Priscilla's Guide To Medicine

Priscillas 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
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) = WILSONS 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
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
PRISCILLAS 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) = CUSHINGS SYNDROME ..................................................................................................................................... 349
MEDICINE (ENDOCRINE) = ACROMEGALY .................................................................................................................................................... 354
MEDICINE (ENDOCRINE) = ADDISONS 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
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
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
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
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; Hills sign)
other features of AR
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)
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
Horners 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 Horners
syndrome. There is also no displacement of the trachea or apex beat.
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 Horners 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 Horners
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
# Brocks 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 Horners 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 patients 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

Cushings 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 patients vitals, performing Pembertons 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 = duputyrens 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 patients 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
Grade 2
Palpable goitre (larger than terminal phalanges of

examiners thumb)
1A = detectable only on palpation
1B = palpable and visible with neck extended
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 (Plummers 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
Grade 2
Grade 3
Grade 4
MR palsy
Lid retraction and Lid lag
Opthalmoplegia
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. Pembertons 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 Hertels exophthalmometer)
5. Associated AI disorders
Vitiligo
Conjunctival pallor pernicious anemia
Myasthenia gravis
Glycosuria T1DM
Hyperpigmentation of palmar creases Addisons 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
anterior pituitary gland
TR
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 + diiodothyrosine
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 = 1.5 days) is 4x more metabolically active than T4 ( T = 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 = Graves disease
* Euthyroid = diffuse non toxic goitre (endemic/physiologic)
* Hypothyroidism = Hashimotos thyroiditis
De Quervains 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
oxidation
anions (per chlorate, thiocyanate)

thioamides (carbimazole, PTU)
Organification
thioamides
iodides
thioamides
coupling
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 and waves
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
Radiation induced cancer
30%)
* 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 = -blockers
* AF = digoxin, -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 7296 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) = Graves 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, Addisons 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 (Plummers 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
* Pembertons sign
Decompensation
* High output cardiac failure
* Thyroid storm
* Fixed opthalmoplegia = usually painful
26
Graves 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, Addisons 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 : Graves opthalmoplegia, pretibial myxoedema, thyroid bruit
*Graves 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
Glycosaminoglycansfibrosis 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)
-blockers ( block sympathetic effects on CVS )
RAI
Subtotal thyroidectomy
Protective eye measures
* Graves 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 hormonescompensatory rise in serum TSH levelshypertrophy and hyperplasia of
Follicular cellsdiffuse goitreinvolution 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
Graves Disease
Younger patients
Diffuse goitre
Eye signs common
AF uncommon
Autoimmune disorders common
Toxic nodular Goitre

Older individuals
Nodular enlargement
Eye signs uncommon
AF and CCF common (40%)
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 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 failurehypotensive 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 aspirininhibits 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 extensionpush goitre into thoracic inlet)
*may cause trachomalaciapost 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 Quervains thyroiditis
(d) autoimmune -> Hashimotos thyroiditis, post-partum thyroiditis, Riedels 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 (Trotters 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
- Tinels 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
* Addisons 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
Hashimotos thyroiditis
* autoimmune inflammation of the thyroid gland usually in middle aged women (45-65 yrs old)
* a/w other AI disorders IDDM, Addisons 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 Hashimotos 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
Riedels 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)
31
* may be mistaken for infiltrating neoplasm

* a/w retroperitoneal fibrosis, sclerosing cholangitis and fibrosing mediastinitis
De Quervains thyroiditis (subacute thyroiditis)
* epidemiology = 20-40 yr old females (much less frequent than Hashimotos 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)
b)
c)
d)
Risk of anesthesia = AMI, CVA

Pain
Wound infection
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)
Chvosteks sign (tapping of facial nerve in front of external auditory meatus will
cause hemifacial spasm
f) Trousseaus 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
Morning stiffness
Aggravating factors
Relieving factors
Systemic complaints
Response to steroids
Inflammatory
1 hr
Rest (unless in severe/ active cases)
Movement
Present
yes
Non-inflammatory
<30mins
Movement
Rest
Absent
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
Septic arthritis
Gout/pseudo gout
Trauma (haemarthrosis)
Seronegative spondyloarthritis
Osteoarthritis
Monoarthritic presentation of a polyarticular
disease
Polyarthritis
Rheumatoid arthritis
Osteoarthritis
Connective tissue like SLE
Reactive arthritis
Gout/ pseudo gout
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 Sjogrens, 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
Eyes
Mouth
Joints
CNS
CVS
Lungs
Renal
Erythematous malar rash sparing nasolabial folds

Photosensitivity
Discoid rash
Alopecia
Nail-fold infarcts, telangiectasia
Raynauds phenomenon (white-blue-red)
Dry eyes (Sjogrens syndrome)
Red eyes (episcleritis, scleritis, anterior uveitis)
Cotton wool exudates (retinal vasculitis)
Oral ulcers
Dry mouth (Sjogrens syndrome)
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 (jaccouds arthropathy)
Psychosis
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)
Pleuritis = serous effusion, fibrinous exudates
Pulmonary fibrosis
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
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
o
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 Coombs 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 Raynauds 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, Raynauds phenomenon, history of phlebitis or APL Ab should not be
treated with OCPs (increases risk of thrombosis)
History taking
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Malar rash
Discoid rash
Photosensitivity
Alopecia, dry eyes and mouth, oral ulcers
Gangrene of fingers, Raynauds phenomenon
Chest pain, dyspnoea
Joint pain
Seizures
Change in urinary frequency and volume, haematuria, frothy urine, loin pain
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
Raynauds 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
Schobers 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 90 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 nonsuppurative 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)
- LoA, LoW, fatigue, fever, rash
- Anemia chest pain, SOB, giddiness, palpitations, fatigue
Extra-articular involvement
- Skin = Raynauds phenomenon, rash
- Head and Neck = red eyes, dry eyes and mouth (Sjgrens 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
48
1. Eyes
Sclera episcleritis, scleritis, scleromalacia, scleromalacia perforans
Conjunctiva pallor, keratoconjunctivitis sicca (Sjgrens syndrome)
Lens cataracts from steroid use
Extra-Ocular Muscles mononeuritis multiplex, myasthenia 2 penicillamine, EOM tendon synovitis
Fundi maculopathy from hydroxycholoroquine use
2. Head and Neck
Mouth ulcers from DMARD treatment, dry mouth and enlarged parotids (Sjgrens)
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 Caplans (rheumatoid nodules in periphery of lung fields a/w coal workers pneumoconiosis)
4. CVS
Pericarditis
Aortic/mitral regurgitation
5. Lympadenopathy
6. GIT
Splenomegaly (5%)
Feltys 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, Raynauds 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, Bakers cysts in popliteal fossae
Lower Leg leg ulcers, calf swelling (ruptured Bakers 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
*
Arthritis and nodules = RA
SLE
RHD
Amyloid arthropathy (usually a/w multiple myeloma)
Investigations
*
FBC
ESR & CRP

Rh factor
ANA
X-ray of joints
C-spine X-ray (lateral, AP, flexion and extension)

Synovial fluid analysis
Monitor drug therapy
NCNC anemia of chronic disease

WCC
Platelets
Raised (c/f SLE, only ESR raised)
Positive in 80%
Also positive in Sjgrens (100%), SLE (30%),
mixed CTD (30%) and systemic sclerosis
Positive in 30%
Soft tissue swelling
Juxta-articular osteoporosis
joint space
Juxta-articular bony erosions
subluxation
complete carpal destruction
Joint dislocation
Atlanto-axial subluxation ( pre-odontoid gap)
Turbid
viscosity
Clots
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
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
6 weeks
Wrist, MCP, or PIP joints among the

symptomatic joints observe
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
2 to Feltys 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, Sjgrens 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
Sjgrens 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
Methotrexate
1st choice for severe

disease
-Better tolerated
S/E = N/V/D, rash, BM depression, oral ulcers,

SJS
Monitor LFT & FBC
CI = pregnancy, liver disease, G6PD deficiency
Do not take with alcohol!!
S/E = N/V/D, lower lobe pulmonary fibrosis,
53
Lefluonomide
Inhibits activated T
cells
Corticosteroids
Indications
Azathioprine, Cyclosporin A,
cyclophosphamide
- vasculitis
- severe disease
- exacerbations not
responding to other
drugs
Severe disease with
failure of other
therapies
transaminitis, no. of rheumatoid nodules

Give with folate to reduce GI S/E
Monitor LFT
Takes months to work
S/E = BM depression, proteinuria, rash,
hepatitis
Monitor LFT, FBC, urinalysis
S/E = metabolic, cosmetic, cataracts,
osteoporosis
Monitor BSL & BP
Rebound disease common on stopping steroids
AZP = BM depression, transaminitis, oncogenic

CSP = gingival hypertrophy, HPT, renal
impairment
Anti-cytokine therapy
-suppress disease activity only during treatment relapse on discontinuation
Infliximab (against TNF)
Etanercept (against TNF receptor)
Progressive RA after 2 S/E = N/V/D, rash, infection (TB reactivation),

DMARDs failure
neutralizing antibodies
Surgery
To improve function, relieve pain and prevent complications
Paramedical services
Others
- Synovectomy & decompression of wrist & tendon sheaths

- tendon repair and transfer
- Arthrodesis
- Osteotomy
- Joint replacement
Physiotherapy
Occupational therapy = adaptive aids, orthoses (eg wrist splints), ADL
training
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 patients 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 3 fingers, Tinels sign (CTS)
Ulnar nerve = FDP of little finger, finger abduction, sensation over medial palm and 1 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.
2.
-
Duration of disease
First presentation: initial clinical picture
Joint pain and swelling: which joints involved
3.
-
Joint stiffness (morning stiffness > 1 hour)

Constitutional symptoms: LOA, LOW, fatigue, fever, anaemia
Initial investigations: x-rays, rheumatoid factors
Initial treatment
Articular involvement
How has the disease progressed?
What joints are affected currently?
Current symptoms: joint pain and swelling
Medications: NSAIDs (renal involvement; BGIT)
Any recent changes

Compliance
Effectiveness
Side-effects
Physiotherapy/occupational therapy= any splints
Surgeries: tendon transfers
Deformities and disabilities:
4.
5.
-
Constitutional symptoms: LOA, LOW, fever, fatigue, anaemia, rash

Eyes: episcleritis (red eyes)
Dry mouth
Cervical spondylosis: neck pain/stiffness, radicular pain and weakness
Lungs: recent lung function test
Skin: vasculitic rash
6.
-
Associated with other AI disorders

IDDM
Vitiligo
Thyroid abnormalities
Pernicious anaemia
Addisons disease
Acute/sudden onset
Character of pain (increase with rest, decrease with movement)
Present everyday or occur in attacks

Frequency of exacerbations and management
Joint stiffness
DMARDS
Anti-cytokine therapy (TB reactivation, increased susceptibility to infection)
Joint stabilization/replacement
ADL
Work
Social recreation
Housework
Home modifications
Dry eyes
Cervical myelopathy: bladder/ bowel involvement

Gait disturbances
LL numbness/ weakness
Pleuritic chest pain, SOB
Raynauds phenomenon
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

Raynauds phenomenon
Esophageal immobility
Sclerodactyly
Telangiectasia
History
Skin
Raynauds (90%)
Edema
Thickened stretched skin
Cutaneous ulcers
Pigmentation, depigmentation (vitiligo)
Dx criteria 1 major or 2 or more minor
Major: scleroderma affecting MCP and MTP
Minor: Sclerodactyly, digital tip pitting or loss of
subst of digital finger pads, bibasal pulmonary
fibrosis
Other organs
Polyarthralgia
Proximal myopathy
Fever
Dysphagia
Lungs
o SOB (due to anemia)
Cardiac
o Chest pain pericarditis
o RHF edema
GI
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
Hands
Arms/Skin
Head
Cachexia
Bird like facies
Raynauds
Oatcinosis, ulcers
Telangiectasia
Arthropathy
Contractures
Thick tethered skin
Pigmentation
Vitiligo
Proximal myopathy
Alopecia
Eyes
Anemia (chronic dz, folate and B12 def, Fe def from chronic esophagitis,
microangiopathic hemolytic anemia)
Sjogrens
Mouth
63
Microstomia: open <3cm max

Roman breastplate tight skin
Pericardial rub
Pulmonary HTN
Fibrosis
Effusion
Chest infections
Alveolar cell carcinoma
Arthropathy
Flexion deformities
BP, urine dipstick for proteinuria
Chest
Lungs
Other joints
Other
Investigations
To confirm diagnosis
To look for complications
Bloods
Urine
Radio
FBC
U/E/Cr
ANA
Anti-centromere Ab
Dipstick
Urinalysis
CXR
2D echo
Anaemia
Renal failure
Nearly always +ve
Proteinuria
Effusion, fibrosis, CA
RHF
Management
Supportive, symptomatic
Pt education
Scleroderma itself
Raynauds
Oesophageal symptoms
HTN
Cytotoxics
Early stages: cyclophosphamide, MTX
Late stage: penicillamine
Vasodilators CA++ blockers, aspirin
Antacids
PPIs
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
Raynauds 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
Raynauds phenomenon
Dry eyes & mouth
Diagnosis
1.
2.
3.
4.
Systemic sclerosis
Limited cutaneous scleroderma (extremities + face)
Diffuse cutaneous scleroderma (extremities + face + trunk)
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
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%)
production of
excretion of uric
purine
acid
Idiopathic
Idiopathic
Genetic enzyme
defects
- Lesch-Nyhan
syndrome (Xlinked
recessive)
Secondary Hyperuricaemia (5%)

turnover of purine
renal clearance
of uric acid
Malignancies
Renal disease
- myeloproliferative
Drugs
disease
- aspirin
- lymphoproliferative
- diuretics
disease
(frusemide,
Chronic haemolytic
thiazides)
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 patients 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
Differentials
-
Gout, DM, HPT, HCL, IHD

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 = duputyrens 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.
2.
-
Initial diagnosis of DM
Age of diagnosis
Type 1/2 DM
Presenting complaint = polyuria, polydipsia, polyphagia, LOW, fatigue
Investigations = random BSL, 2 hr OGTT
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 < 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 dont 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)
Dont 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
Dont 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 doesnt kill but its complications do
Weight loss
-
Diet
-
Decreases insulin resistance

Measure patients height and weight and calculate BMI (Ideal<23)
Advise on ideal weight
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 (Addisons Disease)
Thick greasy skin (Acromegaly)
Papery thin skin (Cushings)
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, Hashimotos thyroiditis, Addisons 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, Turners, Klinefelter syndrome
- Exocrine pancreatic defects: Chronic pancreatitis, Ca pancreas, CF, haemochromatosis
- Endocrinopathies: Cushings 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

Aetiology
Age of onset
Weight
Lab results
- Plasma insulin
-Plasma glucagon
-Anti-islet cell antibodies
Islet cell morphology
Complications
Type 1 DM
Absolute insulin deficiency
- Genetics:
HLA-genes
Twins = 30-70%
concordance
- AI destruction
- Viral infection?
Juvenile (<20 years)
Normal/LOW
Type 2 DM
1. Insulin resistance
- Genetics
no HLA-linkage
Twins = 60-80%
concordance
- Environment: obesity
2. Beta cell dysfunction
Adult-onset (>40 years)
Obese
Absent/Low
High (due to low/no
insulin)
Yes
Insulitis
Marked atrophy and
fibrosis
Diabetic ketoacidosis
Hypoglycaemia
High/Normal
Low
No
No insulitis
Focal atrophy and amyloid
deposition
Hyperglycaemic
Hyperosmolar State
78
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
(BSL=2.8-3.0 mmol/L)
Neuroglycopenia (BSL <2.5-2.8

mmol/L)
- Sweating
- Trembling
- Tachycardia
- Pallor
- Hunger
- Anxiety
Behavioural disturbances
- Irritable
- Aggression
79
Non-specific
- Confused/AMS
- In coordination
- Seizures
- Focal neuro deficits
- Speech difficulty
Drowsy ( GCS)
- Nausea
- Headache
- Tiredness
80
Medicine (Diabetes) = Diagnosis of DM

Asymptomatic AND Random plasma glucose>11.1mmol/L
OR Fasting plasma glucose>7.0 mmol/L
No
Symptomatic AND RPG>11.1

mmol/L OR FPG>7.0mmol/L
Acute metabolic
decompensation
Yes
Repeat
FPG
DM
FPG>7.0m
mol/L
No
Yes
FPG
<6.0mmol
/L
6.16.9mmol/
L
Normal FG
OGTT
>11.1
7.8-11.0
Impaired glucose tolerance
2hr post
challenge
glucose
<7.8
Impaired Fasting Glycemia
81
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
82
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?

Investigations done (renal ultrasound, renal biopsy)
Cause of nephrotic syndrome (if biopsy was done likely glomerulonephritis)
2. Management
83
3.
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?
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.
2.
3.
4.
5.
Smoking
Alcohol drinking
Family set-up? Main caregiver?
Finances
Have to miss a lot of work?
Family History
84
Medicine (Renal) = Nephrotic Syndrome

*in an oedematous patient always test for proteinuria and investigate for nephrotic syndrome if
albustick >= 2+
Definition
1.
2.
3.
4.
Clinical entity
Characterized by classical triad
Proteinuria (> 3g/1.73m3/day)
Hypoalbuminemia (<30g/L)
Oedema
Usually associated with hyperlipidemia and lipiduria
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-Schnlein 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.
2.
Children
Minimal change disease (80%)
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.
2.
3.
4.
5.
6.
Oedema (periorbital, facial, lower limb, genitalia, sacral)

Pleural effusion
Ascites
Xanthelasma
Leuchonychia
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.
3.
Acute renal failure (as a result of hypovolemia)

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
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.
2.
3.
4.
5.
6.
Fluid restriction to < 1L/day

Low salt and low protein diet
Place on I/O charting
Daily weights and albustick
Monitor vitals Q4hourly (inform if systolic BP is <100mmHg or Hr >100/min)
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.
2.
3.
4.
Immunosuppression
PO furosemide with Span K and low salt diet only if oedematous
Monitoring at home with albustick and educate patient on how to escalate therapy and when to admit
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
Conns syndrome (primary hyperaldosteronism)
o Primary hyperaldosteronism
Excess pdn of aldosterone independent of RAA system
Conns 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 conns 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
Conns 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 HippelLindau 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
89
May have no signs

Medullary thyroid cancer
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
Patients 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
93
Medicine (Renal) = Urinary Tract Infection /

Pyelonephritis
Definitions
-
UTI = pure growth of >105 colony forming

units/ml OR 108 CFU/L
o Urethritis
o Cystitis
o Prostatitis
o Pyelonephritis
Bacteriuria = presence of bacteria in urine
o Asymptomatic (covert) only requires
further investigation and treatment if
occurring in infants, pregnant women or
urinary tract abnormalities
o Symptomatic
Abacterial cystitis/urethral syndrome = UTI
symptoms but no Bacteriuria (1/3 of women)
Recurrent UTI = a further infection with a new
organism
Relapse UTI = a further infection with the same
organism
Differential Diagnoses
-
Bladder neck obstruction

o Urethral strictures, BPH/prostate ca,
bladder calculi, bladder tumour, bladder
neck stenosis, Neurogenic bladder,
posterior urethral valve, constipation, ca
cervix/uterus, ca colon, retroperitoneal
fistuli
Reflux uropathy
o Vesico-ureteric reflux (VUR), intra-renal
reflux
Instrumentation
o Urinary catheterization, flexible cystoscopy,
TURP
Immunosuppression
o DM, AIDS, steroids
Organisms
-
E. coli (>70%)
Enterococcus
Enterobacter
Proteus
Klebsiella
Pseudomonas
Symptoms
Acute appendicitis
Diverticulitis
Cholecystitis
Salpingitis
Perinephric abscess
Cystitis
Typical Patient Profile

-
Women = prevalence increases with age

Men = uncommon (usually in 1st year of life or
>60 y/o, a/w BPH)
o Must always rule out urinary tract
abnormalities
Classification
Upper UTI
- Pyelonephritis
Uncomplicated
- Normal renal tract
- Normal renal function
- Normal host defenses
Risk Factors
-
Female
Sexual intercourse
Lower UTI
- Urethritis
- Cystitis
- Prostatitis
Complicated
- Male patients
- Abnormal urinary
tract
- Impaired renal
function
- Impaired host
defenses
- Virulent organisms
Acute Pyelonephritis
- Almost always a/w
lower UTI
(ascending)
- Haematogenous
route less common
Prostatitis
Frequency
Urgency
Nocturia
Dysuria
Haematuria
Suprapubic pain
Cloudy and foul
smelling urine
Obstructive
symptoms
Fever a/w chills and
rigors
Renal colic
Vomiting and
diarrhoea
Symptoms of lower
UTI
Acute renal failure
oliguria
Sepsis
Flu-like symptoms
Lower back ache
Enlarged & tender
prostate
Few urinary
symptoms
Signs
-
Fever
Signs of dehydration
Abdominal tenderness/guarding
Positive renal punch
Renal mass
94
o Hydronephrosis, renal abscess

Bladder distension
Enlarged and tender prostate
o Prostatitis
Prostatitis
-
Complications
-
Perinephric abscess
Pyonephrosis
Necrotizing papillitis in pyelonephritis ARF
Urosepsis
Advice
Investigations
Urine
- Urine
dipstick
- UFEME
- Urine c/s
Bloods
- FBC
- ESR and
CRP
- U/E/Cr
- Blood c/s
Imaging
- KUB
- CT KUB
- Renal U/S
- IVU
- Flexible
cystoscopy
- MCU
- DMSA
- MAG-3
Leukocytes, nitrites, proteinuria,

haematuria
WBC, RBC, casts
WBC and differential count

Inflammatory markers
Renal impairment
If patient is septic
Radio-opaque stones
Highly suspicious of stones
Hydronephrosis
Physiological/anatomical upper
tract abnormalities
Radiolucent stones
Renal function
Lower urinary tract abnormalities
Prevention
trimethoprim (check G6PD

status)
Change as required when urine
c/s results return
Usually treat for 28 days
If severe: IV cephalosporin +
gentamicin
Drink > 2L water per day
Urinate frequently
Double void if reflux present
Wipe from front to back after
micturition
Post-coital voiding
Abx prophylaxis for recurrent
UTI: trimethoprim,
nitrofurantoin
Cranberry juice (inhibits
adherence of E. coli to bladder
cells)
Sterile Pyuria
a)
b)
c)
d)
e)
f)
g)
Renal TB
Inadequately treated UTI
Calculi
Prostatitis
Bladder tumour
Interstitial nephritis
Appendicitis
Urinary Catheters and Lifespan

a) Foleys = 2 weeks
b) Silicon-coated = 4-6 weeks
c) Silicon = 3 months
Reflux uropathy
Renal scarring and differential
renal function (recurring UTI)
Management
Lower UTI
- Empirical Abx: trimethoprim

(check G6PD status),
amoxicillin, nitrofurantoin
- Change as required when urine
c/s results return
- Usually treat for 7 days
Acute
pyelonephritis
- Empirical Abx: broadspectrum

cephalosporin, ciprofloxacin
- Change as required when urine
c/s results return
- Usually treat for 14 days
- Empirical Abx: ciprofloxacin,
Acute
95
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
Body
2/3 water
(60%)
2/3 intracellular
(40%)
1/3 extracellular
(20%)
2/3 interstitial (13%)

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 Kussmauls (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)
96
e.
f.
g.
h.
i.
j.
k.
l.
m.
n.
o.
p.
BP normal, hypertensive
Capillary refill normal
Eyes normal
Mucous membranes normal
JVP normal, raised (>3cm)
Skin turgor normal, increased (taut, non-pliable)
Heart S3 best heard in left lateral position
Lungs bibasal inspiratory crepitations, wheeze
Liver enlarged, tender
Legs normal, oedema
Urine output normal
Lab results dilutional effects
6. Replacement fluids
a. Crystalloids normal saline (limited to extracellular space), Ringers lactate, Hartmanns
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
97
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
98
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
disorder
Metabolic
acidosis
Metabolic
alkalosis
Respiratory
acidosis
Initial
change
Decrease
HCO3
Increase
HCO3
Increase
pCO2
Compensatory
response
Decrease pCO2
Expected compensation
Increase pCO2
pCO2 = 0.6 x [HCO3]
Increase HCO3
Acute = HCO3 increase by 1mmol/L for every

10mmHg increase in pCO2
Chronic = HCO3 increase by 3.5mmol/L for every
10 mmHg increase in pCO2
Respiratory
alkalosis
Decrease
pCO2
Decrease HCO3
Acute = HCO3 decrease by 2mmol/L for every

10mmHg decrease in pCO2
Chronic = HCO3 decrease by 5mmol/L for every
10 mmHg decrease in pCO2
pCO2 = 1.2 x [HCO3]
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
99
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 (Cushings 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 (Conns, Cushings) = treat underlying causes
(d) Severe alkalosis = arginine HCl, NH4Cl, acetazolamides (NAGMA)
100
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
101
Medicine (Renal) = Respiratory Disorders
Check for appropriate HCO3- compensation
Respiratory Acidosis
1. CNS depression
2. Neuromuscular disorder
3. Thoracic cage limitation
4. Impaired lung expansion

5. Pulmonary disease
6. Drugs
1. Anxiety
2. Drugs
3. CNS stimulation
Respiratory Alkalosis
4. Liver disease
5. Pulmonary disease
6. Excessive mechanical
ventilation
102
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
o Biochemical results
K+ , HCO3- , CL-
Normal anion gap
(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
103
o
o
Biochemical results
K+ , HCO3- , CL-
Normal anion gap
(Acidic urine)
Causes
Adrenal disorders (Addisons disease, CAH), R A renal
Hyporeninaemic hypoaldosteronism (interstitial nephritis) R A renal
Pseudohypoaldosteronism R A
Clinical features
Primary renal disease
Adrenal disease
Management
HCO3- supplements
K+ reduction (Eg. Furosemide, thiazides)
Flucortisone
Comparison of Major Types of RTA
Hyperchloraemic
Type 1
Type 2
Type 4
Yes
Yes
Yes
>5.5
<5.5 (but usually >5.5 before the acidosis
<5.5
acidosis
Minimum Urine
pH
Plasma
becomes established)
Low-normal
Low-normal
High
Renal stones
Yes
No
No
Defect
Reduced H+ excretion
Impaired HCO3 reabsorption in proximal
Impaired cation
in distal tubule
tubule
exchange in distal
potassium
tubule
104
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
Cellular death
Shift of intracellular K+ into ECF
Impaired renal K+ excretion
Spurious
K+ containing medications = Span K

High-potassium foods
Haemolysis
Rhabdomyolysis
Burns
Catabolic states = fasting
Acidosis
Hypoxia
Insulin deficiency = DKA, non-compliant DM patient
B-Blockers
Digoxin toxicity
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 = Addisons 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
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.
105
3.
4.
5.
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
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
HO on call
a. Check with sample is not haemolysed
b. Ask for patients 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
106
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
Intracellular shift of
K+
GIT losses
Renal losses
Inadequate dietary intake

IV K+ free fluids
Alkalosis
Insulin = insulinoma, exogenous administraion
Salbutamol
Adrenaline
Vomiting
Diarrhoea
Pyloric stenosis
Villous adenoma
Intestinal fistua
Sequestraion of fluid in bowel (ileus, IO)
Renal tubular acidosis
Drugs = loop diuretics, thiazides
Excess aldosterone =
o primary aldosteronism (conns sydrome, bilateral adrenal hyperplasia)
o secondary aldosteronism (RAS, coarctation of aorta, hypovolaemia)
excess mineralocorticoid = Cushings 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 patients 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
107
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
hyponatraemia
Pseudohyponatraemia
*Causes = lipids,
proteins, glucose
*True Na+ =
Step 2: Urine osmolality
>300mosm
<100mosm
Fluid overload
Hypovolaemi
a
Step 3: Urinary Na+
Step 3: Urinary Na+

<20 mmol/L
1.
2.
3.
4.
>20 mmol/L
Cardiac failure
Nephrotic syndrome
Liver cirrhosis
Protein-losing enteropathy
GIT
1. Vomiting
2. Diarrhea
3. Intestinal
fistula
1. Renal failure
Euvolaemia
Step 3: Urinary Na+
<20 mmol/L
>20 mmol/L
Non-endocrine
1. Drugs
2. 1 polydipsia
Endocrine
1. SIADH
2. Hypothyroidism
3. Addisons disease
<20 mmol/L
>20 mmol/L
Extra renal loss
Renal loss
Skin
1. Burns
2. Excessive
sweating
3. Exudative skin
disease
1. Excess
diuretics
2. Tubulopathy
108
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 Addisons 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
109
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
110
Medicine (Renal) = Hypernatraemia

1. Definition
Na+ > 145 mmol/L
Usually treat when [Na+] > 150 mmol/L
2. Algorithm
Hypernatraemia
Input Disorder
Inc. Salt intake
Drugs
1. Excess
saline
2.Drugs
with high
Na content
3. NaHCO3
after
cardiac
arrest
Urine Osm < Serum

Osm
Excess H20 loss
1. Impaired thirst mech.

2. Limited access to H20
Water Deprivation Test
Pituitary DI
(desmopressin increases urine
Osm)
Hereditary
1. DIDMOAD Syndrome
Urine Osm > Serum

Osm
Impaired ADH
regulation
Dec. H20 intake
Endocrine
1. Conns
2.Cushings
Output disorder
Acquired
1. Head Injury
2. Pituitary
surgery
3. CNS Infection
4. Idiopathic
Renal
1. Osmotic dieresis
-DKA
-Urea
-Mannitol
TPN
Extrarenal
1. Excess
sweating
2.Burns
Nephrogenic DI
(desmopressin does not increases
urine Osm)
Hereditary
Acquired
1. Hypokalaemia
2. Hypercalcaemia
3. Obstructive uropathy
4. Nephrotoxic drugs
111
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 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
112
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
113
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.
2.
3.
4.
5.
Smoking
Alcohol drinking
Family set-up (main caregiver, health of family members, finances)
Lift-landing
Functional status (ADL/iADL)
Family History
114
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. Addisons 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 (Addisons disease)
c. Palmar erythema (CLD hyper estrogenism)
d. Dupuytrens 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 (Virchows node indicating advanced intraabdominal 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 Murphys 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 patients
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. Troisiers sign = presence of a large left supraclavicular lymph node with gastric carcinoma
7. Causes of abdominal distention (6Fs)
a.
b.
c.
d.
e.
f.
Fat = umbilicus buried in fat

Fluid = shifting dullness, fluid thrill, eversion of umbilicus, tense abdominal wall and flanks
Faeces = mass in the left lower quadreant, indentable, non-tender
Flatus
Fetus = umbilicus pushed upwards
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. Cullens 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. Courvosiers 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
Vascular
Infective
Trauma
Autoimmune
Metabolic
Infiltrative
Neoplastic
Haematological
Causes of splenomegaly
Portal hypertension
Viral hepatitis , EBV, CMV
Bacterial (SBE)
Protozoal (malaria, kala-azar)
Haematoma
SLE
RA (feltys syndrome)
Storage disorders (Gaucher, Neimann-Pick, glycogen storage, lipid storage)
Amyloidosis
Sarcodosis
CML (invasive)
Myelofibrosis (massive)
Lymphoma
Lymphoproliferative disorders
Polycythemia ruba vera (massive)
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.
d.
e.
f.
Dull percussion note over spleen but resonant over kidney due to gas filled fowel loops
Kidney is ballotable but not the spleen
Cannot get above the spleen (can get above the kidney)
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 oclock; 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
123
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
Cardiovascular
Congestive cardiac failure
Right heart failure
IVC obstruction
Portal/hepatic vein obstruction
Renal
Acute renal failure
Chronic renal failure
End stage renal failure
Nephritic syndrome
Nephrotic syndrome
GI
Chronic liver disease
Malnutrition
Exudative
Infection
TB peritonitis
Inflammation
Pancreatitis
Intra-abdominal malignancy
Pancreatic/gastric/colonic ca
Ovarian ca
Metastasis to liver
Metastasis to peritonium
Generalised vs Localised
Generalised
Cardiovascular
Right heart failure
Renal
Acute renal failure
End stage renal failure
Nephritic syndrome
Nephrotic syndrome
GI
Localised
Vascular
Portal HPT
a) IVC obstruction
b) Budd-chiari syndrome
c) veno-occlusive disease
d) Liver cirrhosis
e) Portal/splenic vein obstruction
Infection
TB peritonitis
Inflammation
Pancreatitis
124
Malnutrition
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.
2.
3.
4.
BGIT
Sepsis
Recent drug intake
Recent surgery/trauma
Complications (usually of CLD and cirrhosis)
1. Bleeding varices = hematemesis, haematochezia, melena

2. Encephalopathy = lethargy, drowsiness, confusion, personality changes
125
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)

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
126
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
127
Medicine (GIT) = Chronic liver disease and Liver cirrhosis

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 Wilsons 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
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 = duputyrens 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
Childs 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
Albumin
Bilirubin
Coagulopathy (PT)
Distension (ascites)
Encephalopathy
1 point
>35
<34
1-4s
None
none
2 points
28-35
34-50
4-6s
Mild
Grade 1-2
Points
Class
Life expectancy
5-6
7-9
A
B
10-15
15-20 yrs
Candidate for
transplant
1-3months
3 points
<28
>50
>6s
Severe
Grade 3-5
Peri-operative
mortality
10%
30%
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
Liver transplant
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, Wilsons disease, cystic fibrosis,
haemochromatosis, 1-antitrypsin deficiency)
Amyloidosis
Infiltrative
Sarcoidosis
Primary (HCC, hepatic adenoma, hepatoblastoma, hemangioma)
Neoplastic
Secondary (metastasis)
Lymphoma (Hodgkins, non-Hodgkins)
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
132
Chronic Liver disease

Area
Head and neck
Sign
Xanthelesma
(females)
Aetiology to consider
Primary biliary cirrhosis
Must always consider in a middle-aged lady

with splenomegaly and minimal signs of CLD
Slate-grey
Haemochromatosis
(males)
Parotidomegaly Alcoholic liver disease
Raised JVP
Limb
Lungs
Kayserfleischer rings
Duputyrens
contracture
Chorea
Tattoo
Pyoderma
gangrenosum
Lower zone
emphysema
Liver is typically big even if cirrhotic
Right heart failure

Wilsons disease
Alcoholic liver disease
Liver is typically big even if cirrhotic
Wilsons disease
Post-viral (likely Hepatitis B)
Ulcerative colitis
1-antitrypsin deficiency
-thalessemia major
Overall
Pituitary haemosiderosis
Cardiac haemosiderosis
Pancreatic haemosiderosis
Intervention
Request
Short stature
Hyperpigmented
Thalessemic facies (frontal bossing, flat nosebridge,
maxillary hyperplasia)
Looks younger for age
Hypopigmented areolae
Loss of axillary hair
JVP v wave
Pulsatile liver
Lower limb edema
Hypocount marks on fingers
Diabetic dermopathy
Splenectomy
Gonadal examination
Specific conditions
Haemochromatosis
Request to examine for:
a)
b)
c)
d)
Arthropathy pseudogout
CCFcardiomyopathy
Testicular atrophy pituitary involvement
Glycosuria with urine dipstick DM
133
Wilsons Disease
Area
Overall
Eyes
Sign
Short stature
Ptosis
Pallor and jaundice
Kayser-Fleischer rings
Face
Malar Rash
Upper limb
Small hand joint arthritis
Tremor/chorea
Lower limb
Swollen knees
Request urinalysis for glycosuria (proximal RTA)
Interpretation
Rickets secondary to
proximal RTA
Penicillamine-induced MG
Coombs negative
haemolytic anaemia
Copper deposits in
Descemets membrane of
cornea predominantly at 12
and 6 oclock positions. Can
also occur in PBC and
cryptogenic cirrhosis. Look
out for sunflower cataract
as well
Penicillamine-induced
lupus
Penicillamine-induced
lupus
Extrapyramidal syndrome
Pseudogout
Chronic UC
CLD + pyoderma gangrenosum = chronic UC and
a)
b)
c)
d)
e)
Cirrhosis
Chronic active hepatitis
Primary sclerosing cholangitis
Cholangiocarcinoma
Metastatic colorectal cancer
Request to examine
a)
b)
c)
d)
Joints sacroilitis, ankylosing spondylitis, peripheral large joint arthritis

Skin erythema nodosum, pyoderma gangrenosum
Mouth aphthous ulcers
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 (duputyrens
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
134
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.
2.
3.
4.
CCF
Valve replacement mechanical haemolysis
DM, HPT, HCL, AMI, IHD, CVA, cancer, asthma
Previous hospitalizations and surgeries
Drug history
1. Any drug allergies

Social history
1.
2.
3.
4.
5.
6.
7.
8.
Smoker
Alcoholic drinker
Family set-up
Main caregiver
Finances
Type of housing
Lift-landing
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 Glissons capsule; inflammation of
biliary tree)
Bilirubin
end-product of heme degradation heme
biliverdin
Heme
Biliverdin
bilirubin
Formed outside the liver in cells of mononuclear
system
oxygenase phagocyte
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 reexcreted 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 brainkernicterus
- 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, Wilsons disease, haemochromatosis, 1-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
- Rotors 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 stonesscarringstrictures
- 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
Precipitating factor
1st episode
Urine and stools
Anaemia
Progression
Acute
Usually present
Usually not the first time
Dark urine and stools
Usually present, +/- splenomegaly
Usually self-limiting and gradually improves once
precipitating factor is removed
Hepatic jaundice
138
Onset
Pain
Fever
Urine and stools
Progression
Post-hepatic jaundice
Onset
Pain
Fever
Urine and stools
Progression
Onset
Pain
Cholangitis
- Charcots triad
- Raynauds
pentad
2-hit phenomenon
Endocrine insufficiency
Migratory thrombophlebitis
Progression
Viralgradual with prodromal symptoms

Drug/alcohol-inducedacute
Dull and usually insignificant
Usually due to stretching of Glissons capsule
May occur with viral hepatitis
Low-grade and non-specific
Dark urine and stools
Usually self-limiting (die or get better)
Gallstoneacute
Gallstonebiliary colic (tenderness)
Ca pancreasepigastric pain radiating to the back
Hepatomegaly (Stretching of Glissons capsule)congestion
of intra-hepatic biliary spaces
Characteristic of cholangitis (Charcots triad feverRHC
painjaundice)
Spiking with chills and rigors
Dark urine
Acholic stools steatorrhoea
Progressive and relentless
Fluctuating
- periampullary ca (necrosis of tumour may relieve
obstruction)
- Gallstones
Benign (Sx jaundice)
Gallstoneacute
Usually absent
Acute and colicky
Malignant (Sx jaundice)

Usually gradual
LOA, LOW, fatigue, fever
Painless jaundice
Ca pancreasepigastric pain radiating to
back
Courvoisiers 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).
More
Less
-regurgitation of small bowel
-relentless tumour growth eventually leads
contents up biliary tree
to complete obstruction
->90% will have infected bile
-No regurgitation of small bowel contents to
cause infection
Usually obstructs biliary tree
Obstructs both biliary and pancreatic
only
ductssteatorrhoea and LOW
Absent
Worsens existing DM
Newly diagnosed DM
Usually absent
Suggests Ca pancreas (esp body and tail)
Self-limiting if gallstone
Relentless and progressive
passes
Fluctuatingperiampullary 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
HBS sepsis
Malabsorption (protein, fat, vitamins A/D/E/K)
- Protein malnutritionascites, LL oedema pleural effusion
- Hypoglycaemia
- Fat malnutritionsteatorrhoea, LOW, easy bruising
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 hrscholestasis
o Remains prolonged hepatocellular insufficiency
Portal hypertension
- Secondary to long-standing biliary obstructionbiliary 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 Inflammationoedema + neutrophilic infiltrateportal tract fibrosis and cirrhosis
- Cx-ascites, splenomegaly, dilated veins (gastro-oesophageal varices, caput medusa, haemorrhoids),
portal hypertensive gastropathy: mucosal changes.
2.
3.
4.
5.
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 obstructionALP, 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)
140
5.
6.
7.
8.
- Check for coagulopathy

Serum ammonia = measure of liver function
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
Autoimmune markers (anti-ds DNA, ANA, anti-mitochondrial Ab, anti-Sm Ab, ESR, CRP)
Tumour markers = -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
141
Determine hepatic causes of jaundice/grade liver tumour
Decompensated liver cirrhosis

BGIT
Constipation
Sepsis
Drug-inducedalcohol, 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
142
Medicine (GIT) = Acute Hepatitis

Aetiology
Vascular:
Infective:
Drug induced:
Autoimmune:
Metabolic:
Infiltrative:
Neoplastic:
Ischemia
Viral (hepatitis viruses, CMV, EBV, HSV, dengue)
Bacterial (salmonella, shigella)
Parasitic (malaria)
Alcohol, paracetamol, TCM, anti-TB drugs (e.g. isonazid, rifampicin, pyrazinamide),
anti-convulsants (e.g. sodium valporate), satins
Autoimmune hepatitis
Wilsons disease
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)
143
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 = Wilsons disease, haemochromatosis, 1 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
145
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%)
146
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-
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
148
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 IFN combination therapy partial efficacy
No vaccine available; difficult to cover agains the 6 major genotypes
149
Hepatitis D virus
Defective ssRNA virus requires HBsAg coat to infect cells
HBV serves as helper virus
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
Transmission
HAV
Icosohedral capsid,
ssRNA
Picornavirus
Faecal-oral
Incubation period
2 6 weeks
Carrier state
None
Chronic hepatitis
None
Fulminant hepatitis
0.1 0.4%
0.1 1% of blood
donors; 90 95% of
those infected at
birth (vertical
transmission); 1
10% infected as
adults (esp. If
immunecompromised)
5 10% of acute
infections (adults);
90% in infected
neonates
<1%
Hepatocellular Ca
No
Yes
Yes
Vaccine available
Others
Yes
Acute hepatitis
(symptomatic,
asymptomatic)
Yes
No
Fulminant hepatitis
almost never occurs
with HCV
Agent
HBV
Enveloped dsDNA
HCV
Enveloped ssRNA
Hepadnavirus
Parenteral, close
contact, vertical
4 26 weeks
Flavivirus
Parenteral, close
contact
2 26 weeks
0.2 1% of blood
donors; <1% are
healthy carriers
>60%; half then

progress to cirrhosis
Rare
HDV
Enveloped ssRNA
HEV
Unenveloped ssRNA
Calicivirus
Parenteral, close
contact
4 7 weeks
(superinfection)
1 10% of drug
addicts,
haemophiliacs
Waterborne
Flavivirus
Parenteral
2 8 weeks
Unknown
Unknown / none
1 2% of blood
donors
<5% if co-infection
with HBV; 80% upon
super infection with
HBV
3 4% in coinfection
None
None
0.3 3%
20% in pregnant
females
Unknown, but
unlikely
No
Unknown
No increase above
HBV
No
HGV
ssRNA
None
No
At present, not
considered
pathogenic
151
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 Glissons 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*
Duputyrens contracture
Dilated cardiomyopathy displaced apex beat, signs of CCF
Cerebellar signs
Parotidomegaly
Proximal myopathy
Peripheral neuropathy
Dementia
Wernickes encephalopathy classic triad of:
1) encephalopathy (confusion, loss of short-term memory)
2) ataxia
3) ophthalmoplegia (nystagmus, gaze palsies)
Korsakoffs 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
153
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, Cushings 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) = Wilsons disease (Hepatolenticular Disorder)

*History*
Hx of consanguinity Wilsons 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 Wilsons disease
*Physical Examination*
Kayser-Fleischer rings: greenish yellow to golden brown pigmentation at the limbus of the cornea due
to deposition of copper in Descemets 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 Fanconis 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 g/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
o
o
Adequate treatment compatible with normal life expectancy

Genetic screening for rest of the family
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
Hashimotos thyroiditis
Sjogrens 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
158
Immunosuppressants (corticosteroids, cyclosporine A, azathioprine, tacrolimus, methotrexate)

Liver transplant
*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
159
*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, Carolis disease)
Parasitic infections (oriental liver fluke, chronic typhoid carrier state)
160
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-toend bile duct anastomosis)
*clinical presentation: intermittent cholangitis

*investigations: PTC/ERCP (depends on level of narrowing)
*complications
161
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: Whipples 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)
162
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 = Wilsons 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
163
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)
164
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
165
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
166
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, crohns 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)
167
-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
168
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
169
-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 crohns disease
-evident in Jews & Caucasians
-higer rates in monozygotic twine & first-degree relatives
-assoc. with SLE,Hashimotos 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
171
-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)
Crohns 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
Crohns 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
1.Gross pathology
a. location
b. skip lesions
c.stricture formation
d.toxic megacolon
e.fistula/sinus formation
f.pseudopolyps
2.Microscopic Pathology
a. inflammation
b.non-caseating granulomas
c.ulceration
d.fibrosis
e.glands
3.Clinical
a. bloody diarrhea
b.abdominal pain
c.palpable mass
d.perianal disease
e.fat/vitamin malabsorption
f.malignant change
e.recurrence after surgery
UC
CD
Isolated to large bowel
Absent
Absent
Present
Absent
Present
Any part of GIT

-small bowel + colon (50%)
-small bowel (30%)
-colon (20%)
Present (cobblestone mucosa)
Present
Absent
Present
Absent
Mucosa & submucosa

Absent
Superficial
Less
Gland destruction, crypt abscess
Transmural
Present
Deep,linear serpentine
more
Intact glands
Very common
Pre-defecation urgency
Uncommon
Less common
Absent
Greater
Rare
Uncommon
Post-prandial
Frequent (RIF)
More common
Present (in small-bowel involvement)
Lesser
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)
173
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,
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
ampicillin, cephalosporin)
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
Patients vitals
Hydration status
175
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 patients 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/perforationurgent 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
Moderate disease
Severe disease
Oral 5 ASA
5 ASA/steroid enema
Oral prednisolone 40mg OM
IV hydrocortisone x 5/7
177
Maintain remission
Ulcerative colitis or
Crohns colitis
Crohns ileal disease
Sulphasalazine (usu
2g)
Proven benefit in colitis = not for

small bowel CD
Decreases relapse risk from 60%
to 15%
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
completelybovine 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.
2.
3.
4.
DM, HPT, HCL, IHD, CVA, cancer, asthma, TB

If suspect asthmaallergic rhinitis, allergic conjunctivitis, eczema, food allergy, drug allergy
Previous hospitalizations
Previous surgeries
Drug history
1. Any known drug allergy

- If yeswhat 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, fiancs
5. Lift-landing
6. Functional status
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 patients 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
marfans (MVP)
*Harrisons 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 2-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 (horners 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 pectoriloquywhispered 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.
2.
3.
4.
Request for sputum mug, blood pressure and temperature chart

Look for pulmonary HPT (Palpable p2, Parasternal heave, loud p2)
RHF (Raised JVP, hepatomegaly, sacral oedema
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. Pembertons 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
displacement
Chest wall
movement
Percussion
note
Breath sounds
Adventitious
sounds
Consolidation
None
dull
Bronchial with
increased VR
Moderate/coarse
Inspiratory
crepitations
Collapse
Ipsilateral shift
dull
Absent or reduced,
VR resonance
varies
Absent
Pleural
effusion
Apex beat
displaced to the
opposite side
(tracheal
deviation is
massive)
Tracheal
deviation to the
opposite side if
tension
pneumothorax
None
Reduced
over
affected
area
Reduced
over
affected
area,
flattening of
the chest
wall
Reduced
over
affected
area
Stony dull
Absent
Reduced
over
affected
area
Hyperresonant
with loss of
cardiac and liver
dullness
Absent/reduced
over fluid,
bronchial at the
upper border with
decreased vocal
resonance
Absent/reduced
Reduced
bilaterally
Normal/hyper
Resonant
Expiratory
rhonchi
Reduced
bilaterally
Normal/dull
Reduced with
prolonged
expiratory phase
Normal
Pneumothorax
Asthma
Pulmonary
fibrosis
Tracheal
deviation to
affected side if
apical lesion
Absent unless
subcutaneous
emphysema
Fine Inspiratory
crepitations
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, Sjogrens 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 Pembertons sign)
Tracheal compression (stridor, respiratory distress)
Horners 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
CVS
V = pulmonary embolism, Wegeners granulomatosis, Goodpastures 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
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) Wegeners granulomatosis ESR, CRP, ANCA
c) Goodpastures 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

Dyspnoea = subjective feeling of discomfort a/w breathing
Respiratory
Airway
Asthma
COPD (chronic bronchitis, emphysema)
Bronchiectasis
Foreign body obstruction
Cystic fibrosis
Laryngeal/pharyngeal tumor
Bilateral vocal cord palsy
Tracheal obstruction/stenosis
Tracheomalacia/ laryngomalacia
Parenchyma
Pneumonia/TB
Pneumothorax
Pulmonary fibrosis
Pulmonary oedema
Lung ca
Respiratory distress syndrome
Allergic alveolitis
Sarcoidosis
Circulation
Pulmonary embolism
Pulmonary AV malformation
Pulmonary arteritis
CVS
Chest wall and pleura

Pleural effusion
Rib fracture
Ankylosing spondylitis
Kyphoscoliosis
Angina
Acute coronary syndrome (unstable angina, AMI)
Mitral/aortic valve disease

Cardiomyopathy
Pericardial effusion/constrictive pericarditis
Neuromuscular Guillain-Barre syndrome
Myasthenia gravis
Others
Anemia
Hyperventilation
Acidosis
History taking
Date of admission
1. Dyspnoea
Mode of onset (what were you doing?)
Frequency
Duration
Acute/gradual onset
Progressively worsening/getting better
Severity = able to speak in sentences, phrases or words/ activities
affected (NYHA class)
Triggers = exertion (quantify effort tolerance), rest
Aggravating factors
Relieving factors = bronchodilators, rest
a/w orthopnoea and PND
2. aetiology
CVS = chest pain, nausea/vomiting, diaphoresis, palpitations,
giddiness, syncope, ankle oedema, fatigue, intermittent
claudication
RT = fever, cough (+haemoptysis), recent URTI, hoarseness, noisy
breathing, chest pain, night sweats, LOA, LOW, malaise, history of
189
trauma/FB aspiration, history of immobility/recent travel/major

surgery/OCP/HRT/LL swelling
Neuromuscular = generalised weakness and numbness
Others = anemia (pallor, chest pain, SOB, giddiness, palpitations,
fatigue, PR bleeding, menorrhagia), hyperventilation (specific
situations, numbness/tingling/cramps in extremities)
3. Systemic review
Recent changes in urinary/bowel habits
4. Management prior and during admission
5. Has this happened before? Describe? Investigations? Management?
Asthma, COPD, TB, ca
HPT, HCL, DM, AMI/IHD
Previous hospitalisations and surgeries
Drug history
Any known drug allergy
Current medications
Recent drugs = beta blockers, NSAIDs, aspirin, thyroxine
Social history
Smoker (significant smoking history of >10 pack years)
Alcohol
Occupational history
Family set up
Main caregiver
Type of housing/lift landing
Finances
Functional status
Family history
TB, lung ca, asthma, DM, HPT, HCL, AMI/IHD
Investigations
1. ECG and cardiac enzymes = ACS, PE
2. FBC = Hb (anemia), WBC (leucocytosis in infections)
3. U/E/Cr = electrolyte disturbances in acidosis/alkalosis
4. ABG =acidosis/alkalosis, types 1 or 2 resp failure
5. CXR = hyperinflation, rib fracture, pneumothorax, consolidation,
pleural effusion, mass, cardiomegaly, CCF
6. D-dimer = if PE suspected
7. -natriuretic peptide = if CCF suspected
Management
1. Secure patient airway = head tilt chin lift, finger sweep, exclude upper
airway obstruction esp if stridor present, give supplemental oxygen
(COPD/smoker O2 28% by Venturi mask), place on pulse oximetry
2. Ensure pt is breathing spontaneously = auscultate lungs
3. Haemodynamically stable = look for signs of shock, HR/RR/BP, set
large bore IV access, obtain bloods for investigations
4. Resuscitate pt if necessary
5. Obtain history and physical examination once pt is stable
190
Medicine (Respi) = Approach to Chest Pain and Dyspnea

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

Pleural effusion
Rib fracture
Anemia
History
Name/age/race/gender/occupation/drug allergy
Date of admission
1. Chest pain
Mode of onset
Frequency
Duration
Triggers (exertion, palpitations, anxietyCVS, food GIT etc)
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, bronchodilatorsrespi)
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)
191
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
192
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)
193
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
194
Complications
Chronic Bronchitis
Type 2 respiratory failure: low paco2 due to v/q
mismatch from mucous plugging.
Short term: increased paco2 stimulates respiration
Long term: insensitive to high paco2 levels, hence
depend on hypoxic drive
polycythemia
Pulmonary hypertension-> cor pulmonale
Respiratory infections
Obliterative bronchitis(due to mucous plugging)
Emphysema
Type 1 respiratory failure: low po2 and low/normal
paco2
Pneumothorax from ruptured bullae

Pulmonary hypertension-> cor pulmonale
Respiratory infections
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
d) others: increased TLC, FRC, RV
FEV1/FVC > 12%)
195
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%
III=severe
<70%
30-50%
IV= very severe
<70%
<30% or <50%+resp failure
Long acting bronchodilators:

1)LABA (formoterol, salmeterol)
2)LAC (tiotropium)
1) SAB (sympathomimetic)
2) LAB + ICS (prophylactic):
a)seretide= salmeterol +fluticasone
b)symbicort=budesonide+formoterol
1)
2)
3)
4)
LAB + ICS
Theophylline
Pulmonary rehabilitation
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)
196
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
197
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
and SAAC
-example=combivent
-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)
198
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) Kartageners 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
inflammation
Obstruction
Wall damage and fibrosis due to

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

(a) destruction of elastic tissues
(b) contraction of fibrous tissues exerts traction on bronchi
199
(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
Reids 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, Kartageners 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:
200
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
201
- 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
202
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)
203
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)
204
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)
205
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 TBswelling/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 -> Addisons disease
206
o
o
Skin: lupus vulgaris, erythema nodosum

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 0s test by >10mm, means that first Mantoux reactivated
previously exposed immune system, now pt is displaying competent immune
response dont 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
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
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
< 5mm of
induration
Patient is
a child,
adolesce
nt,
and/or is
immunoc
ompromi
sed and
had close
contact
with TB
Initiate
treatment of
latent
tuberculosis
infection
All others
No therapy
10 mm or
more of
induration
5 to 9mm of
induration
All others
Is known to
have or
suspected of
having HIV
infection or
another
cause of
immunocom
promise, is a
close contact
of a person
with
infectious TB
or has a chest
radiograph
suggestive of
previous TB
No risk factors for

reactivation and
low demographic
risk of TB
Risk factors for

reactivation present or
high demographic risk
of TB
No therapy
Less than 15
mm of
induration
No therapy
15 mm or
greater of
induration
Initiate
treatment of
latent
tuberculosis
infection
Initiate
treatment of
latent
tuberculosis
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
-Horners 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 (Wegeners granulomatosis)
c) Extrinsic- Lymphadenopathy, medialstinal masses, aortic aneurysm
2. Request to examine- Vitals, sputum mug, posterior chest-pleural effusion, pembertons sign, abdomenhepatomegaly, 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
Nephrotic syndrome
*Lymphatic obstruction
Tumour compression
Post-radiotherapy
SVCO
*others
Hypothyroidism
Meigs 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)

Cardiac failure
-raised JVP
-Displaced apex beat(heaving)
-S3 heart sound
-Gallop rhythm
Exudate (usually unilateral)

Malignancy
-Radiotherapy marks
-Mastectomy
-cachexia
-clubbing
-nicotine stains
-HPOA
-Cervical lymphadenopathy
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
Gross appearance Straw coloured clear
Cytology
Clinical chemistry
Immunology
Exudate
Yellow turbid
Bloody (trauma, malignancy, TB, PE)
Normal
High WBC
* Neutrophils infection, PE
* Lymphocytes TB, malignancy
* Eosinophils presence of air/blood
Malignant cells
Microorganisms
Protein <30g/L
Protein >30g/L
Lights 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
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) patients 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
Aetiology
Pneumothorax = air in pleural space

Haemothorax = blood in pleural space
Chylothorax = lymph in pleural space
Empyema = pus in pleural space
Spontaneous
(i)
Primary
- No underlying lung disease
- Usually due to connective tissue defect in pleural wall bleb formation and rupture
- a/w Marfans 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 Marfans 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
ABG
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
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, midaxillary 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
Decreased
surfactant
Sudden re-expansion
Sudden inflow of blood, increased

capillary pressure
Increased capillary leak
Alveolar distension
squeezes capillaries
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
221
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
222
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
223
Cardio Vascular System

Medicine (CVS) = History Taking: CVS
Date of admission
1. Cardiovascular symptoms
(a) Chest pain
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)
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
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
224
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
225
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.
2.
3.
4.
5.
Smoking
Alcohol drinking
Family set-up (main caregiver, health of family members, finances)
Lift-landing
Functional status
Family history
226
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.
2.
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 marfans syndrome)

Respiratory rate (15s)
Hands
1.
2.
3.
4.
Pulse rate: hold patients 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)
Radio-radial delay (aortic arch aneurysm, aortic dissection)
Radio-femoral delay (coarcation of the aorta)

Collapsing pulse: ask if there is shoulder pain, lift up patients hand and feel an increase in volume (AR)
Check fingers for:
Cyanosis (R->L shunt)
Clubbing (IE)
Splinter haemorrhages in nail beds (IE, Vasculitis)
Tendon xanthomata (familial hypercholesterolaemia)
Oslers 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.
2.
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)
Check mouth: lips and tongue central cyanosis; teeth, gums, pharynx IE
227
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)
Parasternal heave for RVH (place hand vertically over sternum for 3-5s PS, pulmonary hypertension
Palpable tap of P2 over pulmonary area -> pulmonary hypertension
Thrills for palpable murmurs (place hand horizontally over base of heart) systolic/diastolic
2.
3.
4.
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)
-
228
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
stenosis
Harsh ejection systolic murmur radiating to carotids

Loudest in patient sitting up and in full expiration
Slow rising pulse carotids
Mitral
stenosis
Loud S1
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
229
Legs
1.
2.
3.
4.
Pedal oedema (look at patients face when doing it

Check R/L dorsalis pedis
Check for cyanosis and clubbing of toes
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 (roths 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
230
Medicine (CVS) = Issues for discussion

Clubbing
CVS
Respiratory
GIT
Others
Infective endocarditis
Congenital cyanotic heart disease
Suppurative conditions (empyema,
bronchiectasis, abscess)
Lung carcinoma
Idiopathic pulmonary fibrosis
Cystic fibrosis
Inflammatory bowel disease (eg.
Crohns)
Celiac disease
Biliary cirrhosis
Thyrotoxicosis (acropachy)
Idiopathic
Grading
Grade 1 = fluctuance at nail bed
Grade 2 = loss of nail bed angle
Grade 3 = Increased curvature of nail
(drumstick)
Grade 4: HPOA (Hypertrophic
Pulmonary Osteoarthropathy)
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 korokoffs sounds in expiration and
their apperarance throughout the respiratory cycle
231
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.
b.
c.
d.
e.
Visible but not palpable

Obliterated by finger pressure on vein
Varies with changes in respiration and posture (flatters with inspiration)
Double pulse for every arterial pulse
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
232
a. Raised JVP with abnormal waveform = fluid overload, RHF

b. Raised JVP with absent pulsation = SVCO
c. Raised JVP on inspiration (kussmauls 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
S2
Closure of mitral and tricuspid valves

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
233
Cardiac murmurs
ESM (Ejection systolic
murmur)
Waveform/ Crescendo-decrescendo
Character
murmur with S2 heard
Occurs
when
Causes
Turbulent flow
through the
aortic/pulmonary
valve orifices
Or greatly increased
flow through the
heart
Innocent murmur
(esp in children)
High-output states
(anemia, pregnancy)
Organic (AS, PS,
HOCM)
PSM (Pan-systolic
murmur)
EDM (Earlydiastolic murmur)
Uniform murmur
which merges with S2
High-pitched and
easily missed (listen
for absence of
silence in early
diastole
Organic (AR, PR)
A ventricle leaks to a
lower pressure
chamber/ vessel
Organic (MR, TR,

VSD, MVP)
*MVP late systolic
murmur mid-systolic
click, accentuated by
valsalva manoeuvre
Graham-Steell
murmur = mitral
stenosis
pulmonary
hypertension
pulmonary
regurgitation
MDM (Middiastolic
murmur)
Low-pitched and
rumbling with an
opening snap after
S2
Impaired flow
during ventricular
filling
Organic (MS, TS)
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
Unilateral, pitting
Bilateral, nonpitting
Cardiac (CCF, constrictive pericarditis)

GIT (liver cirrhosis, malnutrition, protein-losing enteropathy)
Renal (nephrotic syndrome, ESRF)
DVT
Compression of large veins by tumour/LAD
Hypothyroidism
Lymphoedema (infection, malignant, congenital)
234
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 radiofemoral 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
Respiratory
Chest wall
Gastrointestinal
Angina (stable, unstable, variant)

AMI
Pericarditis/Myocarditis
Aortic dissection
Pulmonary embolism
Pneumonia with pleurisy
Pneumothorax
Rib fractures
Thoracic herpes zoster
Muscular strain
Costochondritis (Tietzes syndrome)
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
236
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
237
*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.
b.
c.
d.
e.
Sharp or stabbing in nature

Lasts <30s
Pleuritic component
No history of angina/AMI
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
4.
5.
6.
7.
- AR = proximal AD
- Pericardial rub = pericarditis
- Peripheral oedema = CHF, RVF, DVT
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
Abdominal examination
- Guarding and rebound = perforated ulcer
- Epigastric tenderness = PUD
- Generalised abdominal pain = mesenteric infarction from AD
CNS
- Hemiplegia = AD involving carotid artery
Skin
- Herpes zoster = unilateral maculopapular rash/vesicles in dermatomal pattern
239
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.
2.
3.
4.
4 blood tubes = FBC, GXM, U/E/Cr, PT/PTT

Cardiac enzymes (CK, CKMB, troponin-T) and bedside trop-T
ABG
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)
240
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 = samters 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
241
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 =
2.
3.
4.
5.
Central crushing chest pain

Triggered by stress (emotional, exertion)
Relieved by rest
Decubitus angina (severe coronary disease) = on lying down
Nocturnal angina (critical coronary disease) = vivid dreams at night
Prinzemetal/variant angina = rest angina triggered by coronary vasospasm
Higher frequency in women
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
Smoking
- Risk of Ami same as non-smokers
after 2 years
- Risk of angina same as non smokers
after 10 years
Alcohol
Obesity
Physical inactivity
Hypertension
Hyperlipidaemia
Diabetes mellitus
Non-modifiable
Gender (men)
Ethnicity (Indians)
Age (older)
Family history of IHD/AMI
Personal history of IHD/AMI
Homocysteinaemia
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
2.
3.
4.
5.
- Nuclear medicine
- MRI
2D-echocardiogram
- Left ventricular ejection fraction
- Valvular heart disease
MIBI perfusion scan
MUGA functional scan (multiple gated acquisition scan)
Coronary angiogram (delineate exact coronary anatomy in patients going for revascularisation)
Management
Acute
1. Stabilise patient if necessary
- Ensure patent airway
- Ensure spontaneous breathing ->
-
Ensure good circulation ->
Give supplemental O2
Place on SpO2 monitoring (keep SpO2 >95%)
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
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
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 thrombosisDynamic 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
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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
Advantages
Disadvantages
Thrombolysis
Rapid administration
Widely available
Convenient
Does not require expertise
PTCA
Better clinical efficacy
# superior vessel patency
# reduced re-occlusion rates
Less haemorrhagic risk
Early definition of coronary
anatomy
# allows tailored therapy
# more efficient risk stratification
Patency ceiling = vessel patency

restored in only 60 85%
Less clinical efficacy
# optimal reperfusion not
achieved in > 50% of patients
# higher rates of re-occlusion
Haemorrhagic risk
Delay limits efficacy

Less widely available
Requires expertise
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
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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
Most commonly used
Cost-effective
Therapy of choice when risk of
intracranial haemorrhage is high
e.g. elderly patients
Recombinant tPA
< 50 yo
Anterior AMI
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)
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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
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-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)
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
# -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, patients 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 flapischaemia
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
-Dressiers 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. # Starlings 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 (ischaemiafibrosis), cardiomyopathy, myocarditis
(b) Restricted filling = constrictive pericarditis, cardiac tamponade, restrictive cardiomyopathy
(c) Inadequate heart rate = negative inotropic drugs (anti-arrhythmics, -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
Right-sided HF
Biventricular
HF
High-output HF
Systolic dysfn
Diastolic dystn
Decreased LV output
Increased LA or pulmonary venous pressure
Acute = APO
Gradual = reflex pulmonary vasoconstriction pulmonary HPT
Decreased RV output
Causes = dilated CMP, IHD
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
Defective diastolic filling due to decreased LV complianceimpaired 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
- Goldbergs 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 bats 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 patients 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 patients 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 EDVrelieve 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 patients 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 patients 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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(b)
(c)
(d)
(e)
(f)
-
- Monitor vitals and urine output to avoid volume contraction

- Achieve negative balance of 1-2L/day
ACE inhibitors = captopril
- Monitor for hypotension (esp postural), hyperkalaemia and worsening renal function
Nitrates = IV GTN (lower LV EDVrelieve symptoms of pulmonary congestion)
- IV nitroglycerine/nitroprusside
- Contraindicated in inferior/right ventricular infarct or hypotension (SBP must be >90mmHg)
- Continuous BP monitoring needed
Digoxin if hypotensive
Admit = CCU Acute coronary syndrome, intubated
HD CPAP
General ward the rest
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)
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. -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 + -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
Hyponatraemia
Impaired liver
function
Thromboembolism
Arrhythmias
K+-losing diuretics
Hyperaldosteronism (due to RAAS activation)
Impaired aldosterone metabolism due to hepatic
congestion
Diuretics
ADH secretion
Failure of cell membrane ion pump due to ischaemia
Hepatic venous congestion
Ischaemic hepatitis
Low cardiac output
Immobility
Arrhythmias and AF
Intracardiac thrombus due to MS or LV aneurysms
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 patients individual and medical circumstances.
Factors influencing prognosis
Risk Factors for Cardiovascular Disease
Levels of systolic and diastolic BP (Grades 1-2)

Age (Men > 55 yrs; Women > 65 yrs)
Smoking
Family history of premature CVD (Men < 55 years;
Women < 65 years)
Total cholesterol > 6.2 mmol/L (240 mg/dL)

Reduced HDL-C < 1.0 mmol/L (40mg/dL)
Raised LDL-C > 4.1 mmol/L (160 mg/dL)
Diabetes mellitus
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
Ischaemic stroke
Cerebral hemorrhage
Transient ischaemic attack
Heart disease
LVH (ECG, 2DE or CXR)
Myocardial infarction
Angina pectoris
Renal disease
Microalbuminuria (microalbumin-creatinine
ratio > 30 mg/g) or Proteinuria (>0.5 g/24hrs)
Renal impairment [plasma creatinine
concentration > 132 mmol/L(>1.5mg/dl)]
Diabetic nephropathy
Retinopathy
Generalized or focal narrowing of the retinal
264
Coronary revascularization
Congestive heart failure
Vascular disease
Dissecting aneurysm
Symptomatic arterial disease / PVD
arteries
Haemorrhages or exudates
Papilloedema
Atherosclerosis
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 patients
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
(No risk factors)
Systolic
BP
130- LM
139mmHg/ Diastolic
BP 80-89mmHg
Systolic
BP
140- LM + Rx*
159mmHg/ Diastolic
BP 90-99mmHg
Systolic
BP
>160 LM + Rx
mmHg/ Diastolic BP
>100 mmHg
Risk Group B
(1-2 risk factors)
LM
Risk Group C
(>3 risk factors or
Diabetes Mellitus or
TOD/ACC)
LM + Rx
LM + Rx
LM + Rx
LM + Rx
LM + Rx
*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
265
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
Clinical features
Hypertensive retinopathy
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 = Cushings syndrome
Conns 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
267
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
Conns = muscle weakness (hypokalaemic periodic paralysis)

Cushings = 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
269
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 = cushings syndrome
Prognathism, frontal bossing, large hands and feet = acromegaly
Caf 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
S4 heart sound
Bibasal inspiratory crepitations
Peripheral oedema
Carotid bruit
Abdomen
Bilateral ballotable kidneys = APKD
270
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 patients vitals
o Secure airway if patient unconscious
271
o Ensure patient is breathing spontaneously -> give supplymental O2, monitor pulse oximetry
o Obtain patients 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
nitroprusside
First line treatment

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
272
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

273
b) Prototypes
i) Enalopril
- Pro-drug that is converted by de-esterification to
elanoprilat (only IV use)
ii) Captopril
- Competitive ACE inhibitor
- Short T1/2 : TDS dosage
c) Side effects
i) Dry cough
ii) First dose hypotension
iii) Hyperkalemia & metabolic acidosis
iv) Macular rash
v) Neutropenia
vi) Fetotoxicity
vii) Nephropathy
- Reduces glomerular filtration pressure
- Precipitates ARF in patients with impaired renal function
or RAS
- Contraindicated if Cr > 300mmol/L
- Check u/e/cr before and 1-2 weeks after starting Rx
d) Advantages
i) Very effective especially when given with diuretics
ii) Renoprotective = prevents/reduces proteinuria
Stabilies renal function
iii) Extremely useful in Tx of heart failure
iv) Greater fall in Bp in high rennin states
4) Angiotensin 2 Receptor blockers
a) Mechanism of action = competitive inhibition of angiotensin 2
receptors G protein linked
i) Lorsartan
ii) Irbesartan
b) Side effects
i) Hyperkalemia and metabolic acidosis
ii) Nephropathy
iii) Fetoxicity
c) Advantages
i) No dry cough of ACE inhibitors
ii) Renoprotective
iii) More selective than ACE inhibitors for angiotensin effects
iv) More complete inhibition of angiotensin effects of ACE
inhibitors
5) B Blockers
a) Mechanism of action = blocks B-adrenergic actions
i) Negative inotropic and chronotropic effects
- Decrease Hr (decrease Av and SA conduction velocity)
- Decrease contractility decrease cardiac output
- Vasodilatation
- Increase diastolic time increase coronary perfusion
ii) Inhibits B mediated rennin release
b) Contraindications
i) Asthma/COPD
ii) Severe bradycardia
iii) Complete heart block
iv) Peripheral vascular disease
v) Diabetes
c) Drug-drug interactions
i) Avoid verapamil and diltiazam = excessive negative inotropic
effect
ii) Effects decreased in presence of NSAIDS = reduced
production of prostaglandins (vasodilators)
iii) Metabolized by liver = increased concentrations if given with
cimetidine
d) Side effects
i) CVS = bradycardia, hypotension, syncope
ii) CNS = giddiness, irritable, hearing and visual disturbances,
confusion - usually with chronic treatment
iii) GIT = nausea, vomiting, abdominal pain, constipation,
diarrhea
iv) DM = hypoglycemia, mask positive signs of hypoglycaemia
v) Asthma = bronchoconstriction
vi) Withdrawal syndrome after discontinuation of prolonged use

- Tachycardia
- Angina
- Hypertension
- AMI
6) Calcium channel blockers
a) Classification
i) Dihydropyridine
- Amlodipine (norvasc)
- Nifedipine (adalat)
ii) Non-Dihydropyridine
- Verapamil
- Diltiazam
b) Mechanism of action
i) Arteriodilatation = reduces afterlaod
ii) Decreases contractility
iii) Negative inotropic/chronotropic effects (except amlodipine
& nifedipine)
c) Contraindications
i) Heart failure
ii) Prolonged QT syndrome
iii) Heart block
d) Side effects
i) Fluid retention
ii) Constipation
iii) Vasodilatation = dizziness, flushing, headache
7) Diuretics
a) Sites of action
i) Proximal tubule = carbonic anhydrase inhibitors
ii) Thick ascending limb = loop diuretics (frusemide) inhibits
Na/K/2CL
iii) Distal tubule = thiazides inhibits Na/Cl cotransporter
iv) K+ sparing late distal tubules = aldosterone antagonists

spironolactone
b) Carbonic anhydrase inhibitors
i) Acetazolamide (diamox)
ii) Proximal tubule = iso-osmotic reabsorption of water
Secretion of H+ and organic anions
Reabsorption of Na+
iii) MOA = inhibits carbonic anhydrase which catalyses
dehydration of carbonic acid (H2Co3)
- Affects Na+/H+ exchanger
- Inhibits Na/Hco3 reabsorption
iv) Weak diuretic limited clinical utility due to compensation
by Na/Cl cotransporter
v) Side-effects = hypokalemia
Metabolic acidosis
CNS toxicity
vi) Indications = glaucoma
Epileptic seizures
Acute mountain sickness
c) Loop diuretics
i) Example = frusemide (lasix)
ii) Ascending limb of LOH = active NaCl reabsorption/water
impermeable
iii) Most potent diuretic
iv) Mechanism of action = inhibits Na/K/2Cl cotransporter
Induces prostaglandin synthesis
v) Side effects
- Hyponatremia
- Hypokalemia
- Hypochloremia
- Hypomagnesmia
- Calciuria no hypocalcemia as Ca is absorbed in PCT
275
- Metabolic alkalosis
- Auditory and vestibular toxicity
- Venodilatation and hypovolaemia
- Hyperglycemia
- Hyperuricaemia
- Hyperlipidemia
vi) Indications
- CCF
- Oedema
- Acute hyperkalemia and hypercalcemia
d) Thiazides
i) Example = hydrochlorothiazide
ii) Distal tubule = active NaCl reabsorption/impermeable to
water
iii) Mechanism of action = inhibits NaCl cotransporter
Reduces peripheral resistance with
chronic use
iv) Side effects = hypo Na, hypo K, hypo Cl, hypo Mg
Reduced urinary Ca2+
Metabolic alkalosis
Photodermatitis
Venodilatation and hypovolemia
Hyperglycemia, hyperuricaemia,
hyperlipidaemia
e) Aldosterone antagonists (K+ sparing)
i) Examples
- Spironolactone
- Amilonide
Mechanism of action = decreases synthesis of aldosterone
sensitive proteins involved in Na+/K+ ATPase & apical Na+
channels
*aldosterone = Stimulates Na+/H+ exchange

Stimulates K+ excretion
Acts on cytosolic and membrane
receptors
ii) Short T1/2 = 10 mins

Bioactive metabolite (canrerone) has longer T1/2 = 15 hrs
iii) Side effects
- Hyperkalaemia
- Metabolic acidosis
- Anti-androgenic effects = gynacomastia/testicular
atrophy/menstrual disorders/hirstrusim
iv) Mild diuretic used together with other diuretics
f) Osmolar diuretics
i) Examples = mannitol, urea
ii) Characteristics = small inert molecules that are filterable &
non diffusible
Poor oral absorption
Not metabolized
Excreted unchanged
Given IV
iii) Mechanism of action
- Act in segments that are freely permeable to H20 = PCT,
descending limb
- Increases urine volume
- Increases urine flow rate
- Decreases contact time between fluid and tubular
epithelium
- Decreases Na+ reabsorption
iv) Side effects
- Dehydration and hyper Na+ (inadequate hydration;
excessive use)
- ECF volume expansion & Hypo Na+ (may cause Heart
Failure)
v) Indications
- Increased ICP
- Cerebral oedema
- Increased IOP
276
Medicine (CVS) = Guidelines for selecting drug treatment of hypertension

Concomitqant conditions
Heart failure
Angina
Post Myocardial infarction
Isolated systolic Hypertension
Diabetes Mellitus with Proteinuria

(micro or Macroalbuminuria)
Diabetes Mellitus
Post Stroke
Asthma & Chronic Obstructive
Pulmonary Disease
Heart Block
Gout
Bilateral Renal Artery Stenosis
Peripheral Vascular Disease
Pregnancy
Recommended drugs
Diuretics
ACE inhibitors
Angiotensin II receptor blockers
Beta blockers
Calcium channel blockers
Beta-blockers
ACE inhibitors
Diuretic
ACE inhibitors
ACE inhibitors
Angiotensin II receptor Blockers
ACE inhibitors
Diuretics
ACE inhibitors
Contraindicated drugs
Beta Blockers
Diuretics
Beta Blockers
Beta blockers
Diuretics
ACE inhibitors
B Blockers
ACE inhibitors
Medicine (CVS) = Lipids

1. Reference Ranges
Patients w/o preexisting cardiac risk
LDL <3.4 mmol/L
HDL > 1.0 mmol/L
Total <5.2 mmol/L
Patients with preexisting cardiac risk

LDL < 2.6 mmol/L
HDL > 1.0 mmol/L
Total < 4.1 mmol/L
2. Lipid Disorders plays a major role in pathogenesis of CHD

Highest In
- Hypercholesterolaemia
Malays > Chinese > Indians
Clinically relevant risk of CHD begins with min TC =
Males > Females
3.9 mmol/L
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
(Familial, Polygenic)
Mixed Dyslipedemia
(Familial, polygenic
Hypertriglyceridaemia
(TG > 4.5 mmol/L)
Severe Hypertriglyceridaemia
(TG > 10mmol/L)
*main CX = acute pancreatitis
Increased LDL
Increased Cholesterol
Increased LDL, VLDL
Increased cholesterol & TG
Increased VLDL
Increased TG
Chylomicrons
Increased TG
*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
Nephrotic syndrome
Hypothyroidism
Alcohol abuse
Pregnancy
Cholestasis
Drugs (diuretics, B-blockers, OCP, Steroids
Increased TG
Decreased HDL- C
Increased TG
Increased Total Cholesterol
Increased Total Cholesterol
Increased TG
Increased TG
Increased Total cholesterol
Increased TG
May increased Total Cholesterol
Decreased HDL - C
278
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
Mix dyslipidaemia
Hypertriglyceridaemia
Severe hypertriglyceridaemia
Isolated low HDL C
Statin, ezetimibe
Statin + fibrate/nicotinic acid
Fibrate =/nicotinic acid
Fibrate/nicotinic acid + omega 3 fish oils
Fibrate/nicotinic acid
279
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
280
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
Avoid in these
Hyperuricaemia
patients
Hyperglycaemia
281
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
282
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
- 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
- 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
Symptoms
Complications
Course
Asian females
40-45 years old
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
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
Variable = may be slow or rapidly progressing
Management
Symptomatic treatment
Treat complications
Large vessels
Takayasus arteritis
Giant cell arteritis
Medium vessels
Polyarteritis nodosa
Kawasakis disease
Small vessel
HenochSchnlein purpura
Wegeners granulomatosis
Cryoglobulinaemia
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Medicine (CVS) = Valvular heart disease

Murmur
Mid diastolic
-low-pitched
-rumbling
Ejection
systolic
- Crescendodecrescendo
Location of max
intensity
Apex (heard with
bell)
Diagnosis
Signs
Mitral
stenosis
Aortic area
Radiation to carotids
Aortic
stenosis
(ddx: HOCM)
Aortic area
No radiation to
carotids
Pulmonary area
Aortic
sclerosis
Innocent
Pulmonary
stenosis
ASD
Innocent
Innocent
Aortic
General:
Mitral facies (malar flush purple cheeks)
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
Pulse:
Small volume, slow-rising (anacrotic)
Apex beat:
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
Pulse normal
Auscultation: normal S2
Apex
Auscultation:
ESM accentuated with patient sitting up in full inspiration (pulmonary stenosis)
Fixed wide splitting of S2 (ASD)
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Pansystolic
Apex
LLSE
sclerosis
Mitral
regurgitation
Tricuspid
regurgitation
Pulse: normal, tachycardia, AF

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)
General:
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
VSD
Early diastolic
Usually middle/
upper LSE
Aortic
regurgitation
Signs of RV failure: pulsatile hpatomegaly, ascites, peripheral edema

Mild VSD: displaced apex beat (LVH)
Moderately severe VSD: palpable thrill
Severe VSD parasternal heave (RVH)
General:
Marfanoid features
Rheumatoid hands
Spinal deformity (ankylosing spondylitits)
Argylll-Roberston pupil (syphilis)
Head nodding (de Mussets sing)
Nail bed capillary pulsation (Quinkes sign)
Visible carotid pulsation (Corrigans 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:
Traubes sign (systolic pistol-shots over fermoral artery)
Durozlezs sign (to and fro murmur when femorals are compressed by
stethoscope)
Muellers sign (uvular pulsation in time with HR)
Hills 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)
# Ortners syndrome = hoarseness due to left RLN palsy a/w enlarged left atrium
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, Marfans 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
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
Long ESM
o Syncope during or immediately after exercise
S4, left heart failure
o Fatigue (due to reduced cardiac output)
Narrow pulse pressure
o Dyspnoea = exertional, orthopnoea, PND
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

Rheumatic heart disease
Rheumatoid arthritis
o Aortic root disease= calcific AS (degenerative aortic dilation)
Aortic dissection
Syphilis
Seronegtive spondylosis (ankylosing spondyloarthritis, psoriasis, Reiters
syndrome)
Marfan syndrome
History:
o Asymptomatic
291
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:
Wide pulse pressure
o Austin Flint murmur (MDM with no opening snap)
o Presence of S3
Severe HPT functional AR
UL & LL discrepancy
o Hills sign (higher SMP in leg than in arm)
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:
292
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
Apex
S1
S3
MR predominant
Deviated, thrusting
Soft
Present
MS predominant
Not deviated, tapping
Loud
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
Pulse
Apex beat
Pulse pressure
AS predominant
Small volume
Not deviated, heaving
Decreased
AR predominant
Large volume (bounding)
Deviated, thrusting
Increased (wide)
Rheumatic fever
1. Jones criteria for the diagnosis of rheumatic fever
2 major criteria:
Carditis
Arthritis (migratory polyarthritis)
Erythema marginatum
Syndnhams chorea
OR
1 major + 2 minor criteria:

Fever
Arthralgia
Previous rheumatic fever
Raised ESR or CRP
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
strep
2. Pathophysiology
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%
Aortic 40%
Tricuspid 10%
Pulmonary 2%
Incompetent lesions develop during

attack
Stenotic lesions occur years later
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:
294
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
AF & MVR (look for goitre or thyroidectomy)
MS
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 -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
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
296
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 Oslers 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
297
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 patients 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 Dukes criteria is often used
Dukes 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
298
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
299
Priscillas Medicine Add-on

Surgery (Thyroid) = Investigations
1. Serum fT4
2. Serum TSH
Decreased in hyperthyroidism; increased in hypothyroidism
If TSH low and T4 normal request for T3 levels (T3
thyrotoxicosis)
3. Serum thyroglobulin
Used to monitor recurrence of carcinoma
Detect factitious hyperthyroidism (self-medication = T4 +
TSH + T3 + thyroglobulin)
4. Thyroid autoantibodies
Thyroid-receptor autoantibodies (stimulating Graves
disease; inhibitory Hashimotos thyroiditis)
Anti-thyroglobulin (TG) antibodies
Anti-thyroperoxidase (TPO) antibodies
Anti-microsomal antibodies positive in 50% of patients
with Hashimotos thyroditis
5. Thyroid ultrasound
Single or multiple
Consistency (cystic, mixed, solid)
Measurements of mass
Margins (irregular or well-defined)
Microcalcifications (indicative of psamomma bodies in
papillary thyroid CA)
Chick the contralateral lobe for similar lesions
Extra-thyroidal extension into surrounding structures
Cervical lymph nodal involvment
6. Radioisotope scan
Only done in hyperthyroid patients
Procedure:
Radioactive iodine (131I) injected intravenously
Thyroid gland scanned with a detector to map out areas of
high or low uptake
hot nodule
hyper-functioning area; almost never malignant (<5%)
cold nodule
non-functioning area; 20% are malignant
neutral
same as remaining thyroid gland
diffuse uptake
Graves disease
multiple hot
nodules
MNG
increased uptake by
adenoma with
decreased uptake by
remaining tissues
toxic adenoma
Patient with hot or cold nodule can still be euthyroid

7. FNAC (fine-needle aspiration cytology) and biopsy
Single most important test!
Advantages of FNAC:
Simple (can be done in the clinic setting)
Rapid results
Accurate (sensitivity > 90%)
Diagnostic (best test to detect thyroid CA)
Therapeutic (cyst aspiration)
Disadvantages of FNAC:
300
Cannot make distinction between follicular adenoma and

carcinoma (need to see encapsulating capsule, therefore open
biopsy needed)
8. Others
ECG
Hypothyroidism (bradycardia, small complexes

in all leads)
Hyperthyroidism (sinus tachycardia, atrial
fibrillation)
CT
If patient suspected of having retrosternal goitre

Staging of thyroid cancer
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
(inappropriately high
T4)
Isolated TSH
suppression
Isolated TSH
elevation
a)
b)
c)
d)
a)
b)
c)
hormone-binding problems = pregnancy,

increased thyroid-binding proteins,
amiodarone
may affect T3 and T4 levels but fT4/fT3 levels
remain normal TSH normal
subclinical hyperthyroidism
recovery from overt hyperthyroidism
1st-trimester pregnancy
drugs (dopamine, glucocorticoids,
somatostatin)
subclinical hypothyroidism
recovery from overt hypothyroidism
drugs (amiodarone, lithium)
TSH-secreting tumour
thyroid hormone resistance
TSH + T4
primary hypothyroidism
TSH + normal T4
subclinical hypothyroidism
TSH + T3/T4
TSH + normal T4
primary hyperthyroidism
subclinical hyperthyroidism
T3 thyrotoxicosis
pituitary disease (pituitary tumours, postpituitary surgery, post-NPC radiation)
sick euthyroidism (in systemic illness;
typically for everything to be low)
TSH + T3/T4
normal TSH +
abnormal T4
301
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.
302
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 = Sistrunks 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
303
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
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
304
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
Distribution and Joint
Involvement
N.B. arthralgia = presence of
joint pain wout swelling;
arthritis = pain + swelling
Acute / chronic
Getting better / worse
Effect of exercise or rest

Sequence of onset of joint
involvement
Differential
Acute monoarthritis
Septic arthritis, traumatic, gout/pseudogout, haemarthrosis
Chronic monoarthritis
Chronic infection e.g. TB, sero-ve spondyloarthritis,
pigmented villonodular synovitis
Acute polyarthritis
Infection, onset of chronic polyarthritis
Chronic polyarthritis
RA, sero-ve spondyloarthritis, OA, gout, pseudogout, CTD e.g.
SLE, infection
RA symptoms worse aft rest
OA symptoms worse aft exercise
RA/OA symmetrical
Sero-ve spondyloarthritis asymmetrical
Approach to specific symptoms

Back Pain Where, Onset, Aggravation
305
Type
Mechanical
Subset
Characteristics
Well localised
Aggravated by mvt, coughing, straining
Pain in dermatomal distribution
Progressive and unremitting pain
Spinal cord lesion

Non-mechanical
Osteoporosis
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 pts 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
306
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 patients 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
- Opposition strength
Swan neck (hyperextension at
- Practical ability
PIPJ and FFD at DIPJ),
Others
boutonniere (FFD at PIPJ and
- Elbow
extension at DIPJ), Z deformity
(hyperextension of IPJ and FF and
subluxation of MCPJ)
Psoriatic rash
DIPJ Heberdens nodes
Other joints
PIPJ Bouchards nodes
Signs of systemic diseases
Examine this patients feet
Introduction
Sit the pt over the side of the bed
General Inspection
Look
- Skin: swelling, scars
- Bone/joints
Deformity hallux valgus,
clawing, crowding
- Muscle
- Nails
Psoriatic changes
Subtalar joint
Inversion and eversion
Squeeze MTPJ
Tenderness inflammation e.g.
RA
Press upwards from sole of foot just
proximal to the MTPJ of 3rd and 4th
toes
Pain Mortons metatarsalgia
307
Transverse and longitudinal arch

Psoriatic changes pitting,
ridging, onycholysis,
hyperkeratosis, discolouration
Feel & Move
- Ankle
Swelling around lateral and
medial malleoli
- Talar joint
Dorsi and plantar flex
-
Feel and move each individual IPJ

Pain in first MTPJ acute gout
IPJs typically affected in sero-ve
aspondyloarthopathies
Palpate Achilles tendon for
rheumatoid nodules
Simmonds test for Achilles tendon
rupture
Tenderness at inferior aspect of heel
Plantar fasciitis
308
Gottrons sign Erythematous, violaceous smooth or scaly

patches over the dorsal IPJ, MCPJ, elbows, knees, medial
malleoli
o Erythema spares the phalanges (cf SLE phalanges involved,
knuckles spared)
o Erythematous rash may be present on the neck and upper
chest (often in the shape of a V), shoulders (shawl sign),
elbows, knees, malleoli
o Cuticlies may be irregular, thickened, distorted
o Lateral and palmar areas of the fingers rough and cracked
with irregular dirty horizontal lines, resembling those in a
mechanics hands
Neurological examination of the UL/ LL
o Main findings are in the power testing
Proximal muscle weaknes and tenderness of muscles
(muscle wasting absent/ minimal)
Weakness of neck flexors in 2/3 of cases
Intact/ absent deep tendon reflexes
Requests
o If the patient > 40yo, tell the examiner that you would like to
look for an underlying neoplasm
Summary
o Depends on the stem
o If asked to examine UL or LL , say that this is a ___ yo ___ who
has a pattern of proximal myopathy on neurological
examination of the UL or LL, with weakness of shoulder
abduction/ adduction/ of power grade __. There is also muscle
tenderness etc.
o In addition I also noticed cutaneous features suggestive of
dermatomyositis as evidenced by the presence of _____.
o Functionally he/ she is able/unable to stand from the
squatting position/ get up from lying positon/ unable to
swallow (NG tube) etc etc.
o
Medicine (Rheumatology) = Dermatomyositis and Polymyositis

Definition
A number of conditions in which muscles become damaged by a nonsuppurative lymphocytic inflammatory process
Polymyositis inflammation of muscles, Dermatomyositis skin +
muscles
Etiology and Pathophysiology
Polymyositis CD8 cell-mediated muscle necrosis, found in adults
Dermatomyositis B-cell and CD4 immune complex-mediated
perifascicular vasculitis
HISTORY
Adult form usually occurs after the 40 yo
Progressive symmetrical weakness of proximal muscles evolving over
weeks/ mths
o Difficulty in getting up from low chair/ squatting position
o Difficulty in climbing stairs
o Lifting and running
o Inability to raise head (lift head off pillow)
o Inability to get up from bed
Dysphagia (due to weakness of the muscles of the pharynx)
Dysphonia
Muscle pain and tenderness
Raynauds phenomenon
Rash worsened by sunlight (photosensitivity)
PHYSICAL EXAMINATION (stem usu examine this patients UL/ LL)
General inspection
o Cushingoid features?
Skin
o Heliotrope rash or purplish-blue rash around the eyes, back of
hands
o Dilated capillary loops at the base of fingernails
o Gottrons papules pink, violaceous, flat-topped papules
overlying the dorsal surfaces of the IPJ
309
CUTANEOUS MANIFESTATIONS
Heliotrope rash
Periungual telangiectasia
SYSTEMIC MANIFESTATIONS AND COMPLICATIONS
Gottrons sign on knuckles/ elbows
Gottrons papules
FIGURE 3. Shawl sign.

Poikilodermatous macules
appear in a "shawl" distribution
over the shoulder, arms and
upper back.
FIGURE 4. Mechanic's hand.

Fissured, scaly, hyperkeratotic
and hyperpigmented hands are
suggestive of manual labor.
310
INVESTIGATIONS
Confirm diagnosis
o Serum CK elevated. Levels mirrors disease activity
Also in DMD, drugs (statins, chloroquine,
colchicines, px on chronic haemodialysis)
o EMG myopathic changes (spontaneous fibrillation, salvos of
repetitive potentials, short duration of polyphasic potentials of
low amplitude)
o Muscle biopsy necross and phagocytoss of muscle fibres,
interstitial and perivascular infiltration of inflammatory cells.
o Myositis specific auto-antibodies - the aminoacyltransfer RNA
(tRNA) synthetases (anti-Jo-1), the nuclear Mi-2 protein, and
components of the signal recognition particle (SRP).
o CXR
o Serum aldolase, LDH, ALT, AST, FBC, ANA/ENA, U/E/Cr
o Urinalysis, urine myoglobin
DIAGNOSTIC CRITERIA FOR DERMATOMYOSITIS/ 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
probable if fulfil 3 criteria
possible if fulfill 2 criteria
Classification of Dermatomyositis and Polymyositis
TREATMENT
Steroids most patients respond
o Prednisolone is first line drug
Resistant cases methotrexate, azathioprine, cyclophosphamide,

cyclosporine, high-dose IVIg
Malignancy surveillance (regular f/u)
o Detailed history and physical (breast, pelvic, rectal exam)
o CXR, abdominal and pelvic u/s, FOBT, Pap smear,
mammogram
Those with underlying neoplasm may remit after treatment of the tumour
Classification of polymyositis-dermatomyositis (Bohan)

Group I
Primary idiopathic polymyositis
Group II
Primary idiopathic dermatomyositis
Group III Dermatomyositis (or polymyositis) a/w neoplasia
Group IV Childhood dermatomyositis (or polymyositis) a/w vasculitis
Group V Polymyositis (or dermatomyositis) with associated collagen
vascular dz
Overlap syndrome
Dermatomyositis overlaps with systemic sclerosis and mixed connective
tissue dz
o Signs
Sclerotic thickening of dermis
Contractures
Oesophageal hypomotility
Microangiopathy
311
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
312
Medicine (Rheumatology) = History-taking
- triggers = movement (OA), rest (inflammatory arthritis)

- relieving factors = movement (inflammatory arthritis), rest (OA)
name/age/ethnicity/gender/occupation
date of admission
4. Instability (sense of joint giving way)

- a/w locking of the knee?
Symptoms
Priscilla says stupid individuals dont do NS
5. Deformity
- kyphosis
1. Pain
- mode of onset
- frequency
- duration
- acute/sudden onset
- constant/intermittent
- progressively worsening/improving
- site and radiation
- character
- pain score and severity
- triggers = movement (OA), rest (inflammatory arthritis)
- aggravating factors = movement (OA)
- relieving = analgesia, rest (OA), movement (inflammatory arthritis)
2. Swelling
- acute/gradual onset
- history of trauma
- frequency
- duration
- site
- associated with pain, redness and increased warmth
- progressively worsening/improving
3. Stiffness
- duration of early morning stiffness = > 1hr (inflammatory arthritis), < 30
mins (OA)
- site
6. Disability
- functional status = ability to dress, write, bath, transfer, feed
- require walking aids/splints
- ability to stand, walk , run and climb stairs
- impact on social and recreational activities
- mobility within home
- mobility outside home
7. Neurological symptoms
- numbness
- parasthesiae
- weakness
Aetiology
Vascular = bleeding disorder, easy bruisability
Infective = fever, chills, rigors
dysuria, urethral discharge, red eyes, recent URTI/GE (reactive
arthritis)
prolonged cough, haemoptysis, night sweats, LOA, LOW, malaise
Trauma = history of trauma
Autoimmune = other joint involvement (see systemic review)
Metabolic = h/o gouty attacks (gout)
Neoplasia = LOA, LOW, malaise, changes in urinary/bowel habit
Complications (depends on underlying aetiology)
Systemic review
constitutional = LOA, LOW, fever, fatigue
313
anaemia = chest pain, SOB, palpitations, giddiness, fatigue

RA = dry eyes, dry mouth, chest pain, SOB, numbness, parasthesiae, weakness
SLE = alopecia, headache, sudden weakness/numbness, photosensitivity,
malar rash, oral ulcers, chest pain, SOB, changes in urine output, haematuria,
frothy urine, increased susceptibility to infection, petechiae, easy bruising
Sero-ve spondyloarthritis = red and dry eyes, dry mouth, back pain, alternating
constipation and diarrhoea, bloody and mucoid stools,
recurrent abdominal pain
Behcets disease = oral and genital ulcers
smoker
alcoholic drinker
occupation
family set-up and main caregiver
financial status
type of housing and lift-landing
Family history
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
314
Medicine (Rheumatology) = Hand

Permission (& presence of Pain)
Position
Exposure
Examination
Sitting
Exposed elbows
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
Scars
- ganglions and other lumps

- surgical (esp carpal tunnel)
Deformities
Alignment
Effusion
- rheumatoid hand
Atrophy
Discontinuity
- thenar, hypothenar, dorsal interossei
Bones & Joints
Muscles & Tendons
- wrist joint effusion
Nerves
Attitude
Vessels
- ulnar claw, median benediction

sign, wrist & finger drop
Venous
Arterial
Lymphatic
- atrophic skin changes
Feel
Skin
Bones & Joints

(Ligaments)
Temperature
- red, dry skin
Characterise swellings
Bony outline
Tenderness
- 1st extensor compartment, anatomical snuffbox
Effusion
Muscles & Tendons
Subluxation
Tenderness
- along flexor sheath
Thickening
- ulnar at elbow
Nerve
315
Gross sensation
Vessel
Pulse
Pitting edema
- capillary refill
Move
PROM & AROM
Flexion/ extension
Abduction/ adduction
Rotation
Special tests
Stability
Anterior/ posterior
Lateral
Impingement
- Finkelsteins
Fixed deformity
Neurovascular assessment
Pulses
Peripheral nerve
- radial & ulnar

Motor
Sensory
Reflexes
- *see special tests for nerve
Functional assessment
prehension
316
Hand Screen
1. Palms up
4
1
3
Zones
1. thenar- wasting, crease
scar
2. fingers- attitude
3. hypothenar- wasting
4. wrist- scars
2. Finger flexion
Zones
1. joint ROM
2. trigger
317
3. Dorsum up
3
Zones
1. 1st web &
intermetacarpal
spaces- wasting
2. fingersarthropathy
3. wrist dorsumganglion
4. Ulnar border of forearm and elbow
Zones
1. subcutaneous border
of ulna and elbowrheumatoid nodules
318
Nerve screen
Median nerve
Ulnar nerve
Radial nerve
319
Vessel screen
Pulses
Cap refill
320
Allens test- hand
321
Allens 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 Osign
4. Test the power of the APB
Provocative tests
5. Tinels test
6. Phalens 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. Froments test
Provocative tests
8. Tinels 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. Tinels at the spiral groove
323
Wrist
Position
Exposure
Examination
Sitting
Elbows on the table, exposed
Look
Skin
Bones & Joints
Swellings
Scars
- ganglions (volar and dorsal)

- volar and dorsal
Deformities
Alignment
Effusion
- dinner fork deformity

- wrist swelling
Muscles & Tendons

Atrophy
Discontinuity
Nerves
Vessels
Attitude
Venous
Arterial
Lymphatic
Feel
Skin
Bones & Joints

(Ligaments)
Temperature
- radiocarpal joint
Characterise swellings
Bony outline
Tenderness
Effusion
Muscles & Tendons
Subluxation
Tenderness
-radiocarpal joint line

-anatomical snuffbox
- 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
- Finkelsteins
Fixed deformity
Neurovascular assessment
Pulses
- radial & ulnar
Peripheral nerve
Motor
Sensory
Reflexes
Functional assessment
Grip strength
325
Wrist
Position
Exposure
Examination
Sitting
wrist on the table with elbows exposed
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. Finkelsteins test
326
Wrist
Permission (& presence of pain)
sitting
Wrist on table and

elbows exposed
Examination
1. swellingsdiscrete and
diffuse
2. scars
Look
3. dinner fork deformity
4. temperatureradiocarpal joint
Feel
5. Bony tenderness
anatomical snuffbox
*Position change- wrist lifted off the table supported by elbow
327
Wrist
6. radiocarpal joint
tenderness
Feel
Move
Special test
7. tenderness- FCR,
FCU, ECU, 1st extensor
comprtment
8. ROM- extension/flexion,
ulnar/radial deviation,
pronation/supination
9. Finkelsteins test
328
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
Wrists
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)
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
Move
Swelling, increased warmth

Piano-key sign
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)
329
Management
1. Central synovitis
NSAIDs
Low-dose corticosteroids
2nd-line drugs
H&L injections synovectomy
Physiotherapy
3. Reconstruction
Arthrodesis
Arthroplasty
Osteotomy
2. Prevent deformity
Splintage
Tendon repairs/transfers
Joint stabilization
Physiotherapy
4. Rehabilitation
Physiotherapy
Occupational therapy
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)
330
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
osteoporosis (loss of radiological density;
rarefaction)
Loss of joint space
Bilateral involvement
Later Stages
Erosion of femoral head & acetabulum
Gross bone destruction
Can resemble TB arthritis
331
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 (Kussmauls breathing), temperature
Dehydration
respiratory exam
CVS exam
Neurological exam
Complications
DKA
Fluid, electrolyte and acid-base disturbances
332
Acute renal failure

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)
333
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

Plasma glucose
Na +
K+
Urea
Creatinine
Osmolality (mOsm/kg)
pH
HCO3
Ketonuria
Fluid loss
Mortality risk
DKA
> 14 mmol/L
<135 (pseudohypoNa+)
Normal/
Increased
Increased
300-320
< 7.3
<15
++++
4-6 L
Increased
HHNK
>33mmol/L
135-145
Normal
Very Increased
Very Increased
>330
> 7.3
>15
+ or ++
6-10L
Markedly Increased
334
IV insulin sliding scale

<8
Off
8-12
1 U/hr
12-14
2U/hr
14-16
3U/hr
16-18
4U/hr
>18
5U/hr
12-16
6U
16-20
8U
>20
Call Dr
SC insulin sliding scale

<4
Call Dr
4-8
Off
8-12
4U
335
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
Acute renal failure
Thromboembolism (secondary dehydration, occurs on D3) DVT, PE, AMI, CVA
From treatment
Cerebral oedema
336
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 patients 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
o
337
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
338
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 t = 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 (t = 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 t = 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 t = 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 t = 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
339
# 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
pharmacokinetics
# 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
pharmacokinetics
# 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 t = 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
341
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
4.66.4%
Optimal
< 7.0%
Suboptimal
7.18.0%
> 8.0%
Unacceptable
not attainable by most diabetic patients

desired target for pregnant women with GDM or
pregestational diabetes
desired target for diabetic patients
increased risk of hypoglycaemia
attainable for most diabetic patients
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 nondiabetic
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
343
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
Fibrates/Nicotinic acid
TG
- 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 Ps = 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 Buergers test
reduced ABPI
Symptoms
numbness and parasthesiae over palms and soles
burning sensation in soles
Signs
foot deformities = calluses
bunions
hallux valgus
pes cavus
pes planus
344
Poor footwear
hammer toes
clawed toes
charcots 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
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

nurse
at risk
Specialist footcare team
DM footcare education
Annual screening (ankle jerk,
monofilament, vibration sense, ABPI)
DM footcare education
Annual screening (ankle jerk,
monofilament, vibration sense, ABPI)
orthoses / insoles for pressure
distribution
I&D/wound debridement/amputations
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
Type 1 DM
Type 2 DM
Pregestational DM
classification
Non-Proliferative
Retinopathy
(NPDR)
Proliferative
Retinopathy (PDR)
Clinically
Significant Macular
Oedema
1st examination
3-5 yrs after diagnosis
At diagnosis
Prior to conception &
during 1st trimester
Routine minimum f/u

Yearly
Yearly
Depends on 1st
trimester screening
Mild
Moderate
Severe
microaneurysms only
more than just microaneurysms but less than severe NPDR
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
1 or more of the following
neovascularisation
- at the disc
- elsewhere e.g. rubeosis iridis (may obstruct draining angle of eye 2 glaucoma)
vitreous/pre-retinal haemorrhage
Mild
some retinal thickening or hard exudates in posterior pole
but distant from macula
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)
NPDR mild-moderate
severe
PDR
advanced proliferative DR
vitreous haemorrhage
traction RD
Laser treatment (focal/grid)

None
Pan-retinal photocoagulation
Pan-retinal photocoagulation
Vitrectomy
# 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
346
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
Urine PCR (protein:creatinine
Dipstick +
24h UTP
Creatinine clearance
ratio)
Positive
Repeat 2x over 3 mths
Negative
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)
- Charcots 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
348
Medicine (Endocrine) = Cushings 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
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
ACTH Cortisol
Hypothalamus
CRF
Anterior pituitary gland

ACTH
Adrenal cortex
Cortisol
Cushings disease
Adrenal tumour
Ectopic ACTH
Exogenous use
Peripheral tissues
2. Cushings syndrome = chronic glucocorticoids excess from any cause
a. Cushings 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 Cushings syndrome (Rule of 9s)
Etiology
90% exogenous steroid use
10% endogenous steroid production
90% ACTH-dependent
90% pituitary
90% microadenoma
10% ACTH independent
10% ectopic
10% macroadenoma
350
Complications
Abnormality
Fat metabolism
Carbohydrate
metabolism
Clinical features
Moon-like facies, central obesity, dorsal fat pads,
supraclavicular fat pads
Thick violaceous abdominal striae, skin atrophy,
bruising, proximal myopathy
DM (increased hepatic gluconeogenesis + antiinsulin effect)
Others
Hypertension
Protein catabolism
History
Inappropriate fat deposition
Weight gain
Easy bruising
Proximal muscle weakness
History of DM
Hyperglycemia (polyphagia,
polydipsia, polyuria, LOW, fatigue)
Recent BSL
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
Acne
Hirsutism
Menstrual irregularities/
amenorrhaea
Adrenal androgen
production
Acne, hirsutism, menstrual irregularities
MSH activity in
ACTH precursor
molecule
Increased skin pigmentation (extra-adrenal

Cushings syndrome)
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 Cushings syndrome
ii. 24 hour urinary free cortisol
1. Most reliable and practical
2. Accounts for circadian rhythm lost in Cushings
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
e
Detectable
Differentiate between pituitary &

ectopic ACTH
High Dose DST or CRH test
? Adrenal Tumour
Ultrasound/CT/MRI adrenals
Suppresse
d
Pituitary cause (Cushings Disease)

CT/MRI pituitary
Plasma ACTH
High dose DST
CRH test
Inferior petrosal
sinus sampling
Unsuppresse
dd
Ectopic ACTH production

CXR, CT thorax/AP
Undetectable: likely adrenal tumor ultrasound/ CT/ MRI adrenals

Detectable: distinguish pituitary causes from ectopic ACTH high-dose
DST or CRH test
PO dexamethasone 2mg/6h x 2 days
Measure cortisol (plasma + urine) at 0 & 48h
If cortisol suppressed = Cushings disease
If cortisol not suppressed = ectopic ACTH production
IV 100g bovine CRH follow cortisol for 2 hrs
If rise in cortisol = Cushings disease
If no rise in cortisol = ectopic ACTH production
Distinguish Cushings disease vs ectopic ACTH
352
5. Management
(a) Cushings 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-cushings syndrome = increased 24hr urinary free cortisol + absent circadian rhythm + cortisol
suppressed positive DST
D= depression, drugs
O= obesity, OCP
A= alcoholism, acute illness
7. Nelsons 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
Insulin antagonism
Skin
Lipolysis
Connective tissue
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
Tinels 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
CCF (displaced apex beat, JVP, S3, bibasal creps, pedal edema)
CVS examination
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 Bruchs membrane)
Blood pressure = HPT
Urine dipstick = glycosuria
Hypocount = DM
Genitalia = testicular atrophy
Look at old photographs
Macroglossia
Acromegaly
Hypothyroidism
Amyloidosis
Downs syndrome
Indicators of acitivity
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
Etiology
Complications
Serum IGF-1
OGGT with GH measurement
MRI pituitary fossa
Serum Ca (hyperparathyroidism a/w MEN1
syndrome)
CT chest/ abdomen
ECG, CXR
U/E/Cr
TFT, LH/FSH, testosterone, prolactin, short
synacthen test (ACTH def), triple
stimulation test
Skull x-ray
Hand x-ray
Knee x-ray
Feet x-ray
Raised in acromegaly, puberty and pregnancy

Normal = GH suppression
Acromegaly= indadequate GH suppression
Cardiomegaly
Hyperglycaemia (DM)
Hypopituitarism:
Sequence:
o gonadotrophins
o prolactin
o TSH
o ACTH
Large skull
Unusually large frontal sinuses
Frontal bossing
Thick skull table
Occipital prominence
OA c-spine
Prominent jaw
Malocculusion
Dental fillings
Enlarged pituitary fossa
Large spade like hands
turfting to terminal phalanx)
Chondrocalcinosis, OA
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, caf-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 cosecrete 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) = Addisons 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, Hashimotos 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
Sheehans 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
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 Sheehans syndrome
o Withdrawal of chronic glucocorticoids suddenly
Clinical evaluation
o Known patient with Addisons disease = infection, trauma, burns, surgery
o Signs of Cushings 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
Non-pituitary tumors
Misc
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
Adenomas
Others
Craniopharyngiomas
Meningiomas
Gliomas
Chordomas
Ependymomas
Metastases
Infection abscess, meningitis, encephalitis
Infarction --- apoplexia, Sheehans 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
Corticotropin deficiency
Chronic
Acute
Investigative findings
Fatigue, pallor, anorexia

Hypoglycaemia, hypoTN
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
361
Criteria for hormone deficiency

Corticotropic function
Morning cortisol
Morning ACTH
Insulin tolerance test
250 g ACTH test
Thyrotropic function
Free thyroxine
TSH
Gonadotropic function
Women
Clinical
Postmenopausal
Men
Testosterone
Somatotropic function
IGF-1
Insulin tolerane test
GHRH + arginine test
GHRH + GHRP-6 test

Posterior pituitary function
Basal urine and plasma
sample
Water deprivation test
<100nmol/L: hypocortisolism
>500 nmol/L: hypocortisolism excluded
Below upper reference range: secondary adrenal insufficiency
Cortisol < 500nmol/L
Cortisol <500nmol/L after 30min
Low (< 11pmol/L)
Low or normal (occasionally slightly raised)
Oligoamenorrhoea, oestradiol < 100pmol/L, LH and FSH inappropriately low
LH and FSH inappropriately low
Low (<10-12 nomol/L), LH and FSH inappropriately low
Below or in the normal reference range
Adults: growth hormone 3g/L
Children: growth hormone 10g/L
Transition phase: growth hormone 5g/L
Underweight or normal weight (BMI 25): 11.5g/L
Overweight (BMI 25 to <30): 8.0 g/L
Obese (BMI 30): 4.2 g/L
Growth hormone 10g/L
Urine volume (40ml/kg bodyweight per day) + urine osmolality
<300mOsm/kg water + hypernatremia
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!
362
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
Addisons disease
4. Hyperestrogenism
Testicular failure
o Kallmanns syndrome
o Trauma
o Viral orchitis
o Castration (medical, surgical)
o Klinefelters syndrome
Paraneoplastic syndrome (Ca Lung)
5. Uraemia
6. Physcological
Pubertal
Senile
363
Medicine (Renal) = Acute Renal Failure

A sudden decrease in renal function resulting in an inability to maintain fluid
and electrolyte balance and to excrete nitrogenous wastes
Signs and Symptoms
Uraemia
Nausea
Vomiting
LOA
Fatigue
Pruritus
Skin Bruising
Uraemia oesophagitis/gastritis/colitis
Pericarditis
Pleuritis
Seizures
Encephalopathy
Oliguria
Urine output < 400ml/day
Fluid overload
Lower limb oedema
Ascites
Pleural effusion/pulmonary oedema
Facial oedema
Aetiology
Sepsis
Dehydration
Uncontrolled HPT
Recent drug intake
NSAIDs
Aminoglycosides
Contrast
Urinary obstruction LUTS
Haematuria
Backpain
Constipation
Urinary instrumentation
Glomerulonephritis Rash
haemoptysis
Lab findings to suggest ARF
Increased Urea and Cr above baseline
Increase K+ (impaired renal excretion)
Increased PO4 (secondary to decreased secretion from tubule
damage)
Decreased CA2+
Causes of ARF
Pre-renal (40%)
Intrinsic renal (up to 50%)
Post renal (5-10%)
Vomiting
Diarrhea
Poor fluid intake
Fever
Use of diuretics
CCF
Haemoptysis/melena/haematemesis
Compliance with medications
Fluid and salt restrictions
364
Aetiology
Clinical
features
Pre Renal
Decreased renal
perfusion
Sepsis
Dehydration
Shock
Uncontrolled HPT
Sepsis = Fever, Toxic

looking
Post Renal
Urinary Tract Obstruction within the
lumen
Bladder calculi
Bladder tumour
Papillary necrosis
Crystalluria
Urinary tract obstruction within the
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
LUTS (storage and voiding symptoms
Intrinsic Renal
Acute tubular necrosis
Ischaemia
Nephrotoxins
o Aminoglycosides
o Contrast
o Chemo RX
o Rhabdomyolysis
Acute interstitial nephritis

Drug RXN
(penicillin/NSAIDs)
Acute GN
Post strep GN
IgA nephropathy
Rapidly progressive GN
Haematuria
Dehydration =
increased thrist, dry
mucous membranes
Decreased skin turgor,
prolonged capillary
refill time, altered
mental state
Urine Na
(mmol/L)
Urine
osmolality
(mosm/kg)
Sediment
Distended bladder
Enlarged prostate
Shock = tachycardia,
hypotension
<20 (can concentrate
urine)
>500
Variable
>20 (cannot concentrate urine)
<20
>20
<350
<350
>500
<350
Benign/hyaline casts
Normal/RBC/WBC
Granular casts
RBC casts
WBC casts with

eosinophillia
365
Investigations
Urine
UFEME
Haem -> rhabdomyolysis
Casts
o Granular (acute TN)
o RBC (acute GN)
o WBC + Eosinophillia (acute IN)
Urine Osmolality and urine Na+
High/low (pre-renal + acute GN)
Low/High (post renal + acute TN + acute IN)
Complications
Electrolyte imbalances
Hyper/hyponatraemia
Hyperkalaemia
Metabolic acidosis
Hypermagnesaemia
Hyperphosphataemia
Hypocalcemia
Bloods
FBC
Imaging
KUB or CT KUB
Hb (distinguish from CRF)
Eosinophillia (acute IN)
CKMM
Rhabdomyolysis
Bladder catheterization
Rule out urethral
obstruction
Renal U/S
Small atrophied kidneys (CRF)
Hydronephrosis (post-renal)
U/E/Cr
Urea > creatinine (pre-renal)
Electrolyte abnormalities
Autoimmune screen
ANA
Anti-dsDNA
Complement levels
ANCA
Anti-GMB Ab
Fluid overload
Hypertension
Uraemia
Pericarditis
Pleuritis
Encephalopathy
Platelet dysfunction
Pruritus
Oesophagitis/gastritis/colitis
366
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
367
Medicine (Renal) = Chronic Renal Failure

History
Symptoms of renal failure
Complications of renal failure
Unrelated problem
When was the diagnosis made?
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
DM
HTN
GN
o VITAMIN
Vascular (HSP) purpuric rash, joint pain,
abdominal pain
Infections hx of Hep B/C infection
Toxin (gold, penicillamine) drug hx
Autoimmune (SLE) malar rash,
photosensitivity, oral ulcers, joint pain
Metabolic (DM)
Renal
Renovascular disease
Interstitial nephritis drug history
Polycystic kidney hematuria, loin
pain, headache
Analgesic nephropathy analgesic use
Pyelonephritis hx of kidney infection,
fever, loin pain
Reflux nephropathy enuresis,
childhood UTI, cystoscopy treatment
Obstruction dysuria, hematuria, loin
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
368
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
Osteodystrophy
Nutrition
Anemia
Cardiovascular
Skin
Neurology
GIT
Height, weight
Bone pain, fractures
Malnutrition (LOA, LOW)
Pallor, chest pain, SOB, palpitations, giddiness, fatigue
AMI/CCF, HPT, HCL, peripheral vascular disease (intermittent claudication, pain
at night/rest, parasthesia, paralysis, pallor, perishingly cold)
Pruritus, bruising
CVA, seizures secondary to electrolyte disturbances, uremic encephalopathy,
peripheral neuropathy, restless leg syndrome (frequent need to change
position)
Uremic esophagitis/gastritis/colitis (melena, hematemesis, hematochezia,
abdominal pain)
Drug history
Main outcomes of CRF AMI, CVA, PVD

Co-morbidities DM, HPT, HCL, deafness
Previous hospital admissions (esp for renal-related
conditions)
Prior surgeries CTS
Known drug allergy

Current medications
Long-term medications analgesia, TCM
Family history
Social history
Smoker
Alcohol drinker
Days off work/school
Financial difficulty
Family set-up and caregiver
Type of housing and lift-landing
Functional status
Renal failure
Renal diseases APKD, Alports syndrome, IgA
nephropathy
Deafness
DM, HPT, HCL
369
General
(adequate
exposure with
patient inclined at
45 degrees)
Hands/Arms
Face/Chest
Heart
Lungs
Abdomen
Legs
Others
Height, weight
Sallow complexion (dirty-brown appearance due to deposition of urinary
pigments and anemia)
Cachexia
Cushingnoid appearance secondary to steroids
Edema (facial/ascites)
Vital signs (PR, RR hyperventilation), temperature, BP
Mental state (orientated, confused, drowsy, comatose)
Leuconychia
Terrys 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)
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
Raised JVP fluid overload, right heart failure
Carotid artery bruit atherosclerosis
Pericardial rub
Upright position basal crepitations (APO, pneumonia), stony dull percussion
(pleural effusion)
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)
Scratch marks
Edema
Neuropathy sensory > motor deficits
PVD hairless, shiny/dry skin, pallor, cool, gangrene, amputations
Genu varum
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
Etiology
U/E/Cr
Bloods
Urine
Radiology
Complications
Biopsy
Bloods
Radiology
Creatinine to estimate GFR

Plasma glucose and HbA1C DM
ASOT/HBV/HCV infections
ANA/anti-dsDNA/ANCA/anti-GBM/C3/C4 AI
LFT (albumin) nephrotic syndrome
Urine dipstick (proteinuria, hematuria, glycosuria)
UFEME
24h UTP/urine PCR (proteinuria)
KUB stones
Renal U/S cysts, size, symmetry, obstruction, hydronephrosis,
nephrocalcinosis
IVU stones
DMSA/DTPA (radionuclide scans) renal function, renal
scarring
MCU anatomical abnormalities
GN (if proteinuria > 1g/day)
FBC normocytic normochromic anemia
U/E/Cr
Bone panel Ca, PO4, alkaline phosphatase, IPT, Mg, albumin
PT/PTT normal
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

CVS
Prepare for
dialysis
Reduce drug
dosages
Mx = adequate dialysis, repeated blood transfusion, rEPO if not Fe

deficient and Hb < 10g/dL, iron and folate supplementation
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
AVF/AVG 6-8 weeks before HD
Tenchkoff catheter 2-3 weeks before PD
Renal transplant if suitable
Antibiotics = aminoglycosides, cephalosporins, tetracycline
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
1
2
3
4
5 = ESRD
GFR (ml/min/1.73m2)
90
60-89
30-59
15-29
< 15
372
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 (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 Mentzers 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
374
G) Ca/PO4 metabolism in CKD

CKD
Decreased renal
excretion of PO4
Decreased GI Ca
absorption
Decreased serum
Ca
Decreased renal
mass
Acidosis secondary
to decreased H+
excretion
Decreased
hydroxylation of
Vitamin D
Increased iPTH
secretion
Increased bone
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
375
Medicine (Renal) = CRF with fluid overload

Causes
1. CVS event = AMI, CCF
2. Anaemia
3. Sepsis
4. Non-compliance to fluid and salt restrictions
5. Non-compliance to medications
# diuretics
# anti-hypertensives
Investigations
serial cardiac enzymes and ECG = exclude AMI
CXR = cardiomegaly, APO
-natriuretic peptide = exclude CCF
FBC = Hb (anaemia)
WCC and differential count (sepsis)
U/E/Cr = worsening renal function (AoCRF)
Ca/Mg/PO4/albumin/iPTH = renal osteodystrophy
GXM = blood transfusion
LFT = exclude liver pathology
co-morbidities = hypocount, HbA1c, fasting lipids
urine dipstick, UFEME, urine c/s = proteinuria
exclude UTI
Management
Trace old notes
Monitor vitals q4hrly
Fluid restriction 500ml/day (if serum Cr > 400 mol/L)
800ml/day (if serum Cr < 400 mol/L)
Diet = low salt/protein/phosphate/potassium
DM diet
Strict I/O charting
Daily weights
IV frusemide with span K spironolactone
Treatment Orders
1. Diuresis with IV frusemide

120-240 mg/8hrly (if serum Cr > 400 mol/L)
80-120 mg/8hrly (if serum Cr < 400mol/L)
If no response, step up to maximum OR infusion at 30 mg/hr
Urinary catheter if no urine output > 6hrs
2. Exclude cardiac event
Check baseline ECG
If pt has IHD = do CK/CKMB/Trop T and repeat ECG x 3
3. Consider acute dialysis (if APO, severe fluid overload, acidosis or
hyperkalaemia)
PT/PTT, GXM
If for dialysis = trace Hep/HIV status
If results > 6mths = order HBsAg, Anti-HCV, HIV
4. (Day 2) Referral plan
If Cr > 400 mol/L assess ADL
cannot do any one ADL refer MSW
can do all refer renal coordinator and vascular surgeon
If Cr < 400 mol/L refer renal coordinator, MSW and vascular
surgeon
Others = dietician, pharmacist, PT/OT as required
5. (Day 3) If anaemia workup negative, consider EPO therapy
6. (Day 5) Review CXR = if clear, consider switching to oral frusemide
if well on oral frusemide, consider discharge
7. Discharge planning
Fluid restriction
Diet restriction
When to seek medical help = skin turgor, pitting oedema,
weakness, fatigue, muscle cramps,
nausea/vomiting
TCU appointments
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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 Murphys 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
o
o
o
o
o
H&N
o
o
o
o
Back
o
Hypocount marks -> DM from long term steroid therapy

Leukonychia, Terrys Nails, scratch marks, bruising -> ESRF
Gouty Tophi -> cyclosporine A
Thin skin (double pinch test) -> steroids
AVF/AVG -> signs of recent cannulation? (may suggest graft failure)
Proximal myopathy
Eyes
Conjunctival pallor and penguinculae ESRF
Posterior subcapsular cataract -> long term steroid therapy
Oral cavity
Oral thrush -> steroid therapy
Gingivial hyperplasia -> cyclosporine A
Raised JVP -> fluid overload
Buffalo hump, supraclavicular fat pads -> long term steroid therapy
Kyphoscoliosis, step deformity, bony tenderness -> long term steroid therapy
Lungs
o Crepitations -> infection/fluid overload
Lower limbs
o Oedema -> fluid overload
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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
ADL independent
Offsprings
No malignancies
Parents
No PVD
Spouses
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%
Cadaveric doner
No hepatitis B or C
No HIV
No systemic infections
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 Ringers 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
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
o
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, Goodpastures syndrome, MPGN, Alports
syndrome, HUS, TTP
Mx = methylprednisolone, monoclonal antibody, azathioprine
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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
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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)
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, Wegeners granulomatosis, Goodpastures 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, Alports 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
Presence of blood clots

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)
o
o
Aetiology
Renal
o Vascular = purpuric rash over lower limbs, lower limb oedema, joint pain, abdominal pain (HSP)
Haemoptysis (Goodpastures 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 (Alports 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
Hypertension
Deafness (Alports 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

Hypertension
Renal disease
Deafness (Alports 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)
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 Bowmans 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 Wegeners)
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
nephrotic syndrome
(c) membranous GN
(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, Wegeners granulomatosis (*)
(b) infective = Hep B, Hep C, HIV, malaria, post-streptococcal
390
(c)
(d)
(e)
(f)
(g)
(h)
toxins = NSAIDs, captopril, gold, penicillamine, TCM

autoimmune = SLE, Goodpasture syndrome
metabolic = DM
infiltrative = amyloidosis
neoplasia = multiple myeloma, lymphoma
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, Alports 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 (Bergers 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
severity of proteinuria
renal impairment
mean arterial pressure
(hypertension)
Histological
chronic tubulo-interstitial fibrosis
extensive crescents (> 30-50%)
advanced glomerulosclerosis (>
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, Wegeners granulocytosis)
I (Hep B, Hep C, post-streptococcal GN)
T (penicillamine)
A (SLE, Goodpastures 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 = Wegeners granulomatosis, PAN, giant-cell arteritis, Takayasus
arteritis
(b) secondary systemic vasculitis = SLE, HSP, RA, Behcets disease, cryoglobulinaemia
(c) Goodpastures 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
394
(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
Bowmans
space)
crescents eventually obliterate Bowmans 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
395
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
High dependency
Low dependency
(ie relatively healthy)
Eg malignancy, HPT, DM ,
IHD, ADL dependent
Unsuitable for transplant
Perform dialysis (HD or PD)
Suitable for transplant

Aim for living related donor
If no living related donor
available, listed on cadaveric
donor waiting list
Criteria for transplant

Recipient
Living related donor
< 60 YO
Siblings
ADL independent
Offsprings
No malignancies
Parents
No PVD
Spouse
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%
Cadaveric donor
<65 YO
no hepatitis B or C
no HIV
no systemic infections
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

(urine output <50ml/hr)
Immediate graft function

(urine output >50ml/hr)
Exclude inadequate renal perfusion as

cause of delayed graft function
Check CVP
Check perfusion scan
If CVP > 10 cm H2O
Give IV Lasix 80-120mg stat
Impaired
perfusion
Surgery
Normal
perfusion
Lasix
responsive
PRA 25
FK506
+ Azathioprine
+ prednisolone
PRA < 25
Cyclosporine A
+ Azathioprine
+ prednisolone
+ Zenapax
Lasix
unresponsive
+ Delayed
graft function
Determine level of
immunosuppression required based
on PRA
PRA 25
Cyclosporine A
+ MMF
+ prednisolone
+ Zenapax
Determine level of
immunosuppression required based
on PRA (?antigen levels)
PRA < 25
Cyclosporine A
+ Azathioprine
+ prednisolone
+ Zenapax
Mx of Delayed Graft Function

Daclizumab < 6 hrs post
anastomosis
Cyclosporine A: monitor levels to
avoid toxicity
Day 5-7
PT still dialysis
dependent
PT recovering
Renal biopsy of
allograft kidney:
Check for rejection
397
Medicine (GIT) = Hepatosplenomegaly

Causes
Vascular
Infective
Trauma
Autoimmune
Metabolic
Infiltrative
Neoplastic
Haematological
Chronic liver disease with portal hypertension

Viral (hepatitis, IMS, CMV)
Protozoal (malaria)
Haematoma
SLE
RA
Storage disorders (Gaucher = type 1 subtype; NiemannPick)
Amyloidosis
Sarcoidosis
Myeloproliferative disorders
Lymphoma
Lymphoproliferative disorders
Chronic haemolytic anaemia (spherocytosis, G6PD
deficiency, thalessemia)
-thalessemia major
Overall
Pituitary haemosiderosis
Cardiac haemosiderosis
Pancreatic haemosiderosis
Intervention
Request
Short stature
Hyperpigmented
Thalessemic facies (frontal bossing, flat nosebridge,
maxillary hyperplasia)
Looks younger for age
Hypopigmented areolae
Loss of axillary hair
JVP v wave
Pulsatile liver
Lower limb edema
Hypocount marks on fingers
Diabetic dermopathy
Splenectomy
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
Cardiac
Subset
Respiratory
Parenchyma
Airway
Pleura
Haematological
Vasculature
Anemia
Neuromuscular
Psychological
Hyperventilation
Question
Any chest pain? Character?
Any PND?
Any Orthorpnoea?
Leg swelling?
Cough?
Phlegm?
Haemoptysis?
Fever?
Wheeze?
Stridor?
Trauma?
Acute pain followed by SOB?
Prolonged immobility?
Palpitations
Giddiness / Light headedness
Bleeding PR, Menses
Generalised weakness?
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
Lung infection = miliary TB
Inhalants = nitrogen dioxide
sulphur dioxide
Drugs = chemotherapeutic drugs
insecticides
heroin
kerosene
paraquat (pesticide)
Indirect lung injury

Systemic infection (most common)
Shock
Miscellaneous = drowning
high altitude
SLE
air embolism
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
401
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) bats 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 (Cushings 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 Horners 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 Horners 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 nonendocrine origin
(a) Endocrine = ACTH Cushings 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 (Trousseaus 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
409
- 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
410
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 cowsmilk 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 thruout 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
412
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
413
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
415
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 hrhage/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)
- 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
Clinical features
- 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
419
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
+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 <35C or 40C
+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
I
0
Outpatient
II
<70
Outpatient
III 71-90 Inpatient to observe
IV 91-130 Inpatient
V
>130 Inpatient
Mortality %
0.1
0.6
2.8
8.2
29.2
420
Medicine (Respi) = Asthma

Recognise acute asthma clinically and define status asthmaticus.
Describe the severe sequelae arising from inadequate acute management.
Describe the clinical assessment of severity of asthmatic effect.
Describe the immediate steps in management: drugs, dosage and mode of
administration.
List the clinical parameters which should be monitored after initiation of
treatment.
Describe the indications for intubation.
Explain the pathophysiology of acute asthma and the action of the drugs used
in acute management.
Describe the follow-up medical management after the acute attack.
Prevention
Describe the measures to minimize occurrence of severe asthmatic attacks.
Characteristics
3 characteristics:
i) Airflow limitation of changing severity, episodic, reversible
spontaneously or with treatment
ii) Airway hyperresponsiveness to a wide range of stimuli
iii) Inflammation eosinophils, T lymphocytes, mast cells, smooth muscle
hypertrophy, edema, mucosal damage
3 factors contribute to airway narrowing: i) bronchospasm, ii)
inflammation and swelling,
iii) increased mucus production
o Intervals between attacks are characteristically free from respiratory
difficulty, but subtle deficits can be detected by spirometry
Aetiology
Extrinsic (allergic) asthma
- Definite external cause
- Type 1 hypersensitivity reaction
- Elevated serum IgE and eosinophils
- Mediated by Th2 cells release IL 4, IL5 IgE synthesis
sensitization of mast cells
- Triggered by allergen exposure in a sensitised individual mast cell
degranulation
- Early phase (within 1 hr): release of leukotriene D4, PGE2, histamine
- Accompanied by reflex bronchoconstriction due to stimulation of
vagal receptors
- Late phase: recruitment of leukocytes: leukotriene B4, platelet
activating factor, TNF
- Leukocytes damage the epithelium, reducing production of NO, thus
causing smooth muscle contraction
- Eosinophils perpetuate the inflammation
- Eg. Atopic asthma, occupational asthma, allergic bronchopulmonary
aspergillosis
- Often has family history of allergy/atopy
- Develops in childhood
Intrinsic (non-allergic) asthma

- Non immune mechanism, asthmatic diathesis
- IgE antibodies are normal
- Triggered by respiratory infection, aspirin, stress, exercise, cold
(these factors may also trigger asthma in a person with extrinsic
asthma cos of his bronchial hypersensitivity)
- No family history of allergy/atopy
- Develops later in life, late onset
Epidemiology
o Prevalence is increasing
o More common in developed countries
421
Pathogenesis
Atopy
- individuals who readily develop IgE antibodies against common
materials in the environment
- runs in the family
- childhood exposure to allergens has an influence on IgE production:
growing up in a clean environment predisposes towards IgE response
to allergens
Airway hyperresponsiveness
Small airway obstruction due to bronchospasm and thick tenacious
mucous plugs, progressive hyperinflation with air trapping
Remodelling
- deposition of matrix proteins beneath the epithelium
- epithelial metaplasia and increase in goblet cells
- thickened basement membrane
- smooth muscle hyperplasia
Precipitating factors
Environmental allergens: pollen, house dust mite, pets
Occupational: isocyanates (varnish), flour, animals
Atmospheric: cigarette smoke, pollutants
Cold air, exercise (at the end of exercise), emotion
Viral infections: rhinovirus, parainfluenza
Drugs: Aspirin (imbalance in metabolism of arachidonic acid), beta
blockers
Tachypnea
Wheeze, cough
Hyperinflated chest, hyperresonance, diminished air entry
Polyphonic wheeze
Clinical severity: able to complete sentences? Silent chest, bradycardia,
PEF < 33%, cyanosis, feeble respiratory effort, confused
Investigations
FBC: eosinophils
Sputum culture and cytology: eosinophils
Serial peak expiratory flow measurements
- Diurnal variation >20% on 3 days a week for 2 weeks: marked
morning dipping of peak flow
Lung function tests
- Decreased FEV1/FVC ratio and increased residual volume
- Before bronchodilator, after bronchodilator variable airflow
limitation, >15% improvement in PEFR after bronchodilator
CXR: hyperinflation, exclude pneumothorax or allergic
bronchopulmonary aspergillosis
Skin prick test: helps to identify allergens
Histamine or methacholine challenge: to test airway
hyperresponsiveness
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
Classification of asthma
New GINA guidelines
Management
Allergen avoidance eg dust mite, smoking, drugs
Pharmacologic therapy depending on severity/frequency of asthma
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 patients 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
423
Asthma drugs
Beta-2 agonists
- selective for bronchial smooth muscle relaxation and
bronchodilation
- for symptomatic relief (2 puffs prn)
- effective up to 6 hrs
- excessive use (>2 canisters per month) is associated with increased
mortality
Anticholinergic (ipratropium bromide)
- muscarinic receptor antagonists
Long acting beta-2 agonists
- effective up to 12 hours
- for patients who cannot be controlled on 800mcg/day of ICS
Sodium cromoglycate and nedocromil
- blocks chloride channel prevent mast cell activation
Inhaled corticosteroids (ICS)
- any form of persistent asthma (needing relief meds at least once a
week) requires steroid inhaler treatment
- beclometasone, budesonide, fluticasone, triamcinolone
- most of the dose is swallowed or exhaled
- adding a long acting beta-2 agonist is more effective than doubling the
dose of ICS
- side-effects: oral candidiasis, hoarseness, subcapsular cataract,
avascular necrosis of the femoral head, osteoporosis, growth
retardation
- step down treatment after the condition is under control
Oral corticosteroids
- 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
Status asthmaticus
Poor response to drug therapy after 24 hours
Signs of respiratory failure: ABG: PaCO2>6kPa, PaO2<8kPa, pH low and
falling
Risk factors for death from asthma
Past history of sudden severe exacerbation
Prior intubation for asthma
Two or more hospitalisations for asthma in the past year
Three or more emergency care visits for asthma in the past year
Hospitalisation or an emergency care visit for asthma within the past
month
Use of >2 canisters per month of inhaled short-acting B2-agonist
Current use of systemic corticosteroids or recent withdrawal from
systemic corticosteroids
Known difficulty perceiving airflow obstruction or its severity
Comorbidity, as from cardiovascular diseases or chronic obstructive
pulmonary disease
Serious psychiatric disease or psychosocial problems
Low socioeconomic status
Illicit drug use
ABG: PaCO2>6kPa, PaO2<8kPa, pH low and falling
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.
Prolonged bed rest, immobilisation
Surgery, trauma, fractures
Previous stroke or thromboembolism
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
Immobilization or surgery in previous 1 month
Malignancy
Clinical symptoms of DVT
Hemoptysis
Heart rate >100
Other diagnosis less likely than PE
1.5
1.5
1
3
1
1.5
3
0-2 Low probability

3-6 Mod probability
> 6 High probability
Geneva score
Age > 65
Previous DVT or PE
Surgery (under GA) or lower limb fracture within 1 month
Active malignant condition or cured in < 1 yr
Unilateral lower limb pain
Pain on lower limb deep venous palpation and unilateral edema
Hemoptysis
Heart rate 75-94 bpm
Heart rate 95 bpm
1
3
2
2
3
4
2
3
5
0-3 Low probability

4-10 Mod probability
> 10 High probability
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
e probability
High probability
Start tx
D Dimer assay
D Dimer
negative
CTPA
D Dimer
positive
No tx
CTPA
negative
CTPA
CTPA
negative
CTPA
positive
No tx
Start tx
Lower limb
DVT scan
Scan
negative
Stop tx
CTPA
positive
Continue tx
Scan
positive
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 LMWHs 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
PE/DVT
Reversible risk
factor eg. recent
surgery
Warfarin
3-6 months
No identifiable risk
factor
Recurrent episode of
PE/DVT
Irreversible risk
factor eg. ptn C
deficiency, APS
Warfarin
6-12 months,
consider indefinite
therapy
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 Guide To Medicine

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Priscillas Medicine

MEDICINE (RENAL) = URINARY TRACT INFECTION / PYELONEPHRITIS ....................................................................................................94

MEDICINE (CVS) = ISCHAEMIC HEART DISEASE (HISTORY) .................................................................................................................... 242

MEDICINE (RESPI) = PULMONARY EMBOLISM ............................................................................................................................................. 427

Short Cases in Medicine

Medicine = Respi shorts

Chronic obstructive pulmonary disease

Medicine = Renal shorts

Medicine = Endocrine shorts

Medicine = Hands shorts

Not palpable or visible

Palpable goitre (larger than terminal phalanges of

Large goitre visible from a distance

Surface = smooth and diffuse, nodular

5. Palpate for cervical lymphadenopathy (infiltration by carcinoma), carotid artery (displacement/absence

Impaired visual acuity and colour vision

Medicine (Thyroid) = Introduction

anterior pituitary gland

Synthesis of thyroid hormones

Medicine (Thyroid) = Thyroid Lumps

Medicine (Thyroid) = Management of hyperthyroidism

anions (per chlorate, thiocyanate)

Radiation induced cancer

Surgery (Thyroid) = Hyperthyroidism

* Fixed opthalmoplegia = usually painful

Toxic nodular Goitre

Medicine (Thyroid) = Hypothyroidism

- excessively clothed (cold intolerant)

* may be mistaken for infiltrating neoplasm

Surgical (Thyroid) = Thyroid Carcinoma

dyspnea, stridor, cough (airway obstruction)

Surgical (Thyroid) = Thyroidectomy

Reduce thyroid activity -> clinically euthyroid

Papillary lesion ->

Post operative complications

Risk of anesthesia = AMI, CVA

Eyes (scleritis, conjunctival pallor, episcleritis)

Medicine (Rheumatology) = General points about arthritis

Pain and swelling involving joint(S)

5 cardinal signs of inflammation

Inflammatory vs mechanical arthritis

Symmetrical versus asymmetrical

Mono and poly arthritis

Medicine (Rheumatology) = Systemic lupus erythematosus (SLE)

An autoimmune multi system disorder with a remitting and relapsing course

UV light = damages DNA and promotes cell injury

Erythematous malar rash sparing nasolabial folds

Less than 50% of glomeruli affected

Class IV = diffuse proliferative lupus nephritis

Microscopic = proliferation of endothelial and mesangial cells affecting entire

Fixed erythema malar eminences sparing nasolabial

Erythematous raised patches with keratotic scaling and

Unusual reaction to sunlight

Oral or nasopharyngeal ulceration (usually painless)

Non-erosive arthritis involving at least 2 peripheral

Persistent proteinuria >0.5g/day or cellular crisis

Seizures or psychosis in the absence of any known

Hemolytic anemia, Leucopenia, thrombocytopenia,

10. Immunological disorders

Anti-dsDNA Ab, anti-Sm Ab, anti-phospholipid Ab (lupus

NCNC anemia = anemia of chronic disease

Prolonged aPTT in anti phospholipid syndrome

ANA = sensitive but not specific