NURS 6521 PHARM EXAM STUDY GUIDES

Pharmacology for APNs- Cardiovascular Study Guide

HTN: Effect of sympathetic nervous system and RAAS on BP

Goals of treatment of HTN
o JNC 8 recommendations
 BP goal age>60y/o vs <60y/o
 CKD and DM goals- they differ than JNC7, but are controversial and many
nephrologists/endocrinologists will use a lower goal if patient tolerates
therapy well
 Recommendations in African American population- what drugs specifically do
not work well in that population and therefore are not recommended

Drug classes used in treatment- which are first line- etc…

Know the mechanisms of action, pharmacodynamics, adverse effects, warnings,
monitoring, of each of the following drug classes
 Beta blockers (be able to recognize the “lol” drugs
 ACEI (the “pril” drugs)
 Angiotension receptor blockers – ARBs
 Calcium channel blockers- CCB
 Selective Alpha 1 blockers
 Central acting alpha agonists
 Vasodilators
 Nitroglycerin
 Direct renin inhibitor- aliskiren
 Diuretics: Diuretic classes:
o thiazides, thiazide like analogues, loop, aldosterone antagonists, triamterene,
amiloride, carbonic anhydrase inhibitors,

Angina: stable vs unstable, prinzmetal
 Know drug classes used to treat angina
 Organic Nitrates chart

Hyperlipidemia:
 drugs used in treatment, know mechanisms of action, clinical efficacy, adverse effects,
contraindications of the following:
 HMG CoA reductase inhibitors- statins
 Niacin
 Fibrates
 Bile acid-binding resins
 Cholesterol absorption inhibitors


MOA Clinical Efficacy ADE Contraindications

, HMG CoA -Alters sterol 1st line agent Elevated serum Pregnancy and
reductase biosynthesis aminotransferase, lactation
inhibitors - lowers LDL. Most potent for reducing creatine kinase
Statins -Decreases total and LDL chol. Caution: hepatic
oxidative Myopathy disease, ETOH
stress/vascular Patient tolerance: good abuse, polypharmacy
inflammation Constipation (multiple drug
-increases interactions)
stability of Rhabdomyolysis
atherosclerotic (rare)
lesions (statins
initiated post
acute coronary
syndromes
regardless of
lipid levels
Niacin Inhibits VLDL 2nd line Skin flushing (more
secretion  agent/combination so with
Niaspan decreases thearpy ASA/NSAIDS)
B vitamin production of
LDL. Alternative for Pruritis
hypertriglyceridemia/stati Hyperglycemia
Lowers LDL, n intolerant patients Hyperuricemia (can
triglycerides, exacerbate gout)
VLDL – can Patient tolerance: GI complaints
increase HDL reasonable to poor Severe liver
dysfunction

Fibrates Increases Patient tolerance: Good GI complaints Caution: with hx
synthesis of Rash cholelithiasis
lipoprotein lipase Dizziness
by adipose Elevated
tissuedecrease transaminase/alkalin
s triglycerides, e phosphatase levels
may increase Gallstones (rare)
LDL/HDL Myositis
Increased INR in
warfarin patients
Bile acid- Inhibition of bile Reduces LDL 20% at max GI – constipation, Hypertriglyceridemi
binding resins acid reabsorption dose – not very effective bloating, epigastric a
(BARs) fullness, nausea,
Cholestyramine Not as common as they flatulence Caution: take hours
, colestipol, once were after all other drugs
colesevelam Impaired absorption due to drug
of fat-soluble interactions
vitamins (warfarin, thyroxine,