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PHAL303 > Disorders > Flashcards

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
Q

MAOIs

A

Phenelzine (serious adverse effects w cheese/beer, hypotension)
MAOa specific to 5HT - dizziness, insomnia, nausea

26
Q

SSRIs

A

Inhibit 5HT uptake
Fluoxetine, paroxetine, citalopram
Nausea, vomiting, diarrhoea, constipation, sexual dysfunction

27
Q

SNRIs

A

NA uptake
Reboxetine, maprotiline (nortriptyline)

28
Q

Tricyclic vs SSRIs

A

SSRIs first - better side effects and safer in overdose
Greater effect in more severe depression

29
Q

Abrupt discontinuation of SSRIs

A

Dizziness, parasthesia, nausea, movement disorders
Worst if has short half life

30
Q

New antidepressant therapies

A

Ketamine, vortioxitine, vilazidene
Triple monoamine reuptake inhibitors

31
Q

BPD treatment

A

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
Q

Psychedelics

A

Hallucinogens - peyote, psilocybin, ayahuasca, LSD
Hallucinations, emotions, sense of time, compelling sense of reality)

33
Q

Psychedelic mechanism

A

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
Q

Thalamus pathways

A

Pyramidal neutrons -> medial prefrontal cortex inhibit GABA -> thalamus = disinhibition
Increase functional connectivity of thalamus and sensory cortex

35
Q

Ego dissolution

A

“I” no longer exists
Related to default mode network, posterior cingulate cortex - thinking about self, mind wandering, memory about self, planning

36
Q

Psychedelics in depression

A

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

PHAL303 (8 decks)

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