3153 psych > APS > Flashcards

APS Flashcards

(55 cards)

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1
Q

schizo – theory

A

1) dopamine theory: Amphetamine (overactive DA) produce similar sx to acute schizophrenia
* All antipsychotic drugs are D2 antagonists

2) 5HT theory: LSD (blocks 5HT) produce schizo sx

3) glutamate theory: ketamine (block NMDA receptor) produce schizo sx

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2
Q

5 schizo sx domains

A

1) +ve sx (abnormal behaviour)
2) -ve sx (substracted normal behaviour)
3) aggressive sx
4) ANX/ DEP
5) cognitive sx

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3
Q

DA pathways (1) DA theory

A

Nigrostriatal pathway (D1, D2)
- substantia nigra –> dorsal striatum

Mesolimbic pathway (D2, 3)
- ventral tegmental area (VTA) –> Limbic (emotional) brain

Mesocortical (D4)/ mesolimbic pathway
- ventral tegmental area (VTA) –> prefrontal cortex (emotional)

Tuberoinfundibular pathway (D3)
- hypothalamus –> anterior pituitary

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4
Q

Nigrostriatal pathway

A

substantia nigra –> dorsal striatum

Voluntary movement , prevent other movements

  • inhibit D2: EPSE (pseudo-parkinsonism)
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5
Q

Mesolimbic pathway

A

ventral tegmental area (VTA) –> Limbic (emotional) brain
Reward and emotion

  • inhbit D2: reduce +ve sx, reduce schizo sx
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6
Q

Mesocortical pathway

A

ventral tegmental area (VTA) –> prefrontal cortex

motion, cognition, attention
- Higher order thinking
- Executive functions

  • inhibit D2: hypofunction, results in -ve sx
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7
Q

Tuberoinfundibular pathway (D3)

A

hypothalamus –> anterior pituitary (infundibular)

DA inhibits prolactin secretion into blood circ

  • inhibit D2: hyperprolactinemia (more prolactin released)
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8
Q

1st vs 2nd gen

A

BOTH: block dopamine pathways = Control +ve sx of schizo

EPSE in 1st gen > 2nd gen

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9
Q

FGA eg

A

chlorpromazine
haloperidol
sulpiride

  • D2 antagonism
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10
Q

SGA eg

A

clozapine
olanzapine
quetiapine
risperidone
amisulpride
brexipiprazole

  • serotonin-dopamine antagonism (SDA: 5HT, DA) + complex mix
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11
Q

FGA SE

A

○ M1: dry mouth, constipation, blurred vision
○ H1: sedation, weight gain
○ A1: postural hypotension, dizzy
○ DA: EPSE, prolact

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12
Q

EPSE

  • Pyramidal motor pathway is output from primary motor cortex
    ○ via pyramids of medullar oblongata –> spinal cord
    ○ Involves basal ganglia: (striatum, substantia nigra)
A
  • (Tardive dyskinesia + Akathisia) Occur in 20-40% of pt on typical antipsychotics, IRREVERSIBLE dyskinesia
    Upregulation or super sensitivity of dopamine receptors in nigrostriatal system
  • (parkinsonism) block D2 receptor in nigrostriatal, where DA neurons terminate
  • (dystonia) DA hyperactivity in basal ganglia
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13
Q

EPSE description

A
  • Acute dystonia – (posture, spasm)
    * Parkinson-like sx: cogwheel rigidity and tremor at rest, abnormal muscle tone
    * 1st few wks of tx
    * Reversible when drug is stopped
    - Caused by D2 antagonism in nigrostriatal pathway
  • Tardive dyskinesia – uncontrolled facial, jaw movements
    * Slow (tardive) over mnths/ yrs of tx
    * Repetitive (dyskinesia)
    * irreversible
    - stereotyped involuntary movements of face, tongue, limbs
  • Akathisia – restlessness
    * Involuntary movements (akathisia)
    * compulsion assoc with restlessness, ANX, agitation
    - Correlates directly to duration on meds
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14
Q

SGA – atypical

A

produce less EPSE. more metabolic (-ine)
complex mixtures of actions:

  • greater affinity for 5HT2 receptors
  • greater affinity at D4 receptors
  • mixed antagonism: a-adrenoceptor, H1, M1, 5HT2 receptor
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15
Q

diff SGA drug, diff receptor affinity – SE, efficacy

A
  • Amisulpride (D2, D3, reported 5HT7)
    • Fewer SE due to D2,3 receptor selectivity
      ○ D2,3 antagonist: prolactin release incr (breast pain, swell, lact)
      ○ Absence of a1, H1, M1 antagonist SE
  • Clozapine
    • M1: dry mouth, constipation, blurred vision
    • H1: sedation, weight gain
    • A1: postural hypotension, dizziness
      • D1,2,3,4
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16
Q

clozapine ADR

A

Clozapine-induced agranulocytosis
○ <1% of pt but fatal
○ Lack of granulocyte type WBC (monitor regular blood counts)

–> olanzapine (similar effect w/o this ADR)

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17
Q

drug-induced DM

A

clozapine, olanzapine, risperidone

(amisulpride exception)

MOA: unknown - may involve 5HT antagonism
* in hypothalamus
* in pancreatic beta cells

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18
Q

drug-induced weight gain

A

SGA: clozapine, olanzapine, risperidone

MOA: sedation (H1 antagonism) –> incr sedentary behaviour
maybe: A1 , 5HT2 antagonism on hypothalamus & feeding behaviour

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19
Q

WHY SGA < FGA EPSE

A
  • more 5HT2A receptor antagonism > D2 antagonism = less EPS, less -ve sx too
  • high D3 to D2 antagonism ratio (more action on nucleus accumbens > striatum = more DA receptor for EPSE)
  • high D4 to D2 antagonism ration (action in prefrontal cortex > striatum)
    /targets emotion, +ve sx control
  • high D2 to D1 antagonism ratio (less complete blockade of DA function as D2 antagonism at presynapse will iNCR DA RELEASE)
    / presynaptic D2 receptor as a feedback regulation
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20
Q

additional benefits of SGA

A
  • more effective against -ve sx (clozapine, olanzapine, risperidone)
  • cognitive dysfunction sx control (clozapine, risperidone)
  • mood stabilisation (clozapine, olanzapine, risperidone)

FGA: more on +ve sx control (not much for -ve sx, cognition and mood stability)

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21
Q

PK of APS and onset (tmax)

BAO

A
  • SGA
    * (long tmax) olanzapine 6hrs, aripiprazole 3-5hrs, brex 4hrs
  • most FGA, SGA: tmax= 1-3hrs
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22
Q

PK of APS and dosing freq (t1/2)

A

(divided dosing due to risk of hypoTEN, seizure)

  • FGA
    * (divide dose): chlorpromazine, sulpiride
  • SGA
    * (divided dose): amisulpride, clozapine, quet, ziprasidone

most FGA, SGA
* long t1/2: OD dosing
eg haloperidol 12-36hrs

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23
Q

PO APS potency

HOR

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A

low potency: sulpiride, chlorpromazine, Amisulpride, clozapine, quetiapine

high potency: risperidone (2-6mg), haloperidol, olanzapine (5-15mg)

24
Q

dosing freq of LAI

Study These Flashcards
A
  • haloperidol decanoate: 2-4w
  • risperidone: 2wk, suppl PO for first 3 wks reach stabilisation
  • paliperidone: 3mnths
25
relative SE
* FGA * EPSE -- MOST * Prolactin -- ALL * Weight gain -- chlorpromazine, perphenazine * Pro convulsation -- chlorpromazine, cloxapine * Cardiac -- thioridazine * Anticholinergic -- chlorpromazine * Hypotension: chlorpromazine * SGA * Weight gain : clozapine, olanzapine * Anticholinergic : clozapine * Cardiac: clozapine, ziprasidone * Sedation: clozapine
26
EPSE
* acute dystonia (abnormal, prolonged contraction of any muscle grp) ○ anticholinergics * parkinsonism (tremor, muscular rigidity, flattended effect, loss of movement, bradykinesia) ○ anticholinergics * akathisia (restlessness, fidget) ○ BZP, propranolol * tardive dyskinesia (involuntary orofacial muscle) ○ valbenazine
27
EPSE -- dystonia (muscle spasm)
* IM/IV > PO hrs * Risk: high potency, neuroleptic naïve pt, young M * Manage: IM anticholinergics (benztropine, diphenhydramine)
28
EPSE - pseudo parkinsonism manage (tremor, rigid, bradykinesia, salivation)
○ Risk: elder F, previous neurological damage (head injury, stroke) ○ Manage: decr antipsychotic dose, switch to sga ○ Anticholinergics PRN (benztropine)
29
EPSE - tardive dyskinesia (orofacial movement, chew/ tongue protusion, repetitive. Late onset 3-6mnths)
* Risk: FGA > SGA, those develop acute EPSE when started on FGA. Worsens with anticholinergic. May be irreversible * Manage: discontinue anticholinergics ○ Decr dose, switch to SGA (clozapine) ○ Reversible inhibitor of vesicular MAO transporter 2 (VMAT2) = valbenazine 40-80mg/ day ○ BZP: Clonazepam PRN
30
hyperprolactinaemia
* Galactorrhea, amenorrhea, decr libido, gynecomastia (M) * Risk: FGA (Pali =/> RISP > OTHERS) * Manage: decr FGA dose, dopamine agonist (amantadine, bromocriptine) * Switch to aripiprazole
31
metabolic SE
* Weight gain (>7% from baseline), DM incr lipids * Risk: OLAN, CLOZ > CPZ, QUET, RISP > * Manage: lifestyle, tx DM (metformin) & hyperlipidemia * Switch to lower risk agents (Ari, Lura, Zip, Halo)
32
manage CVS - ortho hypoTENsion
* orthostatic hypotension * CPZ, CLOZ > RISP, PALI, QUET * get up slow; switch to olan, zip, ari, sulpiride
33
manage CVS -QTc
* high doses, IV haloperidol, low K+, IHD, Female * avoid: Thio > chlorpromazine > Halo > quet > risp> olan * lower risk agents: Aripiprazole
34
CVS - VTE/ PE
* avoid: low potency FGA: sulpiride, chlorpromazine * prevent, monitor and tx DVT
35
CNS - sedation
Risk: CPZ > CLOZ > QUET > OLAN Manage: switch to lower risk agents. (RISP, PALI, ZIP, ARI)
36
CNS seizure
* Risk: CLOZ > CPZ> OTHERS SGA * High doses, rapid titration, hx of epilepsy * Manage: switch to high potency agents (HALO, RISP)
37
neuroleptic malignant syndrome is __ caused by ___
* DA blockade, cause hypothalamic dysfunction. muscle contraction & temp dysregulation * Muscle rigidity, fever, altered consciousness, high CK, autonomic dysfunct (PR, BP, diaphoresis) * Risk: high potency anticholinergics * Rare, potentially lethal * Onset: hrs - 3days (within 30d) * Other possible causes 1. Succinylcholine/ suxamethonium (muscle relaxant) 2. Antipsychotics D2 blocker 3. Sudden discontinuation Levodopa (LT dopamine agonist)
38
manage NMS
* Manage: IV dantrolene 50mg TDS, PO dopamine agonists (amantadine, bromocriptine) * Supportive measures * Switch to SGA
39
psychogenic polydipsia self-induced water intoxication
* avoid: anticholinergics * manage: fluid restriction, discontinue drug with anticholinergics effect (anta M1, Ach)
40
temp dysregulation
* avoid anticholinergics * manage: hydration, app clothes + shade
41
hepatic SE
* Incr LFT, cholestatic jaundice (CPZ) * Risk: CPZ (FGA), OLAN, QUET > OTHER SGA * Manage: jaundice develops = discontinue and switch to safer agents sulpiride, ami
42
opthalmologic
* Cornea/ lens changes, pigmentary retinopathy * Risk: phenothiazines (CPZ, THIO), Quet * Manage: pt on QUET (eye exam q6mnths)
43
dermatologic
* Maculopapular rash, photosensitive, pigmentation * Risk: CPZ * Manage: protective clothing, sunscreen * Consider switch to other antipsychotics
44
hematologic
* Decr WBC, agranulocytosis (absolute neut count ANC) * Risk: clozapine * Manage: discontinue antipsychotics if severe * WBC < 3x 10*9/L or ANC < 1.5x 10*9/L
45
monitor SE
(every visit) - vitals * BP, PR, temp - SE: * EPSE exam, plasma prolactin (libido, gynecomastia) - mental state: * suicidality, MSE (12wks, annual) - metabolic: * BMI, waist circumference, Fasting blood sugar, lipid panel - ECG (Qtc prolongation) (wkly 18wks, mnthly) - WBC, ANC (clozapine)
46
preg
avoid OLAN, CLOZ: Gestational DM
47
breastfeed
OLAN, QUET suitable CLOZ continue + not breastfeed
48
renal impairment
oral aripiprazole avoid: sulpiride, amisulpride
49
hep impairment
sulpiride, amisulpride preferred
50
elderly
* Avoid drug with high propensity for a1 blockade = hypotension * Avoid drugs with Ach SE = Constipation, urinary retention, delirium ○ Start low, go slow. Simplify regime, avoid DDI, avoid long t1/2 drugs (split) * Caution: FGA, SGA - incr mortality, CVA in dementia pts
51
PD int (6)
* CNS depressants: alcohol, codeine, hydroxyzine, psychotropics * additive effects: anti M1, H1, A1, DA (hypotension) BP meds * Parkinson (nullify effect): dopamine agonist, levodopa * 5HT augmenting agents (antagonise 5HT2A receptor block, decr DA release, worsen EPSE) * EPSE, NMS: metoclopramide, psychostimulants * seizure: lower the seizure threshold, incr seizure risk * incr toxicity: Li, TCAs * agranulocytosis (CBP + cloz)
52
PK int
* P1: oxidation, reduction, hydrolysis ○ CYPP450, 1A2, 3A4, 2D6 * P2 ○ Glucuronidation, coupling
53
CYP1A2
* inducers: rifampicin, PB, PT, smoke * inhibitors: fluvoxamine, ciprofloxacin, quinolones, macrolides, isoniazid, ketoconazole (halo, cloz, olan, zip)
54
CYP2D6
* inducers: rifampicin, PB, PT, CBP * inhibitors: fluoxetine, paroxetine - ssri, duloxetine - snri (halo, risp, ari, olan)
55
CYP3A4
* inducers: barbiturates, CBP, PT, rifampicin, st john's * inhibitors: azoles, TCA, fluvoxamine, isoniazid, macrolides, grapefruit quet, zip, Ari, Risp, brexipip
3153 psych
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