Describe the structure and classification of influenza viruses.

  • ssRNA, bound by nucleoprotein that determines type (A, B or C) and a lipid bilayer that contains both haemagglutinin and neuraminidase (determining subtype eg H1N1)

Pass criteria:

  • Need RNA and major types

What is the difference between antigenic drift and shift?

  • Only in influenza type A
  • Drift – mutation of the haemaglutinin and neuraminidase antigens allowing escape from most host antibodies (epidemic)
  • Shift – antigens replaced via recombination of RNA segments with those of animal viruses (pandemic)
  • Types B and C do not show drift or shift, mostly infect children, who develop antibodies preventing re-infection

Pass Criteria:

  • Bold to pass

How does the human body clear a primary influenza virus infection?

  • 2 mechanisms – cytotoxic T cells and macrophages
  • cytotoxic T cells kill virus infected cells, an intracellular antiinfluenza protein (Mx1)is induced in macrophages by cytokines IFN-a and IFN-b.
  • Future infection is prevented (haemagglutinin Ab) and ameliorated (neuraminidase Ab)

Pass criteria:

  • Bold to pass


What are the pathological features of Alcoholic Liver Disease?

  • Chronic maladaptive state in which cells of the liver respond in an increasingly pathologic manner to alcohol resulting in:
    • Hepatic steatosis (fatty liver)
    • Hepatitis; then
    • Progressive fibrosis to Cirrhosis; Marked derangement of vascular perfusion with secondary portal hypertension

Pass criteria:

  • All three to pass

What changes occur at the cellular level in Alcoholic Hepatitis?

  • Hepatocyte swelling and necrosis: Single or scattered foci, Swelling due to accumulation of fat, water and protein
  • Mallory Bodies: Eosinophilic cytoplasmic inclusions in degenerating hepatocytes, Characteristic but not specific feature
  • Neutrophilic reaction: Accumulate around degenerating hepatocytes
  • Fibrosis: Prominent activation of sinusoidal stellate cells and portal tract fibroblasts

Pass Criteria:

  • At least 3

In end stage alcoholic liver disease, what are the potential causes of death?

  • Hepatic failure and coma
  • Massive GIT bleeding
  • Intercurrent infection (to which these pts are predisposed)
  • Hepatorenal syndrome (following a bout of hepatitis)
  • Hepatocellular carcinoma (3-6%)

Pass criteria:

  • 3 to pass


Please describe the pathogenesis of acute calculous cholecystitis.

Chemical irritation of obstructed GB

  • Mucosal phopholipases hydroylyze luminal lecithins to toxic lysolecithins;
  • Protective glycoprotein mucus layer disrupted;
  • Bile salts – detergent action on mucosal epithelium;
  • PGs contrib. to inflam;
  • GB dysmotility develops;
  • Distension and incr intraluminal press decr blood flow

What conditions are associated with acute acalculous cholecystitis?

  • Postop major surgery
  • Severe trauma
  • Severe burns
  • MOF
  • Sepsis
  • Prolonged IV hyperalimentation
  • Postpartum

Pass Criteria:

  • 2 out of 3 to pass

How do the clinical features of acute acalculous cholecystitis differ from calculous cholecystitis?

  • Acute: RUQ or epigastric pain & tenderness, mild fever, anorexia, tachycardia, sweating, nausea, vomiting
  • *Calculous often more sudden, but can be mild & self-limiting
  • *Acalculous more insidious – may have no GB symptoms –  usually in pt with other illness –risk of complications higher eg perf/gangrene

Pass criteria:

  • Bold to pass

Please describe the pathogenesis of acute calculous cholecystitis.

  • *Bacterial infection: cholangitis, sepsis
  • GB perf & abscess formation; GB rupture & peritonitis; Biliary enteric fistula; Aggravation pre-existing condition


Outline the clinical syndromes which may develop following exposure to hepatitis viruses in an individual not immune to that virus.

  • Acute asymptomatic infection with recovery
    • Incidental finding on serology testing
  • Acute symptomatic infection with recovery
    • Any hepatitis virus (although rarely Hep C)
    • Four phases – Incubation, Symptomatic Pre-icteric, Symptomatic Icteric, Convalescence.
    • Symptomatic – constitutional, Serum sickness in10% (esp Hep B), Liver symptoms
    • Icteric (conjugated) Adults with Hep A, about 50% of Hep B, unusual in Hep C.
    • Recovery in weeks to months with T cell response
  • Chronic Hepatitis
    • Symptomatic, biochemical or serological continuing or relapsing disease for six months or more.
    • Aetiology is the most important predictor of likelihood of progression to cirrhosis.
    • Carrier states eg after vertical childhood Hep B (95%). Variable course, hepatocellular failure, cirrhosis, hepatoma
  • Fulminant Hepatitis
    • Over 2-3 weeks with encephalopathy.
    • Usually A or B (can be reactivation).
    • No stigmata of chronic liver disease, coagulopathy, cardiovascular, renal, ARDS, biochemical disease

Pass criteria:

  • Bold to pass

Describe the morphology of acute hepatitis.

  • Acute enlarged red (green) liver, ballooning degeneration, cholestasis and plugs, isolated cells or clusters necrose, cytolysis / apoptosis, bridging necrosis, architecture disarray.
  • Regeneration hepatocyte proliferation, sinusoidal cell reactive changes (debris in Kupfer cells, influx of monocytes) Portal tract inflammation.


What are the pathological features of Crohn disease?

1.            Transmural inflammation of bowel with skip lesions

2.            Noncaseating granulomata

3.            Fissures and fistulae

Pass: 2/3 Bold needed

What are the extraintestinal manifestations of Crohn disease?
Prompt: What other inflammatory conditions may be seen in Crohn disease?

Migrating polyarthritis, sacroiliitis, ank spondylitis, erythema nodosa, finger clubbing, sclerosing cholangitis (uncommon), Uveitis, mild hepatic pericholangitis, renal disorders due to trapping of the ureters (uncommon). Systemic amyloidosis (rare) GI tract cancer (less common than UC). May occur prior to intestinal symptoms.

Pass: At least three systems


What tissues may be involved in a primary varicella zoster infection?

  1. Mucous membranes
  2. Skin
  3. Neurones
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  1. Reactivation of latent virus
  2. Erodes immune response
  3. Dormant in sensory ganglion
  4. Interstitial pneumonia
  5. Visceral lesions
  6. Encephalitis etc


What are the factors that predispose to ischaemic bowel disease?

  1. 1.       Arterial thrombosis
  2. Arterial embolism, association with AF
  3. Venous thrombosis
  4. Non-occlusive ischaemia eg shock, drugs
  5. Miscellaneous eg radiation, herniae, vasculitis

Pass: 3 of 5. Must include bold.

Regarding acute transmural infarction caused by arterial occlusion, describe the pathological course.


Oedema and haemorrhage in wall

Lumen contains bloody fluid

Mucosal necrosis


Metabolic and cardiovascular derangements eg acidosis/ fluid balance

Perforation often leading to death

Pass: 4 of 7 (must include bold)

What are the outcomes of chronic bowel ischaemia?
Optional Question.

Strictures —submucosal involvement

Segmental, patchy mucosal degeneration


What are the characteristic pathological features of Ulcerative colitis?

Colon only

Continuous, no skip Ieasions

Chronic, relapsing

Crypt abscesses

Mucosal ulceration, with pseudopolyps

Mucosal inflammation only

Epithelial dysplasia

* Comparison of Crohns and UC acceptable

Pass: 4 of 7

What are the complications of UC?
Prompt: What are the extra-intestinal manifestations of Crohn's Disease?

Primary sclerosing cholangitis

Toxic megacolon


Pass: 2 of 3

What are the features of dysplasia/ neoplasia in UC?
Optional Question

Often multi-focal

Carcinomas are often infiltrative without obvious exophytic masses

Pass: 1 of 2


What are the characteristic pathological features of Crohn's Disease?


Skip lesions

Chronic, relapsing

Non-caseating granulomata

Mucosal ulceration

Transmural inflammation

* Comparison of Crohns and UC acceptable

Pass: 4 of 6

What are the complications of Crohn's Disease?

Prompt: What are the extra-intestinal manifestations of Crohn’s Disease?



Malabsorption syndromes

Extra-intestinal manifestations-polyarthritis, ank. Spond.; erythema nodosum, clubbing; pericholangitis, etc

Neoplasia, less common than UC

Pass: 2 of first 3 and one extra-intestinal manifestation


What are the causes of cirrhosis?

Alcoholic liver disease 60-70% ***

Viral hepatitis 10%, biliary diseases 5-10%, primary haemochromatosis 5%, Wilson disease, al-antitrypsin deficiency, idiopathic (cryptogenic) 10-15%, drug induced (a-methyldopa), cardiac disease, galactosaemia tyrinosis

Pass: Alcohol + 2 others

Outline the pathogenesis of cirrhosis.

  1. fibrous septae
  2. parenchymal nodules *
  3. disruption of the architecture of the ENTIRE liver*
  4. Resulting in new vascular channels shunt blood around the parenchyma. Sinusoidal fenestrations are lost, hepatocyte secretion of proteins is impaired. Biliary channels are obliterated *

May also mention- Fibrosis and parenchymal injury are diffuse, nodularity is part of

the diagnosis, vascular architecture is reorganised leading to a functional bypass of the hepatocytes. Fibrosis is the key feature of progressive liver damage and reversal is rare.

Progressive fibrosis and reorganisation of the vascular microarchitecture of the liver leads to a fibrotic nodular liver where delivery of blood to hepatocytes is severely compromised, as is their ability to secrete substances into the plasma Type I and III collagen are laid down in the lobules by perisinusoidal stellate cells (usually fat storage cells). They are activated by cytokines from Kuppffer cells and other inflammatory cells. This leads to robust mitotic activity, a shift in phenotype to myofibroblast and increased capacity for synthesis of extracellular matrix. Activation occurs mainly areas of necrosis and inflammation. Myofibers increase vascular resistance in the parenchyma. Remaining hepatocytes proliferate as nodules within the fibrous septa.

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