Case 3 - alcohol Flashcards

1
Q

how is alcohol absorbed

A

absorbed form the upper small intestine via the portal vein and is then transported to the liver

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2
Q

what is some alcohol in the stomach metabolised by

A

alcohol dehydrogenase

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3
Q

why is womens safe limit less than men

A

they have a lack of alcohol dehydrogenase

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4
Q

where is the rest of alcohol metabolised

A

the liver

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5
Q

what happens in the liver to this alcohol

A

converted to acetaldehyde and excreted by conversion to carbon dioxide in citric acid cycle

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6
Q

what enzyme is involved in the metabolism of alcohol in the liver

A

cytochrome p4502E1

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7
Q

what is alcohol at low levels

A

a stimulant

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8
Q

what happens if there is chronic use of alcohol

A

it has depressant effects on the CNS , mainly depression of cardiovascular and repsiratory centres in the brainstem

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9
Q

at low doses, what does alcohol protect against

A

atheromas

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10
Q

what is Wernicke’s encephalopathy

A

decreased thiamine effects mammiliary bodies in the brain

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11
Q

what is induced in alcohol related disease mechanisms

A

induction of enzyme systems, especially cytochrome p450

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12
Q

what is the biggest nutrient deficiency

A

vitamin B

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13
Q

what is the early change in alcohol liver disease

A

acute fatty change

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14
Q

which area does this acute fatty change usually affect

A

predominantly acinar zone 3 - this area is furthest away from a blood supply

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15
Q

features of acute fatty change

A

Mainly large droplet
May cause acute hepatic failure
Reversible on withdrawal of alcohol

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16
Q

what is alcoholic hepatitis

A

alcoholic steatohepatitis

17
Q

what is alcoholic steatohepatitis

A

fatty change, mainly large droplet

18
Q

what is there an accumulation of in alcoholic hepatitifs

A

Intracytoplasmic accumulation of cytoskeletal components (keratin)

19
Q

what is associated with alcoholic steatohepatitis

A

associated neutrophil polymorph infiltration

20
Q

what is non-alcoholic steatophepatitis

A

Identical features to alcoholic hepatitis
Associated with obesity, diabetes mellitus, hyperlipidemia, drug use (corticosteroids)
May progress to fibrosis and cirrhosis
Reversible on correction of underlying factor

21
Q

what is hepatic fibrosis, where does it start and what is it caused by

A

Starts in acinar zone 3
Initially pericellular fibrosis
Caused by activation of hepatic stellate (ito) cell = facultative myofibroblast
Reversible by TIMPs on withdrawal of alcohol

22
Q

is cirrhosis reversible

A

no

23
Q

what happens when there is liver failure as a result of cirrhosis

A

Protein synthesis: low albumin
Coagulation factors: bleeding
Hyperoestrogenism: gynacomastia, gonadal atrophy, Dupuytren’s contracture, liver palms, spider naevi
Jaundice
Encephalopathy: confusion

24
Q

what are the blood tests that can be done to identify heavy drinkers

A

gamma glutamyl transferase (GGT)
Mean corpuscular volume (MCV)

Screening tools:
CAGE or AUDIT can help

25
Q

what score on the CAGE test is clinically significant

A

2 or greater

26
Q

what is an addict

A

someone who has no control over their behaviour, lacks moral fibre, uses a maladaptive coping mechanism and has an addictive behaviour

27
Q

what is addiction

A

: a need for a drug, the use of a substance that is psychologically and physiological addictive, showing tolerance and withdrawal

28
Q

what is dependency

A

showing psychological and physiological withdrawal

29
Q

what are the three theories of addiction

A

Moral model; addiction as a result of weakness and a lack of moral fibre

Biomedical model; addiction as a disease

Social learning theories; behaviours that are learned according to the rules of the learning theory

30
Q

what is the moral model of addiction

A

addicts are weak, and can overcome a compulsion to use with willpower
Drug abusers choose to use drugs
Drug abusers are anti-social and should be punished
Drugs are evil

31
Q

what is the biomedical model of addiction

A

addiction is a brain disease
Neurotransmitter imbalance
Disease model:
Agent: drug
Vector: dealers
Host: addict
need to stamp out the disease by eliminating drugs
Drug antagonist medicine e.g Wellbutrin, naltrexone, Antabuse

32
Q

what is the social model of addiction

A

drug use is a learned behaviour
Classical conditioning: associative behaviour
Operant conditioning: probability of behaviour occurring Is increased if it is either positively reinforced by the presence of a positive event, or negatively reinforced by the absence or removal of a negative agent
Observational learning/modelling: behaviours are learnt by observing significant others carrying them out
Cognitive factors: factors such as self image, problem solving behaviour, coping mechanisms

33
Q

what does alcohol do to GABA interneurones

A

alcohol inhibits the inhibition of GABA interneurones have on dopamine neurones

34
Q

what happens when dopamine interneurones are dis inhibited

A

increase in dopamine

35
Q

what happens when there is extra dopamine in the brain

A

the dopamine receptors up regulate

36
Q

what happens then, when you are presented with the stimulus of alcohol

A

your response is dampened, therefore you have to drink more to maintain the state of reward sensation and so you become addicted