Ticket N 12 - Propaedeutics of Internal Diseases: Full Answers

1. General Examination Data of Patients with Liver Diseases

Skin and Mucous Membranes

• Jaundice - yellow discolouration of sclera, skin, and mucous membranes due to hyperbilirubinaemia (>34 µmol/L). Pre-hepatic (haemolytic): lemon-yellow. Hepatic: bright yellow. Obstructive (cholestatic): green-yellow.
• Spider angiomata (spider naevi) - dilated arterioles with radiating vessels, found in the SVC territory (face, neck, upper chest, arms). Caused by elevated oestrogens from impaired hepatic metabolism. >5 spiders = significant liver disease.
• Palmar erythema - redness of thenar/hypothenar eminences, also from excess oestrogens.
• Pruritus with scratch marks - especially in cholestatic disease, due to bile salt deposition.
• Caput medusae - dilated periumbilical veins as portosystemic collaterals in portal hypertension.
• Xanthelasmas / xanthomas - in chronic cholestasis (PBC) due to hypercholesterolaemia.
• Dupuytren's contracture - fibrosis of palmar fascia, associated with alcoholic liver disease.

Face and Eyes

• Scleral icterus - earliest sign of jaundice.
• Kayser-Fleischer rings - golden-brown rings at corneal periphery in Wilson's disease (copper deposition).
• Parotid enlargement - in alcoholic liver disease.

Hands and Nails

• Leuconychia (white nails) - hypoalbuminaemia.
• Terry's nails - white proximally, red-brown distally; liver cirrhosis.
• Clubbing - in hepatopulmonary syndrome and biliary cirrhosis.
• Asterixis (liver flap/flapping tremor) - coarse, irregular tremor of outstretched hands; indicates hepatic encephalopathy (metabolic flap).

Body Habitus and Other Signs

• Gynaecomastia and testicular atrophy - excess oestrogens in males with cirrhosis.
• Loss of body/axillary hair - hypo-oestrogenism paradox in females, hypo-androgenism in males.
• Muscle wasting - sarcopaenia common in cirrhosis.
• Oedema - peripheral pitting oedema from hypoalbuminaemia.
• Ascites - abdominal distension, shifting dullness, fluid thrill (portal hypertension + low oncotic pressure).
• Fetor hepaticus - musty, sweet breath from mercaptans produced by gut bacteria; sign of portosystemic shunting.
• Bruising/petechiae - coagulopathy (impaired clotting factor synthesis).

2. S3 and S4 Heart Sounds, Mechanism of Occurrence, Diagnostic Value - Gallop Rhythm

The Fourth Heart Sound (S4)

• Timing: just before S1 (presystolic), i.e., late diastole
• Quality: low-pitched, heard best at the apex with the bell of the stethoscope; patient in left lateral decubitus
• S4 is never present in atrial fibrillation (no atrial contraction occurs)

• Left ventricular hypertrophy (systemic hypertension, aortic stenosis, hypertrophic cardiomyopathy)
• Acute myocardial infarction / active myocardial ischaemia
• Restrictive cardiomyopathy (early)
• Right-sided S4: pulmonary hypertension, pulmonary stenosis - heard at the left lower sternal border, increases with inspiration

The Third Heart Sound (S3)

1. Pathological S3 - high left atrial pressure drives blood rapidly into a stiff, over-loaded LV. The LV diastolic pressure rises steeply (restrictive or pseudo-normal filling pattern - grade III/IV diastolic dysfunction). Indicative of elevated LV filling pressures and heart failure.
2. Physiological S3 - vigorous ventricular relaxation in young, healthy individuals "sucks" blood in with enhanced tissue Doppler velocities. Normal in children, adolescents, athletes, and pregnant women. After age 40, an S3 is almost always pathological.

• Quality: low-pitched, heard at apex with bell, left lateral decubitus position
• Correlates with high E:A ratio and short deceleration time on transmitral Doppler

• Dilated cardiomyopathy / systolic heart failure (most common)
• Severe mitral regurgitation
• Constrictive pericarditis (pericardial knock - slightly earlier, slightly higher pitched than typical S3)
• Volume overload states

Gallop Rhythm

3. Syndrome of Fluid Accumulation in the Pleural Cavity (Hydrothorax / Pleural Effusion)

Definition

Classification by Pathophysiology (Light's Criteria)

Causes

• Transudates: heart failure (most common), hepatic hydrothorax (cirrhosis with diaphragmatic defects, 5-10% of cirrhotics - typically right-sided, 85%), nephrotic syndrome, hypothyroidism
• Exudates: parapneumonic, malignancy (lung, breast, lymphoma), tuberculosis, pulmonary embolism, rheumatoid arthritis, SLE

Clinical Findings (Syndrome description)

• Inspection: decreased respiratory movement on affected side, bulging intercostal spaces in large effusion
• Palpation: reduced chest expansion, tactile fremitus decreased/absent (fluid transmits vibration poorly)
• Percussion: stony dull (absolute dullness) - characteristic of fluid; the upper border forms a curved Sokolov-Damoiso-Ellis line (higher laterally)
• Auscultation: breath sounds absent or markedly reduced; above the effusion - bronchial breathing and egophony (E-to-A change) due to compressed lung; pleural friction rub (in early/resolving exudative effusion)

• Shifting dullness on percussion when patient rolls (distinguishes from consolidation)
• Triangular area of Garland - tympanitic zone above the effusion on the same side (compressed but aerated lung)
• Grocco-Rauchfuss triangle - area of dullness on the contralateral side (mediastinal shift)

4. Coprogram - Diagnostic Value and Features in Enteritis, Colitis, Liver and Pancreas Diseases

Definition

Normal Stool Parameters

Features in Specific Diseases

Enteritis (Small Bowel Inflammation/Malabsorption)

• Consistency: liquid or mushy, large volume ("small bowel type" - large stool)
• Colour: yellow or yellowish-green (unabsorbed bile pigments), possibly grey-yellow
• pH: acidic (fermentation by intestinal bacteria on undigested carbohydrates)
• Microscopy: steatorrhoea (fat droplets - neutral fat, fatty acids, soaps), amilorrhoea (starch grains - iodine positive), creatorrhoea (undigested muscle fibres), mucus mixed throughout stool (not on surface)
• Chemical: increased fatty acids (>7 g/day = steatorrhoea), Sudan III staining positive
• Leukocytes: few (not an infectious enteritis)
• Significance: malabsorption syndrome - deficiency of digestive enzymes and/or reduced absorptive surface area

Colitis (Large Bowel Inflammation)

• Consistency: liquid or semi-formed, small volume, frequent ("large bowel type")
• Colour: with blood - red; purulent/mucus - grey-green
• pH: alkaline (protein putrefaction)
• Mucus: on the surface of or mixed with stool
• Macroscopic blood: present in ulcerative colitis, dysentery, amoebic colitis
• Microscopy: many leukocytes (pus cells, WBC), erythrocytes, colonocytes, mucus
• Occult blood: positive in ulcerative colitis, colorectal cancer
• No fat malabsorption (large bowel does not absorb fat)
• Significance: differentiates infectious colitis (many WBC, bacteria) from IBD

Liver Diseases

• Colour: acholic (clay-coloured, white-grey) stool in obstructive jaundice - complete bile duct obstruction prevents bilirubin/stercobilin from reaching the gut
• In haemolytic jaundice: very dark brown stool (excess stercobilin)
• In hepatocellular disease: pale stool during cholestatic episodes
• Fat: mild steatorrhoea possible in severe hepatic disease (reduced bile salt synthesis → poor fat emulsification)
• Occult blood: may be positive with oesophageal varices or portal hypertensive gastropathy (blood swallowed / enters GI tract)
• Stercobilin: reduced or absent in obstructive jaundice; excess in haemolysis

Pancreatic Disease (Exocrine Pancreatic Insufficiency)

• Most prominent finding: severe steatorrhoea
• Stool: grey, greasy, bulky, foul-smelling, oily sheen ("polyfaecal" - large volume)
• Consistency: paste-like or mushy, difficult to flush
• pH: neutral to acidic
• Microscopy (Sudan III stain):
  • Neutral fat drops (most specific for pancreatic insufficiency - lipase deficiency)
  • Fatty acid crystals
  • Soap deposits
• Creatorrhoea: undigested muscle fibres (protease deficiency)
• Amilorrhoea: starch granules (amylase deficiency)
• No leukocytes, no mucus (not an inflammatory process of the bowel)
• Quantitative stool fat (72-hr collection): >7 g/day confirms steatorrhoea; severe pancreatic insufficiency: >15-20 g/day
• Chymotrypsin/elastase-1 in stool: markedly reduced (diagnostic for exocrine pancreatic insufficiency)
• Significance: pancreatic exocrine insufficiency - chronic pancreatitis, pancreatic cancer, cystic fibrosis

Diagnostic Value Summary Table

Option 2 - Pharmacology of Bronchial Asthma

Question 1. Bronchodilating AND uterolytic effects have:

• Bronchodilation - relaxation of airway smooth muscle (used in asthma/COPD)
• Uterine relaxation (tocolysis) - used to arrest preterm labour (e.g., salbutamol, ritodrine, fenoterol, terbutaline)

• A1-adenosine receptor agonists - cause bronchoconstriction (A1 activation is not bronchodilatory)
• H1-antihistamines - reduce bronchospasm in allergic reactions but have no significant uterolytic (tocolytic) effect
• M-cholinomimetics (muscarinic agonists) - cause bronchoconstriction (not dilation) and increase uterine tone

Question 2. Bronchospasm can be caused by all of the following drugs, EXCEPT:

Question 3. A drug that dilutes sputum and facilitates its excretion:

• Stimulates serous cells of the bronchial glands → increases secretion of low-viscosity fluid
• Activates cilia (mucociliary clearance)
• Stimulates surfactant production by type II pneumocytes
• Reduces sputum viscosity, making it easier to expectorate

• Prenoxdiazine - antitussive (suppresses cough reflex); does not dilute sputum
• Betahistine - H1 agonist/H3 antagonist used for vertigo (Ménière's disease); no mucolytic action
• Butamirate - centrally-acting antitussive (cough suppressant); not a mucolytic
• Betamethasone - corticosteroid; anti-inflammatory; not a mucolytic/expectorant

Question 4. A drug for the basic therapy of asthma that blocks phospholipase A2:

• Prostaglandins (via COX pathway)
• Leukotrienes (via LOX pathway) - major mediators of bronchoconstriction

• Nimesulide - selective COX-2 inhibitor (NSAID); acts downstream of PLA2; can actually trigger aspirin-like bronchospasm
• Montelukast - leukotriene receptor antagonist (blocks CysLT1 receptor); acts even further downstream
• Cromoglycic acid - mast cell stabiliser; prevents mediator release but does NOT inhibit PLA2

Question 5. Prescribe a medication for the basic therapy of bronchial asthma

Budesonide (inhaled, e.g., Pulmicort Turbuhaler) 200 mcg/dose Inhale 1-2 puffs (200-400 mcg) twice daily (morning and evening) #1 inhaler (200 doses) Long-term use; reassess in 3 months

Budesonide/Formoterol 160/4.5 mcg per dose (Symbicort) 1-2 inhalations twice daily - for moderate-severe persistent asthma (ICS + LABA)

• Budesonide is a WHO Essential Medicine and the preferred ICS for asthma (also the only ICS with sufficient safety data in pregnancy)
• Mechanism: inhibits PLA2 via lipocortin → reduces airway inflammation, mucus hypersecretion, and bronchial hyperreactivity
• Controller ≠ reliever: a separate SABA (e.g., salbutamol 100 mcg, 1-2 puffs PRN) should be prescribed for acute relief

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