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GI > Liver > Flashcards

Liver Flashcards

1
Q

A AST:ALT ratio of >2 is indicative of…

A

Alcoholic liver disease

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2
Q

ALT > AST

A

Chronic liver disease

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3
Q

What defines chronic liver disease?

A

> 6mths

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4
Q

What are the two types of cirrhosis and describe the differences?

Give 10 clinical signs of cirrhosis

A

Compensated - asymptomatic
Decompensated - symptomatic

Ascietes
Jaundice
Spider naevi 
Splenomegaly 
Palmar Erthyema
Hepatomegaly 
Gynecomastia
Varices - (in paticular caput medusa) 
Clubbing
Easy bruisinig
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5
Q

What cell activates by injury to cause fibrosis and eventually cirrhosis?

A

Hepatic stellate cells

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6
Q

What are the two types of NAFLD (non-alcoholic fatty liver disease)

A

NAFL - steatosis (fatty acid build up in cells)

NASH - non-alcoholic steatohepatitis (more serious)
- steatosis + Inflammation and scarring

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7
Q

Fibrosis isn’t reversible. true or false?

A

True

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8
Q

When would we suspect NAFLD?

A

Abnormal USS or deranged LFTs >3mnths

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9
Q

How do you treat NAFLD (both NASH and NAFL)?

A

Weight loss

Exercise

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10
Q

Why do we worry more about NASH?

A

Risk of progression to cirrohosis

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11
Q

What are mallory bodies and in what condition do we find it?

What condition is associated with ballooning degeneration (a form of apoptosis which causes hepatocellular swelling)?

A

NASH - steatohepatitis
ALD (most commonly)

Damaged intermediate filaments in hepatocytes

NASH - ballooning

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12
Q

In alcoholic liver disease what causes the damage/fibrosis?

A

Acetaldehyde (metabolite of alcohol)

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13
Q

Microscopic differences between fatty liver, alcoholic hepatitis, alcoholic fibrosis and cirrhosis

A

Fatty liver - fat vacuoles

Hepatitis - hepatocyte necrosis, neutrophils, MALLORY BODIES, fibrosis beginning

Fibrosis - COLLAGEN laid down around cells

Cirrhosis - BANDS OF FIBROSIS separating regeneration nodules of hepatocytes

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14
Q

Important questions with liver disease

A

Alcohol consumption (how much and how long)
Travel
Risk behaviour
Any over the counter/herbal

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15
Q

Treatment of ALD?

A
  1. NO ALCOHOL
  • corticosteroids may be used in acute inflammation
  • ?transplant
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16
Q

‘Speckled’ liver

A

Cardiac cirrhosis (due to R sided heart failure causing hepatic congestion)

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17
Q

How do you diagnose cirrhosis?

A

Biopsy which will show:

Regenerating nodules of hepatocytes
AND
Bands of fibrosis separating these nodules

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18
Q

How is cirrhosis graded?

A

Child-Pugh score

A - well compensated
B - functional compromise
C - decompensated

OR

MELD score - 3 month mortality

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19
Q

What score is used to see if someone qualifies for transplant?

A

UKELD score

  • UK score for end stage liver disease
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20
Q

What is portal hypertension and what does it result from?

A

increase of hydrostatic pressure within portal vein or tributaries

Increase resistance to portal flow
Increase portal venous inflow

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21
Q

How does ascites occur (in relation to liver disease)?

A

Cirrhosis causes increases hydrostatic pressure in splanchci vessels -> release NO (vasodilate) -> decreased blood vol -> baroreceptors in kidneys activate RAAS -> sodium and water retention -> decreased osmotic pressure (from decreased albulium) -> liquid in peritoneum

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22
Q

Signs of ascites?

A 
Huge stomach
Shifting dullness (due to liquid)
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23
Q

Treatment of ascites

A

Decrease salt intake
NO NSAIDS

  1. spironolactone
  2. furosemide - loop diueutics

Paracentesis - drain

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24
Q

Hepatorenal syndrome

A

Kidney failure in those with severe liver damage

RAAS activation causes renal vasoconstriction (to try fix vasodilator)

late complication of decompensated cirrhosis/ascietes

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25
Q

Acute liver failure definiton

Clinical features of acute liver failure

How do you treat it?

A

(Any insult to liver causing damage in previously normal liver)

Defined as causing encephalopathy and impaired protein synthesis

Classic jaundice etc.
N+V & anorexia

Rest = 3-6mnths recovery + monitor

26
Q

Paracetamol and liver

A

Glutathione stores breakdown reactive TOXIC intermediate NAPQ1 into cysteine acid conjugates

27
Q

How do you treat paracetamol overdose?

A

Acetlycysteine - replenishes glutathione stores

28
Q

Diagnostic feature of hydatid cyst?

A

Daughter cysts of the periphery (appears as dark mark on CT)

29
Q

What is the most common liver tumour in non-cirrhotic patients?

A

Haemanginoma

Most often asymptomatic and seen on autopsy

30
Q

Metastatic cancer is more common than primary live cancer in the absence of liver disease. True/False?

A

True

31
Q

How is haemanginoma seen on US?

A

Well demarcated echogenic spot

32
Q

Describe the typical appearance of focal nodular hyperplasia?

A

Central scar with a large artery and radiating branches to the periphery

33
Q

Describe the histological differences between focal nodular hyperplasia and hepatic adenoma?

A

FNH - made up of hepatocytes + bile ducts + sinusoids + KUPPFER CELLS

Hepatic adenoma - just hepatocytes

34
Q

What two drugs is hepatic adenoma associated with?

A

Anabolic steroids (common in bodybuilders)

The pill

35
Q

Hepatic adenoma is more common in what sex?

In what sex is it more likely to become maligant?

A

Females

Males

36
Q

Focal nodular hyperplasia has the potential to become malignant. True or false?

A

False

37
Q

How would you treat hepatic adenomas?

A

Males - always surgical removal

Females >5cm - surgery
<5cm - annual MRI

38
Q

Primary liver tumours are more common than secondary liver tumours. True or false?

A

False

Most liver tumours come from colon mestastes - (think portal system)

39
Q

What is the tumour marker used for HCC?

A

Alpha feto protein (AFP) (>400mg)

must not be diagnosed on this purely - some tumours do not increase levels

40
Q

Patient with HCC may present with ascietes. True or false?

A

True

41
Q

What is the first line of treatment in HCC?

A

Resection followed by transplant

42
Q

What drug can be administered in HCC as a last resort to increase life by months?

A

Sorafebnib

kinase inhibitor -> inhibits proliferation of cancer cells

43
Q

What is the macroscopic difference between ALD and NASH?

A

There is none

The difference is made on a history of patients alcohol consumption

44
Q

What is the difference between diagnosis of the two forms of non-alcoholic liver disease?

A

NAFL - USS

NASH - liver biopsy

45
Q

What is micronodular cirrhosis associated with?

A

Alcoholic liver disease - ALD

46
Q

What liver carcinoma is more common in younger patients, will not cause a rise in AFP and on CT will show stellate scar with radial septa showing persistent enhancement?

A

Fibro-lamellar carcinoma

47
Q

How do you investigate for liver cysts?

A

US

48
Q

What can cause hydatid liver cysts?

How must be looked out for on US as a diagnostic tool?

How is it managed?

A

Echinococcus granulosus (tape worm) -> associated with live stock

Daughter cysts (buzzword)

Surgery - most common

49
Q

What causes polycystic liver disease?

Name the 3 types

A

Embryonic ductal plate malformation -> malformation of bile ducts -> numerous cysts throughout liver

Von Meyenburg Complexes - completely benign and asymptomatic

ADPKD (autosomal dominant polycystic kidney disease) - can have maifestations in liver

Polycystic liver disease - genetic disease - more of a problem

50
Q

How is polycystic liver disease managed?

A

Aim is to halt cyst growth

Most commonly - somatostain analogue - sandostatin (reduces liver volume)

Surgery/transplant if very symptomatic

51
Q

What can cause abscess formation in liver?

How does it present?

How do you investigate?

How do you treat?

A

Pus forming cysts
E.coli, klebsellia and step milleri (most common)

Nausea and vomiting
Jaundice
Abdo pain 
~malaise for several months
(v similar to ascending cholangitis)
Hepatomegaly

US/aspiration - diagnose
CT - for more complex

Broad spectrum IV antibiotics
Aspirate for more specific antibiotic treatment
4 weeks of antibiotic treatment afterwards

52
Q

What is haemochromatosis?

What gene and chromosome is the abnormality found on? What kind of inheritance?

Describe classic presentation

How is it diagnosed?

How is it managed?

A

Excess iron deposits in organs in paticular liver

HFE - chromosome 6 - autosomal recessive

Bronzed diabetic

  • Diabetes mellitus
  • Bronze skin pigmentation
  • Hepatomegaly

Measure serum ferritin (iron)

Venesection - remove excess iron

53
Q

What is Wilson’s disease?

How does it present?

Investigate?

How is it managed?

A

Autosomal recessive disorder causing reduced ceruloplasmin (copper transporter)

Kaysler-Fleisher rings
Liver disease

Increase in urinary copper
reduced serum copper

PENICILLAMINE

54
Q

Where is most copper deposited in the brain in a patient Wilson’s disease?

A

Basal ganglia

55
Q

What should be suspected in young females taking oral contraceptive with deranged LFTs?

What causes it?

A

Autoimmune hepatitis

T cells directed against hepatocyte surface antigens

56
Q

How do you investigate and diagnose autoimmune hepatitis?

A

Raised LFTs
ASMA and ANA +ve - type 1
LKM +ve - type 2
Liver biopsy

57
Q

How do you manage autoimmune hepatitis

A

Corticosteroids + azathioproine

58
Q

What is spontaneous bacterial peritonitis?
How is it diagnosed?
How is it treated?

A

Bacterial infection in the peritoneum
NEUTROPHILS in tap will be >250 - important
Co-trimaxazole

59
Q

What is hepatic encephalopathy?

How does it present?

How is it treated?

A

Increased ammonia in blood (highly toxic)

LIVER FLAP
Confusion
Drowsiness
General mental disfunction

Lactulose
Antibiotics e.g. rifaximin (supress colonic flora)

60
Q

What are ASMA antibodies associated with?

What are AMA antibodies associated with?

A 
ASMA = autoimmune hep
AMA = PBC

GI (26 decks)

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