NR 507 Midterm EXAM NEWEST 2026 ACTUAL EXAM
COMPLETE 200 QUESTIONS AND CORRECT DETAILED
ANSWERS (VERIFIED ANSWERS) ALREADY GRADED
A+BRAND NEW!!.pdf
riggering 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 - ANSWER/-Closing of mitral and tricuspid valve
- Beginning of systole
S2 - ANSWER/- Closure of the aortic and pulmonic valve
- End of systole
Valvular stenosis - ANSWER/the 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 - ANSWER/- LV hypertrophy
- L heart failure
- Pulmonary edema
- Exertional dyspnea
-Syncope
-Angina pectoris
- Systolic murmur
Mitral Stenosis - ANSWER/- LA hypertrophy
-R ventricular failure
- Pulmonary edema
- Orthopnea
- Respiratory infections
,- PH
-Edema
-Atypical chest pain
- Diastolic murmur
Stroke volume - ANSWER/The volume of blood ejected per bear during systole
Cor Pulmonale - ANSWER/right ventricular hypertrophy and heart failure due to
pulmonary hypertension
Cardiac output - ANSWER/HR x SV
-Normal= 5Lpm
-Preload, afterload, contractility, heart rate
Preload - ANSWER/The 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 - ANSWER/The resistance to ejection of blood from the ventricle
total peripheral resistance (TPR)
Systemic vascular resistance (SVR)
Contractility - ANSWER/sympathetic nervous system, epi and norepi) + inotropes
Acetylcholine released from vagus nerve - inotrope
Cytokines released during sepsis impair contractility
O2 < 50% decreased contractility
Troponin - ANSWER/Relaxing 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 - ANSWER/In 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.
Macrophages - ANSWER/-Phagocytic cells
-Involved in the activation of the adaptive immune system
-The primary cells that infiltrate tissue in wounds, remove cells and debris, promote
angiogenesis, and produce cytokines and growth factors that suppress further
inflammation and initiate healing by promoting epithelial cell division, activating
fibroblasts and promote synthesis of extracellular matrix and collagen.
- May appear at inflammatory site at 24 hours (but usually not until 3-7 days later)
- Survive and dive in the acidic inflammatory site
Perfusion - ANSWER/Blood circulating past the alveloi
Bronchioles - ANSWER/Three layer tube like structure surrounding the lumen of air
passageway
transition from cartilage to smooth muscle
Parasympathetic stimulation releases acetylcholine for bronchial constriction=
decreased airflow *dominates*
Sympathetic stimulation by epi binds to b-adrendergic receptors to bronchial
dilation=increased airflow
air trapping in asthma - ANSWER/Mast cell degranulation, triggered by the excessive
amounts of IGE that have formed this individual, will bind the allergen as it enters the
airway. Mast cell degranulation releases chemicals that releases mucus production and
accumulation as well as chemicals that contribute to smooth muscle constriction. that
smooth muscle constriction along with mucus plugs that form, result in hyperinflation of
the alveoli and eventual erosion of airway tissue
Asthma - ANSWER/- inflammation of the bronchial mucosa that causes bronchial
hyperresponsiveness, bronchoconstriction, variable airflow obstruction that is reversible.
-Symptoms: chest constriction, exp wheezing, dyspnea, coughing, tachycardia,
tachypnea
-Beta-agonist inhaler, inhaled corticosteroids,
-Anticholinergic drugs:Block acetylcholine binding in the lung. Promotes bronchodilation
through decrease parasympathetic response (tiotropium, ipratropium)
Polycythemia vera - ANSWER/chronic, progressive disease that is characterized by
overgrowth of the bone marrow, excessive red blood cell production, and an enlarged
spleen and causes headache, inability to concentrate, and pain in the fingers and toes
COMPLETE 200 QUESTIONS AND CORRECT DETAILED
ANSWERS (VERIFIED ANSWERS) ALREADY GRADED
A+BRAND NEW!!.pdf
riggering 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 - ANSWER/-Closing of mitral and tricuspid valve
- Beginning of systole
S2 - ANSWER/- Closure of the aortic and pulmonic valve
- End of systole
Valvular stenosis - ANSWER/the 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 - ANSWER/- LV hypertrophy
- L heart failure
- Pulmonary edema
- Exertional dyspnea
-Syncope
-Angina pectoris
- Systolic murmur
Mitral Stenosis - ANSWER/- LA hypertrophy
-R ventricular failure
- Pulmonary edema
- Orthopnea
- Respiratory infections
,- PH
-Edema
-Atypical chest pain
- Diastolic murmur
Stroke volume - ANSWER/The volume of blood ejected per bear during systole
Cor Pulmonale - ANSWER/right ventricular hypertrophy and heart failure due to
pulmonary hypertension
Cardiac output - ANSWER/HR x SV
-Normal= 5Lpm
-Preload, afterload, contractility, heart rate
Preload - ANSWER/The 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 - ANSWER/The resistance to ejection of blood from the ventricle
total peripheral resistance (TPR)
Systemic vascular resistance (SVR)
Contractility - ANSWER/sympathetic nervous system, epi and norepi) + inotropes
Acetylcholine released from vagus nerve - inotrope
Cytokines released during sepsis impair contractility
O2 < 50% decreased contractility
Troponin - ANSWER/Relaxing 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 - ANSWER/In 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.
Macrophages - ANSWER/-Phagocytic cells
-Involved in the activation of the adaptive immune system
-The primary cells that infiltrate tissue in wounds, remove cells and debris, promote
angiogenesis, and produce cytokines and growth factors that suppress further
inflammation and initiate healing by promoting epithelial cell division, activating
fibroblasts and promote synthesis of extracellular matrix and collagen.
- May appear at inflammatory site at 24 hours (but usually not until 3-7 days later)
- Survive and dive in the acidic inflammatory site
Perfusion - ANSWER/Blood circulating past the alveloi
Bronchioles - ANSWER/Three layer tube like structure surrounding the lumen of air
passageway
transition from cartilage to smooth muscle
Parasympathetic stimulation releases acetylcholine for bronchial constriction=
decreased airflow *dominates*
Sympathetic stimulation by epi binds to b-adrendergic receptors to bronchial
dilation=increased airflow
air trapping in asthma - ANSWER/Mast cell degranulation, triggered by the excessive
amounts of IGE that have formed this individual, will bind the allergen as it enters the
airway. Mast cell degranulation releases chemicals that releases mucus production and
accumulation as well as chemicals that contribute to smooth muscle constriction. that
smooth muscle constriction along with mucus plugs that form, result in hyperinflation of
the alveoli and eventual erosion of airway tissue
Asthma - ANSWER/- inflammation of the bronchial mucosa that causes bronchial
hyperresponsiveness, bronchoconstriction, variable airflow obstruction that is reversible.
-Symptoms: chest constriction, exp wheezing, dyspnea, coughing, tachycardia,
tachypnea
-Beta-agonist inhaler, inhaled corticosteroids,
-Anticholinergic drugs:Block acetylcholine binding in the lung. Promotes bronchodilation
through decrease parasympathetic response (tiotropium, ipratropium)
Polycythemia vera - ANSWER/chronic, progressive disease that is characterized by
overgrowth of the bone marrow, excessive red blood cell production, and an enlarged
spleen and causes headache, inability to concentrate, and pain in the fingers and toes
