Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology I > Antipsychotics Exam 3 > Flashcards

Antipsychotics Exam 3 Flashcards

1
Q

When were the first antipsychotics developed?

A
  • 1950s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Psychosis definiton

A
  • loss of contact from reality

- cannot differentiate fantasy from reality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Schizophrenia

A
  • psychotic episodes but clear sensorium

- marked thinking disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

clear sensorium

A
  • oriented to person, place, and thing but difficulty in perception, thought, affect, daily functioning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Schizophrenia Etiology (cause)

A
  • neurodevelopmental/neurodegenerative disorder
  • has a genetic component –> complex trait, genetic/environmental interactions
  • generally young onset of age (1/2 before age 25)
  • certain birth months higher risk for schizophrenia - viral infections peak at diff times of year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Idental twin with schizophrenia risk?

A
  • 40-65% risk of developing disease if identical twin has it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Positive Schizophrenia symptoms

A
  • present in people w/ schizophrenia but absent in a healthy person
  • reflect excess or dysfunction of normal function
  • delusions, unusual thoughts, hallucinations, disorganized thought and behavior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Negative Schizophrenia symptoms

A
  • present in a healthy person but absent in people with schizophrenia
  • difficulty showing emotions, poverty of speech, decreased pleasure or motivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

alogia

A
  • inability to speak
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

anhedonia

A

inability to feel pleasure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

avolition

A

lack of motiviation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

affective flattening

A
  • loss of emotional expressiveness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cognitive schizophrenia symptoms

A
  • impaired attention, working memory, executive function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which symptoms easiest to treat?

A
  • positive symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Schizophrenia Hypotheses (3)

A
  • Dopamine
  • Serotonin
  • Glutamate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dopamine Hypothesis

A
  • earliest neurotransmitter concept
  • doesn’t explain all aspects of schizophrenia
  • still important for understanding schizophrenia symptoms
  • most/all antipsychotic drugs impact DA signaling (D2 receptors)
  • “out of tune” dopaminergic activity (in some brain regions) may contribute to schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

4 major dopaminergic systems

A
  • Nigrostriatal pathway
  • Mesolimbic pathway
  • Mesocortical pathway
  • Tuberoinfundibular pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Nigrostriatal pathway: DA levels in schizophrenia, what pathway is normally involved in, start and end of pathway regions?

A
  • normal DA levels in schizophrenia
  • pathway part of extra pyramidal nervous system -> motor function and movement
  • pathway also involved in parkinson’s dysfunction
  • substantia nigra to dorsal striatum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Mesolimbic Pathway: DA levels in schizophrenia, what pathway is involved in, start and end of pathway regions?

A
  • DA levels too high
  • thought to drive positive symptoms
  • closely related to behavior and psychosis
  • cell bodies in midbrain ventral tegmentum project to limbic system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mesocortical Pathway: DA levels in schizophrenia, what pathway is involved in, start and end of pathway regions?

A
  • DA levels too low
  • probably contribute to neg and cognitive symptoms
  • closely related to behavior and psychosis
  • cell bodies in midbrain ventral tegmentum project ot neocortex/mesocortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Tuberoinfundibular system: DA levels in schizophrenia, what pathway is involved in, start and end of pathway regions?

A
  • DA levels normal in schizophrenia
  • blocks prolactin release when not needed
  • cell bodies in hypothalamus control DA release into pituitary portal circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Technical def of inverse agonist

A
  • 5HT2A receptors have some constitutive action in ABSENCE of serotonin
  • these inverse agonists would BLOCK this constitutive action when binding
  • will just refer to them as antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Serotonin Hypothesis of schizophrenia

A
  • LSD (Lysergic acid diethylamide) and mesacaline are 5-HT agonists
  • 5-HT2A receptors modulate release of DA in the cortex, limbic region, and striatum
  • 5-HT2C receptor stim also modulates dopaminergic activity
  • atypical antipsychotics antagonize 5-HT2A receptors and can modulate DA release in brain regions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Glutamate Hypothesis of Schizophrenia

A
  • antag on NMDA receptors can mimic schizophrenia symptoms (pos, neg, and cognitive)
  • thought that hypo-function of NMDA receptors may be present in schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

4 families of typicals

A
  • Phenothiazine derivatives
  • Thioxanthene derivatives
  • Butyophenone derivatives
  • miscellaneous structures
  • “The Brother Married Pam”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Phenothiazine Derivatives: 3 subfamilies, most potent, most side effects, 1 fact

A
  • were once the most widely used of the antipsychotics
  • 3 subfamilies: aliphatic, piperidine, piperazine
  • piperazine most potent –> need to be given at lower doses
  • aliphatic and piperidine derivatives more side effects
  • at doses required to have an effect, have effects on other neurotransmitter receptors as well (H1, a1, M)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

1 drug to know for each of the subfamilies of phenothiazines…

A
  • aliphatic: chlorpromazine
  • piperidine: thioridazine
  • piperazine: perphenazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Thioxanthene derivatives 1 fact and 1 drug

A
  • high potency

- thiothixene only one we need to know

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Does lower dose = better efficacy?

A
  • not always
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Butyrophenone derivatives (1) (closely related to which other drug), 1 fact, and how does compare to phenothiazines?

A
  • haloperidol
  • closely related to pimozide (miscellaneous typical)
  • most widely used typical
  • compared to phenothiazines — very good D2 antag, tends to cause D2 side effects (movement-related)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Miscellaneous Structures (typicals): 1 drug, what is it used for

A
  • “Newish” typicals
  • pimozide
  • limited usage b/c of concerns of heart impacts
  • used to control tics in tourette’s
  • dopaminergic dysfunction thought to cause the tics (verbal and motor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Atypicals mech

A
  • block 5-HT2A and D2 receptors

- more activity at 5-HT2A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Very recently approved atypicals (2)

A
  • cariprazine and brexpiprazole (info on note sheet)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Do antipsychotics have affinity for only one receptor?

A
  • no, can fit multiple receptors

- explains both efficacy and adverse profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Dopaminergic Receptors–> how many types, how many families, general info

A
  • 5 types of DA receptors
  • grouped into two families (D1 and D2 families)
  • families can be expressed in diff regions of the brain, diff downstream outputs, some can be found both pre- and post-synaptically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Typical antipsychotic agents in regards to binding dopamine receptors and efficacy

A
  • block D2 receptors stereo-selectively

- binding affinity to D2 but not D1 is very strongly correlated with antipsychotic and extrapyramidal potency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Actions at D3 or D4 or D1 important for antipsychotics?

A
  • nope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Secondary negative symptoms

A
  • neg symptoms caused by treatment itself
  • usually happens with strong D2 antags (typicals)
  • antagonize mesocortical pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Blocking D2 receptors: Nigrostriatal effects

A
  • block D2 results in EPS b/c levels are normal in schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Blocking D2 receptors: Mesolimbic effects

A
  • block D2 results in relief from positive symptoms b/c levels are too high in schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Blocking D2 receptors: Mesocortical effects

A
  • block D2 results in aggravated negative and cognitive symptoms b/c levels are too low in schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Blocking D2 receptors: Tuberoinfundibular effects

A
  • block D2 results in increased prolactin release.. hyperprolactinemia b/c levels are normal in schizophrenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pharmacodynamics: Dopaminergic receptors and blockage

A
  • typical drugs must be given in doses sufficient to achieve 60-75% occupancy of striatal D2
  • some atypicals on lower end of that range
  • Occupancy of striatal D2 receptors >78% run risk for EPS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

dopamine tuner

A
  • aripiprazole

- partial agonist so can increase dopamine when too low and decrease when too high b/c competes for receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Serotonin in the Nigrostriatal tract overview (pharmacodynamics)

A
  • DA levels normal in schizophrenia
  • blocking in this pathway causes EPS
  • Serotonin neuron synapses to DA neuron
  • interneuron is GABA (when 5HT2A on this is bound with antagonist, also disinhibits DA release)
  • 5HT-2A when antagonized, allow DA to be pumped out at its still normal level (serotonin inhibits DA release “dopamine break”)
  • 5HT-1A on the dendrite of the the 5HT neuron when bound with 5HT (agonized), inhibits serotonin release from the neuron and also promotes dopamine release (DA accelerator)
  • 5-HT1A agonists and 5-HT2A antagonists have same effects
46
Q
  • how do second generations help limit EPS in terms of the nigrostriatal pathway
A
  • allow more DA to be released in this tract
  • when you give a drug that is not completely specific for one receptor, cannot control where it goes
  • some of second gen will block D2 receptors
  • by antagonizing 5HT2A, there will be more dopamine released and can overcome D2 block by the same antipsychotic
47
Q

Mesocortical pathway pharmacodynamics

A
  • thought to be too little DA in this pathway in schizophrenia which causes neg and cog symptoms
  • thought either DA neurons aren’t making enough DA OR too much 5-HT (DA brake) at 2A receptors
  • by 5HT2A antagonism, help DA neuron produce more DA
  • might help with neg and cog symptoms
  • controversial but know it wont make them worse
48
Q

Mesolimbic pathway pharmacodynamics

A
  • thought to be too much DA in this pathway causing Pos symptoms
  • all hypothetical theories
  • theory w/ 5HT2A antag in this pathway is that it doesn’t raise levels higher
  • may have indirect effects through glutaminergic neurons.. reduce glutamate release which reduces DA release in this pathway
  • 5HT2A antag may help limit DA release
49
Q

Tuberoinfundibular pathway pharmacodynamics

A
  • thought to be normal DA levels in this pathway in schizophrenics
  • blocking D2 receptors causes hyperprolactinemia because usually dopamine levels keep prolactin in check
  • serotonin also promotes prolactin release, so block 5HT2A, lowers prolactin release
  • diff atypicals can have diff impacts on prolactin levels so mech is still unclear
50
Q

Overall purpose of antipsychotics

A
  • stop positive symptoms and limit the other side effects
51
Q

Side effects of Muscarinic cholinoceptor blockade and what nervous system

A
  • (sympathetic effects) loss of accommodation, dry mouth, difficulty urinating, constipation
  • autonomic nervous system
52
Q

side effects of a-adrenoceptor blockade and what nervous sytem

A
  • orthostatic hypotension, impotence, failure to ejaculate

- autonomic nervous system

53
Q

side effects of dopamine receptor blockade in nigrostriatal pathway and what nervous system

A
  • this is D2 blockade
  • parkinsonism, dystonias
  • central nervous system
54
Q

side effects of supersensitivity of dopamine receptors

A
  • tardive dyskinesia

- CNS

55
Q

Akathisia –> what blockade and what is it?

A
  • unknown mechanism
  • blockade affects CNS
  • feeling of motor restlessness (sometimes grouped as EPS w/ parkinson and dystonias)
56
Q

dopamine-receptor blockade resulting in hyperprolactinemia causes what side effects? and what system

A
  • causes amenorrhea-galactorrhea, infertility, impotence

- affects endocrine system

57
Q

possibly combined H1 and 5-HT2C blockade can cause what side effect?

A
  • weight gain

- most likely due to increased appetite

58
Q

Acute Dystonia

A
  • true EPS
  • mech: acute DA antagonism
  • spasms of muscles of tongue, face, neck, back
  • may mimic seizures
  • NOT HYSTERIA
  • time of maximal risk is 1-5 days when first taking antipsychotics (esp in young that have never taken one before)
  • treatment: curative by antiparkinsonism agents
59
Q

Akathisia

A
  • motor restlessness
  • NOT anxiety or agitation
  • mechanism: unknown (seen too with atypicals)
  • treatment: reduce dose or change drug
  • benzos and propranolol may help
60
Q

Parkinsonism

A
  • true EPS
  • mech: DA antagonism
  • bradykinesia, rigidity, mask tremor, shuffling gait
  • elderly at greatest risk
  • treatment: reduce dose or change drug; antiparkinsonism drugs may help
61
Q

Perioral Tremor (rabbit syndrome)

A
  • like a rabbit moving nose
  • mech: unknown
  • treatment: anti-parkinsonism drugs
62
Q

Tardive Dyskinesia

A
  • oral-facia dyskinesia, widespread choreoathetosis or dystonia
  • elderly at greatest risk, does not appear for months or years taking drug (can also appear on withdrawal)
  • mech: super-sensitivity or upregulation of DA receptors
  • treatment: prevention crucial, treatment is unsatisfactory, may be reversible if caught early enough
63
Q

among typicals highest potency has ____ risk of neurological effects.. also which lowest and why?

A
  • highest potency, highest risk
  • thioridazine has lowest (antimuscarinic activity)
  • in nigrostriatal tract, DA (brake) and ACh (accelerator) have opposite effects on GABA
  • antimuscarinic activity at M1 may help to balance out the D2 blockade
64
Q

Among atypicals, which two have highest risk of neurological effects

A
  • paliperidone and risperidone have highest risk
65
Q

Neuroleptic Malignant Syndrome

A
  • rare but life-threatening
  • thought to be caused by D2 receptor blockade
  • “severe form of EPS”
  • symptoms: parkinsonism, autonomic instability, muscle breakdown/rigidity
  • severe cases can last for a week after discontinuance
  • high potency in high doses generally causes this
66
Q

Tardive Dyskinesia general info

A
  • late-occurring, abnormal choreoathetoid movements
  • most important side effect of antipsychotics b/c no effective treatments (some spontaneous resolve)
  • cause (hypothesis): knee jerk rxn to D2 antag in the nigrostriatal tract (increase sensitivity/upregulation)
  • 15-30% of patients treated long-term
  • elderly and potentially mood disorder patients more sensitive
  • early recognition important because no treatments
67
Q

Pharmacodynamics: Endocrine Effects

A
  • hyperprolactinemia correlates with D2 antagonism
  • most atypicals have a low risk of hyperprolactinemia (exceptions are risperidone and paliperidone)
  • good correlation between high D2 antagonism and highest risk of hyperprolactinemia
  • symptoms in women: amennorhea, galactorrhea, infertility, osteoporosis, abnormal milk production
  • symptoms in men: loss of libido, impotence, abnormal breast growth
68
Q

Adverse Rxns: antimuscarinic effects

A
  • M1 blockade in both CNS and PNS
  • of typicals –> most prominent in low potency phenothiazines (need higher dose to see effect, then get effect from M1 block)
  • of atypicals –> most prominent in clozapine (strongly associated with constipation)
  • concern for anticholinergic effects in elderly
69
Q

Clozapine and antimuscarinic actions

A
  • strongly associated with constipation

- M4 agonism by clozapine –> sialorrhea

70
Q

why is there a concern for anticholinergic effects in the elderly?

A
  • block receptors for ACh, potential to exacerbate dementia
71
Q

Adverse Rxns: Alpha 1 blockade

A
  • orthostatic hypotension
  • elderly patients particular concern –> already poor vasomotor tone
  • low potency phenothiazines also problem with this
  • clozapine and Iloperidone - relative risk higher
  • other atypicals also have effects
72
Q

Adverse Rxns: H1 antagonism

A
  • sedation
  • typicals: low potency phenothiazines
  • of the atypicals, clozapine highest risk but many have effects
  • some tolerance to this may develop (good)
  • rebound insomnia/sleep disturbance
  • elderly are sensitive to this
73
Q

Adverse Rxns: Weight gain

A
  • H1 antagonism, augmented by 5-HT2C antagonism
  • among typicals, low potency agents have highest risk
  • among atypicals, clozapine and olanzapine frequently result in large increases in weight
  • some level of weight gain seen with most antipsychotics (may be because placebo in these trials, during psychotic episodes, tend to lose weight)
74
Q

Adverse Rxns: Metabolic Issues

A
  • two biggest additional metabolic issues
    1. dyslipidemia (primarily elevated serum triglycerides and also cholesterol)
    2. impaired glycemic control (mech unclear)
  • other risk factors can contribute, ex lifestyle factors (80-90% of people with schizophrenia smoke)
  • recommended use of metabolically more benign agents for initial treatment of all patients where long-term treatment is expected
  • patients should receive metabolic monitoring and appropriate pharmacologic/non-pharmacologic (counseling about food intake, exercise) therapies
75
Q

Adverse Rxns: Dyslipidemia

A
  • low potency phenothiazines can raise levels
  • significant elevation seen for clozapine and olanzapine
  • thought to be weight-independent, occurs within weeks of starting medication, resolves within 6 wks after discontinuation
  • weight-independent: can occur before weight gain starts
76
Q

Adverse Rxns: Hyperglycemia

A
  • first noted with low-potency phenothiazines
  • among atypicals, clozapine and olanzapine have greatest risk
  • although no evidence supporting that other atypicals cause this, all atypicals have warning about hyperglycemia
  • USUALLY reversible upon drug discontinuation or switching to a more metabolically benign agent
77
Q

Clozapine and olanzapine extra fact regarding side effects and efficacy

A
  • they are most useful in some patients even though they have these side effects
  • may have use when other drugs fail
78
Q

Adverse Reactions: Ocular Complications (2 drugs)

A
  • Chlorpromazine - commonly causes abnormal pigmentation of eyelids, conjunctiva, cornea, and lens
  • Thioridazine - can cause retinal deposits that are associated with browning of vision
  • maximum daily dose limited to reduce the risk of this complication
79
Q

Pharmacodynamics: EEG effects (brain)

A
  • cause shifts in patterns of EEG freq
  • most LOWER seizure threshold
  • warning for seizure risk on all antipsychotic agents (risk very low except for clozapine [3-5%] and chlorpromazine also higher risk)
  • most can still be used safely in epileptics with careful dose titration and prophylaxis
80
Q

Pharmacodynamics: CV effects

A
  • major concern for antipsychotics is impact on cardiac phys
  • concern about ventricular arrhythmias and SCD
  • all carry warning about QTc prolongation
  • some have black box warnings (torsade/fatal arrhythmias)
  • concern for patients with risk factors for QTc prolongation and interactions with other drugs that prolong QTc
81
Q

QT interval and QTc

A
  • electrical depol and repol of ventricles

- way of normalizing QT intervals in those with different HRs

82
Q

Why do antipsychotics have effects on CV? ex. with one drug

A
  • Thioridazine inhibits NA channels at high doses (also Ca channels potentially), many antipsychotic drugs block the Ikr channel
  • Ikr channel: K efflux channel to repolarize
83
Q

Thought that atypicals had less impact on heart phys.. is this now known to be true?

A
  • no, also dose-dependent risk for sudden cardiac death

- no difference between typicals and atypicals

84
Q

Which drug sometimes associated with myocarditis

A
  • clozapine
85
Q

Dose-dependent increased risk for SCD was found for antipsychotic users of typical and atypical agents alike compared to antipsychotic nonusers

A
  • tru
86
Q

Adverse Rxns: Toxic or allergic rxns - Chlorpromazine

A
  • Chlorpromazine can rarely cause cholestatic jaundice, also can cause skin rxn and photosensitivity
  • cholestatic jaundice thought to maybe be from impurities in early forms of the drug, older formulations w/ higher doses
87
Q

Adverse Rxns: Toxic or allergic rxns - Clozapine

A
  • approx 1% of patients treated with clozapine develop agranulocytosis (loss of immune cells)
  • greatest risk first 6 months
  • serious and potentially fatal
  • discontinue, do not retry
  • appears to be reversible upon discontinuation
  • blood count monitoring is required (at first more often than later on)
  • cause could be genetics combined with toxic metabolites
88
Q

Adverse Rxn: DRESS

A
  • Drug reaction with eosinophilia and systematic symptoms
  • skin eruption (rash), systemic symptoms (including hematopoietic system [bone marrow and lymph nodes]), and visceral involvement
  • lymph node swelling as well
  • only 23 total cases ever
  • 10% mortality
  • immune response to drug, herpes virus reactivation
89
Q

Adverse Rxns: Behavioral Effects

A
  • side effects can lead to non-compliance.. this may be improved by dosing at night w/ sedation
  • drug-induced akinesia may produce “pseudo-depression” that may respond to antiparkinson agents
  • caused by movement disorders or too high of a dose
  • decreasing dose may improve symptoms
90
Q

Psychiatric indications for antipsychotics as a whole (schizophrenia and bipolar)

A
  • primary indication: schizophrenia (except catatonic form)
  • catatonic is more difficult to treat.. with benzos first and then if they get better, antipsychotics
  • psychotic bipolar disorder (BP1)
  • typicals not usually used because of concerns with tardive dyskinesia/ EPS
  • atypicals (w/ some exceptions) are FDA approved for acute mania
  • maintenance therapy in mania becoming more common; some atypicals approved as monotherapy/adjunct for maintenance
91
Q

Psychiatric indications for antipsychotics as a whole (depression, schizoaffective disorder, delusional disorder)

A
  • MDD
  • when psychotic features present
  • atypicals are affective as adjunct therapy in treatment-resistant depression
  • most have limited antidepressant benefit as monotherapies (if they are good as monotherapies, probably b/c of metabolites)
  • Schizoaffective disorders
  • characteristics of both schizophrenia and affective disorders (continuum)
  • delusional disorder (not many studies)
  • more rare, paranoid disorder, delusions prominent
92
Q

Other psychiatric indications for antipsychotics

A
  • substance-induced psychosis
  • tourette’s syndrome (tics)
  • psychotic symptoms of delirium and dementia (off label for dementia - warnings of increased mortality (reason unclear))
  • irritability in autism (a few FDA approved)
  • adjunct in anxiety disorders (OCD, PTSD)
93
Q

Wrongly promoted for which indication

A
  • small doses for relief of anxiety associated with minor emotional disorders
94
Q

Nonpsychiatric indications for antipsychotics

A
  • some phenothiazines with shorter side chains have considerable H1 antagonism
  • Butyrophenone droperidol can be used in neuroleptanesthesia, also used to decrease postoperative or postprocedure nausea and vomiting
  • chlorpromazine: uncontrollable hiccups
  • Prochlorperazine (phenothiazine) is promoted primarily as an antiemetic
95
Q

What receptor does clozapine act on for sialogoge action?

A
  • M4 AGONIST
96
Q

Anti-emetic effects

A
  • DA antagonism in CRT zone/STN (solitary tract nucleus) has antiemetic effects
  • Thioridazine, aripiprazole are exceptions to this
97
Q

CATIE study

A
  • clinical antipsychotic trials of intervention effectiveness
  • 2005 large study of typical vs atypical agents in the US
  • conclusions were no diff between atypicals and typicals
  • but problems with study design: didn’t look at tardive dyskinesia and doses weren’t equal
98
Q

Typicals vs Atypicals drug choice

A
  • with pos symptoms, approx 70% of patients with schizophrenia will experience equal efficacy of typical and atypical agents
  • typicals benefits: cheaper
  • atypicals benefits: less risk EPS, tardive dyskinesia, and hyperprolactinemia but weight gain and metabolic issues with these agents
99
Q

clozapine and suicide risk

A
  • REDUCES suicide risk
100
Q

With exception of ____ and _____, thought that most antipsychotics are equally effective for positive symptoms

A
  • clozapine and olanzapine
101
Q

patient response to drug is static/changing

A
  • can change over time
102
Q

is there a large range of dosages that are effective from one drug to another

A
  • yes
103
Q

most patients who recover from an acute schizophrenic episode do/do not need further drug therapy

A
  • most need

- on an “as needed” basis

104
Q

olanzapine/fluoxetine combo FDA approved for what?

A
  • depression in biopolar disorder
105
Q

Pharmacokinetics of antipsychotics

A
  • absorption quite high
  • many undergo significant first-pass metabolism
  • most highly lipid soluble, membrane or protein bound
  • generally much longer clinical duration of action than estimated from their plasma half lives
  • often takes time for drug effect to take place
  • withdrawal can occur after stopping drug
  • extensively metabolized by CYPs and then conjugations (some exceptions)
  • considerations of interactions: changes in smoking behavior, drugs that impact CYP activity, combining antipsychotics with various other psychotropic drugs
106
Q

do antipsychotics generally interfere with metabolism of other drugs at clinical doses?

A
  • no
107
Q

Time to recurrence of psychotic symptoms

A
  • highly variable
  • average time for relapse: 6 months with exception of clozapine (should never be discontinued abruptly unless side effects are medical emergencies)
108
Q

Use of antipsychotics in special populations

A
  • Pediatric: some approved (sensitive to EPS and weight gain, also hyperprolactinemia)
  • Geriatric: sensitive to EPS, TD, orthostasis, sedation, anticholinergic effects.. potential for drug/drug interactions, weight gain less of an issue for elderly, riskf or cerebrovascular events and all-cause mortality with dementia
109
Q

Use in pregnancy

A
  • Category B or C
  • available data indicate little to no toxicity
  • all antipsychotics cross the placenta
  • decisions should be decided individually
  • issues in breast feeding due to low level of infant hepatic catabolic activity
110
Q

Overdoses

A
  • low potency typicals: risk of torsade and other extensions of known pharmacology
  • high potency typicals: EPS, EKG changes
  • atypicals: less of a risk of torsade, however in combo with other medications it can lead to fatality
111
Q

Non-pharmacological treatment of schizophrenia

A
  • psychosocial support, cognitive, and vocational rehabilitation
  • ECT - last resort

Pharmacology I (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions