NU 578
Unit 3 Study Guide
Key Concepts & Exam Review
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-
minute review. The guide is structured to help students reinforce
understanding, identify weak areas, and prepare confidently for
the assessment.
, Unit 3 Study Guide
r Risk factors of developing ASCVD include: pg 351 - 354
o Advancing age, black race, hypertension, cigarette smoking, and low HDL cholesterol
(positive risk factor) and high HDL (negative risk factor).
o Having diabetes is considered equivalent to having ASCVD as a predictor of a major
coronary event.
r Factors that increase cardiovascular risk include: pg 317
o Heart disease, LVH, Angina pectoris, MI, HFx, CVA/TIA, CKD, PAD, retinopathy, prior
coronary revascularization, smoking, physical inactivity, dyslipidemia, DM,
microalbuminuria, old age, family hx of CVD, diet
r Treatment of Hypertension
o Diuretics pg 291
Most diuretics share the same basic mechanism of action: blockade of sodium and
chloride reabsorption which creates osmotic pressure within the nephron and
prohibits the passive reabsorption of water. The more that the reabsorption of Na &
Cl is blockaded, the greater degree of diuresis.
Great drug to start with for the tx of mild to moderate HTN
When combining diuretics with other meds, you must take it in the morning.
Furosemide – loop diuretic pg 293
MOA: acts in the thick segment of the ascending limb of the loop of Henle to
block reabsorption of sodium and chloride
Very potent. Should be avoided when less efficacious diuretics (thiazides) will
suffice.
Use: Pulm edema a/w CHF, edema of hepatic/cardiac/renal origin that is
unresponsive to less efficacious diuretics, HTN that cannot be controlled with
other diuretics. Can promote diuresis even when renal blood flow and GFR are
low.
ADR/SE: HoNa, HoCl, HoK, dehydration (dry mouth, thirst, oliguria, weight loss),
HoTN, ototoxicity
BBW: All loop diuretics can cause profound diuresis with water and electrolyte
depletion.
DI: digoxin (risk of dysrhythmias d/t HoK), ototoxic drugs
Combo: when paired with K-sparing diuretics, you can reduce risk of HoK.
Loop/Thiazide ADR/DI Table 37.2 pg 294
Hydrochlorothiazide – thiazide diuretic pg 294
Thiazide diuretics have effects similar to those of the loop diuretics. Like the
loop diuretics, thiazides increase renal excretion of sodium, chloride, potassium,
and water. In addition, thiazides elevate plasma levels of uric acid and glucose.
MOA: blocks reabsorption of Na & Cl in the early segment of distal convoluted
tubule. Less potent than loop diuretics due to this.
Ability of thiazides to promote diuresis depends on adequate kidney function.
, Unit 3 Study Guide
Use: HTN, edema
ADR: Same as loop diuretics except thiazides are not ototoxic
Caution with cardiovascular disease, renal impairment, diabetes mellitus, or a
history of gout and in patients taking digoxin, lithium, or antihypertensive drugs.
Chlorthalidone – thiazide diuretic
Spironolactone – Potassium Sparing Diuretic pg 295
Blocks actions of aldosterone in distal nephron. Aldosterone prohibits sodium
uptake in exchange for potassium secretion. Blocking this causes retention of
potassium for increase excretion of sodium. Cardiac protective.
Table 37.4 shows all K+ sparing diuretics pg 295
BBW: Tumorigenic in rats so avoid unnecessary use.
Use: HTN, edema, HFx
ADR: HyperK+, endocrine effects (it is a derivative of steroid hormone)
DI: combined with loop/thiazide diuretic can help prevent K wasting. Use with
caution with K supplements. ARBs/ACEIs can further increase K levels so use
together only when necessary.
o Beta Blockers
Effective in patients who have just had an MI or have headache
Exercise intolerance, patient feels tired
Adherence is crucial pt teaching. If pt is intolerant, medication should be changed
and will need to be weaned off BB.
Labetolol/Carvedilol
Metoprolol
B1 specific
o Calcium Channel Blockers pg 308
Calcium channels are gated pores in the cytoplasmic membrane that regulate entry
of calcium ions into cells. Calcium entry plays a critical role in the function of vascular
smooth muscle (VSM) and the heart. In VSM, calcium channels regulate contractions.
When action potential travels down surface of smooth muscle cell, channel opens
and there in influx of calcium. When channels are blocked, contraction is prevented
and vasodilation occurs.
Lower extremity edema is common and is often confused with heart failure. Elevate
legs or tx with mild diuretic. Check BP to make sure it’s not too low and cause of
edema.
Adherence is crucial pt teaching. If pt is intolerant, medication should be changed
and will need to be weaned off CCB.
Table 39.1 pg 308: CCB class, action, indications
Verapamil pg 308
Direct effects: Blockade of peripheral arterioles cause dilation/reduction of
arterial pressure. Blockade of heart arterioles cause increase coronary
Unit 3 Study Guide
Key Concepts & Exam Review
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-
minute review. The guide is structured to help students reinforce
understanding, identify weak areas, and prepare confidently for
the assessment.
, Unit 3 Study Guide
r Risk factors of developing ASCVD include: pg 351 - 354
o Advancing age, black race, hypertension, cigarette smoking, and low HDL cholesterol
(positive risk factor) and high HDL (negative risk factor).
o Having diabetes is considered equivalent to having ASCVD as a predictor of a major
coronary event.
r Factors that increase cardiovascular risk include: pg 317
o Heart disease, LVH, Angina pectoris, MI, HFx, CVA/TIA, CKD, PAD, retinopathy, prior
coronary revascularization, smoking, physical inactivity, dyslipidemia, DM,
microalbuminuria, old age, family hx of CVD, diet
r Treatment of Hypertension
o Diuretics pg 291
Most diuretics share the same basic mechanism of action: blockade of sodium and
chloride reabsorption which creates osmotic pressure within the nephron and
prohibits the passive reabsorption of water. The more that the reabsorption of Na &
Cl is blockaded, the greater degree of diuresis.
Great drug to start with for the tx of mild to moderate HTN
When combining diuretics with other meds, you must take it in the morning.
Furosemide – loop diuretic pg 293
MOA: acts in the thick segment of the ascending limb of the loop of Henle to
block reabsorption of sodium and chloride
Very potent. Should be avoided when less efficacious diuretics (thiazides) will
suffice.
Use: Pulm edema a/w CHF, edema of hepatic/cardiac/renal origin that is
unresponsive to less efficacious diuretics, HTN that cannot be controlled with
other diuretics. Can promote diuresis even when renal blood flow and GFR are
low.
ADR/SE: HoNa, HoCl, HoK, dehydration (dry mouth, thirst, oliguria, weight loss),
HoTN, ototoxicity
BBW: All loop diuretics can cause profound diuresis with water and electrolyte
depletion.
DI: digoxin (risk of dysrhythmias d/t HoK), ototoxic drugs
Combo: when paired with K-sparing diuretics, you can reduce risk of HoK.
Loop/Thiazide ADR/DI Table 37.2 pg 294
Hydrochlorothiazide – thiazide diuretic pg 294
Thiazide diuretics have effects similar to those of the loop diuretics. Like the
loop diuretics, thiazides increase renal excretion of sodium, chloride, potassium,
and water. In addition, thiazides elevate plasma levels of uric acid and glucose.
MOA: blocks reabsorption of Na & Cl in the early segment of distal convoluted
tubule. Less potent than loop diuretics due to this.
Ability of thiazides to promote diuresis depends on adequate kidney function.
, Unit 3 Study Guide
Use: HTN, edema
ADR: Same as loop diuretics except thiazides are not ototoxic
Caution with cardiovascular disease, renal impairment, diabetes mellitus, or a
history of gout and in patients taking digoxin, lithium, or antihypertensive drugs.
Chlorthalidone – thiazide diuretic
Spironolactone – Potassium Sparing Diuretic pg 295
Blocks actions of aldosterone in distal nephron. Aldosterone prohibits sodium
uptake in exchange for potassium secretion. Blocking this causes retention of
potassium for increase excretion of sodium. Cardiac protective.
Table 37.4 shows all K+ sparing diuretics pg 295
BBW: Tumorigenic in rats so avoid unnecessary use.
Use: HTN, edema, HFx
ADR: HyperK+, endocrine effects (it is a derivative of steroid hormone)
DI: combined with loop/thiazide diuretic can help prevent K wasting. Use with
caution with K supplements. ARBs/ACEIs can further increase K levels so use
together only when necessary.
o Beta Blockers
Effective in patients who have just had an MI or have headache
Exercise intolerance, patient feels tired
Adherence is crucial pt teaching. If pt is intolerant, medication should be changed
and will need to be weaned off BB.
Labetolol/Carvedilol
Metoprolol
B1 specific
o Calcium Channel Blockers pg 308
Calcium channels are gated pores in the cytoplasmic membrane that regulate entry
of calcium ions into cells. Calcium entry plays a critical role in the function of vascular
smooth muscle (VSM) and the heart. In VSM, calcium channels regulate contractions.
When action potential travels down surface of smooth muscle cell, channel opens
and there in influx of calcium. When channels are blocked, contraction is prevented
and vasodilation occurs.
Lower extremity edema is common and is often confused with heart failure. Elevate
legs or tx with mild diuretic. Check BP to make sure it’s not too low and cause of
edema.
Adherence is crucial pt teaching. If pt is intolerant, medication should be changed
and will need to be weaned off CCB.
Table 39.1 pg 308: CCB class, action, indications
Verapamil pg 308
Direct effects: Blockade of peripheral arterioles cause dilation/reduction of
arterial pressure. Blockade of heart arterioles cause increase coronary
