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Pharmacology 200 > 2- antipsychosis > Flashcards

2- antipsychosis Flashcards

1
Q

what is psychosis

A

mental disorders in which there is a loss of contact with reality, affecting abilities to think feel and act

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2
Q

what are the main clusters of symptoms in schizophrenia

A

+, -, mood, and disorganized symptoms

memory deficits

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3
Q

what are the 3 biochemical theories of schizophrenia

A

excess dopamine
reduced serotonin
reduced glutamate or GABA

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4
Q

what is the dopamine hypothesis

A

that psychotic symptoms are caused by an excess of dopamine

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5
Q

how did they come up with the dopamine hypothesis

A

drugs that stimulate DA can cause psychotic symptoms

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6
Q

how do first gen antipsychotics FGAs work

A

they block DA receptors as their main target

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7
Q

how do second gen antipsuchotics work

A

they blcok serotonin receptors

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8
Q

how did they come up with the reduced serotonin theory

A

LSD are serotonin agonists

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9
Q

how did they come up with the reduced glutamate or GABA hypothesis

A

PCP, glu receptor inhibitor, induced +and- symptoms of schizo

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10
Q

what is the mesolimbic/mesocortical system

A

structures that mediate memory, learning, affect and thought organization

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11
Q

what happens when the mesolimbic/mesocortical system is disturbed

A

psychotic Symptoms

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12
Q

what does DA do in the tuberoinfuncibular system

A

effects secretion of some pituitary hormones, like prolactive and growth hormones

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13
Q

what is the nigrostriatal system

A

pathway thought to be involved in parkinson’s life symptoms after using t neuroleptic drugs, like tardive dyskinesias

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14
Q

what do D1 dopamine receptors do

A

stimulate Gs pathway

target for antipsychotics, but it may not be clinically relevant

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15
Q

what do D2 dopamine receptors do

A

Gi pathway (inhibit AC) and couple with other effector systems

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16
Q

what happens when you block the D2 receptor

A

clinical antipsychotic potency

reduce positive symptoms

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17
Q

what happens with 5-HT2A antagonist

A

improves + and - symptoms

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18
Q

how does 5-HT2A reduce positive symptoms

A

positive symptoms by reducing excitation of glutamate neurons in the prefrontal cortex

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19
Q

how does 5-HT2A reduce - symptoms

A

5-HT2A antagonism releases DA in the prefrontal cortex

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20
Q

what happens when there is an increase in DA in the prefrontal cortex (antagonize 5-HT2A)

A

may improve negative, cognitive and affective symptoms of schizophrenia

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21
Q

what do 5-HT1A receptors act as for DA release

A

accelerators

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22
Q

what do 5-HT2A receptors act as for DA release

A

brakes

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23
Q

what does 5-HT1A agonism do

A

increases DA release and decreases glutamate release in prefrontal cortex

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24
Q

what does 5-HT2A antagonism stimulate

A

DA release in nigrostriatal pathway, the increase DA competes with drug at D2 and less receptors binding to drug

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25
Q

what reduces the risk of actrapyramidal symptoms

A

5-HT2A antagonism, because more DA is released and competes with the drug

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26
Q

what do 5HT cells release to communicate to DA neurons

A

GABA

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27
Q

what happens when 5HT blocks 5HT2A receptors on GABA neuron

is it direct or indirect

A

GABA isnt released, and dopamine isnt released

indirect because goes through GABA

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28
Q

are typical antipsychotics gen 1 or 2

A

1

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29
Q

are atypical antipsychotics gen 1 or 2

A

2

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30
Q

how do all 1 gen work

A

target DA receptors

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31
Q

how does 1 gen efficacy depend on

A

D2 receptor antagonism

32
Q

what is haloperidol

A

1st gen

33
Q

what is chlorpromazine

A

1st gen

34
Q

what is clozapine

A

2nd gen

35
Q

what is risperidone

A

2nd gen

36
Q

how do most 2 gen work

A

affinity for 5-HT receptors and D2 receptors

37
Q

why do 2 gen have less dopamine related side effects than gen 1

A

they bind looser and dissociate faster

38
Q

how much D2 occupation is required to produce antispychotic effects

A

60-80%

39
Q

what happens over 80% D2 receptor occupancy with gen 1

A

extrapyrimidal (physical parkinson like symptoms), elevated prolactin and tardive dyskinesias

40
Q

what is haloperidol kinetics

A

fast on slow off compounds

1st gen

41
Q

how does haloperidol work

A

fast rebinding at D2 and hard to insurmound (slow dissociation)

42
Q

what does haloperidol cause

A

increase EPS (extrapyramidal side effects) and increase prolactin release

43
Q

what are chlorpromazine kinetics

A

fast on and fast off

gen 1

44
Q

what happens in chlorpromazine side effects

A

fast rate=high EPS

fast off=normal prolactin

45
Q

what is kinetics of clozapine

A

slow on fast off

46
Q

what symptoms clozapine

A

slow on=less EPS

fast off=normal prolactin

47
Q

what does slow dissociation rates cause

A

high prolactin

48
Q

what does fast dissociation rates cause

A

normal prolactin

49
Q

what does slow binding rates cause

A

normal EPS

50
Q

what does fast binding rates cause

A

high EPS

51
Q

which drug causes agranulocytosis

A

clozapine

52
Q

what is agranulocytosis

A

severe reduction in WBC

53
Q

what are the receptor affinities for haloperidol

A

D2(most), D1, D4, alpha-adrenergic, 5-HT2

54
Q

what are the receptor affinities for chlorpromazine

A

D1(most), D2, 5-HT2A, aloha adrenergic

55
Q

what are the receptor affinities for risperidone

A

low dose: 5-HT2A

high dose: D2 5-HT7

56
Q

what are the main bad side effects of first gen

A

EPS, tardive dyskinesia, prolactin increase

57
Q

what are the main bad side effects of 2 gen

A

cardiovascular bad, metabolic bad, diabetes and weight gain, and life span decrease

58
Q

how long before they start to work

A

hours or days, but 4-6 weeks for full effect

59
Q

where is haloperidol metabolized and by what

half life

A

extensively in liver CYP3A4
1.5days
highly sedating

60
Q

chlorpromazine metabolism and half life

A

accelerates its own metabolism by inducing CYP enzymes, over 100 metabolist, 1 day

61
Q

clozapine metabolism and half life

A

CYP1A2 and CYP3A4 to norclozapine (similar D2 and 5-HT2A affinity as clozapine)
0.5 days

62
Q

risperidone metabolism and half life

A

CYP2D6 indo paliperidone (which is also marketed as an antispychotic)
1day

63
Q

which gen is better for + symptoms

A

both

64
Q

which gen is better for - symptoms

A

second gen

65
Q

what happens when 5HT blocks 5HT2A receptors on DA neuron

is it direct or indirect

A

DA isnt released

directly

66
Q

what happens when 5HT binds to 5HT-1A receptors

A

5HT causes inhibition of its own release
the lack of 5HT results in a disinhibition of DA release
Raises DA

67
Q

what does 5HT1A agonism cause

A

increase DA release in prefrontal cortex

68
Q

what does 5HT2A antagonism cause

A

released DA in prefrontal cortex and in nigrostriatal pathway

69
Q

how does GABA release effect DA release

A

GABA release stimulates DA release

70
Q

which CYP enzymes for haloperidol and what active metabolite

A

CYP3A4

none we know of

71
Q

which CYP enzymes for clozapine and what active metabolite

A

CYP1A2 and CYP3A4

norclozapine

72
Q

which CYP enzymes for chlorpromazine and what active metabolite

A

100 metabolites

induces CYP to accelerate its own metablism

73
Q

which CYP enzymes for risperidone and what active metabolite

A

CYP2d6 into paliperidone

74
Q

which drug is fast on slow off

A

haloperidol

75
Q

which drug is fast on fast off

A

chlorpromazine

76
Q

which drug is slow on fast off

A

chlozapine

Pharmacology 200 (29 decks)

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