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NURS 6521 PHARM EXAM STUDY GUIDES
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NURS 6521 PHARM EXAM STUDY GUIDES
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Pharmacology for APNs- Cardiovascular Study GuideHTN: 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
tissuedecrease 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,
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