Past quest with answer

Question 1

Discuss the causes, pathophysiology, clinical manifestations and investigations of a 50-year-old male patient with chronic liver disease presenting with ascites. (32 marks)

Causes of chronic liver disease (TIMBHO)

1) Toxins – alcohol, drugs (methotrexate)

2) Infection – usually chronic viral Hepatitis B & C

3) Metabolic disease – hemochromatosis, Wilson’s dzz, α-1 antitrypsin

4) Biliary obstruction – 1°/2°(stone,neoplasm) biliary cirrhosis

5) Hepatic venous congestions – cardiac failure, Budd-Chiari malformation

6) Others – autoimmune chronic active hepatitis

Pathophysiology

Under normal circumstances, the portal vein carries blood from the gut & spleen to the liver. Blood vessels enter the liver via hilum and blood passes into the hepatic sinusoids via portal tracts and leave liver through hepatic veins to join the inferior vena cava.

In chronic liver disease, the inflow of portal blood is impeded due to liver parenchymal damage, leading to high pressure in the portal vein causing portal hypertension.

Ascites develop by 3 main mechanisms

1. Portal hypertension

Portal hypertension directly exerts a local hydrostatic pressure which leads to increased transudation of fluid into the peritoneal cavity. It also causes splanchnic vasodilatation, which is mediated by vasodilators (mainly NO₂) which causes shunting of blood into the systemic circulation.

2. Sodium & water retention

Systemic arterial pressure falls due to pronounced splanchnic vasodilatation, and this leads to poor renal perfusion. This results in activation of Renin Angiotensin System with secondary aldosteronism and other neurohumoral pressor system thus promoting sodium and water retention.

3. Hypoalbuminaemia

Poor synthetic function of the liver leads to low serum albumin. This causes low plasma colloid oncotic pressure and increased transudation of fluid due to unopposed hydrostatic pressure in the blood vessels and deficient reabsorption of ascitic fluid.

Clinical manifestation

Symptoms:

· Usually are asymptomatic/ complain of non-specific symptoms particularly fatigue

· More specific symptoms :

ü Right hypochondrial pain – liver distension

ü Abdominal distension & ankle swelling – fluid retention

ü Haematemesis & malaena – GI haemorrhage

ü Pruritus- cholestasis (usually in PBC)

ü Breast swelling, loss of libido – endocrine dysfunction (impaired oestrogen metabolism)

ü Confusion & drowsiness- portosystemic encephalopathy

Physical signs:

1) Hand – clubbing, leukonychia, Dupuytren’s contracture, palmar erythema, hepatic flap, scratch marks, tendon xanthoma

2) Face - Eye -jaundice, xanthelasma, pallor of the conjunctiva, Kayser-Fleischer ring

- Mouth – fetor hepaticus, parotid enlargement, signs of IDA (angular stomatitis, glossitis)

3) Neck - supraclavicular & cervical lymphadenopathy

4) Chest – spider naevi, gynaecomastia, loss of axillary hair

5) Abdomen - dilated veins (caput medusa), everted umbilicus, hepatomegaly, splenomegaly, shifting dullness, fluid thrill

6) Genitalia – testicular atrophy, PR- haemorrhoids

7) Lower limbs – Pitting pedal oedema, pigmented ulcers.

Investigation

v Haematological investigation

Full blood count – looking at the haemoglobin, MCV, MCH white blood cell and platelet

· Normochromic, normocytic anaemia – gastrointestinal hemorrhage

· Chronic blood loss – hypochromic microcytic anemia 2° to iron def

· Alcohol causes macrocytic, sometimes with leucopenia and thrombocytopenia

· WBC- leukocytosis- infection (*SBP)

· Thrombocytosis- may occur in those with active haemorrhage

v Biochemical investigation

1. Liver function test

· Serum albumin – low

· Prothrombin time – preceded by giving IV bolus of vit K – prolonged

2. Liver biochemistry

· Serum AST & ALT – reflecting hepatocellular damage if increased

· Serum ALP and GGT – reflecting cholestasis (PBC)

3. Renal function test

· Watch for any signs of hepatorenal syndrome – high urea & creatinine , and low sodium

4. Viral serology

· Hepatitis B – HbsAg, HbeAg, HBVDNA

· Hepatitis C – HCV DNA

5. Tumour markers – α FP

6. Serum autantibodies

· Antimitochondrial Ab –PBC

· Smooth muscle Ab, ANF – autoimmune hepatitis

7. Ascitic fluid analysis – cytology

8. Serum & urinary copper & serum caeruloplasmin – Wilson’s disease

9. α-1 antitrypsin screening – α-1 antitrypsin deficiency

v Imaging

· Ultrasound liver – nodular liver (cirrhosis) / hepatoma

· Cholecystogram - PBC

· Upper GI endoscopy – esophageal varices/peptic ulcer

Question 2

27-year-old, Chinese – fever, severe headache x 2/52, confusion x 2/7

Examination – T=38⁰c, drowsy, disoriented, oral thrush, neck stiffness, (↑reflexes, upgoing plantar reflex) x right side

a. 3 likely diagnoses and reasons (6 marks)

1. Meningitis – fever (infection), symptoms of meningism (neck stiffness, headache),drowsiness, signs of localized UMN lesion (common in tuberculous meningitis), oral thrush – suspect immunocompromised (risk factor for meningitis)

2. Brain abscess – symptoms of ↑ICP (headache, confusion), fever (infection), and signs of localized UMN lesion

3. Encephelitis – may present with signs of meningism, fever, drowsiness and rarely with localizing features

b. Issues on obtaining consent for investigations in this patient (6 marks)

- Before obtaining consent, the physician has to make sure that the patient is capable of giving consent. The patient is said to be capable if he or she is able to understand the information that is relevant to making a decision about the treatment and must be able to appreciate the reasonably foreseeable consequences of a decision or a lack of decision

- Clinically, if a patient knows who they are, where they are, what are being proposed, and the consequences of the decision they are being asked to make, it is likely safe for a physician to rely on the presumption that the patient is capable.

- If the patient is not capable, informed consent must be obtained whenever possible, from a legally entitled representative (the next of kin).

- If a legally entitled representative is not available, but a medical intervention is urgently needed, consent of the patient may be presumed, unless it is obvious and beyond any doubt on the basis of the patient's previous firm expression or conviction that he would refuse consent to the intervention in that situation.

c. CXR and Ix results interpretation (12 marks)

- CXR – well demarcated consolidation in middle zone of right lung(on AP view), the consolidation is fully radiopaque with no fluid level inside – in this case, highly suggestive for old TB consolidation – fibrosed inactive TB consolidation

- Mantoux test – +ve (≥5mm) because suspected inmmunocompromise due to presence of oral trush – not so specific – false +ve in immunized pt(look for BCG scar), non-tuberculous mycobacteria exposure

- CT, RBS ↔

- CSF – pressure ↑(SAH, bacterial, tuberculous meningitis), WBC ↑, Lymphocyte ↑(viral, tuberculous meningitis), protein ↑(bacterial, tuberculous meningitis) glucose ↓(all except viral)

*Typical CXR presentation for TB

Chest X-Ray Findings that Can Suggest ACTIVE TB

An applicant with any of the following findings must submit sputum specimens for examination.

1. Infiltrate or consolidation—Opacification of airspaces within the lung parenchyma. Consolidation or infiltrate can be dense or patchy and might have irregular, ill-defined, or hazy borders.
2. Cavitary lesion—dark area (lucency) within the lung parenchyma, with or without irregular margins that might be surrounded by an area of airspace consolidation or infiltrates, or by nodular or fibrotic (reticular) densities, or both. The walls surrounding the lucent area can be thick or thin. Calcification can exist around a cavity.
3. Nodule with poorly defined margins (tuberculoma)— Nodules included in this category are those with margins that are indistinct or poorly defined. The surrounding haziness can be either subtle or readily apparent and suggests coexisting airspace consolidation.
4. Pleural effusion—Presence of a significant amount of fluid within the pleural space. This finding must be distinguished from blunting of the costophrenic angle, which may or may not represent a small amount of fluid within the pleural space (except in children when even minor blunting must be considered a finding that can suggest active TB).
5. Hilar or mediastinal lymphadenopathy (bihilar lymphadenopathy)—Enlargement of lymph nodes in one or both hila or within the mediastinum, with or without associated atelectasis or consolidation.
6. Other—Any other finding suggestive of active TB, such as miliary TB. Miliary findings are nodules of millet size (1 to 2 millimeters) distributed throughout the parenchyma.

Chest X-Ray Findings that Can Suggest INACTIVE TB

This category includes findings that are suggestive of prior TB that is inactive. It must be remembered that assessments of the activity of TB cannot be made accurately on the basis of a single radiograph alone. If there is any question of active TB especially if the applicant has any signs or symptoms of TB, sputum smears must be obtained.

1. Discrete fibrotic scar or linear opacity—Discrete linear or reticular densities within the lung. The edges of these densities should be distinct and there should be no suggestion of airspace opacification or haziness between or surrounding these densities. Calcification can be present within the lesion and then the lesion is called a “fibrocalcific” scar.
2. Discrete nodule(s) without calcification—One or more nodular densities with distinct borders and without any surrounding airspace opacification. Nodules are generally round or have rounded edges. These features allow them to be distinguished from infiltrates or airspace opacities. To be included here, these nodules must be noncalcified
3. Discrete fibrotic scar with volume loss or retraction—Discrete linear densities with reduction in the space occupied by the upper lobe. Associated signs include upward deviation of the fissure or hilum on the corresponding side with asymmetry of the volumes of the two thoracic cavities.
4. Discrete nodule(s) with volume loss or retraction—One or more nodular densities with distinct borders and no surrounding airspace opacification with reduction in the space occupied by the upper lobe. Nodules are generally round or have rounded edges.
5. Other—Any other finding suggestive of prior TB, such as upper lobe bronchiectasis. Bronchiectasis is bronchial dilation with bronchial wall thickening

*Mantoux test interpretation

5mm or more is positive in

- HIV-positive person

- Recent contacts of TB case

- Persons with nodular or fibrotic changes on chest x-ray consistent with old healed TB

- Patients with organ transplants and other immunosuppressed patients

10mm or more is positive in

- Recent arrivals (less than 5 years) from high-prevalence countries

- IVDU

- Residents and employees of high-risk congregate settings (e.g., prisons, nursing homes, hospitals, homeless shelters, etc.)

- Mycobacteriology lab personnel

- Persons with clinical conditions that place them at high risk (e.g., diabetes, prolonged corticosteroid therapy, leukemia, end-stage renal disease, chronic malabsorption syndromes, low body weight, etc)

- Children less than 4 years of age, or children and adolescents exposed to adults in high-risk categories

15mm or more is positive in

- Persons with no known risk factors for TB

(Note: Targeted skin testing programs should only be conducted among high-risk groups)

*CSF interpretation

	Normal	SAH	Bacterial M	Viral M	Tuberculous M
Pressure	50 – 180mm	↑	↔/↑	↔	↔/↑
Colour	Clear	Blood stained (xanthochromic)	Cloudy	Clear	Clear/cloudy
RCC	0-4x106/L	↑	↔	↔	↔
WCC	0-4x106/L	↔/slightly ↑	↑(PMN)	↑(lymphocyte)	↑(lymphocyte)
Glucose	>60% of blood level	↔	↓	↔	↓
Protein	<0.45g/L	↑	↑	↔/↑	↑
Microbiology	-	-	+ on gram stain/culture	-/+	Ziehl-Nielson stain/culture +

d. 5 relevant Ix and give reasons (6 marks)

1. CT thorax – better image of the lump – site, size, consistency, extension

2. Blood culture and sensitivity especially for AFB and Zeihl-Nelson culture

3. CSF for acid fast bacilli (AFB) and Zeihl-Nelson culture

4. HIV blood test – risk factor (esp with the presence of oral thrush – common in immunocompromised people)

5. Blood and urine samples for toxin screening for drugs and alcohol

2^nd day of admission – headache worsen, vomit bilious material x2, cough

Examination – T 39⁰c, fundoscopy – bilateral papilloedema, BP 120/70mmHg, PR 90bpm, RR 20bpm, lung – crepitation in middle zone of right chest

e. Explanations for these new development (4 marks)

- Headache, vomiting, bilateral papilloedema - symptoms and signs of ↑ICP – may be due to spread to the cerebral hemisphere (encephalitis) due to nosocomial infection during LP

- ↑ICP may be precipitated by infection introduced during LP

- Develop cough after vomiting → aspiration pneumonia – causing chemical irritation in right side, middle zone (common site)

f. 2 further Ix (4 marks)

1. Brain imaging – CT scan or brain MRI

2. Chest radiograph – to look for underlying cause of his cough

*side effect of lumbar puncture – serious side effects are remarkably rare

- Headache with nausea (spinal headache) – 40% - start within 48 hours and resolves spontaneously within 5 days- responds to analgesics and infusion of fluids and can often be prevented by strict maintenance of a supine posture for two hours after the puncture

- Other side effects that together occur in about 0.3% (1 in 330) of people include the following:

- prolonged headache lasting longer than 7 days (by far the most most common of the rare occurrences on this list

- infection

- nerve root irritation, herniation or transecton

- injury to one of the nerves that exit directly from the head (known as cranial neuropathies

- bleeding (in the head, spine or locally)

- low back pain

- uncal or tonsillar herniation, reversible tonsillar descent or spinal coning depending on which part moves; extremely rare but very serious

- fainting