NSG533 / NSG 533 Exam 3 (Latest 2026 /2027) Advanced Pharmacology | Questions and Verified Answers with Rationales | 100% Correct | Grade A - Wilkes

NSG533 / NSG 533 Exam 3 (Latest 2026 /2027) Advanced Pharmacology | Questions and Verified Answers with Rationales | 100% Correct | Grade A - Wilkes List the novel risk factors for CAD 1) markers of inflammation, ischemia, and thrombosis (elevated high sensitivity C-reactive protein, troponin, fibrinogen) 2) adipokines (leptin, adiponectin) 3) CKD 4) air pollution and ionizing radiation 5) medications (NSAIDs) 6) coronary artery calcification and carotid wall thickness and 7) microbiome 8) small dense LDL particles and lipoprotein(a) 9) Hyperhomocysteinemia List nonmodifiable risk factors for CAD Advanced age, male gender or woman after menopause, and family history (genetics, shared environmental exposure). List modifiable risk factors for CAD Dyslipidemia, hypertension, cigarette smoking, diabetes and insulin resistance, obesity and sedentary lifestyle, and an atherogenic diet. How does dyslipidemia contribute to CAD? High levels of LDL in the bloodstream leads to LDL oxidation, migration into the vessel wall, and phagocytosis by macrophages, all key steps in the pathogenesis of atherosclerosis. Atherosclerosis A chronic inflammatory condition that results in damage to the arteries. Thickening and hardening of the vessels are caused by the accumulation of lipid-laden macrophages (foam cells) within the arterial walls, leading to the formation of a plaque. Optimal lipid panal results Total cholesterol ( 200), LDL ( 100), triglycerides ( 150) What is the response-to-injury hypothesis in the development of atherosclerotic lesions? The earliest event in atherogenesis is injury to the endothelium, which could be triggered by hypertension, circulation of ROS (smoking, pollutants), dyslipidemia, and elevated A1C. When foam cells accumulate in a significant amount within the arterial wall, they form . What is then released? a lesion called a fatty streak; inflammatory cytokines, damaging enzymes, and growth factors. Growth factors released released in atherogenesis stimulate , which . smooth muscle cell proliferation; produce collagen and migrate over the fatty streak to form a fibrous plaque. Plaques that have ruptured are called . complicated plaques Plaque rupture occurs because of the . inflammatory activation of proteinases, apoptosis of cells within the plaque, and bleeding within the lesion (plaque hemorrhage). What happens once a plaque ruptures? The underlying tissue is exposed and causes platelet adhesion, initiation of the clotting cascade, and rapid thrombus formation that can suddenly occlude the vessel, resulting in ischemia and infarction. Stable atheromatous lesions A fibrous plaque that has calcified, protruded into the vessel lumen, and obstructs blood flow, causing chest pain during exercise (stable angina) Unstable atheromatous lesions Plaques that are prone to rupture even before they affect blood flow (clinically silent until rupture). The fibrous cap is typically thinner in an unstable plaque. List the acute coronary syndromes Unstable angina, NSTEMI, and STEMI What are the clinical features and physical exam findings in unstable angina? Chest pain at rest, new-onset, or increasing in severity or frequency. ST segment depression and T wave inversion that often resolves with relief of pain, transient abnormal heart sounds. Possible tachycardia and pulmonary congestion. Patient might be dyspneic, diaphoretic, or anxious. Troponin and CK are normal. What are the clinical features and physical exam findings in a NSTEMI? ST depression and T wave inversion, early peak in CK level, and small elevation in troponin. What are the clinical features and physical exam findings in a STEMI? ST elevation, T wave inversion, and pathological Q waves. Elevation of CK, CK-MB, myoglobin (peaks 1-4 hrs), troponin (begins to rise at 3 hrs), and LDH. Patient has anxiety, cold perspiration and pallor, variable HR and BP response. What are the abnormal heart sounds that might be present in acute coronary syndromes? S3 (systolic dysfunction when blood rushes into an overly compliant ventricle), S4 (ischemia does not allow myocardium to relax and blood is forced into a noncompliant ventricle), and a systolic murmur (mitral regurgitation). What is the most common complication of myocardial infarction? Dysrhythmias. Caused by ischemia, hypoxia, ANS imbalances, lactic acidosis, electrolyte abnormalities, alterations of impulse conduction pathways, possible drug toxicity, and hemodynamic abnormalities. List complications of myocardial infarction. Dysrhythmias, cardiogenic shock, pericarditis, rupture of papillary muscle or chordae tendineae, and ventricular aneurysms. Women often have coronary microvascular; macrovascular. complications rather than complications. What are atypical angina symptoms that women might experience, and why? Prolonged symptoms at rest, SOB, unusual fatigue, and a more frequent pattern of angina. Caused by nonobstructive plaque deposition in the coronary microvasculature. What are some sex-specific precursors that, when combined with known risk factors, can cause a pro-vasculoathic state that could lead to ischemic heart disease? PCOS, hypoestrogenemia, and menopause. Primary hypertension (essential, idiopathic) Most common form of HTN (90-95%) without an identifiable cause. Most likely involving genetics and the environment. Secondary hypertension Directly related to another condition, such as renovascular disease, OSA, drugs/alcohol, primary aldosteronism, etc. Isolated systolic hypertension Elevated systolic BP with a normal diastolic BP ( 90 mmHg). Used to be present in only older adults, now more prevalent in all age groups. Strongly associated with cardiovascular and cerebrovascular events. List modifiable and relatively fixed risk factors for hypertension. Modifiable - cigarette smoking and secondhand smoking, diabetes, dyslipidemia, obesity, sedentary lifestyle, and poor diet. Fixed - CKD, family hx, increased age, low socioeconomic status, male sex, OSA, and psychosocial stress. Classify BP using the AHA and ACC guidelines. Normal: SBP 120 and DBP 80. Elevated: SBP 120-129 and DBP 80. Stage 1: SBP 130-139 or DBP 80-89. Stage 2: SBP 140 or DBP 90. Stage 3: SBP 180 and/or DBP 120. List factors associated with the pathogenesis of primary hypertension. Overactivity of the SNS, overactivity of the RAAS, inadequate natriuretic function, chronic inflammation, endothelial dysfunction, adipokines, insulin resistance. Describe the imbalance of factors affecting vascular tone and structure in hypertension. The growth promoters/constrictors (angiotensin II, catecholamines, endothelin-I, ROS, cytokines, and endothelium-derived constricting factors) have more influence than the growth inhibitors/dilators (nitric oxide, prostacyclin, bradykinin, and endothelium-derived hyperpolarizing factors). What is the definition of heart failure (from the lecture)? A progressive, symptomatic syndrome driven by excessive neuroendocrine (SNS, RAAS) activation and inflammation. What is the universal definition of heart failure? A clinical syndrome with symptoms and/or signs caused by a structural and/or functional cardiac abnormality and corroborated by elevated BNP levels and/or objective evidence of pulmonary or systemic congestion. What is the relationship between the AHA heart failure stages and actual diagnosis of heart failure? Cardiac dysfunction (Stage A & B) + symptoms = heart failure (Stage C & D) AHA Stage A of heart failure At high risk of HF but without structural heart disease or symptoms of HF AHA Stage B of heart failure Structural heart disease but without signs or symptoms of HF AHA Stage C of heart failure Structural heart disease with prior or current symptoms of HF AHA Stage D of heart failure Refractory HF requiring specialized interventions The NYHA functional classification is based on . patient activity tolerance What is a common form of heart failure caused by a parasite? Chagas disease, caused by Trypanosoma cruzi carried by an insect found in central/south American, Mexico, and now Texas. Cardiac remodeling in diastolic heart failure The increases in myocyte length are less than that of myocyte width, resulting in short, thick myocytes and a thick, hypertrophied myocardium that doesn't fill well but has a normal ejection fraction (EF 50%). Cardiac remodeling in systolic heart failure The increases in myocyte length are much greater than that of myocyte width, resulting in long, thin myocytes and a weak, stretched out myocardium that can't contract (EF 40%). What are the actions of circulating angiotensin II in heart failure? Increases ADH, vasoconstriction, sodium reabsorption, and aldosterone secretion What are the actions of tissue-derived angiotensin II in heart failure? Causes myocyte hypertrophy, necrosis, and apoptosis, and causes fibroblast proliferation. How does aldosterone contribute to heart failure? Causes Na+ and water retention, but also K+ and Mg2+ loss (arrythmias), reduced baroreceptor refelx (poor response to BP changes), cardiac fibrosis, ischemia, and sympathetic activation. What are the physiologic actions of B-type natriuretic peptide (BNP)? Balanced vasodilation, decreased aldosterone, endothelin, and norepinephrine, increased natriuresis, and lusitropic, antifibrotic, and antiremodeling effects. B-type natriuretic peptide (BNP) A neurohormone with beneficial effects secreted by the heart in response to stretch. Unfortunately degraded by neprolysin, which is abundant in HF. The gold standard test for diagnosis of HFpEF is . invasive exercise stress testing to measure left ventricular filling pressure (PAWP 15 at rest, 25 during exercise). Also helpful in measuring CO reserve (CO and oxygen consumption in tandem). Current management of HFpEF is currently . control of hypervolemia with diuretics, mineralocorticoid antagonists, and exercise training and control of associated comorbidities (obesity). True or false: HFpEF has grown to become the dominant form of HF worldwide. True. Heart failure with mildly reduced ejection fraction (HFmrEF) EF 41-49% Heart failure with improved ejection fraction (HFimpEF) Baseline EF 40%, but then a 10-point increase from baseline, and a second measurement of EF 40%. White adipose tissue (WAT) The metabolically active visceral and subcutaneous fat that contributes to energy homeostasis. Lipids are stored as one large fat droplet in the adipocytes. Name the adipokines that promote vasoconstriction, inflammation, lipogenesis, and insulin resistance. Angiotensinogen, angiotensin I and II, renin, and ACE. Name the adipokine that promotes inflammation, inhibits appetite, is insulin sensitizing in liver and skeletal muscles, regulates hepatic gluconeogenesis, and glucose and lipid metabolism in liver, muscle, and adipose tissue. Leptin - blood levels are increased in obesity d/t resistance. Name the adipokine that is insulin-sensitizing, anti-inflammatory, and antiatherogenic. Adiponectin - levels are decreased in obesity. Visceral WAT hypertropy leads to . insulin resistance (diabetes), pro-inflammatory conditions (diabetes, cancer, atherosclerosis), altered lipids (NAFLD/NASH, atherosclerosis), and vasoconstriction. Excessive WAt hypertrophy from continued chronic postive energy balance will eventually exceed the supporting vascular supply, leading to . lipotoxicity and WAT cell necrosis (inflammation) Where is brown adipose tissue (BAT) located? Interscapular, perirenal, supraclavicular, and paravertebral. What is the purpose of brown adipose tissue (BAT)? Stores fat as several small droplets throughout the cell, and rich in mitochondria, stores iron, and generates body heat. Not nearly at metabolically active as WAT and inversely related to BMI. Beige adipose tissue (bAT) Develops when brown adipose tissue develops in white adipose tissue from chronic exposure to cold or exercise. Fat is dynamic, and bAT is a promising target for obesity treatments. Obesogens Chemicals in the environment that stimulate the development of fat; thought to be passed down through generations as an epigenetic process. Ex: phytoestrogens, plastics, personal care products, pesticides, household cleaners, medications. List the pathological consequences of leptin resistance 1) Fails to inhibit orexigenic hypothalamic satiety signaling and promotes overeating. 2) Promotes hyperglycemia, hyperinsulinemia, and hyperlipidemia. 3) Stimulates macrophages and endothelial cells to produce proinflammatory mediators. 4) Creates a constant state of lipolysis, which releases VLDL into the blood that are deposited in the liver and arteries. List factors that contribute to the anorexia of aging. Reduced energy needs, diminished sense of taste/smell, decreased saliva, delayed gastric emptying, decreased small intestine motility, medications, medical/psychiatric disorders, social isolation/abuse/neglect. Executive attention functions Planning, problem solving, and goal setting; mediated by the prefrontal areas of the brain. Delirium An acute, transient disorder of awareness that may have either a sudden or gradual onset over 2- 3 days. Pathogenesis of delirium A disruption of the reticular-activating system (RAS) of the upper brainstem and its projections to the thalamus, basal ganglion, and specific areas of the cortex and limbic areas. Associated with ANS hyperactivity. Conditions causing delirium Drug intoxication, alcohol/drug withdrawal, metabolic disorders (hypoglycemia, thyroid storm), brain trauma/surgery, postanesthesia, febrile illness/heat stroke, electrolyte imbalances/dehydration, and heart, kidney, or liver failure. Dementia An acquired deterioration and a progressive failure of many cerebral functions that includes impairment of intellectual processes with a decrease in orienting, memory, language, judgement, and decision making. What is the greatest risk factor for dementia? Age List reversible causes of dementia. Encephalitis, meningitis, neurosyphilis, nutritional deficiences (B vitamins), thyroid abnormalities, brain tumors, medication side effects (anticholingergics, antihypertensives, antihistamines). Intussusception Telescoping of a proximal segment of bowel into a distal segment, 90% of cases are ileo-colic. Only 25% of pediatric cases have an identifiable cause. Causes of intussusception in adults Lead points (polyp/tumor), cystic fibrosis, post abdominal surgery, viruses/bacteria, and the rotavirus vaccine. Clinical manifestations of intussusception Sudden onset, intermittent cramping pain, inconsolable crying, episodic lethargy, legs drawn up to the abdomen, non-bilious vomiting that progresses to bilious, sausage-shaped abdominal mass on the right side, gross or occult blood in stool, and currant jelly stool (late finding). Pyloric stenosis The most common cause of intestinal obstruction in infancy. Thickening of the pyloric muscle fibers resulting in an enlarged, inflexible, and narrowed sphincter. Stomach hypertrophies to compensate. Causes of pyloric stenosis Environmental: maternal gastrin secretion, infantile hypergastrinemia, very innervated myenteric plexus, deficiency of NO synthase-containing neurons, macrolide antiobiotcs, and prostaglandin E administration. Hereditary: pyloric stenosis in the family hx, APO-A1 gene, low serum cholesterol at birth. Clinical manifestations of pyloric stenosis Presents in the first few weeks or months of life in an infant that was previously eating normally and gaining weight. Non-bilious post-prandial projectile vomiting, hungry/irritable, constipation, olive-sized mass in the RUQ. True or false: the severe fluid and electrolyte imbalances, malnutrition, and weight loss in an infant with pyloric stenosis can be fatal within 4-6 weeks. True Vesicoureteral reflux (VUR) The backflow of urine from the bladder, into the ureters, and towards the kidneys caused by an incompetent ureterovesical junction (the ureter opening is too high for a full bladder to compress and prevent reflux). Clinical manifestations of vesicoureteral reflux (VUR) in children Possibly symptoms from recurrent UTIs, but generally unexplained symptoms like fever, poor growth and development, irritability, and feeding problems. List sources of lead in the environment Water, artificial turf, imported candy, alternative medicines and herbal remedies, sindoor, old and imported toys, and occupational hazards. What are the hematological, renal, and skeletal effects of plumbism in children? Anemia, damaged proximal tubules and loop of Henle, interstitial nephritis, nephrotoxicity, decreased metabolism of Vit D (and therefore calcium), slows the growth of long bones and overall decreased growth rate. What are the neurologic effects of plumbism in children? 1) Issues with calcium interferes with synaptic cleft and neuronal transmission 2) increases intracranial pressure and causes cerebral edema, leading to tissue ischemia and irreversible necrosis. 3) behavioral changes, intellectual disabilities. 4) eventual convulsions, coma, and death. What is the "goal" blood lead level (BLL)? What is a normal zinc protoporphyrin (ZPP) level? 5 mcg/dL, although no amount is considered safe; 35 mcg/dL Explain laboratory findings in plumbism Acute poisoning: high BLL, normal ZPP; chronic poisoning: high BLL, high ZPP What are the major pathophysiologic characteristics associated with asthma Wheezing, SOB, Chest tightness, Cough. Contraction of airway smooth muscle, increased mucus production, airway edema, remodeling Asthma Characterized by variable, reversible episodes of brochoconstriction, late inflammation and bronchospasm What are precipitating factors and triggers associated with asthma? Exercise, allergen exposure, weather changes, respiratory infection After a diagnosis is made, what factors are used to determine the components of severity? Daytime asthma symptoms 2X per week, nighttime awakenings, reliever for symptoms 2X per week, activity limitation d/t asthma What are quick relief meds? 1) bronchodilators: Short acting beta agonists (SABA), Short acting anticholinergics (SAMA), 2) systemic corticosteroids Long term controller meds for asthma? Anti inflammatory, Bronchodilators, Long acting anticholinergics (LAMA), Methylxanthines Why is theophylline out of favor? Use is limited due to narrow therapeutic window, multiple drug interactions, questionable efficacy, and adverse effects Inhaled Corticosteroids (ICS) Potent anti-inflammatory agent, they decrease airway inflammation, attenuate airway hyperresponsiveness and minimize mucus production and secretions Examples of ICS Fluticasone, Budesonide, Beclomethasone, Ciclesonide Long Acting Beta Agonists (LABA) Used as add-on therapy for asthma not controlled with ICS alone. Works by stimulating the beta-2 adrenergic receptors in the lungs, resulting in a relaxation of bronchial smooth muscle (bronchodilation) Benefits: improved pulmonary function, more symptom free days, decreased need for SABA Examples of LABA Salmeterol, Vilanterol Long-Acting Muscarinic Antagonist (LAMA) Inhibit effects of acetylcholine on muscarine receptors and protect against cholinergic mediated bronchoconstriction. May cause dry mouth, urinary retention, headache Examples of LAMA Tiotropium (Spiriva) Leukotriene Receptor Antagonists (LTRAs) Anti-inflammatories that inhibit 5-lipoxygenase or completely antagonize the effect of leukotriene D. They improve forced expiratory volume (FEV), decrease symptoms, SABA use, and exacerbations. Can cause neuropsychiatric events. Short acting beta agonists (SABA) Reverse acute airway inflammation and brochoconstriction, increase mucociliary clearance and stabilize mast cell membranes. Side effects: tremors, tachycardia, hypokalemia Examples of SABA albuterol, levalbuterol What is the need for inhaled corticosteroids? ICS are the most potent anti-inflammatory agents. They decrease airway inflammation, attenuate airway hyperresponsiveness and minimize mucus production and secretions. They improve the actions of beta agonists and target the lungs directly Risk factors that may precipitate an asthma attack Uncontrolled asthma symptoms, frequent use of SABA, inadequate ICS therapy, low FEV (60%), psychological or financial problems, smoking or allergy exposure, obesity, pregnancy, hx of intubation, 1 or more of exacerbations in the past year When can step down therapy be initiated for an asthmatic? Once a patient is controlled on a maintenance regimen for 3 months with no symptoms Which beta blockers are not an absolute contraindication for an asthmatic patient Beta 1 (cardioselective) medications such as atenolol and metoprolol Mechanism of action of the Beta Agonist These agents cause smooth muscle relaxation by stimulating adenyl Cyclase to increase formation of cyclic adenosine monophosphate (cAMP) How does smoking influence the dose of theophylline Chemicals in tobacco smoke induce theophylline metabolism and increase its clearance If a patient complains of a dry hacking cough after starting lisinopril, what could you recommend? If coughing will impede compliance, switch to an angiotensin receptor blocker (ARB) For a patient with hypertension and chronic kidney disease, what blood pressure goal would you want the patient to meet Target BP is 130/80 for chronic kidney disease Why would we add a beta blocker to a patients regimen if they have heart failure and HTN? Chronic beta blocker use improves cardiac function through reverse modeling, improves ventricular shape, and reduces LV volumes, and decreases overall mortality. Only start when the patient is euvolemic. Why would we change HCTZ to a Loop diuretic When the patient warrents a stronger diuretic based on congestion and symptoms. Loop diuretics also maintain properties in reduced renal function whereas efficacy of thiazides drops when CrCl 30 mL/min What additional therapy may you have to start for a patient starting a loop diuretic? When adding a loop diuretic you will want to monitor potassium levels. You will likely have to add a potassium supplement to the patients medication regimen Counseling points for heart failure patient starting a beta blocker Dose will start low and be titrated slowly. Monitor for hypotension, bradycardia, orthostasis. Patient education regarding the possibility of the worsening symptoms but improving long-term function and survival is essential to ensure adherence. Signs and symptoms of Digoxin toxicity CNS: fatigue, weakness, confusion, delerium, psychosis GI: nausea, vomiting, anorexia sight: halos, photophobia, color perception problems CV: ventricular tachycardia or fibrillation, nodal block, and bradycardia risk increases with electrolyte disturbances What counseling would you provide to a patient receiving nitrates about using a phosphodiesterase-5 Inhibitor for ED? Phos-5 inhibitors should be avoided when a patient is using nitro due to risk of severe hypotension If a patient had prinzmetals angina, how would this impact your recommendation? Initial therapy for prinzmetals angina can either be a non-dihydropyridine calcium channel blocker (diltiazem/verapamil) or a long acting nitrate. Beta blockers should be avoided in variant angina Which medication recommended for ACS or MI would have no effect on the patients mortality? Nitroglycerin and other vasodilators provide immediate symptom relief in most patients with ACS or MI, but there is no evidence of long term benefits on mortality What medications are used to treat stable angina? Beta blockers, calcium channel blockers, nitrates, ranolazine What can help improve exercise tolerance in patients with stable angina? Beta blockers What additional medication should be given to all patients with ischemic heart disease? Short acting nitrates for acute ischemic symptoms What specific lab test would you monitor if you suspected a patient to be suffering from rhabdo due to a statin CK If you had a pregnant patient with high cholesterol, what medication would be safe if treatment was needed? Avoid statins in pregnancy. Bile Acid Sequestrants are considered safe If a patient had severe rhabdo and you stopped a statin, what would be your next step in treating high cholesterol Once the symptoms resolve you could start the same statin at a lower dose or initiate a different statin Common side effects of niacin and how to prevent it Flushing and hepatotoxicity. ASA or NSAID 30 prior can alleviate flushing symptoms, take with food, slow up-titration Understand the dosing of unfractionated heparin Dosing is weight based, using adjusted body weight for morbidly obese. Continuous infusion is adjusted based on aptt levels Understand the benefits of lovenox vs unfractionated heparin Lower incidence of HIT, osteopenia, osteoporosis. Routine coag labs are not needed Understand the mechanism of action of some of the newer anticoagulants They inhibit a serine protease target within the coagulation cascade, allowing for a linear dose and no anticoagulant monitoring. They have a more rapid onset and shorter half life than warfarin Understand dosing and monitoring of warfarin, as well as how to reverse the effects of warfarin Doses are based on individual patients response and INR. Can be reversed with vitamin K.