Robbins pg. 327-330; 357-363 Flashcards

1
Q

Vascular disease develops through what two principal mechanisms?

A

Narrowing or complete obstruction of vessel lumina, occurring either progressively (e.g., by atherosclerosis) or
acutely (e.g., by thrombosis or embolism)

Weakening of vessel walls, causing dilation and/or rupture

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2
Q

T or F. As arteries narrow to arterioles, the ratio of wall thickness to lumen diameter increases

A

T, to allow more precise regulation of intravascular pressures.

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3
Q

Where does atherosclerosis occur mainly?

A

in larger, muscular arteries

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4
Q

Where does HTN occur mainly?

A

small arterioles

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5
Q

What are the large elastic arteries?

A

aorta, arch vessels, iliac and pulmonary arteries

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6
Q

Describe the structure of large arteries.

A

In these vessels, elastic fibers alternate with smooth muscle cells throughout the media, which expands during systole (storing some of the energy of each cardiac contraction), and recoils during diastole to propel blood distally

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7
Q

What are the medium sized muscular arteries?

A

coronary and renal arteries

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8
Q

Describe the structure of medium sized muscular arteries?

A

The media is composed primarily of smooth muscle cells, with elastin limited to the internal and external elastic lamina. The medial smooth muscle cells are circularly or spirally arranged around the lumen, and regional blood flow is regulated by smooth muscle cell contraction (vaso-
constriction) and relaxation (vasodilation) controlled by the autonomic nervous system and local metabolic factors (e.g., acidosis).

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9
Q

T or F. Arterioles are where blood flow resistance is regulated.

A

T.

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10
Q

How is blood flow regulated in arterioles?

A

As pressures drop during passage through arterioles, the velocity of blood flow is sharply reduced, and flow becomes steady rather than pulsatile.

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11
Q

How big are capillaries?

A

About the size of a single red blood cells

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12
Q

What organs have the highest capillary density?

A

metabolic organs like the heart

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13
Q

Edema and leukocyte emigration characteristic of inflammation occurs preferentially where?

A

in postcapillary venules

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14
Q

Compared to arteries at the same level of branching, how do veins compare? Consequence?

A
  • larger diameter
  • larger lumina
  • thinner walls

Thus, veins are more prone to dilation, external compression, and penetration by tumors or inflammatory processes.

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15
Q

Are endothelial cells similar throughout the body?

A

Although endothelial cells throughout the vasculature
share many attributes, they also show phenotypic variability
depending on the anatomic site and adaptations to local
environmental cues.

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16
Q

What is endothelial activation?

A

endothelial cells respond to various physiologic and pathologic stimuli by modulating their usual (constitutive) functions and by expressing new (inducible) properties

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17
Q

What are some endothelial inducers?

A
  • bacterial/viral products
  • cytokines
  • hemodynamic stress
  • lipid products
  • hypoxia
18
Q

What happens when endothelial cells are activated?

A
  • undergo shape changes,
  • express adhesion molecules, and
  • produce cytokines, chemokines, growth factors, pro- and anticoagulant factors,

and a host of other biologically active products—all presumably intended to respond to the original stimulus.

19
Q

The migratory and proliferative activities of smooth muscle cells are regulated by what?

A
  • PDGF
  • endothelin
  • thrombin
  • fibroblast growth factors, and
  • inflammatory mediators such as IFN-γ and IL-1.
20
Q

Factors that maintain smooth muscle cells in a quiescent state include:

A

heparan sulfate, NO, and TGF-α

21
Q

What are three important congenital vascular anomalies?

A
  • Berry aneurysms
  • Arteriovenous (AV) fistulas
  • Fibromuscular dysplasia
22
Q

What are Berry aneurysms?

A

thin-walled arterial outpouchings in cerebral vessels, classically at branch points around the circle of Willis;

they occur where the arterial media is congenitally attenuated and can spontaneously rupture causing fatal intracerebral hemorrhage

23
Q

What are AV fistulas?

A

abnormal connections between arteries and veins without an intervening capillary bed.

24
Q

What is Fibromuscular dysplasia?

A

a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis.

The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow

25
Q

When does fibromuscular dysplasia occur?

A

It can manifest at any age but occurs most frequently in young women.

26
Q

What are some rules of thumb for distinguishing between benign hemangiomas and malignant angiosarcomas?

A

• Benign tumors usually contain obvious vascular channels
filled with blood cells or lymph that are lined by a monolayer of normal-appearing endothelial cells.

• Malignant tumors are more cellular, show cytologic atypia, are proliferative, and usually do not form well organized vessels`

27
Q

What is Ectasia? Telangiectasia?

A

generic term for any local dilation of a structure

Telangiectasia is used to describe a permanent dilation of preexisting small vessels (capillaries, venules, and arterioles, usually in the skin or mucous membranes) that forms a discrete red lesion.

These lesions can be congenital or acquired and are not true neoplasms.

28
Q

What is nevus flammeus?

A

(a “birthmark”), the most common form of vascular ectasia, is a light pink to deep purple flat lesion on the head or neck composed of dilated vessels.

Most ultimately regress spontaneously.

29
Q

When are spider telangiestasias most common? Association?

A
  • face, neck, or upper chest

- frequently are associated with hyperestrogenic states (e.g., in pregnant women or patients with cirrhosis).

30
Q

What is Hereditary hemorrhagic telangiectasia?

A

(Osler-Weber-Rendu disease) is an AD disorder caused by mutations in genes that encode components of the TGF-β signaling pathway in endothelial cells.

The telangiectasias are malformations composed of dilated capillaries and veins that are present at birth.

The lesions can spontaneously rupture, causing serious epistaxis (nosebleed), gastrointestinal bleeding, or hematuria.

31
Q

T or F. Most hemangiomas regress spontaneously

A

T.

32
Q

While hemangiomas typically are localized lesions confined to the head and neck, they occasionally may be more extensive. What is this called?

A

Angiomatosis- can arise internally. Nearly one third of these internal lesions are found in the liver

Malignant transformation is rare

33
Q

What are some types of hemangiomas?

A
  • capillary hemangiomas
  • juvenile hemangiomas
  • pyogenic granulomas
  • cavernous hemangiomas
34
Q

Describe juvenile hemagiomas.

A

Aka strawberry hemangiomas of the newborn skin are extremely common (1 in 200 births) and can be multiple.

These grow rapidly for a few months but then fade by the age of 1 to 3 years, with complete regression by age 7 in the vast majority of cases.

35
Q

Describe cavernous hemangiomas.

A

composed of large, dilated vascular channels.

Compared with capillary hemangiomas, cavernous hemangiomas are more infiltrative, frequently
involve deep structures, and do not spontaneously
regress.

36
Q

Are cavernous hemangiomas prognostically bad?

A

They may be locally destructive, so surgical excision may be required in some cases. More often the tumors
are of little clinical significance, but they can be cosmetically troublesome and are vulnerable to traumatic ulceration and bleeding.

Brain hemangiomas also are problematic, as they can cause symptoms related to compression of adjacent tissue or rupture.

37
Q

What are glomus tumors?

A

benign, exquisitely painful tumors arising from specialized smooth muscle cells of glomus bodies, arteriovenous structures involved in thermoregulation.

38
Q

How are glomus tumors different from cavernous hemangiomas?

A

Glomangiomas arise from smooth muscle cells, rather than endothelial cells. They most commonly are found in the distal portion of the digits, especially under the fingernails.

Excision is curative

39
Q

What is Bacillary angiomatosis caused by?

A

a vascular proliferation in immunocompromised hosts (e.g., patients with AIDS) caused by opportunistic gram-negative bacilli of the Bartonella family

40
Q

What species of Bartonella are responsible for Bacillary angiomatosis?

A

Bartonella henselae, whose principal reservoir is the domestic cat; this organism causes cat-scratch disease (a
necrotizing granulomatous disorder of lymph nodes) in
immunocompetent hosts.

Bartonella quintana, which is transmitted by human body lice; this microbe was the cause of “trench fever” in
World War I.

41
Q

How do Bartonella cause Bacillary angiomatosis?

A

The bacteria induce host tissues to produce hypoxia-inducible factor-1α (HIF-1α), which drives VEGF production and vascular proliferation.

42
Q

Treatment for Bacillary angiomatosis?

A
The infections (and lesions) are cured by antibiotic
treatment