Pharm Final 2
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- Factors stimulating release of renin
- Decreased blood pressure or sodium level, B-adrenergic agonists, hypokalemia
- Physiological effects of renin
- Increased BP, positive chronotropic and inotropic, vasoconstriction, incr. release of NE, aldosterone, and stimulation of CNS for thirst
- Indications for ACE inhibitors
- Tx of mild to moder. htn, vasodilation to treat moderate to severe CHF
- Contraindications and s/e of ACE inhibitors
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C/I in renal pts.
S/E: hyperkalemia, hypersensitivity, first-dose effect (rapid BP fall) - Nursing implications w/ ACE inhibitors
- Monitor BP before and after dose, K levels, incr. HR, change positions slowly, teach orthostatic hypotn, clear throat feeling r/t incr. secretions in throat, best to take on empty stomach, take at same time (AM) qd
- ACE inhibitor prototype
- captopril (Capoten)
- Why give ACE inhibitors w/ diuretics?
- Better control of htn and K levels
- Angiotensin II Receptor Antagonists
- (ARBs)anti-htn, prevents vasoconstriction and fluidretention, does NOT cause chronic cough that ACE inhibitors cause
- ARB prototype
- losartan (Cozaar)
- Extra kidney functions
- Produce erythropoietin, renin, prostaglandins, involved in synthesis of Vit. D (absorbs Ca)
- Thiazides
- incr. Na and H2O excretion at early distal tubules, give with meals to prevent GI irritation.
- Prototype for Thiazides
- hydrochlorothiazide (hydrodiuril)
- S/E of thiazides
- hyponatremia, hypovolemia, hypokalemia, HYPERglycemia (dilutional), photosensitivity
- Loop diuretics mechanism of action
- Inhibit reabsorption of Na and Cl in proximal and distal tubules but mainly in LOOP, can be given IV
- Loop diuretic prototype
- furosemide (Lasix)
- Side effects of loop diuretics
- Same as all diuretics, OTOTOXICITY
- Potassium sparing diuretics and prototype
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Can be given concurrently w/ other diuretics to counteract K loss
Prototype: triamterene (Dyrenium) - Action of K-sparing diuretics
- Inhibit Na ion pumps in distal tubule for Na reabsorption
- S/E of K-sparing diuretics
- Hyperkalemia
- Osmotic diuretics
- low molecular weight substances that increase plasma osmolarity, glomerular filtration, and tubular fluid retention by remaining in high concentrations in renal tubules. (work in proximal tubule) Inhibits reabsorption
- Indications of osmotic diuretics
- tx glaucoma, ARF, reduction of increased introaocular pressure (before or after surgery), cerebral swelling w/ trauma
- Osmotic diuretic prototype
- mannitol (Osmitrol)
- Carbonic anhydrase inhibitors action
- inhibits carbonic anhydrase->inhibits bicarb reabsorption which alkalizes urine and acidifies blood
- Indications for carbonic anhydrase inhibitors
- adjunct tx for glaucoma, hydrocephalus, petit mal seizures, tx OD of acidic based drugs like ASA or phenobarbital
- S/E and nursing interventions for carbonic anhydrase inhibitors
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s/e: hyponatremia, hypokalemia, hypovolemia, METABOLIC ACIDOSIS
Interventions: I&O, daily weights, labs, BP, dizziness, syncope, same time qd (in am) - Prototype for carbonic anhydrase inhibitors
- acetazolamide (Diamox)
- Causes of essential htn
- Heredity, high sodium diet, smoking, type a personality, stress, hx of atherosclerosis
- Causes of secondary htn
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Pheochromocytoma (tumor of adrenal medulla)
Coarctation of aorta - Cold medications increase BP because...
- increasing vasoconstriction to open nasal airway
- Prototype for B-blockers
- Inderal
- Action of Inderal
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1. Decrease peripheral resistance
2. Decreases renin activity
3. Resets sensitivity of baroreceptors - C/I for B-Blockers
- Cardiac failure, bradycardia, AV conduct. distrubance, Asthma, COPD, diabetics (exacerbates hypoglycemia)
- Centrally acting alpha adrenergic agonists mechanisms of action
- Work in CNS to lower BP (decr. SNS outflow from brain to CV system). Inhibits cardioacceleration and vasoconstriction centers
- Prototype for Centrally acting alpha adrenergic agonist
- Catapres (clonidine)
- Nursing measures for clonidine
- Bradycardia, fatigue, depression. Take at night
- Peripherally acting selective A-adrenergic blockers mechanism of action
- Selectively block a-adrenergic receptors (postsynaptic) in peripheral vasculature->vasodilation
- S/E of peripherally acting selective A-adrenergic blockers
- Reflex action causes + chronotropic and inotropic, inc. renin activity (give w/ B-blocker)
- Direct acting vasodilators mechanism of action
- Directly dilate the arterioles w/out affecting the SNS or adrenergic receptors on smooth muscle cells. Can trigger reflex tachycardia and incr. renin. May require B-blockers
- Examples of direct acting vasodilators
- hydralazine (Apresoline) and nitroprusside (Nipride)
- Nursing interventions w/ hydralazine
- Arteriole dilatore, used more for long-term htn mgt. IV or PO, watch for LUPUS and NEURITIS
- Nursing interventions w/ Nipride
- Arteriole AND veinous dilator, used in ER for sever htn (200/100). Only IV, potent dilator, short durations, thiocyanide is byproduct, given as a continuous drip (not push). Light sensitive
- Class of drugs that abolishes unidirectional blocks
- Group 1B
- Class of drugs that produces bidirectional block
- Group 1A, 2, and 4
- Class 1A Mechanism of action and example
- quinidine (Quinaglute). Given for afib and atrial flutter (superventricular arrhythmias). Slows rate of depolarization, prolongs refractory period
- Interventions w/ quinidine
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v.s., listen to heart sounds, PO w/o food, IV over 30-60 min.
S/E tinnitus, dizziness, visual disturbances, double vision, diarrhea, n/v - Class 1B Mechanism of Action and example
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Example: lidocaine (Xylocaine)
Abolishes unidirectional block (gets impulse through the jello), used for ventricular arrhythmias, - Nursing interventions for class 1B drugs
- Give initial IV bolus, then continuous drip on pump, monitor for extravasation, depresses CNS->drowsiness, confusion, hypotn R/T vasodilation
- Class 2 Drugs Mechanism of action and example
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propranolol (Inderal)
*B-adrenergic blockers. inhibits sympathetic stim. of heart. Tx supraventricular arrhythmias - Class 3 Mechanism of action and example
- amiodarone (Cardarone) Blocks K channels->prolonged refractory, vert. arrythmias, use if pt. can't cardiovert, can be proarrhythmic
- Class 4 mechanism of Action and example
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verapamil (Calan)
Ca channel blocker, prolongs refractory period->depresses myocardium, vasodilation.
Tx: supraventricular arrhythmnias, htn - Nursing interventions for Class 4 drugs
- S/E include constipation, hypotn, syncope, and ortho. hypotn.
- K removing resins mechanism of action and example
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poystyrene sulfonate (Kayexalate)
Bind w/ K (which causes arrhythmias), given orally or as enema. Used when hyperkalemia causing arrhythmias.
S/E: SEVERE DIARRHEA - Organic nitrates mechanism of action
- Directly relax vascular smooth muscle, affect both arterial and venous tone->decr. preload->decr. BP->reflex tachycardia. Used to treat angina and CHF
- Cardiac glycosides action and example
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Digoxin
Act through the inhibition of ATPase->accumulation of Na w/in cell->release of lg. quantities of Ca->more irritable->contracts more freq. Incr. SA node sensitivity, negative chronotropic, slows impulse inside heart, sits at AV node longer (little more time for ventricles to fill) - Indications for digoxin
- CHF, supraventricular arrhythmias
- S/S of digitoxicity
- Blurred vision, white halos, chromatopsia (white looks green or yellow), flickering lights, anorexia, n/v, diarrhea, atrial arrhythmias, SA block, bradycardia
- Antidote for digoxin
- Digoxin Immune Fab (Digibind)
- Heparin action at low and high doses
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Low: prophylaxis, inhibits Factor X, which begins common pathway
High: inactivates thrombin, prevents conversion of fibrinogen to fibrin, pt. already had TIA, CVA, prevent clot from getting worse - Routes of Hep admin.
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IV: immediate action
SC: gradual, longer-acting
NOT IM: erratic absorption and excessive bleedig - Clinical indicator of hep therapy
- APTT (activated partial thromboplastin time). Goal is APTT 1.5-2.0 times normal clotting time (30-40 sec)
- Oral anticoagulants mechanism of action and prototype
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warfarin (Coumadin)
Acts in the LIVER to inhibit the synthesis of active Vit. K clotting factors. - Clinical indicators for coumadin efficacy
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PT 18-30 sec.
INR 2.0-3.0 - Nursing implications w/ Coumadin
- Take same time qd, routine bloodtests, don't change amt. of greens consumed, wait til coumadin therapeutic to take off hep, watch for bleeding, soft bristle tooth brush, electric razor
- Drugs that antagonize coumadin
- Barbituates and dilantin
- Clinical indications for thrombolytic drugs and example
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Ex: streptokinase (Streptase)
Dissolve clots, use w/ CVA if symptoms started w/in last 6hrs. - Nursing interventions w/ streptokinase
- Given IV, use immediately after reconstituting, pump, don't stick more than once, put sandbags over puncture wound, v.s., bleeding, H and H, clotting time
- Antidote to streptokinase
- aminocarproic acid (Amicar) given IV or PO
- Platelet inhibitors mechanism of action and Ex.
- Inhibit plt. aggregation. Ex: ticlopidine (Ticlid) NO ANTIDOTE. Take w/ food
- Hemorrheologic agent mechanism of action and example
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pentoxifylline (Trental)
Improves microcirculation by incr. flexibility of RBCs - Mechanism of action for bile acid sequestrants and example
- cholestyramine (Questran) Inhibits reabsorption of bile-> incr. excretion-> incr. use of cholesterol to make bile->decr. cholesterol. May need to take a laxative and incr. fluids, may decr. fat soluble vitamins
- S/E of nicotinic acid and example
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Niacin (Nicobid, Vit. B3)
S/E: flushing, take ASA 30 minutes before to prevent flushing - Reductase inhibitors mechanism of action and example
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Ex: lovastatin (Mevacor, Zocor, Crestor)
Inhibit enzyme that makes cholesterol. Monitor liver, take w/ meals to decr. GI symptoms, ha - Gompertzian Kinetics
- abnormal growth rate in which cells lack the normal regulating factors->continue to multiply pass the critical mass state
- Clinical manifestations of bone marrow depression in chemo pt. and drugs given to manage
- Neutropenia (give interferon), thrombocytopenia, and anemia (give Epogen or Procrit)
- Toxicities other than bone in chemo tx
- Stomatitis, n/v, diarrhea, alopecia, reproductive toxicity, hyperuricemia (incr. uric acid prod.)
- Subcategories of antimetabolites
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*Folic Acid antagonists
*Purine antagonists
*Pyrimidine antagonists - Pyrimidine antagonists mechanism of action and S/E
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Fluorouracil (5-FU), inhibits pyrimidine synthesis.
S/E: neurotoxicity (monitor for q in LOC), hyperpigmentation, no significant drug interactions - Subcategories of mitotic inhibitors
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Vinca alkaloids
Podophyllotoxins
Taxenes - Vinca alkaloids prototype and mechanism of action
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Vincristine (Oncovin)
Interferes w/ microtubule assembly. - Vinca alkaloids s/e and interactions
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S/e: neurotoxicity, vesicant
Interactions: Phanytoin, digoxin, Ca channel blockers - Podophyllotoxins prototype and mechanism of action
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Etoposide (Vepesid)
Inhibits DNA synthesis so cell doesn't enter mitosis, - S/E and interactions w/ podophyllotoxins
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S/E: bone marrow suppression, alopecia, mild peripheral neuropathy, and sever hypersensitivity, teratogenic and mutagenic risks. GIVE B6.
No significant interactions - Prototype and mechanism of action for Taxanes
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Paclitaxel (Taxol)
Promotes abnormal formation of spindle fibers during interphase - S/E and interactions w/ taxanes
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S/E: bone marrow depression, peripheral neuropathy, cardiotoxicity, severe hypersensitivity, vesicant
Interacts w/ Verapamil, Quinidine, and Ketoconazole - Subcategories of alkylating agents
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Nitrogen mustards
Nitrosureas
Alkylator-like agents - Nitrogen mustard prototype and mechanism of action
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Cyclophophamide (Cytoxan)
Screws up protein matching in double helix (cross-linking) blocks replication - S/E of nitrogen mustards
- Bone marrow depression, hemorrhagic cystitis (blood in urine), alopecia, hepatotoxicity, teratogenic and mutagenic risks. Keep pt. HYDRATED
- Prototype and mechanism of action for nitrosureas
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carmustine (BCNU)
Causes cross-linking, realily crosses BBB - S/E and interactions w/ Nitrosureas
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bone marrow depression, frequent n/v, pulmonary toxicity, hypersensitivity, hyperpigmentation, teratogenic
Interactions: cimetidine, digoxin, and phenytoin - Antitumor antibiotics mechanism for action and prototype and S/E
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Doxorubicin (Adriamycin)
Inhibits DNA and RNA synthesis
S/E: irreversible cardiomyopathy, truns urine pink/red, bone marrow depression, alopecia, hyperuricemia, GI disturbances - Use of corticosteroids in CA pts.
- Used in conjunction w/ xrt, decreases sxs, gradually taper doses, s/e include F/E imbalances,exacerbation of DM, osteoporosis, peptic ulcers, increased infections
- Antiestrogen prototype and mechanism of action
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Tamoxifen (Nolvadex)
Blocks estradiol uptake and is effective w/ tumors that contain high conc. of estrogen receptors. Breast CA prevention - Interferons prototype and S/E
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Interferon alfa-2a
Assist lymphocytes but don't know how.
S/E: flu-like sx, anorexia, diarrhea, dizziness, bone marrow depression, alopecia, cardiotoxicity, neurotoxicity, hyperuricemia - Antigout drugs
- Allopurinol, Colchicine, and Probenecid
- Gout
- Results from inappropriate uric acid metabolism from overproduction or underexcretion of uric acid.