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Robbins Liver & Biliary > Liver path general features > Flashcards

Liver path general features Flashcards

1
Q

What are the major primary diseases of the liver?

A

Viral hepatitis

Alcoholic liver disease

NAFLD (non-alcoholic fatty liver disease)

Hepatocellular carcinoma

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2
Q

Hepatic damage can also occur as secondary result of extra-hepatic diseases, including?

A

cardiac decompensation

Metastasis

Extrahepatic infections

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3
Q

How is the liver able to compensate for mild-moderate damage?

A

There is a large functional reserve

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4
Q

Are liver diseases typically acute or chronic?

A

Chronic (insidious)

Exception is acute hepatitis in viral hepatitis, and fulminant hepatitis

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5
Q

What are the typical cellular signs of liver pathology

A

Hepatocyte degeneration and intracellular accumulations

Hepatocyte necrosis and apoptosis

Inflammation

Fibrosis

Regeneration

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6
Q

How may a liver progress to failure?

A

Through massive parenchymal damage (fulminant hepatitis)

Or through repeated waves of damage over a long period of time (seen in chronic liver diseases)

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7
Q

What is the threshold for hepatocyte loss before the onset of liver failure?

A

80-90%

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8
Q

What is the mortality of liver failure without transplantation?

A

80%

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9
Q

What is the definition of acute liver failure?

A

Progression of liver damage to hepatic encephalopathy within 6 months

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10
Q

Does fulminant liver failure occur quicker than acute liver failure?

A

Yes

Fulminant failure is within 2 weeks, acute is within 6 months

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11
Q

What are the primary causes of acute liver failure?

A

Infection (hep viruses, CMV, yellow fever)

Drugs (paracetamol, isoniazid, halothane)

Toxins (mushroom toxin, tetrachloride)

Vascular (Budd-Chiari syndrome, veno-occlusive disease)

Other (alcohol, haemochromatosis, alpha1-anti-trypsin deficiency, Wilson’s disease, fatty liver of pregnancy)

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12
Q

Does the liver need to undergo overt necrosis to suffer liver failure?

A

No

Hepatocyte function can be viable but unable to perform normal function, as with tetracycline toxicity and acute fatty liver of pregnancy

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13
Q

What are the three categories of liver failures?

A

Acute

Chronic

Failure without overt necrosis

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14
Q

Name 6 clinical features of hepatic failure

A

Jaundice

Asterixis

Hypoalbuminaemia

Hyperammonaemia (contributes to encephalopathy)

Foetor hepaticus (from porto-systemic shunting)

Palmar erythema

Spider angiomas

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15
Q

What is the aetiology of palmar erythema and spider angiomas in liver failure?

A

Impaired oestrogen metabolism in the liver leading to hyperoestrogenaemia

Decreased inactivation of vasoactive endotoxins by the liver (palmar erythema)

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16
Q

What are some major causes of death in hepatic failure?

A

Hepatic encephalopathy

Hepatorenal syndrome

Hepatopulmonary syndrome

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17
Q

Describe the aetiology of coagulopathy in hepatic failure, and the consequence that has back on the liver

A

Impaired hepatocyte function leads to paucity of clotting factors

Gastrointestinal bleeding

Uptake of blood in intestines leads to further metabolic load

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18
Q

What is elevated in the blood to specifically cause hepatic encephalopathy?

A

Nitrogenous wastes, in the form of ammonia

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19
Q

How do astrocytes cause hepatic encephalopathy?

A

They clear the hyperammonaemia with the conversion of glutamate to glutamine

Excess glutamine in the brain causes an osmotic imbalance, resulting in net water shift into neurons -> cerebral oedema

20
Q

What is hepatorenal syndrome?

A

Renal failure in patients with advanced chronic liver disease

21
Q

What diagnosis would be suspected in a patient with pre-renal uraemia and liver failure?

A

Hepatorenal syndrome

22
Q

T/F hepatorenal syndrome responds to fluid replacement

A

False

23
Q

Is urea the best way to measure renal function on a background of liver failure/disease?

A

No; urea is synthesised in the liver

Creatine is better as it does not rely on the liver functioning correctly and better reflects only the kidneys

24
Q

What leads to hepatorenal syndrome?

A

Decreased renal perfusion pressure due to systemic vasodilation

Activation of the renal sympathetic nervous system with vasoconstriction of the afferent renal arterioles

Increased synthesis of renal vasoactive mediators, which decrease GFR

RAAS system activation worsens renal vasoconstriction

25
Q

What is hepatorenal syndrome type 1?

A

Rapidly progressive deterioration in circulatory and renal function

Median survival of <2 weeks

26
Q

What is hepatorenal syndrome type 2?

A

Slow deterioration of circulation and renal function

Median survival of ~6 months

27
Q

How do you treat hepatorenal syndrome?

A

IV albumin + vasoconstrictors (replenish depleted volume)

Haemodyalisis for support

Liver transplant will most likely be needed eventually

28
Q

If a patient has liver failure, what complications need to be monitored for?

A

GI bleeding, esp oesophageal varices

Sepsis

Encephalopathy

Hypoglycaemia

Spontaneous bacterial peritonitis

29
Q

What blood tests should be performed daily on a liver failure patient?

A

FBC, U&E, LFT + INR

30
Q

What special consideration should be given to prescribing drugs to a liver failure patient?

A

Whether the drug has hepatic metabolism

31
Q

What drugs should not be given to a liver failure patient?

A

Diuretics (^ risk of encephalopathy)

Hypoglycaemics (already at risk of hypoglycaemia)

Saline containing IV’s

Sedatives (confuse hepatic encphalopathy diagnosis)

Paracetamol, isoniazid, oestrogen, 6-mercaptopurine and methotrexate, salicylates, tetracycline

32
Q

What characterises hepatopulmonary syndrome?

A

Tried of chronic liver disease, hypoxaemia, and intra-pulmonary vascular dilations (IVPDs)

33
Q

How will a patient with hepatopulmonary syndrome appear when seated upright?

A

They will have dyspnoea and hypoxaemia (platypnea and orthodeoxia respectively)

34
Q

What is thought to cause hepatopulmonary syndrome?

A

Increased hepatic production of, or reduced hepatic clearance of, vasodilators (esp NO)

35
Q

What two processes lead to the symptoms of hepatopulmonary syndrome?

A

Vasodilation causes ventilation-perfusion mismatch (too much perfusion for the same ventilation)

Late in the syndrome there is high output failure (fast blood flow through capillaries lessens time in capillary for RBCs, worsening hypoxia)

36
Q

What are some poor prognostic markers in liver failure/disease?

A

Grade III/IV encephalopathy (stupor, significant confusion/coma)

Albumin 40yrs

Late onset hepatic failure worse than fulminant failure

37
Q

What characterises cirrhosis histologically?

A

Loss of normal hepatic structure throughout entire liver

Extensive fibrosis

Expanding regions of regeneration (gives it the distinctive nodular gross appearance)

38
Q

What are main causes of cirrhosis?

A

Chronic alcohol abuse

NASH

Chronic infection (HBV/HCV)

Autoimmune disease

Haemachromatosis, alpha1 anti-trypsin deficiency, Wilson’s disease

Vascular (Budd-Chiari syndrome)

39
Q

List the three central pathogenic processes of cirrhosis

A

Hepatocyte death

ECM deposition by myofibroblasts (converted from stellate cells)

Vascular reorganisation

40
Q

Is cirrhosis always symptomatic?

A

No

40% of patients are asymptomatic until decompensation or simple disease progression

41
Q

What are some signs found in cirrhosis patients?

A

Leuconychia, clubbing

Hyperdynamic circulation

Dupuytrens contractures

Spider naevi and other signs of portal HTN

Hepatomegaly (or small liver, in late disease)

42
Q

Is coagulopathy a complication of cirrhosis?

A

Yes

Decreased production of clotting factors II, VII, IX and X cause ^ INR)

Also, if cholestasis present, decreased micelle entry into small intestine reduces vit K absorption with resulting lowering of clotting factor production

43
Q

What are some decompensation events for cirrhosis?

A

Superimposed hepatic metabolic load (from systemic infection or GI haemorrhage)

Hepatopulmonary syndrome leading to hypoxia (^ stress)

44
Q

T/F cirrhosis is a major risk factor for hepatocellular carcinoma

A

True

Must screen every 3-6 months in cirrhosis patients

45
Q

How can cirrhosis be treated?

A

Transplant is the only cure

Treat causes (eg infection, alcohol etc)

Treat symptoms (eg support body systems)

46
Q

How can hepatic encephalopathy be treated?

A

Lactulose (moves ammonia into gut lumen)

Antibiotics (lowers ammoniagenic bacteria populations in gut; Rifaximin)

Robbins Liver & Biliary (6 decks)

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