ >3 mOsm/kg/hr (may
ppt cerebral oedema)
2. Restoration of electrolyte balances
 K+ replacement
3. Insulin administration
 Bolus dose not needed as patients are sensitive to insulin
 Continuous low-dose insulin infusion of 0.1 U/kg/hr
o Adjust infusion rate to obtain drop in BSL of 3-4mmol/L/hr
o Monitor BSL hourly
o Adjust until BSL < 14 mmol/L  halve infusion to 0.05 U/kg/hr, add D5% into fluids
4. Treat possible complications
 Thromboembolism = subcut LMW heparin until mobile
5. Treat precipitating factors
 Sepsis  Abx
 AMI  MONA
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Medicine (Diabetes) = Management of Diabetes Mellitus
Management
2. Lifestyle modifications  for 2-4 months unless patient is symptomatic or severely hyperglycaemic (random BSL >
15
mmol/L or fasting BSL > 10 mmol/L)
- quit smoking = nicotine promotes both macro- and micro-vascular disease
- stop alcohol consumption
- exercise regularly
- lose weight
- eat a healthy diet
- reduce stress levels
- control HPT and HCL
(a) Medical nutritional therapy

# weight loss to be attempted gradually = aim for 0.25 – 1 kg per week
- optimal BMI < 23kg/m2
# weight maintenance diet (no longer overweight/obese) = saturated fat < 10% DCI
carbohydrate 50-60% DCI
protein 10-20%
cholesterol < 300mg/day
fibre 20-35g/day
- DM  DCI not more than 1800kCal/day
- HPT  restricted salt intake to < 2g/day
# 3 main meals and 3 snack-times
eat small but frequent meals
avoid saturated fat, refined sugars, sauces, fried food, soft drinks etc
stop smoking and alcohol intake
# aims = abolish symptoms of hyperglycaemia
achieve weight reduction  reduce insulin resistance, hyperglycaemia and dyslipidaemia
avoid hypoglycaemia a/w therapeutic agents
avoid weight gain a/w therapeutic agents (insulin, sulphonylureas, thiazolidinediones)
(b) Physical activity and exercise
# aims = achieve optimal weight
reduces risk of cardiovascular events
improves insulin sensitivity and increases HDL-C levels
# recommendations = 3-5 times/wk
60-85% max heart rate (till patient feels warm or sweats)
20-60 mins each time
aerobic exercises
# complications = exercise-induced hypoglycaemia
avoid activities with significant potential for injuries e.g. soccer (neuropathy)
avoid activities which drastically raised BP e.g. weight-lifting (retinopathy)
# precautions = wear proper footwear
ensure adequate hydration
avoid heavy resistance & isometric exercise
prevent hypoglycaemia (reduce meds prior to exercise, consume simple carbohydrates 30 mins
before and after every 30 mins of exercise, gradual progression of
exercise intensity, avoid late-night exercise)
3. Pharmacological therapy  symptomatic or severely hyperglycaemic

fail to attain target glucose levels after 2-4 mths of lifestyle modifications
# aims = avoid acute complications of hyperglycaemia and DKA
avoid chronic vascular complications
# 1st-line therapy = sulphonylureas (thin)
biguanides (obese)
# monotherapy  combined therapy  insulin therapy
# recommended that each treatment be allowed 6 weeks to work before stepping up therapy
# insulin started if glucose targets are not achieved with lifestyle modifications and OHGA
4. Monitoring of blood glucose control
5. Screening for chronic complications
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Oral hypoglycaemic agents (OHGA)
 Classes of OHGA
(a) insulin secretagogues  promote insulin release
- sulphonylurea
- meglitinide
(b) insulin sensitizers  improve tissue response to insulin
- biguanides
- thiazolidinediones
(c) insulin release sparers  reduce amount of insulin required
- -glucosidase inhibitors
Sulphonylureas
 mechanism of action = inactivate ATP-dependent K+ channels  depolarisation  opening of voltage-gated
Ca2 channels  influx of Ca2  triggers insulin release
(a) 1st-generation
Tolbutamide
- well-absorbed orally
- rapidly metabolised in liver to inactive carboxytolbutamide
- short t½ = 4-5 hrs ( need for TDS dosing)
- advantage = safest sulphonylurea to be used in elderly due to short DOA
- S/E = nephrotic syndrome, hypothyroidism, hepatotoxicity, teratogenicity
Chlorpropamide
- extremely long-acting sulphonylurea (t½ = 36 hrs)
- S/E = severe hypoglycaemia, SIADH, cholestatic jaundice, blood dyscrasia, rash
(b) 2nd-generation
Gilbenclamide (Daonil)
- metabolised in liver to 3 major hydroxylated metabolites (1 has 15% hypoglycaemic effect that of parent drug
and accumulates in liver failure)
- long t½ = 6-12 hrs (given as OM dose)
- S/E = hypoglycaemia not given to elderly who live alone
- CI = hepatic and renal impairment
Glipizide
- metabolised in liver to inactive compounds
- short t½ = 2-4 hrs
- fastest onset and shortest DOA of all the 2 nd generation drugs
- S/E = less likely to cause hypoglycaemia
GIT effects (LOA, nausea, vomiting)
rash
(c) 3rd-generation
Glimepiride
- most potent of all the sulphonylureas!
- metabolised in liver to inactive compounds
- short t½ = 4-5 hrs
- long DOA given as OM dose
- S/E = allergic reactions (due to sulphur content  urticaria, cardiorespiratory failure)
GIT (LOA, nausea, vomiting, abdominal pain, diarrhoea)
less likely to cause hypoglycaemia
Meglitinides  Repaglinide
 mechanism of action = act on binding sites distinct from that of sulphonylureas  inactivate ATP-dependent K+
channels  depolarisation  opening of voltage-gated Ca2 channels  influx of Ca2 
triggers insulin release
 prandial glucose regulator = only to be taken 30 mins before a meal (no meal  no need to take)
 pharmacokinetics
# well-absorbed orally
# metabolised in liver and excreted in bile
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# very fast onset of action (within 1 hr of ingestion)
 used cautiously in patients with hepatic/renal impairment
 S/E = hypoglycaemia
 advantage = can be used in patients with sulphonylurea/sulphur allergy  no sulphur content
Biguanides  Metformin (Glucophage)

 compounds in which 2 guanidine molecules are linked together with the elimination of an amino group
 often prescribed in obese patients
 mechanisms of action
(a) increased density of insulin receptors
(b) direct stimulation of glycolysis in peripheral tissues
(c) reduced hepatic gluconeogenesis  accumulation of lactic acid
(d) decreased GI glucose absorption
(e) reduced plasma glucagons
# not metabolised
# excreted in urine by GF and active secretion
 S/E = GIT (nausea, vomiting, abdominal pain
LOA  due to metallic taste
diarrhoea  reduce dose if persistent and stop metformin if > 1 week)
megaloblastic anaemia (reduced vitamin B12 absorption)
lactic acidosis (serious but rare! more likely to occur in patients with renal/hepatic/CVS impairment)
 CI = renal/hepatic/CVS impairment
 advantages = can be used singly or combined
weight loss in obese patients
no hypoglycaemia
does not depend on functioning pancreatic -cells
reduce hypertriglyceridaemia
may have a role in disease prevention
Thiazolidinediones  Rosiglitazone
 mechanism of action = nuclear regulation of genes involved in glucose and lipid metabolism
- act by binding to PPAR (peroxisome proliferator-activated receptor) found in fat, muscle and lvier
# metabolised in liver
# slow onset and offset of activity  involved gene regulation
 S/E
(a) hepatic impairment
- contraindicated in patients with liver impairment (ALT > 2.5x above upper limit of normal)
- monitor LFT every 2 months
- stop if ALT > 3x above upper limit of normal
(b) fluid retention
- contraindicated in patients with CCF
- results in weight gain and low Hb/Hct/WBC (dilutional effect)
(c) ovulation in pre-menopausal/anovulatory women
- consider OCP
decreases TG levels
decreases LDL/HDL ratio ( HDL >  LDL)
role in disease prevention
-glucosidase inhibitors  Acarbose (Glucobay)

 mechanism of action = competitive inhibition of glucosidase enzymes
- 1000x stronger affinity for binding site of glucosidase enzymes (amylase, dextrinase, isomaltase, maltase and
sucrase but not lactase)
- decreases post-prandial digestion and absorption of starch and disaccharides blunts rise of post-prandial BSL
 S/E
(a) GIT = flatulence, diarrhoea, abdominal pain
- increased undigested carbohydrates in large bowel  increased fermentation by colonic bacteria
- contraindicated in patients with IBS/IO
(b) raised transaminases
340
 contraindications = renal impairment
IBS
I/O (worsened by gas and distension)
role in disease prevention
Insulin therapy
 indications
(a) type 1 DM
(b) failure of lifestyle modifications and OHGAs in glycaemic control of type 2 DM after 6 mths (i.e. 2 consecutive
HbA1c values  8%)
(c) during acute illness/stress in type 2 DM
 manufactured by recombinant DNA technology
 plasma t½ = 10 mins
 insulin preparations = (a) rapid-acting  Aspart (NovoRapid)
Lispro (Humalog)
(b) short-acting  Regular/soluble insulin (Actrapid/Humulin R)
(c) intermediate-acting  Neutral protamine (Insulatard/Humulin N)
Lente (Humulin L)
(d) long-acting  Ultralente (Humulin U)
Insulin glargine (Lantus)
(a) + (b) dispensed as clear solutions at neutral pH  contain small amount of zinc to improve stability and shelf-life
(c) + (d) dispensed as cloudy suspensions at neutral pH except insulin glargine (clear, pH 4)
insulin glargine is the only soluble long-acting insulin
 routes of administration = SC (injection, Novopen, continuous subcutaneous insulin infusion/insulin pump)
IM, IV, IP, aerosol
 current regimes use intermediate/long-acting insulins to provide basal coverage with rapid/short-acting insulin
analogues to meet mealtime requirements
# twice-daily administration (OM and ON) of one of the following regimens
~ rapid-/short- acting insulin analogues with intermediate-acting insulin
~ pre-mixed regular and NPH insulins
~ pre-mixed rapid-acting and their protaminated intermediate-acting analogues
# basal-bolus regimen
~ intermediate-/long-acting insulin ON with rapid-/short-acting insulin analogues before meals
~ BIDS (bedtime intermediate-/long-acting insulin and daytime sulphonylureas) for selected DM type 2 patients
 insulin regimens
- arbitrary dosage = I unit/kg/day
- usually given 30 mins before meals (Lispro and Aspart can be given with or just after meals)
- commonest regimen is twice-daily dosing based on 2/3 : 1/3 rule
# 2/3 total dose given OM before breakfast
# 1/3 total dose given ON before dinner
# each time  2/3 intermediate or long-acting
1/3 short-acting
Insulin lispro
- insulin analogue = inversion of proline-lysine amino acid sequence at positions 28 and 29 on -chain
- features = rapid onset within 15 mins
peak within 1-2 hrs
duration of action 4-6 hrs
- advantages = very useful in toddlers
may improve compliance with adolescents
reduce nocturnal hypoglycaemia
- disadvantages = higher unit cost
frequent injections
Actrapid
- recombinant human insulin
- features = onset within 30 mins
peak within 2-4 hrs
duration of action 6-8 hrs
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Insulin glargine
- insulin analogue
- features = slow and prolonged absorption (soluble at pH 4  micro-precipitates at physiological pH  releases
small amounts of insulin slowly)
peakless
duration of action 24 hrs
- better than ultra-lente = less variability in PK profile
Mixtard 30 (premixed insulin = 30% short-acting; 70% intermediate-acting)

- consists of Actrapid and Insulatard
- features = onset within 30 mins
duration of action 24 hrs
- disadvantage = pre-mixed formulation
 side-effects = factitious hypoglycaemia

true hypoglycaemia
lipodystrophy (lipoatrophy  anti-insulin abs attacking adipose tissue
lipohypertrophy  insulin increases fat stores)
peripheral oedema
weight gain (anabolic hormone)
hypokalaemia  can precipitate cardiac arrest in heart failure patients
allergy
 fasting hyperglycaemia
(a) Somogyi effect = rebound morning hyperglycaemia following nocturnal hypoglycaemia
caused by release of counter-regulatory hormones
Tx  reduce ON insulin dose
(b) Dawn phenomenon = early morning hyperglycaemia in the absence of nocturnal hypoglycaemia
Tx  increase insulin without causing hypoglycaemia
Monitoring of blood glucose control

Targets of glucose control
 tight glucose control reduces risk of microvascular disease (i.e. retinopathy, neuropathy, nephropathy)
- Diabetes Control & Complications Trial (DCCT) in type 1 DM
- UK Prospective Diabetes Study (UKPDS) in type 2 DM with either sulphonylureas or insulin
but increases risk of hypoglycaemia targets must be individualized
 indications for ‘suboptimal’ target levels
(a) older patients with significant atherosclerosis
(b) severe DM complications or co-morbidities
(c) pre-adolescent children = unpredictable food intake and activity level
poor compliance to treatment
Ideal 4.6-  not attainable by most diabetic patients

6.4%  desired target for pregnant women with GDM or
pregestational diabetes
Optimal < 7.0%  desired target for diabetic patients
 increased risk of hypoglycaemia
Suboptimal 7.1-  attainable for most diabetic patients
8.0%
Unacceptable > 8.0%  risk of acute metabolic decompensation and
hyperglycaemia
Monitoring
 indications = patients on insulin therapy (type 1 DM  3-4 times daily; type 2 DM  2-3 times/day on 2-3
days/week)
pregnant women with GDM or pre-gestational DM
patients who failed to achieve glycaemic control
 markers
(a) blood glucose levels
(b) HbA1c= measure of glycaemic control over the previous 3 months
(c) fructosamine (glycated plasma protein) = reflect control over the previous 2-3 weeks
useful in pregnancy to assess short-term control and in
342
haemoglobinopathies which interfere with HbA1c
 advantage = patient can interpret results and modify treatment accordingly
better understanding of own disease
 self-monitoring of blood glucose = pre-meal hypocount  4.0-6.0 mmol/L
post-meal hypocount  6.0-8.0 mmol/L
- visual method  not recommended
- glucometer  recommended
 self-monitoring of glucosuria  not recommended
- inaccurate as raised renal threshold for glucose might mask persistent hyperglycaemia
- only for patients unable or unwilling to perform hypocount
 self-monitoring of ketonuria  recommended in type 1 DM and pregnant women with GDM or pre-gestational DM
- indications = acute illness/stress
persistent hyperglycaemia > 14 mmol/L
symptoms of ketoacidosis (nausea, vomiting, abdominal pain, acetone breath)
Important things to note!

1. Fasting venous glucose = 6.0 mmol/L
HbA1c = 9%
~ possible reasons = (a) non-compliance (patient injected insulin prior to seeing doctor)
(b) wrong insulin regimen (ON dosing  lower FVG in the morning with daytime hyperglycaemia
 convert to BD regimen)
Chronic complications
 microvascular complications  retinopathy, nephropathy, neuropathy
macrovascular complications  CVD, CVA, PVD
 relation to tight glycaemic control
~ DCCT = tight glucose control lowered the risk of a cardiovascular disease event by 42% and the risk of a serious
event (i.e. AMI, CVA) by 58%
~ UKPDS = 1% decrease in HbA1c value correlated to a 35-60% reduction in risk for microvascular complications;
intensive therapy with either sulphonylureas or insulin reduces overall incidence of microvascular
complications by 25% compared to conventional therapy; reduction in mean HbA 1c by 0.9% (from 7.9% to
7.0%) translates into a corresponding reduction in the risk of microvascular complications by 37%
Cardiovascular disease
 importance
- type 2 DM is a major risk factor for atherosclerotic disease
- metabolic changes in DM = hyperglycaemia, HPT, dyslipidaemia, obesity, pro-thrombotic state, endothelial
dysfunction, pro-inflammatory state  prone to CVD
- DM is a coronary heart disease risk equivalent (risk of DM patient suffering an AMI is the same as a non-
diabetic
patient who has already suffered a previous AMI)
- epidemiology = AMI 3-5 times more common in diabetics (also likely to be silent)
~ 60% of DM patients die as a consequence of CVD
case-fatality higher in DM patients (as many as 50% of those suffering their first AMI die)
CVA 2 times more common in diabetics
- main goal of therapy is primary prevention of CVD
 investigations lower incidence of AMI and CVA if LDL-C < 2.1 mmol/L
(a) annual LFT for dyslipidaemia but total mortality is similar in both groups
(b) annual resting ECG and BP
(c) examine for PVD, femoral bruit & carotid bruit
 management
- lifestyle modifications = smoking cessation, medical nutritional therapy, physical activity
- control risk factors
Hypertension
Aim < 130/80 mmHg
Rx Choice of drug depends on additional benefits
- ACE inhibitors are reno-protective
Dyslipidaemia
Aim Total cholesterol  6.2 mmol/L
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LDL-C = very high-risk < 2.1 mmol/L
high-risk < 2.6 mmol/L
intermediate-risk < 3.4 mmol/L
low-risk < 4.1 mmol/L
TG < 2.3 mmol/L (too high at increased risk of acute pancreatitis)
HDL-C  1.0 mmol/L
# priority = LDL-C  HDL-C  TG
 LDL HMG-CoA reductase inhibitor (statin)
- S/E =  liver transaminases (check CK and LFT 2-3 mths after starting Rx, stop if ALT/AST >
3x
upper limit of normal or CK > 10 x upper limit of normal)
myopathy
rhabdomyolysis
- should not use gemfibrozil when combining with fibrates  adversely alter PK of statin
 increased risk of rhabdomyolysis
 TG Fibrates/Nicotinic acid
- S/E = cholesterol gallstone disease
myopathy
rhabdomyolysis
 liver transaminases
- severe  TG = combination of fibrates with omega-3 PUFA
 HDL Fibrates/Nicotinic acid
Cardiovascular events
macrovascular dz low-dose aspirin (100-300 mg/day)
no macrovascular dz DM is a CHD risk equivalent  low-dose aspirin in patients > 45 yrs old
Diabetic foot
 foot ulcers and amputations are major causes of disability & mortality in diabetic patients
 5% of all diabetics develop foot ulcers eventually
 approximately 700 lower extremity amputations performed in diabetic patients annually
 2 types = ischaemic foot (painful, cool peripheries)
neuropathic foot (painless punched-out ulcer, normal skin temperature)
 indications for amputation = dead, dangerous, ‘damn’ nuisance
Risk factors for lower limb amputation

Ulceration or prior LEA
Peripheral vascular Symptoms
disease  intermittent claudication
 rest pain
 6 ‘P’s = pallor, pain, paralysis, parasthesiae, perishingly
cold, pulseless
Signs
 diabetic dermopathy
 pale and cool peripheries
 loss of hair, shiny/dry skin, muscle atrophy, trophic nail
changes
 absent/reduced peripheral pulses
 positive Buerger’s test
 reduced ABPI
Peripheral neuropathy Symptoms
 numbness and parasthesiae over palms and soles
 burning sensation in soles
Signs
 foot deformities = calluses
bunions
hallux valgus
pes cavus
pes planus
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hammer toes
clawed toes
charcot’s joint (rockerbottom feet)
 loss of ankle jerks (1st thing to go)
 negative monofilament sensation (‘glove and stocking’
distribution)
 negative pin prick sensation
 negative turning fork sensation
 loss of proprioception
Poor footwear  open-toe shoes = slippers, flip-flops, thong
 tight or ill fitting shoes
 management
- optimize glycaemic control
- smoking cessation  will worsen PVD
- footcare education
~ inspect feet daily for cuts and injuries especially in between toes
~ dry feet properly after bathing
~ apply moisturizer if skin is dry
~ cut toenails straight across
~ do not use corn plasters or cut calluses
~ f/u with a podiatrist regularly
~ proper footwear = do not go barefooted
wear wide-toed covered shoes
~ do not walk on reflexology footpaths barefooted
~ if a cut is found ( wash with saline and cover with light dressing
see doctor if it does not start to heal within 2 days
not at risk GP & diabetic foot care  DM footcare education

nurse  Annual screening (ankle jerk,
monofilament, vibration sense, ABPI)
at risk Specialist footcare team  DM footcare education
 Annual screening (ankle jerk,
monofilament, vibration sense, ABPI)
 orthoses / insoles for pressure
distribution
 I&D/wound debridement/amputations
Diabetic retinopathy
 leading cause of blindness in Singaporean adults
 pathophysiology
cataracts
- increased metabolism of glucose to sorbitol via polyol pathway
- increased osmotic pressure within the lens  accumulation of water  lens swells  cataracts
retinopathy
- hyperglycaemia increases retinal blood flow  damages retinal endothelial cells and pericytes
- results in impaired vascular auto-regulation and uncontrolled blood flow
- increased production of vasoactive substances and endothelial cell proliferation
~ capillary occlusion
~ chronic retinal ischaemia  stimulate production of growth factors  increases vascular permeability
stimulates angiogenesis
 risk factors for progression
- duration of DM
- glycaemic control = poor glycaemic control in type 1 DM patients increases risk of retinopathy by 8x
intensive glycaemic control reduces risk by 50-75%
1% reduction in mean HbA1c leads to 37% reduction in risk of retinopathy
- HPT = 10mmHg reduction in BP leads to 13% reduction in risk of retinopathy
- HCL = treatment may retard progression of retinopathy
- microalbuminuria and proteinuria = presence should allude to the presence of retinopathy
no clear evidence that treatment has any impact on retinopathy
345
- pregnancy
- anaemia = treatment may retard progression of retinopathy
- smoking
 long-standing poor glycaemic control = intensive insulin therapy and rapid normalisation of blood glucose a/w
worsening retinopathy; especially if retinopathy is past pre-proliferative
stage
- Mx = laser photocoagulation first followed by intensive treatment
 usually develops 10-20 years after onset of DM type 2
 eye examination = fundal photography
indirect ophthalmoscopy with slit-lamp
direct ophthalmoscopy through dilated pupils
1st examination Routine minimum f/u

Type 1 DM 3-5 yrs after diagnosis Yearly
Type 2 DM At diagnosis Yearly
Pregestational DM Prior to conception & Depends on 1st
during 1st trimester trimester screening
 classification
Non-Proliferative Mild  microaneurysms only
Retinopathy Moderate  more than just microaneurysms but less than severe NPDR
(NPDR) Severe Any of the following (4-2-1 rule)
 > 20 intra-retinal haemorrhages in each of the 4 quadrants
 venous beading in  2 quadrants
 prominent intra-retinal microvascular abnormalities (IRMA)
in 1 quadrant and no signs of proliferative retinopathy
Proliferative 1 or more of the following
Retinopathy (PDR)  neovascularisation
- at the disc
- elsewhere e.g. rubeosis iridis (may obstruct draining angle of eye  2 glaucoma)
 vitreous/pre-retinal haemorrhage
Clinically Mild  some retinal thickening or hard exudates in posterior pole
Significant Macular but distant from macula
Oedema Moderate  retinal thickening or hard exudates in posterior pole
approaching the centre of the macula
Severe  retinal thickening or hard exudates in posterior pole
involving centre of the macula
 management
- refer ophthalmologist with annual eye screening
- lifestyle modifications = smoking cessation, medical nutritional therapy, physical activity
- optimal glycaemic control
- control risk factors = HPT, HCL
Macular oedema (moderate-severe) Laser treatment (focal/grid)

NPDR mild-moderate None
severe Pan-retinal photocoagulation
PDR Pan-retinal photocoagulation
 advanced proliferative DR Vitrectomy
 vitreous haemorrhage
 traction RD
# Focal/Grid laser treatment for macular oedema results in at least 50% reduction in risk of visual loss
# Laser photocoagulation should be instituted for severe NPDR and proliferative DR as it results in 50%
reduction
in risk for severe visual loss and need for vitrectomy
~ destroy areas of retinal ischaemia = prevent release of growth factors that stimulate angiogenesis
~ seal leaking microaneurysms
~ obliterate new vessels directly on retina
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DM nephropathy
 leading cause of ESRF in Singapore (> 47% of cases in 2000)
 stages of DM nephropathy
- stage 1 = glomerular hyperfiltration (increased GFR)
- stage 2 = microalbuminuria (30-299 mg/day)
- stage 3 = proteinuria (irreversible from here onwards)
- stage 4 = renal impairment (Cr > 200)
- stage 5 = ESRF (Cr > 900  start preparing for dialysis when Cr ~ 600-700)
 pathophysiology
- hyperglycaemia increases renal blood flow = afferent arteriole vasodilates
efferent arteriole vasoconstricts
- increased intraglomerular pressure  increased single nephron GFR  glomerular hyperfiltration and
hypertrophy  microalbuminuria
- nephrotic range proteinuria lasts ~ 14 yrs
- vessel walls get damaged  thickening of basement membrane, glomerulosclerosis, hyaline arteriosclerosis,
tubular atrophy  ESRF
Dipstick test
 Type 1= annually after 5 yrs
 Type 2 = at diagnosis, yrly
Dipstick + Dipstick –
 24h UTP  Urine PCR (protein:creatinine
 Creatinine clearance ratio)
Positive Negative
 Repeat 2x over 3 mths  Repeat test yearly
 Microalbuminuria diagnosed if 2 out of

3 samples positive
 Limit progression to overt nephropathy
 Monitor every 6-12 mths * Dipstick only detects > 200mg/L albumin
not microalbuminuria
 management
- tight glycaemic control = may be better in ESRF (reduced insulin breakdown in PCT  may have to reduce
insulin and OHGA dosage)
- control HPT = aim for BP < 125/75 mmHg
ACE inhibitors preferred as 1st-line drug (vasodilates efferent arteriole  reduces intraglomerular
pressure; slows rate of GFR decline; reduces proteinuria)
renoprotective effects are independent of BP control
check U/E/Cr 7 days after starting  worsening Cr function, hyperkalaemia
alternative can be non-dihydropyridine CCB (diltiazem, verapamil)
- control HCL = reduces proteinuria and slows rate of GFT decline
- stop smoking
- low-protein diet (0.8 g/kg/day)
- refer nephrologist
DM neuropathy
 can affect sensory, motor and autonomic nerves
(a) sensory
- ‘glove and stocking’ distribution of sensory loss
- parasthesiae and burning sensation in soles
- impaired monofilament sensation, pinprick sensation, vibration and proprioception
- loss of distal reflexes (ankle jerks first to go)
- Charcot’s joint (damage to joint due to impaired sensation)
(b) motor
347
- muscle wasting and weakness only in advanced cases
- clawed toes with wasting of interosseous muscles  pes cavus
- increased pressure on metatarsal heads with callus formation
- loss of plantar transverse arch  pes planus
- diabetic amyotrophy = severe and progressive weakness and wasting of proximal muscles of lower limb
severe pain, parasthesiae and loss of tendon reflexes
due to acute infarction of LMN of lumbosacral plexus
(c) autonomic
- CVS = postural hypotension
- GIT = dysphagia (oesophageal atony)
gastroparesis (abdominal fullness, early satiety, nausea and vomiting)
nocturnal diarrhoea
- GUT = erectile dysfunction  impotence
neurogenic bladder (obstructive symptoms and overflow incontinence)
 management
- neuropathic pain = paracetamol  TCA  gabapentine
- postural hypotension = fludrocortisone
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Medicine (Endocrine) = Cushing’s syndrome
Start
1. Examine the patient on the right side of the bed
2. Introduce yourself and explain purpose
3. Position the patient at 450 with adequate exposure
Inspection
1. Cushingnoid facies = characteristic rounded face, plethora, acne, hirsutism
2. Central deposition of aadiposity
Hands
1. Clubbing and tar stains → small cell lung CA
2. Rheumatoid hands → RA
3. Hypocount marks → DM
4. Skin atrophy (double-pinch tst)
5. Bruises
6. Proximal myopathy
Face
1. Malar rash → SLE
2. Eyes → posterior sub-capsular cataracts
3. Mouth → oral thrush
Neck
1. Supraclavicular fat pads
Back
1. Inspection = dorsal fat pads (‘Buffalo hump’ → fat deposition over interscapular area)
Gibbus/ kyphoscoliosis
2. Palpate spine or bony tenderness and step-deformity → osteoporotic compression fracture
3. Auscultate chest for rhonchi → chronic severe asthma, severe COPD
Fine end-inspiratory crepitations → idiopathic pulmonary fibrosis
Abdomen
1. Thick violaceous abdominal striae → active disease (disruption of collagen fibres in dermis leading to
exposed vascular subcutaneous tissues)
2. Transplanted kidney/liver
3. Splenomegaly → autoimmune haemolytic anaemia
4. Adrenal mass → adrenal adenoma/carcinoma
Legs
1. Diabetic dermopathy
2. Proximal myopathy → squat repeatedly
Request
1. Visual fields for bitemporal hemianopia → pituitary adenoma
2. Fundoscopy → posterior subcapsular cataract
Hypertensive retinopathy
Diabetic retinopathy
Papilloedema/ optic atrophy (raised ICP)
3. Blood pressure → HPT
4. Hypocount for BSL → DM
5. Urine dipstick for glycosuria → DM
Issues for discussion
349
1. Physiology
 Adrenal cortex produces androgens, glucocorticoids (e.g. cortisol) and mineralcorticoids (e.g. aldosterone)
 Cortisol is excreted as urinary free cortisol
Hypothalamus ACTH Cortisol

CRF
Cushing’s disease ↑ ↓
Anterior pituitary gland
ACTH Adrenal tumour ↓ ↑
Adrenal cortex Ectopic ACTH ↑ ↑
Cortisol Exogenous use ↓ ↑
Peripheral tissues
2. Cushing’s syndrome = chronic glucocorticoids excess from any cause

a. Cushing’s disease → ACTH secreting pituitary adenoma
i. Epidemiology = females > males, 30-50 years old
ii. Clinical features = hypopituitarism, hyperpigmentation at back of hands
b. Adrenal cortical tumour → adrenal adenoma/carcinoma
i. Clinical features = abdominal pain & distension, virilisation
c. Ectopic ACTH production → small cell lung carcinoma/ bronchial carcinoid tumour
i. Clinical features = hyperpigmentation at back of hands
d. Exogenous glucocorticoids
i. Hirsutism uncommon due to suprresion of adrenal androgen secretion
3. Etiology of Cushing’s syndrome (Rule of 9s)
Etiology
90% exogenous steroid use 10% endogenous steroid production
90% ACTH-dependent 10% ACTH independent
90% pituitary 10% ectopic
90% microadenoma 10% macroadenoma
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Complications
Abnormality Clinical features History
Fat metabolism Moon-like facies, central obesity, dorsal fat pads, Inappropriate fat deposition
supraclavicular fat pads Weight gain
Protein catabolism Thick violaceous abdominal striae, skin atrophy, Easy bruising
bruising, proximal myopathy Proximal muscle weakness
Carbohydrate DM (increased hepatic gluconeogenesis + anti- History of DM
metabolism insulin effect) Hyperglycemia (polyphagia,
polydipsia, polyuria, LOW, fatigue)
Recent BSL
Others Hypertension History of HPT
Recent BP reading
Management (diet, medications)
Peptic ulcer disease Abdominal pain

Haematemesis
Melena
Nausea/ vomiting
Osteoporosis (anti-vitamin D effect) Bone pain and fractures

Recent DEXA scan result
Regular f/u with orthopaedic Sx
Management (diet, medications)
Immunosuppression Recurrent infections

Poor wound healing
Posterior subcapsular cataracts History of cataracts

Regular f/u with ophthalmologist
Poor vision
Adrenal androgen Acne, hirsutism, menstrual irregularities Acne
production Hirsutism
Menstrual irregularities/
amenorrhaea
MSH activity in Increased skin pigmentation (extra-adrenal
ACTH precursor Cushing’s syndrome)
molecule
4. Investigations
a. Screening tests
i. Overnight dexamethasone suppression test
1. Give PO DExamethasone 1mg at midnight
2. Check serum cortisol before and at 8 am
3. If cortisol suppressed → no Cushing’s syndrome
ii. 24 hour urinary free cortisol
1. Most reliable and practical
2. Accounts for circadian rhythm → lost in Cushing’s
3. Positive test = 3x upper limit of normal (>280nmol/24hr)
4. If raised but < 3x upper limit of normal → measure serum cortisol in late evening
a. If normal → no further testing
b. Mildly raise → re-evaluate in several weeks
b. Localization tests
351
Plasma
ACTH
Undetectabl Detectable
e
Differentiate between pituitary &

? Adrenal Tumour
ectopic ACTH
Ultrasound/CT/MRI adrenals
High Dose DST or CRH test
Suppresse
d
Unsuppresse
dd
Pituitary cause (Cushing’s Disease)
CT/MRI pituitary Ectopic ACTH production
CXR, CT thorax/AP
Plasma ACTH  Undetectable: likely adrenal tumor → ultrasound/ CT/ MRI adrenals
 Detectable: distinguish pituitary causes from ectopic ACTH → high-dose
DST or CRH test
High dose DST  PO dexamethasone 2mg/6h x 2 days
 Measure cortisol (plasma + urine) at 0 & 48h
 If cortisol suppressed = Cushing’s disease
 If cortisol not suppressed = ectopic ACTH production
CRH test  IV 100g bovine CRH → follow cortisol for 2 hrs
 If rise in cortisol = Cushing’s disease
 If no rise in cortisol = ectopic ACTH production
Inferior petrosal  Distinguish Cushing’s disease vs ectopic ACTH
sinus sampling
352
5. Management
(a) Cushing’s disease:
 Surgical resection resection of pituitary adenoma (trans-sphenodial/ frontal approach)
 Pituitary radiation (in children)
 Bilateral adrenalectomy (primary evacuation not possible)
(b) Adrenal tumors:
 Surgery (curative for adenomas; rarely so for carcinomas → chemo + RTx)
(c) Ectopic ACTH:
 Surgery
(d) Exogenous steroids:
 Taper corticosteroid therapy while managing primary pathology
(e) Medications to reduce plasma cortisol
 Ketoconazole
6. Pseudo-cushing’s syndrome = increased 24hr urinary free cortisol + absent circadian rhythm + cortisol
suppressed positive DST
D= depression, drugs
O= obesity, OCP
A= alcoholism, acute illness
7. Nelson’s syndrome = rapid enlargement of pituitary adenoma after bilateral adrenalectomy

a. Characterized by: rapidly growing pituitary adenoma, very high ACTH levels, hyperpigmentation
b. Incidence as high as 50% ∴ regular f/u f plasma ACTH level and imaging for pituitary tumors
353
Medicine (Endocrine) = Acromegaly
Introduction
 Clinical syndrome resulting from excess of growth hormone production after puberty (i.e. after fusion of
epiphyseal growth plate)
(before puberty → giangtism)
 Epidemiology: 30-50 years old
Aetiology
 Excess GH secretion (GHRH independent)
o Pituitary microadenoma
 GH-secreting (commonest cause)
 Mixed GH an prolactin-secreting
o Pancreatic islet cell tumor
 Excess GHRH secretion (GHRH dependent)
o Central = GHRH secreting hypothalamic tumor
o Ectopic secretion =
 Bronchial carcinoid tumor
 Small cell lung Ca
 Medullary thyroid Ca
Pathophysiology
 Due to high levels of GH and GH-dependent insulin-like growth factor-1 (latter produced by the liver)
Somatic Metabolic
Stimulate growth of tissues Nitrogen retention
 Skin Insulin antagonism
 Connective tissue Lipolysis
 Cartilage
 Bone viscera
 Local pressure effects = headache, visual field defects, CN palsies

 Hypopituitary effects= gynecomastia, galactorrhoea, menstrual abnormalities, impotence, testicular
atrophy
History
 Somatic effects
o Excessive sweating (hyperhydrosis)
o Acral and facial changes =
 Increased dental problems (malocclusion)
 Enlarged face, jaw, hands and feet
 Outgrowing wedding ring, dentures, shoes
o OSA = snoring, morning somnolence
o Musculoskeletal=
 Numbness and parasthesia (carpal tunnel syndrome)
 Chronic back ache, radicular pain (spinal stenosis)
 Urinary and bladder problems (spinal cord compression)
 Joint pain (20 OA, chondrocalcinosis)
 Metabolic effects
o Hypertension
o DM = polyuria, polyphagia, LOW, fatigue
 Local pressure effects = headache, visual field defects
 Hypopituitary effects = menstrual disturbances, galactorrhoea, impotence
 Tumors = uterine leiomyomata, colonic polys, CRC
354
Signs/physical examination
Hand Shake hands Large hands with broad palms

Spade like fingers
Sweaty palms
Pinch skin Increased skin thickness
Tinel’s sign Carpel tunnel syndrome
Elbow Feel behind medial epicondyle Ulnar nerve thickening
Axilla Acanthosis nigricans
Skin tags (molluscum fibrosum)
UL Muscle Proximal myopathy
Face From the side Frontal bossing
Promienet supraorbital ridege
Prognathism (protrusion of lower jaw)
From the front Malocclusion (ask patient to clench teeth)
Macroglossia
Broad nose
Thickened lips
Hirsutism
Acne
Neck Posterior Acanthosis nigricans
Anterior Goiter
Chest Inspection Gyaecomastia
Pacity of axillary hair
Galactoroea
Kyphosis
CVS examination CCF (displaced apex beat, ↑JVP, S3, bibasal creps, pedal edema)
Cardiomyopathy (diffusely felt apex beat)
Abdo Hepatosplenomegaly
Bilateral ballotable kidneys
LL Thickened heel pad
Edema (20 to CCF, HTN)
OA knees (from chrondrocalcinosis)
Request to examine
 Visual fields = superior bitemporal hemianopia
 Fundoscopy=
o HPT/DM retinopathy
o Papilloedema/ optic atrophy
o Angioid streaks (degeneration + fibrosis of Bruch’s membrane)
 Blood pressure = HPT
 Urine dipstick = glycosuria
Macroglossia
 Hypocount = DM
 Acromegaly
 Genitalia = testicular atrophy
 Hypothyroidism
 Look at old photographs
 Amyloidosis
Indicators of acitivity  Down’s syndrome
1. Skin tags
2. Hypertension
3. Glycosuria & hyper glycemia
4. Increase goiter/ tumor (with headache, visual field defect)/ hands, feet, mandible
5. Increased sweatiness
355
Algorithm for diagnosing acromegaly
Investigations
Diagnostic Serum IGF-1 Raised in acromegaly, puberty and pregnancy
OGGT with GH measurement Normal = GH suppression
Acromegaly= indadequate GH suppression
Etiology MRI pituitary fossa
Serum Ca (hyperparathyroidism a/w MEN1
syndrome)
CT chest/ abdomen
Complications ECG, CXR Cardiomegaly
U/E/Cr Hyperglycaemia (DM)
TFT, LH/FSH, testosterone, prolactin, short Hypopituitarism:
synacthen test (ACTH def), triple  Sequence:
stimulation test o ↓gonadotrophins
o ↑prolactin
o ↓TSH
o ↓ACTH
Skull x-ray Large skull
Unusually large frontal sinuses
Frontal bossing
Thick skull table
Occipital prominence
OA c-spine
Prominent jaw
Malocculusion
Dental fillings
Enlarged pituitary fossa
Hand x-ray Large spade like hands
‘turfting to terminal phalanx)
Knee x-ray Chondrocalcinosis, OA
Feet x-ray Large feet, thickened heel pad (lat view)
356
Differentials for GH excess
 MEN 1 syndrome = hyperparathyroidism, pituitary tumors, GIT tumors
 McCune-Albright syndrome = polyostotic fibrous dysplasia, precocious puberty, café-au-lait macules
 Carney syndrome
Management
 Trans-sphenoidal surgery
 Pituitary radiation
o Failed surgery
o Older patients
 Conservative
o Growth hormone antagonist (Pegrisomant)
o Dopamine agonisits (bromocriptine, carbageline) → inhibits prolactin secretion in tuotrs that co-
secrete prolactin
o Somatostatin analogues (octreotide) → inhibit GNRH secretion
 Treat complications = DM, HPT, hypopituitarism (steroids, lifelong thyroxine)
Common causes of death (2-3x increased mortality)

 Cardiac failure (CCF, cardiomyopathy, hypertension)
 Tumour expansion (mass effect, haemorrhage)
 Degenerative vascular disease
 CRC
357
Medicine (Endocrine) = Addison’s disease (chronic 10 adrenal insufficiency)
ACTH stimulates adrenal cortex to produce:

1. Cortisol
2. Androgens
3. Aldosterone (still more dependent on RAAS)
Cortisol is require in
1. Carbohydrate metabolism
2. Control of immune system
3. Controls secretion of CRH, ACTH & ADH via feedback mechanism
Eitiology
1. Primary adrenal insufficiency
 Autoimmune adrenalitis
o ↑ adrenal antibodies
o a/w Graves’ disease, Hashimoto’s thyroiditis, MNG, vitiligo, pernicious anaemia
 tuberculous adrenalitis
 AIDS = CMV adrenalitis
 Adrenal hemorrhage =
o Anticoagulants
o Meningococcal septicaemia → Waterhouse-Friederichs Syndrome
o Anti-phospholipid syndrome
2. Secondary adrenal insufficiency

 Pituitary apoplexy
 Sheehan’s syndrome
 Pituitary surgery/ radiation
 Chronic glucocorticoid use
Clinical symptoms
 LOW, LOA
 Fatigue
 Dizziness (may be postural related) → syncope
 Weakness
 GIT = nausea vomiting, diarrhea, abdominal pain
 Depression, psychosis
 Addisonian crisis (see later)
Clinical signs
 Hyperpigmentation (palmar creases, buccal muscosa)
o Due to high ACTH levels 20 decreased cortisol feedback
 Craving for salt
o Due to ↓ aldosterone levels
 Postural hypotension
 Vitiligo
 Goiter
Investigation
 Bloods
o FBC =
 ↓ Hb (mild hemolytic anemia)
 Leukocytosis (infection)
o U/E/Cr=
358
 Hypokalemia
 Hyponatremia
 Hypoglycemia
o Plasma ACTH ↑, renin ↑, aldosterone ↓
 Short synacthen test

o Do plasma cortisol before & 30 mins after administration
 Imaging
o AXR, CXR (if suspecting TB)
o CT abdomen = adrenals
Management
 Patient education
o Warn against stopping steroids abruptly
o Give glucocorticoids IM/suppositories in cases of vomiting
o Medik Awas card
o Double/ triple dose of hydrocortisone during episodes of febrile illness/ injury
 Pharmacotherapy
o Fludrocortisones
 Postural hypotension
 Hypo Na+
 Hyper K+
 ↑ plasma renin
o Hydrocortisone replacement
Addisonian crisis
 Acute adrenocortical failure characterized by nausea, vomiting, hypotension, shock
 Triggers in unknown patient = infection, trauma, burns, surgery
o 1st presentation = bilateral adrenal haemorrhage
 Rare in patients with 20/ 30 adrenalcortical insufficiency
o Pituitary apoplexy
o Sheehan’s syndrome
o Withdrawal of chronic glucocorticoids suddenly
 Clinical evaluation
o Known patient with Addison’s disease = infection, trauma, burns, surgery
o Signs of Cushing’s syndrome = sudden withdrawal of glucocorticoids
 Investigations
o FBC
o U/E/Cr
o Cortisol
o ACTH
 Management
o IV hydrocortisone 100mg start then every 6 hours
o Fluid resuscitation with IV 0.5 % N/S
o Correct hypoglycaemia
o Treat precipitating cuase
o Start mineralocorticoid therapy = fludrocortisones
o Refer endocrinology
359
Medicine (Endocrine) = Hypo-pituitarism
Approach to the Short Case Examination

 Usually a ‘proceed to check for signs of hypopitutarism’ case after detecting bitemporal hemianopia/
hypothyroid features/ hypopigmented areolae
 Examination:
o Inspection:
 Pale but no conjunctival pallor → due to lack of CRH
 Soft skin
 Paucity of axillary and pubic hair
 Atrophy of breast in females/ gynaecomastia in males
o Request to:
 Take BP for postural hypotension
 Check visual fields if not already done
 Examine fundus for optic atrophy
 Examine external genitalia for hypogonadism
 Check for transfrontal scar
 Check for CN III, IV, V, VI palsies
Discussion
360
 Etiology
Brain damage Pituitary tumors are classically the most common caus e of hypopit but new findings imply that causes like
brain damage might outnumber pituitary adenomas in causing hypopituitarism
Traumatic brain injury
SAH
Neurosurgery
Irradiation
Stroke
Pituitary tumors Adenomas
Others
Non-pituitary tumors Craniopharyngiomas
Meningiomas
Gliomas
Chordomas
Ependymomas
Metastases
Misc Infection – abscess, meningitis, encephalitis
Infarction --- apoplexia, Sheehan’s syndrome
Idiopathic
o May be subclinical or present acutely
 ↓ACTH, TSH, ADH are potentially life-threatening
 ↓ gonadotropin and GH cause chronic morbidity
o Signs and symptoms of underlying diseases
 Tumor in sellar region
 Bitemporal hemianopia
 Headace
 Signs of culomotor nerve impairment/ damage to CN 3,4,5,6 in cavernous sinus
o Clinical features/ investigative findings
Clinical features Investigative findings

Corticotropin deficiency
Chronic Fatigue, pallor, anorexia Hypoglycaemia, hypoTN
Acute Weakness, dizziness, n/v, circulatory collapse, fever,
shock
Children Delayed puberty, failure to thrive
N.B. Impt to differentiate between ACTH deficiency and primary adrenal insufficiency with a secondary increase in
ACTH release
 ACTH deficiency does not cause salt wasting, volume contraction and hyperkalemia because it does not result in
clinically important deficiency of aldosterone
 ACTH deficiency does not result in hyperpigmentation
 Both forms of adrenal insufficiency can cause hyponatremia. This abnormalitiy is due to inappropriate secretion
of antidiuretic hormone (vasopressin) that is caused by cortisol (not aldosterone) deficiency
Thyrotropin deficiency
Chronic Tiredness, cold intolerance, constipation, hair loss, Bradycardia, hypoTN
dry skin, hoarseness, cognitive slowing
Children Retarded development, growth retardation
Gonadotropin deficiency
Women Oligoamenorrhoae, loss of libido, dyspareunia, Osteoporosis
infertility
Men Loss of libido, impaired sexual function, mood Decreased muscle mass,
impairment, loss of facial/scrotal/ trunk hair osteoporosis, anemia
Children Delayed puberty
ADH deficiency
Acute Polyuria, polydipsia Decrease urine osmolality,
hypoNa, polyuria
 Investigation
o Imaging
 MRI brain to exclude tumors
o Diagnostic tests
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Criteria for hormone deficiency
Corticotropic function
Morning cortisol <100nmol/L: hypocortisolism
>500 nmol/L: hypocortisolism excluded
Morning ACTH Below upper reference range: secondary adrenal insufficiency
Insulin tolerance test Cortisol < 500nmol/L
250 g ACTH test Cortisol <500nmol/L after 30min
Thyrotropic function
Free thyroxine Low (< 11pmol/L)
TSH Low or normal (occasionally slightly raised)
Gonadotropic function
Women
Clinical Oligoamenorrhoea, oestradiol < 100pmol/L, LH and FSH inappropriately low
Postmenopausal LH and FSH inappropriately low
Men
Testosterone Low (<10-12 nomol/L), LH and FSH inappropriately low
Somatotropic function
IGF-1 Below or in the normal reference range
Insulin tolerane test Adults: growth hormone ≤3g/L
Children: growth hormone ≤ 10g/L
Transition phase: growth hormone ≤5g/L
GHRH + arginine test Underweight or normal weight (BMI ≤ 25): 11.5g/L
Overweight (BMI ≥25 to <30): 8.0 g/L
Obese (BMI ≥ 30): 4.2 g/L
GHRH + GHRP-6 test Growth hormone ≤10g/L
Posterior pituitary function
Basal urine and plasma Urine volume (≥40ml/kg bodyweight per day) + urine osmolality
sample <300mOsm/kg water + hypernatremia
Water deprivation test Urine osmolality <700mOsm/kg
Raito of urine to plasma osmolality <2
 Management
o Treatment of cause
 Non-functioning pituitary adenoma → Transsphenoidal or transcranial surgery
 Craniopharyngioma difficult to access
 Prolactinoma → medical treatment with dopamine agonist
o Hormone substitution
o Follow-up
 Adequate hormone replacement should be monitored at regular intervals
 Tumor → regular ophthalmological f/u & MRI
 Prognosis
o Generally, hypopituitarism is chronic and lifelong, unless successful surgery or medical treatment of
the underlying disorder can restore pituitary function
o Increase mortality
Always replace steroids first before L-thyroxine or else patient can die!
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Medicine (Endocrine) = Gynaecomastia
Definition
 Abnormal amount of breast tissue in males
 Due to increase in estrogen/androgen ratio
Aetiology
1. Liver cirrhosis
2. Drug induced
 Cimetidine
 Spironolactone
 Digoxin
 Others: androgens, estrogns, ACE inhibitors, CCB, chronic alcoholism, isoniazid, ketoconazole
3. Endocrinopathies
 Thyrotoxicosis
 Acromegaly
 Hypopituitarism
 Addison’s disease
4. Hyperestrogenism
 Testicular failure
o Kallmann’s syndrome
o Trauma
o Viral orchitis
o Castration (medical, surgical)
o Klinefelter’s syndrome
 Paraneoplastic syndrome (Ca Lung)
5. Uraemia
6. Physcological
 Pubertal
 Senile
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Recent drug intake NSAIDs
Medicine (Renal) = Acute Renal Failure Aminoglycosides
A sudden decrease in renal function resulting in an inability to maintain fluid Contrast
and electrolyte balance and to excrete nitrogenous wastes Urinary obstruction LUTS
Signs and Symptoms
Haematuria
Uraemia Nausea
Vomiting Backpain
LOA Constipation
Fatigue Urinary instrumentation
Pruritus Glomerulonephritis Rash
Skin Bruising haemoptysis
Uraemia oesophagitis/gastritis/colitis
Pericarditis
Pleuritis Lab findings to suggest ARF
Seizures Increased Urea and Cr above baseline
Encephalopathy Increase K+ (impaired renal excretion)
Peripheral neuropathy Increased PO4 (secondary to decreased secretion from tubule
Oliguria Urine output < 400ml/day damage)
Fluid overload Lower limb oedema Decreased CA2+
Ascites
Pleural effusion/pulmonary oedema Causes of ARF
Facial oedema Pre-renal (40%)
Intrinsic renal (up to 50%)
Aetiology
Post renal (5-10%)
Sepsis
Dehydration Vomiting
Diarrhea
Poor fluid intake
Fever
Use of diuretics
CCF
Haemoptysis/melena/haematemesis
Uncontrolled HPT Compliance with medications
Fluid and salt restrictions
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Pre Renal Post Renal Intrinsic Renal
Aetiology Decreased renal Urinary Tract Obstruction within the Acute tubular necrosis Acute interstitial nephritis Acute GN
perfusion lumen Ischaemia Drug RXN Post strep GN
Sepsis Bladder calculi Nephrotoxins (penicillin/NSAIDs) IgA nephropathy
Dehydration Bladder tumour o Aminoglycosides Rapidly progressive GN
Shock Papillary necrosis o Contrast
Uncontrolled HPT Crystalluria o Chemo RX
Urinary tract obstruction within the o Rhabdomyolysis
wall
Urethral stricture
Bladder neck stenosis
Neurogenic bladder
Urinary Tract obstruction outside the
wall
BPH
Prostate CA
Constipation
CA Cervix/uterus
CA colon
Retroperitoneal fibrosis
Clinical Sepsis = Fever, Toxic LUTS (storage and voiding symptoms
features looking
Haematuria
Dehydration =
increased thrist, dry Distended bladder
mucous membranes
Decreased skin turgor, Enlarged prostate
prolonged capillary
refill time, altered
mental state
Shock = tachycardia,
hypotension
Urine Na <20 (can concentrate Variable >20 (cannot concentrate urine) <20 >20
(mmol/L) urine)
Urine >500 <350 <350 >500 <350
osmolality
(mosm/kg)
Sediment Benign/hyaline casts Normal/RBC/WBC Granular casts RBC casts WBC casts with
eosinophillia
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Investigations
Urine Bloods Imaging Bladder catheterization
UFEME FBC KUB or CT KUB Rule out urethral
Haem -> rhabdomyolysis Hb (distinguish from CRF) obstruction
Casts Eosinophillia (acute IN) Renal U/S
o Granular (acute TN) CKMM Small atrophied kidneys (CRF)
o RBC (acute GN) Rhabdomyolysis Hydronephrosis (post-renal)
o WBC + Eosinophillia (acute IN) U/E/Cr
Urine Osmolality and urine Na+ Urea > creatinine (pre-renal)
High/low (pre-renal + acute GN) Electrolyte abnormalities
Low/High (post renal + acute TN + acute IN) Autoimmune screen
ANA
Anti-dsDNA
Complement levels
ANCA
Anti-GMB Ab
Complications
Electrolyte imbalances Fluid overload Uraemia
Hyper/hyponatraemia Hypertension Pericarditis
Hyperkalaemia Pleuritis
Metabolic acidosis Encephalopathy
Hypermagnesaemia Peripheral neuropathy
Hyperphosphataemia Platelet dysfunction
Hypocalcemia Pruritus
Oesophagitis/gastritis/colitis
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Management
(a) Treat underlying cause (especially if post renal obstruction)
(b) Catheterize and monitor hourly urine output
(c) Fluid replacement – must be balanced against volume status of the patient and ability to PU
Indications for urgent haemodialysis

(a) HCO3 < 10 mmol/L
(b) Urea >20 mmol/L
(c) K+ > 6.0 mmol/L
(d) Uraemic complications = pericarditis, encephalopathy
(e) Oliguria
(f) Pulmonary oedema
(g) Severe and refractory hypertension
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Medicine (Renal) = Chronic Renal Failure
History
 Symptoms of renal failure
 Complications of renal failure
 Unrelated problem

 When was the diagnosis made?
 Presenting complaint
o Urinary symptoms
 Frequency
* urinary concentrating ability is lost early
 Volume of urine passed (polyuria/oliguria/anuria)
 Frothy urine (proteinuria)
 Hematuria
 Loin pain
o Symptoms of fluid overload
 Dyspnea
 Edema (LL/facial/ascites)
o Uremic symptoms
 LOA
 Fatigue
 Nausea/vomiting
o Males – picked up during NS?
Females – any problems during pregnancy?
 Etiology:
Common causes Renal

 DM  Renovascular disease
 HTN  Interstitial nephritis – drug history
 GN  Polycystic kidney – hematuria, loin
o VITAMIN pain, headache
 Vascular (HSP) – purpuric rash, joint pain,  Analgesic nephropathy – analgesic use
abdominal pain  Pyelonephritis – hx of kidney infection,
 Infections – hx of Hep B/C infection fever, loin pain
 Toxin (gold, penicillamine) – drug hx  Reflux nephropathy – enuresis,
 Autoimmune (SLE) – malar rash, childhood UTI, cystoscopy treatment
photosensitivity, oral ulcers, joint pain  Obstruction – dysuria, hematuria, loin
 Metabolic (DM) to groin pain, hx of stones/BPH,
symptoms of obstruction
Extrarenal
 Systemic sclerosis
 Multiple myeloma
 Amyloidosis
 Investigations done
o U/S – anatomical malformations
o Biopsy – GN
 EPO injections
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 Hemodialysis – AV fistula/graft, frequency per week, duration per session, weight gain in between HD
sessions, complications (bleeding/thrombosis/infections/problems with vascular access), fluid and dietary
restrictions, compliance
 Peritoneal dialysis – type of PD (CAPD/APD), type and volume of dialysate used, complications (infections,
catheter blockade), fluid and dietary restrictions, compliance
 On the transplant waiting list?
 Renal transplant – when (year), where (local/overseas), type (cadaveric/living related transplant), recent
graft function (graft pain and swelling, proteinuria, creatinine levels), rejection episodes and treatment,
immunosuppressants (steroids = diabetes, HPT, HCL, obesity, easy bruising, cataracts, proximal myopathy,
osteoporosis, AVN, susceptibility to infections, SCC)
 Current symptoms – urine output, fluid overload, uremia
Complications of disease
Growth Height, weight

Osteodystrophy Bone pain, fractures
Nutrition Malnutrition (LOA, LOW)
Anemia Pallor, chest pain, SOB, palpitations, giddiness, fatigue
Cardiovascular AMI/CCF, HPT, HCL, peripheral vascular disease (intermittent claudication, pain
at night/rest, parasthesia, paralysis, pallor, ‘perishingly’ cold)
Skin Pruritus, bruising
Neurology CVA, seizures secondary to electrolyte disturbances, uremic encephalopathy,
peripheral neuropathy, restless leg syndrome (frequent need to change
position)
GIT Uremic esophagitis/gastritis/colitis (melena, hematemesis, hematochezia,
abdominal pain)
Past medical history Drug history
 Main outcomes of CRF – AMI, CVA, PVD  Known drug allergy

 Co-morbidities – DM, HPT, HCL, deafness  Current medications
 Previous hospital admissions (esp for renal-related  Long-term medications – analgesia, TCM
conditions)
Prior surgeries – CTS
Family history
Social history
 Smoker  Renal failure
 Alcohol drinker  Renal diseases – APKD, Alport’s syndrome, IgA
 Days off work/school nephropathy
 Financial difficulty  Deafness
 Family set-up and caregiver  DM, HPT, HCL
 Type of housing and lift-landing
 Functional status
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General Height, weight

(adequate Sallow complexion (dirty-brown appearance due to deposition of urinary
exposure with pigments and anemia)
patient inclined at Cachexia
45 degrees) Cushingnoid appearance secondary to steroids
Edema (facial/ascites)
Vital signs (PR, RR – hyperventilation), temperature, BP
Mental state (orientated, confused, drowsy, comatose)
Hands/Arms Leuconychia
Terry’s nails (brown arc near the ends of nails)
Palmar crease pallor
Carpal tunnel syndrome
AV fistula – thrill and bruit are important signs of patency
Scratch marks
Bruising
Subcutaneous nodules (calcium phosphate or amyloid deposition)
Asterixis (in terminal CRF)
Face/Chest Fundoscopy – HTN/DM changes (at the end)
Penguinculae (amino acid deposits)
Band keratopathy (calcium deposition in the cornea)
Conjunctival pallor
Uremic fetor (musty smell)
Central line – tunneled/non-tunnelled catheter (HD)
Dehydration – poor skin turgor, dry skin
Tanner staging (breast development)
Rickety rosary ribs
Heart Raised JVP – fluid overload, right heart failure
Carotid artery bruit – atherosclerosis
Pericardial rub
Lungs Upright position – basal crepitations (APO, pneumonia), stony dull percussion
(pleural effusion)
Abdomen Upright position – nephrectomy scar (usually postero-lateral)
Supine position – scar (usually iliac fossa) overlying transplanted kidney
Tenchkoff catheter (PD)
Enlarged bladder
Ascites and fluid thrill
Ballotable kidneys – APKD (look for hepatomegaly)
Renal artery bruit (usually systolic) – RAS
Enlarged prostate (PR)
Legs Scratch marks
Edema
Neuropathy – sensory > motor deficits
PVD – hairless, shiny/dry skin, pallor, cool, gangrene, amputations
Genu varum
Others Bony tenderness (strike vertebral column gently)
Manifestations of DM, HTN, SLE
370
Investigations
 To confirm diagnosis of CRF

 To determine etiology of CRF
 To look for complications of CRF
Diagnosis U/E/Cr Creatinine to estimate GFR

Etiology Bloods Plasma glucose and HbA1C – DM
ASOT/HBV/HCV – infections
ANA/anti-dsDNA/ANCA/anti-GBM/C3/C4 – AI
LFT (albumin) – nephrotic syndrome
Urine Urine dipstick (proteinuria, hematuria, glycosuria)
UFEME
24h UTP/urine PCR (proteinuria)
Radiology KUB – stones
Renal U/S – cysts, size, symmetry, obstruction, hydronephrosis,
nephrocalcinosis
IVU – stones
DMSA/DTPA (radionuclide scans) – renal function, renal
scarring
MCU – anatomical abnormalities
Biopsy GN (if proteinuria > 1g/day)
Complications Bloods FBC – normocytic normochromic anemia
U/E/Cr
Bone panel – Ca, PO4, alkaline phosphatase, IPT, Mg, albumin
PT/PTT – normal
Radiology CXR – cardiomegaly, pleural/pericardial effusion, pulmonary
edema
Bone X-ray – renal osteodystrophy
Management
Refer early to nephrologist

Treat reversible causes = relieve obstruction, stop nephrotoxic drugs, treat hypocalcemia + HPT
Growth failure  Malnutrition – inadequate protein
 Anemia
 Osteodystrophy
 GH resistance
Osteodystrophy  Low phosphate diet – avoid dairy products (milk, cheese, eggs)
 Phosphate binders (CaCO3, Ca acetate, aluminium hydroxide)
 Calcium supplements (CaCO3, Ca acetate) – decrease renal
osteodystrophy, decrease tertiary hyper-pTH
 Vitamin D supplementation
Nutrition  Protein restriction
o HD/PD = give RDA + additional to compensate for dialysis loss
o Restrict in glomerulonephritis (0.8g/kg/day)
 Na+ restriction (2g/day) – control BP, prevent edema
 K+ restriction only if hyperkalemic or acidotic
 Phosphate restriction (800mg/day)
 Fluid restriction in ESRF + fluid overload type CRF = 500ml/day, wt gain <
1 kg/day
 Encourage fluid intake in salt-losing type CRF
Anemia  Keep Hb > 11g/dL
 Work-up (PBF, serum Fe, ferritin/transferrin/TIBC, serum vitamin
B12/folate, UFEME, stool OB, stool microscopy, OGD/colonoscopy)
371
 Mx = adequate dialysis, repeated blood transfusion, rEPO if not Fe
deficient and Hb < 10g/dL, iron and folate supplementation
CVS  HPT (ACE inhibitors/ARB) – decreases rate of loss of renal function even if
normotensive, improves proteinuria, aim for BP < 130/80
 HCL (statins) – may contribute to renal damage, increases risk of CVS
disease, rhabdomyolysis may worsen renal function
 Edema (Lasix/Frusemide) – usually given with K+ supplements
 Control CVS risk factors
Prepare for  AVF/AVG 6-8 weeks before HD
dialysis  Tenchkoff catheter 2-3 weeks before PD
 Renal transplant if suitable
Reduce drug  Antibiotics = aminoglycosides, cephalosporins, tetracycline
dosages  Lithium
 Opiates
 Digoxin
 Insulin
Discussion
A)
Chronic renal failure = substantial, irreversible and usually long-standing loss of renal function, KDOQI
defines CRF as GFR < 60 ml/min/1.73m2 for 3 or more months
Azotemia = raised level of urea and creatinine without symptoms (GFR 20-35% of normal)
Uremia = raised level of urea and creatinine with symptoms (GFR < 20% of normal)
B) Glomerular filtration rate (GFR)

 Defined as volume of blood filtered by the kidneys per unit time
 Estimated by calculating the clearance of creatinine from the blood
 Measure of the adequacy of renal function
 Normal range = 90-120ml/min
 Methods: MDRD study equation, Cockroft-Gault formula
Creatinine clearance = (140-Age) X Mass (in kg)

______________________ X 0.85 if female
72 X plasma creatinine (in mg/dL)
C) Stages of CKD
Stage GFR (ml/min/1.73m2)

1 ≥ 90
2 60-89
3 30-59
4 15-29
5 = ESRD < 15
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D) Complications of CRF
 Dehydration secondary to loss of urinary concentrating ability (early in disease course)

 Fluid overload secondary to loss of urinary excretory ability (later in disease course)
o LL edema
o Facial edema
o Pleural effusion/pulmonary edema
o Ascites
o CCF
 Electrolyte disturbances
o Sodium imbalance
o Hyperkalemia – oliguria, metabolic acidosis
o Hypocalcemia – vitamin D deficiency
o Hyperphosphatemia – secondary hyperparathyroidism
o Hypermagnesemia
o Hyperuricemia (rarely causes clinical gout)
 Renal osteodystrophy (renal bone disease)
o Due to Vitamin D deficiency – failure to hydroxylate 25-hydroxycholecalciferol, decreased Ca
absorption  secondary hyperparathyroidism
o Complications – osteomalacia, osteitis fibrosa cystic (brown tumour), osteosclerosis (enhanced
density of bone in upper and lower vertebral margins, ‘rugger-jersey’ spine), tertiary
hyperparathyroidism
 Anemia
o Failure to produce EPO
o Anemia of chronic disease
o Infections and malignancy
o Decreased lifespan secondary to uremia
o Blood loss secondary to uremic colitis/gastritis/esophagitis
o Malnutrition
 Cardiovascular effects
o Hypertension – failure to excrete Na, fluid overload
o Hypotension – damage to renal tubules leading to sodium loss
 Uremia
o Esophagitis/gastritis/colitis
o Pericarditis/pleuritis
o Anorexia, vomiting, LOA, LOW, fatigue, pruritus
o Platelet dysfunction – bleeding and bruising
o Leukocyte abnormalities – infection
o Anemia
o Encephalopathy
E) Indications for dialysis
 Severe pulmonary edema

 Uremia  uremic encephalopathy, pericarditis, pleuritis
 Hyperkalemia
 Metabolic acidosis
 Severe HPT refractory to conservative management
 Progressive deterioration of renal function (dialyse when Cr ~700-800)
 ARF (HCO3- < 10 mmol/L; hyperkalemia > 6 mmol/L; urea > 20mmol/L in the absence of
BGIT/dehydration; oliguria; pulmonary edema)
373
F) Anemia in CRF
 Investigate if Hb <11g/dL in pre-menopausal and Hb < 12g/dL in post-menopausal women

 Complications – high output cardiac failure, increased risk of IHD (angina, AMI), contributory factor to
cerebral hypoperfusion
 Management:
o Dialyse adequately (reduce urea)
o Repeated blood transfusions
 Cx: blood-borne infections (HBV, HCV, HIV, CMV), ABO-Rh incompatibility, fluid overload
(esp if patient has CCF)
o Epoietin β (Recormon) – IV and SC routes
o Prophylactic folate supplementation for dialysis patients
 Start EPO if Hb < 10g/dL and other causes of anemia have been excluded
o SC 2000-4000U 2x/week
o Target 11g/dL (do not correct to normal or too fast due to increased risk of AMI)
o Anemia causes vasodilatation therefore decrease in peripheral vascular resistance  hypotension
 hyperdynamic circulation
o If anemia is corrected too rapidly  increase in peripheral vascular resistance  vasoconstriction
 hypertension (AMI, CVA, CCF)
o Aim for Hb increase of 1g/dL per month
o S/E: flu-like symptoms, hypertension (not given if BP high)
o Very expensive ($30-50 per 2000U vial)
o If poor response, consider: inflammation/infection/malignancy, malnutrition (low albumin),
aluminium toxicity, insufficient dialysis
 Iron-deficiency anemia
o Must treat as EPO will not be effective  maximize EPO therapy (very ex)
o Transferrin – circulating transporting protein – correlates with TIBC
o Ferritin – iron-binding protein for storage
o Functional iron deficiency – low-circulating iron, high iron stores
Absolute iron deficiency – low-circulating iron, low iron stores
o Investigations:
 FBC – calculate Mentzer’s index (MCV/RBC)
 PBF
 Hemolysis – reticulocyte count, LDH, haptoglobin, Hb electrophoresis
 Iron studies – serum iron, ferritin, transferrin, TIBC, calculate transferring saturation
(iron/TIBC < 15%)
 Serum Vitamin B12 and folate
 Stool OB X 3 +/- stool microscopy
 OGD +/- colonoscopy
o Management:
 Increase dietary iron
 Iron supplements
 Fe fumarate provides more elemental iron than Fe gluconate (Sangobion)
 Latter is 1st line therapy as it contains sorbitol (prevents constipation)
 Advice to patients = take on an empty stomach, S/E include constipation, nausea and
dyspepsia
 Parenteral iron (Venofer)
 Costly
 Never give free iron  free radicals cause hepatitis
 Advantages – avoids GI S/E, compliance ensured
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G) Ca/PO4 metabolism in CKD
CKD
Decreased renal Decreased renal Acidosis secondary

excretion of PO4 mass to decreased H+
excretion
Decreased
hydroxylation of
Decreased GI Ca Vitamin D
absorption
Decreased serum Increased iPTH Increased bone

Ca secretion osteoclastic activity
Management:
 Diet
o First-line therapy
o Low phosphate diet (800mg/day) = avoid milk, cheese and eggs
 Phosphate binders
o CaCO3 (Calcichew)
 Higher elemental Ca load and better tasting
 Taken with meals  reduce phosphate
 Taken without meals  increase calcium
o Ca acetate = higher phosphate binding capacity but large and bad tasting
o MgSO4 = bad tasting, risk of Mg toxicity, common S/E of diarrhea
o Al(OH)3 = aluminium toxicity (encephalopathy, adynamic bone, constipation, dialysis dementia 
slurring of speech, facial grimacing, jerks), anemia, poor BP control, not for use for > 6 weeks
o Seralamer = amino acid polymer, good for control of acidosis but expensive
o Dialysis
o Calcium-phosphate binding product = [Ca] X [PO4]
Calcium product > 55 (calculations in mmol) OR if [Ca] 2.50 mmol/L  avoid Ca-based phosphate
binders in view of risk of metastatic calcium product deposition and accelerated atherosclerosis
o Targets = Stage 3-4 keep [PO4] < 1.5, Stage 5 keep [PO4] < 1.8
 Calcium supplementation
o CaCO3/Ca acetate between meals
o Vitamin D products (Calcitriol)
 Give if iPTH > 21 or 3X normal upper limit
 Contraindications = Ca-PO4 > 55, PO4 > 2.0 or iPTH < 15 (further suppression will impair
bone remodeling and increase risk of fractures)
 Monitoring = 6-monthly in stage 4, 4-6 monthly in stage 5
 Tertiary hyperparathyroidism
o iPTH usually > 100
o Perform U/S or Sestamibi scan to locate pTH glands
o Tx = surgical removal +/- partial reimplantation in deltoids
 Hypocalcemia
o IV CaCl2 = preferably given via CVP or large-bore IV cannula, risk of phlebitis and subcutaneous
necrosis
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1. Diuresis with IV frusemide
Medicine (Renal) = CRF with fluid overload  120-240 mg/8hrly (if serum Cr > 400 μmol/L)
Causes  80-120 mg/8hrly (if serum Cr < 400μmol/L)
1. CVS event = AMI, CCF  If no response, step up to maximum OR infusion at 30 mg/hr
2. Anaemia  Urinary catheter if no urine output > 6hrs
3. Sepsis
4. Non-compliance to fluid and salt restrictions 2. Exclude cardiac event
5. Non-compliance to medications  Check baseline ECG
# diuretics  If pt has IHD = do CK/CKMB/Trop T and repeat ECG x 3
# anti-hypertensives
3. Consider acute dialysis (if APO, severe fluid overload, acidosis or
Investigations hyperkalaemia)
 serial cardiac enzymes and ECG = exclude AMI  PT/PTT, GXM
 CXR = cardiomegaly, APO  If for dialysis = trace Hep/HIV status
 -natriuretic peptide = exclude CCF If results > 6mths = order HBsAg, Anti-HCV, HIV
 FBC = Hb (anaemia)
WCC and differential count (sepsis) 4. (Day 2) Referral plan
 U/E/Cr = worsening renal function (AoCRF)  If Cr > 400 μmol/L  assess ADL
 Ca/Mg/PO4/albumin/iPTH = renal osteodystrophy  cannot do any one ADL  refer MSW
 GXM = blood transfusion  can do all  refer renal coordinator and vascular surgeon
 LFT = exclude liver pathology  If Cr < 400 μmol/L  refer renal coordinator, MSW and vascular
 co-morbidities = hypocount, HbA1c, fasting lipids surgeon
 urine dipstick, UFEME, urine c/s = proteinuria  Others = dietician, pharmacist, PT/OT as required
exclude UTI
Management 5. (Day 3) If anaemia workup negative, consider EPO therapy

 Trace old notes
 Monitor vitals q4hrly 6. (Day 5) Review CXR = if clear, consider switching to oral frusemide
 Fluid restriction 500ml/day (if serum Cr > 400 μmol/L) if well on oral frusemide, consider discharge
800ml/day (if serum Cr < 400 μmol/L)
 Diet = low salt/protein/phosphate/potassium 7. Discharge planning
DM diet  Fluid restriction
 Strict I/O charting  Diet restriction
 Daily weights  When to seek medical help = skin turgor, pitting oedema,
 IV frusemide with span K  spironolactone weakness, fatigue, muscle cramps,
nausea/vomiting
Treatment Orders  TCU appointments
376
Medicine (Renal) = Ballotable Kidneys
Causes of ballotable kidneys
Unilateral
Adult polycystic kidney diease with asymmetrical enlargement
Renal cell carcinoma
Hydronephrosis
o Level of obstruction above the bladder
Renal cyst
Renal abscess
Renal vein thrombosis
Hypertrophy of solitary functioning kidney
o Post – nephrectomy
o Congenital absence
Bilateral
Adult polycystic kidney disease
Renal cell carcinoma
Hydronephrosis
o Level of obstruction at and below the bladder
Early DM nephropathy -> compensatory glomerular hypertrophy
Infiltrative disease
o Amyloidosis
o lymphoma
Short Case Approach

Aims = Confirm Presence of enlarged kidney
Determine aetiology
Signs of ESRF
Inspection
Distended abdomen -> ascites
Grossly enlarged kidneys
Fullness over 1 or both flanks
Vascular access (IJ, subclavian, femoral) -> ESRF
Nephrectomy scar -> hyperfunctioning of solitary kidney
J-shaped scar in iliac fossa overlying rounded mass -> transplanted kidney
Palpation
Describe characteristics of mass = size, shape, surface, edges, tender, consistency
Able to get above the mass
Does not move with respiration
No splenic notch felt
Ballotable
Percussion
Band of resonance due to overlying bowel loops
Auscultation
Bowel sounds
377
Determine Etiology
RCC = cachexic looking
APKD = hepatomegaly, splenomegaly, signs of ESRF
DM = diabetic dermopathy
Renal abscess = positive Murphy’s sign, tenderness
Signs of ESRF
AVF/AVG -> palpable thrill, signs of recent cannulation
Sallow appearance, conjunctival pallor
Uraemia -> bruising, scratch marks, asterixis
Fluid overload -> able to lie flat, ascites, lower limb oedema
Request
Vitals = temperature, BP, HR, RR
Fluid overload = Raised JVP, bibasal inspiratory crepitations
FUndoscopy = diabetic and hypertensive retinopathy
Urine dipstick = glycosuria, haematuria
APKD = CVS (MVP) + Neurological examination ( 3rd nerve palsy, focal neurological deficits, craniotomy)
378
Medicine (Renal) = Transplanted Kidney
Approach to the Short Case Examination
Aims
Confirm presence of transplanted kidney
Graft rejection and failure = tenderness, signs of fluid overload
Assess for immunosuppressant toxicity
Determine aetiology and renal failure
Short Case Approach

General inspection
o Sallow complexion -> ESRF
o Characteristic rounded facies, central obesity, acne, hirsutism, purple abdominal striae -> long
term steroids
Abdomen
o Inspection
 Distended = ascites
 J-shaped transplant scar in iliac fossa overlying a rounded mass
 Presence of tenchkoff catheter
 Surgical scars
o Palpation
 Mass under J-shaped scar -> transplanted kidney
 Determine characteristics of mass = size, shape, surface, edges, tender, consistency, bruit
 Bilateral ballotable kidneys -> aetiology
 Hepatomegaly -> methotrexate induced cirrhosis
Transplant-related hepatitis reactivation
 Hepatosplenomegaly -> transplant related hepatitis B/C induced cirrhosis
Hands
o Hypocount marks -> DM from long term steroid therapy
o Leukonychia, Terry’s Nails, scratch marks, bruising -> ESRF
o Gouty Tophi -> cyclosporine A
o Thin skin (double pinch test) -> steroids
o AVF/AVG -> signs of recent cannulation? (may suggest graft failure)
o Proximal myopathy
H&N
o Eyes
 Conjunctival pallor and penguinculae –ESRF
 Posterior subcapsular cataract -> long term steroid therapy
o Oral cavity
 Oral thrush -> steroid therapy
 Gingivial hyperplasia -> cyclosporine A
o Raised JVP -> fluid overload
o Buffalo hump, supraclavicular fat pads -> long term steroid therapy
Back
o Kyphoscoliosis, step deformity, bony tenderness -> long term steroid therapy
Lungs
o Crepitations -> infection/fluid overload
Lower limbs
o Oedema -> fluid overload
379
o Diabetic dermopathy -> aetiology
Request to
o Measure BP for HPT -> long term steroid therapy
o DO bedside hypocount and urine dipstick -> aetiology (DM)
o Fundoscopy -> aetiology (DM, HPT)
Presentation
Mdm XXX is a (age)(race)(gender) who has a transplanted kidney and is on immunosuppressive therapy.
I say this because she has a J-shaped scar in her left iliac fossa, overlying a rounded mass x cm by x cm, non
tender and firm to touch. She also has evidence of immunosuppression with a characteristic rounded facies,
central obesity, violaceous abdominal striae, oral thrush, gum hypertrophy, bruising and thin skin.
Otherwise, on examination of her abdomen, there is no hepatosplenomegaly or ascites noted.
I looked for but was unable to find any signs suggestive of the aetiology of end stage renal failure such as
bilaterally enlarged ballotable kidneys and diabetic dermopathy.
Functionally, I note that she has a left arteriovenous fistula with a palpable thrill. There are no signs of recent
cannulation which suggests that the graft is functioning well. This is supported by the fact that she does not
have any evidence of uraemia. Her appearance is not sallow, there are no visible bruising or scratch marks and
there is no bilateral lower limb pitting oedema.
Discussion
Criteria for transplant
Recipient Living related doner Cadaveric doner

ADL independent Offsprings No hepatitis B or C
No malignancies Parents No HIV
No PVD Spouses No systemic infections
No IHD 1st or 2nd degree relatives
No CVA No DM
No Active liver disease No HPT
No HBsAg or HBeAg No Hepatitis
No HIV
No Mental retardation
Medical priority cases = vascular access problems, anaemia < 7g%
Benefits of renal transplant over long term dialysis

Better quality of life
Reduced hospital expenses
Reduction in long term risk of death
Surgical processes
Retrieving the doner kidney
o Structures removed = kidney, renal arteries, renal veins, ureter
o Kidney immersed in iced saline or Ringer’s lactate solution while being prepared for
implantation (cold ischemia time)
o Time between retrieval and perfusion of doner organ with cold preservation solution = 1st
warm ischemia time
Implantation
o Kidney transplanted heterotopically (cf transplanted heart, lung and liver which are
transplanted orthotopically)
o Anastomosis = renal vein to external iliac vein, renal artery to external iliac artery
380
o If external iliac vessels too small to allow implantation e.g. paediatric pation -> aorta and IVC
used
o 2nd warm ischemia time = time taken to perform vascular anastomosis after removal from cold
perfusion solution
Location
o Usually in RIF/LIF
o Easy surgical/biopsy access
o Attached to femoral/common iliac vasculature
o Note that the original kidney is usually left in the abdominal cavity
Complications
Steroid toxicity
o Cosmetic effects
o Increased protein catabolism = proximal myopathy, paper thin skin
o Endocrine = HPT, DM, obesity, Addisonian crisis, menstrual irregularities
o Cardiovascular = premature coronary artery disease
o Bone = osteroperosis, aseptic necrosis
o Immunosuppression = opportunistic infections, lymphoma, SCC
o Others = gastritis, posterior subcapsular cataracts, steroid psychosis
Cyclosporin toxicity
o Hepatomegaly
o Hirsutism
o Hyperplastic gums
o Hypertension
o Hypercholesterolaemia
o Hyperkalaemia
o Hyperuricaemia
o Hypomagesaemia
o Haemolytic uraemia syndrome
o Osteoporosis
o Hiccupping
o Neurological
o Nephrotoxicity
o Neoplasia – lymphoproliferative
Graft rejection
o Acute or chronic -> falling urine output, rising creatinine levels
o P/E = tender graft, signs of fluid overload, presence of Tenchkoff/vascular catheter
o Invx = graft biopsy
 Gradually increasing Cr level -> cyclosporine toxicity? Chronic rejection?
 Influences management -> either stop cyclosporine or increase immunosuppression
 Recurrence of GN = FSGS, IgA nephropathy, Goodpasture’s syndrome, MPGN, Alport’s
syndrome, HUS, TTP
 Mx = methylprednisolone, monoclonal antibody, azathioprine
381
Investigations
U/E/CR
o Rising creatinie trend (slightly elevated level is acceptable in patients on cyclosporine A
o Electrolyte disturbances
FBC
o Leucocytosis
 Infection
 Steroids (increased release of mature neutrophils from BM)
o Leucopenia
 Azathioprine (dosing adjusted according to neutrophil count)
LFT (may be deranged with use of cyclosporine A and steroids)
Urine dipstick/UFEME/urine c/s
U/S Kidneys
Prognosis
2 year renal graft survival from LRDT -> 85% cadaveric transplant -> 70%
Poor prognostic indicators for post transplant survival
o Previous rejection
o Host vs Donor disease
o Delayed graft function -> usually presents with oliguria
o Hep B & C infection -> need to treat Hep C with interferon for a year before transplant is carried
out. Treatment not available for Hep B
o Paid donor transplant (e.g. China, India) -> due to higher rates of Hep B, Hep C and HIV
infections and tendency for over immunosuppression
382
Medicine (Renal) = Approach to oliguria
You have been informed that a patient post TURP in the ward has only passed 10ml today
DDX: Oliguria vs Catheter related problems
Blockage
o Kinking of tubing
o Clot/tissue fragments – esp post TURP or TURBT
o Sediment/stones –esp with chronic IDC
Malpositioning
Questions
1. Is the patient stable?
a. Oliguria may indicate patient in shock/impending shock/malignant HTN
2. Is the catheter draining? How has the urine output been?
a. If progressive less U/O -> may be oliguria
b. If sudden -> most likely cath blocked
3. Is there any haematuria/clots?
a. Clot blocking catheter
4. Is there any pain?
a. Peritonitis
b. Bladder distension with obstruction
c. Bladder spasm
When I see the patient, I would first

1. ABCs + vitals to determine if patient is stable
a. Vitals
i. Fever -> sepsis
ii. Tachycardia -> hypovolemia
iii. Malignant HTN
iv. AF -> ?emboli
b. Assess hydration status – fluid depletion vs overload
c. Fundoscopy – chronic HTN changes
d. Heart – S3
e. Lungs – Bibasal creps
f. Abdo – peritonitis, ascites, palpable bladder, bruit of RAS
g. PR – enlarged prostate, masses
2. If catheter not draining well – flush catheter 50ml NS
a. If patient is post-bladder/prostate op, always consult Uro team to do irrigation/change catheter
OR high risk of false passage/disruption of anastomoses
3. If catheter draining well, evaluate patient for oliguria as below
383
Medicine (Renal) = Approach to Proteinuria
Introduction
 normal protein excretion is < 150 mg/day
 earliest sign  microalbuminuria (30-300 mg/day)
 types of proteinuria
(a) glomerular proteinuria = mostly albumin and detected on urine dipstick
severity correlates with renal prognosis (cf haematuria)
(b) tubular proteinuria = LMW proteins (2-microglobulin, Ig light chains)
decreased proximal tubular reabsorption leads to increased excretion
not detectable by urine dipstick  require 24hr UTP
(c) overflow proteinuria = overproduction of Ig light chains in multiple myeloma
exceeds proximal tubular reabsorptive capacity
excreted Ig light chains are also toxic to tubules  further decreases reabsorption
not detectable by urine dipstick  require 24hr UTP
Causes of proteinuria
 V = hypertension
Henoch-Scholein purpura
 I = urinary tract infection
Ig A nephropathy, post-streptococcal GN
 T = drug-induced
 A = SLE
 M = diabetes
 I = amyloidosis
 N = multiple myeloma (UTP +ve, dipstick –ve)
lymphoma
 Others = orthostatic proteinuria, fever, exercise
History-taking
name/age/ethnicity/gender/occupation
past medical history
date of admission
Presentation
- positive dipstick result
- frothy urine
- haematuria
- lower limb oedema (r/o CCF, CLD, protein-losing enteropathy and malnutrition)
Aetiology
(a) Vascular = purpuric rash in childhood (HSP)
(b) Infective
 urinary tract infection
- frequency, urgency, nocturia
- haematuria, dysuria, urethral discharge
- hesitancy, intermittent and weak stream, double voiding, terminal dribbling
- loin to groin pain, nausea, vomiting, diarrhoea
 history of Hep B/C infection
 recent fever, URTI and GE
(c) Drug-induced = TCM, NSAIDs, captopril, gold, penicillamine
(d) Autoimmune = rash, joint pain and swelling
(e) Metabolic = history of DM and symptoms of hyperglycaemia
384
(f) Neoplasia = back pain, LOA, LOW, fatigue, fever
Complications
- oliguria
- lower limb oedema, abdominal distension, dyspnoea, facial oedema
- hypertension
Systemic review
Management
Has this happened before? Please describe

hypertension
childhood GN
diabetes
autoimmune conditions = SLE, PAN
pre-eclampsia during pregnancy
picked up during NS
cardiac or liver problems
Drug history
drug allergies
current medications
 gold and penicillamine  secondary membranous GN
 NSAIDs and penicillin  allergic interstitial nephritis
Social history
Family history
385
Investigations
Urine
 urine dipstick = proteinuria, haematuria, glycosuria
 UFEME
 urine phase contrast microscopy = dysmorphic/isomorphic RBC
 urine c/s (mid-stream catch) = UTI
 24hr UTP/CCT or urine PCR = nephrotic syndrome
Bloods
 FBC = anaemia/leucopenia/thrombocytopenia (SLE)
 U/E/Cr = renal impairment
 Ca/PO4/Mg = renal impairment
 LFT = hypoalbuminaemia
 ESR and CRP
 Hepatitis screen = HBsAg, HBeAg, anti-HCV Ig G
 AI screen = anti-ds DNA, ANA, C3/C4, anti-GBM, ANCA
 fasting glucose and HbA1c = diabetes
 myeloma screen (for those > 45 yrs old) = serum and urine protein electropheresis
Others
 Renal U/S
 Renal biopsy
Management
 orthostatic proteinuria (a/w upright position and in adolescents) = good renal prognosis
no follow-up required
 intermittent isolated proteinuria (a/w stress and exercise) = favourable prognosis
follow-up till proteinuria resolves
 persistent isolated proteinuria = follow-up indefinitely with monitoring of BP and U/E/Cr
 combined microscopic haematuria and proteinuria = most common presentation of GN (esp Ig A
nephropathy)
 fluid overload = fluid restriction
low-salt and protein diet
strict I/O charting with daily albusticks and weights
monitor vitals q4hrly
diuretic therapy (PO Lasix 40mg OM with PO Span K 0.6mg OM)
ACE inhibitors/ARB (PO Losartan 25mg OM)
386
Medicine (Renal) = Haematuria
Introduction
 Microscopic haematuria (≥3 RBC/hpf) should undergo evaluation to exclude renal or urinary tract
pathology
 Evaluate for presence of
o Proteinuria = 24hr urinary protein, urine PCR
o Hypertension = BP
o Renal impairment = U/E/Cr
 Differentials
o Medications = ibuprofen, nitrofuratoin, chloroquine, rifampicin
o Food dye = beets, food colouring
o Metabolites = bile, porphyria, urate, tyrosinosis
Causes of haematuria
Renal – microscopic haematuria
 Vascular = Henoch-Scholein purpura, Wegener’s granulomatosis, Goodpasture’s syndrome
 Infective = post-streptococcal GN, Ig A nephropathy, UTI
 Trauma = blunt abdominal trauma
 Autoimmune = SLE
 Neoplasia = renal cell carcinoma
 Familial = adult polycystic kidney disease (APKD), thin BM disease, Alport’s syndrome (X-linked)
Urinary tract (TITTS) – gross haematuria

 TB
 Infection = cystitis, prostatitis
 Trauma = urinary catheterisation, flexible cystoscopy, post-TURP
 Tumour (bladder, prostate, ureter)
o Kidneys (APKD, RCC, renal vein thrombosis)
o Transitional cell carcinoma of ureters and renal pelvis
o Bladder tumour
o Prostate (BPH, prostatic cancer)
 Stones
Systemic
 Bleeding diasthesis = thrombocytopenia
HISTORY
Drug allergy
Date of admission
 Haematuria
o Microscopic = cloudy/smoky
o Gross = Beginning of flow (urethra)
End of flow (bladder)
Throughout flow (renal)
o Present every time
387
o Presence of blood clots
o Amount of blood loss  symptomatic anemia (pallor, exertional chest pain, palpitations, SOB,
giddiness, fatigue)
o Painful/painless (dysuria, flank/loin pain)
 Proteinuria = frothy urine
 Renal impairment = amount of urine (oliguria, polyuria)
Fluid overload (lower limb oedema, abdominal distension, dyspnoea, facial oedema)
Aetiology
 Renal
o Vascular = purpuric rash over lower limbs, lower limb oedema, joint pain, abdominal pain (HSP)
Haemoptysis (Goodpasture’s syndrome)
o Infective = recent fever and URTI (post-streptococcal GN)
Ongoing fever and URTI/GE (IgA nephropathy)
o Autoimmune = history of SLE
Rash, joint pain and swelling
o Neoplasia = fever, flank pain, palpable abdominal mass (RCC)
o Familial = personal and family history of APKD
History of deafness (Alport’s syndrome)
 Urinary tract
o History of TB
o Infective/stones = frequency, urgency, nocturia, dysuria, urethral discharge, obstructive
symptoms,
loin to groin pain, fever, nausea, vomiting, diarrhea
o History of trauma = history of urinary catheterisation, flexible cystoscopy, TURP
o Tumour = LOA, LOW, fatigue, back pain
 Systemic
o Bleeding diasthesis = gum bleeding, epitaxis, menorrhagia, easy bruising
Systemic review
Management
Has this happened before? Please describe

 Adult polycystic kidney disease
 Hypertension
 Deafness (Alport’s syndrome  secondary membranous GN)
 Urolithiasis
Menstrual history
 Last menstrual period  could be menstrual blood
Drug history
 Drug allergies
 Current medications = penicillamine, rifampicin, hydralazine
 Anticoagulants = TCM, NSAIDs, warfarin, aspirin
Social history
Family history
388
 Adult polycystic kidney disease
 Hypertension
 Renal disease
 Deafness (Alport’s syndrome)
 Urolithiasis
 Skin = purpuric rash, digital vasculitis
 Mouth = injected pharynx, tonsillitis
 Fluid overload = raised JVP, lower limb oedema, hepatomegaly, bibasal inspiratory crepitations
 Enlarged ballotable kidneys
 PR = prostate enlargement
 Vitals = temperature, BP
Investigations
Urine
 Urine dipstick = proteinuria, haematuria
 UFEME
 Urine phase constrast microscopy
o Predominantly dysmorphic  glomerular origin
o Predominantly isomorphic or mixed isomorphic/dysmorphic  urinary tract origin
 Urinary c/s = rule out UTI
Bloods
 FBC = WCC (UTI)
Hb (anemia)
Platelet (thrombocytopenia)
 U/E/Cr = renal impairment
Glomerular origin
 24hr UTP/CCT or urine PCR if urine dipstick ≥ 2+ proteinuria
 ESR, CRP
 AI screen = anti-ds DNA, ANA, C3/C4, ANCA, anti-GBM Ab
 Renal U/S = polycystic kidneys, RCC
 Renal biopsy = glomerulonephritis
Non-glomerular origin
 KUB
 U/S or CT KUB (without constrast)
 IVU
 Urine cytology
 Flexible cystourethroscopy
389
Medicine (Renal) = Glomerulonephritis
Glomerulus
 consists of an anastomosing network of capillaries invested by 2 layers of epithelium
(a) visceral epithelium  incorporated into and part of the glomerular capillary wall
(b) parietal epithelium  lines Bowman’s space
 glomerular capillary wall is the filtering membrane
(a) fenestrated endothelium of capillaries
(b) glomerular basement membrane
- negatively-charged layer  prevent charged solutes from passing through e.g. proteins
- intersecting fibres  limit size of solutes passing through
(c) epithelial slits of visceral podocyte epithelium
- foot processes (pedicels) interdigitate to form filtration slits
 glomerular tuft supported by mesangial cells lying between capillaries = contractile
synthesize collagen and ECM
 allows for plasma ultrafiltration  high permeability to water and small solutes
impermeable to large and charged solutes
 charges on GBM changes in diseased states  proteinuria
Glomerular diseases
2nd leading cause of ESRF  accounts for 1/3 of cases
leading cause is diabetic nephropathy
hallmarks of glomerular disease = haematuria and proteinuria (HPT, renal impairment, oedema)
major clinical syndromes = isolated microscopic/gross haematuria
isolated proteinuria
asymptomatic haematuria and proteinuria
acute nephritic syndrome
nephrotic syndrome
nephritic-nephrotic syndrome
rapidly progressive GN (acute nephritis that results in rapid loss of renal function
over
weeks to months  Goodpasture and Wegener’s)
principles of treatment
(a) acute/immunological phase (immune complexes/cytokine/antibody-mediated injury) =
immunosuppressants
(b) chronic phase (injury due to glomerular hyperfiltration  proteinuria, HPT, azotemia)
- ACE inhibitors/ARB = blocks angiotensin-2 mediated vasoconstriction of efferent arteriole
- dietary protein restriction = reduces macromolecular traffic and afferent arteriolar vasodilatation
 reduces intra-glomerular HPT and glomerular hyperfiltration  less
endothelial
cell and platelet damage
- dipyridamole and warfarin = reduces intra-glomerular coagulation
 Primary glomerulonephritis  kidney is the only organ involved

(a) minimal change disease
(b) focal segmental GN
(c) membranous GN nephrotic syndrome
(d) membrano-proliferative GN
(e) diffuse proliferative GN acute nephritic syndrome
(f) crescentic (rapidly progressing) GN
(g) Ig A nephropathy (can present as both nephrotic and nephritic syndrome)
 Secondary glomerulonephritis  kidney is not the predominant organ involved

(a) vascular = HSP, PAN, Wegener’s granulomatosis (*)
(b) infective = Hep B, Hep C, HIV, malaria, post-streptococcal
390
(c) toxins = NSAIDs, captopril, gold, penicillamine, TCM
(d) autoimmune = SLE, Goodpasture syndrome
(e) metabolic = DM
(f) infiltrative = amyloidosis
(g) neoplasia = multiple myeloma, lymphoma
(h) hereditary disorders = Alport syndrome, Fabry disease
(*) causes systemic vasculitis and crescentic (rapidly progressing) GN
Nephrotic syndrome
Minimal change disease (lipoid nephrosis)

 accounts for 80% of cases in children and 30% in adults
 pathogenesis = primary defect in T cells causes elaboration of factor that affects nephrin synthesis
loss of epithelial foot processes
 LM  glomeruli appear nearly normal
PCT cells often laden with lipids (2 tubular reabsorption of lipoproteins)
FM  negative
EM  diffuse loss of visceral epithelial foot processes
no electron-dense deposits
 clinical features = selective proteinuria (usually albumin)
no renal impairment, HPT or gross haematuria
normal serum complement
steroid-responsive (> 80% achieve complete remission by 16 weeks)
 excellent prognosis (< 5% progress into ESRF)
 relapses less frequent in adults and with increasing age
 disease patterns
(a) complete remission = absence of proteinuria with normal serum albumin levels
(b) partial remission = proteinuria 0.5-3g/day
(c) relapse = reappearance of proteinuria > 3g/day with hypoalbuminaemia
(d) frequently relapsing = initially steroid-responsive but with  2 relapses within 6 months or  4
relapses
within 1 year
(e) steroid-dependent = initially steroid-responsive but relapses during tapering of steroids or
within 4 weeks
of discontinuing steroids
(f) steroid-resistant = no remission after 16 weeks of appropriate steroid therapy ( to repeat
renal biopsy)
Focal segmental GS
 pathogenesis
~ primary (idiopathic)
~ secondary = reflux nephropathy, Ig A nephropathy, Alport’s syndrome, neoplasia, HIV, drugs
 LM  sclerosis affecting some but not all glomeruli (i.e. focal)
involves only segments of each glomeruli (i.e. segmental)
foam cells (monocytes filled with lipid)
increased mesangial matrix
hyalinosis (deposition of hyaline masses)
FM  granular pattern of Ig M and C3
EM  loss of visceral epithelial foot processes
epithelial cell detachment from GBM
 clinical features = non-selective proteinuria
higher incidence of microscopic haematuria and hypertension (> 50% each)
50% progress to ESRF within 10 years of diagnosis if left untreated
recurs in 50% of renal-transplant patients (highest rate)
391
poor response to steroid therapy
 Tx = high-dose prednisolone
cyclophosphamide/cyclosporin A (latter preferred as 2nd-line therapy)
mycophenolate mofetil
tacrolimus
plasmapheresis (but results are disappointing)
Membranous GN
 pathogenesis
~ primary membranous GN  in-situ immune complexes
~ secondary membranous GN  circulating immune complexes
 causes = idiopathic (85%)
infective, drugs (gold, penicillamine, NSAIDs), SLE, neoplasia
 LM  enlarged glomeruli but normocellular (no proliferation)
diffuse thickening of GBM
multiple projections from GBM forming spikes (close over deposits to incorporate them)
FM  granular pattern of Ig G and C3
EM  subepithelial electron-dense deposits
loss of visceral epithelial foot processes
 clinical features = non-selective proteinuria
may not respond to steroid therapy
Membrano-proliferative GN
 pathogenesis
(a) Type 1 MPGN = presents as nephrotic syndrome
- due to circulating immune complexes
- associated with Hepatitis B/C infection and SLE
(b) Type 2 MPGN = presents as either nephrotic or nephritic syndromes
- due to circulating immunoglobulin (C3 nephritic factor)
- C3 nephritic factor reacts with C3 convertase  activates alternative complement pathway
- lab findings = low serum C3 levels
 LM  large glomeruli with proliferation of mesangial cells
thickened GBM (double-contour BM)
FM  type 1 MPGN = granular pattern of C3 and Ig G
type 2 MPGN = granular pattern of C3 (no Ig G)
EM  type 1 MPGN = subendothelial electron-dense deposits
type 2 MPGN = subendothelial extremely electron-dense deposits dense-deposit disease
 poor prognosis = no complete remission
50% progress to ESRF
type 2 MPGN has a worse prognosis and recurs in renal transplant patients
Ig A nephropathy (Berger’s disease)

 epidemiology = most common form of primary GN worldwide and locally (52%)
one of the most common causes of recurrent microscopic/gross haematuria
affects all ages (esp children and young adults  seldom seen in infancy or > 50 yrs
old)
 pathogenesis
(a) defective immune regulation (genetic/acquired)
- Ig A is the main immunoglobulin in mucosal secretions
- increased Ig A synthesis in response to URT or GIT exposure to environmental agents
- immune-complexes get entrapped in mesangium  activate alternative complement pathway
(b) defective Ig A clearance
- abnormality in glycosylation of Ig A reduces plasma clearance
(c) defective immune complex clearance
- defective hepatobiliary clearance of Ig A immune complexes
392
 LM  glomeruli may be normal or show segmental inflammation/mesangial proliferation
RBC casts in tubules
FM  Ig A in the mesangium
EM  electron-dense deposits in the mesangium
 clinical features = asymptomatic haematuria and proteinuria (most common presentation)
gross haematuria (1-2 days after URTI (‘synpharyngitic’) which lasts for several
days and
subsides  recurs every few months; a/w loin pain)
nephrotic syndrome (uncommon presentation)
nephritic syndrome
ARF (uncommon presentation = crescenteric GN; gross haematuria with marked
ATN)
chronic renal failure
 typical patient profile = young male with episodic macroscopic haematuria ppt by infections
(pharyngitis)
recovery usually rapid between attacks
 investigation = elevated serum Ig A (usually low)
 management
(a) isolated haematuria = no specific therapy recommended
monitor every 3-12 mths for HPT, proteinuria and renal impairment
(b) haematuria and proteinuria = < 1g/day  no specific therapy recommended
monitor for HPT, proteinuria and renal impairment
> 1g/day  treat
# ACE inhibitors/ARB = anti-HPT, reduces proteinuria, slows rate of decline of renal function
MOA  reduces intra-glomerular pressure
reduces mesangial proliferation and matrix production
# anticoagulation (dipyridamole and warfarin) = intra-glomerular HPT  endothelial cell
damage 
platelet aggregation and activation of coagulation
# dietary supplementation with fish oil = used when proteinuria > 3g/day
MOA  reduces glomerular/interstitial inflammation,
platelet aggregation and vasoconstriction
results are not conclusive
# steroid therapy = indications  persistent proteinuria > 1g/day
progressive renal impairment despite adequate BP control
(c) nephrotic syndrome = steroids  cyclophosphamide  cyclosporin A
(d) acute renal failure = renal biopsy to determine treatment  may need dialysis
crescenteric GN  methylprednisolone pulse, oral pred/cyclophosphamide,
dipyridamole and warfarin, plasmapheresis/IVIG
 prognosis
- not a benign disease  30-50% eventually develop ESRF after 30 yrs
- prognostic factors
Clinical Histological
severity of proteinuria chronic tubulo-interstitial fibrosis
renal impairment extensive crescents (> 30-50%)
mean arterial pressure advanced glomerulosclerosis (>
(hypertension) 20%)
medial hypertrophy of arterioles
Acute nephritic syndrome

 clinical complex consisting of
(a) gross haematuria (dysmorphic RBC and RBC casts)
(b) hypertension
393
(c) some degree of oliguria and azotemia
(d) mild proteinuria and oedema  not as marked as in nephrotic syndrome
 pathogenesis
- inflammation  capillary wall damage  haematuria and reduction in GFR
- reduced GFR  oliguria and sodium retention  increased plasma volume  decreased renin
activity
- HPT, raised JVP, hepatomegaly
 causes = primary glomerular causes  Ig A nephropathy
secondary causes  V (HSP, PAN, Wegener’s granulocytosis)
I (Hep B, Hep C, post-streptococcal GN)
T (penicillamine)
A (SLE, Goodpasture’s syndrome)
 management
- monitor vitals q4hrly (esp BP)
- fluid restriction in oliguric patients
- low-salt diet
- protein restriction in uraemic patients
- strict I/O charting
- daily weights
- diuretics and anti-hypertensives in mild-moderate HPT
Diffuse proliferative (post-streptococcal) GN

 pathogenesis = immune complexes  exogenous (post-infectious e.g. streptococcal, pneumococcal,
staphylococcal, Hep B/C)
endogenous (SLE)
 post-streptococcal GN usually develops 1-4 weeks after patient recovers from group A
streptococcal infection (-haemolytic streptococcal infection of the pharynx and the skin)
 LM  glomerular proliferation
leukocytic infiltrate
RBC casts in tubules
FM  granular Ig G and C3 deposition
 clinical features = abrupt onset  malaise, fever, nausea, nephritic syndrome
complete recovery in 50-95% of cases
 investigations = low serum complement levels
elevated serum anti-streptolysin O titres
renal biopsy rarely needed
 management = bed rest, salt and fluid restriction, diuretics, anti-hypertensives, dialysis if uraemic
 excellent prognosis (recovery is the rule!) = 20% may develop CRF later
ESRF rarely occurs
Crescentic (rapidly progressing) GN

 clinical syndrome and not a specific aetiologic form of GN
 results in rapid loss of renal function within weeks to months leading to ESRF
 aetiology
(a) primary systemic vasculitis = Wegener’s granulomatosis, PAN, giant-cell arteritis, Takayasu’s
arteritis
(b) secondary systemic vasculitis = SLE, HSP, RA, Behcet’s disease, cryoglobulinaemia
(c) Goodpasture’s syndrome (anti-GBM disease) = anti-GBM Abs may bind to pulmonary alveolar
capillary
basement membrane  pulmonary haemorrhages
Mx = plasmapheresis
(d) primary GN = Ig A nephropathy, membranoproliferative GN, membranous GN
(e) secondary GN = post-streptococcal GN
(f) malignancy = lymphoma, carcinoma
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(g) drugs = penicillamine, rifampicin, hydralazine
 Gross pathology = kidneys are enlarged and pale
petechial haemorrhages on the cortical surfaces
glomeruli may show focal necrosis and thrombosis
 LM  presence of crescents (proliferation of parietal epithelial cells and leukocyte infiltration in
Bowman’s
space)
crescents eventually obliterate Bowman’s space and compress the glomeruli  scarring
distinct ruptures in GBM
 clinical features = loin pain, haematuria, oliguria, non-specific symptoms (malaise, LOA, fever)
death may result from renal failure if untreated
 management = methylprednisolone pulse, high-dose corticosteroids,
cyclophosphamide/cyclosporin A,
plasmapheresis, dialysis, renal transplant
must be treated aggressively! (delay in diagnosis and treatment increases risk of
ESRF)
 poor prognosis = esp if initial serum Cr > 600
may be related to the number of crescents
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Medicine (Renal) = DGIM Renal Transplant
ESRD
 50% are due to diabetes – patients are usually not suitable for transplant due to comorbidities
 other 50% due to other causes suitable for transplant – patients usually do better, have lower mortality and is
cheaper to treat
ESRD
Low dependency High dependency

(ie relatively healthy)
 Eg malignancy, HPT, DM ,
 Suitable for transplant IHD, ADL dependent
 Aim for living related donor  Unsuitable for transplant
 If no living related donor  Perform dialysis (HD or PD)
available, listed on cadaveric
donor waiting list
Criteria for transplant

Recipient Living related donor Cadaveric donor
 < 60 YO  Siblings  <65 YO
 ADL independent  Offsprings  no hepatitis B or C
 No malignancies  Parents  no HIV
 No PVD  Spouse  no systemic infections
 No IHD  1st or 2nd degree relatives
 No CVA  no DM
 No active liver disease  no HPT
 No HepBsAg or HepBeAg  no Hepatitis
 No HIV  no disease
 No mental retardation
Medical Priority cases:
 vascular access problems
 Anaemia <7g%
Poor Px indicators for post-transplant survival

 Previous rejection
 Host Ab vs donor
 Delayed graft function – usually presents with oliguria
 Hep B & C – need to treat Hep C with interferone for a year first and check that it is successfully treated before
transplant is carried out. Treatment not available for Hep B
 Paid donor transplant (eg China, India) – due to high rates of Hep B, Hep C and HIV infections and a tendency
for over immunosuppression with drugs given by overseas doctors.
396
Management pathway for transplant recipient
Check Graft function
Possible Delayed graft function Immediate graft function

(urine output <50ml/hr) (urine output >50ml/hr)
Exclude inadequate renal perfusion as
cause of delayed graft function Determine level of
 Check CVP immunosuppression required based
 Check perfusion scan on PRA (?antigen levels)
If CVP > 10 cm H2O

Give IV Lasix 80-120mg stat
PRA  25 PRA < 25
FK506 Cyclosporine A
+ Azathioprine + Azathioprine
Impaired Normal + prednisolone
+ prednisolone
perfusion perfusion + Zenapax
Surgery Lasix Lasix

responsive unresponsive
+ Delayed Mx of Delayed Graft Function

graft function  Daclizumab < 6 hrs post
anastomosis
 Cyclosporine A: monitor levels to
Determine level of avoid toxicity
immunosuppression required based
on PRA
Day 5-7
PRA  25 PRA < 25

Cyclosporine A Cyclosporine A PT still dialysis PT recovering
+ MMF + Azathioprine dependent
+ prednisolone + prednisolone
+ Zenapax + Zenapax Renal biopsy of
allograft kidney:
Check for rejection
397
Medicine (GIT) = Hepatosplenomegaly
Causes
Vascular Chronic liver disease with portal hypertension
Viral (hepatitis, IMS, CMV)
Infective
Protozoal (malaria)
Trauma Haematoma
SLE
Autoimmune
RA
Storage disorders (Gaucher = type 1 subtype; Niemann-
Metabolic
Pick)
Amyloidosis
Infiltrative
Sarcoidosis
Myeloproliferative disorders
Neoplastic Lymphoma
Lymphoproliferative disorders
Chronic haemolytic anaemia (spherocytosis, G6PD
Haematological
deficiency, thalessemia)
-thalessemia major
Short stature
Hyperpigmented
Overall
Thalessemic facies (frontal bossing, flat nosebridge,
maxillary hyperplasia)
Looks younger for age
Pituitary haemosiderosis Hypopigmented areolae
Loss of axillary hair
JVP v wave
Cardiac haemosiderosis Pulsatile liver
Lower limb edema
Hypocount marks on fingers
Pancreatic haemosiderosis
Diabetic dermopathy
Intervention Splenectomy
Request Gonadal examination
Template for presentation

“In summary this patient has hepatosplenomegaly likely secondary to liver cirrhosis complicated by portal
hypertension. I say this because of
e) Evidence of stigmata of CLD found on peripheral examination
f) Presence of hepatomegaly measuring __cm along the mid-clavicular line and of ___consistency
g) Presence of splenomegaly measuring __cm
h) Features suggestive of portal HPT
This is/is not complicated by hypoalbuminaemia or hepatic encephalopathy”
398
Medicine (Respi) = General Approach to a History of Shortness of Breath
General Questions About SOB

 Tell me about the condition / describe what happened?
 When it started?
 Triggers
 Duration
 Relief
 Progression
Differentials
 Cardiac
 Respiratory
 Anemia
 Psychological
System Subset Question
Cardiac Any chest pain? Character?
Any PND?
Any Orthorpnoea?
Leg swelling?
Respiratory Parenchyma Cough?
Phlegm?
Haemoptysis?
Fever?
Airway Wheeze?
Stridor?
Pleura Trauma?
Acute pain followed by SOB?
Vasculature Prolonged immobility?
Haematological Anemia Palpitations
Giddiness / Light headedness
Bleeding – PR, Menses
Neuromuscular Generalised weakness?
Psychological Hyperventilation Association with certain situations
Tingling in hands / feet?
Cramps?
Severity
 NYHA Score / Effort Tolerance
 Impact on ADL
399
Medicine (Respi) = Acute Respiratory Distress Syndrome (ARDS)
Definition
 Clinical syndrome characterised by acute onset of respiratory distress either caused by direct lung
injury or secondary to severe systemic illness
 worst end of the spectrum for acute lung injury
 Criteria for diagnosis
1. Acute onset
2. Bilateral infiltrates on CXR
3. P/F ratio < 200 [P/F ratio < 300 = acute lung injury]
4. Exclude left heart failure
 Mortality of ARDS ~ 30-50%
Aetiology
Direct lung injury Indirect lung injury

Lung infection = miliary TB Systemic infection (most common)
Inhalants = nitrogen dioxide Shock
sulphur dioxide
Drugs = chemotherapeutic drugs Miscellaneous = drowning
insecticides high altitude
heroin SLE
kerosene air embolism
paraquat (pesticide) acute pancreatitis
liver failure
Aspiration
Pathogenesis
 due to diffuse alveolar damage (epithelial  endothelial damage)
 lungs particularly vulnerable to inflammatory injury = mediators released into bloodstream and
lungs receive entire cardiac output
 pathology = hyaline membrane formation
increased capillary permeability and oedema
interstitial inflammation and fibrosis
damage to type 2 pneumocytes (surfactant abnormalities and alveolar collapse)
 results in hypoxia due to V/Q mis-match and reduced lung compliance
3 stages
1. Exudative stage (0 – 7 days)
- capillary congestion, oedema (increased permeability) and haemorrhage
2. Proliferative stage (1 – 3 weeks)
- proliferation of interstitial fibroblasts and type 2 pneumocytes to replace sloughed type 1 cells
3. Resolution
- diffuse interstitial fibrosis interspersed with dilated distorted air spaces (honeycomb lung)
Complications
 Reduction in lung compliance (stiff lungs) = diffuse interstitial fibrosis
 Respiratory failure = V/Q mismatch
 Pulmonary hypertension = hypoxic vasoconstriction
vascular compression by positive airway pressure
lung parenchymal destruction
 Cor pulmonale = rare but associated with increased mortality if present
 Death
400
Clinical features
History
- Acute onset of breathlessness
- Cyanosis
- Tachypnoea
- Bilateral fine end-inspiratory crepitations
Investigations
 FBC
 U/E/Cr
 LFT
 PT/PTT
 CRP
 ABG
 Bld c/s
 Amylase
 CXR
- diffuse bilateral fluffy alveolar infiltrates with prominent air bronchograms
- absence of heart failure
 Pulmonary artery catheter to measure pulmonary capillary wedge pressure
Management
 Admit to ICU
 Respiratory support = mechanical ventilation
 Rescue therapy
- Recruitment of alveoli = PEEP
- Prone positioning
- High frequency ventilation
 Circulatory support = haemodynamic monitoring, inotropic support, vasodilators, blood
 Treat underlying cause e.g. sepsis
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Medicine (Respi) = Systemic approach to CXR
1. Name, date and projection

 check that it is the correct patient
 check the left/right marker to prevent missing dextrocardia (apex on the right and stomach bubble on
the left)
 AP and supine films are second-best cf PA films
- AP  heart appears enlarged (cannot comment accurately on heart size)
- supine  distension of posterior vessels lung fields appear plethoric
heart appears enlarged
”This is the erect AP/PA chest x-ray of Mr/Mdm ______ taken on the_____..”
2. Rotation, penetration, degree of inspiration

 rotation = medial ends of clavicles should be equidistant from the midline spinous processes
- if one clavicle is nearer than the other  lung on that side will appear whiter
 penetration = vertebral bodies should only just be visible through the cardiac shadow
- too clearly visible  over-penetration
- cannot see at all  under-penetration
 inspiration = 6th anterior rib should cut the midpoint of the right hemidiaphragm in the midclavicular
line
- poorly inspired film  heart appears enlarged, basal shadowing, trachea deviated to the right
“The quality of the film is good = with no rotation, good penetration and taken on full inspiration.”
3. Mediastinum
 trachea = should lie in the mid-line
- comment on the presence of ETT
- pushed away by large pleural effusion, pneumothorax, mediastinal mass or tumour
- pulled by lung collapse or fibrosis
 thin and slender mediastinum = COPD
4. Hilum
 characteristics = mostly formed by the pulmonary arteries with the upper lobe veins superimposed
left hilum is higher than the right
 hilar enlargement = lymphadenopathy, large pulmonary artery
5. Heart
 characteristics = straddles mid-line with 1/3 to the right and 2/3 to the left
right heart border formed by right atrium; left heart border by left ventricle
transthoracic diameter → widest diameter above the costophrenic angles
cardiac diameter → draw a vertical line from the trachea to the heart (assuming no
deviation)
sum of the 2 greatest lengths from the vertical line to both heart
borders
- cardiomegaly = cardiothoracic diameter > 50%
6. Diaphragm
 characteristics = right hemidiaphragm should be higher than the left
 loss of costophrenic angle with meniscus = pleural effusion
 loss of diaphragmatic outline = lower lobe consolidation
 low and flat hemidiaphragms = COPD
 air below the diaphragm = free peritoneal gas (likely perforation)
402
7. Lung fields
 division = apices → lie above the level of the clavicles
upper zone → include the apices to the level of the 2nd costal cartilage
middle zone → lie between 2nd and 4th costal cartilage
lower zone → lie between 4th and 6th costal cartilage
 loss of cardiac silhouette  middle lobe consolidation
 increased translucency  hyperinflation
8. Bone and soft tissue

 rib fractures
 bone metastasis
 subcutaneous emphysema
The heart
 lateral film
- posterior border of heart shadow made up of left ventricle
- anterior border of heart shadow made up of right ventricle
- mitral/aortic valve = draw imaginary line from apex of heart to hilum
# above line  aortic
# below line  mitral
Causes of a white lung

 consolidation
 pleural effusion
 collapse
 fibrosis
 pneumonectomy
 raised hemidiaphragm
Lung collapse
 PA film
(a) lung fields  smaller on the side of collapse
(b) elevation of hemidiaphragms  left may be higher than the right if there is left lung collapse
(c) horizontal fissure (runs from centre of right hilum to level of 6th rib in the axillary line)  pulled up
in right
upper lobe collapse; pulled down in lower lobe collapse
(d) mediastinal deviation  heart should straddle midline with 1/3 to the right and 2/3 to the left
(e) heart borders  blurring of right heart border (right middle lobe collapse)
blurring of left heart border (lingular collapse)
(f) tracheal deviation
 lateral film
(a) displacement of horizontal and oblique fissures
Consolidation
 radiological features
(a) heterogenous shadowing = gets denser and more clearly demarcated at lower border (fluid sinks)
(b) air bronchogram
(c) demarcated by horizontal fissure in right upper lobe pneumonia
Coin lesion
 discrete opacity situated within a lung field
 causes
(a) benign tumour = hamartoma
(b) malignant tumour = bronchial carcinoma, single secondary
403
(c) infection = pneumonia, abscess, TB, hydatid cyst
(d) rheumatoid nodule
 description
- location
- edges = speculated/irregular/lobulated edge  malignancy
well-circumscribed  benign
- nature of shadowing = if centre darker than periphery  cavitation
- calcification (present  unlikely malignant)
- air bronchogram
- air-fluid level
- other coin lesions (likely mets)
- mediastinal LAD or bone mets
Cavitating lung lesion

 causes
(a) lung abscess
(b) neoplasm
- centre of lesion darker than periphery
- air-fluid level may be seen
- thickness of wall (thicker  likely neoplasm)
- white ball seen within cavity  aspergilloma
Left heart failure

(a) upper lobe diversion
- width of upper lobe blood vessel is wider/same size as that of lower lobe vessel
- first sign of heart failure = due to lower zone arteriolar vasoconstriction 2 alveolar hypoxia
- only applicable on erect film  upper lobe diversion normal on supine film
(b) bat’s wing appearance
- severe pulmonary oedema giving rise to confluent alveolar shadowing spreading out from hila
(c) Kerley B lines
- oedema of interlobular septa
- horizontal white lines best seen just above costophrenic angles
(d) cardiomegaly
404
Bronchiectasis
 ring shadows
- ‘bunches of grapes’ appearance
- represent diseased bronchi seen end on
 tramline shadows
- seen at lung peripheries
- consists of 2 thick white parallel lines
separated by black
- represent diseased bronchi seen side on
 tubular shadows
- solid thick white shadows
- represent bronchi filled with secretions
seen side on
 glove finger shadows
- represent group of tubular shadows seen
end on
Pulmonary fibrosis
(a) fine reticulonodular shadows
extending into axillary aspect of
each hemithorax
(b) decrease in lung volume
(c) early  ground-glass appearance
late  honeycomb appearance
(d) mediastinal shift towards
shadowing
405
Medicine (Respi) = Lung Cancer
Epidemiology
 most common cancer in Singaporean males
 2nd most common cancer in Singaporean females
 very strong association with cigarette smoking
Risk factors
1. Smoking
- increases risk by 10-30x
- pathogenesis = genetic damage  squamous metaplasia  dysplasia  CIS  invasive
- cessation of smoking es risk = drops to 2x the risk of a non-smoker if abstain for 10-15 years
- passive smoking doubles the risk of lung cancer
- a/w small cell lung carcinoma and squamous cell carcinoma
2. Genetic predisposition
- cyt p450 polymorphism  increased metabolism of pro-carcinogens  higher risk
- p53 mutation
3. Occupational factors
- radioactive materials
- asbestos
- arsenic
Classification
 Primary lung cancer  usually a single lesion
- Small cell (oat-cell) carcinoma
- Non small cell carcinoma = squamous cell carcinoma
adenocarcinoma (most common)
bronchioalveolar carcinoma
large cell anaplastic carcinoma
 Secondary lung cancer  metastasis
- more common than primary lung cancer
- usually multiple, well-circumscribed “cannonball” lesions on CXR
- exhibit characteristics of primary tumour e.g. mucin-producing GIT tumour
Histological subtypes
1. Small cell carcinoma (20%)
- most aggressive
- metastasise widely very early due to rapid growth
- surgically incurable  mets present at time of presentation
- sensitive to chemo/RT
- derived from neuroendocrine cells  Kulchitsky cells
- paraneoplastic syndrome  ADH (SIADH), ACTH (Cushing’s syndrome)
2. Squamous cell carcinoma (20 - 30%)

- presents as obstructive lesions of the bronchus  collapse, consolidation, bronchiectasis,
localised wheeze
- centrally located hilar/perihilar mass at the bifurcation of bronchi
- late metastasis, local spread more common
- may be surgically curable
- paraneoplastic syndrome  pTH-related peptide (hypercalcaemia)
3. Adenocarcinoma (30 - 40%)

- most common type of lung cancer
- epidemiology = females > males
406
non-smokers (least association with smoking)
- must exclude mets from GIT, ovary and thyroid
- diagnosis = pleural biopsy (percutaneous pleural needle biopsy OR VAT)
- follows adenoma-carcinoma sequence similar to that in the colon
- peripherally located near the pleura
- metastasizes early
4. Bronchioalveolar carcinoma (<1%)

- peripheral solitary nodule
- consists of mucin-secreting bronchiolar cells, clara cells and type II pneumocytes expectoration
of large amounts of mucoid sputum
- “lepidic” growth pattern = tumour cells grow in a monolayer on top of alveolar septa
- minimal stromal invasion  excellent prognosis
- rarely metastasize
5. Large cell anaplastic carcinoma (10%)

- poor prognosis due to early spread
- undifferentiated tumour cells
Clinical features
History
- presenting complaint = chronic productive cough, haemoptysis, dyspnoea, pleuritic chest pain,
hoarseness
- constitutional symptoms = fever, LOA, LOW, fatigue, night sweats
- local effects = dysphagia
- metastasis = bone pain, jaundice, confusion, seizures, focal neurological deficits
- paraneoplastic syndromes = hypercalcaemia (constipation, renal/ureteric colic)
HPOA (pain around UL/LL joints)
- General appearance = cachexia
- Hands = clubbing
tar stains
palmar crease pallor
wasting of intrinsic muscles and weakness of finger abduction (Pancoast tumour)
hypertrophic pulmonary osteoarthropathy
- Head and neck = ipsilateral Horner’s syndrome (Pancoast tumour)
conjunctival pallor
supraclavicular or axillary lymphadenopathy
SVCO (Pancoast tumour)
hoarse voice (RLN palsy)
- Lungs = localised and fixed monophasic wheeze
malignant effusion
consolidation  collapse
- CVS = pericardial effusion (soft heart sounds)
- Metastasis = bony tenderness
hepatomegaly
neurological examination
- Paraneoplastic phenomenon = pigmentation of palmar creases
gynaecomastia
cerebellar syndrome
proximal myopathy
407
Complications
Local growth and spread
(a) Bronchial obstruction  bronchiectasis, lobar collapse, pneumonia
(b) Erosion of vessels  haemoptysis
(c) Parapneumonic pleural effusion
(d) Rib destruction
(e) Dysphagia (oesophageal involvement)
(f) Cardiac involvement  pericardial effusion, pericarditis, tamponade
(g) Pancoast tumour  compression of lower brachial plexus (C8, T1)
ipsilateral Horner’s syndrome
SVCO
(h) Hoarseness (recurrent laryngeal nerve involvement or vocal cord invasion)
(i) Hemidiaphragmatic palsy (phrenic nerve involvement)
Metastasis
(a) Lymphatic spread to regional LN
(b) Haematogenous spread to distant organs  brain, bone, liver, adrenals
(c) Transcoelemic spread to pleural space
Paraneoplastic syndrome
# clinical syndrome due to ectopic production of humoral substances from a malignancy of non-
endocrine origin
(a) Endocrine = ACTH  Cushing’s syndrome
ADH  SIADH
pTH related-peptide  hypercalcaemia
hCG  gynaecomastia
(b) Neuromuscular = cerebellar degeneration
proximal myopathy
Lambert Eaton myasthenic syndrome
(c) Connective tissue = clubbing, HPOA, scleroderma, dermatomyositis, acanthosis nigricans
(d) Haematological = polycythaemia, anaemia, DIVC
(e) Vascular = migratory thrombophlebitis (Trousseau’s syndrome)
Investigations
Bloods
1. FBC = Hb (NCNC anaemia)
2. U/E/Cr = hyponatraemia (SIADH)
3. Ca/PO4/Mg and serum acid phosphatase = hypercalcaemia
bone metastasis
4. LFT = liver metastasis
Sputum cytology/broncho-alveolar lavage (BAL)

- good for endobronchial tumours (SCC and small cell lung carcinoma)
- poor yield for adenocarcinoma
Imaging
1. CXR = primary or secondary lung carcinoma
location
complications (pleural effusion, consolidation, collapse, bony secondaries)
hilar LAD
# If pleural effusion present  thoracocentesis or chest tube insertion
- drain before doing CT
- send fluid for = gram staining, culture/sensitivity, AFB, TB culture, cytology
2. CT thorax = determine exact location and features of lung ca
staging (LN involvement, local spread, distal mets)
408
3. Bronchoscopy = direct visualisation
tissue biopsy
assess operability (inoperable if tumour is within first 2 cm of either bronchus as it
does not allow for sufficient resection margins or
pneumonectomy)
4. Video-assisted thoracoscopy = therapeutic (if need to drain pleural effusion)
direct visualisation of adenoca or bronchioalveolar ca
pleural biopsy
Staging (identify candidates for surgical resection)

1. CT thorax = LN involvement, local spread, distal mets
2. CT abdomen/pelvis = liver and adrenal mets
3. CT head = brain mets
4. Bone scan = bone mets
5. PET scan = mediastinal staging
6. FNAC of peripheral LN = nodal involvement
TNM Staging
Primary tumor (T)
TX = malignant cells in bronchial secretions, no other evidence of tumour
Tis = carcinoma in situ
T0 = none evident
T1 = < 3cm in size, in lobar or more distal airway
T2 = > 3cm in size and > 2cm distal to carina
or any size if pleural involvement/obstructive pneumonitis extending to hilum but not all the lung
T3 = < 2cm from, but not at carina
or involves the chest wall, diaphragm, mediastinal pleura, pericardium
T4 = involves the mediastinum, heart, great vessels, trachea, oesophagus, vertebral body, carina or a
malignant effusion is present
Regional nodes (N)
N0 = none involved (after mediastinoscopy)
N1 = peribronchial and / or ipsilateral hilum
N2 = ipsilateral mediastinum or subcarinal
N3 = contralateral mediastinum or hilum, scalene or supraclavicular
Distant metastasis (M)

M0 = none
M1 = distant metastases present
# If malignant effusion is present  Stage 3b

# Stages 1-3a = surgery
# Stages 3b and 4 = chemo/RT, palliative
Management
Non small cell lung cancer
1. Surgery = lobectomy and pneumonectomy
- excision is the treatment of choice for peripheral tumours with no metastatic spread
- contraindications = metastatic carcinoma
malignant pleural effusion
FEV1 < 1.5 L
severe pulmonary hypertension
uncontrolled cardiac arrhythmias
recent AMI
- neoadjuvant chemotherapy can downstage tumour  shrink to operable size
2. Radiotherapy
- alternative for patients with inadequate respiratory reserve
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- S/E = radiation pneumonitis
pulmonary fibrosis
Small cell tumours

1. Chemo/RT
Palliation
1. Radiotherapy = bronchial obstruction
SVC obstruction
haemoptysis
dysphagia
bone pain
cerebral mets
2. Pleural drainage = cope loop, chest tube, pleurodesis
3. Pain relief = morphine
4. Discuss end of life issues = comfort measures / intensive resuscitation
Prognosis
 Overall 5-year survival = < 15%
 Non small cell without mets = 50% 2yr survival
 Non small cell with mets = 10% 2 yr survival
 Small cell (treated) = 1 year median survival
(untreated) = 3 months median survival
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Medicine (Respi) = Infections – Tuberculosis
Know when to suspect tuberculosis.
Know how to make/confirm a diagnosis of tuberculosis on clinical, radiological and bacteriological grounds.
Explain the basic principles of TB treatment, including the role of DOT, drug resistance.
Describe the common drugs required for treatment of TB including their significant adverse effects.
Describe how to monitor response to treatment.
Prevention
Discuss the public health aspects of Tuberculosis (including the basic principles of TB control), contact tracing,
treatment of latent TB.
Outline the pathogenesis of TB ie TB infection, TB disease, TB relapse.
Outline the protective effect of BCG and the use of the mantoux test.
Describe the basic epidemiology of TB in Singapore and globally.
Epidemiology
 Communicable disease
 Causes 6% of deaths worldwide, making it the most common cause of death from a single infectious
agent (WHO)
 Developing countries
 Incidence is increasing in developed countries as well, due to increasing prevalence of AIDS (most
impt risk factor for devpmt of TB) and migration
 Common in poverty stricken, overcrowded areas, malnutrition
 Common in those with chronic illnesses eg. DM, chronic lung disease, elderly or immunocompromised
(AIDS)
 Notifiable disease
Aetiology
 Mycobacterium tuberculosis (M. bovis from unpasteurised cows’milk is rare)
 Transmission: direct person-to-person transmission via airborne droplets from an active case
(latent disease is not transmissible unless it reactivates in times of immsuppression)
 Pathogenesis:
- Mycobacterium enter macrophages  inhibit microbicidal activity  uncontrolled proliferation of
mycobacterium  bacteremia and seeding of multiple sites
- Recruitment of monocytes which differentiate into epithelioid histiocytes that characterise the
granulomatous response 
- Also results in delayed type tissue hypersensitivity (T lymphocytes)
Pathology
Primary tuberculosis
- Develops in previously unsensitised individuals
- Elderly persons may lose their sensitivity to MTB and hence develop primary TB more than once
- Source of organism is exogenous
- Bacilli deposit near the pleura proliferate in macrophages  form tubercles with caseous necrosis
(Ghon focus)
- Bacilli drain to the regional LN which also undergo caseous necrosis
(Ghon complex = parenchymal lesion + nodal involvement)
- Effective cell-mediated immune (CMI) response develops two to six weeks after infection
- Failure to develop CMI results in progressive destruction of the lung  progressive primary TB
Complications
1. Foci of scarring may harbour viable bacilli for years, and thus be the nidus of reactivation in times
of immunosuppression
2. Progressive primary tuberculosis: disease develops without interruption in immunocompromised
411
individuals eg. AIDS patients with CD4+ counts <200/mm3
- Inability to mount immunological reaction to contain the primary focus
- Absence of characteristic caseating granulomas (non-reactive TB)
- Miliary TB: multiple tubercles evenly distributed thru’out the lung
Latent TB
- Stage inbetween primary and reactivation TB
Secondary tuberculosis (reactivation TB)

- Arises in a previously sensitised host, from reactivation of dormant bacilli when host resistance is
low (only 5% of those with primary disease develop secondary TB)
- Classically localised to the apex of one or both upper lobes (may be due to high oxygen tension)
- Due to hypersensitivity, bacilli excite a prompt and marked tissue response that tends to wall off
the focus (hence the regional LN are less prominently involved in early secondary TB compared to
in early primary TB)
- Cavitation occurs, erosion and dissemination along the airways  sputum positive, person can
spread the disease
Complications
1. Progressive pulmonary tuberculosis: apical lesion enlarges, erodes into surrounding tissue
- Erosion into bronchus creates a ragged irregular cavity
- Erosion of bld vessels leads to hemoptysis
- Dissemination by blood or lymphatics
2. Miliary pulmonary disease
3. Pleural involvement: effusions, tuberculous empyema or obliterative fibrous pleuritis
4. Lymphadenitis: the most common form of extrapulmonary TB
- Typically occurs in the cervical region (“scrofula”)
5. Endobronchial, endotracheal and laryngeal TB
6. Intestinal tuberculosis
7. Pott disease: TB abscesses in the vertebrae (may spread along tissue planes to form “cold abscesses”
which present as a pelvic lump
8. Systemic military tuberculosis
- Hematogenous spread to other organs esp liver, bone marrow, spleen, meninges, adrenals,
kidneys  fatal without treatment
Clinical features
History
- Symptoms: low grade remitting fever, lassitude, anorexia, night sweats, chronic cough, hemoptysis,
pleuritic chest pain, erythema nodosum
- Symptoms of compression by lymph nodes eg. monophonic wheeze, bronchiectasis, lung collapse
- Symptoms of affected organ systems eg. Headaches and seizures for TB meningitis, paraplegia for Pott
disease
- Risk factors: contact/travel history, crowded living conditions, HIV/immunocompromise
- Consolidation in apices is possible
- Effusion
- Wheeze if there is compression
Investigations
 CXR
- cavitation in the apices of the lung
- calcification
- reticulonodular shadowing (for military TB)
- fibrosis ("scarring") with traction
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- enlargement of hilar and mediastinal lymph nodes
- cavity with aspergilloma: air crescent sign
(CXR does not give indication of the activity of the disease; is not diagnostic)
 FBC
 LFT
 CRP
 Sputum AFB smear: MTB binds to Ziehl-Neelson stain and resists decolorisation (acid fast)
- positive AFB smear makes a presumptive diagnosis of TB in a high-risk patient, although a positive
stained smear is not specific for M. Tuberculosis
- 50% of AFB positive locals have MOTT (Mycobacteria other than TB)
- most AFB positive foreign workers have MTB
- if the patient is not able to produce sputum, sputum induction with nebulized, hypertonic 3% saline in
a negative-pressure isolation room is an alternative before more invasive procedures (bronchoscopy)
 Sputum culture is the gold standard (culture on Lowenstein Jensen media requires 12 wks; PCR can
provide faster results) * only culture can provide info on drug sensitivity
 Early morning gastric aspiration: most useful in young children where sputum is more difficult to
obtain, and is best performed following at least nine hours of fasting
 Nucleic acid amplification tests (NAAT), can provide rapid diagnostic information to the clinician,
generally within 24 to 72 hours
 Tuberculin skin test: TB antigen is injected intradermally and the cell mediated response at 48-72 hrs
is recorded. A positive test indicates that the patient has immunity (ie, previously exposed or
vaccinated) A strong positive test suggests active disease. False negatives occur in
immunosuppression eg. Miliary TB, AIDS
 In HIV patients, atypical features include sputum smear negative for AFB, false negative tuberculin test
cos of tuberculin anergy, lack of granulomas in tissues
Management
- Notify CDC, refer to TBCU
- Contact tracing
- Advise HIV testing
- Isolation while infectious
- Ishihara colour vision testing before initiating therapy with ethambutol
- Give anti-TB drugs (directly observed therapy to improve compliance) + monitor liver function
- Monitor CXR weekly during treatment, monthly sputum AFB smear and cultures till two consecutive
negative cultures
- Most persons diagnosed with TB are begun on specific treatment before the diagnosis is confirmed by
the laboratory
TB drugs
 Aims of therapy
- Successful treatment requires more than one drug to which the organisms are susceptible
- Sufficient dose
- Sufficient duration
- Compliance  DOT (polyclinic DOT)
 TB drugs
- First line: Isoniazid (H), Rifampicin (R), Pyrazinamide (Z), Ethambutol (E), Streptomycin (S), Amikacin,
Kanamycin
- Pyridoxine is given to reduce peripheral neuropathy induced by isoniazid
- Pyrazinamide is given for the first two months to kill intracellular bacilli
- 6 month treatment
- Titrate according to body weight
- Initial drug regimen is based on knowledge of the likely drug susceptibility.
- Four drugs are used in the initial phase of treatment when the total duration of treatment is six
months, because of the high incidence of isoniazid-resistant organisms in most communities.
- Usually RHZ or RHEZ
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 Drug resistant TB
 Initial drug regimens need to be modified in areas with a known high prevalence of MDR-TB
 Development of drug resistance after initial drug sensitivity (secondary drug resistance) occurs in
patients who do not comply with treatment regimens, occurs mainly in HIV patients
 Nosocomial transmission significant
 Use 4 drugs, treat for 2 years
 Follow up for 1 year after eradication
 Second line drugs: Ofloxacin, Ciprofloxacin, Cycloserine, Ethionamide, Azithromycin
Drug side effects

 Rifampicin
- induces liver enzymes  caution in drugs and OCP
- stop if liver enzymes are more than 3x elevated
- orange tears, sweat, sputum, urine
 Isoniazid
- peripheral neuropathy
- skin rash
- hepatitis  stop drug
 Pyrazinamide
- precipitates gout
- liver toxicity
 Ethambutol
- dose related optic retrobulbar neuritis, presents with colour blindness, central scotoma, reduction in
visual acuity
 Streptomycin
- irreversible damage to the vestibular nerve
- allergic reactions are more common
TB and HIV
 TB in an HIV patient is an AIDS defining condition
 4 drugs are used instead of the usual 3
 Adverse reactions are common and the prognosis is poor
 Multiple drug resistance occurs in 6%
 M. avium intracellulare is another mycobacterium that can cause pulmonary infection in AIDS patients
Prevention
 BCG vaccination: live attenuated vaccine  protects against miliary and meningeal TB
 Contact tracing
 Chemoprophylaxis for contacts and for HIV patients
414
Mantoux test
- used to identify patients with latent TB
- positive tuberculin skin test indicates infection with M. tuberculosis; it does not diagnose active
disease
- intradermal injection of 0.1 ml of PPD
- interpreted 48 to 72 hours after intradermal administration
- transverse diameter of induration should be measured and recorded in millimetres
- False negatives: newly diagnosed TB, HIV, TB meningitis
- Children who have received the BCG vaccine generally demonstrate PPD skin test reactions of 3 to
19 mm several months after vaccination. Most of these reactions wane significantly with time.
Responses indicative of a new infection include: > 10 mm induration in persons less than 35 years
of age or > 15 mm induration in >35 years old
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Medicine (Respi) = Pneumonia
Definition
Clinical definition
Pneumonia = acute lower respiratory tract illness associated with fever, symptoms and signs in the chest,
and abnormalities on CXR
Pathologic definition
Pneumonia = inflammation of lung parenchyma characterised by consolidation due to exudate in
the alveolar spaces
[ Distinguish from pneumonitis: inflammation affecting the interstitium, which presents clinically
as “atypical pneumonia”]
Causative organisms
CLASSIFICATION BY ACQUISITION
 Community acquired typical (usually bacterial)  Pneumococcus, H influenzae
 Community acquired atypical  Mycoplasma, Legionella
 Nosocomial (usually bacterial)  Pseudomonas, Staph aureus
 Aspiration
CLASSIFICATION BY AGENT
 Bacterial: Strep pneumoniae
Staph aureus: usually 2o, following viral infection, IVDA (assoc w abscesses)
may be 1o in patients with underlying lung disease
H influenzae: usually 2o, following viral infection
most common cause of acute exacerbation of COPD
Klebsiella: affects debilitated patients esp chronic alcoholics
characteristic thick gelatinous sputum (redcurrant jelly)
Legionella: from water storage systems (chlorination and temp control impt)
affects debilitated patients
diarrhoea is a prominent symptom
Pseudomonas: nosocomial infection in patients with CF, on mech ventilation or
neutropenic (can cause pulm artery invasion and h’rhage/infarction)
Mycoplasma (causes atypical pneumonia)
 Viral: Influenza, CMV (cause atypical pneumonia)
 Fungal: Aspergillus: colonise cavities to form aspergilloma; invasive allergic reactions eg. asthma
Candida: causes lung disease in those with chronic lung disease/immcompromise
hematogenous spread
Cryptococcus: opportunistic infection
localised lesion in the lung which can spread to LN and then to other parts
Histoplasma: affects immcompromised, causes granulomatous inflammation
PCP: when CD4 count < 200/mm3 in AIDS patients
perihilar shadowing, dry cough
BAL and immunofluorescence
 Parasites: cause eosinophilic pneumonia: amoeba, paragonimus
 Drugs/chemicals: cause interstitial pneumonitis
Aetiology
CLASSIFICATION BY SITE
Lobar pneumonia
 Etiology/epidemiology
- Causative agent usually Strep pneumoniae (90%), Kleb, Staph, H influenzae (high virulence)
- Can occur at any age in healthy people without underlying lung disease
- Usually follows viral infections
- Pneumococcus is associated with rusty colored sputum
416
Bronchopneumonia
- Causative agents: Staph aureus, H influenzae, Strep, Pseudomonas (low virulence organisms)
 Predisposing factors
- Extremes of age
- Immunosuppression/immunocompromised eg. Chronic disease
- Loss of cough reflex eg. Coma, anaesthesia
- Injury to mucociliary apparatus eg. Smoking, viral disease, genetic disease (CF)
- Interference with phagocytosis or bactericidal action eg. Alcohol, smoking
- Splenectomy
- Pulmonary congestion eg. Cardiac failure
- Accumulation of secretions eg. Bronchial obstruction, prolonged bed rest
- In hospital (nosocomial infections)
Atypical pneumonia
- Causative agents: mycoplasma, chlamydia, viruses (influenza, parainfluenza, RSV, adeno)
- Affects school going children and young adults
- Presents as first as URTI eg. pharyngitis and flu-like symptoms  laryngitis  tracheobronchitis +
pneumonia (LRTI)
- May have headaches and malaise (typical of mycoplasma), erythema multiforme, arthralgia,
autoimmune haemolytic anaemia, myocarditis, hepatitis, DIC
- Cough, fever, modest sputum production, non-specific CXR changes (transient, ill-defined patches),
WBC count only moderately elevated, non-response to antibiotics
- Because the edema and exudatation are both in a strategic position to cause an alveolocapillary
block, there may be respiratory distress out of proportion to the physical and radiologic findings
- Cold agglutinins, rising antibody titre
 Complications
- ARDS
Aspiration pneumonia
 Usually in the right middle lobe cos the right bronchus is straighter
 Especially in unconcscious, drunk, epileptic, stroke patients; may follow after gen anaesthesia, partial
drowning
 Gastric contents: can cause asphyxia if massive; can cause pulm edema + infection
 Necrotising pneumonia, pursues a fulminant clinical course
 Complications: lung abscess, death
Nosocomial pneumonia
 Common in patients with underlying disease, immsuppression, prolonged antibiotic therapy, invasive
devices/foreign bodies, mechanical ventilation
 Commonest causative organisms: Pseudomonas, S aureus and enterobacteriaceae
Clinical features
History
 Symptoms: Fever, rigors, cough, purulent sputum, malaise, dyspnea, pleuritic chest pain
 Diarrhea (legionella)
 Confusion in elderly
 Preceding viral illness
 Hospitalisation/insitutionalisation
 Smoking/alcohol
 Co-morbidities
 Contact/travel/sexual history
417
 Fever, confusion (in the elderly), tachypnea, tachycardia
 Consolidation: diminished chest expansion, dull percussion note, increased vocal fremitus/resonance,
bronchial breathing
 Pleural rub
 Sputum mug
Differentials (non-infectious)
 Chemical pneumonitis / inflammation due to radiotherapy
 Allergic mechanisms, asthma
 Lung cancer
 COPD
Investigations
 FBC: leukocytosis with left shift, CRP
 Bld c/s
 Viral serology if suspected
 CXR: lobar/patchy consolidation (opacity with air bronchograms)
multicentric, likely hematogenous route  IVDA (Staph aureus)
cavitating: TB, anaerobic, kleb, meliodosis, staph aureus
+/- parapneumonic effusions
- CXR changes lag behind clinical course, hence initial CXR may not show typical changes
- CXR may show consolidation after resolution of symptoms, but should clear by 6 wks
 Sputum for microscopy and c/s, AFB smear and culture, TB PCR
- should have < 10 epithelial cells
- > 25 WBCs are abnormal
- lancet shaped diplococci = S pneumoniae
 Urine antigen for legionella, pneumococcus
 Bronchoscopy for immunocompromised patients
 Pleural fluid for analysis (thoracocentesis) if effusion present
Severity
 Two scoring systems to decide outpatient vs inpatient treatment; also of prognostic value
 CURB 65 score
- Confusion (abbreviated mental test score < 8)
- Urea > 7 mmol/L
- Respiratory rate > 30/min
- BP systolic < 90 mmHg
 0-1: treat as outpatient
 2: inpatient treatment
 3 or more: admit to ICU
 PSI (see attached)
- PORT study (Patient Outcomes Research Team)
- Risk class I: no co-morbidities, normal phy exam and age < 50
- Risk class II – V: points are assigned for different comorbidities and abnormal lab findings
 Direct ICU admission if patient is in septic shock requiring vasopressors or intubation
Management
 Outpatient antibiotic treatment: amoxicillin
 Hospitalised patients are generally begun on intravenous antibiotics (ceftriaxone + azithro OR
levofloxacin). Patients who are improving clinically, hemodynamically stable, and able to take oral
medications can be switched to oral therapy.
 If no improvement within 72 hours, consider an organism that is not covered by the initial antibiotic
regimen, including unusual pathogens or drug-resistant organisms
418
 Oxygen: nasal cannula/venture mask/ventilation depending on severity
 IV fluids
 Analgesia
 Vaccines
 Chest physiotherapy
 Follow up CXR in 6 weeks
Antibiotic selection
 Community acquired
- Mild Oral amoxicillin and/or erythromycin, or ciprofloxacin
- Severe IV augmentin or cefuroxime AND erythromycin
- Atypical Clarithromycin (Legionella), tetracycline (Chlamydia), bactrim (PCP)
 Nosocomial
- Gm negs, Pseudomonas, IV aminoglycoside + 3rd gen cephalosporin
IV ciprofloxacin for pseudomonas
Anaerobes IV metronidazole
** if TB cannot be ruled out then do not give quinolones as it may mask the AFB smear
Complications
 Complete resolution is rare in bronchopneumonia  focal fibrosis or bronchiectasis
 Pleural effusion
 Empyema
 Lung abscess
 Respiratory failure
 ARDS
 Sepiticemia
 Brain abscess
 Pericarditis
 Cholestatic jaundice
Causes of poorly resolving pneumonia

 Lung Ca
 Aspiration of foreign body
 Inappropriate antibiotic
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Pneumonia Severity Index
Risk factors Points

Demographic factors
Age for men Age (yr)
Age for women Age (yr) - 10
Nursing home resident +10
Coexisting illnesses
Neoplastic disease (active) +30
Chronic liver disease +20
Congestive heart failure +10
Cerebrovascular disease +10
Chronic renal disease +10
Physical examination findings
Altered mental status +20
Respiratory rate ≥ 30/minute +20
Systolic blood pressure <90 mmH +20
Temperature <35°C or ≥ 40°C +15
Pulse ≥ 125 beats/minute +10
Laboratory and radiographic findings
Arterial pH <7.35 +30
Blood urea nitrogen ≥ 30 mg/dL (11 mmol/L) +20
Sodium <130 mmol/L +20
Glucose ≥ 250 mg/dL +10
Hematocrit <30 percent +10
Partial pressure of arterial oxygen <60 mmHg or an
+10
oxygen saturation of <90 percent on pulse oximetry.
Pleural effusion +10
Class Score Management Mortality %

I 0 Outpatient 0.1
II <70 Outpatient 0.6
III 71-90 Inpatient to observe 2.8
IV 91-130 Inpatient 8.2
V >130 Inpatient 29.2
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Aetiology
Medicine (Respi) = Asthma  Extrinsic (allergic) asthma
Principles of Diagnosis - Definite external cause
Recognise acute asthma clinically and define status asthmaticus. - Type 1 hypersensitivity reaction
Describe the severe sequelae arising from inadequate acute management. - Elevated serum IgE and eosinophils
Describe the clinical assessment of severity of asthmatic effect. - Mediated by Th2 cells  release IL 4, IL5  IgE synthesis 
Principles of Management sensitization of mast cells
Describe the immediate steps in management: drugs, dosage and mode of - Triggered by allergen exposure in a sensitised individual  mast cell
administration. degranulation
List the clinical parameters which should be monitored after initiation of - Early phase (within 1 hr): release of leukotriene D4, PGE2, histamine
treatment. - Accompanied by reflex bronchoconstriction due to stimulation of
Describe the indications for intubation. vagal receptors
Explain the pathophysiology of acute asthma and the action of the drugs used - Late phase: recruitment of leukocytes: leukotriene B4, platelet
in acute management. activating factor, TNF
Describe the follow-up medical management after the acute attack. - Leukocytes damage the epithelium, reducing production of NO, thus
Prevention causing smooth muscle contraction
Describe the measures to minimize occurrence of severe asthmatic attacks. - Eosinophils perpetuate the inflammation
- Eg. Atopic asthma, occupational asthma, allergic bronchopulmonary
aspergillosis
Characteristics
- Often has family history of allergy/atopy
 3 characteristics:
- Develops in childhood
i) Airflow limitation of changing severity, episodic, reversible
spontaneously or with treatment
 Intrinsic (non-allergic) asthma
ii) Airway hyperresponsiveness to a wide range of stimuli
- Non immune mechanism, asthmatic “diathesis”
iii) Inflammation – eosinophils, T lymphocytes, mast cells, smooth muscle
- IgE antibodies are normal
hypertrophy, edema, mucosal damage
- Triggered by respiratory infection, aspirin, stress, exercise, cold
 3 factors contribute to airway narrowing: i) bronchospasm, ii)
(these factors may also trigger asthma in a person with extrinsic
inflammation and swelling,
asthma cos of his bronchial hypersensitivity)
iii) increased mucus production
- No family history of allergy/atopy
o Intervals between attacks are characteristically free from respiratory
- Develops later in life, “late onset”
difficulty, but subtle deficits can be detected by spirometry
Epidemiology
o Prevalence is increasing
o More common in developed countries
421
Pathogenesis
 Atopy Physical examination
- individuals who readily develop IgE antibodies against common  Tachypnea
materials in the environment  Wheeze, cough
- runs in the family  Hyperinflated chest, hyperresonance, diminished air entry
- childhood exposure to allergens has an influence on IgE production:  Polyphonic wheeze
growing up in a clean environment predisposes towards IgE response  Clinical severity: able to complete sentences? Silent chest, bradycardia,
to allergens PEF < 33%, cyanosis, feeble respiratory effort, confused
 Airway hyperresponsiveness
→Small airway obstruction due to bronchospasm and thick tenacious Investigations
mucous plugs, progressive hyperinflation with air trapping  FBC: eosinophils
 Remodelling  Sputum culture and cytology: eosinophils
- deposition of matrix proteins beneath the epithelium  Serial peak expiratory flow measurements
- epithelial metaplasia and increase in goblet cells - Diurnal variation >20% on 3 days a week for 2 weeks: marked
- thickened basement membrane morning dipping of peak flow
- smooth muscle hyperplasia  Lung function tests
- Decreased FEV1/FVC ratio and increased residual volume
Precipitating factors - Before bronchodilator, after bronchodilator  variable airflow
 Environmental allergens: pollen, house dust mite, pets limitation, >15% improvement in PEFR after bronchodilator
 Occupational: isocyanates (varnish), flour, animals  CXR: hyperinflation, exclude pneumothorax or allergic
 Atmospheric: cigarette smoke, pollutants bronchopulmonary aspergillosis
 Cold air, exercise (at the end of exercise), emotion  Skin prick test: helps to identify allergens
 Viral infections: rhinovirus, parainfluenza  Histamine or methacholine challenge: to test airway
 Drugs: Aspirin (imbalance in metabolism of arachidonic acid), beta hyperresponsiveness
blockers
Clinical features
History
 Dyspnea (esp expiration), nocturnal cough, wheezing, chest tightness
 Severity, frequency
 Precipitants: Exercise, cold, stress, infection, drugs eg. aspirin
Allergens, occupational exposure, better when on holiday
 Diurnal variation: worse in the morning
 Other atopic disease: eczema, allergic rhinitis
 Family history
 Social history: occupation, impact on lifestyle
422
Management
 Allergen avoidance eg dust mite, smoking, drugs
Classification of asthma  Pharmacologic therapy – depending on severity/frequency of asthma
New GINA guidelines symptoms
- use step-up or step-down approach
 Education of patient and family:
- Check inhaler technique (avoid excess deposition in mouth)
- Use of spacer to increase lung deposition, decrease the need for
coordination
- Compliance with steroid inhalers
 Asthma action plan
- grades patient’s severity of asthma into the green, yellow and red
zones, according to their symptoms + peak flow rates
- describes the dose, frequency and duration of the appropriate
treatment
- main aim of the asthma action plan is to abort exacerbations by rapid
step up of both reliever and preventor
- also prompts the patient to seek urgent hospital treatment in case of
severe exacerbations and/or failure of self medication.
 SMART approach to asthma (Symbicort Maintenence and Reliever
Treatment)
o 2 puffs BD for maintenence
o 4 puffs BD in exacerbation for rapid relief
o 2 puffs BD when symptoms resolve
o Symbicort = budesonide + formoterol
- Better compliance when using a combined inhaler than two separate
inhalers
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Asthma drugs
 Beta-2 agonists
- selective for bronchial smooth muscle  relaxation and
bronchodilation
- for symptomatic relief (2 puffs prn)
- effective up to 6 hrs Status asthmaticus
- excessive use (>2 canisters per month) is associated with increased  Poor response to drug therapy after 24 hours
mortality  Signs of respiratory failure: ABG: PaCO2>6kPa, PaO2<8kPa, pH low and
 Anticholinergic (ipratropium bromide) falling
- muscarinic receptor antagonists
 Long acting beta-2 agonists Risk factors for death from asthma
- effective up to 12 hours  Past history of sudden severe exacerbation
- for patients who cannot be controlled on 800mcg/day of ICS  Prior intubation for asthma
 Sodium cromoglycate and nedocromil  Two or more hospitalisations for asthma in the past year
- blocks chloride channel  prevent mast cell activation  Three or more emergency care visits for asthma in the past year
 Inhaled corticosteroids (ICS)  Hospitalisation or an emergency care visit for asthma within the past
- any form of persistent asthma (needing relief meds at least once a month
week) requires steroid inhaler treatment  Use of >2 canisters per month of inhaled short-acting B2-agonist
- beclometasone, budesonide, fluticasone, triamcinolone  Current use of systemic corticosteroids or recent withdrawal from
- most of the dose is swallowed or exhaled systemic corticosteroids
- adding a long acting beta-2 agonist is more effective than doubling the  Known difficulty perceiving airflow obstruction or its severity
dose of ICS  Comorbidity, as from cardiovascular diseases or chronic obstructive
- side-effects: oral candidiasis, hoarseness, subcapsular cataract,  pulmonary disease
avascular necrosis of the femoral head, osteoporosis, growth  Serious psychiatric disease or psychosocial problems
retardation  Low socioeconomic status
- step down treatment after the condition is under control  Illicit drug use
 Oral corticosteroids  ABG: PaCO2>6kPa, PaO2<8kPa, pH low and falling
- keep the dose as low as possible
- for those who cannot be controlled on ICS
 Leukotriene-receptor antagonists
- add on therapy
- good for aspirin-intolerant asthma
424
Severity of Asthma Attack
Feeble
Silent
chest
<30%
425
Management of an acute attack
Indications for intubation

- progressive respiratory failure
- altered mental status
- hemodynamic instability
Supportive measures:
- oxygen
Monitoring:
- O2 saturation
- ABG
- PEFR
- Level of consciousness
426
Medicine (Respi) = Pulmonary embolism
Identify risk factors and acquired conditions predisposing to DVT and PE
Enumerate differential diagnoses of DVT (leg swelling) and PE (collapse, chest pain, dyspnea or hemoptysis).
Clinically differentiate between the clinical syndromes of PE, i.e. pulmonary infarction, submassive PE,
massive PE and chronic PE.
Outline the diagnostic work-up of patients with suspected PE, including non-imaging and imaging methods,
and their limitations.
Describe the management of PE including –
a) 1° strategies such as anticoagulants, thrombolysis and surgery.
Detailed knowledge of anticoagulants including contraindications, the types of drugs, route of administration,
indications and maintenance doses, lab monitoring, potential interactive actions to take in case of
overanticoagulation
b) Resuscitative and supportive means for shock, RVF, chest pain
Prevention
Describe the recommended antithrombotic or anticoagulation regimes and mechanical measures for
prophylaxis of DVT.
Know the anticoagulation regimes for secondary prevention of PE.
Describe briefly the role of catheter-based strategies, including inferior vena caval interruption for secondary
prevention of massive PE.
Pathophysiology
Describe the pathophysiology of pulmonary embolism, including the concept of ventricular interdependence.
Predisposing factors
 Prolonged bed rest, immobilisation
 Surgery, trauma, fractures
 Previous stroke or thromboembolism
 Congestive cardiac failure
 Disseminated cancer
 Pregnant women
 Antiphospholipid syndrome
 Drugs: OCP
 Smoking
 Genetic: Factor V Leiden mutation, thrombophilias
Pathogenesis
- Thrombi from deep veins of the leg (95% are from the popliteal vein or the veins above it)
- Clots break off and embolise to the lungs
- Large embolus obstructing the main pulmonary artery  increased pulmonary artery pressure due to
blockage of flow + vasospasm due to release of mediators/neurogenic mechanism  leads to
hypoxemia, acute cor pulmonale (when more than 60% of vasculature is obstructed) and death
- Small thrombi may be clinically silent cos they are rapidly removed by fibrinolytic activity, and the
bronchial circulation maintains the viability of the affected parenchyma till this is achieved
- Smaller thrombi continue traveling distally and are more likely to produce pleuritic chest pain, by
initiating an inflammatory response adjacent to the parietal pleura
- Pulmonary infarction may occur rarely (less likely due to dual blood supply)
- Multiple small emboli may lead to pulmonary hypertension  decreased cardiac output
427
Clinical syndromes of PE
Massive pulmonary embolism
- PE associated with a systolic blood pressure <90 mmHg or a drop in systolic blood pressure of ≥ 40
mmHg from baseline for a period >15 minutes, which is not otherwise explained by hypovolemia,
sepsis, or a new arrhythmia
- a catastrophic entity that often results in acute right ventricular failure and death
Submassive pulmonary embolism

- All PE not meeting the definition of massive PE are considered submassive PE.
Pulmonary infarction
- Infarction only occurs if bronchial circulation is impaired
- The more peripheral the embolic occlusion, the more likely is infarction
Chronic pulmonary embolism

- Occurs when acute PE does not resolve, lasts for years
Clinical features
History
 Acute breathlessness, pleuritic chest pain, hemoptysis, dizziness, syncope
 Risk factors
 Tachypnea, pyrexia, tachycardia, hypotension
 Cyanosis
 Raised JVP, loud P2, 4th heart sound
 Pleural rub or effusion
 Signs of DVT
 Recent surgical scar
Clinical scoring
 Wells score
Previous DVT/PE 1.5
Immobilization or surgery in previous 1 month 1.5 0-2 Low probability
Malignancy 1 3-6 Mod probability
Clinical symptoms of DVT 3
Hemoptysis 1
> 6 High probability
Heart rate >100 1.5
Other diagnosis less likely than PE 3
 Geneva score
Age > 65 1
Previous DVT or PE 3 0-3 Low probability
Surgery (under GA) or lower limb fracture within 1 month 2
Active malignant condition or cured in < 1 yr 2 4-10 Mod probability
Unilateral lower limb pain 3 > 10 High probability
Pain on lower limb deep venous palpation and unilateral edema 4
Hemoptysis 2
Heart rate 75-94 bpm 3
Heart rate ≥ 95 bpm 5
428
Investigations
Nonspecific lab findings
 ESR raised
 BNP raised
 Trop T raised
Specific investigations
 CXR
- Normal
- Atelectasis
- Oligemia of affected segment
- Dilated pulmonary artery
- Small effusion
- Wedge shaped opacities
 ECG
- S1Q3T3 pattern, right ventricular strain, new incomplete RBBB (classical but rare)
- Atrial arrhythmias
- T wave inversion, ST changes
 D dimer: degradation product of cross-linked fibrin
- Sensitivity 95%
 V/Q perfusion scan: look for perfusion defects without corresponding ventilation defects
 CT pulmonary angiography (gold standard)/ “spiral CT”
 Lower limb Doppler ultrasound
Differential diagnoses
PE
 Acute coronary syndrome
 COPD
 Myocarditis
DVT
 Cellulitis
 Superficial thrombophlebitis
429
Algorithm for diagnosis of PE
Suspicion of PE
Perform Wells/Geneva
score
Low/intermediat High probability

e probability
Start tx
D Dimer assay
CTPA
D Dimer D Dimer
negative positive
CTPA CTPA
negative positive
No tx CTPA
Lower limb Continue tx

CTPA CTPA DVT scan
negative positive
No tx Start tx Scan Scan

negative positive
Stop tx Continue tx
430
Management
 Assess ABCs
 Stabilise the patient
- supportive measures eg. supplemental O2
- cautiously administer intravenous fluids (avoid ppting right heart failure)
- vasopressor therapy
 Anticoagulation
- Reduces mortality by preventing recurrent PE
- In those with high probability of PE, start anticoagulation before investigations
- Greatest efficacy if therapeutic heparin levels are initiated within 24 hours
- In hemodynamically stable patients with PE, SC LMWH is preferred
- Patients in whom anticoagulation was initiated during the resuscitative period should remain
anticoagulated during the diagnostic evaluation. Anticoagulation should be discontinued of PE
is excluded
- Long-term anticoagulation with warfarin is indicated if PE is confirmed
 Inferior vena caval filter placement should be considered if anticoagulation is contraindicated (patient
has active bleeding), fails, or causes complications (eg, severe bleeding)
- results in less recurrence of PE
- but recurrent DVT was more common among patients who received an IVC filter
 Thrombolysis should be considered once PE is confirmed
- Accelerates the lysis of acute pulmonary emboli
- Increased likelihood of major hemorrhage
- If thrombolysis is chosen, anticoagulation should be temporarily discontinued then resumed
- No mortality benefit, but shown to improve RV function
- Persistent hypotension due to massive PE is a widely accepted indication for thrombolysis
 Embolectomy
- Removal of embolus using catheters or surgically
- When thrombolysis either fails or is contraindicated
- Catheter emboleeectomy: injecting pressurized saline through the catheter's distal tip, which
macerates the embolus. The saline and fragments of clot are then sucked back into an exhaust
lumen of the catheter for disposal
 Preventive management: elastic stockings, leg exercises, ambulation, long term anticoagulation with
warfarin
431
Anticoagulation regimes
DRUG THERAPY
 LMWH (fraxiparin, enoxaparin)
- results in lower mortality, fewer recurrent thrombotic events, and less major bleeding than UFH
- greater bioavailability, once or twice daily administration, fixed dosing (ie, dose does not require
adjustment), no required laboratory monitoring, and decreased likelihood of thrombocytopenia
- exception: patients who are pregnant or have severe renal failure require anti-Xa assay monitoring
after administration of SC LMWH
 Unfractionated heparin (continuous iv infusion)
- preferred in patients with persistent hypotension due to massive PE; severe renal failure (aPTT
monitoring is easier than anti-Xa assay)
- target 1.5-2.3 x the control aPTT
- protamine sulphate is the antidote for heparin (cannot fully reverse LMWH’s anti-Xa effects)
 Fondaparinux (new)
- synthetic heparin pentasaccharides that catalyse factor Xa inactivation by antithrombin, without
inhibiting thrombin
- may be a viable alternative to unfractionated heparin
 Warfarin
- risk factors for bleeding: age >75, concurrent aspirin therapy, hypertension, CVA, renal insufficiency,
heart disease, cancer
- Vit K and FFP are antidotes for warfarin
DURATION
First episode of Recurrent episode of
PE/DVT PE/DVT
Reversible risk No identifiable risk Irreversible risk

factor eg. recent factor factor eg. ptn C
surgery deficiency, APS
Warfarin
3-6 months Warfarin Indefinite therapy
6-12 months,
consider indefinite
therapy
- Treatment duration among patients with a first episode of PE or deep vein thrombosis (DVT) is
determined by whether a risk factor can be identified and, if so, whether the risk factor is reversible.
- Reversible risk factor eg, immobilization, surgery, trauma: warfarin for 3-6 months
- No identifiable risk factors ie, idiopathic PE or DVT: at least 6 to 12 months, consider indefinite
anticoagulation
- Irreversible risk factor eg. protein C deficiency, protein S deficiency, factor V Leiden gene mutation: at
least 6 to 12 months, consider indefinite anticoagulation
- Indefinite therapy should be administered to patients with recurrent PE or DVT.
Prognosis
 30% chance of developing a second embolus
 Mortality rate of approximately 30 % without treatment, due mainly to recurrent embolism
 Accurate diagnosis followed by effective therapy with anticoagulants decreases the mortality rate to 2
to 8 %
432

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Priscilla’s Medicine

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Prosthetic heart valves

This is most likely due to severe mitral regurgitation

# Request to examine = neurological system (pronator drift for hemiplegia)

This is not complicated by congestive cardiac failure or infective endocarditis

This is not complicated by congestive cardiac failure or infective endocarditis

# Request = BP (narrow pulse pressure)

This is not complicated by congestive cardiac failure or infective endocarditis

# Request = BP (wide pulse pressure; Hill’s sign)

This is not complicated by left heart failure or infective endocarditis

# Request = abdomen (pulsatile liver, hepatomegaly, splenomegaly)

There is no evidence of pulmonary hypertension as there was no parsternal heave or palpable P2

There is no cervical lymphadenopathy or signs of pulmonary hypertension as there was no parasternal

# important to exclude malignancy

Polycystic kidney disease

To end off my examination

Chronic tophaceous gout

Grade 0 Not palpable or visible

 Surface = smooth and diffuse, nodular

Hands and arms

Regulation of thyroid hormone release

Synthesis of thyroid hormones

Thyroid hormone receptors

* Malignant= papillary carcinoma

Medicine (Thyroid) = Management of hyperthyroidism

Radioactive iodine (RAI)

Protective eye measures

Grave’s Disease Toxic nodular Goitre

Thyrotoxic Periodic Paralysis

Compressive effects of goitre

Recurrent laryngeal nerve

Format for examination

De Quervain’s thyroiditis (subacute thyroiditis)

Moderate index of suspicion:

Post operative complications

Complication of the disease

Summary and Request

5 cardinal signs of inflammation

Inflammatory vs mechanical arthritis

Features Inflammatory Non-inflammatory

Mono and poly arthritis

2. discoid rash Erythematous raised patches with keratotic scaling and

3. Photosensitivity Unusual reaction to sunlight

4. Oral ulcers Oral or nasopharyngeal ulceration (usually painless)

5. Arthritis Non-erosive arthritis involving at least 2 peripheral

6. Serositis Pleuritis or pericarditis

7. Renal disorders Persistent proteinuria >0.5g/day or cellular crisis

8. Neurological disorders Seizures or psychosis in the absence of any known

9. Hematological disorders Hemolytic anemia, Leucopenia, thrombocytopenia,

10. Immunological disorders Anti-dsDNA Ab, anti-Sm Ab, anti-phospholipid Ab (lupus

Pregnancy and SLE

Proceed with the following:

Request to look at:

Physical examination (examine patient wearing his underwear only)

FBC  NCNC anemia of chronic disease

 Diagnostic Criteria (revised American Rheumatism Association Criteria (≥4 out of 7)

 Morning stiffness >1 hours

 Arthritis of ≥3 joints Fluid-filled presence of soft tissue swelling in

 Arthritis of hand joints Wrist, MCP, or PIP joints among the

 Rheumatoid nodules Subcutaneous nodules in regions surrounding

 Rheumatoid factor +ve

 Radiological changes Hand and wrist films