PHARM Flashcards
MOA: Blocks Na channels, State dependent- best in rapidly firing neurons
(combined with vasoconstrictors like Epi)
ADE: Arrhythmias, Cardiotoxicity
Local Anesthetics (indicated for minor procedures, and epidurals) **infected tissues need higher doses
MOA: Local anesthetic with 1 “I” in name, blocks NA channels
ADE: prone to causing allergic rxns, arrhythmias
Esters “cocaine, procaine”
MOA: Local anesthetic with 2 “I” in name, blocks NA channels
ADE: prone to LIVER FAILURE (metabolized in liver), arrhythmias, cardiotoxicity
Amides “Bupivacaine, lidocaine”
Local anesthetic that blocks Na channels, Class 1B antiarrhythmic, and use for ventricular dyrhythmias
ADE: “tingling”, respiratory depression, fatigue/drowsy, seizures
Lidocaine (Amide)
-Unknown Mechanism, act on GABA receptors
“HEISM” -HALOTHANE, ENFLURANE, ISOFLURANE, SEVOFLURANE, METHOXYFLURANE, Nitrous Oxide
ADE: resp depression, myocardial depression, bradycardia/hypotension, hepatotoxicity, nephrotoxicity, malignant hyperthermia, expansion of trapped gas
Inhaled Anesthetics
-Halothane: cause hepatotoxicity
-Enflurane: cause seizures
-Methoxyflurane: cause nephrotoxicity
-Nitric oxide: cause exp of trapped gas
-MOA: potentates GABA-A, leads to rapid anesthesia induction
Propofol (IV anesthetic)
-NMDA receptor antagonist (Arylcyclohexylamines), PCP analogs that block effects of glutamic acid at NMDA receptors
ADE: can lead to dissociative amnesia, hallucinations
Ketamine (IV anesthetic)
-Benzo Receptor Antagonist
MOA: reverses benzos via competitive inhibit of the benzo binding site on GABA receptor
ADE: seizures, intensive monitoring is necessary
Flumazenil (Benzo Receptor Antag)
-MOA: increase GABA
ADE: HYPOtension, respiratory depress, confusion, coma, drowsiness
TX: BY FLUMAZENIL
Benzo’s (Midazolam) -zepam/zolam
can be IV anesthetic
MOA: INCREASE Chloride Channel Opening, DECREASING neuron firing
-ultra short acting, IV anesthesia induction, short surgical procedures, *DOES NOT PROVIDE ANALGESIA (just LOC)
-TX: anxiety, seizures
ADE: resp/cardio depression
Barbituates (Thiopental) IV anesthetic
- Gq protein coupled receptor, activates phospholipase C (PIP2–> DAG and IP3)
-DAG–> protein kinase C
-IP3–> phosphorylation
Leads to vasoconstriction, inc BP, pupillary dilator contraction, intestine/bladder sphincter contraction, in smooth muscle, URINARY RETENTION
Alpha 1 Receptor ***EPI PENS
-Gi protein coupled receptor, inhibit CAMP from ATP
-VASOCONSTRICT
-DECREASE sympathetic outflow (NE), insulin release in pancreas, lipolysis in adipose, aqueous humor production (treats glaucoma)
-INCREASE platelet aggregation
Alpha 2 Receptor (Brimonidine) tx: glaucoma
-Gs protein coupled receptor, stimulate adenylate cyclase to activate CAMP pathway–> protein Kinase A
-INCREASE HR/CO, contractility, renin release, lipolysis
Beta 1 Receptor
-Gs protein coupled receptor, stimulate adenylate cyclase to activate CAMP pathway–> protein Kinase A
-VASOLDILATE
-INCREASE CO/contractility/HR, insulin, lipolysis, aqueous humor production in eye, uterus relaxation, RELAX ciliary muscle, bronchodilator (tx asthma)
Beta 2 Receptor tx: asthma/stop early labor
-Cytochrome p450 inhibitors
-Quinidine, Ciprofloxacin, Isoniazid, Grapefruit juice, erythromycin, indinavir, cimetidine, sulfonamides, ketoconazole, amiodarone, Acute alc use
-cytochrome p450 inducers
**be careful taking birth control, can stop ur BC from working or other medications the patient is on
-Griseofulvin, Phenytoin, Carbamazepine, Rifampin, Barbituates, Chronic Alc Use, St. John’s Wort
-Class 1 Antiarrhythmic, fast inward NA currents
ADE: cinchonism, lupus like syndrome
Quinidine
End in “Navir”
-HIV drugs
-Flouroquinolone
-USED FOR GRAM NEG RODS of Urinaty/GI tracts
MOA: interferes with TOP II
-Ciprofloxacin (fluoroquinolone)
-MOA: decreases synthesis of MYCOLIC ACIDS, key components of cell wall of Mycobacterium TB
(only mono therapy prophylaxis against TB)
Isoniazid
-USED FOR B. PERTUSSIS, LEGIONELLA, MYCOPLASMA PNEUMO
-MOA: inhibits protein synthesis by binding to 23S RNA of 50S ribosomal subunit, blocking translocation
Erythromycin (macrolide)
MOA: HIV protease inhibitor that is used as antiretroviral therapy
TX: HIV/AIDS
Indinavir
MOA: Histamine H2 recetor ANTAG
TX: heartburn, decreases stomach acid production
Cimetidine
MOA: INHIBIT fungal ergol sterol synthesis
Tx: systemic mycoses
Ketoconazole
MOA: inhibit 50S ribosomal subunit, broad spectrum
TX: BACT MENINGITIS
(S. Pneumo, H. Influenza, N. Mening) AND ROCKY MOUNT SPOT FEVER
ADE: bone marrow suppress, aplastic anemia, gray baby syndrome (dec UDP glue transfer)
Chloramphenicol (protein synthesis inhibit)
-Antiarrythmic med
Amiodarone
-Oral Antifungal Drug, skin/nails
-MOA: interferes with microtubule function and mitosis of fungus
-Griseofulvin (Antifungal Drug)
-Antiepileptic Drug
-Class 1B anti arrhythmic
MOA: suppress abnormal brain activities by BLOCKING Na channels
Phenytoin (Antiepileptic Drug)
-Anticonvulsant, mood stabilizing drug
TX: epilepsy, trigeminal neuralgia
Carbamazepine (Anticonvulsant, mood stabilizing drug)
MOA: inhibiting DNA dependent RNA polymerase
TX: mycobacterium TB
Rifampin
Competitive muscarinic ANTAG
MOA: BLOCKS ACH in Muscarinic Receptors
-REVERSES “DUMBBeLSS”
Diarrhea, urination, mitosis, bradycardia, bronchoconstriction, lacrimation, salivation, sweating
-INC HR in bradycardia/dilates pupils/cycloplegia/mydriasis, ophthalmic procedures, and TX in organophosphate poisoning
-Use in Malignant glaucoma
-CONTRAINDICATED in narrow angle glaucoma
ADE: hot as a hare, mad as a hatter, red as a beet, dry as a bone
Atropine (anticholinergic)
does NOT block CNS excitation (e in DUMBBeLLS) bc that is by Nicotinic receptors
“B. O. AT. S”- blocks Ach, muscarinic antag
-Benztropine
-Oxybutynin
-Atropine
-Scopolamine
-REVERSES “DUMBBeLSS”
Diarrhea, urination, mitosis, bradycardia, bronchoconstriction, lacrimation, salivation, sweating
Anticholinergics
“PARK my BENZ”
MOA: muscarinic antag, blocks Ach
-can be used with Levodopa therapy to TX Parkinsons to reduce imbalance
ADE: blurry vision, dry mouth, urinary retention, tachy, constipation, psychosis
Benztropine (anticholinergic)
-antispasmodic med
MOA: muscarinic antag, blocks Ach
-TX: bladder spasms, stops frequent urination or urge incontinence
Oxybutynin (anticholinergic)
“SCOPe SICKNESS”
MOA: muscarinic antag, blocks Ach
TX: motion sickness, has sedative properties
Scopolamine (anticholinergic)
MOA: muscarinic antag, blocks Ach
TX: reduces airway secretions/stomach acid (helps in peptic ulcer)
**used with Neostigmine (Nm blocker) to prevent bradycardia
Glycopyrrolate (anticholinergic)
MOA: muscarinic cholinoreceptors AGONIST, increase PSNS activity/Ach
-Bethanechol
-Pilocarpine
-Methacholine
-Carbachol
Direct Cholinomimetics
MOA: muscarinic cholinoreceptors AGONIST, increase PSNS activity/Ach
TX: stimulate bladder contraction/GI motility, prevent urine retention
Bethanechol (direct cholinomimetic)
MOA: muscarinic cholinoreceptors AGONIST, increase PSNS activity/Ach
-Causes Bronchoconstriction, Used as a test in diagnosis of asthma
Methacholine (direct cholinomimetic)
MOA: muscarinic cholinoreceptors AGONIST, increase PSNS activity/Ach
**CONTRACTS Ciliary muscle for open angle glaucoma, and Pupillary/Iris Sphincter for closed angle glaucoma
-Stimulates saliva, sweat, tears, MIOSIS
-RESISTANT to acetylcholinesterase
TX: open angle/closed angle Glaucoma/ xerostomia
ADE: detached retina, decreased visual acuity, eye irritation, RARELY: bradycardia/bronchospasms
Pilocarpine (direct cholinomimetic)
**CONTRAINDICATION: AVOID IN ASTHMA OR BRADYCARDIA
MOA: muscarinic cholinoreceptors AGONIST, increase PSNS activity/Ach
**RELIEVES intraocular pressure, pupillary constriction–> open angle
-TX: open angle glaucoma
Carbachol (direct cholinomimetic)
MOA: DECREASE acetylcholinesterase enzyme to INCREASE Ach (Acetylcholinesterase inhibitors)
ADE: CAUSE “DUMBBeLLS”
DOESN’T CROSS BBB:
-Edrophonium
-Pyridostigmine/Neostigmine
CROSSES BBB:
-Physostigmine
-Donepezil
Indirect Cholinomimetics (Acetylcholinesterase Inhibitors)
CAUSE “DUMBBeLLS” (anticholinergic reverses it- the B.O.AT.S)
MOA: DECREASE acetylcholinesterase enzyme to INCREASE Ach (REVERSIBLE Acetylcholinesterase inhibitor)
USE: to DIAGNOSE Myasthenia Gravis, “tensilon test”, patients immediately show weakness, also to reverse non depolarizing drug blockade
**DOESNT CROSS BBB
Edrophonium (reversible indirect cholinomimetic acetylcholinesterase inhibitor)
MOA: DECREASE acetylcholinesterase enzyme to INCREASE Ach (REVERSIBLE Acetylcholinesterase inhibitor)
TX: MYASTHENIA GRAVIS
**DOESN’T CROSS BBB
Pyridostigmine
Neostigmine (also used to reverse Nm blockers in anesthesia/ Post surgery ileus)
*indirect cholinomimetic acetylcholinesterase inhibitors
MOA: DECREASE acetylcholinesterase enzyme to INCREASE Ach (Acetylcholinesterase inhibitors)
-MORE HYDROPHOBIC that others
TX: atropine/anticholinergic drug overdoses, and induces miosis to help decrease intraocular press in Glaucoma
**CROSSES BBB
Physostigmine (indirect cholinomimetic acetylcholinesterase inhibitor)
MOA: DECREASE acetylcholinesterase enzyme to INCREASE Ach (Acetylcholinesterase inhibitors)
TX: ALZHEIMERS DZ (to help increase Ach)
ADE: N/V, Dizziness
**CROSSES BBB
Donepezil (indirect cholinomimetic-acetylcholinesterase inhibitor)
-CAUSES “DUMBBeLSS”
Diarrhea, urination, miosis, bradycardia, bronchoconstriction, lacrimation, salivation, sweating
TX: Atropine (cross BBB) + Pralidoxime (cant cross)
Acetylcholinesterase Inhibitor Poisoning
Include “CUR”
MOA: Reversible competitive inhibitors of Ach, leads to less receptors available for Ach to bind to
USE: muscle paralysis during mech ventilation or surgery,
-Atracurium
-Mivacurium
-Pancuronium
-Rocuronium
-Tubocurarine
-Vecuronium
Nondepolarizing Nm BLOCKING drugs
TX: with acetylcholinesterase inhibitors (to increase Ach again) Neostigmine, Edrophonium
Tx: to reverse Nondepolarizing Nm Blocking drugs (Ach competitive inhibitors) “cur”
Neostigmine (tx myasthenia gravis) and Edrophonium (diagnoses myasthenia gravis)
**both are acetylcholinesterase inhibitors
-short term paralytic used in hospital
MOA: Nm blocking drug binding to motor nicotinic receptor, Ach AGONIST
-OPENS Na Channels
**keeps the nerve stuck in depolarizing/paralysis
Phase 1: Paralysis, NON reversible
Phase 2: Paralysis, Reversible/Ach receptors are desensitized to Ach (tx with Neostigmine to help reverse and overcome desensitization)
Succinylcholine (Ach receptor Agonist)
**induces paralysis
“AD BAC has HTN”
1- ACE inhibitors, lowers Ang 2 in body, preventing EA constriction in kidney, decreasing GFR, less aldosterone secretion (-“pril”)
2-Diuretics, lower BP by reducing fluid volume (osmotic, carbonic anhydrase inhibitors, loop, thiazide, potassium sparing)
3-Beta Blockers, reduce HR/CO/renin
(-“olol”)
4-Ang 2 receptor blockers, prevents Ang 2 from binding to AT1 receptor, reducing vasoconstriction (-“sartan”)
5-Calcium Chann Blockers (dihydropyridine), decrease resistance (-“dipine”)
Hypertension Medications for high blood pressure
MOA: inhibits ACE/RAAS (-“pril”)
lowers Ang 2 in body, preventing EA constriction in kidney, decreasing GFR, less aldosterone secretion
TX: HTN, CHF, Diabetic Neuropathy
ADE: increases bradykinin (vasodilator), cough CAPTOPRIL MNEUMONIC
ACE inhibitors (-pril)
-ADE: “CAPTOPRIL MNEUMONIC”
-COUGH
-ANGIOEDEMA
-POTASSIUM INCREASE (hyperkalemia)
-TASTE CHANGES
-HYPOTENSION
-PREGNANCY PROBS (can cause stillbirth, baby kidney damage, congenital malformations)
-RASH
-INC RENIN
-LOWER ANG 2
ACE inhibitors (-pril) TOXICITY
**affect EFFERENT ARTERIOLE OF GLOMERULUS
MOA: prevents Ang 2 from binding to AT1 receptor, reducing vasoconstriction, (-“sartan”)
*DO NOT AFFECT BRADYKININ (unlike ace inhibitors)… NO cough
USE: patients who are intolerant to ACE inhibitors, HTN, CHF, diabetic neuropathy
*CONTRAINDICATION: pregnancy
Ang 2 receptor blockers (-“sartan”)
Class 4 antiarrthymic -slow AV conduction (-“dipine”)
USE: angina pectoris, arrhythmias, essental HTN
*CONTRAINDICATED IN HEART BLOCKS
ADE: bradycardia, hypotension, constipation, peripheral edema, gingival hyperplasia
Calcium channel Blockers Verapamil and Diltiazem (non-dihydropyridine),
(-“dipine”)
MOA: inhibit Na-K-2Cl symporter in the THICK ASCENDING limb of loop of henle.
-Lower BP by reducing fluid volume, increases urine production, inhibiting Na/Cl reabsorption
USE: HTN, HYPERCALCEMIA, CHF
ADE: *allergic run, increase GOUT (hyperuricemia), ototoxicity, HYPOCALCEMIA, HYPOKALEMIA, HYPOMAGNESIUM, METABOLIC ALKALOSIS
**FUROSEMIDE is a SULFA drug, CONTRAINDICATED IN PT WITH SULFA ALLERGY
Loop Diuretics (furosemide-sulfa drug)
Ethacrynic Acid (phenoxyacetic acid derivative) is NOT a sulfa drug, so if pt needs a loop diuretic thats allergic to sulfa, can take E. Acid (everything else is same as Furosemide
MOA: osmotic diuretic, decreases water and Na reabsorption in PCT, inc water/Na EXCRETION, decreasing ECF volume, INCREASES URINE FLOW
**INC PLASMA/TUB FLUID OSMOLALITY
USE: high ICP, glaucoma, oliguric renal failure, drug overdoses
ADE: dehydration
Mannitol (osmotic diuretic)
*CONTRAINDICATED IN CHF/ANURIC PATIENTS (if they have no production of urine to begin with)
**FIRST LINE TX FOR HTN
MOA: inhibit NaCl and water reabsorption form DCT by blocking Na/Cl cotransporter (water also blocked)
USE: HTN, HYPOcalcemia, HYPERnatremia, edema
ADE: HYPERglycemia, HYPERlipidemia, HYPERcalcemia, HYPERuricemia, HYPOnatremia, HYPOmagnesium, HYPOkalemia Metabolic Alkalosis, DEHYDRATED
**Hydrochlorothiazide is a SULFA drug, CONTRAINDICATED IN PT WITH SULFA ALLERGY/ DO NOT GIVE TO PT BREASTFEEDING/PREGNANT
Thiazide Diuretics (Hydrochlorothiazide- sulfa drug)
**“thiazides cause hyperGLUC: hyperGLYCEMIA, hyperLIPIDEMIA, hyperURICEMIA, hyperCALCEMIA”
-MOA: inhibits carbonic anhydrase in PCT, leads to sodium bicarb diuresis/reduced bicarb in kidneys/ body, **SULFA drug
USE: glaucoma (dec IOP/dec aqueous humor in eye), altitude sickness, pseudo tumor cerebri, CHF, metab alkalosis
ADE: hyperchloremic metab acidosis, paresthesias, TYPE 2 renal tubular acidosis,
Acetazolamide (Carb Anhydrase Inhibitor)
-Blocking Na Channels/Competitive Aldosterone receptor Antagonist in Cortical Collecting Tubule/collecting duct
USE: CHF, HTN, HYPOKALEMIA (to increase K), HYPERALDOSTERONISM, EDEMA
ADE: HYPERkalemia (muscle weakness, fatal arrhythmias), HYPOaldosterone, HYPOnatremia, Gynecomastia/ED/low libido with spironolactone/Endocrine effects
**TELL PT TO AVOID POTASSIUM SUPPLEMENTS
K+ sparing diuretics (Spironolactone-androgen blocker ADE)/Eplerenone (like spironolactone but no androgen ADE)
**Amiloride and Triamterene are K+ sparing diuretics that act on Epithelial Sodium Channels (ENaC)
MOA: block/slow fast conduction in Na channels, especially depolarized cells
-REDUCES Phase 0 Depolarization SLOPE/rate
-INCREASE ERP/QT/AP/QRS
-INCREASE threshold for firing in abnormal pacemaker cells
-STATE DEPENDENT
TX: Atrial/Ventricular Tachy, Reentranct, Ectopic SVT arrhythmias (Wolfe parkinson), local anesthetics
**CONTRAINDICATED IN HYPERKALEMIA PT (too much K)
Class IA Antiarrhythmics (Na channel blockers)
-Procainamide, Quinidine, Disopyramide
“Double Quarter Pounders”
ALL^ ADE: TORSADES
-Class 1A Antiarrhythmic (Na channel blocker)
-longest half life
-USE: Ventricular Arrhythmias
ADE: Big anticholinergic side effects, worsen heart block/severe HF, TORSADES
DISOPYRAMIDE
-Class 1A Antiarrhythmic (Na channel blocker)
-Similar to others except less GI ADE, and is safer to use intravenously
ADE: DRUG INDUCED LUPUS (anti histone antibodies), TORSADES
PROCAINAMIDE
**only Class 1A that has ADE with drug induced lupus
-Class 1A Antiarrhythmic (Na channel blocker)
USE: SVT and Ventricular Arrhythmias, also used for prevention
ADE: CINCHONISM (dizzy, ringing in ears, diarrhea), thrombocytopenia, TORSADES
QUINIDINE
**only Class 1A that has ADE with cinchonism and thrombocytopenia
-MOA: highly selective for ischemic or depolarized Purkinje/Ventricular tissue, -shorten duration of ERP
-DECREASE AP, QT
-affect ischemic tissue
USE: POST MI TX, ventricular arrhythmias, digitalis overdose, TREATS TORSADES!!! **SEIZURES
ADE: CNS depress (lidocaine), GI probs (mexiletine), Drug induced lupus/ gingival hyperplasia, teratogenic effects, hirsutism/HYPERTRICHOSIS (excessive hair growth) (ALL IN PHENYTOIN), TINGLING
CLASS 1B NA CHANNEL BLOCKERS
-MEXILETINE
-LIDOCAINE
-TOCAINIDE
-PHENYTOIN
“MAYO, LETTUCE, TOMATO, PICKLE”
CLASS 1B NA CHANNEL BLOCKER
ADE: GI probs, abd discomfort
MEXILITINE
“LAST RESORT” Na channel blocker, use dependent in AV NODE/ACCESSORY TRACTS
-INCREASE QRS
-NO EFFECT ON AP, minimal QT
TX: SEVERE V TACH
Flecainide also tx: paroxysmal AFib and Atrial flutter
ADE: CHF, bradycardia, new arrhythmias
**CONTRAINDICATED IN POST - MI, ischemic heart disease
CLASS 1C ANTIARRYTHMICS NA CHANNEL BLOCKER
-PROPAFENONE
-FLECAINIDE
“FRIES PLEASE”
-K CHANNEL BLOCKER
-used when others fail
MOA: INCREASE AP/ERP/QT, they PROLONG depolarization in AV MYOCYTES (do not slow conduction like in Class 1A)
USE: ARRYTHMIAS
VTACH: amiodarone/Sotalol
afib/flutter: ilbutilide, dofetilide
ADE: ilbutilide/sotalol can cause TORSADES
CLASS 3 ANTIARRHTHMICS
K CHANNEL BLOCKER
-AMIODARONE (long half life, always check function tests- causes pulmonary fibrosis, hepatotoxicity, hypo/hyper thyroid)- VTACH
-ILBUTILIDE (afib/a flutter) (ade: TORSADES)
-dofetilide (afib/a flutter)
-sotalol (non selective b blocker) ADE: dizzy, TORSADES (VTACH)
-decrease conduction velocity (SA/AV nodes)
-INCREASE PR/ERP
TX: SVT DUE TO AV NODAL REENTRY/HTN/angina/Raynauds (Verapamil/Diltiazem), subarachnoid hemorrhage (Nimodipine)
ADE: CHF, AV block, sinus node depression, peripheral edema, constipation/gingival hyperplasia (especially verapamil)
CLASS 4 ANTIARRHTHYMICS
CALC CHANNEL BLOCKERS
-VERAPAMIL
-DILTIAZEM
-NIMODIPINE
MOA: inhibit bacterial cell well synthesis, block transpeptidase/bind to PBP
**BACTERICIDAL: cause bacterial cell death
ADE: HS type 3 rxns, vit k deficiency, disulfiram like rx when taken with alcohol, nephrotoxicity when taken with ahminoglycosides, pseudomembranous colitis, AI hemolytic anemia
Cephalosporins (Beta lactams)
*least extensive coverage
*inhibit bacterial cell wall
*P, E, K, S,S *
USE: gram positive cocci bacterial infections (staph/strep), also as pre operative prophylaxis, also gram neg (p. mirabilis, E. coli, Klebs)
*Methicillin sens Staph Aureus (MSSA), with cephalexin
FIRST GEN CEPHALOSPORINS (beta lactams) (FAZ/LEX)
-Cefazolin (IV/IM)
-Cephalexin (oral) -endocarditis prophylaxis
*P, E, K, S,S *
*inhibit bacterial cell wall
-gram neg, gram pos cocci, anaerobes
*P, E, K, H, E, N, S”
P. MIRABILIS
E. COLI
KLEBS
H. INFLUENZ
ENTEROBACTER
N. GON
SERRATIA marcessans
CEFUROXIME: only second gen that can CROSS BBB, (active against H. influenza, N. Gonorrhea, Lyme)
SECOND GEN CEPH (B LACTAMS)
“FOX WEARS FUR CLOTHES”
-cefoxitin
-cefuroxime
-cefaclor- ADE: SERUM SICKNESS
*inhibit bacterial cell wall/block peptidoglycan synthesis
-gram neg, gram pos cocci except enterococcus that are resistant to other gens “serious gram neg”
-TX all bacterial meningitis besides listeria
THEY ALL CROSS BBB
CEFTAZIDIME: ONLY 3RD GEN that can tx pseudomonas
THIRD GEN CEPH (B LACTAMS)
“tax, taz, triax, at dinner”
-cefotaxime
-ceftriaxone
-cefdinir
-ceftaz **only one against pseudomonas
*inhibit bacterial cell wall
-cover pseudomonas/enterococcus
-mod-severe hospital acquired infections by multi resistant bacteria including resistant strep pneumonia/enterococcus
FOURTH GEN CEPH (B LACTAMS)
“fepi the fourth”
-cefepime
*inhibit bacterial cell wall
**MOST COVERAGE, BUT DO NOT HAVE COVERAGE AGAINST PSEUDOMONAS
-specifically created for resistant bacteria like meth res staph aureus (MRSA)
-BROAD spectrum gram pos/neg INCLUDING ENTEROCOCCUS FAECALIS/LISTERIA
FIFTH GEN CEPH (B LACTAMS)
“5 TAR TOBI”
-ceftobiprole
-ceftaroline
MOA: bind to 23S ribosomal RNA in the 50S subunit which catalyzes formation of peptide bond, inhibits protein synthesis by blocking translocation
bacteriostatic
**gram pos cocci, atypical pneumonia, chlamydia
ADE: can lead to QT prolong, TORSADES, diarrhea, p450 inhibit, skin rash, eosinophilia, cholestatic hepatitis
Macrolides “-thromycin” (erythromycin, azithromycin”
**MACRO:
-motility probs
-arrhythmias (torsades)
-cholestatic hep
-rash
-eOsinophilia
-p450 inhibit
MOA: inhibits TOP 2 (DNA gyrase) and 4, prevents bacteria from replicating their DNA
**bactericidal
USE: gram neg rods, pneumonia, GI infxns, UTI, genital infections
ADE: tendon rupture, cartilage damage in young pt, QT prolong/teratogen/diarrhea/headache
Fluoroquinolones (-floxacin)
-Levo/Cipro: have psedommonas coverage
**avoid antiacids/polyvalent cations/TERATOGEN
Cell Wall Inhibitors
“CC is MVP”
*they have a beta lactam ring in their molecular structure
-penicillins
-cephalosporins
-monobactams
-carapenems
-vancomycin
MOA: cell wall inhibitor
-gram neg coverage, useful for penicillin allergies
Aztreonam (monobactam- only important one)
MOA: cell wall inhib
-gram pos, gram neg, anaerobic coverage
**Cilastin is often used with this to prevent breakdown by the kidneys
Carbapenems (imipenem and meropenem)
*they have a beta lactam ring in their molecular structure
-Clavulanic acid, sulbactam, tazobactam
Beta-Lactamase Inhibitors
Penicillins that have activity against pseudomonas:
-Ticarcillin, piperacillin
*they have a beta lactam ring in their molecular structure
-resistant to penicillinase
Penicillins that have activity against S. Aureus:
-Oxacillin, Nafcillin
*they have a beta lactam ring in their molecular structure
MOA: inhibit 30s subunit of ribosome leading to cell death, inhibit formation of initiation complex, resistance by Transferase enzymes
**bactericidal activity
-against gram neg rods (including pseudomonas, enterobacter)
-RESISTANT to anaerobes bc they require O2 for uptake, acetylation, adenylation, phosphorylation
ADE: nephrotoxic (esp w cephalosporins), ototoxic (esp w loop diuretics), teratogen
-Aminoglycosides (-“mycin”
(gentamicin, neomycin, amikacin)
*Neomycin is popular bowel surgery prep