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Fall P2 > IDT - Antipsychotics Filtz > Flashcards

IDT - Antipsychotics Filtz Flashcards

1
Q

Mental Disorder characterized by rifts in rational thought, inappropriate processing of sensory info, and disturbed views of reality and self. Not recognized by the sufferer

A

Psychoses

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2
Q

Abnormal reaction to an external state that is generally recognized as abnormal by the sufferer

A

Neuroses

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3
Q

Psychotic Markers

(Positive) Over Symptoms

A 
Delusions
Paranoia
Hallucinations (auditory > visual)
Disordered thoughts
Loose Ideation
Innappropriate Emotional Responses
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4
Q

Association of a color/temperature/etc with a visual, taste or smell perceptions

A

Synesthesia

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5
Q

In what disease states is Psychoses often seen?

A 
Schizophrenia
Delirium (dementia)
Manic Psychoses
Secondary to severe depression
Post-Traumatic stress disorders
Drug-induced
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6
Q

What type of responses are often seen in Psychoses patients?

A 
Lashing out (verbally)
(less common) Violences in response to fear
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7
Q

What Drugs may induce a psychoses or psychotic symptoms?

A 
Amphetamine
Steroids
LSD
Ketamine
PCP
Sedative/Hypnotics
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8
Q

Why do Dementia patients often experience psychotic symptoms?

A

Delirium causes cognitive decline which may lead to hallucinations and delirium

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9
Q

Why might PTSD display psychotic symptoms?

A

Auditory hallucinations, etc, misinterpreting stimuli

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10
Q

What is the age of onset of Schizophrenia?

A

15-25 yo

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11
Q

What percentage of the population experience schizophrenia psychotic symptoms? What groups affected most?

A

~1% of the population

women and men affected equally

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12
Q

What is the mortality rate/prognosis of schizophrenia?

A

10%, poor long term prognosis

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13
Q

What type of behavior often precedes onset of psychoses?

A

“odd” behaviors

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14
Q

What are “negative” (residual symptoms) of schizophrenia?

A

Flat affect (same expression)
Anhedonia/Apathy (no care)
Anxiety
Lack of volition
Social and emotional withdraw (being called crazy)
Disorganized speech, thinking and behavior
Impaired attention (due to inner dialogue)
Poor Self-care

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15
Q

What is common Etiology of Schizophrenia?

A

Neurodevelopmental Disorders
Genetic Factors
Environmental Factors

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16
Q

What study showed that there are genetic and environmental factors in causation of schizophrenia?

A

Twin studies in monozygotic twins, which looked at anatomic irregularities where only one twin was affected by schizphrenia

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17
Q

What anatomic Irregularities can be seen in schizophrenic patients’ brains?

A

Enlarged Cerebral Ventricles
Reduced Cortical Mass
Hypofrontality (reduced processing in the prefrontal cortex)

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18
Q

What Treatment was often used in the 1940’s and 1950’s for psychoses expressing patients?

A

Frontal Lobotomy, separated prefrontal cortex, which drastically calmed patients, but permanently debilitated them by placing them in a zombie like state.

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19
Q

What Treatment options currently exist for those experiencing psychosis?

A
  • Frontal Lobotomy (not ethical)
  • Psychotherapy
  • Cognitive Behavioral Therapy (no psychoses)
  • Self-medication w/ Nicotine
  • Antipsychotics
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20
Q

When might Cognitive Behavioral therapy be useful?

A

Teaching patients –>
Social skills
Life skills (attendance, housing)
Ability to self-assess

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21
Q

What percentage of psychoses patients self medicate with nicotine?

A

90%

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22
Q

What is the primary effect of Antipsychotic Agents

A

Neuroleptics, Major Tranquilizers

Treat by calming psychotic symptoms
less effect on emotional or social problems

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23
Q

What percentage of individuals do Antipsychotic medications help effectively?

A

70% Respond eventually

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24
Q

What else can Antipsychotic agents be used for?

A

Supplementation with Anesthesia

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25
Q

What is the latency of effectiveness in Antipsychotic agents?

A

Calming (tranquilizing) effect may be seen within minutes to hours
Diminshed psychotic symptoms seen within 24-28 hrs

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26
Q

How long until full antipscyhotics effects evolve?

A

2-8 wks

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27
Q

How long may improvements from antipsychotics continue and what symptoms resolve?

A

6 months

  • fewer hallucinations
  • Less paranoia
  • More rational thinking
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28
Q

What is the action of ALL antipsychotic drugs?

A

D2 receptor antagonism

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29
Q

For the D2 Receptor Agonist drugs concentration to clinical dose curve, what is the most potent drug?

A

Spiroperidol

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30
Q

What Dopamingergic pathways may be changed by antipsychotics?

A

Mesocortical
Mesolimbic
Nigrostriatal
Tuberinfundibular

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31
Q

Where is the Mesocortical pathway?

A

Ventral Tegmental Area to frontal and prefrontal cortex, pathway responsible for reasoning (loose ideation when compromised)

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32
Q

Where is the Mesolimbic pathway?

A

Ventral Tegmental Area to N. Accumbens in limbic area

Pathway responsible for emotional response (social withdrawal and agitation when compromised)

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33
Q

Where is the Nigrostriatal pathway?

A

Substantia Nigra to Striatum (More EPS side effects with D2 antagonism)

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34
Q

Where is the Tuberoinfudibular pathway?

A

Hypothalamus to pituitary (Prolactin side effects with D2 antagonism)

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35
Q

What is the Dopamine Theory of Psychosis?

A

That Psychoses results from over-stimulated dopamine receptors in the cortex (reasoning) and limbic (emotional) areas.

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36
Q

What is Dopamine Hypofrontality?

A

A hypothesized lack of dopamine within the mesocortical pathway that leads to decreased cerebral blood flow

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37
Q

What is the explanation of “positive” psychoses symptoms?

A

Dopamine hyperactivity of mesolimbic that inhibits mesocortical pathway

38
Q

What is the role of Serotonin signaling in psychosis?

A

Some antipsychotics have affinity with 5-HT2 receptors

“Negative” symptoms associated with Serotonin dysfunction

39
Q

What is the role of Glutamate signaling in psychosis?

A

Glutamate antagonists act at NMDA receptors to exacerbate or produce psychoses

40
Q

What drug is known as the “grandparent” of all antipsychotics

A

Chlorpromazine

41
Q

First Gen Phenothiazines or Thioxanthines

A

Chlorpromazine
Thioridazine
Fluphenazine
Thiothixene

42
Q

What are and what is the advantage Butyrophenones?

A

Haloperidol; Pimozide

More D2 selective

43
Q

2nd Generation Dibenzazepine antipsychotics

A

Clozapine
Loxapine
Olanzapine
Quetiapine

44
Q

What are the side effects of blocking Dopamine in the Nigrostriatal pathway?

A
  • Problems with initiation and control of movement/muscle tone
  • Antagonism of D2 receptors in BG (EPS)
45
Q

What are the Acute Extrapyramidal side effects (EPS) of D2 antagonism?

A 
Akathisia (motor restlessness)
Dystonia 
Respiratory Distress
Pseudo-Parkinsonism
 - bradykinesia
 - resting tremor
 - flat affect
46
Q

How do EPS and Dose changes affect individuals?

A

See more EPS with high dose bolus.

Decreasing dose, changing drugs and adding anti-Parkinson agents may help EPS

47
Q

Who are more likely to experience EPS?

A

Women are more sensitive than men.

48
Q

What can EPS lead to?

A

Irreversible Tardive dyskinesias (involuntary movements of tongue, lips, head and neck)

49
Q

What type of drugs can be used to reduce EPS?

A

Muscarinic receptor agonists are inversely correlated with EPS

50
Q

In general, which generation of antipsychotics cause less EPS?

A

2nd Gen

51
Q

How might you treat Tardive Dyskinesia?

A

Withdrawal or reduction in dose of antipsychotic medications
Administration of a-colinomimetic
Vitamin B6 supplementation

52
Q

What normally inhibits Pituitary D2 receptors?

A

Prolactin

  • prolactin levels > 100 ng/ml prolactinomas, increase risk of breast cancer
53
Q

When there is a blockade of D2 inhibition there is?

A

An increased prolactin release

  • gynecomastia and increased lactation
  • disturbed thermal regulation (hypo/hyperthermia)
  • Amennorhea (weird menstruation), infertility and sexual dysfunction
54
Q

When prolactin levels > 100 ng/ml or more

A

Prolactinomas increases the risk of breast cancer

55
Q

On average 2nd generation Antipsychotics have higher?

A

Affinity for 5-HT2 receptors

  • have somewhat lower affinity for D2 dopamine receptor
  • generally, have lower incidence of EPS and endocrine side effects
56
Q

What is recommended as first line therapies for Antipsychotics?

A

2nd generation antipsychotics

- have other side effects

57
Q

Where is the Serotonergic CNS pathways projected from and to?

A 
From the dorsal raphe nuclei in brainstem 
to: 
pre-frontal cortex
Hypothalamus
Limbic areas
Spinal Reflex areas
Basal Ganglia
58
Q

Where is the Serotonergic CNS pathways projected to?

A

pre-frontal cortex, hypothalamus, limbic area, spinal reflex areas and basal ganglia

59
Q

What does the 5HT2 receptors modulate?

A

Dopamine

60
Q

Why are there fewer EPS with antipsychotics that combine 5-HT2 antagonism

A

there is lower affinity D2 antagonism due to 5-HT modulation

61
Q

When there is lower affinity D2 antagonism and more 5HT2 antagonism…

A

5-HT modifies dopamine release in the basal ganglia

62
Q

What Autonomic Effects can be seen from use with antipsychotics?

A

alpha 1 adrenergic antagonism

muscarinic cholinergic antagonism (inc temp, dry skin, cant see, flushing, unstable mood)

63
Q

What can Histamine H1 antagonism lead to?

A

Sedation
Drowsiness
Weight gain
Anti-Nausea

64
Q

When might sedation therapy be difficult or useful in psychoses patients?

A

Difficult –> Patients on prophylactic or chronic therapy, where condition is well controlled.
Useful –> Acute treatment of florid psychoses w/ agitation

65
Q

Why is weight gain/metabolic disorder seen with antipsychoses patients?

A

Serotonin, H1 histamine and alpha 1 adrenergic receptors are blocked

66
Q

What is the result of blockage of serotonin, H1 histamine and alpha 1 adrenergic receptors on metabolism?

A 
Increased appetite
Inc Fat storage
Sleep Apnea
Hypercholesterolemia
Insulin insensitivity and hyperglycemia
67
Q

What antipsychotics are associated with large weight gains?

A

Clozapine, Olanzapine, Chlorpromazine and Thioridazine

68
Q

What APs are associated with moderate weight gains?

A

Risperidone, Quetiapine, Paliperidone, Iloperidone

69
Q

What APs are seen as weight neutral?

A

Ziprasidone, Aripiprazole, Haloperidol, Asenapine

70
Q

Which APs may cause a large increased risk of sudden cardiac death by prolonged QT intervals?

A

Ziprasidone, pimozide, Thioridazine

71
Q

What levels should be monitored in patients on antipsychotic therapy?

A

Lipids
Weight
HbA1c
Blood Pressure

72
Q

What potential fatal cardiotoxicities are exacerbated with use of antipsychotics?

A

Increased QT interval, (Torsades de Pointe)

Black box warning on Antipsychotics

73
Q

Which patient population is on the black box warning for antipsychotic agents?

A

Dementia Patients, elderly

drastically increased mortality rates

74
Q

What is Neuroletpic Malignant syndrome?

A

A rare syndrome that recurs w/ 10% mortality rate in patients with severe EPS

75
Q

What are the symptoms of Malignant Syndrome?

A

Manifestations of Hyperthermia and Diaphoresis (sweating)
Altered Mental Status
Tremors/Muscle rigidity
Acute Renal Failure

76
Q

What is the treatment for Maligant Syndrome?

A

Discontinuation of Antipsychotic medications (patient untreatable)
Dantrolene or Bromocriptine

77
Q

Where do the majority of Hypersensitivity reactions in antipsychotics occur?

A

Phenothiazines
Dermal Reactions (rash and photosensitivity)
Asenapine (serious hypersensitivity/anaphylaxis)

78
Q

What is Clonidine?

A

an Alpha 2 agonist (review for P3 year)

79
Q

Advantages, Toxicities and features of Clozapine?

A

Uniquely effective in 25-30% of treatment-resistant patients (No EPS)
Serious Toxicity!!
- Leukopenia (required WBCs)
- Myocarditis (heart inflammation)
- Cardiovascular Collapse (BP crashes)
- Decreased Seizure threshold
May cause sedation/antimuscarinic effects (constipation)

80
Q

Advantages, Toxcities, and features of Olanzapine?

A

No toxicities of Clozapine
2nd most effective of antipsychotics (not as good as Clozapine)
Weight gain is VERY problematic

81
Q

Advantages and use of Quetiapine?

A

Very Sedating (anxiolytic)
Low EPS
Low adrenergic blockage
Moderate weight gain/Risk of metabolic syndrome

82
Q

Risperidone Pros and Cons?

A

+ Lack of sedations
- restlessness/agitation
- dose needs to be controlled to avoid EPS
+ approved for irritability in autism spectrum disorders (5yo+)

83
Q

Paliperidone Pros and Cons?

A

+ Lack of sedation
+ Sustained release, once monthly dosing
- Restlessness/agitation
- EPS

84
Q

Ziprasidone/Lurasidone Pros and Cons?

A

+ low weight gain
+ Low EPS
- Problems with QT prolongation (Lurasidone less)

85
Q

Iloperidone Pros and Cons

A 
\+ Low EPS
\+ Low anti-cholinergic
\+ low weight gain
\+ low tendency for Metabolic Syndrome
- Hypotension (alpha 1 antagonism)
- Requires dose tiration
86
Q

Asenapine Pros and Cons

A 
\+ Minimal weight gain or metabolic disturbance
\+ Off label to treat PTSD
- Extreme Sedation
- Serious Hypersensitivity
- EPS
- Not very efficacious
87
Q

Aripiprazole Pros and Cons

A 
\+ Good Efficacy
\+ partial D2 agonist
\+ No receptor Sensitization
\+ No endocrine disturbances
\+ Low EPS
- transient Nausea
- Agitating
- alpha 1 antagonism
88
Q

Brexipiprazole Pros and Cons

A 
\+ partial D2 agonist
\+ low risk EPS
- alpha 1 antagonism
\+ low affinity for histamine receptors
- weigh gain, akathesia as side effects
89
Q

Cariprazine Factoids

A

+ D2 partial agonist, 5HT1a Partial agonist, 5HT2 antagonist
+ Low EPS
+ low weight gain
- D3 partial agonist with higher affinity for D3R than D2R

90
Q

APA top 5 recommendatons for choosing wisely

A

1) don’t prescribe APs without appropriate initial evaluation and ongoing monitoring
2) No routine prescribing 2 or more APs
3) No Aps as first choice for behavioral and psychological symptoms of dementia
4) No routine prescription of APs as first line intervention for insomnia
5) No routine prescription as first line intervention for children or adolescents for anything other than psychotic disorders

91
Q

What other indications are APs used for?

A 
Tourette's 
Neuroletanesthesia
Antidpressants (no monotherapy)
Behavioral problems
Bipolar disorder
Severe Nausea/Vomitting
Intractable hiccups
Insufficient lactation

Fall P2 (13 decks)

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