©SOPHIABENNETT@2024-2025 Monday, August 19, 2024 12:35 AM
TEST 3 - Advanced Pathophysiology
Summer 2024 UTA 5315 Practice
Questions and Answers
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
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-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 - 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.
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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 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)
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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
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.
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