Valvular Disease Flashcards
(11 cards)
How is valvular disease diagnosed?
By transthoracic echocardiography (TTE), and/or transesophageal echocardiography (TEE).
Describe mitral stenosis.
Usually results from prior rheumatic fever. Left atrial enlargement and atrial fibrillation are common.
Describe mitral regurgitation.
Arises from disruption of the structural integrity of any of the components of the mitral valve apparatus or their coordinated action.
With chronic MR, left atrial enlargement and left ventricular volume overload are typical.
Describe mitral valve prolapse.
The valve leaflets are elongated and the normal dense collagen and elastin matrix of the valvular fibrosa is fragmented and replaced with loose myxomatous connective tissue.
One or both leaflets bow into the left atrium during systole resulting in a lack of coaptation and mitral regurgitation.
What are the three primary causes of aortic stenosis?
Three primary causes:
1) degenerative calcification of a previously normal trileaflet aortic valve
2) calcification of a congenitally bicuspid aortic valve
3) rheumatic valve disease
Main symptoms are chest discomfort, exertional dyspnea, and exertional light headedness.
Describe aortic regurgitation.
May result either from abnormalities of the aortic valve leaflets or from dilatation of the aortic root.
The hemodynamic deviation if left ventricular volume overload.
Describe tricuspid stenosis.
This is a rare condition, usually a delayed consequence of rheumatic fever.
Describe tricuspid regurgitation.
This condition is typically functional (due to right ventricular enlargement) rather than structural in nature.
Describe pulmonic stenosis.
This condition is rare, and its cause is almost always congenital deformity of the valve.
Describe pulmonic regurgitation.
Most commonly develops in the setting of sever pulmonary hypertension and results from dilation of the valve ring by an enlarged pulmonary artery.
Describe endocarditis.
The pathogenesis of endocarditis requires endocardial surface injury, platelet-fibrin-thrombus formation at the site of injury, bacterial entry into the circulation, and bacterial adherence to the injured endocardial surface.
