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BIOC33H3 Lecture Notes - Subcutaneous Tissue, Passive Smoking, Fecal Occult Blood

Biological Sciences
Course Code
Stephen Reid

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Chapter 38: Vascular Disorders
Peripheral arterial disease (PAD) is a progressive narrowing and degeneration of the
arteries of the neck, abdomen, and extremities. In most cases, it is a result of
PAD typically appears in the sixth to eighth decades of life. It occurs at an earlier age in
persons with diabetes mellitus and more frequently in African Americans.
The four most significant risk factors for PAD are cigarette smoking (most important),
hyperlipidemia, hypertension, and diabetes mellitus.
The most common locations for PAD are the coronary arteries, carotid arteries, aortic
bifurcation, iliac and common femoral arteries, profunda femoris artery, superficial
femoral artery, and distal popliteal artery.
Aortic aneurysms are outpouchings or dilations of the arterial wall.
The primary causes of aortic aneurysms can be classified as degenerative, congenital,
mechanical, inflammatory, or infectious.
Aortic aneurysms may involve the aortic arch, thoracic aorta, and/or abdominal aorta, but
most are found in the abdominal aorta below the level of the renal arteries.
Thoracic aorta aneurysms are often asymptomatic, but the most common manifestations
are deep, diffuse chest pain that may extend to the interscapular area; hoarseness as a
result of pressure on the recurrent laryngeal nerve; and dysphagia from pressure on the
Abdominal aortic aneurysms (AAAs) are often asymptomatic but symptoms may mimic
pain associated with abdominal or back disorders.
The most serious complication related to an untreated aneurysm is rupture and bleeding.
Diagnostic tests for AAAs include chest x-ray, electrocardiogram (to rule out myocardial
infarction), echocardiography, CT scan, and magnetic resonance imaging scan.
The goal of management is to prevent the aneurysm from rupturing.
Surgical repair of AAA involves (1) incising the diseased segment of the aorta, (2)
removing intraluminal thrombus or plaque, (3) inserting a synthetic graft, and (4) suturing
the native aortic wall around the graft.

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Minimally invasive endovascular grafting is an alternative to conventional surgical repair
of AAA and involves the placement of a sutureless aortic graft into the abdominal aorta
inside the aneurysm via a femoral artery cutdown.
Preoperatively, the patient is monitored for indications of aneurysm rupture.
Preoperative teaching should include a brief explanation of the disease process, the
planned surgical procedure(s), preoperative routines, and what to expect immediately
after surgery.
The overall goals for a patient undergoing aortic surgery include (1) normal tissue
perfusion, (2) intact motor and sensory function, and (3) no complications related to
surgical repair, such as thrombosis or infection.
Postoperatively, the patient will have an endotracheal tube for mechanical ventilation, an
arterial line, a central venous pressure or pulmonary artery catheter, peripheral
intravenous lines, an indwelling urinary catheter, a nasogastric tube, and continuous ECG
and pulse oximetry monitoring.
o Monitoring for graft patency and adequate renal perfusion are priorities;
maintenance of an adequate BP is extremely important.
o Antibiotics are given to prevent infection.
o Peripheral pulses, skin temperature and color, capillary refill time, and sensation
and movement of the extremities are assessed and recorded per hospital policy.
o Hourly urine outputs and daily weights are recorded.
On discharge, the patient should be instructed to gradually increase activities but to avoid
heavy lifting for at least 4 to 6 weeks.
Expected outcomes for the patient who undergoes aortic surgery include (1) patent
arterial graft with adequate distal perfusion, (2) adequate urine output, (3) normal body
temperature, and (4) no signs of infection.
Aortic dissection occurs most commonly in the thoracic aorta and is the result of a tear
in the intimal (innermost) lining of the arterial wall allowing blood to “track” between the
intima and media and creates a false lumen of blood flow.
The exact cause of aortic dissection is uncertain, and most people with dissection are
older and have chronic hypertension.
Clinical manifestations include a sudden, severe pain in the anterior part of the chest or
intrascapular pain radiating down the spine into the abdomen or legs that is described as
“tearing” or “ripping.”
Diagnostic studies used to assess aortic dissection are similar to those performed for

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The initial goal of therapy for aortic dissection without complications is to lower the BP
and myocardial contractility with drug therapy.
Surgery is indicated when drug therapy is ineffective or when complications of aortic
dissection are present.
PAD of the lower extremities affects the aortoiliac, femoral, popliteal, tibial, or peroneal
The classic symptom of PAD of the lower extremities is intermittent claudication,
which is defined as ischemic muscle ache or pain that is precipitated by a consistent level
of exercise, resolves within 10 minutes or less with rest, and is reproducible.
Paresthesia, manifested as numbness or tingling in the toes or feet, may result from nerve
tissue ischemia. Gradually diminishing perfusion to neurons produces loss of both
pressure and deep pain sensations.
Physical findings include thin, shiny, and taut skin; loss of hair on the lower legs;
diminished or absent pedal, popliteal, or femoral pulses; pallor or blanching of the foot in
response to leg elevation (elevation pallor); and reactive hyperemia (redness of the foot)
when the limb is in a dependent position (dependent rubor).
Rest pain most often occurs in the forefoot or toes, is aggravated by limb elevation, and
occurs when there is insufficient blood flow to maintain basic metabolic requirements of
the tissues and nerves of the distal extremity.
Complications of PAD include nonhealing ulcers over bony prominences on the toes,
feet, and lower leg, and gangrene. Amputation may be required if blood flow is not
Tests used to diagnose PAD include Doppler ultrasound with segmental blood pressures
at the thigh, below the knee, and at ankle level. A falloff in segmental BP of more than 30
mm Hg indicates PAD.
Angiography is used to delineate the location and extent of the disease process.
The first treatment goal is to aggressively modify all cardiovascular risk factors in all
patients with PAD, with smoking cessation a priority.
Drug therapy includes antiplatelet agents and ACE inhibitors. Two drugs are approved to
treat intermittent claudication, pentoxifylline (Trental) and cilostazol (Pletal).
The primary nonpharmacologic treatment for claudication is a formal exercise-training
program with walking being the most effective exercise.
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