Atypical & Typical Antipsychotics Flashcards

Question

Tardive Dyskinesia

Answer 1

Extrapyramidal side effect Can be IRREVERSIBLE Constant involuntary periorbital muscles CHEWING TARdive Treated with Benadryl

Answer 2

Confusion, Agitation, Hyperthermia (>105 F), Muscular Ridgity, Seizures + Recent Antipsychotic use = NMS! Tx w/ Dantrolene (hint DANtrolene Never Missed a Step)

Answer 3

PO before DEPOT PO to confirm they can tolerate the med b4 giving the med as a Depot IM injection that will be in place and affecting the pt for weeks

Answer 4

FGAs Affects DA-, Ach-, NE-, His- Wide Side Effect Profile Sediment Deposits in Cornea - (hint CHLOR-neal Deposits)

Answer 5

FGAs Affects DA-, ACH- Side effect - retinal deposits (Thioridazine= reTinal deposits

Answer 6

FGAs Affects DA- (more D2 receptor-specific) HOLDol Less anticholinergic, Antihystamic, and Antinoredergic affects Higher rate of extrapyramidal side effects Depot formula is the Decanoate = DECAde

Answer 7

SGAs affects DA- & SE partial agonist Most effective agent against schizophrenia The deadly side effect of agranulocytosis (the loss of all WBC) * watch it CLOZely for agranulocytosis never 1st line Must be registered and the ANC checked prior and serial ANC throughout the 1st year D/C immediately if ANC falls below 1500

Answer 8

SGAs DA- SE+ Second only to clozapine in efficacy but without the side effect of agranulocytosis IS a 1st line treatment for schizophrenia Highest of all prescribed but also the worst for weight gain without increased caloric intake Think Olanzapine and an Obesie person O for Obesity

Answer 9

SGAs DA- SE- NE- His- RISe & Shine (less sedation) RISe to a Pair Low EPS sx High Metabolic syndrome High relation to Gynocomystomy

Answer 10

SGAs DA- SE- NE- HIS- Low EPS sx High Metabolic syndrome Quetiapine = Quiet time (increased sedation)

Answer 11

SGAs DA- SE- NE- HIS- Low EPS sx High Metabolic syndrome Prolongs QT interval Geodon think GEOmetro a Zippy Car (reminding u to do an EKG

Answer 12

Third Generation As DA partial agonist, SE partial agonist Helps with maintenance therapy not acute psychosis Think And Abilify for dopamine and serotonin Antidepressant AND Abilify for refractory cases of MDD

Answer 13

Psychosis is a syndrome, a mixture of symptoms that can be associated with many different psychiatric disorders but is not a specific disorder itself in DSM or ICD diagnostic criteria.

Answer 14

At a minimum, delusions and hallucinations and generally includes symptoms such as disorganized speech, disorganized behavior, and gross distortions of reality.

Answer 15

Paranoid Psychosis - Paranoid Projections; Hostile Belligerence & Grandiose Expansiveness Disorganized/Excited Psychosis - Conceptual Disorganization, Disorientation, Excitement Depressive Psychosis - Psychomotor retardation & Apathy; Anxious Self-Punishment & Blame

Answer 16

Paranoid Projections; Hostile Belligerence & Grandiose Expansiveness

Answer 17

Conceptual Disorganization, Disorientation, Excitement

Answer 18

a mixture of symptoms that are commonly divided into two major categories: Positive and Negative symptoms

Answer 19

Delusion and hallucinations, reflect the development of the symptoms of psychosis; they can be dramatic and may reflect a loss of touch with reality.

Answer 20

Reflect the loss of normal functions and feelings, such as losing interest in things and not being able to experience pleasure. Think alogia, affective blunting or flattening, asociality, anhedonia, avolition & attentional impairment.

Answer 21

The poverty of speech, (talks little, uses few words) Dysfunction of Communication Neg Sx of Schizophrenia

Answer 22

Reduced range of emotions (perception, experience, and expression) ex - feels numb or empty inside, recalls few emotional experiences, good or bad Dysfunction of Affect Neg Sx of Schizophrenia

Answer 23

Reduced social drive and interactions ( little sexual interest, few friends, little interest in spending time with (or little time spent with) friends) Dysfunction of socialization Neg Sx of Schizophrenia

Answer 24

Reduced ability to experience pleasure (finds previous hobbies or interests unpleasurable Dysfunction of capacity for pleasure Neg Sx of Schizophrenia

Answer 25

Reduced desire, motivation, and persistence, (reduced ability to undertake and complete everyday tasks, may have poor personal hygiene) Dysfunction of motivation Neg Sx of Schizophrenia

Answer 26

Positive symptoms - mesolimbic Negative symptoms - mesocortical/ prefrontal cortex Cognitive sx - the dorsolateral prefrontal cortex Aggressive sx - orbitofrontal cortex Affective sx - the ventromedial prefrontal cortex

Answer 27

he mesolimbic dopamine pathway, the mesocortical dopamine pathway, the nigrostriatal dopamine pathway, the tuberoinfundibular dopamine pathway, and a fifth pathway that innervates the thalamus.

Answer 28

The mesolimbic dopamine pathway projects from dopaminergic cell bodies in the ventral tegmental area of the brainstem to axon terminals in one of the limbic areas of the brain, namely the nucleus accumbens in the ventral striatum This pathway is thought to have an important role in several emotional behaviors, including the positive symptoms of psychosis, motivation, pleasure, and reward. It has long been observed that diseases or drugs that increase dopamine will enhance or produce positive psychotic symptoms, whereas drugs that decrease dopamine will decrease or stop positive symptoms. For example stimulant drugs such as amphetamine and cocaine release dopamine, and if given repetitively can cause a paranoid psychosis virtually indistinguishable from the positive symptoms of schizophrenia. All antipsychotic drugs capable of treating positive psychotic symptoms are blockers of the dopamine D2 receptor. These observations have been formulated into a theory of psychosis sometimes referred to as the “dopamine hypothesis of schizophrenia” or “mesolimbic dopamine hypothesis of positive symptoms of schizophrenia.” Hyperactivity of the mesolimbic dopamine pathway hypothetically accounts for positive psychotic symptoms whether those symptoms are part of the illness of schizophrenia, or of drug-induced psychosis, or whether they are positive psychotic symptoms accompanying mania, depression, or dementia. Hyperactivity of mesolimbic dopamine neurons may also play a role in aggressive and hostile symptoms in schizophrenia and related illnesses.

Answer 29

positive psychotic symptoms whether those symptoms are part of the illness of schizophrenia, or of drug-induced psychosis, or whether they are positive psychotic symptoms accompanying mania, depression, or dementia.

Answer 30

play a role in aggressive and hostile symptoms in schizophrenia and related illnesses.

Answer 31

cell bodies in the ventral tegmental area, but projecting to areas of the prefrontal cortex, is known as the mesocortical dopamine pathway. Branches of this pathway into the dorsolateral prefrontal cortex are hypothesized to regulate cognition and executive functions. Branches of this pathway into the ventromedial parts of the prefrontal cortex are hypothesized to regulate emotions and affect. Many researchers believe that cognitive and some negative symptoms of schizophrenia may be due to a deficit of dopamine activity in mesocortical projections to the dorsolateral prefrontal cortex, whereas affective and other negative symptoms of schizophrenia may be due to a deficit of dopamine activity in mesocortical projections to the ventromedial prefrontal cortex.

Answer 32

A deficit of dopamine activity in the mesocortical projections to the dorsolateral prefrontal cortex, whereas affective and other negative symptoms of schizophrenia may be due to a deficit of dopamine activity in the mesocortical projections to the ventromedial prefrontal cortex.

Answer 33

cell bodies in the ventral tegmental area, but projecting to areas of the prefrontal cortex, is known as the mesocortical dopamine pathway. Branches of this pathway into the dorsolateral prefrontal cortex are hypothesized to regulate cognition and executive functions. Branches of this pathway into the ventromedial parts of the prefrontal cortex are hypothesized to regulate emotions and affect. Many researchers believe that cognitive and some negative symptoms of schizophrenia may be due to a deficit of dopamine activity in mesocortical projections to the dorsolateral prefrontal cortex, whereas affective and other negative symptoms of schizophrenia may be due to a deficit of dopamine activity in mesocortical projections to the ventromedial prefrontal cortex.

Answer 34

regulate cognition and executive functions.

Answer 35

to regulate emotions and affect.

Answer 36

Theoretically, increasing dopamine in the mesocortical dopamine pathway might improve negative, cognitive, and affective symptoms of schizophrenia. However, since there is hypothetically an excess of dopamine elsewhere in the brain – within the mesolimbic dopamine pathway – any further increase of dopamine in that pathway would actually worsen positive symptoms. How does one increase dopamine in the mesocortical pathway while simultaneously decreasing dopamine activity in the mesolimbic dopamine pathway? Enters the Atypical Antipsychotics -

Answer 37

Excess Glutamate Decreased GABA NMDA receptor antagonist PCP has been shown to induce the positive, negative, and cognitive symptoms of schizophrenia in healthy patients and cause a resurgence of symptoms in stable patients. These observations led to the NMDA receptor hypofunction hypothesis as an alternative theory for the underlying cause of schizophrenia.

Answer 38

FGAs are also known as typical antipsychotics, conventional or classic antipsychotics, and dopamine receptor antagonists (DRAs) FGAs reduce dopaminergic neurotransmission in the four dopamine pathways by blocking D2 receptors. Although individual effects may vary from patient to patient, in general, conventional antipsychotics share the same primary mechanism of action and do not differ much in their therapeutic profiles. There are, however, differences in secondary properties, such as degree of muscarinic, histaminergic, and/or alpha adrenergic receptor antagonism, which can lead to different side-effect profiles. Largely effective for positive symptoms Highly effective for all disorders that result in psychotic thought processes Acute and chronic neurological side effects can limit their effectiveness Relatively ineffective for negative symptoms Start low and go slow Be sure to review clinical guidelines in Kaplan & Sadock on page 622 paying attention to contraindications under the heading "Dosage & Clinical Guidelines.

Answer 39

potency & side effects, not necessarily effectiveness.

Answer 40

haloperidol, fluphenazine

Answer 41

perphenazine, loxapine

Answer 42

chlorpromazine

Answer 43

Haloperidol (Haldol), Fluphenazine (Prolixin), Thioridazine (Mellaril), Trifluoperazine (Stelazine)

Answer 44

Tardive Dyskinesia (TD)

Answer 45

Benztropine or Trihexyphenidyl or Diphenhydramine

Answer 46

Diphenhydramine

Answer 47

try Trihexyphenidyl or Benztropine

Answer 48

Blockade of the dopamine receptors in the tuberoinfundibular tract results in the increased secretion of prolactin, which can result in breast enlargement, galactorrhea, amenorrhea, and inhibited orgasm in women and impotence in men. The SDAs, with the exception of risperidone (Risperdal), are not particularly associated with an increase in prolactin levels and may be the drugs of choice for persons experiencing disturbing side effects from increased prolactin release. Stimulation of serotonin 2A receptors stimulates prolactin release. Since they have opposing effects on prolactin, adding serotonin 2A antagonism to dopamine 2 antagonism results in a neutral effect on prolactin and may relieve breast secretions caused by dopamine 2 antagonism alone.

Answer 49

Idiosyncratic reaction to dopamine antagonists (more common in patients who are antipsychotic-naive) Capable of producing significant mortality Has been reported with almost all D1 & D2 antagonists including non-psychotropics such as Metoclopramide.

Answer 50

From a clinical perspective: “Atypical antipsychotic” is defined in part by the “atypical” clinical properties that distinguish such drugs from conventional antipsychotics. Atypical antipsychotics have the clinical profile of equal positive symptom antipsychotic actions, but low extrapyramidal symptoms and less hyperprolactinemia compared to conventional antipsychotics. They also have antidepressant actions alone and in combination with other antidepressants. They are “atypical” from what is expected from a classical, conventional, first-generation antipsychotic. Almost all of the agents with this atypical profile came after the introduction of clozapine, sometimes the atypical antipsychotics are also called second-generation antipsychotics. From a pharmacological perspective: Current atypical antipsychotics as a class are defined as serotonin–dopamine antagonists, with simultaneous serotonin 5HT2A receptor antagonism that accompanies D2 antagonism. Pharmacologic actions in addition to 5HT2A antagonism that can hypothetically also mediate the atypical antipsychotic clinical profile of low EPS and less hyperprolactinemia with comparable antipsychotic actions include partial agonist actions at 5HT1A receptors and partial agonist actions at D2 receptors. Atypical antipsychotics as a class have the most complicated pattern of binding to neurotransmitter receptors of any drug class in psychopharmacology, and no two agents have an identical portfolio.

Answer 51

The presumed antipsychotic effects of the SGAs are blockade of D2 dopamine receptors. Where the SGAs differ from older antipsychotic drugs is their higher ratio interactions with serotonin receptor subtypes, most notably the 5-HT2A subtype, as well as with other neurotransmitter systems. Hypothesized that these properties account for the distinct tolerability profiles associated with each of the SGAs. All SGAs have different chemical structures, receptor affinities, and side effect profiles. No SDA is identical in its combination of receptor affinities, and the relative contribution of each receptor interaction to the clinical effects is unknown.

Answer 52

Beyond antagonism of 5HT2A and D2 receptors, atypical antipsychotics interact with multiple other receptor subtypes for both dopamine and serotonin and have effects on other neurotransmitter systems as well. Receptor binding properties linked to various serotonin receptors including 5HT1A partial agonist actions and antagonism of 5HT1B/D, 5HT2C, 5HT3, and 5HT7 receptors. Additional mechanisms linked to antidepressant actions that are shared by various atypical antipsychotics include: Serotonin and/or norepinephrine reuptake inhibition – Only quetiapine (Seroquel) has potency greater than its D2 binding, ziprasidone (Geodon) has weak binding at these sites. Alpha-2 (α2) antagonism – The proven antidepressant mirtazapine is best known for α2 antagonism, but several atypical antipsychotics also have this action with variable degrees of potency, including essentially all the "pines" (higher potency especially for quetia pine [Seroquel] and cloza pine [Clozaril]) and "dones" (higher potency especially for risperi done [Risperidal]) as well as aripiprazole (Abilify).

Answer 53

All antipsychotics are effective for psychotic mania, but atypical antipsychotics appear to have greater efficacy for nonpsychotic mania, leading to the major hypothesis - D2 antagonism/partial agonism combined with 5HT2A antagonism.

Answer 54

Use of atypical antipsychotics for the treatment of various anxiety disorders is controversial. There are some studies which suggest efficacy of various atypical antipsychotics for generalized anxiety disorder, and to augment other agents for other anxiety disorders. Most controversial is their use in PTSD. The one caveat to this is the anecdotal use as well as clinical evidence for utility in various anxiety disorders is greatest for quetiapine (Seroquel).

Answer 55

The good - With short-term treatment, sedation is a desired therapeutic effect, especially early in treatment, during hospitalization, and when patients are aggressive, agitated, or needing sleep induction. The bad - With long-term treatment, sedation is generally a side effect to be avoided because diminished arousal, sedation, and somnolence can lead to cognitive impairment. When cognition is impaired, functional outcomes are compromised. Generally speaking, the pines are more sedating than the dones

Answer 56

Clozapine, quetiapine, olanzapine, and iloperidone. All other antipsychotics have moderate potency, except lurasidone, which has essentially no binding to H1

Answer 57

All atypical antipsychotics share a class warning for causing weight gain and risks for obesity, dyslipidemia, diabetes, accelerated cardiovascular disease, and even premature death.

Answer 58

clozapine, olanzapine

Answer 59

risperidone, paliperidone, quetiapine, iloperidone (weight only)

Answer 60

ziprasidone, aripiprazole, lurasidone, iloperidone (low for dyslipidemia), asenapine

Answer 61

Olanzapine is one of the antipsychotics most associated with weight gain and metabolic risk and would not be a first-line option for patients who have a primary concern about metabolic issues. Quetiapine can lead to weight gain and increased triglyceride levels and may be a second-line option if a primary concern is metabolic issues. Risperidone can lead to weight gain and increased triglyceride levels and may be a second-line option if a primary concern is metabolic issues. Ziprasidone in general seems to be weight neutral and has been shown to lower triglyceride levels. It is therefore a recommended choice for individuals for whom metabolic issues are a primary concern.

Answer 62

weight gain and metabolic risk and would not be a first-line option for patients who have a primary concern about metabolic issues.

Answer 63

weight gain and increased triglyceride levels and may be a second-line option if a primary concern is metabolic issues.

Answer 64

weight gain and increased triglyceride levels and may be a second-line option if a primary concern is metabolic issues. As well as glycomastica Ziprasidone in general seems to be weight neutral and has been shown to lower triglyceride levels. It is therefore a recommended choice for individuals for whom metabolic issues are a primary concern.

Answer 65

weight gain and increased triglyceride levels and may be a second-line option if a primary concern is metabolic issues. As well as glycomastica Ziprasidone in general seems to be weight neutral and has been shown to lower triglyceride levels. It is therefore a recommended choice for individuals for whom metabolic issues are a primary concern.

Answer 66

weight gain and increased triglyceride levels and may be a second-line option if a primary concern is metabolic issues. As well as glycomastica

Answer 67

weight neutral and has been shown to lower triglyceride levels. It is therefore a recommended choice for individuals for whom metabolic issues are a primary concern.

Answer 68

equal positive symptom antipsychotic actions, but low extrapyramidal symptoms and less hyperprolactinemia compared to conventional antipsychotics.

Answer 69

serotonin–dopamine antagonists, with simultaneous serotonin 5HT2A receptor antagonism that accompanies D2 antagonism actions include partial agonist actions at 5HT1Areceptors

Answer 70

Only quetiapine (Seroquel) has potency greater than its D2 binding, ziprasidone (Geodon) has weak binding at these sites.

Answer 71

The proven antidepressant mirtazapine is best known for α2 antagonism Several atypical antipsychotics also have this action with variable degrees of potency, including Essentially all the "pines" (higher potency especially for quetia pine [Seroquel] and clozapine [Clozaril]) And "dones" (higher potency especially for risperi done [Risperidal]) as well as aripiprazole (Abilify).

Answer 72

Generally speaking, the pines are more sedating than the ones The good - With short-term treatment, sedation is a desired therapeutic effect, especially early in treatment, during hospitalization, and when patients are aggressive, agitated, or need sleep induction. The bad - With long-term treatment, sedation is generally a side effect to be avoided because diminished arousal, sedation, and somnolence can lead to cognitive impairment. When cognition is impaired, functional outcomes are compromised.

Answer 73

Clozapine, quetiapine, olanzapine, and iloperidone. All other antipsychotics have moderate potency, except lurasidone, which has essentially no binding to H1

Answer 74

called a psychotic episode. During a period of psychosis, a person’s thoughts and perceptions are disturbed and the the individual may have difficulty understanding what is real and what is not

Answer 75

misrepresentation of a “real” sensory stimulus

Answer 76

defined as the perception of an object or event (in any of the 5 senses) in the absence of an external stimulus, are experienced by patients with conditions that span several fields.

Answer 77

are false beliefs based on incorrect inferences about an external reality that persists despite the evidence to the contrary; these beliefs are not ordinarily accepted by other members of the person's culture or subculture.

Answer 78

 A. Two or more of the following for at least a one-month (or longer) period of time, and at least one of them must be 1, 2, or 3:  1. Delusions  2. Hallucinations  3. Disorganized speech  4. Grossly disorganized or catatonic behavior  5. Negative symptoms, such as diminished emotional expression  C. Duration: Continuous signs of the disturbance persist for at least 6 months. This 6-month period must include at least one month of symptoms (or less if successfully treated) that meet Criterion A (i.e., active-phase symptoms) and may include periods of prodromal or residual symptoms. During these prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or two or more symptoms listed in Criterion A present in an attenuated form (e.g., odd beliefs, unusual perceptual experiences).  D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either (1) no major depressive or manic episodes have occurred concurrently with the active-phase symptoms, or (2) if mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness.  E. The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition.  F. If there is a history of autism spectrum disorder or a communication disorder of childhood onset, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations, in addition to the other required symptoms of schizophrenia, are also present for at least 1 month (or less if successfully treated).

Answer 79

 A. Schizoaffective disorder debut has an uninterrupted period of illness, during which there is an episode of mood disorder (manic or major depressive disorder) concurrent with a schizophrenia episode characterized by 2 or more of the following symptoms present for a considerable part of a 1-month period: * delusions * hallucinations * disorganized speech (e.g., frequent derailment or incoherence) * grossly disorganized or catatonic behavior * negative symptoms (i.e. affective flattening, alogia, or avolition).  B. During this time, there should be a period of at least 2 weeks with delusions and hallucinations, in the absence of prominent mood symptoms during the lifetime duration of illness.  C. Mood symptoms have been present for the majority of the total duration of the active and residual period of illness

Answer 80

The presence of one or more delusions for a month or longer in a person who, except for the delusions and their behavioral ramifications doesn't appear odd and is not functionally impaired can be either with non-bizarre delusions are about situations that could occur in real life, such as being followed, being loved, having an infection, and being deceived by one's spouse or with bizarre delusions that are clearly implauable

Answer 81

The category of unspecified psychotic disorder includes psychotic symptomatology (i.e., delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior) about which there is inadequate information to make a specific diagnosis or about which there is contradictory information, or disorders with psychotic symptoms that do not meet the criteria for any specific psychotic disorder.

Answer 82

Genetic factors The likelihood is correlated with first-degree or second-degree relative with schizophrenia; 50% concordance with monozygotic twins Biochemical Factors  Dopamine hypothesis of too much dopamine-unsure if too much release, too many dopamine receptors, hypersensitivity to dopamine receptors, or combinations  Serotonin-too much?  GABA-inhibitory affect preventing from regulation of dopamine and causing hyperactivity of dopaminergic neurons Neuropathology  Reduced volumes of gray matter and enlarged cerebral ventricles  Reduced symmetry and reduced limbic system  Anatomical abnormality of the pre-frontal cortex

Answer 83

 FGAs are also known as typical antipsychotics, conventional or classic antipsychotics, and dopamine receptor antagonists (DRAs) *  FGAs reduce dopaminergic neurotransmission in the four dopamine pathways by blocking D2 receptors.  Although individual effects may vary from patient to patient, in general, conventional antipsychotics share the same primary mechanism of action and do not differ much in their therapeutic profiles.  There are, however, differences in secondary properties, such as degree of muscarinic, histaminergic, and/or alpha adrenergic receptor antagonism, which can lead to different side-effect profiles.  Largely effective for positive symptoms  Highly effective for all disorders that result in psychotic thought processes  Relatively ineffective for negative symptoms

Answer 84

Chlorpromazine (Thorazine) Prochlorperazine (Compazine) Perphenazine (Trilafon) Trifluoperazine (Stelazine) Fluphenazine (Prolixin) Haloperidol (Haldol) Loxapine (Loxitane) Thioridiazine (Mellaril)

Answer 85

Acute psychotic episodes, schizophrenia, and schizoaffective Maintenance of schizophrenia and schizoaffective disorders Mania Delirium and dementia Substance-induced psychotic disorder Delusional disorder Depression with psychotic symptoms

Answer 86

 S: sedation/sunlight sensitivity skin effects/sexual side effects  T: tardive dyskinesia  A: anticholinergic effects & agranulocytosis  N: neuroleptic malignant syndrome  C: cardiac arrhythmias (orthostatic hypotension)  E: extrapyramidal symptoms /akathisia endocrine effects - increased prolactin eye effects

Answer 87

 Akathisia, Acute Dystonic Reactions, Parkinsonism  Chronic dopamine blockage can lead to Tardive Dyskinesia (TD)  If develops EPS give Benztropine or Trihexyphenidyl or Diphenhydramine  Propranolol more beneficial for akathisia  If develops TD give Diphenhydramine, weak studies Vitamin E use, change to a different antipsychotic with less potential

Answer 88

Stooped posture Shuffling gate Rigidity Bradykinesia Tremors at rest Pill-rolling motion of the hands

Answer 89

Facial Grimacing Involuntary upward eye movement Muscle spasms of the tongue, face, neck, and back (back muscle spasms cause the trunk to arch forward Laryngeal spasms

Answer 90

Restlessness trouble standing still paces the floor feet in constant motion, rocking back and forth

Answer 91

Protrusion and rolling of the tongue sucking and smacking movements of the lips chewing motion facial dyskinesia involuntary movements of the body and extremities

Answer 92

Duration to implement tx - Minutes-hours Tx options - Benztropine or other anticholinergic PO or IM

Answer 93

Duration to implement tx - Days Tx options - Benzodiazepine

Answer 94

Duration to implement tx - Days - Weeks Tx options - Benzodiazepine, beta-blockers

Answer 95

Duration to implement tx - Long term Tx options - Switch to atypical or clozapine, Vesicular Monoamine transporter 2 inhibitor

Answer 96

More common with high potency typical antipsychotics (rare with atypical antipsychotics); D2 blockade Onset in hours to days after antipsychotic started or dose increased; 90% within first 5 days Benztropine 1-2mg 1-twice /day (SE: dry mouth, blurred vision, constipation, urinary retention, cognitive changes) Diphenhydramine 50mg/day If severe, stop the medication and give above agents IV or IV once or twice to stop the dystonia; then prescribe oral medication to prevent another episode

Answer 97

Pseudo parkinsonism---drug induced Parkinson’s like disease (Tremor “pill rolling”, rigidity or cogwheeling, bradykinesia-(slow movement), shuffling gait; slurred speech, mask like face, stooped posture, drooling; cognitive dulling, worse negative symptoms, worse depression. *Decrease the dose or switch to a different antipsychotic *First-line meds: Benztropine 1-2mg once or twice per day; *trihexyphenidyl 2-5mg once or twice per day; diphenhydramine 50mg /day *Symptoms can occur at any time; usually occurs within 1-2 months after antipsychotic initiated; highest risk patients: female, older higher potency agents at higher doses *If the patient is at high risk for parkinsonism—start benztropine (or one of the first-line agents) at the same time as starting the antipsychotic *Can discontinue the anticholinergic agent after several weeks; many patients will not need to remain on it long term *Usually caused by typical agents. Atypical can cause this also. (Meds least likely to cause this: clozapine, quetiapine, and ziprasidone.) *D2 blockade—disruption of balance b/t dopaminergic vs cholinergic neurons

Answer 98

Sense of restlessness, appear fidgety, can’t sit still, rocking motion; can be inner sense of restlessness; can lead to agitation and suicidal ideation; appears in days to weeks after starting medication High potency typical agents most likely to cause this (Haloperidol); atypical aripiprazole, asenapine, brexpiprazole, cariprazine, lurasidone, paliperidone, risperidone; SSRIs/Buspirone); D2 blockade First-line medications to treat: *Propranolol-Start 10mg BID; can go up to 30mg-90mg daily in 2-3 divided doses (SE: dizziness, fatigue, syncope, low BP) *Inderal LA—long-acting propranolol dosed once a day (60- 80mg daily) *Benzodiazepines-any of them will work. (Eg Lorazepam 0.5mg to 1mg BID) or diazepam 10mg BID or more frequently as needed Reduce dose of medication; switch to lower potency agent or different atypical agent *Don’t mistaken akathisia with agitation for psych disorder symptoms; you may worsen akathisia. (Clozapine, quetiapine, and lurasidone cause no more akathisia than placebo)

Answer 99

First line med Deutetrabenazine (Austedo) DOSE 6mg BID for 1 week, then raise based on response by 3mg BID every week max 24mg BID; take with food RISK QTc prolongation, insomnia, nasopharyngitis, possible depression, and suicidality NOTES These usually need to ordered through a specialty pharmacy ($6000/mth) First line med Valbenazine (Ingrezza) DOSE 40mg QHS for 1 week, then 80mg QHS with or without food RISK QTc prolongation, sedation, possible depression and suicidality

Answer 100

Step 1 Prevention-minimizing antipsychotics in patients at risk. Risk factors: Age>50; h/o SUD, brain injury, diabetes, HIV+, female gender, mood disorders, African American race, and presence of EPS * Minimize the dose and duration if taking an antipsychotic * Can decrease duration in mood disorders/not likely in schizophrenia Step 2 Taper off with first signs of TD; discuss risks/benefits to continued treatment with antipsychotic * d/c dose-lower the dose every 2-4 weeks * Can have ‘withdrawal dyskinesias’ with worsening dyskinesias for the first few months after med is stopped * Can be permanent, 30-50% of cases can resolve with discontinuation. Step 3 Switch- if discontinuation is not successful. * Clozapine is the only antipsychotic that does not cause TD (Low level of D2 occupancy) (has other risks) (Quetiapine also has a low level of D2 occupancy & low EPS rates) * Aripiprazole, and olanzapine may be good alternatives Step 4 VMAT2 inhibitor—if tapering and switching do not work-attempt to treat TD * Valbenazine (Ingrezza)—take 1 time a day (1 in 4 response rates) & deutetrabenazine (Austedo) Take BID with food (1 in 7 response rates) (H/o causing depress/suicide in past—has black box warning for Huntington's for suicidality ) * Reduces dopamine hypersensitivity ; Don’t worsen psychosis; actually have been helpful in past for treating psychosis (reserpine) * Take 4-6 weeks to work; continue as long as patient is taking the antipsychotic; or TD will return within a mth of d/c Step 5 Second line agents- dopamine agents that address other pathways such as glutamate antagonist- amantadine-tx’s dyskinesias in Parkinson’s disease; Ginkgo is neuroprotective; benztropine can worsen TD with his anticholinergic effects

Answer 101

NMS is a life-threatening emergency and is fatal in 10% of cases. It usually occurs later in treatment but can occur earlier. It is characterized by:  Reduced consciousness  Increased muscle tone  Autonomic dysfunction (hyperpyrexia, hypertension, tachycardia, tachypnea, diaphoresis, and drooling) *Treatment consists of early detection, discontinuation of antipsychotics, management of fluid balance, temp. reduction, and monitoring for complications.

Answer 102

Anticholinergics-decreases antipsychotic effect Barbiturates-decreases antipsychotic concentrations Carbamazepine-up to 50% reduction in antipsychotic concentrations Cigarette smoking-Reduced plasma concentration of antipsychotic agents Fluvoxamine-increases haloperidol and clozapine concentrations Amphetamines-may exacerbate psychosis Benzodiazepines-Respiratory depression, stupor, and hypotension Clonidine-hypotension or hypertension-potentiate alpha effects Valproate Acid-Increases half-life and levels

Answer 103

Range 1- 40mg daily Decanoate: 10-20 times the previous oral dose/2 weeks How to dose- Oral: 1-15mg/day can give once daily or divided doses; not more than 100mg/day

Answer 104

Range 1-20mg/day Decanoate: 12.5-100mg/2 weeks How to dose Oral: 0.5-10mg/day in divided doses: max: 40mg/day

Answer 105

Range 200-800mg/day How to dose - Initial: dose increased until symptoms controlled

Answer 106

Range 60-100 mg/day in divided doses How to dose - Initial 20mg/day in 2 doses titrate over 7-10 days to 60-100mg/day in 2- 4 doses; max: 250mg/day

Answer 107

Range 12-24mg/day; 16-64mg hospital pts. How to dose - Initial: 4-8 mg TID; 8-16mg BID-QID hospital pts.; Max: 64mg/day

Answer 108

Range 15-20mg/ day How to dose - Initial: 2-5 mg/day BID

Answer 109

From a clinical perspective: * “Atypical antipsychotic” is defined in part by the “atypical” clinical properties that distinguish such drugs from conventional antipsychotics. * Atypical antipsychotics * Have the clinical profile of equal positive symptom antipsychotic actions, but low extrapyramidal symptoms and less hyperprolactinemia compared to conventional antipsychotics. * They also have antidepressant actions alone and in combination with other antidepressants. * Beyond antagonism of 5HT2A and D2 receptors, atypical antipsychotics interact with multiple other receptor subtypes for both dopamine and serotonin and have effects on other neurotransmitter systems as well * They are “atypical” from what is expected from a classical, conventional, first-generation antipsychotic.

Answer 110

 The presumed antipsychotic effects of the SGAs are blockade of D2 dopamine receptors.  Where the SGAs differ from older antipsychotic drugs is their higher ratio interactions with serotonin receptor subtypes, most notably the 5-HT2A subtype, as well as with other neurotransmitter systems.  Hypothesized that these properties account for the distinct tolerability profiles associated with each of the SGAs.  All SGAs have different chemical structures, receptor affinities, and side effect profiles.  Beneficial for both negative and positive symptoms.

Answer 111

Clozapine (Clozaril) Risperidone (Risperdal) Olanzapine (Zyprexa) Quetiapine (Seroquel) Ziprasidone (Geodon) Aripiprazole (Abilify) Paliperidone (Invega) Asenapine (Saphris) Iloperidone (Fanapt) Lurasidone (Latuda) Brexpiprazole (Rexulti) Cariprazine (Vraylar)

Answer 112

Schizophrenia Behavioral disturbances with dementia Treatment-resistant depression Autism Spectrum Disorders Post Traumatic Stress Disorder Anxiety disorders Adjunctive treatment of depression Acute Mania

Answer 113

*Many of the same side effects of FGAs- one disadvantage of atypicals is the tendency to gain weight and put patients at risk for Metabolic Syndrome which consists of : (Weight gain, Dyslipidemia, Altered glucose metabolism, & Hypertension)

Answer 114

Clozapine, Olanzapine

Answer 115

risperidone, paliperidone, quetiapine, iloperidone (weight only)

Answer 116

ziprasidone, aripiprazole, lurasidone, iloperidone (low for dyslipidemia), asenapine

Answer 117

* Olanzapine is one of the antipsychotics most associated with weight gain and metabolic risk * Quetiapine can lead to weight gain and increased triglyceride levels and may be a second-line options if a primary concern is metabolic issues * Risperidone can lead to weight gain and increased triglyceride levels and may be a second-line options if a primary concern is metabolic issues. * Ziprasidone in general seems to be weight neutral and has been shown to lower triglyceride levels.

Answer 118

* Blockade of the dopamine receptors in the tuberoinfundibular tract results in the increased secretion of prolactin, which can result in breast enlargement, galactorrhea, amenorrhea, and inhibited orgasm in women and impotence in men. * The SGAs, apart from risperidone (Risperdal), are not particularly associated with an increase in prolactin levels and may be the drugs of choice for persons experiencing disturbing side effects from increased prolactin release. * Stimulation of the serotonin 2A receptors stimulates prolactin release

Answer 119

* Clozapine is the worst, then olanzapine, quetiapine, and risperidone, paliperidone (in descending order) * Other SGAs are close to a weight neutral in adults. Kids still tend to gain weight despite neutral meds * Weight gain and metabolic effects are the greatest in the pediatric population * All labels with FDA warning for weight gain, hyperglycemia, new-onset or worsening diabetes and hyperlipidemia

Answer 120

* Clozapine, olanzapine, quetiapine are most sedating. ‘Revved up psychosis” will do well on these. * May need an alternative antipsychotic for long-term treatment if too sedating

Answer 121

EKG changes-ziprasidone is most prevalent with increased QT interval and can cause serious arrhythmias * Actual risk is only 0.06%. Others that cause QT prolongation: are thioridazine (Mellaril), iloperidone (Fanapt), quetiapine (Seroquel)

Answer 122

* EPS among the FGAs—Haloperidol and fluphenazine (Prolixin) cause the most EPS * Among the SGAs: risperidone is the highest EPS risk

Answer 123

aripiprazole (Abilify) & brexpiprazole (Rexulti)

Answer 124

Depends on plasma levels; trough level of 350 ng/mL 25mg qhs; increase by 25-50mg every 48-72 hours as tolerated

Answer 125

15-30mg/day schizo and mania 2-10mg/day augment depression Decanoate: 300- 400mg/ 4 weeks Oral: 10-15mg/day initial; max: 30mg/day- schizo/mania 2-5mg/day

Answer 126

2-8mg/day psychosis or bipolar 0.5-2mg/day for children and elderly 12.5mg-50mg IM every 2 weeks 1mg/day orally in BID; increase 1mg each day as tolerated

Answer 127

400-800mg/day- Schizo 300mg/day Bipolar Depression 25mg BID and increase by 25-50mg twice a day each day; max: 800mg Acute mania: 100mg day 1 and increase to 400mg/day on day 4

Answer 128

10-20mg/day 5-10mg/day increase by 5mg once a week until desired efficacy

Answer 129

40mg-200mg/day schizo; 80- 160mg/day Bipolar Schizo: initiate 20mg BID with food/ Bipolar: initiate 40mg BID

Answer 130

6mg/day Sustenna: 39-234mg/month 6mg/day taken in the morning; increase by 3mg/day every 5 days

Answer 131

10-20mg/day BID dose- Sublingual Children: 5mg BID; max 10mg/day 10mg/day- do not eat or drink for 10 mins. after

Answer 132

12-24mg/day in BID dosing 2mg/day 1; 4mg/day 2; 8mg/day 3, 12mg/day on day 4; 16mg day 5

Answer 133

40mg-80mg/day Schizophrenia 20-60mg/day Bipolar Take with food; 40-80mg/day increase as tolerated

Answer 134

2-4mg/day Schizo 2mg/day Depression 1mg/day on days 1-4; 2mg on day 5- 7, and 4mg day 8 if needed

Answer 135

1.5-6mg once daily Schizo 3-6mg/day daily 1.5mg/day on day 1 and can increase to 3mg day 2

Answer 136

 Contraindications of treatment- allergic response history, ingestion of substance that may interact with antipsychotic, severe cardiac abnormality, high risk for seizures, narrow angle glaucoma, and presence of TD.  Usual assessment of CBC, LFTs, and EKG  Elderly and children more sensitive to treatment  Start low and go slow  Maximal effects of particular dose may not be evident for 4-6 weeks  First 3-6 mos. After a psychotic episode are usually considered period of stabilization- dosage can be decreased about 20% every 6 mos. Until minimum effective dose is found.  Persons usually maintained on antipsychotic 1 to 2 years after first psychotic episode; usually 5 years after 2nd episode; lifetime maintenance after 3rd psychotic episode

Answer 137

May overcome problems with compliance IM preparations usually give every 1- 4 weeks May have to adjunct with oral medications initially until dose is therapeutic After 3 to 4 weeks injection dose can be increased to single dose equal to total dose of drug given during period