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microbiology 2 > 21.1 > Flashcards

21.1 Flashcards

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1
Q

acute hepatitis

A

swollen hepatocytes, small areas of necrosis

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2
Q

chronic hepatitis

A

graded ac cording to degree of inflammation, necrosis, fibrosis

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3
Q

cirrhosis

A

reduced hepatocyte mass
fibrosis
nodules of regenerating hepatocytes surrounded by fibrosis
derangement of flow from portal veins to hepatic vein (shunting)
impaired function - filtering of blood from GIT; protein production

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4
Q

LFTs

A

liver function tests

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5
Q

liver enzyme tests

A

ALT
AST
ALP
gammaGT

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6
Q

hepatocyte damage indicative liver enzymes

A

ALT, AST

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7
Q

synthetic function indicative tests

A

albumin
total protein
prothrombin time

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8
Q

excretory function indicative tests

A

bilirubin

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9
Q

true tests of liver function testst

A

albuin
total protein
prothrombin time
bilirubin

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10
Q

ALT

A

alanine aminotransferase

found within hepatocyte cytoplasm

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11
Q

AST

A

aspartate aminotransferase

found within hepatocyte cytoplasm (but also in heart, muscle, intestine, pancreas

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12
Q

presence of these 2 in serum indicates cellular damage

A

ALT and AST

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13
Q

ALP

A

alkalike phosphatase
found within cells lining biliary system (but also in bone, intestine, placenta)
increased synthesis in cholestasis

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14
Q

gammaGT

A

gamma glutamyl transferase
found within cells lining biliary system
raised in cholestasis

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15
Q

bilirubin

A

the laboratory measures conjugated and total bilirubin in the blood
in viral hepatitis, elevated bilirubin may be conjugated, or conjugated + unconjugated

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16
Q

albumin, total protein

A

produced by the liver

decreased levels in chronic liver (or other) disease

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17
Q

prothrombin time

A

increased

reduced synthesis of clotting factors

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18
Q

conjugation of bilirubin in the liver

A

unconjugated bilirubin enters the sinusoids and is taken up by the hepatocytes, where it is conjugated and excreted through the bile ductile

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19
Q

cause of elevated bilirubin in viral hepatitis

A

damaged hepatocytes result in conjugated and unconjugated bilirubin, and liver enzymes, entering the sinusoids and into the circulation

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20
Q

liver function test abnormalities fall into two categories

A

cholestasis and hepatocellular damage

both patterns commonly present together

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21
Q

cholestasis

A

interrupted bile flow between hepatocyte and GIT

cause can be intrahepatic and extrahepatic

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22
Q

signs of cholestasis

A

increased bilirubin and majority is conjugated
increased ALP - suggests liver but may come from other tissues
increased ALP and increased gammaGT - both together indicated liver origin
increased gammaGT - alone suggests alcohol excess
ALT/AST - normal or mildly elevated

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23
Q

increased ALP and gammaGT in chelastasis

A

both at the same time suggests liver origin

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24
Q

increased gammaGT alone in cholestasis indicates

A

alcohol excess

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25
Q

hepatocellular damage

A

enzymes (ALT and AST) are released from damaged cells

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26
Q

hepatocellular damage signs

A

increased ALT
increased AST
increased bilirubin and majority is conjugated

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27
Q

> 10x normal degree of increased AST in hepatocellular damage

A

acute severe insult

  • viral hepatitis
  • toxic drugs - paracetamol
  • hypoxia
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28
Q

<5x normal increased AST in hepatocellular damage

A

other infections
alcohol
some medications

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29
Q

hep B and C both cause

A

chronic infection

serious sequelae - cirrhosis, HCC

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30
Q

hep B

A

DNA virus with double stranded circular genome
a number of components of the virus are antigenic
these, and the host antibodies wot which they give rise, form the basis of the routinely used laboritory tests for infection with this virus

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31
Q

HBsAg

A

hep B surface antigen
found on intact visions or in the form of filamentous or spherical particles
antigen and antibody both detectable in serum

32
Q

HBcAg

A

Hep B core antigen
present in the liver but not detected in blood
not detected in blood
only resulting antibody is detectable in serum

33
Q

HBeAg

A

hepatitis B e antigen
a soluble cleavage product of the core structural polypeptide
both antigen and resulting antibody and detectable in serum

34
Q

HBV DNA

A

hep B DNA
can be detected in serum using PCR tests
HBV DNA and HBV viral load (if quantified)

35
Q

serological response to acute infection

A

70% develop subclinical or antiicteric hepatitis
30% develop icteric hepatitis
HBsAg appears during the incubation period, 4 weeks before evidence of hepatitis (jaundice or elevated liver enzymes)

36
Q

patients with HBsAg are

A

infective

37
Q

if HBsAg is present for 7 weeks or less

A

the patient is unlikely to develop clinically evident hepatitis

38
Q

the appearance of HBeAg roughly correlates with

A

HBsAg

correlates with viral replication and indicates high infectivity

39
Q

testing for HBeAg in acute infection

A

does not usually offer useful information

it’s presence has more significance in persistent infection

40
Q

HBcAb is detectable

A

before the onset of liver damage and persists for years

only detectable through natural infection - does not arise from vaccination

41
Q

indicator of recent infection with Hep B

A

HBcAb IgM

persists for 4 months

42
Q

HBeAb in acute infection

A

shortly after HbeAg disappears, HBaAb appears

persists for a couple of years after resolution of acute infection

43
Q

HBsAb in acute infection

A

doesn’t appear immediately after the disappearance of HBsAg
delay of several months before it appears and then persists for years
HBsAb is a protective antibody and neutralises the virus

44
Q

protective antibody that neutralises the virus

A

HBsAb

45
Q

antibody that may arise from natural infection or from vaccination

A

HBsAb

46
Q

HBV DNA detectable by

A

30 days following acute infection

can be detected 21 days before HBsAg appears in serum

47
Q

if infected with HBV as a neonate

A

almost all cases will remain chronically infected

48
Q

persistence of HBsAg in the serum for 6 months or ore

A

defines chronic infection

or the ‘carrier’ state

49
Q

HBcAb in chronically infected patients

A

develops and persists as it does in those with acute self limiting infection

50
Q

HBsAb in persistent infection

A

does not arise in chronically infected patients

51
Q

HBeAg in chronic patients

A

arises as it does in acute self limiting infection
correlated with HBsAg
may or may not be replaced with HBeAb

52
Q

mutant viruses not producing HBeAg

A

mostly pre-core mutants

don’t produce HBeAg at all

53
Q

core and pre core gene regions

A

HBcAg and HBeAg are a product of a single gene region consisting of the pre-core and core regions
these are two initiation codons, one in the pre-core region and one in the core region

54
Q

how HBeAg and HBcAg are made

A

when translation starts at the pre-core initiation codon, the resulting polypeptide has its ends cleaved off in the host cells endoplasmic reticulum resulting in HBeAg
when translation starts at the core initiation codon, the resulting polypeptide is HBcAg

55
Q

pre core mutant

A

production of a stop codon in the precode region of the genome
viral mutants cannot produce HBeAg
hosts infected with pre core mutants will not have this marker of viral replication and high infectivity in their serum

56
Q

pre core mutants still produce

A

HBcAg

57
Q

pre core mutants cannot produce

A

HBeAg

58
Q

mutation in pre core mutants

A

stop codon in the pre-core region of the genome

59
Q

4 stages of chronic hep B infection

A
  1. immune tolerant
  2. immune clearance
  3. immune control
  4. immune escape
60
Q
  1. immune tolerant stage features
A

seen in those who acquired infection as neonates
persists for 20-30 years
minimal liver damage
low risk of progression

61
Q

immune tolerant stage laboratory

A

positive HBeAg

high viral load

62
Q
  1. immune clearance features
A

active, cytotoxic immune response resulting in liver damage, fibrosis

63
Q
  1. immune clearance stage laboratory
A

HBeAg eventually becomes HeAb
high viral load falls to low levels
ALT elevated but fluctuates

64
Q
  1. immune control features
A

inactive carriers
minimal liver inflammation
low risk of complications
small % flare up and develop complications

65
Q
  1. immune control lab
A

negative HBeAg
low viral load
ALT normal

66
Q
  1. immune escape features
A

virus mutates and no longer produces HBeAg (usually pre core mutant)
can still replicate and get selected
inflammation, significant fibrosis
high incidence of complications

67
Q
  1. immune escape lab
A

negative HBeAg
low viral load
ALT elevated but fluctuates

68
Q

Hep C virus symptomatic illness

A

occurs in only 15-30% of cases

69
Q

Hep C virus incubation time

A

5-12 weeks

70
Q

if HCV RNA still detected at 6 months

A

chronic infection

71
Q

HCV antibody persists

A

regardless of whether infection is cleared

72
Q

ALT levels HCV

A

fluctuate throughout course of infection

73
Q

lab diagnosis of Hep A

A

IgM anti-HAV indicates recent infection, but may persist for up to 12 months
IgG anti-HAV provides evidence of recent or previous infection or immunisation

74
Q

lab diagnosis of Hep E

A

IgG anti-HEV provides evidence of recent or previous infection specific IgM testing not available locally
samples with positive IgG will get HEV PCR testing

75
Q

laboratory diagnosis of Hep D

A

IgG anti-HDV available locally

will only be performed if HBsAg is also present

microbiology 2 (26 decks)

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