NURS 5315 ADVANCED PATHOPHYSIOLOGY EXAM 3 QUESTIONS & ANSWERS 2026-2…
P R O F E S S I O N A L P R A C T I C E M AT E R I A L S
NURS 5315 Advanced
Pathophysiology Exam 3
Questions & Answers 2026-
2027 | UTA | Updated Exam
(Rationales)
Verified Answers Exam Ready With Rationales 173 QUESTIONS
DOCUMENT OVERVIEW
This document contains 173 verified advanced pathophysiology exam questions with
correct answers and detailed rationales, including diagrams. It offers a comprehensive
study resource for cardiovascular, neurological, and immunological conditions. Students
can effectively utilize this material for in-depth learning, exam preparation, and certification
review.
TOPICS
• Valvular Heart Disease • Atherosclerosis & CAD
• Congenital Heart Defects • Heart Failure
• Respiratory Pathophysiology • Shock & Hemodynamics
• Traumatic Brain Injury • Cerebrovascular Disorders
• Seizures & Epilepsy • Neurological Infections &
Degenerative Diseases
• Cranial Nerves
Page 1
, E XA M Q U EST I O N S
Q1 QUESTION 1 OF 173
Mitral Valve Stenosis
CORRECT ANSWER
- 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
Q2 QUESTION 2 OF 173
Mitral Valve Regurgitation
CORRECT ANSWER
-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
Q3 QUESTION 3 OF 173
Aortic Valve Stenosis
Page 2
, CORRECT ANSWER
-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.
Q4 QUESTION 4 OF 173
Aortic Valve Regurgitation
CORRECT ANSWER
-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.
Q5 QUESTION 5 OF 173
Atherosclerosis Causes
Page 3
, CORRECT ANSWER
-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)
RATIONALE
Atherosclerosis initiates with endothelial injury from various insults like toxins, hypertension, or
hyperlipidemia, triggering an inflammatory response that leads to plaque formation. This process
highlights the vascular endothelium's susceptibility to injury as the primary step in atherogenesis.
Q6 QUESTION 6 OF 173
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory Response
CORRECT ANSWER
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.
Q7 QUESTION 7 OF 173
Hyperlipidemia
Page 4
P R O F E S S I O N A L P R A C T I C E M AT E R I A L S
NURS 5315 Advanced
Pathophysiology Exam 3
Questions & Answers 2026-
2027 | UTA | Updated Exam
(Rationales)
Verified Answers Exam Ready With Rationales 173 QUESTIONS
DOCUMENT OVERVIEW
This document contains 173 verified advanced pathophysiology exam questions with
correct answers and detailed rationales, including diagrams. It offers a comprehensive
study resource for cardiovascular, neurological, and immunological conditions. Students
can effectively utilize this material for in-depth learning, exam preparation, and certification
review.
TOPICS
• Valvular Heart Disease • Atherosclerosis & CAD
• Congenital Heart Defects • Heart Failure
• Respiratory Pathophysiology • Shock & Hemodynamics
• Traumatic Brain Injury • Cerebrovascular Disorders
• Seizures & Epilepsy • Neurological Infections &
Degenerative Diseases
• Cranial Nerves
Page 1
, E XA M Q U EST I O N S
Q1 QUESTION 1 OF 173
Mitral Valve Stenosis
CORRECT ANSWER
- 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
Q2 QUESTION 2 OF 173
Mitral Valve Regurgitation
CORRECT ANSWER
-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
Q3 QUESTION 3 OF 173
Aortic Valve Stenosis
Page 2
, CORRECT ANSWER
-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.
Q4 QUESTION 4 OF 173
Aortic Valve Regurgitation
CORRECT ANSWER
-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.
Q5 QUESTION 5 OF 173
Atherosclerosis Causes
Page 3
, CORRECT ANSWER
-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)
RATIONALE
Atherosclerosis initiates with endothelial injury from various insults like toxins, hypertension, or
hyperlipidemia, triggering an inflammatory response that leads to plaque formation. This process
highlights the vascular endothelium's susceptibility to injury as the primary step in atherogenesis.
Q6 QUESTION 6 OF 173
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory Response
CORRECT ANSWER
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.
Q7 QUESTION 7 OF 173
Hyperlipidemia
Page 4
