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Spring 2024 Therapeutics 3 > Exam 4 Schizophrenia > Flashcards

Exam 4 Schizophrenia Flashcards

1
Q

The creation of which schizophrenia drug in the 1950’s lead to the emptying out of mental hospitals?

A

Phenothiazines (chlorpromazine)

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2
Q

What is the most debilitating psychotic disorder?

A

Schizophrenia

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3
Q

What is the onset age of schizophrenia?

A

15-20 years old

(onset late adolescence to early adulthood)

Men: late teens, early 20’s

Women: late 20’s, early 30’s

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4
Q

Why do women have a later onset of schizophrenia than men?

A

Estrogen is protective against schizophrenia onset

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5
Q

What are the 5 etiologies of schizophrenia?

A

Neurodevelopmental/anatomical
Genetics
Environmental
Gene-Environment Interaction
Neurodevelopment-Environment Interaction

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6
Q

What are the neurodevelopmental/anatomical differences seen with schizophrenia?

A

In utero/adolescence:
-Increased ventricle size
-Changes in gray and white matter

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7
Q

What are the environmental etiologies that can result in schizophrenia?

A

-Birth complications
-Infections

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8
Q

Mutations in what gene may cause schizophrenia with the use of marijuana?

A

COMT

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9
Q

What is the cause of schizophrenia?

A

UNKNOWN
-just know some risks

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10
Q

What are positive schizophrenia symptoms?

A

Hallucinations, Delusions, Bizarre Behavior, Thought Disorders

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11
Q

What are negative schizophrenia symptoms?

A

Blunted Emotion, Poor Self Care, Social Withdrawal, Poverty in Speech

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12
Q

What are cognitive symptoms of schizophrenia?

A

*Decrease in cognitive function
-Involves D1 receptors and glutamate receptors

*Newly acknowledged

(Decreased ability to use executive functioning, ex: planning)

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13
Q

What type of schizophrenia symptoms respond well to drug therapy?

A

Positive symptoms

*note: newer agents work better on negative symptoms

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14
Q

What are the 3 types of neurotransmitter hypotheses for schizophrenia?

A

-Dopamine
-Serotonin
-Glutamate

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15
Q

What two hallucinogens is the serotonin hypothesis based on?

A

LSD and Mescaline

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16
Q

What is the serotonin hypothesis?

A

-LSD and Mescaline are 5HT agonists which inspired a search for endogenous hallucinogens

-Studies identified the 5HT2A receptor as a mediator of hallucinations

*Antagonism and inverse agonism are linked to antipsychotic activity

-5HT2A receptors modulate dopamine release, glutamate release, and NMDA receptors

*5HT2C receptors may be beneficial in schizophrenia

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17
Q

What two drugs is the glutamate hypothesis based on?

A

Phencyclidine and Ketamine

**EXACERBATE PSYCHOSIS*

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18
Q

What is the glutamate hypothesis?

A

*Glutamate is a major excitatory neurotransmitter

-Phencyclidine and Ketamine are noncompetitive inhibitors of NMDA receptors. THEY EXACERBATE PSYCHOSIS AND COGNITIVE DEFECTS

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19
Q

What is the dopamine hypothesis?

A

D2 receptor antagonists have a strong correlation between binding affinity and effectiveness

**Dopaminergic agents (L-DOPA, amphetamine) EXACERBATE schizophrenia symptoms

Schizophrenia patients have increased D2 receptor density and increased dopamine release

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20
Q

What does Kd/Ki represent?

A

Estimated concentration at which 1/2 of the receptors are occupied

(used in binding affinity)

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21
Q

When determining a binding affinity, does a high or low number represent tight affinity (good)?

A

LOW

*we want low numbers for binding affinity

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22
Q

What are the dopamine receptors?

A

D1-like: D1 and D5

D2-like: D2, D3, D4

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23
Q

What is the serotonin receptor?

A

5HT

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24
Q

What are the 2 norepinephrine receptors and what effect does blocking them have?

A

a1: Hypotension, Sedation

a2: May be helpful in therapy

(adrenergic receptors)

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25
Q

What are the acetylcholine receptors and what effect does blocking them have?

A

Muscarinic receptors: anticholinergic effects (dry mouth, constipation, tachycardia)

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26
Q

What is the histamine receptor and what affect does blocking it have?

A

H1 Receptor: sedation, weight gain

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27
Q

Which receptor is the key for therapeutic effectiveness in schizophrenia?

A

UNKNOWN
-multiple receptors involved
-different types of schizophrenia may rely on different receptors more

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28
Q

Most antipsychotic drugs function as what towards receptors?

A

Antagonists

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29
Q

Which dopamine receptor (D1 or D2) shows a correlation between binding potency and clinical effectiveness?

(ability to bind to receptor is predicted by the dose and determines effectiveness)

A

D2 receptors

**more effective drug target
*dose does not predict ability to bind to D1

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30
Q

When presynaptic receptors for dopamine are BLOCKED, what affect does it have on dopamine release?

A

When blocked: increased dopamine release + synthesis

-these receptors regulate synthesis and release of dopamine
-when dopamine comes back, it tells the receptors there is too much dopamine in the synapse and the receptors work to decrease synthesis and release
-blocking these keeps dopamine in the system

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31
Q

D2 receptor antagonists block which receptors in the synapse?

A

BOTH pre-and post- synaptic

*even though more dopamine is being released into the synapse, there is not an exacerbation of symptoms because the post-synaptic receptors are blocked not signaling

*not ideal situation but how it works

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32
Q

What affect do antipsychotics have on dopamine metabolites?

A

There is an increase in synthesis and release of dopamine which increases dopamine metabolite levels (note that postsynaptic receptors are blocked)

-overtime, there is an adaptive response that makes metabolite levels go back down

-the eventual normalization of metabolites is associated with increased therapeutic efficacy over time

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33
Q

What part of the CNS is responsible for the primary therapeutic effects in schizophrenia (what we want to target)?

A

Mesolimbic

**only receptors we want to block

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34
Q

If we block dopamine receptors in the Basal Ganglia what happens?

A

Motor effects

(this is where Parkinson’s motor tremors comes from, blocking these receptors cause these tremors)

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35
Q

If we block dopamine receptors in the Mesocortical area what happens?

A

Exacerbation of cognitive defects

*note: this area is already hypo-functioning in schizophrenia

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36
Q

If we block dopamine receptors in the Hypothalamus/ Endocrine System what happens?

A

Increased prolactin release
(normally inhibited by dopamine)

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37
Q

If we block dopamine receptors in the Medulla what happens?

A

DECREASED nausea + vomiting

*ok to block these
-Where anti-emetics work (D2 antagonists)

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38
Q

What percent of dopamine receptors must be lost for symptoms of Parkinson’s to appear?

A

70-80%

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39
Q

How quickly do extrapyramidal symptoms (movement disorders) begin after starting antipsychotic treatment?

A

EARLY (days/weeks)

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40
Q

What are the extrapyramidal symptoms (motor symptoms) that can occur with antipsychotic use?

A

Dystonia
Pseudoparkinsonism (muscle rigidity)
Tremor
Akathisia

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41
Q

What is dystonia?

A

Increased muscle tone

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42
Q

What is akathisia?

A

Restlessness

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43
Q

What do we use to treat drug-induced extrapyramidal symptoms?

A

Anticholinergics:
-Benztropine -Trihexyphenidyl -Akineton

Antihistamines:
-Diphenhydramine

Amantadine (dopamine releasing)

Propranolol (akathisia)

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44
Q

Why do we give anticholinergics to decrease drug-induced extrapyramidal symptoms?

A

Dopamine acts as an inhibitory signal in the neuron to counteract the excitatory signals of acetylcholine

-When dopamine receptors are blocked, there is an increase in excitatory signaling by acetylcholine
-This is why we give anticholinergics

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45
Q

How quickly does the side effect Tardive Dyskinesia occur after starting antipsychotics?

A

LATE (months to a year)

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46
Q

What important fact about Tardive Dyskinesia makes it more severe than some other antipsychotic side effects?

A

IRREVERSIBLE

(want to prevent it)

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47
Q

What are the symptoms of Tardive Dyskinesia?

A

Mouth: rhythmic, involuntary movements

Choreiform: jerking movements

Athetoid: involuntary writhing movements of face or hands

Axial hyperkinesias: “To-and Fro” movements

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48
Q

What is the MOA of Tardive Dyskinesia?

A

Unknown

-possible antagonist-induced hypersensitivity of dopamine receptors

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49
Q

What treatment is available for Tardive Dyskinesia?

A

PREVENTION

  1. Reduce dose of current agent
  2. Change to a different drug, possibly newer agent
  3. Eliminate anticholinergic drugs
  4. VMAT inhibitors (“zine’s”) ***

(use the least risk agent at the lowest dose possible and monitor with the AIMS scale)

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50
Q

How do VMAT2 inhibitors help treat Tardive Dyskinesias?

A

-Prevent dopamine from being packaged into synaptic vesicles

-Allows dopamine to be out in the cell and metabolized (deletes dopamine)

-Super sensitive receptors cannot be activated if there is no dopamine

Drugs: Tetrabenazine, Valbenazine, Deutetrabenazine
“azine”

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51
Q

How quickly after starting antipsychotics does the side effect Neuroleptic Malignant Syndrome (NMS) occur?

A

RAPID***

Note: serious and has high fatality

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52
Q

What are the symptoms of Neuroleptic Malignant Syndrome (NMS)?

A

-Extrapyramidal symptoms with fever
-Impaired cognition (agitation, delirium, coma)
-Muscle rigidity

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53
Q

What is the treatment for Neuroleptic Malignant Syndrome (NMS)?

A

-Discontinue drug

-Dopamine agonists
-Diazepam
-Dantrolene (skeletal muscle relaxant)

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54
Q

How long to antipsychotics take to work?

A

2-3 weeks for effectiveness

6 weeks - 6 months for maximal efficacy

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55
Q

One pharmacological effect of antipsychotics is “Neuroleptic” Syndrome. What is this?

A

-Suppression of emotions
-Reduced initiative and interest

*May resemble negative symptoms

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56
Q

What are the two autonomic side effect mechanisms?

How do these manifest?

A

Muscarinic Cholinoceptor Blockade:
-Loss of accommodation (vision loss)
-Dry mouth
-Difficulty urinating
-Constipation

Alpha Adrenoceptor Blockade:
-Orthostatic hypotension
-Impotence/ Failure to ejaculate

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57
Q

What are the four CNS side effect mechanisms?

How do these manifest?

A

Dopamine receptor blockade:
-Parkinson’s syndrome
-Akathisia
-Dystonias

Supersensitivity of Dopamine Receptors:
-Tardive Dyskinesia

Muscarinic blockade:
-Toxic-confusional state

Histamine (H1) receptor blockade:
-Sedation
-Weight gain

58
Q

What is the endocrine system side effect mechanism?

How does it manifest?

A

Dopamine receptor blockade
Results in hyperprolactinemia

-Amenorrhea-galactorrhea
-Infertility
-Impotence

59
Q

What mechanisms cause weight gain?

A

Combined H1 (histamine) and 5HT blockade

60
Q

Blocking muscarinic receptors causes what?

A

Toxic confusional state

For cholinoceptors (autonomic):
-Loss of accommodation (vision loss)
-Dry mouth
-Difficulty urinating
-Constipation

61
Q

Blocking dopamine receptors causes what?

A

-Parkinson’s syndrome
-Akathisia
-Dystonias

Endocrine blockade resulting in hyperprolactinemia:
-Amenorrhea-galactorrhea
-Infertility
-Impotence

62
Q

New antipsychotics are CONTRAINDICATED with which disease state?

A

Diabetes

63
Q

What was the first antipsychotic?

A

Chlorpromazine

64
Q

What drugs are the aliphatic phenothiazines?
(first gen antipsychotics)

A

Chlorpromazine

Promethazine (used for H1 antagonist property)

65
Q

What property is Promethazine used for and what other indications does it have?

A

H1 antagonism

-Used for nausea/vomiting

66
Q

What is the Piperidine Phenothiazine?

A

-Thioridazine

67
Q

What are the Piperazine Phenothiazines?

A

-Fluphenazine
-Prochlorperazine
-Perphenazine

68
Q

What did the CATIE studies show?

A

Perphenazine is just as effective as newer agents when used in combination with anticholinergics

*this drug is much cheaper as well

69
Q

What is the Thioxanthine drug?

A

Thiothixene

70
Q

What is the Butyrophenone drug?

A

Haloperidol

71
Q

What are the benefits of using Atypical/Second Generation (new) antipsychotics?

A

-Reduced EPS (dual 5HT and D2 blockers)

-Better efficacy for negative symptoms

72
Q

What is the downside of using Atypical/Second Generation (new) antipsychotics?

A

More metabolic problems
-Weight gain
-Linked to diabetes

*can cause compliance issues

73
Q

What affect do presynaptic serotonin receptors have on dopamine?

A

-Control the dopaminergic neuron (which is in charge of making dopamine)

-Activated serotonin receptors lead to decreased dopamine synthesis and release

*Antagonizing these receptors leads to increased dopamine synthesis and release

*D2 receptor agonists compete with dopamine for the receptor which lessens movement disorders

74
Q

What are the Atypical/ 2nd Generation Antipsychotics?

A

-Clozapine
-Olanzapine
-Loxapine

75
Q

What was the first Atypical Antipsychotic?

A

Clozapine

76
Q

What is the most effective Antipsychotic?

A

Clozapine

77
Q

What is a downside to using clozapine?

A

Many side effects!

78
Q

What are the side effects of clozapine?

A

-Agranulocytosis (*requires weekly blood tests)
Anticholinergic
-Antihistamine

*Risk of diabetes

79
Q

What are the side effects of Olanzapine?

A

**Weight gain
-Diabetes

(Causes less N/V and EPS)

80
Q

What atypical antipsychotics have metabolites?

A

Loxapine -> Amoxipine (inhibits NET, antidepressant)

Quetiapine (antidepressant)

81
Q

What are the side effects of Quetiapine?

A

-Hypotension (a1)
-Sedation (H1)
-Diabetes

*low antimuscarinic (blocks both 5HT and D2)
*Low EPS

82
Q

Which antipsychotic is specifically designed to have 5HT and D2 antagonist properties?

A

Risperidone

83
Q

What are the side effects of Risperidone?

A

Weight gain

Some sedation

(low EPS)

84
Q

What makes D2 receptors different than D3 or D4?

A

D2 has very long binding pockets that drugs must be able to enter

85
Q

What atypical antipsychotic has a fast onset?

A

Lurasidone

86
Q

When dosing Lurasidone, what is an important note to make?

A

Low doses have similar efficacy to high doses

87
Q

Which atypical antipsychotic is used to treat Parkinson’s Disease Psychosis?

A

Pimavanserin

88
Q

Which atypical antipsychotic prolongs the QT interval?

A

Ziprasidone

89
Q

What are the 3 D2/D3 partial agonists?

A

-Brexipiprazole
-Cariprazine
-Lumateperone

90
Q

What are the key features that define psychotic disorders?

A

-Delusions
-Hallucinations
-Disorganized thinking and speech
-Disorganized or abnormal motor behavior
-Negative symptoms

91
Q

What are delusions?

A

Fixed false beliefs that are not amenable to change even with conflicting evidence

92
Q

What are positive symptoms?

A

Outward symptoms

93
Q

What are negative symptoms?

A

Symptoms relating to long-term functioning

*impact long-term outcomes and how well a person is able to live alone

94
Q

What substances are associated with schizophrenia?

A

-Smoking

-Marijuana

-Cocaine, Amphetamine

95
Q

How does smoking induce schizophrenia?

A

-Induces 1A2

*not due to nicotine, caused by hydrocarbons produced and inhaled

-Decreases the serum concentration of 1A2 substrate antipsychotics

96
Q

What are the 1A2 substrate antipsychotics?

A

Olanzapine
Asenapine
Clozapine
Loxapine

97
Q

How do marijuana, cocaine, and amphetamine affect schizophrenia?

A

-Hasten the onset of schizophrenia
-Exacerbate symptoms
-Reduce time to relapse

*note: only people with specific genetics are at risk for schizophrenia with marijuana use

98
Q

What is the only substance that can cause schizophrenia?

A

P2P methamphetamine

99
Q

What must be considered when choosing a drug therapy for a patient?

A

-Doses per day
-Side effects
-Previous drug therapy (including family members)
-Cost
-Concomitant therapy
-Need for monitoring

100
Q

What dosage form is considered first-line schizophrenia treatment?

A

Oral therapy

*unless there are reasons why IM would be better

101
Q

Older agents (Typical Antipsychotics) primarily have what function?

A

D2 receptor antagonist

102
Q

True or False: Typical Antipsychotics worsen negative schizophrenia symptoms

A

True

103
Q

What are the partial agonists?

A

-Aripiprazole
-Brexpiprazole
-Cariprazine

104
Q

What function do partial agonists have on dopamine transmission?

A

“Stabilize” dopamine transmission

105
Q

Partial agonists are associated with what side effects overall?

A

*More akathisia than other antipsychotics

*Boxed warning for suicidal thoughts/behavior (depression use)

106
Q

The partial agonists are substrates of what?

A

Aripiprazole + Brexpiprazole: 2D6 and 3A4

Cariprazine: 3A4

107
Q

What is a good antipsychotic to use to avoid weight gain?

A

Aripiprazole

108
Q

Which group of antipsychotics causes the most weight gain?

A

The “pines”

109
Q

What are the “pines”?

A

Asenapine

Clozapine

Olanzapine

Quetiapine

110
Q

The “pines” are substrates of what?

A

Asenapine, Clozapine, + Olanzapine: 1A2

Quetiapine: 3A4

111
Q

Which antipsychotic has a sublingual and patch form?

A

Asenapine

112
Q

Which “pines” are associated with QTc prolongation?

A

Asenapine
Clozapine
Quetiapine

113
Q

Which antipsychotics have a DRESS warning?

A

Olanzapine

Ziprasidone

114
Q

Which antipsychotic causes the most weight gain?

A

Clozapine

115
Q

Which antipsychotic is also a UGT substrate?

A

Asenapine

116
Q

What are the directions for applying an Asenapine patch?

A

Apply one patch every 24 hours
-rotate patch site to minimize application site reactions

117
Q

Clozapine is associated with agranulocytosis which requires blood monitoring while taking this medication. What is the monitoring regimen?

A

Weekly x 6 months

then Biweekly x 6 months

then Every 4 weeks

118
Q

What is the available combination antipsychotic?

A

Lybalivi

(Olanzapine/Samidorphan)

119
Q

When is the combination product Olanzapine/Samidorphan (Lybalvi) contraindicated?

A

*Samidorphan is an opioid antagonist preferring the mu opioid receptor

*Contraindicated in patients currently taking opioids or in opioid withdrawal

120
Q

What 2 antipsychotic meds need to be taken with food to increase absorption and bioavailability?

A

-Lurasidone
-Ziprasidone

121
Q

Which antipsychotic has a CONTRAINDICATION for QTc prolongation?

A

Ziprasidone

122
Q

Which antipsychotic causes hyperprolactinemia?

A

Risperidone

(pseudopregnancy, gynecomastia)

123
Q

Which antipsychotic is renally eliminated?

A

Paliperidone

*requires dose adjustment

124
Q

Which new agent is associated with few side effects?

A

Lumateperone (Caplyta)

125
Q

Which antipsychotic can be used to treat hallucinations/delusions in Parkinson’s Disease?

A

Pimavanserin

126
Q

Which agent is an inverse agonist and antagonist at the 5HT 2A receptor?

A

Pimavanserin

127
Q

What boxed warning do all antipsychotics have?

A

Increased risk of death in ELDERLY patients treated for dementia related behaviors

128
Q

Which antipsychotic is available as a long-acting injection?

A

Haloperidol

129
Q

Why might the long-acting injection of haloperidol not be a great medication choice?

A

Oil-based

*requires a Z-track method of injection to increase area of injection into the deep IM muscle

NOT FIRST-LINE

130
Q

What is the most commonly used immediate release antipsychotic?

A

Haloperidol

131
Q

What is the treatment for acute dystonias?

A

IM anticholinergic NOW

-Benztropine 2mg
-Diphenhydramine 50mg

132
Q

What is the treatment for Drug-Induced Parkinson’s?

A

-Oral anticholinergic

-Benztropine
-Trihexyphenidyl
-Diphenhydramine

133
Q

What is the treatment for Akathisia?

A

Beta-blocker (*propranolol)

Benzodiazepine (*lorazepam)

134
Q

What is the treatment for Tardive Dyskinesia?

A

VMAT inhibitors

135
Q

What are the VMAT inhibitors?

A

Valbenazine (Ingressa)

Deutetrabenazine (Austedo)

136
Q

What are the VMAT inhibitors substrates of?

A

Valbenazine: 2D6/3A4

Deuetrabenazine (2D6)

137
Q

What is a common side effect of the VMAT inhibitors?

A

QTc prolongation

138
Q

True or False:
Future antipsychotic use after development of Neuroleptic Malignant Syndrome is contraindicated

A

False

-still need treatment

139
Q

Which antipsychotics have the highest risk of causing Neuroleptic Malignant Syndrome?

A

Clozapine

Olanzapine

140
Q

Which antipsychotics have the lowest risk of causing Neuroleptic Malignant Syndrome?

A

Ziprasidone

Lurasidone

Aripiprazole

Spring 2024 Therapeutics 3 (24 decks)

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