Peripheral artery disease: Pathology review

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Peripheral artery disease: Pathology review

ETP Cardiovascular System

ETP Cardiovascular System

Introduction to the cardiovascular system
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
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Cardiovascular system anatomy and physiology
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Altering cardiac and vascular function curves
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Pressure-volume loops
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Endocarditis
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Rheumatic heart disease
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Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Cardiomyopathies: Clinical
Congenital heart defects: Clinical
Valvular heart disease: Clinical
Infective endocarditis: Clinical
Pericardial disease: Clinical
Chest trauma: Clinical
Hypertension: Clinical
Pulmonary hypertension
Aortic aneurysms and dissections: Clinical
Raynaud phenomenon
Peripheral vascular disease: Clinical
Heart failure: Clinical
Coronary artery disease: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Fascia, vessels and nerves of the upper limb
Vessels and nerves of the forearm
Vessels and nerves of the hand
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Fascia, vessels and nerves of the lower limb
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Ventilation
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Gas exchange in the lungs, blood and tissues
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Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Trypanosoma cruzi (Chagas disease)
Yellow fever virus
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Arteriovenous malformation
Cerebral circulation

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Tariq is a 52-year-old individual who presents to the clinic complaining of left leg pain. He describes the pain as “cramping” and mostly located in his calf. He also mentions that the pain comes every time he walks from his home to the supermarket, and is relieved when he rests. Tariq also has a known history of hypertension, diabetes mellitus, and a myocardial infarction 2 years ago. On physical examination, there is a noticeable decrease in hair growth on the left side compared to the right, and the skin appears dry and shiny. There is no leg swelling, and there’s no back pain.

Peripheral artery disease is insufficient tissue perfusion due to narrowing or occlusion of the aorta or one of its peripheral branches supplying the limbs. Similar to coronary artery and cerebrovascular disease, the development of an atherosclerotic plaque that narrows or completely occludes an artery is the number one cause of peripheral artery disease, and so these diseases often coexist together.

So on the exam, an important clue may be an individual with a past medical history of a myocardial infarction or a stroke. In addition, look for risk factors of atherosclerosis, such as hypertension, diabetes mellitus, smoking and hyperlipidemia.

The symptoms of peripheral artery disease depend on how bad the occlusion is. In the early stages of the disease individuals may be completely asymptomatic. One of the first symptoms is intermittent claudication. This is characterized by cramping pain in the affected area that comes about during exercise, and is relieved with rest.

Individuals often describe a specific and often consistent distance that brings about the pain, such as walking 2 blocks. The location of the pain can also help give a clue about which artery is occluded. For example, hip claudication indicates aortic or iliac artery occlusion, whereas calf claudication points towards femoral or popliteal artery occlusion.

In addition to claudication, chronic limb ischemia may produce some physical changes. This includes a decrease in the skin temperature, called poikilothermia. Also, hair and nail growth decrease, and sensation can be lost. On physical exam, the pulse distal to the obstruction is weak, and there’s diminished capillary refill in the affected area.

As the arterial narrowing worsens, individuals begin to complain of pain at rest. This is classically worse at night when the individual is sleeping, and gets better when they stand up or hang their leg off of the bed, due to the effect of gravity on blood flow. Eventually, the peripheral tissue dies, which manifests as gangrene and ulcers. The end-stage manifestation is critical limb ischemia, which includes pain at rest as well as tissue loss in the form of gangrenes and ulcers. Critical limb ischemia is limb-threatening if operative intervention is not performed.

For diagnosis, when there’s suspicion of peripheral artery disease, an ankle-brachial index test, or ABI is performed. ABI is the ratio of ankle systolic blood pressure to brachial systolic blood pressure. Normally, both pressures should be equal, and so the ratio should be equal to 1. In individuals with intermittent claudication, the ABI usually lies somewhere between 0.4 and 0.9, since the blood pressure in the ankle is decreased.

In severe peripheral artery disease, usually when the individual begins to develop resting pain, the ABI is less than 0.4. After doing the ABI, the diagnosis is further confirmed with imaging, such as ultrasound or CT angiography.

For treatment, lifestyle changes like exercise programs and diet are the first steps. For medication, Cilostazol, a phosphodiesterase inhibitor, can directly dilate the arteries, easing symptoms. In addition it’s an antiplatelet which can prevent platelet aggregation and decrease the risk of thrombosis. Even without Cilostazol, they should still take an antiplatelet medication like aspirin as prevention for coronary artery disease and stroke. Now, when there’s severe obstruction and tissue necrosis, endovascular or surgical procedures are done to preserve the affected limb.

Now, let’s take a look at some of the other less common causes of peripheral artery disease other than atherosclerosis. Although they’re less common, they make for good exam questions. Think of these when the case is of someone with no atherosclerotic risk factors.

Sources

  1. "Pathophysiology of Heart Disease" Wolters Kluwer Health (2015)
  2. "Lifestyle and Dietary Risk Factors for Peripheral Artery Disease" Circulation Journal (2014)
  3. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  4. "Rapid Review Pathology" Elsevier (2018)
  5. "Medical treatment of peripheral arterial disease" JAMA (2006)
  6. "2016 AHA/ACC Guideline on the Management of Patients With Lower Extremity Peripheral Artery Disease: Executive Summary" Journal of the American College of Cardiology (2017)
  7. "Cilostazol for intermittent claudication" Cochrane Database Syst Rev (2014)