Nursing 324 Adult Health Unit 2 Study Guide, Exams of Nursing

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Nursing 324 Adult Health Unit 2 study guide

Headache: Neurovascular disorder that involves dilation and inflammation of the intracranial blood vessels. Calcitonin gene related peptide (CGRP) and serotonin (5-HT) are key. CGRP promotes migraine and the role of 5- HT is to suppress migraine. Appropriate drugs for prophylaxis: Beta blockers, tricyclic antidepressants, and antiepileptic drugs. Nonspecific analgesics:

• Aspirin like drugs, NSAIDs, Excedrin Migraine (aceta, aspirin, caffeine)
• Opioid Analgesics: Only for severe. Meperidine (Demerol), and butorphanol nasal spray (Stadol). Migraine specific drugs
• Serotonin Receptor Agonists (Triptans) o Constrict intracranial blood vessels and suppressing release of inflammatory neuropeptides o Almotriptan (Axert), Eletriptan (Relpax), Frovatriptan (Frova), Naratriptan (Amerge), Rizatriptan (Maxalt), Sumatriptan (Imitrex), Zolmitriptan (Zomig) o Interactions: Do not combine with other triptans (HTN from vasoconstriction). MAOIs can suppress hepatic degradation of sumatriptan, causing levels to rise. SSRIs (fluoxetine)and SNRIs (duloxetine) indirectly activate serotonin receptors in the brain, which can result in serotonin syndrome (AMS, anxiety, hallucinations).

Indications for Ca++ Channel blockers, Tricyclics (Amitriptyline) For patients who have frequent attacks (three or more a month), attacks that are especially severe, or attacks that do not respond to abortive agents. CC blockers: Verapamil and Nimodipine. Tricyclics: Inhibits reuptake of serotonin, making more of the transmitter available for action. Amitriptyline (Elavil). 25-150mg once daily at bedtime. SE: Hypotension, cholinergic side effects (dry mouth, constipation, urine retention, blurred vision, tachy) Review the indications for topamax (topiramate)

• Several weeks to develop.

• SE: paresthesias, fatigure, and cognitive dysfunction, acidosis, weight loss. Dosage should be low initially and then gradually increased. 25mg daily for 1 week, 25 mg twice daily second week. Up to 50 mg twice daily Meds for cluster HA Cluster HA- 15 minutes to 2 hours. Severe, throbbing unilateral pain in the orbital temporal area. Daily attacks for 2- 3 months. Lacrimation, conjunctival redness, congestion, rhinorrhea, ptsosis, and miosis. Not preceded by an aura, no n/v, more debilitating, no family history
• Prophylaxis is primary therapy. D/C when current cycle of HAs are over.
• Glucocorticoids, verapamil, lithium
• Verapamil is first line treatment
• Lithium is second. Blood levels of lithium must be monitored. 0.66-1.2. SE/Contraindications of drugs such as B-Blockers Beta blockers: Propranolol is used most often. SE: tiredness, fatigue, asthma exacerbation, and may promote depression LOCAL ANESTHETICS : Esters vs Amides Local anesthetics stop axonal conduction by blocking sodium channels in the axonal membrane. Prevent sodium entry, and block conduction. Nonselective modifiers of neuronal function. Block action potentials in all nerons to which they have access. Time: Determined largely by molecular properties. Size, lipid solubility, and degree of ionization at tissue pH. Small size, high lipid solubility and low ionization cross the membrane rapidly. Large size, low lipid solu, and high ionization cross slowly. Termination: Local anesthesia occurs as molecules of anesthetic diffuse out of neurons and are carried away in the blood. Same properties for onset determine termination.

Use with vasoconstrictors: Epinephrine. Decreases local blood flow and thereby delays systemic absorption of the anesthetic. Delaying prolongs anesthesia and reduces the risk of toxicity. Absorption is slowed, then less anesthetic is used. Slowing absorption is more favorable balance is established between the rate of entry of anesthetic into circulation and the rate of its conversion into inactive metabolites. Absorption: determined by blood flow Metabolsim: Ester type are metabolized in the blood by enzymes known as esterases. Amid-type anesthetics are metabolized by enzymes in the liver. AE: CNS excitation followed by depression. Seizures may occur during excitation. Drowsiness to unconsciousness to coma. CV effects suppress excitability in the myocardium and conducting system, and thereby can cause brady, heart block, and reduced contractile force. Allergic reactions are more likely with the ester-type anesthetics than with amides. If allergic to one ester drug, than reactions to all. Opposite in amid drugs. Locals can depress uterine contractility and maternal effort which prolongs labor. Methemoglobinemia: Benzocaine can cause a blood disorder in which HGB is modified such that it cannot release oxygen to tissues.

• Esters: Procaine- Not effective topically. Admin with epi delays absorption. Plasma esterases rapidly convert the drug to inactive, nontoxic products. Allergic response more likely.
• Amid: Lidocaine- rapid and intense, and more prolonged than an equal dose of procaine. Effects can be extended by coadministration of epi. Inactivated by liver. Drugs for Seizures: Actions, side effects, contraindications, monitoring and assessment e.g. phenytoin, valproic acid, Carbamazepine, Phenobarb Dosing with Phenobarb, when can it cause CNS depression, target levels. Actions: Phenytoin, carbamazepine, valproic acid, and lamotrigine, reversible

bind to sodium channles while they are in the inactivated state, and thereby prolong channel inactivation. This returns to the active state, these drugs decrease the ability of neurons to fire at high frequency. Suppression of calcium influx. Promotion of potassium efflux. Antagonism of Glutamate (excitatory transmitter). Potentiation of GABA (inhibitory neurotransmitter). Phenytoin: treats partial seizures and tonic clonic seizures. Selective inhibition of sodium channels. Slows recovery of sodim channels from the inactive state back to the active state. Liver metabolized. Therapeutic effects are only slightly smalled than the doses needed to saturate liver, which would cause levels to rise dramatically.

• Above 20mcg/ml, toxicity can occur. Nystagmus, escessive sedation, ataxia (staggering gait), and diplopia. Gingival hyperplasia, rash, SJS. Tertogen (cleft lip, heart malformations)
• Stimulates drug metabolizing enzymes so it can decrease the effects of other drugs (contraceptives, warfarin, and glucocorticoids. Diazepam, isoniazid, cimetidine, and alcohol can increase phenytoin levels. Carbamazepine (Tegretol): delayed recovery of sodium channels from their inactivated state
• Liver metabolism
• Treats seizures, bipolar, and trigeminal and glossopharyngeal neuralgias.
• AE: nystagmus, blurred vision, diplopia, ataxia, vertigo. Bone marrow suppression (leukopenia, anemia, and thrombocytopenia). Tertogenic. Inhibits renal excretion of water by promoting secretion of ADH.
• Same interactions as Phenytoin. 4-12 mcg/ml Valproic acid (Depakote): All major seizure types.
• Suppresses calcium influx , sodium channels, and it may augment the inhibitory influence of GABA.
• Liver metabolized. Levels of 50-100 mcg/ml are therapeutic.

• AE: N/V. Take with food. Pancreatitis. Teratogenic. Hyperammonemia.
• Decreases Phenobarbital levels. Cause increase in Phenytoin by displacing from binding sites. Ethosuximide (Zarontin): Absence seizures
• Oral admin. 40-100 mcg/ml therapeutic. Inhibition of low threshold calcium currents.
• AE: Drowsiness, dizziness, and lethargy. Phenobarbital
• Suppresses seizures by potentiating effects of GABA.
• Orally. Liver metabolized. Half life of 4 days. 2-3 weeks before plasma levels are reached
• AE: Dependence. Nystagmus and ataxia at toxic levels. Accelerates metabolism of other drugs. Valproic acid can increase plasma levels. Pheno must be reduced when used in conjunction. Understand which drug is appropriate for the type of seizure 24-1 pg 217 Newer seizure meds—what are advantages? How are they used? Consider levetiracitam, Topiramate, Felbamate, Lacosamide,Rufinamide, Vigabatrin, Ezogabine Levetiracitam (Keppra)
• Myoclonic seizures, partial onset seizures and primary generalized tonic clonic seizures.
• Rapid and complete absorption. Does not impair speech, concentration, or other cognitive functions.
• Does not interact with other drugs. Eliminated by kidneys. No interaction with other drugs Topiramate (Topamax) adjunctive treatment of adults and children 2 years and

older with partial seizures, primary generalized tonic clinc seizures, and seziures assoiated with Lennox-Gastaut syndrome. Monotherapy of 10 years and older with parital or primary generalized tonic clonic seizures.

• Rapid absorption and not effected by food. Peak in 2 hours. Eliminated in urine.
• AE: somnolence, dizziness, ataxia, diplopia, nausea, anorexia. Metabolic acidosis, which can lead to hyperventilzation. Hypohidrosis (reduced sweating, then hyperthermia). Cleft lip in pregnancy.
• Pheny and Carb can decrease levels Felbamate: treats severe epilepsy.
• Fatal aplastic anemia and liver failure
• Peak in 1-4 hours and penetrated to the CNS. 20-120 mcg/ml
• AE: GI upset, and CNS effects (insomnia, somnolence, dizziness, HA)
• Increases levels of pheny and valproic acid. Lacosamide: Add-on therapy for partial onset seizures 17 and older.
• Oral and IV are completely absorbed. Peak 1- 4 hours.
• AE: dizziness, HA, diplopia, and nasopharyngitis, vomiting, fatigue, blurred vision
• Cabamazapine, fosphenytoin, pheny, and pheno may decrease the serum concentration of lacosamide. Rufinamide is approved as add-on therapy for seizures associated with Lennox-Gastaut syndrome.
• Oral dosing. Peak 4-6 hours.
• AE: somnolence, vomiting, HA. Reduce the QT interval on ECG.
• Interactions: carbamazepine, pehno, pheny, and primidone can reduce levels of rufinamide. Not metabolized by P450 isoenzymes.

Valproic acid can increase rufinamide levels. Vigabatrin: Add-on therpay of complex partial seizures and monotherapy of infantile spasms in children.

• By mouth. Levels in 0.5 to 2 hours. Eliminated by kidneys
• AE: Vision loss (irreversible damage to the retina), regular vision tests. Ezogabine: first class potassium channel opener. Partial onset seizures.
• AE: Urinary hesitancy or urinary retention from activation of potassium channels. Red color to urine. Dizziness, fatigue, confusion, hallucinations, and psychosis. GENERAL ANESTHETICS : review different types, review mean alveolar concentration. Drugs that produce unconsciousness and a lack of responsiveness to all painful stimuli. Inhalation and IV are 2 groups. Analgesia refers to loss of pain and anesthesia refers not only to loss pain but to loss of all other sensations. Inhalation: Unconsciousness, analgesia, muscle relaxation, and amnesia. Balanced anesthesia refers to the use of a combination of drugs to accomplish what we cannot achieve with an inhalation anesthetic alone.
• Enhancing transmission at inhibitory synapse and by depressing transmission at excitatory synapse. Except for nitrous oxide, all of the agents used today enhance activation of receptors for gamma-aminobutyric acid (GABA), the principal inhibitory transmitter in the CNS.
• Minimum alveolar concentration (MAC): index of inhalation anesthetic potency. Minium concentration of drug in the alveolar air that will produce immobility in 50% of patients exposed to a painful stimulus. Low MAC indicates that the inspired air need contain only low concentrations of the anesthetic. Opposite for high MAC.
• Distribution: Regional blood flow. Rise rapidly in brain, kidney, heart, and liver.

• Elimination: Almost entirely through respiration. Leaves brain first cause of high blood flow.
• Metabolism: Does not effect course of anesthesia.
• AE: Respiratory depression. Increased sensitivity of the heart to stimulation by catecholamines (NE, EPI), most notably enflurane. Malignant hyperthermia except NO (Muscle rigid, high temp, greatest risk with succs). Aspiration of GI contents.
• Interactions: Lowered doses needed when already using opioids, barbs, benzos, and other CNS depressants). Opioids can delay wakening. Alpha adrenergic agonists (clonidine, dexmedetomidine), aids in sedation. Anticholinergic drugs (atropine) may be given to decrease the risk of brady during surgery.
• Divided into gases and volatile liquids.
• Gases: NO
• Volatile liquids: Enflurane, Isoflurane, Desflurane, Sevoflurane o Isoflurane: Low MAC, high potency. Rapid absorption. Weak analgesic. AE: Hypotension, RD, urine retention and impede labe. Eliminated by expired breath o Enflurane: Same as Isoflurane, except can induce seizures. o Desflurane: More rapid induction. Not approved for induction in children and infants because of RD. o Sevoflurane: same as desflurane.
• NO: very low anesthetic potency compared to gases, and it has very high analgesic potency. High MAC and cant be used as induction agent alone. Used as supplement to analgesic effects of primary anesthetic. o Does not effect CNS, CV, or Respiratory, no MH. o SE: N/V. IV

anesthetics Short acting barbs

• Used to induce anesthesia. Only agent is methohexital.
• Methohexital (Brevital): ultrashort acting barb. Analgesic and muscle relaxant effects are weak. Rapid onset and short duration. CV and RD. Benzos
• Given to induce anesthesia.
• Diazepam (Valium): Slower than barbs. Little muscle relaxation and no analgesia. CV and RD are moderate.
• Midazolam (Versed): induction of anesthesia and to produce conscious sedation. Conscious sedation can be produced by combining midazolam with an opioid analgesic (morphine, fentanyl). Propofol
• IV anesthetic. Promotes release of GABA, the major inhibitory neurotransmitter in the brain. Causes CNS depression. Don’t exceed 4mg/kg/hr.
• AE: Hypotension, RD. Risk of bacterial infection because not water soluble, and hence must be formulated in a lipid based medium, which is ideal for growth. Open vials should be discarded within 6 hours to avoid growth. Rare Propofol infusion syndrome (metabolic acidosis, cardiac failure, renal failure, and rhabdo). Ketamine
• Produces dissociative anesthesia in which the patient feels dissociated from his environment. Rapid induction (10-15) minutes. Stimulus free soothing place to avoid psychologic reactions. Benzodiazepines: Side effects, contraindications, antidotes
• First choice for anxiety and insomnia. CNS depressant. Low abuse.

• Used to treat seizure disorders also.
• Reduce anxiety through effects on the limbic system. Promote sleep through effects on cortical areas. Induce muscle relaxation through effects on supraspinal motor areas.
• Main SE are confusion and anterograde amnesia caused by effects on the hippocampus and CC.
• CV system: Orals have no effect on heart and BVs. IV can produce hypotension and cardiac arrest.
• Respiratory: In contrast to barbs, benzos are weak respiratory depressants. MOA: potentiate the actions of GABA, which is an inhibitory neurotransmitter found in the CNS. Not GABA agonists, just binding to specific receptors in supramolecular structure known as GABA receptor-chloride channel complex, intensifies the effects of GABA. Limited by finite amount of GABA, compared to barbs, which are direct agonists.
• Absorption and distribution: high lipid soluble.
• Anxiety: Alprazolam, Clonazepam (Klonopin), Lorazepam (Ativan)
• Insomnia: Estazolam, Flurazepam, Lorazepam (Ativan), Quazepam (Doral), Temazepam (Restoril), Triazolam (Halcion).
• Seizure: Diazepam (Valium), Clorazepate (Tranxene), Lorazepam (Ativan), Clonazepam. AE

• CNS depression (Drowsiness, incoordination)
• Anterograde amnesia especially with Triazolam (Halcion)
• Sleep driving and sleep related complexes
• Paradoxical effects (insomnia, excitation, euphoria, anxiety, and rage) when used to treat anxiety
• Low incidence of RD and abuse
• Cross placental barrier. Use during first trimester is associated with risk of congenital malformations. Interactions
• Unlike barbs, do not induce drug metabolizing enzymes, so they do not accelerate metabolism of other drugs
• Other CNS drugs
• Toxicity from oral is rare, IV causes profound hypotension, RA, and cardiac arrest. Oral can be removed by gastric lavage followed by charcoal and a saline cathartic. Flumazenil is a competitive benzo receptor antagonist. Reverses effects. IV over 15 seconds and may be repeated every minute as needed up to 3mg. Initial dose is 0.2, second is 0.3 and all subsequent doses are 0.5. Good agent for Insomnia & panic attacks (short term use, not a good drug for chronic anxiety) Insomnia benzos
• Safe, effective and lack undesirable properties that typify barbs, low abuse potential, and minimal dependence.
• Decrease awakenings, increase total sleeping time, and decreases interval to sleep onset.
• Triazolam and Flurazepam promote sleep. Triazolam has rapid onset and short duration, ideal for people having difficulty falling asleep, not staying asleep. Flurazepam has long half life and daytime drowsiness. Triazolam has short half life which causes tolerance to hypnotic effects and rebound

insomnia compared to other benzos. Others include Quazepam, (Doral), Estazolam, Temazepam (Restoril). Panic attack drugs Antidepressants (SSRIs, SNRIs, and TCAs, and MAOIs. All four require 6-12 weeks to develop.

• SSRIs: Fluoxetine (Prozac), Paroxetine (Paxil), and sertraline (Zoloft), are approved in Panic disorders. Will benefit both depression and panic attacks. SE: Nausea, HA, insomnia, weight gain, and ED. SSRIs can increase anxiety early in treatment.
• SNRI: Venlafaxine (Effexor). Extended release can induce remission, prevent relapse, and improve quality of life.
• TCAs: Imipramine (Tofranil), Clomimpramine (Anafranil) are second line drugs for panic disorders. SE: sedation, ortho hypo, and anticholinergic effects. Fatal dysrhythmias if taken in OD.
• MAOIs: Phenelzine are effective in panic disorder, but difficult to use. SE: ortho hypo, weight gain, ED. HTN crisis if used with tyramine. Skeletal Relaxants: Review pharmacokinetics & use 2 groups are used. Analgesic anti-inflammatory agents and centrally acting muscle relaxants. Centrally acting
• MOA: Unknown, may be caused by sedative properties.
• Relieves localized spasm resulting from muscle injury. Treatment is almost always associated with sedation. Besides baclofen and diazepam, the central relaxers are not useful for treating spasticity or other muscle disorders resulting from CNS pathology.
• AE: CNS depression (drowsiness, lethargy, and lightheadedness). Tizanidine (Zanaflex), and metaxalone (Skeaxin) can cause liver damage. Chlorzoxazone (Lorzone, Parafon Forte DSC) can cause hepatitis and potentially fatal hepatic necrosis.

• Chronic high dose therapy can cause physical dependence, manifesting as a potentially life threatening abstinence syndrome.
• Carisoprodol, chlorzoxazone, cyclobenzaprine, metaxalone, methocarbamol, orphenadrine, and tizanidine have anticholinergic effects that may create problems for older adults.

Drugs for spasticity

• Movement disorder of CNS origin. Heightened muscle tone, spasm and loss of dexterity. Most common causes are MS and CP.
• Three drugs, baclofen, diazepam, and dantrolene can relieve spasticity. Baclofen and diazepam act in the CNS. Dantrolene acts directly on skeletal muscle.
• Baclofen: o MOA: acts in spinal cord to suppress hyperactive reflexes involved in regulation of muscle movement. Mimics GABA (inhibitory neurotransmitter). AE: CNS (drowsiness, dizziness, weakness, and fatigue), most often during early phase. Withdrawal: Oral baclofen can cause visual hallucinations, paranoid ideation, and seizures when stopped abruptly. Intrathecal baclofen can cause high fever, AMS, exaggerated rebound spastiity, and muscle rigidity, and rhabdo.
• Dizepam: o Valium is a benzo. Mimi GABA in the spinal cord.

o Acts in CNS to suppress spasticity. o AE: Sedation.

• Dantrolene o Acts directly on SM. Suppressing release of cacium from sarcoplasmic reticulum and hence the muscle is less able to contract. o Treats MS, CP, and cord injury. Can cause reduction of strength. o Malignant hyperthermia: hyperthermia is caused by contraction. o AE: Liver toxic. Weakness, drowsiness, and diarrhea. Antipsycho tics: Indications, Actions, SE, Contraindications for first and second generation drugs such as Haldol (haloperidol), Zyprexa (olanzapine), Dantrolene, Thioridazine, Clozapine, Seroquel (Quetiapine), Risperdal (risperidone), paliperidone (Invega), ziprasidone (Geodon) and others. What are key differences between first and second generation antipsychotics? Fall into 2 major groups: Frist gen (FGAs or conventional) and 2 nd^ gen (Atypical) Schizo symptoms
• Positive o Hallucinations, delusions, disordered thinking, disorganized speech, combativeness, agitation, paranoia
• Negative o Social and emotional withdrawal, lack of motivation, poverty of speech, blunted affect, poor insight, poor judgement, poor self- care.

• Cognitive o Disordered thinking, reduced ability to focus attention, and prominent learning and memory difficulties.
• Acute attacks o Delusion and hallucinations are prominent.
• Residual o Acute remits then less vivid symptoms may remain. o Suspiciousness, poor anxiety management, and diminished judgment, insight, motivation, and capacity for self-care. 1 st gen
• Classified as low, medium, or high potency (dose needed to see effects)
• Divided into Phenothiazine (3 subgroups, Aliphatic, Piperdine, Piperzaine), Thioxanthene, Butyrophenone, Dibenzoxazepine
• MOA: Block receptors in and out of CNS. Block DA, acety, histamine, and NE. Main theory is FGAs suppress symptoms by blocking DA because all FGAs block DA.
• AE: o EPS: 4 types. Acute dystonia, parkinsonism, and akathisia occur early, and tardive dyskinesia occurs late. o AD- spasm of muscle of tongue, face, neck and back. Hours- 5 days. Benztropine (muscarinic antagonist). o Park- bradykinesia, mask like facies, tremor, rigid, drooling 5- days. Anticholinergic or switch to 2 nd^ gen. o Akathisia- compulsive, restless movement, anxiety, agitation 5- days. Reduce dose. Give beta blocker or anticholinergic. o TD- Oral facial dyskinesias, choreoathetoid movements (slow wormlike movements of tongue and body). Months to years. DC anticholinergics, give benzo.

• Other AE: o NMS- more likely with high potency. Hyperthermia, dysrhythmias, fluctuations in BP, RF, and CV collapse. o Ortho hypotension- block alpha 1 adrenergic receptors. o Sedation o Neuroendocrine effects: increased prolactin by blocking inhibitory action of DA on prolactin release. Causes gyno and glactorrhea. Drugs should be avoided in patients with prolactin- dependent carcinoma. o Seizures, ED, agranulocytosis, or low WBC, (highest with chlorpromazine and penothiazines). o When used to treate dementia related psychosis, all FGAs and SGAs double the rate of mortality. Not approved for DRP. o Infants exposed during third trimester of preg may experience EPS or withdrawal.
• Interactions: o Anticholinergics intensify. Avoid antihistamines and sleep aids o Levodopa and direct DA receptor agonists- counteracts neuroleptics, and neuroleptics may countact the therapeutic effects of levodopa. Levodopa activates DA and neuroleptics block.
• Toxicity o Hypotension, CNS depression, and EPS. EPS is treated with ant parkinsonism drugs.
• High potency: risk of TD is the same for all FGAs. o Causes early EPS, but less sedation, ▪ Haldol: Early EPS, low sedation, low ortho hypo, can prolong QT. Increased chance of dysrhythmias in hypokalemia,

hyperkalemia, heart attack, and HF. ▪ Fluphenazine: sedation, ortho hypo, anticholinergice effects, gyno, galactorrhea ▪ Trifuluoperazine: sedation, ortho hypo, anticholinergic effects, gyno ▪ Thiothixene. Approved only for Schizophrenia. Anticholinergic effects ▪ Pimozide: Only for Tourette’s. Sedation, Hypotension, EPS. Prolongs QT.

• Medium potency ▪ Loxapine: Only for schizo. Same SEs as Fluphenazine. ▪ Perphenazine: Schizophrenia and other psychotic disorders. SEs same as fluphenazine.
• Low potency: lower chance of EPS. ▪ Chlorpromazine: Treats schizophrenia and schizoaffective disorder and the manic phase of bipolar disorder. Extensive first pass, so oral bioavailability is only 30%. AE: sedation, ortho hypo, and anticholinergic effects. Photosensitivity. Intensifies CNS depressants (antihistamines, benzos, and barbs. ▪ Thioridazine: Prolongs QT. Treats schizophrenia in patients as last resort. Sedation, ortho hypo, anticholinergic effects, weight gain, convulsions, and photosensitivity. ▪ ** Haldol, Thioridazine, and Pimozide prolong QT. 2 nd^ generation (Atypical)
• Less likely to caused EPS, including TD. More serious metabolic effects, weight gain, diabetes, and dyslipidemia. FGAs and SGAs can cause sedation and ortho hypo, as well as increased death when treating DP. Can cause new onset diabetes.

Clozapine

• Most effective agent for schizo
• MOA: Blocks DA and serotonin, affinity for these DA receptors is low, which might be why SGAs cause fewer EPS symptoms
• AE: Sedation, weight gain, OH, dry mouth, blurred vision, urine retention, constipation, and tachy, Neruoendocrine effects. Agranulocytosis (Monitor neutrophil and WBCs). Below 3000 or greater than 2000 (ANC), treatment should be stopped
• Weight gain, diabetes, and dyslipidemia
• Seizures
• Low EPS.
• Myocarditis rarely
• Interactions: Cancer drugs that suppress bone marrow. Drugs that induce cytochrome p450 enzymes (phenytoin, rifampin), can lower clozapine levels, and drugs that inhibit P450 (ketoconazole, erythromycin) can raise levels Risperidone
• Schizo, rapid acting drug.
• AE: EPS low, Increased prolactin levels, weight gain, diabetes, etc. Others
• Paliperidone : acute therpay of schizo. Same as Risperidone
• Olanzapine : for schizo, maintenance therapy, or bipolar, acute agitation with mania, depression. Blocks serotonin, DA, histamine, acety, NE. Low risk of EPS. Olanzapine and clozapine have most serious metabolic effects, w/ diabetes. Leukopenia and neutropenia.
• Ziprasidone (Geodon): bipolar mania. Prolongs QT. AE: Somnolence, OH, and rash. Low risk of diabetes L/N. Avoid in hypok, hypom, brady, MI, HF because QT prolongation. Interactions: QT drugs (TCAs, thioridazine,

amiodarone, clarithryomycin, erythromycin, moxifloxacin). Drugs that induce CYP3A4 (rifampin, phenytoin) can accelerate metabolism.

• Quetiapine: schizo, MD, mania, and depression episodes. Blocks H1, Alpha adrenergic, but does not block acety. Liver metabolized. AE: metabolic effects w/ diabetes. No agranulocytosis. Sedation, OH. Cataract development. Prolongs QT interval. Interactions: Accelerated by drugs that induce CYP3A4.
• Aripiprazole: Contrasts with other SGAs. Is a dopamine system stabilizer (DSSs). Low risk of EPS and TD. Unlikely to cause MEs, hypotension, or prolactin release, and poses no risk of anticholinergic effects or dysrhythmias. Still increase mortality when treating DP. MOA: blocks H1, serotonin (5-HT2), and alpa 1 receptors. Does not block cholinergic receptors. Other SGAs act as pure antagonsits, but aripiprazole acts as a partial agonist. Because of partial agonist, net effects on receptor acitivity will depend on how much DA or serotonin is present. Metabolized by liver enzymes. AE: HA, agitation, nervousness, anxiety, insomnia, n/v and somnolence. Lowest risk of MEs. Drugs that induce CYP3A$ (barbs, barbamazepine, phenytoin, rifampin) accelerate metabolism, and drugs that inhibit CYP3A$ (ketoconazole, itraconazole, fluconazole, erythromycyin), can increase levels.
• Asenapine: MOA: blocks D2, 5-HT2, H1, and alpha adrenergic receptors, but has little effect on muscarinic receptors. Extensive first pass orally. AE: Risk of MEs, prolactin, and AC effects are low. Blockade of H1 can promote drowsiness, and blockade of AA receptors can promote hypotension. Prolongs QT.
• Iloperidone: relative of risperidone. Blocks D2 and 5-HT2. AE: MEs, AC side effects. High risk of weight gain. Low risk of diabetes.
• Lurasidone: AE: somnolence, akathisia, parkinsonism, nausea, agitation, and anxiety. Metabolized by CYP3A4.

Consider the patient’s comorbidities – which meds would you prescribe if the patient has HTN, DM, etc.

• Diabetes or dyslipidemia: FGA, or aripiprazole or ziprasidone. FGAs pose a greater risk of EPS, SGAs pose a significant risk of metabolic effects.

• Resistant: trial with clozapine Treatment for
• Malignant Hyperthermia- Same as Neuroleptic.
• Neuroleptic Malignant Syndrome- Ridid, fever, sweating, sysrhythmias, and fluctuations in BP. Supportive measures include cooling blankets, rehydration, drug therapy with dantrolene, bromocriptine, and immediate withdrawal of the neuroleptic. What meds are good for bipolar patients? Types of moods
• Pure manic: heightened irritable mood, hyperactivity, excessive enthusiasm, and flight of ideas.
• Hypomanic (hypomania): not severe enough to cause marked impairment in social or occupational functioning.
• Major depressive (depression): depressed mood and loss of pleasure or interest in all or nearly all of ones usual activities and pastimes.
• Mixed episode: symptoms of mania and depression Drugs
• Mood stabilizers: relieve symptoms during manic and depressive episodes, prevent recurrence, and do not worsen symptoms. o Lithium, Divalproex sodium (Valproate), and carbamazepine.

• Antipsychotics: Severe manic episode symptoms o Olanzapine, risperidone, etc
• Antidepressants: Always combined with mood stabilizers in BPD. When used alone, antidepressants may elevate mood so much that a hypomanic or manic episode will result o Bupropion, venlafaxine (Effexor), and SSRIs, such as fluoxetine (Prozac), and sertraline (zoloft). Mood Stabilizers: Lithium: o Low TI. Simple inorganic ion that carries a single positive charge. o Treats BPD. Drug of shoice in BPD and for long term prophylaxis against recurrence of mania or depression. o Manic patients reduces euphoria, hyperactivity, and other symptoms, but doe not cause sedation. o Antimaniac effects beign 5-7 days after treatment, full benefits may not develop for 2-3 weeks. o Absorbed evely to all tissue and body fluids. Short half life, because of rapid renal excretion. Must be given in divided daily doses cause of short half life and low TI. o Excretion is reduced when levels of sodium are low because sodium and lithium are processed the same. Kidney senses that sodium levels are low, it retains lithium in an attempt to compensate. Low sodium = toxic levels. Sodium loss from diarrhea, diuretics, and dehydration can cause toxicity. o Monitoring: levels must be below 1.5 meq/L. Levels greater can produce toxicity. Initial therapy for a manic episode range from 0.8- 1.4 meq/L. Once the desired therapeutic effect has been achieved, the dosage should be reduced to produce maintenance levels of 0.4-1 meq/L. Blood tests should be drawn in the morning, 12 hours after the evening dose. During therapy, lithium levels should be measured

every 3-6 months. o AE: 2 cats (effects that occur at excessive levels and effects that occur at therapeutic levels. o Excessive AE ▪ Mild: fine hand tremor, GI upset, thirst, muscle weakness can develop during therapeutic range. ▪ Greater than 2.5: death can occur. o Therapeutic levels AE ▪ Early: GI effects, fatigue, weakness, HA, confusion, and memory impairment. ▪ Tremor: find hand tremor. Can be reduced with beta blocker. ▪ Polyuria: antagonizes effects of ADH. Drink 8-12 glasses per day. Treated with amiloride (Midamor), a potassium sparing diuretic. ▪ Renal toxcicity: Keep dosage low. Assess before treatment and once a year afterwards. ▪ Goiter and Hypothyroidism: Reduces iodine into thyroid hormone, and can inhibit thyroid hormone secretion. Treat with levothyroxine. Levels should be measured beforehand. ▪ Teratogenesis: should be avoided during 1 st trimester. Lithium: When should serum blood levels be drawn? Make sure you understand the difference between starting the meds vs maintenance. o Monitoring: levels must be below 1.5 meq/L. Levels greater can produce toxicity. Initial therapy for a manic episode rangr from 0.8- 1.4 meq/L. Once the desired therapeutic effect has been achieved, the disage should be reduced to produce maintenance levels of 0.4-1 meq/L. Blood tests should be drawn in the morning, 12 hours after

the evening dose. During therapy, lithium levels should be measured every 3-6 months. o Drug levels should be measured every 2-3 days at the beginning of treatment and every 3-6 months during maintenance therapy. o Treatment of OD is supportive. No antidote. Hemodialysis is effective in severely toxic patients. o Maintenance therapy: 0.4-0.1 o Acute therapy: 0.8-1.4 What should patient avoid when on Lithium therapy?

• Diuretics: promote sodium loss, increases risk of toxicity.
• NSAIDs: Increase levels by suppressing prostaglandin synthesis in the kidney, NSAIDs can increase renal reabsorption of lithium, causing levels to rise. Ibuprofen, naproxen, piroxicam, indomethacin, and celecoxib.
• AC drugs: cause urinary hesitancy, coupled with lithium polyuria, can result in considerable discomfort. Other drugs used in the treatment of BPD and other serious mental illnesses; e.g. Aripiprazole, carbamazepine, chlorpromazine, lamotrigine, etc. What other meds are used in combination with lithium for treatment. Antiepileptic drugs
• Divalproex Sodium (Valproate)

o Works faster and higher TI, and more desirable effect than lithium. But lithium is better at preventing suicide, and better at preventing relapses. o Concern for thrombocytopenia, pancreatitis, and lover failure. o Teratogen.

• Carbamazepin (Tegretol) o Treats and prevents manic episodes. o Less effected at treatment and prevention of depression like Valproate. o Plasma level should be 4-12 mcg/ml. o SE: visual distrubances, ataxia, vertigo, unsteadiness, and HA early in treatment o Hematologic effects are rare. CBC should be done at baseline. o Induces cytochrome P450, and can accelerate its own metabolism and other drugs.
• Lamotrigine o Long term maintenance therapy of BPD. o Can be used in combination with other mood stabilizers o SE: HA, dizziness, double vision, and rarely SJS. Understand Parkinson type disorders induced by psychiatric medications. Review peripheral nervous system stimulation as related to side effects of these drugs (e.g. anticholinergic effects). You may need to review autonomic information again. Parkinsonism:
• Bradykinesia, mask like facies, drooling, tremor, rigid, shuffling gait, cogwheeling, and stooped posture.