| Term 
 
        | Loops & Thiazides (action of) |  | Definition 
 
        | prevent Na/Cl reabsorption which pulls water into the renal tubule to be excreted as urine |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | alter Na+ and K+ exchange in the distal tubule to conserve potassium. Always combined with a loop or thiazide to prevent hypokalemia during diuretic therapy |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | Create an osmotic pressure within renal tubule which pulls in water to be excreted as urine; same principal within cranial capillaries: creates osmotic force that pulls excess fluid from the brain into the vascular system |  | 
        |  | 
        
        | Term 
 
        | Loops & Thiazides (side effects) |  | Definition 
 
        | volume depletion; decreased BP; electrolyte imbalances K+ sparing: hyperkalemia
 |  | 
        |  | 
        
        | Term 
 
        | K+ sparing (side effects) |  | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 | 
        |  | 
        
        | Term 
 
        | Which loop, thiazide, or potassium sparing diuretics produce the greatest amount of diuresis? Why? |  | Definition 
 
        | Loops b/c they have the ability to affect the greatest percentage of Na absorption |  | 
        |  | 
        
        | Term 
 
        | What things must be monitored during diuretic therapy? |  | Definition 
 
        | Blood pressure		weight		electrolytes: Na, K, Cl		intake/output |  | 
        |  | 
        
        | Term 
 | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | Hydrochlorothiazide (Hydrodiuril) |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | Spironolactone (Aldactone) |  | 
        |  | 
        
        | Term 
 | Definition 
 | 
        |  | 
        
        | Term 
 
        | Why are diuretics used? Are they used or contraindicated in heart failure? |  | Definition 
 
        | To eliminate excess fluid from the body: pulmonary edema; edema of hepatic or cardiac 	origin; to aid in hypertension therapy. Diruetics are used in heart failure except mannitol.
 |  | 
        |  | 
        
        | Term 
 
        | 3.	Why do we monitor potassium levels in patients taking diuretics? Why is it especially important to monitor potassium when the patient is taking digoxin and diuretics? |  | Definition 
 
        | Hypokalemia is a common side effect of diuretic therapy; thus monitoring K+ levels is 	essential especially in patients taking digoxin because K+ competes with digoxin for 	receptor sites in the heart. If K+ levels are low, then that will allow more dig to bind to 	receptors which could cause toxic effects including ventricular arrhythmias |  | 
        |  | 
        
        | Term 
 
        | What blood pressure numbers would indicate prehypertension, Stage I, & Stage II hypertension? |  | Definition 
 
        | Pre: 120-139/80-89 Stage I: 140-159/90-99 Stage II: greater than 160/100 |  | 
        |  | 
        
        | Term 
 
        | How do ACE inhibitors and Angiotensin II Receptor Blockers (ARBs) work to treat HTN/heart failure? |  | Definition 
 
        | ACEs prevent the conversion of angiotensin I to angiotensin II and ARBs block angiotensin 	II receptors which both lead to decreased vasoconstriction and decreased Na & water retention |  | 
        |  | 
        
        | Term 
 
        | What are the prototypes ARB's and ACE inhibitors? |  | Definition 
 
        | ACE prototype: Captopril (Capoten)  ARB prototype: Losartan (Cozaar) & Valsartan (Diovan) |  | 
        |  | 
        
        | Term 
 
        | What are the major adverse effects of ACE & ARB prototypes? |  | Definition 
 
        | First dose hypotension; dizziness; Hyperkalemia with ACEs; Angioedema |  | 
        |  | 
        
        | Term 
 
        | What are important nursing implications for ARB's and ACE inhibitors? |  | Definition 
 
        | Nursing implications: monitor BP; educate on K+ salts & high K+ foods for ACEs; no use 	during pregnancy; if angioedema occurs the patient should not be given that class of drugs 	again (allergy) |  | 
        |  | 
        
        | Term 
 
        | How do Calcium Channel Blockers work to treat HTN? |  | Definition 
 
        | Block calcium channels of vascular smooth muscle to control contraction which leads to vasodilation. |  | 
        |  | 
        
        | Term 
 
        | What are the prototypes Calcium Channel blockers? |  | Definition 
 
        | Prototypes – Verapamil (cardiac effects ~ can be used for dysrythmias) Nifedipine (little cardiac effect)
 |  | 
        |  | 
        
        | Term 
 
        | What are the major adverse effects of the Ca+ Channel Blocker prototypes? |  | Definition 
 
        | Adverse effects: flushing, headache, peripheral edema; constipation |  | 
        |  | 
        
        | Term 
 
        | What are important nursing implications for calcium channel blockers? |  | Definition 
 
        | Nursing implications: monitor BP; increase fluids/fiber to prevent constipation; education 	re: swallowing sustained release formulation tablets whole |  | 
        |  | 
        
        | Term 
 
        | What is Digoxin used for? |  | Definition 
 
        | Heart failure – to increase cardiac contractility Atrial fibrillation
 |  | 
        |  | 
        
        | Term 
 
        | What is its mechanism of action of digoxin? |  | Definition 
 
        | Promotes Ca+ accumulation within cardiac muscle cells which increases force of contraction. Indirectly decreases afterload and preload |  | 
        |  | 
        
        | Term 
 
        | How do we know if our treatment with Digoxin is effective? |  | Definition 
 
        | Decreased HR; decreased peripheral edema (possibly decreased weight) |  | 
        |  | 
        
        | Term 
 
        | What are important nursing implications of Digoxin? |  | Definition 
 
        | ·	Initial therapy begins with digitalization – loading dose to decrease time to plateau  as half life is 1.5 days ·	Count HR for one full minute before administration – hold and contact MD if rate is less than 60
 ·	Monitor K+ levels – educate re: high K+ foods and salt substitutes
 ·	Monitor dig levels
 |  | 
        |  | 
        
        | Term 
 
        | Which medication is primarily used for angina pectoris? What is the mechanism of action of this drug? |  | Definition 
 
        | nitroglycerine. Dialates veins. |  | 
        |  | 
        
        | Term 
 
        | Discuss important administration and nursing implications for Nitroglycerine. |  | Definition 
 
        | Many administration routes: sublingual, buccal, transdermal, PO, IV Tolerance develops quickly – when taking scheduled doses, there must be at least an 8 hour “nitro 	free” period
 Acute anginal attacks: 1st sublingual dose…call 911 if no relief in 5 min and take 2nd dose
 |  | 
        |  | 
        
        | Term 
 
        | What do anticoagulant drugs do? |  | Definition 
 
        | Decrease coagulation (lengthen clotting time) which decreases blood viscosity & prevents 	intravascular clot formation |  | 
        |  | 
        
        | Term 
 
        | What are the major adverse effects of the anticoagulants discussed? |  | Definition 
 
        | Bleeding – Hemorrhage; thrombocytopenia |  | 
        |  | 
        
        | Term 
 
        | How is Heparin administered and monitored? |  | Definition 
 
        | IV, SC 
 Activated Partial Thromboplastin Time (APTT) should be increased
 |  | 
        |  | 
        
        | Term 
 
        | What is the antidote to Heparin? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | How does Heparin differ from the Low Molecular Weight Heparins? |  | Definition 
 
        | No APTT monitoring required Once daily dosing via SC injection – home therapy
 Less risk of bleeding than unfractioned heparin
 |  | 
        |  | 
        
        | Term 
 
        | How is Coumadin administered and monitored? |  | Definition 
 
        | PO only Prothrombin Time (PT) should be increased	INR should be between 3-4.5
 |  | 
        |  | 
        
        | Term 
 
        | What is the antidote to Coumadin? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What is the definition of high cholesterol (numbers for HDL, LDL, & total cholesterol)? |  | Definition 
 
        | HDL > 60	LDL > 100	total cho < 240 |  | 
        |  | 
        
        | Term 
 
        | HMG-CoA reductase inhibitors mechanism of action. |  | Definition 
 
        | Limits the rate of Cho production and increases LDL receptor sites in the liver |  | 
        |  | 
        
        | Term 
 
        | HMG-CoA reductase inhibitors adverse effects. |  | Definition 
 
        | Adverse effects rare: heatotoxicity, myopathy |  | 
        |  | 
        
        | Term 
 
        | HMG-CoA reductase inhibitors administration and nursing implications. |  | Definition 
 
        | Administered PO at night Life long therapy; liver function monitoring; education re: diet & exercise
 |  | 
        |  | 
        
        | Term 
 
        | Bile Acid-Binding Resins mechanism of action. |  | Definition 
 
        | Form complex with bile acids in intestine…decreased bile triggers liver to produce more which requires cholesterol |  | 
        |  | 
        
        | Term 
 
        | Bile Acid-Binding Resins adverse effects. |  | Definition 
 
        | Adverse effects: GI related – constipation, bloating, indigestion; decreased absorption of fat soluble vitamins. Can bind with certain medications in GI tract |  | 
        |  | 
        
        | Term 
 
        | Bile Acid-Binding Resins administration and nursing implications. |  | Definition 
 
        | Administered PO with plenty of fluid Timing of other drug administration – one hour before or four hours after bile acid binders
 |  | 
        |  | 
        
        | Term 
 
        | Nicotinic Acid mechanism of action. |  | Definition 
 
        | Decreases production of VLDL |  | 
        |  | 
        
        | Term 
 
        | Nicotinic Acid adverse effects. |  | Definition 
 
        | facial flushing/itching due to prostaglandin mediation cutaneous vasodilation (diminishes over time); GI upset |  | 
        |  | 
        
        | Term 
 
        | Nicotinic Acid administration and nursing implications. |  | Definition 
 
        | Administered PO with or after meals |  | 
        |  | 
        
        | Term 
 
        | Hydralazine (Apresoline), Nitroglycerin, Sodium Nitroprusside class? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Verapamil(Isoptin), Nifedipine(Procardia),  Diltiazem (Cardizem)   class? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Heparin,  Warfarin (Coumadin)   class? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | digitoxin, digoxin and deslanoside class? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | digitoxin, digoxin and deslanoside class? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Lisinopril, catopril, elanopril class? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Valsartan(Diovan), Losartan(Cozaar), Candesartan(Atacand) class? |  | Definition 
 
        | ARB's AngiotensinII receptor Blockers |  | 
        |  | 
        
        | Term 
 
        | rosuvastatin (CRESTOR), lovastatin (Mevacor), atorvastatin (Lipitor), pravastatin (Pravachol), fluvastatin (Lescol), pitavastatin (Livalo), and simvastatin (Zocor) class? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Cholestyramine (Questran) Colesevelam (Welchol)
 Colestipol (Colestid)
 Class?
 |  | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 | 
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