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

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
muscles
Medial 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 up
of 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

22. 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

23. • 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

24. 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

25. 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]

26. • 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

27. 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.

28. Learning Objective 3
• Describe the pathophysiology of
atherosclerosis

29. 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

30. Arthrosclerosis

31. 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.

32. Risk factors
Risk factors for hardening of the arteries are:
• Diabetes
• Family history of hardening of the arteries
• High blood pressure
• Smoking

33. 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.

34. 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.)

35. 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.

36. 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

37. Natural history of Atherosclerosis
stable anginaunstable anginaMIcomplicationsdeath

38. 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.

39. 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.

40. 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.

41. 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.”

42. Atheroma with thin fibrous
Initial inflammation cap, no more NO protecting
vessels
Platelet
Endothelial dysfunction
activation/aggregation
Monocyte
Growth factors stimulate
recruitment/differentiation
smooth muscle proliferation
to intima

43. • 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.

44. • 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.

45. • 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).

46. 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

47. 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.

48. 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.

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

50. Learning Objective 4
• Discuss the epidemiology of arteriosclerosis
in Trinidad and Tobago- not worth my time

51. Learning Objective 5
• Discuss the role of diet and exercise with
respect to arteriosclerosis

52. 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).

53. 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.

54. 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

55. 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

56. 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.

57. 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.

58. 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.

59. 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.

60. Learning Objective 6
• Explain the diagnostic tests that could be used
to detect peripheral vascular disease

61. 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.

62. 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.

64. 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.

65. 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.

66. 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.

67. 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.

68. 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.

69. 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.

70. Learning Objective 7
• Discuss the lifestyle changes & treatment
options for peripheral vascular disease

71. • 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.

72. Lifestyle Changes
Quit 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.

73. 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.

74. 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

75. 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.

76. 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.

77. 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.

78. 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.

79. Medications
High 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)

80. 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),

81. • 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.

82. 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

83. 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).

84. 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