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Pharmacology Test #6 > Antipsychotics > Flashcards

Antipsychotics Flashcards

1
Q

Late onset schizophrenia affects

A

post-menopausal women

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2
Q

Positive symptoms of schizophrenia (psychosis)

A

auditory/visual hallucinations, delusions

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3
Q

Negative symptoms of schizophrenia

A

withdrawal, reduced speech, interest, drive, attention, and pleasure

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4
Q

cognitive deficits with schizophrenia

A

attention, memory, executive function

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5
Q

Onset of schizophrenia

A

late adolescence (males earlier than females)

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6
Q

Core symptom of schizophrenia

A

cognitive dysfunction

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7
Q

Etiology of schizophrenia

A

complex interactions between genetic predisposition and environmental risk

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8
Q

Specific genes associated with schizophrenia

A 
COMT - catecholine metabolism;
DISCI - cell morphology, migration;
DTNBPI - axon stability;
GABRB2 - GABA system;
NRGI - cell growth and differentiation
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9
Q

Environmental risks for schizophrenia

A
  1. obstetrical complications (hemorrhage, pre-term, nutrtion, maternal stress)
  2. infections and/or inflammation (more schizo for winter pregnancies and flu epidemics)
  3. cannabis (COMT mutations
  4. immigration (stress?)
    5 smoking rates
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10
Q

What percentage of schizophrenics are smokers?

A

75-90%

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11
Q

Dopamine hypothesis of schizophrenia

A

psychosis or psychotic symptoms are due to a hyperactive DA system/signaling

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12
Q

5 pieces of evidence for the DA hypothesis

A
  1. Correlation between clinical effectiveness and affinity at D2
  2. PRO-DA agents in Parkinson’s can produce psychosis
  3. Increased D2 density in schizophrenia
  4. Increased DA release in schizophrenia and increased DA receptor occupancy
  5. Odd changes in DA metabolism following administration of D2-directed antipsychotics
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13
Q

Evidence against the dopamine hypothesis

A
  1. D2 antagonists are not universally effective
  2. Atypicals - lower D2 affinity and added serotonin pharmacology
  3. Blocking NMDA receptors produces psychosis
  4. Widespread anatomical abnormalities
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14
Q

What does smoking alter?

A

Smoking alters DA transmission

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15
Q

First antipsychotic that worked well

A

Chlorpromazine

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16
Q

First atypical antipsychotic

A

Clozapine

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17
Q

General progression from typicals to atypicals reflects

A
  1. Better affinity at D2 receptors
  2. Addition of activity at 5HT2A and others
  3. Better control over negative and cognitive Sx
  4. Fewer EPS
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18
Q

Selectivity of Chlorpromazine

A

hits multiple targets that are not desirable

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19
Q

Haldol selectivity

A

more selective blocker for D2 than chlorpromazine

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20
Q

Difference between D1-like and D2-like receptors

A

D1-like (D1 and D5) are Gs-coupled (increased cAMP) whereas D2-like (D2, D3, and D4) receptors are Gi-coupled

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21
Q

Dopamine system comprises

A

dopamine-producing cells in the VTA and substantia nigra pars compacta

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22
Q

DA circuits involved in the therapeutic and cognitive activities of D2 antagonists

A

the mesocortical and mesolimbic pathways

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23
Q

Basal ganglia pathway important for motor control

A

nigrostriatal DA pathway from SNc to dorsal striatum

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24
Q

Circuit that extrapyramidal symptoms arise from

A

the nigrostriatal DA pathway from SNC to the dorsal striatum

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25
Manipulation of the dopamine pathway in the hypothalamus causes
hyperprolactinemia
26
Manipulation of the dopamine pathway in the medulla is involved in
the anti-emetic properties of some antipsychotics
27
Efficacy of drugs is likely a combination of
direct antagonism and some long term adaptive changes
28
Adaptive changes known to occur with dopamine antagonists
upregulation of D2 receptors
29
1st generation antipsychotics
Phenothiazines and haloperidol
30
Features of 1st generation antipsychotics
1. Strong D2 antagonism 2. Variable off-target effects 3. Long half life 4. Only (+) symptom control
31
Features of Atypical 2nd generation antipsychotics
1. Acquisition of 5HT pharmacology 2. variable on/off kinetics at D2 receptor (vs. 1st gen) 3. better mangement of cognitive Sx 4. Occupation of other receptors 5. Lower risk of EPS
32
What kind of agonist is Aripirazole?
D2 partial agonist with potent 5HT2 inverse agonism
33
What kind of antagonist is Haloperidol?
D2 antagonist
34
Is complete D2 blockage necessary for antipsychotic efficacy?
No, partial agonism/antagonism may, with 5HT2 effects, be desirable clinically
35
Classical and Early Atypical drugs
Clorpromazine Haloperidol Thioridazine Sulpiride
36
Novel Atypical drugs (Acquisition of 5HT pharm)
``` Clozapine Risperidone Olanzapine Ziprasidone Quetiapine Aripiprazole ```
37
How do you manage schizophrenia in the first few days?
control initial/acute agitation with haldol injections
38
How do you manage schizophrenia within days 7-14?
begin to address the positive symptoms, begin to transition from injection to po route of administration
39
How do you manage schizophrenia long-term?
address the negative symptoms, maintain compliance, prevent relapse
40
Overall treatment goals of schizophrenia
1. control positive symptoms 2. prevent relapse once stabilized 3. reduce severe depression 4. address cognitive dysfunction
41
Other uses of atypical antipsychotics
1. Refractory depression 2. Bipolar depression 3. Tourette's syndrome 4. OCD 5. PTSD 6. Personality disorder 7. Autism 8. Agitation in dementia
42
Atypical antipsychotics for bipolar depression
Quetiapine and olanzapine
43
Atypical antipsychotics NOT for bipolar depression
Aripiprazole and ziprasodone have no benefit
44
Atypical antipsychotics for Tourette's syndrome
Fluphenazine
45
Atypical antipsychotic NOT for Tourette's
Haloperidol not preferred
46
Dystonia
muscle spasms of neck and eyes
47
Akathesia
motor restlessness
48
Parkinsonism
rigidity, shuffling gait, decreased facial expression
49
Tardive dyskinesia
delayed, severe, embarrassing, irreversible uncontrolled movements
50
Neuroleptic Malignant syndrome
EPS, fever, cognitive impairment
51
What is Neuroleptic malignant syndrome treated with
direct DA agonists and muscle relaxants
52
Why do atypicals show lower incidence of inducing EPS?
They have faster OFF kinetics at D2 receptors compared to typicals
53
Describe how parkinsonism develops with antipsychotics
Strongly blocking D2 receptors causes reduced dopamine from SNc and therefore overactivity of indirect pathway striatal neurons, reduced activity of GPe, and overactivity of the STN. This overexcites the Gpi and SNr, which then over-inhibits the thalamus, which then causes reduced activation of the cortex
54
Neuroleptic side effects of antipsychotics
Emotional: apathy and dysphoria Cognitive: impaired thinking
55
Endocrine side effects of antipsychotics
prolactin mediated (increased prolactin secretion, galactorrhea, sexual dysfunction, amenorrhea)
56
Metabolic side effects of antipsychotics
weight gain, diabetes
57
Hematologic side effects of antipsychotics
Agranulocytosis (early atypicals)
58
Anticholinergic side effects of antipsychotics
dry mouth, urinary retention, constipation, blurred vision, sinus tachycardia, confusion, memory impairment
59
Antihistamine side effects of antipsychotics
sedation and confusion
60
Antiserotonin side effects of antipsychotics
weight gain
61
Alpha1-adrenergic antagonism effects of antipsychotics
orthostatic hypotension, reflex tachycardia
62
Notable side effects of Haloperidol
severe EPS
63
Notable side effects of Olanzapine
weight gain
64
Notable side effects of Clozapine
weight gain, sedation, anticholinergic Sx, adrenergic Sx
65
Ideal Antipsychotic drug
Decrease positive symptoms; no EPS effects; no tardive dyskinesia; decrease in negative symptoms; improve cognitive deficits
66
what kind of drugs are the current standard of care for schizophrenia
Atypicals (but are usually not better than typicals for positive Sx and they're more expensive)

Pharmacology Test #6 (12 decks)

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