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Psychopharmacology > Chapter 5: Antipsychotics > Flashcards

Chapter 5: Antipsychotics Flashcards

1
Q

which dopamine pathway has a major role in motivation/reward and why

A

mesolimbic pathway
dopamine neurons target the nucleus accumbens (pleasure center) in the ventral emotional striatum

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2
Q

conventional antipsychotics

A

haloperidol (Haldol)
chlorpromazine (Thorazine)
fluphenazine (Prolixin)
perphenazine (Trilafon)
thioridazine (Mellaril)
trifluoperazine (Stelazine)
Loxapine (Loxitane)
thiothixene (Navane)
pimozide (Orap)

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3
Q

the pines

A

clozapine
olanzapine
quetiapine
asenapine
zotepine

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4
Q

many dones and a rone

A

risperidone
paliperidone
ziprasidone
iloperidone
lurasidone
lumateperone

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5
Q

two pips and a rip

A

aripiprazole
brexpiprazole
cariprazine

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6
Q

Explain how secondary negative symptoms happen with drugs that target MESOLIMBIC/MESOSTRIATAL dopamine D2 receptors and how to treat it

A

dopamine neurons target nucleus accumbens (pleasure center) in the PFC. When dopamine is hyperactive here it causes positive symptoms of psychosis. Blocking D2 receptors here improves positive symptoms but can cause secondary negative symptoms. Treatment is reduce D2 blocker, switch to one that is better tolerated or use adjunctive meds (especially ones that treat depression)

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7
Q

explain how seconday negative symptoms happen by drugs that target MESOCORTICAL D2 receptors

A

in schizophrenia mesocortical pathway in the PFC is hypoactive which leads to negative symptoms. D2 blockers in this pathway make it more hypoactive worsening negative symptoms

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8
Q

Explain how targeting tuberoinfundibular dopamine D2 receptors causes prolactin elevation and what are some side effects of hyperprolactinemia

A

when dopamine binds to D2 receptors in this pathway it inhibits release of prolactin. When dopamine cant bind to these receptors prolactin is not inhibited and levels rise. Associated side effects are galactorrhea, gynecomastia, weight gain, sexual dysfunction

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9
Q

explain how targeting NIGROSTRIATAL D2 receptors cause motor side effects and what are some of these motor side effects

A

affects the reciprocal relationship between dopamine and acetylcholine which is important for normal movement. Causes drug-induced Parkinsonism, dystonia, akathisia, NMS, tardive dyskinesia

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10
Q

what happens with acute and chronic blockade of D2 receptors in the nigrostriatal pathway

A

Normal: dopamine binds to D2 and inhibits release of acetylcholine.
Acute: DIP, akathesia, dystonia
Chronic: Tardive dyskinesia

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11
Q

how does DIP occur from acute blocking D2 receptors in the nigrostriatal pathway and what are symptoms of DIP

A

when dopamine cant bind to its receptors it cant inhibit acetylcholine release. The excess acetylcholine causes increased excitation of postsynaptic M1 receptors on GABA neurons, which causes even more acetylcholine release which inhibits movements. You get akinesia, bradykinesia, rigidity, and tremor

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12
Q

how do you treat drug-induced Parkinsonism and how does the treatment work

A

anticholinergics (benztropine) Blocks the postsynaptic M1 receptors which restores the balance of dopamine and acetylcholine.

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13
Q

peripheral and central side effects of anticholinergics

A

peripheral: dry mouth, blurred vision, urinary retention, constipation
central: sedation and cognitive dysfunction

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14
Q

what happens when there is too high of net anticholinergic action

A

paralytic ileus

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15
Q

what is amantadine used for and how does it work

A

treat drug-induced parkinsonism without anticholinergic side effects
weak antagonism of NMDA glutamate receptors leading to downstream changes in dopamine activity in the indirect and direct striatal motor pathways

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16
Q

what is drug-induced acute dystonia, how does it occur, and how do you treat it

A

twisty-jerkys caused by D2 blockers often with first exposure. treatment with IM anticholinergic injection. Late onset is typically from tardive dyskinesia and anticholinergics actually make this type of dystonia worse

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17
Q

what is drug-induced akathesia and how do you treat it

A

internal and motor restlessness. Treated with benzodiazepines and B-adrenergic blockers blockers

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18
Q

what is neuroletpic malignant syndrome, what are the symptoms, and how do you treat it

A

potentially fatal complication of D2 blockade. Symptoms are extreme muscle rigidity, high fever, coma, death. Treatment is withdrawal of D2 blocker, use of muscle relaxers, and intense supportive treatments

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19
Q

pathophysiology of tardive dyskinesia

A

when there is chronic blockade of D2 receptors in the nigrostriatal pathway it causes upregulation of D2 receptors that are supersensitive to dopamine allowing way too much dopamine in which tells the stop pathway to go go go leading to tardive dyskinesia

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20
Q

How does D2 inhibition of the stop pathway regulate normal movement

A

dopamine in nigrostriatal pathway binds to postsynaptic D2 on GABA neurons. This inhibits the stop pathway, essentially telling it to go

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21
Q

pathophysiology of drug-induced parkinsonism

A

when D2 receptors are blocked, dopamine cant get in to tell the stop pathway to go, so it stops. Too much stop leads to DIP

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22
Q

treatment for tardive dyskinesia

A

VMAT inhibitors reserpine and tetrabenazine-like drugs

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23
Q

how does reserpine work

A

irreversibly binds to VMAT1 and VMAT2 so that dopamine cant get into presynaptic vesicles. Then it is rapidly destroyed by enzyme MAO intracellularly

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24
Q

how does tetrabenazine-like drugs work to treat tardive dyskinesia and how is it metabolized

A

reversibly inhibits VMAT2 so that dopamine cant get into presynaptic vesicles and is rapidly destroyed intracellularly by MAO. tetrabenazine is an inactive prodrug that is metabolized by enzyme carbonyl reductase into 4 active metabolites which are then metabolized by CYP4502D6

25
Q

what are the four active metabolites of tetrabenazine

A

+B (greatest potency for VMAT2 and responsible for most of drug action)
+a
-B
-a
dihydro-entatiomers

26
Q

disadvantages of tetrabenazine

A

short half-life requires TID dosing
DIP/sedation side effects
risk of suicide
requires genetic testing for poor metabolizers
approved for Huntington’s chorea, to TD

27
Q

how is deuterabenazine metabolized, what is deuteration, and what are its advantages/disadvantages

A

deuterabenazine is an inactive prodrug that is metabolized by enzyme carbonyl reductase into four active metabolites that are then metabolized by CYP4502D6. Deuteration changes the drug from a good 2D6 substrate to a poor 2D6 substrate by switching hydrogen atoms for deuterium atoms that are heavier. Allows for a longer half-life for BID dosing. No genetic testing, no suicide warning. Disadvantage must be taken with food. Approved for TD

28
Q

structure of valbenazine, how is it metabolized, what are its advantages

A

amino acid valine is linked to the +a enantiomer of tetrabenazine. When swallowed it is rapidly hydrolyzed into valine and +a-tetrabenazine. carbonyl reductase converts it into +a dihydrotetrabenazine resulting in a long half-life allowing once-daily dosing. No genetic testing, no suicide risk, doesn’t require food. Approved for TD

29
Q

pharmacologic actions of typical antipsychotics other than D2 blockade

A

anticholinergic effects (muscarinic antagonism) - dry mouth, blurred vision, paralytic ileus
antihistaminic action (H1 antagonism) - associated with weight gain/sedation
a-1 adrenergic antagonism - associated with sedation and cardiovascular side effects

30
Q

conditions treated with antipsychotics targeting 5HT2A receptors

A

schizophrenia
parkinson’s disease psychosis
negative symptoms of psychosis in schizophrenia
motors die effects
hyperprolactinemia

31
Q

are 5HT2A receptors pre or postsynaptic

A

postsynaptic

32
Q

are 5HT2A receptors excitatory or inhibitory

A

excitatory

33
Q

Are 5HT1A receptors excitatory or iinhibitory

A

inhibitory

34
Q

Antidepressant actions of 5HT2A/D2 antagonists and d2/5HT1A partial agonists

A

5HT2A antagonism and 5HT1A partial agonism increases dopamine in the PFC
(prescribed in lower doses than in psychosis/mania)

35
Q

antipsychotics with high metabolic risk

A

clozapine
olanzapine
quetiapine
mirtazapine

36
Q

antipsychotics with moderate metabolic risk

A

risperidone
paliperidone
quetiapine
asenapine
iloperidone

37
Q

antipsychotics with low metabolic risk

A

lurasidone
cariprazine
lumateperone
ziprasidone
pimavanserin
aripiprazole
brexpiprazole

38
Q

5HT2A antagonism and/or 5HT1A partial agonism

A

reduced motor side effects
prolactin elevation

39
Q

5HT2A binding of the “pines”

A

higher potency at 5HT2A than D2

40
Q

5HT2A binding for the “dones and a rone”

A

more potency at 5HT2A than D2

41
Q

5HT2A binding of aripiprazole and cariprazine

A

more potency at D2 than 5HT2A

42
Q

which “pine” has monoamine (NET) inhibition in addition to 5HT2A/D2 binding

A

quetiapine
similar potency for NET and 5HT2A
greater potency for NET than D2

43
Q

monoamine transporter binding

A

Ziprasidone binds to NET/SERT
Lumateperone binds to SERT
Quetiapine binds to NET/SERT

44
Q

Alpha-2 binding antipsychotics

A

-All the “pines” to varying degrees
-All the “dones” to varying degrees
-Aripiprazole with less potency than D2

45
Q

which antipsychotic is considered most clinically effective after clozapine

A

olanzapine

46
Q

availability of olanzapine

A

disintegrating tablet
acute IM
long-acting (4 wk) IM

47
Q

Quetiapine at 800mg

A

tx psychosis and mania

48
Q

Quetiapine at 300mg

A

Tx depression

49
Q

Quetiapine at 50mg

A

hypnotic

50
Q

Availability of risperidone

A

2-4 wk depot
oral disintegrating tablet
liquid

51
Q

what is the preferred tx for children with bipolar depression and/or schizophrenia

A

Lurasidone

52
Q

why is less postsynaptic D2 antagonism needed for lurasidone to have antipsychotic action

A

presynaptic D2 AGONISM turns off dopamine synthesis presynaptically to reduce high levels of dopamine

53
Q

what is the only antipsychotic without D2 action

A

pimavanserin

54
Q

what are the classic dopamine pathways

A

tuberoinfundibular
thalamic
nigrostriatal
mesolimbic

55
Q

which dopamine receptors are inhibitory and which are excitatory

A

D1 is excitatory
D2 is inhibitory

56
Q

what area of the brain is associated with euphoria of drug abuse, and delusions/hallucinations in psychosis

A

nucleus accumbens

57
Q

what symptoms are experienced when there is excessive dopamine in the mesolimbic dopamine pathway

A

positive symptoms of psychosis and euphoria from drug abuse

58
Q

what symptoms are experienced when there is deficient dopamine in the mesolimbic dopamine pathway

A

anhedonia, apathy, and lack of energy

Psychopharmacology (13 decks)

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