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SBOMS > Liver > Flashcards

Liver Flashcards

1
Q

Stages of chronic liver disease?

A

Fibrous expansion, bridging, cirrhosis - cancer development

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2
Q

Consequences of decompensation in chronic liver disease

A

Bleeding
Jaundice
Ascites
Encephalopathy

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3
Q

What is Cholestasis?

A

When bile does not enter the duodenum.

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4
Q

Signs/Features of Cholestasis?

A

Pale fatty stools, Dark Urine, Jaundice and raised ALP.

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5
Q

In what situations does ALP increase?

A

ALP is produced by cells lining the biliary ducts in the liver and so will rise in bile duct obstruction (causing cholestasis), intrahepatic cholestasis and infiltrative diseases of the liver.

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6
Q

In what situations are AST and ALT likely to rise?

A

Situations involving liver cell necrosis. Hepatitis, Alcohol induced liver toxicity, shock, sepsis.

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7
Q

What clinical signs are there at end stage liver failure?

A

In order of severity:

ALT raised
Jaundice
INR prolonged
Encephalopathy

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8
Q

Why do we produce bile?

A

Bile salts are crucial for digestion and the absorption of fats and fat soluble vitamins

Removal of endogenous waste products/drugs

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9
Q

Liver disease risk factors?

A 
Alcohol intake
Obesity/Diabetes
Parenteral Virus (hepatitis)
Autoimmune disease
FH
PMH of associated symptoms
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10
Q

Physical signs of Chronic Liver disease?

A 
Jaundice
Palmar Erythema
Spider Naevi
Xanthelasmata
Gynaecomastia
Signs of portal hypertension
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11
Q

What is liver cirrhosis? What can cause liver cirrhosis?

A

Long term liver damage resulting in fibrous tissue replacing the normal liver parenchyma

Alcoholic liver disease
Non-alcoholic fatty liver disease
Hepatitis

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12
Q

Clinical plan when dealing with liver disease?

A

Cirrhotic liver disease
- Look for and try to prevent complications (portal hypertension, cancer risk)

Non-Cirrhotic

  • Diagnose cause of abnormality
  • Prevent progression
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13
Q

What is Hepatic Compensation and Decompensation?

A

Compensation happens in cirrhotic liver disease as it has come on over a longer time, Liver and associated systems have adapted to decreased liver function.

In an acute event such as a Bleed, Sepsis, Hypovolaemia this does not happen which leads to Jaundice, coagulopathy, renal dysfuction, Encephalopathy

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14
Q

Consequences of portal hypertension?

A

Varices (oesophageal, gastric)

Hypersplenism (low platelets)

Ascites (Renal dysfunction, Na+ problems)

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15
Q

How is arterial volume maintained in early and late stage cirrhotic disease?

A

early: Plasma expansion increased cardiac output.

Late: Vasoconstrictor and antinatriuretic factors causing sodium and water retention.

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16
Q

Management of ascites?

A

Salt and water restriction
Diuretics
Seek and treat precipitants

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17
Q

What is Hepatorenal syndrome?

A

Rapid deterioration in renal function in liver disease patients.

18
Q

Pathogenesis of Hepatic Encephalopathy?

A

Ammonia.
CNS GABA receptors.
Central neurotransmitters and circulating aminoacids.
Blood flow and cell swelling

19
Q

Purpose of a Liver biopsy?

A

Surgical:

Confirm presence of Liver neoplasm
Determine the nature of the neoplasm
Exclude underlying pathology

Medical:

Aetiology
Staging

20
Q

Do you need to do HLA matching for transplant livers?

A

No

21
Q

3 Possible Liver autoimmune disorders?

A

Autoimmune chronic active hepatitis

Primary Biliary Cirrhosis

Primary sclerosing cholangitis

22
Q

Difference in type 1 autoimmune hepatitis and type 2

A

Type 1 can affect all ages and is generally less severe than 2, treatment failure is rare and there is a broad range of disease.

Type 2 generally affects pts in childhood, Is more severe and treatment is less successful.

23
Q

Hepatitis causes?

A
  • Viral
  • Fatty liver disease
  • Metabolic (e.g. haemochromatosis)
  • Autoimmune
  • Drugs
24
Q

Risks of Ascites?

A

Spontaneous bacterial peritonitis

25
Q

Treatment for hepatic encephalopathy?

A

Lactulose

26
Q

What cells in the liver promote fibrosis?

A

Stellate cells

27
Q

Differences in nodules in Viral cirrhosis and in Non-alcoholic/alcoholic liver cirrhosis?

A

Viral cirrhosis has larger nodules (macronodular)

The opposite in Non-alcoholic/alcoholic liver cirrhosis, they are smaller, micronodular

28
Q

Examples of medications that can cause liver issues?

A 
Paracetamol (Cell necrosis)
Steroids 
COCP
Allopurinol
Penicillin
29
Q

How can you test for Haemochromatosis and Haemosiderosis?

A

Perls stain.

30
Q

Treatment of spontaneous bacterial peritonitis?

A

Ciprofloxacin and Cefotaxime

31
Q

Consequences of hepatitis?

A

Cell death

Inflammation and release of enzymes from dying cells

Reduced functional capacity:

o Raised transaminases
o Unable to handle bilirubin
o Unable to make proteins

32
Q

How do you assess the Liver protein synthesis function?

A

Albumin level and clotting function

33
Q

What role does the liver have in metabolism?

A
  • Protein, lipid, carbohydrate

* Stores fat and carbohydrate

34
Q

Process of exogenous drug metabolism in the liver?

A

Drug bound to protein enters liver sinusoids

Passive diffusion to space of Disse

Entry to hepatocyte:

o Passive diffusion
o Active transport

Metabolism in hepatocytes:

o Phase 1 (CYP450 etc.)
o Phase 2 (conjugation)

Exit liver:
o Via space of Disse- blood-kidney
o Via bile duct

35
Q

Percentage of compensated liver disease pts with varices?

A

40% increases to 60% if they have ascites

36
Q

Portal pressure where they are at risk of bleeding?

A

> 12mm/hg

Normal = 5mm/hg

37
Q

Testing for hepatic encephalopathy?

A

Neurophysiology

Paper pencil

computerised

38
Q

Main medical types of liver disease?

A

Fatty liver disease e.g alcoholic/non-alcoholic

Chronic hepatitis e.g. viral

Biliary disease e.g. primary sclerosing cholangitis

Iron overload e.g Haemochromatosis, haemosiderosis

Metabolic disease e.g. Wilsons disease.

39
Q

What is AMA?

A

Anti-mitochondrial antibody, present in 95% of Primary biliary sclerosis

40
Q

Features of primary biliary sclerosis

A

AMA seen in 95% of patients

Novosphingobium aromaticivorans may be associated

Female:Male 9:1

Some genetic factors - higher incidence in first degree relatives

SBOMS (18 decks)

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