What is the causative organism of cholera?

  • Vibrio cholera = gram neg bacteria (comma shaped/flagellate)

Pass criteria:

  • Bold points

Describe the pathogenesis of cholera.
Prompt: Describe how the enterotoxin causes diarrhoea.

  • Non invasive
  • Flagella proteins for attachment & colonization
  • Preformed enterotoxin
    • Cholera enterotoxin
      • 5 B subunits
      • 1 A subunit
    • B subunit binds to intestinal (mainly duodenum/jejunum) – epithelial cells
      • Retrograde transport in ER
    • A subunit Tx to cytoplasm
      • A subunit activates G protein
      • Stimulates adenyl cyclase -> c-AMP
      • Opens cystic fibrosis transmembrane conductance regulator (CFTR)
      • Releases Cl– into lumen
        • Secretion of HCO3, Na and H20
        • Massive diarrhoea which overwhelms colonic resorption

Pass criteria:

  • Need 4 bold to pass


Classify portal hypertension giving examples for each.
Prompt: What is the most important hepatic cause?

  • Increased resistance to portal blood flow classified as:
    • Pre hepatic: portal vein thrombosis or narrowing
    • *Hepatic: cirrhosis, granulomatous disease, massive fatty change, schisto, nodular regenerative hyperplasia
    • Post hepatic, R heart failure, constrictive pericarditis, hepatic vein occlusion

Pass criteria:

  • 3 groups including hepatic.
  • Cirrhosis and one other cause

What are the major clinical consequences of portal hypertension due to cirrhosis?

  • Ascites: with potential for infection
  • Porto systemic venous shunts: varices > upper GI bleed. Other sites e.g caput, h’roids, retroperit.
  • Splenomegaly: thrombocytopenia
  • Hepatic encephalopathy > coma

Pass Criteria:

  • At least 3 consequences

What mechanisms are involved in the formation of ascites?
Prompt: What is the most important hepatic cause?

  • Starlings forces: increased pressure, decreased albumin
  • Increased formation of hepatic lymph overwhelms thoracic duct drainage > percolation into peritoneum
  • Intestinal fluid leak: ^pressure in intestinal capillaries and osmotic effect of protein rich ascitic fluid
  • Renal retention of Na and H2O due to secondary aldosterone.

Pass criteria:

  • Starlings forces and one other


Describe how the Hepatitis D virus infects the human body.

  • RNA virus
  • Must always be in conjunction with Hep B
  • Acute infection – indistinguishable from classical acute Hep B. ) Exposure to serum containing both Hep B and D.  HBV must establish first to provide HBsAg necessary for development of complete HDV viridons
  • Superinfection. -chronic HBV carrier exposed to new inoculum of HDV.  Disease develops 30-40 days later
  • Helper-independent latent infection- in liver transplantation patients

Pass criteria:

  • Bold to pass

How does superinfection with HDV manifest?
Prompt: Superinfection is one of the ways that Hepatitis D can infect the human host.

  • Severe acute hepatitis in previously unrecognised HBV carrier
  • Exacerbation of preexisting mild chronic hepatitis B
  • 80-90% chronic progressive disease and cirrhosis

Pass Criteria:

  • 1 out of 3

How is Hepatitis D infection diagnosed?

  • IgM anti-HDV – most reliable marker of recent HDV exposure but late and short lived
  • HBV an HDV coinfection – best with IgM against both HDAg and HBcAg
  • 2 phases –
    • acute phase – active HDV replication, suppression of HBV, high ALT levels
    • chronic phase – HDV replication decreases, HBV replication increases, ALT levels fluctuate, progression to cirrhosis and hepatocellular cancer
  • HDV RNA detectable in blood and liver just prior and in early days of acute symptomatic disease
  • In chronic delta hepatitis, HBsAg is present and IgM and IgG anti-HDV antibodies persist for months

Pass Criteria:

  • At least 1


What are streptococci?

  • Gram-positive cocci growing in pairs or chains.
  • Facultative or obligate anaerobes.
  • Cause variety of suppurative infections and immunologically mediated post-streptococcal syndromes

Pass criteria:

  • Bold to pass

Name some of the different types of streptococci and give examples of diseases they cause.

  • Alpha haemolytic
    • S. pneumonia: pneumonia, meningitis
    • S viridans: endocarditis
  • Beta Haemolytic
    • Group A.  (Pyogenes)
      • pharyngitis, scarlet fever, erysipelas, impetigo
      • Rheumatic fever, Toxic Shock Syndrome, Glomerulonephritis
    • Group B.  (Agalactiae)
      • neonatal sepsis and meningitis, chorioamnionitis
    • Strept. mutans: dental caries

Pass Criteria:

  • 3 major type/group + 6 diseases to pass

What factors in streptococci contribute to their virulence?

  • Capsules
    • pyogenes, pneumoniae
  • M Protein
    • prevents phagocytosis (anti M protein AL  à Rh.F.)
  • Complement C5a peptidase
  • Pneumolysin
    • lyses target cells (S pneumoniae) activates complement
  • Pyrogenic exotoxin-
    • rash and fever
  • High MW glucans:  plaque formation, aggregation of platelets
  • Sucrose à lactic acid (S. mutans).


What are the major pathological sequelae of HIV infection?

  • Attacks CD4+ T cells -> profound immunosuppression -> opportunistic infections, neoplasms, neurologic manifestations

Pass criteria:

  • Placental ischaemia PLUS 1 other point

What are the modes of transmission of HIV?

  • 75% sexual, heterosexual globally more common; female partners of IVDUs.
  • Female to male 1/20th as efficient in US, more in Thailand. Abetted by STDs.
  • Parenteral: IVDUs major, blood products almost eliminated.
  • Mother-to-infant in utero, at delivery, in breastmilk. 7-49%.
  • Not by insect bites. Needle-stick 0.3%


Describe the pathogenesis of primary tuberculosis.

  • Relates to ability to escape macrophages, induce delayed hypersensitivity: cord factor, LAM (lipo arabino mannan), complement activation, heat-shock protein.
  • Cell mediated (Type VI) hypersensitivity causes destructiveness and resistance.
  • Naïve macrophages (hilar lymph nodes) are unable to digest bacilli, which multiply, lyse cell, invade others, may disseminate intravascularly.  3weeks, T-cell mediated reaction –> epithelioid cell granulomas, then caseating granulomas –> calcified scar = Gohn complex


Describe the sequence of events in Plasmodium falciparum infection.

  • Anopheles genus mosquito
    • –>sporozoites
    • –> liver cells.
  • Hepatocyte rupture releases merozoites -> RBCs.
  • In RBCs mainly merozoites rupture cells; some gametocytes form, are sexual, invade mosquito.
  • Mature merozoites change in RBCs to shizont form, cell is rigid, removed in spleen

What are the complications of P. falciparum infection?

  • Anaemia, cerebral malaria, renal failure, pulmonary oedema, hepatosplenomegally, splenic rupture, DIC.


Classify meningitis with examples of important causes.

  • Acute pyogenic: bacterial
  • Aseptic:  viral,   chemical
  • Chronic: infection: TB, infiltration: carcinomatous

Pass criteria:

  • Must have bacterial and viral PLUS one other

What are the likely organisms causing acute bacterial meningitis in different age groups?

  • E coli/Group B strep: neonates
  • Pneumococci: infants/older(all ages beyond neonates really)
  • Meningococci: All ages beyond neonates esp. young adults
  • Haemophilus: Children but decreased incidence with Immunisation
  • Listeria. extremes of age
  • Unusual orgs e.g staph aureus post N/surg. Immuno compromised eg gram negatives.

Pass Criteria:

  • 3 out of 6

What are the typical CSF findings in acute bacterial meningitis?

  • Raised pressure
  • Turbid
  • Raised protein
  • Lower glucose
  • *Raised neutrophils
  • +ve bacteria on gram stain or culture

Pass criteria:

  • Bold PLUS one other


Describe the hepatitis D virus.

  • Unique RNA virus that is replication defective, causing infection only when it is encapusulated by HBsAg
  • A 35nm double shelled particle with a HBsAg outer coat and an internal HD Ag polypeptide with an associated single strand of circular RNA

Pass criteria:

  • Bold PLUS 1 other point

How does hepatitis D virus cause hepatitis?

  • Needs Hep B S Ag
  • Coinfection with HBV.
  • Superinfection of HBV carrier
  • Mild to fulminant (5%). More risk than Hep B alone. Can present as an acute severe hepatitis or can make a mild existing Hep B severe. Can become chronic progressive (mostly and the usual with a superinfection). . HD RNA found when symptoms start. Ig M anti HDV is reliable but occurs late and is short lived

Pass Criteria:

  • At least 2


What is an endotoxin?

Bacterial cell wall Lipopolysaccharides usually from Gram -bacilli. Consists of a generic fatty acid core and a complex polysaccharide coat unique for each species.

Pass: Bold

How does an endotoxin cause septic shock?

Dose dependent activation of neutrophils, macrophages and monocytes —-} mediator release —> local/systemic inflam. response. Activation via: LPS binding prot. + CD14 receptor via IC toll I receptor. Mediators: TNF, IL-I, 6, 8, chemokines —> cytokine release

Low dose: enhanced local inflammatory response and clearance of infection.

Moderate dose: fever, procoagulant activity,

High dose: Syndrome of septic shock

  • Systemic vasodilatation
  • Decreased myocardial contractility
  • Widespread endothelial injury — alveolar capillary damage (ARDS)
  • Activation coag system —, DIC

Pass: 3 of 4 needed

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