{"id":131897,"date":"2024-01-26T17:34:33","date_gmt":"2024-01-26T17:34:33","guid":{"rendered":"https:\/\/learnexams.com\/blog\/?p=131897"},"modified":"2024-01-26T17:34:36","modified_gmt":"2024-01-26T17:34:36","slug":"midterm-exam-nr507-nr-507-latest-2024-2025-update-advanced-pathophysiology-review-questions-and-verified-answers-100-correct-grade-a-chamberlain","status":"publish","type":"post","link":"https:\/\/www.learnexams.com\/blog\/2024\/01\/26\/midterm-exam-nr507-nr-507-latest-2024-2025-update-advanced-pathophysiology-review-questions-and-verified-answers-100-correct-grade-a-chamberlain\/","title":{"rendered":"Midterm Exam: NR507\/ NR 507 (Latest 2024\/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A \u2013 Chamberlain"},"content":{"rendered":"\n<p>Midterm Exam: NR507\/ NR 507 (Latest 2024\/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A \u2013 Chamberlain<\/p>\n\n\n\n<p>Midterm Exam: NR507\/ NR 507 (Latest<br>2024\/ 2025 Update) Advanced<br>Pathophysiology Review| Questions and<br>Verified Answers| 100% Correct |Grade A \u2013<br>Chamberlain<br>Q: Autoimmune disease\u2026<br>Answer:<br>\u2026. can be familial.<br>Q: Hypersensitivity: Type 4<br>Answer:<br>-Delayed<br>-T-cell mediated<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Does NOT involve antigen\/antibody complexes<br>Q: Type 2 &amp; 4 Hypersensitivity relationship<br>Answer:<br>(Type 2) Organ rejection involves cytotoxicity -&gt; (Type 4) T-cells also involved in organ<br>rejection -&gt; (Type 2) Antigens from target cells stimulate T-cells to differentiate into cytotoxic Tcells -&gt; (Type 4) T- cells have cytotoxic activity along with helper T-cells involved in delayed<br>hypersen- sitivity<br>Q: Hypersensitivity Type 4 RASH<br>Answer:<br>-Delayed several days following contact (e.g. poison ivy)<br>-contact dermatitis consisting of lesions only at the site of contact with the allergen<\/li>\n<\/ul>\n\n\n\n<p>Q: Treatment of Type 4 Rash<br>Answer:<br>Topical corticosteroids<br>No epi or antihistamines as doesn&#8217;t act on mast cells\/H1 receptors<br>Q: primary immunodeficiency<br>Answer:<br>Most primary immune deficiencies are the result of a single gene defect<br>*something lacking in the immune system itself<br>Q: secondary immunodeficiency<br>Answer:<br>Immunodeficiency as a complication of some other physiologic condition or disease<br>Q: Example of primary immunodeficiency<br>Answer:<br>B-lymphocyte Deficiency<br>Q: Example of secondary immunodeficiency<br>Answer:<br>Malnutrition is a cause of this<br>HIV pt gets pneumocystis carinii<br>Q: Recycling of RBCs<br>Answer:<\/p>\n\n\n\n<p>Provides the body with most of its iron stores<br>Q: Mean Corpuscular Hemoglobin Concentration (MCHC)<br>Answer:<br>Measure of the av- erage concentration of hemoglobin inside a single red blood cell (color)<br>Q: Normochromic anemias<br>Answer:<br>MCHC 32-36%<br>Hemolytic<br>Aplastic<br>Post-hemorrhagic<br>Q: Hypochromic Anemias<br>Answer:<br>Pale RBCs<br>Sideroblastic anemia Iron deficiency anemia Thalassemia<br>Q: Hyperchromic anemias<br>Answer:<br>Liver disease<br>Sickle cell Hyperthyroidism Hereditary spherocytosis<br>Q: iron deficiency anemia<br>Answer:<br>microcytic, hypochromic<br>Caused by disorder of hb synthesis<br>Powered by <a href=\"https:\/\/learnexams.com\/search\/study?query=\" target=\"_blank\" rel=\"noopener\">https:\/\/learnexams.com\/search\/study?query=<\/a><br>Hypersensitivity: Type 1 -Allergic reaction-Mediated by IgE-inflammation d\/t mast cell degranulation*Most dangerous form is anaphylactic-systemic response-hypotension, sever bronchoconstriction~Main treatment: epi reverses the effects<br>Hypersensitivity: Type 2 -cytotoxic reaction; tissue specific (e.g. thyroid tissue) -macrophages are primary effectof cells involved -can cause tissue damage or alter function-example: Grave&#8217;s disease (hyperthyroidism) is example of altering thyroid function but does not destroy thyroid tissue- incompatible blood type- example of cell\/tissue damage that occurs; severe transfusion reaction occurs and the transfused erythrocytes are destroyed by agglutination or complement-mediated lysis.-organ specific<br>Hypersensitivity: Type 1 Local &amp; Systemic Symptoms -Local: itching, rash-Systemic: wheezing<br>Hypersensitivity: Type 3<br>Scope of damage of SLE- type 3 auto immune rep\u00edtanse Facial rash confine to the cheeks (malar rash)Discoid rash (raised patches, scaling)PhotosensitivityOral or nasopharyngeal ulcersHematological disorders (hemolytic anemia, lymphopenia, or thrombocytopenia). Immunologic disordersNon-erosive arthritis of at least two peripheral jointsSerositis (pleurisy, pericarditis)Renal disorder Neuro disorder (seizure, psychosis)+ANA<br>Alloimmunity Term used to describe what an individuals immune system reacts against antigens on the tissues of other members of the same species<br>Examples of alloimmunity -neonatal disease, where the maternal immune system become sensitize against antigens, expressed by the fetus-Transplant rejection-Transfusion reaction<br>Autoimmunity The alteration in the ability of the body to tolerate its own self antigensCan occur when the immune system overreacts against self antigens to the extent that tissue damage occurs.<br>Autoantibodies T- and B-cells These autoantibodies react in associated body symptoms to produce signs and symptoms in autoimmune disorders<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>ANA Seen and 90% of patients with systemic lupus erythematosus<br>Autoimmune disease\u2026 \u2026. can be familial.<br>Hypersensitivity: Type 4<br>Type 2 &amp; 4 Hypersensitivity relationship (Type 2) Organ rejection involves cytotoxicity -&gt; (Type 4) T-cells also involved in organ rejection -&gt; (Type 2) Antigens from target cells stimulate T-cells to differentiate into cytotoxic T-cells -&gt; (Type 4) T- cells have cytotoxic activity along with helper T-cells involved in delayed hypersensitivity<br>Hypersensitivity Type 4 RASH -Delayed several days following contact (e.g. poison ivy)-contact dermatitis consisting of lesions only at the site of contact with the allergen<br>Treatment of Type 4 Rash Topical corticosteroidsNo epi or antihistamines as doesn&#8217;t act on mast cells\/H1 receptors<br>primary immunodeficiency Most primary immune deficiencies are the result of a single gene defect<em>something lacking in the immune system itself secondary immunodeficiency Immunodeficiency as a complication of some other physiologic condition or disease Example of primary immunodeficiency B-lymphocyte Deficiency Example of secondary immunodeficiency Malnutrition is a cause of thisHIV pt gets pneumocystis carinii Recycling of RBCs Provides the body with most of its iron stores Mean Corpuscular Hemoglobin Concentration (MCHC) Measure of the average concentration of hemoglobin inside a single red blood cell (color) Normochromic anemias MCHC 32-36%Hemolytic AplasticPost-hemorrhagic Hypochromic Anemias Pale RBCsSideroblastic anemiaIron deficiency anemiaThalassemia Hyperchromic anemias Liver disease Sickle cell Hyperthyroidism Hereditary spherocytosis iron deficiency anemia microcytic, hypochromicCaused by disorder of hb synthesis Ferritin level needed to show body&#8217;s total iron stores low serum ferritin iron deficiency anemia Hb hemoglobinOxygen carrying component of red cells Normal hb for men 13.5-17.5 Normal Hb for women 12-15.5 Hct hematocritVolume of cells as % of total volume of cells and plasma in whole blood Normal hct for men 42-45% Normal Hct for women 37-48% Mean Cell Volume (MCV) Mean Corpusular Hemoglobin (MCH) The average weight of hb per RBCNormal is 27 Red Cell Distribution Width (RDW) Quantitative estimate of the uniformity of individual cell size Normal is 11.5-14.5% Labs for IDA (Ferritin, RDW, serum iron, total iron binding capacity, transferrin) Ferritin- lowRDW- highSerum iron- lowTotal iron binding capacity- highTransferrin- low Labs for Thalassemia Ferritin- highRDW- normal to highSerum iron- normal to highTotal iron binding capacity- normalTransferrin- normal to high RDW is increased in \u2026 microcytic and macrocytic anemias Folate deficiency -Can cause megaloblastic anemia-In pregnancy there is increased risk of neural tube defects-ETOH pt high risk d\/t malnutrition Vitamin B12 Deficiency Symptoms FatigueDyspneaPeripheral neuropathy in BLE Those at risk for Vitamin B12 deficiency Older adultsH. Pylori infectionS\/p gastrectomyGastritis pernicious anemia a vitamin B12-deficiency disease, caused by lack of intrinsic factor and characterized by large, immature red blood cells and damage to the nervous system Who is at risk for Hemolytic anemia -Mismatched blood types &#8211; destroys RBCs (cytotoxic type2) -Auto immune hemolytic anemia, due to order antibodies against erythrocytes attack, immune system, and perceives as an antigen, and then attacks it. -Allergic reaction to a drug that causes drug induced hemolytic, anemia -newborn hemolytic disease, Rh incompatibility Acute blood loss anemia # of RBCs lost is greater that # of RBCs produced d\/t direct result of blood loss Causes of blood loss anemia GI BleedingSever traumaSurgeryL&amp;d complications Chronic blood loss from GI aplastic anemia diagnostics Blood test and bone marrow biopsy Blood results in aplastic anemia Low reticulocyte (less or equal to 40&#215;109\/L)Low granulocytes (less than 500\/uL)Platelet count less that 20k causes of aplastic anemia RadiationViral inducedTumorsAbx or other medsCongenital defects (Fanconi&#8217;s)The agent destroys the blood cell producing red bone marrow which is replaced with fatty yellow marrow that cannot produce RBCs\u2026 leads to pancytopenia\u2026 hypoxia\u2026 clotting problems\u2026.. increased infections Sickle Cell Disease (SCD) a group of inherited, autosomal recessive disordersA single amino acid change in the beta-chain Elongated cells (HbS) that do not readily bind with O2 How long until sickled RBCs rupture? 10-15 days SCD is a type of \u2026 \u2026 hemolytic anemia and presents with classic anemia signs plus more SCD pts are at risk for Circulatory iron overloadStrokeSplenic damageKidney damage Thalassemia inherited defect in ability to produce hemoglobin, leading to hypochromia There are many <strong><em>_<\/em><\/strong> with thalassemia. genetic mutations<br>Bicuspid valve Mitral Valve: Between left atrium and ventricle<br>aortic valve The semilunar valve separating the aorta from the left ventricle that prevents blood from flowing back into the left ventricle.<br>tricuspid valve valve between the right atrium and the right ventricle<br>pulmonary semilunar valve heart valve opening from the right ventricle to the pulmonary artery<br>Normal blood flow through the heart superior\/inferior vena cava &gt; r atrium &gt; tricuspid valve &gt; r ventricle &gt; pulmonic valve &gt; pulmonic artery &gt; lungs &gt; l atrium &gt; l ventricle &gt; aorta &gt; body<br>Pulmonary veins carry <strong><em><strong><em>_<\/em><\/strong><\/em><\/strong> blood to the LA Oxygenated<br>Cardiac Output (CO) Amount of blood pumped in 1 minute (ml\/min)<br>Stroke Volume (SV) The volume of blood pumped for each heartbeat (ml\/beat)~ 70 ml<br>Heart Rate (HR) number of heart beats per minute<br>Cardiac output formula CO = HR x SV<br>Preload &#8220;&#8221;&#8221;Volume&#8221;&#8221;Loading heart with blood prior to ejectionDegree of myocardial fiberlength stretch before contraction&#8221;<br>Afterload &#8220;&#8221;&#8221;Pressure&#8221;&#8221;&#8221;&#8221;Unload&#8221;&#8221;The amount of tension the ventricle must develop during systole to open semilunar valves and eject blood&#8221;<br>Contractility ability to shorten when an adequate stimulus is received<br>increases contractility Sympathetic stimuli: FeverAnxiety Increased thyroxine<br>decreases contractility Decreased ATP Levels:IschemiaHypoxiaAcidosisCardiomyopathy<br>Sustained tachycardia will the afterload. decrease<br>causes of increased afterload HTNPulmonary disease (COPD, pulm. HTN)Aortic damage\/stenosis<br>HTN has most immediate effect on the <strong><em><strong>__<\/strong><\/em><\/strong>. \u2026. afterload<br>Decrease la afterload d\/t decreased volume Hemorrhage<br>What does increase preload do to SV in healthy heart? Increases SV<br>Preload decreases with blood volume loss vasodilationcardiac tamponade<br>Major risk factor in developing heart failure Long standing HTN<br>Normal EF 55-70%<br>EDV end diastolic volume Amount of blood in ventricle before systole (~120 ml)<br>ESV Amount of blood in ventricle after systole (50 ml)<br>Afterload decreases with HypotensionVasodilation<br>Three types of heart failure LHFRHFHigh-output failure<br>left heart failure Inability of LV to provide adequate blood flow into systemic circulation<br>Causes of LHF Systemic HTNLV MILV HypertrophyAortic or bicuspid valve damageRHF<br>symptoms of LHF FatigueDecrease urine production Rapid\/irreg heartbeat Congestion Difficulty breathingPink tinged sputum OrthopneaParoxysmal nocturnal orthopneaWeight gain<br>Right heart failure Inability of RV to provide adequate blood flow into pulmonary circulation Cor pulmonale<br>Stage A of HF (ACC\/AHA) Patient has risk factors (CAD) but no symptoms; no structural heart damage<br>Stage B of HF (ACC\/AHA) Patient has structural heart damage(MI), but still has no symptoms<br>Stage C of HF (ACC\/AHA) Patient is symptomatic with alteration in their daily functions due to dyspnea, swelling, etc. This is where the NYHA<\/em> functional classifications come into play.<br>Stage D of HF (ACC\/AHA) End stage heart failure &#8211; have maximize medication&#8217;s to treat it, may need a heart transplant or pacemaker<br>NYHA Functional Classifications Related to the impact on the patients activity caused by the heart failure symptoms<br>NYHA stage I Mild; no limitation of physical activity; ordinary physical activity does not cause symptoms<br>NYHA stage II Mild; slight limitation of physical activity; comfortable at rest; oh no physical activity, results and fatigue, competition, dyspnea, or anginal pain<br>NYHA stage III Moderate; Mark decreasing physical activity; marks, limitation of physical activity; comfortable at rest. Less than ordinary activity, causes fatigue, palpitations, dyspnea, or anginal pain.<br>NYHA stage IV Severe; in ability to carry on any physical activity without discomfort. Symptoms of heart, failure, or the anginal syndrome may be present even at rest. If any physical activities, undertaken, discomfort is increased.<br>aortic stenosis A tight aortic valve impeding blood flow from the left ventricle to aorta.Blood backs up in the left ventricle and decreases blood flow to the body<br>Causes of aortic stenosis Congenital- bicuspid aortic valve Age related calcification (CAD d\/t smoking, HTN, HLD, DM)Rheumatic fever<br>aortic stenosis signs &amp; symptoms<br>aortic stenosis murmur mid-systolic ejection murmur best heard at the 2nd right intercostal space (RU Sternal border)S4 gallopMid-systolic crescendo &#8211; decrescendo murmur, heard loudest at the base and radiating to the neck<br>aortic regurgitation &#8220;&#8221;&#8221;Floppy aortic valve&#8221;&#8221;Blood flows back into LV when aortic valve should be closed&#8221;<br>Aortic regurgitation causes Aneurysmal changes of annulus d\/t:- tertiary syphilis-connective tissues disorder (Marfans, Ehlers) EndocarditisRheumatic fever<br>Aortic regurgitation signs &amp; symptoms FatigueSyncopeSOB that progressively worsensPalpitations Wide pulse pressure (=SBP-DBP)L ventricular dilationCXR pulm edema or cardiomegaly<br>Aortic regurgitation murmur Early diastolic murmur that is high pitched located loudest at the left lower sternal borderDiastolic rumble sound heard at heart&#8217;s apexSystolic crescendo-decrescendo murmur at left upper sternal border<br>Mitral regurgitation &#8220;&#8221;&#8221;Floppy mitral valve&#8221;&#8221;Blood backflows from left ventricle into left atria and into pulmonary circulation&#8221;<br>Causes of mitral regurgitation Anything causing LV dilation:-remodeling post MI-dilated cardiomyopathy Rheumatic fever\/heart diseaseEndocarditis Papillary muscle disfunction\/ruptureChordae tendinae dysfunction\/ruptureCalcification<br>Mitral regurgitation signs &amp; symptoms Acute: papillary muscle rupture-Pulmonary edema\/CHFChronic: dilated ischemic cardiomyopathy-FatigueSOBPulmonary congestion JVDcrackle in basesL atrial enlargement<br>Mitral regurgitation murmur A blowing, holosystolic (pansystolic) murmur at apexRadiates to back and axilla<br>FEV1 forced expiratory volume in 1 second<br>Hypersensitivity Type 1 RASH -Immediate-Atopic dermatitis (widely distributed lesions)<br>mitral valve prolapse When the valve billows or bulges into the left atria.This in itself doesn&#8217;t typically cause a murmur, but if it causes regurgitation it will cause a murmur<br>Mitral valve prolapse causes IdiopathicD\/t connective tissues disorders (Marfans, Ehlers)<br>Mitral Valve Prolapse signs &amp; symptoms Asymptomatic -OR-MVP Syndrome:Atypical chest painPalpitationsSOBdizzinesssyncope<br>Mitral valve prolapse murmur midsystolic click<br>Mitral valve prolapse has increase risk factors for these: Infective endocarditis Certain arrhythmiasProgression to MR<br>mitral valve stenosis &#8220;&#8221;&#8221;Tight mitral valve&#8221;&#8221;Blood cannot pass easily through mitral valve from the left atria to the left ventricle so it backs up in the left atria &amp; in the lungs&#8221;<br>Mitral valve stenosis symptoms S\/s of decrease COFatigueExercise intolerance SOBCoughLA enlargement Pulmonary edema JVDBilat cracklesLVH possibleAfib possible<br>Mitral valve stenosis murmur Diastolic rumbleOpening snap<br>FEV1\/FVC Ratio that is useful in distinguishing between restrictive &amp; obstructive diseases Normal is 70% or less that someone&#8217;s normal<br>Normal FEV1 &gt; 80% predicted<br>Obstructive pulmonary disorders Decreased airflowSOB with exhaleAir trapping after full expirationCOPD &amp; asthma<br>Restrictive pulmonary disorders \u2022Occurs due to decrease compliance of lung tissue\u2022Normal amount of elastin Issue with decreased compliance \u2022Pulmonary fibrosis, decrees compliance equals decrease ventilation, due to amount of air flow into lungs \u2022Not enough in = not enough out<br>TLC for restrictive lung disease &lt; 80% TLC TLC for obstructive lung disease &gt;120 % (hyperinflation)<br>FEV1\/FVC ratio in obstructive disease Less than 70%<br>FEV1\/FVC ratio in restrictive disease Normal or &gt;70%<br>Asthma Chronic disease characterized by airway, inflammation, bronchial, hyperreactivity, and smooth muscle spasm, intermittent, reversible, airflow, obstruction<br>asthma results in Excess mucus production and accumulationHypertrophy of bronchial, smooth muscle Airflow obstruction\/ bronchoconstrictionDecreased alveolar ventilation<br>extrinsic asthma \u2022Triggered by allergic reaction (dust, mold, pollen, pet dander)\u2022 increase IgE levels is diagnostic\u2022 more common in children, males more than females<br>intrinsic asthma \u2022Triggered by a variety of nonallergic factors (chemicals, airborne irritant, infections[viral], exercise, stress, anxiety, GERD, obesity).\u2022No initial elevation in IgE levels\u2022Typically seen in adults over age 40<br>Asthma symptoms CoughingWheezing Shortness of breath TachypneaChest tightness<br>Mucous plugging and pus from inflammatory process in asthma can block alveolar passageways and lead to\u2026.. Air trapping and hyperinflation<br>when are asthma symptoms worse? night and early morning<br>how to diagnose asthma PFT:FEV1\/FVC ration &lt; 70% Methacholine challenge test administer for mildest form of intermittent asthma Short-acting beta2-agonist (SABA) inhalers (albuterol) mild persistent asthma has night symptoms how many days\/month 3-4 Sever persistent asthma has night symptoms how many days\/month Every night COPD diagnosis History of symptomsPhysical examination PFTs- decreased FEV1, unresponsive to bronchodilatorsABG analysis CXR -hyper inflation, flattened diaphragm GOLD staging of COPD GOLD 1: MILD: FEV1 &gt;\/= 80% predictedGOLD 2: MODERATE: FEV1 50-80%GOLD 3: SEVERE: FEV1 30-50%GOLD 4: VERY SEVERE: &lt; 30%<br>Emphysema<br>chronic bronchitis \u2022Damage occurs in the airway\u2022Productive cough w\/ copious amts of sputum \u2022Dyspnea \u2022Wheezing\u2022Rhonchi\u2022cyanosis of skin and mucous membranes\u2022Polycythemia Vera \u2022cor pulmonale<br>Mitral valve stenosis causes Rheumatic fever- group A streptococcus- \u2014 strep pyogenes (pharyngitis) untreated 2-3 weeksEndocarditis<\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"<p>Midterm Exam: NR507\/ NR 507 (Latest 2024\/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A \u2013 Chamberlain Midterm Exam: NR507\/ NR 507 (Latest2024\/ 2025 Update) AdvancedPathophysiology Review| Questions andVerified Answers| 100% Correct |Grade A \u2013ChamberlainQ: Autoimmune disease\u2026Answer:\u2026. can be familial.Q: Hypersensitivity: Type 4Answer:-Delayed-T-cell mediated Q: Treatment of Type 4 RashAnswer:Topical 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