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microbiology 2 > 21.1 > Flashcards

21.1 Flashcards

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
hepatocellular damage
enzymes (ALT and AST) are released from damaged cells
26
hepatocellular damage signs
increased ALT increased AST increased bilirubin and majority is conjugated
27
>10x normal degree of increased AST in hepatocellular damage
acute severe insult - viral hepatitis - toxic drugs - paracetamol - hypoxia
28
<5x normal increased AST in hepatocellular damage
other infections alcohol some medications
29
hep B and C both cause
chronic infection | serious sequelae - cirrhosis, HCC
30
hep B
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
31
HBsAg
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
HBcAg
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
HBeAg
hepatitis B e antigen a soluble cleavage product of the core structural polypeptide both antigen and resulting antibody and detectable in serum
34
HBV DNA
hep B DNA can be detected in serum using PCR tests HBV DNA and HBV viral load (if quantified)
35
serological response to acute infection
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
patients with HBsAg are
infective
37
if HBsAg is present for 7 weeks or less
the patient is unlikely to develop clinically evident hepatitis
38
the appearance of HBeAg roughly correlates with
HBsAg | correlates with viral replication and indicates high infectivity
39
testing for HBeAg in acute infection
does not usually offer useful information | it's presence has more significance in persistent infection
40
HBcAb is detectable
before the onset of liver damage and persists for years | only detectable through natural infection - does not arise from vaccination
41
indicator of recent infection with Hep B
HBcAb IgM | persists for 4 months
42
HBeAb in acute infection
shortly after HbeAg disappears, HBaAb appears | persists for a couple of years after resolution of acute infection
43
HBsAb in acute infection
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
protective antibody that neutralises the virus
HBsAb
45
antibody that may arise from natural infection or from vaccination
HBsAb
46
HBV DNA detectable by
30 days following acute infection | can be detected 21 days before HBsAg appears in serum
47
if infected with HBV as a neonate
almost all cases will remain chronically infected
48
persistence of HBsAg in the serum for 6 months or ore
defines chronic infection | or the 'carrier' state
49
HBcAb in chronically infected patients
develops and persists as it does in those with acute self limiting infection
50
HBsAb in persistent infection
does not arise in chronically infected patients
51
HBeAg in chronic patients
arises as it does in acute self limiting infection correlated with HBsAg may or may not be replaced with HBeAb
52
mutant viruses not producing HBeAg
mostly pre-core mutants | don't produce HBeAg at all
53
core and pre core gene regions
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
how HBeAg and HBcAg are made
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
pre core mutant
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
pre core mutants still produce
HBcAg
57
pre core mutants cannot produce
HBeAg
58
mutation in pre core mutants
stop codon in the pre-core region of the genome
59
4 stages of chronic hep B infection
1. immune tolerant 2. immune clearance 3. immune control 4. immune escape
60
1. immune tolerant stage features
seen in those who acquired infection as neonates persists for 20-30 years minimal liver damage low risk of progression
61
immune tolerant stage laboratory
positive HBeAg | high viral load
62
2. immune clearance features
active, cytotoxic immune response resulting in liver damage, fibrosis
63
2. immune clearance stage laboratory
HBeAg eventually becomes HeAb high viral load falls to low levels ALT elevated but fluctuates
64
3. immune control features
inactive carriers minimal liver inflammation low risk of complications small % flare up and develop complications
65
3. immune control lab
negative HBeAg low viral load ALT normal
66
4. immune escape features
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
4. immune escape lab
negative HBeAg low viral load ALT elevated but fluctuates
68
Hep C virus symptomatic illness
occurs in only 15-30% of cases
69
Hep C virus incubation time
5-12 weeks
70
if HCV RNA still detected at 6 months
chronic infection
71
HCV antibody persists
regardless of whether infection is cleared
72
ALT levels HCV
fluctuate throughout course of infection
73
lab diagnosis of Hep 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
lab diagnosis of Hep E
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
laboratory diagnosis of Hep D
IgG anti-HDV available locally | will only be performed if HBsAg is also present

microbiology 2 (26 decks)

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