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Flashcards in Cardiology Deck (27):
1

Total Cholesterol

< 200 mg/dL

200-240 mg/dL Borderline high

> 240 mg/dL High

2

Triglycerides

< 150 mg/dL

Tx: Diet, exercise, weight loss (BMI > 25), stop smoking, niacin, fibrates, fish oil, contributing drugs

3

HDL

< 40 mg/ dL - Low

> 60 mg/dL - High

Tx: Exercise, niacin, fibrates

4

LDL-C

Primary Prevention:

Less than 2 risk factors LDL-C < 160 mg/dL

2 or more LDL-C < 130 mg/dL

Secondary prevention:

CHD: LDL-C < 100 mg/dL

5

Risk Factors for LDL-C

Smoking, HTN, HDL < 40 mg/dL (HDL > 60 is negative risk factor), family history of premature CHD (male < 55, female < 65), age (male > 45, female > 55)

6

Statins (HMG-CoA Reductase Inhibitor)

MOA

Reduces hepatic cholesterol synthesis and lowers intracellular cholesterol, which stimulates the upregulation of the LDL- C receptor and increases the uptake of non–HDL-C particles from systemic circulation

1st Line in LDL-C lowering

7

Niacin (B3)

MOA

Inhibits the hepatic production of VLDL and
consequently its metabolite LDL-C

2nd line in LDL-C lowering

8

Ezetimibe (Zetia)

MOA

Selective inhibitor of dietary and biliary cholesterol absorption

3rd line in LDL-C lowering

9

Bile Acid Sequestrants

MOA

Binds bile acids in the intestine, decreasing biliary cholesterol absorption.

(Ex. Cholestyramine, Colesevelam, Colestipol)

10

Fibrates

MOA

Peroxisome proliferator-activated receptor alpha
activation

Reduced hepatic secretion of VLDL

Induction of lipoprotein lipase–mediated lipolysis and clearance of TG

Best at lowering TGs

11

Omega-3 Fatty Acids

MOA

Inhibits hepatic secretion of TG and promotes metabolism of TG

12

Pre-HTN

Systolic: 120-139

Diastolic: 80-89

13

Stage 1 HTN

Systolic: 140-159

Diastolic: 90-99

Tx: Thiazide, ACEI, ARBs,  DHP-CCB

14

Stage 2 HTN

Systolic: > 160

Diastolic: >100

Tx: Usually 2-drug, thiazide with an ACEI, ARBs, or DHP-CCB

15

ACE Inhibitors ("prils")

MOA

Prevents conversion of angiotensin I to angiotensin II (potent vasoconstricter) by competitive inhibition of ACE. Results in lower BP secondary to lower levels of angiotensin II, increased levels of plasma renin activity, and a reduction in aldosterone secretion

1st line in HTN

16

Angiotensin Receptor Blockers (ARBs) "sartans"

MOA

Selective, competitive angiotensin II receptor type 1 receptor antagonist, reducing the endorgan responses to angiotensin II. Results in a decrease in total peripheral resistance (afterload) and cardiac venous return (preload) Reduction in BP occurs independently of the status of the renin-angiotensin system.

1st line but normally for intolerance of ACEIs

17

Renin Inhibition

MOA

Direct renin inhibition, decreasing plasma renin activity and inhibiting the conversion of angiotensinogen to angiotensin I

Ex. Aliskiren/Tekturna, not in pregnancy, hyperK wih ACEI

18

Beta-Blockers ("lol")

MOA

Competitive inhibition of βreceptors. Beta 1 receptors found on the heart. Results in decrease heart rate (chronotropic) contractility (inotropic), conduction velocity, and increased ventricular relaxation.

19

Thiazides

MOA

Acts on the kidneys to reduce Na reabsorption in the distal convoluted tubule. By impairing Na transport in the distal convoluted tubule, natriuresis and concomitant water loss is induced

20

Loop Diuretics ("ides")

MOA

Acts by reversibly binding to the Na, K, chloride cotransport mechanism on the luminal side of the ascending loop of Henle, thereby inhibiting the active reabsorption of these ions

HTN management for patients with HF and CKD

21

K+ sparing diuretics

MOA

Blocks the epithelial Na channel on the lumen side of the kidney collecting tubule. Na channel blockers directly inhibit the entry of Na into the Na channels.

22

DHP-CCB ("pines")

MOA

Act by relaxing the smooth muscle in the arterial wall, decreasing total peripheral resistance, and hence reducing BP; in angina, they increase bloodflow to the heart muscle. Increase preload & HR and decrease afterload

1st line option

23

Non DHP-CCB

MOA

Acts as a potent vasodilator of coronary vessels, increasing bloodflow and decreasing the HR by strong depression of atrioventricular node conduction. Also, acts as a potent vasodilator of peripheral vessels, reducing peripheral resistance and
afterload. Has negative inotropic effects

ex. Verapamil, Diltiazem

24

Alpha-1 blockers

MOA

Selective alpha-1 antagonist that works by blocking the action of adrenaline on smooth muscle of the blood vessel walls. Decrease afterload

Used in BPH

25

Aldosterone Receptor Blockers

MOA

Inhibit the effect of aldosterone by competing for intracellular aldosterone receptors in the cortical collecting duct. This decreases the reabsorption of Na+ and water while decreasing the secretion of K+

Ex. Spironolactone, Epleronone

Used in resistant HTN

26

Central alpha-2 agonist

MOA

Stimulates alpha-2 receptors in the brain, which decreases sympathetic outflow cardiac output and peripheral vascular resistance, lowering BP and HR

Ex. Clonidine, Methyldopa, Guanfacine

Used in resistant HTN

 

27

Vasodilators

MOA

Direct-acting smooth muscle relaxant that
acts as a vasodilator primarily in arteries and arterioles

Ex. Hydralazine, Minoxidil

Useful in resistant HTN (use with loop)