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Flashcards in Additional Important Drugs Deck (39)
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CLASS= synthetic analog of endogenous polypeptide hormone somatostatin (produced by the delta cells of the pancreas)


MOA= binds to somaostatin receptors on carcinoid tumors to decrease amount of serotonin released from tumor & decrease vasoactive amines; also inhibits release of GH, VIP, glucagon & insulin; selective vasoconstriction of splanchnic vasculature to redistribute blood flow (tx. esophageal varices)


Pharmacokinetics= 65% PB; onset- rapid; peak- 2 hrs; E1/2- 2 hrs; liver metabolism & excreted 30% unchanged in the urine


SE=decrease glucose tolerance, hyperglycemia, ecreased GI motility, N/V, bradycardia & heart block possible w/ IV boluses


CI= hypersensitivity; caution in DM (exacerbation)

Dose= carcinoid crisis- 50-100 mcg/hr; 25-200 mcg bolus PRN; 25-50 mcg/hr for bleeding varices





MOA= prodrug that irreversibly inhibits H+/K+ ATPase proton pump in gastric parietal cells thereby decreasing gastric acid secretion


Pharmacokinetics= 95% PB; onset- 1 hr; DOA- 72 hrs; metabolized in the liver by CYP450 to inactive metabolites


SE= Crosses BBB=HA, confusion, agitation, dizziness; N/V/D, abdominal pain


CI= hypersensitivity, prolongs the metabolism of diazepam, warfarin, Dilantin


Dose= 40 mg IV



CLASS:   novel modified cyclodextrin molecule- arranged in a ring shape

MOA:  Cycodextrin with 8 sugars arrange in a ring, with a hydrophobic cavity which encapsulates and forms complexes with nondepolarizing NMB rocuronicum and vecurionium,. Has a very high association rate and low dissasociation rate. Can be used to reverse even a deep bockade (1-2 Post tetanic contraction (PTC)

PK: Vd 30L/kg; E1/2 T= 2 hours; metabolism of sugammadex is very limited; excreted predominately unchanged by the kidneys. 

S/E: Hypersentiviity, inadeqaute dose can lead to delayed manifesatation of residual block; bradycardia, N/V, hypotension, pain, HA

CI: Renal impairment (avoid in pt with CrCl <30 mL/.min); known hypersensitivity, safety and FDA approval not established for children under 17 (recently ok'ed 2-17 yo). Hormonal contraceptives can be less effective; contraceptive  back up needed for 7 days

DOSE:  Dependent on level of blockade

  • 2mg /kg recommended if 2/4 twitches present on TOF
  • 4mg/kg recommneded if 1-2 PTC twitches and no twitch responses to TOF stimulation (deep blockade)
  • 16 mg/kg with profound blockade induced by RSI dose of Rocuronium (1.2 mg/kg)



CLASS= bypyridine inotropic/vasodilator agent with phosphodiasterase inhibitor activity


MOA= inhibition of PDE III, which inhibits the degradation of cAMP causing increase intracellular Ca2+ which increase contractility; inhibits the degradation of cGMP causing A&V vasodilation and thus decrease preload & afterload; combined effect cause increase inotropy &decrease  SVR = increase CO; decrease PVR- mild bronchodilator


Pharmacokinetics= onset- 5-20 min; peak- 5 min; E1/2- 2 hrs; metabolized by CYP450 in liver & 80% excreted unchanged in the urine


SE= arrhythmias, mild tachycardia, hypotension, angina, HA, hypokalemia, tremors


CI= aortic or pulmonic valve disease, acute MI, no with digoxin, decrease dose in RF


Dose= 50 mcg/kg IV over 10 min then 0.5 mcg/kg/min gtt



CLASS= dihydropyridine CCB


MOA= binds to the alpha subunit of the L type voltage gated Ca2+ channels in the inactive or closed state & blocks the inward flux of Ca2+ causing preferential peripheral & CA vasodilation to decrease SVR & BP w/ minimal effects on AV & SA conduction


Pharmacokinetics= 90% PB (highly); onset- rapid, E1/2- 3-7 hrs (prolonged in elderly); metabolized by the liver & renal clearance 70% & rest is cleared in bile


SE= reflex tachycardia, flushing, constipation, parenthesis & skeletal muscle weakness, vertigo, HA, potentiate NMB, peripheral edema


CI= abrupt cessation has been associated with CA vasospasm, preexisting hypotension, CHF/HF, renal dysfunction, dantrolene, caution w/ BBs


Dose= 5-15 mcg/kg IV



CLASS= class III K+ channel blocker antiarrhythmic with class I, II & IV properties


MOA= blocks Na+/K+/Ca2+ channels prolonging AP duration & repolarization - decrease general excitability; slowing AV node conduction; alpha & beta adrenergic antagonist; can use for refractory VT, vfib, afib, SVT; 1st line treatment for VT & VF when resistant to defibrillation


Pharmacokinetics= high PB; large Vd; E1/2- 30-100 days; CYP450 hepatic metabolism to active metabolite- N desmethyl amiodarone (DEA) & biliary excretion


SE= hypotension, arrhythmias, AV block, prolonged QTI, torsades de pointes, pulmonary fibrosis, liver toxicity, nephrotoxicity, corneal deposits, photosensitivity, nightmares, thyroid abnormalities, CYP450 inhibitor reducing the clearance of digoxin, warfarin


CI= AV block, iodine allergy, patients on ßB, CCBs, lidocaine, halothane


Dose= 150-300 mg bolus then 1 mg/min x 6 hrs then 0.5 mg/min x 18 hrs



CLASS= non-dihydropyridine  (phenylalkamine) CCB & class IV anti-arrhythmic. most potent


MOA= binds to the alpha subunit of the L-type voltage gated Ca2+ channel in inactive or closed state & blocks the slow inward flux of Ca2+ into myocardial & VSM cells. It is more selective for Ca2+ channels in the heart, thus decrease SA & AV node conduction & decreaseHR & contractility & conduction velocity; also a CA & systemic vasodilator; tx SVT, afib, aflutter, prizmentals angina, HTN


Pharmacokinetics= 90% PB (highly); onset- IV 15 min, PO 30-45 min; E1/2- 6-8 hrs; liver metabolism & excreted 70% unchanged in the urine & bile. active metabolist norverapamil


SE= hypotension, bradycardia, AV block, CV depression, esp with IA’s, AV block, exacerbates HF, nausea, constipation, syncope, gingival hyperplasia, potentiates NMB, can increase LA toxicity, with dantrolene can cause hyperkalemia and CV collapse


CI= HF/HB (especially when combined with ßB); sick sinus syndrome, acute MI/CHF, contraindicated with dantrolene (increase K+) & ßB (CV depression); can increase digoxin levels, NO in VT; myocardial depressiona nd vasodilation with VA


Dose= 2.5-5 mg IV over 2 min then 5-10 mg IV over 15-30 min to max of 20 mg



CLASS non-dihydropyridine CCB (Modified benzothiazepines) & class IV anti-arrhythmic  (Less CV depression than Verapamil)


MOA= binds to the alpha subunit of the L-type voltage gated Ca2+ channel in inactive or closed state & blocks the inward flux of Ca2+ into myocardial & VSM cells. It is more selective for Ca2+ channels in the heart, thus decreaseSA & AV node conduction & decrease HR & contractility; also a CA & systemic vasodilator; tx SVT, afib, aflutter, variant angina, HTN


Pharmacokinetics= 70% PB (highly); onset- rapid; E1/2- 4-6 hrs; extensive liver metabolism by CYP450 & excreted 30% unchanged in the urine


SE= hypotension, bradycardia, AV block, CV depression (esp with IA’s), exacerbates HF, nausea, constipation, syncope, potentiates NMB, can increase LA toxicity, with dantrolene can cause hyperkalemia


CI= HF/HB (especially when combined with ßB), sick sinus syndrome, acute MI/CHF, contraindicated with dantrolene (increase K+) & ßB (CV depression); can increase digoxin levels


Dose= 0.25 mg/kg bolus over 2 min then 5-15 mg/hr



CLASS= endogenous nucleotide not belonging to a specific anti-arrhythmic class


MOA= binds to A1 purine nucleotide receptors & activates G protein coupled adenosine receptors to open K+ channels & increase K+ currents thus hyperpolarizing cardiac tissue; slows SA & AV nodal conduction (SVT); used to terminate SVT or for diagnosis of VT


Pharmacokinetics= very rapid onset & termination of action; E1/2- <10 sec; eliminated by plasma & vascular endothelial cell enzymes


SE= chest pain, dyspnea, facial flushing, hypotension, asystole, nausea, bronchospasm, excessive SA or AV node inhibition


CI= asthma, AV HB, sick sinus syndrome


Dose= 6 mg rapid IVP then repeat in 3 min 6-12 mg



CLASS= cardiac glycoside


MOA= inhibits Na+/K+ ATP pump causing increase intracellular Na+ & Ca2+ thereby incease contractility & decrease HR through increase PNS activity & decrease SA/AV node conduction; decrease HR, preload & afterload; good for management of afib, a flutter (controls the ventricular rate especially when HF); decrease renal reabsorption of Na+ & works synergistically with CCB & ßB


Pharmacokinetics= low PB; large Vd; onset- 30-60 min; E1/2- 36 hrs; excreted in the kidneys 90% unchanged; decrease dose in elderly


SE= prolonged PRI, ST depression, T wave changes, HB, N/V/D/A, HA, hypokalemia, AV block, abx increase absorption, verapamil, amiodarone & quinidine increase digoxin levels


CI= VF/VT, HB, hypertrophic cardiomyopathy, digoxin toxicity potentiated by decrease K+, decreaseMg2+ & increaseCa2+; caution K+ wasting diuretics; do not use in renal disease


Dose= 0.5-1 mg IV over 12-24 hrs; therapeutic window- 0.5-1.2 ng/ml



CLASS= class IA (intermediate) Na+ channel blocker


MOA= depresses phase 0 of AP by blocking Na+ channels which decrease the rate of depolarization & slows conduction velocity, prolonging repolarization & lengthening refractory period; decrease automaticity; decrease contractility & conduction velocity & cardiac excitability; 1st line treatment for VT; used for tachyarrhythmias (a fib, a flutter, WPW syndrome, stable polymorphic VT, stable monomorphic VT, atrial or ventricular in origin)


Pharmacokinetics= low PB; onset- immediate; E1/2- 3 hrs; metabolized to active metabolite N-acetyl procainamide (NAPA) which has class III action & E1/2- 6-8 hrs then excreted 60% unchanged in urine


SE= hypotension, arrhythmias, N/V/D, myocardial depression, blood dyscrasia, wide QRS


CI= AV block, prolonged QTI, hypersensitivity to procainamide or other amide LA, myasthenia gravis, black box warnings- can cause SLE syndrome, don’t use with life threatening arrhythmias, fatal blood dyscrasias & with myocardial depression


Dose= 1-4 mg/min



Class? MOA? Pharmacokinetics? SE? CI? Dose?

CLASS= benzodiazepine antagonist; imidazobenzodiazepine derivative

MOA= competes with benzos for binding to the GABA-A receptor effectively reversing sedation & ventilatory depression effects; also used for differential diagnosis of coma- has high affinity & specificity for GABA-A receptor

Pharmacokinetics= 50% PB; Vd- 0.5L/kg; onset- 1-2 min; DOA- 30-60 min; metabolized by the liver & excreted in the urine; E1/2- 1 hr; can cause re-sedation b/c of short DOA  may need to re-dose

SE= sweating, HA, dizziness, confusion, euphoria, abnormal vision, N/V, pain on injection; no change in HR, BP, or neuroendocrine response


CI= hypersensitivity, DO NOT USE in seizure disorders


Dose= 0.2 mg IV- wait 2 min then repeat at 0.1 mg q 60 sec to a max of 3 mg



MOA? Pharmacokinetics? SE? CI? Dose?

Naloxone/Narcan- nonselective competitive opioid antagonist @ mu, kappa & delta receptors


MOA= reverses narcotic depressant effects & biliary tract spasm by binding to the mu, kappa & delta opioid receptors to reverse respiratory depression sedation & analgesia


Pharmacokinetics= onset- 1-2 min, DOA- 30-60 min; E1/2- 1 hr; metabolized by the liver to form naloxone-3-glucuronide & excreted in the urine


SE= crosses placenta, HTN, tachyarrythmias, severe pain, N/V, PULMONARY EDEMA, seizures


CI= CHF, pregnancy, opioid dependent patients


Dose= 0.1-2 mg IV q 2-3 min- titrated slowly to decrease adverse effects




CLASS= opioid agonist-antagonist


MOA= Mu antagonist & full or partial agonist at the kappa receptor to help with mild-moderate pain w/o respiratory depression effects; can reverse SOO spasm


Pharmacokinetics= onset- 2-3 min; DOA- 3-6 hrs; liver metabolism


SE= analgesia, sedation, N/V/C, pruritus, urinary retention, dose dependent decrease HR, BP, SVR; dysphoria; low probability of dependence; can reverse respiratory depression in opioid OD


CI= allergy, decrease dose in peds & elderly, caution in hypovolemia, pregnancy


Dose= 0.1-0.3 mg/kg



CLASS= opioid agonist/antagonist

MOA= Mu antagonist or partial agonist; & agonist at kappa

Pharmacokinetics= DOA- 2-4 hrs; liver metabolism

SE= analgesia, sedation, N/V/C, pruritus, urinary retention, dose dependent ê HR, BP, SVR;

CI= allergy, decrease dose in peds & elderly, opioid dependent patients, pregnancy

Dose= 0.01-0.04 mg/kg



CLASS= anticonvulsant/ anti-arrhythmic IB

MOA= decrease neuronal excitability & neurotransmission by inhibiting Na+ & Ca2+ transport across neuronal cell membranes

Pharmacokinetics= 90% PB; onset- 30 min; E1/2- 7-42 hrs PO; metabolized by CYP450- 1st order kinetics <10mcg/ml then 0 order kinetics > 10mcg/ml & excreted in urine; INDUCES CYP450

SE= hypotension, bradycardia, arrhythmias, CNS toxicity, GI irritation, anemia; CYP450 inducer, Stevens Johnson syndrome, hepatotoxicity; increase metabolism of NDMRs & many other rx’s


CI= pregnancy; caution w/ liver failure, porphyria, HB, hypoalbuminemia


Dose= 10-15 mg/kg seizures & antiarrhythmic- 50-100 mg IV



CLASS= non-opioid analgesic, antipyretic, anti-prostaglandin central effect


MOA= NMDA receptor blocker in CNS; blocks substance P in SC; lacks peripheral effects (thus weak anti-inflammatory agent)


Pharmacokinetics= c-max 15 min; max fever reduction 30 mins; PO peaks 30-60 min; IV higher peak effect than PO; conjugated & hydroxylated in liver with little excreted unchanged in the urine


SE= renal toxicity b/c metabolites can accumulate; OD= liver failure (depletion of glutathione), ulcers, can impair platelet function


CI= liver & renal disease, hepatitis, alcoholic cirrhosis ( decrease dose)


Dose= 1g IV over 15 min q 4-6 hrs; 325-650 mg PO- not to exceed 4g/day



CLASS= short acting ß2 agonist with 2 isomers R & S (R more affinity for B2; S more affinity for B1)

MOA= acts directly on ß2 receptors coupled to G proteins causing an increase cAMP  causing bronchial SM relaxation (interferes with myosin light chain kinase in SM); increase clearance of mucus by action on the cilia; inhibits mediator release from the mast cells


Pharmacokinetics= onset- 5 min; DOA- 4 hrs with symptom relief up to 8 hrs; E1/2: 4 hrs; hepatic metabolism with 30% excreted unchanged in the urine


SE= (Most r/t systemic absorption) tremors, vasodilation, reflex tachycardia, hyperglycemia, Hypokalemia, Hypomagnesaemia (increase Doses lose selectivity)


CI= hypersensitivity, additive bronchodilatory effect with IAs, caution in CAD (increase HR), caution in DM (increase BG)


Dose= 100 mcg/puff; 2-4 puffs q 4-6 hrs or 2.5-5 mg via neb q 4 hrs



CLASS = anticholinergic, quaternary amine; salt derivative of atropine

MOA= inhibits cGMP by competitively inhibiting the effects of ACh at the muscarinic (M3) receptors causing bronchodilation & decreased mucus secretion, increase PNS activity

Pharmacokinetics= onset- 30-90 min; DOA- 4 hrs; partially metabolized by ester hydrolysis & excreted in the urine

SE= decrease secretions, dry mouth, decrease GI motility, N/V, urinary retention, tachycardia, anaphylaxis, arrhythmias

CI= hypersensitivity, GI/GU obstruction, myasthenia gravis, caution in glaucoma

Dose= 40-80 mcg/puff MDI, rinse mouth; 2-4 puffs 2x/day nebulizer



CLASS = highly sulfated glycosaminoglycan (anticoagulant)


MOA= activates antithrombin III & increase inhibition of thrombin & factor Xa by 1000 fold, thereby decreasing clotting & preventing the conversion of fibrinogen to fibrin; used for DVT prophylaxis, treat PE; ACS, maintain patency of IV catheters


Pharmacokinetics= onset- rapid; E1/2- 1-2 hrs; poor lipid solubility; bound to plasma proteins; hepatic metabolism & 50% excreted unchanged in the urine


SE= bleeding, benign thrombocytopenia, HITT, chest pain, allergy, hyperkalemia


CI= hypersensitivity, HITT, active bleeding, intracranial bleeding, severe thrombocytopenia; bacterial endocarditis, severe HTN;

  • caution:=bleeding disorders, liver disease, renal disease, pts taking platelet inhibitors/other anticoagulants, herbal medications that cause inhibit platelets; decrease body temp prolongs E1/2.
  •  May increase plasma levels of propofol & diazepam; NTG may antagonize heparin effects


Dose= 5000 U SQ prophylaxis q 8-12 hrs & IV for DVT; d/c infusion 4-5 hrs before surgery & check PTT/ACT levels



CLASS = heparin antagonist derived from salmon sperm


MOA= combines with heparin to form an inactive compound with no anticoagulation effects; when used alone it acts on platelets & fibrinogen to produce mild anticoagulative effects; 

from lecture-protamine is alkaline and (+) charge, heparin is acidic and (-) charge---> opposite charges attract and bind


Pharmacokinetics= onset- 5 min (? not on drug cards?) ; DOA- 20 min; metabolized by the reticulo-endothelial system within 20 min; clearance faster than heparin (rebound heparinization may occur)


SE= anticoagulant effects, HISTAMINE release = bronchoconstriction, hypotension, tachycardia, arrhythmias, pulmonary HTN, facial flushing


CI= hypersensitivity- risk for allergy if allergic to seafood; watch in DM if tx.with insulin containing protamine (NPH)


Dose= 1 mg for every 100 U of heparin; administer SLOWLY



CLASS= direct centrally acting muscle relaxant


MOA= reduces muscle tone & metabolism by preventing the ongoing release of Ca2+ from the SR, decreasing muscle contraction; used for treatment of MH & skeletal muscle rigidity by restoring the balance b/t release & uptake of Ca2+


Pharmacokinetics= onset- <5min; DOA- 3 hrs; E1/2- 10-15 hrs; metabolized in the liver & eliminated via the liver & kidneys; reconstitute each 20mg vial with 60ml of bacteriostatic sterile water; Ryanodex (new formula) requires 5mL dilutent for 250 mg vial.


SE= skeletal muscle weakness, tachycardia, labile BP, phlebitis, seizures, does not potentiate the effects of NMB or interfere with reversal of muscle relaxants; hepatitis if used > 60 days


CI= muscular dystrophy, central core disease, preexisting muscle weakness; CCB (can cause HYPERK+ & CV arrest)


Dose= bolus 2.5 mg/kg --> 2 mg/kg q 5 min to a total of 10 mg/kg (unti s/s decrease)--> then 1mg/kg q 6 hours x 72 hours



CLASS = short acting ß2 agonist

MOA= acts directly on ß2 receptors coupled to G proteins causing an increase cAMP & decrease Ca2+, increase K+ conductance causing bronchial SM relaxation; relaxes uterine SM causing tocolytic action

Pharmacokinetics= onset- immediate; DOA- 2 hrs; E1/2: 16hr; hepatic metabolism with 50% excreted unchanged in the urine

SE= tremors, vasodilation, reflex tachycardia, hyperglycemia, Hypokalemia, Hypomagnesaemia (increase Doses lose selectivity)

CI= hypersensitivity, caution in CAD, eclampsia- placental abruption, chorioamnionitis, avoid in MAOIs

Dose= 200 mcg/puff (do not exceed 16-20 puffs); 0.25 mg SQ



CLASS= phenothiazine; H1 & Dopamine 2 antagonist


MOA= blocks DA receptors in CRTZ preventing N/V & antagonizes H1 @ receptors= decrease histamine mediated response in respiratory tract, GI & blood vessels


Pharmacokinetics= 90% PB; onset- 3-5 min; DOA- 2-4 hrs; E1/2- 9-16 hrs; metabolized in the liver including CYP450 & excreted in the urine


SE= extrapyramidal effects, anticholinergic effects, sedation, arrhythmias (prolonged QT), neuroleptic malignant syndrome


CI= hypersensitivity, peds < 2 yrs old, Parkinson’s; caution in renal, hepatic, cardiac, pulmonary disease; caution will potentiate sedative effects of anesthetics


Dose= 6.25-25 mg IV



CLASS= butyrophenone; DA antagonist


MOA= blocks DA at its receptor on the CRTZ of the medulla preventing N/V


Pharmacokinetics= Highly PB; onset- 30 min; DOA- 12 hrs; E1/2- 2 hrs; metabolized in the liver with 5% renal excretion


SE= extrapyramidal effects; black box- torsades, prolonged QTI; decrease BP, sedation, akathesia,


CI= hypersensitivity, Parkinson’s, history of prolonged QT interval, do NOT give with reglan; caution will potentiate sedative effects of anesthetics


Dose= 0.625-2.5 mg IV



CLASS= 1st generation, broad-spectrum cephalosporin c beta lactam ring

MOA= bactericidal- inhibits bacterial cell wall synthesis by binding to Pencillin binding protein and activate autolysins and inhibiting transpetidases& causes cell death; good for joint penetration, endocarditis prophylaxis; preferred choice for perioperative prophylaxis

Pharmacokinetics= 80% (high) PB; E1/2- 2 hrs; metabolized in the liver & 80-100% excreted unchanged in urine

SE= allergy incidence 1-10%;- most commonly displayed as maculopapular rash and/or fever,  anaphylaxis 0.02% (laryngeal edema, bronchoconstriction, severe hypotension);, cross sensitivity with other cephalosporins; cross sensitivity with PCN (1%), thrombophlebitis; hemolytic anemia (rare)

CI= hypersensitivity, , decrease dose in RF; ETOH causes disulfram reaction; probenicid increases DOA

Dose= 1-2 grams IV 30 min preop



CLASS= semi-synthetic narrow spectrum linomycin

MOA= bacteriostatic – inhibits bacterial protein synthesis by binding to 50s ribosomal subunit & preventing peptide bond formation; used for treatment of serious infections of the GI tract, respiratory tract or female GU tract

Pharmacokinetics= peak- 60 min; E1/2- 2 hrs; liver metabolism & excretion in the urine, bile, & feces

SE= anaphylaxis, rash, severe diarrhea= pseudomembranous colitis, CV arrest/hypotension with rapid infusion, jaundice, neutropenia, potnentiates NMB’s d/t OWN NMB properties (these effects are NOT antagonized by Ca/AchEI); increase LFT

CI= increase sensitivity in pt w/ pseudomembranous colitis history; decrease dose in liver disease; crosses placenta. Concurrent admin with NMB can produce profound, lasting NMB

Dose= 600 mg IV preop



CLASS= broad-spectrum glycopeptide antibiotic

MOA= bactericidal - alters bacterial cell membrane permeability & RNA synthesis (from class- binds and inactivates cell wall precursors; inhibits cell wall synthesis); effective for gram + bacteria including MRSA, Cdif, staph, strep & enterococcus infections; good if PCN & cephalosporin allergic; good for cardiac, ortho surgeries, & CSF/shunt infections

Pharmacokinetics= 50% PB; peak 60 min; E1/2- 6 hrs; metabolized in the liver & renal excretion 80-90% unchanged & can take up to 9 days in RF

SE= histamine release & profound hypotension w/ rapid infusion, Red man syndrome, diarrhea, GI upset, oto & nephrotoxic (especially when used with aminoglycosides), thrombocytopenia, potentiates NMB

CI= hypersensitivity, hearing loss, renal failure

Dose= 1 gram in 250 ml NS over 60 min



CLASS= broad-spectrum fluoroquinolone

MOA= bactericidal; prevents transcription & replication by inhibiting the DNA gyrase and topoisomerase, which are critical bacterial enzymes used in DNA replication and cell division.; good for gram + & - bacteria; used to treat GI/GU, bone, soft tissue & respiratory tract infections

Pharmacokinetics= 30% PB; E1/2- 3 hrs; CYP450 metabolism in the liver & 50% excreted unchanged in the urine & 20% excreted unchanged in the feces

SEQT Prolongation!  anaphylaxis, rash, N/V/D, dizziness, photosensitivity, seizures, spontaneous tendon rupture

CI= hypersensitivity, caution in RF= decrease dose; caution with theophylline & pregnancy

Dose= 200-400 mg IV over 60 min



CLASS= 1st generation histamine 1 antagonist; activates muscarinic, serotonin & alpha receptors


MOA= antagonist at the H1 receptor thereby preventing the response mediated by histamine in the respiratory tract, GI tract & blood vessels; prevents bronchoconstriction, vasodilation, edema, itching, & sneezing; used for allergies, hypersensitivity reactions, anti-nausea, sleep, motion sickness


Pharmacokinetics= 78% PB (highly); onset- 30 min; peak- 2-3 hrs; DOA- 4-6 hrs; E1/2- 2-8 hrs; metabolism in liver via CYP450, pulmonary & renal excretion


SE= sedation (crosses BBB), dizziness, seizures, hypotension, tachycardia, dry mouth/nose; urinary retention


CI (caution)= acute asthma, hyperthyroidism, CV disease, increase IOP, glaucoma, neonates


Dose= 10-50 mg IV