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NSG 533 Advanced Pharmacology Exam 3 (2025/2026) Questions And Answers Graded A+ WILKES, Exams of Pharmacology

NSG 533 Advanced Pharmacology Exam 3 (2025/2026) Questions And Answers Graded A+ WILKES What are two classes of medications an individual with HFrEF will be started on? 1. beta blocker (to counter SNS) 2. ACEi (to counter RAAS) what hormones worsen HF - Angiontensin II (RAAS) - catecholamines (SNS) - endothelin - aldosterone hormones that are good for HF - natriuretic peptides (ANP, BNP, CNP) - adrenmedullin - bradykinin - nitric oxide types of ventricular remodeling - concentric (thickened heart wall, diastolic HF, too stiff, HFpEF) - eccentric (thin heart wall, systolic HF, contraction dysfunction, HFrEF)

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2024/2025

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NSG 533 Advanced Pharmacology Exam 3
(2025/2026) Questions And Answers Graded A+
WILKES
What are two classes of medications an individual with HFrEF will be started on?
1. beta blocker (to counter SNS)
2. ACEi (to counter RAAS)
what hormones worsen HF
- Angiontensin II (RAAS)
- catecholamines (SNS)
- endothelin
- aldosterone
hormones that are good for HF
- natriuretic peptides (ANP, BNP, CNP)
- adrenmedullin
- bradykinin
- nitric oxide
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NSG 533 Advanced Pharmacology Exam 3

(2025/2026) Questions And Answers Graded A+

WILKES

What are two classes of medications an individual with HFrEF will be started on?

  1. beta blocker (to counter SNS)
  2. ACEi (to counter RAAS)

what hormones worsen HF

  • Angiontensin II (RAAS)
  • catecholamines (SNS)
  • endothelin
  • aldosterone

hormones that are good for HF

  • natriuretic peptides (ANP, BNP, CNP)
  • adrenmedullin
  • bradykinin
  • nitric oxide

types of ventricular remodeling

  • concentric (thickened heart wall, diastolic HF, too stiff, HFpEF)
  • eccentric (thin heart wall, systolic HF, contraction dysfunction, HFrEF)

blood flow of the heart from right side to left side

  1. deoxygenated blood from the systemic system enters the superior/inferior vena cava
  2. right atrium
  3. tricuspid valve
  4. right ventricle
  5. pulmonary valve
  6. pulmonary artery
  7. lungs where blood is oxygenated
  8. pulmonary veins
  9. left atrium
  10. mitral/bicuspid valve
  11. left ventricle
  12. aortic valve
  13. aorta
  14. oxygenated blood to the systemic system

s/s right sided HF

  • jugular vein distension
  • edema

impairment in:

  • filling
  • relaxation
  • LA pressures

myocardial remodeling HFpEF vs HFrEF

HFpEF: dysfunction is d/t comorbidities and inflammatory markers coming in contact with the endothelium

HFrEF: dysfunction is d/t damage within the actual myocyte

Universal stages of Heart Failure (HF)

  • At-risk for HF
  • Pre HF
  • HF
  • Advanced HF

according to the universal definition, what is "at-risk for HF"?

  • do not have HF, but at risk
  • no current or prior s/s
  • no structural, functional, or biomarker evidence supporting HF

according to the universal definition, what is "HF"

  • clinical syndrome
  • current or prior s/s of HF
  • caused by structural of functional cardiac abnormality
  • elevated natriuretic peptide levels
  • evidence of pulmonary or systemic congestion

who is most at risk for HF

black males and females; older women

two biggest causes of HF

  1. ischemic heart disease (CAD)
  2. HTN

calculate EF

SV/LVEDV

synonym for inotropy

contraction (HFrEF)

synonym for lusitropy

effects of circulating angiotensin II on HF

  • causes vasoconstriction
  • increases secretion of ADH
  • increase aldosterone secretion
  • increases sodium reabsorption

are aldosterone levels high or low in HF?

20x higher than normal

effects of aldosterone on HF

  • increases sodium and water reabsorption
  • decreased potassium and magnesium
  • decreased baroreceptor reflex
  • sympathetic activation

list the comprehensive risk factors of Coronary Artery Disease

  • dyslipidemia
  • genetic studies
  • modifiable risk factors
  • non-modifiable risk factors
  • novel risk factors

what can elevated BNP also be confused with?

HF or renal failure

endogenous effects of BNP

  • lusitropic
  • antifibrotic
  • anti-remodeling
  • balanced vasodilation of veins/arteries
  • decreases aldosterone
  • decreases endothelin
  • decreases norepinephrine
  • increases diuresis

explain dyslipidemia as a risk factor for CAD

  • elevated LDL-C
  • Low HDL-C
  • hypertriglyceridemia
  • advanced age (s/s present 10 years earlier in men; even out around menopause)
  • gender/sex

novel risk factors associated with CAD

  • elevated lipoprotein (a)
  • elevated high sensitivity C-reactive protein
  • elevated fibrinogen
  • elevated LDL particle number
  • small, dense LDL

define atherosclerosis

accumulation of lipid-laden macrophages within the arterial wall, leading to formation of lesions/plaques

what is the leading cause of Peripheral Vascular Disease, Coronary Artery Disease, and Cerebrovascular Disease?

Atherosclerosis

explain the pathophysiology of endothelial cell injury (9 steps)

  • endothelial cell injury d/t modifiable risk factors (HTN, smoking, diabetes)
  • injured cells become inflamed
  • inflamed endothelial cells a) don't make enough antithrombotic and vasodilating cytokines, and b) express adhesion molecules that bind macrophages with inflammatory and immune cells
  • inflammatory process creates toxic oxygen free radicals that cause oxidation of LDL in the vessel intima
  • oxidized LDL a) creates additional adhesion molecule expression, and b) recruits monocytes that differentiate into macrophages --> infiltrate vessel intima --> engulf oxidized LDL --> form foam cells
  • accumulation of foam cells form a lesion called a fatty streak (produce additional toxic oxygen free radicals, inflammatory response/macrophages)
  • macrophages release growth factors that stimulate smooth muscle cell proliferation
  • once proliferating, collagen is produced and migrates over the fatty streak creating an atherosclerotic plaque
  • plaque can calcify and protrude into the lumen, obstructing blood flow to tissues (can be stable or unstable)

define lipoprotein

A fat carrier that enables fats and cholesterol to travel through the lymph and blood (lipids, phospholipids, cholesterol, triglycerides)

three types of lipoproteins

VDL

  1. neurohumoral changes

what are plaques that rupture called?

complicated plaques

what happens when a plaque ruptures?

platelet adhesion, clotting cascade, rapid thrombus formation --> occlusion of vessel --> ischemia or infarction of vessel

list the acute coronary syndromes

unstable angina, NSTEMI, STEMI

what is an acute coronary syndrome?

sudden coronary obstruction caused by thrombus formation over arteriosclerotic plaque

manifestations of unstable angina

  • emergency
  • reversible myocardial ischemia w/ some myocardial damage
  • arteriosclerotic plaque has become a complicated lesion
  • ECG abnormalities
  • treat w/ nitrates, anticoagulants, and antithrombotics

ECG abnormalities of Unstable Angina

ST Depression

T wave inversion

manifestations of stable angina

  • chest pain relieved by rest and nitrates
  • d/t buildup of lactic acid
  • pallor, diaphoretic, dyspnea, substernal chest discomfort

define myocardial infarction

loss of coronary blood flow for an extended period of time that results in myocyte necrosis

two types of MI

STEMI, NSTEMI

s/s STEMI

  • cold, anxious
  • ECG abnormalities
  • elevated CK, CK-MB

complications of myocardial infarction

dysrhythmias, LV failure, RV infarction, cardiogenic shock, pericarditis, LV aneurysm

isolated systolic hypertension

a condition most commonly seen in the older adult in which the systolic pressure is greater than 140 mm Hg and the diastolic pressure is within normal limits (less than 90 mm Hg)

primary/idiopathic hypertension

most common of HTN diagnoses, no specific cause known

secondary HTN

caused by underlying disease or medication that raises PVR or cardiac output

what are some medications that may raise PVR or cardiac output?

oral contraceptives, antihistamines, corticosteroids

risk factors for HTN

obesity, diabetes, increased age, black males, family hx

American College of Cardiology blood pressure categories:

Normal: <120 ; <

Elevated: 120-129 ; > 80

Stage 1: 130-139 ; 80-

Stage 2: >140 ; >

HTN Crisis: >180 ; >

primary factors associated with development of HTN

  1. Neurohumoral Dysfunction
  2. Inflammation
  3. Insulin Resistance

increased PVR and cardiac output leads to sustained HTN -->

atherosclerosis

Six theories of HTN

  1. Hypothesis of Autoregulation
  2. Excess sodium intake
  3. Renal Sodium Retention
  4. Renin Angiotensin Aldosterone System dysfunction
  5. SNS overactivity
  6. Elevated PVR

three categories of irreversible dementia

  1. neurodegenerative
  2. vascular
  3. infectious

three most common forms of dementia

  1. Alzheimer's Disease
  2. Lewy Body
  3. Frontotemporal

hallmark clinical manifestations of dementia

  1. insidious onset (slow, gradual)
  2. progressive decline of cognition, memory, and ability to care for self

define delirium

acute change in attention, awareness, and cognition

four major mechanisms of delirium

  1. neuronal network
  2. vascular dysfunction and metabolic insufficiency
  3. inflammatory effect on glial cells
  1. drugs and stressors that alter neurotransmitters

what are some drugs that alter neurotransmitters in delirium?

anticholinergic, antihistamines, GABAergic sedatives

DSM-V criteria for delirium

  1. disturbance in attention and awareness
  2. disturbance is acute and fluctuates in severity
  3. disturbance in cognition
  4. disturbance cannot be explained by a pre-existing neurocognitive disorder
  5. H&P and labs point to the cause being a direct physiological consequence of another medical condition

function of glial cells

support and protect neurons

three types of glial cells

  1. microglial
  2. astrocytes
  3. oligodendrocytes