MDSC 1102 PBL 3

BY ARVIND SEECHARAN(FUTURE DOCTOR EXTRAORDINAIRE)

Learning Objective 1

• Describe the anatomy of the blood vessels in the lower limbs

Blood vessels of lower limb• Major arteries of lower limb include• Femoral artery• Popliteal artery• Anterior and posterior tibial arteries• Dorsalis pedis artery• Medial and lateral plantar arteries• Plantar arterial arch• Major veins of lower limb:• Deep veins – femoral and popliteal veins• Superficial veins – great and short saphenous veins

• Femoral artery:• Origin:• Continuation of external iliac

artery - behind the inguinal ligament

• Course:• Runs in the femoral triangle

from the base to apex• Runs in the adductor canal • Termination:• Continues as popliteal artery

Femoralartery

ProfundaFemorisartery

Femoralvein

Femoral nerve

• Branches:• Branches in the femoral

triangle:• Superficial epigastric• Superficial external

pudendal• Superficial circumflex iliac• Profunda femoris• Deep external pudendal• Muscular branches• Branches in the adductor

canal:• Descending genicular• Muscular branches

Superficial epigastric

Superficialexternalpudendal

Deepexternalpudendal

• Popliteal artery:• Situated in the popliteal

fossa behind the knee joint

• Origin: • Continuation of femoral

artery• Course: • runs in the popliteal

fossa along with popliteal vein and tibial nerve

• Tibial nerve crosses the artery in the popliteal fossa

Anteriortibialartery

Posteriortibialartery

Tibial nerve

• Termination: • Divides into anterior and posterior tibial

arteries• Branches: • Anterior and posterior tibial arteries• Genicular branches to knee joint• Cutaneous branches• Muscular branches

• Posterior tibial artery:• Situated in the posterior

compartment of leg• Origin: • Branch of popliteal

artery• Course:• Runs down in the

posterior compartment of leg between superficial and deep muscles

• Accompanied by tibial nerve

Posteriortibial artery

Peronealartery

Poplitealartery

Tibial nerve

Medial plantar artery

Lateral plantar artery

• Termination: • Divides into medial and lateral plantar arteries• Branches: • Medial and lateral plantar arteries• Peroneal artery• Circumflex fibular artery• Nutrient artery to tibia• Muscular branches

• Anterior tibial artery:• Artery present in the anterior

compartment of leg• Origin: branch of popliteal artery• Course: runs in the anterior

compartment of leg – deep peroneal nerve

• Termination: Continues as dorsalis pedis artery at the ankle joint

• Branches:• Anterior and posterior tibial

recurrent arteries• Muscular arteries

Anteriortibial artery

Dorsalispedisartery

Deep peronealnerve

• Dorsalis pedis artery:• Artery present in the dorsum of

foot• Origin: continuation of anterior

tibial artery• Course: runs on the dorsum of

foot, enters the sole by piercing 1st dorsal interosseous muscle

• Termination: anatomoses with the lateral plantar artery to form plantar arterial arch

• Branches:• Arcuate artery• Tarsal braches• 1st dorsal metatarsal artery

Doralispedis

Arucate

1st dorsal interosseousmuscle

• Medial and lateral plantar arteries:

• Arteries which supply the sole of the foot

• Branches of posterior tibial artery

• Run in the sole between the 1st and 2nd layer of mucles

• Lateral plantar artery forms plantar arch along with dorsalis pedis artery

LateralPlantar artery

Medialplantarartery

Plantararch

• Plantar arterial arch:• Situated in the sole between the 3rd

and 4th layer of muscles• Formation:• Formed by the continuation of

lateral plantar artery• Completed on the medial side by

the dorsalis pedis artery• Branches:• Four plantar metatarsal arteries

Plantar arterialarch

Plantar metatarsal

Medialplantar

Veins of lower limb• Deep veins and superficial veins• Deep veins:• Run along with the arteries• Major deep veins – popliteal vein

and femoral vein• Popliteal vein:• Situated in popliteal fossa• Formed by the union of veins

accompanying anterior and posterior arteries

• Terminates by continuing as femoral vein

• Receives short saphenous vein

Poplitealvein

Short saphenous vein

• Femoral vein:• Runs in the anterior

compartment of thigh along with femoral artery

• Begins as a continuation of popliteal vein

• Terminates by continuing as external iliac vein

• Receives great saphenous vein

Femoral vein

Great saphenous vein

• Superficial veins:• Runs in the superficial fascia, just deep to

skin• Great (long) saphenous vein:• Longest vein in the body• Begins as a continuation of medial end of

dorsal venous arch• Terminates by opening into femoral vein• Tributaries:• Superficial circumflex iliac vein• Superficial epigastric vein• Superficial external pudendal vein• Short (small) saphenous vein:• Begins as a continuation of lateral end of

dorsal venous arch• Ends by opening into popliteal vein

Dorsal venous arch

Learning Objective 2

• Explain the cholesterol metabolism cycle

Cholesterol metabolism:

•Cholesterol is a sterol, present in cell membrane, brain and lipoprotein•It is a precursor for all steroids•About 1 g of cholesterol is synthesized per day in humans•It is an amphipathic lipid•Lipoproteins transports the free cholesterol in the circulation•Cholesterol ester is a storage form of cholesterol found in most tissues•80% of the liver cholesterol converted to bile acids•Vitamin D3 formed from 7-dehydrocholesterol.•All the steroids have cyclopentanoperhydrophenanthrene ring.Made up of three cyclohexane rings, A,B and C and a cyclopentane ring D•Normal Blood level is 150-200 mg%

Cholesterol metabolism:

• Hypercholesterolemia seen in nephrosis, diabetes mellitus, hypothyroidism and obstructive jaundice

• Increased cholesterol level leads to atherosclerosis• The OH group in the 3rd position can get esterified to fatty

acids to form cholesterol esters. This esterification occurs in the body by transfer of PUFA moiety by Lecithin cholesterol acyl transferase. This step is important in the regulation of cholesterol level.

• It is a poor conductor of electricity

SYNTHESIS• Site: Extra Mitochondrial. The enzymes involved are

found in cytosol and microsomal fractions of the cell.

• Synthesis takes place in liver, skin and intestine and also in adrenal cortex & testis.

• All the 27 carbon atoms are derived from acetyl CoA• 18 acetyl Co A are required

• Acetyl CoA formed in glycolysis and -Oxidation of fatty acid are the precursors for the cholesterol synthesis

Regulation of Cholesterol synthesis• Cholesterol biosynthesis is controlled by the rate limiting enzyme HMG-CO A

reductase

• Feedback control: The end product cholesterol controls its own synthesis of the enzyme by a feedback mechanism. Increase in the cellualar concentration of cholesterol reduces the synthesis of the enzyme by decreasing the transcription of the gene responsible for the production of HMG CoA reductase.

• Hormonal regulation: The HMG CoA reductase exists in two interconvertible forms. – Insulin and thyroid hormones Increase HMG CoA reductase activity

– The dephosphorylated form of the enzyme is more active, phosphorylated is less active. Hormones exert their influence through cAMP

• Glucagon and glucocorticoids decrease HMG-CoA reductase activity

• Inhibition by drugs: The drugs Compactin and lovastatin, mevastatin, simvastin are competitive inhibitors used to decrease the cholesterol.

• HMG CoA reductase is inhibited by bile acids.

• LDL transports cholesterol from the liver to peripheral tissues.

• HDL transports cholesterol from tissues to liver

Compactin, lovastatin [Competitive inhibitors]Mevastin, Simvastin

HMG CoA __

Insulin, thyroxin + HMG CoA Reductase Glucagon(dephosphorylates enz) glucocorticoids

(Phosphorylates enz)Mevalonate Translation

mRNA

Cholesterol _ Transcription

DNA Glucagon and glucocorticoids inactivate the enzyme through phosphorylation Insulin, thyroxin activate the enzyme through dephosphorylation

METABOLIC FATE OF CHOLESTEROL

Cholesterol is converted into following compounds as shown below. Cholesterol is mainly excreted in the form of bile salts in stool.

Steroid hormone (Testosterone, estrogens

Acetyl CoA Cholesterol progesterone,glucocorticoids mineralocorticoids)

Vitamin D3

Bile acids [salts]

• Increased plasma cholesterol results in the accumulation of

cholesterol under the tunica intima of the arteries causing

atherosclerosis. The progression of the disease process leads to

narrowing of the blood vessels. Dietary intake of

polyunsaturated fatty acid (PUFA) helps in transport and

metabolism of cholesterol and prevents atherosclerosis

Role of LCAT:High density lipoprotein (HDL) and the enzyme lecithin-cholesterol acyl transferase (LCAT) are responsible for the transport and elimination of cholesterol from the body. LCAT is a plasma enzyme, synthesized by the liver. LCAT catalyses the transfer of fatty acid from the second position of phosphatidyl choline (lecithin) to the OH group of cholesterol. HDL cholesterol is the real substrate for LCAT and this reaction is freely reversible. LCAT activity is associated with apo-A1 of HDL.

Learning Objective 3

• Describe the pathophysiology of atherosclerosis

What Is Atherosclerosis?• Atherosclerosis is is a disease in which plaque

builds up inside your arteries.

• Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrows your arteries. This limits the flow of oxygen-rich blood to your organs and other parts of your body.

• Atherosclerosis can lead to serious problems, including heart attack, stroke, or even death.

Arthrosclerosis

Causes of Arthrosclerosis• Hardening of the arteries is a process that often

occurs with aging. However, high blood cholesterol levels can make this process happen at a younger age.

• For most people, high cholesterol levels are the result of an unhealthy lifestyle -- most commonly, eating a diet that is high in fat. Other lifestyle factors are heavy alcohol use, lack of exercise, and being overweight.

Risk factors

Risk factors for hardening of the arteries are:• Diabetes

• Family history of hardening of the arteries

• High blood pressure

• Smoking

Symptoms• Hardening of the arteries does not cause

symptoms until blood flow to part of the body becomes slowed or blocked.

• If the arteries to the heart become narrow, blood flow to the heart can slow down or stop. This can cause chest pain (stable angina), shortness of breath, and other symptoms.

• Narrowed or blocked arteries may also cause problems and symptoms in your intestines, kidneys, legs, and brain.

Signs and symptoms

• A health care provider will perform a physical exam and listen to the heart and lungs with a stethoscope. Atherosclerosis can create a whooshing or blowing sound ("bruit") over an artery.

• Some national guidelines recommend having the first screening cholesterol test at age 20. Everyone should have their first screening test by age 35 in men, and age 45 in women. (Note: Different experts recommend different starting ages.)

Signs and symptoms

• A number of imaging tests may be used to see how well blood moves through your arteries

• Doppler tests use ultrasound or sound waves.

Signs and symptoms

• Magnetic resonance arteriography (MRA) is a special type of MRI scan

• Special CT scans called CT angiography• Arteriograms or angiography use x-rays to see

inside the arteries

Natural history of Atherosclerosis

stable anginaunstable anginaMIcomplicationsdeath

Pathology of Atherosclerosis

1. Fatty Streak (yellow streak of lipid-filled macrophage foam cells. Lipid gets deposited first, then macrophages infiltrate and ingest it). Asymptomatic. Does not occlude.

2. Fibrous Plaque (whitish yellow lump occluding lumen of coronary arteries, aorta, and carotids. Includes foam cells and smooth muscle cells). Stable angina.

3. Thrombus (plaque rupture causes exposure of BM, platelet aggregation, and thrombus). Unstable angina or MI.

Pathophysiology of Atherosclerosis

• The endothelium plays a huge role. The intimal endothelium becomes dysfunctional, losing its ability to produce Nitric Oxide, and starting to express selectins/integrins for leukocyte recruitment.

• Endothelial cells normally provide a permeability barrier, reduce clotting, and regulate vascular tone.

Pathophysiology of Atherosclerosis

• NO is a vasoprotective gas released by endothelium. • NO is vasodilatory, anti-thrombotic, and anti-inflammatory. • NO activates guanylate cyclase to generate cGMP, which

causes smooth muscle relaxation/dilation. • NO blocks vascular inflammation by inhibiting endothelial

releaase of inflammatory granules. • It also blocks platelet aggregation. • Endothelial cells lose ability to produce NO due to

inflammation, toxins, atherosclerosis, or oxidized LDL. Endothelial dysfunction leads to monocyte recruitment and atherosclerosis.

Pathophysiology of Atherosclerosis

• ACh stimulates NO release and dilation. In people with atherosclerosis, NO is not generated, and ACh will act directly on smooth muscles to produce “paradoxical vasoconstriction.”

Initial inflammation

Endothelial dysfunction

Monocyte recruitment/differentiation

to intima

Growth factors stimulate smooth muscle proliferation

Platelet activation/aggregation

Atheroma with thin fibrous cap, no more NO protecting

vessels

• Atherosclerosis is an inflammatory disease. This is why levels of C Reactive Protein closely correlate with and predict MI. Aspirin reduces inflammation and can reduce risk of MI.

• Low Density Lipoprotein cholesterol, cigarettes and other toxins initiate vascular inflammation, damage endothelium, and as a result activate macrophages.

• LDL cholesterol can deposit in tissues. Even worse, radicals may oxidize LDL cholesterol.

• Oxidized LDL is very toxic, and directly kills endothelial cells and activates macrophages.

• Monocytes are recruited by rolling (selectins), activation (ICAMs/integrins), adhesion, diapedesis, and migration. Macrophages in the intima will produce growth factors (stimulate smooth muscles and fibroblasts), TNF-α, and superoxide radicals that oxidize LDL.

• Macrophages are a big part of atherogenesis. • Smooth muscle cells become activated (“synthetic”)

by macrophage growth factors. They proliferate in the intima and secrete lots of ECM proteins (collagen, proteoglycan).

Treatment• Atherosclerosis can not be cured, but is manageable and

preventable with proper monitoring and treatment. The best to do is prevention. It will be necessary to make healthy lifestyle changes for improved quality of life.

• Regular exercise - Walking is great, but gym is better

• Control your blood pressure

• Control serum cholesterol and triglyceride levels

• Do NOT smoke

Treatment

• Eat a heart healthy diet of fresh fruits and vegetables, low fat foods, and lean meats

• In the mild stages of this disease, lifestyle changes can slow its progression and help to avoid or delay more advanced treatment.

Treatment

Once symptoms worsen, other treatments be necessary:

• Balloon Angioplasty involves inserting a thin tube into the femoral artery in the groin, or the arm can be used, with aballoon on the end, into the artery. The balloon is inflated which pushes the plaque against the wall of the artery. Often a stent (a mesh tube) is inserted at the same time to keep the artery open preventing re-occlusion.

Treatment

• Your doctor can surgically remove plaque by performing an endarterectomy.

Learning Objective 4

• Discuss the epidemiology of arteriosclerosis in Trinidad and Tobago- not worth my time

Learning Objective 5

• Discuss the role of diet and exercise with respect to arteriosclerosis

Treatment of Arteriosclerosis

• Living a heart-healthy lifestyle which includes eating a healthy diet is often the first line of defense in treating arteriosclerosis.

• You can make diet changes that include eating foods classified as heart-healthy by the American Heart Association (AHA).

More Lean Proteins• An arteriosclerosis diet should focus on the lean proteins. Foods

classified as lean protein need to be included in an arteriosclerosis diet, says the AHA.

• Lean protein contains fewer calories and fat than do other sources of protein known for being rich in saturated fat.

• This category includes fatty fish, such as: – Mackerel – Salmon – Herring– Trout – Sardines – Cod – Halibut – Albacore tuna

• Low-fat dairy foods, legumes and skinless poultry are other lean protein sources.

Avoid Trans Fats• An arteriosclerosis diet should also avoid trans fats.

• To prevent arteriosclerosis, you need to limit fats that are known for harming cardiovascular health (trans fats, cholesterol and saturated fats).

• Trans fats are found in shortening and/or partially hydrogenated oils. Trans fat is known for increasing harmful LDL (low-density lipoprotein) cholesterol levels while also lowering beneficial HDL (high-density lipoprotein) cholesterol levels.

• • Trans fats are commonly found in commercially prepared foods, such as

baked items including snack cakes, pies, cookies, brownies, bagels, croissants, breads, crackers, cakes, muffins and biscuits.

• Other foods known for containing trans fat are boxed cereals and other boxed foods, frozen foods, deli foods, deep-fried items and fast foods

Have a diet low in Saturated Fats, Cholesterol

• Saturated fats and cholesterol are known for increasing LDL cholesterol levels, says the AHA.

• sources of these harmful fats are found in animal-based products, such as:– Beef – Veal– Pork– Venison– Poultry

• Including the animal itself and any meats or byproducts made from that meat. These include sausages, canned meats, sandwich spreads and deli cuts. Whole-fat dairy foods contain large amounts of saturated fats and cholesterol

Eat More Healthy Fats

• Your arteriosclerosis diet should include plant-based fats, which contain heart-healthy unsaturated fats, says the AHA.

• These fats may help lower total cholesterol levels and are found in nuts and seeds, such as:– Walnuts – Flax seeds – Pistachios – Almonds– Peanuts– Nut butters made from these sources are included in this

category. Unsaturated fats are also found in the oils of canola, olives, corn, sunflower seeds and sesame seeds.

More Soluble Fibre• An arteriosclerosis diet needs to include foods rich in soluble fibre. • The Mayo Clinic says your total and LDL cholesterol can be reduced with 10

grams (g) daily of soluble fibre, as it can help remove harmful plaque from arterial walls, thereby lowering levels of harmful cholesterol in the bloodstream.

• Whole grains are rich sources of soluble fibre – Barley– Brown rice– Quinoa– Millet– Triticale– Whole wheat– Wheat bran– Oatmeal

• The Mayo Clinic, in particular, recommends eating oatmeal. A 1 1/2-cup serving of cooked oatmeal contains 6g soluble fiber. Adding a sliced banana to this will add 4g. Other foods rich in soluble fiber include apples, pears, prunes, psyllium seeds and kidney beans.

Exercise and Arteriosclerosis

• Regular exercise can condition your muscles to use oxygen more efficiently.

• Physical activity can also improve circulation and promote development of new blood vessels that form a natural bypass around obstructions (collateral vessels).

• Exercise helps lower blood pressure and reduce your risk of diabetes.

Exercise and Arteriosclerosis

• Ideally, you should exercise 30 to 60 minutes most days of the week.

• If you can't fit it all in one session, try breaking it up into 10-minute intervals.

• You can take the stairs instead of the elevator, walk around the block during your lunch hour, or do some sit-ups or push-ups while watching television.

Learning Objective 6

• Explain the diagnostic tests that could be used to detect peripheral vascular disease

Ankle-Brachial Index

• A simple test called an ankle-brachial index (ABI) often is used to diagnose Peripheral Vascular Disease.

• The ABI compares blood pressure in your ankle to blood pressure in your arm. This test shows how well blood is flowing in your limbs.

Ankle-Brachial Index

• ABI can show whether Peripheral Vascular Disease is affecting your limbs, but it won't show which blood vessels are narrowed or blocked.

• A normal ABI result is 1.0 or greater (with a range of 0.90 to 1.30). The test takes about 10 to 15 minutes to measure both arms and both ankles. This test may be done yearly to see whether Peripheral Vascular Disease is getting worse.

Doppler Ultrasound

• A Doppler ultrasound looks at blood flow in the major arteries and veins in the limbs.

• During this test, a handheld device is placed on your body and passed back and forth over the affected area.

Doppler Ultrasound

• A computer converts sound waves into a picture of blood flow in the arteries and veins.

• The results of this test can show whether a blood vessel is blocked. The results also can help show the severity of P.A.D.

Treadmill Test

• A treadmill test can show the severity of symptoms and the level of exercise that brings them on.

• Patients walk on a treadmill for this test. This shows whether you have any problems during normal walking.

• You may have an ABI test before and after the treadmill test. This will help compare blood flow in your arms and legs before and after exercise.

Magnetic Resonance Angiogram

• A magnetic resonance angiogram (MRA) uses magnetic and radio wave energy to take pictures of your blood vessels.

• This test is a type of magnetic resonance imaging (MRI).

• An MRA can show the location and severity of a blocked blood vessel.

• Patients who have have a pacemaker, man-made joint, stent, surgical clips, mechanical heart valve, or other metallic devices in their body, may not be able to have an MRA.

Arteriogram• An arteriogram provides a "road map" of the arteries. Doctors

use this test to find the exact location of a blocked artery.

• For this test, dye is injected through a needle or catheter (tube) into an arteries.

• Patients may feel mildly flushed. After the dye is injected, an x ray is taken. The x ray can show the location, type, and extent of the blockage in the artery.

• Some doctors use a newer method of arteriogram that uses tiny ultrasound cameras. These cameras take pictures of the insides of the blood vessels. This method is called intravascular ultrasound.

Blood Tests

• Doctors may recommend blood tests to check for Peripheral Vascular Disease. risk factors. For example, blood tests can help diagnose conditions such as diabetes and high blood cholesterol.

Learning Objective 7

• Discuss the lifestyle changes & treatment options for peripheral vascular disease

• The overall goals of treating P.A.D. include reducing symptoms, improving quality of life, and preventing complications. Treatment is based on your signs and symptoms, risk factors, and results from a physical exam and tests.

Lifestyle ChangesQuit smoking• The risk of Peripheral Vascular Disease

increases four times if you smoke. • Smoking also raises your risk for other

diseases, such as coronary heart disease (CHD).

• Talk with doctors about programs and products that can help you quit smoking.

• Also, try to avoid secondhand smoke.

Lifestyle Changes

Lower blood pressure. • This lifestyle change can help you avoid the risk of

stroke, heart attack, heart failure, and kidney disease.Lower high blood cholesterol • Lowering cholesterol can delay or even reverse the

buildup of plaque in your arteries.Lowering blood glucose (sugar) levels• if you have diabetes. A hemoglobin A1C test can show

how well you have controlled your blood sugar level over the past 3 months.

Lifestyle Changes

Become physically active. • Talk with your doctor about taking part in a

supervised exercise program. This type of program has been shown to reduce Peripheral Vascular Disease symptoms

Surgery or Procedures

Bypass Grafting• Your doctor may recommend bypass grafting surgery if

blood flow in your limb is blocked or nearly blocked. For this surgery, your doctor uses a blood vessel from another part of your body or a man-made tube to make a graft.

• This graft bypasses (that is, goes around) the blocked part of the artery. The bypass allows blood to flow around the blockage.

• This surgery doesn't cure P.A.D., but it may increase blood flow to the affected limb.

Surgery or Procedures

Angioplasty and Stenting• Your doctor may recommend angioplasty to restore blood

flow through a narrowed or blocked artery.• During this procedure, a catheter (thin tube) with a balloon

at the tip is inserted into a blocked artery. The balloon is then inflated, which pushes plaque outward against the artery wall. This widens the artery and restores blood flow.

• A stent (a small mesh tube) may be placed in the artery during angioplasty. A stent helps keep the artery open after angioplasty is done. Some stents are coated with medicine to help prevent blockages in the artery.

Surgery or Procedures

Atherectomy• Atherectomy (ath-eh-REK-to-me) is a procedure that

removes plaque buildup from an artery. During the procedure, a catheter is used to insert a small cutting device into the blocked artery. The device is used to shave or cut off plaque.

• The bits of plaque are removed from the body through the catheter or washed away in the bloodstream (if they're small enough).

• Doctors also can do atherectomy using a special laser that dissolves the blockage.

Medications

Cholesterol-lowering medications• You may take a cholesterol-lowering drug called a

statin to reduce your risk factor of heart attack and stroke. The goal for people who have peripheral artery disease is to reduce low-density lipoprotein (LDL) cholesterol, the "bad" cholesterol, to less than 100 milligrams per deciliter (mg/dL), or 2.6 millimoles per liter (mmol/L). The goal is even lower if you have additional major risk factors for heart attack and stroke, especially diabetes or continued smoking.

MedicationsHigh blood pressure medications• If you also have high blood pressure, your doctor may

prescribe medications to lower it. The goal of this therapy is to reduce your systolic blood pressure (the top number of the two numbers) to 140 millimeters of mercury (mm Hg) or lower and your diastolic blood pressure (the bottom number) to 90 mm Hg or lower. If you have diabetes, your blood pressure target is under 130/80 mm Hg.

• ACE inhibitors : enalapril (Vasotec), captopril (Capoten)

Angiotensin II receptor blockers (ARBs) • Are medications that block the action of

angiotensin II by preventing angiotensin II from binding to angiotensin II receptors on the muscles surrounding blood vessels. As a result, blood vessels enlarge (dilate), and blood pressure is reduced.

• Examples of ARB drugs include:– losartan (Cozaar)– Irbesartan (Avapro),

• Beta-blockers• Beta blockers are drugs that block norepinephrine and

epinephrine (adrenaline) from binding to both beta 1 and beta 2 receptors on organs and muscles, including the muscles that cause blood vessels to narrow and the heart to beat. By blocking the effect of norepinephrine and epinephrine, beta blockers reduce blood pressure by dilating blood vessels and reducing heart rate. They also may constrict air passages because stimulation of beta receptors in the lung cause the muscles that surround the air passages to contract.

Medications

Medication to control blood sugar. • If you also have diabetes, it becomes even

more important to control your blood sugar (glucose) levels. Talk with your doctor about what your blood sugar goals are and what steps you need to take to achieve these goals.

• E.G. Pramlintide and Exenatide, Insuilin

Medications

Medications to prevent blood clots. • Because peripheral artery disease is related to

reduced blood flow to your limbs, it's important to reduce your risk of blood clots. A blood clot can completely block an already narrowed blood vessel and cause tissue death. Your doctor may prescribe daily aspirin therapy or another medication that helps prevent blood clots, such as clopidogrel (Plavix).

Medications

Symptom-relief medications. • The drug cilostazol (Pletal) increases blood flow to

the limbs both by preventing blood clots and by widening the blood vessels. It specifically helps the symptom of claudication, leg pain, for people who have peripheral artery disease. Common side effects of this medication include headache and diarrhea. An alternative to cilostazol is pentoxifylline (Trental); however, it's generally less effective. But, side effects are rare with this medication