NR565 Week 3 Study Guide
Chapter 16: Drugs Affecting the Cardiovascular and Renal Systems
Chapter 20: Drugs Affecting the Gastrointestinal System
Chapter 28: Chronic Stable Angina & Low Risk Unstable Angina
Chapter 34: Gastroesophageal Reflux and Peptic Ulcer Disease
Chapter 36: Heart Failure
Chapter 39: Hyperlipidemia
Chapter 40: Hypertension
Chapter 16: Drugs Affecting the Cardiovascular and Renal Systems
ACEIs, ARBs and Direct Renin Inhibitors: MOAs, indications, absolute
contraindications, precautions, monitoring, adverse drug reactions, drug
interactions
Absolute contraindications for all-bilat renal artery stenosis, angioedema, and
pregnancy
Precautions-impaired renal function due to vasodilating affect, hypovolemic or
hyponatremic states, hyperkalemia, hepatic impairment,
Monitoring-Potassium levels, kidney function labs prior to drug, 1 week after,
monthly x3months, and when increasing dose, liver function, vitals, weight,
Adverse Drug Reactions-Angioedema, hypotension, tachyphylaxis, cough, rash,
photosensitivity
Drug Interactions-inhibitors of P450 will cause increased levels of free drug.
Additional hypotensive effects with diuretics, HTN meds, nitrates, ETOH. Potassium
or potassium sparing diuretics may cause hyperkalemia. Antihypertensive
response if reduced by NSAIDS
ACEIs-Improve oxygenation to heart and decreases remodeling after MI or with
heart failure. Lowers BP and reduces adverse effects of DM. Inhibition of ACE
activity results in decreased production or angiotensin II and aldosterone. ACE
facilitates breakdown of bradykinin into inactive fragments-high levels of
bradykinin are thought to be a factor in the cough associated with ACEI use.
Renoprotective for individuals with proteinuria. Prevents diabetic nephropathy due
to a reduction in intraglomerular capillary pressure and slows decline of GFR.
,Crosses placenta and found in breast milk. Excreted in urine. Only short acting is
Captopril. Mult doses daily
ARBs-No indications for use in heart failure, similar role to ACEI related to BP.
Block AT II receptor. No reflex tachycardia. D not prevent diabetic nephropathy but
suppresses the rate of progression. Losartan, extensive first-pass metabolism.
Crosses placenta and found in breast milk. Excreted in feces.
DRI-Directly blocks renin. No indications for HF. NOT used in diabetic patients with
renal function < 60mL/min. Only med is Alsikren. Poorly absorbed
Cardiac Glycosides: indications, MOA, adverse drug reactions, contraindications,
cautions, toxicity, drug and potassium, calcium and Mg interactions, monitoring,
patient education, clinical pearls
Indications-Afib, Paroxysmal SVT, Heart failure (not first line),
MOA-Inhibitors of sodium-potassium adenosine triphosphatase system. Changes in
sodium and calcium result in increased velocity of the shortening of cardiac muscle
with a shift upward and to the left in the ventricular function curve causing an
increase in stroke volume (positive inotropism). These drugs affect all smooth
muscle and the CNS
Adverse Drug Reactions-GI, fatigue, disorientation, hallucinations, yellow vision,
green halos, bradycardia, PVCs, bigeminy, gynecomastia
Contraindications-AV blocks and uncontrolled arrhythmias. Pts with idiopathic
subaortic stenosis may develop worsening outflow tract obstruction. Severe renal
impairment. Digoxin may exacerbate a fib due to WPW syndrome.
Precautions-Use with caution in pts with cor pulmonale. Hypothyroidism and CKD
decrease digoxin's volume necessitating a decrease in loading and maintenance
doses. Use with caution in patients with elyte abnormalities because potassium,
calcium, and mag in extracellular compartment affect sensitivity to CGs and may
result in toxicity.
Toxicity-Toxicity risk increases in the presence of hypoxia from any cause. Low
serum albumin may need lower doses. Toxicity usually caused by excessive
administration of a CG, too much diuresis resulting in hypokalemia, renal
insufficiency, of administration of drugs that interfere with excretion of dig
Drug and potassium-Both inhibit each other’s binding to sodium potassium
ATPase. Hyperkalemia reduces enzyme inhibiting action. Hypokalemia facilitates
actions.
Calcium and Mg Interactions-Calcium facilitates the toxic actions of CGs by
overloading the intracellular calcium stores. Hypercalcemia increased risk for CG
arrhythmias. Mag has OPPOSITE effects of calcium
,Monitoring-lab tests when taking another med that may alter effects of CG, 1-2
weeks after starting new dose, toxicity is suspected, renal function decline. Labs
drawn at least 6 hours after last dose along with lytes and renal function.
Patient education-Take at same time each day, don't stop without speaking with Dr,
avoid high fiber, eat diet high in potassium, moderate calcium, separate milk by one
hour
Clinical Pearls-Digibind for neutralization if expensive, $750 vial. and has a half-life
of 2-6 hours during which the rhythm disturbance that was being treated may occur
and cannot be treated with a CG. CGs should not be used for HF unless clear
evidence of severe chronic systolic dysfunction or a fib. Should not be stopped
unless reversible cause of HF has been completely corrected. ST-T waves do not
correlate correctly with drug levels, do not use them as indication of toxicity-only
drug levels.
Antiarrhythmics-
Procainamide monitoring and dosing- dosing every 6-8 hours, lytes, renal and
hepatic function
Amiodarone indications, supraventricular arrhythmias, especially in children.
Reduces mortality in cardiac arrest survivors
patient education-Take as prescribed, evenly spaced, don't stop suddenly, if missed
Amiodarone dose, do not take one until next day, all others taken as soon as
remembered unless within 4 hours of next dose. Take with food except Sotalol.
Photosensitivity. Bluish skin discoloration. Epididymitis, tremors should be
reported due to sign of toxicity
monitoring; Amiodarone inhibits enzyme that converts T4 to T3 ad iodine is a major
component of this drug. About 5% of pts with predisposition to thyroid disease
develop thyrotoxicosis or hypothyroidism. 5-15% of pt's develop potentially fatal
pulmonary fibrosis. Baseline PFT and thyroid studies. CXR every 3-6 months,
ophthalmic exams, thyroid labs, PFTs. Lytes, renal and hepatic function. EKG,
Vitals,
indications, ventricular arrhythmia
contraindications-bradycardia, heart block, HF, hypotension, shock
MOA for BBs-Block chronotropic impact of norepinephrine.
Class IV CCBs that are indicated for arrhythmias ONLY diltiazem and verapamil
Nitrates:
MOA-Provide more NO to vascular epithelium and arterial smooth muscle causing
all part of vasculature to relax. Affects supply and demand on both sides.
, patient education-Take as prescribed. Keep in closed amber vial, not in heated area
like car of near body, replace bottle 6 months after opening, don't stop suddenly,
discuss new drugs with dr
precautions and contraindications-Head trauma, cerebral hemorrhage, volume
depletion and anemia, closed angle glaucoma, pregnancy category C,
adverse drug reactions-postural hypotension, syncope, tachycardia, headache,
arrhythmias, rebound HTN, N & V, risk of age-related macular degeneration
tolerance-No more effective than placebos after 18-24 hours of continuous therapy.
Only after nitrates have been out of body for 10-12 hours do their effectiveness
return.
drug interactions-hypotension with antihypertensives, drugs with anticholinergic
effects may cause decreased absorption of SL NTG, Aspirin may potentiate
Nitrates, Nitrates may decrease heparin effects,
indications-Angina, HF
Peripheral Vasodilators:
Indications-Resistant HTN and PVD
adverse drug reactions-tachycardia, increased sodium and water retention, lupus-
like syndrome (elevated ANA until 6-8 months after drug stopped, increased hair
growth, pregnancy category C,
drug interactions-Additive effects with other antihypertensives, NSAIDS may
decrease antihypertensive effects, BB and loop diuretics are positive in that they
prevent adverse effects common to PADs
Antilipidemic:
MOAs-Drugs affect the absorption of fat and cholesterol in the intestines or they
increase lipolysis of triglycerides
adverse drug reactions with each class-niacin=flushing, fenofibrate=GI symptoms,
cholelithiasis, Bile-acid sequestrants=constipation, N&V, headache, reduced folate
level, burned smell to urine, Reductase inhibitors=headache, possible intracerebral
hemorrhage, rhabdomyolysis with renal dysfunction; statins=myalgias, GI;
drug interactions-All affect warfarin activity except niacin. Bile acid meds decrease
its effect, other meds increases it. Fenofibrate and gemfibrozil interact with other
antilipidemic. All reductase inhibitors increase dig levels. propranolol decreases
antilipidemic activity or reductase inhibitors. Niacin, emycin, and cyclosporine all
increase risk of rhabdo when given with reductase inhibitors.
rational drug selection-Dependent on nature of lipoprotein abnormality, adverse
effects of drug, cost, age of pt, and degree of CVD risk.
