Cardiovascular I

Question 1

What are the two principle mechanisms of vascular disease?

Answer 1

Narrowing or obstruction of vascular lumina

Weakening of vascular walls, leading to dilation and/or rupture

Question 2

Artherosclerosis

Answer 2

Involves the large and medium arteries
Characterized by atheroma - atheromas protrude into the lumen of the vessel
May weaken the underlying media of the arteria
Plaques can rupture, resulting in catastrophic vessel thrombosis

Question 3

What are the two types of Arteriosclerosis?

Answer 3

Hyaline

Hyperplastic

Question 4

Hyaline Arteriosclerosis

Answer 4

Thickening of basement membrane

Hypertension and diabetes mellitus

Question 5

Hyperplastic Arteriosclerosis

Answer 5

Malignant hypertension

Question 6

Where is Atherosclerosis most and least prevalent?

Answer 6

Most prevalent in western cultures

Least prevalent in eastern cultures and africa

Question 7

What are the non-modifiable risk factors for artherosclerosis?

Answer 7

Age - peak age is 40-60
Gender - men > premenopausal women
Genetics - familial history is the most important factor

Question 8

What are the potentially modifiable risk factors for artherosclerosis?

Answer 8

Cigarette smoking - smoking increases death rate by 200%
Diabetes mellitus
Hypertension
Hypercholesterolemia - specifically LDL

Question 9

Monkeberg’s Medial calcific sclerosis

Answer 9

Medial calcification without luminal narrowing or intimal disruption

Question 10

What is Arteriosclerosis

Answer 10

Hardening of the arteries

Question 11

What are some additional risk factors for artherosclerosis?

Answer 11

Inflammation (CRP levels)
Hyperhomocysteineia
Lipoprotein levels
Metabolic syndrome (obesity)
Type A personality (stress)
Lack of exercise

Question 12

What is the Response-to-Injury Hypothesis?

Answer 12

Endothelial injury results in endothelial dysfunction
LDLs and cholesterols accumulate in the vessel wall
Monocytes migrate and adhere, and differentiate into macrophages and “foam cells” (macrophages that ingested lipids)
Lipids accumulate in the macrophages, with release of inflammatory cytokines
Smooth muscle cell recruitment due to factors released from activated platelets, macrophages, and vascular wlals
Smooth muscle poliferates and ECM (mostly collagen) produciton proliferates
We get fully developed plaque with collage and central lipid core

Question 13

Fatty streaks

Answer 13

Appear in most children independent of geography, gender, race, and environment
Occur at sites both prone and not prone to develop atherosclerosis
Some may progress to atheromas (can also regress)
Characterized by lipid-laden cell in the initia

Question 14

What do plaques contain?

Answer 14

Collagen
Lipid
Myofibroblasts
Macrophafes
Neurovaculature

Question 15

What is the fibrous cap comprised of?

Answer 15

Smooth muscle cells (myofibroblasts) and collagen

Central core of lipid/cellular debris with cholesterol

Question 16

What are some progressive changes in plaques?

Answer 16

Ulceration
Fissure formation
Thrombosis
Embolization
Calcification
Hemorrhage
Medial weakening

Question 17

What are some common sites of atheroma formation?

Answer 17

Major arterial branch points
Abdominal aorta
Coronary arteries
Popliteal arteries
Carotid arteries
Cerebral arteries

Question 18

What are some complications of atherosclerosis?

Answer 18

Ischemic heart disease (MI)
Cerebral vascular accident (stroke)
Gangrene 
Renal artery stenosis
Aortic aneurysm

Question 19

Normal Blood pressure level

Question 20

Mild hypertension BP level

Answer 20

140/90 - 159/104 mmHg

Question 21

Moderate-Severe hypertension BP level

Answer 21

> 160/106 mmHg

Question 22

How common is hypertension in the US?

Answer 22

Approx. 20% of adults have it

Question 23

What are the symptoms of hypertension?

Answer 23

None at early, low and moderate
Headache
Fatigue
Dizziness
Palpitations

Question 24

Essential Hypertension. Prevalence and contributing factors

Answer 24

90-95% of all cases
Contributing factors:
-Genetics
-Stress
-Obesity
-Inactivity
-Smoking
-High salt intake

Question 25

Secondary Hypertension

Answer 25

There are many diseases which may produce hypertension

The hypertension is controlled when the underlying disease is treated

Question 26

Malignant Hypertension

Answer 26

Relatively rapid onset of very high BP
Complications can include cerebral edema, retinal hemorrhage, headache, vomiting, convulsions, transient blindness, encephalopathy, renal failure, heart failure
This is a medical emergency requiring prompt but cautious blood pressure lowering

Question 27

What is the pathogenesis of Essential Hypertension?

Answer 27

Hereditary Factors
Reduced renal Na excretion, increased plasma volume, increase cardiac output
Increased peripheral vascular resistance
Environmental factors

Question 28

What are complications of Hypertension?

Answer 28

Concentric left ventricular hypertrophy: compensated
LVH and ventricular dilation: decompensated
Atherosclerosis and arteriosclerosis
Retinal injury
Nephrosclerosis
Dissecting hematoma of the aorta

Question 29

Compensated Hypertensive Heart disease

Answer 29

Left ventricular concentric hypertrophy provides normal cardiac output

Question 30

Decompensated Hypertensive Heart disease

Answer 30

Hypertrophy is no longer adequate to provide normal CO due to decreased myocardial contractility.
This results in left ventricle dilation and gradual onset of CHF

Question 31

Concentric hypertrophy

Answer 31

Thickening of the left ventricular wall at the expense of the left ventricular chamber with little or no increase in the outside cardiac dimensions