NSG124 Pharmacology Study Test Plan Exam 3., Exams of Nursing

Download NSG124 Pharmacology Study Test Plan Exam 3. and more Exams Nursing in PDF only on Docsity! NSG124 Pharmacology Study Test Plan Exam 3 Antihypertensives • In patients with HF, aldosterone antagonists (e.g., spironolactone, eplerenone) reduce symptoms and prolong life. Benefits derive from blocking aldosterone receptors in the heart and blood vessels. ACE Inhibitors: (-prils) a. Mechanism : i. ACE inhibitors block formation of angiotensin II, promote accumulation of kinins, and reduce aldosterone release. As a result, these drugs cause dilation of veins and arterioles, promote renal excretion of water, and favorably alter cardiac remodeling. 1. By dilating arterioles, ACE inhibitors (1) improve regional blood flow in the kidneys and other tissues and (2) reduce cardiac afterload, which causes stroke volume and cardiac output to rise. 2. By dilating veins, ACE inhibitors reduce venous pressure, which in turn reduces pulmonary congestion, peripheral edema, preload, and cardiac dilation. 3. By suppressing aldosterone release, ACE inhibitors increase excretion of sodium and water, and decrease excretion of potassium. 4. By increasing levels of kinins (and partly by decreasing levels of angiotensin II), ACE inhibitors can favorably alter cardiac remodeling b. Therapeutic : i. Hypertension, heart failure, MI left ventricular dysfunction and nephropathy c. Adverse effects : i. First-dose hypotension, cough, angioedema, hyperkalemia (w/ potassium supplements), renal failure (w/ renal stenosis), fetal injury d. Patient education i. Diuretics may increase first dose hypotension ii. Potassium supplements and K sparking diuretics can cause hyperkalemia iii. Monitor lithium iv. NSAIDS may reduce affects Angiotensin II Receptor Blockers: (-sartans) e. Appropriate choice for pts who cannot tolerate ACE f. Mechanism : i. block access of angiotensin II to its receptors in blood vessels (causing dilation), the adrenals (lowers aldosterone and increase water loss), and all other tissues g. Therapeutic : i. Hypertension, heart failure, MI, stroke prevention and nephropathy h. Adverse effects : i. Less cough, less angioedema, less hyperkalemia, renal failure (w/ renal stenosis), fetal injury i. Patient education i. Do not take with other hypertensive drugs • ARBs share the beneficial hemodynamic effects of ACE inhibitors, but not the beneficial effects on cardiac remodeling. a. In patients with HF, ARBs should be reserved for patients intolerant of ACE inhibitors (usually owing to cough). Aldosterone antagonists: (eplerenone and spironolactone) b. Mechanism : i. block receptors for aldosterone c. Therapeutic : i. hypertension and heart failure • Patient education o avoid potassium supplements and potassium-containing salt substitutes unless they are prescribed by the provider. Potassium-sparing diuretics must also be avoided. ▪ Signs of high potassium – 3.5-5.0 – muscle spasm o possibility of persistent dry, irritating, nonproductive cough with ACEs and ARBs o do not use during pregnancy o seek immediate medical attention if angioedema develops o neutropenia: early signs of infection (fever, sore throat, mouth sores) o minimize NSAID use • Nursing interventions o Stop diuretics o avoiding potassium supplements and potassium-sparing diuretics except when they are clearly indicated o Monitor lithium levels frequently • Nursing considerations o ACEs and ARBs taken without regard to meal o Aliskiren should be taken same time each day at mealtime Calcium Channel Blockers – Verapamil and Nifedipine • nifedipine and the other dihydropyridines act primarily on vascular smooth muscle • verapamil and diltiazem act on vascular smooth muscle and on the heart Verapamil: o Mechanism : vasodilation accompanied by reduced arterial pressure and increased coronary perfusion o Therapeutic : angina (for vasodilation), hypertension (by dilating arterioles), cardiac dysrhythmias (suppressing impulse conduction through the AV node) o Adverse effects : ▪ constipation from blockade calcium channels in smooth muscle of intestine, dizziness, facial flushing, headache, and edema of the ankles and feet from vasodilation ▪ can cause bradycardia, partial or complete AV block ▪ gingival hyperplasia o Patient education ▪ No grapefruit juice ▪ Inform patients about signs of edema (swelling in ankles or feet), and instruct them to notify the prescriber if these occur ▪ Advise patients that constipation can be minimized by increasing dietary o Potassium-sparing diuretics are used to counteract potassium loss caused by thiazide diuretics and loop diuretics o Potassium-sparing diuretics can cause hyperkalemia. By doing so, they can increase the risk of hyperkalemia in patients taking ACE inhibitors or ARBs Beta blockers • BB can prolong survival in patients with HF and are considered first-line therapy • To avoid excessive cardiosuppression, beta-blocker dosage must be very low initially and then gradually increased. • Isosorbide dinitrate (which dilates veins) plus hydralazine (which dilates arterioles) can be used in place of an ACE inhibitor (or ARB) if an ACE inhibitor (or ARB) cannot be used. • BiDil, a fixed-dose combination of hydralazine and isosorbide dinitrate, is approved specifically for treating HF in African Americans. Digoxin • Digoxin and other inotropic agents increase the force of myocardial contraction and thereby increase cardiac output. • Of the available inotropic agents, digoxin is the only one that is both effective and safe when used orally and the only one suitable for long-term use. • Digoxin increases contractility by inhibiting myocardial Na+/K+-ATPase, thereby (indirectly) increasing intracellular calcium, which in turn facilitates the interaction of actin and myosin. • Potassium competes with digoxin for binding to Na+/K+-ATPase. Therefore, if potassium levels are low, excessive inhibition of Na+/K+-ATPase can occur, resulting in toxicity. Conversely, if potassium levels are high, insufficient inhibition can occur, resulting in therapeutic failure. Accordingly, it is imperative to keep potassium levels in the normal physiologic range: 3.5 to 5 mEq/L. • By increasing cardiac output, digoxin can reverse all of the overt manifestations of HF: cardiac output improves, heart rate decreases, heart size declines, constriction of arterioles and veins decreases, water retention reverses, blood volume declines, peripheral and pulmonary edema decrease, water weight is lost, and exercise tolerance improves. Unfortunately, although digoxin can improve symptoms, it does not prolong life. • In patients with HF, benefits of digoxin are not due solely to improved cardiac output; neurohormonal effects are important too. • Digoxin causes dysrhythmias by altering the electrical properties of the heart (secondary to inhibition of Na+/K+-ATPase). • The most common reason for digoxin-related dysrhythmias is diuretic-induced hypokalemia. • If a severe digoxin overdose is responsible for dysrhythmias, digoxin levels can be lowered using Fab antibody fragments [Digifab] • In addition to dysrhythmias, digoxin can cause GI effects (anorexia, nausea, vomiting) and CNS effects (fatigue, visual disturbances). Gastrointestinal and CNS effects often precede dysrhythmias and therefore can provide advance warning of serious toxicity. • Digoxin has a narrow therapeutic range. • Digoxin is eliminated by renal excretion. • Although routine monitoring of digoxin levels is generally unnecessary, monitoring can be helpful when dosage is changed, symptoms of HF intensify, kidney function declines, signs of toxicity appear, or drugs that affect digoxin levels are added to or deleted from the regimen. • Maintenance doses of digoxin are based primarily on observation of the patient: Doses should be large enough to minimize symptoms of HF but not so large as to cause adverse effects • Maintenance doses of digoxin must be reduced if renal function declines. Nursing considerations included assessment of heart rate prior to administration, monitoring for sign/symptoms of hypokalemia, and patient education reference adherence, risks of dysrhythmias, hypokalemia, and toxicity to notify health care provider. Hypertensives in Emergencies & Pregnancy • Therapeutic uses a. hypertensive emergency exists when diastolic BP exceeds 120 mm Hg • Adverse effects a. hypotension, sedation, and sexual dysfunction b. beta blockers can intensify AV block, and hence should not be taken by people with these disorders • Examples a. Sodium nitroprusside (emergency) b. Fenoldopam (emergency) i. indicated for short-term management of hypertensive emergencies ii. lowers BP by activating dopamine1 receptors on arterioles to cause vasodilation iii. helps maintain (or even improve) renal function, by dilating renal blood vessels and promoting sodium and water excretion c. methyldopa or labetalol (pregnancy) i. “severe” hypertension (160/110) requires treatment, whereas “mild” hypertension (140/90) generally does not • Preeclampsia: multisystem disorder characterized elevated BP (above 130/90 mm Hg) and proteinuria (300 mg or more in 24 hours) after the 20th week of gestation (w/ seizures = eclampsia) Reduced cardiac output leads to compensatory responses: (1) activation of the SNS, (2) activation of the RAAS, and (3) retention of water and expansion of blood volume. As a result of volume expansion, cardiac dilation increases. • Nursing interventions o Lifestyle modifications: weight reduction and sodium restriction, DASH diet, alcohol restriction, exercise, smoking cessation, encourage self-monitoring o Simplify the regimen, establish collaborative relationship o Adherence is difficult (1) hypertension has no symptoms (so drug benefits aren't obvious); (2) hypertension progresses slowly (so patients think they can postpone treatment); and (3) treatment is complex and expensive, continues lifelong, and can cause adverse effects • Nursing considerations o The baroreceptor reflex, the kidneys, and the RAAS can oppose our attempts to lower BP with drugs. Counteract the baroreceptor reflex with a beta blocker, the kidneys with a diuretic, and the RAAS with an ACE inhibitor, ARB, DRI, or aldosterone antagonist. o tailor the regimen to the sensitivities of the patient o encourage them to report objectionable responses o Avoid drugs that can exacerbate comorbid conditions • Adverse effects Interactions with oral contraceptives, nonsteroidal anti-inflammatory drugs, glucocorticoids, appetite suppressants, tricyclic antidepressants, monoamine oxidase inhibitors, cyclosporine, erythropoietin, alcohol (in large quantities), and nasal decongestants and other cold remedies. Antidysrhythmics Treat only if there is a clear benefit—and then only if the benefit outweighs the risks Class I: Sodium channel blockers Quinidine: 1A • Mechanism: o blocks sodium channels, quinidine slows impulse conduction in the atria, ventricles, and His-Purkinje system. o delays repolarization at these sites, apparently by blocking potassium channels. o Both actions contribute to suppression of dysrhythmias o Adenosine decreases automaticity in the SA node and greatly slows conduction through the AV node • Therapeutic o Drug of choice for termination of paroxysmal SVT, including Wolff-Parkinson- White syndrome • Nursing: o Adenosine has a very short half-life (less than 10 seconds) and must be given by IV bolus o Remember to avoid grapefruit juice and monitor for edema with calcium channel blockers and amiodarone. Atherosclerotic drugs • HMG-CoA Reductase Inhibitors (Statins) o Beneficial actions : ▪ reduction of LDL, increase in HDL, reduction of triglyceride level, increased bone formation o Therapeutic : ▪ Hypercholesterolemia: most effective drugs for lowering LDL cholesterol ▪ Primary and Secondary Prevention of CV Events ▪ Post MI therapy: better late than never ▪ Diabetes: controlling CV risk factors—especially hypertension and high cholesterol—is as important as controlling high blood glucose o Adverse: ▪ headache, rash, memory loss, or GI disturbances (dyspepsia, cramps, flatulence, constipation, abdominal pain) ▪ myopathy: can cause muscle injury ▪ hepatotoxicity: tatins are contraindicated for patients with viral or alcoholic hepatitis, fatty liver. o Nursing : ▪ Low doses decrease LDL cholesterol by about 25%, and larger doses decrease levels by as much as 63%. Reductions are significant within 2 weeks and maximal within 4 to 6 weeks. • Other: o Niacin removed from use o Bile acid sequestrant (Colesevelam): ▪ reduce LDL cholesterol levels, used as an adjunct / nonabsorbable resin that binds (sequesters) bile acids and other substances in the GI tract and thereby prevents their absorption and promotes their excretion ▪ Cholestyramine and colestipol—but not colesevelam—can impair absorption of fat-soluble vitamins (A, D, E, and K). Vitamin supplements may be required. Colesevelam does not reduce vitamin absorption. o Fibric acid derivatives, also known as fibrates, are the most effective drugs we have for lowering TG levels Antianginal Agents Nitroglycerin o Mechanism : ▪ decreases the pain of exertional angina primarily by decreasing cardiac oxygen demand, by dilating veins, nitroglycerin decreases venous return to the heart, and thereby decreases ventricular filling; the resultant decrease in wall tension (preload) decreases oxygen demand. o Therapeutic : to terminate an ongoing anginal attack, or for acute prophylaxis of angina o Adverse : ▪ Headache, hypotension, reflex tachycardia o Nursing : ▪ Tolerance to nitroglycerin-induced vasodilation can develop rapidly (over the course of a single day) ▪ should be discontinued slowly. If they are withdrawn abruptly, vasospasm may result. ▪ Isosorbide Mononitrate and Isosorbide Dinitrate have pharmacologic actions identical to those of nitroglycerin – differences are in route and dosing Nitrates Decrease oxygen demand by dilating veins, which decreases preload Increase oxygen supply by relaxing coronary vasospasm Beta Blockers Decrease oxygen demand by decreasing heart rate and contractility Not used Calcium Channel Blockers Decrease oxygen demand by dilating arterioles, which decreases afterload (all calcium blockers), and by decreasing heart rate and contractility (verapamil and diltiazem) Increase oxygen supply by relaxing coronary vasospasm Ranolazine Appears to decrease oxygen demand, possibly by helping the myocardium generate energy more efficiently Not used Myocardial Infarction Agents MI is necrosis of the myocardium secondary to acute occlusion of a coronary artery. The usual cause is platelet plugging and thrombus formation at the site of a ruptured atherosclerotic plaque. • STEMI is diagnosed by the presence of chest pain, characteristic ECG changes, and elevated serum levels of cardiac troponins. • Aspirin o suppresses platelet aggregation, decreasing mortality, reinfarction, and stroke. All patients should chew a 162- to 325-mg dose on hospital admission and should take 81 to 162 mg/day indefinitely after discharge. In patients undergoing acute STEMI, beta blockers reduce cardiac pain, infarct size, short-term mortality, recurrent ischemia, and reinfarction. Continued use increases long-term survival. All patients should receive a beta blocker in the absence of specific contraindications. • Oxygen, morphine, and nitroglycerin are considered routine therapy for suspected STEMI. They should be started, as appropriate, soon after symptom onset. • Reperfusion therapy, which restores blood flow through blocked coronary arteries, is the most beneficial treatment for STEMI. • Reperfusion can be accomplished with PCI or with fibrinolytic drugs. Both approaches are highly effective, but PCI is now generally preferred. • PCI usually consists of balloon angioplasty coupled with placement of a drug-eluting stent. • Fibrinolytic drugs dissolve clots by converting plasminogen into plasmin, an enzyme that digests the fibrin meshwork that holds clots together. • Typically, all fibrinolytic drugs are equally effective. However, when treatment is initiated within 4 to 6 hours of pain onset, alteplase is most effective. • The major complication of fibrinolytic therapy is bleeding. Intracranial hemorrhage is the greatest concern. • Heparin is recommended for all patients undergoing fibrinolytic therapy or PCI. • Aspirin (an antiplatelet drug) combined with clopidogrel is recommended for all patients undergoing reperfusion therapy with a fibrinolytic drug. • Glycoprotein IIb/IIIa inhibitors (e.g., abciximab) are powerful IV antiplatelet drugs that can enhance the benefits of primary PCI. • In patients with acute MI, ACE inhibitors decrease mortality, severe heart failure, and recurrent MI. All patients should receive an ACE inhibitor in the absence of specific contraindications. For patients who cannot tolerate ACE inhibitors, an ARB may be used instead. • To lower the risk of a second MI, all patients should decrease cardiovascular risk factors (e.g., smoking, hypercholesterolemia, hypertension, diabetes), exercise for 30 minutes at least 3 or 4 days a week, and undergo long-term therapy with four drugs: a beta blocker, an ACE inhibitor or an ARB, an antiplatelet drug or warfarin, and a statin. Deficiency Anemia Agents • The principal cause of iron deficiency is increased iron demand secondary to (1) maternal and fetal blood volume expansion during pregnancy; (2) blood volume expansion during infancy and early childhood; or (3) chronic blood loss, usually of GI or uterine origin. • The major consequence of iron deficiency is microcytic, hypochromic anemia. • Ferrous sulfate, given PO, is the drug of choice for iron deficiency. • Iron-deficient patients who cannot tolerate or absorb oral ferrous salts are treated with parenteral iron—usually iron dextran administered IV. • The major adverse effects of ferrous sulfate are GI disturbances. These are best managed by reducing the dosage (rather than by administering the drug with food, which would greatly reduce absorption). • Parenteral iron dextran carries a significant risk of fatal anaphylactic reactions. The risk is much lower with other parenteral iron products (e.g., iron sucrose). • When iron dextran is used, a small test dose is required before each full dose. Be aware, however, that patients can experience anaphylaxis and other hypersensitivity reactions from the test dose, and patients who did not react to the test dose may still have these reactions with the full dose. • The principal cause of vitamin B12 deficiency is impaired absorption secondary to lack of intrinsic factor. • The principal consequences of B12 deficiency are megaloblastic (macrocytic) anemia and neurologic injury. • Vitamin B12 deficiency caused by malabsorption is treated lifelong with cyanocobalamin. Traditional treatment consists of IM injections administered monthly. However, large oral doses administered daily are also effective, as are intranasal doses (administered weekly with Nascobal). • For initial therapy of severe vitamin B12 deficiency, parenteral folic acid is given along with cyanocobalamin. • When folic acid is combined with vitamin B12 to treat B12 deficiency, it is essential that the dosage of B12 be adequate because folic acid can mask continued B12 deficiency (by improving the hematologic picture), while allowing the neurologic consequences of B12 deficiency to progress. • The principal causes of folic acid deficiency are poor diet (usually in patients with alcohol use disorder) and malabsorption secondary to intestinal disease. • The principal consequences of folic acid deficiency are megaloblastic anemia and neural tube defects in the developing fetus. • To prevent neural tube defects, all women who may become pregnant should ingest 400 to 800 mcg of supplemental folate daily, in addition to the folate they get in food. Antianxiety agents SRIs, buspirone, and benzodiazepines are first line drugs for GAD SRIs o SRIs (venlafaxine, paroxetine, escitalopram, and duloxetine) are well suited for treating patients who have depression in addition to GAD o With buspirone, venlafaxine, paroxetine, escitalopram, and duloxetine, anxiolytic effects are delayed. Accordingly, these drugs are best suited for long- term management—not rapid relief o SSRIs first line treatment for panic disorder, anticipatory anxiety, OCD, social anxiety o PTSD also treated with psychotherapy and SSRIs/TCAs/MAOIs Buspirone o binds with high affinity to receptors for serotonin and with lower affinity to receptors for dopamine o dizziness, nausea, headache, nervousness, sedation, light-headedness, and excitement. o does not cause CNS depression, has no abuse potential, and does not intensify the effects of CNS depressants. o levels can be increased by erythromycin, ketoconazole, and grapefruit juice. Benzodiazepines o suppress symptoms of GAD immediately. Accordingly, these drugs are preferred agents for rapid stabilization, especially when anxiety is severe. o CNS depressants and hence can cause sedation and psychomotor slowing. In addition, they can intensify CNS depression caused by other drugs. o have some potential for abuse, and hence should be used with caution in patients known to abuse alcohol or other psychoactive drugs. o taken long term, benzodiazepines can cause physical dependence. To minimize withdrawal symptoms, dosage should be tapered gradually—over a period of several months. Bipolar Agents • Bipolar I Disorder—Patients experience manic or mixed episodes and usually depressive episodes too. • Bipolar II Disorder—Patients experience hypomanic or depressive episodes, but not manic or mixed episodes Lithium • Mechanism o Unknown, altered distribution of certain ions, altered synthesis of norepinephrine, serotonin and dopamine and effects on second messengers • Therapeutic o drug of choice for controlling acute manic episodes in patients with BPD and for long-term prophylaxis against recurrence of mania or depression. In manic patients, lithium reduces euphoria, hyperactivity, and other symptoms but does not cause sedation • Adverse o At therapeutic level : tremor, polyuria, renal toxicity with prolonged use, goiter an hypothyroid by reducing iodine, teratogenesis, mild, reversible leukocytosis, skin reactions o At excessive level : Persistent GI upset, coarse hand tremor, confusion, hyperirritability of muscles, ECG changes, sedation, incoordination, ataxia, giddiness, high output of dilute urine, serious ECG changes, fasciculations, tinnitus, blurred vision, clonic movements, seizures, stupor, severe hypotension, coma, death (usually secondary to pulmonary complications) • Nursing o must be kept below 1.5 mEq/L; levels greater than this can produce significant toxicity o because of its short half-life (and high toxicity), the drug must be administered in divided daily doses o toxicity can occur at blood levels only slightly greater than therapeutic levels, monitoring lithium levels is mandatory o Lithium levels can be increased by diuretics (especially thiazides) and by several nonsteroidal anti-inflammatory drugs. o lithium excretion is reduced when levels of sodium are low because the kidney processes lithium and sodium in the same way. Hence, when the kidney senses that sodium levels are inadequate, it retains lithium in an attempt to compensate First-Generation Antipsychotics / Neuroleptics • low potency, medium potency, or high potency o potency refers only to the size of the dose needed to elicit a given response; potency implies nothing about the maximal effect a drug can produce • Mechanism o blocking dopamine2 (D2) receptors in the mesolimbic area of the brain • Therapeutic: o Schizophrenia - effectively suppress symptoms during acute psychotic episodes and, when taken chronically, can greatly reduce the risk of relapse – 1-2 days to 2-4 weeks for full effect o Positive symptoms (e.g., delusions, hallucinations) may respond somewhat better than negative symptoms (e.g., social and emotional withdrawal, blunted affect, poverty of speech) or cognitive dysfunction (e.g., disordered thinking, learning and memory difficulties) • Adverse: o Extrapyramidal symptoms – movement disorders o Acute dystonia - spasm of the muscles of the tongue, face, neck, or back o Parkinsonism - bradykinesia, mask-like facies, drooling, tremor, rigidity, shuffling gait, cogwheeling, and stooped posture o Akathisia o Tardive dyskinesia - involuntary choreoathetoid (twisting, writhing, worm- like) movements of the tongue and face, lip smacking o Neuroleptic malignant syndrome - “lead pipe” rigidity, sudden high fever o CNS: sedation to sleep to general anesthesia. o CV: modest reduction in blood pressure and heart rate, toxic doses hypotension and shock o Hepatic: barbiturates can accelerate their own metabolism and the metabolism of many other drugs • Therapeutic: o Seizures o Anesthesia o Insomnia o Acute mania and delirium o Decrease restlessness in children • Adverse: o Tolerance and dependence ▪ Withdrawal: weakness, restlessness, insomnia, hyperthermia, orthostatic hypotension, confusion, and disorientation, by the third day, major convulsive episodes and psychotic experiences ▪ A long-acting barbiturate (e.g., phenobarbital) may be administered to facilitate the withdrawal process. o Respiratory depression, suicide, abuse o Acute toxicity: respiratory depression, coma, and pinpoint pupils., hypotension and hypothermia Controlled Substance Act & Healthcare Impact • Drugs in Schedule I have a high potential for abuse and no approved medical use in the United States. In contrast, drugs in Schedules II through V all have approved applications. Assignment to Schedules II through V is based on abuse potential and potential for causing physical or psychologic dependence. Of the drugs that have medical applications, those in Schedule II have the highest potential for abuse and dependence. o Sched II : typed, filled out in ink, electronic and signed, no refills (warning label) o Sched III/IV : oral, written, or electronic, refilled up to 5 times (warning label) o Sched V : without Rx, if by pharmacist, limited amount, recipient >17, pharmacist initials, state/local law allows Alcohol Pharmacology & Alcohol Use Disorder • most used and abused psychoactive agent • consumed in moderation, alcohol prolongs life and reduces the risk of dementia and cardiovascular disorders • For those with unhealthy lifestyle : There is clear evidence that people who drink moderately (2 drinks a day or less for men, 1 drink a day or less for women) experience less ischemic stroke, coronary artery disease (CAD), myocardial infarction (MI), and heart failure than do abstainers. o raises HDL cholesterol, decreases platelet aggregation, decreases levels of fibrinogen (the precursor of fibrin, which reinforces clots), increases levels of tissue plasminogen activator (a clot-dissolving enzyme), and suppresses the inflammatory component of atherosclerosis o may decrease the risk for type 2 diabetes • CNS: o (1) general depression of central nervous system function o (2) activation of the reward circuit (from binding with 5-HT3 receptors) • Chronic: o Wernicke's encephalopathy and Korsakoff's psychosis. Both disorders are caused by thiamine deficiency • Cognitive: o Low to moderate drinking helps preserve cognitive function in older people and may protect against development of dementia • Cardiovascular: o acute dose – dilation of cutaneous blood vessels o chronic and excessive – direct damage to myocardium, heart failure, elevation of BP • Adverse: o Erosive gastritis, pancreatitis, sexual dysfunction, fatty liver to hepatitis to cirrhosis, cancer • Alcohol is absorbed from the stomach (20%) and small intestine (80%), metabolized in liver • Interacts with CNS depressants, NSAIDs, acetaminophen, disulfiram, antihypertensives • Alcohol use disorder is a chronic, relapsing disorder characterized by impaired control over drinking, preoccupation with alcohol consumption, use of alcohol despite awareness of adverse consequences, and distortions in thinking, especially as evidenced by denial of a drinking problem – 12 month period o treated with benzos, beta blockers, alpha2 adrenergic agonists, antiepileptic drugs – decreases withdrawal symptoms, prevent sizures o disulfiram, naltrexone, and acamprosate to maintain abstinence Nicotine & Smoking Cessation • CV effects: o Norepinephrine and epinephrine act on the cardiovascular system to constrict blood vessels, accelerate the heart, and increase the force of ventricular contraction. The net result is elevation of blood pressure and increased cardiac work. These effects underlie cardiovascular deaths. • CNS: o increases alertness, facilitates memory, improves cognition, reduces aggression, and suppresses appetite. In addition, by promoting the release of dopamine, nicotine activates the brain's “pleasure system” • Acute poisoning: nausea, salivation, vomiting, diarrhea, cold sweats, disturbed hearing and vision, confusion, and faintness; pulses may be rapid, weak, and irregular. Death results from respiratory paralysis • The overall intervention strategy is summarized in the “5 A's” model for treating tobacco use and dependence: o Ask (screen all patients for tobacco use). o Advise tobacco users to quit. o Assess willingness to make a quit attempt. o Assist with quitting (offer medication and provide or refer to counseling). o Arrange follow-up contacts, beginning within the first week after the quit date. • Nicotine replacement = patch, gum, etc. • Non-nicotine = bupropion, varenicline