UTA NURS 5315 Advanced Pathophysiology
Exam 3 – Questions With Applicable Solutions
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Terms in this set (173)
- 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
Mitral Valve Stenosis
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
, -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
Mitral Valve Regurgitation 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
-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
Aortic Valve Stenosis
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.
, -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)
Aortic Valve
-Acute: increases left ventricular end-diastolic
Regurgitation
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.
, -Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting
Atherosclerosis Causes the blood vessel can weaken it)
Diabetes
Hyperlipidemia (lipids take place of endothelial
cells lining the blood vessel, initiating an
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.
Patho of Atherosclerosis
5. Macrophages engulf the LDL particles.
r/t Hyperlipidemia -
6. Macrophages eat too much LDL, causing them to
Inflammatory Response
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.
Exam 3 – Questions With Applicable Solutions
Save
Terms in this set (173)
- 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
Mitral Valve Stenosis
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
, -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
Mitral Valve Regurgitation 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
-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
Aortic Valve Stenosis
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.
, -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)
Aortic Valve
-Acute: increases left ventricular end-diastolic
Regurgitation
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.
, -Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting
Atherosclerosis Causes the blood vessel can weaken it)
Diabetes
Hyperlipidemia (lipids take place of endothelial
cells lining the blood vessel, initiating an
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.
Patho of Atherosclerosis
5. Macrophages engulf the LDL particles.
r/t Hyperlipidemia -
6. Macrophages eat too much LDL, causing them to
Inflammatory Response
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.
