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Exam 4 Blueprint for PHarmThese are a very good representation of the content covered in the exam and is subject to minor changes of one or two questions.Hope this helps - and happy studying.DrugsNumber of QuestionsAtropine2 Muscarinic Antagonist: AtropinePrototype: atropine (Sal-Tropine)MOA / TE: Competitive blocking of Ach at muscarinic receptors to treat the following:Atropine is dose relatedPre-anesthetic medicationDisorders of the eye (surgery)Bradycardia, raises hrt rateIntestinal hypertonicity and hypermotility Muscarinic agonist poisoning (WMDs)Peptic ulcer disease (Not DOC)Asthmas (Not DOC)Biliary colic bugers bugers bugersAdverse EffectsXerostomia (dry mouth)Blurred vision, photophobia intraocular pressure (glaucoma)Urinary retentionConstipationAnhidrosis (no sweating)TachycardiaThick bronchial secretionsDDAntihistamines, makes drierPhenothiazine antipsychotics, associated with; seretonin reuptace inhibitors, which increase bld pressure. Atropin does sameTricyclic antidepressantsAdverse EffectsXerostomia (dry mouth)Blurred vision, photophobia intraocular pressure (glaucoma)Urinary retentionConstipationAnhidrosis (no sweating)TachycardiaThick bronchial secretions Atropine is dose relatedAnticholinergics1Anticholinergics for OABOxybutynin (Ditropan)1Prototype: oxybutynin (Ditropan)MOA / TE: Partially selective for M3 receptor blocking to target bladder detrusor and alleviate sxms associated with urge incontinence & urinary frequencyAdverse effects – like those of AtropineDRY mouth, constipation, impaired visionAntidote: Physostigmine – CharcoalOther AnticholinergicsScopalamine Like atropine – except: sedative, antiemeticIpratropium Bromide (Atrovent)Inhaled – so fewer SE (dryness less, etc)Urecholine1Muscarinic AgonistsPrototype: Bethanechol (Urecholine)MOA / Uses – binds reversibly to muscarinic cholinergic receptors to activate and selectively produce effects on theHeart (HR)Exocrine glands (sweating, salivation, bronchial secretions, gastric acid)Smooth muscles (constriction of bronchi & tone & motility of GI tract)Contraction of detrusor – relaxation of trigone/sphincter Eye (miosis and accommodation)Principle indication is urinary retentionAdverse effectsHypotension and bradycardia Bloating, cramps, hypersecretions of acid, involuntary defecationBladder rupture in persons with urinary tract obstruction or weak bladder wall. If they have a tumer or something it can cause bladder to rupter Bronchoconstriction Dysrhythmias in hyperthyroid makes you skiny, BP up, high hrt rateAnti-Epileptics (class)3EffectsSuppress discharge of neurons at focus Suppress propagation of seizure activity from focus to other areas of brainMechanisms of actionSuppress sodium influx – reversible bindingSuppress calcium influxAntagonize glutamate – excitatory transmitterPotentiate GABA – an inhibitory transmitterEpilepsy: Therapeutic ConsiderationsDiagnosis and drug selectionDrug evaluation – seizure freq. chartNon-drug therapyNeurosurgery (best success rate) Vagal nerve stimulationKetogenic dietMonitoring plasma drug levelsTraditional AEDsPromoting patient adherenceWithdrawing antiepileptic drugsphenytoin (Dilantin)3MOA / UsesSelective inhibition of sodium channels to suppress cerebral irritability to treat partial and tonic-clonic seizures & selected cardiac dysrhythmias ADME: Varied oral absorptionHalf-life 8 to 60 hoursMetabolism varianceBlood levels (10 mcg/mL)Adverse effectsNystagmus, diplopia SedationAtaxia - gaitCognitive impairmentGingival hyperplasia – floss / gum massageSkin rash – stop therapy (Stevens-Johnson)Effects in pregnancy - teratogen Cardiovascular effects – IV use in SE, heart blocks DDPhenytoin decreases effects oforal contraceptives, warfarin (Coumadin), and glucocorticoids Drugs that increases phenytoin levels:\ diazepam (Valium), isoniazid, cimetidine (Tagamet), alcohol (acute), valproic acid (Depakote)Drugs that decrease phenytoin levelsCarbamazepine, phenobarbital, chronic ETOH ADMEAdministration: po with foodIV – slowly! – compatibility issuesAdditional Nsg considerationsDrivingHazardous work Valproic acid (Depakote)1MOA / Uses: Seizure disorders (all) – including absence seizures, Bipolar disorder, & migraineAdverse effectsGI effectsHepatotoxicity: liver failurePancreatitisTeratogenic effects carbamazepine (Tegretol)2MOA / UsesMuch like phenytoin & used to treat epilepsy (not absence), Bipolar disorder, trigeminal and glossopharyngeal neuralgias – minimal effects on cognitive functionAdverse effectsNystagmus, ataxia, HA, blurred vision, vertigoLeukopenia, anemia, thrombocytopeniaHypo-osmolarity – water excretionRash, photosensitivity reactions & teratogenic DDDecreases effect of warfarin and contraceptivesIs decreased by phenobarbital Is increased by grapefruitNsg considerationsMinimal cognitive impairment effectsTolerance to other SE developsAntiplatelets (class)1Review: Physiology & Pathophysiology of CoagulationHemostasis Stage 1 - Platelet plug via aggregationStage 2 - Intrinsic & Extrinsic pathwaysKeeping hemostasis under controlPhysiologic removal of clotsThrombosisArterial thrombosisVenous thrombosisParenteral Anticoagulants I:Heparin and Related DrugsHeparin and LMW Heparin3Prototype: Heparin (unfractionated)Sources: cattle lungs, pig intestinesMOA / TE / Uses: rapid-acting anticoagulant interfering w Thrombin & Factor to treat;Pulmonary embolism (PE)Evolving stroke, Not hemoragic stroke, but exkemic strokeMassive deep venous thrombosis (DVT)igure 51-1A… 51-2B… is an animal so you can have an allergic reaction with this drug… is a 2 nurse check drugADME – Sub Q only – no po Adverse effectsHemorrhageHeparin- induced thrombocytopenia (HIT) – immune responseHypersensitivity reactionsLong term – osteoporosisWarningsHemophilia, PUD, aneurysm, HTN, threatened spontaneous ABContraindicationsBleeding, thrombocytopenia, surgeries of eye, brain, or spine, (not a lot of room to bleed)Given in units- 2 nurse checkIntermittent via INTermitnetly Continuous – loading dose common, dripDeep subcut – well away from umbilicusLow-dose pre-op prophylactically Protamine sulfate for OD (overdose)MonitoringActivated partial thromboplastin time (aPTT) – Increase from norm (40 sec) 1.5 to 2 timesAbove 80 seconds too longLMW HeparinPrototype: enoxaparin (Lovenox)MOA / TE / Uses: Heparin preparations w shorter molecules than unfractionated that selectively inactivates Factor Xa & used in Prevention of DVT following surgeriesTreatment of established DVTPrevention of ischemic complicationsBenefits over HeparinCan be fixed dose, can be used at home, less thrombocytopenia Adverse effects and interactionsBleedingImmune- mediated thrombocytopeniaCostNursing considerationsHypersensitivity to pork; give 90 degreeThrombolytics1Prototype: Streptokinase [Streptase]MOA / TE: Binds plasminogen to make plasmin to break up clot & is used inAcute coronary thrombosis (acute MI)Deep venous thrombosis (DVT)Massive pulmonary emboliAdverse effectsBleeding, hypotensionAntibody production, feverwarfarin (Coumadin)3Prototype: warfarin (Coumadin) MOA / TE / Uses: Antagonist of vitamin K, blocks biosynthesis of factors VII, IX, X, and prothrombin used inLong-term prophylaxis of thrombosisPrevention of VTE and associated PEPrevention of thromboembolism (in patients with prosthetic heart valves)Prevention of thrombosis during AF, thickens bld ADMELonger onset sec. to circulating clotting factors – may be days on & offSo Some of these different therapies will over lap..Implications for surgery, ok for DDSAdverse effectsHemorrhage, teratogenesis (Cat X)Red-orange urine (not blood)AlopeciaDD & DF (Table 51-4)Drugs that or anticoagulant effectsDrugs that promote bleeding: NSAIDs – including acetominphen, HeparinFoods: broccoli, spinach, dark greens, and grape fruit Nursing considerationsMonitoring INR, PT (Table 51-3)Vit K (the antidote) for OD (po, diluted IV - NO subcut) Vit K1Iron (Fe)3Prototype: Ferrous sulfate (Feosol)MOA / TE: DOC -restores iron for production of hemoglobin to prevent or relieve symptoms of microcytic hypochromic anemiaADMEAbsorbed fr Fe rich foods, uptake in GI tract, stored by liver Lose 1 g / d - requirements r/t rate of RBC production - pregnancy / mensesAdverse effectsGI: N, heartburn, bloating, constipation, & diarrheaAggravation of: PUD ( irritates stomach lining), regional enteritis, ulcerative & colitis – shouldn’t take p.o.Dark green / black stoolsLiquid form – stains teeth, drink through strw ToxicityLeading cause of poison death in kidsTx: Lavage if tabs in gut / deferoxamine DDAntacids – reduce (2 hr B4, 4 hr afterTetracycline - reduceAscorbic acid – increases & potentiates adverse effectsAvoid time- release in elderly - erraticDFAbsorbs best w/o foodFoods protect against bad effects- milk, cereals, dietary fiber, tea, coffee and eggs,may decrease absoption Prototype: Iron dextran (INFeD)MOA / Use: Indicated when orals don’t work – can’t be absorbed – blood loss is excessive – and GI problemsAdverse effectsAnaphylaxis fr. Dextran (test dose of0.5 ml) observe for an1hr, have epiavailable HypotensionPain / tumors at IM sites – intervention? Z trach Can develop tumors at siteExtreme caustion in serious liver inparement Nursing ImplicationsMonitor serum Fe for rise of 2 g /dL – goal is 15 g / dL If unresponsive – monitor for adherenceTherapy possibly for months, if your iron deficient.. May not know in 120 daysBeta-Blockers(Inderal and class)6Therapeutic Effects of Beta Blockade - the “olols and lols”Major effects: heart rate & force of contraction velocity of impulses through AV nodeTherapeutic management of *Angina pectoris & Myocardial infarction*Hypertension *cardiac dysrhythmias Heart failureHyperthyroidism, migraine, stage frightPheochromocytoma GlaucomaNon-Selective Beta () BlockersPrototype: propranolol (Inderal)MOA / TE: as above and as listed previouslyAdverse effectsBradycardia, cause they slow production HRAV heart block*Precipitation of heart failureReduced cardiac outputRebound cardiac excitation w abrupt cessation (ST and VT)Bronchoconstriction (Beta2)Blockade of glycogenolysis (Beta2)A ymptom of hypoglicemia is incresed HR, but with a beta blocker you don’t get an increased HR… need to look at glucose levelPrecautions / contraindications:Severe allergic conditionsIf occurs beta blockade interferes w EPIDiabetesCompensatory glycogenolyis is impairedCan mask sxms of hypoglycemia (ST)Heart failure, AV block, bradycardia, asthma, bronchospasm and depression (crosses easily into CNS)Drug interactionsCalcium channel blockers – esp. verapamil Insulin – sxms of hypoglycemiaNsg ImplicationsTaper off graduallyMasking of hypoglycemia reactionsHeart rates: Brady or Rebound tachy Cardioselective Beta1 BlockersPrototype: metoprolol (Lopressor, Toprol)MOA / TEBeta1 AT THERAPEUTIC DOSESGlobal at higher doses Don’t cause bronchoconstriction – otherwise same as propranolol Adverse effectssame EXCEPT bronchoconstriction and glycgogenolysis safer in asthmatics and diabeticsIndirect-Acting Antiadrenergic AgentsCentrally Acting Alpha2 AgonistsClonidine2Prototype: clonidine (Catapres)MOA / TE: decreases release of norEpi (flight or fight) , limiting vasoconstriction, therefore lowering blood pressure and heart rate. Also used in severe pain of cancer.ADMEEffects start in 30’ and can last for 24 hrsBrain stem or brainYou don’t stop sudenly Adverse Effects Rebound HTN fr. sudden withdrawalDrowsiness, Xerostomia (DRY MOUTH), embryotoxic, constipation, impotence, gynecomastia Administration: PO and patchesACE inhibitors3Drugs Acting on the Renin-Angiotensin-Aldosterone System Physiology of the renin-angiotensin-aldosterone system (RAAS)Angiotensin-converting enzyme inhibitorsAngiotensin II receptor blockersAldosterone antagonistsPhysiology of the Renin-Angiotensin-Aldosterone SystemAngiotensins I, II, & IIIActions of angiotensin II Vasoconstriction Release aldosterone Alter structure of heart & vesselsActions of aldosterone Sodium and waterFibrosis (hardening) of vesselsFormation of Angiotensin IIRenin Released in response to BP, Na+, volume, and renal perfusion Converts angiotensinogen to angiotensin I Angiotensin-converting enzyme (ACE)Catalyzes conversion of angiotensin I (inactive) into angiotensin II (highly active)Regulation of BP by RAASEffect modest in normal hemodynamics & Na+Effect MAJOR in hemorrhage, dehydration, or sodium depletionActs in two waysConstricts renal blood vesselsStimulates release of aldosterone fr. Adrenals thereby ….Tissue (local) angiotensin II productionAngiotensin-Converting Enzyme (ACE) Inhibitors – the “Prils”Prototypes: captopril (Capoten), ramipril (Altace)MOA / TEReduces angiotensin II & increases bradykinin to dilate vessels, excrete Na+ & H20, conserve K+ & help prevent vessel and heart tissue changesUsesHTN, heart failure ( slowing down the production of myocytes) diabetic nephropathy( a key indicator fotr the use of this drug, help keep BP down)( is protective to use this drug), prevention of MI, stroke and deathSpecial benefits of ACE InhibitorsDo NOT interfere with heart reflexes – ok with exerciseSafe in asthmaDo NOT cause hypokalemia(like diurestoics, hyperuricemia, or hyperglycemiaDo NOT induce lethargy, weakness or sexual dysfunctionDO reduce risk of cardiovascular mortality fr. HTN, MI, & stroke (22%)Reduce mortality following MIReduce chance of developing heart failureSlow progression of renal diseaseADMENearly all are POCaptopril and moexipril NOT with foodRenal excretion (monitor who?)anybody with reduced kidney functionAdverse effects1st Dose hypotensionCough, dry hackingHyperkalemia, does not excrete potassium. RF in renal artery stenosis (hardening) can drop GFR to low..Angioedema Neutropenia (rare) prevalent among people w collagen disease or lupis Dysgeusia (taste) and rashDrug DrugDiuretics – withdraw 1 wk prior to starting ace’sAntihypertensive agentsDrugs that raise potassium levels (salt sub)Lithium – raisedNSAIDs (counter effect)Nonsteroidal anti-inflammatory drugslefttopARBs2Angiotensin II Receptor Blockers(ARBs) – the “Sartans”Prototypes: iosartan (Cozaar), valsartan (Diovan)MOA / TEBlocks action of angiotensin II Protects fr. cardiovascular structural changesReduces excretion of K+ and aldosterone Increases renal excretion of Na++ & H2OUseful in migraineDoes the same stuff as the aceMOA cont’dDoes not inhibit kinase II or increase bradykinin MAIN difference between ACEs & ARBs – no cough or hyperkalemia with ARBsADME: All po, All ok with or without foodAdverse effectsSame as ACEs, but less angioedema DrugDrug Antihypertensives Aldosterone AntagonistsPrototype: eplerenone [Inspra]MOA / TESelective blockade of aldosterone receptors for tx of HTN and heart failureRequires 4 weeksBenefit in preventing mortality unknownADMEAbsorption is not affected by foodAdverse effects—hyperkalemia DrugDrug Inhibitors of CYP3A4Can significantly raise levels of eplerenone Drugs that raise potassium levelsCaution when combined with lithium, or other drugs that raise potasium Spironolactone [Aldactone] – older drugMOABlocks aldosterone receptorsBinds with receptors for other steroid hormonesAlso impact other adrenal hormone, BadTherapeutic usesHypertension and heart failureAdverse EffectsHyperkalemia Gynecomastia ( man boobs)Menstrual irregularitiesImpotenceHirsutism (hair in women)Deepening of the voiceAlpha-1 Blocker2Essential hypertensionVasodilation Reverses toxicity fr 1 agonists (EPI)Systemically & extravasation Benign prostatic hyperplasia smooth muscle contraction in bladder neckPheochromocytoma Catecholamine secreting tumorRaynaud’s diseaseVasodilation Selective 1 BlockerMinipress1Prototype: Prazosin (Minipress)MOA / TE: dilates arterioles & veins, relaxes smooth muscle in bladder neck and prostate capsule (off label for BPH)Adverse effectsOrthostatic hypotension (1 % - consciousness – 1st dose – start low – warnings – 1st dose at night)Reflex tachycardia - baroreceptor Inhibition of ejaculation - reversibleNasal congestion - vasodilation Calcium Channel Blockers(CCBs)(Procardia and class)4Normal physiology: Calcium in = contraction / force ofEffects of BlockingDilation of Vascular Smooth Muscles (VSM)= dilated peripheral arterioles / arteries & arteries of heartHeart Ca++ Blocking Effects Inotropic effect ( wrd used to express the contraction or force of the heartSlows conduction thru SA & AV nodesSame effect as Beta1 blockersPrototype: Nifedipine [Adalat,Procardia]MOA / TE: dilates arterioles lowers BP, no cardiac effect, can increase HR via baroreceptor effect, no decreasing contraction force or affect on automaticity of conduction - used in:Angina pectorisHypertensionInvestigational basis to relieve migraine headache and to suppress preterm laborAdverse Effects of nifedipine Flushing - DizzinessHeadachePeripheral edemaGingival hyperplasiaReflex tachycardiaDrugDrug Beta-adrenergic blockersUsed intentionally to prevent reflex tachycardiaFocus on such things as adverse effects, relevant dietary restrictions, drug-drug interactions, patient teaching, labs to monitor, antidotes, patient responses, and actions of the classes, etc. ................
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