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Pharm exam 3
Endocrine & Cardiovascular
| Question | Answer |
|---|---|
| Short Acting Glucocorticoids | Hydrocortisone |
| Intermediate Acting Glucocorticoids | Prednisone |
| Long Acting Glucocorticoids | Betamethasone |
| Main action of Glucocorticoids | Decrease Inflammation |
| Glucocorticoids adverse affects | Birth: Cleft, LBW, Abortion osteoporosis |
| Glucocorticiods drug interactions | Digoxin, thiazide, loop diuretics NSAID Vaccinations |
| Thiazide diuretics | hypokalemia blocks reabsorption of Na&CL Flurosimide is better |
| Loop diuretic | Furosemide Best of ORAL meds K wasting |
| K+ sparing diuretic | Spirinolactone Don't use with ARB, ACE, or aldosterone antagonist |
| Alpha 1 Blocker | blocks receptors on heart dialates blood vessels cause orthostatic BP-zosin |
| Alpha/Beta Blocker | carvedilol, labatelol Blocks stimulation of heart (contraction)increases dilation of arteries and veins |
| Centrally acting alpha 2 antagonist | Clonidine (may be used PRN or maintenance)Methyldopa |
| Adverse Efects Methyldopa & Clonidine | Dry Mouth Sedation Clonidine- may cause rebound hypertension Methyldopa- cause liver problems |
| Antihypertensive Sympatholytic Drugs | Central Acting Alpha 2 Agonist- Clonidine & Methyldopa Alpha/Beta Blockers- Carvedilol, Labetalol Alpha 1 Blockers- Doxazosin, Terazosin Adrenergic Neuron Blockers- Guanethidine & guanadrel, reserpine |
| Direct Acting Vasodilaters | Hydralzine (given for high Systolic presure) & MonoxidilDilates arteries w/o dilating veins |
| Hydralzine Adverse Effects | systemic Lupus & hair growth |
| Calcium Channel Blockers | Dihydropyridines (nifedipine) Non-dihydropyridines (verapamil, diltiazem)Both effect dilation of arterioles & non-dihydropy-also has direct effects on heart |
| Nifedipin Verapamil & Diltiazem | reflex tachycardia (mostly dihydropy & can be substantial b/c they do not block cardiac Ca+2 channels) use in caution in pt with bradycardia & heart failure or AV block b/c of their suppression of the heart |
| Ace Inhibitors | lisinopril, captoprilAntihypertensive drugMay cause cough Less effective for African AmericanContraindicted in Pregnancy |
| Angiotensin II Receptor Blocker (ARB) | losartan, ibersartan blocks I-II if patient has cough when on Ace can switch to ARB (unless patient has angiodema) |
| Aldosterone Antagonist | Spirinolactone eplerterone Excretes Na & H2O |
| Drug Choice for HTN | Thiazide & Beta Blockers are best for decreasing Morbidity & Mortality1st line: Thiazide, BB, A/B BlockersStage 1 HTN: Thiazide Stage 2: Thiazide w/ BB, ACE or ARB |
| Drugs Cause HyperKalemia | Spirinolactone |
| Drugs cause Hypokalemia | |
| Renal Insufficiency | Use caution with K sparing drugs- may cause hyperkalemia |
| Diabetes | Use caution with Thiazide, furosemide- both promote hyperglycemia & BB can mask signs of hypoglycemia |
| Asthma | Beta Blockers & Labetalol |
| Renal Disease | Ace & ARB works best with diuretics. May have to use loop in kidny impaired people |
| HTN drugs during Pregnancy | Patient can continue to use same drugs except for ACE & ARBS |
| HTN initiated during pregnancy | Methyldopa is DOC |
| Adlosterone | Stimulates Na & K exchange |
| Diuretic Classification | Loop- furosemideThiazide- hydrochlorothiazide Osmotic-(mannitol)K+ sparinga. Aldosterone antagonist (spirinolactone)b. Non-aldosterone antagonist (triamterene)Carbonic anhydrase inhibitors (dec. intraocular pressure) |
| Spirinolactone | may cause hyperkalemiais a steriod- gynecomastia, Hirutisim May be given with Loop to spare K Aldosterone blocking |
| Mannitol | Amt of diuresis is directly correlated to the amt of mannitol in the filtrate Administered via IV only |
| Angina | Pain radiates to left shoulder & arm Secondary to another problem |
| Goals for angina | 1) Prevent MI & death2) Prevent pain & myocardial ischemia |
| Angina Drugs | CCB, Nitrates, BB |
| Variant Angina | Beta Blockers are not effective.. Only CCB & Nitrates work |
| MOA for Nitrates | work by dilating vessels and relaxing coronary vasosopasm |
| MOA Beta Blockers | decrease o2 demand by decreasing hr |
| MOA Ca Channel blockers | dilate arterioles which decrease afterload |
| Nitrates | Wait 8-12 hrs between patchesdilates veins headache, hypertension, and reflex tachycardia discontinue long acting slowly store in light resistant container only good 1 yr or 3 months after opening- water gets into pills |
| Stages of CHF | A B C D |
| Stage A CHF Symptoms | No Sx, structural, functional abnormities |
| Stage A CHF treatment | Ace OR ARBLifestyle changes:Stop smoking and drinking |
| Stage B CHF Symptoms | No S/Sx but still have structural heart dz. (LV hypertrophy or fibrosis, LV dilation or hypocontractility, vavular heart dz & previous myocardial infarction (MI) |
| Stage B CHF Goal | Prevent Symptoms and Signs from appearing and stop progression of remodeling |
| Stage B CHF Treatment | Ace OR ARB (like stage 1)PLUS Beta Blocker |
| Stage C CHF Stymptoms | Have structral damage |
| Stage C CHF Treatment | Add Diuretic to ARB or ACE & Beta Blocker (if diuretic doesn't help add Digoxin) |
| Stage C CHF Drug Interactions | Drugs to avoid in Stage C:Antidysrythmic agentsCCB’sNSAID’s (even aspirin) they dec efficacy & intensify toxicity of diuretic & ACE inh |
| Stage D CHF Symptoms | Widespread Damage Symptoms occur at restTreatment is same but now needs heart transplant to survive |
| Drugs used to treat edema from CHF | 1) Diuretics2) Agents that inhibit RAAS3)Beta blockersOthers: Digoxin, dopamine, hydralazine, nesiratide |
| Drugs that prolong cardiac life | ACE, ARB, Aldosterone angtagonist (Spirinolactone, Beta Blockers |
| ACE inhibitors: drugs | Ends in Prilcaptopril, enalapril, ramipril |
| ACE inhibitors drug interactions | Do not use ACE inh if taking triamterine or spirinolactone |
| ARB MOA for treating CHF | only difference between ACE is doesn't cause breakdown of bradykinin and cough- Use ACE first and if cough is unbearable switch to ARB |
| Beta Blockers in CHF | Start dose low to prevent hypocontractility carvedilol, bisoprolol,metoprolol, Prolongs life |
| Digoxin | 2nd line agentWorks by slowing down heart contraction by promoting calcium buildup in myocardial cellsDo not use with other dysrhythmic drugs, use with caution in patients with disrythmias |
| What is most important thing to monitor with Digoxin? | Potassium becuase Digoxin competes for receptor sites with the drug |
| What does Digoxin simulate? | The electrical impulses not the heart muscle- this is helpful in CHF but harmful in arthymias |
| How to treat Digoxin toxicity | Withdraw Digoxin & K wasting diuretics Monitor K GIve Atropine if pt develops AV block |
| What should K levels be when giving Digoxin? | 3.5-5 |
| What is dosage for Digoxin? | 0.5-0.8 ng/ml |
| Digoxin Drug Interactions | Diuretics: thiazide & loop cause K+ loss ACE inh & ARB’s: inc K+ Sympathomimetics: dopamine, dobutamine Quinidine: displaces digoxin from tissue binding sites & reduces renal excretion of digoxinVerapamil (CCB): inc plasma levels of digoxin |
| Digoxin Half Life | 1.5 daystakes 6 days w/o loading dose to acheive plateau |
| Antidysrthymic drugs | Four classes & fifth that includes Digoxin, and adenosine |
| Anti Dysrthmia Class 1 | Na Channel Blockers Largest GroupSlows the action potential by blocking sodium entry which slows the action potential when travelling from SA to AV to perkinjie fibers |
| Class II Antidsyrthmia | Beta Blockers Work by decreasing entry of calcium In SA node, they reduce automaticityIn AV node, the slow conduction velocityIn the atria & ventricles, they produce contractilityThey work almost exactly like CCB |
| Class III Antidysrthymics | K channel blockers prolongs the action potenital duration and the refractory period |
| Class IV Antidsyrthymics | CCB- works same as BB- slows the electrical conduction down sa to av to perkinje |
| Two groups of Dysrthymias | Supraventriculars (not as dangerous- have time to give meds to work on prob- above the ventricles) Ventriculars (dangerous) don't have much room for meds to work on |
| Sustained Ventricular Tachycardia- Treatment of choice | Cardioconversion is Tx of choice or IV amiodarone, alternatives are lidocaine or procainamide |
| Digoxin induced tachycardia | caused by class 1A and III TOC- IV magnesium and cardioconversion |
| Class 1A NA Channel Blockers | Dec conduction velocity in the atria, vent & His-Purkinje systemClass A,B,C sub class |
| Class 1A Na channel blockers drugs | Quinidine, Procainamide, DisopyramideQuinidine used for supraventricular and ventricular |
| Class 1b Na channel blockers drugs | Lidocaine, Mexiletine, Phenytoinonly treats ventricular not supraventricular |
| Class 1c Na channel blockers drugs | Flecainide & Propafenone maintentance of suptravent dysthrmia |
| Class II beta blockers | Propranolol, Acebutolol (non-selective beta 1 & 2 Esmolol (IV), Sotalol (selective beta 1)Sotalol- blocks calcium channels too!!!! |
| Class III K Channel Blockers | Amiodarone- used for lifethreatening ventricular or atrial dusthrytmias, Bretyllium -short term tx of severe ventricular(IV), Dofetilide, Ibutilide (IV), Sotalol (IV) |
| Class IV Calcium Channel Blockers | Verapamil, Diltiazemfor supraventricular dysrthymias |
| Adenosine | Know Adenosine is DOC for terminating paroxysmal and has extrememly short half life |
| Normal PTT time | 40 sec |
| Low Molecular Weight Heparin | Doesn't require PTT time |
| Anticoagulant 1 | Heparin |
| Anticoagulants II | Bivalirudin (angiomax), lepirudin (Refludan), argatroban (Acova) |
| Warfarin | antagonist of vitamin K & bound to albumin |
Created by:
hbissell
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