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ICOM-Cardio > Cardio-Path- Peripheral vascular and aortic disease > Flashcards

Cardio-Path- Peripheral vascular and aortic disease Flashcards

1
Q

What is the innermost layer of medium to large blood vessels?

A

tunica intima

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2
Q

The tunica intima consists of:

A

endothelium, and a thin subendothelial layer

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3
Q

The subendothelial layer of the tunica intima consists of:

A

loose connective tissue sometimes containing smooth muscle fibers

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4
Q

In arteries/veins the intima includes a thin layer, the internal elastic , composed of elastin, with holes allowing better diffusion of substances from blood deeper into the wall.

A

arteries; lamina

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5
Q

What is the middle layer of the medium to larger blood vessels and what does it consist of:

A

tunica media; layers of helically arranged smooth muscle cells.

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6
Q

What other elements are interspersed in the smooth muscle fibers of the tunica media:

A

elastic fibers and elastic lamellae, reticular fibers, and proteoglycans, all of ( which are produced by the smooth muscle cells.)

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7
Q

What is the external elastic lamina and where is it found?

A

In arteries the media may have it separating it from the outermost tunic.

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8
Q

What is the outermost layer of the blood vessel called?

A

adventitia or tunica media

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9
Q

What does the adventitia (tunica media) consist of:

A

connective tissue consisting principally of type I collagen and elastic fibers.

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10
Q

What is the vasa vasorum and where can it be found?

A

: arterioles, capillaries, and venules in the adventitia and outer part of the media in larger vessels

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11
Q

What are abnormally dilated tortuous veins produced by chronically increased intraluminal pressures and weakened vessel wall support?

A

varicose veins

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12
Q

Which veins are typically involve in vericose vein pathology?

A

The superficial veins of the upper and lower leg are typically involved.

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13
Q

What are the statistics of men and women who have vericose veins?

A

Up to a fifth of men and a third of women develop lower-extremity varicose veins.

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14
Q

What major risk factor increases likelihood of vericose veins?

A

obesity

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15
Q

What is the higher incidence of varicose veins in women attributed to?

A

probably reflects the prolonged elevation in venous pressure caused by compression of the inferior vena cava by the gravid uterus during pregnancy

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16
Q

There is/is not a familial tendency toward premature varicosities.

A

is

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17
Q

Describe the pathology of varicose veins?

A

dilation renders the venous valves incompetent and leads to lowerextremity stasis, congestion, edema, pain, and thrombosis.

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18
Q

The most disabling sequelae include which 2 things:

A

persistent edema in the extremity and secondary ischemic skin changes, stasis dermatitis and ulcerations.

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19
Q

What secondary ischemic skin changes are included with sequelae of varicose veins?

A

stasis dermatitis and ulcerations.

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20
Q

Ulcers from varicose veins can become , due to poor wound healing and superimposed infections.

A

chronic

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21
Q

Embolism from these superficial veins is very rare, in contrast with the relatively frequent emboli that arise from thrombosed?

A

deep veins.

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22
Q

Thrombosis of deep leg veins accounts for > 90% of cases of and - venous thrombosis accompanied by inflammation.*

A

thrombophlebitis; phlebothrombosis

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23
Q

In DVT of the legs, what is the most important risk factor?

A

prolonged immobilization resulting in venous stasis

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24
Q

What are thrombophlebitis and phlebothrombosis -

A

venous thrombosis accompanied by inflammation.

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25
Q

What are some independent risk factors of DVT?

A

postoperative state, CHF, pregnancy, oral contraceptive use, malignancy, obesity, male sex, and age over 50 years.

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26
Q

What kind of defects can predispose affected individuals to development of thrombophlebitis?

A

Inherited defects in coagulation factors

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27
Q

Describe venous thrombi that can result from elaboration of procoagulant factors from cancers?

A

the resulting hypercoagulable state can manifest as thromboses in different vascular beds at different times, so-called “migratory thrombophlebitis” or “Trousseau syndrome.”

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28
Q

Thrombi in legs tend to produce many/few reliable signs or symptoms.

A

few

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29
Q

Local manifestations of distal edema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling, and pain can indicate:

A

DVT

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30
Q

In some DVT cases, pain is elicited by pressure over affected veins, squeezing the calf muscles, or forced dorsiflexion of the foot which is called?

A

Homan sign

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31
Q

What is Homan’s sign?

A

pain elicited from forced dorsiflexion of the foot and can indicate DVT

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32
Q

Many DVTs are asymptomatic/symptomatic?

A

asymptomatic, especially if bed ridden

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33
Q

What is is a common and serious clinical complication of DVT, resulting from fragmentation or detachment of the venous thrombus?

A

Pulmonary embolism

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34
Q

In many cases, the first manifestation of thrombophlebitis is what?

A

pulmonary embolus.

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35
Q

refers to an acute inflammation caused by bacterial seeding of the lymphatic vessels.

A

Lymphangitis

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36
Q

What are the physical symptoms on skin of lymphangitis?

A

The inflamed lymphatics appear as red, painful subcutaneous streaks, usually associated with tender enlargement of draining lymph nodes (acute lymphadenitis).

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37
Q

What happens if bacteria are not contained within the lymph nodes?

A

they can pass into the venous circulation and cause bacteremia or sepsis.

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38
Q

What are the 2 causes of primary lymphedema?

A
  1. isolated congenital defect

]2. familial Milroy disease (heredofamilial congenital lymphedema), resulting from agenesis or hypoplasia of lymphatics.

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39
Q

What stems from the accumulation of interstitial fluid behind an obstructed, previously normal lymphatic?

A

Secondary (obstructive) lymphedema

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40
Q

What are 5 causes of Secondary (obstructive) lymphedema?

A

Tumors involving either the lymphatic channels or the regional lymph nodes

✴ Surgical procedures that sever lymphatic connections, e.g., axillary lymph nodes in radical mastectomy.

✴ Postradiation fibrosis

✴ Filariasis

✴ Postinflammatory scarring

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41
Q

Regardless of cause, lymphedema increases the pressure in the lymphatics distal to the obstruction and causes edema.

A

hydrostatic

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42
Q

Chronic edema in turn may lead to deposition of and , producing brawny induration or a peau d’orange appearance of the overlying skin (common in breast cancer).

A

ECM; fibrosis

43
Q

Rupture of dilated lymphatics, typically following obstruction by an infiltrating tumor mass, can lead to milky accumulations of lymph in various spaces designated:

A

chylous ascites, chylothorax, and chylopericardium.

44
Q

What can lead to milky accumulations of lymph in various spaces

designated chylous ascites, chylothorax, and chylopericardium?

A

Rupture of dilated lymphatics,

45
Q

What literally means “hardening of the arteries” reflecting arterial wall thickening with loss of elasticity?

A

Arteriosclerosis

46
Q

Arteriosclerosis (hardening of arteries) can be reflected in which 3 conditions?

A

Atherosclerosis

Mönckeberg medial sclerosis

Arteriolosclerosis

47
Q

What pathology affects small arteries and arterioles and may cause downstream ischemic injury?

A

Arteriolosclerosis

48
Q

What are the 2 variants of Arteriolosclerosis?

A

The two variants are hyaline and hyperplastic arteriolosclerosis

note: hyaline (pink) on the left and hyperplastic on the right (onion skin)

49
Q

What is characterized by calcific deposits in muscular arteries, usually around the internal elastic lamina, and typically in individuals over 50 years of age?

A

Mönckeberg medial sclerosis

50
Q

Mönckeberg medial sclerosis lesions do/do not encroach on the vessel lumen, and usually are/are not clinically significant.

A

do not; are not

51
Q

What are congenital or acquired dilations of blood vessels of the heart?

A

Aneurysms

52
Q

“True” aneurysms involve all layers of the artery (intima, media, and adventitia) or the attenuated wall of the heart; these include atherosclerotic and congenital.*

A

three

53
Q

What are discrete outpouchings ranging from 5 to 20 cm in diameter in an artery, often with a contained thrombus?

A

saccular aneurysm

54
Q

What are circumferential dilations up to 20 cm in diameter in arteries; these most commonly involve the aortic arch, the abdominal aorta, or the iliac arteries?

A

fusiform aneurysms

55
Q

Fusiform aneurysms are circumferential dilations up to 20 cm in diameter; these most commonly involve which 3 types of arteries?

A

the aortic arch,

the abdominal aorta,

or the iliac arteries.

56
Q

What patology involves pressurized blood gains entry to the arterial wall through a surface defect and then pushes apart the underlying layers?

A

arterial dissections

57
Q

When do aneurysms occur:

A

when alterations in SMCs (smooth muscle cells) or ECM compromise the structural integrity of the arterial media.

58
Q

Alterations in SMCs or ECM compromise the structural integrity of the arterial media include these 3 factors:

A

Inadequate/abnormal connective tissue synthesis

Excessive connective tissue degradation

Loss of smooth muscle cells (SMCs) or change in the SMC synthetic phenotype

59
Q

Which growth factor regulates SMC proliferation and matrix synthesis?

A

TGF-β

60
Q

Mutations in receptors or downstream signaling pathways result in defective elastin and collagen synthesis.

A

TGF-β

61
Q

Which condition results defective synthesis of the scaffolding protein fibrillin leading to increased TGF-β in the aortic wall, with subsequent dilation due to dysregulated signaling and progressive loss of elastic tissue?

A

Marfan syndrome

note: the dark purple squiggles are elastin, which is lost in Marfan syndrome

62
Q

Marfan syndrome is an example of or connective tissue synthesis

A

Inadequate; abnormal

63
Q

increased matrix expression by macrophages in atherosclerotic plaque can contribute to aneurysm development by degrading arterial in the arterial wall (media).

This is an example of Excessive connective tissue degradation that can lead to aneurysm

A

metalloprotease; ECM

64
Q

Atherosclerotic thickening of the intima can cause of the inner media by increasing the diffusion distance from the lumen.

A

ischemia

65
Q

Which pathology can cause luminal narrowing of the aortic vasa vasorum, leading to ischemia of the outer media?

A

systemic hypertension

66
Q

What effect does ischemia have on smooth muscle cells of blood of arteries?

A

SMC loss as well as aortic “degenerative changes,” including fibrosis, inadequate ECM synthesis, and accumulation of of proteoglycans.

67
Q

What is cystic medial degeneration of blood vessels?

A

“degenerative changes,” including fibrosis, inadequate ECM synthesis, and accumulation of of proteoglycans.

note: the image on the left is cystic medial degeneration

you can visualize the lost of elastic tissue in the tunica media

68
Q

The two most important predisposing conditions for aortic aneurysms?

A

atherosclerosis and hypertension.

69
Q

Of the two important predisposing conditions for aortic aneurysms are atherosclerosis and hypertension, which is the most dominant factor for abdominal aortic aneurysms?

A

atherosclerosis

70
Q

Of the two important predisposing conditions for aortic aneurysms, atherosclerosis and hypertension, which is the most dominant factor for ascending aortic aneurysms?

A

hypertension

71
Q

Abdominal aortic aneurysms (AAAs) occur more frequently in and in and rarely develop before years of age

A

men; smokers; 50

72
Q

What s is a major cause of abdominal aortic aneurysms?

A

Atherosclerosis, but other factors contribute

73
Q

In the majority of cases, AAA’s results from mediated by proteolytic enzymes released from inflammatory infiltrates in atherosclerotic lesions.

A

ECM degradation

74
Q

What type of enzymes are released from inflammatory infiltrates in atherosclerotic lesions that can lead to abdominal aortic aneurysm?

A

proteolytic ennzymes

75
Q

What 2 effects lead to degeneration and necrosis, which results in arterial wall thinning and AAA?

A
  1. ECM degradation mediated by proteolytic enzymes released from inflammatory infiltrates in atherosclerotic lesions.
  2. Atherosclerotic plaques also compromise the diffusion of nutrients and wastes between the vascular lumen and the arterial wall with negative effects on SMCs in the media.
76
Q

Degeneration and necrosis of artery can lead to :

A

arterial wall thinning

77
Q

Where do abdominal aortic aneurysms typically occur?

A

between the renal arteries and the aortic bifurcation

78
Q

Describe the physical characteristics of AAA?

A

saccular or fusiform, and up to 15 cm in diameter and 25 cm in length.

In the majority of cases, extensive atherosclerosis is present, with thinning and focal destruction of the underlying media.

79
Q

What can the aneurysmal sac of an AAA look like?

A

contains bland, laminated, poorly organized mural thrombus, which can fill much of the dilated segment

80
Q

What are 4 clinical consequences of AAA?

A
  1. obstruction
  2. embolism
  3. abdominal mass
  4. rupture/hemorrhage
81
Q

The risk for rupture is related to which factor of AAAs?

A

size

82
Q

Those cm or less in diameter almost never burst.

A

4

83
Q

Those between cm rupture at a rate of 1%/yr

A

4-5

84
Q

The risk rises to 11%/yr for AAAs cm in diameter, and to 25%/yr for aneurysms > 6 cm in diameter.

A

5 to 6; 6

85
Q

Which size of diameter or larger is manage surgically?

A

5 cm

86
Q

Thoracic aortic aneurysms most commonly are associated with which 3 pathlogies?

A

hypertension, bicuspid aortic valves, and Marfan syndrome

87
Q

What is the condition when blood splays apart the laminar planes of the media to form a blood-filled channel within the aortic wall?

A

aortic dissection

note: devastating if ruptures through adventitia

88
Q

Which 2 age groups are aortic dissections most likely to occur?

A

Men 40 to 60 years of age with previous hypertension (over 90% of cases) •

Younger patients with CT abnormalities that affect the aorta, eg, Marfan syndrome.

89
Q

What is the major risk factor for aortic dissection?

A

HTN

90
Q

What effects does HTN have on the aorta?

A

narrowing of the vasa vasorum associated with degenerative changes in ECM and variable loss of medial SMCs, suggesting that diminished flow through the vasa vasorum is contributory

91
Q

Heritable or acquired connective tissues disorders that can lead to aortic dissections include which 2 conditions?

A

Marfan syndrome

Ehlers-Danlos syndrome IV

92
Q

The trigger for the intimal tear and subsequent intra­mural hemorrhage is/is not known in most cases

A

is not

93
Q

Where does blood under systemic pressure dissect through the media?

A

along laminar planes.

94
Q

What aggressive therapy may be effective in limiting an evolving a dissection?

A

Aggressive pressure-reducing therapy

95
Q

In most dissections, the intimal tear marking the point of origin is found in the aorta within 10 cm of the aortic .

A

ascending; valve

96
Q

What do dissection tears look like?

A

transverse or oblique in orientation and 1 to 5 cm long, with sharp, jagged edges.

97
Q

The dissection plane can extend retrograde toward the heart or distally, occasionally as far as the and arteries, and usually lies between the middle and outer of the media.*

A

iliac; femoral; thirds

note: blood dissecting through media

98
Q

The most serious complications occur with dissections involving which part of aorta?

A

proximal aorta and arch.

99
Q

Describe the 2 classifications types of aortic dissections?

A

Proximal lesions (type A dissections), involving the ascending aorta, with or without involvement of the descending aorta (DeBakey type I or II).

Distal lesions (type B dissections), usually beginning beyond the subclavian artery (DeBakey type III)

100
Q

What is the classic clinical symptom of aortic dissection?

A

sudden onset of excruciating tearing or stabbing pain, usually beginning in the anterior chest, radiating to the back between the scapulae, and moving downward as the dissection progresses

101
Q

The most common cause of death with an aortic aneurysm is?

A

rupture of the dissection into the pericardial, pleural, or peritoneal cavity

102
Q

What is the treatment for type A dissections?

A

rapid diagnosis and institution of intensive anti-hypertensive therapy coupled with surgical repair of the aortic intimal tear can save 65 - 85% of the patients.

103
Q

What is the treatment protocol of type B dissections?

A

managed conservatively; patients have a 75% survival rate whether they are treated with surgery or with antihypertensive medication only.

104
Q
A

ICOM-Cardio (32 decks)

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