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Mdsc 1102 PBL Problem 3

Mdsc 1102 PBL Problem 3
if i have anything wrong or anything can b improved lemme know plz, thanks

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Mdsc 1102 pbl 3 Presentation Transcript

  • 1. MDSC 1102 PBL 3 BY ARVIND SEECHARAN(FUTURE DOCTOR EXTRAORDINAIRE)
  • 2. Learning Objective 1• Describe the anatomy of the blood vessels in the lower limbs
  • 3. 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
  • 4. Femoral nerve• Femoral artery:• Origin:• Continuation of external iliac Femoral artery - behind the inguinal artery ligament Profunda• Course: Femoris artery• Runs in the femoral triangle from the base to apex Femoral vein• Runs in the adductor canal• Termination:• Continues as popliteal artery
  • 5. • Branches: Superficial epigastric• Branches in the femoral triangle:• Superficial epigastric Superficial• Superficial external external pudendal pudendal• Superficial circumflex iliac• Profunda femoris Deep external• Deep external pudendal pudendal• Muscular branches• Branches in the adductor canal:• Descending genicular• Muscular branches
  • 6. Tibial nerve• Popliteal artery:• Situated in the popliteal Anterior tibial fossa behind the knee artery joint• Origin: Posterior• Continuation of femoral tibial artery artery• Course:• runs in the popliteal fossa along with popliteal vein and tibial nerve• Tibial nerve crosses the artery in the popliteal fossa
  • 7. • Termination:• Divides into anterior and posterior tibial arteries• Branches:• Anterior and posterior tibial arteries• Genicular branches to knee joint• Cutaneous branches• Muscular branches
  • 8. • Posterior tibial artery: Popliteal artery • Situated in the posterior compartment of leg Posterior • Origin: tibial artery • Branch of popliteal artery • Course: Peroneal • Runs down in the artery posterior compartment Tibial nerve of leg between superficial and deep musclesMedial plantar artery • Accompanied by tibial nerve Lateral plantar artery
  • 9. • 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
  • 10. • Anterior tibial artery:• Artery present in the anterior compartment of leg• Origin: branch of popliteal artery Anterior• Course: runs in the anterior tibial artery compartment of leg – deep peroneal nerve Deep peroneal• Termination: Continues as dorsalis nerve pedis artery at the ankle joint• Branches:• Anterior and posterior tibial Dorsalis recurrent arteries pedis• Muscular arteries artery
  • 11. • Dorsalis pedis artery:• Artery present in the dorsum of foot• Origin: continuation of anterior tibial artery• Course: runs on the dorsum of Doralis foot, enters the sole by piercing 1st pedis dorsal interosseous muscle• Termination: anatomoses with the lateral plantar artery to form plantar arterial arch• Branches:• Arcuate artery Arucate• Tarsal braches• 1st dorsal metatarsal artery 1st dorsal interosseous muscle
  • 12. • Medial and lateral plantar arteries: Plantar arch• 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 Lateral Medial Plantar artery plantar artery
  • 13. Plantar metatarsal• 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 Medial plantar Plantar arterial arch
  • 14. Veins of lower limb• Deep veins and superficial veins• Deep veins: Popliteal• Run along with the arteries vein• Major deep veins – popliteal vein and femoral vein Short• Popliteal vein: saphenous 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
  • 15. • Femoral vein: Great• Runs in the anterior saphenous vein compartment of thigh along with femoral artery• Begins as a continuation Femoral vein of popliteal vein• Terminates by continuing as external iliac vein• Receives great saphenous vein
  • 16. • 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
  • 17. Learning Objective 2• Explain the cholesterol metabolism cycle
  • 18. 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 upof three cyclohexane rings, A,B and C and a cyclopentane ring D•Normal Blood level is 150-200 mg%
  • 19. 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
  • 20. 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
  • 21. 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
  • 22. • 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
  • 23. Compactin, lovastatin [Competitive inhibitors] Mevastin, SimvastinHMG CoA _ _Insulin, thyroxin + HMG CoA Reductase Glucagon(dephosphorylates enz) glucocorticoids (Phosphorylates enz)Mevalonate Translation mRNACholesterol _ Transcription DNA Glucagon and glucocorticoids inactivate the enzyme through phosphorylation Insulin, thyroxin activate the enzyme through dephosphorylation
  • 24. METABOLIC FATE OF CHOLESTEROLCholesterol 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]
  • 25. • 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
  • 26. Role of LCAT:High density lipoprotein (HDL) and the enzymelecithin-cholesterol acyl transferase (LCAT) areresponsible for the transport and elimination ofcholesterol from the body.LCAT is a plasma enzyme, synthesized by the liver.LCAT catalyses the transfer of fatty acid from thesecond position of phosphatidyl choline (lecithin)to the OH group of cholesterol.HDL cholesterol is the real substrate for LCAT andthis reaction is freely reversible.LCAT activity is associated with apo-A1 of HDL.
  • 27. Learning Objective 3• Describe the pathophysiology of atherosclerosis
  • 28. 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
  • 29. Arthrosclerosis
  • 30. 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.
  • 31. Risk factorsRisk factors for hardening of the arteries are:• Diabetes• Family history of hardening of the arteries• High blood pressure• Smoking
  • 32. 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.
  • 33. 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.)
  • 34. 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.
  • 35. 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
  • 36. Natural history of Atherosclerosisstable anginaunstable anginaMIcomplicationsdeath
  • 37. Pathology of Atherosclerosis1. 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.
  • 38. 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.
  • 39. 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.
  • 40. 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.”
  • 41. Atheroma with thin fibrous Initial inflammation cap, no more NO protecting vessels Platelet Endothelial dysfunction activation/aggregation Monocyte Growth factors stimulaterecruitment/differentiation smooth muscle proliferation to intima
  • 42. • 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.
  • 43. • 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.
  • 44. • 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).
  • 45. 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
  • 46. 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.
  • 47. TreatmentOnce 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.
  • 48. Treatment• Your doctor can surgically remove plaque by performing an endarterectomy.
  • 49. Learning Objective 4• Discuss the epidemiology of arteriosclerosis in Trinidad and Tobago- not worth my time
  • 50. Learning Objective 5• Discuss the role of diet and exercise with respect to arteriosclerosis
  • 51. 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).
  • 52. 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.
  • 53. 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
  • 54. 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
  • 55. 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.
  • 56. 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.
  • 57. 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.
  • 58. Exercise and Arteriosclerosis• Ideally, you should exercise 30 to 60 minutes most days of the week.• If you cant 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.
  • 59. Learning Objective 6• Explain the diagnostic tests that could be used to detect peripheral vascular disease
  • 60. 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.
  • 61. Ankle-Brachial Index• ABI can show whether Peripheral Vascular Disease is affecting your limbs, but it wont 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.
  • 62. 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.
  • 63. 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.
  • 64. 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.
  • 65. 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.
  • 66. 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.
  • 67. 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.
  • 68. Learning Objective 7• Discuss the lifestyle changes & treatment options for peripheral vascular disease
  • 69. • 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.
  • 70. 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.
  • 71. Lifestyle ChangesLower 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.
  • 72. Lifestyle ChangesBecome 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
  • 73. Surgery or ProceduresBypass 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 doesnt cure P.A.D., but it may increase blood flow to the affected limb.
  • 74. Surgery or ProceduresAngioplasty 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.
  • 75. Surgery or ProceduresAtherectomy• 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 theyre small enough).• Doctors also can do atherectomy using a special laser that dissolves the blockage.
  • 76. MedicationsCholesterol-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.
  • 77. 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)
  • 78. 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),
  • 79. • 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.
  • 80. MedicationsMedication 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
  • 81. MedicationsMedications to prevent blood clots.• Because peripheral artery disease is related to reduced blood flow to your limbs, its 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).
  • 82. MedicationsSymptom-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, its generally less effective. But, side effects are rare with this medication