NR-545: PHARM, PHYS ASSMNT & PATHO
NP COMPLETE STUDY & EXAM BUNDLE
(FULL DOCUMENT) STUDY GUIDE,
REVIEW SHEETS, PRACTICE EXAM WITH
RATIONALES (210 QUESTIONS), GRADED A+
HIGH YIELD
========================================
TABLE OF CONTENTS
1. Study Guide ................................ Section 1
2. Review Sheets .............................. Section 2
3. Practice Exam with Rationales (210 Qs) ..... Section 3
• Part A: Multiple Choice (110 Qs with rationales)
• Part B: Multiple Answer/SATA (100 Qs with rationales)
========================================
SECTION 1: STUDY GUIDE (COMPLETE)
1.1 Cardiovascular Pathophysiology & Pharmacology
HEART FAILURE (HF)
HFrEF (Systolic Heart Failure):
• EF <40%
• Causes: MI, dilated cardiomyopathy, chronic alcohol use, viral
myocarditis, chemotherapy (doxorubicin)
,
• Pathophysiology: Reduced contractility → decreased CO →
neurohormonal activation (RAAS, SNS) → ventricular remodeling
→ further decline in function
• GDMT (Guideline-Directed Medical Therapy): ACEi/ARB/ARNI
+ Beta-blocker + MRA + SGLT2i
HFpEF (Diastolic Heart Failure):
• EF ≥50%
• Causes: hypertension (most common), aging, diabetes, obesity,
restrictive cardiomyopathy, infiltrative diseases (amyloidosis,
sarcoidosis)
• Pathophysiology: Impaired relaxation/filling → increased filling
pressures → pulmonary congestion → preserved or hyperdynamic
EF
• Management: SGLT2i (empagliflozin/dapagliflozin), diuretics for
volume, treat underlying cause
Key Assessment Findings in HF:
• S3 gallop (HFrEF) – rapid ventricular filling in dilated ventricle
• S4 gallop (HFpEF with hypertension) – atrial contraction into stiff
ventricle
• JVD, hepatojugular reflux (positive = HF, constrictive pericarditis)
• Crackles (pulmonary edema) – usually bibasilar, may be diffuse in
severe cases
• Peripheral edema, ascites (right-sided HF)
• Paroxysmal nocturnal dyspnea, orthopnea (left-sided HF)
• Weight gain (2-3 lbs/day or 5 lbs/week suggests worsening
volume)
HF Pharmacotherapy:
,
Drug Class Examples Mechanism Key Notes
ACE inhibitors Lisinopril, Vasodilation, First-line for
enalapril, reduces HFrEF; monitor
captopril afterload, K+, Cr; causes
decreases cough (5-20%)
aldosterone
ARBs Losartan, Same as ACEi Alternative if
valsartan, without cough ACEi cough; no
candesartan angioedema
benefit
ARNI Sacubitril/ Neprilysin Superior to
valsartan inhibitor + ARB ACEi; reduce
(Entresto) mortality;
monitor for
hypotension
Beta-blockers Carvedilol, Reduces HR, Only in stable
metoprolol decreases HF; start low, go
succinate, remodeling, slow (2-4 weeks
bisoprolol antiarrhythmic between
increases)
Loop diuretics Furosemide, Reduces volume Symptom relief;
torsemide, overload via Na- no mortality
bumetanide K-2Cl blockade benefit; monitor
in loop of Henle K+, Mg
SGLT2 inhibitors Empagliflozin, Reduces Indicated for
dapagliflozin preload/afterload HFrEF and
, improves HFpEF; reduces
cardiac hospitalizations;
energetics monitor for UTIs
MRAs Spironolactone, Anti-aldosterone Monitor K+;
eplerenone effect, reduces avoid if Cr >2.5
fibrosis (men) or >2.0
(women);
gynecomastia
,
Drug Class Examples Mechanism Key Notes
with
spironolactone
Digoxin Digoxin Na-K-ATPase Second-line for
inhibitor, symptom control
increases in refractory
contractility HFrEF with AF;
no mortality
benefit
HYPERTENSION (HTN)
Primary (Essential) HTN: 90-95% of cases
• Risk factors: obesity, high sodium intake, low potassium intake,
physical inactivity, alcohol, genetics
Secondary HTN causes (suspect if resistant HTN, sudden onset, age
<30 or >55 with new HTN):
• Renal artery stenosis (fibromuscular dysplasia in young women,
atherosclerosis in older adults)
• Primary aldosteronism (most common secondary cause – 5-10% of
all HTN)
• Pheochromocytoma (paroxysmal HTN, headache, sweating,
palpitations)
• Cushing syndrome
• Coarctation of aorta (upper extremity HTN, delayed femoral
pulses)
• Obstructive sleep apnea (most common secondary cause overall)
• Thyroid disease (hyperthyroidism = systolic HTN; hypothyroidism
= diastolic HTN)
NP COMPLETE STUDY & EXAM BUNDLE
(FULL DOCUMENT) STUDY GUIDE,
REVIEW SHEETS, PRACTICE EXAM WITH
RATIONALES (210 QUESTIONS), GRADED A+
HIGH YIELD
========================================
TABLE OF CONTENTS
1. Study Guide ................................ Section 1
2. Review Sheets .............................. Section 2
3. Practice Exam with Rationales (210 Qs) ..... Section 3
• Part A: Multiple Choice (110 Qs with rationales)
• Part B: Multiple Answer/SATA (100 Qs with rationales)
========================================
SECTION 1: STUDY GUIDE (COMPLETE)
1.1 Cardiovascular Pathophysiology & Pharmacology
HEART FAILURE (HF)
HFrEF (Systolic Heart Failure):
• EF <40%
• Causes: MI, dilated cardiomyopathy, chronic alcohol use, viral
myocarditis, chemotherapy (doxorubicin)
,
• Pathophysiology: Reduced contractility → decreased CO →
neurohormonal activation (RAAS, SNS) → ventricular remodeling
→ further decline in function
• GDMT (Guideline-Directed Medical Therapy): ACEi/ARB/ARNI
+ Beta-blocker + MRA + SGLT2i
HFpEF (Diastolic Heart Failure):
• EF ≥50%
• Causes: hypertension (most common), aging, diabetes, obesity,
restrictive cardiomyopathy, infiltrative diseases (amyloidosis,
sarcoidosis)
• Pathophysiology: Impaired relaxation/filling → increased filling
pressures → pulmonary congestion → preserved or hyperdynamic
EF
• Management: SGLT2i (empagliflozin/dapagliflozin), diuretics for
volume, treat underlying cause
Key Assessment Findings in HF:
• S3 gallop (HFrEF) – rapid ventricular filling in dilated ventricle
• S4 gallop (HFpEF with hypertension) – atrial contraction into stiff
ventricle
• JVD, hepatojugular reflux (positive = HF, constrictive pericarditis)
• Crackles (pulmonary edema) – usually bibasilar, may be diffuse in
severe cases
• Peripheral edema, ascites (right-sided HF)
• Paroxysmal nocturnal dyspnea, orthopnea (left-sided HF)
• Weight gain (2-3 lbs/day or 5 lbs/week suggests worsening
volume)
HF Pharmacotherapy:
,
Drug Class Examples Mechanism Key Notes
ACE inhibitors Lisinopril, Vasodilation, First-line for
enalapril, reduces HFrEF; monitor
captopril afterload, K+, Cr; causes
decreases cough (5-20%)
aldosterone
ARBs Losartan, Same as ACEi Alternative if
valsartan, without cough ACEi cough; no
candesartan angioedema
benefit
ARNI Sacubitril/ Neprilysin Superior to
valsartan inhibitor + ARB ACEi; reduce
(Entresto) mortality;
monitor for
hypotension
Beta-blockers Carvedilol, Reduces HR, Only in stable
metoprolol decreases HF; start low, go
succinate, remodeling, slow (2-4 weeks
bisoprolol antiarrhythmic between
increases)
Loop diuretics Furosemide, Reduces volume Symptom relief;
torsemide, overload via Na- no mortality
bumetanide K-2Cl blockade benefit; monitor
in loop of Henle K+, Mg
SGLT2 inhibitors Empagliflozin, Reduces Indicated for
dapagliflozin preload/afterload HFrEF and
, improves HFpEF; reduces
cardiac hospitalizations;
energetics monitor for UTIs
MRAs Spironolactone, Anti-aldosterone Monitor K+;
eplerenone effect, reduces avoid if Cr >2.5
fibrosis (men) or >2.0
(women);
gynecomastia
,
Drug Class Examples Mechanism Key Notes
with
spironolactone
Digoxin Digoxin Na-K-ATPase Second-line for
inhibitor, symptom control
increases in refractory
contractility HFrEF with AF;
no mortality
benefit
HYPERTENSION (HTN)
Primary (Essential) HTN: 90-95% of cases
• Risk factors: obesity, high sodium intake, low potassium intake,
physical inactivity, alcohol, genetics
Secondary HTN causes (suspect if resistant HTN, sudden onset, age
<30 or >55 with new HTN):
• Renal artery stenosis (fibromuscular dysplasia in young women,
atherosclerosis in older adults)
• Primary aldosteronism (most common secondary cause – 5-10% of
all HTN)
• Pheochromocytoma (paroxysmal HTN, headache, sweating,
palpitations)
• Cushing syndrome
• Coarctation of aorta (upper extremity HTN, delayed femoral
pulses)
• Obstructive sleep apnea (most common secondary cause overall)
• Thyroid disease (hyperthyroidism = systolic HTN; hypothyroidism
= diastolic HTN)
