NURS 5315 Advance Pathophysiology - Exam 3 -
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Terms in this set (173)
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 1. Tissue injury to endothelial cells lining the
Hyperlipidemia - Inflammatory blood vessel.
Response 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.
UTA EXAM Questions & Answers, Well
Elaborated | Already Verified Test |100% Verified
solutions | 2026 Latest!!
Save
Terms in this set (173)
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 1. Tissue injury to endothelial cells lining the
Hyperlipidemia - Inflammatory blood vessel.
Response 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.
