Peripheral vascular disease

Question 1

prevalence of PAD

Answer 1

12%

Question 2

Risk factors for peripheral arterial disease

Answer 2

diabetes (x4), smoking (2-3X), lipids (2X), HTN (2X). Diabetes and smoking are most dominant risk factors for PAD with claudication

Question 3

Symptoms of peripheral arterial disease

Answer 3

•Intermittent Claudication (cramping and calf fatigue with exercise that resolves with rest), Ischemic rest pain/ischemic ulcers (Pain in the distal foot or heel, worsened by leg elevation and improved by dependency. Distal, painful ulcers on toes or heel. Blood flow limited at rest and exercise. Symptoms at rest and with exercise)

Question 4

Signs of PAD

Answer 4

• Decreased or absent pulses, Bruits (abdominal, femoral), Muscle atrophy, In severe PAD (critical leg ischemia)-Pallor of feet with elevation and Dependent rubor
• Decreased or absent pulses, Bruits (abdominal, femoral), Muscle atrophy, In severe PAD (critical leg ischemia)-Pallor of feet with elevation and Dependent rubor
• Decreased or absent pulses, Bruits (abdominal, femoral), Muscle atrophy, In severe PAD (critical leg ischemia)-Pallor of feet with elevation and Dependent rubor

Question 5

What are the main components that determine arterial hemodynamics

Answer 5

Perfusion pressure, blood viscosity, arterial stenosis (radius and length), flow velocity (hemodynamic severity increases at higher flow velocities)

Question 6

How does length of stenosis affect drop in pressure and flow across stenosis

Answer 6

Small increases in length of stenosis will not have a major impact

Question 7

How does radius of stenosis affect drop in pressure and flow across stenosis

Answer 7

r^4 is proportional to flow, so a small change in radius will have a large affect on pressure and flow

Question 8

How does blood viscosity affect drop in pressure and flow across stenosis

Answer 8

Blood viscosity has a minimal effect

Question 9

How do drugs that lower systolic BP affect claudication symptoms

Answer 9

May make symptoms worse because driving pressure across the stenosis is decreased thus blood flow to muscles is decreased

Question 10

What is the ankle brachial index

Answer 10

ABI is a resting measure of the hemodynamic severity of the occlusive disease process, with an abnormal ratio defined as < 0.90. It measures the ankle systolic BP and divides it by th arm systolic BP.

Question 11

Role of the atherosclerotic disease process on endothelial function as modulated by nitric oxide

Answer 11

CV risk factors can impair NO mediated arteriolar vasodilation

Question 12

Treatment of claudication

Answer 12

Surgery or angioplasty, exercise training to improve muscle metabolism, drugs

Question 13

Describe the major risk factors for aortic aneurysm

Answer 13

Age, gender, smoking, family history

Question 14

Mechanism of aneurysm formation

Answer 14

Weakened arotic wall (decreased elastin and collagen in media and adventitia), inflammation( lymphocytes, macrophages, cytokines, autoantigens), Proteolytic enzymes (MMP2/9), biomechanical stress (elastin distribution, turbulence)

Question 15

What defines an aneurysm

Answer 15

size and relative change

Question 16

Types of aneurysms

Answer 16

Aneurysms may be fusiform (expansion of the entire vessel circumference) or saccular (evagination of a segment of the circumference). Fusiform aneurysm formation is more common.

Question 17

Why is the abdominal aorta at elevated risk for aneurysm

Answer 17

Abd aorta contains fewer elastic lamellae than thoracic, so it is less able to tolerate loss in elastin. Also vasa vasorum in the AA is less abundant, the AA withstands oscillating blood flow, decreased compliance

Question 18

Understand the relationship between the size of an aortic aneurysm and the subsequent risk of rupture

Answer 18

7cm: 75% rate of 5- year rupture. Risk of rupture increases with diameter of aneurysm

Question 19

What is the 5-year risk of rupture of a 5.5 cm abdominal aortic aneurysm?

Answer 19

25%

Question 20

What is an aortic dissection

Answer 20

Blood dissects into the media

Question 21

Mechanisms for aortic dissection

Answer 21

primary intimal tear or rupture of vasa vasorum (which will cause a hematoma that spreads from the media to the intima)

Question 22

List the key risk factors that initiate aortic dissection

Answer 22

HTN, cocaine, Marfan/Ehlers-Danlos syndrome, bicuspid aortic valve, coarctation, pregnancy, aortitis, trauma

Question 23

What causes an aortic dissection. What part of aorta is most vulnerable

Answer 23

Structural weakness in arterial wall and an initiating event (dilation of aorta and HTN). Ascending aorta is most vulnerable b/c it expands the most during systole and is exposed to greatest stress

Question 24

Clinical manifestation of aortic dissection

Answer 24

Severe pain, rupture and hemorrhage (death), disruption of arterial circulation from false channel leads to stroke (carotid) , syncope (vertebral), MI (coronaries), intestinal ischemia (mesenteric), renal failure (renal).

Question 25

Where is pain located in an ascending aortic dissection? Descending aortic dissection?

Answer 25

Ascending: anterior chest, neck and/or throat. Descending: isolated back

Question 26

Stanford classification system of aortic dissections

Answer 26

Any aortic dissection involving the ascending aorta is type A, and any aortic dissection not involving the ascending aorta is type B.

Question 27

DeBakey classification system of aortic dissections

Answer 27

Type I: ascending and descending aorta affected. Type II: ascending aorta only. Type III: descending aorta only

Question 28

Treatment of aortic dissection

Answer 28

Beta blockers, control BP (nitroprusside, ACEI, Ca channel blockers), Control pain, surgery (acute type A, chronic type A, acute type B with rupture, organ ischemia, or marfans)

Question 29

Describe the stages of venous thromboembolism

Answer 29

stage 1 is swelling. Stage 2 is visible collaterals. Stage 3 is stasis dermatitis. Stage 4 is ulceration

Question 30

For venous thromboembolism, understand the components of Virchow’s triad and mechanistically how each component contributes to thrombosis

Answer 30

Abnormal flow(stasis from immobility), injury (venous trauma from inflammation, diabetes, vascular procedures) and coagulation factors (hypercoagulable state due to anticoag deficiency (potent) or Factor V Leiden (mild))

Question 31

Describe the major sites of action in the clotting cascade of warfarin and heparins

Answer 31

Warfarin inhibits activation of factors II, VII, IX, and X by blocking Vitamin K. Heparin inhibits Factor Xa and activates antithrombin III which inhibits thrombin.

Question 32

Disadvantages of heparin

Answer 32

IV or SC requirement, lack of inhibition of thrombin that is bound to fibrin (but still active) within a developing thrombus, therapeutic drug requirements that can vary with varying ATIII levels, and inhibition of both Xa and thrombin via an ATIII-based mechanism of action (therefore, not Xa-selective).

Question 33

Complications of VTE

Answer 33

include thrombus progression, recurrent VTE (including fatal PE), and development of chronic venous insufficiency (the post-thrombotic syndrome, PTS)