Psych Exam 2 PDF

Psych Exam 2 Antipsychotic Medication Conventional (First-Generation) Antipsychotics ○ Target positive symptoms: Hallucinations Delusions, Disorganized Speech thiothixene (Navane) fluphenazine (Prolixin) haloperidol (Haldol)...

Psych Exam 2 Antipsychotic Medication Conventional (First-Generation) Antipsychotics ○ Target positive symptoms: Hallucinations Delusions, Disorganized Speech thiothixene (Navane) fluphenazine (Prolixin) haloperidol (Haldol) pirozide (Orap) loxaine (Loxitane) molidone (Moban) perphenazine (Trilafon) Chlorpromazine (thorazine) thioriadizine (Mellaril) Atypical (Second-Generation) Antipsychotics ○ Target positive and negative symptoms (negative symptoms-reduced motivation, avolition, cognitive behavior) aripiprazole (Abilify) clozapine (Clozaril) olanzapine (Zyprexa) paliperidone (Invega) quetiapine (Seroquel) risperidone (Risperdal) ziprasidone (Geodon) Conventional ○ Higher risk for: EPS: (involuntary movements) ○ Acute dystonia (Dystonic reaction) Torticollis (wry-neck syndrome), opisthotonus (arched rigid body), oculogyric crisis (eye deviations) Treatment: anticholinergic drugs or diphenhydramine ○ Akathisia-movement, usually below the hips such as marching, rocking while standing ○ Drug-induced parkinsonism ○ Tardive dyskinesia (lip smacking, moving mouth/jaw, tapping feet) NMS (Neuroleptic Malignant Syndrome) – 10-15% death (High fever, confusion, rigid muscles, sweating, erratic b/p) Treatment is symptomatic Dantrolene Orthostatic hypotension Atypical ○ Higher risk for: Risk of metabolic syndrome: Increased weight Increased blood glucose Increased triglyceride levels Insulin resistance Lower risk of EPS ○ Psychopharmacology: Maintenance Therapy ○ Six antipsychotics available in depot injection form:  Fluphenazine in decanoate and enanthate preparations Haloperidol in decanoate Risperidone Paliperidone Olanzapine Aripiprazole ○ May take several weeks of oral therapy to reach stable dosing level before transition to depot injections Adverse effects of receptor blockage of antipsychotic agents Introduction Into Psychotropic Drugs Types of Psychotropic Drugs ○ Antipsychotics: treat delusions and hallucinations ○ Mood stabilizers or antimanic agents: slow down runaway thinking ○ Antidepressants: improve mood ○ Antianxiety drugs: calm anxiety ○ Drugs used for Alzheimer disease: improve thinking ○ Antiparkinsonian drugs: correct problems caused by antipsychotic drugs Nursing Responsibilities ○ Second component of psychotherapeutic management model. ○ Understand key dimensions of psychotropic drug use. ○ Assess drug side effects. ○ Evaluate desired effects. ○ Apply preventive care to reduce potential problems. ○ Determine use of PRN medications. Pharmacokinetics ○ Absorption: getting the drug into the bloodstream ○ Distribution: getting the drug from the bloodstream to the tissues and organs ○ Metabolism: breaking the drug down into inactive and typically water-soluble form ○ Excretion: getting the drug out of the body  Half-Life of Drugs ○ Amount of time required for 50% of the drug to disappear from the body ○ Linear kinetics: The amount of drug in the body decreases by 50% every 4 hours. ○ Washout period: To discontinue a drug, four half-lives are required to eliminate 96% of the drug. Pharmacodynamics ○ Effect that drug has on body: desired effects, side effects, adverse effects Agonists: activate receptors Antagonists: block receptors ○ Down-regulation: Chronic exposure to certain drugs causes receptors to change. ○ Pharmacodynamic tolerance causes reduction in receptor sensitivity. Neurotransmitters and Related Mental Disorders Psychotropic Drugs and Neurotransmitters ○ Block metabolism: some antidepressants and drugs for Alzheimer disease ○ Block reuptake: SSRI and other antidepressants ○ Block receptors: antagonists ○ Stimulate or block autoreceptors ○ Stimulate receptors (agonists) ○ Stimulate receptor affinity ○ Stimulate release of neurotransmitter Receptors ○ Receptor: configured so that precisely shaped molecules fit and cause or prevent a response. ○ Ligand: a transmitter substance that fits and evokes a response from a receptor. ○ Neurotransmitter serotonin fits serotonin receptors. ○ Receptor antagonism: related to blocking that receptor by a psychotropic drug ○ Receptor agonist: a drug that fits and activates the receptor Patient Education ○ Enhances adherence to medication regimen Discuss side effects. Discuss safety issues.  Attitude of patient and nurse about medications. Drug interactions. Discuss cognitive, affective effects. Instructions for older adult patients or children of older patients. Instructions for pregnant or breast-feeding patients. Awareness of metabolic differences in diverse races and ethnicities. Emphasize regular follow-up. Discuss desired effect. Reasons for Nonadherence ○ Sexual dysfunction ○ Side effects, such as dry mouth and insomnia ○ Emotional dulling ○ Cognitive slowing ○ Denial of need ○ Fear of becoming addicted ○ Religious reasons ○ Interference with work Antidepressant Drugs Antidepressant Drugs Treat Mood Disorders ○ Unipolar Depression Major depressive episode ○ Bipolar disorder Bipolar I, Bipolar II ○ Related disorders Dysthymic disorder Cyclothymic disorder Substance-induced depressive or bipolar disorder Seasonal affective disorder Postpartum blues, depression, psychosis, premenstrual dysphoric disorder Nonsuicidal self-injury Etiology ○ Genetic Theory Twin Studies, Adoption Studies ○ Biochemical Theory Serotonin and norepinephrine are two major neurotransmitters involved in depression. ○ Psychosocial Theories The stress–diathesis model of depression Learned helplessness Cultural considerations ○ Cognitive Theory Beck’s cognitive triad:  Negative, self-deprecating view of self Pessimistic view of the world Belief that negative reinforcement will continue Biochemical Theory of Depression ○ Neurotransmitter depletion linked to depression ○ Antidepressants stabilize mood by increasing the intrasynaptic availability of certain neurotransmitters: Norepinephrine (NE) Serotonin (5-HT) Dopamine (DA) Interrelated Biological Hypotheses ○ Include: Receptor dysregulation (receptor/genes change-lag time) Inflammation (stress + inc BBB permeability+ cytokines) Methylation (changes in brain cells and genes) Premature neuronal death (MAO system deregulation) Lack of synaptogenesis/Altered genetic output (cell division-gene mutation) ○ Antidepressant-mediated genetic modification might be the most important current hypothesis. (how the medication affects other genes involved in depression) Antidepressant-Mediated: Genetic Modification ○ Proposed solution: reregulation of the second messenger system ○ Proposed causes: Key genetic products are undersynthesized. Potential deficiency of brain-derived neurotrophic factor causes accelerated cellular apoptosis (genetically programmed cell death). Actual neuronal death from dysregulated monoaminergic systems Lack of synaptogenesis (the growth of new synapses) Antidepressant Treatment ○ Aims to restore normal neurotransmitter levels ○ Cyclic antidepressants (or reuptake-inhibiting antidepressants) Increase the “deficient” neurotransmitters by blocking the reuptake of one or more ○ Enzyme-inhibiting agents (MAOIs) Increase the “deficient” neurotransmitters by preventing/slowing their metabolic breakdown Psychopharmacology ○ Depression SSRI NSSRI Atypical Tricyclic MAOI  ○ Combination of specific psychotherapies & antidepressant therapy may be superior to either psychotherapy or psychopharmacologic treatment alone. ○ Selective serotonin reuptake inhibitors Serotonin syndrome ○ Tricyclic antidepressants ○ Atypical antidepressants ○ MAOI antidepressants Lethal in overdose Hypertensive crisis SSRI’s ○ Selective Serotonin Reuptake Inhibitors ○ First line of treatment for depression and certain anxiety disorders ○ Block the neuronal uptake of serotonin by inhibiting the uptake of serotonin in the nerve terminal, the level of serotonin increases resulting in an antidepressant effect ○ Therapeutic response may take 2-8 weeks ○ Careful monitoring for suicidality during the first few weeks (4-6) of treatment ○ fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil) Side effects include fewer anticholinergic effects than tricyclic agents and nausea and vomiting (N/V). Dizziness, drowsiness, headache, GI Fewer side effects than TCAs Far less dangerous than MAOIs ○ Most Frequently RX: fluoxetine (Prozac) ○ Black box suicide warning ○ Serotonin syndrome -Emergency ○ Antidepressant apathy syndrome - deficit in ADL’s ○ Antidepressant withdrawal/discontinuation syndrome -Flu like symptoms ○ Antidepressant loss of effectiveness -brain less sensitive to the drug ○ Antidepressant-induced suicide –especially in children and young ○ Gastrointestinal symptoms Nausea Diarrhea Loose stools, weight loss or gain Hyponatremia: mainly in older patients Excessive sweating CNS effects Anticholinergic effects: not as common as in TCAs Dry mouth Sedation Excessive sweating: 20% of patients Central nervous system effects Headache Dizziness Tremors  Anxiety Insomnia Sexual dysfunction: 50% of patients Cyclic Antidepressants (or Reuptake-Inhibiting Antidepressants) ○ Serotonin and noradrenaline reuptake inhibitors (SNRIs): venlafaxine (Effexor), desvenlafaxine (Pristiq) duloxetine (Cymbalta), and levomilnacipran (Fetzima). Increases serotonin and norepinephrine. Side effects include fewer anticholinergic effects than tricyclic agents and N/V. ○ Serotonin and noradrenaline disinhibitors (SNDIs): mirtazapine (Remeron) Increases serotonin and norepinephrine. Has antianxiety, antidepressant, and antiemetic effects. Side effects include sedation and weight gain. ○ Norepinephrine dopamine reuptake inhibitors (NDRIs): bupropion (Wellbutrin, Zyban-smoking cessation) Increases dopamine and norepinephrine Sometimes prescribed for weight loss (long-term) SE dry mouth, insomnia, constipation Lower seizure threshold Do not drink ETOH ○ Trazodone (Desyrel) Is not the first choice for antidepressant treatment, but can help with insomnia. Tricyclic antidepressants (TCAs) Nonselective, meaning they block the reuptake of both serotonin and norepinephrine Include: amitriptyline (Elavil), desipramine (Norpramin), imipramine Tofranil), nortriptyline (Pamelor) Indications MDD-not first line due to multiple drug interactions More S/E than SSRI’s, added anticholinergic side effects (drowsiness, blurred vision, etc.) Lethal in overdose Do not use with other serotonin increasing drugs or St John’s Wort Contraindications- MI, hepatic hx Norepinephrine Dopamine Reuptake Inhibitor (NDRI) Bupropion (Wellbutrin, Zyban, Aplenzin) ○ Only antidepressant with dopamine reuptake inhibition as a major mechanism of action.  ○ Does not affect serotonin systems. ○ Good SE profile. ○ Should not be given with drugs that increase dopamine level. ○ Under trade name Zyban, it is marketed for smoking cessation. MAOIs ○ Treatment resistant depression ○ Adverse and toxic effects- inhibits breakdown of tyramine in liver, (hypertensive crisis, CVA, death) ○ Interactions Drugs: Avoid over-the-counter (OTC) medications and SSRI Buspar, Opiates, Demerol Food: Avoid foods containing tyramines (Box 15.8 pg 174) ○ Need to be off MAOI for at least 2 weeks before starting another antidepressant (NO OVERLAP) phenelzine (Nardil) tranylcypromine (Parnate) EMSAM (selegiline transdermal system) delivers monoamine oxidase inhibitors (MAOIs) through the skin. ○ Hypertensive crisis: Occurs if patient ingests tyramine found in some over-the-counter (OTC) medications, beer, wine, aged cheese, organ meats, avocadoes, and other foods. (other medications as previously discussed) ○ Symptoms: HTN, Hyperpyrexia, Tachycardia, diaphoresis, Tremors, Cardiac Dysrhythmias ○ Dietary restriction of tyramine must be maintained for 2 weeks after stopping MAOIs. Serotonin Syndrome ○ Due to central and peripheral serotonin hyper stimulation ○ Symptoms: Confusion, delirium, agitation, irritability, incoordination, tremor, seizures, fever, diaphoresis, n/v, diarrhea, abdominal pain, hypo or hypertension, tachycardia, severe respiratory depression, coma  ○ Develop soon after the addition of a new medication or a dosage increase in current medication ○ A lot of medications affect Serotonin- be Aware of Medications that are being taken which affect Serotonin ○ Treatment Discontinue the medication (that induced the crisis) Treat symptoms Other Medical Treatments and Psychotherapy ○ Electroconvulsive therapy (ECT) Electroconvulsive Therapy (ECT): Treating Severe Depression (youtube.com) ○ Psychotherapy (combined with medications) Interpersonal therapy: relationship difficulties Behavior therapy: positive reinforcement of interactions Cognitive therapy: focus on cognitive distortions ○ Investigational treatments: transcranial magnetic stimulation (TMS) – OCD, MDD Stimulates and resets specific areas of the brain that regulate your mood to provide relief and break the cycle of depression. Antiparkinsonian Normal Extrapyramidal System ○ Normal coordination of involuntary movement. ○ Involuntary movement supports voluntary movement when walking. ○ Balance of two neurotransmitters, acetylcholine (ACh) and dopamine (DA), is required for the normal functioning of the extrapyramidal system. ○ Parkinson’s appear when these two are out of balance. Parkinson Disease and Extrapyramidal SE ○ Cardinal Symptoms Treamors Bradykinesia Rigidity Postural Instability Assocaited Symptoms ○ In addition to the four cardinal symptoms: Difficulty swallowing Drooling Weight loss Choking Impaired breathing Urinary retention Constipation Parkinson Disease Effects ○ Pigmented neurons of the substantia nigra lose their pigmentation and decline dopamine production  ○ Decrease in dopamine transmission to the basal ganglia results in an imbalance with acetylcholine Causes of EPSES vs causes of Parkinson effects ○ PD: imbalance related to neurodegeneration of the substantia nigra at the beginning of the dopamine tracts ○ EPSEs: blockage of dopamine receptors in the basal ganglia at the end of the dopamine tracts Treating ESPES vs Parkinson Disease ○ PD: treated with antiparkinsonian agents that increase dopamine leves: levodopa/carbidopa (SInemet) and levodopa with anticholinergic agents (benztropine [cogentin}) or both ○ EPSEs: treated with anticholinergics only Parkinson-like extrapyramidal side effects ○ Remember: EPSEs are the result of biochemical changes from antipsychotics that are similar to those symptoms found in Parkinson disease (PD) ○ Akathisia Subjective feeling of restlessness Restless legs, jittery feelings, nervous energy Responds poorly to treatment Most common EPSE Reassure patient May need to switch to a different class of antipsychotic medication ○ Akinesia and bradykinesia Akinesia: absence of movement Bradykinesia: slowed movement Includes weakness, fatigue, painful muscles, and anergia (abnormal lack of energy) Be patient, reassure, obtain anticholinergic order Responds to anticholinergics ○ Dystonia Abnormal sustained, contracted postures Caused by involuntary muscle spasms Affects limbs, trunk, neck, mouth Appears early in treatment (w/in 3 days) Responds to anticholinergics In emergency, administer parenterally Types of Dystonia Torticollis: contracted positioning of the neck Oculogyric crisis: contracted positioning of the eyes upward Laryngeal-pharyngeal constriction: can be life-threatening Give antiparkinsonian drug, benztropine (cogentin) or antihistamine diphendhydramine (benadryl) immediately as needed Offer reassurance ○ Drug-induced parkinsonism Tremors, bradykinesia, rigidity, postural instability  Develops early in treatment Assess and report Obtain order for anticholinergic ○ Tardive Dyskinesia Caused by long-term use of antipsychotics (“tardive” means “late appearing”) causing the dopamine receptors in the basal ganglia to be hypersensitive Late appearing, after 6 months or more Lip smacking, teeth grinding Tongue thrusting or writhing Symptoms stop with sleep Worsens with anticholinergics because it is not caused by an imbalance of dopamine-acetylcholine Often irreversible If caught in time, can be averted No treatment yet developed Prevention as important approach ○ Neuroleptic Malignant Syndrome Potentially lethal side effect Hyperthermia: 101F to 103F to 108F Rigidity Autonomic dysfunction Treatment with dantrolene (dantrium) muscle relaxant and bromocroptine (Parlodel) centrally acting dopaminergic Routinely take temperature, assess for symptoms ○ Pisa Syndrome Patient leans to one side Acute or tardive Older adults more vulnerable Higher Risk for Extrapyramidal SE ○ Women ○ First episode of schizophrenia Overtreatment of schizophrenia can cause PD effects To give a dopamine-enhancing drug like levodopa to a patient with schizophrenia can cause increased psychosis ○ Older adults ○ Patients with affective symptoms Anticholinergic Drugs for EPSES in Schizophrenia ○ Schizophrenia is linked to excessive dopamine ○ Antipsychotic drugs block dopamine, which can cause EPSEs ○ Antiparkinsonian drugs can fix the problem that antipsychotics create ○ If dopaminergic antiparkinsonian drugs are given, schizophrenia might worsen ○ Anticholinergics drugs are given to restore ACh-dopamine balance Anticholinergic Drug Dosages for EPSES ○ Benztropine (Cogentin) 1 to 4 mg PO or IM one to twice a day Acute dystonic reactions: 1 to 2 mg IM/IV, then 1 to 2 mg PO BID  ○ Trihexphenidyl (Artane): Start 1 mg daily, increase to usual dosage range, 5 to 15 mg/day Pharmacological Effects ○ Anticholinergic drugs block acetylecholine receptors ○ Anticholinergics are used alone in the treatment of EPSEs ○ Antipsychotic drugs block dopamine receptors, causing EPSEs ○ Blockage of dopamine receptors in basal ganglia produces EPSEs ○ High-potency antipsychotics like haloperidol (Haldol) cause more EPSEs Side Effects of Anticholinergics ○ Central nervous system effects Confusion Cognitive impoverishment Agitation Dizziness Drowsiness Disturbances in behavior Cognitive dysfunction ○ Peripheral nervous system (PNS) effects Dry mouth Nasal congestion Urinary hesitation or retention Blurred vision, photophobia, mydriasis Constipation Decreased sweating Fever Overdose of anticholingeric drugs ○ CNS hyperstimulation Confusion, excitement, hyperpyrexia, agitation, disorientation, delirium, or hallucination ○ CNS depression Drowsiness, sedation, or coma ○ CV, urinary, and GI system, eyes as well ○ Use cautiously during pregnancy ○ Older individuals have more pronounced reaction Interactions with anticholinergics ○ Alert the patient to dangers of OTC drugs and other prescription drugs that intensify the atropine-like effects of anticholinergics ○ Other interactions Intensification of sedative effects when combined with CNS depressants Decrease in absorption when using antacids and antidiarrheal drugs Teaching Patients ○ Avoid discontinuing drugs abruptly ○ Taper over a 1 week period ○ Avoid driving until tolerance develops and drowsiness and blurred vision diminish ○ Avoid over-the-counter medications that have anticholinergic or antihistamine properties  ○ Avoid alcohol ○ Avoid antacids Selected Anticholinergic Drugs ○ Benztropine (Cogentin): most frequently prescribed anticholinergic antiparkinsonian drug ○ Diphenhydramine (benadryl): antihistamine effective for most parkinsonia-like disorders; causes considerable sedation in some; less potent than benztropine ○ Trihexphenidyl (Artane): unavailable parenterally Other treatment options for EPSES ○ Dopamine agnosit - amantadine (symmetrel) ○ Beta Blocker - propranolol (inderal) ○ Benzodiazepines - diazepam (valium), lorazepam (ativan), clonazepam (klonopin) ○ Vitamins E and B6 possibly for TD EPSE Prevention ○ Establish whether patient is from high-risk group Woman Older adult First episode of schizophrenia Has affective symptoms ○ Obtain baseline information about EPSEs Use validated tool ○ Choose drug with lower risk for EPSEs High risk: haldol, prolixin, traditional antipsychotics Lower risk: atypical agents ○ Monitor patient regularly ○ If EPSEs develop Switch to atypical agent If on atypical agent, lower dose; switch to atypical agent with better side effect profile; add antiparkinsonian agent Antimanic Drugs Treatment Goals for Bipolar Disorder ○ Remission ○ Prevention ○ Return to premorbid function Maintenance Therapy for Bipolar Disorder ○ Prevent relapse ○ Reduce suicide risk ○ Improve functioning ○ Reduce subthreshold symptoms Symptoms not quite reaching a level of clinical diagnostic significance Lithium ○ Gold standard for bipolar disorder ○ Naturally occurring element ○ Treatment and prophylaxis of manic phase  Pharmacological Effects ○ Inhibits release of norepinephrine, serotonin, and dopamine ○ Facilitates their reuptake into presynaptic terminals Decreasing the synaptic levels of these neurotransmitters—the very action that one would surmise needs to occur in the hyperactive state of mania. ○ Normalizes a dysfunctional second messenger system Lithium Toxicity Symptoms ○ Symptoms of acute and acute-on-chronic lithium toxicity ○ Early symptoms of acute lithium toxicity include gastrointestinal (GI) problems, like: Nausea and vomiting. Diarrhea. Abdominal pain. Bloated stomach. ○ These symptoms usually develop within one hour of taking excess lithium. Lithium Toxicity ○ If you have moderate to severe lithium toxicity, you’ll likely get neurological symptoms after the gastrointestinal symptoms. These include: Mental status changes that can range from mild confusion to delirium. Uncontrolled shaking (tremors). Coordination and balance issues (ataxia). Muscle twitches (myoclonus). Slurred speech (dysarthria). Overactive reflex responses (hyperreflexia). Uncontrolled eye movements (nystagmus). Hyperthermia (severe cases). Seizures (severe cases). Coma (severe cases). ○ Get immediate medical help if you take lithium and have these symptoms Lithium Toxicity Treatment ○ Stomach pumping (gastric lavage). ○ Whole-bowel irrigation. This involves taking a special solution by mouth or through a tube that goes through your nose and into your stomach. It clears your gastrointestinal system of lithium. ○ Activated charcoal (if you took other medications or substances as well).  ○ Kidney dialysis (hemodialysis). ○ IV fluids. ○ Various medications to treat symptoms. ○ You’ll likely receive treatment in an ER or ICU Lithium Pharmacokinetics ○ Peak blood levels: 1 to 3 hours ○ Absorption: GI tract ○ Excretion: kidneys ○ Plasma half-life: 24 hours ○ Narrow therapeutic index What goes wrong in bipolar disorder ○ Cause: decrease in Na+,K+-ATPase activity Neuronal membranes become irritable, requiring fewer stimuli for cell firing Sodium accumulates, diminishing the hyperpolarizing functions of inhibitory neurotransmitters Neuron fires more easily, but with loss of amplitude. This causes calcium channels to decrease activity, resulting in reduced neurotransmitter release. Patient Guidelines: Lithium ○ Take at same time daily. ○ Mild side effects are transient. ○ Report vomiting, coarse hand tremor, sedation, weakness, and vertigo. ○ Maintain salt intake and a balanced diet. ○ Illness with fever, excessive sweating Might require dose adjustment ○ Lithium level: morning blood draw 8 to 12 hours after last dose Common Side Effects ○ Therapeutic serum level of lithium is 0.6 to 1.2 mEq/L. ○ Common side effects Nausea Dry mouth Diarrhea Thirst Drowsiness Mild hand tremor Polyuria/polydipsia (occur in 70% of patients) Weight gain Bloated feeling Sleeplessness Lightheadedness Toxic Effects ○ Mild to moderate: 1.5 to 2.0 mEq/L. -We do not want lithium to be higher than 1.5. Diarrhea Vomiting  Drowsiness Dizziness Hand tremor (coarse) Muscular weakness Lack of coordination Dry mouth ○ Moderate to severe: 2 to 3 mEq/L -More serious symptoms Previous symptoms, plus… Ataxia Giddiness Tinnitus Blurred vision Large output of dilute urine Delirium Nystagmus ○ Severe toxicity: >3 mEq/L -Manic patients may take their meds too much and become toxic (LETHAL) Previous symptoms, plus… Seizure Organ failure Renal failure Coma Death Key Nursing Interventions ○ Discuss side effects that should subside Nausea, dry mouth, diarrhea, thirst, mild hand tremor, weight gain, bloatedness, insomnia, lightheadedness). ○ Identify the side effects that require immediate notification of the physician Vomiting, severe tremor, sedation, muscle weakness, vertigo) BIG PROBLEM!- Have to be reported to provider ○ Suggest taking lithium with meals to reduce nausea. ○ Suggest drinking 10 to 12 glasses of water per day. Can be juice. Just liquid. ○ Advise elevating feet to relieve ankle edema. ○ Advise consistent dietary sodium intake; increase sodium if a major increase in perspiration occurs. Anticonvulsants ○ Divalproex sodium—Depakote ○ Valproates ○ Carbamazepine—Tegretol ○ Lamotrigine—Lamictal ○ Oxcarbazepine—Trileptal. Side effect is rash. ○ Gabapentin—Neurontin ○ Topiramate—Topamax How Valproates Work ○ Increase in the inhibitory role of GABA ○ Suppression of sodium influx into the neuron ○ Suppression of calcium influx through specific calcium channels Antipsychotics ○ Olanzapine—Zyprexa ○ Risperidone—Risperdal ○ Quetiapine—Seroquel  ○ Ziprasidone—Geodon ○ Clozapine—Clozaril ○ Aripiprazole—Abilify ○ Asenapine—Saphris Monotherapy ○ First-line approaches Either lithium, a valproate, or medication used for acute stage ○ Second-line approach Atypical antipsychotic ○ Third-line approach Carbamazepine or lamotrigine or gabapentin or topiramate Combination Therapy ○ Atypical approach Atypical antipsychotic (e.g., olanzapine) plus lithium or a valproate ○ Benzodiazepine approach Benzodiazepine plus lithium or a valproate ○ Typical approach Typical antipsychotic (e.g., haloperidol) plus lithium or a valproate ○ Mood stabilizers (two or more) Other Treatment Approaches ○ For severe acute mania Lithium or a valproate plus an atypical antipsychotic ○ For bipolar depression First line: lithium or lamotrigine or fluoxetine+olanzapine or electroconvulsive therapy Antianxiety Drugs Models of Anxiety ○ Three causative factors Autonomic nervous system dysregulation Dysregulation of beta-adrenergic receptors ((bad connection of the heart) Inhibition of GABA Neuroendocrine overactivity Faulty thinking Autonomic (adrenergic System) Symptoms of Anxiety ○ Tachycardia ○ Dilated pupils ○ Tremor ○ Sweating Symptoms Associated With Panic Attacks ○ MUCH WORSE THAN ANXIETY- severe ○ Palpitations ○ Sweating ○ Trembling or shaking ○ Shortness of breath ○ Feeling of choking ○ Chest pain (worse than anxiety) ○ Nausea and abdominal distress ○ Feeling dizzy, unsteady, lightheaded, faint ○ Derealization ○ Fear of losing control or going crazy  ○ Fear of dying ○ Tingling sensations ○ Chills or hot flashes Subjective Symptoms of Anxiety Observable by Others ○ Anxious ○ Apprehensive ○ Compulsive ○ Fearful ○ Experiencing feelings of dread ○ Irritable ○ Intolerant ○ Nervous ○ Overconcerned ○ Panicky ○ Phobic ○ Preoccupied ○ Experiencing repetition in motor activities ○ Feeling threatened ○ Wound up ○ Sensitive to shame ○ Worried Medications that can cause anxiety ○ While taking increase symptoms: Asthma medications, e.g., albuterol Beta agonists, e.g., isoproterenol Herbals drugs, e.g., Ma huang, ginseng Corticosteroids Antidepressants, e.g., SSRIs, NDRI, TCAs ○ While “withdrawing”: Alcohol Social drinking (i.e., rebound effect) Nicotine Benzodiazepines (reverse effect) ○ Illegal or abused legal drugs: Methamphetamine (adderal)= stay up at night to study Cocaine Methylphenidate Ecstasy Disorders That Can Cause Anxiety ○ Hypothyroidism ○ Asthma ○ Cardiac arrythmias Antianxiety Drugs ○ Benzodiazepines Acute anxiety Ativan ○ Buspirone 3 times a day Takes edge off Take when about to enter stressful situation Its okay to take less  ○ SSRIs Prozac ○ SNRIs Bupropion ○ Other drugs with antianxiety Clomipramine and other antitricyclics Clonidine Gabapentin Antiepileptics (Pregabalin and Levetiracetam) Propranolol Conditions Amendable to Benzodiazepine Treatment ○ Acute agitation ○ Alcohol withdrawal ○ Antipsychotic-induced akathisia and tremor ○ Catatonia ○ Generalized anxiety disorder ○ Insomnia ○ Panic disorder ○ Social anxiety When Benzodiazepines Are Appropriate for Treating ○ Coadministration for 2 to 4 weeks when initially treating with SSRIs or venlafaxine ○ Patients wanting to avoid sexual side effects of antidepressants ○ Patients taking aspirin or NSAIDs on a long-term basis ○ Patients with comorbid epilepsy or bipolar disorder Frequently Prescribed Benzamidines and Buspirone ○ Alprazolam (Xanax): 0.50 mg ○ Lorazepam (Ativan): 1.0 mg ○ Oxazepam (Serax): 30 mg ○ Temazepam (Restoril): 30 mg ○ Chlordiazepoxide (Librium): 10 mg ○ Clonazepam (Klonopin): 0.25 to 0.5 mg ○ Diazepam (Valium): 5 mg ○ Buspirone (BuSpar): NA= NOT benzo give this before a real benzo Benzodiazepine Side Effects ○ Anterograde amnesia (no new memories) ○ Ataxia ○ Confusion ○ Depression ○ Drowsiness ○ Dysarthria ○ Headache ○ Impairment of mental functions ○ Increased reaction time ○ Lassitude ○ Lightheadedness ○ Motor incoordination ○ Sexual dysfunction ○ Skin reactions ○ Weight gain ○ Physical dependence  ○ Tolerance ○ Withdrawl ○ Drug-drug interactions Symptoms After Benzodiazepine Withdrawal ○ Neurological Convulsions, insomnia, lightheadedness, involuntary movements, headache, weakness ○ Gastrointestinal Nausea, vomiting, diarrhea, weight loss, decreased appetite ○ Psychiatric Anxiety, irritability, cognitive, memory impairment, depression, confusion ○ Other: tachycardia, sweating Major Interactions With Benzodiazepines ○ Alcohol Increased sedation, CNS depression ○ Antacids Impaired absorption rate of benzodiazepine ○ Disulfiram (Antabuse)/cimetidine (Tagamet) Increased plasma level of benzodiazepines that are oxidized (e.g., diazepam) ○ Phenytoin Increased anticonvulsant serum level= seizures ○ TCAs Increased sedation, confusion, impaired motor function ○ MAOIs CNS depression ○ Succinylcholine Decreased neuromuscular blockage Benzodiazepines Patient Teaching ○ Not for minor stresses. ○ Over-the-counter drugs might enhance action. ○ Kava-kava and valerian cause additive effect. ○ Avoid driving until tolerance develops. ○ Do not exceed prescribed dose. ○ Avoid alcohol and CNS depressants. ○ Do not stop abruptly= wean off ADDICTING!!! Buspirone ○ Nonsedating ○ No highs—decreased abuse potential ○ No cross-tolerance with alcohol, sedatives ○ Takes 1 to 6 weeks for full effect ○ No dependence, withdrawal, or tolerance ○ Divided doses ○ Must be taken with food ○ Few drug-drug interactions Other Antianxiety Agents ○ Selective serotonin reuptake inhibitors (SSRIs) SSRIs are first-line agents for anxiety spectrum  Uses: generalized anxiety disorder (GAD), obsessive-compulsive disorder (OCD), panic attacks, posttraumatic stress disorder (PTSD), and social phobias ○ Selective serotonin-norepinephrine reuptake inhibitors (SNRIs) Venlafaxine (Effexor) and duloxetine (Cymbalta) Other Drugs with Antianxiety Properties ○ Clomipramine and other tricyclic antidepressants Clomipramine (Anafranil) ○ Clonidine (Catapres) ○ Gabapentin (Neurontin) ○ Hydroxyzine (Vistaril, Atarax) ○ Antiepileptics: pregabalin and levetiracetam ○ Propranolol Schizophrenia Positive symptoms ○ Hallucinations, delusions, abnormal thoughts, agitation, bizarre behavior, excitement, hostility Negative symptoms ○ Flattened affect, avolition, alogia, anergia, attention deficits, communication difficulties, difficulty with abstractions, poverty of speech