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Muscarinics AtropineMuscarinic 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 relatedSympathomimeticsEpinephrine Therapeutic 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 GlaucomaPrototype: 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 Indirect-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 patchesAnitseizuresphenytoin (Dilantin)MOA / 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 Opiod AgonistStrong: morphine [Duramorph] CIIModerate to strong: codeine [Paveral] CIIIUsual dose of 30 mg = about same relief as 325 mg of ASA or TylenolCombo meds more effectiveExtremely effective cough suppressant at 10 mg dose rangeMOA / TEMimics action of endogenous opioid receptors (mu) to produce analgesia and thereby relieve painOther effects include drowsiness, mental clouding, anxiety reduction, sense of well-beingDosage – Highly individualized Table 28-6Adverse Effects Resp. depressionDiminished by “tolerance” Most common cause of OD deathOthers Constipation, orthostatic hypotension, urinary retention / urgency, cough suppression, biliary colic, emesis, elevated ICP, dysphoria, sedation, miosis, neurotixicity, immune and hormone suppression with prolonged useToxicity Classic triad (coma, resp. depression, pinpoint pupils)ADME (Pharmacokinetics) Nursing implications?Given by several routesSlowest to fastestTime-frame for TE varies by mode of administration Denatured in liverHard to cross blood-brain barrierPrecautions / ContraindicationsDecreased resp reserve, pregnancy, head injury, infants / elderly, hypotension, liver diseaseInteractionsCNS depressants, antihistamines, antihypertensives, MOAIs*, antiemetics, amphetamines, agonist-antagonist, antagonistsADME (Pharmacokinetics) Nursing implications?Given by several routesSlowest to fastestTime-frame for TE varies by mode of administration Denatured in liverHard to cross blood-brain barrierDosage – Highly individualized Table 28-6Administrationpo, IM, IV, SQ, topical Oral associated with chronicPreferably fixed scheduleSite specific – hazards- epidural- effects delayed Special Clinical Concepts r/t Use of OpioidsPain assessment – including evaluation!Dosing amt and scheduleFear of addiction in clinical settingAvoiding withdrawal – 20 days or morePatient controlled anesthesia (PCA)Morphine: DOC - heart attack (MI)Meperidine [Demerol]: DOC OBAvoid opioids in Head Injury…Meperidine [Demerol]Interacts with several drugsToxic metaboliteAvoid use past 48 hrs and not to exceed 600mg/24hr. Opioid Antagonists naloxone [Narcan]MOA – TE / Usecompetes for opiate site and blocks effects of opioid agonists / agonist-antagonists – no significant effect given alone – resulting in REVERSAL of narcoticUsed to reverse the affects of morphineADMERebound effect Adverse effects: acute withdrawalDosage/Admin: 04. mg IM, IV, SubQ Others: naltrexone [ReVia] ETOH/Opioid abuseAntidepressantsGeneral PointsMost common psychiatric disorderMajor treatment method - medicationsFive major groupsGoal? Sxms Depressed mood, loss of pleasure / interest in all or nearly all of one’s usual activitiesUnder-treated More prevalent in womenSuicidal thoughts may increase w RxNursing ImplicationsATI p. 203 (220)Tricyclic Antidepressants (TCAs)Prototype: imipramine [Tofranil]MOA – TE / UseBlocks reuptake of the MAO transmitters NE (norepinephrine) and serotonin. Elevates mood, thereby treating depression.Other uses: bipolar disorder, neuropathic pain, insomnia, fibromyalgia, OCDAdverse effectsOrthostatic hypotension, sedation, anticholinergic effects, sedation, diaphoresis, cardiotoxicity, seizures, hypomania, “yawngasm”Precautions / Interactions TCAs w MAOI can lead to severe HTNPotentiates drugs like NE (norepinephrine)Potentiate CNS depressantsAntidote: activated charcoal after gavage DosingBased on clinical response – don’t give more than a week supplyDose at bedtime once levels achieved – EXCEPT in elderly (cardiac reasons)SSRI AntidepressantsPrototype: fluoxetine [Prozac]MOA / TE / UseSelective serotonin re-uptake inhibitor resulting in elevated serotonin levels – elevating mood and relieving depression.Helps in bulimia nervosaAdverse effectsImpotence, weight gain, Serotonin syndrome, withdrawal syndrome, EPS, bruxism, bleeding, hyponatremia.Interactions: MAOIs, Warfarin, & TCAs MAOI AntidepressantsPrototype: phenelzine [Nardil]MAO / TE / UseEnzyme – deactivates NE, serotonin, dopamine, and tyramine (NE stimulator) from foodsNOT 1st CHOICERelevant P-kineticsTyramine Adverse effects: CNS stimulation – agitation – hypomania – mania – hypotension – HTN crisis – meperidine (hyperpyrexia)Atypical AntidepressantsBupropion [Wellbutrin]Action unclearEffectStimulant ergo no wt gainNo sexual dysfunction – may augmentAdverse effects: agitation, HA, dry mouth, constipation, wt loss, insomnia, tachycardia, seizure Note: St. John’s Wort Box 32-2Classification:Sedative-HypnoticsMajor EffectsCNS depressionTherapeutic UsesRelieve anxiety, facilitate sleep, manage muscle spasms, seizure and panic disorders, augment anesthesia, and manage ETOH withdrawal Barbiturates Prototype: secobarbital [Seconal]MAO / TE / UseMimics GABA and depresses CNS directly causing relaxation and anxiety reduction. Other uses: seizure management, anesthesia, sleep disorders, maniaADMENO CEILING TO LIMITS OF CNS depression Adverse effects:Resp. depression, hypotension in toxic doses, can readily cause death PrecautionsHighly addictive - physical dependence – withdrawal can be severe Caution in elderlyCaution with other CNS agentsCaution with IM injectionBenzodiazepinesBenzodiazepines (CIV)Category DPrototype: diazepam [Valium]Others: clonazepam, lorazepam, clorazepate MOA Depress neuronal function at multiple CNS sites by potentiating endogenous GABA (gamma-aminobutyric acid) and is limited because GABA is finitesafer Cardiac PO effect - heart & blood vessels IV effect – potentially ? Can be vary badRespiratoryMinimal alone, serious if combo or IVPharmacokinetics: Readily absorbed Differ in respect to time of course of action (main indicator for which one chosen for which job)Adverse effectsCNS – daytime vs nighttime impactsAmnesiaParadoxical.. Opposite effect of what you thought you would get AbuseMalnutrition, liver disease and blood levels.. DD w other CNS depressants Dosage: varies by agent Nursing ImplicationsATI pp. 218Benzodiazapine-likes Prototype: Zolpidem [Ambien] CIVMOA – TE / UseAgonists at benzodiazepine receptor site on GABA channel prolonging sleep duration and helps relieve insomniaLow potential for tolerance or abuseAdverse effectsSimilar to benzodiazepines (daytime drowsiness / dizziness)Can intensify CNS depressantsDosage / Administration Before bedtime?DiureticsReview of renal anatomy and physiologyIntroduction to diuretics High-ceiling (loop) diuretics Thiazides and related diuretics PhysiologyThree basic functionsCleanse ECF and maintain volume and compositionMaintain acid-base balanceExcrete metabolic wastes and foreign substances – e.g. ? Relevant Concepts Filtration - non-selectiveRe-absorption – highly selectiveDiuretics interfereActive pumps for organic acids/bases in proximal tubuleSodium-Potassium ExchangeAldosterone Purpose of Diuretics Increase urinary output Major applicationsTreatment of hypertensionMobilization of edematous fluidMaintain urine flow, thereby aids prevention of renal failureHigh-Ceiling (Loop) DiureticsPrototype: furosemide (Lasix)MOA: Acts on the ascending loop of Henle to block re-absorptionADMERapid onset w IV in minutesPO - starts in 1°Therapeutic UsesPulmonary edema of CHF (IV indicated) Edematous states (liver, heart, kidney)HypertensionHypercalcemia Adverse effectsHyponatremia, hypochloremia, and dehydrationHypotension from decreased afterload Loss of volumeRelaxation of venous smooth muscleHypokalemia – esp. with digitalis Symptoms; Nausea, vomiting, general weaknessOtotoxicity – esp. with rapid infusionHyperglycemiaHyperuricemia Use in pregnancyLDL – cholesterol - triglycerides, HDLCalciumMagnesiumDrug interactionsDigoxin Ototoxic drugsPotassium-sparing diureticsLithium Antihypertensive agentsNonsteroidal anti-inflammatory drugsDecreases renal blood flowAce InhibitorsDrugs 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: 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 drugsARBsValsartan Angiotensin 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 Calcium Channel BlockersNormal 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 blockersPrototypes:Verapamil [Calan, Isoptin, Verelan]Diltiazem [Cardizem, Diltia XT]MOA / TEPeripheral arterial dilation, arterial pressure, coronary perfusion, blockade at SA & AV nodes HR, force of contraction aiding in the relief of:Angina pectorisEssential hypertension –1st line for chronicCardiac dysrhythmias – A-flutter / fib / SVTMigraineAdverse Effects of verapamil / diltiazem Constipation – can be severe in elderlyDiltiazem not as constipatingDizziness, Facial flushingHeadacheEdema of ankles and feetGingival hyperplasiaBradycardia Heart block & stroke volumeContraindications? Some one who has a heart block alreadyAnticoagulantsPrototype: 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) B12Prototype: Vitamin B12 (Cyanocobalamin)Stored in liverMOA / Uses: provide B12 for synthesis of DNA to alleviate macrocytic anemia, neuro damage, and GI disturbances from deficiencyADMENot given IV= anaphilaxis A: requires intrinsic factor (IF)E: very slow – stored ______________Routes: PO, IM, deep SubQ, IntranasalAdverse effectsSecondary hypokalemia Dietary sourcesTreatment regimenLifelong if ? IF (intrinsic factor)IronIron Deficiency: Oral TreatmentPrototype: Ferrous sulfate (Feosol)MOA / TE: DOC -restores iron for production of hemoglobin to prevent or relieve symptoms of microcytic hypochromic anemiaADMEAbsorbed from 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 Iron Deficiency: Parenteral TxPrototype: 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 epi, available 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 daysIV – test dose25 mgMonitor 15 minAvoid IM site if possibleTumorsGreatest risk of anaphylaxisProlonged pain / discoloration at siteINSULINS – SHORT, INTERMEDIATE, LONG-ACTINGIn Short:When mixing – draw short-acting first, refrigerated, do not freeze (breaks down cell wall), pre-filled syringes – needle up, agitate before injectionIn Detail:InsulinsHuman Recombinant DNA and analogsBeef and pork (’98 & ’05 respectively)Types: natural and modifiedProlonging effectAttach to protein or alter moleculeMOST are manufactured as clear / colorless suspensionsDiscard if abnormalWhen mixing – draw short-acting first (fast- acting)SubQ, IM, PO, Off label IV Only form also available as U-500SHORT DURATION – RAPID ACTING, not for IV useInsulin lispro (Humalog)Can mix with NPH – right before meal or after mealInsulin aspart (NovoLog)Can mix with NPH – 5 to 10 minutes before mealSHORT DURATION – SLOWER ACTING Regular insulin (Humulin R, Novolin R)30-60 mins before a meal, can be given all routes: subq, IM, PO, off label IV (only one for IV use), only form also available as U-500 (has it’s own syringe), added to TPN to help pt metabolize sugarINTERMEDIATE DURATION Neutral Protamine Hagedorn (NPH) insulinNot intended for postprandial hyperglycemic control, only one that is cloudy – all others are clearCan mix with other drugs or insulins Insulin determir (Levemir)Cannot mix with other insulinsLONG DURATION Insulin glargine (Lantus)Cannot mix with any others, 24 hr durationAE –hypoglycemia (too much insulin): tachycardia, sweating, nervousness. Lipodystrophies (atrophic-hypertrophic), rotation of sites prevents lipodystrophiesTreatment of hypoglycemia – must be rapid! – if conscious: OJ, sugar cubes, honey, corn syrup, non-diet soda, glucose tabs. If unconscious: IV glucose (D50W) or glucagonAdministrationSubcutaneous injectionSyringe and needlePen injectorsJet injectorsInhalationExubera – off market Oct ‘07Subcutaneous infusionPortable insulin pumpsImplantable insulin pumpsIntravenous infusionD/D – hypoglycemic agents, alcohol, hyperglycemic agents (thiazide diuretics, glucocorticosteroids, sympathomimetics-stimulates adrenalin which produces sugar for ForF), beta blockers (slows HR and drops BP-masks sx of hypoglycemia)Antidote – Glucagon: exact opposite of insulin, may see response in 20 mins in unconsious pt, no effect on hypoglycemia of starvation (no sugar to call out), relaxes GI smooth muscleInsulin StorageRefrigeratedDO NOT FREEZECurrent use vial – room temp ok for 1 mo.Pre-filled syringesRefrigerateNeedle upAgitate before injectionTherapy RegimensTight control- produces better management – people who are checking their sugar many times a day??Conventional Therapy (look up) – none at lunch or bedtimeAdverse EffectsHypoglycemia (less than 50 mg/dL)Acute -tachy, palpitations, sweating, nervous, Slow – HA, drowsiness, fatigue, confusionOverdose (of insulin)Food, GI, ETOH, Exercise, and childbirthTreatment – must be rapid!If conscious: OJ, sugar cubes, honey, non-diet soda, glucose tabs, corn syrupIf unconscious: IV glucose (D50W) or glucagonLipodystrophies (atrophic – hypertrophic)D/DHypoglycemic agentsOral hypoglycemicsETOHHyperglycemic agentsThiazide diureticsGlucocorticosteroids (“sweet poison”)SympathomimeticsBeta blockersDelay awareness of hypoglycemia and impairs glycogenesis===========================================================GlucagonExact opposite effect of insulinIn unconscious – may see response in 20 min.No effect on hypoglycemia of starvation Relaxes GI smooth muscleUse in endoscopyAntihistamines: 1st Generation dyphenhydramine [Benadryl] H1 Antagonists (classic antihistamines)MOABlockers (1st Gen)Selectively bind to histaminic receptorsCan also bind to nonhistaminic receptor (muscarinic)Therapeutic Effects (TE)Vessels (If blocks histamine, then ?)Capillaries (If blocks, then ?) shrink,, not ngorged- edema goes downSensory nerves (If, then) – itching reliefMucous membranes (If, then) drynessCNS Therapeutic doses (If, then) - sedationOverdose – stimulation, seizures – esp. in youngOther: relieve N & V, motion sicknessClinical usesMild allergies, seasonal rhinitis, acute urticaria, allergic conjunctivitis, mild transfusion reactionsSome block muscarinic & H1 receptor sites – useful for motion sicknesspromethazine [Phenergan] and dimenhydrinate [Dramamine]Insomnia (diphenhydramine [Benadryl])Adverse EffectsCNSSedation = to excess ETOH (If this, then?)Dizziness, lack of coordination, confusion; take at bed time, don’t drive, elderly and children need to be cautious. Paradoxical: insomnia, excitation, tremors, convulsionsGIN, V, Diarrhea / constipation, loss of appetiteDry mouth, throat nasal passages, thickened secretion, urinary hesitancy, constipation, palpationAnticholinergic effects Cardiac Dysrhythmias w some 2nd Gen.Torsades de pointes, V-fib terfenadine [Seldane] & astemizole [Hismanal]Contraindications – third trimesterPrecautions: asthma ( bronchio constrictions, antihistamines thicken secretion..), children/elderly, urinary retention, HTN, OA(open angal) glaucoma, prostatic hypertrophy D DETOH, barbs/benzos/ opioids ToxicitySxms similar to atropine poisoning (anticholinergic), hyperpyrexiaCan lead to death in children via excitation, hallucinations, convulsion, coma, CV collapse, death.Tx: remove and support – may use charcoal to bind with it followed with cathartics to remove itCox InhibitorsCox 1 vs Cox 2 (sometimes referred to as prostaglandin) Cox 1 Enzyme Onlyhelps prevent gastric ulcers(protects stomach)causes platelet aggregation (bad for heart disease) Cox 1 & 2 Both maintain renal Function, dilation and perfusion Cox 2 enzyme onlyCauses inflammation (bad for RA Causes feverCauses pain Causes feverCOX InhibitorsAnti-inflammatory properties NSAIDs – Non steroid anti-inflammatory drug 1 generation drugs (Asprin)inhibits both cox 1 and cox 2 enzyme 2nd generation (celebrex)Is selective to only inhibiting the effects of COX 2 enzymeNon- anti-inflammatory propertiesAcetaminophen (Tylenol) is a cox inhibitor, but does not have anti-inflammatory propertiesTylenol (2nd generation properties but Anti-inflamtoryMOA - Inhibits prostaglandin synthesis in CNSUses – pain, fever – not anti-inflammatoryBenefits – ? GI (maintain protection in stomach( no ulcer development) ,on bleeding(doesn’t effect platelets), renal impairmentAdverse effectsHepatotoxicity Tylenol has its main affect in the liver…(4g/d)ETOH connection (g/d) lower Tylenol intake Acute Toxicity – Sxms 24-72 h post ODN,V, D, sweating, abd. pain, liver failure, comaMucomyst the antidote for Tylenol overdose if given within 24h Aspirin acetylsalicylic acid (ASA NSAIDs – Non steroid anti-inflammatory drug 1 generation drugs Non-selective(COX Inhibitor of both COX 1&2) MOA / TE / UsesAnalgesic, antipyretic, anti-inflammatorySuppression of platelet aggregation(irreversible for * days, life of plateletTreat / prevent Ischemic stroke (makes blood flow smoothly) not hemorrhagic stroke, TIA, MIs (acute & old), anginas, addition to angioplasty & revascularization Dysmenorrhea (cramps) Cancer preventionPrevention of Alzheimer’s disease, not in treatmentAn initial DOC for RA and juvenile arthritisDose related to use! ADMERapidly absorbed orally, slower rectallyHalf-life (2 h to 20 h)Distributes to all body tissues – pregnant? Contraindicated in pregnancyExcretion pH dependent (increase pH increase excretion 4x)Side effectsGastric distress, heartburn, nauseaAdverse effectsGastrointestinal – (occult (hidden) and overt)BleedingRenal impairment – Signs?acute/reversible – Na+/H2OPre-existing condition dependentCox1 is a broud specrum and 1st generation Imparest the benefit of the cox 2 side, whch means can damage the kidneysSalicylism (over dose of aspirin)– acid/base – tinnitis (symptom of ringing in the ears) often irreversibleReye’s syndrome( liver failure) in children, so contraindicated in use of children.Hypersensitivity – asthma –ranges from rhinorrhe to shockContraindicationsPUD & Bleeding disordersHypersensitivityExtreme caution in pregnancyDDAnticoagulants & other NSAIDsGlucocorticoids supress the effects of prostoglandin.. (gastric ulcertion)Ibuprofen – impairs cardioprotective propertiesAcute PoisoningLD (lethal dose) adult = 20-25 g - LD children = 4 your body becomes acidicSxms Resp excitation depression Hyperthermia, stupor, coma, deathTreatmentSupportive, charcoal, alkalinization of urine to help ecrcretion , and dialysis2nd Gen Selective Cox InhibitorsPrototype: celecoxib (Celebrex)Benefits –lower GI bleeding riskUses OA, RA, Acute pain, dysmenorrhea Familial adenomatous polyposis NOT cardioprotective Adverse effectsDyspepsia, Abdominal painRenal toxicityGI ulceration / bleedingSulfonamide allergyAcetaminophen (Tylenol) is a cox inhibitor, but does not have anti-inflammatory propertiesMOA - Inhibits prostaglandin synthesis in CNSUses – pain, fever – not anti-inflammatoryBenefits – ? GI, bleeding, renal impairmentAdverse effectsHepatotoxicity (4g/d)ETOH connection (g/d) lower Tylenol intake Acute Toxicity – Sxms 24-72 h post ODN,V, D, sweating, abd. pain, liver failure, comaMucomyst the antidote for Tylenol overdose if given with in 24 h Glucocorticosteroids (immunosuppressant) in Non-endocrine Diseases PhysiologyArtificial nearly identical to natural, if you use you loseMetabolic effectsBreakdown of fats, proteins, carbs - glucoseRobs proteins for glucose productionFats redistributed long-term to “moon” faceCardiovascularLow levels – cause permeable vessels, dilated vessels, with hypotensionIncrease RBCs and PMN (polymorhonucular) LeukocytesDecrease Lymphs, Eosins, basophils, and monocytsEffects during stress - define Glucocorticosteroids are produce increasing amount during stressLarge qty glucocorts / epi secretedIf inadequate sreroids – circulatory failure Effects on water and electrolytesAldosterone effect – increased Na+,? H2O, decreases K+; hypokalemia High doses – impair intestinal calcium absorption (hypocalcemia)Respiratory system in neonates – RSDInhibits prostaglandins, leucotriens, and histamines hinder phagocytes and lymphocytes in the inflammatory response TE / UsesAnti-inflammatory and immunosuppressant effects (high doses)Rheumatoid arthritis (Autoimmune disorders)Systemic lupus erythematosus Inflammatory bowel diseaseMiscellaneous inflammatory disordersAllergic conditionsAsthmaDermatologic disordersNeoplasms – toxic to malignant lymphocytesStimulates appetiteSuppression of allograft rejectionPrevention of respiratory distress syndromeAdverse effectsAdrenal insufficiencyOsteoporosis (resorption, rebuilding & calcium)monitor for bone loss, use calcium and Vit D supplementcommon can cause hyperglycemiaInfection – esp. Pneumocystis Carinii Pneumonia (PCP)Glucose intolerance, can cause DiabeticMyopathy Fluid and electrolyte disturbance, monitor for fluid excess(crackes, weight gain edema Growth retardationPsychologic disturbancesCataracts and glaucomaPeptic ulcer disease, Do take wth asprin, choose tylenolIatrogenic Cushing’s syndromeUse in pregnancy and lactationDDInteractions related to potassium loss, whatever Na increases, K decreasesNon-steroidal anti-inflammatory drugsInsulin and oral hypoglycemic Vaccines. Won’t get the inflammation response, or the immune response you looking forAdrenal suppressionAtrophyStress & “flat” response (Alt. day Tx)Glucocorticoid withdrawalDon’t stop taking immunosupreants abruptlyTaper over 7 daysSwitch from multiple doses to single dosesTaper the dosage to 50% of physiologic valuesMonitor for signs of insufficiency, remember if you use the drud the adrenal gland normal exretion of this is limited.. natural soiuHypoTN, hyoglycemia, myalgia, arthralgia & fatigueDrugs Affecting Calcium Levels and Bone MineralizationCalcium Physiology Critical to skeletal, nervous, muscular, and cardiovascular systemsBody stores – review, bones store 99% of caliumAbsorption – occurs in the gut with PTH & vitD Glucocorticoids – effect? Impair absorbtion in the gutExcretion in kidneysCalcitonin augment (Boost) calcium eliminationVitamin D, calcitonin, and parathyroid hormone are essential in the metabolism of calcium.Hypercalcemia: Drug Therapy Usually asymptomatic (don’t know)Causes: PTH, Vit D toxicity, thiazides (diuretic)Drug TherapyPromote urinary excretion – furosemide & IV saline Decrease mobilization from bonecalcitonin, bisphosphonates, inorganic phosphates, gallium nitrateDecrease intestinal absorptionglucocorticoids Hypocalcemia: Drug TherapyIncreases neuromuscular excitabilityCauses: PTH, Vit D & Ca++Clinical presentationTetany, convulsions, and spasm of the pharynx TreatmentTreatmentIV Calcium (calcium gluconate)Vitamin DDrugs for Ca++ Disorders: (IV bisphosphanates)Prototype: Alendronate (Fosamax)MOA – TE – UsesStructural analogs of pyrophosphate of bone incorporated into bone and inhibit resorption by decreasing osteoclast activity and used to treat osteoporosis, glucocorticoid induced osteopororis, Paget’s, and hypercalcemia of malignancy. ADME - CRITICAL! Bioavailability drops if taken with food (0.7%) or drinks other than water (60%)! Remains for decades once incorporatedNever to be taken with cofee or tea, food only with waterAdverse effectsEsophagitis – implications usually with IV adminOcular inflammationOsteonecrosis of the jaw (ONJ) – mostly IVExpectorantsPrototype - guaifenesin (Mucinex)MOA / Use – increases flow of respiratory tract secretionsMakes cough more productiveSympathomimetics (Decongestants) mimics the sympathetic (sympatheic sytem) fight or flightPrototype: phenylephrine (Neo-Synephrine)Action / Uses - Reduce nasal congestion via ?Topical - rapid and intenseOral - prolonged, moderate, systemic effectsAlso used in sinusitis and coldsAdverse effectsRebound congestion depends if allergin is still aroundCNS stimulationCardiovascular caution HTNHemorrhagic stroke w phenylporpanolamine Abuse (pseudoephedrine and ephedrine)Nasal sprays2 – 3 sprays every 4 hours needed – not to exceed 5 consecutive daysPseudoephedrineProton Pump Inhibitors Prototype - omeprazole (Prilosec)Action / Uses – suppress secretion of gastric acid Irreversible - days - up to weeks after cessation; Superior to H2RAsAdverse effectsHA, diarrhea, N & V; Long term may increase risk of CAADME – give 30 min before meal – once dailyD/D, D/FReduced absorption of atazanavir, ketocanazole and itracanazole – NOT recommended concurrently with atazanavirFamotadine (Pepcid)For heartburn, acid indigestion, sour stomachCut dose in renal compromise/ failureNo antiandrogenic effectsNo effect on hepatic metabolism of other drugsHistamine2-Receptor AntagonistsPrototype: cemetadine (Tagamet)First choice for gastric / duodenal ulcersAction / Uses: Promote healing through acid reductionGERD, Aspiration Pneumonitis in obese & gyne prior to anesthesiaAdverse effectsLow incidence of gynecomastia, reduced libido, impotence, CNS depression / excitement, pneumoniaD/ DInhibits hepatic drug metabolism – therefore? Major Drugs of concern – warfarin, phenytoin, theophylline, lidocaineBulk-formingPrototype(s): methylcellulose, psyllium (Metamucil)Action / UseBehave like dietary fiber – nonabsorbable – swell to form viscous solution / gel and softening fecal mass and increasing transit.Temp relief of constipation, diarrhea, irritable bowel, ostomies Adverse effectsEsophageal & intestinal obstruction if not enough fluid ?(If this, then?)StimulantsPrototype(s): bisacodyl (Dulcolax), senna (Senekot)Action / Legitimate UsesDirectly stimulate gut motility, increase secretion of water and ions into intestine, and reduce water and electrolyte absorption.Uses: Treatment of (1) opioid-induced constipation and (2) slow transit constipationDosage: related to formulation administeredTake bisacodyl no sooner than 1 hour after ingesting milk or antacids – do not crushAdverse reactionsBowel rupture can occurCephalosporinsPROTOTYPE: Cefalexin (Keflex) MOA/UseCephs are most widely used of antibiotics (22)Beta-lactam antibioticsSimilar to penicillin – bactericidalADMEUsually given parenterally Renal excretion (Probenacid)Adverse effectsHypersensitivity & anaphylaxisThrombophlebitis AAPMC fr. C-Diff (Antibiotic-Associated Pseudomembraneous ColitisThree agents (cefmetazole, cefoperazine, cefotetan)PTT, Bleeding, Pain at injection siteETOH intoleranceDDProbenacid keeps drug in system longer b/c it impairs excretion from the kidneysETOH intoleranceInduce a state of alcohol intoleranceIngestion of alcohol- disulfiram-like reaction could occur Must not consume alcohol in any formDisulfiram/antabuse First generationCefazolin [Ancef]Highly active against gram + bacteriaMost active of all cephalosporins against staphylococci and nonenterococcal streptococciBe given only to patients with a history of mild PCN allergyEmployed widely for prophylaxis against infection in surgical patientsHave only modest activity against gram – bacteria and don’t reach effective concentrations in CSFAs effective as the newer drugs, less expensive, have more narrow spectrum Second generationCefaclor [Ceclor]Enhanced activity against gram – bacteriaIncrease is due to a combo of factors:Increased affinity for PBPs of gram – bacteriaIncreased ability to penetrate the gram – cell envelopeIncreased resistance to beta-lactamases produced by gram - organismsNone is active against Pseudomonas aeruginoseDon’t reach effective concentrations in CSFUsed against pneumonia caused by H. influenzae, Klebsiella, pneumococci, staphylococciOral is useful for otitis, sinusitis, RTI Third generationCefoperazone [Cefobid]Increased resistance to beta-lactamases, considerabley more active against gram – aerobes than 1st & 2nd generationSome have important activity against P. aeruginosa, other lack activityReach clinically effective concentrations in CSFDrug of choice for meningitis caused by enteric, gram negative bacilli Fourth generation – β-lactamase resistantCefepime [Maxipime]Highly resistant to beta-lactamasesActivity against P. aeruginosa equals that of ceftazidimePenetration to CSF is goodCSF Distribution Curve, & Spectrum of CephsSpectrum, CSF, and Betalatamase susceptibilityHalf lives of cephs range from 30 min to 9 hrs Only 3rd and 4th agents achieve CSF concentrationsMost eliminated by kidneysMany must be absorbed by IM or IV, only 12 can be given orallyMonobactam PROTOTYPE: Vancomycin [Vancocin] **Always try another drug before you use Vanco (used to be this way, but now MRSA is becoming more widespread) Used to fight MRSA (very hard to fight if the infection is in the bones) MOA / UsesDisrupts cell wallUsed in severe infections and DOC MR s. aureus or s. epidermisUsed to treat C. Diff ADMEPoor oral absorptionPoor CSF Adverse effectsOtotoxicity (ear) – esp. when taken w/ othersIf a patient is on Vanco, you need to check patient’s hearing (signs: tingling, ringing in ears, hearing loss) – sometimes reversible, but not alwaysThrombophlebitis – dilutecan cause painful infection & possibly a clot (check IV site regularly – ask patient if it hurts, look for swelling, palpate area)AllergyRed Man Syndrome w rapid infusionTetracyclines PROTOTYPE: tetracycline (Sumycin)MOA / UsesInhibits protein synthesis – broad spect. used in rickettsial disease, Chlamydia trachomatis, lyme disease, acne, PUD, and peridontal diseaseADME absorption w Ca+, Fe-, Mg++, laxatives, antacids, milkAdverse effectsGastrointestinal - esophagealPrevention? Dosing? Meals?Effect on bone and teeth, will become weak and brittle Superinfection - AAPMC Hepatotoxicity Renal toxicity – prevention/contraindication Bone & teeth will become weak and brittle Contraindicated in patients who are renal impaired (patients need to take drug with lots of water) Be careful: congested heart failure patients sensitive to lots of waterPhotosensitivity – preventionSunscreen & limit sun exposure while on drugPregnancy & children under 8Preparations, Dosage, AdministrationSystemic infection- admin. Intermittent infusion over 60+ minUsual adult dosage: 2 mg/day in divided doses at 12 or 24 hr intervalsChildren dosage: 22 mg/kg/day in divided doses at 6 or 12 hr intervalsRenal impairment- dosages reducedPeak blood levels should be drawn at 1.5 hr to 2.5 hr after completing IV infusion- normal = 30 to 40 mcg/mLOral- treatment of antibiotic associated pseudomembranous colitisAdult dosage = 125 to 500 mg every 6 hrChild dosage = 11 mg/kg every 6 hoursRenal impairment- dose not need to be decreased b/c it is not absorbed in GI trackChloramphenicol [Chloromycetin]Broad spectrum antibioticInhibits protein synthesisUses Only for life-threatening infections for which safer drugs are ineffective or contraindicated Adverse effectsReversible bone marrow depressionyour body won’t make as many RBCs, WBCs, and platelets – turns into aplastic anemia (without)Aplastic anemia – potentially fatalSpecial Concepts r/t AnitmicrobialsSelective toxicityAbility to target without harming hostSusceptibility (1+2+3+4+)Sensitive<1ProphylaxisNeutropenia, Surgery, Endocarditis (valvular heart disease or artificial valve have to have prophylactic antibiotic)Combination TherapyUse 2 drugs to achieve a purposeMisuse – non-specific fevers, viruses (antibiotic not indicated but if immunocompromised might use prophylactically)Aminoglycosides: BackgroundResistance is beginning to limit useGentamicin – cheaper but commonly used Used to treat local bugs20 diff aminoglycoside-inactivating enzymesInactivated by 20 enzymesReserve amikacin (Big Guy)Bactericidalconcentration dependentMore you get the more it killsPost-antibiotic effect – several hoursNOT effective against anaerobes (not used in gut)Gentamicin (Garamycin)MOA / Use: narrow spectrum for gram- bacilli – esp. pseud. aerugenosa, E. coli, Klebs., Serratia ADME:Poor CSFNot absorbed orally (so? Typically IV)High levels in gut so will kill gut bugsToxicity w/ wound irrigationHas to have peak & troughAbsorbed into system when used to irrigate woundBinds tightly to renal tissueMonitor closely and reduce dose for renal compromisedExcretion primarily renalDosage varies widely (0.5 mg/kg to 25 mg/kg)Adverse EffectsOtotoxic r/t excess trough levels – sensory hairsWant trough to go below the trough line between doses to keep from being ototoxic HA, N, vertigo then high-pitched tinnitis (Action? Stop the dose first then call Dr)Nephrotoxic r/t Total cumulative doseATN (acute tubular necrosis) (proteinuria, casts (slough), BUN, Creatinine Elderly & youngNeuromuscular blockadeHypersensitivity & blood dyscrasias (rare but can happen)DD p998 PCNs, Cephs, Vanco used in comboPCNs inactivate – schedule issue?Ethacrynic Acid – potenciate the ototoxicity Other nephrotoxics Skeletal Muscle relaxantsResp arrest Special ConcernsNeomycin most nephrotoxic Not used IM, IVPO = sterilize gutTopically usedScheduling once daily – Safer?Post-antibiotic effectWashout – esp. in vestibule and kidneysTypically only measure trough – up to 1hr prior to next dose – level should be ?Antifungals Systemic mycotic (fungal) infectionsOpportunistic – host is immunocompromised/debilitated pts Candidiasis Colonized on you alreadyWarm moist areasThrush in mouthCombination therapies (antifungal, antibiotic, antifungal)aspergillosis, cryptococcosis, Non-opportunisticblastomycosis, histoplasmosis, coccidioidomycosis Superficial mycotic infectionsCandidiasis Dermatophytes Amphotericin B [Fungizone] MOA / TEBroad spectrum antifungal agent binds to ergosterol component of fungal cell wall and increases permeability. DOC for most progressive, potentially fatal systemic mycoses Use when bug is going to kill the personHighly TOXIC to people ADMEHighly toxic (sterols)Breaks down bugs sterols along with personsPoor GI absorption - SLOW IV USE ONLYPoor CSFWatch pt carefully Adverse effects – almost 100% - varyingPhlebitis so give slow Fever, chills, nausea (all common)– pre-treat w benadryl / acetaminophen to reduce effects of side effectsNephrotoxicity – residual if 4 g/day, 1 L NS, Monitor q 3-4 daysTreat c NaCl Monitor urine for protein & serum creatnine Hydration status will change BUNHypokalemia Monitor KBone marrow suppressionDecreased CBC DD: nephrotoxics – flucytosine Drugs for Superficial MycosesDermatophytic infections (e.g., ringworm) Tinea pedis, tinea corporis, t. cruris, & t. capitis Griseofulvin (Grifulvin V)MOA / TESuperficial mycoses only – inhibits fungal mitosis – incorporates into keratin Adverse effectsTransient headache, rash, GIContraindicated in hepatocellular diseaseLiver intensiveClosely monitor if have liver diseaseDDDecreases warfarin AntiviralsDilemmaMutate readily c resistence Live inside the cell nucleusHarder to treat because harder to targetTypesHSV (Herpes-simplex) more sensitive to anti virals Genitalia, mouth, face (HSV-2)VZV (Varicella Zoster) moderately sensitive Chicken pox – ShinglesCMV (Cytomegalovirus) less sensitive = more resistance Prototype: Acyclovir [Zovirax]MOA / TE: Suppress synthesis of viral DNA and is useful in treating HSV1,2 & VZV – no cureAdverse EffectsIntravenous: reversible nephrotoxicity, phlebitisInfuse slowly – hydration – during & 2 hr afterOral: GI, vertigoTopical: stingingNursing ImplicationsResistance – type of clientsAll pt on drugs long termHIV – trying to develop new drugs to decrease resistanceGoal to get viral load low (SVR/VL)If severely immunocompromised then IV therapy is indicatedIV indicated for oral lesions in STI controlNot mean that you are safe if you take the drugHerpes can colonate in other areas besides genitals (can be legs too)Condom not always keeping you safeNo sexual contact during an outbreakTreatment for VZV in elderly and children (w/in 24 hr)ONLY give po (low availability), can be used topically or IV (double check)NO IV bolus, NO IM, or NO SubQ injectionsValacyclovir [Valtrex] – prodrug that increases oral bioavailability (alone not available to use) by 55%Without regard to mealsInterferon alfa (Peg-Intron)immune modulatory, antineoplastic, antiviralMOA / TEBlocks entry of virus, synthesis of viral m-RNA and proteins, and viral assembly. Tx of chronic Hep B & CHep B - vaccinateADMEPegylated - makes drug longer actingOnly parenterally (subQ)Adverse EffectsFlu-like (fever, myalgia, HA, fatigue) & significant depressionLong/High dose – thyroid dysfunction, heart damage, bone marrow suppressionAlopecia (lose hair), GI, injection site pain, bruisingRibavirin (Rebetol)MOA unclearUsed with Interferon A - together are DOC for Hep C (HCV). Therapy 24 to 48 weeks. Goal is SVR – sustained virologic response (loss of detectable viral RNA)Lower the viral load = is goalAdverse effectsHemolytic anemiaBroken RBCs= increased Fe levelsTrash can clot vesselTeratogenic (Category X) – two forms of BCDosage based on weight ................
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