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Block 32- GI/surgery > chronic liver disease > Flashcards

chronic liver disease Flashcards

1
Q

presentation of liver infection (5)

A 
enlarged liver 
lymphadenopathy 
fever 
riggors 
general malaise
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2
Q

enlarged smooth edged liver suggestive of

A

hepatitis

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3
Q

infective causes of hepatomegaly (6)

A
  • infectious mononucleosis
  • viral hepatitis
  • malaria
  • amoebic
  • hydatid cysts
  • leishmaniasis
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4
Q

cancers causing heptomegaly (4)

A

leukemia
lymphoma
hepatocellular carcinoma

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5
Q

signs of liver cirrhosis (3)

A

jaundice
spider naevi
palmar erythema

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6
Q

metabolic causes of liver disease (3)

A

Wilson’s syndrome
Haemochromatosis
acute porphyria

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7
Q

3 drugs causing hepatitis

A

statins
amiodarone
macrolides

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8
Q

2 main liver enzymes -released after hepatocellular injury

A

AST

ALT

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9
Q

which liver enzyme is more specific for hepatic injury

A

ALT

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10
Q

where can AST be found (3)

A

Skeletal and cardiac muscle
hepatocytes
RBCs

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11
Q

ratio of AST and ALT increase in liver injury

A

1:1

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12
Q

alcoholic liver disease ratio of AST to ALT

A

AST>ALT above 2:1

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13
Q

ALP increased in

A

biliary tree obstruction -but not specific to liver

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14
Q

where can ALP be found

A

liver
bone
placenta

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15
Q

if ALP is raised from bone what will be normal

A

GGT

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16
Q

3 tests for hepatic function (not liver enzyme tests)

A

serum albumin
serum bilirubin
PT/INR

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17
Q

cholestatic pattern of liver enzymes

A
  • marked increase ALP and GGT

- mild increase ALT and AST

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18
Q

hepatic pattern of liver enzymes

A
  • marked ALT and AST increase

- minimal to no ALP increase

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19
Q

increase AST + ALT by several 100 = (3)

A
  • chronic hepatitis
  • alcohol induced hepatitis
  • NAFLD
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20
Q

increase AST and ALT by several 1000

A

acute viral heptitis

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21
Q

increase AST and ALT by >10,000 (2)

A
  • toxin related paracetamol (paracetamol)

- liver ischaemia

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22
Q

5 manifestations of liver disease

A
  • coagulopathy
  • ascites
  • hepatorenal syndrome
  • variceal bleeding
  • hepatic encephalopathy
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23
Q

what substances accumulation causes hepatic encephalopathy

A

ammonia

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24
Q

what happens to ammonia in the brain

A

absorbed and removed by astrocyte brain cells

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25
Q

how do the astrocyte cells metabolise ammonia

A

via converting glutamate to glutamine to metabolise the ammonia

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26
Q

what does increasing glutamine stores do to brain cells

A

causes osmotic pressure changes and causing water movement into the brain causing cerebral oedema

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27
Q

mental state changes in hepatic encephalopathy (5)

A
  • forgetfulness
  • confusion
  • irritability
  • inverted sleep pattern
  • personality change
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28
Q

LFTs hepatic encephalopathy

A

increased AST, ALT, albumin, bilirubin, PT,

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29
Q

management of hepatic encephalopathy (5)

A
  • lactulose
  • antibiotics
  • increased protein and kcal diet
  • BCAA and protein supplements
  • transplant
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30
Q

pathology of variceal bleeding

A

fibrosis compresses veins and arteries–> portal hypertension –> high pressure in collateral circulation –> veins in lower oesophagus dilated and prominent –> more prone to damage from coughing/ eating etc –> hematemesis

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31
Q

hepatorenal synrome=

A

rapid deterioration in renal function with cirrhosis or fluminant liver failure

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32
Q

when does hepatorenal syndrome often occur

A

sudden insult to the liver -infection of GI bleed

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33
Q

what happens causing renal hypotension

A

cirrhosis causes release of NO, prostaglandins and other vasoactive substances causing splanchnic vasodilation

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34
Q

what does hypotension in the kidneys trigger

A

RAS - further hypoperfusion of the kidneys -kidney failure

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35
Q

hepatorenal syndrome 1=

A
  • rapid deterioration circulation and renal function -
  • terlipressin resists hypovolemia
  • may need haemodialysis
  • median survival <2 weeks
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36
Q

hepatorenal syndrome 2 =

A
  • steady deterioration
  • may need TIPS
  • 6 months median survival
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37
Q

medical management of hepatorenal syndrome

A

terlipressin
octreotide
midodrine

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38
Q

surgical management of hepatorenal syndrome

A

liver transplant +/- kidney transplant

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39
Q

ascites pathology

A

portal hypertension causing splanchnic vasodilation –> hypoperfusion of kidneys +RAS –> Na+ reabsorption + aldosterone –> fluid retention

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40
Q

aldosterone released from

A

zona glomerulosa of adrenal gland

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41
Q

what in liver failure contributes to ascites formation

A

less albumin formation decreasing osmotic pressure

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42
Q

causes of ascites

A

portal hypertension
hypoalbuminemia
malignancies
infections

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43
Q

complications of ascites (3)

A

bacterial peritonitis
hepatorenal syndrome
thrombosis

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44
Q

3 clinical features of ascites

A

abdominal swelling
SOB
weight gain

45
Q

what does serum ascites albumin gradient (SAAG) determine

A

if ascitic fluid is due to portal hypertension

46
Q

SAAG >1.1=

A

ascites due to portal hypertension

47
Q

SAAG <1.1 =

A

etiology other than portal hypertension -nephrotic syndrome, cancer

48
Q

investigations of an ascitic tap

A 
albumin measurement 
neutrophil count 
amylase 
culture 
cytology
49
Q

2 effects of decreased thrombopoietin synthesis

A

thrombocytopenia

portal hypertension

50
Q

hepatitis acute symptomatic disease (4)

A

Hep A
Hep B
Hep B+D
Hep E

51
Q

possible hepatitis chronic disease

A

Hep B
Hep B+D
Hep C

52
Q

transmission route of Hep A

A

fecal oral route

53
Q

recovery from Hep A

A

99%

54
Q

diagnosis of Hep A

A

high ALT + bilirubin

55
Q

symptoms of Hep A

A

jaundice
epigastric pain
nausea
dark urine/ pale stools

56
Q

Hep B transmission route

A 
blood-blood
sexual 
unsterile needle 
vertical 
tattooing and body piercing
57
Q

Hep B more prevalent in

A

health care workers

58
Q

if Hep B not treated can lead to

A

HCC

59
Q

HBsAg=

A

antigen present of outside of virus

60
Q

HBsAg antibodies without antigens=

A

non-infected immunity

61
Q

HBcAg=

A

core antigen

62
Q

HBcAg indicates

A

active viral replication and infection

63
Q

Hep C infection presentation

A

remains asymptomatic and develops into chronic disease

64
Q

Hep C spread=

A

blood-blood contact

65
Q

test for Hep C

A

Anti-HCV antibody test

66
Q

if anti-HCV positive next step =

A

HCV polymerase chain reaction -positive in chronic infection

67
Q

most common cause of viral hepatitis worldwide=

A

Hep E

68
Q

host of Hep E=

A

pig

69
Q

most cases of Hep E=

A

asymptomatic

70
Q

range of disease in NAFLD

A

steatosis
steatohepatitis
fibrosis
cirrhosis

71
Q

what causes NAFLD

A

fatty deposits in the liver unrelated to alcohol or viral cause

72
Q

metabolic syndrome = 3 of the following (5)

A 
obesity 
hypertension 
diabetes 
hypertriglyceridemia 
hyperlididemia
73
Q

what factor is a major contributor to NAFLD

A

insulin resistance

74
Q

macroscopic view of liver in NAFLD

A

large
soft
yellow
greasy

75
Q

clinical features of NAFLD -My hepatocytes no more fast food

A
  • micro/ macrovesicular steatosis
  • hepatocyte balloon degeneration with necrosis and apoptosis
  • neutrophil rich inflammation
  • mallory denk bodies
  • fibrosis
76
Q

complications of NAFLD

A

cirrhosis

HCC

77
Q

LFTs of NAFLD

A

ALT> AST

78
Q

liver cirrhosis =

A

end stage liver damage by disruption of normal hepatic parenchyma by bands of fibrosis and nodules

79
Q

inflammatory changes in cirrhosis=

A

TGF-beta sub-endothelial fibrosis from stellate cells

80
Q

where are stellate cells

A

beneath endothelial cells lining sinusoids

81
Q

causes of cirrhosis (7)

A

-alcoholic liver disease
-NAFLD
-Chronic hep A and C
-PBC and PSC
-haemochromatosis and wilsons disease
alpha-1 antitrypsin
-cystic fibrosis

82
Q

why do you get palmar erythema

A

hyperestrinism since liver removes estrogen from blood

83
Q

compensated cirrhosis classical presentation (3)

A

fatigue
weight loss
weakness

84
Q

decompensated cirrhosis presentation (6)

A 
confusion 
ascites 
edema 
pruritis 
hematemesis 
melena
85
Q

what score can predict mortality and survival in liver disease

A

Child-pugh score -A BEAP

86
Q

Child-pugh score=

A 
Albumin 
Bilirubin 
Encephalopathy 
Ascites 
PT (INR)
87
Q

liver failure=

A

development of coagulopathy and encephalopathy

88
Q

hemochromatosis=

A

excess iron in body which deposits in tissues

89
Q

primary hemochromatosis =

A

autosomall recessive defect -HFE gene

90
Q

secondary hemochromatosis (3)

A

chronic transfusions
CLD
ineffective erythropoiesis

91
Q

when does hemochromatosis present

A

late adulthood 30-50 years old

92
Q

classical triad of disease from hemochromatosis

A
  • micronodular cirrhosis
  • diabetes mellitus
  • bronze skin
93
Q

complications of hemochromatosis

A 
HCC 
cirrhosis 
CHF 
cardiac arrhythmia's 
thyroid dysfunction 
sepsis
94
Q

treatment of hemochromatosis

A

venesect

avoid iron rich food

95
Q

Wilsons disease=

A

increased copper from

  • lack of copper transport into bile
  • lack of copper incorporation into ceruloplasmin
  • decreased ceruloplasmin secertion into blood
96
Q

when does wilsons disease usually present

A

<30 years old

97
Q

neurological changes of wilsons (4)

A
  • change in behaviour
  • dementia
  • chorea
  • parkinsonian symptoms
98
Q

eye change in wilsons

A

kayser-fleischer rings in descemet membrane of cornea

99
Q

skin changes in wilsons (3)

A
  • blue lunulae in nails
  • grey skin
  • hypermobile joints
100
Q

complications of wilsons (7)

A 
HCC
Coombs 
arthritis
neurological deficits 
psychiatric problems 
amino aciduria 
nephrocalcinosis
101
Q

management of wilsons (6)

A
  • avoid copper
  • lifelong D-penicillamine
  • anticholinergics, GABA antagonist
  • antiepileptics
  • lactulose
  • liver transplant
102
Q

A1 anti-trypsin deficiency =

A

defect in protease inhibitor

103
Q

consequence of a1 anti-trypsin deficiency

A

emphysema and liver

104
Q

when does a1 anti-trypsin present

A

30-40

105
Q

symptoms of panacinar emphysema

A

SOB
wheezing
cough

106
Q

three systems affected with PiZZ genotype of a1 anti-trypsin deficiency

A

lungs
liver disease
skin disease

107
Q

what is affected by the PiSZ genotype of a1 anti-trypsin deficiency

A

predisposed to lung disease

108
Q

management of a1 anti-trypsin (3)

A
  • quit smoking
  • IV augmentation via infusion of pooled human a1 antiprotease
  • transplant

Block 32- GI/surgery (9 decks)

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