PATH 222

Peripheral Vascular Disease

Van Meter & Hubert, Chapter 12
Week 3
Definition
 refers to any abnormality in the arteries or veins outside the heart

Arterial Peripheral Vascular Disease

Pathophysiology
Please refer to the previous notes on the formation of atheromas for discussion of the causes,
development and effects of atheromas.

Common sites for atheroma formation: refer to Figure 10-1 on page 184, 5 th ed.
 abdominal aorta
 femoral artery
 iliac artery
partial or total occlusions of peripheral arteries

decrease in blood supply to the limb

loss of muscle strength and/or sensory function

if the disease progresses to total occlusion and complete loss of blood supply to the limb

development of skin ulcers, necrosis and gangrene (bacterial infection of necrotic tissue)

Signs and symptoms (relate each one to the decreased blood supply to the extremity)
 review the 6P’s
 increasing fatigue and weakness in the legs
 intermittent claudication – define

 sensory impairment – give some examples

 weak or absent peripheral pulses distal to the occlusion

 cold legs and feet
 changes in the skin of the legs and feet: pallor and cyanosis when legs are elevated and rubor
when the feet are dangling
 skin of the legs is dry and hairless
 toenails thick and hardened

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Diagnostic tests – page 261
 Doppler studies
 arteriography

Provide the pathophysiological rationale for the development of gangrene in arterial PVDs.

Aortic Aneurysms
Aneurysm:
Definition:
 a localized dilatation in an arterial wall

Location and Shape:

 most common location is either the abdominal or thoracic aorta; may also occur in the cerebral
circulation
 may have a saccular shape or a fusiform shape – review Figure 12-32 5 th ed. to see the
differences in these two shapes

Pathophysiology:
 develops from a defect in the medial layer; the defect is often associated with turbulent blood
flow at the site – what may cause turbulent blood flow?
 the dilation of the blood vessel enlarges over time
 a thrombus may form in the dilated area and obstruct branching arteries such as the renal
arteries; the thrombus may also be the source of an embolus
 an aneurysm may rupture and cause massive hemorrhage

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Etiology:
 atherosclerosis
 trauma, resulting in tearing of tissues
 syphilis and other infections, resulting in damage to tissues in the arterial wall
 congenital defects in arterial walls
 hypertension is present in 50% of people with aneurysms

Signs and Symptoms

 frequently asymptomatic
 abdominal aneurysms – may present as palpable, pulsating masses with bruits
 early diagnosis may be achieved if the aneurysm compresses nearby structures and causes
symptoms, eg. dysphagia from pressure on the esophagus
 rupture of an aneurysm usually causes severe hemorrhage and death
 signs may include pain and signs and symptoms of shock

Diagnostic tests:
 radiography
 ultrasound
 CT scans
 MRI

Dissecting aneurysm
 develops when there is a tear in the intima which allows blood to flow along the length of the
vessel between the layers of the arterial wall
 causes obstruction of the aorta and its’ branches as the intimal layer of the arterial wall peels
back and blood flow is diverted between the layers
 the dissection tends to progress down the aorta
 causes severe pain, loss of pulses and organ dysfunction

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 Venous Disorders

Varicose Veins
Pathophysiology: please refer to Figure 12-33 on page 263 in Van Meter & Hubert.
 irregular, dilated and tortuous areas of the superficial or deep veins
 most common location is in the legs; varicosities may also occur in the esophagus (esophageal
varices)and rectum (hemorrhoids)
 may contribute to thrombus formation in the veins, particularly when other factors, such as
immobility, are present
 may develop from a weakness in the vein wall

-hydrostatic pressure in the vein causes the vein wall to stretch

-the weight of the blood damages the valve below

-blood backflows into the section of the vein distal to the area of weakness in the vein wall

 may also develop from a defective valve

-reflux of blood into a section of the vein distal to the damaged valve

-veins become overloaded and the walls become stretched and distended with blood

-progressive damage down the vein occurs and some blood may be diverted into other veins,
causing further damage

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Etiology
 familial tendency
 insufficient muscle support for the superficial leg veins
 trauma, which damages the valves
 intravenous administration of fluids and medications
 thrombophlebitis
 factors contributing to increased pressure in the veins, eg. Name some

Signs and symptoms

 irregular, purplish, bulging structures on the legs
 edema in the feet – explain why

 fatigue and aching – explain why

 shiny, pigmented and hairless skin – explain why

 varicose ulcers – explain why

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Thrombophlebitis
 the development of a thrombus in a vein in which inflammation is present
 platelets adhere to the inflamed site and a thrombus develops

Phlebothrombosis
 a thrombus forms spontaneously in a vein without prior inflammation
 the clot is less firmly attached
 thrombus development is silent or asymptomatic

Factors predisposing to the development of a thrombus (Virchow’s triad – review from PATH 122)
 stasis of blood – occurs when immobile or when blood flow is constricted
 endothelial injury, arising from trauma, chemical injury, intravenous injection, inflammation
 increased blood coagulability, which may result from dehydration, cancer, pregnancy or
increased platelet adhesion

Complication of venous thrombosis

 embolism
 What organ will likely be affected first by an embolism originating in a peripheral vein?
Provide your rationale

Signs and symptoms

 may be asymptomatic until an embolus occurs
 positive Homan’s sign may occur, but is not always reliable – explain what this sign is

 superficial vein thrombophlebitis is an inflammatory process – predict the signs and symptoms

 how do the signs and symptoms of deep vein thrombosis differ?

 systemic signs include fever, malaise and leukocytosis

Review the antiplatelet and anticoagulant drugs from PATH 122.