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Pharm: Psych > 2.18: AntiPsycho > Flashcards

2.18: AntiPsycho Flashcards

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1
Q

Indications for antipsychotics?

A
  1. Schizophrenia
  2. Bipolar disorder
  3. Major depression
  4. Delirium / dementia
  5. Substance induced psychosis
  6. Tourettes
  7. OCD
  8. Anxiety / Agitation
  9. Autism
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2
Q

What are the 4 dopamine (DA) tracts?

A
  1. Mesolimbic
  2. Mesocortical
  3. Nigrostriatal
  4. Tuberoinfundibular
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3
Q

Which of the dopamine (Da) tracts seems to be sources of psychosis?

A
  • Mesolimbic: hyperactivity in this region leads to symptoms

- Also where antipsychotics work

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4
Q

What is the dopamine hypothesis?

A
  • Psychosis caused by too much dopamine
  • Antipsychotics were blocking DA receptors: those with higher affinity = more affective
  • Drugs that increased DA increased psychosis
  • Schizos seen to have increase DAr
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5
Q

What is FGA?

A

First generation antipsychotics

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6
Q

Problem with dopamine hypothesis of antipsychos?

A
  • FGAs were not very effective with negative signs
  • 35% ptns relapsed annually
  • 30% didnt have adepuate response
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7
Q

Which are the FGA’s?

A 
Low Potency:
1. Chlorpromazine: ***Most important to remember 
2. Thioridazine
3. Perphenazine
4. Thiothixene: moderate potency
High potency
1. Haloperidol ****Most important 
2. Fluphenazine
3. Trifluoperazine
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8
Q

MOA of antipsychotics?

A
  • Block D2 receptors in mesolimbic tract

* ***Occur when 60% of receptors here are blocked

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9
Q

How do side effects of antipsychotics occur?

A
  1. Unintended D2 blockage in nigrostriatal and tuberoinfundibular tracts: Increased prolactin / EPS
  2. Muscarinic receptors
  3. Adrenergic receptors
  4. Histamine receptors
    * ***Occurs when 80% of receptors here are blocked
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10
Q

Window of antipsychotics?

A

> 60%

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11
Q

Side effects for low potency FGAs?

A

Chlorpromazine: Corneal deposits
Thioridazine: retinal deposits

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12
Q

What does increased prolactin cause?

A
  • **Caused by tuberoinfundibular tracts interaction:
    1. Gynecomastia
    2. Galactorrhea
    3. Sexual dysfunction
    4. Menstrual irregularity/infertility
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13
Q

Dopaminergic side effects of chlorpromazine?

A
  1. Extrapyramidal
  2. Increased prolactin
  3. Decreased bone density
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14
Q

What are the histaminic side effects of chlorpromazine?

A
  1. Sedation

2. Weight gain

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15
Q

What are the adrenergic side effects of chlorpromazine?

A
  1. Orthostasis: fall risk
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16
Q

What are the muscarinic effects of chlorpromazine?

A 
"Anticholinergic"
1. Blurred vision 
2. Urinary retention 
3. Dry mouth 
4. Constipation 
"Cant pee, cant see, cant spit, cant shit"
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17
Q

Relation of dopamine and ACh?

A
  • In nigrostriatal pathway, dopamine suppresses Ach
  • When DA blocked, ACh suppression is released = EPS
  • Low potency antipsychotics are anticholinergic = self treating for EPS
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18
Q

What is EPS?

A

Extrapyramidal systems

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19
Q

How do identify FGAs?

A
  • “Phenothiazines” end in “azine”

- Haloperidol and thiothixene exceptions

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20
Q

Side effects of high potency antipsychotics?

A
  1. Dopaminergic side effects are greater

2. NO muscarinic, adrenergic, or histaminic side effects are seen

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21
Q

What are the EPS side effects?

A

“Drug induced movement disorders” (50 - 90% develop):
EPS:
1. Parkinsonian: resting tremor, bradykinesia, stiffness
2. Dystonia
3. Akathisia
4. Tardive dyskinesia: involuntary movement (20-50%)

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22
Q

What is dystonia? Who is at higher risk?

A
  • Sustained abnormal posture / muscle contraction
  • Made worse by activity
  • Young males at higher risk
  • Often seen early in treatment, may be reported as allergy
23
Q

What is akathisia?

A
  • Feeling of restlessness and need to move

- Women 2x risk of men

24
Q

What is tardive dyskinesia?

A
  • Classically seen from taking DA blockers
  • Involuntary movements
  • Classically seen in lower face and tongue
  • Does not remit even after taken off drugs
25
Q

What are SGAs?

A

Second Generation antipsychotics

26
Q

What are the endings of the SGAs?

A
  1. “idone”
  2. “Apine”
  3. Aripiprazone
27
Q

Broad mechanism of the SGAs?

A
  • Dual antagonism of DA / 5HT receptors
28
Q

What does blocking D2 receptors in nigral striatal pathway lead to?

A
  • Extrapyramidal side effects
  • Tardives
  • **Our target is blocking D2 in mesolimbic system, at higher [] in other tracts other D2 receptors begin to be blocked leading to side effects
29
Q

Impact of 5HT on DA?

A
  • When serotonin binds Dopaminergic neuron, DA release is decreased
30
Q

Why is it important that SGAs are blocking 5HT?

A
  • Blocking 5HTr releases more DA into synapse
  • This DA is competing with the drug to bind DA receptor
  • at > 80% binding of drug, side effects are seen
  • By releasing more DA via dual action, we compete with Drug for DA-receptors = decreased side effects
31
Q

What is the hit and run concept?

A

SGAs bind more loosely to DA receptor meaning it works enough to get antipsychotic effects but not long enough for EPS

32
Q

Side effect profile of SGAs?

A
  • Less extra pyramidal side effects via over blockade of DA in areas outside of mesolimbic
  • Side effect profiles vary for histamine and muscarinic receptors and are often worse in this regard than haloperidol
33
Q

What are some metabolic syndromes?

A
  1. Weight Gain
  2. Hyperlipidemia
  3. Glucose intolerance
34
Q

New side effects found in SGAs?

A

Metabolic syndromes

35
Q

Which SGAs have least weight gain?

A
  1. Ziprasidone

2. Aripiprazole

36
Q

Mechanisms of Aripiprazole?

A
  • Partial antagonism of DA-r
  • In low DA environment, binds DA-r acting as agonist keeping 65% or receptors blocked
  • ***Keeps % un therapeutic window
37
Q

Cost benefit of clozapine?

A 
Benefit:
1. Great efficacy for negative symptoms 
2. Great efficacy in patients unresponsive to others 
3. Lowers risk of suicide
Costs:
1. Agranulocytosis
2. Myocarditis
3. Decreased seizure threshold
38
Q

When can clozapine be used?

A

Only after 2 other drugs have failed

39
Q

What is agranulocytosis?

A

Bone marrow stops producing blood cells

40
Q

More commone side effects of clozapine?

A
  1. Weight gain
  2. Very sedating
  3. Metabolic Syndrome
  4. Anticholinergic
41
Q

What is NMS?

A

“Neuroleptic malignant syndrome”

  • Can be caused by SGA or FGA: same risks for all DA blockers
  • Dopamine system goes haywire
42
Q

Signs of NMS?

A
  1. Mental status changes
  2. Muscle rigidity: Increased CPK
  3. Fever
  4. Dysautonomia
43
Q

Treatment for NMS?

A
  1. Stop meds
  2. Supportive
  3. Dantrolene
  4. Bromocriptine: D2 agonist
44
Q

What has black box warning of sudden death?

A
  • FGAs and SGAs

- Seen in elderly, usually CV in nature

45
Q

Who should you take extra care in prescribing antipsychotics to?

A

Elderly: sudden death black box warning

46
Q

Protein binding of anti psychotics? Halflife?

A
  • Highly protein bound
  • Unbound portion crosses BBB for effects
  • 20 hours
47
Q

Longest 1/2 life of antipsychotics?

A

Aripiprazole: 72 hours

- Most others are 20

48
Q

Which drug has risk of increased qTc interval as side effect?

A

Ziprasidone

49
Q

Which drug has long lasting injectable form?

A
  1. Risperidone
  2. Olanzapine
  3. Aripiprazole
  4. Haldol
    * **Good for patient with low compliance
50
Q

Drug only available in sublingual form?

A

Asenapine

51
Q

What is risperidone metabolized to?

A

Palliperidone

52
Q

How is paliperidone excreted?

A

80% renal

53
Q

What to use if patient has liver disease?

A

Paliperidone

54
Q

What to avoid if patient has renal disease?

A

Paliperidone

Pharm: Psych (7 decks)

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