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Antimicrobials Flashcards

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1
Q

4 mechanisms of antibacterial resistance

A

alteration in receptor target, decreased entry/efflux, alteration in metabolic pathway, inactivate drug

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2
Q

Penicillin mechanism of action

A

bind PBP (transpeptidase that cross links NAG and NAM, autolysins, endopeptidase, carboxypeptidase)

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3
Q

4 mechanisms of antebacterial resistance to penicillin

A

modification of PBP, active pumping out of drug, cleave B lactam ring, altered porins in gram negative bacteria.

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4
Q

When penicillins are combined with drugs that are _____, pharmacologic antagonism results.

A

bacteriostatic

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5
Q

With oral contraceptives, gut bacterial normally cleave _____ conjugates, allowing estrogen to be reabsorbed and recycled via the ______ pathway.

A

estrogen-glucuronide conjugates, enterohepatic recirculation

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6
Q

Which types of penicillins are given for gram positive bacteria?

A

natural penicillins, penicillinase resistant penicillins

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7
Q

Which types of penicillins are given for gram negative bacteria?

A

amino, anti-pseudomonal

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8
Q

What are the common natural penicillin drugs?

A

Penicillin G and penicillin V

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9
Q

How is penicillin G administered?

A

intravenously or intramuscularly–> it is readily destroyed in acidic environments

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10
Q

How is penicillin V administered?

A

it is more stable than penicillin G so it is administered orally, but on empty stomach

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11
Q

What are the common aminopenicillins?

A

amoxicillin, ampicillin

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12
Q

How is ampicillin administered?

A

enterally or parenterall, oral must be on empty stomach

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13
Q

How is amoxicillin administered?

A

orally, with or without food because it is more stable

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14
Q

Rate penicillin G, V, amoxicillin, and ampicillin based on stability in an acidic enviornment.

A

Pen G, ampicillin and V, amoxicillin

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15
Q

What are the common penicillinase-resistant penicillins?

A

dicloxacillin, oxicillin, methicillin, naficillin

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16
Q

Mechanism of action of penicillinase resistant penicillins

A

they contain side groups that protect them from being inactivated by B-lactamases

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17
Q

Which penicillinase resistant penicillin is given orally?

A

dicloxacillin

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18
Q

What are the common anti-pseudomonal penicillins?

A

carbenicillin, ticarcillin, piperacellin, mezlocillin

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19
Q

Which antipseudomonal penicillin is given orally?

A

carbenicillin

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20
Q

Where are the therapeutic levels of carbenicillin found and what does this imply?

A

urinary tract: limits utility to UTI and prostate infections

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21
Q

What are the common irreversible inhibitors or B lactamases?

A

clavulanic acid, sulfbactam, tazobactam

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22
Q

Cephalosporins structurally resemble _____. Why?

A

penicillins, they have a B lactam back bone

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23
Q

What penicillin might be given to treat a prostate infection?

A

carbenicillin

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24
Q

Adverse effects of cephalosporins

A
  1. cross reactivity with penicillin allergy
  2. GI irratiation, take with food
  3. disruption of normal flora may cause secondary infections
  4. renal toxicity
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25
What pre-existing disease indicates need for caution when administering cephalosporin?
renal disease
26
Common carbapenem drugs
dorypenem, imipenem/cilastatin, ertapenem, meropenem
27
MAO of carbapenems
bacteriocidal, inhibit cell wall synthesis, different B lactam ring, so resistant to B lactamases
28
MAO of telavancin, vancomycin
Inhibit cell wall synthesis by binding D-Ala D-Ala portion of cell walls. Telavancin disrupts membrane potential and changes in permeability due to lipophilic side chain moiety
29
MAO of cycloserine
inhibits cell wall synthesis in gram positive, negative but reserved for resistant TB
30
MAO of polymyxin B
bacteriocidal to all gram - bacilli (not Proteus). Cationic detergent that disrupts lipoproteins in cell walls thus increasing permeability
31
Common aminoglycosides
streptomycin, tobramycin, amikamicin, neomycin, kanamycin, netilmicin
32
Aminoglycosides bind to the ____ ribosomal subunit.
30S
33
4 ways aminoglycosides interfere with protein synthesis
formation on initiation complex, misread RNA, ribosomes separate from mRNA. formation of monosome
34
How are aminoglycosides administered?
parnterally. they are highly polar cations so they are too water soluble
35
PK of aminoglycosides
short half live, ototoxic, nephrotoxic, postantibiotic effect
36
Are aminoglycosides used for gram neg or pos?
negative
37
Tetracycline drugs
tetracyclines, doxycycline, demecycline, oxytetracyline, tigecycline
38
Tetracyclin MOA
Binds 30S preventing binding of aminoacyl-tRNA, interfere with peptide growth. Bacteriostatic against G- and G+
39
What are glycylcycline?
antibiotics derived from tetracycline that are designed to overcome two common mechanisms of tetracycline resistance (efflux pumps and ribosomal protection). Tigecycline
40
Of all the tetracycline derivatives, _____ is most closely related to minocycline.
tigecycline
41
Mode of penetrance in tetracycline
G-: passive, G+: active
42
Tetracycline PK
gastric absorption is inhibited by chelation due to divalent cations or bile acid resins. Best to administer on empty stomach
43
Which tetracycline is the safest option for patients with renal dysfunction?
Doxycycline: metabolized hepatically, excreted in feces
44
Tetracycline resistance
G+: acquire resistance to tetracyclines by actively pumping out via. G-: alterations in outer membrane proteins
45
Chloramphenicol MOA
Bacteriostatic, binds 50S, blocks incoming amino acids, interferes with peptidyl transferase
46
How is chloarmphenicol metabolized?
via glucuronidation
47
What are dangers of giving chloramphenicol to someone with hepatic disease?
ineffiecient glucuronidations resulting in gray baby
48
Lincosamide drug
clindamycin
49
MOA lincosamide
binds 50S, prevents translocation from A to P site
50
Macrolide drug
erythromycin base, estolate, stearate, ethylsuccinate, clarithromycin, axithromycin
51
Macrolide MOA
inhibit protein synthesis by binding to 50S--> prevent translocation from A to P site, can be bacteriocidal or static depending on concentration
52
What cross-resistance can occur with macrolides?
because it shares the same binding site with clindamyin and chloramphenicol, they can interfere with each other and cause cross resistance
53
How can microorganisms become resistant to macrolides?
altered permeability, methylate 50S, develope enzymatic mechanisms to destroy the drugs
54
Erythromycin adverse effects
GI distress, cholestatic hepatitis (estolate salt), inhibiting P450 3A4 can cause toxicity, prolong QT interval--> torsades do pointes
55
Clarithromycin adverse effects
prolongs QT interval, inhibits P450 3A4, but less GI distress than erythromycin
56
Azithromycin adverse effects
does NOT prolong QT interval or inhibit P450 3A4,
57
Ketolide drugs
Telithromycin
58
MOA ketolides
inhibits 50S by binding 2 separate subunits. This means that 2 mutations would be needed to develop resistance. Poor substrate for efflux.
59
Retapamulin drug
ointment, pleuromutilin
60
Retapamulin MOA
interferes with peptidyl transferase by binding to unique spot on 50S.
61
Mupirocin MOA
topical cream and ointment that inhibits tRNA with ile
62
___ has no cross resistance with any other antimicrobial.
Mupirocin
63
Linezolid
interferes with protein synthesis by binding to 50S that prevents formation of the functional 80S complex
64
Streptogramins drugs
quinipristin and dalfopristin
65
Streptogramins MOA
acts at bacterial ribosomes and intereferes with protein synthesis. Quinupristin blocks late in protein synthesis, dalfopristin inhibits early.
66
When are streptogramins used?
treat life threatening infections caused by vancomycin resistant enterococci and skin infections caused by MRSA
67
Sulfanoamide drugs
sulfadiazine, silver sulfadiozine, sulfisoxazole, sulfmethoxazole, sulfacetamide, sulfasalazine
68
Sulfonamide MOA
compete with para-aminobenzoic acid at first biosynthetic step of the folic acid pathway
69
What can cause adverse effects with sulfanoamides?
1. highly protein bound, can displace other drugs like warfarin. 2. Displaces bilirubin: bad in pregnant women and infants younger than 2 months. Hyperbilirubinemia can cause kerincterus
70
How does bacteria develop resistant to sulfanoamides?
reduced uptake of drugs, alternate metabolic pathways, production of excess para-aminobenzoic acid, alterations in dihyropteroate synthase
71
how are sulfanoamides metabolized?
hepatically via acetylation, oxidation, glucuronidation--> slow acetylators may be at risk for hypersensitivity reaction . excreted renally
72
Trimethoprim MOA
inhibits dihyrofolate reductase, the enzyme that catalyzes the last step of bacterial folic acid synthesis
73
How can bacteria develop resistance to trimethoprim?
reduced uptake, alterations in dihydrofolate reductase, overproduction of dihydrofolate reductase
74
Fluoroquinolone drugs
besi-, cipro-, gati-, gemi-, levo-, moxi-, nor-, of- floxacin
75
MOA fluorquinolones
bacteriocidal. inhibit gyrase or topioisomerase IV.
76
Why is it hard for bacteria to develop resistance to gemifloxacin?
inhibits both gyrase and topioisomerase IV
77
What affects absorption of fluorquinolones?
food/cations: calcium, iron, aluminum, magnesium, zinc, sucralfate
78
Distribution of fluoquinolones
minimal to CNS, all other compartments
79
Lipopeptide drug
daptomycin
80
lipopeptide MOA
daptomycin binds bacteria membrane--> depolarization--> RNA, DNA, protein synthesis stopped --> cell death
81
how is daptomycin excreted?
unchanged in the urine
82
Metronidazole MOA
absorbed by anerobic bacteria and sensitive protazoa, reduced by ferrdoxin (generated by pyruvate/ferredoxin oxido-reductase--> toxic metabolites--> inhibition of DNA synthesis, degradation of DNA, etc.. death...mutagenic/carcinogenic. Not given in first trimester
83
nitazoxanide moa
interferes with pyruvate/ferredoxin oxido-reductase enzyme dependent electron transfer essential for anaerobic metabolism...carcinogenic/mutagenic. Not given in first trimester
84
Tinidazole moa
cytotoxicity via damage to DNA and inhibiting DNA synthesis
85
How is metronidazole used?
penetrates the CNS so it can be used to treat meningitis and brain abscesses caused by anerobes.
86
Rifaximim MOA
rifampin derivative that inhibits bacterial RNA synthesis by binding to bacterial DNA dependent RNA polymerase
87
Rifaximin PK
drug excreted unchanged in feces, does not interfere with p450
88
Isoniazid MOA
inhibits synthesis of mycolic acids
89
Isoniazid distribution
total body water including CNS
90
Metabolism of isoniazid
acetylation
91
Rifampin MOA
inhibits bacterial RNA polymerase by suprressing initation of RNA chain formation
92
Why are drug-drug interactions a major concern for rifampin?
it is a potent inducer of drug metabolism and alters the levels of many drugs
93
pyrazinamide MOA
unclear--> lowers pH and inhibit growth?
94
Ethambutol MOA
inhibits RNA synthesis and decreases replication of tubercle bacillia
95
Clofazimine MOA
binds mycobacterial DNA and inhibits RNA polymerase actions. Slow acting
96
treatment options of mycobacterial infections
isoniazid, rifampin, pyrazinamide, ethambutol, clofazimine

Pharmacology (4 decks)

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