NR 546 Week 4 Midterm Study Guide, Exercises of Nursing

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Typical antipsychotics (conventional) (FGA) • Treats positive (+) symptoms only appropriate for the acute and chronic management of schizophrenia and psychosis. • Non-selectively blocks dopamine D2 receptors, specifically in mesolimbic pathway; also blocks Ach (Muscarinic), histamine, NE Five main SE of FGAs • Sedation • Postural Hypotension • Lower seizure threshold • Anticholinergic side effects • Photosensitive Haloperidol-High-Appropriate for acute, severe agitation and aggression-Butyrophenones • Initial oral dose 1-15mg/day (can give once daily or divide; • Usual dose 1-40mg/day (orally); • Max dose 100mg/day • Tablets 0.5, 1, 2, 5, 10, 20mg; Concentrate 2mg/ml; Injection 5mg/ml • Half-life 13-38 • Higher risk for EPS and TD • Avoid in older adults due to increased risk of cerebrovascular accident (CVA), cognitive decline, and death in persons with dementia and with dementia-related psychosis. Fluphenazine-Medium-Psychotic D/Os • Initial oral dose 0.5-10mg/day divided doses; • Usual dose 1-20mg day; • Max dose40mg/day • Tablet 1, 2.5, 5, 10mg; Elixer 2.5mg/ml; Concentrate 5mg/ml • Half-life 15 hours Thiothixene-Medium • Initial dose 5-10mg/day; • Usual dose 15-30mg/day; • Max dose 60mg/day divided • Capsules 2, 5, 10mg • Half-life 3.4-34 hours Thioridazine-Low-2nd line due to QTc issues • Initial dose 50-100mg/3xday/increase gradually; • Usual dose 200-800mg divided; • Max dose 800mg/day • Tablets 10, 15, 25, 50, 100mg • Metabolized by CYP450 2D6 Chlorpromazine-Low-2nd line due to QTc issues -schizophrenia-DA 2 antagonist • Usual dose 200-800mg divided; maximum 800mg/day • Psychosis-increase dose until symptoms are controlled; after 2 weeks reduce to lowest effective dose • Can improve in one week but may take several weeks for full effect on behavior • Tablet 10, 25, 50, 100, 200mg • Half-Life 8-33 hours • Phenothyazine • SXS-Dry mouth, pupil dilation, blurred vision, cog impair, constipation, urinary retention, tachycardia Mesoridazine-Low-off market due to dangerous side effects, including irregular heartbeat and QT prolongation. *Low potency meds require higher doses to achieve efficacy *Low potency meds have more anticholinergic, antihistaminic, and α 1 properties resulting in more sedation than higher potency meds. *High risk for developing hyperprolactinemia and EPS (negative symptoms aren’t affected by FGAs only positive symptoms) Neurolepsis is a term to describe antipsychotic medication effects on psychotic clients, with respect to cognition and behavior. Newer medications (SGA) do not necessarily have these same effects. Neurolepsis syndrome has three major features. Examine the image below to learn more about the PEA acronym. • Psychomotor slowing - extreme form of slowness or absence of motor movement (nigrostriatal pathway) • Emotional quieting - worsening of negative and cognitive symptoms (mesocortical pathways) • Affective indifference - worsening of affective symptoms (mesocortical pathway) Atypical antipsychotics (SGA) Developed to treat both positive (+) and (-) negative symptoms • SGAs are considered serotonin-dopamine antagonists, as they maintain D2 antagonism but also have simultaneous serotonin 5HT2A antagonism • Lower affinity for D2 and higher affinity for 5HT • Effective for treatment-resistant clients • Does not increase prolactin levels • Treats positive and negative symptoms • Lower risk of EPS Ziprasidone(Geodon)-Schizophrenia 10 and older • MOA- • SE-moderate metabolic risk • Serotonin-Dopamine antagonist • Special Comments: IM dosing in acute agitation associated with schizophrenia • Low metabolic risk • Lowest risk for weight gain • AVOID IN PREGNANCY! • Avoid in older adults due to increased risk of cerebrovascular accident (CVA), cognitive decline, and death in persons with dementia and with dementia-related psychosis. • Contraindicated in clients with QT, recent myocardial infarction, or uncompensated heart failure • High incidence of rash/urticaria related to Stevens-Johnson syndrome and Drug Reaction with Eosinophilia and Systemic Syndrome (DRESS) • Iloperidone-Schizophrenia; Schizophrenia maintenance • Usual dose 12-24mg /d (divided in two) • Max dose is 32mg/d • Max dose is 16mg/d for those who are poor 2D6 metabolizer • If prescribed with a CYP 3A4 inhibitor dose should be 8mg/d • MOA- • Moderate risk for weight gain • Low risk for hyperlipidemia Lurasidone-(latuda)Schizophrenia 13 and older • MOA • SE-low metabolic risk • Serotonin-Dopamine antagonist • TAKE WITH FOOD, AT LEAST 350 CALORIES FOR MAX ABSORPTION • Blocks DA2 receptors reducing (+) sxs of psychosis and stabilizing affective symptoms; Blocks 5HT2A receptors causing enhancement of dopamine release in certain brain regions and thus reducing motor side effects and possibly improving cognitive and affective sxs Aripiprazole-(Abilify)Schizophrenia 13 and older • Listed as SGA or TGA • partial agonist at D2, 5HT1a, 5HT2 • When DA levels are high it reduces DA output improving positive sxs • When DA levels are low it increases DA output improving negative sxs, mood and cog • Usual dose15-30mg/d for SP and mania • Initial dose 10-15mg/d • Max dose 30mg/d • Max dose is 15mg/d for those who are poor 2D6 metabolizer • If prescribed with a CYP 3A4 inhibitor dose should be 7.5mg/d • MOA • Low metabolic risk • Low risk for weight gain • Low risk for orthostatic hypotension • BLACK BOX WARNING: Increased risk of suicide in children. • Brexpiprazole-(Rexulti) AKA a (TGA)-Schizophrenia • Usual dose 2-4mg /d • Max dose is 4mg/d • Max dose is 2mg/d for those who are poor 2D6 metabolizer • If prescribed with a CYP 3A4 inhibitor dose should be 1mg/d • MOA-Partial agonism at dopamine 2 receptors • SE-Low metabolic risk • Special Comments: Considered precognitive • Dopamine-Serotonin Partial Agonist Cariprazine (Vraylar)-schizophrena • MOA • SE_Low Metabolic risk *Order fasting Glucose, Lipids, EKG, BMI, BP when on SGAs Prescribing Considerations 1. Start with the lowest dose, evaluate tolerance, then slowly titrate dose to efficacy. Titrating helps prevent undesirable side effects. 2. There is no evidence that high antipsychotic doses are more effective than standard doses. 3. Dose adjustments should be made after two weeks of taking medication. 4. Establish efficacy and an effective medication dose before switching to a long-acting injectable (LAI). The prescribed dose of LAI will be the same as the effective oral dose. 5. Most antipsychotic side effects and adverse effects are dose-related. 6. Begin with monotherapy. The use of multiple antipsychotics can increase the risk of QT prolongation (a measure of delayed ventricular repolarization). Combinations should be considered only after single medications have provided an inadequate response. • Negative symptoms are more difficult to treat successfully than positive symptoms. • The need to effectively address negative symptoms led to the development of second- generation, or atypical, antipsychotics (SGA), which treat both positive and negative signs of psychosis. • SGAs are considered serotonin-dopamine antagonists, as they maintain D2 antagonism but also have simultaneous serotonin 5HT2A antagonism. Serotonin (5HT) can regulate DA release directly or indirectly, producing various effects on dopamine (DA) neurons. 5HT1A and 5HT2A receptors have opposite actions on dopamine release. • Stimulation of 5HT1A receptors increases dopamine release (a DA accelerator). Once bound to 5HT1A receptors, 5HT causes inhibition of its release, which results in increased dopamine output. • All four dopamine pathways have presynaptic 5HT2A receptors and work differently. Stimulation of 5HT2A receptors inhibits the release of dopamine (a DA brake). Blocking presynaptic 5HT2A receptors in the striatum increases DA release. • The imbalance between acetylcholine (ACh) and dopamine (DA), characteristic in FGAs, is less prominent in SGAs. Due to the antagonism of serotonin, SGAs generally have fewer EPS and prolactin effects than FGAs making them the first-line choice when prescribing medications for schizophrenia. • Cross titration over several days to weeks is required to prevent side effects. • Abrupt discontinuation is only relevant for those experiencing NMS. Can increase symptoms and cause withdrawal reactions. NOT RECOMMENDED WHEN D/C CLOZAPINE • Cross titration could be beneficial for those who are stable and experiencing side effects but could lead to breakthrough psychosis due to sub-therapeutic doses of both agents • Delayed withdrawal beneficial when relapse is a concern. Keep current and start new meds, but can increase side effects. Pregnancy • Risk of withdrawal symptoms in the newborn: extrapyramidal symptoms may be present at delivery. • In pregnancy, atypical antipsychotics appear more harmful than typical antipsychotics due to increased risk of gestational metabolic complications, increased gestational age weight, and increased birth weight. Avoid the use of Clozapine, Ziprasidone, olanzapine, risperidone, and quetiapine in pregnancy, especially in the third trimester. Breastfeeding • All antipsychotics are assumed to be secreted in breast milk. It is recommended that either the drug is discontinued or the infant bottle feeds. CYP450 Inducers: Can increase the rate of another drugs metabolism by 2-3-fold developing over a week. The rate of metabolism is greater and the effect of the med is reduced=therapeutic failure 1A2-carbamazepine, phenobarbital, rifampin, tobacco 2B6- carbamazepine, phenobarbital, phenytoin 2C9-carbamazepine, phenobarbital, phenytoin, rifampin 2C19-carbamazepine, phenytoin, rifampin, VTA to NA in the limbic system: Regulates emotional behaviors and is associated with reward, motivation, and pleasure: Overactivation leads to positive symptoms Mesocortical-(Memory note* CORE EMOTIONAL DISTURBANCE CAN CAUSE NEGATIVE SXS) VTA to PFC: Regulates cognition, executive function, emotions, and affect: Hypoactivation of the pathway may result in affective, cognitive and negative symptoms Nigrostriatal-Substantia nigra to the basal ganglia: Part of the EP nervous system and controls posture and voluntary motor movements: Imbalance causes movement disorders like EPS and TD secondary to chronic blockade (D2 antagonism) of this pathway. Tuberinfundibular- (Memory Note* OVARIAN TUBES AND FUNDUS IN WOMAN INCREASE BREAST SIZE AND MILK SECRETION) Hypothalamus to the anterior pituitary gland: Dopamine inhibits prolactin release from the pituitary so prolactin levels rise causing prolactinemia: Can cause gynecomastia and galactorrhea in males and females. SSRI’s- Inhibits the reuptake of serotonin, which can cause nausea, agitation, headache, and sexual dysfunction SNRIs- Inhibits the reuptake of serotonin and norepinephrine, which can cause nausea, sweating, insomnia, tremors, sexual dysfunction TCA’s • Inhibits the reuptake of serotonin and norepinephrine, which can cause sexual dysfunction • Blocks norepinephrine receptors, which can cause hypotension and tachycardia • Blocks histamine receptors, which can cause sedation and weight gain • Blocks acetylcholine receptors, which can cause dry mouth, constipation, blurred vision, and urinary retention MAOI’s- Increases norepinephrine and serotonin by inhibiting the enzyme that inactivates it, which can cause sedation, dizziness, sexual dysfunction, and hypertensive crisis Benzodiazepines- Increases the receptor affinity for GABA, which can cause dependence and confusion Bupropion- Inhibits the reuptake of norepinephrine and dopamine, which can cause insomnia, dry mouth, tremors, and seizures Benzodiazepines-GABA increase with use causing a calming effect Phosphodiesterase inhibitor-(Viagra) may be needed after 4-6 weeks of treatment with SSRI *Do not use St. Johns wort with SSRI as it can cause Serotonin Syndrome *One-third of psychotropic drugs bind to a neurotransmitter, and one-third bind to G-protein- linked receptors SYMPTOMS OF SCHIZOPHRENIA: Positive symptoms • Hallucinations • Delusions • Thought disorder • Hostility • Excitability Motor symptoms • Motor delay • Dyscoordination • Extrapyramidal side effects (EPS), e.g., o Parkinsonism o Dyskinesia Affective symptoms • Depression • Anxiety • Suicidality Cognition • Attention • Working memory • Verbal memory • Visual memory • Executive functioning • Processing speed • Social conditioning Negative symptoms • Affective flattening • Alogia • Anhedonia • Amotivation • Asociality *Hallucinogens stimulate 5HT2A receptors and excitate glutamate receptors *Extreme caution should be taken when prescribing antipsychotics for clients with metabolic disorders. SGAs are associated with hyperglycemia and type 2 diabetes, dyslipidemia, and hypertension Symptoms of Neuroleptic Malignant Syndrome (NMS) • Altered mental status • Hyperthermia • Muscle stiffness • Diaphoresis • Anxiety • Tachycardia • Tachypnea NMS is considered a medical emergency. If NMS is suspected, the provider should stop the administration of antipsychotic medications and provide supportive therapy. Treatment and pharmacologic management may include hydration, benzodiazepines, and muscle relaxants. Although serious, the syndrome is typically reversible when caught early. Medication Adherence • Adverse effects of medication • Lack of housing • Substance use • Younger age • New diagnosis • Financial constraint LEGAL CONSIDERATIONS • In cases of extreme agitation and violence, a short-acting intramuscular antipsychotic medication, such as haloperidol can be given, often in combination with adjuvant medications. • EPS related to the use of haloperidol may be controlled by co-administration of promethazine. • An injectable benzodiazepine, such as lorazepam, may help relieve emotional distress, insomnia, and other behavioral disturbances secondary to psychosis until antipsychotic medications take effect. • Inhaled loxapine may also be used to treat agitation in acute psychosis due to its rapid onset of action. Loxapine is well tolerated and less challenging to administer compared to oral or intramuscular antipsychotics. Rationale: Fear can trigger an adaptive respiratory response which can exacerbate asthma or other chronic breathing disorders. This explains client reports of not being able to breathe during a panic attack. Sympathetic nervous stimulation causes increased heart rate, dry mouth, constipation, urinary retention, and increased blood sugar. When autonomic nervous system symptoms become chronic, there is an association with hypertension, cardiac ischemia, myocardial infarction, and sudden death. MEDICATION MANAGEMENT FOR ANXIETY: Antidepressants • SSRIs • SNRIs Anxiolytics • azrapirones • benzodiazepines Other • alpha 2 delta ligands • beta blockers • histamine receptor agonists Selective serotonin reuptake inhibitors (SSRI) are the first-line drugs to treat anxiety disorder(s) • generalized anxiety disorder • panic disorder • obsessive-compulsive disorder • post-traumatic stress syndrome • social anxiety disorder Rationale: SSRIs are the first-line drugs to treat all anxiety disorders. SSRI Selective serotonin reuptake inhibitors (SSRIs) are used for the treatment of all anxiety disorders. They act by preventing the reuptake of 5-HT by synapses in the brain. • Drugs o citalopram (Celexa) o escitalopram (Lexapro) o fluoxetine (Prozac) o fluvoxamine (Luvox, Luvox CR) o paroxetine (Paxil, Paxil CR) o sertraline (Zoloft) • Adverse Effects o anorexia o diarrhea o headache o weight gain o sexual side effects o serotonin syndrome • Monitoring o akathisia, increased anxiety, suicidal ideation • Clinical Pearls o Each agent in the class has a unique pharmacological profile. o Dosage should be started at half the recommended dose for depression; increase dosage after 2-4 weeks as needed to control anxiety. o SSRIs should not be stopped abruptly because it can result in rebound anxiety. o PAROXETINE CONTRAINDICATED IN PREGNANCY SNRI Serotonin-norepinephrine reuptake inhibitors (SNRIs) are used to treat all anxiety disorders except obsessive-compulsive disorder. SNRIs work by preventing the reuptake of 5-HT and norepinephrine (NE) by synapses in the brain. Compared with venlafaxine and desvenlafaxine, which have serotonin reuptake inhibition (SRI) activity and dose-related affinity for norepinephrine reuptake inhibition (NRI) primarily, duloxetine has more balanced SRI and NRI activities. Levomilnacipran has higher activity at NRI than SRI. • Drugs o desvenlafaxine (Pristiq) o duloxetine (Cymbalta) o venlafaxine (Effexor, Effexor XR) o levomilnacipran (Fetzima) • Adverse Effects o elevated blood pressure o sweating o anxiety o dizziness o insomnia o constipation o serotonin syndrome • Monitoring o increased anxiety o suicidal ideations • Contraindications o liver problems o hypertension • Clinical Pearls o Due to the presence of norepinephrine, SNRIs can exacerbate anxiety. o Dosage should be started at half the recommended dose for depression to minimize side effects. Buspirone Azapirones are Federal Drug Administration (FDA) approved for short-term anxiety treatment and are used alone or as an adjunct to antidepressants. They bind to serotonin and dopamine receptors in the brain and increase norepinephrine metabolism in the brain. • Drug o buspirone (BuSpar) • Adverse Effects o dizziness o headache o sedation o nervousness o nausea • Contraindications o severe renal impairment o severe hepatic impairment o concurrent use of monoamine oxidase inhibitors (MAOIs) • Clinical Pearls o Buspirone is not habit-forming, does not have abuse potential, causes withdrawal reactions, or potentiates alcohol and sedative-hypnotic effects. o It is prescribed for two or three times a day due to the short half-life; it is not prescribed as needed (PRN). o It has a gradual onset of action of 2 weeks, but over time provides the same efficacy as a benzodiazepine. o BuSpar may decrease sexual side effects when used in combination with an SSRI. Alpha 2 Delta Ligands Alpha 2 delta ligands are used off-label for general anxiety disorder (GAD). They bind with glutamate calcium channel blockers (Glu-CB) to inhibit the release of several neurotransmitters. Pregabalin has anxiolytic properties with selective binding to the α-2-delta subunit of voltage- gated calcium channels. • Drugs o pregabalin (Lyrica) o gabapentin (Neurontin) • Adverse Effects o sedation, dizziness, impaired attention, confusion • Social anxiety disorder o sertraline o paroxetine o Drug therapy takes 4 weeks to see effects • Post-traumatic stress disorder o paroxetine o sertraline Roleplay: patient has tolerated Paroxetine (Paxil) without difficulty for 12 weeks however has not seen improvement in symptoms of anxiety. What step-wise approach would be done for maximum relief? Drugs requiring a taper due to withdrawal symptoms: • Paroxetine-SSRI • Sertraline-SSRI • Fluvoxamine-SSRI • Desvenlafaxine-SNRI • Duloxetine-SNR • Venlafaxine-SNRI • Pregabalin-Alpha 2 Delta Ligand • Gabapentin-Alpha 2 Delta Ligand Switch medications. 1. Switch from one SSRI to another. (Paroxetine to Escitalopram) 2. Switch from SSRI to SNRI. (Escitalopram to Cymbalta) 3. Augment with buspirone. (Cymbalta and Buspar) 4. Augment with pregabalin. 2. If standard drugs are not effective, nonstandard drugs approved for other anxiety disorders may be used. 1. hydroxyzine 2. benzodiazepine (if clinically justified) are for short-term use only Rationale: Use a stepwise plan to change drug treatment if the initial medication was either ineffective or poorly tolerated. Paroxetine requires a taper while you start the new medication. Do not stop abruptly due to discontinuation syndrome. BENZODIAZEPINES: • Benzodiazepines (BZOs) are used to treat acute anxiety symptoms. • BZOs provide short-term relief of acute anxiety but do not treat the underlying cause. • Benzodiazepines are controlled substances and not intended for long-term use due to the risk of tolerance, dependence, and an uncomfortable withdrawal process. • Abrupt cessation of BZOs can lead to severe withdrawal symptoms including seizures and death. • BZOs enhance gamma-aminobutyric acid's (GABA's) inhibitory effects in the brain by acting on GABA receptors outside of the receiving neuron to open a channel that allows negatively charged chloride ions to pass into the neuron. The negative ions "supercharge" the neuron making it less responsive to neurotransmitters that would normally excite it. • BZOs will induce calm but will also affect higher-level thinking. • Excitatory neurotransmitters, including norepinephrine, serotonin, acetylcholine, and dopamine, are necessary for alertness, memory, muscle tone, coordination, emotional responses, endocrine gland secretions, heart rate, and blood pressure control. • BZOs increase GABA's inhibitory activity, leading to the decreased output of excitatory neurotransmitters resulting in the adverse effects related to BZO use *Equivalence dosing is compared to the standard 10mg Diazepam Alprazolam IR (Xanax) • Short-acting • Use: GAD, panic disorder • Half-life: 12-15 hours • Equivalence: 0.5 mg Dosage: • anxiety: 0.75-1.5mg/day in divided doses; max dose 4 mg/day • panic: 1.5mg/day in divided doses; dosing may exceed 4 mg, increase slowly Additional Information: • rapid onset, less sedating • can cause sedation, fatigue, forgetfulness, hypersalivation • useful adjunct to SSRI/SNRI • recommended use: lowest effective dose for shortest period of time • risk for respiratory depression, especially when taken with CNS depressants • contraindicated in angle-closure glaucoma • tapered dosing when discontinuing, risk of seizures with withdrawal Lorazepam (Ativan) • Short-acting • Use: agitation, anxiety • Half-life: 10-20 hours • Equivalence: 1 mg Dosage: • 2-6 mg/day; BID-TID dosing; max 10 mg/day • elderly: 1-2 mg/day in divided doses Additional Information: • rapid onset • can cause sedation and fatigue (anterograde anesthesia) • safe with liver disease; use lower dosage with liver and renal impairment • increased risk of drug hangover due to longer half-life • increased depressive effects with opioids- do not prescribe together • caution with sleep apnea • contraindicated in angle-closure glaucoma, breastfeeding, and pregnancy • tapered dosing when discontinuing Clonazepam (Klonopin) • Long-acting • Use: panic disorder • Half-life: 30-40 hours • Equivalence: 0.5 mg Dosage: • 0.5-2 mg/day in divided doses or at bedtime • starts at 0.25 mg and increases slowly Additional Information: • rapid onset and less sedating, but does cause some sedation and fatigue • longer duration of action • only Category C benzodiazepine; not recommended with breastfeeding • increases salivation • contraindicated with liver disease • easier to taper dosing than other BZOs due to the long half-life Diazepam (Valium) • Long-acting • Use: acute myocardial infarction-related anxiety, night terrors, alcohol withdrawal • Half-life: 20-50 hours • Equivalence: 10 mg Dosage: • Withdrawal symptoms tend to occur faster with shorter-acting agents (within 2 to 3 days) than with longer-acting agents (within 5 to 10 days). • The Ashton Model recommends reducing daily dosing by 10-20% every 1-2 weeks SPECIAL LIFESPAN CONSIDERATIONS: Pregnancy • Paroxetine is contraindicated in pregnancy due to the risk of atrial septal defects. • Hydroxyzine is contraindicated in the 1st trimester. • Benzodiazepines cross the placenta, so there is an increased risk of neonatal complications even with therapeutic doses. Use of benzodiazepines during pregnancy can cause: o intrauterine growth restriction o oversedation at birth can cause floppiness, difficulty breathing, and difficulty feeding o potential for learning disabilities, autism, and attention-deficit/hyperactivity disorder (ADHD) o neonatal withdrawal syndrome Breastfeeding Contraindicated when breastfeeding: • gabapentin • benzodiazepines • histamine receptor agents • alpha 2 ligands Older Adult With advancing age, a decline in renal and liver function may contribute to the prolonged elimination of medications leading to increased sedative effects and fall risk. Consider decreasing the dosage of sedative-hypnotics when prescribing for older adults; taper whenever possible. 2019 American Geriatric Society (AGS) Beers Criteria include the following recommendations: • avoid barbiturates (increased dependence, tolerance, risk of overdose) • avoid benzodiazepines (increased sensitivity, decreased metabolism) • avoid gabapentin and pregabalin (falls due to sedation) • avoid hydroxyzine (clients with dementia, cognitive impairment, delirium, lower urinary symptoms, or benign prostatic hyperplasia [BPH]) Children • Anxiety disorders often begin in childhood and are often comorbid with depression or bipolar disorder. • For children and adolescents, psychotherapy is the first choice of treatment. SSRIs may be used for severe symptoms or when psychotherapy is not effective. There is an increased risk of suicide in clients less than 30 years using SSRIs. • Gabapentin is not approved for anxiety in children, it may only be used for seizures. Blocking histamine 1 receptors in the brain, it can cause sedation and possibly weight gain, antiemetic effects Blocking alpha 1 adrenergic receptors can cause dizziness, hypotension, drowsiness, and syncope Blocking muscarinic cholinergic receptors can cause dry mouth, blurred vision, urinary retention, constipation, and paralytic ileus Acute blockade of dopamine 2 receptors in the striatum can cause drug-induced parkinsonism, dystonia, or akathisia Chronic blockade of dopamine 2 receptors in the striatum can cause tardive dyskinesia By blocking dopamine 2 receptors in the pituitary, it can cause elevations in prolactin By blocking pancreatic M3 muscarinic receptors Insulin regulation may be impaired Blocking alpha 1 adrenergic receptors can cause dizziness, hypotension, and syncope Partial agonist actions at dopamine 2 receptors in the striatum can cause akathisia and drug- induced parkinsonism Partial agonist actions at dopamine 2 receptors can Also cause nausea, occasional vomiting, and activating side effects Blocking muscarinic cholinergic receptors can cause dry mouth, blurred vision, urinary retention, constipation, and paralytic ileus Blockade of dopamine 2 receptors in the tuberoinfundibular pathway causing sexual dysfunction