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*B32 GI and Surgery* > Acute liver disease > Flashcards

Acute liver disease Flashcards

1
Q

What are the 3 different antigens of Hep B

A

Hb surface antigen = HBsAg
Hb E antigen = HBeAg
Hb Core antigen = HBcAg

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2
Q

HBsAg +ve indicates

A

Infection

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3
Q

HBsAg +ve for >6 months =

A

Chronic infection

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4
Q

HBeAg +ve indicates

A

In acute phase of infection (virus replicating)

marker of infectivity so ↑ levels = ↑ infectivity

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5
Q

Anti-Hbs +ve indicates

A

current infection

If all others negatives = previous immunisation against Hep B

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6
Q

Anti-HBc -ve but HBsAg +ve

A

Previous Hep B but not a carrier

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7
Q

anti-HBc +ve and HBsAg +ve

A

Previous Hep B and carrier

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8
Q

If IgM Anti-HBc +ve it means..

A

Acute infection

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9
Q

If IgM Anti-HBc -ve it means

A

Chronic infection

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10
Q

Hep B serology explained

A

HBsAg indicates infection

HBeAg indicates infectivity (2nd marker)

Anti-HBs =recovery and immunity

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11
Q

Pre-hepatic causes of portal hypertension

A

Portal vein or splenic vein thrombosis

Infiltration of vessel by tumour (pancreatic cancer)

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12
Q

Hepatic causes of portal hypertension

A

Cirrhosis
Hepatocellular cancer
Schistosomiasis
Sarcoidosis

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13
Q

Post-hepatic causes of portal hypertension

A

Hepatic vein thrombosis -> can lead to Budd-Chiari
Heart failure
Restrictive pericarditis

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14
Q

Portal hypertension complications

A 
Esophageal varices
Anorectal varices 
Caput Medusae (dilated veins in abdo wall)
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15
Q

Budd-Chiari syndrome

A

Thrombosis of hepatic vein = occlusion

Presents with RUQ pain, ascites, hepatomegaly

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16
Q

Risk factors for Budd-Chiari syndrome

A 
Contraceptive pill use 
Pregnancy
Post-partum period
Polycythaemia vera, essential thrombocytosis
Hypercoagulable states
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17
Q

Varices =

A

Dilated veins due to elevated pressure in the portal venous system

Leads to weakened vessels walls

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18
Q

Varices develop in patients w/ cirrhosis when portal pressure is.

A

> 10mmHg

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19
Q

Variceal bleed can occur when portal pressure is

A

> 12mmHg

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20
Q

Causes of ↑ ALT

A

Hepatocellular damage

Acute hepatocellular injury, alcholic hepatitis, cirrhosis

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21
Q

Drugs causing increase in ALT

A 
Paracetamol overdose (AST and ALT)
Phenothiazines, chlorpromazine
Barbiturates
Tetracycline, isoniasid, nitrofurantoin
Morphine, codeine
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22
Q

AST found to be released during

A

Damage of cardiac muscle, liver, skeletal muscle, brain

V. non-specific - not used a lot

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23
Q

↑ ALP

A

Usually due to biliary or liver pathology

Use GGT to confirm

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24
Q

↑ ALP but normal GGT or

isolated ↑ ALP and normal other LFTs

A

Bone origin = Bone mets, hyperparathyroidism

check calcium

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25
Q

Tests of hepatic dysfunction

A

Albumin (reduced)
Prothrombin time (increased)
Bilirubin (increased)

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26
Q

↑ Conjugated Bilirubin indicates

A

Obstructive jaundice

Bile duct stone
Head of pancreas carcinoma
Pancreatitis
Cholangiocarcinoma
Biliary atresia
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27
Q

absent bilirubin but raised urobilinogen in urine = ___________ jaundice

A

Haemolytic jaundice/pre hepatic jaundice

due to increased amount of bilirubin production from breakdown of cells

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28
Q

Raised bilirubin but normal/absent urobilinogen in urine = ___________ jaundice

A

Obstructive jaundice/post hepatic jaundice

Remember: urobilinogen made in small intestines and reabsorbed into blood -> urine. If obstruction then no formation of urobilinogen

29
Q

Causes of Pre-hepatic jaundice

A

Excessive RBC breakdown -> Unconjugated hyperbilirubinaemia

Haemolytic anaemia
Gilbert’s syndrome
Criggler-Najjar syndrome

30
Q

Causes of Hepatic jaundice

A

Due to dysfunction of liver (may not be able to conjugate- so mixed bilirubinaemia is seen)

Alcoholic liver disease
Hepatitis (Viral/autoimmune)
Medication
Haemochromatosis
Primary biliary cirrhosis/Primary sclerosing cholangitis
Hepatocellular carcinoma
31
Q

Causes of Post-Hepatic jaundice

A

Mainly obstruction of biliary drainage (conjugated hyperbilirubinaemia as already passed through liver)

Gallstones
Cholangiocarcinoma 
Strictures
Drug-induced cholestasis
Pancreatic cancer or abdominal masses (e.g. lymphomas)
32
Q

Normal urine and normal stools

Pre hep/hepatic/post hep jaundice?

A

Pre hepatic jaundice

33
Q

Dark urine and normal stool

Pre hep/hepatic/post hep jaundice?

A

Hepatic jaudice

34
Q

Dark urine and pale stools indicates what?

Pre hep/hepatic/post hep jaundice?

A

Post-hepatic jaundice

35
Q

↑ bilirubin
↑ ALP
↑ GGT

A

Cholestatic pattern

36
Q

↑ INR
↓Albumin
↓ Platelets

Whats the problem?

A

Poor liver function - problem with synthesis

37
Q

↑ Bilirubin only - diagnosis?

A

Gilbert’s syndrome (↑ unconjugated:conjugated bilirubin) =

38
Q

What is Gilbert’s syndrome?

A

Hereditary unconjugated hyperbilirubinaemia

Reduced activity of UDP glucuronosyltransferase

39
Q

When does Gilbert’s syndrome typically cause jaundice?

A

During prolonged fasting Illness

Stressful periods

40
Q

What is Criggler-Najjar Syndrome

A

Hereditary unconjugated hyperbilirubinemia (absent UDP-glucuronosyltransferase enzyme)

Presents early in life
Severe brain damage at infancy

41
Q

Symptoms of viral hepatitis

A

of viral hepatitis
General malaise, fever, anorexia, arthralgia

RUQ pain, jaundice, hepatosplenomegaly

42
Q

Which Viral hepatitis: Unusual to have acute symptomatic disease

A

Hep C

43
Q

Hep ___ and ____ never/rarely cause chronic disease

A

Hep A and Hep E

44
Q

Hepatitis __ almost always causes chronic disease

A

Hep C

Chronic infection also seen in Hep B and D

45
Q

Hep ___ and ___ = faecal oral route of transmission

A 
Hep A (common amongst travelers)
Hep E

ingestion of faeces contaminated food and water

46
Q

In Viral serology IgM Ab indicates what

A

Active infection

47
Q

In Viral serology IgG Ab indicates what

A

Recovery from infection or vaccination

48
Q

Hepatitis ___ is dangerous in pregnant woman

A

Hep E

Can lead to acute liver failure

49
Q

Hepatitis __ is a DNA virus

A

Hep B

Rest are RNA viruses

50
Q

How is viral hepatitis detected

A

HepA = IgM/IgG
Hep B = HBsAg/HbeAg
Heb C =PCR/immunoassay HCV IgG/ELISA

51
Q

Hep ___ needs Hep B to complete viral replication and transmission cycle

A

Hep D

52
Q

Hep ___, ___ and ____ transmission route is parenteral

A

Hep B, C, D

Transmission via blood and body fluids - Needles, sexual intercourse, MTCT, razors, toothbrushes

53
Q

Vaccination available for Hepatitis ___ and Hepatitis ____

A

Hep A and B

54
Q

What is Hep D Co-infection and superinfection?

A

Co-infection: HepB and Hep D infection at the same time

Superinfection: A hep B surface antigen +ve patient subsequently develops a hep D infection (can quickly progress to cirrhosis)

55
Q

Hep C treatment

A

Direct acting antivirals (DAAs)

Sofosbuvir, Simeprevir with ribavirin

56
Q

Hep B treatment

A

Vaccination and supportive treatment

Avoid alcohol

57
Q

Heb A and Hep E treatment

A

Self-limiting

58
Q

Acute liver failure=

A

Rapid onset of hepatocellular dysfunction leading to complications

59
Q

Acute liver failure causes

A

Paracetamol overdose
Alcohol
Viral hepatitis (usually A or B)
Acute fatty liver of pregnancy

60
Q

Features of acute liver failure

how does it differ from Wernicke’s encephalopathy

A 
Jaundice
Coagulopathy: raised prothrombin time
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure (hepatorenal syndrome')

Wernicke’s encephalopathy is due to a deficiency of thiamine whilst acute liver failure encephalopathy is due to high levels of ammonia in the blood stream due to liver failure

61
Q

Patients at risk of paracetamol overdose

A

Suicidal patients

Use of certain drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)

Malnourished patients (anorexia, bulimia, CF, hep C, HIV)

Alcoholic liver disease

Patients who haven’t eaten for a while

62
Q

Paracetamol overdose pathophysiology

A

Paracetamol metabolised by cyto P450
NAPQI produced which is toxic but gets metabolised by glutathione

In overdose -> depletion of glutathione -> NAPQI build up -> hepatotoxicity

63
Q

Management of paracetamol overdose

A

Acetylcysteine (precursor to glutathione so increases levels)

Activated charcoal if soon after ingestion

64
Q

Causes of raised ALP

A

Bone mets

Paget’s disease, osteomalacia, rickets, bone fractures, primary bone tumours, pregnancy (as it is released by the placenta), hyperparathyroidism

Tests to exclude other causes: PTH, calcium, PSA and a skeletal survey

65
Q

Hepatorenal syndrome

A

Rapid deterioration in kidney function in individuals with cirrhosis or fulminant liver failure (liver failure THEN acute renal failure)

Will see rise in creatinine

66
Q

Wernicke’s encephalopathy

A

Confusion, ataxia and ophthalmoplegia
Due to thiamine deficiency -> treat with thiamine replacement

Occurs with alcohol excess, the malnourished and in pregnancy

CAN LEAD TO KORSAKOFFS (irreversible)

67
Q

Most common organism that causes SBP

A

E coli (2nd is klebsiella)

68
Q

SBP features, diagnosis and treatment

A

Ascites
Abdominal pain
Fever

Diagnosis
Paracentesis: neutrophil count > 250 cells/ul and culture (Usually E-coli)

Management = intravenous cefotaxime is usually given

*B32 GI and Surgery* (9 decks)

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