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Pharmacology - Exam 2 > Antipsychotic Therapy > Flashcards

Antipsychotic Therapy Flashcards

1
Q

Name the 4 schizophrenic symptoms that are considered “Positive” (enhancement of function). Where are these symptoms originating? Why?

A

Nucleus Accumbens (Mesolimbic)= too much DAergic activity

  1. Hallucinations
  2. Delusions
  3. Behavioral disorganization
  4. Positive formal thought disorder
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2
Q

Name the 6 schizophrenic symptoms that are considered “Negative” (deficit of function). Where are these symptoms originating? Why?

+

Name the one schizophrenic symptoms that fits into neither positive or negative as a category. Where is this symptom originating? Why?

A

Frontal cortex (Mesocortical)= too little DAergic activity​

  1. Alogia
  2. Affective blunting
  3. Avolution
  4. Asociality
  5. Anhedonia
  6. Attentional Impairment

____________

Frontal cortex (Mesocortical)= too little DAergic activity​

Also, COGNITIVE (own category)

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3
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Hallucinations

A

Positive

Nucleus Accumbens (Mesolimbic)= too much DAergic activity

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4
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Delusions

A

Positive

Nucleus Accumbens (Mesolimbic)= too much DAergic activity

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5
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Behavioral disorganization

A

Positive

Nucleus Accumbens (Mesolimbic)= too much DAergic activity

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6
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Positive formal thought disorder

A

Positive

Nucleus Accumbens (Mesolimbic)= too much DAergic activity

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7
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Alogia

A

Negative

Frontal cortex (Mesocortical)= too little DAergic activity​

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8
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Affective blunting

A

Negative

Frontal cortex (Mesocortical)= too little DAergic activity​

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9
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Avolution

A

Negative

Frontal cortex (Mesocortical)= too little DAergic activity​

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10
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Asociality

A

Negative

Frontal cortex (Mesocortical)= too little DAergic activity​

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11
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Anhedonia

A

Negative

Frontal cortex (Mesocortical)= too little DAergic activity​

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12
Q

Schizophrenic symptom: Positive or negative? Location? DA activity level?

Attentional impairment

A

Negative

Frontal cortex (Mesocortical)= too little DAergic activity​

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13
Q

What receptor do ALL antipsychotic drugs block?

A

Dopamine (DA)

D2 receptor

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14
Q

Which dopamine pathway in the brain has too little DAergic activity? What types of symptoms is it responsible for?

A

Frontal cortex (Mesocortical)= too little DAergic activity

NEGATIVE AND COGNITIVE SYMPTOMS

  1. Alogia
  2. Affective blunting
  3. Avolution
  4. Asociality
  5. Anhedonia
  6. Attentional impairment
  7. Cognitive (neither negative nor positive, own category)
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15
Q

Which dopamine pathway in the brain has too much DAergic activity? What types of symptoms is it responsible for?

A

Nucleus Accumbens (Mesolimbic)= too much DAergic activity

POSITIVE SYMPTOMS

  1. Hallucinations
  2. Delusions
  3. Behavioral disorganization
  4. Positive formal thought disorder
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16
Q

Identify the APS:

  • First Generation/typical
  • Category: Phenothiazines
  • Tricyclic

Pros

  • Generic
  • Inexpensive
  • Slight extrapyramidal syndrome

Cons

  • Many adverse effects, especially autonomic
  • Neuroleptic (Potentiated anesthesia)
  • 800 mg/day limit
  • Cardiotoxicity
  • Increased risk of tardive dyskinesia
  • No paraenteral form
A

Chlorpromazine (thorazine)

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17
Q

Identify the APS:

  • First generation/typical
  • Category: Butyrophenones

Pros

  • Major advantages over phenothiazines include lower sedation and less alpha-block
  • Generic
  • Cheap

Cons

  • Severe extrapyramidal syndrome
A

Haloperidol

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18
Q

Identify the APS:

  • 2nd generation/atypical
  • Category: Dibenzodiazepine

Pros

  • No EPS: Somehow was selective for causing DPI ONLY in mesolimbic pathway
  • Benefit to treatment resistant patients
  • Higher potency at 5HT2
  • Better against negative symptoms

Cons

  • Agranulocytosis risk requires weekly WBCs
  • Diabetes
  • Weight gain
A

Clozapine

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19
Q

Identify the APS:

  • 2nd generation/atypical
  • Category: Benzisoxazole

Pros

  • Broad spectrum w/ few or no EPS at low dose
  • No evidence of agranulocytosis risk
  • Long acting injectable available

Cons

  • high dose EPS
  • high dose hypotension
A

Risperidone

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20
Q

Identify the APS:

  • 2nd generation/atypical
  • Category: Thienobenzodiazepine

Pros

  • Benefit in negative symptoms
  • Little or no EPS
  • No risk of agranlocytosis

Cons

  • Diabetes
  • Hypotension
  • Serious Weight gain
  • Smaller increase in serum PRL than haloperidol
A

Olanzapine

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21
Q

Identify the APS:

  • 2nd generation/atypical
  • Category: Dihydroindolone

Pros

  • similar to other atypicals
  • perhaps less weight gain/diabetes risk

Cons

  • QT prolongation
A

Ziprasidone

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22
Q

Identify the APS:

  • 2nd generation/atypical
  • Category: quinolinone

Pros

  • Different mechanism (partial agonist at D2 receptors)
  • Modest affinity at 5-HT2 receptors (antagonist)
  • Partial agonist at 5-HT1a receptors
  • Less effect on prolactin levels
  • No apparent risk of diabetes

Cons

  • No long term studies
A

Aripiprazole

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23
Q

Drugs that increase synaptic DA produce ______

(ex. Amphetamine toxicity; overdoses of L-DOPA)

A

psychosis

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24
Q

Successful treatment with Anti-psychotics (increases or decreases) DA metabolites

A

Increases DA metabolites

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25
Q

True or false: DA receptor density changes in schizophrenia

A

true

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26
Q

How does Amphetamine enhance DA release?

A

Amphetamine enhances DA release via reversal of the transporter

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27
Q

How does L-DOPA produce psychosis?

A

By increasing DA synthesis by providing more precursor, it may produce psychosis

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28
Q

Other than dopamine, what two other neurotransmitter may play a role in Schizophrenia?

A
  1. Serotonin (5-HT2 receptors)
  2. Glutamate (NMDA receptors)
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29
Q

In the treatment of psychosis, is there proven clinical efficacy for treating with a 5-HT2 block (serotonin receptor block)?

A

No; correlation of clinical efficacy with 5-HT2 block is poor

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30
Q

Approximately how long does it take for anti-psychotic treatment to become effective? Successful management corresponds to what?

A
  • 4-6 weeks
  • Corresponds to the development of “depolarization inactivation”=DPI
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31
Q

Identify stage of TX:

  • Location: Nucleus Accumbens
  • Numerous synaptic D2 receptors
  • Numerous pre-synaptic D2 receptors
  • Steady firing of pre-synaptic neuron
A

Untreated

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32
Q

Identify stage of TX:

  • Location: Nucleus Accumbens
  • Some synaptic D2 receptors blocked
  • Some pre-synaptic D2 receptors blocked
  • Pre-synaptic neuron fires LIKE CRAZY
A

Acute TX

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33
Q

Identify stage of TX:

  • Location: Nucleus Accumbens
  • ALL Synaptic D2 receptors blocked
  • ALL Pre-synaptic D2 receptors blocked
  • Pre-synaptic neuron wears out; no firing (too depolarized)
  • State of depolarization inactivation
A

Chronic TX

(4-6 weeks)

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34
Q

What state must be reached for schizophrenic patient to experience relief of symptoms?

A

State of deplarization inactivation corresponds to therapeutic benefit

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35
Q

What brain pathway is the substrate for schizophrenia?

A

Mesocorticolimbic system

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36
Q

Which brain pathway is responsible for Parkinsonian-like symptoms (extrapyramidal symptoms: EPS) when using a dopamine D2 receptor blockade?

A
  • Nigrostriatal Projection
  • Substantia nigra, which connects to the striatum
  • Blockage of D2 in striatum results in EPS
  • For physiology, refer to Parkinson’s lecture
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37
Q

How is it possible to have both the Nucleus Accumbens (Mesolimbic)= too much DAergic activity and the Frontal cortex (Mesocortical)= too little DAergic activity​ at once in schizophrenia?

A
  • Brain stem dopaminergic neurons
    • There are brain stem dopaminergic neurons that connect to the pre-frontal cortex (mesocortical)
    • There are brain stem dopaminergic neurons that connect to the limbic areas (nucleus accumbens/mesolimbic)
  • The pre-frontal cortex has feedback to the limbic areas and feedback to the brain stem dopaminergic neurons. The limbic areas DO NOT have feedback to the brain stem dopaminergic neurons.
  • The connection between the brain stem dopaminergic neurons and prefrontal cortex breaks (neurons die).
  • Thus, prefrontal cortex is not getting dopamine. In feedback, the pre-frontal cortex tells the brain stem it needs more dopamine.
  • However, the prefrontal cortex is unable to get more dopamine because the connection between the brain stem and dopaminergic neurons is broken (dead), so nothing is fixed on the prefrontal cortex side
  • BUT, stimulated by the prefrontal cortex feedback, the brain stem makes more dopamine, and the connection between the brain stem dopaminergic neurons and limbic system is connected, so it releases more dopamine to the limbic system
  • result: prefrontal cortex too little dopamine/limbic system too much dopamine

**Important to note that the limbic system does not have a feeback of its own to the brain stem dopaminergic neurons, only the pre-frontal cortex has this connection**

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38
Q

Prolonged treatment with D2 blockers causes what pathophysilogical response in the Nigrostriatal projection? What side-effect is the result of this response?

A
  • Prolonged treatment with D2 blockers produces D2 receptor supersensitivity (neuron makes more D2 receptors to compensate)
  • Side effect=Tardive dyskinesia (disorder that results in involuntary, repetitive body movements)
  • THIS IS A LONG TERM EFFECT OF ANTI-PSYCHOTIC DOPAMINE D2 RECEPTOR BLOCKERS
39
Q

What are the four neurological pathways of dopamine? What happens if you take an anti-psychotic (dopamine D2 receptor blocker)?

A

Pathways and effects of dopamine D2 receptor blocker

Schizophrenia pathways

  1. Mesocortical (Frontal cortex)
    • Responsible for negative and cognitive symptoms
    • Worsen negative and cognitive symptoms
  2. Mesolimbic (Nucleus Accumbens)
    • Responsible for positive symptoms
    • Relieve positive
    • symptoms

Other dopamine pathways

  1. Nigrostriatal
    • EPS side effects
    • Prolonged: Tardive Dyskinesia
  2. Tuberoinfundibular
    • Prolactin (PRL) release increase (gynecomastia, galactorrhea-increased lactation)
  3. Medullary-perventricular neurons
    • Eating behavior+weight gain
  4. Chemotrigger zone (CTZ)
    • Anti-emetic response
40
Q

Two traits of “atypical” anti-psychotic drugs?

A

– Lower incidence of EPS compared with the typical antipsychotics

– Increased ratio of 5-HT2:D2 receptor blockade

41
Q

True or false: Currently atypicals (2nd generations) are used more than typicals because of lower incidence of EPS and superiority in treatment of negative symptoms.

What’s the exception?

A

True; exception is Clozapine

42
Q

What types of drugs would you like to avoid in the elderly? Which APS drugs are best for avoiding those side effects?

A

Alpha block

  • +++ Chlorpromazine (thorazine)
  • +++ Risperidone (Risperidal)

_____

Best drugs for avoiding alpha block:

  • +/- Aripriprazole (abilify)
    • Haloperidol (haldol)
43
Q

What types of drugs can cause confusion? Which drugs are best for avoiding confusion?

A

Ach block

  • +++ Clozapine (Clozaril)
  • +++ Olanzapin (Zyprexa)

_____

Best drugs for avoiding Ach blocks:

  • Most 2nd gen APS are +/- on this side effect, excepting the two listed above
44
Q

If a patient has diabetes risk, which APS drugs shoud you avoid?

A
  1. ++++ Clozapine
  2. ++++ Olanzapine
  3. Also, ++ Risperidone
45
Q

Which drug may have cardiotoxicity risk?

A

Thioridazine

46
Q

If a patient has depressive symptoms, which two APS drugs should you consider using?

A
  1. Aripiprazole
  2. Quetiapine
47
Q

If a patient is non-compliant with taking their APS medication, which administration form may be most beneficial?

A

Depot form

48
Q

Differentiate: Low potency or high potency? Give an example APS in this category.

  • Low incidence of neurological side effects
  • High incidence of autonomic side effects
A

Low potency

ex. chlorpromazine

49
Q

Differentiate: Low potency or high potency? Give an example APS in this category.

  • Higher frequency of neurological and endocrinological side effects
  • Fewer autonomic side effects
A

High potency

ex. haloperidol

50
Q

Low potency APS need a high dose to get an antipsychotic effect. What is the minimum effective dose?

A

Need high dose to get antipsychotic effect

(100 mg min effective dose)

ex. chlorpromazine

51
Q

High potency APS need a low dose to get an antipsychotic effect. What is the minimum effective dose?

A

Need low dose to get antipsychotic effect

(2 mg min effective dose)

ex. haloperidol

52
Q

Compare/contrast receptor binding profile of first generation APS Chlorpromazine v. Haloperidol?

  • Sedation
  • Ach block
  • D2 block
  • Alpha1 block
  • 5-HT2 block
A

Sedation

  • +++ Chlorpromazine
  • +/- Halperidol

Ach block

    • and +/- About equal

D2 block

    • Chlorpromazine
  • +++Haloperidol

Alpha1 block

  • +++ Chlorpromazine
    • Haloperidol

5HT2 block

  • ++ Equal
53
Q

Which APS has a “dose-dependent” EPS? What is the dose for which EPS becomes a concern?

A
  • Risperidone
  • Any dose <6mg no EPS; any dose >6mg risk of EPS
54
Q

Which APS is a partial agonist for Dopamine D2 receptor block?

A

Aripiprazole (Abilify)

55
Q

Which APS may result in QTc interval prolongation?

A

++ Zipresidone

56
Q

Which drug has a tricyclic structure? What does this imply?

A

Chlorpromazine; LOTS OF SIDE EFFECTS

57
Q

Which APS does not cause EPS side effects?

A

Clozapine (no D2 supersensitivity)

58
Q

How does blocking 5-HT2 receptors help negative symptoms and avoid EPS?

A
  • When serotonin binds to 5-HT2 receptors in cortex and striatum, it blocks dopamine release
  • If you block this, then dopamine is more readily released

Note:

  • Frontal cortex (Mesocortical)= too little DAergic activity. This prevents the too little dopamine.
  • EPS occurs when DA is blocked in striatum
59
Q

How does a partial agonist work? What is the drug that has this mechanism?

A
  1. Partial agonist blocks access of dopamine where dopamine is high
  2. Partial agonist increases dopaminergic activity where dopamine is low

Aripriprazole

60
Q

Based on total profile, what is the preferred APS of choice?

A

Aripriprazole

61
Q

What are 6 neurological side effects of APS (early appearing)?

A
  1. Acute dystonia (spastic retrocollis or torticollis)
  2. Akasthisia (motor restlessness)
  3. Parkinsonism (EPS)
  4. Neuroleptic Malignant Syndrom (NMS)
  5. Sedation
  6. Lower seizure threshold

**note that not all of these side effects are present for all drugs**

62
Q

If a patient is experiencing acute dystonia (spastic retrocollis or torticollis), what might you do to treat?

A

Could use an anticholinergic antiparkinson agent

63
Q

If a patient is experiencing akasthisia (motor restlessness), what should you do?

A

Reduce drug or change treatment; a benzodiazepine or propranolol may help

64
Q

If a patient is experiencing Parkinsonism (EPS), what can you do?

A

Can give anticholinergics

65
Q

What early appearing side effect of APS drugs is potentially fatal? How long to appear? What are the symptoms? What are the treatments? What should you NEVER give?

A

Neuroleptic Malignant Syndrome (NMS)

Timecourse

  • Occur within weeks
  • Can persist after stopping APS

Symptoms

  • Catatonia
  • Stupor
  • Fever
  • Unstable Blood Pressure
  • Myoglobinemia

Treatment

  • Stop drug IMMEDIATELY
  • Give Bromocriptine or dantrolene
  • DO NOT GIVE ANTICHOLINERGICS
66
Q

Patient starts an APS, and upon return to clinic, presents with:

  • Catatonia
  • Stupor
  • Fever
  • Unstable Blood Pressure
  • Myoglobinemia

What is the cause? What should you do?

A

Neuroleptic Malignant Syndrome (NMS)

Cause

  • Probably due to D2 block in hypothalamus

Treatment

  • Stop drug IMMEDIATELY
  • Give Bromocriptine or dantrolene
  • DO NOT GIVE ANTICHOLINERGICS
67
Q

Which types of APS should you be wary of with an epileptic patient or a patient withdrawing from CNS depressant?

A

low potency APS and clozapine because it can lower the seizure threshold

68
Q

What are the two late occuring neurological side effects of APS?

A
  1. Perioral syndrome (Rabbit syndrome)
  2. Tardive dyskinesia

**note that not all of these side effects are present for all drugs**

69
Q

If a patient is experiencing Perioral syndrome (rabbit syndrome), how might you treat?

A

Antiparkinson drugs often helpful

70
Q

What is crucial with regard to Tardive Dyskinesia? Why?

_______

What should you NEVER give a patient with Tardive Dyskinesia? Why?

A

Prevention is CRUCIAL b/c treatment is unsatisfactory

_______

NEVER give an anticholinergic; this will only make the balance worse by supressing the cholinergic interneuron on GABAergic outflow.

71
Q

How can EPS be treated?

A

EPS can be treated by adding an anticholinergic

72
Q

What symptom could result from alpha 1 receptor blockade?

A

orthostatic hypotension+reflec tachycardia (dangerous in elderly)

73
Q

Three ANS side effects of APS drugs

A
  1. Alpha: Orthostatic hypotension + reflex tachycardia
  2. Alpha: Altered sexual function by preventing ejaculation without affecting erection
  3. Anticholinergic effects (dry mouth, blurred near vision, constipation, and urinary retention)

**note that not all of these side effects are present for all drugs**

74
Q

One endocrine side effect of APS

A

Increased prolactin secretion which results in galactorrhea and amenorrhea in women (due to D2 receptor blockade)

**note that not all of these side effects are present for all drugs**

75
Q

Which drug does NOT increase PRL (prolactin) secretion?

A

Olanzapine

76
Q

Which drugs cause an increased risk of diabetes AND hyperlipidemia?

A

Primarily high risk in Olanzepine and Clozapine, but low risk exist in all atypicals

77
Q

Which drug may cause a potentially fatal agranulocytosis? As a result, how must this drug be monitored?

A

Clozapine

Weekly white blood cell counts

78
Q

Which transmitters are most likely to be dysregulated in schizophrenia?

a) Serotonin and Norepinephrine
b) Serotonin and Dopamine
c) Acetylcholine and Dopamine
d) GABA and Dopamine

A

b) Serotonin and Dopamine

79
Q

Of the following antipsychotic drugs, which is/are considered atypical or second generation?

  1. Haloperidol
  2. Chlorpromazine
  3. Risperidone
  4. Aripiprazole
A

Risperidone and Aripripazole

80
Q

Which of the following is considered a neurological side effect of treatment with an antipsychotic?

a) diabetes
b) orthostatic hypotension
c) phototoxicity
d) tardive dyskinesia

A

d) tardive dyskinesia

81
Q

A patient develops extrapyramidal symptoms while taking his haloperidol. Which of the following is NOT an appropriate strategy?

  1. increase his dose of haloperidol
  2. switch patient to ariprazole
  3. switch patient to a low dose of risperidone
  4. Administer an anticholinergic
A

Option 1: increase his dose of halperidol

82
Q

What is the mechanism underlying tardrive dyskinesia?

  1. 5-HT receptor blockade
  2. dopamine receptor supersensitivity
  3. high levels of GABA release in striatum
  4. D2 blockade in hypothalamus
A
  1. dopamine receptor supersensitivity
83
Q

What are four other potential side effects of APS?

A
  1. blood dyscrasias (agranulocytosis)
  2. metabolic (weight gain/diabetes/hyperlipidemia)
  3. skin reactions/phototoxicity
  4. cardiac toxicity

**note that not all of these side effects are present for all drugs**

84
Q

Which APS is sometimes used in an acute psychotic episode for treatment?

A

Chlorpromazine (thorazine)

85
Q

Describe absorption of APS

A

Somewhat erratic; decreased by food, antacids, anticholinergics

86
Q

Where do APS drugs concentrate (what kind of tissues?)

A

Fatty tissues; APS highly protein bound

87
Q

APS drugs are:

  • Oxidized or demethylated by _________ system
  • conjugated by ______
A
  • hepatic microsomal system
  • glucocuronic acid
88
Q

APS drug interactions:

Potentiation with what?

A

CNS depressants

89
Q

APS drug interactions:

What enhances metabolism of APS

A

Barbiturates

90
Q

APS drug interactions:

What can interfere with digitalis?

A

Ziprasidone; quinidine-like effect in some drugs

91
Q

APS drug interactions:

Which agents are enhanced by alpha 1 block properties of APS?

A

antihypertensive agents

92
Q

APS drug interactions:

What can be exacerbated if patient is on other anticholinergics by an APS drug with muscarininc block?

A

confusion

93
Q

List the APS drugs of the section

A

1st Gen “Typical”

  1. Chlopromazine
  2. Haloperidol

2nd Gen “Atypical”

  1. Clozapine
  2. Risperidone
  3. Olanzapine
  4. Ziprasidone
  5. Aripiprazole

Pharmacology - Exam 2 (14 decks)

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