Hepatology Flashcards
What is HVWP an indirect measure of?
Sinusoids pressure
HVWP is raised in extra-hepatic causes of portal HTN. T/F
False. Raised in infra-hepatic causes e.g. Cirrhosis
Describe the risk factors for varices bleeding
Pressure on varix
Variceal size
Tension on variceal wall
Severity of liver disease (Child-Pugh)
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
What percentage of patients with varices bleed each year
7%
What is the 6 week mortality following a variceal bleed:
- Childs Pugh A
- Child Pugh C
- 0%
2. 30%
Treatment options in gastric varix
- Cyanoacrylate (glue)
2. TIPSS
Describe the mechanism of beta-blockers in oesophageal varices
Reduce portal pressure by reducing cardiac output and producing splanchnic bed dilatation
How do we grade oesophageal varices
Based on size
- Small = grade 1 - collapse to inflation of oesophagus to air
- Medium = grade 2 - inbetween
- Large = grade 3 - large enough to occlude the lumen of the endoscope
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
Why may a patient have further haematemesis after banding
Variceal bleed
Ulceration from banding
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
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
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
Describe the pathogenesis of hepatorenal syndrome
- Nitric oxide released
- Splanchnic arterial vasodilatation
- Reduced peripheral vascular resistance
- Splanchnic bed resistant to endogenous vasoconstrictors (angiotensin 2)
- Elsewhere, vasoconstrictors cause renal/hepatic/cerebral vasoconstriction
- Renal vasoconstriction occurs secondary to RAA system. Renal perfusion more sensitive to change in MAP
- Compensatory hyperdynamic circulation to meet tissue demand
- Over time cardiac function declines causing hypoperfusion of kidneys
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
The finding of renal epithelial cells on microscopy suggests…
ATN
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
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
When to offer secondary prevention in SBP and what
SAAG > 11
Ciprofloxacin
Causes of SAAG >11
Cirrhosis
Right heart failure
PVT
TB (lymphocyte >250)
Causes of SAAG<11
Exudate: Cancer Peritonitis TB Connective tissue disease Malnutrition Nephrotic syndrome
Treatment of cholestasis of pregnancy
Happens in 2-3rd trimester
Risk of premature labour
UDCA relieves pruritis, lowers ALT, lowers bile acids
What blood marker remains unchanged in pregnancy
Bilirubin
Aminotransferases
PT
What blood marker is reduced in pregnancy
Gamma globulins
Hb (in later pregnancy)
What blood markers increase in pregnancy
WBC
cholesterol
ALP
Fibrinogen
How do we calculate Maddreys discriminate function
4.6xPTprolongation + bil/17
What Maddreys score is classed as sever and suggests possible use of steroids
> 32
As these patients have a 50% mortality at 1/12
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
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)
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
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
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)
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
CT findings of HCC
Hypervascular in arterial phase
Washout in portal venous phase
Ct findings of hydatid cyst
Cysts have a thick wall with focal or circumferential calcification
Define acute liver failure
Encephalopathy
Coagulopathy
<26 weeks onset
Which virus is a significant cause of acute liver failure in Asia
Hepatitis E
It is more severe in pregnancy
What herbal product used to treat menopausal Sx has reports of liver failure
Black Cohosh extract
What percentage of patients with acute hepatitis B develop acute liver failure
8%
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
What percentage of patients have no identifiable cause in acute liver failure
17%
Parameters for consideration of liver transplant assessment in paracetamol overdose
PH <7.3
PT>100 (INR>6.5)
Creat >300
Encephalopathy 3/4
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
Describe phase 1 drug metabolism
CP450 enzyme.
End product can be toxic
Describe phase 2 drug reaction
Increasing water solubility by conjugation
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
Which drugs cause a predominantly cholestatic liver injury
Ibesartan
Co-amoxiclav
Mirtazapine
Tricyclics antidepressants
There is no evidence, but can use ursodeoxycholic acid
What is the strongest predictor for cirrhosis in hep B
HBV DNA
Hep B - vaccinated patient serology
HBsAb +Ve
Rest negative
Hep B - susceptible serology
HbSAg negative
Anti-HBc negative
HBSAb negative
Hep B - serology of a resolved infection
HbSAg negative
Anti-HBc positive
HBSAb positive
Acute HBV serology
HBSAg positive
Anti-HBc positive
HBSAb negative
Anti-HBc IgM positive
Chronic hep B serology
HBsAg positive
Anti-HBc positive
HBsAb negative
Anti-HBc IgM negative
Describe the natural history (5 phases) of hepatitis B
- Immune tolerance = high DNA, normal ALT, HBeAg positive
- Immune reactive = high DNA, raised ALT, HBeAg positive
- Immune control = low DNA, normal ALT, HBeAg negative, HBeAb positive
- Immune escape = high DNA, raised ALT, HBeAg negative, HBeAg positive (CONSIDER RX)
- HbSAg negative - undetectable DNA, HBSAg negative with or without HBSAb. At risk of reactiveation if immunosuppressive and anti-HBc positive
When should hep B treatment be commenced
Raised liver enzymes and or high HBV DNA levels (>2000)
Active disease on liver Bx or fibroscan
Treatment options for HBV
Tenofovir
Entacavir
These two less risk of resistance and safe to use in cirrhosis
Interferon (s/c)
Lamivudine
Treatment of hep C genotype 2 & 3
Pegylated interferon and ribaviron
80% response rate
Hep C genotype 1 Rx
Boceprevir
Telaprevir
With pegylated interferon and ribaviron
How can we define response to treatment in PBC
- Paris criteria - bil<17, ALP <3 times ULN, ALT<2xULN
Barcelona criteria - normalisation or 40% reduction in ALP
Treatment in PBC
Ursodexoycholic acid
15mg/kg/day
Protects damaged cholangiocytes against bile salts
When can we do ERCP and dilatation in PSC
CBD structure <1.5mm
L and R hepatic ducts <1mm
Stent when dilatation fails
What is the risk of gallbladder cancer when a mass in identified in the gallbladder in patients with PSC?
50%
Histology of autoimmune hepatitis
Interface hepatitis (inflammation of hepatocytes @ junction of hepatic parenchyma and portal tracts)
Portal branching fibrosis
Plasma cell infiltration
Perilobular necrosis
Describe the histological duct lesions staging in PBC
S1 = florid bile duct lesion S2 = ductular proliferation S3 = septal fibrosis and bridging S4 = cirrhosis
How long should PBC patients in remission stay on Rx for
2yrs or 12 months after transaminases normalise
The left hepatic artery supplies which segments of the liver
2, 3, 4 (a, b)
The right hepatic artery supplies which segments of the liver
1, 5, 6, 7, 8
Cause of hydatid liver disease
Tape worm
Echinococcus granulosis
Who commonly gets hydatid liver disease
Africans
Farmers
How is hydatid liver disease contracted
Contaminated food with infected dog faeces
Describe the cycle of hydatid disease
Egg penetrates intestine wall
Enter portal system
Enter liver
How do we diagnose hydatid liver disease
Echinococcus ELISA
CT shows ‘daughter cysts’
Treatment of hydatid liver disease
Surgery
Mebendazole on effective in 30%
Is there evidence for beta carotene in NASH cirrhosis
No
NASH histology
Steatosis
Hepatocyte ballooning degeneration
Mild diffuse lobular acute and chronic inflammation
Perivenular collagen deposition
Findings (bloods, genetics, etc) in Wilsons
Low ALP LOW copper LOW caeruloplasmin ATP7A gene on C13 (AR) Raised urinary copper Gallstones (pigmented) Cirrhosis
Treatment in Wilson’s disease
Penicillamine - increases copper excretion
Zinc - reduces GI copper absorption
Next step after finding patient is homozygous for C282Y mutation
ORAL GLUCOSE TOLERANCE TEST
THEN ARRANGE VENESECTION IF SYMPTOMATIC OR LFTS ABNORMAL
Which autoimmune condition is not associated with a raised ferritin
HYPOTHYROIDISM
Hepatosplenic schistosomiasis:
- It is acquired through…
- Symptoms patient experiences
- Eggs that do not pass out of the body get lodged where?….
- Contaminated water with blood fluke
- Swimmers itch (due to eggs), tenesmus, pr bleeding, colitis
- Lodged in liver causing presinusoidal venous obstruction and portal HTN (non-cirrhosis) = hepatomegaly, splenomegaly, low plt
Visceral leishmaniasis:
- How contracted
- What is Kala-azar
- Symptoms
- Sand fly bite
- Gray hyperpigmented spots on skin
- Popular lesion at site of bite, fever, weight loss, diarrhoea, painful hepatosplenomegaly
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
Treatment of schistosoma
Praziquantel
Cause of hydatid cysts
Enterococcal infection
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
Signs of congenital Porto systemic shunt
Encephalopathy
High ammonia
NO cirrhosis
Main risk factors for developing HCC
Obesity
Smoking
ETOH
Hep C
