Liver + Biliary 1 Flashcards

1
Q

How is bilirubin metabolised?

A

Haem by haem oxidase to iron and biliverdin then into unconjucated bilirubin

Unconjucated -> (UDPGT) conjucated -> into bile -> biliary system -> stercobilinogen/urobilinogen

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2
Q

Pre-hepatic jaundice causes?

A

Haemolysis and Gilberts
(normal urine)

Raised bilirubin only

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3
Q

Hepatocellular jaundice causes?

A

Hepatitis, cirrhosis, liver mass and haemochromotosis

Dark urine (conj bilirubin)

Raised AST/ALT

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4
Q

Post-hepatic jaundice causes?

A

Gallstone, pancreatic cancer, cholangiocarcinoma, PSC, PBS and drugs

Dark urine + pale stools + pruritis (bile salts)
Raised ALP/GGT

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5
Q

Caused of raised AST and ALT?

Symptoms?

A

Alcoholic, NASH, viral, drugs and autoimmune

RUQ pain, jaundice,hepatomegaly, joint pain, nausea, fatigue, dark urine

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6
Q

Progress and Sx of alcholic liver disease>

A

Steatosis (after a few days of drinking, no Sx) -> Alcoholic hepatitis ( after long term, nausea, anrexia, weiht loss, hepatomegaly. Severe = fever, jaundice, tachycardia, tender, bruising, encephalopathy, ascites) -> cirrhosis

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7
Q

What mediates damage of the liver?

A

Mediated b NAD+ which promotes fatty infiltration -> inflammation

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8
Q

Ix for alcoholic hepatitis?

A

FBC = macrocytic anaemia
LFTs: AST/ALT ratio >2, increased bilirubin, alp, GGT and decreased albumin
Increased prothrombin time

Hepatc USS and liver biopsy

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9
Q

What histological marker indicates alcoholic hepatitis?

A

Mallory bodies

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10
Q

Mx for alcoholic hepatitis?

A

Alcohol abstinence + withdrawal (diazepam)
Nutrition
Weight loss and stop smoking
Steroids if severe

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11
Q

Progression of NAFLD?

RFs and Ix?

A

Steatosis -> NASH -> cirrhosis

Rfs: obesity, insulin resistance and diabetes, hyperlipidaemia, HTN, metbalic syndrome, short bowel syndrome, TPN

LFTS AST:ALT elevated <1, GGT/ALP eleavted and check glucose

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12
Q

Signs of insulin resistance?

A

Polyuria, polydipsia, ancanthosis nigricands

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13
Q

Mx for NAFLD?

A

diet and exercise, control RFs e.g. statsins for hyperlipidaemia, good blood sugar control with metformin

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14
Q

Features of Viral Hep A and E

A

Acute, faeco-oral, supportive management. Avoid alcohol and excess paracetomol
A= acute so travel and water
E = enteric, epidemic, expecting mothers and immunocompromised

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15
Q

Hep B features?

A

80% acute with RUQ, jaundice, N+V, anorexia

HCC risk
Birthing, blood, Babymaking (sex/MSM)

Coinfection with D increases the risk of liver failure
Treatment for coinfection = peginterferon-a-2a and tenofovir/entecavir

Acute -> supportive

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16
Q

Hep C features?

A

Chronic
HCC Rf
Blood spread

Treatment = sofosbuvir, ledispavir, grazoprevir

17
Q

Drug features of hepatitis?

A

Paracetomol (also NSAIDS< GCs, isonazid, fluclox, erythromycin)

AST/ALT in 1000s

N-acetylcysteine

18
Q

Autoimmune hepatitis features?

A

other AI presentation e.g. T1DM, hashimotos, coeliac. F>M

AST/ALT,
ANA, ASMA, AMA

Biopsy = interface hepatitis + plasma cells

19
Q

What drugs can cause cholestasis?

A

Co-amoxiclav, nitrofurantoin, OCP

20
Q

What are the main organs affected by haemochromotosis and types?

A

LIVER, PANCREAS, skin, pituitar, hearts and joints

Primary : autosomnal recessive and cannot stop GI tract Fe absorption

Secondary: iron overload e.g. multiple transfusions

21
Q

Primary haemochromotosis pathophysiology?

A

HFE gene mutation means transferrin binds poorly to receptor to less hepcidin production

22
Q

Clinical features of haemochromotosis?

A

75% Asx
Hepatomegaly, bronze skin, DM onset, artharlgia, male incompetence

M earlier than F
May progress to cirrhosis and HCC

23
Q

Ix for haemochromotosis?

A
1st transferrring satuation (raised) and serum ferritin (raised)
Gene typing for HFE
Liver Biopsy (gold)
24
Q

What is Wilsons, epi + clinical features?

A

impaired copper excretion so accumulates in liver and brain

Autosomnal recessiver (onset 5-25)

Hepatitis + dementia + parkinsonism i young person

hepatosplenomegaly, abdo pain, jaundice, ascites portal HTN
Kayser-fleischer rings

25
Q

Ix for Wilsons disease?

A

1st LFTS (raised transaminases/bilirubin), 24hr urinary copper, slit lamp exam

Decreased serum caeruloplasmin, increased serum free copper and urinary cooper excretion

Genetic testing and liver biopsy are gold standard

26
Q

Aetiology of Cirrhosis?

A

alcohol, viral (B/C), autoimmune, haemochromotosis, NASH and chronic biliary disease

27
Q

Nodule cirrhosis size?

A
Macronodular = viral
Micronodular = alcoholic
28
Q

Signs of chronic liver disease?

A

Clubbing, gynaecomastia, dupuytrens contracture, palmar erytherma, spider naevi, jaundice, easy bruising

29
Q

Where does blood flow from to porto-systemic circulation?

A

Lower oesophagus, anal canal, imbilicus, splenorenal

30
Q

What can cause portal hypertension?

A

Increase pressure in portal vein due to cirrhosis or a clot in hepatic vein e.g. Budd-chiari syndrome

31
Q

Signs of portal hypertension?

A

Clubbing, spider naevi, dupuytrens, palmar erytherma, gynaecomastia, brusing

+

Caput medusae, ascites, oesophageal varices

32
Q

What is the management of cirrhosis?

A

Treat cause and avoid hepatotoxic drugs
Monitor risk of complications (MELD score, 6 month USS, endoscopy)
Manage complications

33
Q

What is a complication of cirrhosis?

A

Portal hypertension

Encephalopathy = treat precipitating event + short term protein restriction, oral lctulose and phosphate enema, avoid sedatives

34
Q

What are the risk factors for encephalopathy with cirrhosis and MOA?

A

MOA: increased ammonia metabolised to glutamine = symptoms

RFS: infection, GI bleeding, constipation, high protein diet, zinc deficiency, benzodiazepines

35
Q

How do you manage ascites?

A

sodium restriction +- diuretics (spir/fures) +- large vlume paracentesis

36
Q

How to manage spontaneous bacterial peritonitis?

A

Abx = cefuroxime + metronidazole

37
Q

Definition of SBP?

A

> 250 neutrophils per mmcubed ascitic fluid in absence of other reason e.g. organ inflammation or perforation

Commonly E.coli

38
Q

Management of varices?

A

Primary prohphylaxis = Non selective beta blocker, EVL if large

Ruptured (haematemesis) = ABCDE, IV bloods and fluid. If Hb<7g/dl then terlipressin + abx
EVL after resus when stable

Secondary prophylaxis = non selective beta blocker
TIPS procedure if all else fails