Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

🄼💊 CARDIO PATH/RX > PATH - 9-25 - Vascular, Valvular Dz and Atherosclerosis > Flashcards

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

1
Q

A: ______ Thickening is the Vascular response to injury.

B: What are the 3 Steps to this process

A

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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A: Describe Arteriosclerosis

B: List the 3 possible types

A

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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

B: Muscular arteries affected by Atherosclerosis? (5)

A

Elastic arteries affected:

– Aorta (abdominal more than thoracic)

– Carotid

– iLiac

B: Muscular arteries affected: [MC gave CPR]

– Coronary

– Popliteal

– Renal

– Mesenteric

-Circle of Willis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • 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

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • 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

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • 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?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
A

Atherosclerotic Cholesterol Emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A: What does the D represent?

B: What does the C represent?

A

D = Dense Plaque

C = Calcification of a Dense [Atherosclerotic Plaque]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

B: Why Aren’t these a problem?

C: What happens if this progresses?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

A:

  1. Hyaline Arteriolosclerosis
  2. Hyperplastic Arteriosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hyaline Arteriosclerosis

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

B: Findings (3)

C: This is 1 of 2 types of ______

A

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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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 ______

A

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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
A

Hyaline arteriolosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
A

Hyperplastic arteriolosclerosis

“Onions are Plastic”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Identify these Aneurysm Types

A

A: Normal Vessel

B: [Saccular True Aneurysm] = 1 side

C: [FusiForm True Aneurysm] = 2 SIDES

D: False Aneurysm

E: Dissection (Tear in Intima)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

3 Characteristics of Aneurysm Pathogenesis

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A: What are the asterisk representing

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

A

A: [Cystic medial Degeneration]

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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?

A

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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

A: Describe the 2 Classifications for Aortic Dissection

B: Which Classification involves all of the Aorta?

A

[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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

B: Clinical Presentation (3)

C: Tx (2)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

2 Causes of Vasculitis

A
  1. Direct invasion of vascular wall by Pathogen
  2. Immune-mediated inflammation
25
Q

How are Foam Cells produced during ATHerosclerosis?

A

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

26
Q

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

A

There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism

Type 1 Phenotype

A: Chylomicrons INC

B: [TriAcylGlycerides (Exogenous)] INC

C: [LPL- Lipoprotein lipase] gene

D: No Atherogenicity

27
Q

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

A

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

28
Q

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

A

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 TriAcylGlycerides] INC

C: [LDL Receptor gene] OR [apoB gene]

D: +3

29
Q

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

A

There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism

Type 3 Phenotype

A: [Chylomicron Remnants] and IDL INC

B: [Cholesterol and TriAcylGlycerides] INC

C: [Apo E gene]

D: +3

30
Q

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

A

There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism

Type 4 Phenotype

*Most Common*

A: VLDL

B: TriAcylGlycerides (endogenous)

C: [LPL- Lipoprotein lipase] gene

D: +1

31
Q

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

A

There are 6 Categories of [Primary Genetic Disorders] in Lipid/Lipoprotein Metabolism

Type 5 Phenotype

A: [VLDL and Chylomicrons] INC

B: [Cholesterol and TriAcylGlycerides] INC

C: [Apo C2 gene] OR [LPL gene]

D: +1

32
Q

Total Cholesterol Plasma Levels (mg/dL)

A: Optimal

B: Borderline

C: HIGH

A

A: Less than 200

B: 200 - 239

C: GREATER THAN 240

33
Q

LDL Plasma Levels (mg/dL)

A: Optimal

B: Borderline

C: HIGH

D: VERY HIGH

A

A: Less than 100 ( +29 = near optimal)

B: [130 - 159]

C: [HIGH = 160 - 189]

D: VERY HIGH = GREATER THAN 190

34
Q

HDL Plasma Levels (mg/dL)

A: Optimal

B:BAD

A

A: Greater than 60

B: lower than 40

35
Q

Describe [General Risk Categorization #1] for Assessing 10-year Coronary Heart Disease

A: Risk Level

B: Risk Factor Tx?

C: Type of pharmacotherapy

D: When is pharmacotherapy indicated

A

[General Risk Categorization #1] for Assessing 10-year Coronary Heart Disease

A: Low Risk

B: Just for Reassurance

C: May delay Cardiovascaular assessment for 5 years

D: Pharmacotherapy if [LDL ≥ 190]

36
Q

Describe [General Risk Categorization #TWO] for Assessing 10-year Coronary Heart Disease

A: Risk Level

B: Risk Factor Tx?

C: Type of pharmacotherapy

D: When is pharmacotherapy indicated

A

[General Risk Categorization #TWO] for Assessing 10-year Coronary Heart Disease

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]

37
Q

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

A

[General Risk Categorization #3] for Assessing 10-year Coronary Heart Disease

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

38
Q

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

A

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]

39
Q

-Triglyceride Plasma Levels (mg/dL)

-Tx regimen for each

A: Optimal

B: HIGH

C:VERY HIGH (3)

A

A:Lower than 150–> Lifestyle changes

B: HIGH: 200-499 –> [Reduce LDL/VLDL 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

40
Q

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]?

A

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

41
Q

A: Minimum amount of years after Rheumatic Fever onset before [____valve stenosis] sx begin?

B: Sx of [Chronic ____valve Stenosis (4)

A

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
42
Q

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?

A

[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)

43
Q

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]]

A

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]]

44
Q

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

A

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

45
Q

Tx for Rheumatic Heart Disease (5)

A
  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)
46
Q

Common causes of [Acute Mitral Regurgitation] (7)

A

[HIP Treats Leaky Mitral Valves]

  • Infectious endocarditis
  • Trauma
  • Myxomatous Degeneration
  • [LSLE - Libman Sacks Lupus Erythematosus]
  • Heart Ischemia: CAD /MI /ischemia/myocarditis
  • LV dysfunction
  • Prosthetic valve dysfunction
47
Q

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
A
  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
48
Q

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]?

A

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

49
Q

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

A
  1. [ACEk2 inhibitor]–> Reduce Afterload (similar to CHF tx)
  2. Hydralazine–> Reduce Afterload (similar to CHF tx)
  3. Valve Replacement with OPTIMAL TIMING
50
Q

[Auscultation Physical Exam finding] for

Mitral Valve Prolapse

B: [T or F] MOST [MVP Syndromes] are not accompanied with [Mitral Regurgitation]

A

Mid Systolic Click

B: TRUE

51
Q

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

A

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

52
Q

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

A

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.

53
Q

A: Why are Aortic Stenosis sx so dangerous?

A

A: Onset of Severe sx has a poor mortality

54
Q

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)

A

A: “I can hear a SIE in this Aortic Stenosis pt”

  1. Systolic murmur thts cooing or musical when [Aortic Stenosis] becomes severe; associated with a precordial thrill
  2. Inaudible S2 due to calcification and immobility of aortic valve
  3. Ejection 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
55
Q

A: Tx for [Aortic Valve Stenosis] (2)

B: What type of complications are associated with tx

C: When do these complications present?

A
  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.

56
Q

A: 2 primary causes of [Aortic Regurgitation]

B: How does [Aortic Regurgitation] affect Stroke Volume?

C: Auscultation Findings (2)

A

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.
57
Q

[Aortic Regurgitation] Treatment

A: Symptomatic pts

B: Asymptomatic pts (2)

C: Which Asymptomatic pts remain stable without cardiac failure or death? (2)

A

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 Need Drugs”

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]

58
Q

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?

A

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

🄼💊 CARDIO PATH/RX (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions