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NLM2 > Alcohol week > Flashcards

Alcohol week Flashcards

1
Q

Daily units for men and women?

A

3-4 Men

2-3 Women

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2
Q

Criteria for alcohol dependence syndrome?

A

A strong desire/compulsion to consume alcohol

Impaired capacity to control drinking

physiological withdrawal state

Evidence of alcohol tolerance

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3
Q

Neurological alcohol related disabilities?

A

Epilepsy

Peripheral neuropathy

Cerebellar degeneration

WKS

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4
Q

GI alcohol related disabilities?

A

Gastritis

Peptic ulceration

Pancreatitis

Oesophageal varices

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5
Q

Psychiatric alcohol related disabilities?

A

Alcohol dependence

Depression/anxiety

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6
Q

Steps of normal ethanol metabolism in the liver?

A

Ethanol to Acetaldehyde (catalysed by Alcohol dehydrogenase) - NAD to NADH

Acetaldehyde to Acetate (Acetaldehyde dehydrogenase) NAD to NADH

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7
Q

How much alcohol is metabolised in the normal system and how much in the MEOS system?

A

80-90% in normal

10-20% in MEOS system

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8
Q

What are the steps of alcohol metabolism in the MEOS system?

A

Ethanol to acetaldehyde (catalysed by CYP2E1)

During: NADPH + H+ + O2 = NADP+ + 2H2O

Stops there

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9
Q

What damage is done by acetaldehyde?

A

Flushing (dilated capillaries

Nausea and Vomiting

Liver Damage from free radicals

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10
Q

How does acetaldehyde cause liver damage?

A

Inhibits glutathione which protects agains H2O2 damage

Binds and inhibits enzymes that prevent free-radical damage

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11
Q

How are alcoholics treated pharmacologically, how’s it work?

A

Disulfiram - inhibits ALDH (which breaks down acetaldehyde into acetate)

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12
Q

How are there differences in people’s ability to process alcohol?

A

ADH, ALDH and CYP2E1 can all have genetic differences that can make them more or less effective.

Drinking history - levels of gastric ADH decrease and levels of CYP2E1 increase

Gender - females have lower gastric ADH

Quantity - as more alcohol is consumed more is processed by the MEOS pathway

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13
Q

Stages of liver damage?

A

Fatty Liver

Hepatitis/Fibrosis

Cirrhosis

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14
Q

What causes an increased NADH to NAD ratio in alcohol consumption?

A

The conversion of ethanol to acetaldehyde by ADH

The Conversion of acetaldehyde to acetate

Both produce NADH from NAD

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15
Q

What does the increased NADH to NAD ratio cause?

A

Fatty liver

Ketoacidosis

Lacticacidosis

hyperuricaemia

Hypoglycaemia

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16
Q

How does an increased NADH to NAD ratio cause a Fatty Liver?

A

NADH increases the availability of glycerol-3-phosphate

This means triacylglycerides are converted to VLDS

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17
Q

How does increased NADH lead to ketoacidosis?

A

Fats that are oxidised to acetyl CoA are encouraged to enter ketogenesis rather than the TCA cycle due to the presence of high concentrations of NADH

High amounts of alcohol also increases the amount of acetate, which is a preferential fuel to ketones and means there are more ketones in the body

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18
Q

How are lacticacidosis and hyperuricaemia caused by the increased NADH to NAD ratio?

A

NADH encourages lactate to be formed instead of pyruvate after glycolysis producing lacticacidosis

lactic acid decreases uric acid excretion = hyperuricaemia

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19
Q

How is hypoglycaemia caused by the high NADH to NAD ratio?

A

The reduction of gluconeogenesis

Reduced as less pyruvate is formed (lactate instead)

Other factors prevented from entering Gluconeogenesis as well, such a:s oxaloacetate

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20
Q

Presenting signs of an alcoholic?

A

Resting tachycardia

Hepatomegaly

Ascites (belly)

peripheral neuropathy

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21
Q

An alcoholics blood results? Why?

A

Reduced RBC + Haemoglobin, increased clotting time, hyperbillirubic due to reduced liver function

HCHb (Hb per cell) is normal there is just reduced cells

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22
Q

Why do alcoholics have a decreased appetite? why is this problematic?

A

Due to high calorie content of alcohol, problematic as will eat less and will get less nutrition.

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23
Q

Main nutrients that are deficient in alcoholism?

A

Thiamin, Folate, B12

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24
Q

What does thiamin deficiency cause?

A

Initially: Weight loss, irritability

Later: peripheral neuropathy, tachycardia, headache

25
Q

What does folate deficiency cause?

A

Megaloblastic anaemia due to altered RBC formation

26
Q

What does B12 deficiency cause?

A

Megaloblastic anaemia and also it is used to form myelin and so neuropathy

27
Q

What does Lowered albumin cause?

A

Decreased synthesis of clotting factors

Expansion of ECF = ascites

28
Q

What is Wernicke-korsakoff syndrome (WKS)?

A

Confusion, Ataxia and Opthalmoplegia

29
Q

Nutritional management of alcoholic?

A

Parentovite (thiamin + others)

Complete multivit/min

Folate

30
Q

Differentiate between decriminalisation and legalisation of drugs?

A

Decriminalisation - making the possession of drugs no longer a criminal offence

Legalisation - Making drug use, possession, production and distribution legal, but strictly controlled

31
Q

Reasons to decriminalise drugs?

A
  • Public health approach could be taken, perhaps improving the ability to tackle a major health issue
  • Purity and potency could be controlled
  • Reduce burden on police
  • Reduced Crime
  • Taxes will make money
  • Could boost economy/provide jobs
32
Q

Reasons not to decriminalise drugs?

A
  • Could give the impression drug use is safe
  • Not lead to reduced crime
  • More people at risk of harm
33
Q

What do drugs of abuse target in the brain to bring about their addictive quality?

A

Mesolimbic dopaminergic pathway and the nucl

34
Q

Main categories of drugs of abuse and examples?

A

Narcotic analgesics - opioids

Psychomotor stimulants - cocaine, amphetamines, nicotine

Psychomimetic stimulants - LSD, Cannabis, MDMA

CNS depressants - Alcohol, Benzodiazepines, solvents

35
Q

Definition for tolerance?

A

An increased dosage needed to obtain the same effects as in the past

36
Q

Two types of dependence and their definitions?

A

Physical dependence - a state in which the person only functions normally under the influence of the drug

Psychological - consists of cravings

37
Q

Pharmacological approaches to treating opioid withdrawal?

A

Methadone - to alleviate withdraw and long term substitution

Buprenorphine and lofexidine can also be used to allieveiate withdrawal symptoms

38
Q

Effects of cocaine?

A

Euphoria

Alertness

Increased confidence

Increased sexual feelings

39
Q

Mechanism of cocaine’s action?

A

Inhibits re-uptake of 5-HT, NA and DA in the synaptic cleft

Blocks Na+ channels, a1-adrenoceptor agonist

40
Q

Effects of amphetamines and their mechanism of action?

A

Euphoria and excitement

Increased stamina

acute schizophrenic attack

Displaces NA and DA and inhibits their action

41
Q

Formula to work out units of alcohol?

A

%ABV x vol (ml) / 1000

42
Q

Why do we use a BDZ to help with alcohol withdrawal?

A

It acts on GABA receptors, which alcohol acts on and so will produce relief of some withdrawal symptoms, but will not become dependent

43
Q

Alcohol withdrawal symptoms?

A

Uncomplicated:

Insomnia
Increased BP
Tachycardia
Pyrexial
Anxiety

Complicated:

Seizures
Hallucinations
Delirium
Delusions

(can use antipsychotic)

44
Q

What is Wernicke-Korsakoff syndrome, what causes it?

A

Ataxia, Loss of memory activity and memory (can be severe), visual changes

Caused by a lack of thiamine (vit. B1)

45
Q

Symptoms of opioid OD?

A 
Pin point pupils
depressed respiratory rate
Hypotension
Bradycardia
Cool Moist skin
46
Q

Adverse effects of amphetamines?

A

Anxiety irratibility and restlessness

Tolerance/dependence

47
Q

Pharmacological treatments for nicotine dependence?

A

Alleviate withdrawal: Clonidine (a2 adrenoceptor agonist)

Nicotine replacement therapy

Block responses: Mecamylamine

Modification of cravings: Bupropion (antidepressant)

48
Q

Mechanism of cannabis’ action?

A

Binds to CB1 cannabinoid receptors

49
Q

Pharmacological treatments for alcohol dependence?

A

BDZ, or clonidine (a2 receptor agonists)

Disulfiram (induve unpleasant response to alcohol)

Bupropion (antidepressant)

50
Q

How is dopamine involved in reward circuits?

A

Mesolimbic pathways: D2 receptors inhibit cAMP production in the NAcc, It inhibits activity in the medial forebrain which is inhibitory projecting to the prefrontal cortex, this is disinhibition to the prefrontal cortex

51
Q

What are the neuroanatomical factors of addiction?

A

Drug associated cues activate dopamine and endorphin release in the: Amygdala, striatum and other areas

52
Q

What is the biological basis of dependence and tolerance?

A

Repeated use of the drug leads to down-regulation of neurotransmitter release and upregulation of autoreceptors, this produces tolerance, meaning more is required to bring about the same response

Synaptic plasticity alters the weight of existing connections in the mesolimbic pathway, there is excessive NA output from the locus ceruleus

53
Q

What two areas do drugs of dependence have an effect on?

A

The VTA and the NAcc

54
Q

The tree groups of harms of substance misuse?

A

Social, psychological, Physical

55
Q

How many units do men and women have to be having daily to be at an increased risk drinking group, and a higher risk drinking group?

A

Above 3-4 for men to be increased, 2-3 for women

More than 8 units a day for men and 6 for women to be at a higher risk group

56
Q

What are teratogens?

A

Agents that cause defects or malformations in the developing embryo or foetus

57
Q

Clinical features of Foetal Alcohol Syndrome?

A

Thin upper lip, Flat mid-face

Growth retardation

Learning difficulties, hearing loss

58
Q

What amounts of drinking give a particular risk to FAS?

A

above 5 units in one session in first trimester

3-4 units a day

59
Q

The vomiting centre and the CTZ use what receptors?

A

Vomiting centre: Muscarinic and Histamine

CTZ: 5HT3 and dopamine

NLM2 (14 decks)

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