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CPR II > (1) Blood Vessels; Part 1 (Martin) > Flashcards

(1) Blood Vessels; Part 1 (Martin) Flashcards

1
Q

***Self Review***

What are the three layers within a blood vessel?

A

Intima

Media

Adventitia

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2
Q

***Self Review***

What differentiates the intima from the media?

A

Internal elastic lamina

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3
Q

***Self Review***

What is the clinical importance of the internal elastic lamina?

A

VERY common site for damage within vessels

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4
Q

***Self Review***

Describe a elastic artery

A

High elastin content

–> Allows for expansion during systole and recoil during diastole

Becomes less compliant with age

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5
Q

***Self Review***

Describe a muscular artery

A

Circumferentially oriented smooth muscle

Contribues to arteriolar:

Contraction=vasoconstriction

Relaxation=dilation

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6
Q

***Self Review***

Describe arterioles

A

Main point of physiologic resistance to blood flow

Resistance to fluid flow is INVERSELY proportional to the fourth power of the diameter

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7
Q

***Self Review***

What is contained within the adventitia?

A

Vasa Vasorum

“Vessels of the vessels”

Small arterioles supply O2 to the outer media of large arteries

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8
Q

***Self Review***

Describe the characteristics of capillaries

A

Diameter of RBC

No media

contains pericytes

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9
Q

***Self Review***

Describe the characteristics of veins

A

Most inflammatory reactions ooccur here

Larger lumens, thinner and less organized walls

Contains about 2/3 of total blood volume

Less rigid

Reverse flow due to gravity prevented in the extremities by venous valves

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10
Q

***Self Review***

Describe lymphatics

A

Thin walled, lined by specialized endothelium

Returns interstinal tissue and inflammatory cells to the bloodstream

Transports bacteria etc, tumor cells

*THE PATHWAY FOR DISEASE DISSEMINATION

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11
Q

Where does gas and nutrient exchange occur in the vasculature?

A

Capillary

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12
Q

Where is blood pressure regulated within the vasculature?

A

Arteriole

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13
Q

What structure is contained within veins but NOT arteries?

A

ONE WAY VALVES

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14
Q

What are the three primary vascular anomalies?

A
  • Aneurysms
  • Arteriovenous malformations (AVM)
  • Fibromuscular dysplasia
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15
Q

What is an aneurysm?

A

Localized abnormal dilation of a blood vessel or the heart

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16
Q

How does an aneurysm develop?

A

NOT present at birth

Develops over time due to underlying defect in the media of the vessel

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17
Q

Describe what arteriovenous malformations (AVM) are:

A

When arteries directly connect with veins without intervening capillaries

They are tangle, worm-like vascular channels with significant PULSATILE arteriovenous shunting with high blood flow

Large or multiple AVMs may shunt blood leading to cardiac failure

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18
Q

Describe what fibromuscular dysplasia is

A

Focal irregular thickening

in medium and large muscular arteries

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19
Q

How does fibromuscular dysplasia typically arise?

A

USUALLY developmental defect

rarely rises from trauma

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20
Q

Berry Aneurysms

Where does this commonly occur?

A

Circle of Willis

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21
Q

​Berry Aneurysms

What is the most common clinical report of patients with Berry Aneurysms?

A

“The worst headache I’ve ever had”

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22
Q

​Berry Aneurysms

Anatomically, where are they frequently found within the circle of willis?

A

Branch points of the anterior circulation

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23
Q

​Berry Aneurysms

Most frequent cause?

A

Subarachnoid hemorrhage (SAH)

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24
Q

​Berry Aneurysms

Typical size?

A

>10 mm in diameter

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25
Q

​Berry Aneurysms

Approximatly 1/3 of ruptures are associated with…

A

Acute increases in intracrainal pressure

eg Straining at stool, Sexual orgasm…nice

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26
Q

​Berry Aneurysms

Fatality percentage?

A

25-50% die with first rupture

-Repeat bleeding common in survivors

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27
Q

What is a mycotic aneurysm?

A

Can be one of the three…

  1. embolization of a SEPTIC EMBOLUS which is usually a complication of infective endocarditis
  2. an extension of an adacent suppurative process
  3. circulating organisms directly infecting the arterial wall
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28
Q

What are the 4 types of aneurysm?

A
  1. Saccular (berry) ***most common
  2. Giant
  3. Fusiform
  4. Mycotic
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29
Q

Describe the appearance of an AVM:

A

Wormy, tangled

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30
Q

Why would you surgically induce an AVM?

A

To generate a arteriovenous fistula to provide vascular access for chronic hemodialysis

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31
Q

Describe the appearance of fibromuscular dysplasia

A

“String of beads”

Focal irregular thickening in medium and large muscular arteries

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32
Q

What population is highly susceptible to fibromusclar dysplasia?

A

1st degree relatives

YOUNG WOMEN

33
Q

What is one of first responses of the vascular wall to injury?

A

Intimal thickening

34
Q

Basal and Activated Endothelial Cell States

What are some aggrevating factors that can activate an endothelial cell?

A

Turbulent flow

Hypertension

Cytokines

Complement

Bacterial products

Lipid products

Hypoxia

Viruses

CIGARETTE SMOKE

35
Q

Basal and Activated Endothelial Cell States

What occurs once an endothelial cell is ACTIVATED?

A
  • Increased expression of procoagulents, adhesion molecules and proinflammatory factors
  • Altered expression of chemokines, cytokines and growth factors
36
Q

Describe the response to vascular injury in three steps

A
  1. Recruitment of smooth muscle cells TO the intima
  2. Smooth muscle cell mitosis
  3. Elaboration of extracellular matrix
37
Q

Define Hypertensive vascular disease

A

Sustained…

Diastolic >89

or

Systolic >139

38
Q

What is a highly associated pathology associated with hypertensive vascular disease?

A

Atherosclerosis

39
Q

What are the three subtypes of hypertension?

A

Secondary HTN

Essential HTN

Malignant HTN

40
Q

What are the causes of:

Seconary HTN

Essential HTN

Malignant HTN

A

Seconary HTN = underlying renal/adrenal dz

Essential HTN = idiopathic

Malignant HTN= pre-existing benign HTN

41
Q

Which is the MOST and LEAST common?

Seconary HTN

Essential HTN

Malignant HTN

A

Seconary HTN (LEAST) 5%

Essential HTN (MOST) 90-95%

Malignant HTN (LEAST) 5%

42
Q

What population is at risk for essential HTN?

A

Increases with age

African-american

43
Q

Describe the origin of secondary HTN

A

The hypertension is secondary to renal artery stenosis which is caused by increased production of renin from the ischemic kidney

44
Q

What is the BP of a malignant HTN patient?

A

Systolic >200mmHg

Diastolic >120mmHg

45
Q

Neural factors that influence peripheral resistance

What are the constrictors?

What are the dilators?

A

Constrictors = alpha adrenergic

Dilators = beta adrenergic

46
Q

Humoral factors that influence peripheral resistance

What are the constrictors?

What are the dilators?

A

Constrictors = Angtiotensin II, Catecholamines, Thromboxane, Leukotrienes, Endothelin

Dilators = Prostaglandins, Kinins, NO

47
Q

Describe how blood volume and vascular tone are modified and maintained

A

RAAS System

  • With low volume/resistance, RENIN is released by JGG cells
  • RENIN cleaves angiotensinogen–> angiotensin I
  • Angiotensin I is cleaved to form angiotensin II by ACE
  • Angiotensin II also stimulates release of aldosterone which causes renal reabsorption of Na+ and H2O
48
Q

What are the two forms of small blood vessel disease?

A
  1. Hyaline arteriolosclerosis
  2. Hyperplastic arteriolosclerosis
49
Q

Describe the appearance of Hyaline arteriolosclerosis

A

Increase in smooth muscle matrix synthesis

Homogenous pink (hyaline) thickening of the vessel wall

(in nephrosclerosis, aquire glomerular scarring therefore non-functional)

50
Q

When does Hyperplastic arteriolosclerosis occur?

What does it look like?

A

Occurs in SEVERE HTN

Smooth muscle cells form concentric lamellations (“onion skinning”) –> luminal narrowing

51
Q

What does arteriosclerosis literally mean?

A

“hardening of the arteries”

-Arterial wall thickening and loss of elasticity

(generic term)

52
Q

What is Monckeberg medial sclerosis?

Population affected?

A

Calcification of muscular arteries, internal elastic membrane invloved. UNIQUE b/c there is NO narrowing of lumen and NO clinical significance

>50y/o

53
Q

What causes more deaths in the western world than any other disorder?

A

ATHEROSCLEROSIS

It accounts for aprox. half of all deaths in western world…damn

54
Q

Describe what an artherosclerotic plaque is:

A

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

55
Q

What impacts can an artherosclerotic plaque have clinically?

A

Mechanically obstructing blood flow

Atherosclerotic plaques can rupture, leading to catastrophic obstructive vascular thrombosis

Can increase diffusion distance from the lumen to the media

56
Q

What is the most significant risk factor for atherosclerosis?

A

Hypercholesterolemia

57
Q

Clinically, what does C Reactive Protein (CRP) help predict?

A

Cardiovascular risk

58
Q

What are the two most important factors contributing to the pathogenesis of atherosclerosis?

A
  1. Hemodynamic turbulence
  2. Circulating lipids
59
Q

IMPORTANT IMAGE

Describe the arterial wall response to injury

A
  1. Chronic endothelial injury
  2. Endothelial dysfunction
  3. Macrophage activation
  4. Macrophages and smooth muscle cells engulf lipid
  5. Smooth muscle proliferation + collagen + ECM deposition
60
Q

What are the major immunologic contributors to inflammation in atherosclerosis?

A

IL-1

T-lymphocytes

Macrophages

61
Q

What is this image an example of?

A

Fatty streaks

62
Q

What are these images?

A

A) Mild aortic atherosclerosis

B) Severe aortic atherosclerosis

63
Q

What are the potential consequences of stenosis of the arterial lumen?

A

May lead to chronic ischemia of myocardium, bowel, brain, the extremities, etc.

64
Q

What is Critical stenosis?

A

Approx. 70% of lumen is occluded

65
Q

Here’s a summary of the clinical complications of atherosclerosis

A
66
Q

What is the difference b/w a vulnerable and stable plaque?

A
67
Q

What is the difference b/w a “true” vs “false” aneurysm?

A

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

False= defect through the wall of the vessel, or heart, communicating with an extravascular hematoma that freely communicates with the intravascular space

68
Q

What is an arterial dissection?

A

Blood enters a defect in the arterial wall and tunnels between it’s layers

69
Q

When would an aneurysm occur?

A

Whenever the connective tissue of the vascular wall is weakened

  1. Defective vascular wall CT
  2. Net degredation of vascular wall CT
  3. Weakening of the vascular wall by ischemia
70
Q

Tertiary syphilis is…

A

ischemia of outer media (thoracic aorta)

71
Q

Describe the appearance of normal vs marfan elastin within the blood vessel

A
72
Q

Where do abdominal aortic aneurysms (AAA) occur?

What usually causes?

How is it detected?

A

Usually below the renal arteries

typically caused by atherosclerosis

Pulsating mass in the abdomen

73
Q

AAA’s that are __ cm or greater are usually managed surgically

A

5cm

74
Q

AAA are due to:

A

Hypertension

or

Marfans

75
Q

What is Marfan?

A

AD

Defective synthesis of fibrillin

Leads to aberrant TGF-beta

76
Q

What is the most characteristic description of an aortic dissection?

A

Sudden onset of severe chest pain that…

RADIATES to the back b/w the scapulae

and moving downwards as the dissection progresses

77
Q

Most aortic dissections occur in the…

A

Ascending aorta w/in 10cm of the aortic valve

78
Q

Describe the Stanford classification scheme os dissections

A
79
Q
A

CPR II (30 decks)

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