Lilly Chapter 8 Part 1 Valvular Heart Disease

Front 1

3 Etiologies of Aortic stenosis.

Back 1

Congenital, Rheumatic Valve Disease, Age-related calcification

Front 2

What is the physiologic compensation mechansim for Aortic Stenosis?

Back 2

Concentric LV hypertrophy leading to concomitant LA hypertrophy

Front 3

What are 3 the major symptoms, not structural changes, in advanced Aortic Stenosis and Why do they occur?

Back 3

Angina (supply can't meet demand); Syncope (can't increase CO with exercise), CHF (with time LVEDV increase, insurmountable AL, leading to congestion)

Front 4

What are the PE findings (murmurs, carotid pulse change, S2 effect) in Aortic Stenosis?

Back 4

coarse late peaking systolic ejection murmur; weak Carotid upstroke pulse; S4; loss of aortic portion of S2

Front 5

What is used to confirm AS? Treatment for Aortic Stenosis?

Back 5

Confirmed by Cardiac catherization, treatment by AVR onces LV dysfunction is great enough + prophylaxis

Front 6

What are the 2 mechanisms that cause Aortic Regurgitation?

Back 6

Aortic leaflet disease; dilatation of the aortic root

Front 7

How does Acute Aortic Regurgitation present? Treatment?

Back 7

MEDICAL emergency appears with normal LV but quick volume overload has caused pulmonary edema; AVR STAT!

Front 8

Describe compensation in Chronic Aortic Regurgitation.

Back 8

Compensatory adaptation to volume overload has occurred (dilatation and to a lesser degree LV hypertrophy);

Front 9

What condition gives you a Widened Pulse Pressure?

Back 9

Hallmark of Aortic Regurgitatoin

Front 10

What are the most frequent patient complaints when presenting with chronic Aortic Regurgitation?

Back 10

dyspnea on exertion, fatigue, forceful heartbeat;

Front 11

Describe Treatment for Asymptomatic & Symptomatic AR.

Back 11

If Asymptomatic follow closely LV function and prophylaxis for endocarditis; Symptomatic: some efficacy with VDs/CCBs/diuretics to delay AVR prior to decompensation;

Front 12

TRUE/FALSE - Tricuspid Stenosis is common and often a complication related to Rheumatic Heart Disease.

Back 12

False - rare but related to RHD

Front 13

What are the Common PE findings (JVP, murmurs, palpations, etc) in Tricuspid Stenosis.

Back 13

JVD with large a wave; Opening Snap with diastolic murmur; hepatomegaly/abdominal distention

Front 14

Treatment for Tricuspid Stenosis.

Back 14

Valvuloplasty or Replacement

Front 15

Describe what usually causes Tricuspid Regurgiation.

Back 15

Functional, in that RV dilatation prevents full closure.

Front 16

Common PE findings (JVP, murmurs, palpations,etc) in Tricuspid Regurgitation.

Back 16

Prominent v waves in jugular veins (RA dilation), systolic murmur, pulsatile liver (back pressure from ventricle)

Front 17

TRUE/FALSE - Often treatment for Tricuspid Regurgitation requires complete replacement.

Back 17

False - treat the underlying RV enlargement

Front 18

TRUE/FALSE - Pulmonic Stenosis is rare and usually a congenital lesion treated by ballon valvuloplasty.

Back 18

TRUE

Front 19

What is the most frequent cause of pulmonic regurgitation?

Back 19

Severe pulmonary HTN

Front 20

What is main negative for the long lasting mechanical valves when compared to bioprosthetic valves? Often recommended to what group?

Back 20

thrombogenic surface requiring lifelong anticoagulation; Younger patients

Front 21

What is the main negative for porcine valves when compared to mechanical valves? Often recommended to what group?

Back 21

less durable requiring more frequent replacement; the elderly( more negatives with anticoagulation)

Front 22

TRUE/FALSE - All valve replacements require lifetime abx prophylaxis for endocarditis.

Back 22

True

Front 23

Describe the 2 conditions for Acute Bacterial Endocarditis.

Back 23

Acute, fulminant endocardial infection with highly virulent and invasive microbe (if less virulent, SBE)

Front 24

Describe the pathogenesis of Endocarditis.

Back 24

1. endocardial surface injury (often via turbulent flow);
2. thrombus formation;
3. bacteria entry into circulation (usually G+);
4. bacterial adherence to fibrin laid down by Platelets (then coated and protected);
5. Possible embolism leading to infarcts;

Front 25

Right Sided Infective Endocarditis is seen often in (blank).

Back 25

Intravenous Drug users

Front 26

What is the Treatment strategy for infective endocarditis?

Back 26

1st obtain blood culture, 2nd IV abx can be directed at the microorganism,3rd if persistent bacteremia then valve replacement

Front 27

Normal Aortic Valve

Back 27

?

Front 28

Congenital Pulmonary Stenosis

Back 28

?

Front 29

Combined aortic and mitral stenosis seen with LA dilation and LV hypertrophy

Back 29

?

Front 30

TRUE/FALSE - Marantic Endocarditis is non inflammatory, non destructive and non infective but can still cause thrombotic embolization.

Back 30

True

Front 31

Marantic Endocarditis

Back 31

Disease process?

Front 32

What heart disease process is associated with SLE & Collagen Vascular Disease?

Back 32

Libman-Sacks Endocarditis

Front 33

Libman Sacks Endocarditis

Back 33

?

Front 34

Carcinoid Heart tumors from the GI tract cause valvular fibrosis via production of (blank).

Back 34

vasoactive metabolites (serotonin)

Front 35

What disease condition is Distinguished by large atrial gelationous mass?

Back 35

Cardiac Myxoma