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GASTROENTEROLOGY SCE > Hepatology > Flashcards

Flashcards in Hepatology Deck (88):
1

What is HVWP an indirect measure of?

Sinusoids pressure

2

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

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

3

Describe the risk factors for varices bleeding

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

4

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

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

5

What percentage of patients with varices bleed each year

7%

6

What is the 6 week mortality following a variceal bleed:

1. Childs Pugh A
2. Child Pugh C

1. 0%
2. 30%

7

Treatment options in gastric varix

1. Cyanoacrylate (glue)
2. TIPSS

8

Describe the mechanism of beta-blockers in oesophageal varices

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

9

How do we grade oesophageal varices

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

10

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

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

Grade 1 - carvedilol
Grade 2-3 = band ligation

11

Why may a patient have further haematemesis after banding

Variceal bleed

Ulceration from banding

12

Describe the different types of gastric varices

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

13

How do we diagnose hepatorenal syndrome

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

14

Differentiate between type 1 and type 2 HRS

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

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

15

Describe the pathogenesis of hepatorenal syndrome

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

16

Treatment options for hepatorenal syndrome

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

17

The finding of renal epithelial cells on microscopy suggests...

ATN

18

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

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

Urine Na is LOW

Urine Osmolality is HIGH

renal tubule integrity is maintained

19

What features/findings may suggest a secondary cause of peritonitis

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

20

When to offer secondary prevention in SBP and what

SAAG > 11

Ciprofloxacin

21

Causes of SAAG >11

Cirrhosis
Right heart failure
PVT
TB (lymphocyte >250)

22

Causes of SAAG<11

Exudate:
Cancer
Peritonitis
TB
Connective tissue disease
Malnutrition
Nephrotic syndrome

23

Treatment of cholestasis of pregnancy

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

24

What blood marker remains unchanged in pregnancy

Bilirubin
Aminotransferases
PT

25

What blood marker is reduced in pregnancy

Gamma globulins
Hb (in later pregnancy)

26

What blood markers increase in pregnancy

WBC
cholesterol
ALP
Fibrinogen

27

How do we calculate Maddreys discriminate function

4.6xPTprolongation + bil/17

28

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

>32

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

29

What Glasgow hepatitis score suggests poorer outcomes

9

28 day 52% without steroids
78% survival with steroids

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

30

Describe the UKELD and it uses

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)

31

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

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

Hepatopulmonary syndrome

32

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

Oxazepam - short acting

Do fixed dose Vs front-loading Vs symptom triggered

33

Describe liver abscess findings on CT

Low density
Smooth margins
Contrast enhancing peripheral rim

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

34

CT findings of an hepatic adenoma

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

35

CT findings of HCC

Hypervascular in arterial phase
Washout in portal venous phase

36

Ct findings of hydatid cyst

Cysts have a thick wall with focal or circumferential calcification

37

Define acute liver failure

Encephalopathy
Coagulopathy
<26 weeks onset

38

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

Hepatitis E

It is more severe in pregnancy

39

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

Black Cohosh extract

40

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

8%

41

Causes of acute liver failure

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

42

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

17%

43

Parameters for consideration of liver transplant assessment in paracetamol overdose

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

44

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

PT >100 (INR>6.5)

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

45

Describe phase 1 drug metabolism

CP450 enzyme.

End product can be toxic

46

Describe phase 2 drug reaction

Increasing water solubility by conjugation

47

Describe an idiosyncratic drug reaction

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

Which drugs cause a predominantly cholestatic liver injury

Ibesartan
Co-amoxiclav
Mirtazapine
Tricyclics antidepressants

There is no evidence, but can use ursodeoxycholic acid

49

What is the strongest predictor for cirrhosis in hep B

HBV DNA

50

Hep B - vaccinated patient serology

HBsAb +Ve
Rest negative

51

Hep B - susceptible serology

HbSAg negative
Anti-HBc negative
HBSAb negative

52

Hep B - serology of a resolved infection

HbSAg negative
Anti-HBc positive
HBSAb positive

53

Acute HBV serology

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

54

Chronic hep B serology

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

55

Describe the natural history (5 phases) of hepatitis B

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

When should hep B treatment be commenced

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

Active disease on liver Bx or fibroscan

57

Treatment options for HBV

Tenofovir
Entacavir

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

Interferon (s/c)
Lamivudine

58

Treatment of hep C genotype 2 & 3

Pegylated interferon and ribaviron

80% response rate

59

Hep C genotype 1 Rx

Boceprevir

Telaprevir

With pegylated interferon and ribaviron

60

How can we define response to treatment in PBC

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

Barcelona criteria - normalisation or 40% reduction in ALP

61

Treatment in PBC

Ursodexoycholic acid

15mg/kg/day

Protects damaged cholangiocytes against bile salts

62

When can we do ERCP and dilatation in PSC

CBD structure <1.5mm

L and R hepatic ducts <1mm

Stent when dilatation fails

63

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

50%

64

Histology of autoimmune hepatitis

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

65

Describe the histological duct lesions staging in PBC

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

66

How long should PBC patients in remission stay on Rx for

2yrs or 12 months after transaminases normalise

67

The left hepatic artery supplies which segments of the liver

2, 3, 4 (a, b)

68

The right hepatic artery supplies which segments of the liver

1, 5, 6, 7, 8

69

Cause of hydatid liver disease

Tape worm
Echinococcus granulosis

70

Who commonly gets hydatid liver disease

Africans
Farmers

71

How is hydatid liver disease contracted

Contaminated food with infected dog faeces

72

Describe the cycle of hydatid disease

Egg penetrates intestine wall
Enter portal system
Enter liver

73

How do we diagnose hydatid liver disease

Echinococcus ELISA
CT shows 'daughter cysts'

74

Treatment of hydatid liver disease

Surgery

Mebendazole on effective in 30%

75

Is there evidence for beta carotene in NASH cirrhosis

No

76

NASH histology

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

77

Findings (bloods, genetics, etc) in Wilsons

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

78

Treatment in Wilson's disease

Penicillamine - increases copper excretion
Zinc - reduces GI copper absorption

79

Next step after finding patient is homozygous for C282Y mutation

ORAL GLUCOSE TOLERANCE TEST

THEN ARRANGE VENESECTION IF SYMPTOMATIC OR LFTS ABNORMAL

80

Which autoimmune condition is not associated with a raised ferritin

HYPOTHYROIDISM

81

Hepatosplenic schistosomiasis:

1. It is acquired through...
2. Symptoms patient experiences
3. Eggs that do not pass out of the body get lodged where?....

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

Visceral leishmaniasis:
1. How contracted
2. What is Kala-azar
3. Symptoms

1. Sand fly bite
2. Gray hyperpigmented spots on skin
3. Popular lesion at site of bite, fever, weight loss, diarrhoea, painful hepatosplenomegaly

83

The schistosomes life style is...

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

Treatment of schistosoma

Praziquantel

85

Cause of hydatid cysts

Enterococcal infection

86

Describe the cycle of enterococcal infection

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

87

Signs of congenital Porto systemic shunt

Encephalopathy

High ammonia

NO cirrhosis

88

Main risk factors for developing HCC

Obesity
Smoking
ETOH
Hep C