NURS 5315 Advance Pathophysiology - Exam 3 -
UTA EXAM Questions & Answers, Well Elaborated
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- 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
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-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 atrium and
Aortic Valve Stenosis 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.
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-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 Regurgitation -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.
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-Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the
Atherosclerosis Causes 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.
5. Macrophages engulf the LDL particles.
Patho of Atherosclerosis
6. Macrophages eat too much LDL, causing them to
r/t Hyperlipidemia -
burst and become foam cells (under a microscope
Inflammatory Response
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.
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