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GASTROENTEROLOGY SCE > Hepatology > Flashcards

Hepatology Flashcards

1
Q

What is HVWP an indirect measure of?

A

Sinusoids pressure

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2
Q

HVWP is raised in extra-hepatic causes of portal HTN. T/F

A

False. Raised in infra-hepatic causes e.g. Cirrhosis

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3
Q

Describe the risk factors for varices bleeding

A

Pressure on varix
Variceal size
Tension on variceal wall
Severity of liver disease (Child-Pugh)

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4
Q

Describe the high risk feature found on endoscopy that predict variceal bleeding

A

Red whale mark - red streaks on varix
Cherry red spot - flat and overly the varix
Haematocystic spots - raised discreet red spots (blood blisters)
Diffuse erythema - diffuse red colour of varix

These happen due to changes in variceal wall structure and tension due to formation of micro-telangiectasia

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5
Q

What percentage of patients with varices bleed each year

A

7%

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6
Q

What is the 6 week mortality following a variceal bleed:

  1. Childs Pugh A
  2. Child Pugh C
A
  1. 0%

2. 30%

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7
Q

Treatment options in gastric varix

A
  1. Cyanoacrylate (glue)

2. TIPSS

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8
Q

Describe the mechanism of beta-blockers in oesophageal varices

A

Reduce portal pressure by reducing cardiac output and producing splanchnic bed dilatation

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9
Q

How do we grade oesophageal varices

A

Based on size

  1. Small = grade 1 - collapse to inflation of oesophagus to air
  2. Medium = grade 2 - inbetween
  3. Large = grade 3 - large enough to occlude the lumen of the endoscope
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10
Q

What primary prophylaxis can be offered to a patient with oesophageal varices

A 
Oesophageal band ligation
Beta blocker (non-selective; carvedilol)

Grade 1 - carvedilol
Grade 2-3 = band ligation

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11
Q

Why may a patient have further haematemesis after banding

A

Variceal bleed

Ulceration from banding

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12
Q

Describe the different types of gastric varices

A

Type 1 - continuous with oesophageal varices and extend 2.5cm below GOJ along lesser curvature

Type 2 - above and extend beyond the GOJ into the funds of the stomach

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13
Q

How do we diagnose hepatorenal syndrome

A

Creat>133 despite few days Rx (IVI, HAS, holding nephrotoxics), cirrhosis with ascites, euvolaemic, no signs of shock, off all nephrotoxic drugs

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14
Q

Differentiate between type 1 and type 2 HRS

A

Type 1 - rapidly progressive, precipitated by SBP, potentially reversible

Type 2 - moderate renal failure with a slow progressive course. Patients with refractory ascites

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15
Q

Describe the pathogenesis of hepatorenal syndrome

A
  1. Nitric oxide released
  2. Splanchnic arterial vasodilatation
  3. Reduced peripheral vascular resistance
  4. Splanchnic bed resistant to endogenous vasoconstrictors (angiotensin 2)
  5. Elsewhere, vasoconstrictors cause renal/hepatic/cerebral vasoconstriction
  6. Renal vasoconstriction occurs secondary to RAA system. Renal perfusion more sensitive to change in MAP
  7. Compensatory hyperdynamic circulation to meet tissue demand
  8. Over time cardiac function declines causing hypoperfusion of kidneys
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16
Q

Treatment options for hepatorenal syndrome

A

Terlipressin - 0.5-2mg 4 hourly (want <25% reduction in creatinine after 3 days). It increases BP, reduces renin and increases GFR

HAS 1g/kg day one, then 20-40g/day

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17
Q

The finding of renal epithelial cells on microscopy suggests…

A

ATN

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18
Q

In HRS the urinary sodium is ……. (high or low)

The urine osmolality is……. (high or low)

A

Urine Na is LOW

Urine Osmolality is HIGH

renal tubule integrity is maintained

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19
Q

What features/findings may suggest a secondary cause of peritonitis

A

PMN>250
Multiple organisms
2 of: total protein >1, LDH>ULN for serum, glucose<50
Failure to respond to therapy for SBP

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20
Q

When to offer secondary prevention in SBP and what

A

SAAG > 11

Ciprofloxacin

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21
Q

Causes of SAAG >11

A

Cirrhosis
Right heart failure
PVT
TB (lymphocyte >250)

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22
Q

Causes of SAAG<11

A 
Exudate:
Cancer
Peritonitis
TB
Connective tissue disease
Malnutrition
Nephrotic syndrome
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23
Q

Treatment of cholestasis of pregnancy

A

Happens in 2-3rd trimester
Risk of premature labour
UDCA relieves pruritis, lowers ALT, lowers bile acids

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24
Q

What blood marker remains unchanged in pregnancy

A

Bilirubin
Aminotransferases
PT

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25
Q

What blood marker is reduced in pregnancy

A

Gamma globulins

Hb (in later pregnancy)

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26
Q

What blood markers increase in pregnancy

A

WBC
cholesterol
ALP
Fibrinogen

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27
Q

How do we calculate Maddreys discriminate function

A

4.6xPTprolongation + bil/17

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28
Q

What Maddreys score is classed as sever and suggests possible use of steroids

A

> 32

As these patients have a 50% mortality at 1/12

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29
Q

What Glasgow hepatitis score suggests poorer outcomes

A

9

28 day 52% without steroids
78% survival with steroids

Score based on age, wbc, urea, pt, bil

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30
Q

Describe the UKELD and it uses

A

U.K. Version of MELD used to stratify patients for liver transplant

Na, creat, nil, INR

> 49 score = 1 year mortality >9% (this is the minimum criteria for entry into waiting list)

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31
Q

What two conditions are indicators for transplant that the MELD doesn’t reflect the mortality

A

HCC (one nodule <5cm OR 3 nodules, none larger than 3cm

Hepatopulmonary syndrome

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32
Q

Which benzo do we use in ETOH withdrawal in patient with hepatic impairment

A

Oxazepam - short acting

Do fixed dose Vs front-loading Vs symptom triggered

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33
Q

Describe liver abscess findings on CT

A

Low density
Smooth margins
Contrast enhancing peripheral rim

Amoebic liver abscess - leucocytosis, +Ve anti-amoebic serum antibodies (90% +Ve for indirect haemagglutination)

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34
Q

CT findings of an hepatic adenoma

A

Enhance early in arterial phase as blood supply is from the hepatic artery

Linked with COCP and anabolic steroid use.

Malignant potential so resection advised. Can watch if <5cm

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35
Q

CT findings of HCC

A

Hypervascular in arterial phase

Washout in portal venous phase

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36
Q

Ct findings of hydatid cyst

A

Cysts have a thick wall with focal or circumferential calcification

37
Q

Define acute liver failure

A

Encephalopathy
Coagulopathy
<26 weeks onset

38
Q

Which virus is a significant cause of acute liver failure in Asia

A

Hepatitis E

It is more severe in pregnancy

39
Q

What herbal product used to treat menopausal Sx has reports of liver failure

A

Black Cohosh extract

40
Q

What percentage of patients with acute hepatitis B develop acute liver failure

A

8%

41
Q

Causes of acute liver failure

A 
Autoimmune
PCM OD
Ischaemia
DILI
Hep B
Hep C
Hep A
Hep E
Budd-Chiari
Wilson syndrome
Pregnancy - HELLP, fatty liver, 
Toxins - mushrooms
42
Q

What percentage of patients have no identifiable cause in acute liver failure

A

17%

43
Q

Parameters for consideration of liver transplant assessment in paracetamol overdose

A

PH <7.3
PT>100 (INR>6.5)
Creat >300
Encephalopathy 3/4

44
Q

Parameters for consideration of liver transplant assessment in non-paracetamol overdose

A

PT >100 (INR>6.5)

OR 3/5 of:
Age <10, >40
Jaundice to encephalopathy >7/7
PT>50
Bil>300
45
Q

Describe phase 1 drug metabolism

A

CP450 enzyme.

End product can be toxic

46
Q

Describe phase 2 drug reaction

A

Increasing water solubility by conjugation

47
Q

Describe an idiosyncratic drug reaction

A

Unrelated to dose

Metabolic reaction - accumulation of toxic metabolites in hepatocytes = inflammation (isoniazid, ketonazole, valproate)

Can get hypersensitivity 1 week after exposure. Rash, fever, eosinophilia and recur after exposure

48
Q

Which drugs cause a predominantly cholestatic liver injury

A

Ibesartan
Co-amoxiclav
Mirtazapine
Tricyclics antidepressants

There is no evidence, but can use ursodeoxycholic acid

49
Q

What is the strongest predictor for cirrhosis in hep B

A

HBV DNA

50
Q

Hep B - vaccinated patient serology

A

HBsAb +Ve

Rest negative

51
Q

Hep B - susceptible serology

A

HbSAg negative
Anti-HBc negative
HBSAb negative

52
Q

Hep B - serology of a resolved infection

A

HbSAg negative
Anti-HBc positive
HBSAb positive

53
Q

Acute HBV serology

A

HBSAg positive
Anti-HBc positive
HBSAb negative
Anti-HBc IgM positive

54
Q

Chronic hep B serology

A

HBsAg positive
Anti-HBc positive
HBsAb negative
Anti-HBc IgM negative

55
Q

Describe the natural history (5 phases) of hepatitis B

A
  1. Immune tolerance = high DNA, normal ALT, HBeAg positive
  2. Immune reactive = high DNA, raised ALT, HBeAg positive
  3. Immune control = low DNA, normal ALT, HBeAg negative, HBeAb positive
  4. Immune escape = high DNA, raised ALT, HBeAg negative, HBeAg positive (CONSIDER RX)
  5. HbSAg negative - undetectable DNA, HBSAg negative with or without HBSAb. At risk of reactiveation if immunosuppressive and anti-HBc positive
56
Q

When should hep B treatment be commenced

A

Raised liver enzymes and or high HBV DNA levels (>2000)

Active disease on liver Bx or fibroscan

57
Q

Treatment options for HBV

A

Tenofovir
Entacavir

These two less risk of resistance and safe to use in cirrhosis

Interferon (s/c)
Lamivudine

58
Q

Treatment of hep C genotype 2 & 3

A

Pegylated interferon and ribaviron

80% response rate

59
Q

Hep C genotype 1 Rx

A

Boceprevir

Telaprevir

With pegylated interferon and ribaviron

60
Q

How can we define response to treatment in PBC

A
  1. Paris criteria - bil<17, ALP <3 times ULN, ALT<2xULN

Barcelona criteria - normalisation or 40% reduction in ALP

61
Q

Treatment in PBC

A

Ursodexoycholic acid

15mg/kg/day

Protects damaged cholangiocytes against bile salts

62
Q

When can we do ERCP and dilatation in PSC

A

CBD structure <1.5mm

L and R hepatic ducts <1mm

Stent when dilatation fails

63
Q

What is the risk of gallbladder cancer when a mass in identified in the gallbladder in patients with PSC?

A

50%

64
Q

Histology of autoimmune hepatitis

A

Interface hepatitis (inflammation of hepatocytes @ junction of hepatic parenchyma and portal tracts)
Portal branching fibrosis
Plasma cell infiltration
Perilobular necrosis

65
Q

Describe the histological duct lesions staging in PBC

A 
S1 = florid bile duct lesion
S2 = ductular proliferation
S3 = septal fibrosis and bridging
S4 = cirrhosis
66
Q

How long should PBC patients in remission stay on Rx for

A

2yrs or 12 months after transaminases normalise

67
Q

The left hepatic artery supplies which segments of the liver

A

2, 3, 4 (a, b)

68
Q

The right hepatic artery supplies which segments of the liver

A

1, 5, 6, 7, 8

69
Q

Cause of hydatid liver disease

A

Tape worm

Echinococcus granulosis

70
Q

Who commonly gets hydatid liver disease

A

Africans

Farmers

71
Q

How is hydatid liver disease contracted

A

Contaminated food with infected dog faeces

72
Q

Describe the cycle of hydatid disease

A

Egg penetrates intestine wall
Enter portal system
Enter liver

73
Q

How do we diagnose hydatid liver disease

A

Echinococcus ELISA

CT shows ‘daughter cysts’

74
Q

Treatment of hydatid liver disease

A

Surgery

Mebendazole on effective in 30%

75
Q

Is there evidence for beta carotene in NASH cirrhosis

A

No

76
Q

NASH histology

A

Steatosis
Hepatocyte ballooning degeneration
Mild diffuse lobular acute and chronic inflammation
Perivenular collagen deposition

77
Q

Findings (bloods, genetics, etc) in Wilsons

A 
Low ALP
LOW copper
LOW caeruloplasmin
ATP7A gene on C13 (AR)
Raised urinary copper
Gallstones (pigmented)
Cirrhosis
78
Q

Treatment in Wilson’s disease

A

Penicillamine - increases copper excretion

Zinc - reduces GI copper absorption

79
Q

Next step after finding patient is homozygous for C282Y mutation

A

ORAL GLUCOSE TOLERANCE TEST

THEN ARRANGE VENESECTION IF SYMPTOMATIC OR LFTS ABNORMAL

80
Q

Which autoimmune condition is not associated with a raised ferritin

A

HYPOTHYROIDISM

81
Q

Hepatosplenic schistosomiasis:

  1. It is acquired through…
  2. Symptoms patient experiences
  3. Eggs that do not pass out of the body get lodged where?….
A
  1. Contaminated water with blood fluke
  2. Swimmers itch (due to eggs), tenesmus, pr bleeding, colitis
  3. Lodged in liver causing presinusoidal venous obstruction and portal HTN (non-cirrhosis) = hepatomegaly, splenomegaly, low plt
82
Q

Visceral leishmaniasis:

  1. How contracted
  2. What is Kala-azar
  3. Symptoms
A
  1. Sand fly bite
  2. Gray hyperpigmented spots on skin
  3. Popular lesion at site of bite, fever, weight loss, diarrhoea, painful hepatosplenomegaly
83
Q

The schistosomes life style is…

A

Larvae -Snail host - enter skin - liver - worms - mesenteric vessels - female lay eggs - go to intestine - eggs pass in faeces - eggs deposited in water - snail

84
Q

Treatment of schistosoma

A

Praziquantel

85
Q

Cause of hydatid cysts

A

Enterococcal infection

86
Q

Describe the cycle of enterococcal infection

A

Sheep ingest eggs (indeterminate host) - dogs ingests cyst (definitive host) - humans ingest eggs - small intestine - circulation - hydatid cyst in liver

87
Q

Signs of congenital Porto systemic shunt

A

Encephalopathy

High ammonia

NO cirrhosis

88
Q

Main risk factors for developing HCC

A

Obesity
Smoking
ETOH
Hep C

GASTROENTEROLOGY SCE (11 decks)

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