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CPR II Week 1 > Robbins Ch 11 Vascular Pathology part 1 > Flashcards

Robbins Ch 11 Vascular Pathology part 1 Flashcards

1
Q

What part of the blood vessel is characterized as a single layer of endothelial cells sitting on a basement membrane underlaid by a thin layer of extracellular matrix?

A

Intima

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2
Q

What part of the blood vessel is characterized as concentric smooth muscle layers in arteries while it is disorganized in veins?

A

Media

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3
Q

In elastic arteries, what is there is a greater amount of to help change shape with the pulse?

In muscular arteries, what is there more of to allow the artery to change shape as the body need?

A

1) Elastin

2) Concentric smooth muscle layers

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4
Q

What does atherosclerosis mainly affect?

What does HTN mainly affect?

A

1) Elastic and muscular arteries

2) Small muscular arteries and arterioles

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5
Q

What are direct connections between arteries and veins that can be made surgically?

What does it provide vascular access for?

A

1) AV fistulas

2) Chronic hemodialysis

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6
Q

What are characterized by focal irregular thickenings in medium and large muscular arteries?

What classic appearance does it have?

What population is it seen most commonly in?

A

1) Fibromuscular dysplasia
2) String of beads
3) Young women

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7
Q

Vascular wall response to injury is always?

A

Intimal thickening

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8
Q

What are the relaxing factors involved in vascular injury?

What are the contracting factors?

A

1) NO, kinins, and prostaglandins

2) Endothelin, angiotensin II, and catecholamines

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9
Q

What cells are motile, acquire new biosynthetic capabilities, and move from the media to the intima?

A

Neointimal smooth muscle cells

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10
Q

Individual with a blood pressure above what are more at risk of atherosclerotic disease?

A

140/90

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11
Q

Hypertensive vascular disease will lead to?

A

Left ventricular hypertrophy

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12
Q

Most hypertensive vascular disease patients are asymptomatic until late in the course and 50% of untreated patients will die of?

Another 33% die from?

A

1) Ischemic heart disease or congestive heart failure

2) Stroke

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13
Q

What blood pressure is defined as malignant HTN?

A

BP > 200/120

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14
Q

What is seen when aldosterone causes the BP to rise by increasing Na+ reabsorption in the DCT?

A

Increased preload

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15
Q

What is the most common form of secondary HTN?

A

Aldosterone metabolism

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16
Q

Arterioles that show homogenous pink (“glassy”) thickening with associated luminal narrowing describes the morphology of?

A

Hyaline arteriolosclerosis

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17
Q

Hyaline arteriolosclerosis is due to excess hemodynamic stress that causes there to be?

A

More matrix deposition and plasma proteins to leak across the endothelial cell membrane

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18
Q

Diabetic microangiography lesions are that of?

A

Hyaline arteriolosclerosis

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19
Q

Vessels show concentric laminated (“onion skin”) thickening of the walls with luminal narrowing describes the morphology of?

A

Hyperplastic arterioles

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20
Q

When is estrogen therapy beneficial in treating atherosclerosis?

When is there no benefit from the therapy?

A

1) Younger postmenopausal women

2) Older postmenopausal women

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21
Q

What is the most common cause of left ventricular hypertrophy?

A

Chronic HTN

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22
Q

What is the best biomarker to look for inflammation?

A

C reactive protein (CRP)

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23
Q

In the pathogenesis of atherosclerosis, macrophages phagocytose lipids and become?

A

Foam cells

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24
Q

The two most important causes of endothelial dysfunction are?

A

1) Hemodynamic disturbances

2) Hypercholesterolemia

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25
Q

What are the dominant lipids in plaques?

A

Cholesterol and Cholesteryl esters

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26
Q

What creates a stable plaque?

What creates an unstable plaque?

A

1) Smooth muscle cells synthesize extracellular matrix (collagen)
2) Inflammatory cells in atheromas may increase breakdown of extracellular matrix components

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27
Q

What may fatty streaks evolve into?

A

Plaques

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28
Q

Atherosclerotic plaques are more likely to occur at places of?

A

Turbulent flow like branch points

29
Q

What are the most commonly involved arteries for atherosclerotic plaque?

A

1) Lower abdominal aorta
2) Coronary arteries
3) Popliteal arteries
4) Internal carotid arteries
5) Circle of Willis

30
Q

What occurs if an atheroma ruptures, ulcerates, or erodes?

A

Exposes highly thrombogenic substances such as tissue factor and leads to thrombosis

31
Q

What is the point at which there is a 70% decrease in cross-sectional area?

A

Critical Stenosis

32
Q

How do plaques that are responsible for myocardial infarction and other acute coronary syndromes present?

A

Often asymptomatic before the acute change

33
Q

What destabilizes the mechanical integrity of the fibrous cap?

A

Plaque inflammation which is the net increase in collagen degradation and reduced collagen synthesis

34
Q

What does a true aneurysm involve?

A

An attenuated but intact arterial wall or thinned ventricular wall of the heart

35
Q

What is characterized as a defect in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space?

What type of aneurysm is it?

A

1) Pulsating hematoma

2) False aneurysm

36
Q

What is defective in Marfan syndrome?

What does this lead to?

A

1) Fibrillin synthesis

2) Hyperactive TGFβ signaling which leads to cardiovascular abnormalities

37
Q

What is defective in Loeys-Dietz syndrome?

What does this lead to?

A

1) TGFβ receptor mutations

2) Hyperactive TGFβ signaling which leads to cardiovascular abnormalities

38
Q

Why is the balance of collagen degradation and synthesis altered by inflammation and associated proteases?

A

Increased MMPs and/or decreased TIMPs

39
Q

What is characterized by ischemia of the medial media which leads to aortic changes with smooth muscle cell loss leading to scarring, lack of matrix synthesis and production of amorphous ground substance?

A

Cystic medial degeneration

40
Q

What is characteristic of late-stage syphilis?

What does tertiary syphilis lead to?

A

1) Obliterative endarteritis

2) Thoracic aortic aneurysm

41
Q

What is the greatest risk factor for Abdominal Aortic Aneurysm?

What is it for ascending aortic aneurysm?

A

1) Atherosclerosis

2) HTN

42
Q

What population is most affected by AAA?

Where does it commonly occur?

A

1) Male smokers > 50 yo

2) Below renal arteries above iliac bifurcation

43
Q

How do inflammatory AAA commonly present?

A

Younger patients who present with back pain

44
Q

Immunoglobulin G4 (IgG4)-related disease AAA responds well to?

A

Steroid therapy

45
Q

What size is an AAA at risk of rupture?

A

6 cm = 25% / year

46
Q

What noticeable sign and symptom is seen with thoracic aortic aneurysm?

What is it due to?

What is this called?

A

1) Chronic cough
2) Recurrent laryngeal nerve palsy
3) Ortner syndrome

47
Q

What is the major risk factor for aortic dissection?

A

HTN

48
Q

What type of aortic dissection is more dangerous?

What does it invovle?

A

1) Proximal lesion (Type A)

2) Ascending aorta

49
Q

Where does the Distal lesion (Type B) of aortic dissection occur?

When does it involve the ascending aorta?

A

1) Distal to the subclavian artery

2) Never

50
Q

What is the most common cause of death from aortic dissection?

A

Rupture into pericardial, pleural or peritoneal cavities

51
Q

The clinical manifestations of aortic dissections include?

A

1) Cardiac tamponade
2) Aortic insufficiency
3) Widened mediastinum

52
Q

What antibodies are seen with Microscopic Polyangiitis and Churg-Strauss Syndrome?

What are seen with Wegener’s granulomatosis (polyangiitis)?

A

1) p-ANCA = MPO-ANCA

2) c-ANCA = PR3-ANCA

53
Q

Immune Complex Associated Vasculitis is associated with antibodies directed against?

A

Drugs or streptokinase

54
Q

Kawasaki disease has antibodies to?

It is the leading cause of?

What is the Tx for it?

A

1) Endothelial cells
2) Acquired heart disease in kids
3) Aspirin

55
Q

What is the most common form of vasculitis among adults over 50 in the United States and Europe?

A

Giant Cell (Temporal) Arteritis

56
Q

Why is Giant Cell (Temporal) Arteritis a medical emergency?

A

Permanent blindness

57
Q

What is characterized by severe luminal narrowing of great vessel branches?

What clinical feature does it lead to?

What does it classically involve?

A

1) Takayasu Arteritis
2) Weakening of pulses in UE
3) Aortic arch

58
Q

Because the clinical features and histology are very similar between Giant Cell Arteritis and Takayasu Arteritis, the diagnosis is usually made based on?

A

1) patients < 50 years = Takayasu Arteritis

2) patients > 50 years = giant cell arteritis/aortitis

59
Q

30% of patients with polyarteritis nodosa (PAN) have a vasculitis attributable to immune complexes composed of?

What does PAN spare?

What population is it most common in?

A

1) HBsAg and HBsAb
2) Pulmonary circulation
3) Young adults

60
Q

How are the lesions characterized in microscopic polyangiitis?

What is found in 90% of patients?

What is also commonly seen?

A

1) All lesions are the same stage and distributed widely
2) Necrotizing glomerulonephritis
3) Pulmonary capillaritis

61
Q

What is Churg-Strauss Syndrome associated with?

What is it characteristically accompanied by?

A

1) Asthma

2) Granulomas and eosinophils

62
Q

The triad of Oral aphthous ulcers, Genital ulcers, and Uveitis is diagnostic of?

What is the most likely cause of mortality due to this disorder?

A

1) Behcet disease

2) Rupture of vascular aneurysms

63
Q

Granulomatosis with Polyangiitis (Wegener Granulomatosis) resembles what condition?

A

PAN but with respiratory involvement

64
Q

Thromboangiitis Obliterans (Buerger Disease) involves what arteries?

What population is affected?

A

1) Tibial and radial arteries

2) Heavy smokers younger than 35 yo

65
Q

What will classically show red, white, and blue changes from most proximal to most distal of the extremities?

What do the red and blue color changes mean?

A

1) Raynaud Phenomenon

2) Red is vasodilation, blue is vasoconstriction

66
Q

Which type of Raynaud’s affects the extremities asymmetrically?

Symmetrically?

A

1) Secondary

2) Primary

67
Q

Greater than 20 minutes of vasoconstriction in a coronary artery can lead to?

A

MI

68
Q

What may we see with myocardial vessel vasospasm?

A

Contraction band necrosis

CPR II Week 1 (7 decks)

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