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NURS 5315 Advance Pathophysiology -
Exam 3 - UTA EXAM Questions &
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Mitral Valve Stenosis - (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
Mitral Valve Regurgitation - (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
,2
-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 - (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.
Aortic Valve Regurgitation - (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
,3
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 - (ANSWER)-Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the blood vessel can weaken it)
Diabetes
, 4
Hyperlipidemia (lipids take place of endothelial cells lining the blood vessel,
initiating an inflammatory response)
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory Response -
(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.
Hyperlipidemia - (ANSWER)Leading cause of coronary artery disease
NURS 5315 Advance Pathophysiology -
Exam 3 - UTA EXAM Questions &
Answers, Well Elaborated | Already
Verified Test |100% Verified solutions |
Latest!!
Mitral Valve Stenosis - (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
Mitral Valve Regurgitation - (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
,2
-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 - (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.
Aortic Valve Regurgitation - (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
,3
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 - (ANSWER)-Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the blood vessel can weaken it)
Diabetes
, 4
Hyperlipidemia (lipids take place of endothelial cells lining the blood vessel,
initiating an inflammatory response)
Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory Response -
(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.
Hyperlipidemia - (ANSWER)Leading cause of coronary artery disease
