NR 507: Advanced Pathophysiology Midterm Exam (Latest 2024/ 2025 Update), Exams of Pathophysiology

Download NR 507: Advanced Pathophysiology Midterm Exam (Latest 2024/ 2025 Update) and more Exams Pathophysiology in PDF only on Docsity! 1 / 26 NR 507: Advanced Pathophysiology Midterm Exam (Latest 2024/ 2025 Update)  1.Asthma: Chronic disease due to bronchoconstriction and an excessive inflam- matory response in the bronchioles 2.What are 5 s/s of asthma: coughing wheezing shortness of breath rapid breathing chest tightness 3.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 4.Bronchioles: smaller passageways that originate from the bronchi that become the alveoli 5.3 layers of the bronchioles: innermost layer middle layer - lamina propria 2 / 26 outermost layer 6. lamina propria: the middle layer of the bronchioles 7.structure of the lamina propria: embedded with connective tissue cells and immune cells 8.purpose of the lamina propria: white blood cells are present to help protect the airways 9.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 10.What does the innermost layer of the bronchioles contain: columnar epithe- lial ells and mucus producing goblet cells 11.What does the outermost layer of the bronchioles contain: smooth muscle cells 12.what does the outermost layer of the bronchioles do: control the airways ability to constrict and dilate 13.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 14.how does hyperinflation occur?: the ongoing inflammatory process of asthma produces mucus and pus plug that the bronchial walls collapse around 15.Effect of hyperinflation of the alveolar: -expanded thorax and hypercapnia (retention of CO2) 5 / 26 29.What does smooth muscle hypertrophy do in lungs?: causes increased bronchoconstriction 30.Hypertrophy and hyperplasia of goblet cells do what in the bronchials: pro- motes hypersecretion of mucus 31.What are characteristics of epithelial cell metaplasia?: squamous cells be- come nonciliated and are less protective; allow passage of toxins and WBCs 32.What does the migration of WBCs to the bronchials do?: increases inflam- mation of the cite and causes fibrosis in the bronchial wall 33.How does the thickening and rigidity of bronchial basement membranes effect the lungs?: leads to further narrowing of the bronchial passageways 34.What acid-base disorder is seen in chronic bronchitis?: respiratory acidosis 35.how does chronic bronchitis lead to respiratory acidosis?: hyperinflation of the alveoli causes CO2 retention 36.Where does air enter the body?: naso and oropharynx (mouth and nose) 37.Where does air go after it passes through the nose and mouth?: it passes through the trachea 38.After air passes through the trachea where does it go?: goes into the left or right bronchi 39.Where does air flow after the bronchi?: into the smaller bronchioles 40.Where does air flow after the bronchioles?: into the alveoli 6 / 26 41.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 42.What is the formula for cardiac output: CO = HR x SV 43.cardiac reserve: difference between resting and maximal CO; should be about 4-5x as high but does decrease 1% per year after age 30 44.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 45.What is preload?: the degree of stretch on the heart before it contracts/ amount of blood entering the ventricles during diastole 46.average amount of preload?: 120-130 mls 47.When fibers stretch during diastole how does that effect contraction?: con- traction 7 / 26 is stronger 48.What happens when cardiac fibers overstretch during diastole?: decreased contraction due to fibers being unable to snap back 49.What can cause increased preload: CHF and hypervolemia 50.What can cause decreased preload: cardiac tamponade and hypovolemia 51.What are two common causes of hypovolemia: dehydration and hemorrhage 52.Afterload: the amount of resistance to open the semilunar valves and eject of blood from the ventricle 53.what influences afterload (3): ventricle wall thickness (muscle strength) arterial pressure (resistance to ejection) ventricle chamber size (blood volume capacity) 54.what can cause an increase in afterload: systemic hypertension valve disease COPD (pulmonary hypertension) 55.what can decrease afterload: hypotension or vasodilation 56.what influences cardiac contractility (inotropic state): levels of electrolytes High levels of ATP level of oxygen available synchronous muscle contraction 57.What electrolytes are used for cardiac muscle contraction?: sodium potas- sium and calcium 10 / 26 adequate blood flow into systemic circulation 81.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 82.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 83.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 84.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 85.How does heart failure progress from hypertension?: - high systemic vascu- lar 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 11 / 26 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 pul- monary tissues 86.What does fluid in the pulmonary tissue result in: the areas are flooded and results in pulmonary edema and dyspnea 87.cor pulmonale: right-sided heart failure 88.right sided heart failure: inability of the right ventricle to provide adequate blood flow into the pulmonary circulation 89.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 90.What is the most common cause of right sided heart failure: pulmonary hypertension 91.Progression of right sided heart failure: - damage causes the right ventricle to 12 / 26 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 92.signs and symptoms of right sided heart failure: jugular vein distension hepatosplenomegaly peripheral edema 93.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 94.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 95.High output failure: inability of the heart to pump sufficient amounts of blood to 15 / 26 104. Erythropietin: Produce: Kidney (small amount in liver) Released: Kidney Target: Bone Marrow Functions: Stimulates bone marrow to produce more red blood cells 105. hematopoietic stem cells: The stem cells that give rise to RBC WBC and platelets through the process of haematopoiesis. 106. How does a hematopoietic stem cell produce a red blood cell: hematopoi- etic stem cells produces an unndifferentiated hemocytoblast - erythropoietin binds to it and createsa a proerythroblast - cell develops into an erythrocyte 7 days later 107. Erythrocyte function: transport oxygen and carbon dioxide 108. Erythrocyte life span: 120 days 109. anemia risk factors: acute or chronic blood loss, increased hemolysis, inade- quate dietary intake or malabsorption, bone marrow suppression, age 110. 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. 111. causes of anemia: - impaired RBC production 16 / 26 - excessive blood loss - increased RBC destruction 112. hemolytic anemia: premature destruction of RBCs 113. causes of hemolytic anemia: infection transfusion reaction hemolytic disease of the newborn (Rh incompatibility) autoimmune reaction drug induced 114. development of anemia due to gastrectomy: loss of intrinsic factor from surgery results in the loss of protein necessary for vitamin B12 absorption an can lead to anemia 115. what kind of anemia can result from incorrect blood transfusion: hemolytic anemia 116. normocytic normochromic anemia: Characterized by red cells that are rela- tively normal in size and hemoglobin content but insufficient in number 117. hemolytic anemia is what kind of anemia: normocytic normochromic anemia 118. polycythemia vera: condition characterized by too many erythrocytes; blood becomes too thick to flow easily through blood vessels 119. Kidney Anatomy: renal artery renal vein cortex, medulla, renal pelvis 17 / 26 ureter renal pyramid nephron 120. Nephron Anatomy: 1. glomerulus 2.bowman's capsule 3.collecting duct 4.tubule 5.capillary 121. Bladder anatomy: - ureter - bladder -urethra 122. reabsorption (kidney): movement of solutes from filtrate to blood things taken back that were secreted of filtered by the kidney 123. what solutes are typically reabsorbed: glucose, ions, amino acids and urea 124. Where is most of the solute reabsorbed?: proximal convoluted tubule 125. What effects amount of water and solute reabsorption: ADH and aldos- terone 126. secretion (kidney): movement of solutes from blood to filtrate anywhere be- sides bowman's capsule able to secrete salts, acids, bases and urea directly into the tubule via *active or passive transport* 20 / 26 are present at birth 133. polycystic kidney disease: - Mutant PKD genes cause fluid accumulation in kidney tubules "cysts" -The cysts can be the size of grapes or oranges and compress and destroy nephrons 134. Why are kidneys and bladders at high risk for cancer: - UT is the route of excretion for many toxins and contains highly mitotic cells 135. Descending infection: The blood can carry bacteria from a focus of infection in another part of the body to the kidneys. The bacteria then pass with the urine down the ureters to the bladder. 21 / 26 136. Ascending infection: - urethra to bladder, and then to kidney - due to: bacteria from residual fecal contamination 137. glomerulonephritis: inflammation of the glomeruli of the kidney 138. tubular necrosis: the renal tubules cells are highly sensitive to low oxygen levels or presence of toxins and leads to tubular necrosis 139. Causes of tubular necrosis: - being post operative - severe sepsis - burns - trauma - contrast chemical use in medical imaging procedures 140. Pathophysiology of tubular necrosis: - ischemia or nephrotoxin exposure occurs to the renal tubules - inflammation and tubular injury occur - cast formation and tubular obstruction occurs - tubular injury, leakage, increased glomerular pressure causes decreased capillary perfusion further decrease in GFR occurs - oliguria results 141. Acute Kidney Injury: Sudden decline in kidney function with a decrease 22 / 26 in GFR and an increase in plasma creatinine and BUN levels -results in oliguria 142. Prerenal disease: decreased blood flow to and through the kidney 143. prerenal disease causes: - hypotension - decreased cardia output - decreased blood volume 144. What are most cases of AKI caused by?: prerenal issues 145. Intrarenal disease: disease or damage within the kidney 146. Causes of intrarenal disease: ATN Acute glomerulonephritis 147. postrenal disease: obstruction in the lower urinary tract that prevents urine flow from the kidneys 148. Causes of postrenal disease: BPH Calculi Inflammation Tumors 149. Chronic kidney disease: progressive, irreversible deterioration in renal func- tion Labs: elevated BUN, Cr Phosphorus. Rx: meds for hypertension, statins, epoetin, diuretics, calcium, LOW protein, low salt, restrict K, phosphorus (no chicken, milk, legumes, carbonated drinks), dialysis. 25 / 26 160. Why is there azoetmia with renal failure?: Decreased GFR means waste is remains in the bloodstream and is not excreted 161. Why is there oliguria with renal failure?: when the glomerual structure has sustained enough damage the nephron structure is no longer functional as a filtration unit 162. What happens in renal failure when the coagulation cascade is activated- : fibrin is deposited in the glomerular structure and decreases capillary perfusion by causing blockages and further decreases GFR further 163. blood hydrostatic pressure: the pressure produced by a fluid against a sur- face 164. angiotensin converting enzyme (ACE): an enzyme that converts angiotensin I to angiotensin II 165. What does angiotensin II do?: increases blood pressure by vasoconstriction 166. Role of macrophages: -In Innate: 1.Phagocytosis PRR or opsonization w/ complement 2.Secrete Cytokines: Recruit more cells, inflammation, fever, etc. -In Adaptive: 1.Phagocytosis: opsonization with complement or Abs 26 / 26 2.Secrete cytokines: recruit more cells etc. 3.Antigen presentation: peptides from the broken down pathogen are displayed on surface of the cell.