Alcoholism & Hepatitis - 205 Flashcards

1
Q

What is the most common cause of liver disease in the UK?

A

Alcohol

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2
Q

What is the mechanism for a fatty liver in alcoholism?

A

NAD is used up in the metabolism of ethanol, this means that there is less available for gluconeogenesis, so less glucose is made resulting in a build up of fatty acids.

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3
Q

What hepatic manifestations does alcoholic liver disease encompass?

A

Fatty liver, alcoholic hepatitis, hepatic fibrosis/cirrhosis

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4
Q

How common is a fatty liver in alcoholics?

A

90% of alcoholics have a fatty liver

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5
Q

What is alcoholic hepatitis and what causes it?

A

Inflammation of the liver - caused by the toxic effect of acetaldehyde. It presents acutely.

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6
Q

Name 3 causes for chronic liver disease

A

Alcoholic Liver Disease
Chronic Viral Hepatitis
Obesity

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7
Q

What is the route of transmission of Hepatitis A and Hepatitis E?

A

Oral-faecal

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8
Q

What is the route of transmission of Hepatitis B and Hepatitis C?

A

Parenteral

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9
Q

In the prodromal phase of hepatitis what might patients complain of?

A

Flu-like symptoms, anorexia, nausea, vomiting, fatigue, malaise, low-grade fever (<39.5), myalgia and mild headache.

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10
Q

In the icteric phase of hepatitis what might patients complain of?

A

Dark urine, pale stools, GI symptoms, malaise, R upper quadrant pain, hepatomegaly, jaundice, fever

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11
Q

What investigations would you do in a patient that you expect might have viral hepatitis?

A

FBC, U&E, LFTs, clotting, serology, PCR

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12
Q

Is there a vaccine present for Hepatitis A, B and E?

A

Yes! There is NOT a vaccine for Hep C or D

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13
Q

Which viral hepatitis is there PEP (post exposure prophylaxis) available for?

A

Hepatitis B

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14
Q

Which viral hepatitis is more common in gay men?

A

Hep. C

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15
Q

Which viral hepatitis’ are treated with drugs? Which drugs?

A

Hep. B and C.
Hepatitis B -> Peg IFN, Tenofovir, Entercavir
Hepatitis C -> Peg IFN, Ribavirin, DAAs

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16
Q

In what situation in Hepatitis D present?

A

In the presence of active Hepatitis B.

17
Q

What is the difference in metabolism between 1st and 2nd pass metabolism of alcohol?

A

1st pass uses alcohol dehydrogenase which is found in the cytoplasm
2nd pass uses microsomal ethanol oxidising system
- Both are used when the concentration of ethanol is so high that 1st pass metabolism cannot deal with it all.

18
Q

What is the risk of hypoglycaemia in someone that has just consumed a large amount of alcohol?

A

If the large alcohol metabolism were to coincide with a period when blood glucose is falling it could lead to hypoglycaemia

19
Q

What factors can exacerbate fatty liver progression to hepatitis?

A

Diet high in unsaturated fat

Deposition of excess iron in the liver

20
Q

What ion channels/receptors does ethanol affect?

A

GABA, NMDA, calcium channels

21
Q

What affect does ethanol have on the activity of GABA?

A

It enhances its effect. GABA is an inhibitory neurotransmitter and alcohol increases the inhibition

22
Q

What affect does ethanol have on glutamate?

A

Glutamate is an excitatory neurotransmitter and it’s effect is reduced by alcohol. (NMDA receptors inhibited)

23
Q

What is responsible for memory loss and alcohol consumption?

A

NMDA receptor inhibition.

24
Q

What is the definition of tolerance?

A

Decreased response to effects of a drug concentration after continued use

25
Q

What are some mechanisms underlying chronic alcohol tolerance?

A

Increase in number of and activity of enzymes that metabolise ethanol. More NMDA receptors -> different function

26
Q

What is the Himmelsbach hypothesis regarding withdrawal?

A

Withdrawal happens when the adaptations that characterise tolerance take place without the drug in the system

27
Q

Give an example of an opioid receptor antagonist that can be used to treat alcoholism

A

Naltrexone and Nalmefene

28
Q

What receptor does caffeine act on?

A

Adenosine receptor antagonist

29
Q

What is the triad of symptoms in Wernicke’s encephalopathy?

A

Encephalopathy, oculomotor disturbance, gait ataxia

30
Q

What is thought to cause Wernicke’s encephalopathy? (What is it?)

A

Acute neurological symptoms due to CNS damage caused by thiamine deficiency. WE can progress to Korsakoff’s syndrome and this occurs more commonly in patients who abuse alcohol

31
Q

How is Wernicke’s encephalopthy treated? How is Korsakoff’s syndrome treated?

A

WE -> thiamine supplements

Korsakoff’s -> pabrinex and lactulose

32
Q

When might ALT and AST levels be raised? (LFTS)

A

ALT and AST are found in hepatocytes and released in hepatocellular disease.

  • If ALT and AST are raised by 10x or more -> acute viral hepatitis (HAV), O/D
  • If ALT and AST are raised by 5x or more -> chronic hepatitis (HBC, HCV), alcoholic hepatitis
33
Q

When might ALP or GGT be raised? (LFTs)

A

They are released in response to damage to bile canaliculi and cholestatic disease

34
Q

If LFTs show increased levels of unconjugated bilirubin what could this point to?

A

Haemolysis or a congenital disorder such as Guilberts.

35
Q

If LFTs show increased levels of conjugated bilirubin what could this point to?

A

Infection, cholestasis.

36
Q

What could high levels of unconjugated bilirubin on a LFT be suggestive of?

A

Haemolysis. E.g. Guilbert’s Disease