Hepatobiliary II

Question 1

Acute Hepatitis VS Chronic Hepatitis histo

Answer 1

BOTH SAME mononuclear lymphocytic inflitrate
- lymphplasmacytic
Chronic is just denser inflitrate

Acute - Lobular Hepatitis; ballooning, apoptosis
Chronic 6 mths - Portal Hepatitis: fibrosis, cirrhosis, ductular reaction. Portal bridging fibrosis

Question 2

TB description [4]

Answer 2

Granulomatous Inflammation
Epitheloid Histiocytes
Langhan's giant cells - Multinucleated giant cells
Lymphocytes
Caseating Necrosis

• ZN stain for Acid-fast bacilli

Question 3

Entamoeba description [4]

Answer 3

• Friable
• CONCENTRIC Nucleoli
• Hematophagous trophozoites
• Liquefactive necrosis - hence cant see inflammatory cells

4 nucleoli in Schizonts

Question 4

Alcoholic liver disease pathophysiology

Answer 4

Steatosis

• NADH from alcohol metab increase fat synthesis; decrease lipoprotein export, increase peripheral fat catabolism
• ROS oxidative stress and Acetaldehyde damages liver cells;
• Gut bacteria produces endotoxin - inflammation, HSC activation, fibrosis

Question 5

Alcoholic liver disease histology - [3++] !!!

impt af

Answer 5

Ballooning degen and Necrosis - hence Neutrophils
- Swelling of cells w excess fats, fluids
Mallory-Denk bodies - protein aggregates which are pink! – eosinophilic
– most common in alcoholic liver stuff, HCC can also

Cirrhosis, Chicken wire fence Pericellular fibrosis
Centrilobular Steatosis
Neutrophils (inflammation)

Question 6

Non-alcoholic FLD pathophysiology, risk factors [2]

Answer 6

Associated w Metabolic Syndrome
- Insulin resistance - increase fatty acid delivery from adipose to liver, increased unopposed glucagon on HSL, increase fatty acid production in the liver

– Then fat laden cells - prone to lipid peroxidation - oxidative injury

Risk factor: Obesity & Type 2 Diabetes

Question 7

Whats Wilsons disease

Answer 7

Metabolic disease, AR
- failure of copper excretion - toxic to liver

• can accumulate in Basal Ganglia
• • Parkinsonism

Question 8

Whats A1-Antitrypsin Deficiency

Answer 8

Metabolic disease, AR

• poor protein folding IN LIVER, then deficient in A1-antitrypsin A1AT
• hence less inhibition of protease (trypsin is protease) from neutrophils in Lungs, lung damage
• — EMPHYSEMA smoking pathogenesis
• Liver cirrhosis develops as A1AT not secreted properly, accumulates in Liver