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Chamberlain College of Nursing NR 508 Midterm Exam

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NR 508 Midterm Exam Consist of 50 Questions From a Random Test Bank of Questions from Chapters 1-4 (including Week 4 Content) and All Embedded Recorded Lectures. Information is taken from the follow... ing Areas: Highlighted areas are areas to help you understand the concepts better they are in NO way an indication of what you are guaranteed to see on the exam. Remember these are random some of your classmates may not have the same question that appear on your exam. PLEASE NOTE that this study guide may not be inclusive of all topics you may see on the exam 1 NP Practice 1-2 Questions 2 Birth Control Contraindications 1-2 Questions 3 Treatment of CHF 5-15 Questions  Know First Line Treatment in CHF  Side Effects of Diuretics  Side Effects of Ace Inhibitors 4.Treatment of Hypertension 5-6 Questions  Know First Line Treatment in Hypertension  Side Effects of Diuretics  Side Effects of Ace Inhibitors 5. Treatment of Fungal infections 3-5 Questions  Know How to Treat Various Fungal Infections  Common Uses 6. Treatment of Abnormal Heart Rhythms 4-5 Questions  Know Treatment of Arrhythmia 7. Treatment of Depression& Anxiety 4-5 Questions 8. Treatment of Parkinson 4-5 Questions  Know Treatment of Parkinson Disease 9. Treatment of Alzheimer’s 4-5 Questions 10. Treatment of Acne 1-2 Questions 11. Clotting Factor in Vitamin K1-2 Questions CONGESTIVE HEART FAILURE (CHF): *Refer to your CHF PowerPoint Slides  EPIDEMIOLOGY: o Most common cause of hospitalization over 65 years of age. o Afflicts more than 2 million Americans annually. o 900,000 hospitalization per year. o PROGNOSIS: Poor  Untreated, 82% of men die within 6 years of onset.  Untreated, 67% of women die within 6 years of onset.  Treated, mortality was reduced to 40% Causes: Myocardial Infarction, hypertension, coronary artery disease, Hyperthyroidism, Beriberi, anemia, arteriovenous shunts.  HEMODYNAMIC PROPERTIES: Consequences of CHF o Subnormal Cardiac Output ------> decreased exercise tolerance, tachycardia, pulmonary edema, cardiomegaly o Neurohumoral Reflexes: Reflex tachycardia, increased sympathetics, increased Renin. o Myocardial Hypertrophy occurs, to maintain cardiac performance.  Ventricular dilation helps to maintain cardiac output to an extent (due to Starling's Law), but past a certain point it can no longer help. o Factors affecting cardiac performance:  Higher preload: due to increased blood volume and venous tone.  Higher afterload: due to hypertension, increased arterial tone.  Lower contractility ------> lower inotropic state  Higher heart rate, due to reflex tachycardia o Edema: Especially pulmonary edema, but also peripheral. Results from decreased Cardiac Output, by two mechanisms:  Decreased CO ------> impaired venous return ------> higher capillary hydrostatic pressure  Decreased CO ------> decreased renal perfusion ------> activate renin angiotensin system RAS ------> aldosterone causes higher Na+ and fluid retention.  TREATMENT: o CARDIAC GLYCOSIDES: See CHF PowerPoint Slides : o MECHANISM: Inhibit Na+ /K+ -ATPase Pump ------> increased intracellular Na+ in myocardium ------> decreased expulsion of Ca+2 in myocardium ------> tonically higher levels of intracellular Ca+2 ------> increased myocardial contractility o MECHANICAL ACTION on HEART:  Increased myocardial contractility  Bradycardia, due to reduced sympathetics.  Increased Cardiac Output, due to reduced TPR (from reduced sympathetics) and increased inotropic state. o ELECTRICAL ACTION on HEART:  Direct Effect on AV Node: Increase risk of heart block  Decrease the rate of rise of Phase-0 depolarization at AV node.  Prolong refractory period at AV-Node  Decrease conduction velocity at AV-Node.  Direct Effect on Purkinje Fibers:  Increase automaticity ------> increased risk of arrhythmias. This occurs by two mechanisms:  Increase the slope of Phase-4 depolarization.  Elevate the resting membrane potential of the SA-Node, as a consequence of inhibiting the Na+ /K+ -ATPase  Decrease conduction velocity  Parasympathomimetic Effects: Digitalis increases vagal stimulation, by three mechanisms:  Baroreceptor Sensitization  Central Vagal Stimulation  Facilitate muscarinic transmission at myocardial cells  Hypokalemia potentiates the cardiotoxic effects of Digitalis, since digitalis deprives cardiac cells of K+ . This effect of K+ is opposite to the effect seen with quinidine. o KIDNEY DIURESIS: Digitalis effect on kidney is indirect -- resulting from improved cardiac output. If cardiac output does not improve, then there will be no diuresis. o ACE INHIBITORS: They have significantly decreased mortality due to CHF.  ACTION: They inhibit the activation of the renin-angiotensin system, which is hyperactive in CHF, due to increased sympathetics.  They reduce afterload: Reduce circulating levels of AngiotensinII  They reduce preload: Reduce Aldosterone ------> reduce blood volume.  INDICATIONS: ACE Inhibitors are recommended in the following patients:  All patients with symptomatic CHF due to LV systolic dysfunction.  Asymptomatic patients with severe LV systolic dysfunction, HTN, or valvular regurgitation (aortic incompetence, mitral regurgitation).  Post-MI patients at risk for complications. o VASODILATORS:  Sodium Nitroprusside: IV, used to treat acutely decompensated CHF, where brain and kidney perfusion is compromised.  Hydralazine: It maintains renal blood flow. Used to treat CHF in the presence of kidney dysfunction. o LOOP DIURETICS: Goal in this case is to reduce blood volume, not reduce blood pressure. o XANTHINES: Theophylline can produce coronary vasodilation and bronchodilation, both of which can be therapeutic in CHF. LOOP DIURETICS:  MECHANISM: They inhibit the Na+ /K+ /2Cl- transporter, essentially shutting down the counter-current multiplier ------> profuse natriuresis.  INDICATIONS: o Edema, caused by CHF, cirrhosis, or nephrosis. o Management of hyponatremia or hypercalcemia. Given in combination with saline infusion. o Increase K- and H+ excretion in patients with distal renal tubular acidosis.  PHARMACOKINETICS: o Furosemide is secreted by a probenecid-sensitive transport mechanism into proximal tubule. Thus indomethacin or NSAID's decrease its effectiveness. o Bioavailability 50-70%. Extensively binds to plasma albumin.  ADVERSE EFFECTS: o Metabolic effects:  Hyponatremia, hypomagnesemia, metabolic acidosis.  Hypokalemia: can be counteracted with K+ -sparing diuretic, or with supplemental K+ .  Hypochloremic Alkalosis: Increased delivery of Na+ to distal tubules ------> increased RAS and aldosterone ------> increased secretion of K+ and H+ ------> hypokalemic alkalosis. o Hyperuricemia, hypercholesterolemia o Ototoxicity, especially in patients with impaired renal function. THIAZIDE DIURETICS:  MECHANISM: They inhibit Na+ /Cl- antiport ------> natriuresis.  ADVERSE EFFECTS: Also see thiazides under Anti-HTN o Metabolic Effects:  Marked hyponatremia.  Hypokalemia and Hypomagnesemia: can be particularly bad in folks with CHF (taking glycosides), cirrhosis, MI, arrhythmias.  Slight hypercalcemia  Hyperuricemia  INDICATIONS: o Hypertension o Kidney stones o Hypercalcuria o Diabetes Insipidus POTASSIUM-SPARING DIURETICS:  INDICATIONS: Modest diuresis o Adjunct therapy with other diuretics o Primary (Conn's Disease) or secondary (glucocorticoid therapy) hyperaldosteronism.  ADVERSE EFFECTS: o Hyperkalemia ------> fatal arrhythmias. Especially at risk for folks with renal failure, or in those receiving K+ supplements. o Hyperchloremic metabolic acidosis ANTI-ARRHYTHMICS:  NORMAL RHYTHM: o Phase-4 Depolarization results in automaticity of the cardiac action potential, in normal SA nodal cells.  AV nodal cells and Purkinje fibers also have spontaneous Phase-4 depolarization, but their automaticity is slower than SA node, thus under normal circu [Show More]

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