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Pharmacology > Antimicrobials III > Flashcards

Antimicrobials III Flashcards

1
Q

mechanism of vancomycin

A

binds to D-Ala-D-Ala terminus of nascent peptidoglycan pentapeptide –> inhibition of transglycosylase –> inhibiting further elongation of peptidoglycan and cross-linking –> peptidoglycan and cell wall synthesis inhibition –> cell lysis

pay back 2 D-ALAs for VANdalizing

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2
Q

how are enterococci resistant against vancomycin

A

terminal D-Ala is replaced with D-lactate hence vancomycin not being able to bind to its target

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3
Q

clinical use of vancomycin

A
  • against serious gram positive bacteria only – especially those that are beta lactam resistant or allergic
  • ex: C. difficile pseudomembrane colitis and staph enterocolitis
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4
Q

when is vancomycin used to treat enterococci

A

it is used together with aminoglycosides against E. faecalis or E. faecium in enterococcal endorcarditis

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5
Q

adverse effect of vancomycin

A

PORN

  • Phlebitis
  • Red man or Red neck syndrome: flushing of the face or upper torso due to release of histamine
  • Ototoxicity and Nephrotoxicity: esp if renal insufficiency or given with aminoglycosides
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6
Q

mechanism of daptomycin

A

binds to cell membrane of bacteria via calcium dependent insertion of lipid tail –> depolarization of cell membrane and potassium efflux –> rapid cell death

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7
Q

clinical applications of daptomycin

A
  • vancomycin resistant enterococci and staph aureus

- MRSA, MSSA, VRE

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8
Q

what do you not use daptomycin to treat and why

A

not used to treat pneumonia because pulmonary surfactant antagonizes daptomycin

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9
Q

adverse effects of daptomycin

A

constipation, nausea, headache, insomnia

-myopathy and possible increase in creatinine phosphokinase

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10
Q

mechanism of bacitracin

A

interferes with dephosphorylation in cycling of the lipid carrier that transfers peptidoglycan subunits to growing cell wall –> cell wall synthesis inhibition

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11
Q

clinical application of bacitracin

A

topical treatment of mixed bacterial infections of skin, wounds, or mucous membrane

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12
Q

adverse effect of bacitracin

A

nephrotoxic if administered systemically hence why used topically

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13
Q

mechanism of fosfomycin

A

inhibits enolypyruvate transferase which is a cytoplasmic enzyme used in early stages of cell wall synthesis

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14
Q

clinical application of fosfomycin

A

uncomplicated lower urinary tract infections

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15
Q

what are the protein synthesis inhibitors

A

TAMGOS [CC FML]

Tetracyclines
Aminoglycosides
Macrolides
Glycylcylines
Other: Chloramphenicol, Clindamycin, Fidaxomicin, Mupirocin, Linezolid
Streptogramins: Dalfopristin/Quinupristin

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16
Q

what part of the bacteria do protein synthesis inhibitors work on and why is there still adverse effects?

A
  • they work on ribosome 70S found only in bacteria (compare to 80S found in mammalians)
  • adverse effects seen because mammalian ribosome closely resembles bacterial ribosome
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17
Q

what are the tetracyclines

A

Tetracycline
Doxycycline
Minocycline

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18
Q

mnemonic for protein synthesis inhibitors for what does what part of the 70s ribosome

A

Buy AT 30, CCEL at 50

30S:
Aminoglycosides (bactericidal)
Tetracyclines (bacteriostatic) (glycylcylines as well since it is derived from tetracyclines)

50S: 
Chloramphenicol (bacteriostatic)
Clindamycin (bacteriostatic)
Erythromycin (all macrolides) (bacteriostatic)
Linezolid (variable)
19
Q

mechanism of tetracyclines

A

binds to 30S and prevents attachment of aminoacyl-tRNA –> inhibition of AA to growing peptide

20
Q

clinical application of tetracyclines (name them)

A

tetracycline, doxycycline, minocycline

  • most common: severe acne and rosacea (flushed appearance of cheeks and nose)
  • Chlamydia, Cholera, Anthrax, Rickettsia, Lyme diseases, Mycoplasma
21
Q

what cations impair absorption of tetracyclines

A

Ca2+, Mg2+, Fe2+

22
Q

adverse effects of tetracyclines (name them)

A

Tetracycline, Doxycycline, Minocycline

  • Discoloration and Hyperplasia of teeth and stunting of growth (affects fetus and kids less than 8)
  • Dizziness and Vertigo
  • Photosensitization
  • Nephrotoxicity
  • Hepatotoxicity
  • GI disturbances (most common)

first three are more testable

23
Q

what is the glycylcylines

A

Tigecycline

24
Q

mechanism of glycylcyline (name it)

A

Tigecycline

binds to 30S but more tightly than tetracyclines and overcome resistance associate with acquired efflux pumps and ribosomal protection

25
Q

what is intrinsically resistant to glycylcyline (name it)

A

tigecycline

Proteus
P. aeruginosa

26
Q

clinical application of glycylcylines (name it)

A

tigecycline

complicated skin, soft tissue, and intra abdominal infections

-MRSA, VISA, VRE

27
Q

adverse effects of glycylcylines (name it)

A

tigecycline

  • same as tetracyclines
  • Discoloration and hyperplasia of teeth and stunting of growth
  • Photosensitization
  • Dizziness and Vertigo
  • Nephrotoxicity and Hepatotoxicity
  • GI disturbances (also most common here as well)
28
Q

who are glycylcylines and tetracyclines contraindicated in and why

A

pregnant women and children under 8 due to discoloration and hyperplasia of teeth and stunting of growth

29
Q

what are the aminoglycosides

A

Mean (aMINoglycosides) GNATS caNNOT kill anaerobes – all bactericidal

Gentamicin
Neomycin
Amikacin
Tobramycin
Streptomycin

NNOT are the adverse effects - Nephrotoxicity, Neuromuscular blockade, Ototoxicity (esp with loop diuretics), and Teratogen

30
Q

mechanism of aminoglycosides (name them)

A

GNATS - gentamicin, neomycin, amikacin, tobramycin, streptomycin

irreversible inhibition of initiation complex via binding the 30S subunit –> protein wall synthesis inhibition

31
Q

aminoglycosides initially cross the outer membrane of the bacteria via passive diffusion. how can this step be inhibited

A

divalent cations
anaerobic environment
acidic pH
increased osmolality

32
Q

how can resistance to aminoglycosides occur (name them)

A

GNATS: gentamicin, neomycin, amikacin, tobramycin, streptomycin

  • inactivating drug by phosphorylation, adenylylation, and acetylation
  • receptor protein on 30S can be altered or deleted due to mutation
  • decreased accumulation of drug by impaired entry into cell or increased efflux
33
Q

pharmacodynamic property of aminoglycosides (name them)

A

GNATS: gentamicin, neomycin, amikacin, tobramycin, streptomycin

post antibiotic effect (PAE): suppression of bacterial growth even after drug has been removed

concentration dependent killing: higher conc induces more rapid and complete killing of organism hence why a larger, single dose is more effective than smaller, multiple doses

34
Q

clinical application of aminoglycosides (name them)

A

GNATS: gentamicin, neomycin, amikacin, tobramycin, streptomycin

  • severe gram neg rod infections
  • gentamicin plus penicillin/vancomycin for infective endocarditis
  • streptomycin for plague caused by yersinia pestis
  • neomycin for hepatic encephalopathy (lactulose is first line though)
35
Q

adverse effects of aminoglycosides (name them)

A

Mean (aMEANoglycosides) GNATS caNNOT kill anaerobes

GNATS: gentamicin, neomycin, amikacin, tobramycin, streptomycin

NNOT
Nephrotoxicity
Neuromuscular blockade
Ototoxicity (esp if taken with loop diuretics)
Teratogen
36
Q

contraindication of aminoglycosides

A 
pregnant women (teratogen)
myasthenia gravis (due to neuromuscular blockade)
37
Q

what are the macrolides

A

Macrolides CEAT

Clarithromycin
Erythromycin
Azithromycin
Telithromycin

38
Q

mechanism of macrolides (name them)

A

Macrolides CEAT: clarithromycin, erythromycin, azithromycin, telithromycin

bind to 50S –> inhibition of transpeptidation, translocation, chain elongation, and protein synthesis

39
Q

mechanism of resistance in macrolides (name them)

A

Macrolides CEAT: clarithromycin, erythromycin, azithromycin, telithromycin

  • reduced membrane permeability or active efflux
  • makes esterase –> hyrolyzation of drug
  • modification of ribosomal binding site via chromosomal mutation or methylase
40
Q

clinical application macrolides (name them)

A

Macrolides CEAT: clarithromycin, erythromycin, azithromycin, telithromycin

  • erythromycin: whooping cough
  • infection by by Hemophilus, Strep pneumo, staph, enterococci
41
Q

of all the macrolides, which one is only one available as an IV

A

azithromycin

42
Q

safest macrolide for pregnancy

A

erythromycin

43
Q

drug interactions of macrolides

A
  • CET (clarithromycin, erythromycin, telithromycin) leads to increase in plasma conc of drugs that are metabolized by CYP3A4, theophylline, anticoagulants, carbamazepine
  • erythromycin increases plasma levels of digoxin
44
Q

adverse effects of macrolides (name them)

A

Macrolide CEAT: clarithromycin, erythromycin, azithromycin, telithromycin

MACRO
Motility issues
Arrhythmias due to long QT interval
Cholestatic hepatitis
Rash
eOsinophilia

Steven Johnson Syndrome

Pharmacology (79 decks)

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