Medicine Cases

Dr. Maiada
Edited
 This sheet is the work of Dr. Maiada.
We are very thankful for her great efforts .

Participants in typing of the sheet:

Qassawer (Batch 88)

Asmaa Mahmoud

Aya Abdullah Altayeb

Ekram Siddig

Hibat Allah Mohammed

Khansaa Alamin

Romaisaa Ismaiil

Rawya Abdullah

Sara Yahya Ali

Samar Wagih

Waad Mohammed

Islam Siddig (Batch 93)

Marwa Haider (Batch 91)

Misan Murshid (Batch 90)

Revised by: Muram Elmamoun

Contents

Respiratory………………………………………………………………….……1
Cardiovascular………………………………………………………………..15
Neurology……………………………………………………………………….28
Tropical + Endocrine………………………………………………………41
Gastroenterology…………………………………………………………..52

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‫قف على ناصية الحلم وقاتل‬
 Respiratory System
1) A 62 yrs old man was admitted to the hospital with progressive cough, mucoid sputum
and hemoptysis for the past 3 weeks. He had smoked 20 cigarettes per day for over 40
yrs, he is unsuccessfully treated with a course of antibodies and there is no history of
chest pain, palpitation, urinary or bowl problems.
O/E: not pale, JVP not raised, no lymphadenopathy, there is clubbing of the figures,
trachea was central, he had area of bronchial breathing and few crepitations at his Rt
base.
CVS
GTT NAD
CNS
After admission he developed epileptic fit. Blood glucose, urea, and K are normal.

Questions:
A- What is the most likely diagnosis?
CA Bronchus most likely small cell CA.

 DDx of non-resolving pneumonia:

1- Atypical pneumonia
2- TB
3- CA Bronchus

 DDx of massive hemoptysis:

1- Brochoectasis
2- T.B
3- Aspergilloma
4- Adenoma

B- Give 4 investigations to help you in diagnosis?

 3 categories of investigations:
1- To confirm is this cancer or not?
2- Staging of the cancer
3- Assessment of the fitness of the pt. for surgery

 To confirm the cancer:

1- plain cx ray
 cavitation /collapse /consolidation /effusion/ hailer lymphadenopathy

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  Central lesion → squamous or small cell ca.
 Peripheral lesion → usually adenoma or large cell ca.
2- CT → shape and area of the lesion, assess operability.
3- Bronchoalveolar lavage / sputum for cytology.
4- Biopsy
 bronchoscopic for central lesion
 transthoracic needle aspiration for peripheral lesion

 To stage the cancer: CT brain / abdominal ultrasound / bone scan.

 Assess patient’s fitness for surgery;

 pulmonary function test
 investigations for para-neoplastic syndrome.
C- What is the most likely cause of the epileptic fits?
1- mets to brain
2- paraneoplastic syndrome > hyponatremia due to SIADAH

D- If surgery is to be performed for treatment of this condition, mention 2 major

contraindications for surgical treatment.
1- distal Mets .
2- FVC <1.5 litter
3- Malignant pleural effusion
4- SVC Obstruction
5- Central lesions 2 cm from carina
6- Comorbidities
7- Small cell lung cancer

 Treatment
 small cell cancer → palliative
 non-small cell cancer → curative

 Notes in lung cancer :

 squamous → commonest
 Complications :
1- Local → collapse, consolidation, pleural effusion, Horner syndrome , SVC obstruction,
recurrent laryngeal nerve infiltration.
2- Metastatic → BLABEL mnemonic

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3- Endocrinological:
 squamous : high PTH → hypercalcemia , high prolactin → gynecomastia
 small cell : ACTH → Cushing, ADH → SIADH → hyponatremia
 Adenocarcinoma → gynecomastia
 Squamous cell CA is the commonest one associated with clubbing.

4- paraneoplastic nonmetastatic syndrome:

 Lambart -Eaton syndrome

 Myelopathy
 Dermatomyositis
 Acanthosis nigrigans
 Thrombophelbitis migrans
 Pure red cell aplasia (also associated with SC injection of erythropoietin in pts.
with chronic renal failure)
Treatment:
 Para-pneumonia effusion: no ttt except if pt. is symptomatic → drainage.
 Empyema : surgery → decorticate surgery (remove the pleura + chest tube)
 Recurrent malignant pleural effusion: pleurodesis ( talc / tetracycline / bleomycin)
 Treat the underlying cause.
 Adenocarcinoma → associated with non-smoker, more common in females
 Adeno ca 30%
 Squamous ca 30%
 Small ca 30%
 Risk factors: smoking, asbestosis, radiation, age
 Signs:
Anemia, cachexia, clubbing, LN enlargement + HPOA (hypertrophic pulmonary
osteoarthropathy)
+ Local signs in chest + Mets + Paraneoplastic syndrome

 Treatment of non-small cell lung CA:

 surgical or chemotherapy (Cyclophosphamide, Methotrexate, Vincrist)
 Neo-adjuvant → shrink tumor size
 Adjunct → prevent the recurrence

 Small + metastatic → palliative

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 Note:
 Hemoptysis + ANCA +ve → Wegener,s granulmatosis .
 Hemoptysis +B ANCA +ve → Churg-Strauss
 Hemoptysis + anti BM Abs +ve → Good Pasture’s syndrome

2) A 30 years old male presented with one year history of gradually progressive dyspnea
and cough, there was no chest pain or fever. He had whooping cough as a child.
O/E: - There was 3rd degree finger clubbing, bilateral basal crepitations.
Questions: -
A- What are the 2 possible diagnoses?
1-bronchiatesis 2- idiopathic lung fibrosis

 DDx of clubbing :
1- Suppurative lung diseases (bronchiectasis , lung abscess)
2- CA bronchus
3- Mesothelioma
4- Fibrosing alveolitis
5- Complicated TB
N.B: Cystic fibrosis need long history to be diagnosed.

B- What point in the history may help you to differentiate between the two?
Bronchiectasis ILF
 Large amount (copious sputum)
 Foul smelling, yellow greenish
 Change in amount with change in Dry cough
posture
 hemoptysis

O/E O/E
 fine end inspiratory crackles (opening
of
Coarse crackles
fibrosed alveoli)
(also found in Pulmonary edema)
CXR CXR
 ring shadow - tram line shadow bilateral reticulonodular shadow →

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 Feature of fibrosis ground glass appearance then honey
 Features of hyperinflation combing

 Features of hyperinflation:
1- increase translucency of lung shadow
2- wide horizontal space between ribs
3- 6 ribs can be counted anteriorly and d 10 ribs posteriorly
4- low set or flat diaphragm
5- elongated tubular heart

 Investigations:
1- high resolution CT(HRCT) (diagnostic for brochoectasis)
 dilated cyst, ↓ bronchioles
2- lung biopsy (diagnostic for ILF)
3- Sputum > organisms
4- Pulmonary Function Test:
 Bronchoectasis → obstructive pattern may be found
 ILF → Restrictive pattern may be found
5- for both two diseases assess the respiratory function:
Pulse oximetry, ABG, PFT

C- Outline briefly the management of each?

ttt of bronchiectasis:
1- chest physiotherapy (postural drainage)
2- antibiotics (Cipro for pseudomonas )
3- bronchodilator (salbutamol, ipratropium)
4- vaccination(pneumococci, influenza)
5- surgical:
If there is massive hemoptysis / good PFT/ local disease (not bilateral)
ttt of ILF → definitive ttt is lung transplant.

Causes of bronchiectasis:
 Congenital :
1- Ciliary dysfunction syndrome
Kartagner’s syndrome (bronchiectasis, situs invertus, sinusitis)
2- cystic fibrosis

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 3- Young’s syndrome → (sinusitis, bronchitis, infertility)
4- 1ry hypogammaglobulinemia

 Acquired:
 Children: TB, whooping cough, measles, foreign bodies, HSV
 Adults:
suppurative Pneumonia, TB, lung tumor, pulmonary esinophilia, aspergillosis, RA,
idiopathic.

3) A 62 years old lady was admitted with 2 months history of progressive shortness of
breathing on exercise, tiredness, poor appetite and wt loss. She had cough but denied
any haemoptysis.
O/E: - she was dysponiec, JVP is not raised, she was pale, not cyanosed, the trachea is
deviated to the left. There is slight dullness on percussion over the right base
posteriorly, with absent breath sounds, vocal fermitus, vocal resonance and no added
sounds.
CVS, GIT, NAD.

Questions:-
A- What is the most likely diagnosis?
Right sided massive pleural effusion

B- What are the most common 2 causes of this diagnosis?

1- Parapneumonic effusion 2- TB 3- Malignancy
C- What are the 3 investigations will you ask for in this pt?
1- CXR or CT :
 Homogenous opacity obliterating the costophrenic angle & Rt border of the
heart with upper concavity toward the axilla and shifting of the mediastinum.
o The most sensitive investigation for pleural effusion is USS.
2- Pleural tab for → (microscopy, bacterial, cytology, immunology)
3- Pleural biopsy
D- If the finding in the Rt side of the chest are also present in the Lt side mention 4
causes for this presentation?

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 Causes of unilateral pleural effusion:
1- TB
2- malignancy
3- MEIG,s syndrome (right side only)
4- Pulmonary infarction
5- SLE/ RA
Causes of bilateral pleural effusion:
1- CHF 2- Liver failure 3- Nephrotic syndrome 4- Hypothyrodism
Transudate vs exudate
 Protein < 25g/l = transudate
 Protein > 35g/l = exudate
 If in between apply the Light criteria

4) A 45 years old female was admitted to the surgical ward for cholecystectomy, 2 days
after an uneventful surgery she developed cough initially dry then productive of yellow
sputum. One day later she develop right side chest pain that increased with deep
breathing and cough, she had received amoxicillin capsule 500 ml 12 hourly for one
week and was discharged home on day 7 of the surgery, she was a smoker. 3 weeks
later she presented with an increase in her cough associated with very large amounts of
sputum that was greenish and foul in smell, she particularly noticed an increase in the
amount of the sputum when she lay on her left side, she also had low grade fever and
sweating.
O/E:- She appeared ill and overweight, Temp 38C, PR 110 beat/min. BP 120/80, No
palpable lymph nodes, trachea was central.
Chest/Ex:- revealed coarse crackles and loud bronchial breathing on the right side of
the chest inferiorly. The rest of examination was normal.

Questions:-
A- What is the most likely diagnosis?
Rt side lung abscess:
 pleuritic chest pain, ↑ with deep breathing , cough and large amount of foul
smelling sputum.
B- Mention 3 risk factors from the given data for her most likely diagnosis?
 Post-operative, smoker, over wt → aspiration pneumonia> atelectasis OR

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  Rupture of sub-pherenic abscess during abdominal surgery.
C- Mention 2 other differential diagnoses?
1- Empyema 2- Parapneumonic effusion

D- Mention 4 appropriate investigations, which will help reaching this diagnosis.

1- CXR → air fluid level + cavity.
2- sputum analysis → culture , microbiology
3- Blood tests → CBC (leukocytosis) / blood culture / CRP / ESR.
4- CT chest → size / site / nature
E- Outline the treatment in two headings?
1- long term antibiotics:
 If this is hospital acquired pneumonia:
Aminoglycosides + antipseudomonal penicillin or 3rd generation cephalosporin (
cephtiazidime ).
 If community acquired >amoxicillin + clarithromycin ( B lactams + macrolides ) then
change according to culture and sensitivity.
 Plus: O2 →if hypoxic, analgesic → if there is chest pain

2- Drainage:
 Postural or CT guided needle aspiration with antibiotic instillation.
 Chest drainage if empyema.

o Poor prognostic features of pneumonia: (CURB65)

1- Confusion
2- Urea >7 mmol/l
3- RR ≥30
4- BP < 90/60
5- 65 age or more
+ comorbidity + more than one lobe affected.

5) A 29 year old soldier presented with a four week history of progressively worsening
dyspnea on excretion. He also complained of a non-productive cough. Over the two
days preceding admission the patient had become breathless at rest and was started on
oral coamoxiclav by his GP.

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O/E: he was febrile 38C and looked unwell and wasted. Candida was noted on the
tonsillar pillars. Oxygen saturation was 95% on room air. But fell to 85% following a bout
of coughing. No wheeze or crackles were heard in his chest.

Questions:

A- What is the possible diagnosis?

Atypical pneumonia due to Pneumocystis Jerovicii

B- What is the risk factor in this patient?

 Immunocompromised patient (HIV) → peritonsillar candidiasis.
 Had exercise and cough induced desaturation (characteristic).

C- What further investigations you would ask for?

1- CXR → bilateral peri -hailer shadowing Or normal.
2- Bronchoalveolar lavage → organism
3- lung biopsy → diagnostic
4- CD4 count → less than 200

D- Outline the treatment of this condition?

1- High dose of co-trimoxazole +/- pentamidine if fail
2- Antiretroviral therapy if not taken.
3- After treatment give the patient 2dry prophylaxis

 NB: HIV patients are prone to:

 TB
 Aspergillosis
 Cryptococcal meningitis
 Pneumocystis jirovicii

Other problems not in the sheet:

6) 28 year female, 7 days Hx of malaise, headache, myalgia, dry cough and fever. She
took amoxicillin but she did not improve. After that she developed cough and mild
dyspnea.

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O/E; unwell, temp. 39°C, maculopapular rah, fine crackles in the mid zone, mild neck
stiffness and wheeze.
Reticulocyte = TWBC = 8000 x
Hb = 8.4 mg/dl platelets = 120 x
Na = 129 K= 5.2
GGT= 48

A- What is the most likely diagnosis?

Atypical pneumonia
Why ???
1- Presence of prodromal symptoms
2- Not responding to antibiotics
3- Extra respiratory involvement.

B- What is the DDx?

Legionella pneumonia, Mycoplasma pneumonia

C- What is the treatment?

 Legionella → clarithromycin ( ttt of choice), rifampicin
 Mycoplasma → Macrolides ( 1st line), tetracycline

D- What are the extra respiratory manifestations?

Legionella Mycoplasma
Prodrome of flu like symptoms Prodrome of flu like symptoms
Renal impairment Autoimune Hemolytic anemia
( caused by cold agglutinins)
GI upset Erythema multiform
Hyponatremia ( SIADH)

 Other manifestations:
1- ↑ liver enzyme activity

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2- Neurological involvement
3- GBS
4- Arthralgia

7) 45 yr old patient treated from TB recently came complaining of massive hemoptysis.

A- What is the differential diagnosis?
1) Aspergilloma(commonest)
2) Bronchiactesis
3) Recurrence
4) Malignancy( Ca lung)

 N.B. Aspegilloma follows:

1- Tb 2- Malignancy 3- Silicosis

B- What is the most likely diagnosis?

Aspergilloma (commonest)

C- Discuss the management of this patient?

1- ABC \ massive hemoptysis, good positioning of patient.
2- CXR - high resolution CT  site/size/ nature of the lesion.
3- Sputum analysis:
 TB  microscopy  culture
 Malignancy  cytology
 Ag detection of aspergilloma
4- Bronchoscopy \ biopsy
 If aspergilloma :
1. Needle intracavitary instillation of amphotericin.
2. Surgery → local , unilateral , good pulmonary function test (PFT)
 N.B. ttt of ABPA (Allergic Bronchopulmonary Aspergillosis) :
1. Steroids (prednisolone) ± O2
2. Bronchodilation for asthma
3. itraconazole
4. Bronchoscopic aspiration of mucus plug.

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 If TB (recurrence):
 Add another drug, increase the duration and consider Multi drug resistance.

 ttt of malignancy and bronchiectasis → see above

8) 30 year patient presented to ER with sudden Rt sided pleuritic chest pain and
dyspnea , O/E  unwell , dyspnic , Rt side is hyper-resonant , trachea is shifted to the Lt
and the Rt side moving less.

A- What is the diagnosis?

Rt sided tension pneumothorax

B- List the causes for this condition?

1- Traumatic  RTA / iatrogenic
2- Spontaneous :
 Primary  tall / thin / black healthy male.
 Secondary  asthma , COPD , pneumonia (staph/TB) , malignancy

C- What investigation do you want to do and the findings?

1- Chest Xray:
 Homogenous black shadow
  lung markings
 Visceral line
 Manifestations of the cause

But diagnosis is CLINICAL.

D- What is the treatment of this patient?

 If traumatic :
 Wide bore cannula in the 2nd intercostal space , midclavicular line , upper border
of the lower rib + chest tube
 If spontaneous :
1- Depends on the distance between the chest wall and visceral line :
 <2cm  conservative: O2 + observation

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  >2cm  pleural aspiration by wide bore cannula, if it fails insert a chest
tube.

o If you need to do percutaneous aspiration you can use a 3 way valve → used only
in primary NOT in recurrent pneumothorax.
 If secondary pneumothorax → treat the cause

9) 45 yr old patient with long history of productive cough of whitish sputum.

O/E  distressed , tachypneic , hyperinflated chest (absence of normal dullness

over the heart and liver but not cyanosed .

A- What is the most likely diagnosis??

COPD – Emphysema

COPD Asthma

Irreversible or poorly Reversible

reversible

Emphysema Chronic bronchitis

wasted edematous
Tachypnic – distressed No tachypnic
Noy cyanosed cyanosed
JVP (cor purmonale)
Respiratory Not sensitive
Sensitive to Co2

 N.B: Emphysema and chronic bronchitis mostly occur together.

 Both diseases are associated with smoking → chronic irritation of the airway
epithelium  hypertrophy of mucous glands  accumulation of mucous  obstructs
the airway and produces cough.
 Smoking produces free radicals:
 Macrophages and neutrophils secrete elastase  destructs lung tissue.
 congenital deficiency of alpha1 antitrypsin ( which inhibits elastase activity) 
destruction of lung tissue.

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B- How will you diagnose this patient?
Clinically: pt. has productive cough on most days of the weeks for at least 3 consecutive
months for 2 consecutive years.

C- What investigations you want to do to confirm the diagnosis?

1- CXR → features of hyperinflation.
2- Lateral CXR → increase retrocardiac / ↓ retrosternal space.
3- PFT → FEV1/FVC (obstructive pattern)
4- Sputum analysis.
5- Alpha 1 antitrypsin serum level.

D- How would you manage the acute exacerbation of this condition?

1- ABC.
2- Oxygen.
3- Bronchodilator→ salbutamol, hydrocortisone, ibratopium bromide
4- If not improving add aminophyllin
5- Antibiotics.
6- CXR: to know the cause of exacerbation ( e.g: pnemothorax ),
7- monitor CO2 level:
 if ↑ → type 2 respiratory failure ;
 Admit pt to ICU;
 Give controlled O2 by ventori mask ( maximum 60%)
 Start by low dose 24% then if CO2 ↓ move to 28%... , but if CO2 isstill ↑↑
move to ventilation:
1. non invasive ( if fail )
2. intubation of mechanical ventilation ( if fails)
3. doxapvam ( respiratory stimulant )!!
E- What is the long management of the pt?
1- Lifestyle modification → stop smoking, exercise, balanced diet.
2- Pharmacological:
 Mild: bronchodilator on demand (salbutamol)
 Moderate: regular bronchodilator →salbutamol ( LABA )+ Beclomethazone.
 Severe: LABA+ Hydricortisone + Ibratopium bromide.
3- long term O2 therapy > 15 hr/ day
 pulse oximetry < 88%
 PO2 < 7.3 kpa.

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  PO2 >7.3 kpa + pulmonary HTN or polycythemia.
4- Pulmonary rehabilitation.
5- Volume reduction surgery

Cardiovascular System
1). A 50 years old driver was admitted with several hours of substernal pressure with
nausea, vomiting and restlessness, he denied any previous history of chest discomfort or
known heart disease, he used to smoke cigarettes and there was family history of
hypertension.
O/E:- BP 80/55, pulse 88 beat/min regular, pale, lethargic, JVP was raised, lungs are
normal, heart sounds are normal and there was S4, there was pansystolic murmurs all
over pericardium, but maximally over 3rd and 4th left intercostals spaces near the
sternum.
Questions:-
A- What is the most likely diagnosis?
VSD due to MI in sinus rhythm without pulmonary HTN, no HF, no feature of IE or
thromboembolic phenomena.
B- Mention 2 non-invasive investigations to confirm the diagnosis?
1- ECG
 ST segment elevation ( > 2mm in chest leads, > 1 square in limb leads)2-
 Tall T wave.
 Pathological Q wave.
 wide QRS complex
2- Cardiac enzymes:
 Myoglobin → first appear.
 Troponin → highly sensitive.
 CK MB ; specific to heart, and the first enzyme to disappear so useful in diagnosis
of reinfarction.
 LDH with pathological Q wave → old MI.
3- Base line investigations → RFT, LFT, lipid profile, RBG.
4- Angiography → site, size of the lesion, vessel affected
5- Echo → detect any valvular lesion or abnormal wall motion (both are complications)
6- CXR → heart failure as a complication

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To diagnose MI (2 of 3 criteria):
1- ECG changes
2- high cardiac enzymes
3- Clinical:
 Sub sternal pressure radiated to the left arm, axilla, jaw , umbilicus
 Autonomic symptoms  sweaty, palpitation, vomiting , nausea , SOB .

Site of MI IN ECG:
 Ant.  V1, V2, V3
 Septal  V3, V4
 Lateral  V5, V6, AVL, I
 Inferior  II, III, AVF
 Posterior  reciprocal changes in V6 + Depression in V3, V4

C- Mention 10 complications which may develop in this patient?

1-Due to pump failure:
 Cardiac death  cardiogenic shock-hypotension  heart failure  pulmonary
edema
 Stagnation of blood  intramural thrombi
 Thromboembolic phenomena  stroke, ischemic colitis etc.

2- Rhythm:
A- tacy-arrhythmias:
 Tachycardia , Ventricular ectopics, Supraventricular tachycardia,
Ventricular and atrial fibrillation (causes of death)
B- Brady- arrhythmias:
 Bradycardia, Heart block associated with inferior MI (because it affects the Rt.
coronary artery that supplies the SA and AV node.

3- Mechanical complications:
 Rupture of papillary muscle  valve regurge
 Rupture of septal muscle  VSD
 Rupture of ventricular wall  cardiac tamponade
 Ventricular aneurysm  arythmogenic tissue
4- Dressler’s syndrome
5- Acute pericarditis

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D- Mention 5 important steps for the management of this pt.
A- initial management:
1- Admission
2- cardiac bed
3- O2
4- Morphine + Metoclopramide
5- Sublingual nitrate
6- Aspirin
 N.B : to inhibit thromboxane use aspirin or clopidogril or glycoprotin IIb/ IIIa
antagonists.
7- B lockers
8- ACEIs
9- Wide bore cannula for investigations

B- If there is no ST segment elevation (NSTEM) :

1- Heparin - B. blockers - SV nitrate

Stable not stable

(increasing pain or Troponin not decreasing) Modify risk
factor

Tirofiban (glycoprotin IIb/ IIIa antagonist)

2- Revascularization PCI (percutaneous coronary intervention)

Coronary artery bypass

C- If there is ST segment elevation (STEM):

 NO HEPARINE ( bz it will induce rupture of wall)
 Revascularization PCI – bypass

Thrombolytic agents (streptokinase – urokinase – altepase)

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 D- Long term management
1- IH complications
2- 2- secondary prevention : B blockers , ACEI , aspirin , control DM and HTN
,statin and fibrates
3- Life style modification : stop smoking ,diet , exercise
4- Cardiac rehabilitation

 ttt of Pulmonary edema :

 Cardiac bed , O2 , diamorphine (venodilator) , sublingual nitrate , furosemide 40-
80mg

If not improve: ( go to the management written under it)

 IV nitrate
 Second dose of furosemide
 Ventilator
 Venesection of 500 ml of blood
 ICU and treat as cardiogenic shock by inotrope

Diagnosis of pulmonary edema CXR:

A → Alveolar edema (bat wing appearance)
B → Kury B lines (interstitial edema)
C→ Cardiomegaly (50% or 55% of chest)
D → Dilated prominent lobe vessels
E → Pleural Effusion

 Phenytoin is contraindicated in cases of pulmonary edema

2). A 60 years old man who smokes and who has history of obstructive airway disease is
diagnosed as having angina on exertion.
A- What drug therapy might be given to:
1. Abort the attack.
2. To prevent further attacks.
ANSWER :
1- Sublingual nitrate ( to abort the attack)

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 2- Ca channel blockers – statins ( to prevent further attacks)

B- What is nitrate tolerance and how can it be avoided?

 It’s when an increase in the dose is needed to reach the previous effect.
 Avoided by (nitrate free period)  stop nitrate for 8-14 hrs (decrease the dose
and increase the duration )

C- He uses nebulized high dose salbutamol for his chest problem but he noticed that this
tends to bring on an attack of angina why might this be?
 B agonist  increases HR  precipitates attack of angina

3). A 29 yrs old house wife presented with 2 weeks history of fever, fatigue, weight loss
and poor appetite. There was no history of cough, chest pain, palpitation or sweats. She
had no urinary or bowel symptoms. There was no history of RHD.
O/E:- she was pale, BP 120/70, PR 88 beat/min regular. There is finger clubbing but no
cyanosis. JVP is not raised. She had peticheal haemorrhages in her Lt Conjunctiva. Heart
was in sinus rhythm. S1 was loud and she had a middiastolic murmur at the apex.
Splenic tip was palpable, but there was no hepatomegaly or ascites.
RS and CNS were normal

Questions:
A- What is the most likely diagnosis?
MS due to R fever, in sinus rhythm , no HF , no pul. HTN , features of sub-acute IE ,no
thromboembolic features .

 Major criteria:
1- Blood culture  at peak of fever , 3 sets , 3 times from 3 different sites.
2- Evidence of endocardial involvement
 infective vegetation ,
 myocardial abscess ,
 dehiscence of prosthetic valve
3- New developed MR

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  Minor criteria:
1- Fever
2- Culture and Echo findings that do not meet the major criteria
3- Pre-existing cardiac disease
4- Immunological manifestation
5- Thromboembolic manifestation

B- Mention 5 investigations to help you in confirming the diagnosis?

1- Blood culture
1- CBC ,RFT, Coagulation profile, LFT
2- Echo → (aortic root abscess )
3- ECG: Lt ventricular hypertrophy, LBBB, heart block, p mitrale, Afib
4- CXR → features of heart failure, Lt atrial enlargement, mitral valve calcification
5- Blood serology, Urine general  microscopic hematuria.

C- Name 4 complications of this condition?

1- Vegetation  valve stenosis / regurgitation.
2- Embolism  brain abscess ,liver abscess , septic gangrene ,disseminated
infection ,GIUs , aortic root abscess ,
3- Heart failure ,
4- Heart block

D- What are the fundal changes which can occur in this condition?
 Roth spots, Petechial haemorrhage , Subconjuctival hemorrhage.

 ttt of Infective Endocarditis:

1- Broad spectrum, IV, imperial antibiotics
 Normal valve  benzyl penicillin + gentamycin
 Prosthetic valve  rifampicin – vancomycin ( Staph Saprophiticus )
 Acute IE + IV drugs abuser  fluxacillin
2- Surgery → indications

4). A 35 years old farmer presented with exertional fatigue, dyspnea and ankle edema. He
had mild fever but no history of Rheumatic fever.

20
O/E: - slightly pale, not cyanosed, 2nd degree finger clubbing, BP 110/70, pulse 95
beat/min, regular. JVP was 9cm of H2O. The apex in the 6th intercostals left to the
midclavicular line, there was 3rd heart sound, middiastolic murmur localized to the
apical region, with pansystolic murmur radiating to the axilla. 2nd heart sound is loud in
the pulmonary area, the liver was enlarged and tender and the spleen was just palpable,
edema was present.

Questions:-
A- What are the valvular lesions which occurred in this patient?
MR, MS
B- Mention 2 causes for this valvular lesion?
1- Rheumatic fever 2-Infective Endocarditis
C- Mention 3 complications which had occurred in this patient?
1- IE 2- Pul. HTN 3- HF

D- Mention 5 important measures for treatment of CHF?

1- life style modifications (exercise, diet, stop smoking , salt and water restriction
2- Control risk factors  DM , HTN , Hyperlipidaemia , anemia, infection, annual
vaccination by Flu Vaccine
3- Diuretic therapy 
 furosemide (if no response)
 spironolactone (if not response)
 thiazide
 ACEI and slow, low dose B blockers
 if not digoxin
 If not  hydralazine
4- Assisted pump therapy
5- Heart transplant

 Digoxin toxicity is aggregated by hypocalcemia because it acts on the Na/K ATPase

pump:
 nausea , vomiting , yellow vision ,ventricular arrhythmia, heart block , heart
failure

21
  ttt of Digoxin toxicity:
1- Stop the drug
2- Correct K
3- Eliminate its action by Lidocaine or Mg
4- Abs. against digoxin

5). A 56 yrs old retired worker suddenly collapsed during digging of the ground. He was
taken to the hospital immediately. He had no previous known cardiac disease. He was
not smoker and there was no history of DM or HT.

O/E: the pt was cyanosed, the femoral and carotid pulse was absent he was unconscious
and respiration was absent, the pupil start to dilated, no papilledema.

Questions:
A- What is the diagnosis?
Cardiac arrest

B- What the immediate steps to be taken?

CPR steps

6). A 34 years old man was brought to the casualty complaining of shortness of breath for
the last month. His ankles were swollen and stomach distended. He had no chest pain,
fever or join pains. He used to be a heavy cigarette smoker and had Thyroidectomy 10
years ago.
When examined there was massive edema, ascites and bilateral pleural effusion. His
liver was 2 cm BCM, BP unrecordable, pulse 130/minute, JVP elevated to ears and more
prominent in inspiration. Heart sounds were faint. An added sound was present and the
apex beat was not palpable.
CXR showed bilateral pleural effusion and large cardiac shadow. ECG was of low voltage
with electrical alternans of the axis. Renal function was normal. Hb was 13.8gm, WBCs
=9.000 and ESR = 90 mm 1hr.
Questions:
A- What is the most likely diagnosis?
Cardiac tamponade:
Beck’stirade (Kaussmul sign, hypotension, muffled heart sounds)

22
B- Mention 3 likely causes.
1- Pericarditis  TB, viral (mumps, Coxsackie virus)
2- Hypothyroidism
3- IHD
4- Malignancy
5- CT diseases ( RA , SLE )
6- CA Bronchus

C- Mention 3 useful investigations

1- base line investigations  CBC,CRP,ESR
2- TFT , cardiac enzymes , RFT
3- CXR → enlarged globular heart
4- ECG → pericarditis
 saddle shape ST elevation in all leads
 P-R depression
 Tamponade / effusion → low voltage ECG, axial deviation
5- Echo → fluid ( <2mm = acute, < 4mm = chronic)

D- What is the immediate therapeutic measure you would do?

1- Pericardiocentesis
2- Pericardial window xiphisternum
3- Thoracotomy
 ttt of pericarditis → analgesia + steroids

 DDx of Kussmaul’s sign +ve:

1- Cardiac tamponade
2- Constrictive pericarditis
3- Restrictive cardiomyopathy
4- Rt. atrial myxoma

23
7). A 40 years old lady had past history of Rheumatic fever at the age of 15 years from
which she made a good recovery after hospitalization and treatment. She started to
become dyspnoeic over the last few months and developed sever hemoptysis. She had
sudden pain in her right lower limb which became pale and cold. She was confined to
bed because of the pain. 10 days later she developed severe central chest pain. She was
ant coagulated before. Two months later she developed left lion pain and frank
hematuria.
O/E: the apex beat was not displaced. A murmur was heard at the mitral area.
Questions:-
A- What is the most likely cause diagnosis?
MS due to RH. Fever features of thrombosis no HF no pul. HTN no IE

B- What are the possible causes of hemoptysis?

1- MS ( cardiac asthma)
2- Pulmonary infarction
3- Rupture of pulmonary vennule

C- What are the possible causes for the chest pain?

1- Pul. embolism from DVT (immobilization)
2- MS → Afib → thrombus → Acute Coronary Syndrome

D- What are the likely abnormalities of the ECG before the chest pain?
 P mitral, AF, RT ventricular hypertrophy, Rt axis deviation  p pulmonale
 After chest pain → ST segment elevation

 N.B: When MS changes to AF  loss of presystolic accentuation.

8). A 52 years old male was admitted to hospital with increasing dyspnea over the last few
weeks. His past history was unremarkable apart from mild chest pain which did not
disturb him and long standing hypertension.
O/E:- He was breathless, BP 160/105, PR 120 beat/min. irregular and of poor volume.
His JVP was raised 6cm and precordial examination showed gallop rhythm with a
pansystolic murmur at the mitral area. There were bibasal crackles and the liver was
3cm BCM.
ECG showed AF with T inversion in V4&V5. CXR showed cardiomegally with pulmonary

24
 oedema. ECHO showed enlargement of both atria and ventricles. The left ventricle was
poorly contracting with an ejection fraction of 40%.

Questions:
A- What is the most likely diagnosis?
 MR due to dilated cardiomyopathy, with HF ,no thromboembolic phenomena,
no IE, no pul. HTN not in sinus rhythm (T wave inversion )

B- Mention two possible underlying causes in this patient?

 Idiopathic - HTN- DM - alcohol – peri or postpartum - Coxaki virus – drugs (e.g.
chemotherapy)-HIV

C- Mention the medications and their effects that are used for
treatment of this condition?
1- ttt of heart failure → diuretics, digoxin , ACEI , B blockers
2- Anticoagulant → prevent thrombosis
3- Antiarrhythmic

D- Mention two other therapeutic modalities?

1- ICD  implantable cardiac defibrillator
2- Bichamber pacing → increases the contractility
3- Cardiac transplant

 N.B : Causes of angina in young people:

1- Congenital aortic stenosis
2- HOCM
3- Familial hyperlipidaemia

9). A previously healthy 30 years old man suddenly collapsed at home and developed
short generalized seizure but recovered well in a few minutes. On examination, his Bp
110/95 and there was an ejection systolic murmur in the precordium. The chest X-ray
showed slight cardiomegaly.

Questions:-

A- Mention the differential diagnosis.

1- Aortic stenosis

25
 2- HOCM
3- Pulmonary stenosis
4- Coarcitation of the Aorta
5- HEMIC (short E.S murmer) → anemia
6- ASD
7- Aortic stenosis 2dry to aortic regurgitation.

B- Mention the signs that you would look for to rule out the differentials.

AORTC STENOSIS HOCM

Slow rising pulse Jerky pulse

Dicplaced heaving apex Double apex

Opening snap No

Soft heart sounds Normal heart sounds

S4 S4

Carotid shedder (palpated like thrill ) No

↑ with expiration ↑ with valsava

↓ with squatting ↑ with squatting

↓ with sustained hand grip ↓ with sustained hand grip

AORTIC STENOSIS HOCM

ECHO : ASH – SAM (asymmetrical septal
hypertrophy – systolic anterior
ECHO : AS –left vent . dilatation
movement of leaflets of mitral valve )
F hx of sudden death; seizure.

 N.B :
Mitral prolapse murmur is like HOCM (Increase with valsava and squatting) but unlike
HOCM it’s also increased with sustained hand grip.

26
 DDx of S4 :
1-AS 2 - HOCM 3- HTN 4 –IHD

 After syncopal attack if the patient postictally is;

 drowsy → CNS problem
 If normal → cardiac problem
 Signs of Coarctation of aorta :
1- Radio femoral delay.
2- BP high in upper limbs and low in lower limbs but later on there is generalized
HTN.
3- Inter scapular bruit.

C- What investigations will you do and what are the findings that you expect for each
differential?
1- CXR → post stenotic dilatation = coarctation of aorta
2- ECHO → stenotic valve , ↓velocity of blood ejection
HOCM → ASH – SAM
3- ECG → LT vent. Hypertrophy (HOCM)
4- CBC → Anemia

 N.B : In combination of MS /MR ttt is

 Asymptomatic → diuretics and ACEIs
 Symptomatic → valve replacement

Treatment of HOCM:

 B –blockers
 Septostomy
 Cardiac transplant

27
 NEUROLOGY
1).A man of 43 yrs old had flu like illness, which was self-treated with analgesics and course
of antibiotics. He felt better for the first 3 days but later started getting excessively tired,
lost his appetite and became generally unwell. He had great difficulty in walking. His
wife reported that he couldn’t swallow his food, therefore he was admitted to the
medical unit for further investigations.
O/E:- He was mentally alert. JVP was not raised. There was no digital clubbing or
lymphadenopathy.
PR 78 beat/min, regular. BP 130/70 mmHg. CVS, RS and GIT were normal.
He had weakness of all four limbs with reduced tone and absent tendon reflexes. There
was some loss of t6ouch and pain sensations in both lower limbs below the knees. All
cranial nerves were normal except he had bilateral VII cranial nerves paralysis.

Questions:
A- What is the most likely diagnosis? GBS
DDx :
 Transverse myelitis
 Poliomyelitis
 Diphtheria
 Cord compression

B- What 4 investigations will you carry & what are the expected results?
1- CBC → infection.
2- LP → CSF analysis :cyto albumin dissociation (↓cells -↑ proteins)
3- Nerve conduction studies → demylinating pattern (slow conduction)
4- Electromyogram → denervation pattern
5- Imaging (CT, MRI spine) → to exclude others.

C- Outline the management of this patient?

1- Admit to ICU
2- ABCs
3- NG tube
4- Continous monitoring : vital capacity, Arrhythmia (fatal), Renal failure
5- SPECIFIC → IV IG/ Plasmaphoresis

DDx of bilateral facial nerve palsy:

 GBS – Sarcoidosis – Leprosy - Lyme disease
28
2). A 52 yrs old man presented with gradually progressing weakness in both arms over the
last one year. prior to his presentation at the same time he experienced parasthezia and
numbness over the hands, few months later he starts to feel numbness in the lower
limbs with dragging of them during walking, no history of trauma.
O/E:- BP 130/90, the higher functions were normal, cranial nerve were normal, CVS, RS,
GI were normal.
Hand wasting with flaccid paralysis weakness extending till the proximal muscle of both
upper limbs, reflexes were lost. Diminished temp and pin prick in both upper limbs.
Lower limb showed spastic weakness, brisk reflexes, up going planter response.
Questions:-
A- Mention the most likely 2 differential diagnosis?
1- Syringomyelia and intra medullary tumors
2- Cervical spondylitis
3- Cervical cord tumors

B- Where is the level of lesion?

C5 - T1 (respiration is normal)
C- Name 3 investigations to help in reaching final diagnosis?
1- MRI cervical cord → syringomyelia / cord tumor / spondolysis
2- CSF → malignant cells ( cord tumor)
3- Ct brain → associated with Chiari malformation

D- What type of sphincteric disturbance to be expected in this patient?

Urine retention
 Any pathology that causes UMNL in the lower limbs causes urine retention except
Amyotrophic Lateral Sclerosis and Subacute combined degeneration of the spinal
cord.
 Treatment of syringomyelia → neurosurgery

Cervival spondyolsis:

 Proliferation and fusion of bone → narrowing

 The 1st movement to be lost is rotational movement
 Treatment:
1- Conservative: collar, exercise
2- Surgical laminectomy or laminoplasty

29
 N.B. In spondyolisis the LL are affected before the UL.

3). A 69 years old lady was admitted with 2 months history of confusion unsteady gait, no
loss of appetite or weight.
O/E:- she was moderately confused, BP 140/75, pulse 88 beat/min regular, JVP is not
raised, no thyroid or lymph node enlargement, no clubbing or tremor.
CVS, RS, NAD
Spleen was 2 cm enlarged, no hepatomegaly or ascites.
L.L power and tone were reduced in both, absent ankle jerks bilateral brisk knee
reflexes. Up going planter response bilaterally.
Touch, pain, vibration and sensation were impaired below the knee on both.
Investigations:-
HB 8.2 g/dl, serum bilirubin 3.1 mg/dl, WBCs was 3.5 x 1000, neutrophils seen.

Questions:-
A- What is the most likely diagnosis?
Subacute degeneration of the spinal cord due to vitamin B12 deficiency.
B- What are 3 investigations to confirm the diagnosis?
1- CBC → macrocytic anemia associated with ↑ MCH, MCV
2- Serum B12 and folic acid
3- Peripheral blood picture → hyper-segmented neutrophils
4- Bone marrow aspiration → Megaloblasts (immature cells)
5- Schilling test:
1. Give the pt high dose of vitamin B12 → saturation of all tissues with vit.
B12.
2. Give radioactive B12 orally.
3. Measure urinary levels of vit. B12
Normal → nutritional
↓ or absent → intrinsic factor deficiency or terminal ileum problem.
4. Give intrinsic factor → normal

C- How do you explain the presence of jaundice?

Jaundice → increased destruction of RBCs due to ineffective erythropoiesis.

30
D- Name 4 causes of the diagnosis?
1- Nutritional ( strict vegetarians)
2- Pernicious anemia (the most common cause of vit. B12 deficency)
3- Gastrectomy / atrophic gastritis
4- Terminal ileum disease e.g. Chron’s
5- Blind loop syndrome
6- Infection → Diphyllobothrium parasite
7- Drugs → phenytoin

 N.B investigations for pernicious anemia:

1- detection of Parietal cells Abs
2- Detection of intrinsic factor Abs
E- Name one other serious complication?
1- Optic atrophy
2- Psychosis ( Megaloblastic madness)
3- Sterility

F- What is the cause of confusion in this pt?

Due to vit. B12 deficiency anemia

 N.B
 Absent ankle jerk
 Brisk knee reflexes combination of UMNL and LMNL
 Up going plantar reflexes

DDx: MAST mnemonic

1- Multiple sclerosis
2- MND ( Motor Neuron Disease)
3- Ataxia ( Friedreich’s ataxia)
4- SCDSC ( vit. B12 deficency)
5- Syringomylia
6- Tabes dorsalis

Friedreich’s ataxia:
 The most common type of early onset ataxia ( young age)

31
  Autosomal recessive
 Pes cavus, kyphoscilliosis
 Dilated cardiomyopathy (cause of death)

4).A 40 years old male who develop fever and headache on the next day he became
drowsy and his relative quickly brought him to the hospital.
O/E:- Not place, not jaundiced or cyanosed, temp 39 C.
CVS, RS, GIT, NAD.
Normal fundus but there were signs of meningeal irritation.
Questions :-
A- Mention 3 signs of meningeal irritation?
1- Kernig’s sign
2- Neck stiffness
3- Brudziniski’s sign

 DDx of Headache + fever → meningeal irritation:

1- Meningitis
2- ↓ level of consciousness ( LOC) → encephalitis
3- Focal lesion → brain abscess
 Headache + meningeal irritation without fever → SAH with or without focal signs

B- Mention 3 causes which might causes the above mentioned clinical picture?
1- Meningitis
2- Meningo-encephalitis
3- Atypical pneumonia
4- Severe UTI
5- Cerebral malaria

C- Mention 3 important investigations that are helpful in the diagnosis?

1- CBC, Hb, CRP, ESR
Platelet → DIC → Meningococcemia
2- CT for meningitis ( with contrast) → Meningeal enhancement
3- MRI for encephalitis (BEST):
 Brain edema
 Temporal lobe abscess → herpes virus infection

32
 4- LP ( no ↑ ICP):
 Turbid → bacterial
 Xanthochromia → Subarachnoid hemorrhage ( SAH)
 Hemorrhagic → injury by needle or SAH ( to differentiate do serial
aspirations)
o CSF analysis and culture:
 Bacterial : ↓ glucose, ↑ neutrophils, ↑ protein
 Viral: normal glucose, ↑ lymphocyte, ↑ protein
5- PCR for Herpes Virus and Blood film for Malaria.

D- Outline 5 important steps in the management of any one of the 3 causes?

1- Admission
2- Do imaging studies
3- Start imperical antibodies
 3rd generation cephalosporins + gentamycin +ampicillin for listeria
monocytogenes ( old age, alcoholic, immunocompramised).
 If enecephalitis is suspected add acyclovair
 In Sudan add quinine for malaria
4- Do CSF / Blood culture and change according to culture and sensitivity
5- If it is Bacterial meningitis add steroids to ↓inflammation of the brain.

 In case of SAH:
1- Admit to the ICU AND GIVE o2
2- Give Nimodopine
3- Control blood pressure
4- Refer to a neurosurgeon

 Subarachnoid hemorrhage is associated with:

1- Co-arctation of the aorta
2- Aortic regurgitation
3- Autosomal dominant Polycystic Kidneys
4- Hepatic cyst
5- Ehlers-Danlos syndrome

33
  The commonest sites for intracrebral hemorrhages are:
1- Internal capsule
2- Basal ganglia ( thalamus)
3- Pons
4- Cerebellum

 If the manifestations are:

 Pure motor → internal capsule
 Pure sensory → thalamus
 Ataxic hemiparesis → Cerebellar
 Clumsy hands and dysarthria → pons

5). A 64 years old man admitted with 3 months history of progressively increasing
weakness of his arms and legs with painful cramps and difficulty in walking, he had
started using a walking stick for the past 2 months but during the past 2 weeks he could
hardly stand without the help for his wife.
O/E:- He was mentally alert, BP 160/80, pulse 80, thyroid and lymph node not enlarged,
there was no clubbing or anemia.
CVS, RS, GIT NAD
Cranial nerves were normal, there was marked bilateral wasting and weakness of
shoulder girdle muscles. He has claw hand deformity in the Lt hand, there was marked
fasciculation over both upper limbs and thighs.
There was some wasting and weakness of muscles of both upper limbs, tendon reflexes
were depressed in the upper limbs, but brisk in the lower limbs with up going planters,
no sensory impairment.
Questions : -
A- What is most likely diagnosis?
MND (Motor Neuron Disease)

 5 things that will NEVER occur in MND:

1- No cognitive impairment
2- No extraocluar muscle involvement
3- No sensory impairment
4- No sphincteric disturbance
5- No sexual impairment
34
  Types of MND:

1- Amyotrophic Lateral Sclerosis

2- Primary lateral Sclerosis

3- Progressive muscular atrophy

4- Progressive Bulbar Palsy

 The cause of death →Respiratory distress syndrome, respiratory failure

B- What 4 investigations will you ask for?

1- EMG → features of loss of motor innervation ( denervation)
2- Nerve Conduction studies
3- imaging CT/MRI → to exclude pathologies
4- LP /CSF analysis → to exclude infections and malignancy

C- Outline the management?

Symptomatic → (multidisciplinary team):
1- NG tube for nutrition
2- 2- O2 if needed
3- Sphincteric care
4- Skin care (bedsore) → mobilize every 2hr
5- Drugs;
 spasticity → dantorlene
 Amitriptyline for hyper salivation

6- Chest physiotherapy
7- Psychotherapy
 Riluzole (Antiglutamatergic drugs) →increases survival expectancy by about 3month.

6). A 50 yrs old male presented with a sudden onset right sided weakness of 3 hours
duration. His condition was associated with convulsions. He had no past history of
diabetes or hypertension, but history of angina pectoris for which he was taking glyceryl
trinitrate. He had a strong family history of myocardial infarction. Two of his brothers
had died suddenly before their age reaches forty.
One of his sisters had myocardial infarction then she was thirty years.

35
O/E:- Pulse 88/min regular and have normal volume. BP 140/95.
Neurological examination revealed right upper motor neuron facial palsy and right sided
hemiplegia.
Examination of the heart, chest and abdomen revealed no abnormality.
Examination of the neck revealed weak carotid pulsations with a thrill on the left side.
Questions : -
A- What is the most likely cause of his hemiplegia?
Embolic infarct of brain due to atherosclerosis of cerebral artery

B- What is the most likely underlying problem in the family and how would you confirm
that? Mention two tests.
Autosomal dominant familial hyperchlestrolemia type 2b because both his sisters and
brothers affected).

Family Hx of IHD diseases:

 Male < 55 years
 Female < 65 years

Mention two tests:

1- Lipid profile (cholesterol/triglyceride)
2- Karyotyping

C- Mention 2 investigations you would order, and explain how each would affect the
management?
1- CT brain
2- carotid Duplex

D- Outline the management of the familial disorder in 2 steps?

 If carotid stenosed >60% carotid endartiotomy
 If < 60% if symptomatic / asymptomatic → conservative

Management of the family members:

1- Lifestyle
 Stop smoking ,decrease Wt, exercise, control HTN and DM,
 Diet ( green vegetables, white meat)

36
 2- lipid lowering drugs:
 Statins: ↓ cholesterol
 Clofibrate: ↓ TG

 Statin is given mainly at night because the enzyme HMG,co reductase is active at
night.

7). A man of 60 yrs old presented with 2 days history of convulsion of the left side of his
body followed by loss of consciousness?

A- Mention 3 possible causes?

SOL – Epilepsy – Stroke

B- Mention how the history and examination would help you in differentiation
between these causes?

HISTORY:
1- Onset:
 Sudden (within seconds) → Embolic
 Acute (within 6 hours) → hemorrhage, meningitis
 Evolving ( ≥ 6 hours) → thrombosis , SOL
2- Duration:
3- Progression:
 Progressive → SOL, thrombotic
 Regressive → hemorrhage
 Static → infarction

4- Relation to activity
 At start of activity → embolic
 Mid of activity → hemorrhage
 At rest → thrombosis
5- Associated symptoms:
 ↑ ICP → SOL
 Sensory, sphincteric or cranial nerves involvement
 Fever → abscess
 LOC → hemorrhage ( cerebral)
 HTN → risk for hemorrhage

37
 6- Past medical history:
 Hemiparesis – hematological disorders – hepatic disease – polycystic kidney
disease ( associated with aneurysm)
7- Family history
8- Drug history → combined oral contraceptives pills (COCP)

EXAMINATION:
Cranial nerves- sensation – higher function → to localize the lesion
 Frontal lobe → psychotic symptoms, motor aphasia
 Temporal → auditory impairment, sensory aphasia, upper quandrantopia.
 Parietal → Gerstmann’s syndrome
 Occipital → visual impairment

C- What treatment would you offer such pt?

Acute phase:
 ABCs – elevate head of bed – NPO - non-contrast CT scan – Baseline investigations.
If ischemic stroke:
< 4 hours → thrombolysis
> 4 hours → aspirin
 Lower the ↑ BP if it is ≥ 220/ 120
 In pt who recently had thrombolysis , or pt. with severe cardiac disease ( ↓ BP by
20% of MAP)

If hemorrhagic:
 ICU
 Lower the BP if it is > 160/100
 Elevate the head of the bed
 ↓ fluid intake
 Controlled ventilation
 Manitol
 Steroids ( only if it’s caused by a tumor)
Long term management → modify the life style

 3 P’s:
1- Pulmonary aspiration:
Elevate the head of the bed, NPO, speech therapist, Ng tube if the pt. can’t swallow.
2- Pulmonary embolism:
Ted stocking, prophylactic heparin
3- Physiotherapy, psychotherapy , occupational therapy

38
  3 Bs: Bowel care, Bladder care, Bed sores prevention

8). A 20 yrs old male known to have grand mal epilepsy presented to the causality with
recurrent attacks of fits without regaining consciences between the attacks for 3 hours,
he was already taking phenytoin 200mg B.D but in spite of that he developed the
epileptics fits.

Questions:
A- Name 3 drugs and their route of administration which can be given for treatment of
this pt?
1- Diazepam infusion
2- IV bolus lorazepam
3- IV phenytoin

B- Mention 5 side effects of phenytoin?

1- Megaloblastic anemia
2- Polyneuropathy
3- Gum hypertrophy
4- Ataxia, nystagmus
5- Depression
6- Dysarthria
7- Myopathies

C- Name one drug that interacts with phenytoin apart from its antiepileptic use?
Warfarin (↑s metabolism of phenytoin so the dose should be increased)

D- How dose phenytoin cause megaloblastic anemia?

1- ↓ vit. B12 absorption
2- By causing hypothyroidism leading to vit. B12 deficiency.

E- What is the usual duration of antiepileptic drug therapy used in case of grand mal
epilepsy?
After being free of seizures for 2 years:
i.e. CNS normal , IQ normal, EEG normal, no Juvenile myoclonus epilepsy.

39
 Neurology cases not in the sheet:
9). 40yrs old women had headache and blurring vision, she is overweight and also has
acne, on oral contraceptive pill.

CVS, Respiratory and GIT systems are normal.

A- What is most likely diagnosis?

3 Fs (Fat, Fertile, Female) = Idiopathic Intracranial HTN (Benign intracranial HTN)

B- what investigations would you like to do?

 Ct brain: dilated 4th ventricle / exclude other pathologies
 LP( no ↑ IC P) → increase opening pressure

C- How would you treat this pt.?

1- Life style changes → decrease Wt ,stop Vi.t A derivatives
2- Acetazolsmide
3- Serial Lumbar Puncture
4- Optic nerve fenestration
5- Surgery → ventricular peritoneal shunt

10) 70 yr old male brought to the casualty by his daughter and she tells that he has
worsening confusion which has continued for several weeks and before 8 hours he lost
his sphenteric control. O/E pulse is normal, BP 130/90
Normal GI, Cardiovascular and respiratory
CNS examination is well except for unsteady gate.

A- What is the most likely diagnosis

Normal pressure hydrocephalus → (dementia, ataxia , sphenteric disturbance)

B- What investigation do you want to do?

1- Ct scan → dilated ventricular system
2- LP normal (because it’s due to ↓ absorption of CNS)

C- How would you treat the pt.?

Ventricular peritoneal shunt

40
 TROPICAL + ENDOCRINE
1). A Female of 20 yrs, from Khartoum city presented with fever for 2 weeks which does
not respond to a full course of injectable chloroquine. The fever was of high grade
without rigors or sweating, she had no other symptoms.
O/E: looked toxic, ill, had a dry coated tongue, temp 39C, pulse 80/min regular, BP
120/60. Liver was 2 cm enlarged, soft not tender.
Investigation: urine clean, Hb 95%, TWBCS 2100 cell/cumm.

Questions:
A- What is the most likely diagnosis?
Typhoid Fever

B- Mention 3 investigations which would help you to confirm the diagnosis?

1- Blood culture in the 1st week
2- Widal test ( agglutination test) → in the 2nd week
3- Urine and stool analysis → 3rd week
4- Bone marrow → Gold standard
5- CBC → Leucopenia (mentioned in the problem)

C- Mention 3 important complications of this disease and discuss briefly how to

manage it?
1- Acholuric cholycystitis ( which also occurs in burn / sepsis)
2- GIT hemorrhage / perforation
3- Abscess formation
4- Acute pyelonephritis / pancreatitis
5- Osteomyelitis
6- Degeneration of the anterior abdominal wall
7- Psychotic changes:
 1st week:
Persistent frontal headache , fatigue, abdominal pain, nausea , anorexia, constipation
 2nd week:
Step ladder fever, Rose spots, diarrhea , relative bradychardia
 3rd week → complications
 4th week → recovery or death

DDx of relative bradycardia i.e. normal pulse despite the fever (Faget’s sign):
1- Typhoid fever
2- Yellow fever
3- Tonsillitis

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 4- ↑ ICP
5- Drug overdose

Treatment of Typhoid Fever:

A- Symptomatic antipyretic (fever), analgesic ( headache) , rehydration
B- Specific
1- Ciprofloxacine (2wks) → 1st line S/E:
 Rupture Archilis tendon
 Arthropathy
 Cartilage damage
2- Chloramphenicol
S/E : grey body syndrome - B.M.suppression
3- Ceftriaxone
4- Septrin
5- Azithromycine

2). A 28 yrs old man from Babanosa presented with a history of intermittent fever for 6
months duration. He complained of discomfort in the left side of his abdomen.
O\E: He was anemic and wasted. Lymphadenopathy was detected in the neck, both
axillae and the inguinal regions. Temp was38.5 C , pulse 108 beat/min , RR 16/min, BP
110/60 mmHg, other abnormal finding were confined to the abdomen The liver was
enlarged 6cm below the right costal margin, firm with smooth surface. The spleen was
enlarged 14cm below the costal margin.
Investigations: - Hb =6.4 g/dl . WBC =12000/ml. Platelets =90.000/ml. serum albumin
=2.8 g/dl. Serum globulins = 5.8 g/dl.

Questions:
A- What is the most likely diagnosis?
Visceral Leshmeniasis

B- Mention three alternative diagnoses?

DDX of Hepato-splenomegaly+ generalized lymphadenopathy + chronic fever:
1- Visceral leshmeniasis
2- Schistosomasis (portal HTN)
3- Chronic Brucllosis
4- CML
5- Hodgkin’s lymphoma
6- Milliary TB

42
 C- How would you confirm the diagnosis chosen in 1?
1- DAT(direct agglutination test)
2- Lymph node excisional biopsy (65%)
3- B.M. biopsy (80%)
4- Spleen biopsy(95%) → dangerous
5- ICT
Leshmanin test
CBC →pancytopenia
ESR → (3 Figures)

D- What is the treatment of choice and mention the most serious side effects of the
drug or drugs given?
1- IV Pentostam 10mg/Kg (in Sudan)
S/E: 1- Cardiotoxic 2-Nephrotoxic
2- Ribosomal amphotersine (amphotresome)

 Diseases causing Hyper gama- globulinimia:

1- Kalazar
2- Autoimmune diseases
3- Connective tissue diseases

 DDx of 3 figures ESR:

1- Vis.leshmenaisis. 2- TB
3- Multiple Myleoma. 4- Nephrotic syndrome
5- Connective tissue disease

 DDX of bilateral epitrochlear LN.enlargement:

1-Vis. Leshmeniasis 2- HSV 3-sarcoidosis
4- 2dry Syphilis 5- Lymphoma 6- CLL

 DDX of unilateral epitroclear LN:

Trauma – infection - Scratch disease

3). A 52 years old female coming from Elmanagel presented to the causality with dragging
pain in her left hypochondrial region for 3 months, on asking her direct questions she
said she had low grade fever and moderate loss of weight.
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O/E:- found to be pale but not jaundiced, temp was 37.8 C, no lymph node
enlargement. Abdomen : showed enlarged liver 4 cm, no ascites.
CVS, RS, CNS / NAD.
Questions: -
A- Mention 4 differential diagnoses for this presentation?
1- Schistosomiasis
2- Brucellosis
3- Malaria
4- Typhoid fever
5- Vis. leshmaniasis
6- CML

B- Mention 5 investigations which may help you to reach a final diagnosis?

1- Blood tests:
Blood film for malaria, LFT( ↑↑),Serology (Brucellosis, Typhoid)
2- Stool for hatching test, serology, cathodic\anodic Abs
3- U\S → PERIPORTAL FIBROSIS - Portal vein diameter
4- Endoscopy for esophageal varices
5- CBC & B.M biopsy for: blastcells and immunohistochemistery
6- CXR \ECG \ ECHO---for complication of Schitosomiasis ( pul. HTN , tricuspid
regurgitation)

C- If the patient develops hypersplenism give 3 criteria that help to diagnose this
condition?
1- Pancytopenia
2- Splenomegaly
3- Normal or hyper active BM
 Treatment of hypersplenism is splenectomy

D- Give 4 indications for splenectomy?

1- Surgical (emergency) → most common
2- Hereditary spherocytosis
3- G6PD deficiency
4- Hypersplenism
5- Sequestration crisis

44
 Treatment of Shistosomiasis
 Praziquentil 40 mg\kg
 Oxamniquine → for mansoni only
 Metrifonate → for hematopium only

4). A 25 years old from damazin was admitted to Khartoum hospital because of fever
which is for 3 months, his appetite was little affected, he had lost moderate amount of
weight, he had dry cough, his past medical history was otherwise not significant.
O/E:- The patient was found to be febrile, ill and anemic, his CVS , RS were normal.
Abdomen: - liver was enlarged 4 cm bcm, firm, the spleen was 8 cm bcm firm, no
ascites, there were bilateral inguinal lymphadenopathy discrete and firm.

Questions:-
A- Mention probable causes of his problem?
 VIS. LESHMENIASIS, CML, Military TB, Chronic brucellosis - Hodgkin lymphoma

B- Discuss the mechanism of hepatosplenomegaly in this pt.

Kuppfer cell hyperplasia
C- Mention 6 important investigations which will help you to reach a final diagnosis?
SEE ABOVE

5). A 22 years old Sudanese girl who lived in Banat in since she was 5 years old in her
holiday in Sudan she complained of a constant frontal headache with fever which had
been presented for ten days. Treatment with chloroquine in full dose had not produced
any improvement, on enquiry she complained of anorexia, abdominal discomfort and
constipation. She had a dry cough and muscular aches and pains. On physical
examination she looked ill and had rather sunken facies.
Vital signs: - Temp 40 C. PR 92 beat/min BP 120/70 mm Hg. RR 18/min.
On abdominal palpation there was generalized abdominal tenderness, but no rigidity or
guarding, Bowel sounds were present, her spleen was palpable at 2 cm below the left
costal margin.
Investigations: - Hb 11g/dl, WBC 2.1 x 109 L-1, CXR and urine microscopy were all
normal. BFFM is negative.

45
 Questions: -
A- What is the most likely diagnosis?
Typhoid fever

B- How would you confirm this diagnosis?

SEE ABOVE
C- What complication may occur? ( mention two )
D- What is the correct treatment? Mention the drug, dose and duration of treatment.
Ciprofloxcicine 500mg BDS for 1-2 wks → not given to pregnant (cartilage damage) or
epileptic pt.

 N.B.
 Chloramphicel → idiosyncratic aplastic anemia
 Cotrimoxazol → Steven Jonson syndrome
 azithromycin (MDR) → used in pregnants & children
 Steroids are given to severely ill pts.

6). Male of 35 yrs old presented with 4 months history of increasing weakness, tiredness
and fatigability, his appetite is normal but lost 4 kilos of weight in the past 4 months.
Bowel habit was normal and no urinary symptoms. He denied cough, dyspnea, chest
pain headache or blurring of vision.
O/E:- He had asthenic built, BP 100/50, pulse 80 beat/min regular, pale but not
jaundiced or cyanosed, no clubbing or edema. JVP not raised, there were some brown
discolorations of the mucus surface of his lips and buccal mucosa, the teeth and gums
are normal.
CVs
RS NAD
GIT
CNS

Questions:-
A- What is the most likely diagnosis?
Addison disease

46
B- Give 5 possible causes for this condition?
Primary Addison’s:
1- Autoimmune (most common)
2- TB (most common in Sudan), Anti -Tb
3- Sarcoidosis
4- hemochromatosis
5- Water-house- Friederichsen’s syndrome (Meningiococemia)
6- Nelson syndrome
7- HSV
Secondary: iatrogenic → sudden steroid withdrawal

C- Mention 5 investigations which will help you in your diagnosis?

1- blood
 CBC → leukocytosis—eosinophilia
 RFT → pre renal failure
 Electrolytes level→ hyponatremic – kalemic alkalosis
 Serum cortisol→ ↓
 Blood glucose→ ↓
2- Short ACTH stimulation test (Synacthen):
 Give I.M or I.v ACTH then measure the plasma cortisol level →
if increased the test is +ve then:
 If ACTH level is elevated → 1ry adrenal insufficiency
 If ACTH level is normal or low → 2dry adrenal insufficiency

3- Imaging → abdominal CT or US
 Large adrenal → malignancy, amyloidosis.
 Calcification in adrenal gland→ TB
4- HIV screening
5- CXR & manteaux test for TB
6- Serology → Abs against 21 alpha hydroxylase enzyme if +ve do autoimmune
screening:
7- Autoimmune screening → thyroid, celiac disease, pernicious anemia, DM.

D- Mention 3 drugs used in this condition?

Acute phase → hydrocortisone, methotrexate, Prednisolone, fludrocorticoid

47
 Then follow up:
 Steroids
 Give steroid card and advise wearing a bracelet declaring steroid use.

7). A 35 years old man was brought to the causality with 7 days history of fever chills,
backache, headache, and arthralgia. There was no history of cough, chest pain,
palpitation, urinary or bowel symptoms.
O/E:- The patient oriented, BP 140/85, pulse 98 heat/min regular, temp 39C
The patient was sweaty, no anemia, cyanosis or jaundice.
CVS, RS were normal.
Abdomen: - the spleen is moderately enlarged and soft, liver is not palpable.
Lymph node in the axillary region are soft, discrete and tender, there was tenderness
over the spine and both sacroiliac joint.
Questions: -
A- What is the most likely diagnosis?
Acute Brucellosis
 Groups at risk: Farmers, Butchers, Medical staff

B- Give other 2 important differential diagnoses?

Malaria, military TB, visceral leshmeniasis (no joint involvement)

C- Name 3 blood test to help in diagnosis?

1- General:
 CBC: leucopenia with relevant lymphocytosis
 ESR CRP: ↑↑
2- DAT:
 Widal test→ high titer or rising titer
3- Blood culture - PCR (90%) - Bone marrow (not affected by use of Abx)

D- Mention 5 major complications of this diagnosis?

1- Neurobrucellosis meningitis , encephalitis ,psychosis→ suicide( most common
cause of death)
2- Endocarditis
3- Sacroilitis , arthritis

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 4- Epidydemitis, orchitis, cord compression
5- Liver→ abscess, necrosis, hepatitis
6- Uveitis
7- Respiratory→ pneumonia

E- Name 3 drugs used in the treatment of this condition?

1- Doxycycline + streptomycin → 6wk
 If no response doxycycline+ rifampicin → 6wk
 If major complication occur continue for 6 mnth
2- Pregnancy → Rifampicin
3- Children → Cotrimoxazol +Rifampicin
 Surgery for abscess, joint effusion

8). A 30 years old male developed polyuria and increased thirst for the last 2 months, he
passed large amount of urine with day/ night frequently 6-8/2-3, no history of loss of
appetite or wt loss. No history of past illness. He was not taking any drugs, he appear to
be fit BP 130/75, pulse 74 and regular, JVP is not raised, no edema, clubbing, thyroid or
lymphadenopathy
CVS, RS , GI, CNS were normal.
Investigations: - Normal blood glucose, calcium, urea and electrolytes. Urinary
osmolality was low.
Questions:-
A- What the most likely diagnosis?
Diabetes Insipidus
B- Give 6 causes of polyuria?
1- DI
2- DM
3- Psychogenic polydipsia
4- polyuric phase of Chronic renal failure
5- alcohol overdose
6- drugs → thiazide

C- If blood glucose was found to be 400mg /dL mention 4 drugs which can be used to
treat this condition?
49
 1- Insulin
2- Metformin
3- Sulfonylurea(glibenclamide)
4- Glituzone
5- Glycosidase inhibitor
6- Glib tins
7- Meglibrimide

How to test for DDx of D.I:

1- Water deprivation test ( 8 hours):
 if urine concentrated → NOT DI
 if urine NOT concentrated → DI
2- Then give ADH:
 if urine concentrated → Central DI
 If urine NOT concentrated peripheral (nephrogenic) DI.

CAUSES OF DI:
A- Central DI:
1- Craniopharingioma
2- Post-surgery
3- Trauma
4- TB
5- Sarcoidosis
6- Granulomatous disease
B- nephrogenic DI:
1- Electrolyte disturbance(most common)
A. Any cause of hypokalemia(↓K⁺)
B. Any cause of hypercalcaemia (↑Ca)
2- Congenital
3- Renal disease
4- Sickle cell disease
5- Drugs: lithium, demeclocyclin

Management of DI:
 Central → good hydration + desmopressin
 Nephrogenic → good hydration + thiazide.

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10). A 29 years old female presented with a 6 weeks history of weight loss, painful ankles,
weakness and fatigue. Her appetite is depressed, no history of chest pain, cough or
palpitation, she had experienced redness over her cheeks in the past 10 days.
O/E: - BP, Pulse, Temp were normal, not pale or jaundice, no thyroid or lymph node
enlargement. She had an erythematous rash over her face covering both cheeks and the
center of the nose. Joints of the hands and ankles appear somewhat swollen but their
movement was satisfactory.
CVS, RS, CNS, NAD
Abdomen: - spleen was 2 cm bcm, tender, liver was not enlarged no ascites.
Skin: - There was loss of hair in the scalp with some vasculitic rash.
Questions:-
A- What the most likely diagnosis?
SLE
B- Mention 3 investigations to confirm the diagnosis?
C- Mention 4 main features of this condition not present in this lady?

Criteria for SLE:

Useful mnemonic A RASH POINTS AN MD
1- Non erosive Arthritis → involving ≥2 peripheral joints
2- Renal disorders → persistent proteinuria or cellular casts.
3- Antinuclear Abs (ANA): +ve in 95%
4- Serositis → Pleuritis, Pericarditis
5- Hematological:
 hemolytic anemia or
 leukopenia on ≥2 occasions or
 lymphopenia on ≥2 occasions
 Thrombocytopenia in the absence of drug effects.
6- Photosensitivity
7- Oral ulcers → recurrent usually painless
8- Immunological disorder:
 Anti-dsDNA Abs
 Anti-smooth muscle Abs
 Ant phospholipid Abs
9- Neurological disorders: seizures, psychosis.

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 10- Malar (butterfly) rash
11- Discoid rash

Gastroenterology
1). A 47 yrs old female was admitted with history of nausea, vomiting and jaundice for 2
weeks, she had low grade fever with rigor .she denied any previous systemic illness or
blood transfusion.

O/E: she was wasted, febrile, moderately jaundiced not pale, no clubbing or
lymphadenopathy.
CVS NAD,
RS NAD

Abdomen: liver was 6cm bcm enlarged and tender, smooth and regular edges, no
splenomegaly or ascites

Questions:
A- What is the most likely diagnosis?
Acute hepatitis most likely viral hepatitis
 2 wks duration → acute
 2—4 wks → sub acute
 <4 wks → chronic
- Tinge of jaundice (lemon like) → hemolytic ( jaundice + pallor)
- yellow → hepatic
- Deep golden→ post hepatic

In the case:
 No clubbing → no chronic liver disease
 No lymph nodes → no sero –ve hepatitis (CMV - EBV)

Causes of hepatitis:
1- Viral
2- Autoimmune:
 Female
 DM 1

52
  Anemia
 Menstrual disturbances (premature ovarian failure)
3- Alcohol
4- Drugs: paracetamol, methyl dopa, anti TB except streptomycin, anticonvulsants,
antifungal, antibiotics, pethidine, contraceptives.
5- Metabolic:
 Wilson’s D {not associated with HCC}
 Hemochromatosis
 Alpha 1 antitrepsin deficiency

DD of tender hepatomegaly:
1- Infections:
 parasites (Ameobic L.A - infected hyadatid cyst)
 Bacteria (……………..)
 Viruses (viral hepatitis)
2- Non infectious: congestive hepatomegaly (Rt sided heart failure, congestive
heart failure, Budd chiari syndrome, constrictive pericarditits, pericardial
efussion)
3- Others: (HCC, poly cystic liver disease, autoimmune, alcohol)

 In hepatitis remember to ask for:

1- Blood transfusion
2- Recent contact
3- Joint pain, rash, malaise
4- Odd relationship
5- Drug abuse
6- Vaccination

N.B other DD of this case is Primary biliary cirrhosis

B- Name other 3 symptoms could be asked for to help in diagnosis?

1- Symptoms of anemia
2- Extra hepatic manifestations (joint pain, rash, malaise)
3- Obstructive symptoms

C- Name 2 other signs help you in confirming the diagnosis?

1- signs of chronic liver disease

53
 2- signs of decompensated liver disease (ascites, encephalopathy, edema)
3- other : (scratch marks , joint swelling, Kayser Fischer ring, bronze skin
pigmentation, drug injection site)

D- Name 4 other investigations you should ask for?

Investigations to prove this is liver disease:

1- LFT, Albumin, PT, INR → To assess the synthetic function.
 state of biliary tree (alkaline phosphatase)
 State of hepatocytes (transaminase)
2- Serum Bilirubin (secretory function)
3- USS
4- Urine analysis (bilirubin)

Investigations to know the cause:

 PCR (hep C) , HBsAg , serology (hep E, CMV), monogput test (EBV)
 Auto Abs → (ANA, ASMA),
 Urinary copper

Base line investigations: CBC, Glucose (impaired), RFT(imp)

Treament→ Supportive:
IV fluids, bed rest, good diet (no diet restriction) , stop unnecessarily drugs

2). A 53 yrs old man from Deleng gave a three months history of pain and swelling in the
upper abdomen. Together with distension, flatulence, nausea and anorexia, he was
constipated and had lost 10 kg during the previous three months. He gave a history
suggestive of previous malaria.
O/E:- He appeared ill and emaciated but was a febrile. He was not jaundiced. The liver
was enlarged and tender, extending to about 9 cm bcm, enlargement seemed to be
confined to the left lobe which was hard and a solid feel. There was shitting dullness,
but fluid thrill could not be elicited.
Investigations:-
Hb = 7.9 g/dl. TWBC= 7900/cum. ESR 70mm/hr. Serum bilirubin & AST were normal.
Alkaline phosphatase was 30 KA unit/dl.

54
Questions:-
A- Mention 3 most likely diagnoses?
1- Primary HCC,
2- Secondary HCC, Schistosomiasis,
3- pyogenic (Ameobic L.A)

 Left lobe enlargement → Schistsoma, HCC

 Hard, irregular→ secondary mets
 Bruit → HCC, hemangioma, alcoholic hepatitis

- The most common cause of HCC is liver cirrhosis

- HBV, aflatoxin → can cause HCC without cirrhosis
alphaprotien is used in:
 great cell tumor,
 gonadal cancer

B- What other physical signs that could be elicited in such a case?

1- Stigmata of chronic liver disease
2- Features of compensated liver disease
3- Bruit in auscultation

 HCC → causes Paraneoplastic Syndrome:

 Polycythemia → erythropoiten
 Hyperglycemia → insulin like growth factor
 Hypercalcemia → Parathyroid hormone
 Porphyria
 Hyperlipidemia
 Other signs of malignancy: Virchow LNs, Sister Mary- Josef LN

C- What other investigation that you carry out & discuss the relevance of their
investigation to the diagnosis mentioned.
1- Baseline Investigations:
 CBC (polycythemia), LFT, RFT, clotting profile, glucose
2- USS, USS guided biopsy (liver features, ascites, biliary system)
3- Triphasic CT → DIAGNOSTIC

55
 4- Alpha feto protein → increased
 N.B: Ovarian CA = CA125, Pancreatic CA = CA19
5- Upper GI endoscopy and biopsy→ Stomach CA
Lower GI endoscopy and biopsy → Colonic CA

Note:
 smooth surface → acute hepatitis, Rt sided HF
 nodular → HCC
 firm→ abscess

3). A 36 years old male came to the outpatient complaining of discomfort at the Rt upper
abdomen with malaise and swinging fever for 2 weeks, he also had a cough, pain felt in
the Rt shoulder, he had nausea, vomiting, the bowel habits were normal, he lost some
of his weight.
O/E: - looked ill, febrile but not pale or jaundiced.
CVS, RS, NAD
Abdomen:- spleen is not enlarged, liver was enlarged and tender, point tenderness in
the lower Rt intercostals space was present, no ascites.
TWBCs was increased.
Questions:-
A- What is the most likely diagnosis?
Ameobic liver abcess

 Point tenderness is characteristic for:

1- ALA
2- Pyogenic associated with infection e.g acute appendictitis, Mickel diverticulitis,
umbilical sepsis

B- Give one important differential diagnosis?

1- Pyogenic liver abcess
2- Infected hydatid cyst

N.B: GIT symptoms are present in 20% of patients with ameobic liver abcess.

C- Give other 2 investigations to confirm the diagnosis?

1- Imaging: US abdomen – Ct scan abdomen
2- Aspiration of abcess → Anchovy sauce
56
 3- Baseline CBC → Neutrophil leukocytosis
4- Serology → direct haemagglutination test – ELISA
5- Stool analysis → cyst

D- Mention 3 drugs used in the treatment of this condition?

 Trophozoite → Metronidaxole, Tinidazole
 Cyst → Dialoxide, chloroquine

Complications of ALA:
Rupture – Fistula – Pleural effusion – Pericardial effusion

4). A 28 yrs old man presented with 2 weeks history of cervical lymphadenopathy,
weakness, fatigue, night sweats and generalized pruritis. He has poor appetite and some
loss of weight, there was no history of cough, chest pain, no urinary or bowel symptoms.
O/E:- looked pale, temp 37.8C, BP 135/80, no clubbing, lymph node were enlarged in
the Lt anterior cervical and Lt axillary region.
CNS, Respiratory examinations were normal. No hepatosplenomegally or ascites, urine
analysis, ECG, CXR were normal, mantoux test was negative.
Questions:-
A- What is the most likely diagnosis?
Hodgkin’s lymphoma
 Hodgkin lymphoma has bimodal distribution( young 20-30 / old 50-60)
 Non-Hodgkin’s 45 years of age
 stage 2, 3 has bad prognosis
 Characteristic:
1- Generalized pruritis
2- Alcohol induced pain in the affected L.N ( 2-5%)
DDx of generalized pruritis:
1- Hodgkin’s lymphoma
2- Obstructive jaundice
3- Severe iron deficiency anemia
4- Anaphylaxis
5- Uremia
6- Polythycemia Rubravera ( after hot bath)
7- Scabes

57
DDx of drenching sweat → Brucella – T.B – Hodgkin’s Lymphoma
DDx of cervical lymphadenopathy → T.B – Lymphoma – Leukemia – Tonsillitis
DDx of PUO → Hodgkin’s – T.B – Leishmania

B symptoms Wt loss < 10%

(One is enough) Drenching seating
Fever < 38 C
Annarbar Classification (clinical):
Stage 1 → one group of L.N in one side of the diaphragm
Stage 2 → 2 groups of L.N in one side of the diaphragm
Stage 3 → Both sides
Stage 4 → reticulendithilial system
 A → no systemic symptoms
 B→ presence of systemic symptoms ( one symptom is enough).

B- Give 4 further investigations help in diagnosis and management?

1- General : ESR – CRP – LFT – RFT – LDH ( very high) –
2- Specific : CBC → Immature lymphocytes
Bone marrow aspiration :
Blast: < 25 leukemia
> 25 % lymphoma
Lymph node excisional biopsy
Histology → Reed- Sternberg cell
3- Staging investigations

C- What are the characteristic findings in histological examination?

Reed- Sternberg cell
D- Mention 4 drugs used in the treatment of this condition?
 1,2 → Radiotherapy
 3 or B or depleted lymphocyte type (poor prognosis) → chemotherapy
Chemothreputic drugs: Actinomycin, Bleomycin, Vinblastine, Darbazine

58
5). A 45 years old lady was referred from Rabak with a 6 months history of intermittent
jaundice. She was anorexic and vomited occasionally. She had no itching and her bowel
habits were normal.
O/E:- She looked unwell and was deeply jaundiced, her pulse was 78 beat/min regular.
BP 140/90. No palpable lymph nodes. The liver was enlarged and tender with a smooth
surface.
Investigations:-
Blood count & ESR were normal
LFs:-
- AS 240 u.L ( normal 15 – 40 )
- Alkaline phosphatase 78 u.L ( Normal 25-115)
- Total serum bilirubin 16mg/dl
- Total protein 96gm.L ( Normal 62-80)
- Hepatitis Bs Ag negative ,Hepatitis C antibodies Negative

Questions: -
A- What other relevant information in the history would you like to obtain?
Rash – arthritis – amenorrhea – fever

B- What further physical signs would you look for? Mention two.
Features of chronic liver disease – features of decompensation

C- What further investigation would you arrange? Mention three.

1- CBC → pancytopenia
2- Liver biopsy → mononuclear infiltration of portal and peripheral areas +
piecemeal necrosis.
3- Detection of Abs ( ANA, ASMA, LKM1)
4- MRCP to exclude primary biliary cirrhosis

D- What the most likely diagnosis?

Autoimmune hepatitis

59
E- Considering the most likely diagnosis, outline your management of the patient.
1- Supportive
2- Immunosuppressant : prednisolone, azathioprine
3- Liver transplant

‫ بالتوفيق‬

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