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Microbiology- Antibiotics Flashcards

1
Q

Penicillin G, V- MOA, CU, Tox, Res

A

Prototype beta-lactam antibiotitcs
MOA: Bind PBP, block transpeptidase x-linking of peptidoglycan in cell wall.

CU: Mostly for G(+) organisms: (S. pneumo, S. pyogenes, Actinomyces) also for G(-) Cocci (N. meningitidis) and spirochetes (T. pallidum). Penicillinase sensitive.

Tox: Hypersens reac., hemolytic anemia

Res: Penicillinase in bacteria

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2
Q

Amoxicillin, Ampicillin- MOA, CU, Tox, Res

A

aminopenicillins
MOA: Same as penicllin, bind PBP. Also combine with clavulonic acid to protect against beta-lactamases. Think: “AMinoPenicillins are AMP-ed up beta-lactams” and “AmOxicillin has better Oral bioavailability than ampicillin.”

CU: Extended-spectrum penicillin (H. influenze, H. pylori, E. coli, Entercocci, L. moncytogenes, P. mirabilus, Salmonella, Shigella) Think: “Ampicillin/Amoxicillin HHEeLPSS.”

Tox: Hypersens reac., rash, pseudomembranous colitis

Res: Penicillinase in bacteria

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3
Q

Dicioxacillin, Nafcillin, Oxacillin- MOA, CU, Tox

A

Penicillinase resistant penicillins
MOA: Binds PBP. Bulky R group blocks access of of beta-lactamases to beta-lactam ring.

CU: Narrow spectrum. (MSSA) Think “Use Naph for Staph”

Tox: Hypersens reac., interstitial nephritis

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4
Q

Piperacillin, Ticarcillin- MOA, CU, Tox, Res

A

Anti-pseudomonals
MOA: Binds PBP. Combine with beta-lactamase inhibitors

CU: Extended spectrum. Use against Pseudomonal spp. and G(-) Rods

Tox: Hypersens. reac.

Res: Penicillinase in bacteria

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5
Q

Clavulonic Acid, Sulbactam, Tazobactam

A

Beta-lactamase inhibitors

Think: “CAST”

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6
Q

Cefazolin, Cephalexin- MOA, CU, Tox, Res

A

1st gen Cephalosporins
MOA: Bind PBP, beta-lactams that are less susceptible to penicillinase.

CU: Proteus mirabilis, E. coli, K. pneumoniae. Cefazolin used prior to surgery to prevent S. aureus infections.
Think: “PEcK”

Tox: Hypersens reac., autoimmune hemolytic anemia, disulfram-like reaction, vit. K def., X-reactive with penicllins, increase nephrotoxicity of aminoglycosides.

Res: Change of structure of PBP

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7
Q

Cefoxitin, Cefaclor, Cefuroxime- MOA, CU, Tox, Res

A

2nd gen Cephalosporins
MOA: Bind PBP, beta-lactams that are less susceptible to penicillinase.

CU: G(+) cocci: (H. inlfuenzae, Enterobactor aerogenes, Neisseria spp., P. mirabilis, E. coli, K. pneumoniae, S. marcesens. Think: “HEN PEcKS”

Tox: Hypersens reac., autoimmune hemolytic anemia, disulfram-like reaction, vit. K def., X-reactive with penicllins, increase nephrotoxicity of aminoglycosides.

Res: Change of structure of PBP

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8
Q

Ceftriaxone, Cefotaxime Ceftazidime- MOA, CU, Tox, Res

A

3rd gen Cephalosporins
MOA: Bind PBP, beta-lactams that are less susceptible to penicillinase.

CU: Serious G(-) infections resistant to other beta-lactams.
Ceftriaxone- meningitis, gonorrhea, disseminated Lyme disease.
Ceftazidime- anti-psuedomonas

Tox: Hypersens reac., autoimmune hemolytic anemia, disulfram-like reaction, vit. K def., X-reactive with penicllins, increase nephrotoxicity of aminoglycosides.

Res: Change of structure of PBP

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9
Q

Cefepime- MOA, CU, Tox, Res

A

4th gen Cephalosporins
MOA: Bind PBP, beta-lactams that are less susceptible to penicillinase.

CU: G(-) species with enhanced activity against Pseudomonas and all G(+) organisms.

Tox: Hypersens reac., autoimmune hemolytic anemia, disulfram-like reaction, vit. K def., X-reactive with penicllins, increase nephrotoxicity of aminoglycosides.

Res: Change of structure of PBP

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10
Q

Ceftaroline- MOA, CU, Tox, Res

A

5th gen Cephalosporins
MOA: Bind PBP, beta-lactams that are less susceptible to penicillinase.

CU: Broad G(+) and G(-) coverage, including MRSA. Doesn’t cover Psuedomonas(!)

Tox: Hypersens reac., autoimmune hemolytic anemia, disulfram-like reaction, vit. K def., X-reactive with penicllins, increase nephrotoxicity of aminoglycosides.

Res: Change of structure of PBP

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11
Q

Imipenem, Meropenem, Ertapenem, Doripenem- MOA, CU, Tox

A

Carbapenems
MOA: Imipenem is a broad-spectrum beta-lactamase-resistant carbapenem. Always administered with Cilastatin (inhibitor of renal dehydropeptidase I) to decrease the inactivation of the drug in the renal tubules
Think: “The kill is lastin’ with Cilastatin.”

CU: G(+) cocci, G(-) rods and anearobes. Ertapenem has limited psuedomonas coverage. Meropenem has a decreased risk of seizures and is stable to DHP I.

Tox: Significant side-effects limit use to life-threatening infections. GI distress, skin rash, and CNS toxicity (seizures) at high plasmas levels.

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12
Q

Aztreonam- MOA, CU, Tox

A

Monobactam
MOA: Less susceptible to beta-lactamases. Binds specifically PBP3. Synergistic with aminoglycosides,. No cross-allergenicity with penicillins.

CU: G(-) rods only (!) No activity against G(+) or anaerobes. For penicillin allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

Tox: Usually nontoxic. Occasional GI upset.

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13
Q

Vancomycin- MOA, CU, Tox, Res

A

MOA: Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursers. Bactericidal. Non-susceptible to beta-lactamases.

CU: G(+) only. Serious, MDR organisms. MRSA, S. epi., Enterococcus, C. diff.

Tox: Well tolerated in general. Can result in Nephrotoxicity, Ototoxicity, Thrombophlebitis, and diffuse flushing. Red Man Syndrome. Prevent by slowing infusion or adding antihistamines. Think “NOT without side effects.”

Res: Bacteria change D-ala D-ala linkages to D-ala D-lac

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14
Q

Gentamicin, Neomycin, Amikacin, Tobramyxin, Streptomysin– MOA, CU, Tox, Res

A

Aminoglycosides
MOA: Bactericidal. Irreversible inhibition of initiation complex through binding to the 30S subunit. Require O2f for uptake, therefore ineffective against anaerobes.

CU: Severe G(-) rod infections. Synergistic with beta-lactams. Neomycin is used for bowel surgery.

Toxicity: Nephrotoxiticy, Neuromuscular blockade, Ototoxicity (espc. with loop diuretics) Teratogen.

Res: Bacterial transferase enzymes inactivate the drug through acetylation, phosphorylation or adenylation.

Think: “Mean (aMINoglycosides) GNATS (Gentamicin, etc..) can NNOT (Nephrotox., etc…) kill anaerobes.”

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15
Q

Tetracycline, Doxycycline, Minocycline- MOA, CU, Tox, Res

A

Tetracyclines
MOA: Bacteriostatic(!). Bind to 30S subunit. Limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Do not tetracyclines with milk, antacids or iron-containing preps because divalent cations inhibit drugs absorption in gut. Drug can accumulate intracellularly, so good for certain intracellular infections.

CU: Correlia, M. pneumoniae, Rickettsia, and Chlamydia. Tick-borne diseases(!) Also used to treat acne.

Tox: GI distress, discoloration of teeth and inhibition of bone growth in children. Photosensitivity. Contraindicated in pregnancy.

Res: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pump.

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16
Q

Chloramphenicol- MOA, CU, Tox, Res

A

MOA: Bacterstatic(!) Blocks peptidyltransferase at 50S subunit.

CU: Meningitis d/t H. influenzae, N. meningitidis, S. pneumoniae and Rocky Mtn. Fever (Rickettsia)

Tox: Anemia, aplastic anemia, grey baby syndrome(!) in premature infants because they lack liver UDP-glucuronyl transferase.

Res: Plasmid-encoded acetyltransferase inactivates the drug.

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17
Q

Clindamycin- MOA, CU, Tox

A

MOA: Bacteriostatic. Blocks peptide transfer at 50S subunit.

CU: Anerobic infections(!) (bacteroides spp., C. perfringens) in aspiration pneumonia, lung abscess and oral infections. Also effective against invasive GAS infections. Think “Treats anaerobes ABOVE the diaphragm while metronidazole treats anaerobes BELOW the diaphragm.”

Tox: Psuedomembranous colitis (C. diff overgrowth), fever diarrhea.

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18
Q

Linezolid- MOA, CU, Tox

A

Oxazolidinones
MOA: Inhibit protein synthesis by binding 50S subunit

CU: G(+) spp. including MRSA and VRE.

Tox: Bone marrow supression (espc. thrombocytopenia) peripheral neuopathy, serotonin syndrome(!)

Res: Point-mut of rRNA

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19
Q

Name 2 30S inhibitors and 3 50S inhibitors

A

30S
Aminoglycosides-Bactericidal
Tetracylines-Bacterstatic

50S
Chloramphenicol-static
Clindamycin-static
Erythromycin (Macrolides)-static
Linezolid-variable

Think: “Buy AT 30 CCEL at 50.”

20
Q

Azithromycin, Clarithromycin, Erthromycin– MOA, CU, Tox, Res

A

Macrolides
MOA: Static. Inhibit translocation by binding to 23S rRNA subunit of the 50S ribosome.

CU: Atypical pneumonias. (Mycoplasma, Chlamydia, Legionella), STIs (Chlamydia), G(+) cooci (Streptococcal infections in pts. allergic to penicillins) and B. pertusis.

Tox: MACRO: Gastrointestinal motility issues, Arrhythmias d/t prolonged Q/T intervals, acute Cholestatic hepatitis, Rash, eOsinophila. Increases serum concentration of theophyllines, oral anticoagulants,. Clarithromycin and Erythromycin inhibit cyt P-450

Res: Methylation of 23S rRNA

21
Q

Trimethoprim– MOA, CU, Tox

A

MOA: Static. Inhibits bacterial dihydrofolate reductase.

CU: Used in combination with SMX (TMP-SMX) causing sequential blockade of folate synthesis. Combination used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii, pneumonia treatment and prophylaxis, and toxoplasma prophylaxis.

Tox: Megaloblastic anemia, leukopenia, granulocytopenia. May alleviate with supplemental folinic acid) Think: “TMP Treats Marrow Poorly.”

22
Q

Sulfamethoxazol (SMX), sulfisoxazole, sulfadiazine– MOA, CU, Tox, Res

A

Sulfonamindes
MOA: Static alone, Cidal w/ TMP. Inhibit folate synthesis.

CU: G(+) organisms, G(-), Nocardia, Chlamydia, Triple sulfas or SMX for simple UTI.

Tox: Hypersens reac., hemoylsis if G6PD deficient, nephrotoxicity, photosensitivity, kernicterus in infants, displace other drugs from albumin (esp. warfarin).

Res: Altered target enzyme, decreased uptake, or increased PABA (upstream substrate) synthesis.

23
Q

Ciprofloxacin, norfloxaxin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enoxacin- MOA, CU, Tox, Res

A

Fluoroquinolones
MOA: Cidal. Do not take with antacids. Inhibit prokaryotic enzymes Topo II and Topo IV.

CU: G(-) rods of UTI and GI tract. (Psuedomonas, Neisseria, some limited G(+) coverage

Tox: GI upset, superinfections, Contraindicated in pregnant women and children d/t cartilage damage. May cause tendonitis or rupture in elderly and and patients taking prednisone.

Res: Chromosome encoded mutations in DNA gyrase. Plasmid mediated resistance by expression of efflux pumps.

Think: “F-LONES bad for BONES”

24
Q

Daptomycin- MOA, CU, Tox

A

MOA: Lipopeptide that disrupts cell membrane of G(+) cocci

CU: S. aureus skin infections, especially MRSA (!), bacteremia, endocarditis, VRE. Not for pneumonia d/t reaction with surfactant.

Tox: Myopathy, rhabdomyolysis

25
Q

Metronidazole- MOA, CU, Tox

A

MOA: Cidal. Anti-protozoal and anit-bact. Forms toxic free radical metabolites in the bacterial cell that damage DNA.

CU: Giardia, Entamoeba, Trichomonas, Gardnerella, Anaerobes (Bacteroides, C. diff). Used in combo with PPI and clarithhromycin for “Triple Therapy” against H. pylori.

“GET GAP on the Metro.” Treats anaerobic infections BELOW the diaphragm whilst Clinda treats ABOVE.

Tox: Disulfram-like reaction with alcohol. headache. metalic taste.

26
Q

M. tb prophylaxis

A

Isoniazid

27
Q

M. avium-intracellulare prophylaxis

A

Azithromycin, rifabutin

28
Q

M. leprae treatment

A

Long-term with dapsone and rifampin for tuberculoid form. Add clofazimine for lepromatous form.

29
Q

M. tb treatment

A

Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE for treatment)

30
Q

M. avium- intracellulare

A

More drug resistant than M. tb. Azithromycin or clarithromycine + ethambutol. Can add rifabutin or ciprofloxacin

31
Q

Rifampin, Rifabutin- MOA, CU, Tox, Res

A

Rifamycin
MOA: Inhibit DNA-dependent RNA poly

CU: M. tb., meningococcal prophylaxis and chemoprophylaxis in contacts of children with HiB.

Tox: Minor hepatoxicity, and drug interactions Cyt P450, orange body fluids (!), Rifabutin favored over Rifampin in pts with HIV infection d/t less Cyt P450 activation.

Res: Mutations reduce drug binding to RNA poly.

“Rifampin’s 4 R’s” RNA poly inhibitor, Ramps up P-450, Red body fluids, Rapid resistance if used alone.

“Rifampin AMPS P-450 rifaBUTan does not.”

32
Q

Isoniazid- MOA, CU, Tox, Res

A

MOA: decreased synthesis of mycolic acids. Bacterial catalaze-peroxidase needed to convert INH to active metabolite.

CU: M. tb., the only agent used as solo prophylaxis against M. tb(!)

Tox: Neurotox, Hepatotox, Pyridoxine (B6) can prevent neurotox. “INH injures Neurons and Hepatocytes”

Res: Mut leading to underexpression of KatG (cat/peroxidase gene)

33
Q

Pyrazinamide - MOA, CU, Tox

A

MOA: Uncertain, prodrug that is converted to pyrazinoic acid.

CU: M. tb

Tox: Hyperuricemia, hepatotox

34
Q

Ethambutol- MOA, CU, Tox

A

MOA: decrease carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase.

CU: M. Tb

Tox: Optic neuropathy (red-green color blindness)

“Pronounce EYEthambutol”

35
Q

Prophylaxis for dental procedures

A

Amoxicillin

36
Q

Prophylaxis for gonorrhea exposure

A

Ceftriaxone

37
Q

Prophylaxis for Hx of recurrent UTIs

A

TMP-SMX

38
Q

Prophylaxis for exposure to meningococcal infection (3)

A

Ceftriaxone, ciprofloxacin, or rifampin

39
Q

Prophylaxis for pregnant women carrying GBS

A

Penicillin G

40
Q

Prophylaxis for prevention of gonococcal conjunctivitis in newborn

A

Erythromycin ointment

41
Q

Prophylaxis for postsurgical infection d/t S. aureus

A

Cafazolin

42
Q

Prophylaxis for strep pharyngitis in child with prior rheumatic fever

A

Benzathine penicillin G or oral penicillin V

43
Q

Prophylaxis for exposure to syphilis

A

Bezathine penicillin G

44
Q

Treatment of MRSA (5)

A

Vancomycin, daptomycin, linezolid, tigecycline, ceftaroline

45
Q

Treatment of VRE (2)

A

Linezolid and streptogramins

46
Q

Treatment of Mdx P. aeruginosa, Acinetobacter (2)

A

Polymyxins (B) and (E)

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