NURS 5315 Advanced Pathophysiology
Final Exam Questions and Answers (2026 /
2027) (Real Exam Verified Answers)
• Mitral Valve Stenosis -✓✓- 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 -✓✓-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
-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 -✓✓-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 -✓✓-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)
-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 -✓✓-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 -✓✓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.
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 -✓✓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 -✓✓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 -✓✓-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)
Maternal Risk Factors:
Age over 45, prior child with heart defect, poorly controlled diabetes during pregnancy,
alcohol, congenital infection during pregnancy (rubella), aspirin, lupus,
Dilantin/phenytoin/diphenylhydantoin for seizures
• LEFT to RIGHT shunt (Congenital heart defect) -✓✓-Oxygenated blood from the left
side of the heart mixes with unoxygenated blood in the right side of the heart.
-Oxygen saturation on left side is usually 95%, whereas right side is 75%
- As blood mixes, right side's oxygen saturation increases to 80% or more
-VOLUME OVERLOAD occurs on RIGHT side of heart occurs, leading to PULMONARY
HYPERTENSION, which causes RIGHT VENTRICULAR HYPERTROPHY, (secondary
to pulm. hptn.), and LEFT VENTRICULAR HYPERTROPHY(secondary to blood being
returned to left ventricle)
Eisenmenger Syndrome: Reversal of left to right shunt to a right to left shunt.
• Eisenmenger Syndrome -✓✓1. Increased blood flow returns to lungs rather than to the
rest of the body.
2. Blood vessels become stiff and narrow - permanent damage.
3. Increased pressure of the blood flow in the lung becomes so great that the direction
of blood flow through the shunt reverses.
Final Exam Questions and Answers (2026 /
2027) (Real Exam Verified Answers)
• Mitral Valve Stenosis -✓✓- 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 -✓✓-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
-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 -✓✓-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 -✓✓-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)
-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 -✓✓-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 -✓✓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.
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 -✓✓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 -✓✓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 -✓✓-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)
Maternal Risk Factors:
Age over 45, prior child with heart defect, poorly controlled diabetes during pregnancy,
alcohol, congenital infection during pregnancy (rubella), aspirin, lupus,
Dilantin/phenytoin/diphenylhydantoin for seizures
• LEFT to RIGHT shunt (Congenital heart defect) -✓✓-Oxygenated blood from the left
side of the heart mixes with unoxygenated blood in the right side of the heart.
-Oxygen saturation on left side is usually 95%, whereas right side is 75%
- As blood mixes, right side's oxygen saturation increases to 80% or more
-VOLUME OVERLOAD occurs on RIGHT side of heart occurs, leading to PULMONARY
HYPERTENSION, which causes RIGHT VENTRICULAR HYPERTROPHY, (secondary
to pulm. hptn.), and LEFT VENTRICULAR HYPERTROPHY(secondary to blood being
returned to left ventricle)
Eisenmenger Syndrome: Reversal of left to right shunt to a right to left shunt.
• Eisenmenger Syndrome -✓✓1. Increased blood flow returns to lungs rather than to the
rest of the body.
2. Blood vessels become stiff and narrow - permanent damage.
3. Increased pressure of the blood flow in the lung becomes so great that the direction
of blood flow through the shunt reverses.
