Case 3 - alcohol Flashcards

(36 cards)

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

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
what score on the CAGE test is clinically significant
2 or greater
26
what is an addict
someone who has no control over their behaviour, lacks moral fibre, uses a maladaptive coping mechanism and has an addictive behaviour
27
what is addiction
: a need for a drug, the use of a substance that is psychologically and physiological addictive, showing tolerance and withdrawal
28
what is dependency
showing psychological and physiological withdrawal
29
what are the three theories of addiction
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
what is the moral model of addiction
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
what is the biomedical model of addiction
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
what is the social model of addiction
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
what does alcohol do to GABA interneurones
alcohol inhibits the inhibition of GABA interneurones have on dopamine neurones
34
what happens when dopamine interneurones are dis inhibited
increase in dopamine
35
what happens when there is extra dopamine in the brain
the dopamine receptors up regulate
36
what happens then, when you are presented with the stimulus of alcohol
your response is dampened, therefore you have to drink more to maintain the state of reward sensation and so you become addicted