Peripheral vascular disease Flashcards
prevalence of PAD
12%
Risk factors for peripheral arterial disease
diabetes (x4), smoking (2-3X), lipids (2X), HTN (2X). Diabetes and smoking are most dominant risk factors for PAD with claudication
Symptoms of peripheral arterial disease
•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)
Signs of PAD
- 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
What are the main components that determine arterial hemodynamics
Perfusion pressure, blood viscosity, arterial stenosis (radius and length), flow velocity (hemodynamic severity increases at higher flow velocities)
How does length of stenosis affect drop in pressure and flow across stenosis
Small increases in length of stenosis will not have a major impact
How does radius of stenosis affect drop in pressure and flow across stenosis
r^4 is proportional to flow, so a small change in radius will have a large affect on pressure and flow
How does blood viscosity affect drop in pressure and flow across stenosis
Blood viscosity has a minimal effect
How do drugs that lower systolic BP affect claudication symptoms
May make symptoms worse because driving pressure across the stenosis is decreased thus blood flow to muscles is decreased
What is the ankle brachial index
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.
Role of the atherosclerotic disease process on endothelial function as modulated by nitric oxide
CV risk factors can impair NO mediated arteriolar vasodilation
Treatment of claudication
Surgery or angioplasty, exercise training to improve muscle metabolism, drugs
Describe the major risk factors for aortic aneurysm
Age, gender, smoking, family history
Mechanism of aneurysm formation
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)
What defines an aneurysm
size and relative change
Types of aneurysms
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.
Why is the abdominal aorta at elevated risk for aneurysm
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
Understand the relationship between the size of an aortic aneurysm and the subsequent risk of rupture
7cm: 75% rate of 5- year rupture. Risk of rupture increases with diameter of aneurysm
What is the 5-year risk of rupture of a 5.5 cm abdominal aortic aneurysm?
25%
What is an aortic dissection
Blood dissects into the media
Mechanisms for aortic dissection
primary intimal tear or rupture of vasa vasorum (which will cause a hematoma that spreads from the media to the intima)
List the key risk factors that initiate aortic dissection
HTN, cocaine, Marfan/Ehlers-Danlos syndrome, bicuspid aortic valve, coarctation, pregnancy, aortitis, trauma
What causes an aortic dissection. What part of aorta is most vulnerable
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
Clinical manifestation of aortic dissection
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).
Where is pain located in an ascending aortic dissection? Descending aortic dissection?
Ascending: anterior chest, neck and/or throat. Descending: isolated back
Stanford classification system of aortic dissections
Any aortic dissection involving the ascending aorta is type A, and any aortic dissection not involving the ascending aorta is type B.
DeBakey classification system of aortic dissections
Type I: ascending and descending aorta affected. Type II: ascending aorta only. Type III: descending aorta only
Treatment of aortic dissection
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)
Describe the stages of venous thromboembolism
stage 1 is swelling. Stage 2 is visible collaterals. Stage 3 is stasis dermatitis. Stage 4 is ulceration
For venous thromboembolism, understand the components of Virchow’s triad and mechanistically how each component contributes to thrombosis
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))
Describe the major sites of action in the clotting cascade of warfarin and heparins
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.
Disadvantages of heparin
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).
Complications of VTE
include thrombus progression, recurrent VTE (including fatal PE), and development of chronic venous insufficiency (the post-thrombotic syndrome, PTS)
