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NR 507 – Advanced Pathophysiology Midterm Review Practice Questions Study Guide Latest Edition (2026)

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This document provides a comprehensive study guide for NR 507 Advanced Pathophysiology midterm examination preparation, updated for 2026. It includes revision materials and practice questions covering essential concepts such as cellular adaptations, genetic and developmental disorders, inflammation and immunity, fluid and electrolyte imbalances, acid-base disturbances, and pathophysiological alterations affecting the cardiovascular, respiratory, endocrine, renal, gastrointestinal, neurological, and hematologic systems. The material is designed to support structured revision, reinforce critical disease process concepts, and improve preparedness for examinations and advanced nursing practice. References to “correct answers” are intended as study support and should not be interpreted as official examination materials or guarantees of future performance.

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ADVANCED PATHOPHYSIOLOGY
MIDTERM REVIEW NR507 LATEST
UPDATE PRACTICE QUESTIONS WITH
CORRECT ANSWERS 2026
Glomerulonephritis - ans-The glomerular-capillaries can trap blood-borne Ab & Ag-
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Ab complexes
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- Causes: PRIMARY: infection, drugs, toxins, vascular disorders, ischemia, immunolo
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gic responses, free radicals. SECONDARY: DM, CHF, HIV, Lupus
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Triggering event (infection)- Ag-Ab complex formation & deposition in glomerulus-
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Activation of complement system & WBC infiltration- Glomerular injury & leakage-
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Proteinuria/hematuria- edema, increase creat, azotemia, oliguria
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OR
after glomerular injury & leakage-
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Coagulation cascade activation & FIbrin deposition- Decreased capillary perfusion-
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decreased GFR- edema, increase creat, azotemia, oliguria
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S1 - ans--Closing of mitral and tricuspid valve
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- Beginning of systole
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S2 - ans-- Closure of the aortic and pulmonic valve
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- End of systole
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Valvular stenosis - ans- ws ws ws


the valve orifice is constricted and narrowed, impeding the forward flow of blood and
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increasing the workload of the cardiac chamber proximal to the diseased valve. Intr
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aventricular or atrial pressure increases in the chamber to overcome resistance to fl
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ow through the valve. Increased pressure causes the myocardium to work harder, c
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ausing myocardial hypertrophy.
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Aortic stenosis - ans-- LV hypertrophy
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- L heart failure
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- Pulmonary edema
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- Exertional dyspnea
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-Syncope
-Angina pectoris ws


- Systolic murmur
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, Mitral Stenosis - ans-- LA hypertrophy
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-R ventricular failure
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- Pulmonary edema
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- Orthopnea
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- Respiratory infection s
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- PH
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-Edema
-Atypical chest pain ws ws


- Diastolic murmur
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Stroke volume - ans-The volume of blood ejected per bear during systole
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Cor Pulmonale - ans-
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right ventricular hypertrophy and heart failure due to pulmonary hypertension
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Cardiac output - ans-HR x SV
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-Normal= 5Lpm ws


-Preload, afterload, contractility, heart rate
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Preload - ans-The volume inside the ventricle at the end of diastole
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Determined by: ws


- Amount of venous blood returning to the ventricle during diastole
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- The amount of blood in the ventricle after systole
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Afterload - ans-The resistance to ejection of blood from the ventricle
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total peripheral resistance (TPR)
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Systemic vascular resistance (SVR) ws ws ws




Contractility - ans-sympathetic nervous system, epi and norepi) + inotropes
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Acetylcholine released from vagus nerve - inotrope ws ws ws ws ws ws




Cytokines released during sepsis impair contractility
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O2 < 50% decreased contractility
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Troponin - ans-Relaxing proteinws ws ws ws




Troponin T- aids in binding the troponin complex to actin and tropomyosin
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Troponin I- Inhibits the ATPhase of actomyosin
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