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D2 - FALL - Par 3 > Path - Blood vessels > Flashcards

Path - Blood vessels Flashcards

1
Q

Vasculogenesis

A

De novo formation of blood vessels during embryogenesis.

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2
Q

Angiogenesis

A

The process of new vessel formation in the mature organism (Neovascularization)

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3
Q

Arteriogenesis

A

Remodeling of existing arteries in response to chronic changes in pressure or flow.

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4
Q

What is the predominant cellular element in the vascular media?

A

vascular smooth muscle cells

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5
Q

What is intimal thickening?

A
  • stereotypic response to vascular injury
  • Vascular injury → endothelial cell loss/dysfunction → muscle cells growth and matrix synthesis → intimal thickening (neointima)
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6
Q

What is the difference between neointimal SM cells & medial SM cells?

A

Neointimal smooth muscle cells do not contract, but are able to divide.

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7
Q

What are the steps of the intimal thickening process?

A
  1. Migration of smooth muscle cells to the intima
  2. Smooth muscle cells mitosis
  3. Elaboration of extracellular matrix
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8
Q

At what blood pressure is it considered hypertensive? Malignant hypertensive?

A

HYPERTENSION
Systolic > 139 mmHg, Diastolic > 89 mmHg

MALIGNANT
> 200/120 mmHg

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9
Q

What are the 2 classification of hypertension, and which one is more common?

A
  1. idiopathic/primary/essential hypertension
  2. secondary hypertension

idiopathic/primary/essential is more common.

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10
Q

What is the difference between the 2 classifications of hypertension?

A
  1. idiopathic/primary/essential hypertension
    - hereditary - familial/genetic factors
  2. secondary hypertension
    - caused by an identifiable underlying secondary cause
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11
Q

Hypertension causes what effects to the walls of large & medium arteries? What about to small blood vessels?

A 
large & medium arteries:
- aortic dissection
- cerebrovascular hemorrhage
small blood vessels
- hyaline arteriolosclerosis
- hyperplastic arteriolosclerosis
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12
Q

What is an aortic dissection?

A

separation of aorta walls; tear in inner wall of aorta causes blood to flow betw layers of the wals of aorta, forcing layers apart

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13
Q

What is a cerebrovascular hemorrhage?

A

intracranial hemorrhage that occurs w/i brain tissue

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14
Q

What is hyaline arteriolosclerosis?

A

thickening/hardening of arteriole walls by deposition of hyaline material; narrowed lumen

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15
Q

What is hyperplastic arteriolosclerosis?

A

narrowed lumen; caused by malignant hypertension; prominent in kidney, can lead to schemia & acute renal failure

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16
Q

What are the 3 general patterns of arteriosclerosis? “Briefly” describe each of them.

A
  1. Atherosclerosis – affects large elastic arteries (aorta and major branches) like heart attacks etc
  2. Monckeberg’s medial calcific sclerosis – affects medium muscular arteries (arms and legs)
  3. Arteriolosclerosis – affects arterioles
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17
Q

Between the ages 40 & 60, what has a fivefold increased incidence?

A

myocardial infarction

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18
Q

Why do males have a higher risk of atherosclerosis?

A

estrogen has an atheroprotective effect.

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19
Q

What is the “bad cholesterol” and what does it do?

A

Low-density lipoprotein (LDL) cholesterol - form of cholesterol delivered to peripheral tissue.

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20
Q

What is the “good cholesterol” and what does it do?

A

High-density lipoprotein (HDL) mobilizes cholesterol from tissue, transporting to the liver.

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21
Q

Higher levels of HDL have been correlated with reduced risk of atherosclerosis. T/F?

A

True!

On the other hand, higher levels of LDL are correlated with increased risk of atherosclerosis.

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22
Q

Hypertension increases risk of ____ by approx 60% and causes left ventricular hypertrophy.

A

IHD (ischemic heart disease)

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23
Q

Diabetes increases the risk of stroke and a 100-fold increased risk for what?

A

atherosclerosis-induced gangrene of lower extremeties

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24
Q

What is C-reactive protein?

A

C-reactive protein (CRP) is an acute phase protein and its concentration in serum reflects the inflammatory condition of the patient

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25
Q

What is the morphology of an atheromatous plaque?

A

a raised lesion w/ a soft, yellow, grumous core of lipid (mainly cholesterol) covered by a white fibrous cap

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26
Q

What is the pathogenesis of atherosclerosis?

A
  1. chronic endothelial injury
  2. endothelial dysfunction
  3. smooth muscle emigration from media to intima & macrophage activation
  4. macrophages & SM cells engulf lipid
  5. SM proliferation & other ECM deposition & extracellular lipid
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27
Q

What are some complications of atherosclerosis plaque changes?

A
  1. Rupture, ulceration, or erosion → thrombosis → ischemia
  2. Hemorrhage into a plaque
  3. Atheroembolism
  4. Aneurysm formation
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28
Q

What is the difference between vulnerable & stable atherosclerotic plaques?

A
  • Vulnerable plaque, susceptible to rupture, ulceration or erosion of the luminal surface, with a thin fibrous cap, a large lipid core, and active inflammation (macrophages)
  • Stable plaque, with densely collagenous and thickened fibrous cap with minimal inflammation
29
Q

How can statins help reduce atherosclerosis formation/risk?

A

statins = a class of drugs which lowers circulating cholesterol levels (inhibit HMG-CoA reductase)

30
Q

Difference between true and false aneurysm?

A

True aneurysms have an INTACT attenuated arterial wall or a thinned ventricular wall, while a false aneurysm involves a ventricular RUPTURE with an extravascular hematoma.

31
Q

2 types of aneurysms?

A

sacular & fusiform

32
Q

2 most important disorders predisposing to aortic aneurysms are?

A

atherosclerosis & hypertension

33
Q

What is a berry aneurysm?

A

aka congenital aneurysm due to congenital weakness at bifurcation in Circle of Willis.

34
Q

Aortic dissection usu occurs in what two groups?

A
  1. Men aged 40-60 with hypertension
  2. Younger patients with systemic or
    localized abnormalities of connective tissue affecting the aorta (Marfan syndrome)
35
Q

What is the morphology of an aortic dissection?

A
  • Usually initiates w/ an intimal tear → extending the dissecting hematoma
  • No inflammation
  • Cystic medial degeneration as the most frequent pre-existing histologically detectable lesion
36
Q

Difference between the 2 classifications of dissections? Which one has more serious complications?

A

A – Involves the ascending aorta and/or aortic arch, and possibly the descending aorta. It includes DeBakey types I and II.

B – Involves the descending aorta or the arch (distal to the left subclavian artery), without involvement of the ascending aorta. It includes DeBakey type III.

*The serious complications predominantly occur in type A dissections.

37
Q

What is an example of a small vessel vasculitis?

A

granulomas, no asthma (Wegener granulomatosis)

38
Q

What is an example of a medium vessel vasculitis?

A

immune complex mediated (polyarteritis nodosa)

39
Q

What is an example of a large vessel vasculitis?

A

granulomatous disease (giant cell arteritis, Takayasu arteritis)

40
Q

What is the most common form of vasculitis among old people in US & Europe? And describe it briefly.

A

Giant-cell (temporal) arteritis: chronic, granulomatous inflammation of large to small-sized arteries; predominantly in head.

  • has nodular intimal thickening, reduced luminal diameter, medial granulomatous inflammation, elastic lamina fragmentation
  • ex. of large vessel vasculitis
41
Q

What is an oral manifestation of giant-cell (temporal) arteritis?

A

tongue necrosis

42
Q

What is polyarteritis nodosa (PAD)?

A
  • systemic vasculitis of small or medium-sized muscular arteries (usu renal & visceral aa’s)
  • starts w/ segmental transmural necrotizing inflamm
  • may lead to thrombosis
43
Q

What is Wegener Granulomatosis?

A
  • Acute necrotizing granulomas of U/L respiratory tract or both
  • Necrotizing or granulomatous vasculitis affecting small to medium-sized vessels
  • Renal disease (necrotizing glomerulonephritis)
44
Q

What is a useful marker of Wegener Granulomatosis’s disease activity?

A

PR3-ANCAs

45
Q

What is an oral manifestation of Wegener Granulomatosis?

A

strawberry gingivitis, palatal ulcers & perforation

46
Q

What is Thromboangiitis Obliterans (Buerger Disease)?

A
  • Segmental, thrombosing, acute and chronic inflammation of medium-sized and small arteries (tibial and radial arteries)
  • Almost exclusively in heavy smokers, > 35 years old
47
Q

What are early manifestations of Thromboangiitis Obliterans (Buerger Disease)? What are the chronic manifestations?

A

Early manifestations:

  • Superficial nodular phelebitis
  • Cold sensitivity of the Raynaud type in the hands
  • Pain in the foot induced by exercise (instep claudication)

Chronic ulcerations followed in time by frank gangrene

48
Q

What is the Raynaud Phenomenon?

A
  • Fingers become white due to lack of blood flow, then blue as vessels dilate to keep blood in tissues, finally red as blood flow returns (RED, WHITE, & BLUE, BBY! ‘MURICA)
  • Results from an exaggerated vasoconstriction of digital arteries and arterioles
49
Q

What are varicose veins?

A
  • Abnormally dilated, tortuous veins
50
Q

What is the cause of varicose veins?

A

prolonged, increased intraluminal pressure and loss of vessel wall
support

51
Q

What is the diff betw Thrombophlebitis and Phlebothrombosis?

A
  • Thrombophlebitis - inflammation of a vein w/ blood clot formation inside the vein
  • Phlebothrombosis - thrombosis in vein w/o primary inflamm
52
Q

Where are the majority of deep venous thrombosis (DVT)?

A

in deep leg veins (>90% of cases)

*Pulmonary embolism as a serious complication of DVT

53
Q

What is Homan sign?

A

pain in the calf of the leg upon dorsiflexion of the foot with the leg extended that is diagnostic of thrombosis in the deep veins of the area

54
Q

What is a vascular ectasia?

A
  • Nevus Flammeous = most common form of vascular ectasia
  • ectasia = local dilation
  • telangiectasia = permanent dilation of pre-existing small vessels forming a red lesion
55
Q

What is Sturge-Weber Syndrome (Encephalotrigeminal Angiomatosis)?

A
  • a congenital disorder that is a special form of nevus flammeous
  • ipsilateral venous angioma in cortical leptomeninges
  • includes mental retardation, seizure, & hemiplegia ( paralysis of the arm, leg, and trunk on the same side of the body)
56
Q

What is an arterio-venous (vascular) malformation?

A
  • Uncommon errors on vascular morphogenesis
  • Distinct from hemangioma (tumor of the endothelial cells that line BV’s)
  • Not a neoplasm
  • Present at birth but may not clinically evident
  • Consist of abnormal channels lined by normal endothelium
57
Q

What are the differences between vascular malformations VS infantile hemangioma?

A

Vascular malformation: present at birth, no rapid inc in size, no involution

Hemangioma: not always present at birth, rapid inc in size, involution

58
Q

What is a pyogenic granuloma?

A
  • Reactive Vascular Proliferations (Tumor-like Conditions)
  • common, fast-growing lesion of the skin and mucous membranes
  • Focal reactive growth of fibrovascular or granulation tissue with extensive endothelial cells proliferation
  • gingiva = common site
59
Q

Most common soft tissue tumors of infancy? And the common place for these tumors?

A

hemangioma (type of benign neoplasm); head & neck

60
Q

What are the 2 types of lymphangiomas mentioned Describe them.

A

Lymphangiomas = benign neoplasms
- Types:
1. Simple (capillary) lymphangiomas:
raised lesions, up to 1-2 cm, predominantly seen in head, neck, and axillary subcutaneous tissues
2. Cavernous lymphangiomas (cystic hygromas): found in the neck or axilla of children, up to 15 cm in size

61
Q

What is an angiosarcoma?

A
  • malignant endothelial neoplasm affecting older adults
  • could get angiosarcoma in setting of lymphedema in pts w/ breast cancer after radical mastectomy
  • associated w/ radiation
62
Q

What compound is associated w/ lung cancer & angiosarcomas of the liver and brain?

A

Polyvinyl Chloride

63
Q

What is an endothelial marker for angiosarcoma?

A

diffuse positivity of tumoral cells for CD31

64
Q

What is Kaposi Sarcoma (KS)?

A
  • a malignant vascular neoplasm that is caused by humans herpesvirus 8 (HHV8)
  • highly associated w/ AIDS
  • 4 forms of KS: classic, endemic african, transplant-associated, AIDS-associated (epidemic)
65
Q

What is the classic type of Kaposi Sarcoma?

A
  • A disorder of older men
  • Associated with malignancy or altered immunity but not with HIV infection
  • As multiple red-purple skin plaques or nodules
  • Usu in distal lower extremities
66
Q

What is the Endemic African type of Kaposi Sarcoma?

A
  • In HIV-seronegative individuals
  • Younger than age 40
  • Lymph nodes /visceral involvement
  • Aggressive course
67
Q

What is the transplant-associated type of Kaposi Sarcoma?

A
  • In solid organ transplant recipients in the setting of T-cell immunosuppression
  • Aggressive course
  • Lymph nodes, mucosa, and visceral involvement
68
Q

What is the AIDS-associated type of Kaposi Sarcoma?

A
  • Most common HIV-related malignancy
  • Often oral mucosa and lymph nodes involvement
  • Palate and gingiva as most common locations in the mouth

D2 - FALL - Par 3 (10 decks)

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