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CV II Exam 2 > Blood Vessels > Flashcards

Blood Vessels Flashcards

1
Q

Identify the blacked out portions of the artery shown

A
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2
Q

What are the primary regulators of arterial blood pressure?

A

Arterioles (and small muscular arteries)

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3
Q

What is the typical diameter of arterioles?

A

20-100 um

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4
Q

What is the Hagen-Poiseuille equation?

A
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5
Q

What are the categories of arteries?

A
  1. Large or elastic
  2. Medium-sized or muscular
  3. Small (less than or equal to 2 mm in diameter)
    - vasa vasorum
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6
Q

In veins, what is the site of leukocyte exudation and vascular leakage?

A

Postcapillary venules

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7
Q

What is the approximate diameter of a capillary?

A

7-8 um or roughly the diameter of a red blood cell

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8
Q

What size lymph vessels have valves?

A

larger lymph vessels

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9
Q

Endothelial cells contain Weibel-Palade bodies. What the hell are these?

A

membrane-bound storage organelles that contain vWF

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10
Q

What are the three types of capillaries?

A

Continuous

Fenestrated

Discontinuous

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11
Q

What are three typical locations for continuous capillaries?

A

fat

muscle

nervous system

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12
Q

What are three typical locations for fenestrated capillaries?

A

intestinal villi

endocrine glands

kidney glomeruli

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13
Q

What are three typical locations for discontinuous capillaries?

A

liver

bone marrow

spleen

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14
Q

Endothelial cells can elaborate anticoagulant, antithrombotic and fibrinolytic regulators. What are four of these?

A

Prostacyclin

Thrombomodulin

Heparin-like molecules

plasminogen activator

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15
Q

Endothelium can elaborate prothrombotic molecules, what are three examples of these?

A

vWF

Tissue factor

Plasminogen activator inhibitor

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16
Q

Endothelial cells have the ability to produce ECM, including collagen and proteoglycans. What are some examples of how they do this?

A

Modulation of blood flow and vascular reactivity

vasoconstrictors: endothelin, ACE

Vasodilators: NO and prostacyclin

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17
Q

In what ways to endothelial cells contribute to regulation of inflammation and immunity?

A

IL-1

IL-6

chemokines

Adhesion molecules

  • VCAM-1

ICAM

E-selectin

P-selectin

Histocompatibility antigens

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18
Q

In what ways does endothelium regulate cell growth?

A

Growth stimulators: PDGF, CSF, FGF

Growth inhibitors: heparin, TGF-β

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19
Q

Vascular smooth muscle is responsible for vasoconstriction and dilation. What are they regulated by?

A
  1. promoters
  2. Inhibitors
  3. RAAS
  4. Catecholamines
  5. Estrogen and osteopontin
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20
Q

What does vascular smooth muscle do in response to injury?

A

Migrates to the intima and proliferates

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21
Q

What does vascular smooth muscle synthesize post injury?

Elaborate?

A

Synthesizes

  • collagen
  • elastin
  • proteoglycans

Elaborate

growth factors

cytokines

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22
Q

What are the three vascular anomalies that we discussed? Which can rupture?

A
  1. Developmental (congenital, berry) aneurysms
  2. Arteriovenous Fistulas.
  3. Fibromuscular dysplasia

1 and 2 can rupture

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23
Q

Focal irregular medial and intimal hyperplasia with thickening of walls of medium and large muscular arteries… would describe what?

A

Fibromuscular dysplasia

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24
Q

Which component of blood pressure is more important in determining cardiovascular risk?

A

Systolic BP

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25
Q

What are five things htn is a risk factor for?

A
  1. Aortic dissection
  2. cerebral vascular accidents
  3. hypertensive heart disease
  4. coronary artery disease
  5. renal failure
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26
Q

HTN is sustained chronically elevated pressure. What are the numbers we need to remember for Dr. Gomez?

A

140/90

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27
Q

BP is proportional to cardiac output and peripheral vascular resistance. What are some major facctors that determine blood pressure?

A

Age

Gender

BMI

Diet

Genetic variations in RAAS

Na+ retention

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28
Q

controlled hypertension with no short term problems describes what?

A

Benigh (essential HTN)

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29
Q

What are the guidlines for hypertensive urgency?

A

•systolic >220 mm Hg or diastolic >120 mm Hg with no evidence of target organ damage

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30
Q

What is described here?

•significant increase in B. P. associated with target organ damage (flame-shaped hemorrhages or exudates of fundus, renal failure, headache, angina, etc.)

A

Accelerated hypertension

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31
Q

What are the types of hypertensive emergencies we discussed?

A

Accelerated HTN

Malignant hypertension

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32
Q

Describe the process of renovascular hypertension

A

Renal artery stenosis

→↓glomerular flow +/- ↓pressure in the glomerulus afferent arteriole

→ ↑renin secretion

→ ↑angiotensin I

→ ↑angiotensin II

→1) vasoconstriction

→↑ peripheral resistance

→ 2) ↑ aldosterone

→↑ sodium reabsorption

→↑ blood volume

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33
Q

What is Liddle syndrome?

A

Liddle Syndrome – moderately severe salt sensitive hypertension due to Increased distal tubular reabsorption of Na+ with aldosterone stimulation

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34
Q

What disease process is shown here?

Where does this typically occur?

A

Atherosclerosis

primarily in elastic arteries and muscular arteries

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35
Q

What is this?

Where does it occur?

A

Arteriosclerosis

small arteries and arterioles

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36
Q

What is shown here?

Where does it typically occur?

In what populations?

A

Monckeberg Medial Calcific Sclerosis

Muscular arteries of those over 50 y/o, with no vessel lumen narrowing (can ossify)

37
Q

What is shown here?

Who is this seen in?

A

1.Hyaline arteriolosclerosis - Protein deposition (hyalinized)

Seen in

  • aging
  • diabetes mellitus
  • benign nephrosclerosis (hypertension)
38
Q

What is shown here? When is this seen?

A

Hyperplastic arterioloslerosis,, cell death (onion skinning) with or without arteriolitis

Seen in malignant HTN

39
Q

How does licorice cause HTN?

A

It contains aldosterone analogues. Someone who regularly eats licorice will have elevated Na+ concentrations and thus HTN.

40
Q

What are some endocrine causes of HTN?

A
  • Adrenocortical hyperfunction (Cushing syndrome, primary … aldosteronism, congenital adrenal hyperplasia, licorice ingestion)
  • Exogenous hormones (glucocorticoids, estrogen [including … >> >>pregnancy-induced and oral contraceptives], sympathomimetics
  • and tyramine-containing foods, monoamine oxidase inhibitors)
  • Pheochromocytoma
  • Acromegaly
  • Hypothyroidism (myxedema)
  • Hyperthyroidism (thyrotoxicosis)
  • Pregnancy-induced
41
Q

What are some renal causes of HTN?

A

Acute glomerulonephritis

Chronic renal disease

Polycystic disease

Renal artery stenosis

Renal vasculitis

Renin-producing tumors

42
Q

What are the cardiovascular causes of HTN?

A

Coarctation of aorta

Polyarteritis nodosa

Increased intravascular volume

Increased cardiac output

Rigidity of the aorta

43
Q

What are some neurologic causes of HTN?

A

Psychogenic

Increased intracranial pressure

Sleep apnea

Acute stress, including surgery

44
Q

How do oral contraceptives contribute to HTN?

A

Increased Angiotensinogen

45
Q

How does a 11B-hydrozylase deficiency contribute to HTN?

A

Increased aldosterone production, similar to effects from an aldosteronoma

46
Q

What areas are prone to atherosclerosis?

A

Those with turbulent flow and low shear stress

47
Q

Laminar flow induces endothelial genes for products that protect againts?

A

atherosclerosis (superoxide dismutase)

48
Q
  1. What characterizes Type I atherosclerosis?
  2. What is its sequence in the atherosclerotic progression?
  3. What is the main growth mechanism?
  4. When is the onset?
  5. What is the clinical correlation?
A
  1. Isolated macrophage foam cells - “fatty dots”
  2. First in the sequence, progresses to Type II
  3. Mainly lipid accumulation
  4. From first decade
  5. Clinically silent
49
Q

What characterizes Type II atherosclerosis?
What is its sequence in the atherosclerotic progression?
What is the main growth mechanism?
When is the onset?
What is the clinical correlation?

A
  1. Mainly intracellular lipid accumulation - “fatty streak” lesions
  2. Step II, progresses to step III
  3. Lipid accumulation
  4. First decade
  5. Silent clinically
50
Q

What characterizes Type III atherosclerosis?
What is its sequence in the atherosclerotic progression?
What is the main growth mechanism?
When is the onset?
What is the clinical correlation?

A
  1. Type II changes and core small extracellular lipid pools.
  2. Third, progressed to fourth
  3. Third decade
  4. Silent
51
Q

What characterizes Type IV atherosclerosis?
What is its sequence in the atherosclerotic progression?
What is the main growth mechanism?
When is the onset?
What is the clinical correlation?

A
  1. Type II changes and a core of extracellular lipid
  2. Step 4, progresses to step five OR six
  3. lipid accumulation
  4. third decade
  5. silent OR overt
52
Q

What characterizes Type V atherosclerosis?
What is its sequence in the atherosclerotic progression?
What is the main growth mechanism?
When is the onset?
What is the clinical correlation?

A
  1. Fibroatheroma - lipid core and fibrotic layer, or multiple lipid cores and fibrotic layers, or mainy calcific or mainly fibrotic
  2. step five, progresses to step 6
  3. Accelerated smooth muscle and collagen increase
  4. Fourth decade
  5. silent or overt
53
Q

What characterizes Type VI atherosclerosis?
What is its sequence in the atherosclerotic progression?
What is the main growth mechanism?
When is the onset?
What is the clinical correlation?

A
  1. complicated lesion - surfacce defect, hematoma-hemorrhage, thrombus
  2. step6, final step
  3. fourth decade
  4. silent or overt
54
Q

What stage of atherosclerosis is shown in this sample from the aorta of a 45 y/o male recently deceased from a CVA?

A

Stage IV, with diffuse and complicated lesions including an ulcerated plaque (open arrow) and a lesion with an overlying thrombus (closed arrow)

55
Q

What is shown here?

A

Stage II atherosclerosis

Note the fatty streaks indicated by arrows on gross image and the presence of Fatty dot, macrophage derived foam cells.

56
Q

Is this an example of complicated lesions?

A

No, this is mild atherosclerosis only, with fibrous plaques

57
Q

Identify!

A

This is a coronary artery with atheromatous plaque

A - masson’s trichrome stain

B- elastin stain

C- hematoxylin and eosin stain (revealing calcification and neovascularization)

58
Q

Identify the indicated portions of the atherosclerotic plaque

A
  1. Fibrous cap
  2. necrotic center
  3. media
59
Q

Which example of these two vessels is more likely to rupture?

A

The one on the left, due to the narrow fibrous cap.

60
Q

Is this plaque likely to rupture?

Why?

A

Yes, due to the invaginated and thin fibrous cap.

61
Q

What is shown here?

A

A ruptured atherosclerotic plaque with a superimposed thrombus

62
Q

What are the non-modifiable (constitutional) risk factors for atherosclerosis?

A

Genetic Abnormalities - familial hypercholesterolemia

Family history

Increasing age

Male gender

63
Q

What are some modifiable risk factors for atherosclerosis?

A

Hyperlipidemia

HTN

Smoking

DM I or II

Inflammation

64
Q

If you have two risk factors, how much does this increase your risk for atherosclerosis?

3 risk factors?

A

2 risk factors - 4 times the risk

3 risk factors - 7 times the risk

65
Q

What constitutes metabolic syndrome?

A

Obesity

Dyslipidemia

hypertension

Insulin resistance

(may also see hypercoagulation and inflammatory state)

66
Q

What is an example of a drug that inhibits HMG-CoA reductase?

A

Statins

67
Q

Characterize cholesterol metabolism!

A

2/3 via LDL receptor pathway

1/3 via scavenger receptor pathway (oxidized LDL)

68
Q

Where are most LDL receptors located?

A

~75% on hepatocytes

69
Q

What does the LDL receptor bind?

What is the process that this event leads to?

A

Apolipoproteins B-100 and E on LDL and IDL.

  1. →Endocytotic internalization
  2. →↑Cytoplasmic cholesterol
  3. → Inhibition of cholesterol synthesis
70
Q

In what ways does LDL receptor binding inhibit cholesterol synthesis? (3)

A
  1. Inhibition of 3-hydroxy-3-methylglutaryl (3-HMG) coenzyme A reductase, which is the rate limiting step in the synthetic pathway.
  2. activates acyl-CoA: cholesterol acyltransferase (ACAT), which favors esterification and storage of excess cholesterol.
  3. Down regulates the synthesis of cell surface LDL receptors
71
Q

In addition to the inhibition of HMG-CoA reductase, what other effect do statins have on cholesterol metabolism?

A

They promote synthesis of LDL receptors

  • ↓intracellular cholesterol allows ↑LDL receptor formation
72
Q

What is the number for LDL that is where a patient is in need of therapy?

A

LDL-C > or equal to 190 mg/dL

73
Q

↑LDL, ↓ HDL and ↑Lp(a) are associated with ?

A

Increased atherosclerosis

74
Q

What impact do estrogens have on lipid levels?

A

•↑ HDL &↓ LDL

75
Q

What impact does estrogen replacement therapy have on the risk of heart attacks in post menopausal women?

A

None

76
Q

What is the risk increase for coronary artery disease with oral contraceptives in women over 35 who also smoke?

A

2x Increased risk of coronary artery disease

77
Q

What is mutated in familial hypercholesterolemia?

A

LDL receptor gene is mutated, leading to elevated LDL and IDL cholesterol in plasma.

78
Q

What pathway for lipid elimination takes over in familial hypercholesterolemia?

A

Oxidized LDL receptors take over - the scavenger pathway

79
Q

What is the most common class of familial hypercholesterolemia?

A

Type II - Transport to the golgi complex from the endoplasmic reticulum is impaired d/t abnormal protein folding.

80
Q

What is the inheritance pattern of familial hypercholesterolemia?

A

Autosomal dominant

81
Q

What are the three things shown in these images of a patient with familial hypercholesterolemia?

Is this patient hetero or homozygous?

A
  1. Planar xanthoma
  2. xanthelesma
  3. Arcus Juvenilis (senilis in adult)

Homozygous

82
Q

To what degree are heterozygous patients with familial hypercholesterolemias plasma cholesterol levels elevated?

A

2-3x

83
Q

How much higher are plasma cholesterol levels in a patient who is a homozygote for the familial hypercholeterolemia mutation?

A

5x normal

84
Q

What are the complications that arise d/t familial hypercholesterolemia?

A
  1. Severe atherosclerosis
  2. mitral valve stenosis
  3. corneal arcus
  4. Xanthomas
85
Q

What are four other risk factors for atherosclerosis that we covered?

A
  1. Elevated homocysteine
  2. presence of lipoprotein a
  3. Elevated plasminogen activator inhibitor 1
  4. infections from Chlamydia pneumoniae, herpes virus and CMV
86
Q

What is C-reactive protein? Where is it produced?

A

•Acute-phase reactant synthesized primarily by the liver

87
Q

What are the roles of C-reactive protein?

A
  • Has roles in opsonizing bacteria and activating complement
  • Involved in endothelial adhesion of WBCs and thrombosis
88
Q

What does C-reactive protein strongly and independently predict the risk for?

(4 things)

A
  1. MI
  2. Stroke
  3. peripheral artery disease
  4. sudden cardiac death
89
Q

Does lowering CRP reduce cardiovascular risk?

A

No evidence of this… although smoking cessation, weight loss, statins and exercise lower C reactive protein and decrease risk.

CV II Exam 2 (8 decks)

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