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PSYCH - PHARMACOLOGY Flashcards

1
Q

ANTI-PSYCHOTICS
What are the two types of anti-psychotics?

A
  • Typical/1st generation
  • Atypical/2nd generation
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2
Q

ANTI-PSYCHOTICS
what is the general mechanism of action for anti-psychotics?

A

psychosis is thought to be caused be an excess of dopamine
therefore anti-psychotics aim to reduce dopamine by blocking receptors

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3
Q

ANTI-PSYCHOTICS
Give an example of a typical (1st generation) anti-psychotic.

A

haloperidol,
flupentixol
zuclopenthixol (decanoate = depot)
chlorpromazine

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4
Q

ANTI-PSYCHOTICS
Give examples of atypical (2nd generation) psychotics.

A

olanzapine,
risperidone (depot),
clozapine,
aripiprazole (depot),
quetiapine

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5
Q

ANTI-PSYCHOTICS
What is the mechanism of action of typical (1st generation) anti-psychotics?

A
  • D2 receptor antagonist
  • Reduced release of dopamine from dopaminergic neurones + so reduced electrical activity in dopaminergic pathways
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6
Q

ANTI-PSYCHOTICS
What pathway do typical (1st generation) anti-psychotics work on to have anti-psychotic effect?

A

Mesolimbic pathway (reduces +ve Sx)

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7
Q

ANTI-PSYCHOTICS
What is the mechanism of action of atypical (2nd generation) anti-psychotics?

A
  • Antagonists at dopamine D2 receptors but more selective in dopamine blockade + so block serotonin 5-HT2a
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8
Q

ANTI-PSYCHOTICS
What is the most crucial adverse effect of clozapine?

A
  • Severe life-threatening agranulocytosis
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9
Q

ANTI-PSYCHOTICS
What are the 5 broad categories of SEs caused by anti-psychotics?

A
  • Extra-pyramidal side effects (EPSEs)
  • Hyperprolactinaemia
  • Metabolic
  • Anticholinergic
  • Neurological
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10
Q

ANTI-PSYCHOTICS
What are the extra-pyramidal side effects (EPSEs) of anti-psychotics?

A
  • Acute dystonic reaction
  • Parkinsonism
  • Akathisia
  • Tardive dyskinesia
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11
Q

ANTI-PSYCHOTICS
How does Parkinsonism present?

A
  • Bradykinesia, rigid, resting pill-rolling tremor + postural instability
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12
Q

ANTI-PSYCHOTICS
How does akathisia present?

A
  • Motor restlessness, typically lower legs (can’t sit still)
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13
Q

ANTI-PSYCHOTICS
How does tardive dyskinesia present?

A
  • Purposeless involuntary movements (chewing, lip smacking, blinking, tongue protrusion)
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14
Q

ANTI-PSYCHOTICS
What are the SEs from hyperprolactinaemia?

A
  • Sexual dysfunction (+ anti-adrenergic)
  • Osteoporosis risk
  • Amenorrhoea
  • Galactorrhoea, gynaecomastia + hypogonadism in men
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15
Q

ANTI-PSYCHOTICS
What are the metabolic SEs?

A
  • Weight gain (esp. olanzapine)
  • Hyperlipidaemia, risk of stroke + VTE in elderly
  • T2DM risk + metabolic syndrome
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16
Q

ANTI-PSYCHOTICS
What are the anticholinergic SEs?

A

Can’t see, pee, spit, shit –
- Blurred vision
- Urinary retention
- Dry mouth
- Constipation
+ tachycardia

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17
Q

ANTI-PSYCHOTICS
What are the neurological SEs?

A
  • Seizures
  • Postural hypotension (anti-adrenergic)
  • Sedation
  • Headaches
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18
Q

ANTI-PSYCHOTICS
What baseline investigations are done for people starting on anti-psychotics?

A
  • FBC, U+Es, LFTs, lipids, BMI, fasting glucose, prolactin, BP, ECG (QTc prolongation) + smoking status (can reduce effects by enhancing metabolism so issues if suddenly stop)
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19
Q

ANTI-PSYCHOTICS
What regular investigations are done for people on anti-psychotics?

A
  • Lipids + BMI at 3m
  • Fasting glucose + prolactin at 6m
  • Frequent BP during dose titration
  • FBC, U+Es, LFTs, lipids, BMI, fasting glucose, prolactin + CV risk yearly
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20
Q

ANTI-PSYCHOTICS
What specific monitoring is required for clozapine?

A
  • FBC at baseline + weekly for 18w, fortnightly until 1y + monthly after
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21
Q

ANTI-PSYCHOTICS
What happens if a patient does not take their clozapine for 48 hours?

A

If not taken for 48hr needs retitrating

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22
Q

ANTI-DEPRESSANTS
What monitoring is needed when starting someone on an anti-depressant?

A
  • 2 weekly to ensure dose working + patient stable, may take up to 6w to start working,
  • weekly if <30y as increased suicide risk
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23
Q

ANTI-DEPRESSANTS
How should anti-depressants be stopped?
Why?

A
  • Gradual dose reduction over 4w
  • Sudden cessation can cause severe withdrawal effects (mostly GI) – pain, diarrhoea, vomiting, restlessness, sweating + mood change
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24
Q

ANTI-DEPRESSANTS
What is the mechanism of action of SSRIs?
Give some examples

A
  • Prevents reuptake + subsequent degradation of serotonin from synaptic cleft by inhibiting its reuptake transporter on the post-synaptic membrane
  • Prolonged serotonin in synaptic cleft = prolonged neuronal activity
  • Citalopram, sertraline, fluoxetine
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25
Q

ANTI-DEPRESSANTS
What are the side effects of SSRIs?

A
  • GI Sx most common (N+V, hyponatraemia, abdo pain, bowel issues, increased bleed risk)
  • Sedation + sexual impotence
  • Citalopram + QTc prolongation (dose-dependent)
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26
Q

ANTI-DEPRESSANTS
What are some cautions for SSRIs?

A
  • Suicidal thoughts may increase initially, esp. younger patients
  • May precipitate manic phase in bipolar
  • 1st trimester risk of CHD, 3rd trimester risk of persistent pulmonary HTN
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27
Q

ANTI-DEPRESSANTS
What are some interactions for SSRIs?

A
  • NSAIDs + aspirin = increased risk of bleeding, co-prescribe PPI
  • Can lower seizure threshold
  • Do not start until 2w after stopping MAOI + vice-versa as increased risk of serotonin syndrome
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28
Q

ANTI-DEPRESSANTS
What is the mechanism of action of SNRIs?

A
  • Prevents reuptake + subsequent degradation of serotonin AND noradrenaline from synaptic cleft by inhibiting reuptake transporters on post-synaptic membrane
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29
Q

ANTI-DEPRESSANTS
Give some examples of SNRIs?

A

Venlafaxine, duloxetine

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30
Q

ANTI-DEPRESSANTS
What are some side effects of SNRIs?

A
  • GI (N+V, constipation),
    central/peripheral effects (SIADH, rhabdomyolysis)
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31
Q

ANTI-DEPRESSANTS
What is the mechanism of action of monoamine oxidase inhibitors (MAOI)?

A
  • Inhibits monoamine oxidase enzyme which reduces breakdown of adrenaline, noradrenaline + serotonin so increases level
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32
Q

ANTI-DEPRESSANTS
Give some examples of monoamine oxidase inhibitors (MAOI)?
Give some examples.

A
  • Selegiline is selective MAO-B inhibitor which also increases dopamine
  • Isocarboxazid, phenelzine
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33
Q

ANTI-DEPRESSANTS
What are some side effects from MAOIs?

A
  • Sexual dysfunction, weight gain + postural hypotension
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34
Q

ANTI-DEPRESSANTS
What are some cautions with MAOIs?

A
  • Increased risk of serotonin syndrome if used with other serotonergic drugs
  • Hypertensive crisis with ingestion of foods containing tyramine (aged cheeses, smoked/cured meats, pickled herring, Bovril, Marmite)
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35
Q

ANTI-DEPRESSANTS
What is the mechanism of action of tricyclic antidepressants (TCAs)?

A
  • Prevents reuptake + subsequent degradation of serotonin + noradrenaline from synaptic cleft by inhibiting reuptake transporters on post-synaptic neuronal membrane
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36
Q

ANTI-DEPRESSANTS
Give some examples of tricyclic antidepressants (TCAs)?

A

Amitriptyline, dosulepin, imipramine

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37
Q

ANTI-DEPRESSANTS
What are the side effects of TCAs?

A
  • Anticholinergic (can’t see, pee, spit, shit)
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38
Q

ANTI-DEPRESSANTS
What cautions are there for TCAs?

A
  • Caution in CVD, avoid following MI
  • Cardiotoxic in overdose so caution in suicidal patients (QTc prolongation)
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39
Q

ANTI-DEPRESSANTS
In terms of TCA overdose…

i) mild-moderate Sx?
ii) severe Sx?

A

i) Dilated pupils, dry mouth, urinary retention, increased tendon reflexes + extensor plantars
ii) Fits, coma, cardiac arrhythmias > arrest

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40
Q

ANTI-DEPRESSANTS
In terms of TCA overdose what are the ECG signs?

A

Sinus tachy,
wide QRS,
prolonged QT interval

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41
Q

ANTI-DEPRESSANTS
What is the management of a TCA overdose?

A

Sodium bicarbonate

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42
Q

ANTI-DEPRESSANTS
What is the mechanism of action of mirtazapine?

A
  • Blocks alpha-2 adrenergic receptors > increased release of neurotransmitters
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43
Q

ANTI-DEPRESSANTS
What are some side effects of mirtazapine?

A

Increased appetite + weight gain + sedation are big ones, also increased triglyceride levels

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44
Q

MOOD STABILISERS
What are some examples of mood stabilisers?

A

Lithium (first line)
AEDs such as valproate, carbamazepine, lamotrigine

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45
Q

MOOD STABILISERS
What is the mechanism of action of mood stabilisers?

A

Lithium inhibits cAMP production which inhibits monoamines

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46
Q

MOOD STABILISERS
What is important to note about mood stabilisers?

A

Narrow therapeutic range 0.4–1.0mmol/L

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47
Q

MOOD STABILISERS
What are the side effects of lithium?

A

LITHIUM –
- Leukocytosis
- Insipidus (diabetes, nephrogenic)
- Tremors (fine if SE, coarse if toxicity)
- Hydration (easily dehydrates, renally cleared)
- Increased GI motility (N+V, diarrhoea)
- Underactive thyroid
- Mums beware (Ebstein’s anomaly)

Can cause weight gain + derm (acne, psoriasis) long-term too

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48
Q

MOOD STABILISERS
What drugs does lithium interact with?

A
  • NSAIDs, ACEi, ARBs + diuretics may increase lithium levels
  • Diuretics = dehydration,
    NSAIDs = renal damage
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49
Q

MOOD STABILISERS
What baseline measurements are taken for lithium?

A
  • FBC, U+Es, eGFR, TFTs, BMI + ECG
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50
Q

MOOD STABILISERS
What regular monitoring is done for lithium?

A
  • Weekly serum lithium after initiation + dose changes until stable then every 3m for a year, then every 6m (sample taken 12h after dose)
  • 6m = TFTs, U+Es, eGFR
  • Annual = BMI
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51
Q

MOOD STABILISERS
What might carbamazepine and lamotrigine interfere with?

A
  • Contraceptive pill
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52
Q

HYPNOTICS
What is the mechanism of action of hypnotics?

A
  • GABA agonists on alpha2-subunit of GABA(A)-BDZ receptor/Cl- channel complex
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53
Q

HYPNOTICS
Give some examples

A

Zopiclone, zolpidem, BDZs used for hypnotic effect (lorazepam, temazepam)

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54
Q

HYPNOTICS
What are the adverse effects?

A

Same as BDZs
- Amnesia, ataxia (esp elderly = falls risk), confusion, drowsiness, dizziness next day (hangover effect), tolerance
- Monitor for resp depression (caution in resp disease)

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55
Q

ANTI-PSYCHOTICS
What are the issues for typical anti-psychotics?

A

Not selective so can bind to other dopaminergic pathways causing generalised dopamine receptor blockade

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56
Q

ANTI-PSYCHOTICS
What pathway do typical anti-psychotics work on to cause side effects?

A

Nigrostriatal (Parkinsonism),
tuberoinfundibular (prolactin)

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57
Q

ANTI-PSYCHOTICS
What is the benefit of atypical anti-psychotics?

A

More useful in treating -ve Sx of schizophrenia + less likely to cause EPSEs

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58
Q

ANTI-PSYCHOTICS
What anti-psychotic has a reduced SE profile and why?

A

Aripiprazole as it is a partial dopamine agonist

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59
Q

ANTI-PSYCHOTICS
What is the most crucial adverse effect of clozapine?

A
  • Severe life-threatening agranulocytosis
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60
Q

ANTI-PSYCHOTICS
What is the most common adverse effect of clozapine?
What other adverse effects may it have?

A
  • Constipation (big issue in elderly)
  • Reduced seizure threshold, hypersalivation (Rx hyoscine hydrobromide)
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61
Q

ANTIPSYCHOTICS
what is the effect of smoking on clozapine?

A
  • when smoking a higher level of clozapine may be required to get therapeutic dose
  • if stopping smoking a lower dose of clozapine may be required
62
Q

ANTI-PSYCHOTICS
How is parkinsonism managed?

A

Reduce dose or switch to atypical anti-psychotic

63
Q

ANTI-PSYCHOTICS
Why is akathisia dangerous?

A

It is a massive risk factor for suicide in young men with schizophrenia

64
Q

ANTI-PSYCHOTICS
How is akathisia managed?

A

Reduce dose, introduce beta-blocker (propranolol)

65
Q

ANTI-PSYCHOTICS
When does tardive dyskinesia present?

A

After months-years of Tx

66
Q

ANTI-PSYCHOTICS
How is tardive dyskinesia managed?

A

Prevention crucial,
switch to atypical anti-psychotic,
tetrabenazine used if mod–severe but unlikely to completely resolve

67
Q

ANTI-DEPRESSANTS
When can an anti-depressant be stopped?

A
  • Carried on 6m after Sx resolved even if patient feels better
68
Q

ANTI-DEPRESSANTS
What are some interactions of SNRIs?

A
  • NSAIDs
    warfarin (increased risk of bleeding),
    lower seizure threshold
69
Q

BDZs
What is the mechanism of action of anxiolytics/benzodiazepines (BDZs)?

A
  • Enhance effect of inhibitory GABA by increasing frequency of Cl- channels + flow of Cl- ions causing hyperpolarisation of membrane + so prevention of further excitation
70
Q

BDZs
Give some examples of BDZs?

A
  • Diazepam (longer duration), lorazepam + temazepam (shorter duration), clonazepam, chlordiazepoxide
71
Q

BDZs
What are they suitable for?

A

Short-term Tx (<4w), sedation + anxiolytic

72
Q

BDZs
What are some adverse effects of BDZs?

A
  • Amnesia, ataxia (esp elderly = falls risk), confusion, drowsiness, dizziness next day (hangover effect), tolerance
  • Monitor for resp depression (caution in resp disease)
73
Q

BDZs
What drugs can BDZs interact with?

A
  • Anti-hypertensives as enhanced hypotensive effect
74
Q

BDZs
How would you manage an overdose?
What is the risk of using this?

A

IV flumazenil (danger of inducing status epilepticus or death though)

75
Q

SUBSTANCE ABUSE
What is an addiction?

A
  • Compulsive substance taking behaviour with physiological withdrawal state
76
Q

SUBSTANCE ABUSE
What is an addictive behaviour?

A

Behaviour which is both rewarding + reinforcing

77
Q

SUBSTANCE ABUSE
Why is something addictive?

A

Related to dopamine + mesolimbic reward system a motivational circuit

78
Q

SUBSTANCE ABUSE
What are the physical effects of dependent drug use?

A
  • Acute = injecting complications, SEs, OD, poor pregnancy outcomes
  • Chronic = BBV transmission, chronic illnesses
79
Q

SUBSTANCE ABUSE
What are the…

i) psychological
ii) social

effects of dependent drug use?

A

i) MH issues, fearing withdrawal, craving, guilt, pre-occupation with finding next fix
ii) Effects on relationships, criminality + imprisonment, social exclusion, poverty (no money for food)

80
Q

SUBSTANCE ABUSE
What is dependence?

A
  • The inability to control the intake of a substance to which one is addicted to
81
Q

SUBSTANCE ABUSE
List 8 features of dependence

A
  • Withdrawal
  • Cravings
  • Continued use despite harm
  • Tolerance
  • Primacy/salience
  • Loss of control
  • Narrowed repertoire
  • Rapid reinstatement
82
Q

SUBSTANCE ABUSE
What is withdrawal?
Give an example

A
  • Physiological withdrawal state when substance stopped with Sx + substance use to prevent
  • Early morning drinking
83
Q

SUBSTANCE ABUSE
What are cravings?

A
  • Very strong desire for the substance
84
Q

SUBSTANCE ABUSE
What is continued use despite harm?
Give an example

A
  • Despite clear problems caused by substance, person cannot stop
  • Injecting heroin despite abscess formation
85
Q

SUBSTANCE ABUSE
What is tolerance?
Give an example

A
  • Larger doses required to gain the same effect as previously (NB: individuals often show no signs of being on a drug at dose ordinary people would)
  • Opiate-dependent people may inject enough heroin to kill a non-tolerant person
86
Q

SUBSTANCE ABUSE
What is primacy/salience?
Give an example

A
  • Obtaining + using substance becomes so important other interests are neglected
  • Not eating to save money for drugs
87
Q

SUBSTANCE ABUSE
What is loss of control?
Give an example

A
  • Difficulties controlling starting, stopping or amounts used
  • Becomes hard to say no
88
Q

SUBSTANCE ABUSE
What is narrowed repertoire?
Give an example

A
  • Less variation in types of substances used
  • Dependent drinker will drink same amount of same drink in same way (usually cheapest)
89
Q

SUBSTANCE ABUSE
What is rapid reinstatement?
Give an example

A
  • When a user relapses after period of abstinence, risk of returning to previous dependent pattern quicker
  • Someone who used to smoke 10/d may quickly return to this after 1 fag
90
Q

SUBSTANCE ABUSE
What are some primary care interventions for drug users?

A
  • Health checks + BBV screening
  • Contraception, smear + sexual health advice
  • General immunisation status + hep A/B
  • Information on local drug services (needle exchange)
91
Q

SUBSTANCE ABUSE
How can harm be reduced in drug users?

A
  • Not injecting or safe injecting (don’t share, new one each time)
  • Not mixing resp depressants or using drugs alone
  • Reduce amount taken after intervals tolerance is lost
92
Q

ALCOHOL DEPENDENCE
What is alcohol abuse?

A
  • Regular or binge consumption of alcohol which is sufficient to cause physical, neurological, psychiatric or social damage
93
Q

ALCOHOL DEPENDENCE
How do you calculate number of units in a drink?

A
  • % ABV x volume (L)
94
Q

ALCOHOL DEPENDENCE
What is 1 unit of alcohol?

A

10ml or 8g

95
Q

ALCOHOL DEPENDENCE
What is the recommended weekly units for men and women?

A

14 units/week

96
Q

ALCOHOL DEPENDENCE
What are the components to alcohol abuse?

A
  • Psychological dependence = feelings of loss of control, cravings, pre-occupation
  • Physiological dependence = physical withdrawal Sx
  • +ve reinforcement = drinking to feel euphoric
  • -ve reinforcement = drinking to avoid withdrawal Sx
97
Q

ALCOHOL DEPENDENCE
What areas of the brain can alcohol affect?

A
  • Amygdala + nucleus accumbens
  • Cerebral cortex
  • Pre-frontal cortex
  • Cerebellum
  • Hypothalamus + pituitary
  • Medulla
98
Q

ALCOHOL DEPENDENCE
How does alcohol affect…

i) amygdala + nucleus accumbens?
ii) cerebral cortex?
iii) pre-frontal cortex?
iv) cerebellum?
v) hypothalamus + pituitary?
vi) medulla?

A

i) Euphoria, pleasure + reward centre
ii) Slows thinking + speech
iii) Slow behavioural inhibition centres (confident + relaxed)
iv) Slows movement + impairs coordination
v) Alters mood + hormones (libido increases)
vi) Decreases breathing, consciousness + body temp

99
Q

ALCOHOL DEPENDENCE
How does alcohol affect the activity of neurotransmitters in the brain?

A
  • Ethanol > ADH > acetaldehyde > ALDH > acetate > CO2 + H2O
  • Ethanol binds to GABA + makes inhibitor/depressant effect stronger
  • Glutamate antagonism which decreases excitatory neurotransmission
  • Activates opioid receptors to release endorphins
  • Release dopamine + serotonin
100
Q

ALCOHOL DEPENDENCE
What are some causes/risk factors for alcohol dependence?

A
  • Genetics – more likely if FHx, M>F, less likely if acetaldehyde dehydrogenase deficiency
  • Occupation – army, Drs
  • Culture/beliefs/background – high in Scottish, Irish, lower in Muslims + Jews
  • Cost of alcohol
  • Early use of substances
  • Social reinforcement
  • Chronic illnesses
  • Traumatic life events
101
Q

ALCOHOL DEPENDENCE
What are the acute effects of alcohol intoxication?
When is it classed as alcohol dependence?

A
  • Euphoria, impaired judgement, reduced anxiety, ataxia, vomiting
  • ≥3 features of dependence
102
Q

ALCOHOL DEPENDENCE
What are the 3 stages of alcohol withdrawal?

A
  • 6–12h = tremors, diaphoresis, tachycardia, anxiety, irritability + aggression
  • 36h = seizures
  • 48–72h = delirium tremens
103
Q

ALCOHOL DEPENDENCE
What are some chronic complications of alcohol dependence?

A
  • Cardiac = dilated cardiomyopathy, arrhythmias
  • Liver etc – fibrosis, cirrhosis, oesophageal varices, pancreatitis
  • Wernicke’s + Korsakoff’s
104
Q

ALCOHOL DEPENDENCE
What are some common causes of death in alcohol dependence?

A
  • Accidents + violence
  • Malignancies (head + neck, pancreatic, stomach, colon, hepatic, breast + gynae)
  • CVA, IHD
105
Q

ALCOHOL DEPENDENCE
What are some blood markers for alcohol consumption?

A
  • Red blood cell mean corpuscular volume (MCV) raised
  • Gamma glutamyl transpeptidase (GGT) raised
  • Carbohydrate deficient transferrin (CDT) raised
106
Q

ALCOHOL DEPENDENCE
What are some clinical tools for assessing alcohol dependence or withdrawal?

A
  • CAGE
  • AUDIT
  • Clinical Institute Withdrawal Assessment
107
Q

ALCOHOL DEPENDENCE
What are the CAGE questions?

A
  • Have you ever felt you need to CUT down on your drinking?
  • Have people ANNOYED you by criticising your drink?
  • Have you ever felt GUILTY about your drinking?
  • EYE-opener – ever felt you need drink first thing in morning to steady your nerves?
108
Q

ALCOHOL DEPENDENCE
What are the AUDIT questions?

A
  • How often do you have a drink containing alcohol?
  • How many units of alcohol do you drink on a typical day?
  • How often did you have >6 units on a single occasion in the past year?
109
Q

ALCOHOL DEPENDENCE
What is blood alcohol content?
How is it affected?
What is the drink drive limit?

A
  • mg ethanol/100ml blood
  • Affected by amount of ethanol consumed, person’s blood volume (males have increased), if eaten, any meds
  • Illegal to drive with BAC ≥0.08%
110
Q

ALCOHOL DEPENDENCE
What are public health measurements to help prevent alcohol abuse?

A
  • Increasing tax on alcohol + restricting advertisement on alcohol
  • Drinkaware + know your limits campaign
  • Keeping alcohol out of site (behind counter + having to ask for it)
  • School alcohol education to reduce long-term alcohol use + binge drinking
111
Q

ALCOHOL DEPENDENCE
What are the indications for an inpatient detoxification?

A
  • Withdrawal seizures or delirium tremens in past
  • Significant mental/physical illness, including suicidality
  • Lack of stable home environment
112
Q

ALCOHOL DEPENDENCE
What is the regime for acute detoxification?

A
  • Chlordiazepoxide 1st line (2nd = diazepam) for withdrawal Sx + preventing seizures
  • Thiamine (PO or IV)
  • Rehydrate with fluids (often IV), correct electrolyte disturbance
  • Reducing regime (slowly reduce doses over days)
113
Q

ALCOHOL DEPENDENCE
What factors make detoxification more likely to work?

A
  • Younger users with less time addicted + lower level of drug use
114
Q

ALCOHOL DEPENDENCE
What are the 3 biological treatments used in alcohol dependence?

A
  • Naltrexone
  • Acamprosate
  • Disulfiram
115
Q

ALCOHOL DEPENDENCE
What is the mechanism of action of naltrexone?

A
  • Opioid receptor antagonist
  • Blocks euphoric effects of alcohol
  • Helps people stick to detox programme + avoid relapse
116
Q

ALCOHOL DEPENDENCE
What is the mechanism of action of acamprosate?

A
  • NMDA antagonist acts on GABA to reduce cravings + risk of relapse
117
Q

ALCOHOL DEPENDENCE
What is the mechanism of action of disulfiram?
What affects does it have?

A
  • Inhibits acetaldehyde dehydrogenase > build-up of acetaldehyde
  • Produces hangover-like Sx when alcohol is drunk = deterrent (flushing, headaches, anxiety, nausea, reduced BP)
118
Q

ALCOHOL DEPENDENCE
What are some psychological treatments for alcohol dependence?

A
  • Motivational intervention
  • Aversion therapy
  • CBT, prevention measures (relapse prevention strategies)
119
Q

ALCOHOL DEPENDENCE
What is motivational intervention?

A
  • Discuss potential harm caused, reasons for changing behaviour, cover obstacles to change, strategies to combat obstacles > motivation
120
Q

ALCOHOL DEPENDENCE
What is aversion therapy?

A
  • Designed to put the patient off the undesirable habit by causing them to associate it with an unpleasant effect
121
Q

ALCOHOL DEPENDENCE
What is the social management of alcohol dependence?

A
  • Housing, economical + employment issues
  • Alcoholics anonymous
  • Developing social routines that are not reliant on alcohol
122
Q

OPIATES/OPIOIDS
What are opiates?

A
  • Derived from opium poppy, synthetic compounds with similar properties are called opioids with heroin most commonly abused
123
Q

OPIATES/OPIOIDS
How do opioids work?

A
  • Bind to m-receptor > endogenous endorphins causing cortical inhibitor effects (analgesia) almost immediately
  • Addictive as high reward for minimal effort
124
Q

OPIATES/OPIOIDS
What routes can opioids be taken via?
How long does it take for withdrawal symptoms to develop?
What are some examples?

A
  • Smoking, PO, snorted, parenterally (IM/IV)
  • 6h post-dose
  • Morphine, diamorphine (heroin), codeine, methadone
125
Q

OPIATES/OPIOIDS
What are some complications from opioids?

A
  • Resp depression, constipation, N+V, coma, OD + death
126
Q

OPIATES/OPIOIDS
What are some complications with injecting heroin?

A
  • Abscesses, cellulitis, infective endocarditis, BBV (hep B/C, HIV), VTE
127
Q

OPIATES/OPIOIDS
With opioids, what is the…

i) psych effect?
ii) physical effect?

A

i) Euphoria, relaxation, drowsiness, analgesia
ii) Resp depression (esp. OD), pinpoint pupils, bradycardia, constipation

128
Q

OPIATES/OPIOIDS
With opioids, what are the symptoms of withdrawal

A

“Goose flesh” (piloerection),
raised HR/BP,
fever,
pupil dilatation,
abdo cramps,
insomnia,
agitation
(everything runs > D+V, lacrimation, rhinorrhoea, diaphoresis)

129
Q

OPIATES/OPIOIDS
What is the management of opioid overdose?

A
  • 400mg IV naloxone
  • M-receptor inverse agonist > blockade (almost immediate)
130
Q

OPIATES/OPIOIDS
What are some maintenance therapies for opioids?

A
  • Methadone (full opioid agonist) or buprenorphine (partial agonist/antagonist)
  • Start low + titrate up
131
Q

OPIATES/OPIOIDS
What are the pros of methadone?

A
  • Reduces mortality, drug-related morbidity, crime, spread of BBV
132
Q

OPIATES/OPIOIDS
How does maintenance therapies help?

A
  • Don’t get high but reduces cravings
  • Less dangerous than heroin + safe in pregnancy (risk of miscarriage if stop in pregnancy)
133
Q

OPIATES/OPIOIDS
What drug can be used to prevent relapses?

A
  • Naltrexone
  • Opiate antagonist which prevents lapse > relapse
134
Q

OPIATES/OPIOIDS
What is the first line detox management in opioids?
How long does detox last?

A
  • Motivational intervention
  • Alternative therapies = exercise, art therapy, counselling
  • 4w = inpatient, 12w = community
135
Q

SEDATIVES
What are some types of sedatives?
What is a ‘date-rape’ drug?
What routes can it be taken?

A
  • BDZs, barbiturates (increased duration of Cl- channels) often taken for their anxiolytic effects
  • Rohypnol > intoxicant, aphrodisiac + anterograde amnesia
  • PO + IV
136
Q

SEDATIVES
What are the…

i) psych
ii) physical

effects of sedatives?

A

i) Euphoria + disinhibition, hallucinations, paranoid, agitation, time passes slowly
ii) Unsteady gait, dysarthria, hypotension, nystagmus
iii) Sweating, myalgia, tremors, risk of seizures

137
Q

SEDATIVES
What are the withdrawal effects of sedatives?

A

Sweating,
myalgia,
tremors,
risk of seizures

138
Q

STIMULANTS
What is the action of stimulants?

A
  • Potentiate mood enhancing neurotransmission (dopamine, serotonin, noradrenaline) by blocking their uptake + increase cortical excitability
139
Q

STIMULANTS
What are some examples?

A

Cocaine,
ecstasy (MDMA),
amphetamines (speed)

140
Q

STIMULANTS
What are the…

i) psych
ii) physical

effects of stimulants?

A

i) Euphoria, increased alertness + endurance, grandiosity, hallucinations, aggression, impulsivity
ii) Tachycardia, HTN, N+V, pupil dilation, CP + convulsions

141
Q

STIMULANTS
What are the withdrawal effects of stimulants?

A

Psychomotor agitation,
dysphoric mood,
insomnia
bizarre/unpleasant dreams

142
Q

STIMULANTS
What different routes of taking these drugs?

A
  • Cocaine inhaled or IV
  • MDMA + amphetamines PO
  • Crack cocaine releases all dopamine straight away when smoked
143
Q

STIMULANTS
What are some other adverse effects of cocaine?

A
  • Arrhythmias, MI + damage to nasal septum if used chronically
144
Q

CANNABINOIDS
Why is cannabis addictive?
What can heavy use lead to?

A
  • Addictive as causes release of dopamine, anxiolytic
  • Anxiety + depression, use in youth > schizophrenia
145
Q

CANNABINOIDS
What are the…

i) psych
ii) physical

effects of cannabinoids?

A

i) Euphoria + disinhibition, hallucinations, paranoid, agitation, time passes slowly
ii) Increased appetite, dry mouth, tachycardia

146
Q

CANNABINOIDS
What are the withdrawal effects of cannabinoids?

A

Anxiety,
irritable,
tremor,
conjunctival injection

147
Q

HALLUCINOGENS
Give some examples of hallucinogens

A
  • LSD, magic mushrooms (PO)
148
Q

HALLUCINOGENS
What are some psych + physical effects of hallucinogens?

A
  • Hallucinations, illusions, depersonalisation + derealisation, paranoia, impulsivity, anxiety, magic mushrooms > euphoria as serotonin release
  • Tachycardia, palpitations, sweating, blurred vision
149
Q

VOLATILE SOLVENTS
Give some examples of solvents.

A
  • Aerosols, paint, glue, petrol (inhaled)
150
Q

VOLATILE SOLVENTS
What are some psych + physical effects of solvents?

A
  • Apathy, lethargy, impaired judgement, psychomotor retardation
  • Decreased consciousness, unsteady gait, diplopia
151
Q

VOLATILE SOLVENTS
Are the effects of solvents dangerous?

A

Very –laryngospasm due to cold temp, brain damage, hypoxia

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