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
What are some mechanisms underlying chronic alcohol tolerance?
Increase in number of and activity of enzymes that metabolise ethanol. More NMDA receptors -> different function
26
What is the Himmelsbach hypothesis regarding withdrawal?
Withdrawal happens when the adaptations that characterise tolerance take place without the drug in the system
27
Give an example of an opioid receptor antagonist that can be used to treat alcoholism
Naltrexone and Nalmefene
28
What receptor does caffeine act on?
Adenosine receptor antagonist
29
What is the triad of symptoms in Wernicke's encephalopathy?
Encephalopathy, oculomotor disturbance, gait ataxia
30
What is thought to cause Wernicke's encephalopathy? (What is it?)
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
How is Wernicke's encephalopthy treated? How is Korsakoff's syndrome treated?
WE -> thiamine supplements | Korsakoff's -> pabrinex and lactulose
32
When might ALT and AST levels be raised? (LFTS)
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
When might ALP or GGT be raised? (LFTs)
They are released in response to damage to bile canaliculi and cholestatic disease
34
If LFTs show increased levels of unconjugated bilirubin what could this point to?
Haemolysis or a congenital disorder such as Guilberts.
35
If LFTs show increased levels of conjugated bilirubin what could this point to?
Infection, cholestasis.
36
What could high levels of unconjugated bilirubin on a LFT be suggestive of?
Haemolysis. E.g. Guilbert's Disease