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Cardiovascular Exam I > Vascular Anomalies, HTN, Atherosclerosis, Aneurysms/Dissections > Flashcards

Vascular Anomalies, HTN, Atherosclerosis, Aneurysms/Dissections Flashcards

1
Q

3 concentric histologic layers of blood vessels

A

Intima (single layer of endothelial cells)

Media (well organized in arteries, haphazard in veins)

Adventitia (external to media, often separated from it by wide external elastic lamina)

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2
Q

Describe media component in elastic arteries

A

High elastin content — allows expansion during systole, recoil during diastole —> propels blood toward organs

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3
Q

What changes occur in the media component of elastic arteries with age?

A

Becomes less compliant with increasing age —> increased systolic BP

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4
Q

Describe media component in muscular arteries

A

Circumfirentially oriented smooth muscle; arteriolar smooth muscle contraction = vasoconstriction, or relaxation = vasodilation

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5
Q

______ are the principle point of physiologic resistance to blood flow — wherein resistance to fluid flow is inversely proportional to the fourth power of the diameter

A

Arterioles

[Small changes in vasoconstriction at this level has profound effects on BP]

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6
Q

Small arterioles that supply O2 to the outer media of large arteries

A

Vaso vasorum

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7
Q

Most inflammatory reactions affect what type of blood vessel?

A

Veins — leads to vascular leakage and leukocyte exudation

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8
Q

Describe architecture of veins

A

Larger lumens, thinner and less organized walls

Less rigid = susceptible to dilation and compresion, as well as infiltration by tumors and inflammatory processes

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9
Q

Reverse flow d/t gravity is prevented in the extremities by ____ ____

A

Venous valves

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10
Q

Describe architecture and function of lymphatic vessels

A

Thin walled, lined by specialized endothelium

Return intestinal fluid and inflammatory cells to the bloodstream

Transport bacteria etc. and tumor cells, making them a pathway for disease dissemination

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11
Q

Blood pressure control occurs at the level of the _______

Gas and nutrient exchange occur at the level of the _____

A

Arteriole

Capillary

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12
Q

ADPKD is associated with what type of vascular anomaly?

A

Berry aneurysm (circle of willis)

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13
Q

Anomaly characterized by abnormal connection between arteries and veins; in other words, capillaries are not present

A

Arteriovenous malformations (AVM)

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14
Q

Large or multiple AVMs may shunt blood from arterial to venous circulation, forcing the heart to pump additional volume leading to ______

A

High-output cardiac failure

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15
Q

Focal irregular thickening in medium and large musclar arteries, including renal, carotid, splanchnic, and/or vertebral vessels

A

Fibromuscular dysplasia

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16
Q

With fibromuscular dysplasia, first degree relatives have an increased incidence, as do young _____.

Medial and intimal hyperplasia leads to _____ _____

This condition displays on angiography as ___________-appearing due to marked attenuation of adjacent media

One of the major complications is development of an ______

A

Women

Luminal stenosis

“String of beads”

Aneurysm

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17
Q

Fibromuscular dysplasia of renal arteries leads to what complication?

A

Renovascular HTN

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18
Q

Cell type that creates nonthrombogenic surface, maintaining blood in fluid state and modulating the medial smooth muscle tone, metabolizing hormones (angiotensin), regulating inflammation, and affecting growth of other cell types (especially muscle cells)

A

Endothelial cells

[note that endothelial dysfunction results in proinflammatory and prothrombogenic state, resulting in thrombus formation, atherosclerosis, and vascular lesions of HTN]

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19
Q

Describe vascular smooth muscle cells

A

Ability to proliferate (can be maladaptive)

Synthesize collagen, elastin, and proteoglycans

Elaborate growth factors and cytokines

Vasoconstriction and/or dilation

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20
Q

Stereotypical response of a vessel wall to ANY insult

A

Intimal thickening

[associated with endothelial cell dysfunction or loss; stimualtes sm m cell recruitment and proliferation and associated matrix synthesis]

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21
Q

Neointimal sm m cells are motile, undergo cell division, and acquire new biosynthetic capabilities

T/F: smooth muscle cells can not return to nonproliferative state even if endothelial layer is normalized

A

False — these cells CAN return to nonproliferative state with normalization of endothelial layer (a change that may take place with lifestyle modifications, medication, etc.)

However, the healing response can result in intimal thickening that may impede blood flow

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22
Q

What is the initial event following vascular injury?

A

Endothelial cell activation!

Insults d/t turbulent flow, HTN, cytokines, complement, bacterial products, lipid products, hypoxia, acidosis, viruses, cig smoke, etc. —> increased expression of PROCOAGULANTS, ADHESION MOLECULES, and proinflammatory factors as well as altered expression of chemokines, cytokines, and GROWTH FACTORS signify “activated state”

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23
Q

Response to vascular injury:

  1. Recruitment of smooth muscle cells or smooth muscle precursor cells to the _____
  2. Smooth muscle cell _____
  3. Elaboration of ______
A

Intima

Mitosis

ECM (thrombogenic!)

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24
Q

Definition of hypertensive vascular disease as it relates to increased risk of atherosclerosis

A

Sustained systolic > 139 mmHg, or sustained diastolic >89 mmHg associated with increased risk of atherosclerosis

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25
Q

Causes of secondary HTN

A

Primary aldosteronism, Cushing syndrome, or pheochromocytoma

[other causes — renal disease, exogenous hormones, acromegaly, thyroid conditions, pregnancy, coarctation of aorta, polyarteritis nodosa, psychogenic, sleep apnea, acute stress, increased ICP]

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26
Q

HTN secondary to __________ is caused by increased production of renin from the ischemic kidney.

A _____ can be heard on auscultation of the affected kidneys

A

Renal artery stenosis

Bruit

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27
Q

What pt populations are at increased risk of essential (primary) HTN? What are some complications?

A

Risk factors: increasing age, African Americans have higher prevalence

Complications: cardiac hypertrophy and heart failure, multi-infarct dementia, renal failure

50% of untreated HTN pts die of ischemic heart disease (IHD) or CHF; another 1/3 die of stroke

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28
Q

Signs and symptoms of malignant HTN

A

Systolic > 200 mmHg, diastolic > 120 mmHg

Severe HTN, renal failure, retinal hemorrhages and exudates, +/- papilledema; often superimposed on pre-existing benign HTN

Untreated leads to death within 1-2 years

29
Q

BP is a function of what 2 physiologic processes?

A

Cardiac output — HR and stroke volume (strong influence by blood volume — relationship with renal sodium excretion vs. reabsorption)

Peripheral vascular resistance — regulated at level of arterioles; influenced by neural and hormonal inputs

30
Q

Humoral and neural factors that cause constriction in peripheral vessels

A 
Humoral: 
Angiotensin II
Catecholamines
Thromboxane
Leukotrienes
Endothelin

Neural:
Alpha-adrenergic

31
Q

Humoral and neural factors that cause dilation in peripheral vessels

A

Humoral:
Prostaglandins
Kinins
NO

Dilators:
Beta-adrenergic

32
Q

The volume expansion resulting from activation of the RAAS induces myocardial release of ______, leading to Na+ excretion and diuresis as well as vasodilation - thus lowering BP

A

ANP

33
Q

What condition in the kidney might result in RAAS activation and ANP release?

A

Renal artery stenosis

34
Q

Compare/contrast the 2 forms of small blood vessel disease result from HTN

A

Hyaline arteriolosclerosis — homogenous pink (hyaline) thickening of the vessel wall, with associated luminal narrowing

Hyperplastic arteriolosclerosis — occurs in SEVERE HTN, smooth muscle cells form concentric lamellations (“onion skinning”) with resultant luminal narrowing

35
Q

What condition tends to occur in those >50 y/o and is characterized by calcification of muscular arteries, involving internal elastic membrane, but there is NO narrowing of the lumen, and thus NO clinical significance?

A

Monckeberg medial sclerosis

36
Q

Raised lesion with a soft grumous core of lipid covered by a fibrous cap

A

Atheroma = atheromatous = atherosclerotic plaque

[used interchangeably]

37
Q

Why are premenopausal women somewhat protected from atherosclerosis?

A

Atheroprotective effects of estrogen

38
Q

Major risk factor for atherosclerosis that is sufficient to initiate atheroma development even in the absence of other factors

A

Hypercholesterolemia

39
Q

How does metabolic syndrome contribute to atherosclerosis risk?

A

Insulin resistance, HTN, dyslipidemia, hypercoagulability, and proinflammatory state may contribute to endothelial dysfunction and/or thrombosis

40
Q

What serum marker may be used to predict cardiovascular risk?

A

C reactive protein (CRP)

41
Q

Atherosclerosis does not occur randomly in vessels, nor does it occur everywhere uniformly. Where do most lesions tend to occur and why?

A

Most lesions tend to occur at opening of exiting vessels, branch points, posterior abdominal aorta, etc. — due to HEMODYNAMIC TURBULENCE and other flow disturbances in these locations

42
Q

Lipids in atheromatous plaques are predominantly cholesterol and cholesterol esters; they accumulate in the _____, are taken up by macrophages and partially oxidized.

This modified LDL further accumulates in macrophages and ______ cells, forming _____ cells and a lesion known as a “fatty streak”. this stimulates an inflammatory response to accumulation of this toxic form of LDL

A

Intima

Smooth muscle; foam

43
Q

As part of the pathogenesis of atherosclerosis, accumulatioin of cholesterol crystals within macrophages is recognized by the inflammasome, which leads to ____ secretion. More macrophages and ______ are recruited and activated. Inflammatory cytokines further activate endothelial cells, and growth factors stimulate smooth muscle cells to migrate to the intima and proliferate.

A

IL-1; T-lymphocytes

44
Q

Several growth factors are implicated in smooth muscle proliferation. What are some examples?

A

PDGF (released by locally adherent platelets)

Fibroblast growth factor

TGF-alpha

45
Q

Once there is initial formation of an atheromatous plaque, the soft fibrofatty structure becomes covered with a fibrous cap (dense collagen fibers). The center of the plaque is _______, containing lipid, debris, foam cells, and thrombus, surrounded by a zone of inflammatory and smooth muscle cells

A

Necrotic

46
Q

Common sites of atherosclerosis involvement

A

[in decreasing order of frequency]:

Abdominal aorta
Coronary arteries
Popliteal arteries
Internal carotid arteries
Circle of willis
47
Q

Complications of atherosclerotic plaques

A

Rupture and ulceration — may lead to thrombosis

Hemorrhage — may follow plaque rupture

Embolism — may follow plaque rupture

Aneurysm formation

48
Q

One of the consequences of atherosclerosis is gradual shrinkage of vessel lumen, eventually leading to ischemia downstream. At a point known as _____ _____, approximately 70% of the vessel is occluded which may lead to chronic ischemia of myocardium, bowel, brain, the extremities, etc.

A

Critical stenosis

49
Q

What are some characteristics of atheromatous plaques that are more prone to rupture?

A

Those in which the fibrous cap is continually being remodeled

Those with increased inflammation — which can accelerate cap degradation and inhibit its resynthesis, thus reducing the amount of collagen in the cap and weakening it

Physical stresses can cause plaque rupture — like changes in BP, vasoconstriction, etc.

50
Q

T/F: there is a direct relationship between plaque thickness and likelihood of rupture

A

True — the thicker the plaque, the more vulnerable it is to rupture

51
Q

What is the difference between true vs. false aneurysm?

A

True aneurysm = an intact (but thinned) muscular wall at the site of dilation

False aneurysm = defect through the wall of the vessel, communicating with an extravascular hematoma

52
Q

What connective tissue disorder is associated with increased risk of aneurysm formation?

A

Marfan syndrome — defective fibrillin synthesis

53
Q

Conditions in which there is net degradation of vascular wall CT can predispose pts to aneurysms, this includes inflammatory conditions like atherosclerosis, which result in increased ________

A

Matrix metalloprotease

54
Q

What are some conditions that predispose to aneurysm by weakening the vascular wall by ischemia?

A

Atherosclerosis —> ischemia of inner media

HTN —> ischemia of outer media

Tertiary syphilis —> ischemia of outer media (thoracic aorta)

55
Q

How does tertiary syphilis contribute to ischemia of the outer media (particularly in thoracic aorta)

A

Obliterative endarteritis (characteristic of late-stage syphilis) shows a predilection for small vessels, including those of the vasa vasorum of the thoracic aorta

This leads to ischemic injury of the aortic media and aneurysmal dilation which sometimes involves the aortic valve annulus (aortic valve regurgitation) — sometimes referred to as “tree barking”

56
Q

During pathogenesis of aneurysms, loss of vascular wall elastic tissue, or ineffective elastin synthesis leads to cystic medial degeneration, with disrupted and disorganized elastin filaments and increased ground substance (proteoglycans). Cystic medial degeneration is a final common result of different conditions, including ischemic medial damage and _____ syndrome.

However, the 2 MOST IMPORTANT causes of aortic aneurysms are ______ and ______

A

Marfan

Atherosclerosis; HTN

57
Q

Where do mycotic aneurysms originate from? (multiple)

A

Septic emboli (usually complication of infective endocarditis)

Extension of an adjacent suppurative process

Circulating organisms directly infecting the arterial wall

58
Q

AAAs are characterized by severe _______ of the aorta, covered with mural thrombus. They may be detected as a _________ mass in the abdomen

A

Atherosclerosis; pulsating

59
Q

AAAs occur in the abdominal aorta, usually below the _____ arteries and often involve the _______ arteries

A

Renal; common iliac

60
Q

Complications of AAA

A

Rupture and hemorrhage

Occlusion of branching arteries and downstream ischemia

Embolism

Impingement on another structure

61
Q

AAA rupture risk is related to aneurysm ______

A

Size! — aneurysms 5cm or greater are usually managed surgically

62
Q

Thoracic aortic aneurysms are often d/t _____, or less commonly congenital defects in CT: Marfan syndrome. Marfan is a _____ inherited disorder resulting in defective synthesis of fibrillin (FBN1), leading to aberrant ______ activity that weakens elastic tissue

A

HTN

AD

TGF-B

63
Q

Clinical presentation of thoracic aortic aneurysm

A

Clinical presentation is often d/t impingement of: lower respiratory tree, esophagus, recurrent laryngeal nn

Aortic valvular insufficiency

Rupture

64
Q

Complication of aortic aneurysm in which blood enters a defect in the intima and travels through a tissue plane within layers of the aortic media

Who is most at risk for this complication?

A

Aortic Dissection

Most commonly occurs in hypertensive males age 40-60, or younger patients with Marfans

[primary risk factor is HTN]

65
Q

Classic presentation of aortic dissection

A

Sudden onset of severe chest pain (usually beginning in anterior chest), radiating to the back between the scapulae, and moving downward as the dissection progresses

—can be confused with AMI!

66
Q

What is a “double-barreled aorta”?

A

If dissecting aorta hematoma re-enters the lumen of the aorta through a second distal intimal tear, a new false vascular channel is created — creating appearance of double-barreled aorta

This averts a fatal extraaortic hemorrhage, and over time, such false channels can be endothelialized to become recognizable chronic dissections

67
Q

With aortic dissection, blood enters aortic wall via an intimal tear (cause is generally unknown), forming an intramural hematoma. Usually in hypertensive patients, there is some degree of cystic medial degeneration. Where do most aortic dissections arise?

A

Most arise in the ascending aorta, within 10 cm of the aortic valve

68
Q

Aortic dissections can rupture through the _______ leading to massive hemorrhage or _____ ______ (hemorrhage into pericardial sac)

A

Adventitia; cardiac tamponade

69
Q

Classifications of aortic dissections and which are more common

A

Type A = DeBakey I and Debakey II

Type B = DeBakey III

Type A dissections (involving the ascending aorta) are more common and associated wtih higher morbidity and mortality. They are treated with antihypertensive therapy and an attempt to surgically repair the intimal tear

Cardiovascular Exam I (8 decks)

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