NURS 5315 ADVANCE
PATHOPHYSIOLOGY EXAM
QUESTIONS AND ANSWERS 100% PASS
2026/2027
Mitral Valve Stenosis - ANS - Characterized by NARROWING of mitral valve
- Normal is 4-6 cm
-Narrowed is less than 2.5 cm
- Caused by RHEUMATIC FEVER
-More common in WOMEN
-Oxygenated blood comes back into heart into the left atrium and down through the mitral
valve to the left ventricle
- Complex: Stenosis leads to volume/pressure in left atrium, which results in atrial
hypertrophy/dilation, which increases pressure/volume in the pulmonary circulation & causes
PULMONARY EDEMA
- Simplified: Skinny mitral valve doesn't let blood pass through easily, so blood backs up into the
left atrium and causes it to swell, then backs up into the lung and causes resp. symptoms
-S/sx: dyspnea, hemoptysis, a-fib, dysphagia, pulmonary hypertension
Mitral Valve Regurgitation - ANS -Characterized by INCOMPLETE CLOSURE of mitral valve
-Caused by MITRAL VALVE PROLAPSE (flaps don't close together properly, leaving valve ajar);
more common in WOMEN; STICKING CHEST PAIN
@2026 ALLRIGHTS RESERVED 1
,-Blood in left ventricle backs up to left ventricle during systole (mitral valve should be closed
during systole/contraction of heart)
-Leads to atrial dilation/hypertrophy, increased pulmonary vascular pressure/volume,
PULMONARY EDEMA
-S/sx: Dyspnea, rales, pansystolic murmur, S3 & S4 heart sounds
Aortic Valve Stenosis - ANS -Most common valvular disease
-Most common causes are aortic valve CALCIFICATION (stiffening) in people over 60; congenital
aortic valve stenosis in people less than 30
-Normal valve 3 cm; symptoms seen when valve less than 1 cm; severe when valve is less than
0.5 cm
-Narrowed valve prevents outflow from left ventricle to aorta. This backs up blood to the left
atrium and ultimately floods the lung causing PULMONARY EDEMA
S/Sx: Pulmonary hypertension/edema, poor outflow of aorta to body (aorta sends out
oxygenated blood to body), causing fainting or chest pain
Simplified: Aorta is stiff and can't send out oxygenated blood properly to the body, depriving
tissues of oxygen. Blood gets backed up into lungs, causing pulmonary edema.
Aortic Valve Regurgitation - ANS -Valve is TOO WIDE or TOO NARROW, blood doesn't pass
through effectively, causing back flow of blood into the left ventricle
-Marked by EARLY DIASTOLIC MURMUR (on systole, heart contracts and pushes blood up the
aorta, but on diastole, heart relaxes and ineffective aortic valve is not able to hold blood up in
aorta, so blood falls and makes a swish sound, which is the murmur)
-Most commonly caused by AORTIC ROOT DILATION(starting point of aorta is too wide)
-Other causes: infective endocarditis, rheumatic fever, aortitis from syphilis, coarctation
(congenital narrowing of aorta), aortic dissection (tear), ankylosing spondylitis (inflammatory
arthritis)
@2026 ALLRIGHTS RESERVED 2
,-Acute: increases left ventricular end-diastolic pressure (LVEDP) (increased blood back down in
the left ventricle increases pressure), decreased stroke volume (not much blood is being pushed
from left ventricle because blood's backed up and overwhelming left ventricle), normal or
decreased pulse pressure, decreased cardiac output (aorta is not effectively pumping blood
from heart)
Chronic: Body adjusts; LVEDP normalizes, systolic bp increases (compensation: harder
contraction to push blood out of aorta before it falls back down to left ventricle), diastolic bp
decreases (compensation: decreased relaxation of heart to stop blood from seeping back out of
aorta), cardiac output is normal, pulse pressure is increase. Blood ultimately is backed up into
the left atrium and pulmonary circulation.
Atherosclerosis Causes - ANS -Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the blood vessel can weaken it)
Diabetes
Hyperlipidemia (lipids take place of endothelial cells lining the blood vessel, initiating an
inflammatory response)
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory Response - ANS 1. Tissue injury to
endothelial cells lining the blood vessel.
2. Endothelial cells become inflammed and unable to produce sufficient antithrombotic and
vasodilating cytokines, increasing risk for clot formation and creating a tighter space for plaques
and clots to grow.
3. Macrophages and platelets are called to the area of injury, further congesting the growing
plaque area.
4. LDL replaces endothelial cells in the lining of the blood vessel.
5. Macrophages engulf the LDL particles.
@2026 ALLRIGHTS RESERVED 3
, 6. Macrophages eat too much LDL, causing them to burst and become foam cells (under a
microscope they look like sea foam)
7. Accumulation of foam cells causes a fatty streak. Fatting streak further triggers inflammatory
responses, repeating the whole cycle, and growing the fatty streak.
8. Smooth muscle hyperplasia from all the inflammation grows, produces collagen, and covers
the fatty streak to create a fibrous plaque.
9. The plaque may calcify, protrude into the vessel, and occlude blood flow, resulting in ischemia
or infarction.
Hyperlipidemia - ANS Leading cause of coronary artery disease
Most commonly affects promximal portions of coronary arteries, larger branches of carotid
arteries, circle of Willis (base of brain), large vessels of lower extremities, renal arteries,
mesenteric (intestinal) arteries
Consequences of Atherosclerosis - ANS Reduced blood flow
Coronary artery disease, myocardial infarction, carotid artery disease, cerebral vascular disease,
stroke, mesenteric ischemia, peripheral vascular disease, renal artery stenosis
Congenital Heart Disease - ANS -Most common heart disease affecting children
-Etiology is unknown in 90% of cases
Causes:
Genetic/environmental factors (multifactorial factors)
Primary genetic factors (single gene disorders, chromosome disorders)
Sole environmental factors (Accutane/isotretinoin for acne, alcohol, maternal rubella infection)
@2026 ALLRIGHTS RESERVED 4
PATHOPHYSIOLOGY EXAM
QUESTIONS AND ANSWERS 100% PASS
2026/2027
Mitral Valve Stenosis - ANS - Characterized by NARROWING of mitral valve
- Normal is 4-6 cm
-Narrowed is less than 2.5 cm
- Caused by RHEUMATIC FEVER
-More common in WOMEN
-Oxygenated blood comes back into heart into the left atrium and down through the mitral
valve to the left ventricle
- Complex: Stenosis leads to volume/pressure in left atrium, which results in atrial
hypertrophy/dilation, which increases pressure/volume in the pulmonary circulation & causes
PULMONARY EDEMA
- Simplified: Skinny mitral valve doesn't let blood pass through easily, so blood backs up into the
left atrium and causes it to swell, then backs up into the lung and causes resp. symptoms
-S/sx: dyspnea, hemoptysis, a-fib, dysphagia, pulmonary hypertension
Mitral Valve Regurgitation - ANS -Characterized by INCOMPLETE CLOSURE of mitral valve
-Caused by MITRAL VALVE PROLAPSE (flaps don't close together properly, leaving valve ajar);
more common in WOMEN; STICKING CHEST PAIN
@2026 ALLRIGHTS RESERVED 1
,-Blood in left ventricle backs up to left ventricle during systole (mitral valve should be closed
during systole/contraction of heart)
-Leads to atrial dilation/hypertrophy, increased pulmonary vascular pressure/volume,
PULMONARY EDEMA
-S/sx: Dyspnea, rales, pansystolic murmur, S3 & S4 heart sounds
Aortic Valve Stenosis - ANS -Most common valvular disease
-Most common causes are aortic valve CALCIFICATION (stiffening) in people over 60; congenital
aortic valve stenosis in people less than 30
-Normal valve 3 cm; symptoms seen when valve less than 1 cm; severe when valve is less than
0.5 cm
-Narrowed valve prevents outflow from left ventricle to aorta. This backs up blood to the left
atrium and ultimately floods the lung causing PULMONARY EDEMA
S/Sx: Pulmonary hypertension/edema, poor outflow of aorta to body (aorta sends out
oxygenated blood to body), causing fainting or chest pain
Simplified: Aorta is stiff and can't send out oxygenated blood properly to the body, depriving
tissues of oxygen. Blood gets backed up into lungs, causing pulmonary edema.
Aortic Valve Regurgitation - ANS -Valve is TOO WIDE or TOO NARROW, blood doesn't pass
through effectively, causing back flow of blood into the left ventricle
-Marked by EARLY DIASTOLIC MURMUR (on systole, heart contracts and pushes blood up the
aorta, but on diastole, heart relaxes and ineffective aortic valve is not able to hold blood up in
aorta, so blood falls and makes a swish sound, which is the murmur)
-Most commonly caused by AORTIC ROOT DILATION(starting point of aorta is too wide)
-Other causes: infective endocarditis, rheumatic fever, aortitis from syphilis, coarctation
(congenital narrowing of aorta), aortic dissection (tear), ankylosing spondylitis (inflammatory
arthritis)
@2026 ALLRIGHTS RESERVED 2
,-Acute: increases left ventricular end-diastolic pressure (LVEDP) (increased blood back down in
the left ventricle increases pressure), decreased stroke volume (not much blood is being pushed
from left ventricle because blood's backed up and overwhelming left ventricle), normal or
decreased pulse pressure, decreased cardiac output (aorta is not effectively pumping blood
from heart)
Chronic: Body adjusts; LVEDP normalizes, systolic bp increases (compensation: harder
contraction to push blood out of aorta before it falls back down to left ventricle), diastolic bp
decreases (compensation: decreased relaxation of heart to stop blood from seeping back out of
aorta), cardiac output is normal, pulse pressure is increase. Blood ultimately is backed up into
the left atrium and pulmonary circulation.
Atherosclerosis Causes - ANS -Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the blood vessel can weaken it)
Diabetes
Hyperlipidemia (lipids take place of endothelial cells lining the blood vessel, initiating an
inflammatory response)
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory Response - ANS 1. Tissue injury to
endothelial cells lining the blood vessel.
2. Endothelial cells become inflammed and unable to produce sufficient antithrombotic and
vasodilating cytokines, increasing risk for clot formation and creating a tighter space for plaques
and clots to grow.
3. Macrophages and platelets are called to the area of injury, further congesting the growing
plaque area.
4. LDL replaces endothelial cells in the lining of the blood vessel.
5. Macrophages engulf the LDL particles.
@2026 ALLRIGHTS RESERVED 3
, 6. Macrophages eat too much LDL, causing them to burst and become foam cells (under a
microscope they look like sea foam)
7. Accumulation of foam cells causes a fatty streak. Fatting streak further triggers inflammatory
responses, repeating the whole cycle, and growing the fatty streak.
8. Smooth muscle hyperplasia from all the inflammation grows, produces collagen, and covers
the fatty streak to create a fibrous plaque.
9. The plaque may calcify, protrude into the vessel, and occlude blood flow, resulting in ischemia
or infarction.
Hyperlipidemia - ANS Leading cause of coronary artery disease
Most commonly affects promximal portions of coronary arteries, larger branches of carotid
arteries, circle of Willis (base of brain), large vessels of lower extremities, renal arteries,
mesenteric (intestinal) arteries
Consequences of Atherosclerosis - ANS Reduced blood flow
Coronary artery disease, myocardial infarction, carotid artery disease, cerebral vascular disease,
stroke, mesenteric ischemia, peripheral vascular disease, renal artery stenosis
Congenital Heart Disease - ANS -Most common heart disease affecting children
-Etiology is unknown in 90% of cases
Causes:
Genetic/environmental factors (multifactorial factors)
Primary genetic factors (single gene disorders, chromosome disorders)
Sole environmental factors (Accutane/isotretinoin for acne, alcohol, maternal rubella infection)
@2026 ALLRIGHTS RESERVED 4
