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Year 5 > Psych 4 > Flashcards

Psych 4 Flashcards

1
Q

Alcohol detoxification management

A
  • Where: home, partial hospitalisation, inpatient
  • General support/advice
  • Drug of choice- longer acting benzodiazepines
  • Regular monitoring: observe for withdrawal/ over-sedation. BAC/CIWA
  • Treat withdrawal: symptoms triggered/ fixed dose etc. Risk of undertreatment (DT’s/fits). Risk of overtreatment (over-sedation)
  • Oral/IM vitamins as indicated
  • Reducing regime
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2
Q

Alcohol withdrawal treatment plan

A
  • ABC
  • +DEFG!
  • Physical observations, ECG
  • Bloods – incl. FBC, U and E, LFTs, clotting, amylase +/- CK +/- blood cultures
  • IV thiamine
  • Diazepam / chlordiazepoxide; likely symptom triggered
  • PRN medication in case of seizure; midazolam/ diazepam as per policy
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3
Q

Alcohol withdrawal symptoms

A
  • 6-12 hours: tremor, sweating, headache, craving and anxiety
  • 12-24 hours: hallucinations
  • 24-48 hours: seizures
  • 24-72 hours: delirium tremens
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4
Q

Delirium tremens

A
  • Medical emergency associated with alcohol withdrawal
  • Symptoms: acute confusion, severe agitation, delusions and hallucinations, tremor. tachycardia, hypertension, hyperthermia, ataxia, arrhythmias
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5
Q

Drugs

A

Drugs= a substance which produces a non-nutritional physiological effect when introduced to the body.

Almost half of all drug poisonings involve an opiate, over half of all drug poisonings involve more than one drug.

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6
Q

Withdrawal

A

WITHDRAWAL is the experience of a set of unpleasant symptoms following the abrupt cessation or reduction in dose of a psychoactive substance; it has been consumed in high enough doses and for a long enough duration for the person to be physically or mentally dependent on it. Withdrawal symptoms are, essentially, opposite to those that are produced by the psychoactive substance itself.

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7
Q

Acute intoxications and overdose

A

ACUTE INTOXICATION is a transient condition following intake of a psychoactive substance resulting in disturbances of consciousness, cognition, perception, affect, or behaviour.

OVERDOSE is the use of any drug in such an amount that acute adverse physical or mental effects are produced.

Cannabis is the most widely used illegal drug

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8
Q

Dependence >= 2 of

A
  • Control (Powerlessnes): over onset, intensity, duration, termination, frequency, context
  • Precedence: over other aspects of health (bio-psycho-social)
  • Physiological: tolerance, withdrawal, use to prevent/alleviate withdrawal
  • Time course: >12 months (or 3 months if continuous)
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9
Q

Harmful use

A
  • Control (Powerlessnes): over onset, intensity, duration, termination, frequency, context
  • Precedence: over other aspects of health (bio-psycho-social)
  • Physiological: tolerance, withdrawal, use to prevent/alleviate withdrawal
  • Time course: >12 months (or 3 months if continuous)
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10
Q

Diacetylmorphine (Heroin)

A
  • Heroin and other opiates are depressants of the nervous system: Act via opioid receptor. Brain, spinal cord, peripheral neurons, and digestive tract.
  • They slow down body functioning and are strong painkillers.
  • The effect is usually to give a feeling of warmth, relaxation and detachment with a lessening of anxiety.
  • Effects start quickly and can last several hours.
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11
Q

Opiate withdrawal

A
  • Early= agitation, muscle ache, restlessness, anxiety, increased tearing, runny nose, excessive sweating, yawning often
  • Later= Diarrhoea, abdominal cramping, nausea and vomiting, skin goose bumps, dilated pupils, rapid heartbeat, high blood pressure
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12
Q

Diagnosing substance misuse

A
  • History: Substance, quantity, pattern, recent events. Control (initiation, cessation etc). Impact on life, other info sources
  • Examination: features of withdrawl/intoxication. Needle marks
  • Investigation: UDS/ formal toxicology
  • Alcohol and other drugs
  • Needle sharing and other risky behaviour
  • Mental/physical/social health
  • General examination
  • BBV (blood born virus) screening
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13
Q

Pharmacological treatment of opioid dependence (agonism)

A
  • Short acting (heroin assisted treatment)
  • Long acting (methadone)
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14
Q

Pharamcological treatment of opioid dependence: partial agonism

A
  • Long acting (buprenorphine)
  • Very long acting (extended release buprenorphine)
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15
Q

Pharmacological treatment for opioid dependence: antagonism

A
  • Short acting: naloxone
  • Long acting: naltrexone
  • Very long acting: extended release naloxene
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16
Q

Features of opioid misuse

A
  • rhinorrhoea
  • needle track marks
  • pinpoint pupils
  • drowsiness
  • watering eyes
  • yawning
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17
Q

Complications of opioid misuse

A
  • viral infection secondary to sharing needles: HIV, hepatitis B & C
  • bacterial infection secondary to injection: infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis
  • venous thromboembolism
  • overdose may lead to respiratory depression and death
  • psychological problems: craving
  • social problems: crime, prostitution, homelessness
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18
Q

Emergency management of opioid overdose

A

IV or IM naloxone: has a rapid onset and relatively short duration of action

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19
Q

Drug addiction: harm reduction interventions may include

A
  • needle exchange
  • offering testing for HIV, hepatitis B & C
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20
Q

Management of opioid dependence

A
  • patients are usually managed by specialist drug dependence clinics although some GPs with a specialist interest offer similar services
  • patients may be offered maintenance therapy or detoxification
  • NICE recommend methadone or buprenorphine as the first-line treatment in opioid detoxification
  • compliance is monitored using urinalysis
  • detoxification should normally last up to 4 weeks in an inpatient/residential setting and up to 12 weeks in the community
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21
Q

What is cocaine and crack

A
  • Natural product of coca-leaves
  • Processed to produce cocaine hydrochloride (powder), acid- insufflated or injected
  • Freebase (inc. crack): solid (rocks), alkaline w/low melting point- smoked
22
Q

Comparing powdered cocaine and crack

A
  • Powdered cocaine (acid): mainly snorted (+/- inj). Starts in a few mins, full high at 15-30 mins, gradual come down. £40-50 per gram
  • Crack: crystalised (alkaloid), mainly smoked (+/- inj). Starts in a few seconds but very short with rapid come down. £15-20per rock, smaller rocks are cheaper
23
Q

Cocaine and other amphetamine like stimulants

A
  • Binds to monoamine transporters increasing Dopamine, Serotonin and Noradrenaline in the synaptic cleft.
  • Dopamine transporters are all throughout the brain
  • Important action on the limbic system (emotional responses and memories): dopamine responsive cells are highly concentrated in this system. Nucleus accumbens important in cocaine high
24
Q

Cocaine: effects

A
  • Excited, confident and/or anxious, happy, panicky, risk-taking
  • Tachycardia, tachypnoea, hypertension, hyperthermia, nausea, sweating, shaking
  • If use continues: Decreased need for sleep, appetite suppression, paranoia, hallucinations, mood swings/depression
  • The way the drug affects memories of the euphoric sensation, keeps users coming back to it, chasing the first high
  • The way the brain adapts to the disrupted dopamine and other mono-amines produces mood instability or depression.
25
Q

Management of cocaine toxicity

A
  • in general, benzodiazepines are generally first-line for most cocaine-related problems
  • chest pain: benzodiazepines + glyceryl trinitrate, if myocardial infarction develops then primary percutaneous coronary intervention
  • hypertension: benzodiazepines + sodium nitroprusside
  • the use of beta-blockers in cocaine-induced cardiovascular problems is a controversial issue: The American heart association advises against it but some cardiologists still do
  • if a reasonable alternative is given in an exam it is probably wise to choose it
26
Q

Adverse effects of cocaine

A
  • Cardiovascular= coronary artery spasm → myocardial ischaemia/infarction, both tachycardia and bradycardia may occur. Hypertension, QRS widening and QT prolongation, aortic dissection
  • Neurological= seizures, mydriasis, hypertonia, hyperreflexia
  • psychiatric effects= agitation, psychosis, hallucinations
  • others= ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding. Hyperthermia, metabolic acidosis, rhabdomyolysis
27
Q

Cocaine abuse: education

A
  • Risks of specific combinations
  • Not dangerous to stop suddenly
  • Health risks: Stroke, MI, Cognitive impairment, Parkinsons disease, seizures, Psychotic illness, Anxiety/depression
28
Q

Cocaine abuse: harm reduction

A
  • BBV testing & treatment
  • Safe injecting advice
  • Safe environment
  • Clean equipment + avoid home made pipes
  • Mucous membrane care (Vaseline)
  • Eat before using
  • Stay hydrated
  • Buy less (effect reduces after the first hit anyway)
29
Q

Cycle of change

A
  • Pre-contemplation: no intention of changing behaviour
  • Contemplation: aware a problem exists but with no commitment to action
  • Preparation: intent on taking action to address the problem
  • Action: active modification of behaviour
  • Maintenance: sustained change, new behaviour replaces old
  • Relapse: fall back into old patterns of behaviour
30
Q

Drug abuse; other psychological interventions

A
  • Psychoeducation
  • Practical strategies to reduce safely
  • Harm reduction
  • Mutual help groups
  • Online self help
  • Carer support
  • Employment and Accommodation support
31
Q

MoA of different drugs

A
  • Cocaine: blocks reuptake of dopamine by the presynaptic membrane
  • MDMA: stimulates the release of Serotonin and blocks its reuptake
  • Methamphetamine: stimulates release of dopamine and block its reuptake
  • Alcohol/Benzo: stimulate GABA receptors
  • LSD: stimulates serotonin receptors particularly 5-HT2A
  • Cannabis: stimulates cannabinoid receptors (CB1 and CB2)
  • Pregabalin/Gabapentin: blocks voltage gates calcium channels in the presynaptic membrane. Reducing release of excretory neurotransmitters
  • Nicotine: stimulates nicotinic acetylcholine receptors
32
Q

Medications to stop smoking

A
  • Nicotine replacement therapy (e.g., patches, gum or lozenges)
  • Bupropion
  • Varenicline
33
Q

Wernicke’s encephalopathy

A
  • A condition of acute thiamine (vitamin B1) deficiency
  • Triad: ophthalmoplegia, fluctuant mental state (confusion) and ataxia
  • Urgent treatment with thiamine replacement is essential due to rapid progression of irreversible neurological damage
  • Most commonly occurs in chronic alcoholics
34
Q

Wernicke’s encephalopathy symptoms

A
  • Neurological: ophthalmoplegia, Nystagmus, ataxia
  • Cognitive: confusion, memory deficits, apathy or agitation
  • Other clinical features: Hypothermia, altered consciousness, N+V, tachycardia
35
Q

Wernicke’s encephalopathy investigations

A
  • Tends to be diagnosed clinically but can measure serum thiamine
  • Blood tests: FBC, Urea and Electrolytes, Liver Profile, Clotting, Bone Profile, Magnesium
  • Neuroimaging: MRI can show typical changes in specific regions of the brain, as well as mamillary body atrophy in Korsakoff’s syndrome.
36
Q

Wernicke’s encephalopathy management

A
  • Urgent administration of parenteral (not oral) thiamine for a minimum of 5 days
  • Thiamine must be administered before or concurrently with any glucose administration (glucose can lower thiamine levels)
  • Adressing underlying cause: i.e. counselling for alcohol use disorder
37
Q

Korsakoff syndrome

A
  • Memory impairment (retrograde and anterograde)
  • Confabulation: patients fabricate memories to mask their memory deficit
  • behavioural changes
  • Often irreversible and results in patients needing full time institutional care
38
Q

Management of Korsakoff’s syndrome

A
  • Ongoing thiamine replacement
  • Cognitive rehab: To improve residual cognitive function and adapt to the memory loss
  • Management of patients environment: to reduce confusion and disorientation
  • Treatment of underlying cause i.e. alcoholism
39
Q

Typical antipsychotics

A
  • Mechanism of action: Dopamine D2 receptor antagonists blocking dopaminergic transmission in the mesolimbic pathways
  • Adverse effects: Extrapyramidal side-effects and hyperprolactinaemia common
  • Examples: Haloperidol, Chlopromazine
40
Q

Atypical antipsychotics

A
  • Mechanism of action: acts on a variety of receptors (D2, D3, D4, 5-HT)
  • Adverse effects: extra-pyramidal side effects and hyperprolactinaemia less common, metabolic effects (weight gain, dyslipidaemia and glucose metabolism)
  • Weight gain, clozapine is associated with agranulocytosis and hyperprolactinaemia
  • Examples: Clozapine, Risperidone, Olanzapine
41
Q

Antipsychotics: extrapyramidal side effects

A
  • Parkinsonism: instead change to an alternative (quetiapine/olanzapine) or prescribe anticholingeric medication
  • Acute dystonia: sustained muscle contraction i.e. torticollis, oculogyric crisis. May be managed with procyclidine
  • Akathsia (severe restlessness)
  • Tardive dyskinesia (late onset of choreoathetoid movements, abnormal, involuntary. May occur in 40% of patients, may be irreversible. Most common is chewing and pouting of jaw

Specific risks in elderly patients: increased risk of stroke, venous thromboembolism

42
Q

Antipsychotics: other side effects

A
  • antimuscarinic: dry mouth, blurred vision, urinary retention, constipation
  • sedation, weight gain
  • raised prolactin= may result in galactorrhoea, due to inhibition of the dopaminergic tuberoinfundibular pathway
  • impaired glucose tolerance
  • neuroleptic malignant syndrome: pyrexia, muscle stiffness
  • reduced seizure threshold (greater with atypicals)
  • prolonged QT interval (particularly haloperidol)
43
Q

Adverse effects of clozapine

A
  • agranulocytosis (1%), neutropaenia (3%)
  • reduced seizure threshold - can induce seizures in up to 3% of patients
  • constipation
  • myocarditis: a baseline ECG should be taken before starting treatment
  • hypersalivation
44
Q

Antipsychotics: monitoring

A
  • FBC, U&E, LFT= at start of therapy, annually. Clozapine requires more frequent monitoring of FBC (initially weekly)
  • Lipids, weight= at the start of therapy, at 3 months, annually
  • Fasting blood glucose, prolactin= at start of therapy, at 6 months, annually
  • Blood pressure: baseline, frequently during dose titration
  • ECG: baseline
  • Cardiovascular risk assessment: annually
45
Q

Smoking and psychotropic drugs

A
  • 7-12 cigarettes a day is sufficient for maximum induction of CYP1A2
  • In smokers the clozapine metabolism is increased reducing clozapine plasma levels
  • Smokers require higher doses of clozapine to achieve same plasma levels
  • On stopping smoking you should reduce the clozapine dose gradually
46
Q

Antipsychotics and physical risks

A

Long term risks: Cardiovascular, Dyslipidaemia, Weight gain, Diabetes, Hyperprolactinaemia, EPSE

47
Q

Qtc and antipsychotics

A
  • Dose dependent
  • May present as: increased QT interval, torsades de pointes, ventricular fibrillation, sudden death
  • Normal QTc= Women <470ms, Men <440ms
  • A QT prolonged to 450ms is of some concern. >500ms can lead to torsades de points and requires prompt review and action
48
Q

Dyslipidaemia and anti=psychotics

A

Olanzapine and clozapine associated with the greatest risks. Discuss dietary and lifestyle on initiation/ early in treatment. Full lipid profile at baseline, 3 months and annually. If QRISK above 10% prescribe a Statin.

49
Q

Antipsychotics and hyperprolactinaemia

A
  • Dopamine antagonists increase prolactin levels, can be caused by all antipsychotics
  • Less risk= Clozapine, olanzapine, quetiapine and ariprazole
  • Symptoms include: galactorrhoea, amenorrhoea, gynaecomastia, hypogonadism, sexual dysfunction
  • Linked with osteoporosis and breast cancer
50
Q

1st and 2nd gen antipsychotic side effects

A

1st generation antipsychotics tend to cause movement disorders whilst 2nd generation cause more metabolic disturbance

Year 5 (24 decks)

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