INTERNAL MEDICINE Clerkship PDF

MUHIMBILI UNIVERSITY OF HEALTH AND ALLIED SCIENCES
CLINICAL SUMMARIES OF INTERNAL MEDICINE
AUTHOR: Elton, MD class of (2013-2018).
Email: ellierolland@gmail.com
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INTRODUCTION
These are just summaries of different clinical case presentations in Internal Medicine
department and some important aspects of discussion about the particular diagnosis. They are
clinical cases that one might encounter in internal medicine department. I found this worthy
during my ample time to leave behind something that others can quickly refer especially when it
is their first exposure to clinical rotation. Read every line in it.
Contents in this document are for use among clinical students if it pleases them. It has been my
pleasure sharing moments with so many people during my stay at MUHAS and I would love to
recognize their untiring support and encouragement during my stay. I dedicate this to my
beautiful classmates and teachers.
Special thanks to my lovely friends Francis Kazoba, Humphrey Medarakini, Cornel Sizimwe, and Davis
Amani for their unconditional support when I needed them. A Special recognition to our lovely CR Eveline
Ngoli for making internal medicine a smooth eight weeks of learning. Life is always beautiful, with good
people around, and I have always been grateful to Victoria for her wise advice and support in the
accomplishment of this piece of work.
How can I be so rude not to mention TAMSA and JKM for they have made me grow both academically
and spiritually.
Below is a story of a blind girl.
THE BLIND GIRL

There was a blind girl who hated herself just because she was blind. She hated everyone except her
loving boyfriend who was always there for her. She said if she could only see the world, she would marry
her boyfriend.
One day someone donated a pair of eyes to her and she could see everything, including her boyfriend.
Her boyfriend asked her “now that you see the world, would you marry me?”. The girl was shocked when
she saw her boyfriend was blind too, and refused to marry him. Her boyfriend walked out in tears and
later wrote a letter saying “just take care of my eyes love”.
LESSON
This is how human mind changes when the status is changed. Only a few remember what life was
before. Its best to remember what life was before and put a ladder to let others climb.
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Table of Contents
INTRODUCTION...........................................................................................................................................2
THE BLIND GIRL...........................................................................................................................................2
HISTORY TAKING..........................................................................................................................................5
HEMATOLOGY...........................................................................................................................................12
CHRONIC MYELOID LEUKEMIA..............................................................................................................12
MULTIPLE MYELOMA.............................................................................................................................13
CASE -APLASTIC ANEMIA.......................................................................................................................15
DISCUSION.............................................................................................................................................18
NEUROLOGY..............................................................................................................................................21
STROKE..................................................................................................................................................21
CASE-NEUROLOGY.................................................................................................................................23
CASE - CIDP............................................................................................................................................25
CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY(CIDP)...............................................35
GUILLAIN BARRE SYNDROME................................................................................................................37
DIAGNOSTIC CRITERIA OF GBS...........................................................................................................38
CASE 3-ADULT ONSET SEIZURE..............................................................................................................39
PARAPLEGIA...........................................................................................................................................49
TB SPINE................................................................................................................................................49
TRANSVERSE MYELITIS..........................................................................................................................49
CARDIOLOGY.............................................................................................................................................50
HEART FAILURE......................................................................................................................................51
CARDIOMYOPATHIES.............................................................................................................................52
PERICARDIAL SYNDROMES....................................................................................................................54
PERICARDITIS.....................................................................................................................................55
PERICARDIAL EFFUSION.....................................................................................................................56
CARDIAC TAMPONADE......................................................................................................................56
CONSTRICTIVE PERICARDITIS.............................................................................................................56
RHEUMATIC HEART DISEASE.................................................................................................................57
INFECTIVE ENDOCARDITIS.....................................................................................................................58
CORONARY ARTERY DISEASE.................................................................................................................59
HYPERTENSION......................................................................................................................................62
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CASE 4-HEART FAILURE..........................................................................................................................64
TENSION HEADACHE..............................................................................................................................69
CASE -HEART FAILURE............................................................................................................................70
NEPHROLOGY............................................................................................................................................81
ACUTE KIDNEY INJURY...........................................................................................................................81
CHRONIC KIDNEY DISEASE.....................................................................................................................81
RESTLESS LEG SYNDROME AND CKD......................................................................................................85
MALARIA AND RENAL DISEASE..............................................................................................................85
CASE -POLYCYSTIC KIDNEY DISEASE.......................................................................................................86
DISCUSSION...........................................................................................................................................93
GASTROINTESTINAL SYSTEM.....................................................................................................................95
INFLAMMATORY BOWEL DISEASE.........................................................................................................95
IBD RISK FACTORS..............................................................................................................................95
LIVER CIRHOSIS......................................................................................................................................97
HEPATOPULMONARY SYNDROME.....................................................................................................99
HEPATORENAL SYNDROME...............................................................................................................99
HEPATIC ENCEPHALOPATHY............................................................................................................100
ACUTE PANCREATITIS..........................................................................................................................101
HEPATOCELULAR CARCINOMA............................................................................................................102
CASE -PUD...........................................................................................................................................103
CASE- JAUNDICE..................................................................................................................................105
INFECTIOUS.............................................................................................................................................112
MENINGITIS.........................................................................................................................................112
RARE DIAGNOSIS.....................................................................................................................................113
CASE- SLE.............................................................................................................................................113
CASE- HEREDITARY TALENGECTASIA...................................................................................................128
CASE-CASTLEMAN DISEASE.................................................................................................................130
CASE- DENGUE.....................................................................................................................................135
CASE-SLE..............................................................................................................................................148
CASE-PHEOCHROMOCYTOMA.............................................................................................................153
COMMON QUESTIONS............................................................................................................................159
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HISTORY TAKING
1. Particulars of a patient
 Name of the patient- introduce the patient by three names.
 Age of the patient- in years. For pediatric patients can be in months, weeks or years as well.
 Sex- do not ignore as some patients are trans gender or hermaphrodites. Some disease are
more prevalent in certain sex, example breast cancer is common in females.
 Residence – It’s important to know where the patient comes from because it can tell the
diagnosis also. Some diseases are common in certain areas, example Schistosomiasis is
common in lake zone.
 Religion- this is not so much important but if one asks its best to mention. It could help in
some diagnosis. Possibly not to think of pig tape worm among Muslims.
 Hospital registration number is also important and the ward the patient is residing for easy
allocation. If possible with the bed number. ( but this is not so important for you as a student
in your clinical exams presentation)
 Parity and gravidity-gravidity referring to the number of times this woman has been pregnant.
If it is her second pregnancy then you report gravid 2. Parity is the number of live births. If this
is her third pregnancy and had previous two live births you report as gravid 3 para 2. (G3P2). If
this is her third pregnancy and she had one live birth and one abortion you write (G3P1+1)
that means one live birth plus an abortion.
 Last normal menstrual period- is important to estimate the expected the date of delivery for
pregnant women. So you ask when was her last menstrual period. Example it was 3/1/2017.
To get the expected date of delivery (EDD) we use naegele’s rule by adding one year,
substracting three months and add seven days to the LNMP. So when we add one year there
we get 2018, substracting three months it becomes October and adding seven days to date it
becomes 10. So EDD is 10/oct/2018.
 Expected date of delivery.
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2. A short introduction of a patient/an opening statement- this includes mentioning the number of
days the patient has stayed in the ward, if referred where is he or she referred from and a referral
diagnosis if possible. ( In an exam setting you may not be able to see the file or see the referral letter
so its best you end up mentioning from where he or she is referred otherwise examiners will poke
your eyes). In the introduction remember mentioning if it’s a re-admission at that hospital or it’s the
first one. If it’s a re-admission remember to ask for the reason of previous admission and the
condition at discharge if possible get a look at the discharge summary at the file. Mention if there is
any chronic illness that is known of the patient. Example known patient with HIV on
regular/irregular medication for 3years now.
3. Main complains- this is what brought the patient to hospital. So ask the patient, what made you
seek health care today? It could be that the patient has pain for the past six months, but why didn’t
he come last month? So did it worsen to necessitate him or her to attend the hospital? Remember
to put complains in an order from the one which begun first to the recent one. If all complains
started at the same time then arrange them in the order of severity, beginning with the most severe
symptom.
4. History of presenting illness- this is the story of the current illness. How it started, when, anything
that gives a relief of the condition, anything that worsens the condition and whether there are
accompanying symptoms. This helps you arrive at the diagnosis. Take an example of a patient having
a swelling at the forehead. He tells you it has been there for the past two hours, grew up slowly,
painful, nothing worsens it but has been massaging it and it is fading away.
It was preceded by a fist from an angry loyal citizen that hit his forehead. There you definitely know the
diagnosis. The rule here is DONPARA
 D- DURATION
 O-ONSET
 N-NATURE OF THE CONDITION
 P-PERIODICITY
 A-AGGREVIATING FACTORS
 R-RELIEVING FACTORS
 A-ASSOCIATED SYMPTOMS
In the history of presenting illness we also ask for risk factors regarding the diagnosis you are thinking
about, complications of the disease you are suspecting, and ask for symptoms of the disease that may
mimic the disease you are suspecting to just be sure it’s not some other disease, and this is what we call
ruling out other conditions. Mention if there are any efforts the patient has done regarding his illness
along the course and if any interventions were done and lastly ask for the progress in the ward.
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5. Review of other systems- there could be coexistence of other conditions despite the illness the
patient has. If you have more than one pathologies, sometimes one is primary the others are
secondary. So you might be dealing with renal failure only to forget this patient may have
secondarily hyper parathyroidism.
6. Pre natal history, natal and post natal history follows incase it’s a pediatric case. Pre natal history
involves asking how many times the mother attended clinic while carrying this particular baby in her
womb, what was the gestation age at her first visit and ask for any drugs given during the visits and
if there was any illness like skin rash during pregnancy to just be sure she never suffered things like
rubella. Natal history involves asking for mode of delivery, time of labor, was it at term or not as
some conditions are common among pre term such as necrotizing enterocolitis, ask for the birth
weight too in the natal history and if the baby cried and sucked immediately. Postnatal events
involves the events afterwards, so ask if the baby ever got ill, jaundice or anything. These only
appear in pediatric cases and are written under separate headings, don’t include all at once as I did
in this paragraph.
7. Immunization history- this is important in pediatric cases. This can be obtained from the RCH card.
Conclude if at all they are appropriate for the child’s age. If the child missed the vaccine we conclude
it as “missed opportunity for vaccination”
8. Developmental milestones- report what the child can do and conclude if appropriate for his or her
age. Example for a 9months old baby not be able to sit unsupported is delayed milestones.
9. In obstetrics and gynecology we don’t include the parts no. 6, 7 and 8 instead follows past
gynecology and obstetrics history immediately after history of index pregnancy.
10. Past medical history- this follows review of other systems in an adult male case, otherwise it follows
after pre natal, natal, post natal, immunization and milestones history in pediatric case. For a female
adult case it follows after past gynecological history and obstetric history and if pregnant history of
index pregnancy. Past medical history includes any history of surgery, blood transfusion or any
chronic illness. Report any illness of relevance the patient suffered in the past. Example past history
of recurrent schistosomiasis could explain the bladder ca the patient has now. Any allergy to drugs
or foods should be mentioned.
11. Family and social history- here we are interested of the conditions that run in families, if there is any
social activity that is related to the patient’s illness. Example a long distance driver is at risk of HIV,
smokers have a risk of lung cancer. Alcohol is a risk to liver cirrhosis.
12. Dietary history- mention number of meals, what he eats and amount. And has it changed since he or
she became ill.
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13. Summary of the history- remember summary is the mini skirt of the history. It should be short
enough and contains important information. It should have important positives and important
negatives. If one had a history of bleeding, mentioning in the summary that so and so with history of
bleeding and symptoms of anemia not in failure, symptoms of anemia are important positives here.
One is interested to hear did this patient bleed so much? And saying not in failure is an important
negative, atleast one wants to hear has this patient gone to failure.
PHYSICAL EXAMINATION
1. GENERAL EXAMINATION- a head to toe. Report whatever you see. Example normal hair
distribution, conjunctiva pallor, conjunctiva hemorrhage, any oral lesions such as candidiasis,
ulceration, examine the hands for stigmatas of liver or heart diseases such as duptreyn
contracture, finger clubbing, mention if there is any palpable lymph nodes and finally lower
limb edema. Lymph nodes to palpate are pre and post auricular, sub mandibular, mental,
along the borders of sterno cleido mastoid, supra and infra clavicular, axillary and inguinal
nodes.
2. LOCAL EXAMINATION- in cases of local pathologies.
3. SYSTEMIC EXAMINATION. Begin with inspection, then palpation, percussion and finally
auscultate.
SYSTEMIC EXAMINATION
RESPIRATORY SYSTEM-on inspection report respiratory rate then look for the appearance of the chest
and movement. In appearance look for scars if present, shape of the chest which normally is elliptical
with antero-posterior diameter being shorter. Observe the chest movements. Are the movements
symmetrical? Then palpate for lymph nodes (though most of the times it is covered in general
examination and therefore not reported in respiratory examination), palpate for the trachea if its central
and chest expansion. Percussion is done while comparing the two sides of the chest, start with infra
clavicular then mammary and infra mammary, then percussion of the axial and finally three areas at the
back. Normal percussion is resonant. Ascultate same areas you did percussion and finish with
auscultation of the lung basis. Normal breath sounds are reported as vesicular. (more details refer
Hutchson text book)
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CARDIOVASCULAR SYSTEM- Patient should be at lying on bed inclined at 45 degrees.
We follow an inverted J and more palatable we mention it as hockey stick approach. Begin with the
radial pulse, say the rate rhythm, synchronicity, is it of good volume and whether its collapsing or not.
Then measure the blood pressure. See if there are distended neck veins, and you may need two rulers to
measure the jugular venous pressure- with one ruler at sternal angle and the other at the highest point
of jugular pulse and the rulers perpendicular to each other. Normal jugular venous pressure is 6-8 cm of
H20 from right atrium. Then inspect precordium if there is any hyper activity, locate the apex beat in
relation to mid clavicular line, palpate for heaves and thrills and finally auscultate four areas- apex,
lower left sternal border, upper left sternal edge and upper right sternal edge and these correspond to
mitral , tricuspid, pulmonary, and aortic valves. (details are in Hutchison)
PER ABDOMEN- inspect for any scars, therapeutic marks. Report if the abdomen is distended, does it
move with respiration. Palpate to see if there is any tenderness and report according to the nine
abdominal regions eg tender at hypogastric region. Palpate for the liver, spleen and kidneys( hutchson
demonstrates well). Percussion note normally is tympanic, if dull then there is fluid or something else.
Auscultate bowel sounds. Hutchson mentions just to the right of the umbilicus is best and stethoscope
should be kept for one minute. Auscultate for vascular bruits particularly renal bruits 2cm above and
2cm lateral to umbilicus. Then finish abdominal exam with digital rectal examination.
Remember to examine the gravid uterus- that is Leopold maneuver. Leopold maneuver includes fundal
palpation to know what occupies the fundus, lateral palpation to know the lie and finally pelvic grip to
know if the baby is engaged or not.
In gynecology cases remember the per vaginal digital examination and speculum.
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CENTRAL NERVOUS SYSTEM EXAMINATION
This is the most interesting per say. So begin the higher centres. Is the patient oriented to time, place
and person. Ask him whether he is aware if its day time or night to know his orientation to time as it is
difficult one to say the exact clock time like its 1245hrs. Ask him or her of where he or she is to know the
orientation to place and finally identify if can recognize people. While talking to him you must have
known the speech so report it if its slurred, normal or mute. Report memory both long and short term
memory.
You can ask him or her if he or she recalls her forexample when his or her first child was born to assess
long term memory, you can ask her your name if you introduced yourself before you begun taking
history to see if he or she remembers and that could assess short term memory. Then examine cranial
nerves
Cranial nerve examination
We know the cranial nerves and we report their functions only. Forexample
Cranial nerve 1- can smell
Cranial nerve 2- can read from a 6metre distance, has no color blindness (if at all you had ishihara plates
to test), pupils equally in size, reactive to light and measure 2-3mm, fundoscopy not done- obviously for
a medical student to not do fundoscope.
Cranial nerve 3,4 and 6- can move eyes in all directions
Cranial nerve 5- has intact facial sensations, good contraction of the temporalis and masseters.
Cranial nerve 7- it’s the facial nerve. Report if there is any facial symmetry, can blow out the cheeks?
Cranial nerve 8- can hear
Cranial nerve 9 and 10- uvula centrally located, positive gag reflex.
Cranial nerve 11- can shrug shoulders, turn neck against resistance.
Cranial nerve 12- can protrude tongue, no fasciculations, no muscle atrophy
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MOTOR EXAMINATION
Mnemonic is BIG TPR.
B-Bulkiness of all groups of muscles in upper and lower limbs
I-see if there are any Involuntary movements
G-observe the GATE
T-mucle Tone
P-Power in all groups of muscle
R- Reflexes both superficial and deep tendon reflexes ie knee, ankle, elbow and wrist places you hit with
patella.
COORDINATION
Assess coordination- finger to nose test, or heel to shin test.
SENSATION
Then test for sensation following the dermatomes.
GO THROUGH THIS LINK FOR MORE ON CNS EXAMINATIONS OR HUTCHSON-

https://googleweblight.com/i?u=https://meded.ucsd.edu/clinicalmed/neuro2.htm&hl=en-
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HEMATOLOGY
CHRONIC MYELOID LEUKEMIA
It’s a common case in hematology. It’s an abnormality in production and proliferation of mature and
maturing granulocytes. Granulocytes are white blood cells with secretory granules, that means can
secrete something. These are such as eosinophils, basophils.
A definition that will earn you a credit on CML is when you say it is “a myeloproliferative disorder
characterized by dysregulated production and uncontrolled proliferation of mature and maturing
granulocytes with fairly normal differentiation”
It’s a result of fusion of 2 genes. BCR gene on chromosome 22 fuses with ABL1 gene on chromosome 9.
The two genes have tyrosine kinase activity and once they fuse it results to dysregulated tyrosine kinase
activity.
CLINICAL FEATURES
The disease has three phases
1. Chronic phase- in which majority of the patients you will clerk are in this phase
2. Accelerated phase- a stage production of white cell is severly uncontrolled and can not be taken
down by treatment
3. Blast crisis- time when even immature cells uncontrollably proliferate to resemble acute
leukemias in which there are immature cells.
20-50% of patients are asymptomatic and may be discovered by routine investigations. Even those
symptomatic have non specific symptoms such as
1. Fatigue
2. Malaise
3. Weightloss
4. Excessive sweating
5. Abdominal fullness- due to splenomegally
6. Bleeding tendencies due to platelet being affected.
7. Abdominal pain and discomfort may include left upper quadrant pain and early satiety due to
enlarged spleen with or without perisplenitis and/or splenic infarction
8. Tenderness over the sternum due to the bones that produce cells are highly active and
expanding.
Frequently seen picture is massive splenomegally, anemia and high white cell count. If you mention
these and report its CML, just chill and wait for credits.
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INVESTIGATIONS
1. Peripheral smear where you will definetly see a lot of white cells
2. Leucocyte alkaline phosphatase when scored will be low. To just be sure these many white cells
arenot because there is an ongoing infection that they are fighting check for leucocyte alkaline
phosphatase that healthy leucocytes make.
3. Full blood picture- same thing many white cells
4. Bone marrow biopsy- granulocyte hyperplasia with maturation pattern
5. Genetic testing for Philadelphia chromosome and BCR-ABL1 gene.
TREATMENT
As I said earlier the problem is tyrosine kinase activity so we find tyrosine kinase inhibitors which are
Imatinib, Disatinib and dilotinib. The “nib” drugs
They give hydroxyl urea in the wards because its cytotoxic it just goes to kill the cells and reduce their
numbers and just give a relief.
MULTIPLE MYELOMA
Its simply a cancer. There is uncontrolled division of plasma cells. They divide rapidly in bone marrow
destroying bones. Since they destroy bones calcium from bones is released into the system. Remember
these cells that divide uncontrolled produce immunoglobulins that are proteins, hence a lot of proteins
will be in blood.
So the above explanation give you a clear picture in summary what multiple myeloma is and how it will
present. Its clinical features will be
1. Bone pain with lytic lesions seen on X ray

2. Increased total serum protein concentration
3. Hypercalcemia
4. Renal failure
5. Signs of malignancy as unexplained anemia
The best way to remember multiple myeloma is the mnemonic CRAB
C-calcium high
R- renal failure
A-anemia
B-bone pain
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MANAGEMENT
The best one is HEMATOPOIETIC STEM CELL TRANSPLANTATION (which is not so far applicable in our
setting).
Its complicated just remember they use the drug Mephalan. If you want to know management better
read further but trust me its not so worthy your time.
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CASE -APLASTIC ANEMIA
NAME XXXX
AGE 29
SEX FEMALE
RESIDENCE DAR
DAYS IN THE WARD 16
Chief complaints- recurrent PV bleeding
Lower abdominal pain
Easy fatigability
Awareness of heart beats.
HISTORY OF PRESENTING ILLNESS
She reports to experience recurrent episodes of PV bleeding, sudden on onset, profuse, not period
specific, not precipitated by contact. The bleeding is not associated with clots. She changes the pad
three times a day. No history of using anticoagulant and denies any other discharge that is foul smelling.
She also reports lower abdominal pain, crampy in nature, gradual on onset, not period specific with no
known aggravating or relieving factors.
She complains of awareness of heart beats and easy fatigability. She doesn’t cough.
No history of Recurrent fevers, Nose bleeds or gum bleeds, Easy bruising, Bone pains, Shortness of
breath, LL swelling or Difficulty in lying flat
She has had a black stool once. No history of vomiting blood and has never been diagnosed to have
peptic ulcer disease.
Initially admitted to gyn ward and later referred to hematology due to a report of pancytopenia.
REVIEW OF OTHER SYSTEMS
Nothing was significant
PAST MEDICAL HISTORY
First admission at BMC. She was admitted with similar complains. She was found to have polycystic
ovarian syndrome and pancytopenia whose cause was not determined. She was being treated
supportively with transfusion of packed RBC and platelets. When given hormonal therapy stops
bleeding.
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No history of allergy or surgery.
She was on following medications- cyclosporine, primolut, metformin, bromocriptine and tranexemic
acid. She also developed malaria 20 mps/200 WBC and was treated.
GYNECOLOGICAL AND OBSTETRIC HISTORY
She is para 0. She sees has been seeing cycles normally until 5months ago when this illness begun. She
used to have a 28day cycle and exchange pads up to twice a day not fully soaked
FAMILY AND SOCIAL HISTORY.
She is single. She is a university student from Shinyanga. All parents are HIV positive. There is no history
of blood transfusion or easy bleeding from other family members.
EXAMINATION
General examinations- alert, afebrile, not dyspneoic, pale, not jaundiced, no petechiae or ecchymoses,
no pedal or facial edema, no lymphadenopathy, no hirsuitism, no acanthosis nigricans and has no gum
hypertrophy.
PER ABDOMEN- scaphoid abdomen with no traditional or therapeutic marks. It moves with respiration,
soft non tender with no hepatosplenomegaly. Tympanic note heard on percussion and normal bowel
sounds heard on auscultation.
RESPIRATORY SYSTEM- elliptical chest, syemtrical, trachea centrally located and resonant note on
percussion. Vesicular breath sounds heard on auscultation.
CVS- normal
CNS- normal
INVESTIGATIONS
Full blood picture results.
WBC-0.482
NEUTROPHIL-0.095
LYMPHOCYTES-0.33
HB-5.14
MCV -83.0
PLATELET-4.58
Peripheral blood film showed pancytopenia. The cause still not known
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It was suggested to do
1. Reticulocyte count whereby the results came it was 2%.

2. Bone marrow aspiration which showed features of erythroid hyperplasia and no evidence of
malignant infiltrations.
To rule out megaloblatic anemia it was suggested to check B12 levels and folic acid and the results were;
B12= 41.37 (the normal range is 19-119) and folic acid=14.2 (normal range is 7.2-15.4)
Bone marrow histology- trephine biopsy showed hypocellular marrow features of evolving aplastic
anemia. No malignant infiltrate.
Other investigations done
1. Serum ferritin- >1000

2. PT-7.85
3. INR=0.71
4. Hormonal assays were done- FSH,LH, THYROID HORMONES, ESTRADIOL, TESTOSTERONE AND
PROGESTERONE.
5. Creatinine- 54, urea-3, urinalysis revealed blood +2
6. SGPT=64, SGOT=53
7. Abdominal pelvic ultrasound- Polycystic ovarian syndrome
8. HIV test was negative.
Provisional diagnosis
Severe anemia not in failure secondary to menorrhagia. The cause? Polycystic ovarian syndrome?
Aplastic anemia?
DDx of Pancytopenia
– Pancytopenia due to failure of cell production probably due to
• Bone marrow Infiltration: leukemia, myeloma, MF, lipidoses
• Severe B12/FA deficiency
• Myelodysplastic syndrome
• HIV infection
• Aplastic or Hypoplastic anemia
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– Pancytopenia due to peripheral cell destruction-
• Splenomegally
• Overwhelming infection (sepsis)
• SLE (systemic lupus erythematosus)
• PNH (paroxysmal nocturnal hemoglobinuria)
DISCUSION
APLASTIC ANAEMIA
• Causes
– Congenital eg. Fanconis anemia
– Acquired
• Idiopathic
• Drugs
– Dose dependent: Cytotoxics, benzene
– Idiosyncratic: Chloramphenicol, NSAIDS
• Radiation
• Viral: nonA, nonB, nonC hepatitis, EBV
• PNH
• Pathophysiology could be due to any of the following mechanisms-
– Damage to the multipotent hemopoietic stem cells
– Impaired self renewal
– Stem cell depletion
– Damage may be due to: drugs, viruses, immunological
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• Clinically
– Anemic symptoms- as easy fatigability, awareness of heart beats, dizziness.
– Thrombocytopenic symptoms- bleeding, bruising easily
– Neutropenic symptoms- repeated infections.
– Splenomegally is rare, when present consider alternative diagnoses
• Hematological findings
– Normo or macrocytic anemia
– Low reticulocyte count
– Pancytopenia
– Elevated erythropoetin levels
– Markedly hypocellular marrow
– Fatty
– May contain some foci of normal or increased cellularity
• Use trephine bx
• Treatment
– Remove causative exposure if identified
– Supportive therapy
– Platelet transfusions and alloimmunization
– Limit transfusions of blood products if marrow transplantation is planned.
– Non transplanted patients may benefit from: ATG, Cyclosporin A, methyl pred
– Combination therpay > monotherapy
– Addition of G – CSF has produced encouraging results
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• Prognosis
– Only approx 10% make a complete hematological recovery
– Poor prognostic feature
• Platelet < 20 * 109
• Neutrophil < 0.2 * 109
• Reticulocyte count < 10 * 109
• Marked hypocellularity of the marrow
WAY FORWARD TO OUR PATIENT WAS
• Gynecological review
• Supportive treatment meanwhile
• Start hormonal treatment if bleeding re starts
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NEUROLOGY
STROKE
Is simply lack of blood supply to the brain. It could be maybe a vessel has ruptured (hemorrhagic stroke)
and no more blood supply distal to it or there is blockage or blood doesn’t reach despite vessels being
intact (ischemic stroke).
Types of stroke- ischemic and hemorrhagic stroke.
Categories of ischemic stroke
1. Thrombotic type where the cause is thrombosis. Under this there are only two subtypes
thrombosis of larger vessel and thrombosis of smaller vessels in the brain
2. Embolic type where the cause is embolism. Under the embolic type we have subcategories
• Those with emboli whose source is known is from the heart
• Those whose source is not known but is thought to be probably the heart or aorta.
• Those whose source is an artery
• Those whose source is not known
3. Systemic hypoperfusion. Maybe the blood pressure is low that heart cant pump enough blood
to the brain
Categories of hemmorhagic stroke
1. Intracerebral hemorrhage
2. Subarachnoid hemorrhage
CLINICAL FEATURES OF STROKE
Depends on the area of brain affected because each area in brain has specific functions. Commonest
vessel involved in stroke is the middle cerebral artery. So just find out where middle cerebral artery
supply to know the areas affected and how one will present.
ANTERIOR CEREBRAL ARTERY STROKE
Patients usually have weakness and sensory loss in the lower legs and foot opposite to the hemisphere
affected and may have behavioural change
MIDDLE CEREBRAL ARTERY STROKE
Patient will have contra lateral hemiparesis and hemisensory loss of the face, upper and lower
extremities. Functions of the lower extremity are not very affected as it is in anterior cerebral stroke. If
it’s the left dominant hemisphere MCA affected they have speech problems, if it’s the right one they will
have perceptual deficits.
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POSTERIOR CEREBRAL ARTERY STROKE
Remember the visual centre is at the occipital region. So they will have visual problems. This also
supplies the thalamus, so failure to supply the thalamus which is the sensory relay centre the brain will
perceive every stimuli as pain and they will end up with central post stroke pain where the patient will
be experiencing pin and needle sensations. Another presentation is Alexia without agraphia ( that is a
patient cant read but can spell and write)
SUBARACHNOID HEMMORHAGE- a patient will report to have a prior history of abrupt onset of sudden,
severe headache. Patients are usually very ill and sometimes with reduced alertness.
HEMMORHAGIC STROKE- gradual progression of symptoms during minutes or hours. It can also be
preceded by headache. Patients are usually very ill and sometimes with reduced alertness.
ISCHEMIC STROKE- you have sudden onset of paralysis maybe without even a headache prior. The
symptoms may improve with time. It can be precipitated by getting up at night to urinate. So someone
may report it happened when he or she woke up at night to urinate.
HISTORY IN STROKE
1. Age – most ischemic strokes occur in patients with age above 40. So if is an elderly patient start
thinking of ischemic type
2. Hypertension- is associated more with hemmorhagic stroke
3. Pre existing heart diseases such as valvular heart disease, infective endocarditis gives you a clue
it is a stroke due to embolism of cardiac origin
4. Smoking is a risk to atherosclerosis and hence ischemic stroke.
5. Diabetes also increases the risk of ischemic stroke. So it is important to know if your patient has
diabetes.
6. A previous transient ischemic attack is also a risk factor.
COMPLICATIONS OF STROKE
1. Pulmonary complications- aspiration pneumonia if it affects the nerves that deal with
swallowing. They also get what we term as neurogenic pulmonary edema.
2. Genitourinary complications- UTI since they need to be catheterized
3. Post stroke seizures happen since after ischemia a scar remains in brain and these could disturb
the brain impulse travel and lead to seizures
4. Hematological- thromboembolism due to long term immobility.
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CASE-NEUROLOGY
NAME TUTUTUTU
AGE 51
SEX FEMALE
RESIDENCE TANGA
Referred from BOMBO were was treated as a patient with Paraplegia.
Main complaints are upper and lower limb weakness for 2years.
Recurrent episodes of UL and LL weakness, 3 episodes /2years gradual onset progressively worsening
with time.
1st episode –Started on the Lt foot, gradual onset, preceded with hx of falling down when she was
walking on a wet surface and stepped on a fruit, weakness was also preceded with a cold sensation,
numbness and pricking sensation and later weakness involving the whole Lt lower limb. Weakness
ascends up to the level of the knee and involve the Rt. LL trunk, chest and upper limbs after 3 days with
similar character, left side > affected than the Right sides. Patient was not able to walk, or stand.
LL weakness was associated with inability to pass stool despite diet containing roughages and fluids also
associated with generalized abdominal distension and discomfort especially after a meal, nausea, loss of
appetite. No history of vomiting and was able to pass flatus normally, relieved by medication and
manual fecal evacuation of bulky, hard stool, not blood stained. Normal micturition habit
2nd episode –Gradual onset, more severe, with more difficulties on walking, severe numbness (sandals
drop out unaware, relative constipation, normal micturition, affect UL > LL, Left UL > Rt UL and had
minimal improvement after physiotherapy and medication.
3months before admission experienced: Low grade fever without history of neck stiffness/ pain ,
vomiting or convulsion. Associated with difficulty in breathing and sweating especially the upper part of
her body, relative constipation and was not able to control the bladder together with progressive
worsening of weakness and numbness ( not able to sit unsupported or lift the legs)
These symptoms were associated with headache: More marked at the back, associated with blurred
vision, not associated with vomiting or nasal congestion/ tearing, dizziness or fainting episodes
Denied history of fever or neck pain or stiffness before the onset of illness, No history of chronic cough
or straining during defecation before the onset of the illness. No history of nasal congestion, difficult in
swallowing or DIB
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Nothing significant
Nothing ringing the bells
GYNECOLOGICAL HISTORY, FAMILY AND SOCIAL AND DIETARY HISTORY all don’t have anything
significant
EXAMINATION FINDINGS
CNS
Higher centres and cranial nerves normal findings
Motor examination- bulkiness reduced in all groups of muscles in upper limbs but normal in lower limbs.
Tone reduced in all groups of muscles both upper and lower limbs. Power 1/5 in all muscles in lower
limbs while 3/5 in all muscles in upper limbs. Deep tendon reflex lost in ankle and knee bilaterally. No
clonus or babinski sign. Sensation lost in all limbs.
Other systems had normal findings except per abdomen where DRE noted fecal impaction
PROVISIONAL DIAGNOSIS
• Central Cord Syndrome
• Transverse Myelopathy
• Anterior Horn Syndrome
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CASE - CIDP
NAME ZYZ
AGE 15
SEX FEMALE
RESIDENCY MWANZA
SEEN ON OUTPATIENT NEUROLOGY CLINIC
CHIEF COMPLAINTS- lower limb weakness for 2years, upper limb weakness for 1 year, failure to pass
stool 2months and difficulty in swallowing for 2months.
Prior to the onset LL weakness the patient had episodes of diarrhea which were acute on onset initially
watery later blood stained and could have >10motions/day. No history of vomiting, fever or headache.
No history of diarrhea from other family members at home during her illness. She was once treated for
UTI. Two weeks later following the onset of diarrhea the patient experienced LL pain (both), described
as burning in nature with pin and needle sensation. No history of loss of sensation. It was temporally
relived by applying oils and Paracetamol. A month later she noted heaviness of the LL, described as
difficulty in rising from the sitting position or squatting, difficulty in climbing stairs or small hills she used
to climb. No history of falls. It progressed to the extent he could not stand or walk. She was able to walk
with support initially but 2wks later she was completely unable to walk even with support.
She dropped school and was unable to do her normal daily activities. No history of change in bowel or
micturition habit. She received treatment at Bugando hospital and was given prednisolone, neurotone
and ant pain plus physiotherapy. She attended traditional healers. She was given oils to apply in the LL
and oral medicines plus traditional marks around the joints of LL.
Some months later she improved. She could flip the toes, lift the legs against gravity. As time went she
improved and could walk again which made her mother stop her from the medications. A few months
passed and she got a second episode of LL weakness. This time it was more severe but same pattern and
character as the 1st episode. It was associated with severe lower back pain, non radiating,and loss of
sensation (numbness) of both LL symmetrically ascending in nature. It was not preceded by febrile
illness. Sometimes slippers fell off without her awareness.
2months later following the second attack she noticed herself dropping a glass of water, plates, couldn’t
comb her own hair and realized her upper limbs were also weak. She was later not able to sit or support
her head. No history of difficulty in breathing.
Two months prior to admission she developed inability to pass stool despite taking adequate fluids,
water and roughages. She developed generalized abdominal swelling, nausea, early satiety and loss of
appetite but was able to pass flatus. No history of vomiting. She then lost sensation of urge to urinate.
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Along with that she developed difficulty in swallowing preceded by painful swallowing, more with solid
than liquids. She could still feel the taste of food. No history of drooling of saliva or abnormal tongue
movements. No facial asymmetry or abnormal facial sensation. No neck bulging or coughing during
swallowing. She has noted weight loss, loosening of clothes and has difficulty in articulating words and
swallowing.
She denied history of blurred vision, double vision or loss of vision. Symptoms not aggravated after
taking hot baths. No complains of fever or body malaise. No history of neck trauma or spine surgery
neither radiotherapy. No history of heat or cold intolerance. No history of joint pain or swelling or skin
lesions. No history of seizures or confusion. She has never had a genital ulcer, per vagina discharge or
bleeding.
Progress in the ward still the same can’t sit unsupported, feeds by NGT.
• 2nd Admission
• 1st admission Bugando Hospital.
• h/o herbal use for 3 months,
• No history use of medications for chronic illness
• No history of BT
• No history of HT/Dm
• No history of surgery
DIETARY HISTORY
• Breakfast: Tea/porridge/ bread, rice, chapati
• Lunch: one full plate of either rice, banana, potatos with veg/ occ meat/ fish/ beans, or fruits
• Dinner: As lunch
• Adequate in Quality and quantity
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FAMILY AND SOCIAL HISTORY
• Father 50yrs- doctor- vet nary medicine- private
• Mother 42yrs, Food vender
• Index is the 5th born in a family of 6 sibling
– 1st born 22yrs, completed form iv 3yrs ago, doing well
– 2nd born 20 yrs completed form IV 2yrs ago, doing well
– 3rd born 17yrs form II, doing well
– 4th born 15 yrs STD 6, doing well
– 6TH born 8 yrs STD 2, doing well
• No hx of DM/HT
• No hx of similar illness in the family or surrounding community
SUMMARY
Presented G.J, 15 years of age, STD IV self referral from Mwanza, with the history of remitting relapsing
progressive LL weakness (accompanied with features of length-dependent large and small fiber
neuropathy) preceded by a febrile illness, and autonomic dysfunction with no eye signs. She has a
worsening dysphagia and odynophagia. No associated constitutional symptoms
EXAMINATION
• Lethargic, not dyspneic, had NGT, afebrile (36.5 ◦C), not pale, not jaundiced, oral ulcers, no oral
thrush, no lymphadenopathy, soft neck, clawed hands, no clubbing, secondary sexual
characteristics, therapeutic marks on knees, no bed sores, no contractures, pes cavus, no LL
edema.
• Weight: 35kg
• Ht: 1.52m
• BMI: 15.1 BMI – below 5 th percentile
• CONCLUSION- she is underweight.
CNS EXAMINATION
Higher centers- were okay.
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Cranial nerve examination
CNS- Cranial nerves
– C1- could not be assessed
– C2- Visual acuity,visual fields, color could not be assessed, and had normal fundoscopy
results -Red reflex was there, the macula and optic disc were normal, retinal vessels
were normal. No RAPD
– C3,4,6 Can move eyes in all directions and pupillary reflex normal bilaterally- normal
shape and size.
– C5- clench teeth normally, sensation (pain) was intact in the face
– C7- Facial symmetry, sensory not assessed
– C9,10 - Gag reflex present
– C12- No tongue deviation or fasciculation
MOTOR EXAMINATION
UL-RT UL-LT LL-RT LL-LT

Bulk reduced reduced Reduced Reduced
Fasciculation No No No No
Tone Hypo Hypo Hypo Hypo
Power 0/5 0/5 0/5 0/5
Reflex Absent Absent Absent Absent
Clonus Absent Absent
Babinski Absent Absent
SENSORY EXAMINATION
– Light touch, vibration and proprioception were not tested. But pain in upper limbs the
level was C5-8 and lower limbs L1-S1.
– Spine examination- it was of normal contour and no tenderness or swelling.
– Other systems were essentially normal.
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SUMMARY
Presented G.J, 15 years of age, STD IV self referral from Mwanza, with the history of remitting
relapsing progressive LL weakness (accompanied with features of length-dependent large and
small fiber neuropathy) preceded by a febrile illness, and autonomic dysfunction with no eye
signs. She has a worsening dysphagia and odynophagia.
No associated constitutional symptoms. On examination Lethargic, had NGT, oral ulcers, clawed
hands, pas cavus, normal gag reflex and signs of Peripheral nerve lesion.
1. Peripheral Neuropathy? Cause
– Post infectious: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)
– Hereditary: Motor and sensory neuropathy Charcot-Marie-Tooth
– Metabolic Neuropathy: Hypothyroidism/ Vitamin B12 deficiency/ Diabetic Neuropathy
2. Muscular dystrophy: Limb Girdle Muscular Dystrophy
Differentials with reasons supporting it
1. Post infectious/ chronic inflammatory demyelinating polyradiculoneuropathy (CIPD). The

features that appear in the history that convince us of the diagnosis are:
• Precipitous onset of symptoms which occurs in 20-30% of patients
• Insidious onset of symptoms progressing to chronic
• Recurrent and progressive symptoms for atleast two months
• Initial limb weakness more than sensory (50% of the patients have sensory
disturbances)
• Symmetric involvement of arms and legs
• Proximal muscles involved along with distal muscles
• Autonomic system dysfunction
• Reduced deep tendon reflex.
2. Hereditary motor and sensory neuropathies of charcot marie tooth disease. The features that
appear in our patient and convince us of the diagnosis are:
• Onset usually in childhood
• Slowly progressive distal weakness
• Motor symptoms predominate over sensory symptoms
• Muscle atrophy, pes cavus and claw hands
• Absent deep tendon reflex
• Sensory loss
• Family history
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3. Metabolic neuropathies
• Vitamin B12 deficiency- common in vegetarians, they have visual changes, spastic
paresis, positive babinski sign and features of pernicious anemia,
• Hypothyroidism- poor ability to tolerate cold, feeling of tiredness, weight gain and
anterior neck swelling
• Diabetic neuropathy- but our patient is not known to be diabetic and no family history
of diabetes.
Provisional Diagnosis
Muscular dystrophy: Limb girdle muscular dystrophy- reasons being;
⁺ Symmetric progressive proximal muscle weakness
⁺ Dysphagia
⁺ Onset in childhood or teens
⁺ Muscle wasting, hypotonia and absent reflexes
No sensory neuropathy or autonomic or visceral dysfunction.
INVESTIGATIONS
1. Motor conduction studies:
CMAPs were low in ulna, median and peroneal nerves, with normal distal latency and velocity sensory
conduction:
Sensory conduction velocity was low in ulna and sural nerves with prolonged distal latency
Conclusion:
Motor sensory axonopathy predominant, multifocal polyneuropathy.
2. CSF Examination
Macroscopically: clear fluid, normal opening pressure
Biochemistry:
• CSF protein 0.17g/L (0 – 0.43)
• CSF glucose 3.96 mmol/L, Blood glucose 5.5mmol/L
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CSF EXAMINATION
• Cytology: Acellular smear
Microscopy
• Incapsulated yeast cells-Absent
• Polymorphs-Absent
• Lymphocytes-Absent
• Gram positive cocci-Absent
• Gram negative cocci-Absent
• Gram positive bacilli-Absent
• Gram negative bacilli-Absent
• Yeast-Absent
• Acid fast bacilli-Absent
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TOTAL SPINE MRI
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BRAIN MRI
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OTHER INVESTIGATIONS DONE
Serum Vitamin B12 level: 450 pg/mL
Serum Creatinine Kinase level: 156 U/L (53 – 269 U/L)
Thyroid function test:
Total T3 – 2.90 nmol/L
Free T4 – 1.24 ng/dL
TSH – 1.0500 µIU/mL
Hepatitis B Surface antigen negative.
HIV 1 and 2 antibodies negative.
VDRL-negative
Hepatitis c antibody- negative
Hepatitis b surface antibody- positive
Hepatitis A Igm antibody-negative.
Full blood picture results were normal. Liver enzymes were all within the normal range.
Creatinine and urea were all normal.
Urinalysis results were all normal.
FINAL DIAGNOSIS
Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)
⁺ History and physical findings
⁺ Confirmed by NCT (Nerve Conduction Studies) - Motor sensory axonopathy predominant multifocal
polyneuropathy.
CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY(CIDP)

Is a chronically progressive, stepwise or recurrent proximal and distal weakness and sensory dysfunction
of all extremities, developing over at least 2months with absent or reduced tendon reflexes in all limbs
and sometimes cranial nerve involvement.
A rare acquired disease of peripheral nerves and nerve roots. It is usually a continuum of Acute
inflammatory demyelinating polyradiculopathy (GBS). Sometimes it is secondary to systemic disorders
such as SLE, HIV, hepatitis. It’s a immunologically based disorder with multiple triggers.
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CIDP – DIAGNOSTIC CRITERIA
-Progression over at least two months
-Weakness more than sensory symptoms
-Symmetric involvement of arms and legs
-Proximal muscles involved along with distal muscles
-Reduced deep tendon reflexes throughout
-Increased cerebrospinal fluid protein without pleocytosis
- Nerve conduction evidence of a demyelinating neuropathy
- Nerve biopsy evidence of segmental demyelination with or without inflammation
CIDP – VARIANTS
• Lewis-Sumner syndrome: Multifocal acquired demyelinating sensory and motor neuropathy

(MADSAM)
• Sensory-predominant CIDP
• Distal acquired demyelinating sensory neuropathy (DADS)
• Pure motor CIDP
• CIDP with CNS involvement
PATHOLOGY
Characteristically segmental demyelination and remyelination, and onion bulb formation on nerve
biopsy. There may be associated axonal degeneration.
CIPD TRIALS
Mainstay treatment is IVIG1, glucocorticoids and plasma exchange. Other modalities suggested are
cyclosporine, cyclophosphamide, methotrexate and rituximab.
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MANAGEMENT
• Tabs Prednisolone 40mg OD – 6 weeks

• IV Methylprednisolone 1000mg OD – 5 days. (now she is on 30mg on alternate days)
• Tabs Gabapentin 100mg BD
• Tabs Pantoprazole 40mg OD
• Tabs Calcium + Vitamin D OD
• Feeding via NGT
• Metronidazole oral gel
• Nursing: Turning every 3-4 hours to prevent bed sores
MONITORING
Monitor RBG regularly. Do daily neurological and disability assessment and watch out for side effects of
prednisolone. The side effects of prednisolone are gastritis, oral ulcers, cataracts, osteoporosis, weight
gain, easy bruising.
One can use the rasch built overall disability scale to monitor patients progress or the online neuropathy
limitation scale.
FOLLOW UP
Every 3-6 months
COUNSELLING
• Mother has been explained on the nature of the disease and its chronicity
• Possibility of recovery at this stage of presentation may be low
• She has been encouraged to continue feeding, physiotherapy and general nursing care.
PROGNOSIS
 30% achieve cure or remission1

 Studies mainly done in early stages of CIDP
 Lack of long-term follow up data
 Overall prognosis is poor
GUILLAIN BARRE SYNDROME

This simply includes all polyneuropathies( diseases affecting different peripheral nerves) that are
immune mediated (meaning it’s the immune attacking own nerves) and acute on onset (meaning
progress rapidly).
So usually there is a preceding infection with microbes whose antigens resemble host nerves, then the
body mounts an immune response that attacks both the infectious agent and the nerves.
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Which is why you will hear history of diarrhea preceding it forexample. Campylobacter jejuni infection is
the most commonly identified precipitant of GBS. Others are such as cytomegalovirus, EBV, HIV and Zika
virus.
CARDINAL CLINICAL FEATURES
 Progressive fairly symmetric muscle weakness accompanied by absent or depressed deep
tendon reflexes. The presentation could be mild difficulty in walking to nearly complete paralysis
of all extremity, facial, respiratory and bulbar muscles.
 The weakness usually begins in the legs though in 10% it may begin in arms or facial muscles.
 Paraesthesia in the arms and feet accompany the weakness in more than 80%. Pain occurs due
to nerve root inflammation.
 Dysautonomia (abnormal functioning of autonomic nervous system which could be either hyper
or hypo functioning)-where one can have diarrhea or constipation, urine retention, etc
 Severe respiratory muscle weakness necessitating ventilator support.
It usually progresses over a period of two weeks. The disease progression of more than 8weeks probably
it has gone to a chronic form (CIPD). CIPD and GBS are literally almost similar with difference in time
period of disease.
INVESTIGATION
CSF- one will find high protein with normal white cell count just as in CIPD and we call it
albuminocytologic dissociation.
GBS VARIANTS
• AIDP (acute inflammatory demyelinating polyradiculopathy)
• Acute motor axonal neuropathy- same as GBS all explanation but here only motor neurons are
affected.
• Acute motor and sensory axonal neuropathy- here all motor and sensory neurons are affected.
• Miller fisher syndrome- this affects nerves to eye muscles. Remember opthalmoplegia, ataxia
and areflexia is the key presentation.
DIAGNOSTIC CRITERIA OF GBS

1. Progressive weakness of legs and arms.
2. Areflexia
3. Progression of symptoms over days to four weeks
4. Relative symmetry
5. Mild sensory symptoms or signs
6. Autonomic dysfunction
7. Pain
8. No fever at the onset
9. Elevated protein on CSF
10. Recovery starting from two weeks to four weeks after progression stops.
Things that can make you doubt the diagnosis of GBS are such as
1. Bowel and bladder dysfunction at onset
2. Asymmetry of the weakness
3. Fever at onset
4. CSF high white cell count
5. Severe sensory symptoms
MANAGEMENT
IVIG, and plasma exchange.
Supportive treatment- includes management of pain if one has pain give gabapentin or carbamazepine
and bowel and bladder care as they may not be able to pass urine so you may have to put catheter etc.
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CASE 3-ADULT ONSET SEIZURE
NAME WWWW
AGE 39YRS
SEX MALE
RESIDENCE MWENGE
DATE OF ADMISSION MARCH 2018
Informant- wife and patient himself.
Refered from Ardhi dispensary with the diagnosis of traumatic brain injury
Chief complains are: loss of consciousness for seven hours.
He was referred to MNH after being involved in a motor traffic crush. Prior to the accident the patient
reports a history of general body malaise and lightheadedness for 1 wk .Before the accident he was at
work he felt unwell and decided to drive home. After a short drive (few meters) he felt dizzy and
experienced blurring of vision. The patient does not recall anything. Until he found himself in the
hospital bed 7hrs later.
In the event was he found unconscious and had an episode of generalized tonic clonic convulsions,
associated with frothing, tongue biting and eye rolling. Had a history of urine incontinence no fecal
incontinence. This took about 3 Min.
After waking up 7hrs later the patient was confused, agitated and had slurred speech this state resolved
in 3hrs. No focal neurological deficit noted. Confusion state lasted 1hr. He became fully conscious but he
does not recall anything around the accident. No history of external injuries, no history of bleeding from
ears or nose. No history of abnormal smell before the onset. No history of epigastric pain. No history of
fever. He had normal breakfast. Had a history of headache.
No history excessive alcohol use. No history of vomiting/ history of nausea. No history of tooth
extraction/dental abscess. No history of alcohol withdrawal. No history of DM or HT and not known to
be epileptic. No history of using ilicit drugs. Not on any medication. No prior history of Motor Traffic
Accident.
No history of Polyuria, polydipsia, polyphagia. No history of Cough, Chest pain, Orthopnea/ PND, Lower
limb swelling. No history of Excessive night sweats, loss of weight. No history of Heat /cold intolerance
No history of joint pains. Normal sleeping pattern. No history of snoring during sleep.
Was admitted in the ward for 2wks evaluated and started on medication. No repetition of the event in
the ward.
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AS PER HPI
• No history of prior admission
• No history surgery or BT
• No history of epilepsy, asthma, DM.
• No history of drug or food allergy
• No history of prolonged use of medication
• 1st born in a family of 3, PHD holder
• He is a lecturer
• History of Alcohol use 4 beers everyday no cigarette smoking
• Married with three children wife is an administrator at IFM
• No similar illness in the family
• No history of DM, epilepsy or asthma in the family
DIETARY HISTORY
• Breakfast - One cup of tea/milk with bread, chapati, potatoes, cassava.
• Lunch - rice or stiff porridge, banana with vegetables, beans or meat
• Dinner - pork meat and banana and occasionally rice or stiff porridge, banana with vegetables,
beans or meat.
• He can complete a plate full at single serving with a fruit a day
• Conclusion – Adequate in quantity and quality with excessive pork
SUMMARY
Mr. WWW 39yr old, lecturer from UDSM presented with first ever seizure in his life that presented with
tonic clonic pattern and a history of urine incontinence associated with LOC >7hrs. On recovery he was
confused and agitated but no focal neurological deficit or acute medical condition.
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• Fully conscious, Middle aged man
• GCS 14/15
• No neck stiffness
• Kernig’s sign negative
• Not obese
• Not Dyspneic
• Afebrile
• No conjuctival, mucous membrane and palmar Pallor.
• Not cyanosed
BMI 27.34Kg/m2.
No finger clubbing, no leuconychia or koilonychia. No palmar erythema. No duptreyns contracture, no

flapping tremors, no parotid swelling.
No discharge per ear or nose, no oral thrush, no peri orbital or facial edema, no palpable peripheral
lymphadenopathy, no lower limb edema.
CNS EXAMINATION
HIGHER CENTRES- fully conscious, oriented to time place and person. He had impaired both short and
long term memory.
CRANIAL NERVE EXAMINATION
CN I Olfactory
• can smell
CN II Optic
• Normal Visual field,
• VA 6/6(R/e), 6/6le ,
• Normal pupil reflex
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CN III, IV ,VI ; Oculomotor, trochlear, Abducens
• Vertical and lateral eye movement normal
• Corneal reflex normal
CN V Trigeminal
• clench teeth with temporalis prominence
• normal facial sensation
• normal corneal reflex
CN VII Facial
• Able to
-frown
-close eyes against resistance
-whistle
-show teeth without facial deviation
CN VIII- Vestibulochochlea
• Able to hear
CN IX Glosopharyngeal
• Able to say “ah” without uvula deviation
CN X valgus
• Able to swallow
CN XI Accessory
• can shrug shoulders/turn the head against resistance
CN XII hypoglossal
• no tongue wasting/fasciculation, deviation on protrusion
MOTOR EXAMINATION- NORMAL
CARDIOVASCULAR SYSTEM EXAMINATION-all were normal except had elevated systolic blood pressure.
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SKIN AND APPENDAGES- normal hair texture, no skin rashes or excoriations.
RESPIRATORY EXAMINATION AND PER ABDOMEN-all normal
SUMMARY
Mr. WWW 39yr old, lecturer from UDSM presented with first ever seizure in his life that presented with
tonic clonic pattern and a history of urine incontinence associated with LOC >7hrs. On recovery he was
confused and agitated but no focal neurological deficit or acute medical condition. On examination he
had impaired long and short term memory, and elevated systolic blood pressure while the rest of the
findings were normal.
1. Adult onset seizure secondary to

- Neurocysticercosis
- Tuberculoma
- Tuberculous abscess
- CNS toxoplasmosis
- Brain tumor
2. Mild traumatic brain injury
POINTS TO DEFEND THE DIAGNOSIS
ADULT ONSET SEIZURE
The following are the points supporting the diagnosis of adult onset seizures
i) Headache
ii) Lightheadedness
iii) Loss of consciousness
iv) Generalized convulsion
v) Post ictal confusion
vi) Urine incontinence.
The only negative point that goes against the diagnosis is absence of stool incontinence.
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NEUROCYSTICERCOSIS (NCC)
The following support the diagnosis of NCC
i) Headache
ii) Dizziness
iii) Nausea
iv) Seizure
v) Dysarthria
vi) Confusion
vii) History of eating pork
The points against NCC are absence of neurological deficit and normal gait.
TUBERCULOMA/ABSCESS
The points to support it
i) Headache ‘
ii) Nausea
iii) Confusion
iv) Visual impairment
v) Seizure
The points against are fever and focal neurological deficit.
BRAIN TUMOR
The points to support it
i) Headache
ii) Dysarthria
iii) Visual impairment
iv) Seizure
v) Confusion
The points against are such as he doesn’t vomit, and has no focal neurological deficit. The age also is not
supporting.
TOXOPLASMOSIS
The points to support this are headache, nausea, seizure, and confusion. The points against are no fever,
no focal neurological deficit or vomiting.
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MILD TRAUMATIC BRAIN INJURY
The points that convince us about the diagnosis are a history of being involved in a motor traffic crush,
lost consciousness, had nausea, seizure and confusion
Points against are such as no focal neurological deficit, no vomiting and no bleeding from the ear and
nose.
FINAL DIAGNOSIS
ADULT ONSET SEIZURE SECONDARY TO EITHER NCC OR BRAIN TUMOUR.
INVESTIGATIONS DONE
I. HIV ELISA TEST- NEGATIVE

II. Stool analysis- no oval seen
III. Serum cryptococall antigen negative
IV. Serum toxoplasmosis- Igm negative but IgG positive
V. Serum adenosine deaminase 7.9IU/L (normal range is 0.01-35)
VI. CSF examination- clear, normal white cell count and the differentials, protein was 40mg/dl,
csfglucose was 4.4mmol/l. Zn stain negative, culture no growth, cryptococal antigen negative,
Indian ink negative and ADA 2IU/L.
VII. Full blood picture results were all normal
VIII. Hepatitis panel negative
IX. Echo normal findings
X. ECG normal
XI. IMAGING STUDIES WERE DONE
T2W1
T2 MRI you can tell this because the subarachnoid space/CSF is white. And notice the white
matter is darker than the gray matter (which is reverse in T1)
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FLAIR
There is surrounding edema that is bright on T2 and FLAIR images that predominantly involves
the white matter, in a pattern consistent with vasogenic edema
FLAIR is a sequence that looks like a T2, but the CSF is dark. You can tell this is a FLAIR because
the CSF is dark, but that the white matter is darker than the gray matter. This sequence is useful
to highlight areas of edema.
DW1
No central restriction – hypointense center – central necrosis – tuberculoma. Why isolated?
46 | P a g e
PLAIN CHEST XRAY OF THE PATIENT
WAY FOWARD
Explore his concerns about driving and explain to the patient that unexplained loss of
consciousness poses a risk to him and other road users
NCC TREATMENT
Follow Tanzania guidelines.
Studies were done and they were as follows:
 Group A (150 patients) were treated with 15 mg/kg/day albendazole for 14 days, plus 2 mg
dexamethasone orally at 8-h intervals for 14 days, plus antiepileptic drugs at appropriate doses.
The dexamethasone was tapered off over time.
 Group B (150 patients) were treated with antiepileptic drugs and placebo.
Results of the trials were:
 During the first year of treatment the incidences of seizure, encephalopathy, and readmission
were greater for group A than group B.
 Two patients in group A died from intractable seizures and encephalopathy in the first 3
months of treatment.
 The proportion of patients with complete resolution of lesions was greater in group B than in
group A
 The proportion of patients with calcification of lesions was greater in group A than in group B.
 Calcified lesions may be the focal pathology for seizure recurrence. ( in our patient he had
calcified lesion in the cortex)
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OUR PATIENT WAS PUT ON
 Albendazole 400mg bd po 28/7
 Carbamazapine 200mg po bd 1/12
 Prednisolone 20mg po bd 1/52 (tapering down)
 prednisolone 15mg po od 5/7
 prednisolone 10 mg po od 5/7
WHY NOT SURGERY?

SURGERY IN NCC IS RESTRICTED FOR
 Placement of ventriculo-peritoneal shunts for hydrocephalus
 Excision of single big cysts causing mass effect
(Which our patient did not have any of the above)
IN A NUT SHELL,
 Treatment with albendazole plus antiepileptic drugs has no benefit over treatment with
antiepileptic drugs alone.
 Albendazole treatment may cause problems or have adverse effects with regard to increased
seizure frequency, encephalopathy and hospital readmissions in the early part of the treatment.
(Gracias et al 2013)
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PARAPLEGIA
Is the paralysis of both legs.
Causes are best categorized as
1. Traumatic and
2. Non traumatic causes
Non traumatic causes are further classified as in the table below
classification Examples
1.compressive causes TB spine, metastasis in cancers, cervical
a)extradural compressive causes spondylosis,
Epidural abscess, echinococcus cyst
b)Subdural compressive causes
i)Extramedullary subdural compression Neurofibroma,meningioma
ii) intramedullary subdural Astrocytoma, tuberculoma, syringomyelia
compression
2.Non compressive
a)transverse myelopathy HIV, HTLV-1, syphilis
b)vascular non compressive causes Sickle cell, AV fistula
c)hereditary Familial spastic paraplegia
d)deficiencies Vitamin B12
TB SPINE
History of back pain over weeks/months worsened with weight bearing plus features of TB as fever night
sweats and weight loss. Also history of TB contact.
Clinical signs- tenderness at the back and gibus formation.
X RAY- will show features of loss of disc space at the site of infection with destruction and wedging of
adjacent vertebrae. CT scan is helpful if Xray is inconclusive.
TRANSVERSE MYELITIS
An episode of inflammation affecting the spinal cord which results in acute paraplegia and can be
following an infection or autoimmune.
Features include flaccid paralysis developing over hours or days, loss of sensation in the trunk and lack
of bowel and bladder control.
CSF analysis will show high white cell count and protein.
Treatment-high dose IV steroids and anti virals as viruses are commonly behind this. IV methyl
prednisolone 1000mg/day for 5days followed by oral prednisolone 60mg/day tapered in 2-3weeks plus
acyclovir 10mg/kg to a maximum of 800mg thrice daily for 10days.
49 | P a g e
CARDIOLOGY
All cardiac patients you will see its always heart failure, your job is to find what caused the heart failure.
The conditions of importance we will touch here and that are likely to be asked are Infective
endocarditis, rheumatic heart disease, pericarditis and cardiomyopathies plus hypertension.
HEART FAILURE
To diagnose heart failure we use Framingham criteria. Where if one has two major or one major plus
two minor criteria we say its heart failure.
Major criteria
1. Neck vein distention

2. Paroxysymal nocturnal dyspnoea
3. Cardiomegally
4. Acute pulmonary edema
5. Positive hepatojugular reflex.
Minor criteria
1. Ankle edema
2. Dyspnoea on exertion
3. Hepatomegaly
4. Nocturnal cough
5. Pleural effusion on xray
6. Tachycardia
NYHA (NEW YORK HEART ASSOCIATION) Classification of severity
Class 1- asymptomatic
Class 2- heart failure symptoms give slight limitation of activity to the patient.
Class 3- marked limitation of activity
Class 4 symptoms at rest
50 | P a g e
MANAGEMENT
It depends on the forrester classification of heart failure. This includes four categories
1. Warm and dry (normal meaning no heart failure. The extremities are warm meaning the
perfusion is there, and dry here refers to lungs no pulmonary edema). Here no treatment.
2. Warm and wet- here the perfusion is there but lungs are wet. The treatment here is vasodilators
and diuretics.
3. Cold and dry- extremities cold and lungs dry. This is rare and such patients such give fluids to
increase the circulating volume and improve perfusion. Consider ionotropics to improve heart
pumping activity.
4. Cold and wet- extremities cold meaning hypoperfusion and still lungs are congested wet. Here
we need to push the heart to pump (ionotropics) to improve perfusion at the same time
decongest the lungs(diuretics). So its ionotropics plus diuretics.
Most patients will be wet and warm the ones you meet in the wards.
You will hear of mortality benefit drugs and morbidity benefit drugs.
Morbidity benefit drugs are simply the symptom relievers. When one has lung congestion that gives
difficulty in breathing we give diuretics to relieve the symptoms.
Mortality benefit drugs these are drugs that have shown to reduce mortality in heart failure patients
and these are the beta blockers.
CARDIOMYOPATHIES
As the name is its pathology of the cardiac muscles. It is defined as heterogeneous group of diseases of
the myocardium associated with mechanical and/or electrical dysfunction that usually but not
invariably exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes
that are frequently genetic
Types
1. Dilated cardiomyopathy
2. Restrictive cardiomyopathy
3. Hypertrophic cardiomyopathy
4. Arrythmogenic right ventricular cardiomyopathy
RESTRICTIVE CARDIOMYOPATHY
Its simply the disease due to infiltration of the cardiac muscles with some materials that render them
rigid and unyielding (not relaxing to allow filling).
Such substances that infiltrate the cardiac muscles are such as amyloids. Amyloid cardiomyopathy
remains a prominent cause of restrictive cardiomyopathy leading to heart failure. Amyloids are simply
body proteins that are misfolded and get deposited in different places including the heart muscles.
51 | P a g e
Other causes that can cause restrictive cardiomyopathy
1. Hemachromatosis- where iron deposits in heart muscles making them rigid

2. Radiation- radiation generates oxygen reactive oxygen species and these cause inflammation
and finally fibrosis.
3. Loefflers syndrome- when eosinophils accumulate in heart muscles.
4. Sarcoidosis
5. Endomyocardial fibrosis
Types of cardiac amyloidosis (not frequently asked. Know it to jus add knowledge)
1. Light chain immunoglobulin amyloidosis

2. Familial cardiac amyloidosis
3. Senile cardiac amyloidosis- occurs in elderly where proteins misfold.
HYPERTROPHIC CARDIOMYOPATHY
Occurs when the walls of the ventricles get thick, heavy and hypercontractile. The muscles as they
hypertrophy take more room leading to reduced space in chambers and reduced filling. There is
asymmetric left ventricular hypertrophy meaning the interventricular septum grows relatively larger
relatively to the free walls leading to ventricular outflow.
The intensity of the murmur depends on the degree of obstruction. On standing position blood
returning to the heart is reduced and obstruction is increased because there is no enough blood to push
the hypertrophied muscles occupying the chambers to relieve the obstruction.
In squatting position venous return is increased a lot enough to push the obstruction and the intensity of
the murmur changes.
And since the muscle is hypertrophied but still the blood supply is the same so some muscle will lack
blood end ischemic and so risk of arrhythmias and sudden cardiac death.
Causes – inherited most of the time. It is also linked to some other condition not important to know
which is Friedrich’s ataxia.
DILATED CARDIOMYOPATHY
Its when heart chambers dilate and fail to contract. The muscles get weak and walls get thin and
chambers dilate. It is the commonest and most important to know about.
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CAUSES
Mnemonic for the causes- Dilated Hearts End In Terrible Infiltration Inside
D- Dietary causes such as thiamine deficiency
H-Hereditary. Familial dilated cardiomyopathy, muscular dystrophies
E- Endocrine causes like hypothyroidism, thyrotoxicosis
I-Infections such as HIV, Cocksackie B virus
T-Toxins like Alcohol, drugs like cyclophosphamide
I-Infiltrative conditions as sarcoidosis, hemachromatosis.
I-Ischemic causes.
Other causes being stress induced and peripartum cardiomyopathy
PERICARDITIS
Its discussed under the heading of pericardial syndromes
PERICARDIAL SYNDROMES
These different clinical presentations of pericardial diseases with distinctive signs and symptoms that
can be grouped into specific syndromes.
The four classical pericardial syndromes are
1. Pericarditis
2. Pericardial effusion
3. Cardiac tamponade
4. Constrictive pericarditis
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PERICARDITIS
Acute pericarditis is an inflammatory pericardial syndrome with or without pericardial effusion.
DIAGNOSTIC CRITERIA
Clinical diagnosis can be made if one ha two of the following of criterias
1. Chest pain (which occurs in 85-90% of the cases). The pain is sharp, pleuritic, improved by sitting
or leaning foward
2. Pericardial friction rub (occurs in less or equal to 33% of the patients) it’s a superficial scratchy
or squeaky sound best heard with the diaphragm of the stethoscope over the left sterna border
3. ECG changes with new wide spread St elevation or PR depression in the acute phase (60% of the
cases)
4. Pericardial effusion (which occurs in 60% of the cases)
5. Additional markers include raised ESR, CRP and white cell count or evidence of pericardial
inflammation from an imaging technique.
Types of pericarditis
1. Incessant pericarditis- the one that lasts for more than 4-6 weeks but less than 3months
2. Recurrent pericarditis- after a documented first episode of acute pericarditis and symptom free
interval of 4-6weeks
3. Chronic pericarditis lasting for more than 3months
Wide spread ST elevation has been reported as a typical hall mark sign of acute pericarditis. However
changes on ECG imply inflammation of the epicardium since the parietal pericardium is electrically inert.
Markers of inflammation can be used to monitor progress of the disease and efficacy of treatment.
Xray is usually normal unless the effusion is more than 300mls
Most of the times the cause is TB.
Causes as usual you can group them as
1. Infections- viral like HIV, could be bacterial like TB.

2. Toxins
3. Radiation
4. Idiopathic
5. Malignancies
MANAGEMENT
Treat the cause. If its Tb treat TB.
They say aspirin can also be used. 750-1000mg tds for 1-2weeks then tapered in 4weeks.
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Myopericarditis- is simply pericarditis that has extended to affect cardiac muscles. Its defined as acute
pericarditis with evidence of elevated markers of myocardial injury without newly developed focal or
diffuse impairment of left ventricular function in echo. If there is left ventricular function impairment
then it is perimyocarditis. Jus the vice versa. (if it confuses you just catch the highlighted sentences)
PERICARDIAL EFFUSION
Normally pericardial sac has fluid of 10-50mls. So when this fluid increases its what we say effusion.
The causes could be either production of that fluid is increased or its reabsorption is reduced
Classification
Can be classified depending on
1. Onset- where we have acute, sub acute and chronic

2. Distribution- where we have circumferential and loculated pericarditis
3. According to hemodynamic impact- we have non cardiac tamponade and effusive constrictive
type
4. According to composition- exudative and transudative
5. According to size of effusion- mild, moderate and large effusion
Symptoms- dyspnoea, orthopnea. If heart enlarges can compress the esophagus and cause dysphagia.
CARDIAC TAMPONADE
It’s a life threatening rapid or slow compression of the heart due to pericardial accumulation of fluid
The three classic features that we call the becks triad are
1. Raised JVP/ distended neck veins

2. Distant heart sounds
3. Hypotension
Other symptoms are- tachycardia, pulsus paradoxus and decreased voltage on ECG with electrical
alterans
Causes are TB, trauma, iatrogenic, neoplasia and all causes of pericarditis apply here.
This is an emergency- urgent pericardiocentesis is recommended
CONSTRICTIVE PERICARDITIS
Is the result of scarring and consequent loss of normal elasticity of pericardial sac.
There are two forms
1. Effusive constrictive
2. Transient constrictive
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RHEUMATIC HEART DISEASE
Is a systemic post streptococcal non suppurative inflammatory disease principally affecting the heart,
skin, joints, subcutaneous tissues and central nervous system.
Mostly in children between 5-15 years.
The etiological role of preceding throat or skin infection with beta hemolyticus streptococcal group A is
well accepted. There are epidemiological and immunological evidences to support the fact this comes
after infection with group A beta hemolyticus streptococcus.
EPIDEMIOLOGICAL EVIDENCE
1. There is often a history of infection of the pharynx or upper respiratory tract 2 to 3weeks prior
to the onset of this disease
2. Subsequent attacks of streptococcal infection in patients with rheumatic heart disease has
shown to exercebate the condition.
IMMUNOLOGICAL EVIDENCE
1. Cell wall polyssacharide of group A beta hemolyticcus streptococcus make the body form
antibodies that can attack own cells of the cardiac valves.
2. The hyaluronate capsule of group A beta hemolyticus streptococcal is identical to human
hyaluronate present in joint tissues
CLINICAL MANIFESTATION
Simply refer to the definition and see what organs it affects. Manifestations will depend on the organ it
affects.
Heart- carditis, skin-erythema marginatum, joints- migratory polyarthritis, CNS- syndenham chorea, and
subcutaneous tissues- subcutaneous nodules.
The same mentioned above are the ones in the major criteria in JONES criteria.
Then your clinical evaluation (fever, polyarthralgia), lab investigations ( raised ESR, CRP) and your ECG
(prolonged PR interval) give you the minor criterias in JONES criteria.
MANAGEMENT
Benzathine penicillin im injection 1.2 million units single dose.
If they have carditis and arthritis give aspirin. For carditis you can add prednisolone. For the case of
Synedenham chorea give haloperidol.
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INFECTIVE ENDOCARDITIS
It’s the infection of the endocardial surface of the heart. It’s the infection of one or more valves.
Risk factors
1. Having an artificial (prosthetic) valves

2. IV drug use
3. Indwelling intravenous catheter
4. Immunosupression
5. Recent dental or surgical procedure
To make a diagnosis here we use modified Dukes criteria
Simple mnemonic Be Everywhere FIVE PM
MAJOR CRITERIA
B-blood culture positive for an organism causing IE and conditions are any of the following. +ve blood
culture:
i. For a typical micro organism in two separate cultures

ii. Persistently positive blood culture drawn 12hrs apart
iii. Single culture for coxiella burnetti
E- endocardial involvement
i. Be it evidenced by echocardiogram or
ii. Hearing a new vulvular regurgitation
MINOR CRITERIA
F- Fever
I-Immunological phenomena (glomerulonephritis, oslers nodes, roths spot)
V-vascular phenomena(major arterial emboli, intracranial hemorrhage, conjunctiva hemorrhage,

janeway lesions)
E-Echocardiographic findings but not definitive
P-Predisposed individual like ones with pre existing heart disease
M-Microbiologic evidence. Positive blood culture for organisms that are not typical for infective
endocarditis.]
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MANAGEMENT
Benzyl penicillin G 18-24 million IU/24 hrs for 4-6weeks +cloxacilin 2g IV 6hrly for 4-6weeks +
Gentamycin 1-1.5mg/kg for atleast 2weeks. (I used to remember it as a mnemonic of Be (benzyl
penicillin G) Close(cloxacilin) Gentleman(gentamycin). So just say Be Close Gentleman)
If one has the artificial valves then you do the above management and add rifampicin.
Infective Endocarditis Prophylaxis
Antibiotic prophylaxis should be considered for patients at highest risk for IE:
1. Patients with any prosthetic valve, including a trans catheter valve, or those in whom any
prosthetic material was used for cardiac valve repair.
2. Patients with a previous episode of IE.
3. Patients with Congenital Heart Disease (CHD):
A. Any type of cyanotic CHD.
B. Any type of CHD repaired with a prosthetic material, whether place surgically or by
percutaneous techniques, up to 6 months after the procedure or lifelong if residual shunt or
valvular regurgitation remains.
Antibiotic prophylaxis is not recommended in other forms of valvular or CHD
CORONARY ARTERY DISEASE

Simply it’s the disease of the coronary arteries the vessels that supply the heart with blood. So its either
these artery narrow(by atherosclerosis) or are blocked and blood supply to the heart is compromised
and heart muscles die. As the heart muscles die because of ischaemia one gets chest pain which they
term it as angina pain.
Angina pectoris is a symptom complex caused by transient myocardial ischemia.
Characteristics of Angina
1. Central chest pain

2. Could be a chest discomfort or breathlessness
3. Excercebated by activity or any form of stress (such as cold exposure, intense emotion and one
that comes after taking heavy meal the one we call post prandial angina) and relieved by rest
Atherosclerosis (which is the cause of angina most of the times)
It’s the cause of whole this angina thing. The pathophysiology is simple. The whole process starts with
injury to inner lining of the blood vessels be it by high blood pressure, smoking or diabetes. When
injured the inner ling of blood vessels leaves a gap through which LDL cholesterol can pass to enter the
walls of a blood vessel. Apart from that, injured endothelial cells express some molecules that attack
white blood cells (it’s like they are calling out for help).
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Once white cells go to this area they also pass through the gap that has been broken in the injured inner
lining of a vessel and enter the wall of a blood vessel as LDL. Inside there white cells eat LDL because
they get hungry there (to make the story interesting). Once they eat the LDL, they get fat and since
these LDL are white they appear foamy and hence called foam cells (these fat cells that have eaten fat).
Some fat cells die release the fat that others eat to be fat too. The accumulation of foam cells, LDL inside
the wall of the blood vessel create a bump that keep increasing narrowing the vessel and this is what we
call a plaque.
This plaque is being covered by endothelial cells as the injured place heals endothelial cells start
covering the gap. Sometimes this bump may grow until disrupts the endothelial lining trying to cover it
up and hence making it more possible to form a clot as blood clots inside a vessel whenever it finds a
rough surface. This clot we call it a thrombus. If this clot dislodges and travels we call it an embolus.
Causes of angina (coronary heart disease)
1. Atherosclerosis (of importance to remember)

2. Aortitis
3. Polyarteritis
4. Other connective tissue disease
Risk factors for atherosclerosis and angina
1. Diabetes Mellitus – so ask if he or she is diabetic

2. Hypertension – ask if he or she is hypertensive and if yes does he use the drugs well/attend
clinic.
3. Central obesity: waist circumference ≥ 94 cm (men) and ≥ 80 cm (women)
4. Dyslipidaemia (fasting levels): Total cholesterol > 5 mmol/L, or LDL> 3 mmol/L, or HDL< 1 mmol/
L in men and < 1.2 mmol/L in women
5. Smoking
6. Age: Men > 50 years, Women > 60 years
7. Family history of early onset cardiovascular disease; Male relatives < 55 years and Female
relatives < 65 year
8. Alcohol – excess alcohol is associated with risks of hypertension.
TYPES OF ANGINA
1. Stable angina- where pain occurs in exercise and stops at rest

2. Unstable angina- pain occurs even at rest and is a risk for cardiac muscle death (myocardial
infarction- the one we call Non ST elevation myocardial infarction)
3. Prinzmental angina- in which there is vasospasm. Pain comes and goes wether at rest or at work
just depending or coronary vessel spasms.
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MANAGEMENT OF STABLE ANGINA
Pharmacological Treatment:
A: Aspirin soluble 75 - 100mg daily oral. (long-term prophylaxis for arterial thrombosis)
AND
C: Isosorbide mononitrate 10mg/20mg twice daily oral, or Isosorbide dinitrate 20mg/40mg twice
daily oral preferably at 8:00 and 14:00 hours for both medicines to provide a nitrate free period to
prevent tolerance.
If nitrates cannot be tolerated especially due to nitrate induced severe headache consider stepwise
adding other anti-angina medicines below;
Add stepwise other anti-angina medicines
Step 1: add ß-blocker if not contraindicated eg
C: Atenolol12.5/25mg daily oral
OR
D: Metoprolol 25/50mg daily oral.
If ß-blocker cannot be tolerated or is contraindicated, consider long acting calcium channel blocker.
Step 2 adds long acting calcium channel blocker.
D: Verapamil 30mg 2-3 times daily oral
OR
D: Diltiazem 30mg 2-3 times daily oral, if suspects Prinzmetal Angina.
And lipid lowering drugs as well such as atovartstatin.
UNSTABLE ANGINA
Is a medical emergency because one can end up with non st elevation myocardial infarction the one we
call NSTEMI.
Patient at a stage of NSTEMI have a chest pain that is increasing in frequency or severity/ occurring even
at rest.
Management of unstable angina
1. Give something to relieve the pain. give IV morphine. (dosage if interested is 1-2mg/min a
maximum dose is 10mg and repeat every four hours)
2. Give antiplatelets- aspirin 300mg stat then 75mg daily plus clopidogrel 300 mg stat followed by
75mg daily
3. Add atorvastatin 80mg stat then 40mg daily
4. Then anticoagulant enoxaparin 1mg/kg body weight
5. Consider beta blockers if there left ventricular dysfunction
6. Give ACE inhibitors
STEMI- which is ST elevation myocardial infarction simply is when coronary arteries are either
completely or partially occluded. Its also a medical emergency. The management is same as NSTEMI
above in unstable angina except here the definitive management is reperfusion therapy where you can
use thrombolytics to break the thrombi and reperfuse the heart.
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HYPERTENSION
The new guideline says any systolic blood pressure of 130mmhg and above or diastolic of 80mmg and
above its considered hypertension.
Normal values are systolic less than 120 and diastolic less than 80. Systolic between 120 and 130 is just
termed as elevated blood pressure but not hypertension.
Systolic of 130-139mmhg or diastolic of 80-89mmhg is stage 1 hypertension. Any values beyond

140/90mmhg is stage 2.
We have primary hypertension (when the cause is not known) and secondary hypertension (when
hypertension is because of something else ie secondary to some other problem).
MANAGEMENT
Non pharmacological way of dealing with it is
1. Diet salt restriction

2. Control weight
3. DASH diet (Dietary Approaches to Stop Hypertension) which is high in vegetables, fruits, low fat
dairy products, whole grains, poultry, fish, and nuts, low in sweets, sugar, sweetened beverages
and no red meat.
4. Exercise
5. Low alcohol intake
Pharmacological
There are two categories here: hypertensive with diabetes/ckd or hypertensive without diabetes or ckd.
HYPERTENSION WITHOUT CKD/DM
1. Start with thiazide diuretic or calcium channel blocker alone or in combination

2. If still blood pressure doesn’t go down insist on lifestyle modification and the non
pharmacological measures. If still fails titrate the doses of the drugs you started him or her with
to a maximum dose.
3. If still it fails consider adding the third drug ACE inhibitors or ARB. If on addition of these still no
improvement find out he or she is using the drugs correctly, find out about life style
modifications like dietary salt.
4. If all are taken care and still high then one can add a beta blocker on top.
5. If hypertension is still high despite the use of a combination of three antihypertensive or more,
and titrated to a maximum dose and one among the drugs is a diuretic then that hypertension
we call it refractory hypertension. (that is for a specialist. Above your pay grade dude, chill enjoy
your loan from loan board)
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HYPERTENSION WITH CKD OR DM
1. Initiate treatment with either ACE inhibitors or ARB’s. Monitor blood pressure, if no changes
keep titrating the doses to maximum while insisting the life style modifications.
2. If no improvement yet keep adding other drugs CCB then if still nothing add THIAZIDES.
3. The last drug to add is a beta blocker. Then if all these fail same point as above.
HYPERTENSIVE URGENCY VS EMERGENCY
Urgency is simply blood pressure with systolic 180 and above or diastolic 120 and above without
threatening symptoms is an urgency.
If there are already threatening symptoms its an emergency.
Management of Hypertensive urgency and emergency
For urgency- give long acting calcium chanel blocker and ACE inhibitor ( ACE inhibitor begin with low
dose initially).
Hypertensive emergency- preferably IV therapy. Drugs to use are labetalol, nitrogylecerine and
hydralazine.
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CASE 4-HEART FAILURE
NAME DIRISHA
AGE 18years
SEX male
RESIDENCE CHANIKA
Referral from Amana with complains of shortness of breath for 4months, lower limb edema for 3months
and headache for 3months
Reports shortness of breath for 4months: Gradual onset, progressively increasing in severity with time,
initially experienced at exertion, but then at rest, associated with difficulty in breathing on lying flat, at
home he uses about two pillows, also associated with easy fatigability on exertion, heartbeat
awareness ,general body malaise and dry cough
No history migratory joint pain, swellings underneath skin or sore throat, no history of bluish
discoloration of lips/tongue or squatting down to rest with exertion. No known history of recurrent
chest infection or fever. There is no history of Failure to thrive or Poor growth
Lower limb edema - gradual onset, bilateral, worsening with time, not painful, increased in severity on
sitting, not accompanied by facial, abdominal or scrotal swelling, reduced on raising limbs.
Has no history of reduced urine output, no discomfort during micturition, no history of blood in urine,
neither yellowish discoloration of skin/eye nor body itching. No history of rashes or abnormal body
movements.
Headache- Gradual onset, unilateral, on right side, squeezing , not pulsating, mild or moderate intensity
aggravated by routine physical activity but not by eating chocolate , drinking tea or coffee, radiating to
the right neck posterior. No nausea/vomiting/ running nose/ear ache or discharge, no aura, light or
sound sensitivity, no loss or blurring of vision, no history dizziness, LOC or convulsions, no weakness or
numbness of the limb.
He has a history of vomiting 3rd day post admission, No history of difficulty swallowing, dyspepsia,
epigastric pain, vomiting blood, constipation , diarrhoea or melena. No h/o bleeding from the nose,
gums. No h/o prolonged bleeding after minor cuts. No reported bone or muscle pain.
In the ward he developed fever, abdominal pain and vomiting which was presumed to be malaria and
was treated with Artemether ; Gentamycin and Xpen were also given with improvement
On cardiac symtoms he was treated with Valsartan, carvedilol, furosemide and aldactone. His
symptoms improved from NYHA 4 on admission and currently he is class 2.
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As per HPI
• 2nd admission – 1st was at Amana for a week
• No history of trauma to the chest
• No history of surgery or BT
• No HTN , DM or Asthma
• Orphan staying with guardian
• Form four leaver – withhold his further studies
• Not alcoholic/smoker/drug user/risk sexual behavior
• No family history of congenital or inherited disease
• No history of DM, HTN in the family
• Parents died of HIV at the age of 9yrs
• staying with aunty h/wife and uncle works – petty trader
DIETARY HISTORY
Adequate
SUMMARY
A 18yrs, male orphan from chanika, referral from Amana who has been in ward for 2/12 came with
history of : shortness of breath, lower limb edema suggestive of biventricular heart failure in class IV on
admission but currently class 2 after treatment. Has non-migraine headache , no history of head injury.
No positive history suggestive of acute RHD or Congenital HD
Awake , afebrile 37.5⁰c, Not dyspnoeic , not cyanosed, Normal hair texture and distribution, No neck
stiffness, de’musset sign, scalp swelling or tenderness, Pale , not jaundiced, No oral thrush or high
arched palate /uvula central and non pulsating and no dental caries or extraction, No lymphadenopathy,
No finger clubbing , arachnodactyly , wrist sign, Arm span to height ratio is normal, no skin hardening or
subcutaneous nodules, No purpura, scars or marks seen, No sacral or LL edema ,Bwt and height : 45 kg
and 160cm BMI: 17.5
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CARDIOVASCULAR SYSTEM EXAMINATION
• PR 86bpm , regular with good volume, normal character
• BP : Left -100/50mmhg
Right - 90/50mmHg
• No Pulse Discrepancy or Radial-femoral delay
• Raised JVP 4cm above sternal angle ( v- wave)
• Precordial hyperactivity but no bulging
• Left parasternal heave
• Apex beat at 7th ICS lateral to MCL
• Normal S1 and S2 heard
• No added sound or murmur
• No pericardial rub
RESPIRATORY SYSTEM- only bilateral crepitations was the abnormality.
PER ABDOMEN- the only positive findings were a tender right upper quadrant and positive
hepatojugular reflex
CNS normal findings.
SUMMARY
 HEART FAILURE SECONDARY TO:
- Rheumatic Heart Disease
- Congenital Heart Disease
- Dilated cardiomyopathy
- Infective Endocarditis
 TENSION HEADACHE
DEFENDING THE DIAGNOSIS
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BIVENTRICULAR HEART FAILURE
Features of right sided heart failure
• Liver congestion
• LL edema
• RUQ abd. Pain
• ↑ JVP and positive HJR
Features of left sided heart failure
• Dyspnoea (PND)
• Fatigue
• Basal creptation
Hence biventricular heart failure.
Why do we think of rheumatic heart disease?
Points to support are
• Age
• Developing country
• Systolic murmur
The point that don’t support the diagnosis are there are no following symptoms
• Sore throat
• Migratory poly arthritis
• Sydenham chorea
• Erythema marginatum
• Subcutaneous nodules
• Recurrent fever
CONGENITAL HEART DISEASE
Points to support the diagnosis is only age.
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DILATED CARDIOMYOPATHY
Points to support the diagnosis
• Displaced apex
• Idiopathic ?viral
Points that don’t support the diagnosis
• Age
• Family history
• No secondary risk factors
– Alcohol
– Hiv
– Diabetes
– HTN
– Drug use
– malnutrition
INFECTIVE ENDOCARDITIS
Points to support the diagnosis. The patient has:
• Fever
• Headache
• Pallor
• Rales
• Weight loss
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Why are we not convinced of this diagnosis is because the patient has no
• Petechiae
• Splinter hemorrhage
• Osler nodes
• Roth spots
• Pleural or percardial rub
TENSION HEADACHE
The things that make us say its tension headache that the patient has are the headache is
• Unilateral (which is true in 10 -20% of people)
• constant
• Tight /pressure
• Non pulsatile
• No aura
• No sensitivity
• Cause : stress and sleep deprivation
It’s not tension headache because of the following
• Often bilateral
• No scalp muscle tenderness
• No Lacrimation
• Normal findings on general examination
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CASE -HEART FAILURE
NAME MMMM
AGE 23
SEX MALE
RESIDENCY UCHIRA
DATE OF ADMISSION MARCH 2018
Referred from KCMC with diagnosis of pulmonary stenosis and cardiac cirrhosis
Chief complain- abdominal distention for 9years.
Abdominal distention gradual onset, progressively increasing with time, painless relieved by meds
and tapping associated with painless lower limb but no facial swelling. It is associated with early
satiety but no abdominal pain. The abdominal distention has been severe to the extent of
preventing him from doing his daily activities including going to school.
Associated with 9yrs history of weight loss quantified as his clothes are loose on the lower waist,
easy fatigability and awareness of heart beats on exertion. He also has difficulty in breathing on lying
flat but has never woke up due to air hunger.
Denies history of heartburn, constipation, Black tarry stools, blood in stools, diarrhea, vomiting
blood, difficulty swallowing, yellow coloration of eyes, or change in skin color
Denies history of cough, chest pain, changing skin and lips blue, wheezing, nasal discharge nor post
nasal drip, night sweats, fever, blood in urine, painful urination, frothy urine, or reduced urine
output.
He dropped out STD 4 due to progression of his illness- in Jan 2006. Slow growth and poor weight
gain since he was 14yrs that was since the onset of his illness
He denied history of sore throats, subcutaneous nodules, abnormal movements, joint pains, IV drug
use, recurrent chest infections, sudden death in the family, alcohol / smoking. No history ofLithium ,
barbiturates use in mother during pregnancy. Not a fan of Cassava, so he doesn’t them on regular
basis.
Denies history of blood transfusions, sexual activities, tattooing, drug use like amiodarone,
methyldopa, anthracyclines, ergotamine, serotonin. No history of loss of consciousness, right/left
sided weakness, or seizures.
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He has been attending at KCMC hosp since 2008 and has been admitted 4 times. He was admitted
last (4th )at KCMC in march 2017 for a month due to the same problems and was diagnosed to have
pulmonary stenosis and cardiac cirrhosis and was treated with furosemide, aldactone, captopril and
frequent abdominal fluid tapping-yellow colored fluid with recurrence of his abdominal distension
and so he was referred to MNH for further management.
• 4 admissions at KCMC hosp.

• No history of major or minor surgery.
• No known drug or food allergies.
• No known history of DM, Asthma.
BIRTH HISTORY
• Antenatal History: uneventful.
She has attended ANC clinics - 3 visits
No history of rash, fever, drug use, herbal use or chemical exposure, alcohol, smoking during
pregnancy
• Natal History: delivered via SVD at home, BWT?. Cried immediately and started Breast feeding
in the first hour of life
• Post-natal Hx: uneventful
-Immunization- received all
-Growth: adequate weight gain acc to mother during infancy
DIETARY HISTORY
• Previous meal at home
-Makande
-Cooked banana
-Rice/ugali+beans
-meat 4per mnth
• meal at the Hospital
-Breakfast-fresh milk, eggs and mandazi
-Lunch- Cooked banana+ meat, cheps, water melon, orange
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- Dinner- Rice beans, vegetables
• Conclusion: inadequate in quality and quantity
• Lives in Uchira Moshi with his parents and siblings
• 2nd born in a family of 4 children.
• All other siblings are alive and health
• He dropped out of school during the last week of completing grade 4 due to his illness
• No hx of chronic diseases including heart d’se
• Both parents are farmers, their income per month≈ 300,000Tshs
• Sponsor ready to sponsor for his treatment
• Both parents have completed grade 7.
SUMMARY
23 yrs old Male with a 9 yr history of painless gradual onset of abdominal distension with exertional
palpitation, fatigue, orthopnea, poor growth and poor weight gain. He is a school dropout due to his
illness.
During his illness he has been attending hosp and been treated with frusemide, aldactone, captopril
and ascitic tapping with recurrence of abdominal swelling in few days.
No history of alcohol use. No history of night sweats, abdominal pain, fever. No history of similar
disease in the family.
EXAMINATION
Fully conscious, oriented, not dyspnoeic, normal hair, cachexic,stunted, afebrile, not jaundiced, not
pale, not cyanotic, no parotid swelling, no lymphadenopathy including virchow’s nodes. No
duptreyns contracture, no clubbing, no koilonychias, no leuconychia, no splinter hemorrhages, no
janeway lesions, no palmar erythema, no oslers nodes, peripherals not cold, no flapping tremors, no
axillary or pubic hair. No spider naevi, bruises, or scratch marks, no darkening of skin, testicular
atrophy, sacral edema or lower limb edema.
MUAC =15cm, ht=1.52m, weight =43kg
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CARDIOVASCULAR SYSTEM
- PR: 80beats/min, regular, normal volume, not collapsing , synchronous with other peripheral
pulses
- BP supine: 100/70
standing: 90/60mmHg
no pulsus paradoxus
- JVP raised, no kussmaul’s sign
- No Precordial hyperactivity.
Apex beat at 6th ICS – LMCL
- No parasternal heave, no thrill
-Normal 1st and 2nd heart sound with wide splitting of 2nd heart sound heard on inspiration
- No murmur heard
- no pericardial rub or knock
PER ABDOMEN
Grossly distended- symmetrical, no marks,surgical scars or striae, moves with respiration, distended
veins drain downwards. The umbilicus is everted. Hepatomegally with liver span by scratch test was
16cm, non tender. The spleen was not palpable. Dull percussion note, shifting dullness negative, fluid
thrill positive, bowel sounds heard from distant.
DRE: Normal anal verge and sphincter tone. No hemorrhoids, no masses felt and gloved finger was
stained with normal colored stool, no blood.
Conclusion: Hepatomegally and massive ascites.
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RESPIRATORY SYSTEM EXAMINATION
RR 17breaths/min, regular. SP02- 98%
– Chest elliptical in shape, no therapeutic marks, no surgical scars
– Normal chest expansion bilaterally
– Trachea centrally located
– No areas of tenderness or mass felt
– Normal Tactile vocal fremitus bilaterally
– Resonant percussion note through out the chest
– Vesicular breath sounds heard
– Normal vocal resonance in all zones. No added sounds
CNS EXAMINATION- normal
SUMMARY
23 yrs old Male with a 9 yr history of painless gradual onset of abdominal distension with exertional
palpitation, fatigue, orthopnea, poor growth and poor weight gain. He is a school dropout due to his
illness.
During his illness he has been attending hosp and been treated with frusemide, aldactone, captopril and
ascitic tapping with recurrence of abdominal swelling in few days.
No history of alcohol use. No history of night sweats, abdominal pain, fever. No history of similar disease
in the family.
On examination was cachexic, stunted with no axillary or pubic hair. He had features of right sided heart
failure and hepatomegally of 16cm with no stigmatas for infective endocarditis.
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Right sided heart failure NYHA class 1 secondary to
• Endomyocardial fibrosis
• Ebstein’s anomaly
• Restrictive cardimyopathy
• Constrictive pericarditis
• Rheumatic heart d’se - tricuspid valve
2. Liver cirrhosis
3. TB peritonitis
4. Malnutrition/ Stunted growth
POINTS THAT SUPPORT THE DIAGNOSIS
ENDOMYOCARDIAL FIBROSIS
The following are the strong reasons that concur with the diagnosis
i) Coming from tropical regions

ii) Occurs in children/young adults
iii) Malnutrition
iv) Presence of right sided heart failure
v) Orthopnea, lower limb edema
vi) Ascites out of proportion to mount to peripheral edema.
Points against the diagnosis are:
No history of taking cassava and sex (common in females)
Endomyocardial fibrosis- is simply fibrosis of the endocardium. Once fibrosis occurs normal heart
expansion to allow filling fails. It is common the fibrosis of the endocardium at the apex of right ventricle
or sometimes left ventricle or even both. Once filling is impaired blood returns to where it comes. This
leads to either right sided or left sided heart failure.
What causes fibrosis obviously its inflammation, what causes the inflammation now that is not known
but there are speculations. Some scientists think some infections such as toxoplasmosis, rheumatic
fever, malaria or helminthic infections could induce some sort of inflammation that can also affect the
heart and end up with fibrosis.
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Environmental exposure such as cassava eating is also linked. Cassava has linamarin which liberates
cyanide in the gut. This cyanide is a poison that may go affect the endocardium and cause fibrosis.
The disease is common in children and young adults from rural poverty tropical regions.
EBSTEIN ANOMALY
The positive features for the diagnosis are
• Ascites, congested liver, LL edema, JVP
• fatigue, palpitations- atrial tachyarrythmias- that affect 20-30%
The things that were negative and don’t agree with the diagnosis are such as
• cyanosis
• Lithium intake during pregnancy
RESTRICTIVE CARDIOMYOPATHY
The positive findings consistent with the diagnosis are
• Fatigue
• Palpitations, wt lose
• Hepatomegaly
• Edema
• Ascities
• JVP↑
The things that go against the diagnosis are common in elderly.
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CONSTRICTIVE PERICARDITIS
The positive features to support
• Fatigue
• Orthopnea
• cachexia
• LL edema
• Ascites
• Hepatomegaly
• JVP↑
Things that were negative that give us a doubt on the diagnosis are
• No kussmaul’s sign
• Apical impulse impalpable
• No Pericardial knock
• No TB
RHEUMATIC HEART DISEASE OF TRICUSPID VALVE
The only things that support the diagnosis is the poor social economic status and the age. The negatives
that make us doubt is no history of sore throat, Sydenham chorea, migratory polyarthritis, erythema
marginatum, subcutaneous nodules or pansystolic murmur.
LIVER CIRHOSIS
Features that can convince us are such as absence of pubic or axillary hair, ascites, cachexic and fatigue.
The findings that make us doubt the diagnosis are no risk factors for liver cirrhosis such as alcohol etc.
TB PERITONITIS
The only positive finding are weight loss and ascites. Otherwise he has no night sweats, no fever, no
abdominal pain and the duration of the disease also gives us the doubt.
INVESTIGATIONS DONE
I. FBP WAS ONE AND ALL WERE NORMAL EXCEPT THE HB, MCV AND MCH WERE LOW.
II. Urinalysis results were normal.
III. Liver enzymes were checked, AST alone was raised to 41.
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IV. Serum albumin was low and the serum albumin ascetic gradient was more than 11.1g/l.
V. Ascetic fluid macroscopically is straw colored, Protein 42g/l, glucose 5.9 and albumin 18g/l, WBC
5/microlitre and there were no RBC. And AFB negative.
VI. AOT- negative, HIV serology negative, PT PTT and INR all within normal range.
VII. Hepatitis panel all negative.
VIII. Chest Xray film below
ECG, ECHO, ABDOMINAL USS were all done.
ABDOMINAL USS FINDINGS
• Enlarged liver-16cm with normal homogeneous echotexture, smooth margins
• Hepatic veins are dilated- 2.2cm , portal vein 9mm
• Spleen is normal in size and shape
• Kidneys normail in size with good corticomedullary differentiation
• Massive ascites
FINAL DIAGNOSIS
Ebstein’s anomaly complicating into right sided heart failure NYHA class 1 and malnutrition/ Stunted
growth
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DISCUSSION
Ebstein Anomaly- simply a congenital malformation of tricuspid valve and the right ventricle.
• There are heterogeneous genetic factors, most cases are sporadic; rarely familial
• No gender predilection
• Occurs in 1/ 20,000 live births
• Mortality at all age is 12.5%
There is usually an association with maternal use of lithium in early pregnancy. Once it occurs screen for
other congenital heart diseases because they usually accompany it. Check ASD, VSD, etc.
Normally the tricuspid valve has three leaflets that separate from the myocardium during development
failure to do so is what results to this anomaly that’s a simple way to explain it. So simply the valves
reduce the volume of the right ventricle.
There are of four types. Type A,B,C and D. The types jus differ in severity. Type A the right ventricle
volume is adequate. Type B part of the right ventricle is above the tricuspid since the valve attaches way
below the myocardium of right ventricle and we call this atrialization of the right ventricle. Type C RV
outflow tract obstruction by anterior leaflet of tricuspid. Type D is almost almost complete atrialization
of right ventricle.
MANAGEMENT
• Surgical: Cardiac surgery in recommended by ACC/AHA 2008 guideline indication being :
– Symptoms or deteriorating exercise capacity
– Cyanosis (oxygen saturation < 90%)
– Paradoxical embolism
– Progressive cardiomegaly on chest x-ray
– Progressive right ventricular (RV) dilation or reduction of RV systolic function
Otherwise medical treatment you need to just give prophylaxis for endocarditis, treat heart failure with
diuretics, digoxin and ACE. Treat arrhythmias with amiodarone, beta blockers and give warfarin to lower
the risk of thromboembolism.
WAY FORWARD
• Surgery - Repair of TV
- Right atrialized ventricular Plication
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In our set up????
• Medical treatment – lasix , aldactone and warfarin
• Prognosis if no surgery (predictors of poor prognosis)*
– Male sex
– Early age onset
– Cardio Thoracic Ratio > 0.65 on CXR
– NYHA class II – IV
– GOSE score of > 1.5
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NEPHROLOGY
ACUTE KIDNEY INJURY
Its abrupt decrease in kidney function resulting in retention of wastes that are normally excreted by the
kidney.
DIAGNOSTIC CRITERIA
There is the KDIGO, RIFLE and AKIN criteria. Knowing one of them is enough.
KDIGO defines it as
• Increase in serum creatinine by greater or equal to 0.3mg/dl within 48hrs.

• Increase in serum creatinine to greater or equal to 1.5 times baseline which is known or
presumed to have occurred within the prior seven days
• Or urine volume of less than 0.5mls/kg/hr for 6hours
RIFLE criteria;
R-RISK urine output <0.5mls/kg/hr in 6hrs
I-INJURY urine output <0.5ml/kg/hr in 12 hrs
F-failure urine output <0.5ml/kg/hr in 24 hrs or no urine at all for 12 hours
L-loss complete loss of renal function >month
E-end stage renal disease
Notice the game above its all urine less than 0.5ml/kg/hr what changes is time, 6, 12, 24.. that’s the
pattern
CHRONIC KIDNEY DISEASE

It’s defined as presence of kidney damage or progressive loss of kidney function for three months or
more irrespective of the cause.
We say the kidney is damaged when there is a pathological abnormality confirmed either by imaging
studies such as (CT scan, MRI), biopsy results or inferred from markers that indicate the kidney is
damaged such as presence of albumin in urine is a marker that shows something is wrong up there in
the kidney.
Kidney damage can be identified by following markers
1. Albuminuria- albumin in urine is an indicator of kidney damage.

2. Presence of white cells or red cells in urine. It is what we call urine sedimentation abnormalities.
3. Imaging abnormalities
4. Evidence from biopsy
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Once kidney’s are damaged the glomerular filtration rate is affected. It’s according to how the
glomerular filtration rate is affected we stage the CKD. The normal CKD is 125ml/min
STAGING CKD
Stage 1- early disease where GFR is normal or >90ml/min
Stage 2- GFR 60-89ml/min
Stage 3- 30-59ml/min
Stage 4-15-29ml/min
Stage 5- the severe one- less than 15ml/min (should be on dialysis)
CALCULATING GFR
There are three formulas (just know their names no need to know how to calculate. They will ask you in
exam only the names of these formulas not how to calculate)
i. Cocroft formulas
ii. Chronic kidney disease epidemiology collaboration (CKD-EPI)
iii. Modified diet in renal disease
But it’s not bad to know how to calculate: lets see the cocroft formula
Estimated GFR= (140-age in years)x weight in kg x k
Serum creatinine
K is constant which is 1.44 for males and 1.02 for females.
CAUSES OF CKD
Anything that can damage the kidneys can bring CKD. A way to remember use the mnemonic VITAMINS
1. Vascular causes- vasculitis, renal artery stenosis

2. Infections- such as malaria, hepatitis B and C. when you clerk a case make sure you ask if one
sleeps in insect treated nets (to rule out malaria), if has multiple sexual patners or injects drugs
and if has any symptoms of liver disease as jaundice, bleeding easily etc. (to rule out hepatitis
infections)
3. Toxins- drugs. Ask if he or she has a history of taking drugs like NSAIDS. Some people use herbal
drugs that can damage the kidneys. So its worthy your time reporting no history of using herbal
medications.
4. Autoimmune diseases- so check out SLE symptoms.
5. Metabolic diseases such as diabetes, and gout. So its important to say if he is a known diabetic.
Ask for gout symptoms like joint pain and swelling.
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6. Infiltrative diseases- such as sarcoidisis and multiple myeloma
7. Neoplastic conditions including polycystic kidney disease.
8. Systemic hypertension
9. To add up, there are hereditary conditions you need to ask in history. Alport syndrome is a
genetic condition characterized by kidney disease, hearing loss and eye abnormalities. So its
worthy your time asking if there is any member in the family with kidney issues, any family
history of deafness? Just report it may give you credit
CLINICAL FEATURES
Once kidneys fail the urea cant be excreted and it circulates in blood and can affect every system. So we
will look the symptoms at every system that need to appear in your history
GASTRO INTESTINAL TRACT
Mouth- they will report unpleasant taste due to urea in saliva. The tongue will appear dry, and may be
ulcerated. The reason of mouth dryness is due to mouth breathing. On examination the tongue will
appear dirty, brown or white coated.
Stomach-they can have abdominal pain and vomit blood as urea erodes the gastric mucosa they get
gastritis. They will have anorexia, nausea and vomiting. They can get hiccough if phrenic nerve is
irritated.
Intestinal- they may report constipation due to dehydration. Sometimes may have diarrhea or bloody
stool due to urea deposition in colon and erodes the colon. In severe cases one may bleed per rectum
NEUROLOGICAL
If it goes to the brain- headache, lassitude, drowsiness, insomnia and change of sleep pattern are
common symptoms that you need to report in your history.
Neuro muscular symptoms- they can have symptoms of peripheral neuropathy such as pin and needle
sensations, or numbness. They can report convulsion which occurs due to hypocalcemia in CKD as
kidney is important to regulate calcium. They will have muscle weakness too. On examination you can
observe flapping tremors
HEMATOLOGICAL AND CARDIOVASCULAR
Anemia symptoms such as easy fatigability, dizziness, awareness of heart beats and it may end up to
heart failure too. They can hav bleeding tendency since urea in blood affects the quality of platelets.
Urea can go to the pericardium and one ends with uremic pericarditis that presents with chest pain and
on auscultation you will hear a pericardial rub.
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CUTANEOUS MANIFESTATIONS
Ask them if they have itchy skin because calcium deposits irritate the sensory nerves. They will be
dehydrated so the skin will be dry and on examination you will see uremic frost on the skin (looks like
sand on the skin. If you ever observed someone from beach with sand particles on skin)
Nail changes- these one may simply report as my nails have also changed but technical terms will be
used to report nail changes in examination. They may end up with either TERRY’S nails, MUEHERCKE’S
nails or LINDSAY’S nails.
OCULAR MANIFESTATIONS
Red eyes due to conjuctival congestion. They will report visual problems so you need to ask. They can
have retinopathy or the one we call it uremic amaurosis.
MUSCULOSKELETAL
Skeletal- renal osteodystrophy. Bone calcium is used up by the body and hence weak bones.
Muscle- fatigue, and wasting
GONADAL
They can complain decreased sexual drive (libido), impotence or develop gynecomastia for males.
ENDOCRINE ABNORMALITIES
They have secondary hyperparathyroidism, increased rennin activity and they lack erythropoietin that is
produced by the kidneys. Insulin is excreted in kidneys too so if kidneys have a problem insulin will
circulate longer
WHY CHANGE OF SLEEP PATTERN IN CKD PATIENTS?
There are two theories (just to add knowledge. Not very much asked, but if asked it add you credit)
1. According to HILDRETH, patients with CKD often exhibit sympathovagal imbalance due to baro
receptor reflex function impairment in which there is hyperactivity of sympathetic nervous
system and decreased vagal tone. In normal healthy individuals sleep is accompanied by
decrease in sympathetic activity and increase in vagal tone that leads to nocturnal dipping of
blood pressure.
2. Melatonin a hormone secreted in pineal gland is responsible for sleep wake circadian rhythm. Its
secreted in small amounts during the day and increases at night. In one study it was found
melatonin levels in renal failure patients at night is quite reduced.
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MANAGEMENT OF CKD
Mnemonic goes by “BEANS”
B- blood pressure control
E- erythropoietin injection for end stage disease
A-access for long term dialysis
N-nutritional care
S-specialist referral
RESTLESS LEG SYNDROME AND CKD

It’s a sensory motor disorder manifested by unpleasant nocturnal(night) sensations in the lower limbs
that are relieved by movement. These sensation occur deep within the muscles but patients occasionally
report feeling them on the skin. 2/3 of patients have it bilateral and 1/3 have it unilateral and most
common is upper calf.
Pathophysiology
Brain iron dysregulation plays a role possibly during transport across BBB. Since iron is an essential co
factor in the production of dopamine, low iron levels could explain the changes in dopamine metabolism
in restless leg syndrome. The syndrome is worsened by iron deficiency.
End stage renal patients are susceptible to acquire this because neuropathy due to uremia complicates
and overlaps the whole picture
MALARIA AND RENAL DISEASE

The four ways malaria leads to renal problems in summary
1. Heme toxicity- as plasmodium hemolyse red cells heme is released and gets deposited in the
kidneys damaging the kidneys
2. Immune mediated- as immune system attacks own tissues
3. Immune complex deposition- antibodies bind to plasmodium antigens creating complexes that
may get deposited in the kidney causing damage.
4. Rossete formation- its when non infected red cells surround those that are infected they create
what we call rossetes. These rossetes block the micro vessels later affecting the kidneys.
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CASE -POLYCYSTIC KIDNEY DISEASE
NAME RRRRR
AGE 45
SEX FEMALE
RESIDENCY UKONGA
OCCUPATION HOUSEWIFE
Referred with the diagnosis of uncontrolled hypertension.
Main complain is abdominal pain for 7months.
Patient was diagnosed with hypertension in June 2013, after a routine check at a clinic she had visited to
seek attention for UTI. She had been on/off antihypertensive medications since she was diagnosed. In
May 2017, she was diagnosed with stroke with right sided weakness at Amana Hospital. The episode
was preceded by abdominal pain on the day she suffered the stroke (No CT Scan was done)
During her admission at Amana Hospital, she remained unconscious for three days. She was discharged
home a week after admission with anti hypertensives (Losartan-H and Amlodipine), which she was
adherent to post-discharge, she was still not completely oriented, reporting to have episodes of
confusion with the right sided weakness showing slow improvement. She recovered fully from the
stroke after a month, after which she was well oriented to her environment and her weakness had
resolved
Four months later, in September 2017, she started experiencing on and off abdominal pain,dull in
nature, involving mostly the right upper abdomen and the flanks. No specific periodicity. No apparent
aggravating or relieving factors. Not radiating to the shoulder, scapula or groin. It has persisted for the
last seven months. No change in the severity of the pain over the last the seven months. Not associated
with nausea, vomiting, diarrhea or constipation.
She denies history of abdominal distension, difficulty swallowing, weight loss, rectal bleeding, yellowish
discoloration of eyes, and itching. Occasionally she gets episodes of heartburn. She does report being
treated for UTIs in the past but currently denies any pain, frequency or urgency of micturition. No
history of blood or froth in urine. Has normal urine output. No urine or fecal incontinence. Normal
appetite
Denies history of: Fever, Headache, Excessive Sweating, Visual impairment, Dizziness, Seizures, Anxiety
attacks, Neck pain, Speech difficulties, Neck swelling, Heat intolerance, Tremors, Awareness of
heartbeats, Difficulty breathing, Hair loss, Weight loss or gain.
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Denies history of Skin changes, Facial hair, Fractures, Sleep disturbances, Trauma, Chest pain, Fainting
episodes, Cough, Easy fatigability, Pain on walking, Limb swelling or pain,Numbness in the limbs or Oral
or genital ulcers
She denies history of drug use prior to this illness (except for anti-HTN), smoking or alcohol
consumption. She is post-menopausal – normal menstruation in the past. Has never used oral
contraceptive/hormonal replacement. Has eight children, no history of gestational hypertension. Her
father was hypertensive, and two of her children get anxiety attacks occasionally.
The patient remained in the ward for 4 days and was discharged with anti-hypertensives and was
followed up as outpatient to complete investigations. The abdominal pain is still present, with episodes
of no pain on some days. No new symptoms have developed
• This was her second admission
• First admission at Amana in November 2013 due to stroke
• No history of major or minor surgery
• No history of blood transfusions
• No known drug or food allergies
• No history of DM or asthma
GYNECOLOGICAL HISTORY
• Post-menopausal for 3 years
• Menarche at 13 years
• Has had normal menstruation with regular cycles and flow throughout until menopause
DIETARY HISTORY
• Mainly three meals a day
– Breakfast: Black tea with bread
– Lunch: Rice/Ugali with fish
– Dinner: Rice/Ugali with fish
– Has fruits and vegetables when available
• Conclusion: Adequate in quality and quantity
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• Married in a monogamous relationship
• Has eight children, last born in 2010 – all vaginal deliveries.
• BTL done after her last delivery
• She is a housewife
• Husband is retired teacher
• No smoking, alcohol or illicit drug use
• No history of DM, renal or cardiac disease in the family
• HTN in the father and anxiety attacks in two children
SUMMARY
A 45 year old female, with history of uncontrolled hypertension and stroke one year ago, presenting
with a 7 month history of dull aching abdominal pain more in the right upper abdomen and flanks. She
has history of frequent UTIs and family history of hypertension and anxiety attacks in her children
GENERAL EXAMINATION
Fully Conscious, Oriented, Afebrile(36.5°), Not pale, No jaundice, Not dyspneic, Not cyanotic, No LL
edema. No lymphadenopathy, Not wasted, No tremors, No anterior neck swelling, BP: 174/100 mmHg,
PR: 76 bpm, RR: 22 bpm, SpO2: 100% RA.
PER ABDOMEN
• Normal abdominal contours
• No marks or surgical scars
• Moves with respiration
• No distended veins
• Mild tenderness at the right hypochondrium
• Liver enlarged – span 16cm, firm, nodular (3x4cm)
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CARDIOVASCULAR SYSTEM
• PR: 76/min, regular, good volume, synchronous with other peripheral pulses and non-collapsing
• JVP not raised
• No precordial hyperactivity
• Apex 6th ICS – Left MCL
• No heaves or thrills
• Normal first and second heart sound
• No added sounds
RESPIRATORY SYSTEM
• Normal thoracic cage, with no marks or scars
• Normal chest expansion and movements
• Trachea centrally located
• No areas of tenderness or mass felt
• Normal TVF in all lung zones
• Resonant percussion note in all lung zones
• Normal air entry and vesicular breath sounds in all lung zones
• No added sounds
CNS – NORMAL
SUMMARY
45 year old female, with history of uncontrolled hypertension and stroke one year ago, presenting with
7 month history of dull aching abdominal pain more in the right upper abdomen and flanks. She has
history of frequent UTIs and family history of hypertension and anxiety attacks in her children
Examination revealed persistently elevated BPs; enlarged, nodular, mildly-tender liver and a displaced
apex beat
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• Cystic Diseases of the Liver
• Simple Liver Cyst
• Polycystic Liver Disease
• Polycystic Kidney Disease
• Hepatocellular Carcinoma
• Hepatic Abscess
POINTS TO DEFEND THE DIAGNOSIS
SIMPLE LIVER CYST
Positive
• Nodular liver
• Occurs in 2-7% of population
• Female predilection
What goes against is that its generally asymptomatic.
POLYCYSTIC LIVER DISEASE
Positive
• Enlarged liver
• Nodular liver
• RUQ pain
What makes us doubt the diagnosis is that it is very rare and no family history.
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POLYCYSTIC KIDNEYS
POSITIVE FEATURES THAT SUPPORT IT
• Flank pain
• Hypertension
• Frequent UTIs
• RUQ pain
• Enlarged liver
• Nodular liver
• Common in females
What makes us doubt is kidneys are not bimanually palpable and no family history.
HEPATOCELULAR CARCINOMA
Positive features pointing towards the diagnosis
• Enlarged liver
• Nodular liver
• RUQ pain
Negative
• No systemic signs of malignancy e.g. weight loss, fever
• No signs of decompensated liver disease e.g ascites, edema, bleeding tendencies
• No known risk factors
HEPATIC ABSCESS
Positive
• Enlarged liver
• Nodular liver
• Right upper quadrant pain
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Negative
• No fever, chills
• Flank pain
• No preceding history of diarrheal illness (mostly are due to amoeba- amoebic liver abscess)
• Chronic presentation
INVESTIGATION DONE
I. FBP- Only Hb was low

II. Urinalysis- turbid urine, and leucocytes 10/hpf
III. Liver enzymes normal
IV. Serum creatinine raised but normal BUN. Calculated GFR=35.8
V. Total cholesterol is also high.
VI. Abdominal uss was done.
VII. Chest Xray were cardiac size enlarged, no pleural or pulmonary lesions. No hilar nodes
VIII. ECHO findings were as follows
• Normal uniform contractility
• Normal valves
• Good systolic function – EF 68%
• Diastolic dysfunction Grade I
• No RWMA
• Mild Concentric LVH
• No thrombus
• No pericardial effusion
ix. virology was done and HIV was negative and hepatitis negative.
FINAL DIAGNOSIS
• Polycystic Kidney Disease associated with multiple liver cysts, secondary hypertension and CKD
Stage 3 with anemia and UTI. (UTI because of the urinalysis results being turbid and leucocytes)
• Hypercholesterolemia
• Cholelithiasis
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DISCUSSION
POLYCYSTIC KIDNEY DISEASE
• Commonly inherited disease
• Two forms exist
• Autosomal Dominant PKD (ADPKD)
• Autosomal Recessive PKD (ARPKD)
• ADPKD occurs due to mutation in PKD1 (85%) or PKD2 (15%) which code for polycystin-1 and
polycystin-2, respectively
• Occurs in 1:400-1000 worldwide
• Family history in 95% of cases
CLINICAL FEATURES
• Features include abdominal discomfort, hematuria, UTIs, abdominal masses, hypertension,

elevated serum creatinine and cystic kidneys on imaging
• End stage renal disease develops in 60% of those with ADPKD1 by age of 70 years
• ADPKD2 tends to be of later onset and slower progression
• Polyuria and nocturia indicate decreased concentrating ability of the kidney
• Dull, persistent, abdominal and flank pain due to enlargement of the renal and liver cysts
• Cysts may rupture, be infected, or hemorrhage
• Nephrolithiasis (kidney stones) occurs in 20% of patients
• Extra-renal features
• Intracranial aneurysms in 4 – 10%. Can be detected by MRA in at-risk patients
• Aortic root and annulus dilatation
• Cardiac valvular abnormalities in 25%, especially Mitral valve prolapse and Aortic
regurgitation.
• Colonic diverticulae
• Hepatic cysts occur in > 80%, with chances of hemorrhage, infection and rupture.
Women tend to have larger cysts
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HOW TO MAKE A DIAGNOSIS
• Diagnosis is made by positive family history and evidence of cysts on imaging
• Ultrasound is the modality of choice. Criteria for diagnosing ADPKD by Pei et al. in 2009:
• For asymptomatic individuals aged 40 – 59 years: Presence of two or more cysts in one
or both kidneys with a sensitivity of 90% and specificity of 100%
TREATMENT
• No treatment has been approved for cyst growth reduction or to prevent decline in kidney
function
• Goals of treatment are:
• Control hypertension with a target of 130/80mmHg (JNC VIII)
• Multidrug approach for hypertension that includes RAAS inhibitors
• Lipid soluble antimicrobials (TMP-SMX and fluoroquinolones) for infected cysts
• Managing pain with analgesia, cyst drainage or sclerotherapy
• Renal Replacement Therapy for ESRD (Dialysis)
WAY FORWARD TO THIS PARTICULAR CASE
• Pain management
• Anti-hypertensive therapy
• Lipid lowering agents
• Salt and oil restriction
• Counselled on screening other siblings
• Preparation for renal replacement therapy
• Regular follow-up on hypertension and renal function
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GASTROINTESTINAL SYSTEM
INFLAMMATORY BOWEL DISEASE
• Comprises of Ulcerative Colitis(UC) and Chrons Disease(CD).
• UC:
• Colon involvement is continuous. And as its name it affects the colon.
• Mucosal layer only affected
• CD:
• Skip Lesions. Not continuous.
• Transmural inflammation meaning it can affect all the four layers of the GI mucosa,
submucosa to serosa.
• May involve the entire GI not as UC affects colon, this can even affect the mouth.
IBD RISK FACTORS

1. AGE- common between 15-40years and 50-80years
2. SEX- slight male predominance in UC
3. About 10-25% of patients have first degree relative with either of the two. Ask for family history
always.
4. SMOKING- increases the risk of chrons disease and reduces the risk of UC.
5. OBESITY
6. GI INFECTION
7. DIET
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CLINICAL FEATURES
• Diarrhea associated with blood and mucus, accompanied by colicky abdominal pain, urgency,
tenesmus and incontinence
• Fever, weight loss, anemia, and peripheral edema may occur in some
• Extra Intestinal Manifestations- so don’t forget to ask symptoms from other systems too.
• Musculoskeletal e.g. Ankylosing spondylitis
• Eye e.g. Uveitis
• Skin e.g. Psoriasis
• Hepatobiliary e.g. Primary Sclerosing Cholangitis
• Hematopoeitic/Coagulation e.g. Thromboembolism
• Pulmonary e.g. Airway inflammation
INVESTIGATIONS IN IBD
• Colonoscopy:
• Non-specific findings
• Loss of vascular markings due to mucosal edema, giving it a erythematous appearance
• Severe cases may be associated with ulcerations, profuse bleeding and copious exudates
• Biopsy:
i. Crypt abscess, crypt branching, shortening and disarray and crypt atrophy.
ii. Diffuse inflammation
PSORIASIS AND IBD
It is more frequent in patients with chrons disease. Patients with psoriasis commonly have microscopic
inflammation in the colon even in the absence of bowel symptoms. Susceptibility genes have been
tracked to nearby regions of chromosome 6p.
IL-23 has a regulatory role Th1-inflammation, and drugs that target IL-23 have shown activity in both
psoriasis and IBD.
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MANAGEMENT
• Acute episodes are best treated topically i.e. with suppositories or enemas
• 5-aminosalicylic acid
• Steroids
• Maintenance is indicated in patients with more than one episode per year (proctitis) or in all
patients with proctosigmoiditis
• 5-aminosalicylic acid every night
• Steroids are avoided
• Extensive disease may require combination therapy
• For severe UC, oral glucocorticoids, high-dose oral 5-ASA and topical 5-ASA or steroids are
recommended
• Antibiotics in the presence of systemic toxicity
• IV glucocorticoids in patients who fail to respond to initial treatment
• 6-MCP/AZA or Anti-TNF agents are potential options is relapsing and refractory cases
LIVER CIRHOSIS
It is simply fibrosis of the liver and nodule formation. Its when you have chronic inflammation of the
liver and it ends up with fibrosis.
Worldwide most common causes of liver cirrhosis are viral hepatitis (hepatitis b, c), prolonged excessive
alcohol consumption and non alcoholic fatty liver disease.
It can occur secondary to damage or obstruction of the bile path such that bile accumulates and injures
the liver and end with fibrosis. Such conditions that which can lead to this are such as primary biliary
cirrhosis, primary sclerosing cholangitis and post surgical billiary stricture.
It can also occur secondary to diseases that obstruct liver drainage such as budd chiari syndrome which
is a veno occlusive disorder.
Causes of liver cirrhosis
1. Alcohol- so in your history ask if one takes alcohol, how much, how frequent, for how long has
he or she been taking and what type of alcohol is taking.
2. Viral hepatitis- ask for risks to acquire hepatitis viruses such as multiple sexual patners, IV drug
use etc.
3. Non alcoholic fatty liver disease
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4. Immune mediated such as autoimmune liver disease
5. Biliary causes –anything obstructing bile flow such primary biliary cirrhosis
6. Genetical conditions such as alpha 1 antitrypsin deficiency, hemachromatosis.
7. Chronic venous outflow obstruction as in budd chiari syndrome
PATHOPHYSIOLOGY
Simple explanations. You injure liver cells, they release what they had inside after dying, this signals the
guards of the liver who are the kupffer cells that something is wrong we are attacked.
The kupffer cells panick start shooting all over (their bullets are cytokines). The bullets kill and other liver
cells, as you understand war has collateral damage where good civilians die. These cytokines also
transform the stellate cells which are just cool cells chilling in the liver in the perisunusoidal spaces to
become myofibroblasts (wear bullet proofs). These stellate cells end up creating fibrosis thinking they
are protecting something.
So there is progressive fibrosis and widespread hepatocyte loss leading to distortion of normal liver
architecture disrupting even the blood vessels in the liver ending with blood by passing the liver what
we call portosystemic shunting.
CLINICAL PRESENTATION
Just think of all liver functions destroyed and you will get the clinical picture
1. Jaundice- liver is responsible for bilirubin metabolism

2. Bleeding tendency- liver makes clotting factors
3. Ascites- liver makes albumin, if no albumin no oncotic pressure
4. Splenomegally- remember after blood comes from spleen it goes to liver so if there is blockage it
goes back and accumulates making the spleen big
5. Portal hypertension since the pathway is obstructed and blood all flows back to the portal
vessels
6. Endocrine changes since the liver is also responsible for metabolism of hormones like estrogen.
If it fails then males end with gynecomastia, loss of pubic hair, and testicular atrophy.
7. Liver size can be big if the cause is alcohol or hemachromatosis in which a lot of iron is
deposited. The liver size is reduced in cases of viral hepatitis and autoimmune liver causes
where they eat up the liver.
How to determine the prognosis in liver cirrhosis we use the CHILD PUGH SCORE.
1 2 3
Encephalopathy none Mild Marked
Bilirubin <2 2-3 >3
Ascites None Mild Marked
PT(secs) <4 4-6 >6
Albumin (g/dl) >3.5 2.8- <2.8
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3.5
A score if adds up to less than 7 is CHILD PUGH A, 7-9=B and more than 9 CHILD PUGH C.
TREATMENT
Treat the underlying cause. If its lcohol should stop it.
Treat complications such as portal hypertension and hepatic encephalopathy
HEPATOPULMONARY SYNDROME
This is when the liver disease leads to pulmonary problems.
It is simply abnormal arterial oxygenation caused by intrapulmonary vasculature dilatations in a setting

of liver disease, portal hypertension or porto systemic shunting.
Why is there even pulmonary vessel dilatation? The simple way to explain it is to just know the liver is
the master in metabolizing almost everything including the chemicals that cause vasodilatation and
make them inactive after they have been active for sometime. Failure of the damaged liver to clear the
circulating pulmonary vasodilators is the key thing to recall.
So you have vessels dilate, a lot of blood flows through them with same amount of oxygen to diffuse so
a lot of blood will go without oxygen. To complicate it we say its VQ mismatch as a consequence of
increased blood flow through dilated vessels with preserved alveolar ventilation.
Clinically- dyspnoea will be the feature as one tries to add more oxygen.
HEPATORENAL SYNDROME
Same story here there is arterial dilatation in the systemic circulation hence hypotension, but preserved
resistance in the kidney. The reason the resistance is high in the kidneys is that as systemic circulation
dilates there is hypotension, and this leads to activation of rennin angiotensin system and sympathetic
nervous system. The activation of all these makes the vessels that let blood to the kidney be resistant
and at the end less blood to the kidney and then kidney damage.
The whole picture begins with liver disease failure to clear vasodilators plus blood pulling back to the
systemic circulation after failing to pass through the liver bringing this whole thing of systemic
vasculature dilatation and hemodynamic changes.
Types of hepatorenal syndrome
i. Type 1- defined by 2fold increase in serum creatinine in a 2weeks period or less

ii. Type 2- less severe and they have ascites resistant to diuretics.
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HEPATIC ENCEPHALOPATHY
Once the liver fails to do its functions some toxins circulate and enter the brain and disturb its functions.
These neurotoxins have not yet been found but they think it’s the nitrogeneous substances from the gut
that go through the portal vessels to the liver and fail to be cleared go disturb the brain.
Initially as it begins its mild but as it progresses they develop apathy, inability to concentrate, confusion,
disorientation, drowsiness, slurring of speech, and eventually coma. They can also get convulsions.
Precipitants of hepatic encephalopathy ( things you should consider if one has hepatic encephalopathy)
1. Drugs
2. Dehydration
3. Infections
4. Hypokalemia
5. Constipation
6. Portosystemic shunting
GRADING
Grade 1-poor concentration, slurred speech, disordered sleep pattern
Grade 2- drowsy but easy to wake him or her up
Grade 3-drowsy responds to pain and voice, or has marked confusion
Grade 4- unresponsive to voice. May or may not respond to pain.
TREATMENT
Our lovely professor Mugusi used to say the way to remember its management is only to say “the
treatment is to rest the liver”. Make the liver rest because all this it’s because it has a disease and you
work it.
So they give lactulose to make sure nothing is absorbed in GI so that the liver rests from all the materials
that come to it through the portal vessels.
You give one IV glucose to make sure the liver doesn’t toil to think on how to do gluconeogenesis.
If there is infection treat, if dehydration correct.
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ACUTE PANCREATITIS
Common cause is Alcohol where one will report to have taken a lot of alcohol maybe the previous day.
The following cause is gall stones.
Less common causes are trauma, drugs, post ERCP and hypertryglyceridemia.
The mechanism at which it occurs simple way to remember: pancrease has enzymes that it stores them
in packages that open up in the GI. In pancreatitis these active enzymes open up in pancrease and digest
the pancrease itself. How are these enzymes released? It’s when there is damage to pancrease as one
takes a lot of alcohol or trauma, or certain drugs injure the pancrease cells that have the enzymes and
make them released inside the pancrease.
CLINICAL FEATURES
Severe constant upper abdominal pain of sudden onset. it radiates to the back. Nausea, vomiting and
marked epigastric tenderness in early stages. You meet a male patient with very severe upper
abdominal pain that started suddenly and comes at Friday night to hospital, ask him “where you
drinking?” if he denies then proceed to find other causes.
COMPLICATIONS
After enzymes digest own cells there is fluid and tissue debris accumulation in the pancrease. If these
collections becomes surrounded by fibrous capsule on healing of the process they create what we call
pancreatic pseudocyst. if this fluid leaks to the peritoneal cavity is what we call pancreatic ascites.
When maybe the pancreatic ducts rupture and this fluid enters the lesser sac we term it as pancreatic
fluid collections. It may leak to the thoracic cavity and this we call it pleura pancreatic fistula.
Remember the pancrease makes insulin, once damaged one can end with diabetes as a complication.
INVESTIGATIONS
You will notice raised serum amylase and lipase which are pancreatic enzymes. Amylase is excreted by
the kidneys so if measured 24-48hrs after onset of acute pancreatitis it may be found normal. Persistent
elevated serum amylase implicates formation of a pseudocyst.
MANAGEMENT
• NIL per oral. No eating to rest the pancrease.

• Anaelgesics to control pain. opiates like tramadol 100mg bd.
• Fluids should be given because one is not feeding can be dehydrated
• Put catheter to monitor urine output
• NGT for aspirating materials if there is paralytic ileus
• Give oxygen for hypoxic patients
• Antibiotics can be given. As the process can be superimposed with infection.
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HEPATOCELULAR CARCINOMA
RISK FACTORS
1. Alcohol and tobacco

2. Environmental toxins- Aflatoxins from stored groundnuts
3. Liver cirhosis
4. Hepatitis viruses b and c
5. Obesity
6. Hemachromatosis
7. Dietary factors- red meat and saturated fat diets.
Clinical presentation is same as cirrhosis all liver functions are disturbed and in addition maybe
symptoms of malignancy as weightloss, anemia of chronic illness and symptoms of metastasis.
Tumour marker- alpha fetal protein
Investigations include imaging modalities as CT, MRI and biopsy of the liver may be required.
SPINAL MENINGIOMA
• Account for 10% of cases of meningioma
• Spinal meningiomas occur most commonly within thoracic spine
• Typically slow growing, invasive lesions
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CASE -PUD
NAME MMM
AGE 22
SEX MALE
RESIDENCE TANGA
Readmitted
Main complaints are recurrent abdominal pain for 8years and recurrent vomiting blood for 2years.
The patient was apparently well till 8 yrs ago, when he started experiencing recurring abdominal pain
more on the epigastric region burning in nature, radiates to the back. No specific periodicity though the
pain have been Increasing in frequency and severity over time . Some time experience severe pain that
interferes with his daily activity including schooling. Aggravated by hunger, Relieved by food temporally.
Antacids provided relieves initially for few weeks to few months but its effect kept on wearing off after
4 years of treatment, thereafter remained with mild abdominal pain that was almost always there.
Abdominal pain has been associated with: loss of appetite, abdominal fullness, early satiety, Nausea
and vomiting. He occasionally had watery diarrhoea lasting for 3-5 days, and weight loss. Not associated
with history of: Bone pain, joint pains or swelling, difficult /Painful swallowing or constipation.
Recurrent history of vomiting blood for the last 2 yrs initially blood mixed with food, Later on vomits
fresh blood and clots, preceded by epigastric pain. He vomited about 100mls (1/2 cupful) at a time,
having an average of 2-3 times before reaching hospital. Has a total of four vomiting episode for last 2
yrs and the interval between vomiting episodes has been lessening over time and the interval between
3rd and 4th episode was 1 month.
In the last two episodes, reported excessive vomiting blood (1 cupful=200mls @ time) compared to the
previous episodes, ~ 4 times prior to hospitalization and it necessitated 3 units of BT. Each episode
necessitated admission for an average of one week.
He reports all episodes of vomiting blood to be associated with history of: Passage of black tarry stool,
weakness, increasing easy fatigability, awareness of heart beats chest pain, Headache, and dizziness
He denied history of having: DIB, orthopnea, PND, LL swelling.
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No history of: Easy bruising, prolonged bleeding from minor trauma, gum bleeding or bleeding from any
other natural orifice Use of NSAIDs , anticoagulant or herbal medications, yellowing of mucous
membranes, Skin itching or discoloration, Fever, loss of consciousness, confusion, seizures, numbness of
extremities.
During the course of this illness: In 2012 abdominal pain/ vomiting became more frequent and was
advised to come to DSM for investigation. He underwent several investigations at different hospitals
here at DSM. He 1st attended AKH in which 1st OGD was performed (PUD, H. pylori -Negative Verbal
report), Kept on PPI for 3 consecutive months; Symptoms subsided but not completely ameliorated and
reoccurred when off medication for 2-3 months hence retreated intermittently. In Mid 2013 he reported
history of passing dark stool and was attended at Temeke; before being referred to MNH for further
evaluation
Several OPD attendances at MNH due to same complaints. Received PPIs, anti emetics, Ferrous sulphate
5 admissions in the last 2 yrs (MNH). 1st and 2 nd admissions- due to vomiting blood. 3rd admission- for
Surgery. 4th and 5th admissions- due to vomiting blood
1st and 2nd admission OGD confirmed Gastritis and multiple Duodenal ulcer involving 2 nd part of the
duodenum. 3rd admission he had features of GOO confirmed by OGD, antrectomy and
gastrojejunostomy performed. For 4th and 5th had history of vomiting blood and OGD showed Gastritis,
multiple Jejunal ulcers. Received PPIs, Ferrous sulfate, Blood transfusion in all admission and post
discharge ).Histology: section showed duodenal mucosa, and few gastric mucosa. A large number of
lymphocytes and plasma cells, neutrophils were infiltrated in the stroma mild atypia in focal glands.
Conclusion : Chronic Inflammation
Nothing significant
PAST MEDICAL
Nothing also
The only thing positive is that the mother has PUD. The rest do not contribute anything to our diagnosis.
SUMMARY
22 years old male patient with history suggestive of peptic ulcer disease and has a positive family history
of peptic ulcer disease.
ON EXAMINATION no positive findings
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Recurrent PUD secondary to :
1. Zollinger Ellison Syndrome
2. Retained Antrum Syndrome
3. G- cell Hyperplasia
4. Crohn’s Disease
CASE- JAUNDICE
NAME SSSSS
AGE 29
SEX MALE
RESIDENCE KIWALANI
Referred from Amana hospital, currently attended at Gastro enterology OPD
Main complaints being yellowish discoloration of the sclera for 4months and swelling at the anal
opening for 2weeks
Gradual onset of yellowish discoloration of the sclera, persistent and progressive, associated with
anorexia and nausea, accompanied by pruritis, darkening of urine (black tea colored urine) and
lightening of stool color, low grade intermittent fevers with no specific periodicity. He has a +ve history
of weight loss. No abdominal pain, no vomiting. Denied history of diarrhea, or abdominal distention.
He reported a history of easy fatigue and awareness of heartbeat. No hx of cough, DIB, chest pain or
chest tightens. No hx of joint/bone/muscle pain, no joint swelling, Bleeding tendency, reduced
frequency of micturition, headache, confusion, or edema/swelling. No history of loss of balance,
numbness or weakness of the limbs.
No history of prior episodes of jaundice, or recent history of blood transfusion or body piercing. He has
never been exposed to jaundiced individual. He reports alcohol intake for more than 10 years (quantify
if possible). He has a history of cigarette smoking (……..pack years), and cannabis abuse. He has a history
of using herbal medications during this illness. He has been having multiple sexual partners. He denied
history of IV drug abuse. He had not been exposed to any known hepatic toxins. No history of previous
biliary/abdominal surgeries. He is not known to have sickle cell disease (SCD) or other blood disease. No
family members with similar presentation. He has taken deworming drugs just lately and reports
sleeping in insect treated mosquito net.
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He also reported gradual onset of a swelling at the anal verge progressively increasing in size associated
with anal itching and irritation. He experiences intense pain during defecation (bleeding PR?). He has a
history of chronic constipation. He denied history of chronic cough or heavy lifting
The patient remained in the ward for 17 days. He is given Supportive treatment with cholestyramine and
annusol suppository with minimal improvement of the symptoms. No new symptoms have developed.
He was discharged for further work out and management as an outpatient.
REVIEW OF OTHER SYSTEM AS PER HPI
• 1st admission
• Known patient with Glaucoma and had undergo bilateral eye surgery at childhood
• On daily timolol eye drop
• No hx of major or minor abdominal surgery
• No known history of HT, DM or Asthma
DIETARY HISTORY
Mainly 3 meals per day
• B/fast:
o 1 cup of tea, doughnuts, chapati
• Lunch:
o ugali, beans, banana, meat and vegetables occasionally
• Supper:
o Rice & beans, fish and vegetables occasionally
o Fruits: infrequently: seasonal
• Conclusion: inadequate in quality, reduced quantity.
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• 3rd born in a family of 5 children
• Married three times, divorced with the 1 st wife 3yrs ago, 2nd wife died 1 year ago, currently living
with a third wife (any relevant history of 2 nd wife’s death)
• Father of two children, 6yrs old F, and a 7/12 old male, doing fine
• Family h/o of HTN and DM
SUMMARY
29 years old male from kiwalani, referral from Amana with a history suggestive of obstructive jaundice
and anal mass. He agrees to have multiple sexual patners, take alcohol and smoke cigarette.
EXAMINATION
• Alert, afebrile, jaundiced, not pale, no lymphadenopathy, no lower limb oedema, No kayser
flescher ring, wasted, has generalized skin excoriation on upper and lower limbs.
• P/A: normal contour, skin scratches, macular rash scattered, liver palpable 4cm below the right
coastal margin, gall bladder, spleen and kidney not palpable. negative Murphy’s sign.
• CVS: S1 & S2 heard
OBSTRUCTIVE JAUNDICE secondary to:
1. Choledocholithiasis
2. Acute cholecystitis
3. Cholangitis (fever, abd pain and jaundice)
4. Pancreatic carcinoma/ Neoplastic obstruction
5. Drug-induced cholestasis
6. Alcoholic hepatitis
7. Viral hepatitis
8. Malignant nodes at porta hepatis
HEMMORHOIDS
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DISCUSSION POINTS
• Pancreatic carcinoma features to support our diagnosis
– Commonest neoplasm producing obstructive jaundice
– Progressive and deep jaundice
– Weight loss
Features against the diagnosis of pancreatic carcinoma
– No abdominal pain radiating into the back
– Courvoisier’s sign is negative
• Metastatic cancer
– Subcutaneous nodule
– No other primary site could be elicited
• Hepatocellular carcinoma
– uncommon to rupture into the biliary system
EXPLANATIONS ON OBSTRUCTIVE JAUNDICE ARE WELL EXPLAINED IN MY SURGERY SUMMARIES.

OBSTRUCTIVE JAUNDICE IS A SURGICAL CASE.
INVESTIGATIONS DONE
I. FBP- only Hb was low and Hematocrit

II. Liver enzymes were all normal
III. Renal functions were okay
IV. Urinalysis- macroscopically deep yellow, bilirubin 2++, blood 3, and rbc present >100/hpf
V. Serology- HIV 1 and 2 antibodies positive, all hepatitis negative.
VI. Chest xray ordered
VII. Abdominal CT- showed hepatomegally
VIII. MRCP NORMAL
IX. FNAC of the subcutaneous nodule
• Hyperchromatic tumor composed of plump spindle cells, large ovoid cells, and abnormal mitotic
figures
• Conclusion: malignant subcutaneous mesenchyma tumor (sarcoma).
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FINAL DIAGNOSIS
HIV DISEASE Stage ….. With:
• Cholestasis
• Hemorrhoids
• Malignant mesenchyma tumor
MECHANISM OF CHOLESTASIS
To make it simple cholestasis means the stasis of bile. Bile doesn’t get to move.
How does it happen now? Lets go through it slowly.
Liver cells is where bile is made through uptake and production of organic anions, bilirubin and bile salts.
Bile salts are conjugated inside liver cells to make them water soluble and later excreted into the billiary
tree. The process of excretion of the bile salts from liver cells to out could depend on Na+ coupled
channels, or these salts could be packed in vesicles and released out we call it vesicular transport
mechanism or could be the other way out we call it carrier mediated channels. This all is not a must to
strain to recall.
So what impairs these transport mechanisms and make bile static? They say inflammations. Its simple to
end there and know endotoxins that stimulate inflammatory processes affect bile salts transport in the
liver. To complicate it more see the explanations below.
Endotoxins are potent stimuli for activating cytokine production from macrophages and have acute
cholestatic effects on hepatic bile production. Endotoxins and several proinflammatory cytokines (TNF
alpha, IL-1, and IL-6) down regulate hepatic transport mechanisms that determine bile acid-dependent
bile flow, affecting both bile acid uptake and canalicular secretion. Proinflammatory cytokines activate
neutrophils and T and B cells, increase the expression of intercellular adhesion molecules (ICAMs), and
may promote tissue damage by direct action. It is proposed that these portal tract inflammatory events
can contribute to the down regulation of hepatocellular bile salt transport and hence aggravate
cholestasis.
VANISHING BILE DUCT SYNDROME
• Vanishing bile duct syndrome, acquired disorder characterized by progressive destruction and
loss of intrahepatic bile duct (ductopenia), ultimately result in cholestasis
• Ductopenia, by definition, is loss of interlobular bile ducts in more than 50% of portal tracts in a
pathologic specimen
• Promoted biliary epithelial apoptosis due to various insults
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Acquired causes of ductopenia
I. Hodgkin disease
II. Histiocytosis
III. Infectious causes
IV. Viral infection
a. CMV
b. EBV
c. HBV
d. HCV
V. Enteric organisms, Eg E.Coli
VI. Parasite, Eg cryptosporidium
VII. Ischemic
VIII. Drugs and toxins
WAY FORWARD TO OUR PATIENT
• CD4 and referral to CTC for initiation of ARVs
• Inj. Vit K 10mg I/M for 7/7
• Control PT,PTT and INR
• Liver Biopsy
• Referral to ORCI for chemo/radiotherapy
CUSHING SYNDROME
• Cushing's disease refers to hypercortisolism secondary to excess production of ACTH from a

corticotroph pituitary adenoma or due to excess production of hypothalamus CRH
(Corticotropin releasing hormone).
• This causes the blood ACTH levels to be elevated along with cortisol from the adrenal gland.
• The ACTH levels remain high because the tumor is unresponsive to negative feedback from high
cortisol levels.
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EPIDEMIOLOGY OF CUSHING
• Most cases of Cushing disease are sporadic, which means they occur in people with no history of
the disorder in their family
• Incidence 10- 15/mil/ year cases
• Age 20 – 50 year F:M ratio 5:1 (Female 70% cases)
• Pituitary adenomas account for > 70% cases in adults (60-70% cases in
children and adolescents)
• Sometimes there is ectopic ACTH production due to lung cancer/ paraneoplastic syndrome
CAUSES
• Prolonged/excess exposure to cortisol as a result of: Long-term use of corticosteroid hormones

such as cortisone or prednisone
• Tumor/abnormal adrenal gland, which causes the body to produce excess cortisol
• Tumor/abnormal pituitary gland Eg: pituitary tu (70%cases)
• Other : tumors of the lungs(SCC 13%), thyroid, kidney, pancreas, or thymus gland produce
hormones that trigger the syndrome
RISK FACTORS
• Factors that increase risk of Cushing's syndrome include:
– Chronic use of corticosteroid medicines
– Age: 20-50 years
• Sex: female (much more common in women)
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INFECTIOUS
MENINGITIS
Is simply the inflammation of the tissues surrounding the brain and spinal cord.
Classic triad is fever, neck stiffness and change in mental status. Headache is also common. Other
symptoms are photophobia, convulsion and vomiting.
On examination they will have positive brudzinski and kernig signs.
KERNIG SIGN- ask the patient to lie flat, flex the hip with the knee at right angle then later extend the
knee it stretches the meninges). If these give pain then its meningitis.
BRUDZINSKI SIGN- Flex the neck of the patient as the patient lies flat. If one has meningitis will flex his
hips.
Laboratory investigation to never forget is lumbar puncture. In lumbar puncture observe
1. Opening pressure- mostly it is high except in viral meningitis where it is not high.
2. The color of CSF- turbid in bacteria infections and TB meningitis. The rest give clear CSF
3. Send CSF to lab for cytology. If its lymphocytes are many then its viral men, if neutrophils are
high kill them bacteria doctor.
4. CSF for biochemistry. If its bacteria infection, bacteria eat glucose so CSF glucose will be low and
protein will be high.
5. CSF gram stain
Other investigations- blood culture, urine culture, brain CT etc.
MANAGEMENT
Ceftriaxone IV .
OTHER INFECTIOUS DISEASES HIV, TB follow specific guidelines.
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RARE DIAGNOSIS
CASE- SLE
NAME MYYY
AGE 18
SEX
RESIDENCY TANGA
Referred from Mwananyamala
Main complains being recurrent fevers and joint pain for four years
Fever: Low grade recurrent, about 2-3 episodes a week. No specific periodicity, relieved by paracetamol.
Associated with generalized joint pain
Joint Pain: Started out as weakness and severe, dull in nature affecting the lower extremities (knee &
ankle) and later involved also the wrist and fingers. Currently pain is localized to the fingers, wrist,
elbow, neck and lower back. The pain is associated with stiffness. Stiffness is more pronounced in the
morning, lasting about an hour. No associated swelling of the joints. Denies any relation of episodes to
sunlight
Condition has progressively worsened with time to the point that she is unable to sit or walk without
support due to excessive weakness. Also reports deformity of both hands which has restricted
movement in the hands (since 4 months). Has history of unintentional weight loss over the last five
years. Has occasional mild numbness in the hands, not related to activity, which resolves spontaneously.
Also reports easy fatigability and awareness of heartbeats
Denies history of: Seizures, headache, double vision, dizziness, loss of consciousness, difficulty breathing,
excessive night sweats, cough, hemoptysis or sore throat
Denies history of: Chest pain, abdominal pain, nausea, vomiting, diarrhea, constipation, yellowish
discoloration of eyes, difficulty swallowing, vomiting blood or passing blood per anum.
Denies history of: Eye, ear, nose or vaginal discharge, Blood or froth in urine, Difficulties with
micturation , Pain in micturation , Increased frequency of micturation , Urine/Bowel incontinence,
Dryness of eyes and mouth, Any swelling of any part of the body, Oral or genital ulcers, Any skin lesion
anywhere, Hair loss or Abnormal movements.
Denies: Drug use prior to beginning of illness, Any or recurrent infections prior to illness, Smoking, or
Family history of similar disease
Patient has been treated for TB (diagnosed clinically) in 2011, completed the 6 month course.
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She has also been on haematenics and other medications which she is unable to recall. In MNH:
Prednisolone, haematenics with subjective feeling of improvement and reduction in number of episodes
of fever and joint pain
• Has been in good health overall
• No history of major or minor surgery
• Prior to this illness, has never been admitted to any hospital
• No known history of DM, Asthma
DIETARY HISTORY
• Mainly 4 meals a day:
Morning: Millet porridge
Late morning: Tea with bread
Lunch: Ugali with spinach/beans
Dinner: Rice with fish/meat
• Single, lives in Tanga with her mother
• 5th born in a family of 7 children. All others are alive and well
• Disease started when she was in Form 2 and worsened in the first week of Form 3, for which she
had to drop out of school
• Unemployed
• No history of smoking, illicit drug use or alcohol intake
• Menarche at 13 years
• Regular periods since then.
• Last menstrual period in March 2014
• Denies engaging in any sexual activity
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SUMMARY
18 year old M.O, with a 4 year history of recurrent low-grade fevers, associated with joint pain involving
the neck, lower back and symmetrical involvement of the fingers, wrists and elbows with deformities in
the hands. She also has unintentional weight loss and generalized weakness which has caused her to be
unable to sit or walk without support and drop out of school due to her illness
Fully Conscious, Oriented, Afebrile, Moderate conjunctival pallor, No jaundice, Not dyspneic, Not
cyanotic, No LL edema, No lymphadenopathy, Wasted, Angular cheilitis, Microstomia, Obvious
deformities seen in the small joints of the hands
• BP: 108/69 mmHg
• PR: 118/min
• RR: 22/min
SYSTEMIC EXAMINATION
• CVS:
• Precordial hyperactivity
• Apex beat 6th ICS – MCL
• Systolic murmur radiating to the axilla
• RS:
• Normal thoracic cage
• Dull percussion on right side
• Absent breath sounds on left side, normal vesicular breath sounds on right side
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• PA:
• Normal contours
• No areas of tenderness
• No organomegaly
• Normal bowel sounds
CNS: Uneventful
MSS-SPINE
• Normal curvature
• Bony prominence at the S3-S4 joint with mild tenderness
• Cervical
– Rotation L
– Flexion L
– Extension L
– Lateral bending L
– No paraesthesia
• Thoracic and Lumbar
– Extension L
– Lateral bending N (N= normal)
– Flexion N
– Rotation N
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MSS-SHOULDER
• Non tender, not swollen, no joint crepitus, no local oedema
• Movement neutral
– Adduction N
– Abduction N
– Rotation in adduction N
– Rotation in abduction N
– Flexion L
– Extension L
– Elevation L
MSS- THE ELBOW
• No deformity, muscle wasting, non tender, not swollen, no joint crepitus, no local oedema
• Movement
Flexion L
Hyperextension L
MSS FOREARM
• No deformity, muscle wasting, non tender, not swollen, no joint crepitus,
• Movement
• Supination L
• Pronation N
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MSS- WRIST EXAMINATION
• Muscle wasting, non tender, not swollen, no joint crepitus, no local oedema
• Movement
• Dorsiflexion L
• Palmar flexion L
• Ulnar deviation L
• Radial deviation L
MSS- HAND EXAMINATION
• Muscle wasting at thenar and hypothenar
• Impaired hand and pinch grip
• Ulnar deviation of the fingers at the MCP
• Thumb
– Z – deformity (L), muscle wasting , non tender, not swollen, no joint crepitus,
– Movements
• Extension L
• Flexion L
• Opposition L
• Abduction L
• Fingers:
– Boutonnière deformity, swan-neck deformity, muscle wasting , mild tenderness at the

MCP, swollen MCP of the index and middle fingers, no joint crepitus
– Flexion limited at MCP (Metacarpal phalangeal), PIP (proximal interphalangeal) and DIP
(distal interphalangeal) joints
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MSS THE HIP EXAMINATION
• Wasting of the gluteal and thigh muscle
• Movements
• Flexion L
• Abduction N
• Adduction N
• Rotation in flexion L
• Rotation in extension L
• Extension N
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THE KNEE
• No deformity, muscle wasting quadriceps, no swelling, no joint crepitus, normal patella, non
tender, normal ligaments
• Movement
– Extension N
– Flexion N
THE ANKLE
• Muscle wasting calf and interosseous
• No deformity
• Movement
• Dorsiflexion N
• Plantar flexion N
THE FOOT
• Normal posture, no deformity, no swelling
• Reduced muscle bulkiness
• Movement
– Eversion N
– Inversion N
– Adduction N
– Abduction N
– Flexion N
– Extension N
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SKIN AND APPENDAGES
– Tightened skin on the face
– Reduced facial expression
– Microstomia
– Normal hair texture
– Normal nail structure
RESPIRATORY SYSTEM EXAMINATION
– Normal thoracic, with no marks or scars
– Normal chest expansion
– Trachea centrally located
– No areas of tenderness or mass felt
– Tactile vocal fremitus reduced bilaterally in the lower zones
– Dull percussion note on the lower zones bilaterally
– Reduced air entry on the lower zones
– Reduced vocal resonance in the lower zones
CARDIOVASCULAR SYSTEM EXAMINATION
– PR: 96/min, regular, synchronous with other peripheral pulses
– JVP not raised
– Precordial hyperactivity noted
– Apex 6th ICS – Left MCL
– No heaves or thrills
– Normal first and second heart sound
– No added sounds
NORMAL ABDOMINAL FINDINGS
CNS- REDUCED MUSCLE BULKINESS AND REDUCED POWER IN ALL GROUPS OF MUSCLES WAS THE ONLY
POSITIVE FINDING
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SUMMARY
18 year old M.O, with a 4 year history of recurrent low-grade fevers, associated with joint pain involving
the neck, lower back and symmetrical involvement of the fingers, wrists and elbows with deformities in
the hands. She also has unintentional weight loss and generalized weakness which has caused her to be
unable to sit or walk without support and drop out of school due to her illness
Examination revealed the patient is anaemic, wasted, has angular cheilitis and microstomia with
tightened facial skin. There were multiple joint deformities in the small joints of the hands with reduced
range of motion and reduced power. Patient also had a displaced apex beat with signs of bilateral
pleural effusion
• Systemic lupus erythematosus
– Ddx – Juvenile rheumatoid arthritis
• Scleroderma
• Anemia
– Iron deficiency anemia
– Anemia of chronic disease
POINTS SUPPORTING AND THOSE AGAINST
SLE
POSITIVE POINTS TO SUPPORT
• + Arthritis
• +Serositis (pericardial rub)
• +Anemia (Palor)
• + Fever
• African
• Female
NEGATIVE POINTS AGAINST
No malar rash, discoid rash or oral ulceration
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JUVENILE RHEUMATOID ARTHRITIS
POSITIVE FEATURES IN LINE WITH THE DIAGNOSIS
• Joint pain
• + Joint stiffness (morning)
• + Duration > 6 weeks
• + Symmetrical distribution of involved joints
• + pallor (extra articular)
• + onset <16yrs
SCLERODERMA
Positive features
• Tightening of facial features
• + Microstomia
• + Sclerodactyl
Whats against is no hard tight skin on other parts
WHY ANEMIA?
• Easy fatigue
• Palpitation
• Pallor
• Angular cheilitis
• Long standing illness
What is against anemia as a diagnosis
• Adequate diet
• - No obvious h/o blood loss
• - No Jaundice as an evidence of hemolysis.
• - Normal menstruation
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INVESTIGATIONS DONE
i. FBP- HB=5.1, MCV,MCHC,MCH were all low and RBC number was low.
ii. ESR=130mm/1st hr
iii. Stool analysis normal
iv. Urinalysis normal results
v. Biochemistry results of electrolytes were all normal
vi. Serum feritin 1502ng/ml (normal is 22-112)
vii. ANA positive, Anti-dsDNA- positive and rheumatoid factor negative
viii. HIV 1 and 2 negative
ix. Urine total protein is 1.07g/24hr (normal is 0-0.07)
x. PERIPHERAL SMEAR
• Red blood cells – Microcytic hypochromic
• White blood cells – Adequate
• Platelets – Plentiful
• Conclusion: Feature suggestive of iron deficiency anemia
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To the left is of the left hand and to the right is the one of the right hand.
ECHO FINDINGS
• Pericardial effusion approximately, no pericardial thickening.
• Dilated right heart with pulmonary hypertension
• Conclusions: Features of Cor-pulmonale
ECG WAS DONE TOO
FINAL DIAGNOSIS
• Systemic Lupus Erythematosus
– Non-erosive arthritis
– Hematological: Lymphopenia: <1500 cells/ᶙL (1310, 620)
– Pericardial effusion – ECHO, ECG
– Renal disorder: 24hrs urine protein > 0.5
– ANA
– Immunological: Anti-dsDNA
IRON DEFICIENCY ANEMIA AND ANEMIA OF CHRONIC ILLNESS ARE OTHER DIAGNOSIS HERE.
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DISCUSION ON SLE
• SLE is an autoimmune chronic inflammatory condition which run a remission and relapse course
CRITERIA TO DIAGNOSE SLE
4 out of 11 of the following features that go by the mnemonic SOAPBRAINMD if one has then its
definitely SLE.
S- Serositis. Inflammation of any serosal be it lungs, pericardium etc
O- Oral ulceration
A-arthritis
P-photosensitivity
B- blood issues be it anemia, leukopenia
R- renal issues like proteinuria
A-ANA
I-IMMUNOLOGICAL such as anti ds-DNA
N-neurological symptoms like seizures or any
M-Malar rash
D-Discoid rash
• Nephritis and infections are the leading cause of mortality in the 1 st decade of disease
• Lupus nephritis (LN) is one of the most serious SLE complications and it is the major predictor of
poor prognosis1
• The LN cumulative incidence is higher in Asians (55%), Africans (51%), and Hispanic (43%)
compared with Caucasians (14%)2
• 25% of these patients develop ESRD 10yrs after onset of renal compromise 3
• Dx and classification of LN require a renal biopsy examination
• Indication of renal biopsy in SLE – proteinuria ≥0.5 g/24h especially with glomerular haematuria
and/or cellular casts
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LUPUS NEPHRITIS CLASSIFICATION
I. Class I minimal mesangial lupus nephritis
II. Class II mesangial proliferative lupus nephritis
III. Class III focal lupus nephritis
IV. Class IV diffuse lupus nephritis
V. Class V membranous lupus nephritis
VI. Class VI advanced sclerosis lupus nephritis 5
MANAGEMENT
Class 1 and 2- mantainance of blood pressure and give ACE to reduce proteinuria
Class 3 and 4- immunosuppressive therapy
Current is on
• Tabs prednisolone 30mg od
• Tabs Paracetamol 1g tid
• Tabs FESO4 200mg tid
• Tabs FA 5mg od
• Fever – subsided
• Joint pain - decreased
Wish list
• Kidney biopsy
• Skin biopsy
• Anti-centromere antibody
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CASE- HEREDITARY TALENGECTASIA
NAME PRURURUJ
AGE 48
SEX MALE
RESIDENCE LUSHOTO
Self referral, a petty trader with grade 7 education
Main complaint is recurrent nasal bleeding for 30 years.
He reported nasal bleeding spontaneous in onset from both nostrils of no specific periodicity but more
at night. For the first 29 years; small in amount, about 20mls per episode (he could soak a quarter of a
handkerchief for every bleed) fresh reddish in color, painless, last for about 2-3minutes. About 2
episodes per months, however not all months, he could be free from bleeding for 6 to 8 months in a
year. The nasal bleed had never required admission during this period of 29 years.
However in the past 1 year the frequency and amount of bleeding has been progressively increasing to
about 6 episodes per month and amount approximately 100mls per episode, no aggravating factors,
relived by pinching the nose and application of cold wet towel on the nasal bridge and fore face.
For the past 1 year it has been associated with: Easy fatigability and awareness of heart beats, feeling of
sense of swallowing during episodes, occasional passing of black stool during episodes, not associated
with: Headache, loss of consciousness, convulsion, blurred vision, chest pain, DIB, cough, orthopnea,
PND, LL swelling, vomiting, abdominal pain or swelling, or gum bleeding.
Not associated with: Easy bruising, prolonged bleeding from minor trauma, yellowing of mucous
membranes, skin itching or discoloration, fevers, weight loss, loss of appetite, consuming salted fish,
neck swelling, numbness or focal weakness, or change of voice.
Moreover, no history of: recurrent nasal discharge, irritation or sneezing bouts, loss of smell sensation,
regular nasal picking, bone pains or head trauma. No history of; Snorting drugs, use of antiplatelets or
anticoagulants, use nasal spray or breathing aids. No skin color change/loss of sensation or nodular skin
lesion. Remarkable history of the same illness in the family tree, however no consanguinity
On the course of illness the patient was first admitted in December 2014 before the current admission
he presented with epistaxis, melena and features of anemia (Hb=1.08gm/dl), stool for ocult blood –
positive, endoscopy was done: OGD – Gastric Angiodysplasia, and Colonoscopy – Normal. He received 3
units of blood (PRBCs) and haematinics supplement (FeSo4, Folic Acid)
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There was nothing significant
PAST MEDICAL HISTORY AND DIETARY HISTORY all were not significant
• Grade 7 leaver who was originally living in Lushoto-Tanga but shifted to DSM 8 yrs ago for
search of good life.
• He is married living with his wife and they have four living children
• First born female- 24 years old, affected, grade 7 leaver
• 2nd born male- 15years old, affected, form 3 student
• 3rd born female, 8 years old, affected, grade 3 pupil
• 4th born male, 4 years old, affected
• Pt is currently unable to work due to illness and his medical expenses are covered by his uncle
who is working at Azam industry
• However he got exempted in some investigations
• Wife is occasionally working as a petty trader
• Living in rented house wit three small rooms paying 60,000/month
• Family monthly income ~ 300,000 Tshs
• No history of drug abuse- alcohol, smoking or IDU
• No history of HTN, DM or ATOPY in the family
PROGRESS IN THE WARD
He has had 2episodes of epistaxis about 300mls of blood. Transfused 6 Units of PRBCs. Nasal packing
was done. Haematenics were given. Now able to walk a long distance and climb up stairs without fatigue
or palpitation
SUMMARY
A 48yr old male, petty trader & peasant from Kimara, a father of 4 children presented with 30 years
history of epistaxis, and chronic anemia, remarkable familial history suggestive of inherited
haemorrhagic disorder. No history of atopy, night sweat, fevers, weight loss. No history suggestive liver
diseases or malignancy. No history of use of anticoagulants
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EXAMINATION FINDINGS IN SUMMARY
On examination, middle aged man, alert, severe pallor, afebrile, not tachypnoic, not cyanosed and no LL
edema. He has features of mucocuteneous and visceral vascular ectasia. No echymosis and petechiae.
He has features suggestive of cardiomegaly with Mitral regurgitation and Tricuspid rgurgitation
Hereditary hemorrhagic talengectasia with a differential of von willebrand disease
CASE-CASTLEMAN DISEASE
NAME MMED PHD
AGE 55
SEX MALE
RESIDENCE KOROGWE TANGA
Referred from BOMBO hospital
Main complaints being awareness of heart beats, fever, frequent urination and thirst and multiple
swelling on the neck for 6months.
Awareness of heartbeat: Insidious onset, no specific periodicity, associated with general body malaise
and dizziness. He reported a single brief episode of loss of consciousness for 10-15min(as reported by
his wife) , not associated with convulsion, tongue bite ,stool or urine incontinence. It is not postural
related, neither associated with chest pain nor cough, no history of air hunger at night or DIB. Not
associated with bilateral lower limb swelling
Fever: Gradual in onset, low grade, no specific periodicity, with history of night sweat. No Hx of
yellowish discoloration of the eyes, or skin. No history of headache, body rash, joint pain, or bone pain
or recurrent sore throats. Its temporarily relieved by PCM
Frequent urination: Gradual onset, more during the night, associated with excessive thirst ,loss of
appetite and loss of weight (clothing), not painful /blood stained, no Hx of vomiting , diarrhea,
constipation or blood in stool. No hx of loss of vision, libido, erectile dysfunction ,numbness or tingling
sensation or joint pain. No heat or cold intolerance
Multiple swellings on the neck and axilla: Gradual onset, started on the Rt side of the neck, later
appeared on the Lt side of the neck and Lt axilla, increasing and decreasing in size and number.
Mobile ,Wax and waning course, not warm , not painful, no skin changes, not ulcerating not associated
with hoarseness of voice or difficulty in swallowing.
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Denied history of: Pruritus, easily bruising, nose or gum bleeding, Joint, bone or back pain, long term
medication use eg: phenytoin, radiation or chemotherapy, or blood transfusion prior to sickness
At Bombo Hospital Hospital: Admitted for 10days, diagnosed with Dm and HTN, received 2unit of blood,
losartan, Inj. insulin (during acute phase) and Lasix and got mild improvement.
Second admission at regency where he was diagnosed with hypothyroidism and third at MNH.
• 1st admission Bombo Hosp.
• 2nd Regency MH
• 3rd at MNH
• Recurrent blood transfusions 7times
• Newly diagnosed with HTN, DM and hypothyroidism
• HIV test done -ve
DIETARY HISTORY- nothing significant.
FAMILY AND SOCIAL HISTORY- nothing significant
SUMMARY
A 55yrs old male from Tanga, presenting with 6/12 with symptoms of anemia, B symptoms, multiple
neck and axillary swellings with waxing and wanning coarse and history of multiple BT(7times). Recently
diagnosed with DM and HTN on medication.
Pale+++, painless palpable lymphadernopathy in cervical, submandibular, sub mental, axilla, inguinal and
has splenomegaly
Chronic lymphocytic leukemia
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DEFENDING THE DIAGNOSIS
CHRONIC LYMPHOCYTIC LEUKEMIA
Positive points that support my diagnosis
• Commonest
• Male (2X) , age >50 years
• Insidious onset
• Peripheral lymphadenopathy + Splenomegaly
• Symptoms and signs of anemia
• Anorexia, night sweats and fever
Negative
No symptoms of thrombocytopenia
NON HODGKIN LYMPHOMA
Positive
• Age (median age 50 years)
• Constitutional symptoms (40%)
• Anemia (BM involvement occurs in 60%)
• Peripheral LN enlargement (2/3)
Negative
• Low grade fever
• Severe anemia
• Hepatomegaly (40% of indolent NHL)
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TB LYMPHADENITIS
Positive
• Constitutional symptoms
• Peripheral lymphadenopathy
• Symptoms and signs of anemia
Negative
• Presence of severe anemia
• LN description ( not matted, warm and inguinal LN are rarely involved)
GIANT LYMPH NODE HYPERPLASIA (CASTLEMAN DISEASE)
Positive
• Age (mean age 50 -65years)
• Male (65 -75%)
• Insidious onset (MCD variant, HIV -VE)
• Wax and wane (MCD, plasma cell variant)
• Inflammatory symptoms (90%)
• Peripheral LN splenomegaly(80 – 92%)
• Anemia
Negative
• Respiratory symptoms of effusion
• Severe anemia
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POEMS SYNDROME
Positive
• Splenomegaly and lymph node enlargement
• Hypothyroidism and hyperglycemia (T2DM)
• Anemia
• Male (2.5:1)
Negative
• Monoclonal plasma proliferative disorders
• Polyneuropathy/pulmonary sx
• Skin changes (hyperpigmentation/clubbing)
• Ocular symptoms and signs
• Severe anemia
FINAL DIAGNOSES
1. Multicentric Castleman disease, plasma cell variant, HHV 8 negative with anemia
2. Type 2 DM
3. HTN
DISCUSSION
CASTLEMAN DISEASE
Its a rare disease of lymph node and related tissues. It is usually associated with HIV and HHV8. The
cause is unknown but it is said anything stimulating lymphnodes to be highly reactive can cause. HHV8
increases production of Interleukin 6 in lymph nodes one ends up with this disease. There occurs nodal
expansion.
If there is expansion of lymphoid organs so expect lymphadenopathy and splenomegally since the
spleen is a lymphoid organ too.
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CASE- DENGUE
NAME FYEKELEA
AGE 23
SEX FEMALE
RESIDENCE KIBAHA
Self referral
Known patient of sickle cell disease since 8months of age attending clinic at MNH
Main complaints are abdominal pain and joint pain for 1week and fever and chest pain for two days.
Abdominal Pain: 1 wk duration. Gradual onset, sharp in nature, not colicky, progressively worsening with
time, initially localized on the epigastrium, then became generalized, no specific periodicity. No specific
aggravating or relieving factors
Abdominal pain was associated with: Loss of appetite, nausea, vomiting –one day prior to admission.
Initially she vomited recently eaten food. Later she was vomiting everything, not projectile, not bloody,
not foul smelling. She had >5 episodes prior to admission. Other associated features being relative
constipation and yellowish coloration of the eyes. But denied difficulty swallowing or abdominal
distention.
She also reported Joint pain 1 wk duration. Acute on onset, and progressive, started at right elbow then
became generalized. It was associated with moderate swelling and joint stiffness together with
generalized bone and muscle pain but denied history of ulceration of the legs.
Fever: 2 days prior to admission. It was acute on onset, high grade, intermittent, with no specific
periodicity, no specific aggravating factor and its unresponsive to Paracetamol. Fever was associated
with: Headache, generalized body weakness, dizziness, sweating and chills. She used to spit blood
stained saliva – Dental caries???? She reported blood stained urine – (rangi ya tai yako), altered mental
state and finally – Loss of consciousness --- taken to ICU
Fever was not associated with: Weight loss, or any rash, sore throat, convulsions, visual disturbances or
difficulty in speaking. Neither was it associated with Frequency in urination, Dysuria, abnormal Urethral
or PV discharge or even Loin pain
Chest pain: Started 2 days prior to admission, acute onset, progressive, generalized, dull aching in
nature, no specific periodicity, no specific aggravating or relieving factors.
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Chest pain was associated with: shortness of breath particularly on exertion but later even at rest,
palpitations, easy fatigability, dry cough, not postural related, not paroxysmal, made worse on exertion.
But not associated with: wheezing or hemoptysis.
EVENTS IN THE WARD (this is to make you understand the case but you don’t include it in your
clerkships as part of your presentations. You understand review of other systems should have followed
here)
On Admission day:
• Quite stable with GCS = 15.
• PR= 102b/min regular but weak.
• BP = 100/52mmHg
• SpO2 = 95% in room air
• Febrile – with 38oC
• But jaundiced, pale and dehydrated
• Managed as a pt with
• SCD in painful crisis
• Moderate anemia
• Dehydration
• Septicaemia
Two days later:
• Joint pain became severe
• Fever persisted
• With Mod tender abdomen without guarding
• Done in addition:
Abdominal USS
Blood Transfusion one unit
Antibiotics were given
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The following day
• The abdomen – had rebound tenderness
• Acute abdomen secondary intestinal perforation was queried.
• NGT was put and the materials were greenish, foul smelling
• Urethral catheter – drained dark brownish urine(1800mls)
Surgical consultation was made same day
• P/A: - Only rebound tenderness
– Bleeding PV but normal vaginal mucosa
• RS: - Crepitations bilaterally
• CVS: - Gallop rhythm with murmur
• Impression:
– Acute abdomen secondary to painful crisis
– Dehydration
– Severe anemia in failure
The following were done: CXR, Plain Abd X ray. She was given 40mg of IV Lasix BD and transferred to WD
1. Before the transfer she became very dyspnoeic her condition worsened and was transferred to ICU
for mechanical ventilation.
• Confirmed SCD patient at 8 months of age
• She has had several admissions and several BTs.
• But never admitted in the ICU before
• No h/o surgery before
• But she is allergic to majani ya maboga but not to other vegetables
• No h/o any other chronic illness.
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• Attained menarche at 20yrs
• With irregular flow of 2 – 3 days every 2 wks to 30 days
• Change pads 3 – 4 times a day
• No clots
• No dysmenorrhea
• No menorrhagia
• No h/o contraception
• Last born in a family of 10.
– 1 died in an accident
– 1 died due to an illness???
– 1 mentally retarded since 3 yrs
– Others – ok
• She has a distant cousin who has SCD
• Form IV leaver
– Perfomance – not good following recurrent hospitalizations
• Recently married – 2 months ago
• Neither drinks alcohol, Nor smokes cigarette
DIETARY HISTORY
• Breakfast: Chapati/scones, Milk, Beans
• Lunch: Ugali or Rice, Bananas with meat, Beans, Green vegetables
• Dinner: As for lunch
• Impression: initially Adequate quality and quantity but now it has been affected by her illness.
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SUMMARY
She is a 23 year old married female, a peasant from Visiga Kibaha, known SCD patient since the age of
8mo with multiple past admissions and BTs. Attending SCD Clinic regularly. Readmitted due to main
complaints of Abdominal pain for 1 wk, Joint pain for 1 wk, Fever for 2 days, and Chest pain for 2 days
prior to admission associated with headache, vomiting, Loss of consciousness, hematuria and spitting
blood stained saliva.
GENERAL EXAMINATION
Semi-conscious on mechanical ventilator, NGT, catheterized (normal urine color). GCS=E 4VtM4=9t/15
intubated. She was Afebrile T 37 0C. Not wasted, pale, had a tinge of jaundiced, and skull bossing
Oral exam: mal-occluded dentition with no gum bleeding.
She had mild finger clubbing, polished nails, no abnormal skin pigmentation (petechiae), no
lymphadenopathy, no neck mass, no breast mass, no LL edema or ulceration.
RESPIRATORY EXAM- only bilateral crepitations, the rest were normal.
PER ABDOMEN- normal findings
CARDIOVASCULAR SYSTEM- normal findings
CENTRAL NERVOUS SYSTEM EXAMINATION
• GCS=E4VtM4=9t/15 intubated
• Cranial Nerves:
– II, III. Equal sized pupils with normal reaction to light (both direct and consensual)
– VII. No facial asymmetry
– VIII. Could hear (opened eyes on verbal command)
Motor examination- all were normal except power was 1/5 in all groups of muscles.
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PROBLEMS IN THIS PATIENT (POSSIBLE DIAGNOSIS)
1. SCD in painful crisis
– Vasoocclusive
– Hemolytic
– ACUTE CHEST SYNDROME
2. Vomiting – Dehydration – Electrolyte imbalance – Paralytic ileus - ?? Intestinal obstruction
3. Pneumonia - SCD prone to encapsulated bacteria
4. UTI – gram –ve - +ve urine nitrite
5. Septicaemia - same reason
6. Anemia in failure - Pulmonary edema
7. Renal insufficiency - ?? Hematuria
8. Malaria
9. Jaundiced – hemolysis – but a primary liver pathology can not be excluded?? Hepatitis.
10. Dengue Hemorrhagic Fever ?? – complicating the whole picture??
139 | P a g e
INVESTIGATIONS DONE
I. Urinalysis done- protein 3+, urobilinogen 3, bilirubin 2+, PH 5, WBC 10/hpf, RBC 20/hpf and
nitrites positive. The rest were normal.
II. FBP- has leucocytosis, neutrophilia, low Hb and low platelet.
III. Creatinine is high
IV. PT, PTT and INR are all raised.
V. Other tests
• BS-Negative
• MRDT - Negative
• HBsAg-Negative
• HIV – Negative
• Blood Culture – Negative
• Urine culture - Negative
• Dengue IgM/IgG - POSITIVE
Chest xray showed mild pleural effusion (cardiogenic pulmonary edema).
Plain abdominal xray showed fecal impaction.
Echo showed early features of dilated cardiomyopathy.
ECG is normal.
FINAL DIAGNOSES
1. SCD in Crisis
2. Dengue Fever with Complications.
DENGUE FEVER
Epidemiology in Tanzania
• First outbreak - May 2010- Japanese tourists
• 2013 – 20 students IFM
• April 2014 – 58/120 at MNH EMD
• MNH - 15-20 pts/day with signs and symptoms of dengue
140 | P a g e
ETIOLOGY
• Dengue Virus (DENV)
• Single-stranded RNA virus
• Family Flaviviridae
• Genus Flavivirus
• Four serotypes: 1,2,3,4.(Red = severe forms)
• Infection with one dengue serotype confers lifelong homotypic immunity and a very brief period
of partial heterotypic immunity
• But each individual can eventually be infected by all 4 serotypes.
• Several serotypes can be in circulation during an epidemic.
TRANSMISSION
• Mosquito borne
• Aedes aegypti
– Predominantly highly efficient vector
– Bite during the day,
– Grows in clear water
141 | P a g e
PATHOGENESIS
• Humans are the primary reservoir for dengue.
• Certain nonhuman primates in Africa and Asia also serve as hosts but do not develop dengue
hemorrhagic fever.
• Mosquitoes acquire the virus when they feed on a carrier of the virus.
• Persons with dengue viruses in their blood can transmit the viruses to the mosquito 1 day
before the onset of the febrile period.
• The patient can remain infectious for the next 6-7 days.
• The mosquito can transmit dengue if it immediately bites another host.
• Usually transmission occurs after 8-12 days of viral replication in the mosquito's salivary glands
(extrinsic incubation period).
• The virus does not adversely affect the mosquito.
• The mosquito remains infected for the remainder of its life.
• The life span of A aegypti is usually 21 days but ranges from 15 to 65 days
• Incubation period of 3-14 days (average 4-7 days)
• Viral replication takes place in the RES such as dendritic cells,hepatocytes, and endothelial cells
• Result in the production of immune mediators in response to both the initial and subsequent
infections
• Capillary damage – plasma leakage to the interstitium + hemorrhage
142 | P a g e
• The majority (~75%) of DENV infections are asymptomatic.
• Among persons with symptomatic DENV infection (dengue), the illness occurs in three phases
– Acute phase:
– The critical phase
– The convalescent phase
• 2–7 days of fever, which is often accompanied by one or more of the following:
– Headache
– Retro-orbital eye pain
– Joint pain
– Muscle and/or bone pain,
– Rash
– Mild bleeding manifestations (e.g., nose or gum bleed, petechiae, or easy bruising)
– Low white cell count.
• Begins at defervescence
• 24 to 48 hour period in which
• Compensated or decompensated shock may occur due to increased capillary permeability with
plasma leakage that produces ascites, pleural effusions and “third spacing” of fluids.
• The presence of these signs and/or symptoms is now called severe dengue rather than DHFor
DSS.
143 | P a g e
WARNING SIGNS OF DENGUE
• Abdominal pain
• Vomiting
• Thrombocytopenia
• Mild to severe hemorrhagic manifestations
– Easy bruising
– Petechiae
– Menorrhagia
– Mucous membrane bleeding of the nose or gums.
CONVALESCENT PHASE
• Later stage of the illness when the patient recovers and returns to normal, but
• May continue to be a source of infection even if feeling better.
• Lasts for 4-7 days
HOW TO MAKE A DIAGNOSIS
PCR- to detect viral RNA
Serology –ELISA test.
Points to remember
• Patients who have IgM antibodies to dengue detected in their serum specimen ELISA and had
either
– A negative PCR result in the acute phase specimen or
– Did not submit an acute phase specimen,
144 | P a g e
Are classified as having a recent probable dengue infection.
• This is because IgM antibodies for dengue may remain elevated for 2 to 3 months after the
illness.
• The elevated IgM observed in a sample could be the result of an infection that occurred 2 to 3
months ago.
• Often times both an acute and convalescent phase specimens are needed to make a diagnosis of
dengue infection.
• This is especially true for those who submit a day 5 acute specimen because the virus and IgM
antibodies may be at undetectable levels.
Immunological response
• The acquired immune response following a dengue infection consists of the production of IgM
and IgG antibodies primarily directed against the virus envelope proteins.
• The immune response varies depending on whether the individual has a 1 o or 2o infection.
PRIMARY INFECTION
• Characterized by a slow and low titer antibody response.
• IgM antibody is the first immunoglobulin isotype to appear.
• Anti-dengue IgG is detectable at low titer at the end of the first week of illness, and slowly
increases.
SECONDARY INFECTION
• Antibody titers rise extremely rapidly and antibody reacts broadly with many flaviviruses.
• High levels of IgG are detectable even in the acute phase and they rise dramatically over the
proceeding two weeks
• IgM levels are significantly lower thus some anti-dengue IgM false-negative reactions are
observed during secondary infections.
• 80% of all dengue cases have detectable IgM antibody by day five of illness, and
• 93-99% of cases have detectable IgM by day six to ten of illness, which may then remain
detectable for over 90 days*
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MANAGEMENT
• Mainly conservative
• Syndromic approach
• In our patient with SCD it is complicated
• Corticosteroids should be avoided.
• NSAIDs should also be avoided
• IM injections – avoid also
• Careful attention to fluid management and proactive treatment of hemorrhage.
COMPLICATIONS
• Cardiomyopathy
• AKI
• Encephalitis
• Hepatic injury
• Pneumonia
• Severe hemorrhage – shock – death
• Multiple organ failure
PROGNOSIS
• Dengue fever is typically a self-limiting disease with a mortality rate of less than 1%.
• When treated, dengue hemorrhagic fever has a mortality rate of 2-5%.
• When left untreated, dengue hemorrhagic fever has a mortality rate as high as 50%.
• Survivors usually recover without sequelae and develop immunity to the infecting serotype
146 | P a g e
CASE-SLE
NAME MD PHD
AGE 34
SEX female
RESIDENCE Dar es salaam
OCCUPATION Primary school teacher
Referred from Mwananyamala with a referral diagnosis of pruritic drug eruption for dermatological
review
Main complaints being nose bleeding for 6/12, skin rash 4/12 and joint pain for 2/12
She reported nose bleeding for the past 6months, four (4) episodes, 1 week apart, each episode lasted
about 10 minutes, sudden onset, unprovoked and painless from both nostrils, quarter to half filled cup
of tea (100-150mls) per episode, was controlled by nasal packing, no h/o nasal discharge or trauma prior
onset. No h/o gum bleeding, easy bruising, vomiting blood, abnormal PV bleeding or passing fresh
bloody stools. She had received multiple blood transfusions during the course of this illness.
She also developed skin rash, gradual onset, first appeared on her cheeks, started as fluid filled rashes
(clear fluid), small, round, easily ruptured, later(1 week), evolved to cover the nasal bridge and parts of
both arms and legs then progressed to involve the trunk sparing the buttocks and the thighs. With time
the lesions became black and dry with scar formation, itching in nature, non painful and burning
sensation on sun exposure. Associated with oral ulcerations, non painful spontaneous hair loss, easily
pluckable during combing but no nail changes reported
Joint pain 2/12: Gradual onset and progressive involving multiple joints, non migratory initially involved
small joints (MCP, PIP), later(2 weeks), large joints (wrist, elbow and shoulder) were involved
symmetrically. The pain was dull in nature, and had no limitation of activities or interference with sleep.
Not aggravated by cold environment or change in color of fingers when handling cold substances,
relieved by rest and paracetamol, no joint swelling or morning stiffness, no deformity reported. No
history of trauma. It was the first episode
During the course of this illness; Low grade, intermittent fever, generalized body weakness, awareness
of heart beats, dizziness and decreased exertion tolerance. She also had weight loss where she noticed
by loose/ unfitting cloths
However; No history of dryness of eyes and mouth, Cough, DIB on lying flat or air hunger at night. No
history of Chest pains at rest, during any movement or sleep.
147 | P a g e
No history of yellowish discoloration of the eyes, abdominal pains, nausea, vomiting, diarrhea,
headache, convulsions, confusion, numbness, loss of memory or abnormal behaviors, reduced urine
output, froth urine, bloody urine, facial swelling or lower limb swelling. No history of heat/cold
intolerance, tremors, recurrent pregnancy loses. She does not know her HIV status. No history of similar
illness in the family
• She had 3 admissions at Mwananyamala
• Where she received multiple blood transfusion.
• No known food or drug allergies
• No known history of DM, Asthma
• Menarche at 12yrs of age.
• Normal and regular cycles of 4/28, usually changing 2 pads per day
• No h/o oral contraceptive use
• No h/o abortion
DIETARY HISTORY
 Mainly 3 meals a day;
• Breakfast: tea with chapati /porridge
• Lunch: stiff porridge/ rice with beans or meat ± green vegetables
• Dinner: same as lunch
• She was unable to finish her plate
 Conclusion: Adequate in quality but reduced quantity
148 | P a g e
• 2nd born out of 4 (other siblings are doing fine)
• Diploma holder in education
• Primary school teacher, not married, 2 children of the same father, who are doing fine
• Non alcoholic, not smoking
• No family h/o atopic diseases, diabetes
SUMMARY
34 year old female, presented with h/o recurrent epistaxis, poly arthralgia, wide spread pruritic skin
lesion and photosensitivity. Associated with hair loss, oral ulcerations and features suggestive of anemia.
GENERAL EXAMINATION
Middle aged female, Fully conscious, Calm, Notably wasted, No periorbital edema, Soft scalp hair,
diffuse alopecia, severe conjunctival pallor, Not jaundiced, No petechial or ecchymosis, No gum
bleeding, No angular cheilitis, Oral ulcerations, No digital clubbing, No koilonychia, No palmar No lower
limb edema. No palpable peripheral lymph nodes.
ERECT BP: 108/64mmhg SUPINE 106/62mmHg, PR: 120/min, RR: 17/min
Temp= 37celcius, RBG= 6.2mmol/l
Weight= 52kg, height= 174cm
BMI: 17.2 (Underweighterythema, No dupuytren’s contracture, No flapping tremor, No spider nevi
INTEGUMENTARY SYSTEM EXAMINATION
• Wide spread hyper-pigmented, scaly, xerotic patches.
• Distributed on the sun exposed areas, face, upper trunk, and extremities.
• Face: hyper-pigmented patches spread all over the face sparing the nasal labial folds.
• Coalescing patches with erythromatous centres.
• Purpura, scars and excoriations seen all over the affected sites.
• Diffuse alopecia with skin on the scalp intact.
• Normal nails
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MUSCULOSKELETAL SYSTEM EXAMINATION
UPPER LIMBS NORMAL
HANDS NORMAL
SPINE NORMAL
CARDIOVASCULAR SYSTEM EXAMINATION- the only abnormality was tachycardia and gallop rhythm
CNS, RESPIRATORY AND PER ABDOMEN ALL NORMAL.
SUMMARY
34 year old female, presented with h/o recurrent epistaxis, poly arthralgia, wide spread pruritic skin
lesion and photosensitivity. Associated with hair loss, oral ulcerations and features suggestive of anemia.
O/E: Severely pale, tachycardia and underweight, diffused alopecia, malar rash and wide spread hyper-
pigmented, scaly, xerotic patches on the sun exposed areas. Normal nails.
SYSTEMIC LUPUS ERYTHEMATOSUS with a differential of rheumatoid arthritis
TO DEFEND THE DIAGNOSIS
POINTS SUPPORTING THE DIAGNOSIS
• Gender – Females 90%
• Age 20-30’s
• Constitutional symptoms 50-100%
• Malar rash, photosensitivity
• Non scarring alopecia 20%
• Oral ulcers
• Arthralgia 62%
• Hematological (Anemia)
150 | P a g e
POINTS AGAINST THE DIAGNOSIS
Our patient doesn’t have
• Serositis which occurs in 24%
• Renal involvement (Lupus nephritis 50-60% of cases)
• Neurological involvement.
RHEUMATOID ARTHRITIS
POINTS SUPPORTING
• Joint involvement
– Pain
– Symmetrical, PIP, MCP wrist, shoulder joint.
– Number of joints
• Duration > 6 weeks
• Sex (female 3X)
• Age 35-50
• Arthralgia
POINTS AGAINST..features that are not present
• Serositis
• Joint deformity(active>1yr)
• Morning stiffness for more than 1 hour.
• Joint swelling.
• Rheumatoid nodules.
151 | P a g e
After several investigations the final diagnosis was:
• Systemic Lupus Erythematosus
– Malar rash
– Non-scarring alopecia
– Non-erosive arthritis
– Hematological: pancytopenia (from full blood picture results)
– ANA was found +
– Anti-Sm was found +
CASE-PHEOCHROMOCYTOMA
NAME RURURUR
AGE 22
SEX MALE
RESIDENCE SHINYANGA
Referred from Victoria hospital with main complaints of excessive sweating for 11months and
generalized body malaise and headache for 5months.
Excessive sweating: abrupt onset, generalized, occurs while awake and sleeping, not associated with
fever or unintentional weight loss and disrupts his daily activities and he was unable to sleep inside the
house and the condition wakes him from sleep.
General body malaise: Sudden onset, no specific periodicity, not related with exertion nor does it
improve with rest, limit his daily activities, not associated with dyspnea nor dizziness, not associated
with fever or loss of appetite, not associated with any significant weight loss or weight gain, not
associated with polyuria or polydipsia, not associated with muscle weakness or muscle cramps.
Headache: Abrupt onset, lasts for an hour,frontal, associated with palpitations and tremors not
associated with blurred vision, or change in mental status, convulsions or Loss of consciousness, not
associated with fever, nasal discharge, post nasal drip or hearing impairment, not associated with
nausea or vomiting, not relived by rest, made worse by moving
At Home: Used traditional herbs, boiling roots and flowers of certain plants and drink the residuals with
no relief of symptoms after approximately three months
152 | P a g e
At Bugando Hospital- was diagnosed with Hypertension. He was kept on: Atenol 50mg, Amilodipine
10mg, Telmisatan 80mg, Indapamide 1.5mg and Furosemide 40mg od. Despite medications given, his BP
persistently remained high.
At Victoria Hospital- Was treated as hypertensive patient but there was no relief of symptoms and
referral BP was 250/190mmg
• No joint pains, rash, or joint deformities
• No constipation, diarrhea, or discomfort on swallowing
• No neck swelling
• No cough
• No hx of increased urination at night, painful urination, no blood in urine, or reduced urine

output
• No numbness or loss of sensation ,
• no h/o weakness of any limb
• 1st admission, previously well prior to these symptoms
• h/o herbal use for 3 months, no chronic medications like beta blockers, tricyclic antidepressants
• No hx of major or minor surgery
• No hx of BT
• No known history of HT, DM, HIV or Asthma
DIETARY HISTORY- NORMAL
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• Last born in a family of three
• Married with one child
• Never attend any kind formal education
• Both parents are peasant- Shinyanga
• Non in the family with similar disease
• No Hx of DM or HT in the family
• No hx of smoking, illicit drug use, or alcohol intake
• No known family hx of Cancer
SUMMARY
S.N.N, 22yrs,M Shinyanga, presenting with 8/12 hx of paroxysmal episodes of generalized sweating
which occurs during awake and sleeping, palpitations not provoked, general body malaise and
headache. Managed as hypertensive patients with no improvement
On examination patient had high blood pressure with sustained LV impulse and grade 2 retinopathic
changes. The rest of the findings were normal
Secondary HTN(hypertension) with complications 2 0
• Pheochromocytoma
• Hyperthyroidism
• Renal artery stenosis
• Primary hyperaldosteronism
Why do we say secondary hypertension? It occurs at the age below 35yrs where one has high blood
pressure.
154 | P a g e
Why pheochromocytoma? The following are reasons that convince us of the diagnosis
Unprovoked paroxysmal-
+Headache
+Sweating
+General body weakness
+Awareness of heartbeats
+Tremors
+Hypertension
What points discourage the diagnosis? The age (pheochromocytoma is common in 4 th and 5th decade)
and also the race (its less in blacks)
RENAL ARTERY STENOSIS
Age (common in young age) convinces us but the race (less common in African American), symptoms
(does not include excessive sweating,tremors,palpitations) and Absence of renal bruit make us doubt it.
HYPERTHYROIDISM
POSITIVE POINTS FOR IT
+HTN
+Excessive sweating
+Palpitations
+Tachycardia
POINTS THAT MAKE US DOUBT IF IT REALLY IS THE ONE
-No weight loss
-No increased appetite
-No opthalmopathy
-No palpable thyroid mass
155 | P a g e
PRIMARY HYPERALDESTORINISM
POINTS FOR IT
+HTN
+Black race
+Headache
+No pedal edema
What gives us a doubt is no muscle weakness or muscle cramps.
FINAL DIAGNOSIS AFTER ALL INVESTIGATIONS
• Secondary HTN 2 left suprarenal pheochromocytoma with complications
– CKD stage 3/4
– Grade 2 retinopathy
– LVH
DISCUSSION ON SECONDARY HYPERTENSION
Elevated blood pressure that results from an underlying, identifiable, often correctable cause.
Causes :
• Endocrine-Phechromocytoma,Hyperthyroidism,Cushing’s syndrome, Primary

hyperaldosteronism
• Renal - Renal artery stenosis, Renal parenchymal disease
• Cardiac -Coarctation of the aorta
• Drugs
• Diet
156 | P a g e
PHEOCHROMOCYTOMA
• Catecholamine-secreting tumors that arise from chromaffin cells of the adrenal medulla and the
sympathetic ganglia.
• Rare
• Most common in the 4th to 5th decade
• Equally common in men and women
• 10% extra adrenal. 10% malignant. 10% familial. 10 % bilateral
The classic triad of symptoms :
• Episodic headache-90%
• Sweating-60-70%
• Tachycardia
About half have paroxysmal hypertension
PRECIPITATING FACTORS
• Exertion
• Trauma
• Anesthesia
• Surgery
• Surgical manipulation of the tumor
• Certain drugs :Tricyclic antidepressants, glucagon, metoclopramide, phenothiazines, and

naloxone
• Foods or beverages-cheeses or red wine that contain tyramine.
• The β-blockers may cause a paradoxical rise in blood pressure.
157 | P a g e
MANAGEMENT
Preoperative management:
• Alpha-adrenergic blockade (Phenoxybenzamine )
— 10 to 14 days preoperatively -normalize BP and expand the contracted blood volume.
• Blood pressure monitoring — twice daily in the outpatient setting with the patient in the
seated and standing positions. Target BP< 120/80 mm Hg (seated), with SBP> 90 mm Hg
(standing).
• High sodium diet — On the second or third day of alpha-adrenergic blockade- catecholamine-
induced volume contraction and the orthostasis associated with alpha-adrenergic blockade
• Beta-adrenergic blockade
- After adequate alpha-adrenergic blockade has been achieved
-Blockade of vasodilatory peripheral beta-adrenergic receptors with unopposed alpha-adrenergic

receptor stimulation à further elevation in blood pressure.
• Calcium channel blockers
• ACEIs
BUT SURGERY IS THE SOLUTION. ADRENALECTOMY WETHER LAPARASCOPIC OR OPEN.
POST OPERATIVE COMPLICATIONS
• Hypotension
• Hypoglycemia
COMMON QUESTIONS
What are the indications of dialysis in renal patient?
Indications of dialysis- mnemonic A E I O U
A-acidosis
E-electrolyte imbalance not responding to treatment. (Intractable Hyperkalemia)
I-intoxication
O-fluid overload not responding to treatment
U-Uremia
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What is the danger of hyperkalemia and how do we manage it?
Hyperkalemia can lead to arrhythmias.
Management of hyperkalemia involves three steps
1. Stabilize cardiac membrane so that one doesn’t get arrhythmias- by calcium gluconate then,
2. Make potassium shift into cells, so give insulin then,
3. Make the body excrete potassium that has failed to shift into cells- by give furosemide
What are the precipitants of DKA? REMEMBER THE 4S
1. Surgery
2. Stress like infection
3. Sugar- high sugar maybe missed dose of insulin
4. Substance -alcohol
Symptoms of DKA- mnemonic DKA
D- diabetes
K-ketones in urine
A-Acidosis + wide anion gap.
MANAGEMENT OF DKA PRINCIPLES
1. Correct dehydration. Give a lot of fluid

2. Correct hypokalemia
3. Give insulin. Short acting, IV, and low dose (0.1IU/Kg). rate of fall of glucose at a rate of
5.6mmol/hr.
4. Treat the precipitating factors if they are treated
5. Prevent complications
6. Provide education and make follow up.
What is the best immunological marker of disease progression?
ANSWER: CD4 cell count.
CD4 is usually measured as baseline before starting ART and when you suspect treatment failure or IRIS.
If its <350cells/mm3 follow up 6monthly if above 350cells then no need unless there is indication of
treatment failure or IRIS.
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What is the preferred monitoring approach to diagnose and confirm early HIV treatment failure?
Answer HIV VIRAL LOAD
Viral load is checked 6months after initiation of treatment. If the viruses are less than 1000copies/ml
repeat after 6months if still less than 1000copies/ml test every after one year.
If the viral load is more than 1000copies/ml insist adheherence and repeat after three months the test
and if still viral load is more than 1000copies/ml but >0.5log drop continue insisting adheherence then
check after three months, but if the drop is <0.5log drop even after adherence consider 2 nd line
treatment.
If you find unconscious patient what would you think of the causes?
A-Alcohol withdrawal/ abuse of substance
E-Electrolyte imbalance/ encephalopathy/ epilepsy
I-infection
O-overdose of drugs, oxygen deficiency
U-uremia
T –trauma, brain tumor
I-insulin (overdose maybe hypoglycemia)
P- poisoning, psychogenic
S-stroke,shock, space occupying lesion
160 | P a g e
CLOSING NOTE
Internal medicine is very wide but above is the best I could summarize. Don’t ignore everything but
don’t put too much effort on rare diagnosis. Don’t also rely in this and forget books.
161 | P a g e

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MUHIMBILI UNIVERSITY OF HEALTH AND ALLIED SCIENCES

CLINICAL SUMMARIES OF INTERNAL MEDICINE

AUTHOR: Elton, MD class of (2013-2018).

Below is a story of a blind girl.

THE BLIND GIRL

 Name of the patient- introduce the patient by three names.

 Expected date of delivery.

 N-NATURE OF THE CONDITION

2. LOCAL EXAMINATION- in cases of local pathologies.

Cranial nerve examination

Cranial nerve 1- can smell

Cranial nerve 3,4 and 6- can move eyes in all directions

Cranial nerve 8- can hear

Cranial nerve 12- can protrude tongue, no fasciculations, no muscle atrophy

Mnemonic is BIG TPR.

B-Bulkiness of all groups of muscles in upper and lower limbs

I-see if there are any Involuntary movements

G-observe the GATE

P-Power in all groups of muscle

Assess coordination- finger to nose test, or heel to shin test.

Then test for sensation following the dermatomes.

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The disease has three phases

1. Bone pain with lytic lesions seen on X ray

The best way to remember multiple myeloma is the mnemonic CRAB

DAYS IN THE WARD 16

Chief complaints- recurrent PV bleeding

Lower abdominal pain

Awareness of heart beats.

HISTORY OF PRESENTING ILLNESS

REVIEW OF OTHER SYSTEMS

Nothing was significant

PAST MEDICAL HISTORY

GYNECOLOGICAL AND OBSTETRIC HISTORY

FAMILY AND SOCIAL HISTORY.

Full blood picture results.

1. Reticulocyte count whereby the results came it was 2%.

Other investigations done

1. Serum ferritin- >1000

– Pancytopenia due to failure of cell production probably due to

• Bone marrow Infiltration: leukemia, myeloma, MF, lipidoses

• Severe B12/FA deficiency

• Aplastic or Hypoplastic anemia

• Overwhelming infection (sepsis)

• SLE (systemic lupus erythematosus)

• PNH (paroxysmal nocturnal hemoglobinuria)

– Congenital eg. Fanconis anemia

– Dose dependent: Cytotoxics, benzene

– Idiosyncratic: Chloramphenicol, NSAIDS

• Viral: nonA, nonB, nonC hepatitis, EBV

• Pathophysiology could be due to any of the following mechanisms-

– Damage to the multipotent hemopoietic stem cells

– Impaired self renewal

– Stem cell depletion

– Damage may be due to: drugs, viruses, immunological

– Anemic symptoms- as easy fatigability, awareness of heart beats, dizziness.

– Thrombocytopenic symptoms- bleeding, bruising easily

– Neutropenic symptoms- repeated infections.

– Splenomegally is rare, when present consider alternative diagnoses

– Normo or macrocytic anemia

– Low reticulocyte count

– Elevated erythropoetin levels