PATH - 9-25 - Vascular, Valvular Dz and Atherosclerosis

Question 1

A: ______ Thickening is the Vascular response to injury.

B: What are the 3 Steps to this process

Answer 1

A: Intimal Thickening is the Vascular response to injury.

1st: Smooth m. cells from [Tunica Media] are recruited into the [Tunica intima]
2nd: Those Smooth m. cells undergo mitosis inside [Tunica intima]
3rd: Extracell matrix starts to “elaborate”

Question 2

A: Describe Arteriosclerosis

B: List the 3 possible types

Answer 2

Arteriosclerosis is “Hardening of the arteries” (arterial wall thickening and loss of elasticity) with 3 possible types:

– Atherosclerosis (Tunica intima Dz)

– MMcS - Monckeberg’s medial calcific sclerosis

– [HIA - HTN induced Arteriosclerosis]

Question 3

A: Name the Elastic arteries affected by Atherosclerosis? (3)

B: Muscular arteries affected by Atherosclerosis? (5)

Answer 3

Elastic arteries affected:

– Aorta (abdominal more than thoracic)

– Carotid

– iLiac

B: Muscular arteries affected: [MC gave CPR]

– Coronary

– Popliteal

– Renal

– Mesenteric

-Circle of Willis

Question 4

Who’s more at risk for ATHerosclerosis development? (8)

Answer 4

Girls Having PMS Can DEC Hyperlipidemia

• Genetics
• HTN
• Postmenopausal women (ESTROGEN IS PROTECTIVE)
• MALES
• Smokers cigarettes
• Pt with Chronic Inflammation ( [high sensitive CRP] is a normal lab parameter for athersclerosis now)
• DM
• Hyperlipidemia pts

Question 5

A: ATHerosclerosis is an _____ Wall _____ response to _____—> that involves the interaction of 4 components. It eventually leads to —-> _____ _____.

What 4 components interact during ATHerosclerosis?

C: Which hypothesis is this?

D: Which size arteries are mostly affected by ATHerosclerosis? (2)

Answer 5

A: Arterial Wall [Chronic Inflammatory response] to [Chronic Endothelilal Injury] that involves interaction of TLC-m:—> “arterial hardening”

• Lipoproteins
• [monocyte macrophages]
• [T-lymphocytes]
• Cellular Constituents

C: :Response to Injury”

D: Large to [muscle medium] size arteries

Question 6

• Atheromas* consist of
  1. Fibromuscular Cap
  2. Cellular area beside the Cap
  3. [Lipid Necrotic Core]

B: Describe the Composition of the Fibromuscular Cap (2)

C: In which Tunica are Atheromas located

Answer 6

• Atheromas* consist of
  1. Fibromuscular Cap
  2. Cellular area beside the Cap
  3. [Lipid Necrotic Core]

B: Fibromuscular Cap:

-[Smooth muscle cells] + [Dense Connective Tissue Fiber]

C: TUNICA INTIMA

Question 7

• Atheromas* consist of
  1. Fibromuscular Cap
  2. Cellular area beside the Cap
  3. [Lipid Necrotic Core]

B: Describe the Composition of the Cellular area beside the Cap (3)

C: In which Tunica are Atheromas located

Answer 7

• Atheromas* consist of
  1. Fibromuscular Cap
  2. Cellular area beside the Cap
  3. [Lipid Necrotic Core]

B: Cellular area beside the Cap:

- macrophage

-[smooth muscle]

-T-lymphocytes

C: TUNICA INTIMA

Question 8

• Atheromas* consist of
  1. Fibromuscular Cap
  2. Cellular area beside the Cap
  3. [Lipid Necrotic Core]

B: Describe the Composition of the [Lipid Necrotic Core] (4)

C: In which Tunica are Atheromas located

D: Where does neovascularization of the Atheroma occur?

Answer 8

• Atheromas* consist of
  1. Fibromuscular Cap
  2. Cellular area beside the Cap
  3. [Lipid Necrotic Core]

B: [Lipid Necrotic Core]: is a ..

“Lipid Filled Plasma Cake”

*Cholesterol Crystals

*[Lipid filled Foam Cells]

*Fibrin

*Plasma Proteins

C: TUNICA INTIMA

D: Periphery of Lesion

Question 9

Answer 9

Atherosclerotic Cholesterol Emboli

Question 10

A: What does the D represent?

B: What does the C represent?

Answer 10

D = Dense Plaque

C = Calcification of a Dense [Atherosclerotic Plaque]

Question 11

Fatty Streaks

A: Possible Precursor of what?

B: Color? Shape? Composition(3)?

C: What demographic are they found in?

D: Where in the vessel do they occur?

Answer 11

Fatty Streaks

A: Possible Precursor of an [Atherosclerotic Plaque]

B: Yellow / Flat lesions made of [Lipid filled foam cells] / T-lymphocytes / [Extracell debris]

C: FOUND IN EVERYONE OVER 10 YEARS OLD

D: Near Branch Points of vessel

Question 12

A: Where are [MMcS - Monckeberg’s Medial calcific Sclerosis] found?

B: Why Aren’t these a problem?

C: What happens if this progresses?

Answer 12

A: [MMcS - Monckeberg’s Medial calcific Sclerosis] are Calcific depositis found within [Tunica Media] of [muscular medium arteries]

B: They are NON-Obstructive

C: If calcification progresses, arteries may be more appreciable

Question 13

A: What are the 2 forms of [HIA - HTN induced Arteriosclerosis]

Answer 13

A:

1. Hyaline Arteriolosclerosis
2. Hyperplastic Arteriosclerosis

Question 14

Hyaline Arteriosclerosis

A: What pt demographics are at risk? (3)

B: Findings (3)

C: This is 1 of 2 types of ______

Answer 14

Hyaline Arteriosclerosis

A: Seen in patients with

• hypertension,
• DM
• normotensive elderly

B: Findings:

• -Homogeneous pink hyaline thickening of arterioles*
• lumenal narrowing from plasma protein leakage across injured endothelial cells
• increased smooth muscle cell matrix in response to hemodynamic stress.

C: This is 1 of 2 of [HIA - HTN induced Arteriosclerosis]

Question 15

Hyperplastic Arteriosclerosis

A: What pt demographics are at risk?

B: Findings (2)

C: What Disease does this cause of untreated?

D: This is 1 of 2 types of ______

Answer 15

Hyperplastic Arteriosclerosis:

A: Seen in

1. severe acute elevation of blood pressure - (malignant HTN where diastolic BP > 120 mmHg)

B: Findings:

*Onion skin concentric thickening of arteriole wall.

*Laminations made of smooth muscle cells with thickened reduplicated basement membranes.

C: Lumen narrowing —> end organ ischemia

D: This is 1 of 2 types of [HIA - HTN Induced Arteriosclerosis]

Question 16

Answer 16

Hyaline arteriolosclerosis

Question 17

Answer 17

Hyperplastic arteriolosclerosis

“Onions are Plastic”

Question 18

Identify these Aneurysm Types

Answer 18

A: Normal Vessel

B: [Saccular True Aneurysm] = 1 side

C: [FusiForm True Aneurysm] = 2 SIDES

D: False Aneurysm

E: Dissection (Tear in Intima)

Question 19

3 Characteristics of Aneurysm Pathogenesis

Answer 19

1. Poor intrinsic quality of vascular wall connective tissue (Marfan syndrome / Ehlers Danlos)
2. Altered balance of collagen degradation and synthesis (INC [Matrix Metalloproteinases])
3. Weakened vascular wall from loss of smooth muscle cells or inappropriate synthesis of [extracellular matrix] (caused by Ischemia from Atherosclerosis or HTN—> AORTIC Aneurysms)

Question 20

A: What are the asterisk representing

B: This is a common finding of ____ and caused by ______

Answer 20

A: [Cystic medial Degeneration]

B: Common finding of Aneurysms caused by loss of smooth muscle cells —> “cystic” spaces

Question 21

A: Describe the 2 Step Etiology of [Abdominal Aortic Aneurysm]

B: Where does a AAA typically occur? (2)

C: What type of Aneurysm can it form into? (2)

D: What are the 3 Demographics most at risk?

Answer 21

Abdominal Aortic Aneurysm

A: Etiology:

1st: Atheromas compress [aortic media] —> Ischemia and eventual Degeneration of [Tunica Media]—> weakning and thinning!
2nd: Inflammatory infiltrates then come and release [Matrix Metalloproteinase] which worsen the condition —> AAA!

B: Infrarenal and above aortic bifurcation

C: Can be [Saccular True Aneurysm] OR [FusiForm True Aneurysm]

D: Men / Smokers / [Pt over 50]

Question 22

A: Describe the 2 Classifications for Aortic Dissection

B: Which Classification involves all of the Aorta?

Answer 22

[Type A - DeBakey type 1 and 2] - PA12
i. Proximal lesions involving

• ascending and descending aorta = Type 1
• ascending aorta only = Type 2

vs.

[Distal - Type B - DeBakey type 3] - DB3

i. Distal - does not involve ascending aorta and begins distal to subclavian artery

Question 23

A: #1 Cause of Aortic Dissection and 2 Contributing factors?

B: Clinical Presentation (3)

C: Tx (2)

Answer 23

Aortic Dissection

A:

1. Etiology: 90% caused by HTN (Mechanical Pressure vs. Ischemic injury)

Contributing factors for this are:

• Medial hypertrophy of vasovasorum
• Degenerative changes of media 2º to Connective Tissue Disorder (Marfans Syndrome)

B:

1. Sudden onset of ripping chest pain radiating to back
2. CXR with [mediastinal widening]
3. Proximal Dissection–> [pulse and neurological deficit] + [Aortic Regurgitation]

C: Tx:

*Blood Pressure Control

*Surgery for acute proximal dissection

Question 24

2 Causes of Vasculitis

Answer 24

1. Direct invasion of vascular wall by Pathogen
2. Immune-mediated inflammation

Question 25

How are Foam Cells produced during ATHerosclerosis?

Answer 25

1- [Chronic Endothelial Injury] to Tunica Intima allows **_Lipids_ to leak into [Tunica Intima]** 2-_Lipids_ are eventually **oxidized** and Macrophages come to scavenge them using [scavenger receptors] 3- Macrophages + [Oxidized Lipids] = **FOAM CELLS**

Question 26

There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism **Type 1 Phenotype** A: Which _Lipoprotein_ is INC B: Which _Lipid_ is INC C: Defective Gene D: Atherogenicity as a result of the Disorder

Answer 26

There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism **Type 1 Phenotype** A: Chylomicrons INC B: [**T**ri**A**cyl**G**lycerides (Exogenous)] INC C: [LPL- Lipoprotein lipase] gene D: No Atherogenicity

Question 27

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 2 A Phenotype** A: Which _Lipoprotein_ is INC B: Which _Lipid_ is INC C: Defective Gene (2) D: Atherogenicity as a result of the Disorder

Answer 27

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 2 A Phenotype** A: LDL INC B: Cholesterol INC C: [LDL Receptor gene] OR [apoB gene] D: **+3**

Question 28

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 2 B Phenotype** A: Which _Lipoprotein_ is INC (2) B: Which _Lipid_ is INC (2) C: Defective Gene (2) D: Atherogenicity as a result of the Disorder

Answer 28

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 2 B Phenotype** **\*Much more common\*** A: [LDL and VLDL] INC B: [Cholesterol AND **T**ri**A**cyl**G**lycerides] INC C: [LDL Receptor gene] OR [apoB gene] D: **+3**

Question 29

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 3 Phenotype** A: Which _Lipoprotein_ is INC (2) B: Which _Lipid_ is INC (2) C: Defective Gene D: Atherogenicity as a result of the Disorder

Answer 29

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 3 Phenotype** A: [Chylomicron _Remnants_] and IDL INC B: [Cholesterol and **T**ri**A**cyl**G**lycerides] INC C: [Apo E gene] D: **+3**

Question 30

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 4 Phenotype** A: Which _Lipoprotein_ is INC B: Which _Lipid_ is INC C: Defective Gene D: Atherogenicity as a result of the Disorder

Answer 30

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 4 Phenotype** **\*Most Common\*** A: VLDL B: **T**ri**A**cyl**G**lycerides *(**endo**genous)* C: [LPL- Lipoprotein lipase] gene D: **+1**

Question 31

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 5 Phenotype** A: Which _Lipoprotein_ is INC (2) B: Which _Lipid_ is INC (2) C: Defective Gene (2) D: Atherogenicity as a result of the Disorder

Answer 31

*There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism* **Type 5 Phenotype** A: [VLDL and Chylomicrons] INC B: [Cholesterol and **T**ri**A**cyl**G**lycerides] INC C: [Apo C2 gene] OR [LPL gene] D: **+1**

Question 32

**Total Cholesterol** *Plasma Levels (mg/dL)* A: Optimal B: Borderline C: HIGH

Answer 32

A: Less than 200 B: 200 - 239 C: GREATER THAN 240

Question 33

**LDL** *Plasma Levels (mg/dL)* A: Optimal B: Borderline C: HIGH D: VERY HIGH

Answer 33

A: Less than 100 *( +29 = near optimal)* B: [130 - 159] C: [HIGH = 160 - 189] D: **VERY HIGH = GREATER THAN 190**

Question 34

**HDL** *Plasma Levels (mg/dL)* A: Optimal B:BAD

Answer 34

A: Greater than 60 B: lower than 40

Question 35

Describe [General Risk Categorization #**1**] for Assessing 10-year Coronary Heart Disease A: Risk Level B: Risk Factor Tx? C: **T****ype** of pharmacotherapy D: **When** is pharmacotherapy indicated

Answer 35

[General Risk Categorization #**1**] for Assessing 10-year Coronary Heart Disease ## Footnote A: Low Risk B: Just for Reassurance C: May delay Cardiovascaular assessment for 5 years D: Pharmacotherapy if [**LDL ≥ 190**]

Question 36

Describe [General Risk Categorization #**TWO**] for Assessing 10-year Coronary Heart Disease A: Risk Level B: Risk Factor Tx? C: **T****ype** of pharmacotherapy D: **When** is pharmacotherapy indicated

Answer 36

[General Risk Categorization #**TWO**] for Assessing 10-year Coronary Heart Disease ## Footnote A: HIGH Risk B: All Risk Factors need to be tx C: [Aggressive management] + Aspirin to lower LDL under 100 D: Pharmacotherapy if [**LDL \> 100**]

Question 37

Describe [General Risk Categorization #**3**] for Assessing 10-year Coronary Heart Disease A: Risk Level B: Risk Factor Tx? C: **When** is pharmacotherapy indicated D: What is different about this Categorization

Answer 37

[General Risk Categorization #**3**] for Assessing 10-year Coronary Heart Disease ## Footnote A: Intermediate Risk B: Do **NOT** qualify for Risk Factor Tx C: Pharmacotherapy if [**LDL \> 160**] D: Most [Coronary Vascular Disease] events occur in Intermediate Risk patients

Question 38

A: LDL Goal for Pt who **have Coronary Heart Disease** B: LDL Goal for Pt with 2 Risk Factors for CHD C: LDL Goal for Pt with 0-1 Risk Factors for CHD

Answer 38

A: HAVING [Coronary Heart Disease] = [LDL Goal is Under 100] B: 2 Risk Factors for CHD = [LDL Goal is Under 130] C: 0-1 Risk Factors for CHD = [LDL Goal is Under 160]

Question 39

**-Triglyceride** *Plasma Levels (mg/dL)* *-*Tx regimen for each A: Optimal B: HIGH C:**VERY HIGH** (3)

Answer 39

A:Lower than 150--\> Lifestyle changes B: HIGH: 200-499 --\> [Reduce LDL/**V**LDL using Statin or add (Niacin / Fibrates)] C: [**MORE THAN 500] but can PREVENT PANCREATITIS WITH [NIACIN/FIBRATES]** and then address LDL goals once levels are lower than 500

Question 40

A: The predominant cause of [mitral stenosis] is ______ and most are \_\_\_\_\_\_[*male/female*]. B: Rheumatic fever results in four forms of [mitral valve _fusion]_ that leads to \_\_\_\_\_\_. What are they? C: Rheumatic Fever can cause both [Mitral Stenosis] and [Mitral Regurgitation]. What condition INC chance of [Mitral Regurgitation]?

Answer 40

A: The predominant cause of mitral stenosis (MS) is [Rheumatic fever] and most are **FEMALE**. *(some even have mitral regurgitation as well)* B: Rheumatic fever results in four forms of fusion of the mitral valve apparatus leading to stenosis :(1) commissural (2) cuspal (3) chordal (4) combined. C: When rheumatic fever results exclusively / predominantly in [contraction and fusion of chordae tendineae], with little fusion of valvular commissures---\> dominant MR

Question 41

A: Minimum amount of years after Rheumatic Fever onset before [\_\_\_\_valve stenosis] sx begin? B: Sx of [Chronic \_\_\_\_valve Stenosis (4)

Answer 41

A: 2 years (but is commonly 3rd/4th decade before sx commense and pts in temperate climates have longer delay) B: * Enlargement and Calcification of L atrium * resultant elevation of the left main stem bronchus, * development of mural thrombi, * obliterative changes in pulmonary vascular bed

Question 42

This photo demonstrates \_\_\_\_*(dz)*\_\_\_\_\_ with what 4 key findings? B: What is the principal **symptom** of this dz? C: What is a common Echocardiogram finding for this dz?

Answer 42

[Severe rheumatic mitral stenosis] with * small left ventricle (lv) * enlarged left atrium (la), * Calcified stenotic valve (arrow) * Subvalvular changes (double arrows). B: Dyspnea w/cough and wheezing C: Hockey Stick Deformity *(note there are other manifestations)*

Question 43

A: 4 Potential Sx of Mitral Stenosis B: Which sx is most common in [Pts older than 35 with aFib , [low Cardiac Ouput] and dilation of [L atrial appendage]]

Answer 43

A: 1. Dyspnea w/cough and wheezing 2. Thromboembolism\*\* 3. Infective endocarditis 4. Compression of [L recurrent laryngeal nerve]--\> Hoarseness B: **Thromboembolism** is more common in [Pts older than 35 with aFib and dilation of [L atrial appendage]]

Question 44

How do you calculate **[Mitral Valve Area]** *(cm²)* ?

Answer 44

220 / [**PHT**- Pressure Half Time (milliseconds)]

Question 45

Tx for **Rheumatic Heart Disease** (5)

Answer 45

1. Penicillin Px for [Strep Pyogenes Group A] 2. Px for infective endocarditis 3. [Digitalis glycosides] in pts **with aFib** ---\> [slows Ventricular HR] and treats [right heart failure] 4. Beta Blockers in pts with sinus or aFib rhythm (INC exercise capacity) 5. Surgical (*Mitral valve replacement vs. valvuloplasty*)

Question 46

Common causes of [**Acute** Mitral Regurgitation] (7)

Answer 46

[**HIP T**reats **L**eaky **M**itral **V**alves] * **I**nfectious endocarditis * **T**rauma * **M**yxomatous Degeneration * [**LSLE** - Libman Sacks _Lupus Erythematosus_] * **H**eart Ischemia: CAD /MI /ischemia/myocarditis * **L**V dysfunction * **P**rosthetic valve dysfunction

Question 47

Common causes of [**CHRONIC** Mitral Regurgitation] (5) * List Examples of each* 1. Inflammatory (2) 2. Degenerative (3) 3. Infective Subactue Endocarditis 4. Structural (5) 5. Congenital

Answer 47

1. • Inflammatory (Rheumatic Fever vs. SLE) 2. • Degenerative - MVP,Marfans ,MAC 3. • Infective Subacute Endocarditis 4. • Structural-Ruptured chordae ,CAD , LV dilatation,Hypertrophic CM ,Prosthetic valve dysfunction 5. • Congenital

Question 48

A: When do Sx of Chronic [Mitral Regurgitation] typically develop? How long do they last compaired to [Mitral Stenosis]? B: Acute pulmonary edema occurs **less** frequently in Mitral _____ [*Stenosis/Regurgitation*] C: Why do patients with [Mitral Stenosis] have a slight benefit than those with [Mitral Regurgitation]?

Answer 48

A: Symptoms usually do not develop in patients with chronic [Mitral Regurgitation] until [left ventricle fails]. Sx are longer and exceeds 2 decades. B: Acute pulmonary edema occurs less frequently in chronic MR than in MS, C: In contrast, patients with MS have the benefit of an “early warning system. By the time [Mitral **Regurgitation** symptoms become apparent, [left ventricular dysfunction may have developed

Question 49

Tx for Acute/Chronic [Mitral **Regurgitation]** (3)

Answer 49

1. [ACEk2 inhibitor]--\> *_Reduce Afterload_ (similar to CHF tx)* 2. Hydralazine--\> *_Reduce Afterload_ (similar to CHF tx)* 3. Valve Replacement with OPTIMAL TIMING

Question 50

[Auscultation Physical Exam finding] for **Mitral Valve Prolapse** B: [*T or F*] MOST [MVP Syndromes] are _not_ accompanied with [Mitral Regurgitation]

Answer 50

Mid Systolic Click B: TRUE

Question 51

A: What's the most common cause of [Aortic Stenosis] in adults B: Risk Factors for this lesion? (2) C: What type of [Aortic Stenosis] develops in pts with severe hypercholesterolemia

Answer 51

A: In degenerative (senile) calcific AS, the cusps are immobilized by a deposit of calcium along their flexion lines at their bases. This . A2: Both DM and hypercholesterolemia(can cause 2) B: atherosclerotic aortic valvular stenosis

Question 52

How is it possible to have an Aortic valve that is **both** Stenotic AND Regurgitant?

Answer 52

Rheumatic [Aortic Stenosis] results from fusions and adhesions of the commissures and cusps and then vascularization of the leaflets of the valve ring --\> leading to retraction and stiffening of the free borders of the cusps, with calcific nodules on both surfaces and an orifice reduced to a triangular opening.

Question 53

A: Why are Aortic Stenosis sx so dangerous?

Answer 53

A: Onset of Severe sx has a _poor mortality_

Question 54

A: Potential Auscultation Findings for [**Aortic Stenosis**] (3) B: What do these Auscultation findings depend on? (2) C: *Where* are these Auscultation findings best heard (3)

Answer 54

A: "I can hear a **SIE** in this Aortic Stenosis pt" 1. **S**ystolic murmur thts cooing or musical when [Aortic Stenosis] becomes severe; associated with a precordial thrill 2. **I**naudible S2 due to calcification and immobility of aortic valve 3. **E**jection sound of Aorta occurs simultaneously with halting upward movement of aortic valve B: - mobility of the valve cusps - auscultation findings disappears when they become severely calcified. C: Usually late-peaking and heard best at * *base of the heart* but is often well transmitted * *along carotid vessels* and to the * *apex*

Question 55

A: Tx for [**Aortic Valve Stenosis**] (2) B: What type of complications are associated with tx C: When do these complications present?

Answer 55

1. Balloon Aortic Valvuloplasty 2. [Aortic Valve Repair - *2nd option*] B: balloon valvuloplasty in adults with [critical calcified AS] may develop ReStenosis due to scarring --\> option only for [bridge to Replacement] / [Severe CHF pts] / [Non surgical pts] C: occurs in about half of the patients within 6 months.

Question 56

A: 2 primary causes of [Aortic **Regurgitation**] B: How does [Aortic **Regurgitation**] affect Stroke Volume? C: Auscultation Findings (2)

Answer 56

A: 1. Aortic Root Dz 2. Rheumatic Fever B: [INC Stroke Volume] BUT [DEC **EFFECTIVE** Stroke Volume] C: * [Early diastolic murmur] tht proceeds immediately from second heart sound and is characterized as *early crescendo followed by long DeCrescendo* * [Prominent midSystolic flow murmur] across an unobstructed aortic valve.

Question 57

[Aortic **Regurgitation**] *Treatment* A: Symptomatic pts B: Asymptomatic pts (2) C: Which Asymptomatic pts remain stable without cardiac failure or death? (2)

Answer 57

A: Symptomatic = [Aortic Valve Replacement *(better survival rate if PreOp Ejection Fraction is good!)*] B: Asympatomatic pts with severe [Aortic **Regurgitation**​] = "*No Sx? Ok, you'll **N**eed **D**rugs"* 1st choice: Nifedipine 2nd choice: Digoxin C: Asymptomatic pts with both: * [end-systolic diameter less than 40 mm] * [ejection fraction greater than 50%] *All others may pass from [L ventricle dysfunction]*

Question 58

A: Most common cause of [tricuspid **regurgitation**] is not from _______ but is rather from _____ (2) B: What is [Carvallo's sign] and how is it diagnostic for [tricuspid **regurgitation**]? C: When is tx _NOT_ indicated?

Answer 58

A: most common cause of [tricuspid **regurgitation**] is _not intrinsic involvement of the valve itself_ but from \*[R ventricle Failure ---\> (R ventricle) and (tricuspid annulus) _Dilatation_] B: [tricuspid **regurgitation**] is usually augmented during inspiration = *(Carvallo’s sign)* C: If no pulmonary HTN is present, [tricuspid **regurgitation**] does _not_ require surgical *(Carpentier's suturing annulus to a right prosthetic ring)* tx