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GI Revision Concise Cards > Revision Week 6 Liver > Flashcards

Revision Week 6 Liver Flashcards

1
Q

What is Glisson’s capsule?

A

fibrous protective lining on the liver

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2
Q

What divides the left and larger right lobe?

A

falciform

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3
Q

What does each segment have?

A

Own portal vein, artery and bile duct

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4
Q

What does fenestrated endothelium mean?

A

Liquid has access but blood does not

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5
Q

What are the stages in Phase I of drug metabolism in the liver?

A
  • Oxidation
  • reduction
  • hydrolysis
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6
Q

What is Phase II of drug metabolism?

A

Conjugation

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7
Q

How are drugs excreted from body?

A
  • Kidneys
  • faeces (bile from liver)
  • lungs (water vapour)
  • sweat/tears
  • milk, saliva
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8
Q

What does Phase 1 do in drug metabolism?

A

Increases drug polarity

-creates a new chemically reactive group permitting conjugation

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9
Q

What happens in phase 2

A

further increases polarity

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10
Q

What do LFTs distinguish in liver?

A

Hepatocellular injury or cholestasis

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11
Q

What are LFTs?

A
  • ALT
  • AST
  • ALP
  • GGT
  • Bilirubin
  • Albumin
  • PT
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12
Q

Why are bilirubin, albumin and pt called true LFTs?

A

Measures of protein synthesis in liver

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13
Q

ALT

A

marker for hepatocellular injury

-mainly exists in liver

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14
Q

AST

A
  • also in heart, skeletal muscle,brain, RBC

- may be elevated because of diseases associated with other areas its in

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15
Q

Where can ALP be found?

A

-present in liver, bile duct, bone and placenta

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16
Q

altered levels raising ALPs?

A
  • biliary obstruction
  • liver disease
  • bone problems
  • hyperthyroidism, hyperparathyroidism
  • renal osteodystrophy
  • pregnancy
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17
Q

When does ALP synthesis increase?

A

During cholestasis

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18
Q

In what cells in bone can ALP be found?

A

osteoblasts

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19
Q

GGT present where?

A
  • liver/bile duct
  • kidneys
  • pancreas
  • gallbladder
  • etc. etc.
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20
Q

hepatocellular injury?

A

ALT increased

AST increased

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21
Q

cholestasis

A

ALP increased

GGT increased

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22
Q

What is cholestasis?

A

Blockage of bile duct

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23
Q

If ALP and GGT both increased what does that suggest?

A
  • suggests biliary epithelial damage and bile flow obstruction
  • GGT increase confirms that ALP increase is from liver
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24
Q

GGT and alcohol

A

GGT raised with lots of alcohol

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25
Q

albumin function

A

maintains intravascular osmotic pressure

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26
Q

bilirubin

A

breakdown product of haemoglobin, gets conjugated in liver and excreted

27
Q

What causes darker urine

A

conjugated bilirubin passes to liver causing darker urine

28
Q

pre-hepatic jaundice

A

excessive red blood cell breakdown

29
Q

hepatocellular jaundice

A

jfpsf

30
Q

post-hepatic

A

liver fine, obstruction biliary drainage but bilirubin still conjugated

31
Q

pre-hepatic jaundice causes

A
  • Gilbert’s syndrome

- Haemolytic anaemia

32
Q

hepatocelullar jaundice acute causes

A
  • poisoning e.g. paracetamol
  • infection
  • liver ischaemia
33
Q

hepatocellular jaundice chronic causes

A
  • cirrhosis

- etc

34
Q

obstructive jaundice causes

A
  • gallstones
  • strictures
  • tumours
  • congenital biliary atresia
35
Q

When is chronic liver disease chronic

A

longer than 6 months

36
Q

compensated cirrhosis

A

asymptomatic stage

LFTs show damage

37
Q

decompensated cirrhosis

A

symptomatic:

  • ascites
  • jaundice
  • variceal haemorrhage
  • hepatic encephalopahty
38
Q

what cells are activated in liver when damaged and produce fibrosis

A

heapptonfn

39
Q

what is steatosis

A

fatty acid build up in cells in liver

40
Q

NASH

A

steatosis + inflammation and scarring

41
Q

When is it not reversible

A

fibrosis

42
Q

What is mainly responsible for liver disease in alcohol?

A

acetaldehyde

43
Q

What are scores for grading cirrhosis

A

CHild-Pugh

-…

44
Q

UKELD score for transplant

A

49

45
Q

ascites diagnosis

A
  • shifting dullness

- USS

46
Q

What is treatment for ascites?

A
  • treat underlying disease
  • look for infection
  • decrease salt intake
  • no NSAIDs
  • spironolactone first line
  • loop diuretics
  • paracentesis
  • TIPSS or transplant
47
Q

What is first line medication for ascites?

A

Spironolactone -mineralocorticoid receptor antagonist

48
Q

What is hepatorenal syndrome?

A

Kidney failure seen in those with severe liver damage

49
Q

What activates RAAS system in kidneys?

A

decreased perfusion of glomeruli

50
Q

Treatment for hepatorenal syndrome?

A
  • Transplantation

- TIPSS

51
Q

Spontaneous bacterial peritonitis?

A

bacterial infection in the peritoneum, despite the absence of an obvious source of infection

52
Q

What antibiotics for SBP? (Mild and severe?)

A

Mild - co-trimaxazole PO

Severe -

53
Q

What is hepatic encephalopathy?

A

build up of ammonia -> hyperammonaemia

54
Q

What is hyperammonaemia toxic to?

A

CNS - disturbs astroytes

55
Q

treatment for hepatic encephalopathy?

A
  • lactulose

- antibiotics

56
Q

What is definition of acute liver failure?

A

causing encephalopathy and impaired protein synthesis

57
Q

hep A

A

igM

58
Q

hepA and igG

A

means theyve had vaccination

59
Q

How is Hepatitis B transmitted? (3 Bs)

A
  • Bone (sex)
  • Baby
  • Blood
60
Q

What are children with Hep B more likely to get?

A

Chronic Hep B

61
Q

Surface antigens Hep B HBsAg

A

present in all infectious individuals

62
Q

HBeAg

A

marker for how infectious individual is - usually related to acute

63
Q

Hep B virus DNA

A

measure response to antiviral therapy

-used for prognosis

GI Revision Concise Cards (4 decks)

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