Microbiology- Pharmacology Flashcards

1
Q

How do Penicilin G IV, IM), V (PO) work?

A

bind penicillin-binding proteins (transpeptideases) and block PEP cross-linking of peptidoglycan in cell walls

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2
Q

AEs of Penicillin?

A

Hypersensitivity rxns, hemolytic anemia

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3
Q

Resistance to penicillin?

A

pencillinase in bacteria (B-lactamase)

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4
Q

What is the MOI of amoxicillin, ampicillin?

A

Same as penicillin but iwth wider spectrum (still penicillinase sensitive)- can combine with clavulinic acid to protect aginst B-lactamases

NOTE: Amoxicillin has greater bioavailabilty than ampicillin

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5
Q

What are the main uses of Amoxi/Ampicillin?

A

H. influenzae, H. pylori, E. Coli, Listeria, Proteus, Salmonella, and Shigella

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6
Q

AEs of amp/amoxicillin?

A

Hypersensitivity rxn, rash, pseudomembranous colitis

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7
Q

What is the MOI of dicloxacillin, nafcillin, oxacillin?

A

Same as penicllin, but narrow spectrum and penicillinase resistant because of a bulky R group blocks access of B-lactamase

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8
Q

What are the main clinical uses of dicloxacillin, nafcillin, oxacillin?

A

S. aurues (except MRSA- resistant due to altered penicillin-binding protein target site)

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9
Q

What are the AEs of dicloxacillin, nafcillin, oxacillin?

A

Hypersensitivity rxns, interstitial nephritis

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10
Q

What is the MOI of piperacillin and ticarcillin?

A

Same as penicillin, extended spectrum

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11
Q

What are the main uses of piperacillin and ticarcillin?

A

Pseudomonas spp. and gram neg rods; susceptible to penicillinase (use with a B-lactamase inhibitor)

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12
Q

What are the main B-lactamase inhibitors?

A

Clavulanic acid, sulbactum, taxobactam

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13
Q

How do cephalosporins work?

A

B-lactam drus that inhibit cell wall synthesis but are less susceptible to B-lactamases (bactericidal)

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14
Q

cephalosporins are ineffective against what bugs?

A

LAME

Listeria

Atypicals (Chlamydia, Mycoplasma)

MRSA (except ceftaroline)

Enterococci

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15
Q

What are the 1st gen cephalosporins?

A

Cefalozin and cephalexin

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16
Q

What are the uses of Cefalozin and cephalexin?

A

mostly gram pos cocci, Proteus, E. Coli, and Klebsiella

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17
Q

What are the 2nd gen cephalosporins?

A

Cefoxitin, Cefaclor, and Cefuroxime

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18
Q

What are the uses of Cefoxitin, Cefaclor, and Cefuroxime?

A

gram positive cocci, H. influenzae, Enterobacter, N. spp, Proteus, E. coli, and Klebsiella, Serratia

HEN PEcKS

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19
Q

What are the 3rd gen cephalosporins?

A

Ceftriaxone, Cefotaxime, and Ceftazidime

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20
Q

What are the uses of Ceftriaxone, Cefotaxime, and Ceftazidime?

A

severe gram neg infetions resistant to others (Ceftriaxone- meningitis, gonorrhea, disseminated Lyme disease; Ceftazidime-Pseudomonas)

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21
Q

What are the uses of 4th generation cephalosporins?

A

Cefepime- mainly gram neg organisms with icnreased activtiy against Pseudomonas

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22
Q

Main AEs of cephalosporins?

A

Hypersensivity rxns, autoimmune hemolytic anemia, disulfram-like rxns, vitK deficiency

cross reativity with penicillins

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23
Q

What are the carbapenems?

A

Imipenem, meropenem, Ertapenem, etc

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24
Q

How do carbapenems work?

A

Imipenem is a broad spectrum B-lactamase resistant carbapenem always given with cilastatin which is a renal dehydropeptidase I inhibitor

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25
Q

What are the Monobactams?

A

Aztreonam

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26
Q

How does Aztreonam work?

A

Less susceptible to B-lactamases; prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. Synergisitic with aminoglycosides (no cross-allergy with penicllins)

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27
Q

Uses of Aztreonam?

A

Gram neg rods only (no activity against gram pos or anaerobes)

good for penicillin allergic pts and those with renal insufficiency who cannot tolerate aminoglycosides

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28
Q

How does Vancomycin work?

A

Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall percursors (bactericidal; not susceptible to B-lactamases)

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29
Q

What are the uses of Vancomycin?

A

Gram + bugs only - serious, multidrug resistant including MRSA, S. epi, sensitive Enterococcus spp. and C. difficile

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30
Q

AEs of Vancomycin?

A

Well tolerated but may cause nephro-, ototoxicity, thrombophlebitis, diffuse flushing (prevent with pretreamtnet with antihistamines)

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31
Q

How do antimicrobial protein synthesis inhibitors work?

A

Target the 30S or 50S subunits, leavin human 80S unaffected

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32
Q

What are the 30S inhibitors?

A

Aminoglycosides (bactericidal)

Tetracyclines (bacteriostatic)

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33
Q

What are the 50S inhibitors?

A

Chloramphenicol, Clindamycin (bacteriostatic)

Eryhtromycin (macrolides); bacteriostatic

Linezolid

Buy At 30, CCEl at 50

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34
Q

What are the Aminoglycosides?

A

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

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35
Q

How do Aminoglycosides work?

A

Bactericidal by binding to the 20S and causing mRNS misreading and blocking translocation

require O2 for uptake and therefore inneffective against anaerobes

36
Q

What are the main uses of Aminoglycosides?

A

Severe gram neg rod infections. Synergistic with B-lactams

Neomycin for bowel surgery

37
Q

AEs of Aminoglycosides?

A

nephrotoxicity, neuromuscular blockade, ototoxicity, teratogen

38
Q

What are the tetracyclines?

A

tetracycline, Doxycycline, Minocycline

39
Q

How do tetracyclines work?

A

Bacteriostatic by binding to the 30S and preventing attachment of the aminoacyl-tRNA (limited CNS penetration)

NOTE: Doxy is fecally eliminated and can be used in pts with renal failure. Also, dont taketetracyclines wth milk, antiacids, or iron containing preps because divalent cations inhibit its absorption

40
Q

How does chloramphenicol work?

A

Blocks peptidyltransferase at 50S ribosomal subunit; bacteriostatic

41
Q

What are the uses of Chloramphenicol?

A

Meningitis (H. influ, N, men., S. pneumo) and RMSF (Rickettsia rickettsii)

Limited use due to toxicities

42
Q

What are the AEs of Chloramphenicol?

A

Anemia (dose dependent)

aplastic anemia (dose independent)

grey baby syndrome (in premature infants because they lack liver UDP-glucuronyl tranferase)

43
Q

How does Clindamycin work?

A

Blocks translocation at the 50S subunit. Bacteriostatic

44
Q

What are the uses of Clindamycin?

A

Anaerobic infections (e.g. Bacteriodes, Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections

Also effective against invasive GAS infections

Treats anaerobic infections above the diaphragm vs. metronidazole which treats below

45
Q

What are the AEs of Clindamycin?

A

Pseudomembranous colitis, fever, diarrhea

46
Q

How does Linezolid work?

A

Inhibits protein synthesis by binding to the 50S subunit and inhibiting formation of the initiation complex

47
Q

What are the uses of Linezolid?

A

gram positive species including MRSA and VRE

48
Q

What are the AEs of Linezolid?

A

Bone marrow suppression (especially thrombocytopenia), peripheral neuropathy, serotonin syndrome

49
Q

What are the macrolides?

A

Azithromycin, clarithromycin, erythromycin

50
Q

How do macrolides work?

A

Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S subunit;; Bacteriostatic

51
Q

What are the AEs of Macrolides?

A

MACRO

GI motility issues

arrythmia caused by QT prolongation

Cholestatic hepatitis

Rash Eosinophilia

52
Q

How does trimethoprim work?

A

Inhibits bacterial dihydrofolate reductase (bacteriostatic) (similar to pyrimethamine)

53
Q

What are the uses of trimethoprim?

A

Used in combo with sulfonamides (trimethoprim-sulfamethoxazole), causing sequential blockade of folate synthesis- commonly used for UTIs

Shigella, Salmonella, Pneumocystitis jivroceii

toxoplasmosis prophylaxis

54
Q

What are the AEs of trimethoprim?

A

Megaloblastic anemia

leukopenia

granulocytopenia

55
Q

What are the sulfonamides?

A

Sulfamethoxazole (SMX), Sulfisoxazole, Sulfadiazine

56
Q

What is the MOI of sulfonamides?

A

Inhibit folate synthesis- PABA antimetabolites inhibit dihydropteroate synthase

57
Q

What are the AEs of sulfonamides?

A

hypersensitivity rxns, hemolysis if G6PD deicient, nephrotoxicity, photosensitivity, kernicterus in infants

58
Q

What are the Fluoroquinolones?

A

Ciprofloxacin, -floxacins

59
Q

What is the MOI of Fluoroquinolones?

A

Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and IV. Bactericidal (dont take with antacids)

60
Q

What are the AEs of Fluoroquinolones?

A

GI upset, skin rashes, HA, dizziness

Leg cramps and myaglaias

Contraindicated in pregnant women, nursing mothers, and children less than 18 yo due to possible cartilage damage.

tendonitis/tendon rupture

QT prolongation

61
Q

How does Daptomycin work?

A

Lipopetide that disrupts cell membranes of gram-positive cocci (good for S. aureus skin infctions, endocarditis, VRE)

NOTE: Dont use for pneumonia (inactivated by surfactant)

62
Q

What are the AEs of Daptomycin?

A

Myopathy, rhabdomyolysis

63
Q

How does Metronidazole work?

A

Forms toxic free radical metabolites in the bacterial cell that damage DNA. Bactericidal

64
Q

What are the AEs of Metronidazole?

A

Disulfram-like rxn (severe flushing, tachycardia, hypotension), metallic state

65
Q

What is the prophylaxis of Mycobacterium TB?

A

Isoniazid

66
Q

What is the prophylaxis of Mycobacterium avium?

A

Azthromycin or rifabutin

67
Q

How is M. avium tx?

A

More drug resistant than M. tb. tx with azitrho or clarithromycin + ethambutol (can add rifabutin or ciprofloxacin)

68
Q

Mycobacterium cell wall

A
69
Q

What are the rifamycins?

A

Rifampin, rifabutin

70
Q

How do rifamycins work?

A

Inhibit DNA-depedent RNA polymerase

71
Q

Major uses of rifamycins?

A

M. tb; delay reisstance to dapsone when used for leprosy

Used for meningococcal prophylaxis and chemoprophylaxis in contract of childrens with H. influenzae type B

72
Q

AEs of rifamycins?

A

Minor hepatotocixity and DDIs (induce CYP450)

orange body fluids (nonhazardous side effect)

Rifabutin favored over rifampin in pts with HIV infection due to less cyp activation

73
Q

What are the 4 R’s of Rifampin?

A

RNA polymerase inhibitor

Ramps up CYPs

Red/orange body fluids

Rapid resistance if used alone

74
Q

How does Isoniazid work?

A

Decreased synthesis of mycolic acids

NOTE: Bacterial catalase-peroxidase (encoded by katG) needed to convert INH to activate metabolites

75
Q

AEs of Isoniazid?

A

neurotoxicity, hepatotoxicity

Pyridoxine (VitB6) can prevent neurotoxicity

76
Q

How does pyrazinamide work?

A

Mehcanism uncertain but it is a prodrug that is converted to the active compound pyrazinoic acid

77
Q

AEs of pyrazinamide?

A

Hyperuricemia and hepatotoxicity

78
Q

How does ethambutol work?

A

Decreased carbohydrtae metabolism of mycobacterium cell walls by blocking arabinosyltransferase

79
Q

AEs of ethambutol?

A

Optic neuropathy (red-green color blindness)

80
Q

What is the preferred prophylaxis for AIDs pts with CD4 less than 200 cells/mm3?

A

TMP-SMX (protect against pneumocystis jivroceii)

81
Q

What is the preferred prophylaxis for AIDs pts with CD4 less than 100 cells/mm3?

A

TMP-SMX

82
Q

What is the preferred prophylaxis for AIDs pts with CD4 less than 50 cells/mm3?

A

Azithromycin or claitromycin (protect against mycobacterium avium)

83
Q

How should MRSA be tx?

A

Vanco, daptomycin, linezolid, tigecycline ceftaroline

84
Q

How should VRE be tx?

A

Linezolid or tigecycline

85
Q

How should Mmulti-drug resistant P. aeruginosa or multidrug resistant Acinetobacter baumannii be tx?

A

polymyxins B and E (colistin)