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Flashcards in Liver Deck (31):
1

What are the 7 key functions of the liver?

-Glucose homeostasis - gluconeogenesis & glycogen storage
-Synthesis of clotting factors
-Drug & toxin metabolism
-Bilirubin conjugation & clearance
-Albumin synthesis
-NH3 metabolism
-Immune functions

2

If ALT > AST in an acute presentation, what 3 aetiologies should you be most suspicious of?

-Acute viral hepatitis
-Acute drug toxicity
-Liver ischaemia

3

If LFTs show AST > ALP, what 3 aetiologies does it raise the suspicion of?

-Alcohol
-Cirrhosis
-Paracetamol

4

What 3 parameters of the LFTs are mostly greatly affected in cholestasis?

Bilirubin, GGT, ALP

5

What are some of the definitions of acute liver failure?

-Rapid deterioration of liver function in a previously normal liver
-INR >1.5 or any encephalopathy that develops in under 26 weeks
-'Jaundice to encephalopathy in

6

Name the 4 broad causes of acute liver failure.

-Paracetamol toxicity
-Acute viral hepatitis
-Ischaemia
-Other drug reaction

7

What intervention can improve the outcome of acute liver failure from paracetamol toxicity?

N-acetylcysteine

8

What intervention can improve the outcome of acute liver failure from hepatitis B?

Anti-virals

9

What intervention can improve the outcome of acute liver failure from Wilson's disease?

Chelation/exchange

10

What intervention can improve the outcome of acute liver failure from Budd-Chiari syndrome?

Shunt insertion (TIPS - transjugular intrahepatic portosystemic shunt)

11

What intervention can improve the outcome of acute liver failure from acute fatty liver of pregnancy?

Delivery

12

What intervention can improve the outcome of acute liver failure from autoimmune hepatitis?

Steroids

13

What abnormalities would you expect on liver biopsy following paracetamol overdose?

-Panlobular necrosis
-Relative preservation of portal tracts
-No early inflammatory response

14

Outline the pathogenesis of acute liver failure in paracetamol toxicity.

-Paracetamol is normally metabolized by hepatic glutathione, which conjugates it to glucuronide & excretes it in bile
-When this path is saturated, paracetamol is metabolized via the CYP450 pathway, and becomes a toxic metabolite - NAPQI
-Glutathione normally conjugates NAPQI to make it non-toxic
-When glutathione stores are depleted, the NAPQI accumulates & becomes hepatotoxic

15

What is considered a toxic dose of paracetamol?

200mg/kg or 10g, whichever is less

16

How does N-acetylcysteine work & how soon after paracetamol OD does it need to be given?

NAC works by acting as a glutathione donor (so paracetamol can be excreted even when hepatic glutathione stores are depleted)
-it needs to be given within 8 hours of OD to be 100% effective

17

Name 4 steps in the management of acute paracetamol overdose.

-Reduce absorption: give activated charcoal
-Symptomatic care: anti-emetics
-Risk assessment: dose based/plasma paracetamol concentration
-Specific treatment: NAC

18

Name the causes of chronic liver disease under the following headings - Big 3, Metabolic 3, Autoimmune 3, Other 3:

Big 3: alcohol, hepatitis B, hepatitis C
Metabolic 3: Wilson's disease, A1AT deficiency, haemochromatosis
Autoimmune 3: Autoimmune hepatitis, Primary sclerosing cholangitis, Primary biliary cirrhosis
Other 3: fatty liver disease, Budd-Chiari, chronic biliary obstruction

19

What are 5 symptoms of chronic liver disease?

-Fatigue
-Weight loss or gain
-Abdominal distension
-Confusion
-Bleeding

20

What are 9 signs of chronic liver disease?

-Jaundice
-Spider naevi
-Caput medusae
-Ascites
-Encephalopathy
-Asterixis
-Clubbing
-Dupuytrens contracture
-Splenomegaly
-Leukonychia
-Palmar erythema
-Parotidomegaly (only alcohol)
-Gynaecomastia
-Bruising

21

Outline the stages of liver fibrosis from F0 to F4.

F0 = no fibrosis
F1 = periportal fibrosis, no septa
F2 = periportal fibrosis, some periportal septa
F3 = numerous septa, no architectural distortion
F4 = architectural distorsion & nodule formation

22

Name 5 major complications of CLD and how they should be managed.

1. Oesophageal varices - beta-blockade, band ligation, endoscopic banding
2. Fluid retention - fluid & salt restriction, diuresis
3. Jaundice - no specific treatment
4. Osteoporosis - vitamin D supplementation, regular surveillance of BMD
5. Encephalopathy - supportive care, withdraw potential precipitants

23

What are 5 findings to suggest decompensated liver disease?

Jaundice, coagulopathy, ascites, variceal bleeding, hepatorenal syndrome

24

What is the difference between type 1 and type 2 hepatorenal syndrome?

Type 1 is acute & a more severe renal failure
Type 2 is a more insidious renal failure that is less severe

25

Name a pre-hepatic, a hepatic & a post-hepatic cause of portal hypertension.

Pre-hepatic: portal vein thrombosis, stenosis or compression of the hepatic blood supply
Hepatic: cirrhosis, schistosomiasis, severe steatosis, sarcoidosis
Post-hepatic: hepatic vein obstruction, severe RHF, constrictive pericarditis

26

Outline the biopsy findings in hepatocellular carcinoma.

-Abnormal bile canalicular architecture
-Thickened trabeculae >3 cells
-Pseudo-bile duct spaces
-a-fetoprotein positive

27

What serum marker is usually elevated in HCC?

Alpha-fetoprotein

28

What 2 autoantibodies are present in type 1 autoimmune hepatitis?

Anti-nuclear antibodies
Anti-smooth muscle antibodies

29

What is primary biliary cirrhosis? Name 2 biopsy findings.

Primary biliary cirrhosis is an autoimmune disease causing non-suppurative cholangitis.
Biopsy:
-Florid bile duct lesions
-Chronic cholestasis
-Loss of small bile ducts
-Variable periportal hepatitis

30

What is the mainstay of treatment of primary biliary cirrhosis?

Ursodeoxycholic acid (responds poorly to steroids, unlike autoimmune hepatitis)

31

Name 4 causes of hepatic granuloma & granulomatous hepatitis.

-Tuberculosis
-Sarcoidosis
-Primary biliary cirrhosis
-Drugs