NR 507 PATHOPHYSIOLOGY EXAM QUESTIONS ANSWERED CORRECTLY LATEST UPDATE 2026

NR 507 PATHOPHYSIOLOGY EXAM QUESTIONS ANSWERED CORRECTLY LATEST UPDATE 2026 Oxygen transportation step 1 - Answers Air is inhaled through the process of ventilation (mechanical movement of gas or air into or out of the lungs) Oxygen transportation step 2 - Answers oxygen diffused from the alveoli into pulmonary capillaries, moving oxygen from the pulmonary veins to the left side of the heart to the aorta into systemic arterial circulation Oxygen transportation step 3 - Answers Perfusion (exchange of O2 and CO2 in the blood stream, which occurs via the alveoli and pulm capillaries) of the systemic capillaries with oxygenated blood Oxygen transportation step 4 - Answers oxygen is diffused from the systemic capillaries to each and every cell Gas CO2 transport step 1 - Answers Diffusion of blood (deoxygenated) from cells into systemic capillaries Gas CO2 transport step 2 - Answers Perfusion of the systemic capillaries with deoxygenated blood through the venous circulation, to the vena cava into the right side of the heart, to the pulmonary arteries (ART carry deoxygenated blood) Gas CO2 transport step 3 - Answers Diffusion of the CO2 from pulmonary arteries into alveoli through pulmonary capillaries Gas CO2 transport step 4 - Answers Exhalation of air by ventilation of lungs from removal of CO2 What are bronchioles? - Answers smallest of the conducting airways, branch out from the alveoli and connect to the alveoli What are the three layers of the bronchioles? - Answers Epithelial layer (inner layer) mucous containing goblet cells, and ciliated cells. Connective tissue (middle layer) lamina propia- cartilage and WBC's Smooth muscle layer (outer layer) outer layer to constrict and dilate What are the bronchioles controlled by? - Answers The autonomic nervous system Parasympathetic stimulation- mediated via vagus nerve--- release neurotransmitter acetylcholine binds to cholinergic receptors-- leading to bronchial constriction (decreased air flow). Dominates to limit exposure to external substances Sympathetic stimulation- stimulation of neurotransmitter epinephrine-- binds to beta 2- adrenergic receptors-- leading to bronchial dilation What is asthma? - Answers chronic inflammatory disorder of the bronchial mucosa caused by bronchial hyper-responsiveness, construction of airways, and variable airflow obstruction that is reversible. Asthma signs and symptoms - Answers Those are asymptomatic between attacks. Beginning of attacks--chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachypnea, and tachycardia Severe attacks-- use of accessory muscles of respiration, wheezing during both inspiration/expiration, pulsus paradoxus- decrease in SBP during inspiration Anti-cholingeric drugs for asthma - Answers Tiotropium and Ipratropium- these drugs block acetylcholine binding--- leading to bronchodilation through decrease in the parasympathetic response What causes bronchitis and associated pathogenesis? - Answers acute causes- infection or inflammation chronic causes- usually caused by viruses with a nonproductive cough Chronic bronchitis - Answers Inflammation of the bronchi persisting over a long time. Productive cough that continues for at least three months for a year for 2 years consecutive years. Enhanced chronic inflammatory response in the airways to noxious particles or gases. Inspired irritants-- bronchial inflammation-- bronchial edema increase in mucous glands and goblet ells in airway, smooth muscle hypertrophy with fibrosis, narrowing of airways Hypersecretion of thick muscus and cannot be cleared due to impaired ciliary function-- increasing susceptibility to infection contributing to airway injury and ineffective repair. Initially only affects larger bronchi-- eventually all airways involved Chronic bronchitis and acid/base disturbances - Answers narrowed airway--obstruction-- ventilation-perfusion mismatch with hypoxemia Hypercapnia develops as air trapping worsens and the work of breathing increase Reduced tidal volumes-hypoventilation-- respiratory acidosis Polycythemia vera - Answers chronic neoplastic, nonmalignant condition that is characterized by overproduction of red blood cells (often with an increase levels of WBC and platelets) and splenomegaly chronic bronchitis (marked hypoxemia) leads to ... - Answers polycythemia and cyanosis what is an essential component of polycythemia vera - Answers Erythrocytosis; clonal proliferation of erythoid progenitors occurs in the bone marrow independent of erythropoietin, even though the cells express a normal erythropoietin receptor alveolar hyperinflation with asthma - Answers airway obstruction increases airflow resistance and decreases flow rate--- impaired expiration causes air trapping, hyperinflation distal to obstruction and increased work of breathing-- continued air trapping increase intrapleural pressure and alveolar gas pressures-- decreased alveolar perfusion-- hyperventilation is triggered in response to increased lung volume and obstruction (early hypoxemia without Co2 retention and respiratory alkalosis)-- With progressive obstruction of expiratory airflow, airflow trapping more air leading to lungs and thorax hyperexanded, decrease respiratory muscles resulting in a decrease tidal volume and increase in CO2 retention-- causing respiratory acidosis Blood flow between heart and lungs - Answers The superior and inferior vena cava carry systemic DEoxygenated blood to the right atrium-- the tricuspid valve opens to allow for blood flow into the right ventricle-- the pulmonary semilunar valve opens to allow blood flow into the pulmonary truck; a large blood vessel that divides to form the left and right pulmonary arteries that carry blood to the lungs and eventually into the alveolar capillaries where gas exchange occurs-- The pulmonary veins return oxygenated blood to the left atrium-- the bicuspid valve opens to allow blood flow into the left ventricle-- the aortic semilunar valve opens to allow blood flow into the aorta; a large blood vessel that divides into brachiocephalic, left common carotid and subclavian arteries that will further branch to carry blood to the rest of the body. cardiac cycle - Answers atrial systole, atria contracts-- blood pushes through open tricuspid and mitral valves into ventricles. Semilunar valves are closed-- Beginning of ventricular systole, ventricular contract-- increased pressure in ventricles. Tricuspid and Mitral valves close (1st heart sound). As pressure rises, semilunar valves open when ventricles pressure-- atrial pressure-- blood pushed into aorta and pulmonary arteries. Beginning of ventricular diastole, pressure in relaxing ventricles drop below that in the arteries and semilunar valves close (2nd heart sound) As pressure falls, blood flow from veins into relaxed atria. Tricuspid and mitral valves open when pressure ventricle falls below atrial pressure. atrioventricular (AV) node - Answers mitral (left AV valve) and tricuspid (right AV valve) What happens during ventricular relaxation (systole) - Answers the two AV valves (mitral and tricuspid) blood from the atria to the ventricles. Once pressure is high in the ventricles the valves close to prevent from back flow into the atria as the ventricles contract (S1- 1st heart sound) What are the semilunar valves? - Answers pulmonary (RV-- lung) and aortic (LV-- body) what happens during ventricular contraction (Diastole) - Answers The pulmonary and aortic valves open when there is pressure and blood flows out of the ventricle and into the systemic and pulmonary circulation---after ventricular contraction and ejection the pressure decreases and the semilunar valves close when pressure is in the ventricles-- the closure is to prevent back flow into the right and left ventricles (S2- 2nd heart sound) What is cardiac output? - Answers HR x SV; normal CO in healthy adults is about 5L/min What four factors affect CO? - Answers Preload, afterload, heart rate and myocardial contractility. What is Ejection fraction? - Answers SV/ EDV (end diastolic volume) What increase EF? - Answers factors that increase contractility (sympathetic nervous system activity) What would a decrease in EF indicate? - Answers Ventricular failure What is stroke volume? - Answers volume of blood ejected per beat during systole Average SV is 70 mL SV and HR relationship - Answers Inverse relationship-- high HR= shorter fill time= low SV or low HR= longer fill time= high SV What factors determine force of contraction (Contractility)? - Answers Changes in preload Intropic stimuli changes O2 and CO2 levels the available Ca+ and its interaction with actin-myosin actin- myosin turn towards each-other (inotropic) and together create muscle fiber contraction troponin releases Ca+= muscle relaxation decreased in ischemia, hypoxia and decreased ATP what are inotropic stimuli changes for contractility? - Answers Fever, anxiety and SNS neurotransmitters: epi and norepi (positive agents) result in increased contractility Vagus nerve (Acetycholine- negative agent) results in a decreased contractility How does the O2 and CO2 levels change in contractility? - Answers Severe hypoxemia= contractility is decreased Moderate hypoxemia= catecholamines can increase contractility calcium binding and troponin? - Answers In resting muscles- calcium ions are stored in the sarcoplasmic reticulum Action potential reach the muscle cells-- T tubules carry action potential deep into the sarcoplasm-- causing sarcoplasm reticulum to release store of calcium ions-- in resting muscles, myosin binding sites are covered by troponin and tropomyosin. Calcium ions are released into the sarcoplasm as a result of action potential bind to troponin--- tropomysin and troponin move out of the way of the myosin binding sites leaving myosin heads free to bind to the actin microfilament--- ATP is used as an energy molecule to the myosin cross bridge-- the release of the stored energy provides force needed for each cross-bridge to move back to its org position, pulling actin along-- each cross bridge will bing to an actin molecule until another ATP molecule binds to it and pulls it back into a resting position. What is preload? - Answers degree of myocardial stretching before contraction-- the volume inside the ventricle at the END of diastole ((Ventricular end-diastolic volume (VEDV) and pressure (VEDP)) What two factors affect preload? - Answers 1)the amount of venous blood returning to the ventricle during diastole 2) the amount of blood in the ventricle after systole (end- systolic volume) What is starlings law? - Answers The volume of blood in the heart at the end of diastole (the length of the muscle fibers) is directly related to the force of the contraction during the next systole. What causes an increase in preload? - Answers CHF and hypervolemia what causes a decrease in preload? - Answers decrease in external pressure on the heart ( Cardiac tamponade and hypovolemia) What is afterload? - Answers amount of tension each ventricle must develop during systole to open semilunar valves and eject blood What causes a decrease in afterload? - Answers low aortic pressure, enables the heart to contract more rapidly hypotension or vasodilation example- shock what causes a increase in after-load? - Answers high aortic pressure, slow contraction and cause higher workloads against which the heart function to eject blood-- usually the result of systemic vascular resistance. systemic hypertension, valve disease, or COPD resulting in pulmonary hypertension What is diastole? - Answers period of relaxation, blood fills the ventricles What is systole? - Answers period of contraction, follows diastole. propels blood out of the ventricles and into the pulmonary and systemic circulation What is stenosis? - Answers valve orifice is constricted and narrowed. What happens during stenosis? - Answers stenosis impedes forward flow of blood-- increases the workload of the cardiac chamber proximal to the diseased valve intraventricular and atrial pressure increases in the chamber to overcome resistance to flow through the valve-- causing the myocardium to work harder-- resulting in myocardium hypertrophy what is the most common stenosis? - Answers Aortic stenosis What is the cause of aortic stenosis? - Answers calcification related to aging, inflammatory damage from rheumatic heart disease, congenital bicuspid valve What happens with aortic stenosis? - Answers aortic semilunar valve narrows-- diminishing blood flow from the left ventricle into the aorta-- increase left ventricular pressure-- causing left ventricular hypertrophy-- resulting in an increase in myocardial oxygen demand What can happen if someone has aortic stenosis? - Answers dysrrhytmias, MI, heart failure, decreased stroke volume, reduced SBP, and narrowed pulse pressure, heart rate is often slow and pulses are faint What is mitral stenosis? - Answers narrowing of the mitral valve and impairment in blood flow from the left atrium to the left ventricle What is the main cause of mitral stenosis? - Answers rheumatic heart disease What occurs during mitral stenosis? - Answers autoimmune activation of lymphocytes and macrophages leading to inflammatory damage and scarring of the valve leaflets. Scar tissue causes the leaflets to become more fibrous and fused-- and the chordae tendineae becomes shortened-- leading to impedance to blood flow-- resulting incomplete emptying of the left atrium and elevated atrial pressure as the chamber tries to force blood through the stenotic valve. Continued increase in left atrial pressure and volume leas to chamber dilation and hypertrophy--- causing pulmonary hypertension What can mitral stenosis result in? - Answers Atrial dysrhymias (afib)-- induced thrombi decreased cardiac output-- mainly on exertion JVD and peripheral edema-- pulmonary congestion and right heart failure What is heart failure? - Answers Heart is unable to generate adequate cardiac output-- leading to inadequate perfusion to the tissues-- diastolic filling pressure of the left ventricle or both-- causes pulm capillary pressure to increase What is the most common cause of heart failure? - Answers ischemic heart disease and hypertension What are other causes of heart failure? - Answers age, smoking, obesity, stress, renal failure, MI, congenital heart disease or excessive alcohol use Left heart failure (congestive heart failure) - Answers Systolic heart failure Inability of the heart to generate adequate cardiac output to perfuse tissues Ventricular remodeling Causes include myocardial infarction, myocarditis, cardiomyopathy neurohormonal activation in attempt to increase cardiac output-- SNS activation and renin-angiotension-aldosterone system activation (RAAS) long standing activation of SNS can lead to decrease in contractility due to decreased sensitivity to catecholamine and reduced inotropic response Activation of RAAS leads to increase in sodium and water retention and vasoconstriction leading to an increase in blood pressure and blood volume Neurohormonal changes--increase venous tone and peripheral vasoconstriction-- causing an increase in afterload. Diastolic heart failure Pulmonary congestion despite normal stroke volume and cardiac output Causes include myocardial hypertrophy and ischemia, diabetes, valvular and pericardial disease What are the s/s of left sided heart failure? - Answers fatigue, tachycardia, dyspnea, (left = lungs), pulmonary congestion, crackles, orthopnea, frothy sputum, hypotension/hypertension, and S3 gallop Right heart failure - Answers inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure-- as pressure in the pulmonary circulation rises-- the resistance to right ventricular emptying increases-- right ventricle hypertrophies increased workload-- pressure will rise in the systemic venous circulation-- JVD, peripheral edema and hepatosplenomegaly occurs What may cause right sided hear failure? - Answers Severe left heart failure-- when the increased left ventricular filling pressure is reflected back into the pulmonary circulation physiologic response to HR symptoms - Answers impaired ventricular function and reduced contractility, SV, CO are decreased-- increase in preload-- increase left atrial pressure resulting in pulmonary venous congestion blood volume increase due to activation of RAAS-- increases sodium and water retention-- increase blood volume and pulm congestion contribute to SOB-- and not being able to breath laying flat. What is cor pulmonale? - Answers right-sided heart failure in the absence of left-sided heart failure; right side is failing due to a pulmonary disease process in the lungs-- most commonly by pulmonary hypertension - increased pulmonary resistance because of a respiratory disease (COPD or cystic fibrosis) or from primary pulmonary arterial hypertension -pulmonary artery hypertension-- chronic pressure overload in the right vent-- increased workload of the right vent--hypertrophy of the heart muscle-- compromises right vent myocardial perfusion-- increased pressure-- decreased perfusion of the right coronary arteries-- leading to ischemia, decreased contractility and right vent overload right vent. usually fails when pulm artery = systemic blood pressure What is hypertension? - Answers SBP greater than 130 or DBP greater than 80. It is caused by an increase in cardiac output, total peripheral resistance or both. Most cases are primary hypertension or essential hypertension and these cases have an unknown cause Why does cardiac output increase? - Answers It increase by any condition that increase HR or SV. -Peripheral resistance is increased by factors that increase blood viscosity or reduces vessel diameter (vasoconstriction) -Overactivity of the SNS may result from increased production of catecholamines (epi/norepi) or from increased receptor reactivity -shift in the pressure-natriuresis relationship- increased vascular volume is related to a decrease in renal excretion of salt. - over-activity of the RAAS contributes to salt and water retention and increased vascular resistance What are risk factors for an increase cardiac output - Answers obesity, insulin resistance, and high intake of sodium What is complicated HTN? - Answers Hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling. when continued fibrosis has occured-- reduced blood flow and dysfunction perfused to other organs is affected causing inevitable damage (kidneys, brain, heart, eyes, etc) What are complications of HTN? - Answers angina pectoris, left ventricular hypertrophy (leading to CHF or L sided HF), CAD, MI or even sudden death What is a macrophage? - Answers a large phagocytic cell found in stationary form in the tissues or as a mobile white blood cell, especially at sites of infection. Circulating in the blood and must first leave the circulation and migrate to the sire of inflammation before initating phagocytosis (process in which cell ingests and gets rid of damaged cells and foreign material) - Monocytes- are a precursor of a macrophage that are found in the tissue. -Monocytes macrophages from the circulation may appear at the site as soon as 24 hours after inital neutrophil infiltration but usually arrive 3 to 7 days later (late inflam response) -Activated macrophages also secrete factors that stimulate the growth, differentiation and activation of other inflammatory cells -promotes wound healing What is hematopoiesis? - Answers production of blood cells