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My Pathoma Unit 4 > Chapter 7 Blood Vessels > Flashcards

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
Q

What two conditions is hyaline arteriolosclerosis a consequence of? what is the etiology of each?

A

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
Q

What does hyperplastic arteriolosclerosis involve? What is the classic appearance?

A

Thickening of vessel wall by hyperplasia of smooth muscle (onion skin appearance)

27
Q

What size vessels does arteriolosclerosis effect?

A

small

28
Q

What does hyaline arteriolosclerosis result in?

A

reduced vessel caliber with end organ ischemia; classically produces glomerular scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure.

29
Q

What is the cause of hyperplastic arteriolosclerosis?

A

malignant HTN

30
Q

What does hyperplastic arteriolosclerosis result in?

A

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
Q

What is monckeberg calcific sclerosis? what are its symptoms?

A

calcification of the media of muscular (medium sized) arteries; nonobstructive. Not clinically significant; seen as an incidental finding on x-ray or mammography

32
Q

What is an Aortic dissection?

A

Intimal tear with dissection of blood though the media of the aortic wall

33
Q

Where do aortic dissections typically occur?

A

Occurs in the proximal 10 cm of the aortic (high stress region) with preexisting weakness of the media.

34
Q

What are two common causes of weakness of the media leading to aortic dissection?

A

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
Q

How does aortic dissection present?

A

Presents as sharp, tearing chest pain that radiates to the back

36
Q

What complications can arise from aortic dissection?

A

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
Q

What is a thoracic aneurysm?

A

Balloon-like dilation of the thoracic aorta

38
Q

What are thoracic aneurysm due to and what are they classically seen in? What is their classic gross appearance?

A

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
Q

What is a major complication in a thoracic aneurysm?

A

dialtion of the aortic valve root, resulting in aortic valve insufficiency

40
Q

What are some other complications of a thoracic aneurysm?

A

compression of mediastinal structures ( eg airway or esophagus) and thrombosis/embolism due to disruption of blood flow

41
Q

Where do abdominal aortic aneurysms usually occur?

A

Below the renal arteries and above the bifurcation.

42
Q

What is AAA primarily due to? who is it seen in?

A

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
Q

How does AAA present?

A

pulsatile abdominal mass that grows with time

44
Q

What is a major compication of an AAA? what is the classic triad seen in this.

A

rupture, especially when >5 cm in diameter; presents with triad of hypotension, pulsatile abdominal mass, and flank pain

45
Q

What are some other complications of an AAA?

A

compression of local structures (eg ureter) and thrombosis/embolism

46
Q

What is a hemangioma? when does it usually present? what structures does it most often involve? does it blanch?

A

Benign tumor comprised of blood vessels.
commonly present at birth; often regresses during childhood
most often involves skin and liver
Blanches

47
Q

What is an angiosarcoma? what are the common sites? what exposures can predispose?

A

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
Q

What is Kaposi sarcoma and what is it associated with? What grade malignancy is it?

A

Low grade malignant proliferation of endothelial cells; associated with HHV-8

49
Q

How does Kaposi sarcoma present?

A

presents as purple pathces, plaques, and nodules on the skin; may also involve visceral organs

50
Q

What three populations is kaposi sarcoma classically seen in? how does it present and how is it treated?

A

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.

My Pathoma Unit 4 (3 decks)

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