Disorders Flashcards

1
Q

Types of hypnotics

A

Benzodiazepines - pams and chlordiazepoxide
Barbituates - pentobarbital, thiopental
Zopiclone (non-BDZ)
Ethanol
Anaesthetics - propofol, etomidate

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2
Q

Benzodiazepines

A

Increase the effect of GABA on GABAa receptors (PAM)
increase inhibition and decrease anxiety
can be hypnotic (triazolam) = memory impairment
Gamma2 subunit on GABAa important for full response

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3
Q

GABA inhibition

A

NAM - FG-7142
antagonist - flumazenil
anxiogenic

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4
Q

GAD

A

general anxiety disorder
Treat with SSRI, cognitive therapy
seconds line - pregabalin or buspirone
Quetiapine - atypical antipsychotic (5HT2a and D2)

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5
Q

Insomnia

A

Cognitive-behaviour therapy
Benzos, antidepressants, melatonin, orexin antagonist, gabapentin

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6
Q

Benzodiazepines adverse effects

A

High therapeutic index
Drowsiness, decreased alertness, ataxia, tolerance (less binding sites), dependance (mostly to sedative and ataxic effects), withdrawal

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7
Q

Seizures

A

Epileptic - epilepsy, acute symptomatic, febrile
Non-epileptic - vasovagal faint, day dreaming, tics, parasomnia

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8
Q

Epilepsy

A

Recurring seizures (2 more than 24 hours apart and ongoing)

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9
Q

Types of seizures

A

Focal - one place, discrete (may be aware)
Generalised - widespread, bilateral, tonic-clinic, absence

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10
Q

Tonic-clonic

A

abrupt onset of bilateral tonic (increased muscle tone), jerking (clonic), unaware with no warning event, confused and drowsy

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11
Q

Absence seizure

A

Abrupt and less than 10 seconds
Normal after seizure
Eyelid flutter/blinking

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12
Q

Focal seizures

A

Limited network in one hemisphere, distribution varies, may mirror focus
Aware, impaired, focal to bilateral tonic clonic

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13
Q

Causes of seizures

A

Increase synaptic excitation, decrease inhibition, increase intrinsic excitability

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14
Q

Anti-epileptic drugs

A

Focal and generalised = valproate, carbamazepine, phenytoin
Absence = valproate, ethosuximide
Gabapentin

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15
Q

Status epileplicus drugs

A

Midazolam, phenytoin, phenobarbital

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16
Q

Epilepsy drug MoAs

A

Carbamazepine, valproate, phenytoin = increase inactive Na2+ channels
Ethosuximide, valproate = inhibit T-type Ca2+ channels
Vigabatrin = inhibits GABA transaminase
Tiagabine = inhibits GABA reuptake
Benzos = PAMs

17
Q

Other uses of anti-epileptic drugs

A

BPD, migraine, anxiety, neuropathic pain, tinnitus

18
Q

Anti-epileptic side effects

A

Carbamazepine - nausea, dizziness, drowsiness, agranulocytosis, blurred vision
Lamotrigine - rash, blurred vision , dizziness, drowsiness
Valproate - weight gain, bleeding, hair loss, autism in pregnancy
Levetiracetam - lethargy, fatigue
Phenytoin - narrow therapeutic index, vertigo, headache, confusion, hyperplasia of gums, hepatitis, etc

19
Q

Depression

A

Noradrenaline and serotonin
Depressed mood, fatigue, weight change, insomnia, cognitive impairment, feelings of worthlessness, suicidal ideal action, anhedonia

20
Q

Bipolar depression

A

Depressed and manic (gambling, speeding, risks)

21
Q

BPD drugs

A

Lithium, carbamazepine, valproate (D2 antagonist), gabapentin
Electroconvulsive therapy

22
Q

Monoamine hypothesis

A

Deficiency of NA and 5HT
May be more one than another
Evidence = muted response to DL-fenfluramine (interference with release), PET scan shows less serotonin
Stress -> gene transcription -> change neurogenesis in brain
No good evidence

23
Q

Anti-depressants

A

SSRIs - selective serotonin reuptake inhibitors
SNRIs - selective noradrenaline reuptake inhibitors
MAOIs - monoamine oxidase inhibitors
TCAs - tricyclic antidepressants
Mianserin, trazodome, mirtazapine

24
Q

TCAs

A

Imipramine, amitriptyline
Block 5-HT and NA reuptake (and ACh, alpha NA, histamines) = non selective
Take 2-3 weeks to work
Cardiotoxicity, dry mouth, blurred vision, constipation, tachycardia

25
MAOIs
Phenelzine (serious adverse effects w cheese/beer, hypotension) MAOa specific to 5HT - dizziness, insomnia, nausea
26
SSRIs
Inhibit 5HT uptake Fluoxetine, paroxetine, citalopram Nausea, vomiting, diarrhoea, constipation, sexual dysfunction
27
SNRIs
NA uptake Reboxetine, maprotiline (nortriptyline)
28
Tricyclic vs SSRIs
SSRIs first - better side effects and safer in overdose Greater effect in more severe depression
29
Abrupt discontinuation of SSRIs
Dizziness, parasthesia, nausea, movement disorders Worst if has short half life
30
New antidepressant therapies
Ketamine, vortioxitine, vilazidene Triple monoamine reuptake inhibitors
31
BPD treatment
Lithium - don’t know exact mechanism, dopamine antagonist when manic, does something to phosphatidy inositol, narrow therapeutic index, cerebellar ataxia, cognitive deterioration Carbamazepine, gabapentin, dopamine antagonist
32
Psychedelics
Hallucinogens - peyote, psilocybin, ayahuasca, LSD Hallucinations, emotions, sense of time, compelling sense of reality)
33
Psychedelic mechanism
Bind to 5HT2a in prefrontal cortex, posterior cingulate cortex, visual cortex Thalami nuclei = reticular nucleus, medial dorsal nucleus, pulvinar Bottom up processing ( thalamus to cortex), remove filter Ketamine = antagonist
34
Thalamus pathways
Pyramidal neutrons -> medial prefrontal cortex inhibit GABA -> thalamus = disinhibition Increase functional connectivity of thalamus and sensory cortex
35
Ego dissolution
“I” no longer exists Related to default mode network, posterior cingulate cortex - thinking about self, mind wandering, memory about self, planning
36
Psychedelics in depression
Open mind to accepting ideas, bigger splash Reduce rumination via default mode network Improve patient-therapist relationship Increase synaptogenesis, increase AMPA + NMOA downstream effects Clinical trial = worked but need more studies, fewer side effects, persisting perception disorder, tolerance