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pharm final

What is hemostasis Bleeding stops.
What are the 2 stages of hemsotasis? 1. formation of platelet plug 2. coagulation
What is the extrinsic fibrin pathway? Extrinsic pathway: (AKA: tissue factor pathway). This is activated when there is trauma to the vascular wall. Causes release of thromboplastin.
What is the intrinsic fibrin pathway? Intrinsic pathway: contact activation pathway. activated when blood makes contact with collagen as a result of trauma to blood vessel. Through a series of actions, this pathway eventually becomes the same as the extrinsic pathway. two pathways converge.
What is thrombophlebitis? inflammation of vein, associated with blood clot, typically seen in lower extremities. Can be seen in any vein accessed by an IV
What are the parts of Virchow’s triad? Venous stasis, endothelial damage, hypercoagulability
What are some causes of hypercoagulability? Estrogen therapy, high doses of vitamin E, dehydration, increased platelets, neoplasms (ovarian and visceral)
What are the 4 coagulation modifying agents? Anticoagulants, antiplatelets, thrombolytics, antifibrinolytics.
What is the lab value PT? Prothrombin time. Time to form fibrin clot (10-13.4 sec); therapeutic range
What is the lab value INR? (Internationalized Normalized Ratio): basically the same thing as PT only “standardized” (2-3 times the normal value). Use to monitor warfarin (Coumadin).
What is the lab value APTT or aPTT? (activated partial thromboplastin time): test includes an activator of the clotting process. Often done in combination with PT. Normal aPTT is 40 sec. Range with heparin
Which factors are involved in coagulation? Factors II, VII, IX, X
Coagulation factors need ____ to be synthesized Vitamin K
What is the MOA of anticoagulants? MOA: work on clotting pathways in varying methods (e.g., warfarin works on particular clotting factors II, VII, IX, X)
What are the prototypes of anticoagulants? Heparin (unfractionated), heparin (low molecular weight), warfarin (Coumadin)
What lab values should you monitor for heparin? aPTT
What is the aPTT range for heparin? 60-80 seconds
What is normal aPTT time? 40 seconds
What lab values should you monitor for warfarin (Counmadin)? INR, PT
How does heparin work as an anticoagulant? Binds to antithrombin III, inactivates clotting factors
How does enoxaprin (Lovenox) work as an anticoagulant: which clotting factor? More specific for factor X.
How does unfractionated heparin work as an anticoagulant? inactivates several clotting factors, particularly factor II (thrombin) & factor X
What are some AE for unfractionated heparin? bleeding; thrombocytopenia (reduced platelet count); hypersensitivity
What are some contraindications for unfractionated heparin? NSAIDs, aspirin
What is the heparin antagonist? Protamine sulfate
What is low molecular weight heparin? heparin preparations made of smaller molecules. Easier to use as they can be given on a fixed dose without lab monitoring (note: aPTT will still be done as needed to monitor the overall coagulation)
What is the MOA of LMW heparin? similar to heparin; more specific to factor X; more predictable response
What are some AE of LMW heparin? bleeding (note: much less than unfractionated heparin); neurologic injury when using in spinal anesthesia/puncture (Note: particularly serious when given with other anticoagulants)
How does warfarin (Coumadin) work as an anticoagulant? Affects the vitamin K dependent clotting factors (II, VII, IX, X). Reduces the activation of vitamin K, and is not an antagonist to vitamin K actions
Does warfarin (Coumadin) ‘thin’ the blood? No. should not be referred to as a blood thinner – it does not change either the viscosity nor the thickness of the blood
What are indications for warfarin (Coumadin)? prevention of long term thrombosis; atrial fibrillation; mechanical heart valves; reduce TIA development; reduce risk of MI
What are indications for LMW heparin (enoxaprin, lovenox)? recovering post-operative clients; immobile or “bedridden” clients; DVT; unstable angina; Note: they are safe for outpatient clients
What are indications for unfractionated heparin? pulmonary embolism (PE), DVT, recovering open heart surgeries, renal dialysis, DIC, addition to thrombolytic agents in treatment for MI
What are some AE for warfarin (Coumadin)? bleeding (hematuria, melena, petechiae, ecchymosis); N/V; Abdominal cramping; ulcerations; osteoporosis; anaphylaxis
What are ways to manage AE of warfarin? Stop medication, administer vitamin K
What are contraindications for warfarin (Coumadin)? hypersensitivity; pregnancy/lactation; hemorrhagic disorders; thrombocytopenia; serious inflammation; vitamin K deficiency; liver disease; alcoholism; prior to surgery (particularly eye, spinal cord, brain)
What are the 3 groups of antiplatelets? aspirin, ADP or adenosine diphosphate receptor antagonists, glycoprotein IIb/IIIa receptor antagonists
What do antiplatelets do? Primary action: work in the initial phase of the clotting process (platelet formation) as contrasted with other anticoagulants which work throughout the clotting process
What is the MOA of antiplatelets? prevents platelet adhesion which prevents activation of several substances that attract more platelets to site of injury
What are indications for ADP receptor antagonists? CVA, ACS
What is the prototype of ADP receptor antagonists? Clopidogrel (Plavix)
What are indications of clopidogrel (Plavix)? used to reduce MI, ischemic stroke, ACS, prevent blockage of coronary stents
What is the MOA of ADP receptor antagonists? alters platelet membrane and can’t receive a signal to form a clot
What are AE of ADP receptor antagonists? chest pain; HTN, flu-like Sx; abdominal pain; Nausea; rash/pruritis
What is the MOA of glycoprotein IIb/IIIa receptor antagonists? Inhibits final stage of platelet aggregation; prevents clotting by all factors
What are indications for glycoprotein IIb/IIIa receptor antagonists? ACS (unstable angina, MI); post angioplasty (PCI
What are AE of glycoprotein IIb/IIIa receptor antagonists? severe bleeding; usually does not lend itself to causing hemorrhagic stroke; research shows very questionable to give longer term
What is the MOA of thrombolytic agents? converts plasminogen to plasmin and breaks down the thrombus & “digests” the fibrin
What are indications of thrombolytic agents? acute MI; DVT; PE; CNS clots
What are AE of thrombolytic agents? bleeding; antibody production; hypotension
What is nursing care for thrombolytic agents? assess for bleeding tendencies; review serum anticoagulant lab findings (e.g., PT, aPTT, Hct, platelet count)
What is the prototype for thrombolytics? Tissue plasminogen activator (tPA)
What do antifibrinolytic agents do? prevent the lysis of fibrin, promotes clot formation. Prevents lysis of fibrin, which MAINTAINS clot formation
What is the prototype of antifibrinolytics? Desmopressin (DDAVP), aminocaproic acid (Amicar)
What is Desmopressin (DDAVP)? Antifibrinolytic. an analog of ADH, increases platelet aggregation
What are SE/AE of desmopressin? fluid retention; hyponatremia
What is angina pectoris? Principle symptom of ischemic heart disease. Characterized by sudden, severe substernal pain or pressure
What is the primary cause of angina? imbalance between myocardial oxygen demand and oxygen supplied by coronary vessels. This imbalance may be due to: a decrease in myocardial oxygen delivery or an increase in myocardial oxygen demand
What are major determinants of myocardial oxygen consumption? Ventricular wall stress: preload (end-diastolic pressure) and afterload (end-systolic pressure). Heart rate. Inotropic state (contractility). Myocardial metabolism (glucose vs fatty acids)
What causes stable/exertional angina? atherosclerosis (reduced oxygen delivery). exercise, cold, stress, emotion, or eating
What classes of antianginal medications are used to treat chronic stable/exertional angina? Organic nitrates, beta blockers, calcium channel blockers
What is variant/Prinzmetal’s/vasospastic angina? Angina that is caused by coronary artery spasms. These spasms decrease myocardial blood flow
Compare variant angina to stable angina Stable anginal episodes are brought on with exercise, etc. Variant angina can happen at night, at rest, or any time. The two types of angina can occur together with one another
What is the management goal for variant angina? Goal is to increase oxygen supply, whereas, stable angina goal is to reduce oxygen demand.
What classes of antianginal medications are used to treat variant angina (vasospastic or Prinzmetal's)? Variant angina can be treated with calcium channel blockers and organic nitrates.
What is unstable angina? change in the character, frequency, and duration of angina in patients with stable angina, and episodes of angina at rest.
What are management goals for unstable angina? To increase oxygen supply, and decrease oxygen demand
What classes of antianginal medications are used to treat unstable angina? Nitroglycerin, beta blocker, O2, morphine sulfate, ACE-I, aspirin, clopidogrel (Plavix) ADP receptor antagonist, or specific glycoprotein IIb/IIIa inhibitors. Antiplatelets.
Emergent meds: ranolazine (Ranexa).
What are the 4 classes of antianginal medications? Organic nitrates, calcium channel blockers, beta-adrenergic blockers, pFox Inhibitors
What do nitrovasodilators do? peripheral vasodilation, increase coronary blood flow, inhibition of platelet function
What are AE of nitrovasodilators? due to excessive vasodilation: Orthostatic hypotension; Tachycardia; Severe throbbing headache; Dizziness; Flushing; Syncope
Contraindications of organic nitrates/nitrovasodilators? Elevated intracranial pressure, erectile dysfunction meds alcohol
What is the drug of choice for acute angina? nitroglycerin
What is the MOA of nitroglycerin? decreases pain by decreasing cardiac oxygen demand by: dilating veins, which decreases venous return to the heart (note: it does not dilate coronary arteries)
What are the prototypes of nitroglycerin? short acting (nitroglycerin) and long acting isosorbide (Isordil)
What is tolerance, and which drug is it associated with? A resistance to the effects of a substance after repeated exposure: common problem with nitrates
How is sublingual nitroglycerin absorbed? directly through oral mucosa; lower doses are effective because it bypasses the liver (note: these are not effective if swallowed)
How are nitroglycerin tabs taken during ‘acute’ anginal attack? take one tab and if pain isn’t relieved in 5 minutes call 911; then take a second and a third tab in 5 minute intervals
What is reflex tachycardia? Associated with nitrates, when too quick of vasodilation and the heart responds with an increased HR.
How do calcium channel blockers work as antianginals? Improve oxygen delivery to ischemic myocardium: vasodilate coronary arteries. May inhibit platelet aggregation. Reduce myocardial oxygen consumption. Decrease afterload (no effect on preload)
What are some drug interactions of calcium channel blockers? Beta-blockers, digoxin, quiidine
What are prototypes of calcium channel blockers? Diltiazem (Cardiazem), verapamil
How do beta blockers work as antianginals? Ability to slow HR (negative chronotropic effects) and reduce contractility (negative inotropic effects)
Beta-blockers are NOT used to treat which type of angina? Variant angina. Used mainly for stable angina
What are AE of beta blockers? May cause bradycardia. May exacerbate heart failure
What are contraindications of beta blockers? bronchial asthma; vasospastic angina. Should be used with caution in patients with diabetes. May depress contractility and heart rate and produce AV block in patients receiving calcium channel blockers
What are pFox inhibitors? First new class of antianginals in more than 25 years. Does not decrease HR, BP or vascular resistance. Used as a “backup” when the other medications have not worked
What is the MOA of pFox inhibitors? Unclear, Acts by partially inhibiting fatty acid oxidation in the myocardium, thus shifting metabolism to glucose which requires less oxygen to metabolize. Used for chronic angina
What are AE of pFox inhibitors? prolonged QT interval and potentially increase ventricular dysrhythmias; may raise BP (particularly in patients with renal history); constipation, nausea, H/A
What are drug interactions of pFox inhibitors? quinidine, CCBs (note: grapefruit juice also contraindicated with pFox inhibitors), hepatic dysfunction
What is the prototype for pFox inhibitors? ranolazine (Ranexa)
Ranexa and pFox inhibitors are less effective in _____ women
What is STEMI? S-T elevated myocradial infarction. Heart muscle is damaged by lack of blood flow in coronary arteries from platelet plugs and thrombus formation (from atherosclerotic plaque)
What is an MI? necrosis of the heart muscle resulting from local ischemia
Compare the etiology of MI vs STEMI MI: blockage of coronary arteries (partial or complete); STEMI: complete blockage of coronary arteries
What medications are used to treat STEMI? oxygen, ASA, Morphine, Beta blockers, Nitroglycerin. Note: NSAIDS NOT used due to risks
What is reperfusion therapy? restoration of blood flow through the blocked coronary arteries in the STEMI. 1.Percutaneous Coronary Intervention 2.Fibrinolytic therapy (e.g., tPA, Streptokinase)
What are medications used with reperfusion therapy? PCI, fibrinolytics, Heparin, Antiplatelet agents, ACE Inhibitors, ARBs
What is an ionotropic effect? Affects strength of heart: contractility
What is a chronotropic effect? Affects heart rate
What is a dromotropic effect? Affects speed of conduction of heart
What is heart failure? progressive disorder of the heart known by reduced cardiac output, ventricular dysfunction, decreased tissue perfusion, and signs of fluid retention.
What are some signs of heart failure? heart is unable to meet the metabolic demands of the body. May be asymptomatic at first, then begins to progress with deoxygenation (shortness of breath, decreased tissue perfusion), peripheral edema, and pulmonary edema
What are some compensatory mechanisms of heart failure? increased: dilation of the heart size, heart rate, contractility, venous/arterial tone. fluid retention
What are the mechanisms of fluid retention in HF? 1.RAAS is stimulated 2.renal system does not receive as much blood, decreases GFR. This decreases UO & fluid is retained
What are the stages of HF? Stage A: high risk for HF, without structural disease Stage B: Structural hd, but w/o symptoms Stage C: Structural hd, w prior/current HF symptoms Stage D: advanced structural hd w marked Sx at rest & req specialized interventions
What are medications used in HF? Diuretics, ACE inhibitors, ARBs, Aldosterone antagonists, Direct renin inhibitors, Beta adrenergic blockers, Sympathomimetics, Phosphodiesterase inhibitors, Vasodilators, Cardiac glycosides
Describe direct renin inhibitors treatment of HF useful in treatment of hypertension, but not successful in management of HF
What is the prototype of thiazide diuretics? hydrochlorothiazide (Hydrodiuril)
What is the prototype of high-celing (loop) diuretics? furosemide (Lasix)
What is the prototype of potassium-sparing diuretics? spironolactone (Aldactone)
What medications are used as a first line in volume overload? Diuretics
What is the MOA of Ace Inhibitors? block production of angiotensin II, and decrease release of aldosterone. Improve hemodynamics and decrease cardiac remodeling
What are AE of ACE-I? Hypotension, hyperkalemia, cough, angioedema. Note: can cause fetal alterations, particularly in 2nd & 3rd trimester
What causes the dry cough of ACE-I? Increase in levels of bradykinins
What are prototypes of ACE-I? captopril (Capoten) and enalapril (Vasotec)
What is the MOA of angiotensin receptor blockers? Very similar to ACE Inhibitors (improve ejection fraction, reduce Sx, increase exercise intolerance, etc.)
What is the critical difference between ACE-I and ARBs? ARBs do not increase kinins, which means they do not decrease cardiac remodeling as effectively as ACE inhibitors. ARBs do not produce cough
Aldosterone antagonists are also called _____ Potassium-sparing diuretics
What is the MOA of aldosterone antagonists? block aldosterone receptors in heart and blood vessels. 
What effects does aldosterone have on the heart?
What are AE of aldosterone antagonists? causes renal retention of potassium and causes hyperkalemia
What is the prototype of aldosterone antagonists? spironolactone (Aldactone)
Aldactone is an antiandrogen. What does this mean? Causes reduction in testosterone which causes men to have: impotence, erectile dysfunction, gynecomastia, weakness. For women: reduces facial hair (hirsutism), and acne. Usually not used for prolonged period of time to treat HF.
Do direct renin inhibitors manage HF? No. Is useful in treating hypertension
What is the MOA of direct renin inhibitors? Suppress RAAS; similar “strength” as ACE Inhibitors, ARBs, and CCBs
What are SE of direct renin inhibitors? diarrhea; causes less problems with hyperkalemia, or cough
What is the prototype for direct renin inhibitors? aliskiren (Tekturna)
What is the MOA of beta-adrenergic blockers? improves ejection fraction; slows HF progression, increases ability to exercise, and prolongs survival of HF
What should you monitor for with beta adrenergic blockers? fluid retention, fatigue, hypotension, and bradycardia
What are prototypes of beta adrenergic blockers? metoprolol, propranolol
What are sympathomimetics? Medications that mimic the effects of transmitter substances of the SNS
What are prototypes of sympathomimetics? Dopamine, dobutamine
What is dopamine? Sympathomimetic. Catecholamine that increases myocontractility, increases HR, increases renal blood flow. Given for acute & severe HF
What is dobutamine? synthetic catecholamine and same actions as Dopamine, except it does not increase vascular resistance. Given for short term management of acute HF
What are phosphodiesterase inhibitors? A group of inotropic agents that inhibit an enzyyme, phosphodiesterase. Labeled an inodilator because blocking this enzyme causes: 1.positive inotropic effects, and 2. vasodilation.
Phosphodiesterase inhibitors are used for whom? Due to toxicity issues: usually reserve their use for patients who have not responded well to ACE Inhibitors or other cardiac meds
What are contraindications for phosphodiesterase inhibitors? Drug allergy; severe aortic/ pulmonary valve disorders
Overdose of phosphodiesterase inhibitors cause ____. Is there an antagonist? Hypotension. No antagonist.
What are prototypes of the heart failure class of phosphodiesterase inhibitors? Inamrinone; Milrinone
What are 4 types of vasodilators? Isosorbide dinitrate (ISDN, Dilatrate) used with hydralazine, nitroglycerine, sodium nitroprusside (Nitropress), nesiritide (Natrecor)
Isosorbide dinitrate (ISDN, Dilatrate) is given in combination with _____ to cause _____ Hydralazine. Dilation of veins. First group of meds approved for use with ethnic group (african americans)
What does nesiritide (Natrecor) do? Vasodilator. Causes vasodilation of arteries and veins. Relatively new vasodilator.
What are cardiac glycosides? Second line of drug used to treat HF.
What is the prototype of cardiac glycosides? Digoxin (Lanoxin, Lanoxicaps)
What is the MOA of cardiac glycosides? Increases myocardial contractility by inhibiting sodium pump which increases calcium concentration. Decreases electrical conduction, affects area bw the atria &ventricle, causing cells to remain longer in depolarization, decreases the rate of response
Cardiac glycosides cause a positive ____ response, and negative _____ response, which cause what? Positive inotropic effect which increases force/velocity of contractions; increases stroke volume; reduces heart size; decreases venous BP; increases coronary circulation; reduces heart rate with negative chronotropic effects
What are contraindications for cardiac glycosides? drug allergy; heart block conditions; females with increased caution; V.Tach
What are signs of digoxin toxicity? bradycardia; h/a; malaise; fatigue; confusion; convulsions; GI (anorexia, nausea, diarrhea); colored vision/flickering lights
What drug is used as a digoxin antagonist? Digibind
What is depolarization? the process or act of neutralizing polarity. less negative.
What is repolarization? return to resting potential
What is automaticity? the ability of a cell to depolarize itself and then initiate an action potential
What is sinus rhythm? referring to normal cardiac electrical pathway
What are the 2 pacing mechanisms of the heart? SA & AV nodal rhythms
What is ectopic foci? an area in the heart that initiates abnormal beats
What is ejection fraction? proportion of blood that is ejected during ventricular contraction (normal is 60%)
What is the refractory period? period of time when impulse is unresponsive (e.g., SA node)
What is preload? amount of blood in ventricle before it contracts; pressure at the end of diastole
What is afterload? the load, or resistance, against which the left ventricle must eject its volume of blood during contraction
What diseases cause dysrhythmias? Hypertension; Valve disease; CAD; Medications; MI; CVA; Diabetes Mellitus; HF
What symptoms are associated with dysrhythmias? dizziness, weakness, decreased exercise tolerance, dyspnea, syncope, paleness
Which drugs are Vaughn Williams class I? Sodium channel blockers
Which drugs are Vaughn Williams class II? Beta adrenergic blockers
Which drugs are Vaughn Williams class III? Potassium channel blockers
Which drugs are Vaughn Williams class IV? Calcium channel blockers
The Vaughn Williams classifications are derived from...? The four classes are derived from the stage in which they affect the action potential
What is the MOA of calcium channel blockers? They block sodium channels and prevent depolarization; also suppress ectopic pacemaker activity which decreases dysrhythmias
What are the 3 classes of sodium channel blockers? Class I A procainamide (Procanbid); quinidine. Class I B lidocaine (Xylocaine); phenytoin (Dilantin). Class I C flecainide (Tambocor)
What is the MOA of beta adrenergic blockers? blocks cardiac beta 1 (and 2) receptors; slows heart rate and conduction velocity; suppresses dysrhythmias
What is the prototype of beta adrenergic antidysrhythmics? propranolol (Inderol)
What are indications of beta adrenergic antidysrhythmics? Dysrhythmias caused by sympathetic stimulation (blocks it)
What are contraindications for beta blocker antidysrhythmics? heart block; bradycardia; asthma d/t bronchoconstriction
What is the MOA of potassium channel blockers? block potassium (this lengthens repolarization) within the myocardial cells. Note: when cells are in the repolarization state, they depend upon removal of potassium from the cell
Which class of antidysrhythmics are used for hard to treat dysrhythmias? potassium channel blockers
What are the prototypes of potassium channel blocker antidysrhythmics? amiodorone (Cordarone)
What does amiodorone (Cordarone) do? Prolongs refractory time
Which antidysrhythmic can cause hypo or hyper thyroidism? Potassium channel blockers. amiodorone (Cordarone)
What is the most severe AE that potassium blockers can cause? Pulmonary toxicity with dyspnea and cough
What do calcium channel blockers do in regards to dysrhythmia? Provide cardiac conduction. slow flow of calcium into the channels. This limits the activity to atria and AV node, where conduction is prolonged and therefore controls the ventricular response to atrial fibrillation
What is the general MOA of calcium channel blockers? strong vasodilator to smooth muscle; decrease oxygen demand; reduce cardiac workload; increase oxygen to the myocardium
What are the 2 prototypes of calcium channel blocker antidysrhythmics? Diltiazem (Cardizem) and verapamil (Calin)
What are 2 other antidysrhythmic drugs that do not belong in the Vaughn Williams classes? adenosine (Adenocard), digoxin
What is the MOA of adenosine? decreases automaticity in the SA node and slows conduction through the AV node; very short half-life
What are the indications of adenosine (Adenocard)? Paroxysmal SVT (e.g., Wolff-Parkinson-White syndrome) What the fuck is this thanks for explaining rick
What are SE of adenosine (Adenocard)? sinus bradycardia; dyspnea from bronchoconstriction; hypotension; vasodilation which can cause FACIAL FLUSHING; chest discomfort
What are drug interactions of adenosine (Adenocard)? methylxanthines (e.g., aminophylline, caffeine) block receptors for adenosine; dipyridamole (antiplatelet) intensifies its effects
What is digoxin used to treat? Atrial dysrhythmias. Heart failure.
What are the functions of the renal system? Urine formation; Ultrafiltration; Regulation of water balance; Regulation of acid-base balance; Production of erythropoietin; Production/secretion of renin; Activation of vitamin D
What are the 3 main processes of the kidneys? filtration, reabsorption, active tubular secretion
What is ADH? regulates the concentration of body fluids by altering the permeability of the kidneys. Causes more water to be absorbed, which concentrates the urine. Reabsorb water not salt.
What condition causes low levels of aldosterone? Diabetes insipidus. Diluted urine, reabsorbing not enough water.
What is SIADH? Syndrome of inappropriate (excessive) ADH
How does hypertension affect the kidneys? can damage blood vessels and cause hardening of the kidneys (nephrosclerosis). This eventually causes chronic renal disease
What is the leading cause of chronic kidney disease? Type 1 diabetes
What are the 3 categories of causes for acute renal disorders? Prerenal, intrarenal, postrenal
What are prerenal causes of acute renal disorders? conditions caused by circulation changes leading to the kidney (e.g., MI)
What are intrarenal causes of acute renal disorders? conditions caused within the kidney organ itself (e.g., cancerous tumor)
What are postrenal causes of acute renal disorders? conditions caused by changes in the “outflow” from the kidney (e.g., renal calculi)
What are some causes of chronic kidney disease? diabetes mellitus, hypertension, glomerulopathies, hereditary nephropathies (small kidney), obstructive uropathies, renal vascular disease
What are the primary therapies of chronic renal disease? diuretics, antihypertensives, agents affecting volume and ion content of body fluids
What are the 4 categories of diuretics? high-ceiling diuretics, thiazide diuretics, potassium sparing diuretics, osmotic diuretics
What is the 5th group of diuretics? carbonic anhydrase inhibitors. OSMOTIC DIURETICS. lower intraocular pressure (IOP). They are not used to increase U/O.
What is the MOA of diuretics? A drug that increases urine output. Block sodium reabsorption in the nephron which sends more sodium in the urine. Water molecules travel with sodium which increases urination volume.
What is the most commonly administered loop (high-ceiling) diuretic? Furosemide (Lasix)
What is the MOA of furosemide (Lasix)? its actions take place in the ascending limb of Henle’s loop. It blocks sodium and chloride, which prevents reabsorption of water
What are the indications of furosemide (Lasix)? edema throughout body locations (e.g., peripheral, pulmonary); hypertension
What are SE/AE of high-ceiling (loop) diuretics? Fluid loss can cause dehydration, loss of electrolytes (hypokalemia, hypochloremia, hyponatremia); CNS: dizzy, h/a, tinnitus, blurred vision; GI: n/v, diarrhea
What are some drug interactions of high-ceiling (loop) diuretics? potassium-sparing diuretics; ototoxic agents; digoxin
What is the prototype of thiazide diuretics? Hydrochlorothiazide (Hydrodiuril)
What is the MOA of thiazide diuretics? blocks the reabsorption of sodium and chloride in the early distal convoluted tubule. Diuretic actions somewhat lower than high-ceiling diuretics. They are chemical derivatives of sulfonamides
What are the indications of thiazide diuretics? hypertension, edema, hypercalcemia, diabetes insipidous, adjunctive medications for: hepatic cirrhosis; HF
What are contraindications of thiazide diuretics? allergies; anuria; severe renal failure; pregnancy (note: the “normal” interstitial buildup of fluids in pregnancy is not an indication for diuretics)
What are SE/AE of thiazides? electrolyte imbalances (e.g., hypokalemia, hyponatremia, hypochloremia); GI; dizzy; vertigo; h/a; impotence
What are the 2 categories of potassium-sparing diuretics? Aldosterone antagonists and nonaldosterone antagonists
What are potassium sparing diuretics, how are they used? Relatively weak diuretics and primarily used to prevent hypokalemia. Very common to use these in combination with other diuretics. Note: they cause a “slight” increase in urine production
What should you watch for with potassium sparing diuretics? Hyperkalemia. Potassium is retained which can contribute to hyperkalemia
What is MOA of spironolactone (Aldactone)? blocks the action of aldosterone which decreases loss of potassium.
Aldactone is an _______ and causes a reduction in testosterone Antandrogen
What are contraindications of Aldactone? renal insufficiency; hyperkalemia; pregnancy or lactation
What is the prototype of nonaldoesterone antagonist? triamterene
What is the MOA of triamterene? directly inhibits exchange of potassium and sodium. Keep potassium and kick out sodium (usually kick out both)
What are indications of triamterene? hypertension; edema. Often used in combination with other diuretics. Note: relatively mild in its diuretic capabilities
What are SE/AE of triamterene? hyperkalemia; n/v; dizziness, leg cramps
What is the MOA of osmotic diuretics creates osmotic force in the nephron and most of the drug stays in the nephron. This increases urine flow. There is not any significant loss of potassium (or other electrolytes).
What is the prototype of osmotic diuretics? mannitol (Osmitrol)
What are indications of osmotic diuretics? Reduce increased intracranial pressure. Prevent renal failure. Decrease intraocular pressure (IOP)
What are AE of osmotic diuretics? Mannitol can worsen edema by drawing fluid into tissues. It can also cause: h/a; n/v; fluid/lyte imbalances. Must be used with caution in patients with HF or pulmonary edema.
What are crystalloid agents? Fluids that supply water/sodium to maintain the osmotic gradient between ECF & ICF
What is the MOA of crystalloid agents? sodium content maintains the osmotic gradient
What are indications for crystalloid agents? Indications: body fluid deficits; manages specific fluid/electrolyte imbalances; liver failure; burns; DVT; renal dialysis; shock syndrome
What are contraindications for crystalloid agents? Contraindications: hypervolemia; severe electrolyte imbalances, edema
What are SE/AE of crystalloid agents? can leak into plasma and result in edema throughout the body. They do not carry oxygen and their effects are short lived
Which crystalloid agent does not cause cells to swell or shrink? Isotonic solution
Which crystalloid agent is composed of 0.9%NaCl? Isotonic solution
Which solution draws fluid from cells? Hypertonic solution
Which solution contains more solutes than normal plasma? Hypertonic solution
Which crystalloid agent is D10, or one with 3.0% NaCl? Hypertonic solution
Which solution draws fluid into the extracellular fluid? Hypertonic solution
Which solution has less solute concentration than normal plasma? Hypotonic solution
Which crystalloid agent contains 0.45% NaCl or .225% NS? Hypotonic solution
Which solution pushes fluid into cells? Hypotonic solution
What is volume contraction? Decrease in total body volume. Hypovolemia
What is volume expansion? Increase in total body volume. Hypervolemia
What is isotonic contraction? Water and salt is lost in equal proportions. Loss of total volume, but osmolality remains same.
What are some causes of isotonic contraction? Diarrhea, vomiting, diuretics
What is used to treat isotonic contraction? Isotonic solution
What is hypertonic contraction? Loss of more water than sodium. Increases osmolality and draws water out of cells. Leaves more sodium than water in ECF.
What is used to treat hypertonic contraction? Hypotonic solution
What causes hypertonic contraction? Diaphoreses, osmotic diuresis, extensive burns
What is hypotonic contraction? Loss of more salt relative to water. Decreases osmolality and pushes water into cells. Leaves more water than sodium in ECF.
What is used to treat hypotonic contraction? Hypertonic solution, draws water from cells
What causes hypotonic contraction? Diuretics, chronic kidney disorders
What is hypokalemia? Low potassium levels. Below 3.5 mEq/L
What are some causes of hypokalemia? diuretic therapy; increased renal excretion of potassium; vomiting
What are SE/AE of hypokalemia? n/v, abdominal pain, diarrhea
How is hypokalemia treated? IV potassium chloride
What is hyperkalemia? Excessive potassium levels above 5mEq/L
What are some causes of hyperkalemia? tissue trauma; acidosis; potassium-sparing diuretics
How is hyperkalemia treated? decrease potassium in diet; hold potassium diuretics; counteractive medications to protect the CV system (calcium salts)
What is an antagonist to hyperkalemia? Kayexalate which absorbs potassium
What causes hypomagnesemia? diarrhea, hemodialysis, renal disease, IV administration without magnesium
What are symptoms of hypomagnesemia? tetany from increased neurotransmission; disorientation; seizures
How is hypomagnesemia treated? Magnesium gluconate; magnesium hydroxide
What can happen from administering magnesium? Neuromuscular blockade; ECG changes (Can deteriorate into life threatening dysrhythmia of ventricular fibrillation). Torsades de pointes
What causes hypermagnesemia? renal disorders; antacids that contain Mg
What are symptoms of hypermagnesemia? muscle weakness; sedation; ECG changes
What is used to treat hypermagnesemia? IV calcium
Created by: kangaloo



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