NURS 5334 Study Questions and Answers Exam 2

NURS 5334 Study Questions and Answers Exam 2 • What are the basic mechanisms by which neuropharmocologic agents act? o Can modify the disease process o Act at the sites of actions which is the axons versus synapses and steps in synaptic transmission and effects of drugs on the steps of synaptic transmission • Transmittter synthesis is the first step in transmission. What are the other 4 steps? o Transmitter storage, transmitter release, receptor binding, and termination of the transmission • True or False: Neuropharmacologic drugs have high selectivity. o True—the nervous system uses many different receptor types • Information needed: o Type of receptors—through which the drug acts ▪ Alpha and beta o Normal responses to the activation of those receptors ▪ Agonists vs. antagonists o What the drug in questions does to the receptor function • What are the 3 functions of ANS? o Regulates the heart o Regulates the secretory glands, saliva glands, gastric, sweat, and bronchial o It regulates smooth muscles: bronchi, blood vessels, urogenital system, and the GI tract • What are the regulatory functions of the parasympathetic NS? o Seven regulatory functions ▪ Slowing the heart rate ▪ Increasing the gastric secretions ▪ Emptying the bladder ▪ Emptying the bowel ▪ Focusing the eye for near vision, ▪ Constricting the pupil ▪ Contracting the bronchial smooth muscle o It also regulates the digestion of food, excretion of waste, control of vision and conservation of energy • What are the functions of the sympathetic NS? o Regulation of the cardiovascular system ▪ Maintaining blood flow to the brain ▪ Redistributing blood and compensating for the loss of blood o Regulation of body temperature ▪ Regulates blood flow to the skin ▪ Promotes the secretion of sweat ▪ Induces piloerection (erection of the hair) o Implementation of the fight or flight reaction ▪ Increase HR and BP ▪ Blood shuts away from the skin and visera ▪ Bronchi dilate 2 ▪ Pupils dilate ▪ Use energy that had been stored • What is the baroreceptor reflex? o The receptors near the heart monitor BP changes and send the information to the brain o The brain then activates the Autonomic NS to restore blood pressure to normal o When BP falls, this reflex causes vasoconstriction and increases cardiac output. o When BP rises, it causes vasodilation and reduces cardiac output • Where is acetylcholine employed? o Most junctions at the peripheral nervous system • Where is epinephrine and norepinephrine released? o Norepinephrine—postganglionic neurons o Epinephrine—adrenal medulla • What are the cholinergic receptors mediated by? What are the subtypes? o Receptors that mediate responses to acetylcholine o Subtypes: ▪ Nicotinic ▪ Muscarinic • Whare are adrenergic receptors mediated by? What are the subtypes? o Mediate responses to epinephrine and norepinephrine o Subtypes: ▪ Alphas ▪ Betas ▪ Dopamine • What are the functions of each adrenergic subtype? o Alpha 1—vasoconstriction, ejaculation and contraction of the bladder neck, and prostate o Alpha 2—(located in presynaptic junction)—minimal clinical significance o Beta 1—control the heart ▪ Increase HR, increase force of contraction and velocity of conduction in the AV node; stimulate renin released in the kidney o Beta 2—bronchial dilation, relaxation of the uterine muscle, vasodilation, glycogenolysis o Dopamine—dilates renal blood vessels • Epinephrine can activate all alpha and beta receptors but not dopamine receptors • Norepinephrine can activate alpha1, alpha2, and beta receptors but not beta2 or dopamine receptors • Dopamine can activate alpha1, beta1 and dopamine receptors • Muscarinic agonists mimic the effects of acetylcholine at muscarinic receptors • Muscarinic antagonists selectively blood the effects of acetylcholine (and other muscarinic agonists) at muscarinic receptors • What are therapeutic uses of Bethanechol? o Urinary retention o Investigational GI uses—off label GI reflux • What are actions on smooth muscle, exocrine glands, and eye? o Smooth muscle— 3 ▪ lung by causing constriction of the bronchi ▪ the GI system by increasing tone and motility ▪ the bladder by contraction of the detrusor muscle ▪ relaxation of the trigone and sphincter o Exocrine glands—increased sweating salivation, bronchial secretions and secretion of gastric acid o Eye—causes miosis and contraction of the ciliary muscle • Adverse Effects? o Hypotension o Abdominal cramps o Diarrhea o Increased salivation o Exacerbate asthma o Can cause dysrhythmias in patients with hyperthyroidism • What are cevimeline, pilocarpine, and acetylcholine used for? o Cevimeline—treat dry mouth and Sjogren’s syndrome o Pilocarpine—topical treatment of glaucoma as well as dry mouth from Sjogren’s syndrome o Acetylcholine—rapid myosis after delivery and cataract surgery • Anticholinergics o Competitively block the actions of acetylcholine as muscarinic receptors o Most muscarinic receptors are on structures innervated by parasympathetic nerves o Also known as parasympatholytic drugs, antimuscarinic drugs, muscarinic blockers, and anticholinergic drugs o Anticholinergic drugs: produce selective blockade of the muscarinic receptors (not all cholinergic receptors) o Can’t pee, see, spit or shit • What are the pharmacologic effects of atropine? o The heart—increases in rate o The exocrine glands—decrease secretions o Smooth muscle—relaxes the bronchi, decreases the tone of the urinary bladder detrusor and decreases the tone motility of the GI tract o Mydriasis and cycloplegia in the eyes o Mild excitation to hallucinations and delirium in the Central Nervous system • Therapeutic Uses of Atropine? o Pre-anesthetic medication to help dry up secretions o Disorders of the eye o In codes for bradycardia, intestinal hypertonicity and hypermotility o Muscarinic agonist poisoning o Peptic ulcer disease o Asthma o Biliary colic • Side effects of Atropine 4 o Dry mouth o Blurred vision o Photophobia o Elevation of interocular pressure o Urinary retention o Constipation anhidrosis o Tachycardia o Asthma • Overactive bladder o Oxybutyin—acts on M3 muscarinic receptors ▪ Highly lipid soluble ▪ Metabolized CYP3A4 ▪ Very short ½ life and must be dosed frequently o Darifenacine— ▪ Can reduce OAB symptoms while having no effect or M1 receptors in the brain or M2 receptors in the heart ▪ Greatest degree of M3 selectivity o Solifenacin—at high dose can prolong QT interval o Tolterodine—nonselective muscarinic antagonist o Fesoterodine—nonselective muscarinic antagonist o Trospium-nonselective muscarinic antagonist • Scopalamine o Uses? ▪ Motion sickness ▪ Production of a cytoplegia and mydriasis for ophthalmic procedures ▪ Production of pre-anesthetic sedation and obstetric amnesia o Side effects? ▪ Xerostomia (dry mouth) ▪ Blurred vision ▪ Photophobia ▪ Urinary retention ▪ Constipation ▪ Hyperthermia ▪ Tachycardia • Ipratropium Bromide o Uses? ▪ Treat asthma, COPD and rhinitis caused by allergies or common cold o Side effects? ▪ Not associated with typical anti-muscarinic side effects • What are mydriatic cycloplegics? o Atropine, homatropine, scopolamine, cyclopentolate and tropicamide o Used to produce mydriasis and cyclopedia in ophthalmic procedures • Muscarinic Poisoning 5 o Cause? ▪ Direct-acting muscarinic agonist and cholinesterase inhibitors ▪ Symptoms result from excessive activation of the muscarinic receptors o Treatment? ▪ Muscarinic blocking agent—atropine • Cholinesterase inhibitors o Reversible ▪ Neostigmine • Uses? o Management of myasthenia gravis o Irreversible ▪ Highly toxic ▪ Used—as insecticides ▪ Only clinical application is glaucoma • Catecholamines o Cannot be used orally due to short half life and they become inactivated in the liver before they reach circulation o Have brief durations of action o Cannot cross blood-brain barrier • Noncatecholamines o Metabolized slower ▪ Not metabolized by COMT o Can be given orally o Less polar and can cross blood-brain barrier • Receptors o Alpha 1—vasoconstriction (1st) then mydriasis ▪ Therapeutic application • Hemostasis—epinephrine • Nasal decongestion—phenylephrine (topical) and pseudophedrine • Adjuct to local anesthesia to delay absorption • Mydriasis—dilation of pupil ▪ Activation-vasoconstriction ▪ Adverse effects due to vasoconstriction? • Hypertension • Necrosis of tissues • Bradycardia o Alpha 2 ▪ Activation—reduction of sympathetic outflow to the heart ▪ Pain relief o Beta 1 ▪ Activation-heart o Beta 2- ▪ Activation-lung and uterus o Dopamine 6 ▪ Renal vasodilation • Adrenergic Agonists 2 o Epinephrine ▪ Receptor—alpha 1, alpha 2, beta 1, and beta 2 ▪ Uses—delays absorption of local anesthetics, can control superficial bleeding, can elevate BP, can overcome AV heart block, restore cardiac functions, cause bronchodilation, treating anaphylactic shock o Norepinephrine ▪ Receptors—alpha 1, alpha 2, and beta 1 ▪ Uses—hypotensive states in cardiac arrest o Isoproterenol ▪ Receptors—beta 1 and beta 2 ▪ Uses—AV block and cardiac arrests o Dopamine ▪ Receptors—dose dependent specificity—dopamine, beta 1 and alpha 1 (only at high doses) ▪ Uses—shock (can decrease renal perfusion and do more damage to kidneys) o Dobutamine ▪ Receptors—beta 1 ▪ Uses—heart failure o Phenylephrine ▪ Receptors—alpha 1 ▪ Uses—nasal congestion and sometimes epistaxis, elevate BP, dilate pupils o Albuterol ▪ Receptors—beta 2 ▪ Uses-asthma (bronchodilation) o Ephedrine ▪ Receptors—alpha 1, alpha 2, beta 1 and beta 2—poor selectivity ▪ Uses—decongestants, stimulant, diet products, asthma (bronchodilation) • Adrenergic Antagonists o Alpha-adrenergic blocking agents ▪ Uses? • Essential hypertension • Reversal of toxicity from alpha-1 agonists • Overdose of alpha-adrenergic agonist (epinephrine) • Hypertension due to excessive activation of alpha 1 receptors on blood vessels • Used as reversal for an alpha blocking agent • Used for extravasated necrosis • Blocks vasoconstriction and prevents injurty • Benign prostatic hyperplasia o Symptoms—dysuria, increased frequency of daytime urination, noctura, urinary hesitancy, urinary agency, a sensation of 7 incomplete voiding and reducation in size and force of urinary stream • Pheichromocytoma—causes uncontrolled hypertension • Raynaud’s disease—prevents vasoconstriction ▪ Side effects? • Orthostatic hypotension • Reflex tachycardia • Nasal congestion • Impotence (reversible and resolves once drug is d/c) • Sodium retention and increase blood volume o Due to retention of sodium and water ▪ Combined with diuretic when used for hypertension o Beta-adrenergic blocking agents ▪ Uses? • Antianginal therapy • Hypertension • Reduce peripheral vascular resistance (long-term use) • Cardiac dysrhythmias—excess of electrical activity in the sinus node and atria • MI • Heart failure o Only three are effective—carvedilol, bisoprolol, metoprolol • Hyperthyroidism • Migraine prophylaxis • Stage fright • Pheochromocytoma • Glaucoma ▪ What are non-selective beta blocking agents? • Produce a broader spectrum of adverse effects ▪ Adverse effects? • Bradycardia • Reduced cardiac output • Can cause AV heart block • Can cause rebound cardiac excitation • Bronchoconstriction • Hypoglycemia ▪ Need to be discontinued slowly • Indirect-acting anti-adrenergic agents o Clonidine ▪ Uses • Hypertension • Severe pain • ADHD 8 • Off-label use—opioid and methadone withdrawal, smoking cessation, conduct disorder and oppositional defiant disorder in children, Tourette Syndrome ▪ Adverse effects? • Drowsiness—35% • Xerostomia (dry mouth)—40% • Rebound hypertension if stopped abruptly o Guanabenz and Guanfacine ▪ Use? • Hypertension • ADHD ▪ Side effects • Xerostomia • Sedation • Rebound hypertension if not weaned o Methyldopa and methyldopate ▪ Uses? • Lower blood pressure in supine and standing subjects • Vasodilation and not cardiosuppression ▪ Pregnancy use? • Hypertension during pregnancy • Reserpine o Discontinues in the US • What is Parkinson’s? o A neurodegenerative disorder of the extrapyramidal system associated with the disruption of neurotransmission of the striatum and is characterized by dyskinesias and akinesia o Cardinal signs? ▪ Tremor at rest ▪ Rigidity ▪ Postural instability ▪ Bradykinesia ▪ Tremor ▪ Autonomic disturbances, depression, psychosis and dementia o Only 2 of 6 cardinal signs to be diagnosed with Parkinson’s ▪ One must be either bradykinesia or tremor at rest o Therapeutic goals? ▪ Improve the patient’s ability to carry out the activities of daily life o Drugs ▪ Dopaminergic—most common • Promote activation of dopamine receptors • levodopa ▪ Anticholinergic • Prevent activation of the cholinergic receptors 9 • Levodopa • Benztropine ▪ Monoamine oxidase-B (MAO-B) inhibitor • Selegiline or resagiline ▪ Catechol-O-methyltransferase (COMT) inhibitors o Downfalls? ▪ Beneficial effects diminish over time o Combined with? ▪ Carbidopa • Allows for smaller dose of levodopa to be given • Decreases diskinesias o Foods that interfere? ▪ High protein foods o How long before therapeutic response? ▪ Several months of treatment for full response o When does the therapeutic response turn to pretreatment stage? ▪ End of five years o What is an “off” period? How can wearing off be treat? ▪ When drug levels drop to sub therapeutic levels ▪ Treatment • Shorten dosing interval, give it more frequently • Give a drug that prolongs plasma half-life • Give direct acting dopamine agonist • COMT inhibitors help too o Adverse effects? ▪ N/V ▪ Dysrhythmias, especially in heart disease pts ▪ Postural hypotension ▪ Psychosis, visual hallucinations, vivid dreams, paranoid ideation ▪ Anxiety, agitation, memory and cognitive impairment ▪ Insomnia, nightmares, problems with impulse control ▪ Behavioral changes (promiscuity, gambling, binge eating and alcohol abuse) ▪ Dyskinesias ▪ Darkening of sweat and urine o Carbidopa adverse effects? ▪ None • Dopamine Agonists o Non-ergot derivatives ▪ Pramipexole (Mirapex) ▪ Ropinrinole ▪ Rotigotine ▪ Apomorphine o Ergot derivatives ▪ Bromocriptine 10 ▪ Carbergoline • COMT o Entacapone o Tolcapone o Levodopa/Carbidopa/Enacapone • MAO-B Inhibitors o Selegiline o Rasagiline • Central Acting Anticholinergic Drugs o Benztropine (Cogentin) o Trihexyphenidyl (Artane) • Amantadine—antiviral found to be effective in Parkinson’s • Nonmotor symptoms of parkinson’s? o Dementia o Psychosis • Treatment of non-motor symptoms? o Clonazepam o Quetiapine • Alzheimer’s disease o Risk factors? ▪ Advancing age ▪ Family history ▪ Female ▪ Head injury ▪ Low education level ▪ Production of the apolipoprotein E4 ▪ High levels of homocysteine ▪ Low levels of folic acid ▪ Estrogen and progesterone therapy ▪ Nicotine in cigarette smoke ▪ Sedentary lifestyle o Goal of treatment? ▪ Improve the symptoms ▪ Reverse the cognitive decline o Drugs? ▪ None, may only slow the loss of memory and cognition and prolong independent function o What are the 4 drugs approved for Alzheimers? ▪ Cholinesterase inhibitors—indicated for mild to moderate AD • Donepezil • Galatamine • Rivastigmine ▪ Neuronal receptor blocker (NMDA receptor antagonist)—moderate to severe • Memantine 11 • Muscle relaxants o Diazepam o Tizanidine o Metaxalone—least sedating o Chlorzoxazone o Cyclobenzaprine ▪ All are sedating ▪ All can be addictive • Movement disorders o Baclofen o Diazapem o Dantrolene • Epilespy o Goal? ▪ Reduce seizures to a level that allows the patient to live life as normal as possible ▪ Balance the desire for complete seizure control with acceptable side effects o Non-pharm options ▪ Neurosurgery ▪ Vagal nerve stimulation ▪ Ketogenic diet o Traditional Antiepileptic Drugs ▪ Phenytoin ▪ Fosphenytonin ▪ Carbamazepine ▪ Valproic acid ▪ Ethosuximate ▪ Phenobarbital ▪ Primidone o Newer AEDs ▪ Oxcarbazepine ▪ Lamotrigine ▪ Gabapentin ▪ Pregabalin ▪ Topiramate ▪ Tiagabine ▪ Zonisamide ▪ Felbamate ▪ Rufinamide ▪ Ezogabine o Treat Status epilepticus? ▪ Maintain ventilation ▪ Correct hyperglycemia 12 ▪ Drug choices—benzodiaepines (lorazepam (1st line), diazepam (if lorazepam is not readily available)) ▪ Initiate or continue long term suppression drugs (phenytoin) • Antipsychotics o First-generation antipsychotics (FGAs) or conventional antipsychotics ▪ Block receptors for dopamine in the central nervous system (CNS) ▪ Cause serious movement disorders known as extrapyramidal symptoms (EPS) o Second-generation antipsychotics (SGAs) or atypical antipsychotics ▪ Produce only the moderate blockade of dopamine receptors; stronger blockade for serotonin ▪ Fewer EPS (Extrapyramidal symptoms o Used to treat schizophrenia o Main side effects: extrapyramidal movements o High potency: ▪ Haloperidol ▪ Fluphenazine o Low Potency ▪ Chlorpromazine ▪ Thioridazine • Atypical antipsychotic Agents o Clozapine (first SGA) ▪ MOA—blocks dopamine and serotonin ▪ Therapeutic uses • Schizophrenia • Levodopa-induce psychosis ▪ Pharmacokinetics: taken orally. • Metabolized by the CYP450 • 12 hours half o Respiradone o Paliperidone o Olanzapine o Ziprasidone o Quetiapine o Aripiprazole o Asenapine o Iloperidone • Depot preparations o Depot antipsychotics: long acting, injectable formulations used for the long-term maintenance therapy of schizophrenia • Schizophrenia drug therapy o Three major objectives ▪ Suppression of acute episodes ▪ Prevention of acute exacerbations ▪ Maintenance of the highest possible level of functioning 13 o Drug selection: efficacy, safety and cost o No one size treatment. May be trial and error. Try to individualize. ▪ Example: a patient is treatment resistant, trial with clozapine might be reasonable ▪ Patient with a history of diabetes or dyslipidemia, an FGA might be a good choice, as might aripiprazole or ziprasidone, two SGAs with a low risk for metabolic effects. ▪ If there’s no clinical reason to select an SGA over an FGA, cost considerations would suggest choosing an FGA • Depression o The usual drugs of first choice are SSRIs, SNRIs, bupropion, and mirtazapine. Older antidepressants—TCAs and MAOIs—have more adverse effects and are less well tolerated than the first-line agents and hence are generally reserved for patients who have not responded to the first line drugs o Start low and gradually increase o 4-8 weeks if no success, increase med, switch to drug in same or different class or add another med • SSRI o Fluoxetine o Sertraline o Fluvoxamine-long half life o Paroxetine o Citalopram—can cause prolonged QT o Escitalopram o MOA: produces selective inhibition of serotonin reuptake and central nervous system excitation o Serotonin Syndrome? ▪ Usually starts 2-72 hours after treatment ▪ s/s • altered mental status • agitation • confusion • disorientation • anxiety • hallucinations • poor concentration ▪ syndrome resolves spontaneously after discontinuation ▪ increased risk if given with MAOI and other drugs o Main side effectS? ▪ Increased sweating ▪ Bleeding disorder (impeded platelet aggregation) ▪ Sexual dysfunction (impotence, delayed or absent orgasm, delayed or absent ejaculation, general decreased sexual interest)—70% of patients get this side effect 14 • SNRI • Treat—bupropion ▪ Weight gain o Venlafaxine o Desvenlafaxine o Duloxetine o Levomilnacipran o MOA: blocks norepinephrine and serotonin uptake ▪ Does not block cholinergic, histaminergic, or alpha-1 adrenergic receptors o Side effects? ▪ Nausea ▪ Headache ▪ Anorexia ▪ Nervousness ▪ Sweating ▪ Somnolence ▪ Weight loss ▪ Sexual dysfunction • Tricyclics o Most common adverse effects: sedation, orthostatic hypotension, and anticholinergic effects o Long and variable half-lives ▪ Usually single daily dose ▪ Requires individualization of dosage o Amitriptyline o Amoxapine o Desipramine o Doxepin o Imipramine o Nortriptyline o Protriptyline o Trimipramine • MAOI o Isocarboxazid o Phenelzine o Tranylcypromine o Selegiline (transdermal) o Used for patients that have not responded to other therapy. o Multiple side effects ▪ Hypertensive crisis • Dietary tyramine (aged cheese and cured meats) • Atypicals o Burpropion 15 ▪ Mechanism by which depression is relieved is unclear but may be related to blockade of dopamine or NE reuptake ▪ Does not cause sexual dysfunction ▪ Decreases appetite ▪ Used for smoking cessation ▪ Increases seizure risk ▪ Can be given with SSRI to counteract sexual dysfunction o Mirazapine-can help with sleep o Nefazodone—Black box warning—liver failure o Trazodone o Vilazodone o Amoxapine • Bipolar Disorder o What are types of mood episodes seen with bipolar disorder? ▪ Manic and depression o What are the 3 types of meds used to treat bipolar? ▪ Mood stabilizers (lithium) ▪ Antipsychotics—severe manic episodes ▪ Antidepressants—during depressive episodes o What are the nonpharm treatments for bipolar? ▪ Stable sleep pattern ▪ Maintaining regular pattern of activity ▪ Get regular exercise ▪ Avoid alcohol and psychoactive street drugs ▪ Support from family and friends ▪ Reduce stress at work ▪ Mood chart (monitor progress and see how they are doing) ▪ Psychotherapy (individual, group or family) ▪ ECT—last resort • Lithium o Pharmacokinetics? ▪ Well absorbed orally ▪ Distributes evenly to all tissues and body fluids ▪ Short half-life ▪ Excreted by kidneys ▪ Reduced in patients with low sodium levels ▪ Plasma levels: 0.8-1.4 o What is therapeutic index? ▪ 0.8-1.4 o Side effects? ▪ Toxicity—outside of therapeutic level ▪ GI effects ▪ Tremors ▪ Polyuria 16 ▪ Renal toxicity ▪ Goiter ▪ Hypothyroidism ▪ Teratogenic o Drug/Drug interactions? ▪ Diuretics ▪ NSAIDs ▪ Anticholinergic drugs • Antiepileptic Drugs o What are the antiepileptic drugs used in treatment of bipolar disorder? ▪ Divalproex sodium ▪ Valproate ▪ Carbazepine o What are they used to treat? ▪ Helps reduce symptoms ▪ Protect against mania and depression • What are the 5 antipsychotic drugs used to treat bipolar? o Olanzapine o Quetiapine o Risperidone o Ariprprazole o Ziprasidone • Sedative/Hypnotic Drugs o Benzodiazepine/Benzodiazepine receptor agonists ▪ Therapeutic uses? • Manage seizure disorders • Muscle spasms • Panic disorder • Withdrawal from alcohol • Anxiety • Insomnia • Perioperative applications ▪ Pharmacologic effects? • CNS o Reduce anxiety o Promote sleep o Too high dose—hypnosis and stupor • Cardio o No effect—orally o IV—profound hypotension, even cardiac arrest • Respiratory system o Little effect as respiratory depressants ▪ Do they readily cross blood brain barrier? • Yes, high-lipid solubility 17 ▪ Adverse effects? • CNS o Depression o Anterograde amnesia o Sleep driving o Paradoxical effects • Respiratory depression off use ▪ Drug interactions • CNS depressants ▪ Can they cause physical dependence? • Yes, but relatively low o Benzodiazepine-like drugs ▪ What are the four drugs? • Zolpidem (Ambien) • Zaleplon (sonata) • Eszopiclone (Lunesta) • Ramelteon (rozerem) ▪ Used for? • Treatment of insomnia • Anxiety disorders o 5 types? ▪ Generalized Anxiety Disorder ▪ Panic Disorder ▪ OCD ▪ Social anxiety disorder ▪ PTSA • Generalized Anxiety Disorder o Benzodiazepines, buspirone, venlafaxine, paroxetine, escitalopram, and duloxetine are approved drugs for treatment o Buspirone—first line drug for GAD o Drug/Drug Interactions? ▪ Erythromycin ▪ Ketoconazole ▪ Grapefruit Juice • Panic Disorder o Drug therapy ▪ Antidepressants • SSRIs—fluoxetine, paroxetine, and sertraline • Venlafaxine XR (SNRI) • Tricyclic antidepressants—imipramine and clomipramine o These are second line(less well tolerated than SSRI) • MAOIs (Phenelzine) o Not used much ▪ Benzodiazepines 18 • First-line drugs for panic disorder • OCD o SSRIs ▪ First line drugs ▪ Citalopram ▪ Escitalopram ▪ Fluoxetine ▪ Fluvoxamine ▪ Paroxetine ▪ Sertraline o Clomipramine (Anafranil) ▪ Less tolerated ▪ Second-line drug o Benzodiazepines can be used—clonazepam and alprazolam • Social Anxeity Disorder o Drug therapy ▪ SSRIs (paroxetine (paxil) and sertraline (zoloft)) • PTSD o Evidence of efficacy is strongest for 3 SSRIs (fluoxetine, paroxetine and sertraline) and one serotonin/norepinephrine reuptake inhibitor (venlafaxine) • Stimulants o Therapeutic uses? ▪ ADHD ▪ Narcolepsy o Side effects? ▪ CNS stimulation ▪ Weight loss ▪ Cardiovascular effects ▪ Psychosis ▪ Acute toxicity • Dizziness, confusion, hallucinations, paranoid delusions, palpitations, dysrhythmias, hypertension • Addiction • Alcohol o Most commonly used and abused psychoactive agent o Primarily used for nonmedical purposes o Moderate consumption actually prolongs life and reduces risk of demential and cardiovascular disorders o Excessive consumption diminishes both quality and quantity of life o CNS depressant o Enhances GABA-mediated inhibition o Dose-dependent—activated the reward circuit o Chronic Use ▪ Two Neuropsychiatric syndromes 19 • Wernicke Encephalopathy o Confusion o Nystagmus o Abnormal ocular movements • Korsakoff Psychosis o Polyneuropathy or inability to convert to short term memory into long term memory and confabulation o Not reversible ▪ Can impact cognitive function ▪ Effects sleep ▪ Cardiovascular system • Damage to the myocardium • Increased risk of heart failure • Increase risk of elevated BP ▪ Interferes with glucose metabolism and bone health o Depresses respiratory system o Can cause non-viral hepatitis, erosive gastritis and pancreatitis o Diuretic o Increases risk for Breast and colorectal cancer o Can cause Fetal Alcohol Spectrum disorder or fetal alcohol syndrome ▪ If used during pregnancy or in lacation o Intoxication is anything from 0.08% and above for blood levels ▪ Earliest effects start at 0.05% ▪ Risk for death at 0.4% and higher o Therapeutic uses—topical, oral, local injections for nerve blocks, etc o Relapsing disorder ▪ Preoccupation with alcohol consumption ▪ Use of alcohol despite awareness of adverse consequences ▪ Causes distortions in their thinking ▪ Influenced by genetics as well as psychosocial and environmental factors o Drugs that facilitate ▪ Withdrawal • Benzodiazepines and adjuncts to benzodiazepines • Carbamazepine (antieleptic) • Clonidine (alpha-andrenergic blocker) • Atenolol • Propranolol ▪ Abstinence • Disulfiram—antabuse • Naltrexone • Acamprosate ▪ Treatment of alcohol use • B Vitamins • Fluid replacement 20 • Antibiotics