Chapter 7 Blood Vessels Flashcards

1
Q

What two circulation system can increased blood pressure be seen?

A

Pulmonary and systemic

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2
Q

What is systemic HTN defined by and what two types is it divided into?

A

BP >140/90

divided into primary and secondary

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3
Q

What is systolic pressure a function of?

A

Stroke Volume

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4
Q

What is diastolic pressure a function of?

A

TPR

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5
Q

What are 6 risk factors from Primary HTN?

A
Age
race (increase in blacks, decreases in asians)
Obesity
Stress
lack of physical activity
high salt diet
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6
Q

What is primary HTN due to? and what percentage of HTN cases does it encompass?

A

Unknown etiology

95%

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7
Q

What percentage of HTN cases are secondary?

A

5%

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8
Q

Describe how Renal artery stenosis leads to renovascular HTN

A

Stenosis decreases renal blood flow. JGA responds by secreting renin, which converts angiotensinogen to angiotensin 1. AT 1 gets converted to AT 2 by ACE in lungs. AT 2 raises BP

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9
Q

How does AT 2 raise BP? 2 ways

A

1 contracting arteriolar smooth muscle and increasing TPR

2 Promoting adrenal release of aldosterone, which increased reabsorption of sodium in the DCT and CD.

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10
Q

What signs are seen in renovascular HTN?

A

Increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary HTN.

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11
Q

What are two important causes of stenosis in secondary HTN, and what demographic are they seen in?

A

atherosclerosis (elderly males) and fibromuscular dysplasia (young females)

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12
Q

What is fibromuscular dysplasia? What size vessels, what common vessel?

A

Developmental defect of the blood vessel wall, resulting in irregular thickening of large and medium sized arteries, especially the renal artery.

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13
Q

Describe benign HTN and its symptoms and pathophys.

A

a mild to moderate elevation in BP; most cases of HTN are benign. Clinically silent; vessels and organs are damaged slowly over time

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14
Q

Describe malignant HTN, how common it is, how it arises, and its symptoms and its effects on BV?

A

Severe elevation in BP (>180/120 or >200/120); comprises <5% of HTN cases. It may arise from preexisting benign HTN or de novo. Presents with acute end organ damage (eg acute renal failure, HA, and papilledema) and is a medical emergency. Can also cause fibrinoid necrosis of BV walls.

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15
Q

What is Arteriosclerosis and what are the three pathological patterns?

A

literally “hard arteries” due to thickening of the blood vessel wall.
Atherosclerosis
Arteriolosclerosis
Monckeberg medial calcific sclerosis

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16
Q

What is atherosclerosis?

A

Intimal plaque that obstructs blood flow. Consists of a necrotic lipid core (mostly cholesterol) with a fibromuscular cap; often undergoes dystrophic calcification.

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17
Q

What size arteries does atherosclerosis affect? What are the 4 most common

A

involves large and medium sized arteries; abdominal aorta, coronary artery, popliteal artery, and internal carotid artery are commonly affected.

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18
Q

What 4 modifiable risk factors of atherosclerosis?

A

HTN, hypercholestremia, smoking, diabetes

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19
Q

What are 3 non modifiable risk factors for atherosclerosis?

A

age (number and severity of lesions increases with age)
gender( increased risk in males and postmenopausal females; estrogen is protective)
genetics (multifactorial, but family history is highly predictive of risk)

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20
Q

Describe the pathogenesis of atherosclerosis?

A

1 damage to endothelium allows lipids to leak into intima
2 lipids are oxidized and then consumed by macrophages via scavenger receptors resulting in foam cells
3 Inflammation and healing leads to deposition of extracellular matrix and proliferation of smooth muscle and fibromuscular capsule

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21
Q

Describe the morphological stages of atherosclerosis?

A

1 Begins as fatty streaks (flat yellow lesions of the intima consisting of lipid laden macrophages); arise early in life (present in most teenagers)
2 progresses to atherosclerotic plaques.

22
Q

What are 4 complications of atherosclerosis?

A

1 stenosis of medium sized vessels results in impaired blood flow and ischemia leading to peripheral vascular disease (lower extremity arteries), angina (coronary arteries), ischemic bowel disease (mesenteric arteries)
2 Plaque rupture with thrombosis results in MI )coronary arteries) and stroke (Middle cerebral arteries)
3 Plaque rupture with embolization results in atherosclerotic emboli, characterized by cholesterol crystals within the embolus (Cholesterol clefts)
4 Weakening of vessel wall results in aneurysm (abdominal aorta) due to diffusion barrier causing media and adventitia to become weak and atrophic

23
Q

What is arteriolosclerosis, what two types is it divided into?

A

Narrowing of small arterioles; divided into hyaline and hyperplastic types

24
Q

What is hyaline ateriolosclerosis caused by and what can be seen on microscopy??

A

caused by proteins leaking into the vessel wall, producing vascular thickening; proteins are seen as pink hyaline on microscopy

25
What two conditions is hyaline arteriolosclerosis a consequence of? what is the etiology of each?
Long standing benign HTN - high blood pressure forces protein into the wall Diabetes - non enzymatic glycosylation damages BM and makes it leaky and proteins get into wall.
26
What does hyperplastic arteriolosclerosis involve? What is the classic appearance?
Thickening of vessel wall by hyperplasia of smooth muscle (onion skin appearance)
27
What size vessels does arteriolosclerosis effect?
small
28
What does hyaline arteriolosclerosis result in?
reduced vessel caliber with end organ ischemia; classically produces glomerular scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure.
29
What is the cause of hyperplastic arteriolosclerosis?
malignant HTN
30
What does hyperplastic arteriolosclerosis result in?
Results in reduced vessel caliber with end-organ ischemia. may lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure with a characteristic "flea bitten" appearance due to pinpoint hemorrhages.
31
What is monckeberg calcific sclerosis? what are its symptoms?
calcification of the media of muscular (medium sized) arteries; nonobstructive. Not clinically significant; seen as an incidental finding on x-ray or mammography
32
What is an Aortic dissection?
Intimal tear with dissection of blood though the media of the aortic wall
33
Where do aortic dissections typically occur?
Occurs in the proximal 10 cm of the aortic (high stress region) with preexisting weakness of the media.
34
What are two common causes of weakness of the media leading to aortic dissection?
1 Hypertension results in hyaline ateriolosclerosis of the vasa vasorum; decreased flow causes atrophy of the media 2 Marfan Syndrome (fibrillin) and Ehler's Danlos (Collagen) syndrome classically lead to weakness of the connective tissue in the media (cystic medial sclerosis)
35
How does aortic dissection present?
Presents as sharp, tearing chest pain that radiates to the back
36
What complications can arise from aortic dissection?
complications include pericardial tamponade ( dissection goes back toward heart, most common cause of death), rupture with fatal hemorrhage, and obstruction of branching arteries (eg. coronary or renal) with resultant end organ ischemia.
37
What is a thoracic aneurysm?
Balloon-like dilation of the thoracic aorta
38
What are thoracic aneurysm due to and what are they classically seen in? What is their classic gross appearance?
Due to weakness in the aortic wall. Classically seen in tertiary syphilis; endarteritis of the vaso vasorum results in luminal narrowing, decreased flow, and atrophy of the vessel wall. Results in a 'tree-bark' appearance of the aorta.
39
What is a major complication in a thoracic aneurysm?
dialtion of the aortic valve root, resulting in aortic valve insufficiency
40
What are some other complications of a thoracic aneurysm?
compression of mediastinal structures ( eg airway or esophagus) and thrombosis/embolism due to disruption of blood flow
41
Where do abdominal aortic aneurysms usually occur?
Below the renal arteries and above the bifurcation.
42
What is AAA primarily due to? who is it seen in?
Primarily due to atherosclerosis; classically seen in male smokers >60 years old with HTN. atherosclerosis increases the diffusion barrier to the media, resulting in atrophy and weakness of the vessel wall.
43
How does AAA present?
pulsatile abdominal mass that grows with time
44
What is a major compication of an AAA? what is the classic triad seen in this.
rupture, especially when >5 cm in diameter; presents with triad of hypotension, pulsatile abdominal mass, and flank pain
45
What are some other complications of an AAA?
compression of local structures (eg ureter) and thrombosis/embolism
46
What is a hemangioma? when does it usually present? what structures does it most often involve? does it blanch?
Benign tumor comprised of blood vessels. commonly present at birth; often regresses during childhood most often involves skin and liver Blanches
47
What is an angiosarcoma? what are the common sites? what exposures can predispose?
Malignant proliferation of endothelial cells; highly aggressive. Common sites include skin, breast, and liver. Liver angiosarcoma is associated with exposure to PVC, arsenic, and thorotrast (old imaging dye)
48
What is Kaposi sarcoma and what is it associated with? What grade malignancy is it?
Low grade malignant proliferation of endothelial cells; associated with HHV-8
49
How does Kaposi sarcoma present?
presents as purple pathces, plaques, and nodules on the skin; may also involve visceral organs
50
What three populations is kaposi sarcoma classically seen in? how does it present and how is it treated?
1 Older Eastern European males - tumor remains localized to skin; treatment involves surgical removal 2 AIDS- tumor spreads early; treatment is antiretroviral agents (to boost immune system) 3 Transplant recipients - tumor spreads early; treatment involves decreasing immunosuppresion.