ASCVD Pathology Flashcards

(42 cards)

1
Q

what is Arteriosclerosis

A

Vascular disease manifested by thickening and inelasticity of arteries

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2
Q

what are the 3 patterns of arteriosclerosis

A

atherosclerosis (AS)
Monckeberg’s medial calcific sclerosis
arteriolosclerosis

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3
Q

what is Medial Calcific Sclerosis

A

Calcification of muscle wall (media) of arteries
May ossify
No narrowing of vessel lumen
Patients older than 50 years.

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4
Q

what are the two types of Arteriolosclerosis� and are associated with

A

Thickening and narrowing of vascular walls of small arteries and arterioles,Associated with hypertension and diabetes

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5
Q

what are the two types of Arteriolosclerosis

A

hyaline and hyperplastic

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6
Q

what is Atherosclerosis

A

Intimal fibrofatty plaques
narrow vascular lumen
weaken arterial wall (media)

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7
Q

what are the major targets of Atherosclerosis

A

aorta, coronary arteries, cerebral arteries

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8
Q

what is the epidemiology and risk factors of Atherosclerosis.

A

Responsible for half of all deaths in the western world
Ubiquitous in developed nations
Less common in Central and South America, Africa, Asia, Japan
Begins in early childhood

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9
Q

What has caused a reduction in Atherosclerosis

A

Life-style changes (diet, smoking, control of HTN)
Improved therapy for IHD
Prevention of recurrences

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10
Q

what are the constitutional RF for Atherosclerosis

A

Age 40 to 60 year olds have 5X incidence of MI
Sex (males have 5X death rate from IHD until menopause
same MI frequency by 7th to 8th decade)
Genetics (familial clustering of other risk factors
genetic defects (eg familial hypercholesterolemia)

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11
Q

what are the acquired risk factors for Atherosclerosis

A

Hyperlipidemia
Hypertension 160/95 has 5X risk IHD than < 140/90
Smoking 1ppd X years has 200% increase in death rate from IHD
Diabetes 2X incidence of MI, increased risk of stroke, 100X risk of gangrene
C-reactive protein
“Soft” risk factors`

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12
Q

What does C-Reactive protein tell us

A

Systemic marker of inflammation synthesized by liver

Level correlates with risk of IHD/MI, stroke, PVD, SCD

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13
Q

what reduces CRP

A

smoking cessation, weight loss, exercise, statins

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14
Q

what is the role of HDL

A

Reverse transport of cholesterol from cells/plaque to liver for excretion in bile

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15
Q

what elevated HDL

A

Exercise and ETOH

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16
Q

what reduces HDL

A

Obesity and smoking reduce HDL

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17
Q

True of False risk factors are not additive

18
Q

what are other RF for AS

A
Inadequate physical activity
Type A personality
Obesity
Estrogen deficiency
High carbohydrate diet
Hardened (trans) unsaturated fat intake
Chlamydia pneumoniae
19
Q

what is Hyperhomocystinemia

A

Inborn error of metabolism resulting in high levels of circulating homocysteine
Can also be caused by low folate and vitamin B intake
Level correlates with CAD, PVD, stroke and venous thrombosis

20
Q

what is Lipoprotein Lp (a)

A

Altered form of LDL (apolipoprotein B-100 of LDL linked to apolipoprotein A)
Correlation between increased lipoprotein Lp(a) and coronary and cerebral vascular disease

21
Q

Response to Injury Hypothesis

A

Focal chronic endothelial “injury”
Endothelial dysfunction and monocyte adhesion/emigration
Smooth muscle cell emigration and macrophage activation
Macrophages and SMCs engulf lipid
Proliferation of SMCs, ECM deposition, extracellular lipid.

22
Q

Cellular Events in AS

A
Endothelial injury
Lipids
Macrophages
Smooth muscle cells
Infection
23
Q

Endothelial Injury

A
Endotoxin		
Hypoxia	
Smoking 
Viruses
Immune reactions
Homocysteine
 Hemodynamics
Hypercholesterolemia
24
Q

Hemodynamics

A

Shear stress and turbulent flow
plaques occur at branch points and posterior abdominal aorta
Lesion protected areas associated with induction of atheroprotective genes

25
Severity of AS correlates with total
LDL cholesterol levels
26
``` AHA classifications of lesions Type I - Type II - Type III - Type IV - Type V - Type VI - ```
``` Fatty dot Fatty streak Intermediate lesion Atheroma Fibroatheroma Complicated plaque ```
27
what is an Aneurysms
Abnormal dilatation of arteries/veins due to weakening of vessel wall
28
What is the most common cause of aortic aneurysms
Atherosclerotic Aneurysms
29
Ischemic Heart Disease
Also called coronary heart (artery) disease (most common cause is atherosclerosis) Most common cause of death (1/3 of all deaths) in developed countries
30
Ischemic Heart Disease 4 syndromes
angina pectoris sudden cardiac death myocardial infarction chronic IHD
31
Coronary Artery Thrombosis
Plaque rupture exposes thrombogenic lipids and subendothelial collagen Complete occlusion results in AMI Incomplete occlusion results in U/A or sudden death or microinfarcts downstream
32
other causes of IHD
``` Emboli from vegetations Vasculitis Systemic hypotension Systemic hypertension Valvulopathy ```
33
Angina Pectoris
Intermittent chest pain due to reversible myocardial ischemia
34
Three types of angina pectoris
stable angina Prinzmetal's or variant angia unstable angina
35
Stable Angina
Episodic chest pain associated with exertion or stress Chest pain is crushing, squeezing, may radiate to left arm Fixed lesions > 75% vessel lumen Relieved by rest, NTG (reduces preload and augments coronary blood flow)
36
Prinzmetal’s Angina
Also called variant angina Chest pain occurs at rest or while sleeping Vasospasm near plaque Responds to vasodilators
37
Unstable Angina
Also called crescendo and preinfarction angina Increasing frequency of chest pain More intense and longer duration Due to acute plaque change
38
Myocardial Infarction
Local ischemia leading to corresponding myocardial necrosis | Single most common cause of death in industrialized nations
39
Pathogenesis of MI
``` Coronary artery thrombosis most common cause of MI preexisting plaque disrupted Vasospasm Platelet aggregation Hypoperfusion ```
40
Infarct location
LAD (40 to 50%) - anterior/apical infarcts RCA (30 to 40%) - posterior/basal infarcts LCX (15 to 20%) - lateral
41
Complications of MI
``` Papillary muscle dysfunction Rupture Mural thrombi Acute pericarditis Ventricular aneurysm ```
42
Clinical Features of MI
Severe crushing substernal chest pain +/- radiate to neck, jaw, epigastrium, shoulder, left arm for hours to days unrelieved by NTG Rapid weak pulse, diaphoretic, dyspnea (pulmonary edema), shock (if >40% of LV infarcted)