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173 Cards in this Set
- Front
- Back
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The body, mostly the ___, produces essentially all of the cholesterol needed for normal functioning—about 1,000 mg a day.
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liver
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The major cholesterol carrier in the blood.
Take cholesterol away from the organs and vessels and bring it into the liver either to store it or to make bile |
HDL
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produces steroids, bile acid production, cell membrane
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cholesterol
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takes cholesterol into the vessels or other organs
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LDL
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main risk factors for development of artherosclerosis
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LDL
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main risk factor for ischemic heart disease
Not enough blood flow to the heart due to an occlusion of coronary arteries Increases oxygen demand |
Atherosclerosis
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hard thick layer – narrows vessel-> leads to a decreased blood flow to the heart → causes muscle soreness→
Pain→ due to lactic acid build up |
stable plaque
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thin fibrous layer of plaque
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unstable plaque
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progressive build up of plaque- leads to non stemi elevation bc of incomplete occlusion of the vessel-
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Angina
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coronary artery disease may present without st elevation- means that there is no __
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necrosis
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st segment elevation – happens more often due to the rupture of thin plaque – activates the coagulation cascade- platelets → end product is fibrin which seals and causes clots
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complete occlusion of blood flow
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__clot= reversible with platelets
Once fibrin arrives= __ clot= irreversible ST segment elevation → necrosis |
white
red |
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anti-platelet NSAID
Nonselective Blocks COX1 and COX2 COX1= inhibit platelet aggregation Worry about bleeding- especially gastric bleeding, renal issues, tinnitus |
Asprin- to treat angina
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main energy storage in our bodies
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triglycerides
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an elevation of blood lipid levels.
considered a risk factor for the following disorders: atherosclerosis, coronary artery disease, and thromboses. |
hyperlipidemia
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Total cholesterol= ___
LDL: __→ L=lethal HDL: AT LEAST __IDEALLY __→ H=healthy |
200
100 40-60 |
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Diet- Increase veggies decrease met
Encourage weight loss Increased physical activity |
lifestyle changes dealing with high cholesterol
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First line drug
Lowers blood cholesterol levels by inhibiting the enzyme responsible for converting HMG-CoA It’s needed for cholesterol biosynthesis |
statins
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Increased HDL by bringing it from the vessel back into the liver and decreases LDL bc there is less cholesterol being taken into the vessel
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statin
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Main side effect- hepatotoxicity- monitor LFTs- beginning of therapy, 3 months and 6 months and periodically
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statin
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Taken orally
Highly liver-toxic lowers LDL and increase HDL |
statin
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atorvastatin (Lipitor), rosuvastatin (Crestor), simvastatin (Zocor)
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statin
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statin that gives Blurred vision, must take with evening meal
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lovastatin
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Cholesterol level, pruritus prior to Rx
Will check serum levels q4weeks & prn Active liver disease and pregnancy LFTs monitored• ACE-I can lead to increase K+ |
statin
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Increases bleeding risk with coumadin Rx
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Lovastatin & simvastatin
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in statins, assess for muscle and joint aches due to
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Rhabdomyolysis (rare)
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Rapid destruction of skeletal muscle
Risk increases with other cholesterol GI main test used= CPK |
Rhabdomyolysis (rare)
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Main treatment- IV fluids +/- bicarbonate
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Rhabdomyolysis (rare)
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High first-pass effect. Highly protein bound. Excreted primarily through the gastrointestinal tract.
Constipation |
statin
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statin taken in the evening
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simvastatin
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Pt who needs __ therapy
• Overweight • Poor diet • Low exercise levels • Smoker • Drinker |
statin
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• Monitor labs, including CK if c/o muscle pain
LFTs, K+, folic acid • Watch urine for color change • Sunscreen (photosensitive) • Monitor for vitamin deficiency |
statin- risk for injury
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• 2-3 L fluid daily
• No ETOH- protect liver • Health diet & exercise plan • Weight reduction • Reduce Tylenol |
altered nutrition for statin
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• Common side effect- pruritis and itchiness
• Hives=adverse |
statin
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• Lowers LDL and increases HDL
• Adjunct therapy • Prevents bile from being reabsorbed and recycled allowing it to be excreted in the stools, consequently lowering cholesterol. |
o Bile acid resins (Sequestrants)
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• Allows for more empty receptors at level of the liver→ increases HDLs and lower LDLs
• Can interfere with absorption of Dig, hydrocortisone, Coumadin • Can decrease absorption of propranolol, lasix, HCTZ, and fibrates |
o Bile acid resins (Sequestrants)
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• Watch for gallbladder inflammation & gallstones→ don’t take this medication bc it works in the duct system of the liver
• Hepatotoxicity is an issue |
o Bile acid resins (Sequestrants)
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cholestyramine (Questran)
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o Bile acid resins (Sequestrants)
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• Lowers LDL and increases HDL
• Adjunct therapy- Sometimes can order by itself but usually when the statin isn’t working add a low dose of niacin* |
o Nicotinic Acids
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• High dose of vitamin B3
• Potent vasodilator • Take with aspiring to make the flushing better • Don’t give to DM, bleeders, or liver Dz Can cause hyperglycemia |
o Nicotinic Acids
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• The best cholesterol lowering medication
• Increases HDL the most and decreases LDL the most but it has the greatest amount of side effects • Patients don’t tolerate it well • Hepatotoxic |
o Nicotinic Acids
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• Can be given w statins but the FDA doesn’t recommend it because it increases the likelihood of hepatotoxicity and rabdomyalisis
• HOWEVER many doctors and NPs will prescribe them together • Don’t give too high a dose |
o Nicotinic Acids
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• Normally used to lower triglycerides ***
• Heart problems aren’t associated with triglycerides but they can become lethal → can increased the likelihood of pt developing pancreatitis • Adjunct therapy |
o Fibric acid derivatives
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• Increase effect of coumadin & insulins
Watch your diabetics and bleeding risk patients • Serum monitoring same as for statins • Also: blood sugar, CBC, uric acid Blood sugar can increase- bouts of hyperglycemia • Watch out for liver &/or renal disease |
o Fibric acid derivatives
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fenofibrate (Tricor), gemfibrozil (Lopid) and Triplix
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o Fibric acid derivatives
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• Lowers LDL
• Little effect on HDL • Worry about hepatotoxicity, renal disease (somewhat nephrotoxic), usually not given by itself (hence adjunct- usually w a statin |
o Fibric acid derivatives
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• Only one medication in this class→ not popular
• Adjunct therapy • Same adverse and side effect as statins, but also watch for: Back pain, CP, cough, sinusitis |
o Cholesterol absorption inhibitors
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prevents absorption of cholesterol at level of intestines
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Zetia (ezetimibe)
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Zetia (ezetimibe)
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o Cholesterol absorption inhibitors
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• Complain of fatty stools, bloating, gas and anal leakage
• Need to be monitored routinely for vitamin depletion • May effect the absorption (lower) of certain meds such as digoxin and Coumadin |
o Cholesterol absorption inhibitors
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o Leading risk factor for development of heart disease, renal failure and stroke
o Silent killer o Staggering, insidious process |
HTN
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o May develop renal insufficiency secondary to proteinuria
o May develop heart disease in many forms→ one by increases systemic vascular resistance- increases workload of the heart- increase O2 demand |
HTN
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Main etiologies of congestive heart failure→ mostly left sided
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HTN
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clot at level of brain leads to thrombotic stroke
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In HTN, shearing force increases
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__ doesnt work if you already have a clot
Main risk= bleeding—start bleeding from every orifice |
asprin
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the following is used when?
• CT scan (CAT scan) • To determine if they can have aspirin because it tells you if the pt has bleeding in the brain (with 98% sensitivity) • CT isn’t sensitive for clots |
hemorrhagic stroke-> aneurism burst
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BP= __+__
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BP= CO+PR
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Main drugs for HTN
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Diuretics
Ace inhibitors ARBs Beta blockers Calcium Channel Blockers Alternative medications Alpha 1 blockers Alpha 2 agonist Direct vasodilators |
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o Main drug to effect stroke volume=
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diuretics
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o Main drug to effect contractility-
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beta blocker, calcium channel blockers
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alpha 1 antagonist, alpha 2 agonists used for
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vasoconstriction
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o Vasodilators or direct vasodilators
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nitroglycerine
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__inhibitors block RAAS- produce vasodilation
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ACE
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angiotensin receptor blockers→ produce vasodilation (indirectly)- prevent attachment of angiotensin 2 to its receptors
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arbs
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effect RAAS system – reduce amount of renin
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beta blockers
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Initial treatments:
• Lifestyle modifications • Diet- Decrease alcohol and sodium • Exercise • Smoking cessation—big one • Changes in body habitus |
HTN
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Medications for HTN are used in conjunction with?
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lifestyle modifications
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Medications used for
pre-hypertention hypertension 1 hypertension 2 |
Patient should AT LEAST do lifestyle modification
thiazide like diuretic→ HCTZ if they have no other disease and LSM LSM, HCTZ, beta blocker or ace inhibitor or calcium channel blocker |
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when medication HTN2 if pt has;
Chronic renal problems uses__ Heart failure use__ |
ace inhibitors
beta blockers or ace inhibitors |
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first line drug for HTN
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diuretics
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What does D-I-U-R-E-T-I-C stand for when dealing with HTN
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• DIET- Increase K+ (except Aldactone)
By supplementation or diet Peaches, mangoes, oranges, sweet potatoes and bananas • I&O- daily weights Report 2lb gain in a day and 5 lb gain in a week • Same time everyday in same type of clothes • Undesirable effects- fluid/electrolyte imbalances • Hypovolemia- hypotension • Hypokalemia • Hyponatremia • Hypocalcemia • Review HR,BP & LYTES • Monitor HR and BP • Elderly- careful E-evening dose no • Nocturia- get up run to the bathroom, fall, break a hip • Take with or after meals in am • Increased risk orthostatic hypotension • Risk for falls • Cancel cigs, ETOH • Reduce as much as possible but best to avoid • Many diuretics are nephrotoxic |
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lowers effectiveness of diuretic and increases likelihood of nephrotoxicity
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NSAID
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Pt is at risk for falls – be aware of safety WHEN taking?
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Diuretics
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works on distal convoluted tubule to Inhibit sodium & chloride reabsorption
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thiazide (HCTZ)
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most common thiazide
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o Hydrochlorothiazide (HCTZ)
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S/S- hypovolemia, hypokalemia and hyponatremia
cross reaction with sulfur |
THIAZIDE
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• Encourage potassium containing foods
• Administer in the morning • Nephrotoxicity is a big issue |
thiazide
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• Never want to discontinue any BP med all of the sudden bc of the risk for __
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rebound HTN
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may cause postural hypotention
May cause K+ depletion & hypokalemia o Monitor K+ levels o Monitor for muscle cramps & weakness o Encourage high K+ foods o May require K+ supplements |
thiazide
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• More potent than thiazide diuretics
• Prevents reabsorption of sodium & chloride in the Loop of Henle • Prevent reabsorption of water, sodium, and potassium |
loop
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• Potassium wasting diuretic
• Remains effective even if pts have renal insufficiency • Widely used with the elderly |
loop
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types of loop diuretics
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bumex and lasix
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• Also a vasodilator
• Develop hypotension even before they start to diurese • Lead to hypotension, dehydration, renal failure, and tinnitus • Tinnitus can happen w fast IV push • Poorly absorbed through the GI although we have the PO form • Better bioavailability IV |
o Furosemide (Lasix)-
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• 40x stronger than Lasix
• Reserved for pts w renal problems and Lasix isn’t working |
bumex- loop
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Nsg Dx: Fluid Volume, Injury
Watch for: • Ototoxicity & transient deafness, hypokalemia, hyperglycemia, hypovolemia |
diuretics
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o Ototoxicity
Give SLOW IV -> Hypokalemia o May require supplements o Monitor for digoxin toxicity o T wave flattens |
loop- lasix
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o T wave flattens
o Premature ventricular contractions- PVCs 3 or more PVCs is v tachycardia Be careful for v fib and v tach o Magnesium and lost through use of diuretics o Hypomagnesaemia- can give multifocal ventricular fib – torsades de pointes |
loop- lasix
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• Spironolactone (Aldactone)
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potassium sparing
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Aldosterone promotes sodium and water retention, so if you inhibit this you reduce the amount of fluid reabsorbed
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k- sparring
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• Can have hyperkalemia
• Contraindicated is K+ is greater than 5.5 • Not good for people w renal disease • Shouldn’t be taken w ace inhibitors bc they also increase the likelihood of hyperkalemia |
k- sparring
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• Not potent diuretics
Usually combined with K+ depleting diuretics to decrease risk of hyperkalemia/hypokalemia |
k-sparring
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• Monitor for Hyperkalemia
Avoid salt substitutes • Males may develop gynecomastia - develop enlargement of breast tissue |
aldactone
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• Combination __ & thiazide diuretics
The combo drugs help decrease risk of K depletion (or retention depending on the drug) and increase antihypertensive effects So, it decreases chances of adverse effects since most are related to K imbalances. Also, pt only hast o take one pill instead of 2 |
k-sparring
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• Not for HTN
• Produce a profound diuretic effect • Usually used in increased ICP or intraocular pressure • May be used to treat renal failure |
osmotic diuretic
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• Mannitol
o IV administration o Used primarily to treat increased intracranial pressure NOT for HTN |
osmotic diuretic
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• Remove sodium and water from the body by inhibiting reabsorption of sodium
• Used to treat: • Edema • Ascites- in pt w liver failure, liver disease or congestive heart failure (can move all the way to the periphery) • HTN • Congestive heart failure |
Carbonic Anhydrase Inhibitors- diuretic
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• When alpha-1 receptors are stimulated, they cause peripheral constriction, and blood pressure increases as a result.
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adrenergic receptors
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Alpha 1 blockers used is heart problems (3)
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prazosin ( Minipress)
tamsulosin (Flomax) Doxazosin (Cardura) |
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A1 blockers used to HTN
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prazosin ( Minipress)
Doxazosin (Cardura) |
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A1 blocker used for BPH or to pass kidney stones
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tamsulosin (Flomax)
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• Take it at night to avoid first dose phenomenon
• Main issue= orthostatic hypotension |
A1 blockers
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• Reduce systemic vascular resistance→ decreases workload of the heart → afterload reducer
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A1 blockers
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• Don’t discontinue all of the sudden→ rebound HTN
• Don’t effect HR- monitor BP • Sometimes can have tachycardia—not common |
A1 blockers
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Decrease NE released by the brain→ decrease vasoconstrictor- lead to vasodilation
watch for sedation |
A2 agonist
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prototype of A2 Agonist
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Catapress (clonidine) *
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Don’t stop all the sudden- rebound tachycardia and HTN
can also be used for smoking cessation Also can be used in pts w autism, for anxiety (off label use) or migraines |
catapress (clonidine)
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receptor sites are located primarily in the heart and kidneys.
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Beta 1 blockers
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can be selective or non selective
• First monitor HR—HR<60bpm—hold medication unless otherwise indicated • Because it decreases HR, contractility and firing action • Need to teach pts to take their pulse |
beta 1 blockers
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use for HF bc it stops remodeling or growth of heart
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beta 1 blockers
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• Decreases likelihood of developing deadly arrhythmias in pts w MI and CHF
• May also decrease the symptoms of hypoglycemia – monitor blood sugar bc they can have hypoglycemia but without the symptoms |
beta 1 blockers
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• If pt develops leg swelling or SOB they need to report bc they are signs of HF- ___ can throw you into acute exacerbations of HF
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beta 1 blockers
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• Metoprolol (Lopressor, Toprol)
• Atenolol (Tenormin) • Labetalol (Normodyne) |
selective beta blocker
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• Propanolol (Inderal)
• Carvedilol (Coreg)- blocks alpha 1, beta 1 and beta 2 |
non selective beta blocker
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blocks alpha 1, beta 1 and beta 2
• Pts w asthma, COPD, or pneumonia can get worse w this drug *** • Bronchospasm |
coreg
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• Adrenergic blocking agent that has a nonspecific beta-blocking action at both the beta-1 and beta-2 receptor sites, and a selective alpha-1 blocking action.
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o Alpha 1 and beta blockers
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labetalol (Normodyne, Trandate)
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o Alpha 1 and beta blockers
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• Use caution with Beta Blockers in heart block
• No B-2 or non selective blockers with asthma patients |
o Alpha 1 and beta blockers
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• Can induce CHF btu can also go into decompensated CHF bc the medicine
• Usually given with other diuretics (thiazide & Loop) |
o Labetalol- normodyne
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• Nsg Dx: decreased Cardiac Output; Injury
• Interventions: IV only in hospital setting, watch orthostatic hypotension- lie down, not for heart block Dx, can induce CHF, • Watch Dm carefully- it masks s/s hypoglycemia…may need to adjust insulin |
o Labetalol- normodyne
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clonidine (Catapres).
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o Centrally acting alpha 2 agonist
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• 2nd-line anti-hypertensive agent
• Don’t stop abruptly, rebound htn and angina Rebound angina bc the heart works harder and exerts itself more |
clonidine (Catapres).
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• Watch for: sedation, dry mouth, dizzy
• Transdermal patch changed q 7 days • Can develop a tolerance – stop for at least 8 hrs a day w patch- usually at night |
clonidine (Catapres).
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• First line treatment for compensated heart failure
• Used to be digoxin but NOT ANYMORE • This fixed contractility AND underlying problem which is RAAS--- need to stop RAAS to prevent remodeling |
o ACE inhibitors
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stops RAAS
Prevent conversion of angiotensin I to angiotensin II at level of lung |
o ACE inhibitors
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• Prevent breakdown of bradykinin
Can lead to a dry, nagging cough Can change to an ARB or other ace inhibitor |
o ACE inhibitors
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deals with Renin, which is synthesized by the kidneys, produces angiotensin I.
• Angiotensin I is a basically inactive substance until it is converted to the active angiotensin II • Angiotensin II is a potent vasoconstrictor. The ACE inhibitors prevent the conversion of angiotensin I to angiotensin II. |
o ACE inhibitors
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first-line antihypertensives if the patient has comorbidities.
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o ACE inhibitors
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lisinopril (Zestril)
enlapril (Vasotec) captopril (Capoten) end in "peril) |
ace inhibitors
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• Prototype drug: captopril (Capoten)
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o ACE inhibitors
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• Most are prodrugs
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o ACE inhibitors
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___ that are NOT PRODRUGS: captopril and lisinopril
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ace inhibitor
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how to treat Angioedema
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First line drug for this= EPI followed by histamine 1 blockers (benadyl) and glucocoritcosteroids (methylprednisolone)
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• Nephroprotective in pts w chronic renal problems
• Contraindicated during acute renal failure • Lead to hyperkalemia • Potassium >5 or 5.5 don’t put on ace inhibitor • Worry about hypotension—monitor HR and BP |
ace inhibitors
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• Lisinopril (Zestril)
• Enlapril (Vasotec) • Captopril (Capoten) |
o Angiotensin II receptors blockers (ARBs)
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block the action of angiotensin II from all the different pathways where it is formed.
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o Angiotensin II receptors blockers (ARBs)
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• Decrease the amount of adolsterone- hyperkalemia, hypotension
• Indicated for pts who cannot handle ace inhibitors- pts who develop angioedema for example • Many prevent remodeling but not as thoroughly studied |
o Angiotensin II receptors blockers (ARBs)
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first-line treatment for severe hypertension with electrocardiographic (ECG) evidence of left ventricular hypertrophy
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o Angiotensin II receptors blockers (ARBs)
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losartan (Cozaar)
valsartan (Diovan)* |
o Angiotensin II receptors blockers (ARBs)
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o Used alone or with other agents
• Usually a diuretic o Great for Type II DM (renal protection, NOT DURING ACUTE RENAL FAILURE |
o Angiotensin II receptors blockers (ARBs)
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o Monitor BUN & creatinine levels
o Monitor BP and renal function o SE: cough/tickling in throat, high K+ Not an ACE cough Don’t take K+ supplements Salt substitutes contain K+ o Patch may take days to take effect Check for skin reactions |
o Angiotensin II receptors blockers (ARBs)
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o Nsg Dx: Injury, Fluid Volume
• Hypotensive effects- slow when rising • Weigh daily • Watch for URI, diarrhea • Notify MD |
o Angiotensin II receptors blockers (ARBs)
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• The use of ACE inhibitors and ARBs alone does not protect organs from damage completely because the body uses renin-angiotensin-aldosterone system escape mechanisms.
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o Selective aldosterone blocker
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___, when added to either ACE inhibitor therapy or ARB therapy, provide added benefit
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o Selective aldosterone blocker
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• Lower BP by decreasing volume- retain potassium secrete sodium and HF
• Worry about hyperkalemia and hypotension |
o Selective aldosterone blocker
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• Nsg Dx: Injury- LYTES
• Monitor labs K+ (high) & Na (low) Renal function Not recommended for DM w/renal Dz • Avoid St John’s Wort & grapefruit juice • Flu-like s/s • Takes 4 weeks to see full results |
o Selective aldosterone blocker
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eplerenone (Inspra)*
*spironolactone (Aldactone) |
o Selective aldosterone blocker
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• Used for treatment of HTN, Pritzmental angina and cardiac arrhythmias
• Decrease development of angina bc they decrease the workload of the heart and decrease O2 demand so you allow more O2 to be carried to the cells |
calcium channel blockers
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• Divided in selective and non selective.
• Selective only work in the vessels, non selective have effect on vessels and heart muscle. |
calcium channel blockers
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• Norvasc (Amlodipine)
• Works mostly on the vessels – at level of the vessels—does not effect cardiac conduction |
selective calcium channel blockers
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• Diltiazem (Cardizem), Verapamil (Calan) older medication (used for atrial arrhythmias such as a fib, flutter). → most commonly prescribed
o Bradycardia, hypotension, arrhythmia o Verapamil gives you more constipation o Also used for atrial arrhythmias—a fib, atrial flutter o Oral and IV form |
non-selective calcium channel blockers
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• Not only block calcium at level of the vessels but also at the level of the myocardium decreasing the conduction system or the action potential
• Work also as antiarrhythmics • To remember about antiarrhythmics- can give you a worse arrhythmia (like a heart block) |
non-selective calcium channel blockers
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Prototype drug: nitroprusside (Nitropress)
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Drug used in HTN crisis
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• Directly relaxes vascular smooth muscle, allowing dilation of peripheral arteries and veins.
• Infusion rate for nitroprusside must be titrated to reduce blood pressure without compromising organ perfusion. |
nitroprusside (Nitropress)
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• Watch for Cyanide toxicity
• Main issues- hypotension and it produces a byproduct of cyanide→ cyanide toxicity→ this drug should not be given at maximum dose for more than 10 minutes bc risk for cyanide toxicity |
nitroprusside (Nitropress)
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o Inability of the ventricles to pump enough blood to meet the body’s metabolic demand (Adams, 2011).
o Can be classified as Right or Left or both, systolic or diastolic. |
heart failure
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____- presents with peripheral symptoms
___- presents w lung symptoms – SOB, cough, dyspnea |
r-sided HF
L-sided HF left=lung |
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o Symptoms will vary according to the side of the heart that is affected.
o Pt may present with SOB, chest pain, JVD, ascites, abd pain, nausea, vomiting, anorexia, cough, leg edema, hepatomegaly, splenomegaly |
HF
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Causes or catalysts
• CAD, • mitral stenosis • MI • HTN • Diabetes Mellitus Main drug used- ACE inhibitors |
HF
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o Research suggests that the clinical benefits of ACE inhibitors and beta blockers are related to modifying the changes that occur in the left ventricle with CHF.
o Additionally, the following agents should be given to selected patients: cardiac glycosides (digoxin), aldosterone antagonists, ARBs, and the combination |
CHF
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Vasodilator–antianginal (hydralazine–isosorbide)
diuretics nitrates Dobutamine (Dobutrex) IV drip Hydralazine- Digoxin Cardiac glycoside |
CHF medication
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use for for African descend patients.
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o Vasodilator–antianginal (hydralazine–isosorbide)
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used when patients have fluid overload
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o Diuretics such as loop and thiazide diuretics
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can decrease pulmonary congestion and edema
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o Nitrates such as Nitroglycerin
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IV drip can be used to increase inotropicity in the heart in acute episodes of CHF decompensation
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o Dobutamine (Dobutrex)
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decrease work on the heart
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o Hydralazine
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increases strength of contraction of the heart (pos inotrope) but reduces the HR (negative chronotrope
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digoxin
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• Reserved for pts w later stages of HF when you need to increase contractility
• Unlike ACE inhibitors it does not decrease mortality • Doesn’t prevent remodeling- makes it worse- increases likelihood heart will remodel • Keeps pt out of the hospital- pt feels symptom free |
Digoxin
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• Main prob- narrow therapeutic level- 0.8-2.0
• Digoxin has a narrow therapeutic index. • It is important to monitor the serum levels of digoxin. |
digoxin
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• Education should include importance of:
• Med adherence • BP & HR monitoring • Serum levels • S/S toxicity |
digoxin
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____ toxicity- plethora of symptoms
• Early- anorexia, nausea, vomiting and abdominal pain • Later- tachyarrhythmias, bradyarrhythmias, or halos around the lights (visual disturbances) • Main reversal agent- digibind • Hypokalemia increases rate • Monitor HR before giving—held if HR <60bpm • Class five antiarrhythmic • Can worsen arrhythmia |
digoxin
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• The cardiac glycosides also are known as digitalis preparations or digitalis glycosides.
• Digoxin is used to maintain clinical stability and improve symptoms, quality of life, and exercise tolerance in patients with all phases of CHF. |
o Cardiac glycoside
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• Current AHA/ACC guidelines recommend that digoxin can be added if patients also have atrial fibrillation.
• Digoxin is not used as the primary treatment • Digoxin increases the force of cardiac contraction, increasing cardiac output. |
o Cardiac glycoside
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h
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h
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