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GASTROENTEROLOGY SCE > Hepatology > Flashcards

Hepatology Flashcards

(88 cards)

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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
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

GASTROENTEROLOGY SCE (11 decks)

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