NURS 5315/ NURS5315 Exam 3 V2 – Advanced Pathophysiology Guide
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Question:
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
Question:
Mitral Valve Regurgitation
Answer -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
Question:
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.
Question:
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)
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)
Question:
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.
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.
Question:
Hyperlipidemia
Answer
Leading cause of coronary artery disease
Most commonly affects promximal portions of coronary arteries, larger branches of carotid arteries, circle of Willis
(base of brain), large vessels of lower extremities, renal arteries, mesenteric (intestinal) arteries
Question:
Consequences of Atherosclerosis
Answer
Reduced blood flow
Coronary artery disease, myocardial infarction, carotid artery disease, cerebral vascular disease, stroke, mesenteric
ischemia, peripheral vascular disease, renal artery stenosis
Question:
Congenital Heart Disease
Answer -Most common heart disease affecting children -Etiology is unknown in 90% of cases
Causes:
Genetic/environmental factors (multifactorial factors)
Primary genetic factors (single gene disorders, chromosome disorders)
Sole environmental factors (Accutane/isotretinoin for acne, alcohol, maternal rubella infection)
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