PATH - 9-25 - Vascular, Valvular Dz and Atherosclerosis Flashcards
A: ______ Thickening is the Vascular response to injury.
B: What are the 3 Steps to this process
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”
A: Describe Arteriosclerosis
B: List the 3 possible types
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]
A: Name the Elastic arteries affected by Atherosclerosis? (3)
B: Muscular arteries affected by Atherosclerosis? (5)
Elastic arteries affected:
– Aorta (abdominal more than thoracic)
– Carotid
– iLiac
B: Muscular arteries affected: [MC gave CPR]
– Coronary
– Popliteal
– Renal
– Mesenteric
-Circle of Willis
Who’s more at risk for ATHerosclerosis development? (8)
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
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: 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
- 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
- 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
- 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
- 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
- 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?
- 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
Atherosclerotic Cholesterol Emboli
A: What does the D represent?
B: What does the C represent?
D = Dense Plaque
C = Calcification of a Dense [Atherosclerotic Plaque]
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?
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
A: Where are [MMcS - Monckeberg’s Medial calcific Sclerosis] found?
B: Why Aren’t these a problem?
C: What happens if this progresses?
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
A: What are the 2 forms of [HIA - HTN induced Arteriosclerosis]
A:
- Hyaline Arteriolosclerosis
- Hyperplastic Arteriosclerosis
Hyaline Arteriosclerosis
A: What pt demographics are at risk? (3)
B: Findings (3)
C: This is 1 of 2 types of ______
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]
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 ______
Hyperplastic Arteriosclerosis:
A: Seen in
- 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]
Hyaline arteriolosclerosis
Hyperplastic arteriolosclerosis
“Onions are Plastic”
Identify these Aneurysm Types
A: Normal Vessel
B: [Saccular True Aneurysm] = 1 side
C: [FusiForm True Aneurysm] = 2 SIDES
D: False Aneurysm
E: Dissection (Tear in Intima)
3 Characteristics of Aneurysm Pathogenesis
- Poor intrinsic quality of vascular wall connective tissue (Marfan syndrome / Ehlers Danlos)
- Altered balance of collagen degradation and synthesis (INC [Matrix Metalloproteinases])
- Weakened vascular wall from loss of smooth muscle cells or inappropriate synthesis of [extracellular matrix] (caused by Ischemia from Atherosclerosis or HTN—> AORTIC Aneurysms)
A: What are the asterisk representing
B: This is a common finding of ____ and caused by ______
A: [Cystic medial Degeneration]
B: Common finding of Aneurysms caused by loss of smooth muscle cells —> “cystic” spaces
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?
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]
A: Describe the 2 Classifications for Aortic Dissection
B: Which Classification involves all of the Aorta?
[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
A: #1 Cause of Aortic Dissection and 2 Contributing factors?
B: Clinical Presentation (3)
C: Tx (2)
Aortic Dissection
A:
- 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:
- Sudden onset of ripping chest pain radiating to back
- CXR with [mediastinal widening]
- Proximal Dissection–> [pulse and neurological deficit] + [Aortic Regurgitation]
C: Tx:
*Blood Pressure Control
*Surgery for acute proximal dissection
2 Causes of Vasculitis
- Direct invasion of vascular wall by Pathogen
- Immune-mediated inflammation
How are Foam Cells produced during ATHerosclerosis?
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
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
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
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
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
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
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
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
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
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
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
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
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
Total Cholesterol Plasma Levels (mg/dL)
A: Optimal
B: Borderline
C: HIGH
A: Less than 200
B: 200 - 239
C: GREATER THAN 240
LDL Plasma Levels (mg/dL)
A: Optimal
B: Borderline
C: HIGH
D: VERY HIGH
A: Less than 100 ( +29 = near optimal)
B: [130 - 159]
C: [HIGH = 160 - 189]
D: VERY HIGH = GREATER THAN 190
HDL Plasma Levels (mg/dL)
A: Optimal
B:BAD
A: Greater than 60
B: lower than 40
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
[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]
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
[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]
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
[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
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: 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]
-Triglyceride Plasma Levels (mg/dL)
-Tx regimen for each
A: Optimal
B: HIGH
C:VERY HIGH (3)
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
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: 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
A: Minimum amount of years after Rheumatic Fever onset before [____valve stenosis] sx begin?
B: Sx of [Chronic ____valve Stenosis (4)
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
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?
[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)
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:
- Dyspnea w/cough and wheezing
- Thromboembolism**
- Infective endocarditis
- 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]]
How do you calculate [Mitral Valve Area] (cm2) ?
220 / [PHT- Pressure Half Time (milliseconds)]
Tx for Rheumatic Heart Disease (5)
- Penicillin Px for [Strep Pyogenes Group A]
- Px for infective endocarditis
- [Digitalis glycosides] in pts with aFib —> [slows Ventricular HR] and treats [right heart failure]
- Beta Blockers in pts with sinus or aFib rhythm (INC exercise capacity)
- Surgical (Mitral valve replacement vs. valvuloplasty)
Common causes of [Acute Mitral Regurgitation] (7)
[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
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
- • Inflammatory (Rheumatic Fever vs. SLE)
- • Degenerative - MVP,Marfans ,MAC
- • Infective Subacute Endocarditis
- • Structural-Ruptured chordae ,CAD , LV dilatation,Hypertrophic CM ,Prosthetic valve dysfunction
- • Congenital
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: 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
Tx for Acute/Chronic [Mitral Regurgitation] (3)
- [ACEk2 inhibitor]–> Reduce Afterload (similar to CHF tx)
- Hydralazine–> Reduce Afterload (similar to CHF tx)
- Valve Replacement with OPTIMAL TIMING
[Auscultation Physical Exam finding] for
Mitral Valve Prolapse
B: [T or F] MOST [MVP Syndromes] are not accompanied with [Mitral Regurgitation]
Mid Systolic Click
B: TRUE
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: 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
How is it possible to have an Aortic valve that is both Stenotic AND Regurgitant?
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.
A: Why are Aortic Stenosis sx so dangerous?
A: Onset of Severe sx has a poor mortality
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: “I can hear a SIE in this Aortic Stenosis pt”
- Systolic murmur thts cooing or musical when [Aortic Stenosis] becomes severe; associated with a precordial thrill
- Inaudible S2 due to calcification and immobility of aortic valve
- 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
A: Tx for [Aortic Valve Stenosis] (2)
B: What type of complications are associated with tx
C: When do these complications present?
- Balloon Aortic Valvuloplasty
- [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.
A: 2 primary causes of [Aortic Regurgitation]
B: How does [Aortic Regurgitation] affect Stroke Volume?
C: Auscultation Findings (2)
A:
- Aortic Root Dz
- 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.
[Aortic Regurgitation] Treatment
A: Symptomatic pts
B: Asymptomatic pts (2)
C: Which Asymptomatic pts remain stable without cardiac failure or death? (2)
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]
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: 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
