NR566 Week 3 Study Outline
Many questions are written to assess your clinical application of
the material from the textbook, in real-world scenarios.
Chapter 16: Drugs Affecting the Cardiovascular & Renal
Systems
• Know the pharmacodynamics, pharmacotherapeutics clinical
use, drug interactions and adverse drug reactions for:
o o Angiotensin converting enzyme inhibitors (ACEI): pregnancy D
Benazopril Captopril Enalapril Fosinopril Lisinopril Moexipril
o vasodilators
o Not as effective for African-American patients
o When combined with a diuretic, race no longer an issue
o Adverse drug reactions (ADRs): dry cough (bradykinin- mediated), hypotension, loss
of taste, angioedema, blood dyscrasias, teratogenicity, hyperkalemia, acute renal
failure, cholestatic jaundice, pancreatitis, rash
•
o o Angiotensin receptor blockers (ARBs) pregnancy D
Pharmacokinetics
o Losartan: CYP 2C9
o Extensive first-pass metabolism resulting in 33% bioavailability
o Inducers: rifampin, barbituates
o Inhibitors: lovastatin, SMZ/TMP, fluconazole, fluvastatin, fluvoxamine, sertraline
o
Angiotensin II Receptor Blockers SARTANS : losartan, esporsartan,
olmesartan, telmisartan, valsartan, candesartan, irbesartan
o Like ACEI orthostasis with dose changes
•
o o Calcium channel blockers (CCB)nifedipine cat safe and
Functionally act as vasodilators, lowering calcium (Ca++) influx into smooth muscles
o Two major classes
, o Type I – Non-dihydropyridines: affect conduction through the atrioventricular (AV)
node and have negative chronotropic effects
o Why it is used in treating supraventricular tachycardia
o Diltiazem (Cardizem), verapamil (Calan)
o Type II – Dihydropyridines: do not affect conduction through the AV node
o Nifedipine (Procardia), amlopidine (Norvasc), felodipine (Plendil)
• amlodipine cat C, methyldopa very safe
o Cardiac glycosides and antiarrhythmics
Digoxin
o Well-absorbed orally
o NOT extensively metabolized, excreted unchanged by kidneys Half-life is 36 to 48 hours
o In the absence of oral or intravenous loading, steady state is achieved in four half-
lives or 1 week
o Reduced clearance of digoxin with drug interaction
o Quinidine, amiodarone, verapamil, diltiazem
o ADRs
o Gastrointestinal (GI) most common: anorexia, nausea/vomiting, diarrhea
o Central nervous system: fatigue, disorientation, depression, hallucinations,
visual disturbances – yellow vision and green halos around lights
o Toxicity: atrial arrhythmias/tachycardia in children
o Cardiac: bradycardia, premature ventricular contractions, junctional and AV
block arrhythmias, and bigeminy
o Avoid using in patients with normal left ventricular systolic function
o Monitoring
o Diagnosis of toxicity is based on both clinical and laboratory data
o Toxicity commonly occurs with serum levels greater than 2 ng/mL
o Monitor potassium levels
•
• o Nitrates and peripheral vasodilators nitrates work on veins
and reduce preload, hydralazine is a vasodilator
, • o Anti-lipidemics
• o Diuretics treat symptoms of congestions, help the
body get rid of excess fluid, reduce symptoms that
result in excess fluids like shortness of breath doing
this it reduces heart failure (aldosterone inhibitors)
• Also know:
• o ACEIs & ARBs benefits in other conditionsHTN, HEART
FAILURE, SLOWING RENAL DISEASE ,
CARDIOVASCULAR DISEASE AS WELL
• o Dosing schedules
• o Management of ACEI side effects
• o Therapeutic monitoring for cardiac glycosides and
antiarrhythmics
• Chapter 28: Chronic Stable Angina & Low Risk Unstable
Angina
Differentiate between myocardial oxygen supply & demand
Angina: Ischemia caused by the imbalance between myocardial oxygen supply (MOS) and
myocardial oxygen demand (MOD) produces pain referred to as angina.
• Ischemia occurs when demand exceeds supply
• Chronic stable angina (exertional angina) is caused by narrowing of the arterial lumen and
hardening of the arterial walls so that the affected vessels cannot dilate in response to the
increased MOD associated with physical exertion or emotional stres
•
Etiology, diagnosis and risk factors The major risk factors for CAD are age, family
history, smoking, hypertension, hypercholesterolemia, low HDL cholesterol, and diabetes mellitus.
These risk factors are used in the Framingham equations for calculating the 10-year risk for the
development of coronary heart disease (Anderson et al, 2007) and in the new risk equations that aim
at uncovering a 7 year risk In addition, conditions that decrease oxygen supply and increase oxygen
Many questions are written to assess your clinical application of
the material from the textbook, in real-world scenarios.
Chapter 16: Drugs Affecting the Cardiovascular & Renal
Systems
• Know the pharmacodynamics, pharmacotherapeutics clinical
use, drug interactions and adverse drug reactions for:
o o Angiotensin converting enzyme inhibitors (ACEI): pregnancy D
Benazopril Captopril Enalapril Fosinopril Lisinopril Moexipril
o vasodilators
o Not as effective for African-American patients
o When combined with a diuretic, race no longer an issue
o Adverse drug reactions (ADRs): dry cough (bradykinin- mediated), hypotension, loss
of taste, angioedema, blood dyscrasias, teratogenicity, hyperkalemia, acute renal
failure, cholestatic jaundice, pancreatitis, rash
•
o o Angiotensin receptor blockers (ARBs) pregnancy D
Pharmacokinetics
o Losartan: CYP 2C9
o Extensive first-pass metabolism resulting in 33% bioavailability
o Inducers: rifampin, barbituates
o Inhibitors: lovastatin, SMZ/TMP, fluconazole, fluvastatin, fluvoxamine, sertraline
o
Angiotensin II Receptor Blockers SARTANS : losartan, esporsartan,
olmesartan, telmisartan, valsartan, candesartan, irbesartan
o Like ACEI orthostasis with dose changes
•
o o Calcium channel blockers (CCB)nifedipine cat safe and
Functionally act as vasodilators, lowering calcium (Ca++) influx into smooth muscles
o Two major classes
, o Type I – Non-dihydropyridines: affect conduction through the atrioventricular (AV)
node and have negative chronotropic effects
o Why it is used in treating supraventricular tachycardia
o Diltiazem (Cardizem), verapamil (Calan)
o Type II – Dihydropyridines: do not affect conduction through the AV node
o Nifedipine (Procardia), amlopidine (Norvasc), felodipine (Plendil)
• amlodipine cat C, methyldopa very safe
o Cardiac glycosides and antiarrhythmics
Digoxin
o Well-absorbed orally
o NOT extensively metabolized, excreted unchanged by kidneys Half-life is 36 to 48 hours
o In the absence of oral or intravenous loading, steady state is achieved in four half-
lives or 1 week
o Reduced clearance of digoxin with drug interaction
o Quinidine, amiodarone, verapamil, diltiazem
o ADRs
o Gastrointestinal (GI) most common: anorexia, nausea/vomiting, diarrhea
o Central nervous system: fatigue, disorientation, depression, hallucinations,
visual disturbances – yellow vision and green halos around lights
o Toxicity: atrial arrhythmias/tachycardia in children
o Cardiac: bradycardia, premature ventricular contractions, junctional and AV
block arrhythmias, and bigeminy
o Avoid using in patients with normal left ventricular systolic function
o Monitoring
o Diagnosis of toxicity is based on both clinical and laboratory data
o Toxicity commonly occurs with serum levels greater than 2 ng/mL
o Monitor potassium levels
•
• o Nitrates and peripheral vasodilators nitrates work on veins
and reduce preload, hydralazine is a vasodilator
, • o Anti-lipidemics
• o Diuretics treat symptoms of congestions, help the
body get rid of excess fluid, reduce symptoms that
result in excess fluids like shortness of breath doing
this it reduces heart failure (aldosterone inhibitors)
• Also know:
• o ACEIs & ARBs benefits in other conditionsHTN, HEART
FAILURE, SLOWING RENAL DISEASE ,
CARDIOVASCULAR DISEASE AS WELL
• o Dosing schedules
• o Management of ACEI side effects
• o Therapeutic monitoring for cardiac glycosides and
antiarrhythmics
• Chapter 28: Chronic Stable Angina & Low Risk Unstable
Angina
Differentiate between myocardial oxygen supply & demand
Angina: Ischemia caused by the imbalance between myocardial oxygen supply (MOS) and
myocardial oxygen demand (MOD) produces pain referred to as angina.
• Ischemia occurs when demand exceeds supply
• Chronic stable angina (exertional angina) is caused by narrowing of the arterial lumen and
hardening of the arterial walls so that the affected vessels cannot dilate in response to the
increased MOD associated with physical exertion or emotional stres
•
Etiology, diagnosis and risk factors The major risk factors for CAD are age, family
history, smoking, hypertension, hypercholesterolemia, low HDL cholesterol, and diabetes mellitus.
These risk factors are used in the Framingham equations for calculating the 10-year risk for the
development of coronary heart disease (Anderson et al, 2007) and in the new risk equations that aim
at uncovering a 7 year risk In addition, conditions that decrease oxygen supply and increase oxygen
