Abdominal Aortic Aneurysm

Question 1

Pathogenesis of atherosclerosis

Answer 1

1. Endothelial injury/dysfunction - increased capillary permeability, leukocyte adhesion, thrombus formation
2. Accumulation of lipoproteins (LDL) in vessel wall
3. Monocyte adhesion to endothelium
4. Platelet adhesion
5. Factor release from platelets –> smooth muscle cell recruitment
6. Smooth muscle cell proliferation, extracellular matrix production, recruitment of T cells
7. Lipid accumulation

Question 2

Metoprolol

Answer 2

Selective inhibitor of beta1-adrenergic receptors; competitively blocks beta1-receptors, with little or no effect on beta2-receptors

Question 3

Hydrochlorothiazide

Answer 3

inhibits sodium reabsorption in the distal tubules causing increased excretion of sodium and water as well as potassium and hydrogen ions

Question 4

Amlodipine

Answer 4

• Inhibits calcium ion from entering the “slow channels” or select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization –> producing a relaxation of coronary vascular smooth muscle and coronary vasodilation
• increases myocardial oxygen delivery in patients with vasospastic angina.

Question 5

Fluticasone/salmeterol

Answer 5

Fluticasone belongs to a group of corticosteroids which utilizes a fluorocarbothioate ester linkage at the 17 carbon position; extremely potent vasoconstrictive and anti-inflammatory activity

Question 6

Simvastatin

Answer 6

methylated derivative of lovastatin that acts by competitively inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis

Question 7

Cholesterol Biosynthesis

Answer 7

3 Acetyl CoAs –> HMG-CoA –> Mevalonate –> STEPS –> cholesterol
HMG-CoA Reductase catalzyes HMG-CoA to mevalonate

Question 8

Ankle-Brachial Index

Answer 8

helps diagnose peripheral artery disease

- systolic ankle pressure/systolic brachial pressure

Question 9

Cilostazol

Answer 9

-inhibitor of phosphodiesterase III –> increase cAMP (inhibition of platelet aggregation) –> vasodilation and inhibition of VSM proliferation

Question 10

Atorvastatin

Answer 10

• inhibits HMG-CoA Reductase (RLS of cholesterol synthesis) –> leads to compensatory increase in LDL receptor expression –> LDL catabolism

Question 11

LDL

Answer 11

“bad” cholesterol - it is the complex that delivers cholesterol to our tissues

Question 12

HDL

Answer 12

“good” cholesterol - it is complex that delivers cholesterol to liver to be excreted as bile

Question 13

Niacin

Answer 13

Decrease synthesis and secretion as VLDL (same indication for use as previous drugs) == decrease cholesterol, triglyerides, VLDL, IDL, and LDL but increase HDL (Yayy!) - side effect is flushing of the skin, can be counteracted with aspirin- controversy in the significance

Question 14

Bile Acid Resin

Answer 14

(they contain chloride ion they exchange it for bile salt to form insoluble complex that gets excreted in the feces. The body also increases LDL receptors with this drug.) - use with an LDL greater than 190 or greater than 160 with 2 risk factors == decrease cholesterol and decrease LDL but increase triglycerides, VLDL, and HDL - Limit the bioavailability of fats

Question 15

Fibrates

Answer 15

decrease VLDL

increase lipolysis of lipoprotein and triglycerides

Question 16

Claudication

Answer 16

pain caused by decreased blood flow during exercise

- caused by peripheral artery disease