NR 508 Midterm Exam Consist of 50 Questions Completed with Answers
NR 508 Midterm Exam Consist of 50 Questions From a Random Test Bank of
... [Show More] Questions
from Chapters 1-4 (including Week 4 Content) and All Embedded Recorded Lectures.
Information is taken from the following 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 Disease9. 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 circumstances, they are already depolarized before reaching the
automatic depolarization.
o Reentrant Excitation: Retrograde conduction and unidirectional block are
required for reentrant excitation to occur. Anti-Arrhythmics stop reentry excitation by prolonging the refractory
period at the ectopic site. In this way the unidirectional block becomes a
bidirectional block, and the cycle is stopped.
GENERAL EFFECTS of ANTI-ARRHYTHMICS: Anti-arrhythmics also cause
arrhythmias. All anti-arrhythmics also have local anesthetic effects.
o Reduce the slope of Phase-4 Depolarization ------> reduce automaticity.
o Decrease conduction velocity.
o Reduce threshold potential.
o Terminate reentrant excitation, by prolonging the refractory period of the
initiation point.
ANTI-HYPERTENSIVE DRUGS:
ORAL DIURETICS:
o SUBTYPES:
THIAZIDE DIURETICS: Most commonly used for HTN.
Hydrochlorothiazide, Chlorthalidone, Indapamide
ACTION: Lowers blood volume by depleting body Na+ stores, by
increasing Na+ excretion in the kidney.
LOOP DIURETICS: Rarely used for HTN, often used for CHF.
POTASSIUM-SPARING DIURETICS: Weak; used in conjunction with
thiazides to help alleviate hypokalemia.
o PATIENT POPULATION: Thiazides can be used as monotherapy.
Old, black males respond best to Thiazide diuretics.
Cheap drug
For patients with moderate HTN, and normal kidney and cardiac function.
o SIDE EFFECTS: Sexual impotence, as is potentially true with any anti-hypertensive
Hyperuricemia, gout
Reflex increase in renin secretion (can be counteracted with ACE
Inhibitor)
Potassium depletion: Can be potentially countered with (1) supplemental
potassium, or (2) potassium-sparing diuretic
Muscle cramps
Arrhythmias
Impaired glucose tolerance, hyperinsulinemia.
Atherogenesis: Thiazides increase LDL and increase the LDL/HDL ratio.
Hyperlipidemia
o DOSING: Very low dose (6-12 mg/day) is required for lowering blood pressure,
as compared to that which is required for diuresis (100-200 mg/day). This helps to
alleviate side-effects.
SYMPATHOLYTICS:
o CENTRALLY ACTING: alpha2-agonists. Clonidine, Guanabenz, Guanfacine,
Methyldopa.
ADVERSE EFFECTS: Not recommended for monotherapy.
CNS: Dizziness, sedation, nightmares, depression
Dry Mouth
beta-BLOCKERS:
o CLASSES: Non-selective (beta1, beta2), cardioselective (only beta1), partial
agonists.
o MECHANISM: Blocks beta-receptors in 3 places:
Block beta1-receptors on heart: Reduce heart rate and inotropic state. Block beta1-receptors on kidneys: Reduce renin secretion.
Block beta-receptors in CNS: Reduce sympathetic outflow ------> reduce
vasomotor tone.
o INDICATIONS:
Lower blood pressure
Improve myocardial oxygen supply ------> treat angina
They do not, however, increase blood supply to the myocardium.
Often combined with nitrates.
Do not use with variant angina. beta-blockers slow heart rate
------> prolonged ejection time and increased LVEDV ------>
increased myocardial oxygen supply.
Normalize heart rate
Prevent myocardial infarct (less O2 demand of myocardium)
Limit the size of myocardial infarct [Show Less]