Liver Function + Pathology Flashcards

1
Q

Functions of the liver

A
  • Storage: e.g. glycogen, vitamins, iron, copper
  • Synthesis: e.g. glucose, lipids, cholesterol, bile, clotting factors, albumin
  • Metabolic: e.g. bilirubin, ammonia, drugs, alcohol, carbs, lipids
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2
Q

Investigations of liver pathology

A
  • LFTs
  • gamma GT
  • FBCs (thrombocytopenia)
  • bilirubin, albumin
  • USS of liver
  • hep B+C serology
  • HIV screen
  • autoantibodies
  • clotting times
  • ferritin + transferrin (haemochromatosis)
  • caeruloplasmin (wilson’s disease)
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3
Q

What is involved in liver screen?

A
  • hep B+C serology
  • Ferritin + transferrin saturation
  • autoantibodies + immunoglobuins
  • alpha 1 antitrypspin
  • coeliac serology (tissue transglutaminase)
  • TFTs, lipids + glucose
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4
Q

Symptoms of liver pathology

A

Jaundice
Oedema/ascites
Bleeding
Confusion

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5
Q

Signs of chronic liver disease

A
  • spider naevi
  • clubbing
  • palmar erythema
  • ascites
  • Dupuytren contracture
  • leukonychia
  • asterixis - flapping tremor
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6
Q

What can cause acute liver failure?

A

Excessive alcohol
Paracetamol overdose
Virus
Medications e.g. aspirin

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7
Q

What is acute liver failure?

A

Sudden onset of liver pathology symptoms with no previous background of liver disease

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8
Q

Why do we avoid giving children aspirin?

A

Can cause acute liver failure

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9
Q

What is cirrhosis

A

Permanent damage to the liver which results to impaired function + distortion of liver architecture in response to chronic inflammation of the liver

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10
Q

Key feature of liver cirrhosis

A

Nodules
Due to bands of fibrosis

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11
Q

Causes of liver cirrhosis

A
  • alcohol related liver disease
  • non-alcoholic fatty liver disease
  • hep B+C
    .
    rare causes:
  • hemochromatosis
  • wilsons disease
  • alpha 1-antitrypsin deficiency
  • primary sclerosing/biliary cholangitis
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12
Q

What is the best imaging for cirrhosis?

A

FibroScan
determines the degree of fibrosis

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13
Q

Management of chronic liver disease

A
  • treat underlying cause
  • monitoring + managing complications
  • liver transplant
  • Child-Pugh Score
  • MELD score every 6 months
  • USS + alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • endoscopy every 3 years of oesophageal varices
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14
Q

When is a liver transplant considered?

A

when there are features of decompensated liver disease

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15
Q

Features of decompensated liver disease

A

AHOY
- Ascites
- Hepatic encephalopathy
- Oesophageal varices bleeding
- Yellow (jaundice)

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16
Q

What score is used to assess the severity of cirrhosis + prognosis?

A

Child-Pugh Score

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17
Q

Outline the Child-Pugh Score

A
  • assesses the severity of cirrhosis + prognosis
  • each factor scored 1-3
  • ABCDE:
  • Albumin
  • Bilirubin
  • Clotting (INR)
  • Diltation (ascites)
  • Encephalopathy
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18
Q

Complications of cirrhosis

A
  • malnutrition + muscle wasting
  • portal hypertension, oesophageal varices + bleeding varices
  • ascites + spontaneous bacterial peritonitis
  • hepatorenal syndrome
  • hepatic encephalopathy
  • hepatocellular carcinoma
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19
Q

What investigation should be done on all patients with ascites?

A

diagnostic ascitic tap
to look for spontaneous bacterial peritonitis

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20
Q

Stepwise progression of alchol realted liver disease

A
  • alcoholic fatty liver (hepatic steatosis)
  • alcoholic hepatitis
  • cirrhosis
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21
Q

What happens to the liver in alcoholic liver disease over weeks?

A
  • Fatty changes due to fatty deposits > Hepatomegaly
  • Normally reversible
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22
Q

What happens to the liver in alcoholic liver disease over years?

A
  • alcoholic hepatitis
  • inflammatory cells + fatty change
  • jaundice
  • right upper quadrant pain
  • Hepatomegaly
  • leads to cirrhosis
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23
Q

What is Wernicke-Korsakoff syndrome?

A

alcohol excess > thiamine deficiency > Wernicke’s encephalopathy + Korsakoff syndrome

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24
Q

Features of Wernicke’s encephalopathy

A
  • confusion
  • disturbance of eye movements
  • ataxia
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25
Q

Features of Korsakoff syndrome

A
  • memory impairment
  • behavioural changes
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26
Q

Management of alcohol related liver disease

A
  • stop drinking (turning point) (disulfiram)
  • cognitive behavioural therapy
  • nutritional support - high vitamins + protein diet
  • treat complications of cirrhosis
27
Q

What infections can cause chronic liver damage?

A
  • Hepatitis B: vaccine but no cure | symptomatic
  • Hepatitis C: cure but no vaccine | asymptomatic
28
Q

Outline non-alcoholic fatty liver disease

A
  • associated with insulin resistance
  • accumulation of triglycerides
  • inflammation over time > NASH non alcoholic steatophepatitis
29
Q

Stages of non-alcoholic fatty liver disease

A
  • non-alcoholic fatty liver disease
  • non-alcoholic steatohepatitis NASH
  • fibrosis
  • cirrhosis
30
Q

Describe the two mechanisms that lead to fatty deposition on liver

A
  • excessive intake of dietary fats: increased triglyceride accumulation in liver
  • regarding insulin resistance: impairs ability of liver to respond to insulin > increased breakdown of fats in adipose > accumulation in liver
31
Q

Management of non-alcoholic fatty liver

A
  • weight loss
  • healthy diet (Mediterranean)
  • exercise
  • limit alcohol intake
  • smoking cessation
  • control of diabetes, BP + cholesterol
32
Q

Outline hereditary haemochromatosis

A
  • increased absorption of iron from small intestines
  • leads to excessive deposition within liver
  • autosomal recessive
  • associated with high levels of ferritin
33
Q

Presentation fo haemochromatosis

A

presents after 40
- chronic tiredness
- joint pain
- bronze skin
- testicular atrophy
- ED
- amenorrhea
- hepatomegaly
- mood + memory disturbance

34
Q

Diagnosis of haemochromatosis

A
  • high ferritin
  • high transferrin
  • genetic testing for mutation of HFE gene
35
Q

Complications of haemochromatosis

A
  • liver cirrhosis + hepatocellular carcinoma
  • ED
  • reduced fertility
  • cardiomyopathy
  • hypothyroidism
  • chondrocalcinosis > arthrisi
  • secondary diabetes
36
Q

Treatment of hereditary haemochromatosis

A

Venesection
Reduces iron in circulation

37
Q

Outline Wilson’s disease

A
  • decreased copper secretion from liver to be removed
  • leads to increased deposition in liver
  • low levels of caeruloplasmin
  • can effect CNS (seizures, memory loss)
  • autosomal recessive
38
Q

Presentation of Wilson’s disease

A
  • Kayser-Fleischer rings in cornea (brown ring)
  • chronic liver disease features
  • abnormal behaviour
  • depression
  • cognitive impairment
  • tremor
  • dysarthria
39
Q

Investigations of Wilson’s disease

A
  • serum caeruloplasmin (low)
  • 24-hour urine copper assay
  • genetic testing
  • MRI brain - double panda sign
40
Q

Management of Wilson’s disease

A
  • copper chelation using penicillamine or trientine
  • zinc salts - inhibits GI copper absorption
  • liver transplant
41
Q

What autoimmune conditions can damage the liver?

A

Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis

42
Q

Why can liver disease can jaundice?

A

Build up of bilirubin as liver cannot metabolise it effectively

43
Q

Why can liver disease cause oedema or ascites?

A
  • decreased synthetic function
  • decrease albumin production
  • decreases osmotic pressure
  • fluid moves out more easily
    .
  • fibrosis > compression of liver sinusoids
  • exerts back pressure on portal vein
  • portal hypertension
  • fluid moves out into abdominal cavity
44
Q

Why can liver disease cause bleeding issues?

A

Decreased synthesis of clotting factors
e.g easy bruising, nosebleeds, long bleeding time

45
Q

What is portal hypertension?

A

When there is increased hydrostatic pressure within the portal venous system due to fibrotic changes in the liver

46
Q

Complications of portal hypertension

A

Ascites
Splenomegaly
Varices

47
Q

What are varices?

A

Dilated veins

48
Q

What is heptaorenal syndrome?

A

Presence of acute or rapidly deteriorating kidney function due to underlying liver cirrhosis + portal hypertension

49
Q

What are the three location for varices in portal hypertension?

A

Oesophagus
Umbilical
Anorectal

50
Q

How does portal hypertension cause oesophageal varices?

A
  • left gastric vein normally drains the lower part of the oesophagus
  • in portal hypertension, varices divert blood to the azygous vein which drains into the SVC
51
Q

Symptoms of anorectal varices

A

Rectal bleeding > anaemia
Pain
Discomfort

52
Q

What are umbilical varices also called?

A

Caput medusae

53
Q

Venous drainage of the oesophagus

A

Upper 2/3: oesophageal veins > azygous vein > SVC
Lower 1/3: left gastric vein > portal vein

54
Q

Prophylaxis of bleeding for oesophageal varices

A

first line: B blockers propanolol
variceal band ligation in B blockers are contraindicated

55
Q

How does hepatorenal syndrome occur?

A
  • presence of cirrhosis + portal hypertension increases NO in gut vasculature
  • results in splanchnic vasodilation
  • body perceives as a drop in circulating volume
  • RAAS activated > systemic vasoconstriction
  • decreased perfusion to kidney > acute kidney injury
56
Q

Why might someone with liver disease become confused?

A

Unconjugated bilirubin can pass the blood brain barrier

57
Q

Name the underlying change that causes liver enlargement following chronic alcohol intake

A

Steatosis (fatty liver)

58
Q

What causes Budd Chiari syndrome?

A

Hepatic vein becomes blocked or narrowed

59
Q

What is the triad of Budd-chiari?

A

Abdominal pain
Ascites
Hepatomegaly

60
Q

How does cirrhosis cause hepatic encephalopathy?

A
  • due to build up of ammonia produced by intestinal bacteria
  • in cirrhosis, the liver cells have a reduced ability to metabolism ammonia into harmless waste products
  • and, collateral vessels between portal + systemic circulation mean that ammonia bypasses the liver
61
Q

Grading of hepatic encephalopathy (presentation)

A
  • Grade 1: reversed sleep pattern, psychomotor slowing, poor memory
  • Grade 2: lethargy, disorientation, asterixis, agitation
  • Grade 3: drowsy
  • Grade 4: coma
62
Q

Management of hepatic encephalopathy

A
  • lactulose
  • antibiotics: e.g. rifaximin to reduced intestinal bacteria
  • nutritional support
63
Q

How does lactulose reduce ammonia?

A
  • speeds up transmit time + reduces constipation > removes ammonia before it is absorbed
  • promotes bacterial uptake of ammonia for protein synthesis
  • makes the intestines more acidic > killing the bacteria