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PC/MC > Antipsychotics > Flashcards

Antipsychotics Flashcards

1
Q

Striatal interneuron

A

Ach Containing

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2
Q

Nigrostraital

A

A9 Dopamine neuron Substantia nagra pars compacta- Corpus striatum
DA release in straitum is essental for normal extrapyramidal motor function

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3
Q

Striatonigral

A

GABAnergic Neuron VTA-Corpus Striatum

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4
Q

Mesolimbic

A

A10 DA neuron VTA- Nucleus accumbens

DA release is important for normal affect, orderly thinking, drive states, pleasure/reward

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5
Q

DA receptor subtypes

A

D1 (D1,D5)

D2 (D2,D3,D4) Exist in 2 isoforms D2 long, D2 short

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6
Q

D1 receptors

A

Stimulate adenylate cyclase and increase cAMP
Affinity for phenothiazines > butyrophenones
small intracellular loop, large carboxy tail

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7
Q

D2 receptors

A

Not associated w/stimulation of Adenyate cyclase and may inhibit it
Affinity for butyrophenones > phenothiazines
Large intracellular loop, small carboxy tail

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8
Q

DA receptors are…

A

GPCRs

7 transmembrane spanning receptors

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9
Q

D1 couple

A

Gs, Golf

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10
Q

D2 couple

A

Gi/o

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11
Q

Symptoms and diagnosis of psychosis

A

Charecterized by impared behavior. Inability to think coherrently and comprehend reality.
+ve symptoms- “added” hallucinations, delusions, paranoia etc.
-ve symptoms- withdrawl, depersonalization
cognative- impared attention, deficits in learning and memory.

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12
Q

Organic Psychosis

A

Known cause. Can be due to:

Impared cerebral tissue function, intellecutual decline, drug abuse, tramua etc.

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13
Q

Idiopathic psychosis

A

Cause is not known. May have a genetic component (twin studies)
Schizophrenia

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14
Q

Dopamine theory

A

Upregulation of dopamine, excessive DA transmission- in limbric striatum and cortical areas innervted by A10 causes Schizophrenia.
* Terminal regions of A10 Dopamine pathways- Limbic cortex, and nucleus accumbens

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15
Q

Evidence for DA theory

A

Drugs blocking D2 like receptors reduce psychotic symptoms (+ve)
Drugs increasing synaptic DA cause psychosis (amphetamines, LDOPA)

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16
Q

Problems with DA theory

A

Other transmitter systems (seratonin, glutamate) and brain areas (Cortex, thalamus) are also likely involved
This theory alone is not enough to explain schitzophrenia. Multiple genes/systems are likely involved
Upregulation of dopa- negative symptoms??!

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17
Q

Pharmacological basis of therapuetics in Schizophrenia

A

Reduce DA transmission in terminal regions (A10 mesolimbic)
D2 blockers
Therapeutic problems arise as its difficult to block DA receptors only in limbic terminal areas (leading to SAs)

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18
Q

Classes of Antipyschotics

A

Typical- older generation- blockade D2 w/greater affinity than 5-HT2A
Atypical- newer generation- blockade 5-HT2A> D2 receptors. 2nd & 3rd Generation

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19
Q

Typical antipsychotic classes

A

Phenothiazine
Thioxanthene
Butyrophenone

Miscellaneous

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20
Q

Chlorpromazine

A

Phenothiazine

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21
Q

Thioridazine

A

Phenothiazine

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22
Q

Trifluoperazine

A

Phenothiazine

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23
Q

Perphenazine

A

Phenothiazine

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24
Q

Fluphenazine

A

Phenothiazine

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25
Q

Haloperidol

A

Butyrophenone

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26
Q

Pimozide

A

Misc.

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27
Q

Loxapine

A

A-typical

dibenzoxazepine

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28
Q

Clozapine

A 
dibenzodiazepine
A-typical
No extrapyramidal SAs
May suppress tardive dyskinesia
Effective in drug resistant cases- reduces +/- symptoms
Blocks many receptors besides DA- muscarinic, 5-HT2A, a1, h1. 
D4 blockade as well
D4=a1>5HT2A>D2=D1
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29
Q

Risperidone

A

A-typical

Low incidence of extrapyramidal and tardive dyskinesia. D2 5HT receptor blocking

30
Q

Quetiapine

A

A-typical
H1>a1>D2>5HT2A
low incidence of extrapyramidals
+/- symptoms

31
Q

Olanzapine

A 
A-typical
5HT2A>H1>D4>D2
\+/- Symptoms
Low incidence of extrapyramidal
Weight gains!
32
Q

Ziprasidone

A

A-typical
Acute treatment for agitated or violent encounters
Serious cardiac arrhythmias

33
Q

Aripiprazole

A

A-typical- 3rd generation
Partial agonist D2=5HT2A>D4>A1=H1»D1
DA stabilizer since its a partial.
No extrapyrmaidals

34
Q

Receptors

A

All have similar binding pockets, all ligands are monoamine NTs

35
Q

CNS SA’s

A

Sedation- tolerance
Antianxiety- +ve!
Suppression of spontaneous movement, lack of initative, disinerest, lack of pleasure

36
Q

Endocrine SA’s

A

Increased Prolactin- causing breast enlargement in males. Increased female and decreased male libido. Inc appetite, weight gain.

More prominent in typical antipsychotics and risperidone

37
Q

Autonomic SA’s

A 
Anticholinergic- muscarinic blockade (ACh) blurred vision, dry mouth
Antiadrenergic effects (GPCR)- orthostatic hypotention and reflex tachycardia
38
Q

Cardio SA’s

A

Hypotention

39
Q

Blood Disorders

A

Decrease WBC- leukopenia
Increase certain elements (eosinophilia)
Clozapine- can cause bone marrow suspension and frank agranulocytosis

40
Q

EPS SA’s

A

More common w/typical.

41
Q

Parkinsonian

A

EPS

5-30 day onset.
Treatment w/anticholinergic drugs

42
Q

Acute Dystonic Rxn

A

1-5 day onset- spasms of muscles in face, back, mimic seizures
Treatable w/anticholinergics

43
Q

Akathisia

A

5-6 day onset; restlessness

Reduce dose of antipsych to treat

44
Q

Neuroleptic Malignant Syndrome

A

Onset is weeks.
Can persist for days after stopping a neuroleptic.
Fever, unstable BP, can be fatal
STOP antipsychotic, dantrolene or bromocriptine may help.

45
Q

Tardive dyskinesia

A

Months to years
Irreversible orofacial dyskinesias
No effective treatment
Prevention- use lowest effective dose of antipyscs.

46
Q

Skin Reactions

A

Phenothiazines

47
Q

Lowering of seizure threshold

A

Contraindicated during alc withdrawl or CNS depression

48
Q

Interactions

A

Potentiates effects of CNS Depressents, sedative/hypnotics, alcs, antihistamines, opiates.

49
Q

Asenapine

A

Atypical
Schizophrenia and acute manic episodes BPD
Reduced extrapyramidal symptoms, no changes in prolactin

50
Q

Lurasidone

A

Atypical
MDD BPD
Blocks 5HT2A, D2, AND 5HT7 w/high affinity
Extrapyramidal- akathisia (restlessness)

51
Q

Other uses

A

Huntingtons

Tourettes

52
Q

1st Generation Antipsyhcs

A

Typical, block +ve symptoms.

Little to no discrimination between D2-D1

53
Q

2nd Generation Antipsychs

A

Selective for D2, HT2A

+’ve symptoms, -ve symptoms

54
Q

3rd Generation Antipsychs

A

Partial agonists.

No metabolate syndrome

55
Q

Phenothiazine Derivatives

A

Phenol, Sulfer, Nitrogen.
Non-selective DA antagonist.
Lipophobic- good to pass BBB
some Hydrophillic properties- needed to dissolve and absorb in GI

56
Q

Long Acting Neuroleptics

A

Increase patient compliance. More lipophillic in nature, injected IM.
Prodrug design- not active. Bioactivation occurs via esterases in blood stream.

57
Q

Alkyl chain size for optimal antipsychotic activity

A
  1. 2c- antihystamines
    1c, 4c+ do not work
58
Q

Antipsychotic potency trend

A

Piperazine>piperidine>aliphatics

59
Q

EPS frequency trend

A

Piperazine>piperidine>aliphatics

60
Q

Sedation trend

A

Aliphatics~piperidines>piperazines

61
Q

Hypotensive effects

A

Aliphatics>piperidines>piperazines

62
Q

Metabolism of Phenothiazines and Thioxanthenes

A

Oxidase Demethylate, -OH addition, sulfoxides, sulfones

63
Q

Butyropheones SAR

A

3’ Amino group is essential for neuroleptic activity
Variations on 3’ amino group, ie rings retain activity
Lengthening alkyl chain- reduces activity (dont want >3carbons)

64
Q

-OH/COOH on a butyrophenone

A

Conversion top a LA Neuroleptic. Esterify it.

65
Q

Metabolism of Haloperidol

A

Extensively metabolized in the body. See pic

Potentt neuroleptic- associated with high incidence of TD.

66
Q

Dibenzazepines

A

Neuroleptics that utilize Tricyclic dibenzazepine heterocyte.
Lipophillic, weakly basic.

67
Q

Dibenzodiazepine

A

X substituted for: NH

ex. Clozapine, Olanzapien

68
Q

Dibenzoxazepine

A

X substituted for: O

ex. Loxapine, Amoxapine

69
Q

Dibenzothiazepine

A

X substituted for: S

ex. Quetiapine

70
Q

Benzisoxazoles

A

Risperidone
balanced DA/5HT2A antagonism
Reduced EPS, +/- effects

71
Q

Risperidone Metabolism

A

Alicyclic hydroxylation, Oxidative N-dealkylation, Benzisooxazole Ring clevage

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