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Mental Health > Typical and atypical Psychotics > Flashcards

Typical and atypical Psychotics Flashcards

1
Q

High potency typical antipsychotics

A

Haloperidol strongest potency

Fluphenazine

Trifluroperazine

“Hal Tries to Fly HIGH”

Block Dopamine D2 receptors and need very little doses to take affect

tend to have more EPS symptoms as ADRs

also tend to have higher chances of developing neuroleptic malignant syndrome in genetically predisposed patients

lower off target ADR profile

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2
Q

Indications for antipsychotics

A

Schizophrenia

  • typical only treats primary symptoms, atypical treats both primary and secondary. therefore atypical antipsychotics are preferred and first-line.
  • *clozapine specifically for treatment-resistant schizophrenia

Psychosis
- drug-induced
- Parkinson-induced (best used is quetiapine)
- depression-induced
- dementia-induced
(Must be careful in dementia thou since elderly with dementia-related psychosis treated with atypical antipsychotics have increased stroke risk)

Bipolar disorder

Delirium

Tourette syndrome

Huntington’s disease

OCD

Manic episodes

  • atypicals are is first line in non pregnant patients
  • haloperidol is first line in 1st trimester pregnant patients
  • quetiapine is first line in all trimesters

Anxiety and Irritability in severe autism for children 6-17 yrs
- risperidone and aripiprazole are the best

Pruritis

  • blocks histamine receptors
  • NOT first line

Intractable hiccups
- chlorpromazine only (after trying everything else in the book)

Preoperative sedatives

Possess Antiemetic effects: (lowers vomiting/nausea) in patients with syndromes that are assocaited with increased vomiting/nausea

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3
Q

Targets for typical antipsychotics

A

D2 receptors that are most commonly found in the mesolimbic and mesocortical pathways
- also blocks the dopamine receptors in the nigrostriatal pathway and tuberoinfundibular which causes the ADRs

because of this, positive symptoms go away, but negative symptoms often stay or get worse

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4
Q

Mesolimbic and mesocortical pathway

A

Controls motivation and desire and the emotions of the patient

  • common site for antipsychotic treatments
  • mesolimbic dysregulation due to hyperactivity of dopamine receptors causes the positive symptoms seen in schizophrenia and psychosis.
  • mesocortical dysregulation due to hypoactivity of dopamine receptors causes the negative symptoms seen in schizophrenia and psychosis.

this is why adding levodopa/amphetamines/bromocriptine/apomorphine (dopamine agonists) to a non-psychotic patient can induce psychosis as a symptom

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5
Q

Drugs that can induce psychosis de novo or increase schizophrenia psychosis

A

Levodopa

Amphetamines

Bromocriptine

Apomorphine

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6
Q

Nigrostriatal pathway

A

Pathway that is used by motor neurons that bypass the medullary pyramids

Controls involuntary movements and coordination
- blocking of this pathway via antipsychotics can induce EPS and motor disturbance ADRs.

  • The site of ADRs associated with EPS symptoms*
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7
Q

Tuberoinfundibular pathway

A

Pathway that keeps prolactin in check by releasing dopamine
- bloackage of D2 receptors causes hyperprolactinemia

more common in high potency typical and atypical antipsychotics (haloperidol, risperidone, etc.)

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8
Q

Medullary periventricular pathway

A

Pathway that regulates eating behavior

blocking this pathway causes over indulgence in eating and lowered metabolism, hence why obesity, hyperglycemia and dyslipidemia are common ADRs among antipsychotics

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9
Q

Low potency typical antipsychotics

A

Thioridazine

Chlorpromazine

Thiothixene

“Cheating Thieves are LOW”

Block dopamine (D2) receptors and require high doses to take effects

tend to have lower on target ADR profiles (EPS “ADAPT” and hyperprolactin), but higher off target profiles (sedation/weight gain/ANTI-SLUD/orthostatic hypotension/etc).

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10
Q

EPS side effects of antipsychotics

A

“ADAPT”

Typical antipsychotics cause these ADRs more often than atypical

1) hours -> days after beginning treatment
- Acute Dystonia (muscles spasms) of the face/tongue/neck/back, and/or oculogyric crisis
* treatment = benzotropine or diphenhydramine*
* *also can give amantadine, but not 1st line since it can override the antipsychotic**

2) days -> months after beginning treatment
- Akathisia (restlessness)
* treatment = BBs, clonazepam or benzotropine*

  • Parkinsonism (bradykinesia and mask facies)
  • treatment = Benzotropine or amantadine*

3) Months -> years after beginning treatment
- Tardive dyskinesia (chorea often of the face, but can be of the body also)

  • must discontinue use if #3 is seen, since it is irreversible*
  • # 1-2 are treatable and reversible*

** amantadine (dopamine agonist) also works in replacement of benztropine, however it less used since it counters the antipsychotic drug effect directly where as benztropine does not (anticholinergic drug)

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11
Q

Neuroleptic malignant Syndrome (NMS)

A

A life-threatening EPS that can occur in patients who have a pregenetic disposition for it and take antipsychotics
- more common in high potency typical agents

“Looks like severe Parkinsonism with autonomic instability”

Basic Symptoms: (starts days-> weeks after tx)

  • confusion
  • seizures
  • agitation
  • hyporeflexia*
  • normal pupils*
  • hyperthermia throughout body
  • = ways to tell this apart from serotonin syndrome *

Severe symptoms: (starts days-> weekly after tx)

“Malignant FEVER”

  • Myoglobinuria
  • Fever
  • Encephalopathy
  • Vitals are unstable
  • increased Enzymes
  • muscle Ridgitiy
  • death = coma

Treatment:

  • take off medication and give dantrolene or bromocriptine
  • the earlier caught the better

Note: that even with proper treatment, NMS can still persist for more than a week after proper treatment. If this is the case = high mortality so need to watch patient closely.

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12
Q

Non-dopamine related side effects of antipsychotics

A

Orthostatic hypotension and lightheadedness :
- blockage of a1 receptors

Anti cholinergic (ANTI-SLUD)
- blockage of Muscarinic receptors

Sedation and weight gain

  • blockage of Histamine H1 receptors
  • low potency antipsychotics have a high chance of causing this*

Prolonged QT intervals

Metabolic disorders
- hyperglycemia/dyslipidemia

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13
Q

What are the specific ADRs associated with chlorpromazine and thioridazine?

A

Corneal and retinal calcium deposits respectively

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14
Q

Atypical psychotics

A

Aripiprazole

  • highest D2 potency of atypicals
    • is a dopamine and 5-HT(1a) partial-agonist*
  • antagonist at all receptors it hits

Asenapine

Clozapine

  • lowest D2 potency of atypicals
  • highest D4 receptor potency

Olanzapine

  • highest serotonin inverse agonism
  • binds strongest to 5-HTA2 receptors

Quetiapine

  • highest histamine potency, lowest serotonin inverse agonism
  • highest odds of sedation and weight gain among atypicals
  • least likely to cause EPS of all antipsychotics
    • best used in patients who have Parkinson-induced psychosis

Iloperidone

Paliperidone

Risperidone
-high potency for D2 as well

Lurasidone

Ziprasidone

  • MOA is not fully understood but most work as inverse agonists for serotonin (5-HT2A) and antagonists for dopamine (D2 and D4) receptors*
  • apripiprazole = partial dopamine agonist
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15
Q

Why does atypical antipsychotics possibly work on negative symptoms of schizophrenia?

A

Blocks the inhibitory serotonin neurons located in the mesocortical Pathway
- these neurons keep dopamine levels low when active, but when blocked raise levels of dopamine in the pathway. This “cures” the negative symptoms

note: it doesn’t actually cure, rather than just not make them get worse or slightly improve them

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16
Q

Clozapine only specific ADRs

A

Agranulocytosis, leukopenia, granulocytopenia, and dose-related seizures

    • rare but fatal*
  • must monitor WBCs and bone marrow while on it.
  • ** discontinue if the WBC count is below 3,000cells/mm or granulocyte is below 1500cells/mm**
  • patients are also more susceptible to atypical infections

Myocarditis and cardiomyopathy

  • rare but fatal if not caught
  • must monitor patients for chest pain, dyspnea, fever, tachypnea

Severe small bowel constipation

  • can cause obstruction and subsequent rupture of intestines fatal
  • MUST use in conjunction with stool softeners if constipation develops.

because of these it is usually last-line only and used only for treatment resistant psychosis/schizophrenia

** also is known to cause drooling/hypersalivation, even though it has anti-cholinergic side effects. Treatment of this ADR = glycopyrrolate**

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17
Q

Tuberoinfundibular side effects of antipsychotics

A

Blockage of dopamine receptors in this pathway causes hyperprolactinemia since there is no regulation of this hormone present (dopamine is responsible for this)

Symptoms:

  • amenorrhea
  • galactorrhea
  • gynecomastia

risperidone is the most commonly associated antipsychotic with these symptoms (but all can cause it)

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18
Q

Why do typical antipsychotics generally cause more EPS symptoms than atypical antipsychotics

A

Because typical antipsychotics bind tightly to D2 receptors (non competitive binding), and atypical antipsychotics bind loosely (competitive binding) so atypical can be overridden in high doses of dopamine.

potency of typical = haloperidol > fluphenazine > chlorpromazine > thioridazine

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19
Q

What is unique about clozapine and olanzapine pertaining to ADRs?

A

These two are the most common antipsychotics to see metabolic syndrome in

  • weight gain
  • new onset diabetes
  • dyslipidemia
  • increase CV risks

must monitor weight, A1C, BMI

Contraindicted in patients with family/personal history of diabetes, dyslipidemia, CVD and uncontrolled HTN

20
Q

If a psychiatric patient is experiencing Parkinsonian symptoms from dopamine antagonist use, why should you NOT give dopamine agonists as treatment?

A

For reasons not fully understood, it actually makes the psychosis worse.

Instead, lower dose of dopmiane antagonist or switch antipsychotic completely and give anticholinergic drug benzatropine.

21
Q

Can you give benzatropine to a psychiatric patient experience tarditve dyskinesia?

A

NO

  • Doesn’t work must give valbenazine (VMAT inhibitors) and switch to atypical antipsychotic
  • reason for this is unknown*

can also switch to clozapine if severe tardive dyskinesia is present

22
Q

In adult psychiatric patients who are severely violent and have psychosis and need to be sedated, what IM mixture is given to them?

A

Lorazepam and Haloperidol

  • lorazepam to calm the patient down
  • haloperidol to quickly act on the psychosis

NOTE: Haloperidol is contraindicated in Parkinson patients, whom can show psychosis episodes due to overuse of L-dopa. In this case just give lorazepam

23
Q

Chlorpromazine specific ADRs

A

Blue pigment changes in cyanotic patients

Severe photophobia
- causes 3rd degree burns in extensive sun exposure

24
Q

Which atypical antipsychotics are the best at treating acute manic episodes?

A

Olanzapine and risperidone

25
Q

How often do you monitor clozapine patients for agranulocytosis?

A

Once a week for first 6 months

Once every 2 weeks for the next 6 months

Once every month Indefinitely afterwards

if it is discontinues, must check weekly for at least 4 weeks from discontinuation or until WBC = 3500 or greater

26
Q

What are all the receptors that clozapine specifically acts on

A

D1

D2

D4

Histamine-1

Muscarinic

A1 receptors

5-HT(2/3)

27
Q

Which atypical antipsychotic is often first line in Parkinson patients with psychosis or schizophrenia patients with Parkinsonian symtpoms?

A

Clozapine

  • spares the nigrostriatal dopaminergic system for unknown reasons
  • only one to do this
28
Q

How to treat hyperprolactinemia ADR in psychotic patients

A

Reduce dose of current antipsychotic or change antipsychotic altogether.

If not feasible to either above, give bromocriptine in conjunction or use aripiprazole.

29
Q

What ADRs are chlorpromazine and thioridazine more closely associated with and why?

A

Sedation, weight gain, dyslpidemia, hypertriglyceride.

Due to low potency typical antipsychotics having a stronger effect on H1 receptors

thioridazine is hardly ever used though since it has also the highest rates of QT elongation and torsades de pointes production

30
Q

What is the most commonly used typical antipsychotic?

A

Haloperidol

  • has the highest incidence of EPS symptoms thou
  • lowest potential for weight gain, sedation and orthostasis

Used most often since it is the best for LAI dosage in non compliant patients (only have to give every month instead of weekly)

31
Q

Difference between atypical and typical antipsychotic MOAs

A

Typical = antagonism of the D2 receptors

Atypical = antagonism of the D2 receptors and inverse agonism of the 5-HT(2a) receptors
- inverse agonism = antagonizes agonist molecules and stabilizes the transmitter in its inactive form (kind of like an indirect non-competitive antagonist)

32
Q

Dopamine hypothesis Of schizophrenia

A

Positive symptoms (hallucinations/delusions) are a cause of hyperactivity of dopamine in the mesolimbic pathway

Negative symptoms (emotional blunting, social withdrawal, lack of motivation, altered working memory) Are a cause of hypofunction of dopamine in the prefrontal cortex/ mesocortical pathway

33
Q

What formulations for antipsychotics should be used for select patient populations?

A

IM = emergency interventions or agitated inpatients

ODT = for paranoid inpatients and patients who hide normal oral tablets in their cheeks “cheeking”

LAI = for non compliant patients

34
Q

Which antipsychotic is allergic responses reported with?

A

Clozapine

35
Q

difference between EPS symptoms and dystonia/akathesia vs tardive dyskinesia

A

EPS = blockage of dopamine receptors acutely causes DA/ACh balance to be off

  • ACh > DA
  • this causes sustained contractions and motor restlessness
  • is reversible*

Tardive dyskinesia = blockage of dopamine receptors chronically causes sensitization of dopaminergic receptors

  • neuronal motor responses now are hyper sensitive to dopamine vs cholinergic ACh receptors
  • DA> ACh (due to excess dopamine receptors rather than excess dopamine physically)
  • causes excess and involuntary movements of the jaw mouth and tongue mostly.
  • is almost always irreversible*
36
Q

VMAT inhibitors

A

Are vesicle molecular amine transport inhibitors that block dopamine from being released in synapses

Includes:

  • valbenazine
  • deutetrabenazine

for mental healthy, just known these are used to treat tardive dyskinesia, with low efficacy, but are textbook treatment.

37
Q

Behavioral toxicity from antipsychotics

A

Blockage of both D1 and D2 receptors can result in:

  • akinesia: (apathy, withdrawal, depression)
  • dysphagia: (state of unease/dissatisfy)
  • confusion
  • “pseudo-dementia”

more common in typical antipsychotics than atypical

38
Q

Cardiovascular effects of antipsychotics

A

Low potency typical antipsychotics more commonly affect a1 receptors
- causes orthostatic hypotension and tachycardia

39
Q

How does inverse agonism work for atypical antipsychotics?

A

Prevents agonists to bind and forces the receptors into the inactive form.

Are actually more effective antagonists than antagonists themselves

As it pertains to atypical antipsychotics, they are inverse agonists for 5-HT(2a) receptors
- reduces serotonin receptor activity and therefore turns off glutamtergic neurons and slightly lowers dopamine activity as well.

40
Q

Olanzapine specific ADRSs

A

Somnolence and increased anti-SLUD

Increased chances of developing diabetes

Elevated AST levels

  • Cardiorespiratory arrest and sudden death*
  • rare but MUST catch if develops. Must monitor closely for at least 3 hours when it will develop usually
41
Q

Quetiapine specific ADRs

A

is the preferred agent in patients with Parkinson disease who develop psychosis

High odds of sedation and weight gain

Also very high chances of DDIs with drugs that also increase QTc intervals
- contraindicated in patients using other drugs that prolong QT interval

42
Q

What antipsychotics are usually first line in non-specific first break psychosis in younger patients?

A

Risperidone and aripiprazole

  • due to rather Low chances of EPS
  • does have high prolactin secretion thou

Also shows fewer relapses

43
Q

how are most antipsychotics metabolized?

A

First-pass through CYP2D6, CYP1A2 AND CYP3A4

are highly lipid soluble so not very blood bound (be careful with commitment use with warfarin)

44
Q

average time of relapse after getting of antipsychotic drugs if they come back

A

6 months

Exception is clozapine which is faster

45
Q

Factors contributing to selecting the proper antipsychotic for clinical use

A

1) patient response
- all antipsychotic drugs have similar efficacy, but response can vary based on patient to patient
- also cost is and availability

2) ADR avoidance
- while all antipsychotic drugs have similar efficacy, they vary in mechanism and ADR profile
- always try to begin with “best” ADR profile and move to “worse” if needed

3) acute psychotic episode vs chronic maintance
- time spent on a drug matters for ADRs
- combination therapy should only be used in refractory patients

4) situation for dose:
- IM = emergency intervention/agitated aggressive patients
- ODT = paranoia patients
- LAI = noncomplaint patients

46
Q

Overdose of antipsychotics

A 
Rarely fatal (with the exception of thioridazine) 
- induces fatal ventricular tachyarrhythmias

Symptoms:

  • drowsiness -> coma (if not treated)
  • agitation
  • NMJ excitability -> convulsions (if not treated)
  • mitotic pupils and DTR decrease
  • hypotension and hypothermia

Mental Health (46 decks)

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