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117 Cards in this Set
- Front
- Back
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Right Ventricle Failure
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increases peripheral vascular capillary pressure>fluid leak edema increases right ventricular pressures>jugular venous distension |
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Left Ventricle Failure
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increases back pressure of blood into the pulmonary circulation (edema) life threatening |
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Vasodilators
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decreasing cardiac work decreasing oxygen consumption increasing cardiac output |
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Vasodilators
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isosorbide dinitrate hydralazine |
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Vasodilators Side Effects
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reflex tachycardia |
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Diuretics
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eliminating excess sodium and water from the kidneys reduce volume overload (edema) |
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Diuretics
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Loops (most efficient/high ceiling; drug of choice) potassium sparing (helps minimize potassium loss from thiazides and loops) |
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Beta-Blockers
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decrease heart rate and force of contraction Metoprolol, Carvedolol calms the heart down to prevent further damage |
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Cardiac Glycoside
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inhibits Na+/K+ ATPase indicated for: severe left ventricular insufficiency (+Acel & Diuretic) increases contraction in the atrial and ventricular myocardium |
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Blood Flow
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-into right ventricle -contraction forces pulmonary valve open -into pulmonary trunk -blood unloads CO2 & loads O2 -left atrium contraction of left ventricle forces aortic valve open -aorta>body>venae cavae |
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Electrocardiogram
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Cardiac Action Potential |
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Vaughan-Williams Classification of Antiarrhythmic Drugs |
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Quinidine
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Class 1A (Sodium Channel Blockers) -also blocks K+ channels, 1st antiarrhythmic used,good oral bioavailability -side effects: ventricular paroxysmal tachycardia -Anticholinergic properties: GI disturbance & cinchonism |
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Cinchonism
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tinnitus, blurred vision, sweaty skin |
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Procainamide
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similar to quinidine except side effects include lupus erythematosus-like syndrome (long time use) but also less toxic can be used as a local anesthetic |
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Lidocaine
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-drug of choice for acute ventricular tachycardias, emergency termination of VT, post cardioversion or during open heart surgery -least cardiotoxic Na+ channel blockers -administered IV ONLY |
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Mexiletine
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can promote synergism |
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Flecainide
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-poorly tolerated and limited to experienced providers -reserved for life threatening supraventricular arrhythmias |
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Propranolol, Metoprolol, and Esmolol
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Class 2-Beta Blockers -antiarrhythmic agents by depressing automaticity; also has direct effect on cardiac membrane receptors -Adverse Effects: bradycardia, hypotension, fatigue, bronchospasm -safe drugs with few serious side effects |
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Propranolol
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Drug of choice for treating cardiac arrhythmias resulting from hypertension |
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Metoprolol
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most widely used beta-blockers for arrhythmias less bronchospasms than propranolol |
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Esmolol
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very short acting for acute emergency therapy (IV only) |
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Amiodarone
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Class 3- K+ Channel Blocker very broad spectrum antiarrhythmic & very potent, most commonly used antiarrhythmic mainstay of therapy for atrial fibrillation |
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Amiodarone Side Effects and Other Considerations |
Drug can accumulate in many different tissues including the heart, eye (corneal microdeposits), skin (photodermatits), and lungs (pulmonary toxicity) drug will be discontinued in over half of patients |
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Two Classes of Ca++ Channel Blockers
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Non-Dihydropyridines- angina, arrhythmias, decrease conduction velocity and the firing rate |
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Verapamil & Diltiazem
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Verapamil has greater action in the heart than on vascular smooth muscle Major Indication: Supraventricular tachycardia |
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Adenosine
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-Inhibits Ca++ & K+ channels (decreases conduction velocity at the AV node) -Drug of choice for abolishing acute PSVT -Extremely short duration -Side Effects: facial flushing, headache, hypotension, and shortness of breath |
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Arrhythmias are caused by:
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electrolyte disturbances and overstimulation of the heart and can originate anywhere in the heart |
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Common Types of Arrythmias are:
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-Premature contractions (Ventricular) -Flutters (atrial and ventricular) -Fibrillations (atrial and ventricular) |
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Ischemia
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Sudden, severe, pressing chest pain starting substernal & radiate to left arm caused by an imbalance between myocardium oxygen requirement and oxygen supply |
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Effort Angina
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-fixed obstruction in the coronaries -triggered by exercise, cold, stress, or heavy metals -therapeutic goal is to increase oxygen delivery (vasodilation) |
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Variant Angina |
-spasms of coronaries -triggered by alcohol, drinking cold liquids, REM sleep (occurs at rest or at work) -goal is to increase oxygen delivery (decrease vasospasms) |
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Unstable Angina |
recurrent episodes of small platelet clots which can also precipitate local vasospasm goal is to increase oxygen delivery (decrease platelet aggregation) |
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Nitrovasodilators
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Stable Angina/Effort Angina |
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Nitroglycerin
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-Donates Nitric Oxide which promotes increased myocardial blood supply & decreased pre-load (venous vasodilation) and afterload (arterial vasodilation) -Drug of Choice for stable angina -preferred route: sublingual (prophylactic therapy-transdermal patch) |
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Nitroglycerin
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Tolerance (nitrate-free periods) Reflex tachycardia (paradoxical increase in oxygen demand) |
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Isosorbide Dinitrate
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same as nitroglycerin except duration of action is considerably longer |
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Ca+ Channel Blockers
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Ca++ Dihydropyridines
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increase smooth muscle relaxation (vasodilation) |
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Ca++ Non-Dihydropyridines
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Angina- increase smooth muscle relaxation, decrease heart rate and contractility |
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Diltiazem
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variant and unstable angina- has greater effect in the vasculature than does Verapamil & therefore produces more incidence of reflex tachycardia |
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Verapamil
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Ca++ Channel Blocker -Relatively selective for the myocardium and is less effective as a systemic vasodilator -Primary effect: depress SA node and AV conduction (decrease O2 demand & vasospasms) -Good choice for prophylaxis |
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Nifedepine & Nicardipine
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Prototype of the dihydropyridine group -Causes arterial vasodilation Chronic Stable & Unstable Angina -not as effective as other vasodilators or beta-blockers |
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Drug of Choice for Treating Variant Angina
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Non-Dihydropyridines |
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Beta-Adrenergic Receptor Blockers
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Hypertension, Arrhythmias, Myocardial Infarction, Angina (decrease heart rate & contractility, reduce work) |
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Propranolol
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contraindicated in asthmatics & patients with COPD |
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Metoprolol
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generally safer in patients with asthma and diabetes |
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Other Therapies for Angina
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Clopidogrel- decrease platelet aggregation Atorvastatin- HMG-CoZ Reductase Inhibitor |
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The ABCs of Angina Management
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Be: more physically active Control: blood pressure, cholesterol, body weight |
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Calculating Blood Pressure
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BP=COxPVR Cardiac Output: heart rate, contractility PVR: smooth muscle tone (kidney plays a major role in regulation) |
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Controlling Moment-to-Moment Blood Pressure
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Blood pressure>Baroreceptors "stretch">signaling to VMC>sympathetic/parasympathetic outflow>heart rate, stroke volume(arterial & venous dilation/constriction)>cardiac output/TPR>BP returns to normal |
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Mechanisms Responsible for Long-term Blood Pressure Control |
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Beta-Blockers
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Highly recommended for first-line therapy in hypertension when concomitant disease is present Use cautiously in patients with acute heart failure or diabetes Side Effects: hypotension, fatigue, bradycardia |
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Beta-Blockers for Hypertension
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-Propanolol -Metoprolol-most commonly used |
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Labetalol
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effects (3:1) B1:A1 this combined effect is desirable for treating hypertensive emergencies & pheochromocytoma |
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Esmolol
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very short half life, used for hypertensive emergencies |
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A1-Blockers
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-First dose syncope -Seldom used as monotherapy in hypertension -Primarily used to treat benign prosthetic hypertrophy Side Effects: syncope, reflex tachycardia, orthostatic hypotension, sexual dysfunction |
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Prazosin
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selective antagonist, decreases PVR rarely used as single agent to treat hypertension |
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Phentolamine
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primarily used to manage pheochromocytoma & another hypertensive emergencies |
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Vasodilators
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-Decrease PVR Oral: Hydralazine&Minoxidil (long-term) Parenteral: Nitroprusside(short-term) Ca+ Channel Blockers(Verapamil, Diltiazem, & Nifedipine) Side Effects: hypotension, reflex tachycardia |
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Hydralazine
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-oral -Almost always given with beta-blocker, a diuretic and/or a nitrate Monotherapy is accepted in gestational hypertension |
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Minoxidil
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-used for moderately severe hypertension -Almost always given with beta-blocker, a diuretic and/or a nitrate *hypertrichosis* |
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Sodium NItroprusside
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-Parenatal (must be given by IV infusion) -Used for hypertensive crisis, malignant hypertension, and severe heart failure -Contains cyanide (poison risk) |
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Calcium Channel Blockers (Hypertension) |
Non-Dihydropyridine: more cardioselective -decrease in PVR -safe to use in asthmatics -Side Effects: constipation, flushing, hypotension |
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ACE Inhibitors
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-Reduces PVR with no reflex cardiovascular response -inhibits the enzyme that hydrolyses angiotension 1 to angiotension 2 -ACE inhibitors also directly inhibit the degradation of Bradykinin Side Effects: dry cough, hypotension, skin rash |
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Captopril
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first-line antihypertensive and a good choice for initiating therapy in patients with severe heart failure Contraindicated: pregnancy, angioedemia |
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Lisonopril (and all other -prils) |
all prodrugs |
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Losartan (and other -sartans) |
-Developed as alternatives to ACE inhibitors -Block Angiotensin Receptor (AT1) |
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Hydrochlorothiazide
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-Block Na+/Cl- transporter thereby inhibiting NaCl reabsorption |
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Reserpine
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Blocks release of neurotransmitter (NE) at postganglionic terminal -First effect therapy to be used -Side Effects: sedation, nightmares, mental confusion, depression |
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Clonidine and a-Methyldopa
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a-Methyldopa- nightmares, mental confusion, and depression (used to treat hypertension during pregnancy) |
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General Risk Factors for Hypertension
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obesity family history high salt diet smoking excessive alcohol consumption African American diabetes |
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Therapeutic Uses for Diuretics
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-Congestive Heart Failure -Chronic Renal Failure -Pulmonary Edema -Cerebral Edema -Hypertension -Glaucoma -Hypercalcemia |
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Acetazolamide
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-MOA: inhibition of CA> inhibition of bicarbonate reabsorption -Benefits: Glaucoma (most common), mountain sickness -Adverse Effects: potassium wasting, allergic rxns |
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Dorzolamide
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Carbonic Anhydrase Inhibitor -MOA: same as Acetazolamide -Benefits: glaucoma -Differences: site of action, topical admin, minimal side effects |
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Mannitol
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-MOA: no utilization of a transport system; always administered IV -Benefits: mainstay of treatment of patients with acute renal failure, good for decreasing brain volume and intracranial pressure Side Effects: dehydration & hypernatremia |
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Furosemide
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(Most Efficacious Diuretic Available) -MOA: inhibits the Na+,K+,2Cl- symporter -Indications: congestive heart failure, hypertension, drug of choice for acute pulmonary edema & peripheral edema, acute renal failure -Adverse Effects: ototoxicity, hypotension, dehydration, allergic rxn |
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Hydrochlorothiazide |
-most widely used diuretic -MOA: block Na+,Cl- transporter thereby inhibiting NaCl reabsorption -Indications: hypertension, CHF, diabetes insipidus Adverse Efects: hyponatremia & hypotension, hyperlipidemia, allergic rxns |
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Spironalactone
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(not very efficacious) -MOA: synthetic steroid that inhibit aldosterone receptors in the collecting tubule -Benefits: drug of choice in hepatic cirrhosis, useful in counteracting K+ wasting associated with other drugs, CHF, hyperaldosteronism Adverse Effects: hyperkalemia, gynecomastia |
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Three Phases of Clot Formation
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2. Platelet Phase 3. Coagulation Phase |
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Vascular Phase
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damage to the blood vessels lead to vascular spasm of the smooth muscle in the vessel wall |
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Platelet Phase
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-damaged endothelium release von Willebrand Factor, which makes the surfaces of the endothelial cells "sticky" -platelets sticking to the surfaces of endothelial cells change morphology becoming "activated" and release ADP & TXA2 -the clump initiate the coagulation phase (thrombin, fibrinogen, and fibrin) |
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Coagulation Phase
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-fibrin entraps and stabilizes the initially loose platelet plug
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Strategies to Prevent Thrombosis
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-inhibit platelet function -inhibit fibrin formation |
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Heparin
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-indirect inhibitor of thrombin -anticoagulant (cofactor for anti-thrombin 3) -arterial emboli, acute deep vein thrombosis, MI &DIC -drug of choice for pregnant women -bolus IV injection followed by continuous infusion -Adverse Effects: bleeding, hypersensitivity |
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Warfarin
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-inhibits production of activated vitamin K ("new" coagulation factors) -primarily to prevent formation of venous thrombi -100% oral bioavailability -excessive bleeding, teratogen |
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Factors that Regulate Platelet Function
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Aspirin
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inhibits TXA2 production -makes platelets less "sticky" sot that clot cannot form Adverse Effects: excessive bleeding |
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Clopidogrel
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Antiplatelet-inhibits function ADP -makes platelets less "sticky" so that clot cannot form -highly recommended in patients undergoing placement of coronary stint |
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Alteplase (tPA)
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-"fibrin selective" drug -preferentially binds to and activates plasminogen that is bound to fibrin VERY EXPENSIVE |
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Protamine Sulfate
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antidote for Heparin toxicity |
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Vitamin K1
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antidote for Warfarin toxicity |
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Hemostasis
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after being damaged |
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Thrombosis
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formation of a blood clot inside a blood vessel |
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Extrinsic Pathway
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-very rapid but only good for small clots |
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Intrinsic Pathway
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-slow but produces larger clots |
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Hypochromic Anemia
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(microcytic, hypochromic) results from iron deficiency |
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Megaloblastic Anemia
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(macrocytic, normochromic) Results from B12 or Folic Acid deficiency |
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Ferrous Sulfate
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Absorption-small intestine (vitamin C can help) |
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Deferoxamine
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(iron overdose) |
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Cobalamin
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-megaloblastic: helps regulate adequate production of tetrahydrofolate -neurologic damage: regulates the conversion of methylmalonyl-CoA to succinyl-CoA |
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Folic Acid Deficiency
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Susceptible: strict vegetarians/vegans, pregnant, alcoholics |
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Folic Acid
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helps regulate adequate production of tetrahydrofolate (required for DNA synthesis), anemia can occur within months -oral ingestion |
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Causes of Anemia
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-Increased Demand -Decreased Production -Blood Loss -Bone Marrow Disease -Sickle Cell Disease |
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Type 1 (Familial Hyperchylomicronemia)
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-Deficiency of lipoprotein lipase -not associated with increase in CHD Therapy: low fat diet |
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Type 2A (Familial Hyperchylomicronemia)
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-defect in synthesis/processing of LDL -increases risk for ischemic heart disease Therapy: Diet, Niacin+BABR |
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Type 2B (Familial Combined Hyperlipidemia)
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-overproduction of VLDL -similar to above Therapy: Diet, Niacin+BABR |
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Type 3 (Familial Dysbetalipoproteinemia)
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-defect in apolipoprotein E -increases risk for vascular disease Therapy: Niacin + Fibrate |
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Type 4 (Familial Hypertriglyceridemia)
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-overproduction/ decreases removal of VLDL TG -increases risk for ischemic heart disease Therapy: Diet, Niacin and/or Fibrate |
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Type 5 (Familial Mixed Hypertriglyceridemia)
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-elevated cholesterol and greatly elevated TG -overproduction/decreased removal of VLDL and CM Therapy: Diet, Niacin and/or Fibrate |
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Atorvastatin
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-useful in all types of hyperlipidemias -increases LDL receptors -small increase in HDL levels -contraindicated in pregnancy/nursing mothers |
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Niacin
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-most effect agent for increasing HDL -most prominent side effect: prostaglandin-induced cutaneous flushing |
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Bile Acid Binding Resins
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Primary role: to facilitate the formation of micelles which promote processing of dietary fat |
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Colestipol & Cholestyramine
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-lower cellular cholesterol -increase LDL receptors -Gritty, may affect the absorption of other drugs |
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Genfibrozil & Fenofibrate
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increase VLDL clearance adverse reactions are rare |
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Ezetimibe
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selectively inhibits NPC1L1 (a transport protein) |
