NR 507 Advanced Pathophysiology Midterm Review Latest Update 2024/2025 Questions, Exams of Nursing

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NR 507

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Pathophysiology

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NR 507 Midterm Exam

Asthma Chronic disease due to bronchoconstriction and an excessive inflammatory response in the bronchioles What are 5 s/s of asthma coughing wheezing shortness of breath rapid breathing chest tightness Pathophysiology of asthma (5) -airway inflammation, bronchial hyper-reactivity and smooth muscle spasm -excess mucus production and accumulation -hypertrophy of bronchial smooth muscle -airflow obstruction -decreased alveolar ventilation

Bronchioles smaller passageways that originate from the bronchi that become the alveoli 3 layers of the bronchioles innermost layer middle layer - lamina propria outermost layer lamina propria the middle layer of the bronchioles structure of the lamina propria embedded with connective tissue cells and immune cells purpose of the lamina propria white blood cells are present to help protect the airways How does the lamina propria effect the lungs in regards to asthma the WBCs protective feature goes into overdrive causing an inflammatory response that damages host tissue

What does the innermost layer of the bronchioles contain columnar epithelial ells and mucus producing goblet cells What does the outermost layer of the bronchioles contain smooth muscle cells what does the outermost layer of the bronchioles do control the airways ability to constrict and dilate alveolar hyperinflation When air is unable to move out of the alveolar like it should due to bronchial walls collapsing around possible mucus plug thus trapping air inside how does hyperinflation occur? the ongoing inflammatory process of asthma produces mucus and pus plug that the bronchial walls collapse around Effect of hyperinflation of the alveolar

-expanded thorax and hypercapnia (retention of CO2)

• respiratory acidosis What are two anticholinergic drugs used for asthma tiotropium and ipratropium What do anticholinergics do in the lungs? These drugs block the effects of the parasympathetic nervous system
• increasing bronchodilation MOA of anticholinergic drugs for asthma the parasympathetic system is stimulated by the vagal nerve to release acetylcholine which binds to the cholinergic receptors of the respiratory tract to cause bronchial constriction = decreased airflow
• blocking the cholinergic receptors prevents acetylcholine binding preventing the bronchial constriction bronchitis inflammation of the bronchial tubes

3 characteristics of bronchitis bronchial inflammation hypersecretion of mucus chronic productive cough for at least 3 consecutive months for at least 2 successive years Perfusion The supply of oxygen to and removal of wastes from the cells and tissues of the body as a result of the flow of blood through the capillaries. results of chronic bronchitis/ low perfusion cyanosis right to left shunting chronic hypoxemia Why is there cyanosis with chronic bronchitis there is hypoxia due to unfavorable conditions for gas exchange Right to left shunting

when blood passes from the right ventricle through the lungs and to the left ventricle without perfusion Causes of bronchitis -long term exposure to environmental irritants -repeated episodes of acute infection (RSV infection in early infancy) -Factors affecting gestational childhood lung development (preterm birth) Pathogenesis of bronchitis -Exposure to airborne irritants

• Irritant activates bronchial smooth muscle constriction and mucus secretion
• Triggers release of inflammatory mediators from immune cells located in the lamina propria most common irritant with bronchitis is? tobacco product smoke what does long term exposure to irritants promote in bronchitis? (5)
• smooth muscle hypertrophy

• hypertrophy and hyperplasia of goblet cells
• epithelial cell metaplasia
• migration of more WBC to site
• thickening and rigidity of bronchial basement membrane What does smooth muscle hypertrophy do in lungs? causes increased bronchoconstriction Hypertrophy and hyperplasia of goblet cells do what in the bronchials promotes hypersecretion of mucus What are characteristics of epithelial cell metaplasia? squamous cells become nonciliated and are less protective; allow passage of toxins and WBCs What does the migration of WBCs to the bronchials do? increases inflammation of the cite and causes fibrosis in the bronchial wall

How does the thickening and rigidity of bronchial basement membranes effect the lungs? leads to further narrowing of the bronchial passageways What acid-base disorder is seen in chronic bronchitis? respiratory acidosis how does chronic bronchitis lead to respiratory acidosis? hyperinflation of the alveoli causes CO2 retention Where does air enter the body? naso and oropharynx (mouth and nose) Where does air go after it passes through the nose and mouth? it passes through the trachea After air passes through the trachea where does it go? goes into the left or right bronchi

Where does air flow after the bronchi? into the smaller bronchioles Where does air flow after the bronchioles? into the alveoli Describe how blood flows to become oxygenated

• deoxygenated systemic blood flows from the vena cava to R atrium
• Tricuspid valve opens to flow to R ventricle -Pulmonary semilunar valve opens and blood flows to the alveolar capillaries for gas exchange from the pulmonary trunk and L & R pulmonary arteries
• blood goes from alveolar capillaries to pulmonary veins to return oxygenated blood to the left atrium
• bicuspid valve opens to allow blood to go to left ventricle
• aortic semilunar valve opens and blood goes to the aorta
• aorta pushes oxygenated blood out to the body What is the formula for cardiac output CO = HR x SV

cardiac reserve difference between resting and maximal CO; should be about 4-5x as high but does decrease 1% per year after age 30 What type of relationship does heart rate and stroke volume have? inverse low HR = longer fill time = increase stroke volume high HR = lower fill time = lower stroke volume What is preload? the degree of stretch on the heart before it contracts/ amount of blood entering the ventricles during diastole average amount of preload? 120-130 mls When fibers stretch during diastole how does that effect contraction? contraction is stronger

What happens when cardiac fibers overstretch during diastole? decreased contraction due to fibers being unable to snap back What can cause increased preload CHF and hypervolemia What can cause decreased preload cardiac tamponade and hypovolemia What are two common causes of hypovolemia dehydration and hemorrhage Afterload the amount of resistance to open the semilunar valves and eject of blood from the ventricle what influences afterload (3) ventricle wall thickness (muscle strength) arterial pressure (resistance to ejection) ventricle chamber size (blood volume capacity)

what can cause an increase in afterload systemic hypertension valve disease COPD (pulmonary hypertension) what can decrease afterload hypotension or vasodilation what influences cardiac contractility (inotropic state) levels of electrolytes High levels of ATP level of oxygen available synchronous muscle contraction What electrolytes are used for cardiac muscle contraction? sodium potassium and calcium What increases cardiac muscle contraction sympathetic stimulation; fear anxiety and increased thyroxine

what decreases cardiac muscle contraction low ATP levels; ischemia hypoxia or acidosis Stimulation of what set a resting HR (chronotropic state) parasympathetic system what stimulates the parasympathetic system the vagus nerve What does the parasympathetic system do? It releases acetycholine which decreases heart rate and causes vasodilation What can extreme vagal response result in? life threatening bradycardia What mediates the sympathetic system epinephrine and norepinephrine

What does the sympathetic system promote in the cardiac system vasoconstriction and increased HR What can uncontrolled tachycardia lead to? reduced stroke volume and fatigue What are the two parts of the cardiac cycle? diastole and systole What causes blood to move from the atria to the ventricles gravity and atriole systole What causes the S1 heart sound? Bicuspid/Mitral and Tricuspid valves closing What are the atrioventricular valves? tricuspid and bicuspid (mitral) valves

What are the semilunar valves? pulmonary and aortic valves What causes the semilunar valves to open? As ventricles contract and intraventricular pressure rises, blood is pushed up against the SL valves, forcing them to open ejection fraction measurement of the volume percentage of left ventricular contents ejected with each contraction What causes the semilunar valves to close? ventricles relax and intraventricular pressure falls, blood flows back from the arteries, and fill the cusps of the semilunar valves What causes the S2 heart sound? closing of semilunar (aortic and pulmonary) valves What prevents the backflow into the ventricles semilunar valves

Stenosis of heart valve A narrowing of the valve opening, causing turbulent flow and enlargement of the emptying chamber Stenosis of a heart valve, may result in what? Narrowing of the heart valves means that blood moves with difficulty out of the heart. Results may include chest pain, edema in the feet or ankles, and irregular heartbeat. and hypertrophy heart failure cardiac dysfunction caused by the inability of the heart to provide adequate CO resulting in inadequate tissue perfusion Left sided heart failure characteristic inability of the left ventricle to provide adequate blood flow into systemic circulation Causes of left sided heart failure systemic hypertension left ventricle MI LV hypertrophy

Aortic SL valve or bicuspid valve damage Secondary to right heart failure How does LV hypertrophy lead to left sided heart failure The hypertrophy is secondary to cardiac damage resulting in an enlarged by weaker structure that holds more blood How does Aortic SL valve or bicuspid valve damage lead to heart failure damage leads to back flow into the left atrium or ventricle after ejection Biventricular failure unresolved left sided heart failure will increase pressure on the right side of the heart contributing to right sided heart failure as well How does heart failure progress from hypertension?

• high systemic vascular pressure causes high after load requires the left ventricle to increase contraction force to eject the blood
• damage causes reduced ejection fraction and left ventricle gets tired and becomes unable to eject normal amount of blood

• increased amount of blood remaining in left ventricle and increased left ventricle preload causes the left atrium unable to eject the normal amount of blood into the left ventricle
• blood volume and pressure backs up into the pulmonary veins
• increased pressure will force fluid from the pulmonary capillaries into the pulmonary tissues What does fluid in the pulmonary tissue result in the areas are flooded and results in pulmonary edema and dyspnea cor pulmonale right-sided heart failure right sided heart failure inability of the right ventricle to provide adequate blood flow into the pulmonary circulation Causes of right sided heart failure
• pulmonary disease

• pulmonary hypertension
• RV MI
• RV Hypertrophy
• pulmonary SLV or tricuspid valve damage
• secondary to left heart failure What is the most common cause of right sided heart failure pulmonary hypertension Progression of right sided heart failure
• damage causes the right ventricle to increase contraction force to eject/unload the blood
• over time EF is reduced and right ventricle us unable to eject the normal amount of blood
• the blood remaining in the RV increases and RA preload increases until the RA is unable to eject the normal amount of blood into the RA
• the amount of blood remaining in the right atrium increases causing an increase in RA preload
• blood volum enad pressure then backs up into the vena cava and systemic veins

signs and symptoms of right sided heart failure jugular vein distension hepatosplenomegaly peripheral edema Why does hepatosplenomegaly develop in right sided heart failure the large volume of blood flow through the liver and spleen causes these areas to be engorged why does peripheral edema occur in right sided heart failure Increased pressure forces fluid from the systemic capillaries into the peripheral tissues and flood those areas High output failure inability of the heart to pump sufficient amounts of blood to meet the circulatory needs of the body despite normal blood volume and cardiac contractility causes of high output failure Severe anemia

Nutritional deficiencies Hyperthyroidism Sepsis Extreme febrile state Process of high output failure

• impaired oxygen delivery of excessive tissue oxygen demands cause tissue hypoxia
• catecholamines initiation increase HR and stroke volume
• increased cardiac output is produced but depletes cardiac muscle reserve overtime and leads to low output failure over time Troponin-Calcium Binding Calcium binds to troponin on the thin filament sliding filament theory theory that actin filaments slide toward each other during muscle contraction, while the myosin filaments are still Hematopoiesis

formation of blood cells Where does blood cell formation occur in a fetus 3 weeks - yolk week 8 - fetal liver and spleen 5th month - bone marrow Blood cell formation in chidren 0-5 years old red marrow of all bones to make blood cells blood cell formation in adults over 20 red marrow in large bones -illium, vertebrae, cranium, jaw, sternum, ribs, humerus, and femur Erythropietin Produce: Kidney (small amount in liver) Released: Kidney Target: Bone Marrow Functions: Stimulates bone marrow to produce more red blood cells

hematopoietic stem cells The stem cells that give rise to RBC WBC and platelets through the process of haematopoiesis. How does a hematopoietic stem cell produce a red blood cell hematopoietic stem cells produces an unndifferentiated hemocytoblast

• erythropoietin binds to it and createsa a proerythroblast
• cell develops into an erythrocyte 7 days later Erythrocyte function transport oxygen and carbon dioxide Erythrocyte life span 120 days anemia risk factors acute or chronic blood loss, increased hemolysis, inadequate dietary intake or malabsorption, bone marrow suppression, age

function of hemoglobin In red blood cells, carries oxygen from the lungs to body's tissues and returns carbon dioxide from tissues back to lungs. It also maintains the shape of red blood cells. causes of anemia

• impaired RBC production
• excessive blood loss
• increased RBC destruction hemolytic anemia premature destruction of RBCs causes of hemolytic anemia infection transfusion reaction hemolytic disease of the newborn (Rh incompatibility) autoimmune reaction drug induced