TEST 3 - Advanced Pathophysiology Summer UTA 5315
- Characterized by NARROWING of mi-
tral 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 ventri-
cle
- Complex: Stenosis leads to vol-
Mitral Valve Stenosis ume/pressure in left atrium, which re-
sults in atrial hypertrophy/dilation, which
increases pressure/volume in the pul-
monary circulation & causes PUL-
MONARY 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, dys-
phagia, pulmonary hypertension
-Characterized by INCOMPLETE CLO-
SURE 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
Mitral Valve Regurgitation left ventricle during systole (mitral valve
should be closed during systole/contrac-
tion of heart)
-Leads to atrial dilation/hypertrophy,
increased pulmonary vascular pres-
sure/volume, PULMONARY EDEMA
-S/sx: Dyspnea, rales, pansystolic mur-
mur, S3 & S4 heart sounds
,TEST 3 - Advanced Pathophysiology Summer UTA 5315
-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
Aortic Valve Stenosis 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 pul-
monary edema.
,TEST 3 - Advanced Pathophysiology Summer UTA 5315
-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 MUR-
MUR (on systole, heart contracts and
pushes blood up the aorta, but on dias-
tole, 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 aor-
ta), aortic dissection (tear), ankylosing
Aortic Valve Regurgitation spondylitis (inflammatory arthritis)
-Acute: increases left ventricular end-di-
astolic pressure (LVEDP) (increased
blood back down in the left ven-
tricle increases pressure), decreased
stroke volume (not much blood is be-
ing pushed from left ventricle because
blood's backed up and overwhelming left
ventricle), normal or decreased pulse
pressure, decreased cardiac output (aor-
ta is not effectively pumping blood from
heart)
Chronic: Body adjusts; LVEDP normal-
izes, systolic bp increases (compensa-
tion: harder contraction to push blood out
of aorta before it falls back down to left
ventricle), diastolic bp decreases (com-
pensation: decreased relaxation of heart
, TEST 3 - Advanced Pathophysiology Summer UTA 5315
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 pul-
monary circulation.
-Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the
blood hitting the blood vessel can weak-
Atherosclerosis Causes
en it)
Diabetes
Hyperlipidemia (lipids take place of en-
dothelial cells lining the blood vessel, ini-
tiating an inflammatory response)
1. Tissue injury to endothelial cells lining
the blood vessel.
2. Endothelial cells become inflammed
and unable to produce sufficient an-
tithrombotic and vasodilating cytokines,
increasing risk for clot formation and cre-
ating 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.
Patho of Atherosclerosis r/t Hyperlipi-
4. LDL replaces endothelial cells in the
demia - Inflammatory Response
lining of the blood vessel.
5. Macrophages engulf the LDL particles.
6. Macrophages eat too much LDL, caus-
ing 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
