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Examen

ADVANCED PATHOPHYSIOLOGY Midterm REVIEW NR507 QUESTIONS WITH Verified Answers

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Glomerulonephritis - ANSWERSThe glomerular-capillaries can trap blood-borne Ab & Ag-Ab complexes - Causes: PRIMARY: infection, drugs, toxins, vascular disorders, ischemia, immunologic responses, free radicals. SECONDARY: DM, CHF, HIV, Lupus Triggering event (infection)- Ag-Ab complex formation & deposition in glomerulus- Activation of complement system & WBC infiltration- Glomerular injury & leakage- Proteinuria/hematuria- edema, increase creat, azotemia, oliguria OR after glomerular injury & leakage- Coagulation cascade activation & FIbrin deposition- Decreased capillary perfusion- decreased GFR- edema, increase creat, azotemia, oliguria S1 - ANSWERS-Closing of mitral and tricuspid valve - Beginning of systole S2 - ANSWERS- Closure of the aortic and pulmonic valve - End of systole Valvular stenosis - ANSWERSthe valve orifice is constricted and narrowed, impeding the forward flow of blood and increasing the workload of the cardiac chamber proximal to the diseased valve. Intraventricular or atrial pressure increases in the chamber to overcome resistance to flow through the valve. Increased pressure causes the myocardium to work harder, causing myocardial hypertrophy. Aortic stenosis - ANSWERS- LV hypertrophy - L heart failure - Pulmonary edema - Exertional dyspnea -Syncope -Angina pectoris - Systolic murmur Mitral Stenosis - ANSWERS- LA hypertrophy -R ventricular failure - Pulmonary edema - Orthopnea - Respiratory infections - PH -Edema -Atypical chest pain - Diastolic murmur Stroke volume - ANSWERSThe volume of blood ejected per bear during systole Cor Pulmonale - ANSWERSright ventricular hypertrophy and heart failure due to pulmonary hypertension Cardiac output - ANSWERSHR x SV -Normal= 5Lpm -Preload, afterload, contractility, heart rate Preload - ANSWERSThe volume inside the ventricle at the end of diastole Determined by: - Amount of venous blood returning to the ventricle during diastole - The amount of blood in the ventricle after systole Afterload - ANSWERSThe resistance to ejection of blood from the ventricle total peripheral resistance (TPR) Systemic vascular resistance (SVR) Contractility - ANSWERSsympathetic nervous system, epi and norepi) + inotropes Acetylcholine released from vagus nerve - inotrope Cytokines released during sepsis impair contractility O2 50% decreased contractility Troponin - ANSWERSRelaxing protein Troponin T- aids in binding the troponin complex to actin and tropomyosin Troponin I- Inhibits the ATPhase of actomyosin Troponin C- Binding sites for the calcium ions involved in contraction. I & T and released into the blood during myocardial injury calcium binding and troponin - ANSWERSIn resting muscle the myosin-binding sites are covered by troponin and tropomyosin. The calcium ions released into the sarcoplasm as a result of the action potential bind to the troponin. This binding causes the tropomyosin and troponin to move out of the way of the myosin-binding sites, leaving the myosin heads free to bind to the actin microfilament.

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ADVANCED PATHOPHYSIOLOGY
Midterm REVIEW NR507 QUESTIONS
WITH Verified Answers
Glomerulonephritis - ANSWERSThe glomerular-capillaries can trap blood-borne Ab &
Ag-Ab complexes
- Causes: PRIMARY: infection, drugs, toxins, vascular disorders, ischemia, immunologic
responses, free radicals. SECONDARY: DM, CHF, HIV, Lupus

Triggering event (infection)- Ag-Ab complex formation & deposition in glomerulus-
Activation of complement system & WBC infiltration- Glomerular injury & leakage-
Proteinuria/hematuria- edema, increase creat, azotemia, oliguria
OR
after glomerular injury & leakage- Coagulation cascade activation & FIbrin deposition-
Decreased capillary perfusion- decreased GFR- edema, increase creat, azotemia,
oliguria

S1 - ANSWERS-Closing of mitral and tricuspid valve
- Beginning of systole

S2 - ANSWERS- Closure of the aortic and pulmonic valve
- End of systole

Valvular stenosis - ANSWERSthe valve orifice is constricted and narrowed, impeding
the forward flow of blood and increasing the workload of the cardiac chamber proximal
to the diseased valve. Intraventricular or atrial pressure increases in the chamber to
overcome resistance to flow through the valve. Increased pressure causes the
myocardium to work harder, causing myocardial hypertrophy.

Aortic stenosis - ANSWERS- LV hypertrophy
- L heart failure
- Pulmonary edema
- Exertional dyspnea
-Syncope
-Angina pectoris
- Systolic murmur

Mitral Stenosis - ANSWERS- LA hypertrophy
-R ventricular failure
- Pulmonary edema
- Orthopnea
- Respiratory infections

, - PH
-Edema
-Atypical chest pain
- Diastolic murmur

Stroke volume - ANSWERSThe volume of blood ejected per bear during systole

Cor Pulmonale - ANSWERSright ventricular hypertrophy and heart failure due to
pulmonary hypertension

Cardiac output - ANSWERSHR x SV
-Normal= 5Lpm
-Preload, afterload, contractility, heart rate

Preload - ANSWERSThe volume inside the ventricle at the end of diastole

Determined by:
- Amount of venous blood returning to the ventricle during diastole
- The amount of blood in the ventricle after systole

Afterload - ANSWERSThe resistance to ejection of blood from the ventricle

total peripheral resistance (TPR)

Systemic vascular resistance (SVR)

Contractility - ANSWERSsympathetic nervous system, epi and norepi) + inotropes

Acetylcholine released from vagus nerve - inotrope

Cytokines released during sepsis impair contractility

O2 < 50% decreased contractility

Troponin - ANSWERSRelaxing protein

Troponin T- aids in binding the troponin complex to actin and tropomyosin

Troponin I- Inhibits the ATPhase of actomyosin

Troponin C- Binding sites for the calcium ions involved in contraction.

I & T and released into the blood during myocardial injury

calcium binding and troponin - ANSWERSIn resting muscle the myosin-binding sites are
covered by troponin and tropomyosin. The calcium ions released into the sarcoplasm as

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Subido en
3 de agosto de 2025
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2025/2026
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