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IP > Peripheral Arterial Disease > Flashcards

Peripheral Arterial Disease Flashcards

1
Q

define intima

A

the inner-most layer of a blood vessel, including the endothelial monolayer and the elastic extracellular matrix of connective tissue

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2
Q

define platelets

A

small megakarocyte cell fragments that contribute to the formation of clots during vascular injury

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3
Q

define stenosis

A

an abnormal narrowing in a blood vessel or other tubular organ or physiological structure

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4
Q

define foam cell

A

monocyte-derived macrophages that have absorbed high concentrations of oxidized LDL particles

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5
Q

define embolism

A

the migration of material, often from an existing thrombus or clot, though the circulation, leading to formation of a new occlusion in another part of the body

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6
Q

define ischemia

A

a reduction or cessation of blood flow that results in damage to the tissue

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7
Q

blood leaves the heart in (arteries or veins)?

A

arteries

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8
Q

blood returns to the heart in (arteries or veins)?

A

veins

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9
Q

this layer of a blood vessel responds to signals from sympathetic nerves to control the circumference of the vessel

A

media

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10
Q

this is the outer layer of blood vessel and is comprised of connective tissue and collagen-producing fibroblast cells

A

adventitia

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11
Q

the level of resistance of blood flow can be altered by what properties?

A

changes in the viscosity of blood, the length of the blood vessels, and the vessel diameter

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12
Q

name two inhibitory factors that are secreted by the vascular endothelial cells that prevent aggregation of platelets in circulating blood

A

nitric oxide (NO), prostacyclin (PGI2)

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13
Q

what is the leading cause of PAD?

A

patients over 40 with narrowing or occlusion of the arteries of the limbs due to atherosclerosis

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14
Q

strongest risk factors for PAD

A

smoking and DM

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15
Q

response-to-injury hypothesis

A

a mechanism that describes a chronic inflammatory and healing response of arterial vessels to injury and leads to the development of atherosclerosis

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16
Q

how does an atherosclerosis form?

A
  1. LDL particles collect in the intima of the arterial vessel and may be retained there by binding to the macromolecules that make up the extracellular matrix (e.g., glycosaminoglycans). This makes up a “fatty streak”
  2. Oxidized LDL particles recruit white blood cells (leukocytes) through two mechanisms
    - they initiate an inflammatory response that recruits lymphocytes to the site of the fatty streak
    - they stimulate cells of the vascular wall to secrete cytokines to attract mononuclear phagocytes
  3. phagocytic macrophages absorb the lipoproteins through receptor-mediated endocytosis and may become converted to foam cells
  4. foam cells secrete growth factors and cytokines which cause smooth muscle cells to migrate into the intima
  5. smooth muscle cells synthesize collagen, creating a rigid area where is should be elastic
  6. circulating platelets become activated by exposure to collagen and other components of the ECM that normally makes up the external layer of the vessel and aggregate around the site
  7. activated platelets stimulate the formation of a blood clot (thrombus) via the molecule thromboxane (TXA2)
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17
Q

what is thromboxane (TXA2) synthesized from?

A

arachidonic acid

18
Q

synthesis of TXA2 requires the activity of what enzyme?

A

cyclooxygenase (COX1)

19
Q

what are the 3 main components of atherosclerotic plaques?

A
  1. cells (smooth muscle cells, macrophages, and T lymphocytes)
  2. extracellular matrix (collagen, elastic fibers, and proteoglycans)
  3. intracellular and extracellular lipid
20
Q

is platelet aggregation dependent on low or high levels of cAMP?

A

low

21
Q

what happens when ADP binds to P2Y12 receptors expressed on platelet mebmranes?

A

G proteins get activated which then inhibit the enzyme responsible for the synthesis of cAMP, called adenylyl cyclase

22
Q

name the enzyme that synthesizes cAMP

A

adenylyl cyclase

23
Q

what happens to cAMP when you inhibit P2Y12 receptors?

A

cAMP levels would increase inside the cell, thus inhibiting platelet aggregation

24
Q

what happens to intracellular cAMP levels when PDE isoforms are activated?

A

intracellular cAMP levels decrease

25
Q

what happens to intracellular cAMP levels when you inhibit PDE enzymes?

A

intracellular cAMP levels increase and inhibit platelet aggregation

26
Q

what are some common characteristics of patients with PAD?

A

over 40 years old, history of HTN, dyslipidemia, DM2, CKD, CAD, and/or smoking

27
Q

what is intermittent claudication?

A

a term used to describe fatigue, discomfort, cramping, pain, or numbness in the extremities (i.e., buttock, thigh, or calf) during exercise that resolves within a few minutes of rest

28
Q

what physical exam findings indicate decreased blood flow to the extremities?

A

cool skin temperature, shiny skin, thickened toenails, lack of hair on the calf, feet, and/or toes

29
Q

what diagnostic test is used to diagnose PAD?

A

ankle-brachial index (ABI)

30
Q

what are the goals of therapy for PAD?

A

increase maximal walking distance, duration of walking, and amount of pain-free walking, improve quality of life, achieve glycemic control, smoking cessation, goal BP <130/80 mm Hg, prevent limb amputations, prevent cardiovascular events and mortality

31
Q

nonpharmacotherapy for PAD

A

smoking cessation, waling exercise program (30 minutes at least 3 times/week for at least 12 weeks), bypass surgery or balloon angioplasty (for patients with CLI or PAD patients who have not responded well to other therapies)

32
Q

name 3 therapeutic agents used to PAD

A

aspirin, clopidogrel, cilostazol

33
Q

is aspirin best absorbed at low or high pH?

A

low (aspirin pKa = 3.5)

34
Q

why shouldn’t you take antacids with aspirin?

A

antacids will raise the stomach pH to around 4 and since aspirin is absorbed in its unionized form and its pKa is 3.5, a pH of 4 will ionize aspirin and it will not get absorbed

35
Q

what class of medication is aspirin?

A

COX-1 inhibitor

36
Q

what class of medication is clopidogrel (Plavix)?

A

platelet P2Y12 receptor inhibitor

37
Q

what class of medication is cilostazol (Pletal)?

A

phosphodiesterase inhibitor (PDE3 inhibitor)

38
Q

what is cilostazol (Pletal) used for?

A

intermittent claudication

39
Q

what medication(s) should be recommended for all patients with PAD?

A

aspirin or clopidogrel

40
Q

which function group on aspirin is responsible for its anti-platelet activity?

A

the acetyl group

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