Additional Important Drugs

Question 1

Octreotide

Answer 1

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

Question 2

Omeprazole

Answer 2

CLASS= PPI

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

Question 3

Sugamamadex?

Answer 3

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)

Question 4

Milrinone

Answer 4

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

Question 5

Nifedepine

Answer 5

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

Question 6

Amiodarone?

Answer 6

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; 1^st 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

Question 7

Verapamil

Answer 7

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

Question 8

Diltiazem?

Answer 8

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

Question 9

Adenosine

Answer 9

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

Question 10

Digoxin

Answer 10

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

Question 11

Procainamide

Answer 11

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; 1^st 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

Question 12

Flumazenil?

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

Answer 12

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

Question 13

Naloxone?

MOA? Pharmacokinetics? SE? CI? Dose?

Answer 13

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

Question 14

Nalbuphine

Answer 14

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

Question 15

Butorphenol

Answer 15

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

Question 16

Phenytoin?

Answer 16

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- 1^st 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

Question 17

Acetaminophen?

Answer 17

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

Question 18

Albuterol

Answer 18

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

Question 19

Ipratropium

Answer 19

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

Question 20

Heparin

Answer 20

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

Question 21

Protamine

Answer 21

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

Question 22

Dantrolene

Answer 22

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

Question 23

Terbutaline

Answer 23

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

Question 24

Phenergan

Answer 24

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

Question 25

Droperidol

Answer 25

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

Question 26

Cefazolin

Answer 26

CLASS= 1^st 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

Question 27

Clindamycin

Answer 27

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

Question 28

Vancomycin

Answer 28

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

Question 29

Ciprofloxacin

Answer 29

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

SE= QT 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

Question 30

Diphenhydramine?

Answer 30

CLASS= 1^st 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

Question 31

Sodium Citrate/ Bicitra

Answer 31

CLASS= nonparticulate antacid; pH = 8.4

MOA= pH of 8.4 & directly neutralizes gastric acid to NaHCO3; increase gastric acid pH to prevent Mendelsson syndrome

Pharmacokinetics= onset- 15-30 minutes effectiveness; metabolized as NaHCO3 in the kidneys & <5% excreted unchanged in the kidneys

SE= unpleasant taste, increase gastric volume, N/V

CI= low Na+ diet, severe renal impairment, patients taking aluminum antacids

Dose= 15-30 ml 15-30 min preop

Question 32

Regular insulin

Answer 32

CLASS= pancreatic hormone that is structurally identical to endogenous insulin with zinc ions added for stability

MOA= binds to insulin receptors on pancreatic beta cells to increase translocation of GLUT 4 transporters into the cell membrane = facilitates diffusion of glucose into cells, facilitates the storage of glucose as glycogen, facilitates protein synthesis, & uptake of amino acids, K, Mg, & Ph

Pharmacokinetics= SQ- Onset 30-60 min; peak 1-5 hours; DOA 5-8 hours; IV- rapid plasma clearance after injection; DOA 60 min; E1/2 T 5-10 minutes;

all tissues metabolize insulin but main site is the proteolytic enzymatic breakdown in liver & kidney

SE= hypoglycemia, lipid dystrophy at the site of injection; insulin resistance

CI= hypoglycemia, caution in hepatic & renal disease (prolonged effect & greater risk of hypoglycemia)

Dose= 1U regular will decrease BG by 30-50 units; 0.05-0.1 U/kg/hr titration based on BG

Question 33

Glucagon

Answer 33

CLASS= synthetic analog of endogenous polypeptide hormone glucagon (produced by the alpha cells of the pancreas)

MOA= activates adenylate cyclase = increase cAMP = (1) increases glycogenolysis & gluconeogenesis= increase BG, increase insulin release; (2) induces catecholamine release, increase contractility & increase HR; (3) relaxes smooth muscle; used for hypoglycemia, SOO spasm & ßB OD

Pharmacokinetics= onset- rapid; DOA- 1hr; E1/2- 5 min; metabolized in the liver, kidney & tissues to inactive metabolites

SE= Hyperglycemia, hypoglycemia (paradoxical), hypokalemia, decrease gastric motility, N/V, incrase RBF; relax sphincter of Oddi; tachycardia with Afib

CI= hypersensitivity, pheochromocytoma, insulin-secreting tumor; caution DM

Dose= 1-5 mg IV over 5 min or 20 mg/hr; 0.3 mg IV for SOO spasm

Question 34

Arginine Vasopressin

Answer 34

CLASS= exogenous antidiuretic peptide & vasopressor

MOA= V1- arterial smooth muscle contraction causing profound vasoconstriction (large doses) V2= collecting duct in nephron, increased H2O permeabiliyt/reabsoprtion back into circulation. V3= increases ACTH release; PromotEs hemostasis by increasing VWF and factor VIII; causes peristalsis by stimulating GI smooth muscle

Pharmacokinetics= onset- rapid E1/2- 10-20 min; metabolized by tissue peptidases (33%) & urinary excretion

SE= increase BP, angina, arrhythmias, CA spasm, increase peristalsis, N/V, abdominal pain, bronchoconstriction; decrease platelet count

CI= CAD (caution), renal disease, asthma, GI obstruction; NSAIDS increase effect

Dose= 40 U IVP for CV arrest ACLS; 20 Units IV for varices; 0.04U/min gtt for sepsis

Question 35

Octreotide

Answer 35

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

Question 36

Oxytocin

Answer 36

CLASS= endogenous posterior pituitary hormone

MOA= binds to oxytocin receptors on the uterus= SM contraction; used to induce or augment labor & contract the uterus post-delivery & decrease chance of hemorrhage

Pharmacokinetics= onset- 1 min; DOA- 1 hr; E1/2- 5 min; metabolized by the liver & kidney; broken down by plasma oxytocinase & metabolism in mammary gland

SE= mom- anaphylaxis, N/V, PP hemorrhage, uterine rupture, arrhythmias & PVCs; baby- Bradycardia, problematic fetal positioning, fetal distress; high doses = decrease SVR & weak vasopressin activity & H2O retention

CI= fetal distress, hypertonic contractions, hypersensitivity

Dose= 0.5-2 mU/min (increase gtt q 15 min by 0.5-2 mU/min until contractions are 2-3 min apart); post partum uterine atony = up to 40mU/min

Question 37

Ampicillin

Class? MOA? Pharmacokinetis? SE? CI? Dose?

Answer 37

CLASS= broad spectrum ß lactam 2^nd generation penicillin

MOA= bactericidal - Binds to PBP and inhibits transpeptidases and activates autolysins inhibits bacterial cell wall synthesis by interfering w/ the production of peptidoglycan, which is an essential component of the cell wall; ß lactam covalently binds with transpeptidases causing autolysis & cell death;

- good for endocarditis prophylaxis & GI/GU & dental procedures

Pharmacokinetics= 20% (poor) PB; E1/2- 2 hrs (can be up to 20 hrs in RF); metabolized in the liver & excreted 90% unchanged in the urine

SE= highest incidence of rash, anaphylaxis, diarrhea, GI upset, hemolytic anemia; drug induced SLE, interstitial nephritis

CI= increase sensitivity to PCN & cephalosporins; potentiates warfarin; with rapid infusion can cause seizures (give over 10-15min); decrease dose in RF

Dose= 2 grams IV 30 min preop

Question 38

Gentamycin?

Answer 38

CLASS=broad-spectrumaminoglycoside

MOA= bactericidal – inhibits bacterial protein synthesis inside the bacteria by inducing mRNA misreading, (binds to 30s subunit ribosome and block initiation of protein synthesis) which causes cell death;

–good for endocarditis, sepsis, respiratory, bone, soft tissue, abdominal & urinary tract infections

Pharmacokinetics= < 30% (poor) PB; E1/2- 2 hrs (20-40 fold increase in RF); almost 100% renal excretion unchanged

SE= anaphylaxis, rash, N/V/D, neuro, oto, nephrotoxicity; decrease release of ACh= skeletal muscle weakness & potentiates NMB (inhibits prejunctional release of ACh and decreases post synaptic sensitivity to Ach- can be reveresed with Ca or neostigmine)

CI= hypersensitivity, decrease dose in RF, vestibulocochlear impairment; caution in pts w/ muscle weakness & myasthenia gravis; increases nephrotoxic potential of other drugs such as loop diuretics, NSAID’s & other abx; synergistic with vancomycin

Dose= 60-120 mg IV; toxic levels @ >9 mcg/ml – monitor levels

Question 39

Metronidazole

Answer 39

CLASS= synthetic antibacterial & antiprotozoal agent

MOA= bactericidal; broken down & activated by anaerobic organisms & form cytotoxic compounds that bind to bacteria & damage it;

• good for many gram – species but also some gram + species; used to treat CSF infections, abdominal & pelvic infections & pseudomembranous colitis

Pharmacokinetics= < 20% PB; E1/2- 8 hrs; liver metabolism with 70% excreted unchanged in the urine & fecal elimination

SE= anaphylaxis, rash, N/V/D, seizures, encephalopathy, confusion, optic & peripheral neuropathy, neutropenia, flu-like symptoms; dry mouth, metallic taste, nausea, avoid ETOH- antabuse

CI= hypersensitivity, caution in seizure history & CHF,hepatic dx; potentiates warfarin; preg Cat B

Dose= 500 mg over 10-20 min