pharm 3 set 3

IV Nitro needs special tubing b/c it sticks to plastic

• Stable angina
• used preventative, not for acute setting

• Pt. will be given Ca++ blockers (arteriole dilation and relax cornary spasm
• Pt will also be given Beta Blocks (slow HR, Inc. coronary flow time, and reduce atrial pressure)

• Reduces accumulation of Na+ and Ca+ in muscle cells
• Not sure how, but does help muscle cells use energy more efficiently

SE=dysrrhythm, HTN, GI

Reserved for refactory cases when all other drugs fail

• anti-coag
• Inactivates Thrombin and Factor 10a
• -fibrin production is reduced, clotting suppressed
• -short 1/2

Used for PE, Embolic stroke, MI, DIC

Monitor aPTT (22-34 sec.)

Risk for Bleeding

Antidote for heparin induced bleeding

• IV intermittent - during cath procedure or the like
• - Not done often

• IV continuous - given by weight and managed protocol
• - Q6h after dose given or change made

Low dose therapy - to prevent DVT's

low molecular weight heparin 

• Fractionated - use part of long hep chain
• Does NOT affect aPTT so don't need t monitor
• -only affects Factor 10a (not thrombin)
• can be done at home

• oral anti-coag
• Vit K antagonist

Monnitor PT and INR

• risk for bleeding
• many drug reactions

• Direct Thrombin Inhibitor
• non-valvular A-Fib clot prevention
• Thromboembolism
• Inc. incidence of bleeding
• GI SE
• Unstable
• No blood monitoring

• Anti-platelet
• prevent platelet aggregation
• prevent thromboses in arteries

• Interrupts clotting by interfering with Thromboxane
• SE= GI bleed

• Anti-platelet drugs
• More specifically, ADP Receptor Antagonists
•  - Irreversible blockage of platelet ADP (prevent aggregation)

• T= 1st but hematologic SE
• P= 2nd gen
•  = less side effects, very popular
• E= 3rd gen
•  = less clotting, but more major bleeding

• Anti-platelet
• *Glycoprotein receptor antagonist
• -reversible blocking of receptor to prevent agg

Given IV short term for ACS and PCI ONLY

• Anti-platelete
• used ONLY for prevention of thromboembolism AFTER heart valve replacement
• used in conjunction with coumadin

A= Persantin combined with ASA to reduce incidence of strokes

Anti-platelet

Platelet inhibitor and vasodilator

DOC for intermittent Claudication

• remove thrombi that have formed
• convert plasminogen to plamin
• -plasmin degrades the fibrin cap
• Indication: acute MI, DVT, PE; lead to ischemic stroke

this drug has risk of bleeding

Thrombolytics

S= 1st drug, but allergic rxns b/c is made from strptococci

• A= 2nd gen.
•  = Short 1/2

increase urine output

• -Tx of HTN
• -Mobilization of edematous fluid
• -Prevent renal failure
•   =when fluids are low on this pt. we give fluids and diuretics to flush kindeys out

• filtration
• reabsorption
• secretion

• Hypovolemia
• -dehydration, orthostatic hypoTN, thirst
• Acid/Base imbalance
• Disturbances of electrolyte levels

• Loop (high ceiling) Diuretic
• Works in the Ascending loop of Henle
• -depends on prostaglandin availability (which dec. with ibuprofen use)
• Blocks Na+ and Cl- reabsoprtion
• DOC for fluid overload

SE= Hypokalemia

• Thaizide diuretic
• Blocks Na and CL reabsorption
•  ->much LESS h2o and electrolyte loss than loops
• Doesn't work well with low GFR rate, so not given for Renal Failure
• Used for HTN and Edema
• BAD for Gout (uric acid build up)

Paradoxical (reverse) effects on Diabetes Insipidus (decreases urine in a disease that increases urine

• K+ sparing diuretic
• -used with other diurs.

• Aldosterone Antagonist
• Inc. Na+ excretion so Kidney saves K+

Limited urine production but dec. K+ loss

K+ sparing diuretic

• Non Aldosterone Antagonist
• Inc. Na+ (h2o) loss
• Directly blocks K+ loss
•  ->given with loops b/c of blocking effect

• Creates an osmotic effect in the nephron
• -inhibits passive reabsorption of h2o
• NO Metab effect, just a big molecule that attracts h2o
• Moves fuild from tissue into vascular space
• MUST be given IV and use a filter needle
• Given mainly to Dec. ICP, also used for edema

• C= part of cell membran
• = essential for bile production
• =made in liver

• L= carry cholest
• -LDL= carry chol to body (bad chol)
• -HDL= carry excess chol to liver for metab

HMG reductase provides for cholest product

Inhibitors are called Statins -> DOC for dec. LDL and inc. HDL

• Dec. LDL
• INc. HDL
• Promote plaque stability
• Also, an Inc in Hepatic LDL receptors

take drug at night b/c most chol production is done at night

create risk for liver failure and muscle breakdown

Headache, rash, GI

Hepatotoxicity major SE, monitor every 6 months

Muscle inflamm and breakdown

Grapefruit juice

Statin

• statin
• NEVER more than 80mg

statin

• 2nd gen statin
• very potent (dec dose, dec SE in theory)
• Rhabdomyolysis is big issue with Crestor

• try every other day statin dosing
• check thyroid imbalances
• check Vit. D status
• Consider Coenzyme Q10
• -studies suggest it can help prevent muscle issues

• Dec. triglycerides and LDL production
• Inc HDL better than any other drug
• Reduces coronary risk and mortality

SE= skin flushing, GI, hepatotoxicity, hyperglycemia

Niacin= slow release form

Bile Acid Sequestrant

• Binds with bile acids in gut to prevent reabsorption
• Dec. bile acid creates demand for more production
• Choilesterol is used to make bile acids, so liver creates more LDL receptors

SE= constipation, indigetion, nausea (with food)

Dec uptake of fat soluble drugs, so take Coumadin 1 hr before Questran

• new Bile Acid Sequestrant
• 2nd gen
• Better tolerated, less constipation and nausea
• does NOT afftect fat soluble drugs/vit.s
• $$$

• Cholesterol Absorption Blocking
• Block absoption in sm. intestine
• Affects dietary and cholesterol secreted in bile (which is often reabsorbed)
• well tolerated, careful in liver failure

Fibric Acid Derivative  "Fibrates"

• Most effective for lowering triglycerides
• can Inc HDL, NO affect on LDL
• accelerated breakdown of triglys

SE= gall stones, myopathy