Biliary + liver Flashcards
Causes of jaundice
Pre-hepatic
= haemolytic anaemia
= unconjugated bilirubin, normal urine
Hepatic
= liver disease
= mixed conjugated bilirubin
Post-hepatic
= gallstones, obstructing Ca-CBD (head of pancreas)
= conjugated bilirubin, pale stools, dark urine
Main causes of CLD
I. Alcoholic liver disease (small liver) II. Viral hepatitis (hep B + C; chronic) III. Fatty liver (NAFLD) IV. AIH (women, young, Cushingoid) V. Congenital (A1AT, Wilson's, HH - all AD)
Hep A summary card
Oro-anal sex; faeco-oral spread, acute, asymptomatic (usually) = Faecal-oral transmission = 2 weeks incubation period = Africa/Asia high risk = RFs: poor hygiene = Rarely chronic
*improperly cleaned shellfish from contaminated water
Hep B summary card
Learn your serology, most adults clear it; never acute whilst children are carriers = Bodily fluids transmission = 4-12 week incubation period = Africa high risk = RFs: health workers = Chronic in children, 5% adults
Serology: IgM(an that’s acute), IgG(one, chronic!)
Hep B serology
HbsAg: now/around
= -ve if cleared/past vaccine
= +ve if acute/chronic infection
HbeAg: infective
Anti-Hbs: immune, IgG
= past clearance/vaccination
Anti-Hbc: caught in past, IgM
= +ve natural immunity and cleared
Hep C summary card
Blood production spread, most adults chornic carries, leads to HCC, 80% asymptomatic = Bodily fluids transmission = 2 weeks-6 months incubation period = Eastern Mediterranean high risk = RFs: IVDU = Chronic in 60-80%
Hep D summary card
Superinfection of B, requires HBV surface antigen to access liver cells = Bodily fluids transmission = 4-12 weeks incubation period = Africa high risk = ONLY coninfects with hep B = Rarely chronic
Hep E summary card
Morbidity in pregnant women, expectant mothers beware!! Usually acute and self-limiting = Faeco-oral transmission = 5-6 weeks incubation period = Occurs in areas with poor water supply = RFs: immuncompromised, pregnant = Rarely chronic
Sx of hepatitis
Fever, jaundince, increase in both AST/ALT thus liver problem (transaminitis in all except hep B)
Mx of hepatitis
A
= supportive, all resolves by 6 months
B
= supportive for acute
= anti-virals and pega-interferon for chronic
= viral suppresion in 90% of chronic carriers
C
= supportive for acute
= direct acting anti-virals for chronic (elbasvir/glecaprevir or ritonavir + rinavirin)
= mortality at 79% at 10 years for chronic cases
What can you interpret from these LFT results?
a) transaminitis in 1000s
b) increased AST + ALT
c) increased GGT + ALP
d) AST:ALT is 2:!
e) decreased urea
f) increased urea (>10)
g) decreased albumin
a) paracetamol OD, ischaemic hit, viral
b) hepatic problem
c) cholestatic/obstructive picture, EToH, biliary damage
d) alcoholic hepatitis when S > L
e) pregnancy, malnutrition, severe liver disease (synthesis down)
f) dehydration/AKI, UGIB/large protein meal
g) poor synthetic function of liver
Who is NASH?
Non-alcoholic steatohepatitis
=> umbrella for steatosis and steatohepatitis
RFs: obesity, TIIDM, HTN, high cholesterol, smoking, age > 70yo
Usually an incidental finding as no sx in early stages
Increased risk of DM, MI, stroke
20% go on to develop cirrhosis
Ix and mx of NASH
Ix show
- LFTs: raised ALT/AST
- raised fasting triglycerides, low HDL
- steatosis liver on USS
Mx is to control RFs
- BP, diabetes, cholesterol, wt loss, smoking cessation, exercise, reduce alcohol
Complications of cirrhosis
Ascites Oeseophageal varices Hepatic encephalopathy Hepatocellular carcinoma End-stage liver failure
Presentation of alcoholic hepatitis
Hx of 15-20 years of heavy drinking Typically asymptomatic Mild sx - epigastric pain, nausea, malaise Severe sx - jaundice, abdo discomfort/swelling, swollen ankles, GI bleed
Ix findings of alcoholic hepatitis
Bloods
- FBC; low Hb, high MCV, high WCC, low plts
- LFTs; AST:ALT, 2:1, high bilirubin, ALP, GGT, low albumin
- U&Es; low urea and potassium
- prolonged PT
UGI endoscopy ?varices
Liver biopsy to distinguish from other heps
EEG ?encephalopathy
USS ?malignancy
Acute mx of alcoholic hepatitis
Acute
- thiamine + vitamens => pabrinex
- monitor K+, Mg2+, glucose
- restrict proteins, oral/NG tube
- manage ascites => diuretics
- treat encephalopathy => oral lactulose/phosphate enemas
What would histopathology show for an alcoholic liver?
Degeneration and necrosis of hepatocytes Steatosis Neutrophilic inflammation Cholestasis Mallory-hydraline inclusions
Complications of alcoholic hepatitis
Acute liver decompensation Hepatorenal syndrome (due to increased RAAS activation) Cirrhosis (within 1-3 years if continues drinking)
Mortality 1st month = 10%, 1st year = 40%
Wilsons disease summary card
Copper accumulation due to defective liver transporters (ATP7B gene on chr 13)
=> copper deposits in basal ganglia and eyes
=> Kayser-Fleische rings (slit-lamp ix) pathognomonic
=> early onset neuropalsy sx/Parkinsonism
=> renal tubular acidosis (Fanconi’s syndrome)
Ix show
- decreased serum ceruloplasmin (copper transport protein)
- increased urinary copper
- decreased serum copper (paradoxical so not reliable)
Haemochromatosis sx
Starts 40-60 years old
- arthropathy arthralgias, weakness, fatigue, erectile dysfunction, heart problems
Late presentations
- diabetes, cirrhosis, neuro/psych sx, cardiomyopaty, arrhytmias, hepatomegaly, bronzed skin
What is haemochromatosis?
Dysregulated increased iron absorption
= HFE gene; C282Y + H63D (most common mutations)
= AR inheritence
= 90% problem with hepcidin
= deposits in liver, pancreas and pituitary gland
Haemochromatosis ix and mx
Ix
- Check CRP, ALT, chronic EToH to rule out other reasons for increased ferritin
- Bloods show increased ferritin + transferrin saturation and decreased transferrin + TIBC
Mx
- Avoid iron overload in early stages
Differentiate the gallbladder diseases
Biliary colic
= stone in Hartmann’s pouch
= RUQ, colicky pain due to GB spasm against stone
Acute cholecystitis
= GB inflamed
= RUQ continuous pain, fever, Murphys +ve
Ascending cholangitis
= GB infection
= Charcot triad: RUQ pain-fever-jaundice
= Rarely Reynold’s pentad: “ “ + hypotension, confusion