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PSYCH AND EXTRA CONDITIONS Flashcards

1
Q

MENTAL HEALTH ACT 1983
What are the main principles of the MHA?

A
  • Respect for pts wishes + feelings (past + present)
  • Minimise restrictions on liberty
  • Public safety
  • Pts well-being + safety
  • Effectiveness of treatment
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2
Q

MENTAL HEALTH ACT 1983
What is the purpose, duration, location + professionals involved, evidence needed for a Section 4?

A

P – emergency order
D – 72h
L – anywhere in community
P – 1 S12 Dr, 1 AMHP, nearest relative
E – same as S2 but only in an urgent necessity when waiting for a second dr (for a S2) would lead to undesirable delay/outcome

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3
Q

DEPRESSION
What are 2 theories speculating the causes of depression?

A
  • Stress vulnerability = someone with high vulnerability will withstand less stress before becoming mentally unwell
  • Monoamine hypothesis = depression caused by deficiency in monoamines (serotonin, noradrenaline) hence why Tx works
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4
Q

BIPOLAR DISORDER
What are the 4 types of bipolar?

A
  • Bipolar 1 = mania + depression in equal proportions, M>F
  • Bipolar 2 = more episodes of depression, mild hypomania (easy to miss), F>M
  • Cyclothymia = chronic mood fluctuations over ≥2y (episodes of depression + hypomania, can be subclinical)
  • Rapid cycling = ≥4 episodes of (hypo)mania or depression in 1 year
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5
Q

BIPOLAR DISORDER
In order to differentiate a manic and hypomanic episode, psychotic symptoms must be present.
What are some of these?

A
  • Grandiose idea may be delusional
  • Persecutory delusions sometimes
  • Pressure speech may become so great that it’s incomprehensible
  • Irritability > violence
  • Preoccupation with thoughts > self-neglect
  • Catatonia ‘manic stupor’
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6
Q

SCHIZOPHRENIA
What is schizophrenia?

A
  • Splitting or dissociation of thoughts, loss of contact with reality
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7
Q

SCHIZOPHRENIA
What is the neurotransmitter hypothesis in schizophrenia?

A
  • Excess dopamine + overactivity in mesolimbic tract = +ve Sx
  • Lack of dopamine + underactivity in mesocortical tracts = -ve Sx
  • Overactivity of dopamine, serotonin, noradrenaline + underactivity of glutamate + GABA
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8
Q

SCHIZOPHRENIA
What are some risk factors?

A

Strongest RF = FHx,
others = Black Caribbean, migrants, urban areas, cannabis use + traumatic pregnancy (emergency c-section)

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9
Q

SCHIZOAFFECTIVE
What is schizoaffective disorder?

A
  • Features of both affective disorder + schizophrenia present in equal proportion
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10
Q

GAD
What model can be used to explain the causes of GAD?

A

Triple vulnerability –
- Generalised biological
- Generalised psychological (diminished sense of control)
- Specific psychological (stressful events)

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11
Q

GAD
What are some organic differentials for GAD?

A
  • Endo = hyperthyroidism, pheochromocytoma, hypoglycaemia
  • CVS = arrhythmias, cardiac failure, anti-hypertensives, MI
  • Resp = asthma (excessive salbutamol), COPD, PE
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12
Q

PANIC DISORDER
What is the stepwise management of panic disorder?

A
  • Recognition + diagnosis with treatment in primary care
  • CBT or drug therapy (SSRIs 1st line, if C/I or no response after 12w then imipramine or clomipramine)
  • Psychodynamic psychotherapy + specialist MH services if severe
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13
Q

OCD
What are some risk factors for OCD?

A
  • Genetics = FHx of OCD or tic disorder
  • Abuse, neglect, teasing + bullying
  • Parental overprotection
  • Paediatric neuropsychiatric disorders associated with streptococci (PANDAS)
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14
Q

OCD
What is the biological management of OCD?

A
  • 1st line SSRIs = sertraline
  • 2nd line = clomipramine (TCA) with specific anti-obsessional action
  • ?Psychosurgery (stereotactic cingulotomy if intractable > 2 antidepressants, 3 combination Tx, ECT + behavioural therapy
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15
Q

PTSD
What are the 4 core symptoms of PTSD?
How long do they need to be present for to diagnose?

A

HEAR (≥1m) –
- Hyperarousal
- Emotional numbing
- Avoidance + rumination
- Re-experiencing (involuntary)

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16
Q

ANOREXIA NERVOSA
What is the diagnostic criteria for anorexia?

A

FEED ≥3m with absence of binge eating –
- Fear of fatness
- Endocrine disturbance
- Extreme weight loss
- Deliberate weight loss

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17
Q

ANOREXIA NERVOSA
How may endocrine disturbance present?

A
  • Amenorrhoea
  • Reduced libido/fertility
  • Abnormal insulin secretion
  • Delayed/arrested puberty if onset pre-pubertal
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18
Q

ANOREXIA NERVOSA
What screening tool can be used in anorexia?

A

SCOFF –
- Do you ever make yourself SICK as too full?
- Do you ever feel you’ve lost CONTROL over eating?
- Have you recently lost more than ONE stone in 3m?
- Do you believe you’re FAT when others say you’re thin?
- Does FOOD dominate your life?

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19
Q

ANOREXIA NERVOSA
What are the biological treatments for anorexia nervosa?

A
  • Fluoxetine, chlorpromazine + TCAs may be used for weight gain
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20
Q

ANOREXIA NERVOSA
What is the pathophysiology of refeeding syndrome?

A
  • Reduced carb consumption leads to reduced insulin secretion so the body switches from carb > fat + protein metabolism
  • Electrolyte stores depleted as needed to convert glucose>energy
  • Reintroducing food causes abrupt shift from fat>carb metabolism + insulin secretion surges, driving electrolytes from serum>cells to help convert glucose>energy causing further serum concentration decrease
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21
Q

ANOREXIA NERVOSA
What is the clinical presentation of refeeding syndrome?

A
  • Fatigue, weakness, confusion, dyspnoea (risk of fluid overload)
  • Abdo pain, vomiting, constipation, infections
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22
Q

ANOREXIA NERVOSA
What are the biochemical features of refeeding syndrome?

A
  • Hypophosphataemia main disturbance due to role of converting glucose>energy
  • Hypokalaemia, hypomagnesaemia + thiamine deficiency too
  • Abnormal fluid balance
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23
Q

ANOREXIA NERVOSA
What should be monitored before + during refeeding?

A
  • U+Es (Na+, K+), phosphate, magnesium, glucose, ECG, fluid balance
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24
Q

BULIMIA NERVOSA
What is the diagnostic criteria for bulimia?

A

BPFO ≥2 a week for ≥3m –
- Behaviours to prevent weight gain
- Preoccupation with eating (compulsion to eat but regret after)
- Fear of fatness
- Overeating ≥2/week

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25
Q

BULIMIA NERVOSA
What metabolic abnormalities may be present?

A
  • Hypochloraemic hypokalaemic metabolic alkalosis due to vomiting
  • Hypokalaemia > muscle weakness + arrhythmias
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26
Q

PERSONALITY DISORDERS
What are some differentials of schizotypal personality disorder?

A
  • Autism
  • Asperger’s
  • Schizophrenia (50% may develop it)
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27
Q

PERSONALITY DISORDERS
What are some investigations for personality disorders?

A
  • Assessed (Hx + MSE) more than once
  • Minnesota Multiphasic Personality Inventory (MMPI)
  • Eysenck Personality Inventory + Personality Diagnostic Questionnaire
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28
Q

PERSONALITY DISORDERS
What is the biological management of personality disorders?

A
  • Only use to treat comorbid conditions or if Sx distressing (e.g. antipsychotics in group A to reduce suspiciousness)
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29
Q

KORSAKOFF’S
What are some causes of Korsakoff’s?

A
  • Heavy alcohol drinkers
  • Head injury, post-anaesthesia
  • Basal or temporal lobe encephalitis
  • CO poisoning
  • Other causes of thiamine deficiency (anorexia, starvation, hyperemesis)
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30
Q

LITHIUM TOXICITY
What is the clinical presentation of lithium toxicity?

A
  • Ataxia, dysarthria, confusion (drunk)
  • COARSE tremor, blurred vision, hyperreflexia
  • N+V, diarrhoea
  • Myoclonus, seizures + coma if severe
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31
Q

LITHIUM TOXICITY
What are some complications of lithium toxicity?

A
  • Arrhythmias (VT)
  • Acute renal failure
  • Syndrome of irreversible lithium-effectuated neurotoxicity (SILENT) after cessation of lithium >2m = truncal ataxia, ataxic gait, scanning speech, incoordination
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32
Q

LITHIUM TOXICITY
What is the management of lithium toxicity?

A
  • ABCDE approach as emergency
  • Stop + check lithium levels, serum creatinine, U+Es
  • IV fluids (bolus + 1.5–2x maintenance
  • ?Whole bowel irrigation with polyethene glycol for severe, acute ingestion
  • Haemodialysis
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33
Q

NMS
What is the pathophysiology of neuroleptic malignant syndrome (NMS)?

A
  • Dopamine antagonism often due to typical antipsychotic OD or acute withdrawal of Parkinson’s meds
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34
Q

NMS
What is the clinical presentation?

A

Bodybuilder–
- Pyrexia >38 + diaphoresis
- Muscle rigidity (diffuse “lead-pipe” rigidity)
- Confusion, agitation, altered consciousness
- Tachycardia, high/low BP
- Hyporeflexia

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35
Q

NMS
What are some investigations for NMS?

A
  • FBC (leukocytosis)
  • Low serum iron
  • U+Es, Ca2+, phosphate
  • Urinary myoglobin (raised)
  • Serum creatinine phosphokinase (CPK) may be raised
  • CK raised
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36
Q

NMS
What is the management of NMS?

A
  • ABCDE approach
  • Stop antipsychotic (wait >2w before restarting, consider atypical)
  • Give L-dopa if dopamine withdrawal in Parkinson’s
  • IV dantrolene or lorazepam to reduce rigidity 1st line (amantadine second)
  • Bromocriptine prophylaxis
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37
Q

SEROTONIN SYNDROME
What is the clinical presentation of serotonin syndrome?

A

Sx onset + recovery fast–
- Neuro = confusion, agitation
- Neuromuscular = myoclonus, tremors (incl. shivering), hyperreflexia, ataxia
- Autonomic = hyperthermia, diarrhoea, tachycardia, mydriasis

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38
Q

SEROTONIN SYNDROME
What are some investigations for serotonin syndrome?

A
  • FBC, U+Es, biochemistry (Ca2+, Mg2+, phosphate), CK, drug toxicology scren
  • ECG monitoring for prolonged QRS or QTc interval
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39
Q

SEROTONIN SYNDROME
What is the management of serotonin syndrome?

A
  • ABCDE
  • Stop offending agent
  • IV access to correct volume + reduce risk of rhabdomyolysis as in NMS
  • BDZs like slow IV lorazepam for agitation, seizures + myoclonus
  • Serotonin receptor antagonists like PO cyproheptadine or chlorpromazine if severe
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40
Q

SEROTONIN SYNDROME
What is the management of serotonergic drug OD?

A
  • ?Gastric lavage ± activated charcoal
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41
Q

LEARNING DISABILITIES
What is the triad in learning disabilities?

A
  • Low intellectual performance (IQ < 70)
  • Onset during birth or early childhood
  • Wide range of functional impairment
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42
Q

LEARNING DISABILITIES
What physical disorders may be present in those with learning disabilities?

A
  • Motor disabilities (ataxia, spasticity)
  • Epilepsy
  • Impaired hearing/vision
  • Incontinence
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43
Q

AUTISM SPECTRUM
What are some risk factors for autism?

A
  • M>F
  • Obstetric complications
  • Perinatal infection (rubella)
  • Genetic disorders (Fragile X, Down’s)
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44
Q

AUTISM SPECTRUM
What are the 3 areas of impaired functioning that need to be present in autism?

A
  • Social interaction
  • Communication (speech + language)
  • Behaviour (imposition of routine with ritualistic or repetitive behaviour)
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45
Q

TIC DISORDERS
What is Tourette’s syndrome?

A
  • Development of tics that are persistent for >1y
  • More severe expression of the spectrum of tic disorder
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46
Q

ADHD
What are some risk factors for ADHD?

A
  • Epilepsy, low socioeconomic status, learning difficulties
  • Premature or LBW
  • Brain damage (in vitro or after severe head injury later)
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47
Q

ADHD
What is the triad of symptoms in ADHD?

A
  • Inattention
  • Impulsivity
  • Hyperactivity
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48
Q

ADHD
What is the management for severe ADHD?

A
  • CNS stimulants like methylphenidate (increase monoamine pathway activity, not addictive)
  • S/E = appetite suppression, insomnia, psychosis, important to monitor growth, baseline ECG (cardiotoxic)
  • Atomoxetine (SE = liver dysfunction, suicidality)
  • (Lis)dexamfetamine
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49
Q

GENDER DYSPHORIA
What are some risks of the hormone therapy?

A
  • Oestrogen = clots, gallstones, high triglycerides
  • Testosterone = polycythaemia, acne, dyslipidaemia
  • Both = elevated LFTs, infertility, weight gain
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50
Q

SCHIZOAFFECTIVE
What are the two types of schizoaffective disorder?

A

Manic type or depressive type

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51
Q

SELF-HARM
What are some risk factors for self-harm?

A

Female
Social deprivation,
Single or divorced,
LGBTQ+,
mental illness

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52
Q

SCHIZOPHRENIA
What are the features of simple schizophrenia?

A

Pts never really experienced +ve Sx, mostly -ve

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53
Q

TIC DISORDERS
What might cause them?

A
  • Stress, gestational + perinatal insults, PANDAS
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54
Q

TIC DISORDERS
How does Tourette’s syndrome present?

A
  • Multiple motor tics + at least 1 phonic tic (coprolalia)
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55
Q

OCD
What is a potential cause of OCD?

A

Neurochemical dysregulation of 5-HT system

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56
Q

PHENOMENOLOGY
Define psychosis

A

Severe mental disturbance characterised by a loss of contact with external reality (schizophrenia)

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57
Q

PHENOMENOLOGY
Define illusion

A

The false perception of a real external stimulus

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58
Q

PHENOMENOLOGY
Define hallucination

A

An internal perception occurring without a corresponding external stimulus. The person experiences it as they would a real perception.

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59
Q

PHENOMENOLOGY
Define delusion

A

A fixed, false, unshakable belief which is out of keeping with the patient’s educational, cultural + social norms. It’s held with extraordinary conviction + certainty (even despite contradictory evidence)

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60
Q

PHENOMENOLOGY
What is capgras syndrome?

A

Capgras = idea someone has been replaced by an imposter.

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61
Q

PHENOMENOLOGY
what is Fregoli syndrome?

A

Fregoli = idea various people are the same person

62
Q

PHENOMENOLOGY
What is intermetamorphosis?

A

Intermetamorphosis = one significant relative is replaced by another (father is son).

63
Q

PHENOMENOLOGY
Define delusional perception and give an example

A

A primary delusion of two components – where a normal perception is subject to delusional interpretation
E.g. – traffic light changed red so that means I am the son of God

64
Q

TIC DISORDERS
What is the epidemiology of tics?

A
  • Transient simple tics affect 10% of children
  • May be associated with OCD, ADHD + ASD
  • M>F, usually present around or after 5y
65
Q

TIC DISORDERS
What are the two types of tics?
How may they manifest?

A
  • Simple
  • Complex
  • May be invisible to observer (abdo tensing, toe crunching)
66
Q

TIC DISORDERS
Give some examples of simple tics

A
  • Throat-clearing
  • Blinking
  • Sniffing
  • Head jerking
  • Eye rolling
67
Q

TIC DISORDERS
Give some examples of complex tics

A
  • Physical movements (twirling on spot, touching objects)
  • Copropraxia (obscene gestures)
  • Coprolalia (obscene words)
  • Echolalia
68
Q

TIC DISORDERS
What improves or worsens tics?
What sensations are felt before tics?

A
  • Stress + stimulant meds worsen, distraction improves
  • Premonitory = pts feel urge to perform tic, often several times to get relief from that urge (can be suppressed but internal tension builds)
69
Q

TIC DISORDERS
What is the management of mild tics?

A
  • Watch + wait (usually improve over time
  • Education + reassurance
  • Avoid caffeine + stress
70
Q

TIC DISORDERS
What is the management of severe tics?

A
  • Habit reversal training
  • ERP
  • Antipsychotics considered in VERY severe cases
71
Q

CONDUCT DISORDER
What can be used as a last resort in conduct disorder?

A
  • Antipsychotic like risperidone to reduce aggressive tendencies
72
Q

CONVERSION DISORDERS
What are the features of conversion disorders?

A
  • Paralysis (any pattern)
  • Aphonia (complete loss or whispered speech)
  • Sensory loss (area may cover patient’s beliefs about anatomy)
  • Seizure (NEAD)
  • Amnesia (short-term memory loss usually too severe for forgetfulness)
73
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
74
Q

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

A
  • Acute dystonic reaction
  • Parkinsonism
  • Akathisia
  • Tardive dyskinesia
75
Q

ANTI-PSYCHOTICS
What are the SEs from hyperprolactinaemia?

A
  • Sexual dysfunction (+ anti-adrenergic)
  • Osteoporosis risk
  • Amenorrhoea
  • Galactorrhoea, gynaecomastia + hypogonadism in men
76
Q

ANTI-PSYCHOTICS
What are the metabolic SEs?

A
  • Weight gain (esp. olanzapine)
  • Hyperlipidaemia, risk of stroke + VTE in elderly
  • T2DM risk + metabolic syndrome
77
Q

ANTI-PSYCHOTICS
What are the anticholinergic SEs?

A

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

78
Q

ANTI-PSYCHOTICS
What are the neurological SEs?

A
  • Seizures
  • Postural hypotension (anti-adrenergic)
  • Sedation
  • Headaches
79
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)
80
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
81
Q

ANTI-PSYCHOTICS
What specific monitoring is required for clozapine?

A
  • FBC at baseline + weekly for 18w, fortnightly until 1y + monthly after
82
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
83
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)
84
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
85
Q

ANTI-DEPRESSANTS
What are some side effects from MAOIs?

A
  • Sexual dysfunction, weight gain + postural hypotension
86
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)
87
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
88
Q

ANTI-DEPRESSANTS
What are the side effects of TCAs?

A
  • Anticholinergic (can’t see, pee, spit, shit)
89
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)
90
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

91
Q

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

A
  • Blocks alpha-2 adrenergic receptors > increased release of neurotransmitters
92
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

93
Q

MOOD STABILISERS
What drugs does lithium interact with?

A
  • NSAIDs, ACEi, ARBs + diuretics may increase lithium levels
  • Diuretics = dehydration,
    NSAIDs = renal damage
94
Q

MOOD STABILISERS
What baseline measurements are taken for lithium?

A
  • FBC, U+Es, eGFR, TFTs, BMI + ECG
95
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
96
Q

HYPNOTICS
What is the mechanism of action of hypnotics?

A
  • GABA agonists on alpha2-subunit of GABA(A)-BDZ receptor/Cl- channel complex
97
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

98
Q

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

A

Nigrostriatal (Parkinsonism),
tuberoinfundibular (prolactin)

99
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)
100
Q

ANTI-PSYCHOTICS
Why is akathisia dangerous?

A

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

101
Q

ANTI-PSYCHOTICS
How is akathisia managed?

A

Reduce dose, introduce beta-blocker (propranolol)

102
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

103
Q

ANTI-DEPRESSANTS
What are some interactions of SNRIs?

A
  • NSAIDs
    warfarin (increased risk of bleeding),
    lower seizure threshold
104
Q

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

A

Amitriptyline, dosulepin, imipramine

105
Q

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

A

Sinus tachy,
wide QRS,
prolonged QT interval

106
Q

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

A

Sodium bicarbonate

107
Q

ANTI-DEPRESSANTS
What are some side effects of mirtazapine?

A

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

108
Q

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

A

Lithium inhibits cAMP production which inhibits monoamines

109
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)

110
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
111
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)

112
Q

SUBSTANCE ABUSE
Why is something addictive?

A

Related to dopamine + mesolimbic reward system a motivational circuit

113
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
114
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)

115
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
116
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
117
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
118
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
119
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
120
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
121
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?
122
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?
123
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
124
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
125
Q

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

A
  • Naltrexone
  • Acamprosate
  • Disulfiram
126
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
127
Q

ALCOHOL DEPENDENCE
What is the mechanism of action of acamprosate?

A
  • NMDA antagonist acts on GABA to reduce cravings + risk of relapse
128
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)
129
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
130
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
131
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

132
Q

OPIATES/OPIOIDS
What are some complications with injecting heroin?

A
  • Abscesses, cellulitis, infective endocarditis, BBV (hep B/C, HIV), VTE
133
Q

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

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

STIMULANTS
What are some examples?

A

Cocaine,
ecstasy (MDMA),
amphetamines (speed)

135
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
136
Q

STIMULANTS
What are the withdrawal effects of stimulants?

A

Psychomotor agitation,
dysphoric mood,
insomnia
bizarre/unpleasant dreams

137
Q

STIMULANTS
What are some other adverse effects of cocaine?

A
  • Arrhythmias, MI + damage to nasal septum if used chronically
138
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
139
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

140
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
141
Q

BDZs
What drugs can BDZs interact with?

A
  • Anti-hypertensives as enhanced hypotensive effect
142
Q

SUBSTANCE ABUSE
What is an addiction?

A
  • Compulsive substance taking behaviour with physiological withdrawal state
143
Q

SUBSTANCE ABUSE
What is an addictive behaviour?

A

Behaviour which is both rewarding + reinforcing

144
Q

OPIATES/OPIOIDS
What are some complications from opioids?

A
  • Resp depression, constipation, N+V, coma, OD + death
145
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)

146
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

147
Q

STIMULANTS
What is the action of stimulants?

A
  • Potentiate mood enhancing neurotransmission (dopamine, serotonin, noradrenaline) by blocking their uptake + increase cortical excitability
148
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

149
Q

CANNABINOIDS
What are the withdrawal effects of cannabinoids?

A

Anxiety,
irritable,
tremor,
conjunctival injection

150
Q

HALLUCINOGENS
Give some examples of hallucinogens

A
  • LSD, magic mushrooms (PO)
151
Q

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

A
  • Apathy, lethargy, impaired judgement, psychomotor retardation
  • Decreased consciousness, unsteady gait, diplopia
152
Q

VOLATILE SOLVENTS
Are the effects of solvents dangerous?

A

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

C TO REVISE - PHASE 3A (11 decks)

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