Anti-Microbials Flashcards

(43 cards)

1
Q

What does selective toxicity mean in respects to anti-microbial?

A

anti-microbials’ MoA do not harm the host (us), only do damage to bacteria, ex.:
- disrupt cell wall of BacT
- inhibit an enzyme unique to BacT
- disrupt bacterial protein synthesis

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2
Q

Antimicrobial Classes (5)

A

Narrow-spectrum (active against few bugs)
Broad spectrum (active against a variety of bugs)
Virus (antiviral)
Fungus (antifungal)
Protozoa (antiprotozoal)

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3
Q

Beta-Lactam Anti-microbials MoA/classes

A

MoA: inhibit bacterial growth by interfering with a specific step in bacterial cell wall synthesis
BACTERICIDAL
classes: penicillins, cephalosporins, monobactams, carbapenems

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4
Q

Narrow spectrum penicillins & route

A
  • penicillin G - IV
  • penicillin VK- PO
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5
Q

Narrow spectrum penicillins (anti-staphylococcal)

A
  • nafcillin
  • oxacillin
  • cloxacillin (PO)
  • dicloxacillin
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6
Q

Broad spectrum penicillins & route

A

(aminopenicillins)
- ampicillin- IV, PO
- amoxicillin- PO

*improved activity against gram -, but destroyed by B-lactamases

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7
Q

Extended-spectrum penicillins & route

A

(anti-pseudomonal)
- Piperacillin (IV)
- Ticarcillin (IV)

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8
Q

bacterial mechanisms of resistance to B-lactams

A
  1. Inactivation of antibiotic by B- lactamase
  2. Modification of target PBP’s
  3. Presence of efflux pump
  4. Impaired penetration of drug to target PBP’s
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9
Q

Penicillin AEs

A

very safe, least toxic; AEs due to hypersensitivity
- rash most common

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10
Q

Penicillin anaphylaxis

A
  • Immediate: urticartia, anaphylaxis, laryngeal edema
  • accelerated: urticartia, less severe
  • Late: maculopapular rash, drug fever, hemolytic anemia, thrombocytopenia, interstitial nephritis

**avoid all other B-Lactams

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11
Q

Cephalosporin changes with generation

A

The higher up in generation
- increasing ability to reach CSF
- increasing resistance to destruction by B-lactamases
- increasing activity against gram - bacteria and anaerobes

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12
Q

1st generation Cephalosporins/spectrum/use

A

Cefadroxil - PO
Cefazolin - IV
Cephalexin - PO

  • active against gram + cocci
  • for UTI, minor staph lesions, cellulitis
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13
Q

2nd Generation Cephalosporins/spectrum/use

A

Cefoxitin - IV
Cefotetan - IV
Cefuroxime - PO and IV
Cefaclor

  • less active against gram -; more against gram +
  • for sinusitis, otitis, and lower respiratory infections
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14
Q

Cephamycins drugs (sub group of 2nd gen)

A

Cefocitin
Cefotetan

  • active against anaerobes
  • for diverticulitis, peritonitis, abdominal/colorectal surgical prophylaxis
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15
Q

3rd Generation Cephalosporins/spectrum/use

A

Cefotaxime- IV
Ceftrazidime - IV
Ceftriaxone - IV/IM

  • more active against gram -; crosses BBB, used in HAIs
  • for complicated CAIs of resp. tract, blood, intra-abdominal, skin/soft tissue, and UTI
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16
Q

4th Generation Cephalosporins/spectrum

A

Cefepime - IV/IM

  • good gram - & + coverage, with activity against Pseudomonas
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17
Q

5th Generation Cephalosporins/spectrum

A

Ceftaroline - IV

  • broad gram-positive and gram-negative organism coverage, including MRSA; does not cover Pseudomonas
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18
Q

“6th” Generation Cephalosporin/use

A

Cefiderocol - IV

Clinical Uses: hospital acquired pneumonia, complicated UTI

19
Q

AE of Cephalosporins

A

patients with anaphylaxis, hives, angioedema, to penicillins should not get cephalosporins
- opportunistic infections with broader spectrum
- hypoprothrombinemia if on warfarin

20
Q

Carbapenems drug/class

A

*drugs in this class end in -penem
- Imipenem
BACTERICIDAL

21
Q

AE of Carbapenems

A

HA
Seizures
Nausea
Lowers valproic acid concentrations

22
Q

Monobactam drug

A

Aztreonam (Azactam)

23
Q

Other B-lactam drugs/use

A
  • Clavulanic acid
  • Sulbactam
  • Tazobactam
  • inhibit B-lactamases protecting penicillins from inactivation; used only in combo with PCNs
24
Q

Glycopeptides drug, moa, use

A
  • Vancomycin - IV (targets gram + bacteria)
  • moa: inhibit cell wall
  • use: sepsis or endocarditis caused by MRSA, meningitis with highly penicillin resistant pneumococcus
25
Lipoglycopeptides drug/moa/use
- Telavancin - moa: inhibits cell wall synthesis and disrupts BacT cell membrane - complicated skin and skin structure infections, covers VRE, MRSA
26
Tetracyclines drugs/acting time
- tetracycline --> short - demeclocycline --> intermediate - doxycycline, minocycline --> long acting
27
Tetracyclines spectrum/use
- *BACTERIOSTATIC* inhibits protein synthesis - broad spectrum for gram + & - - DOC for mycoplasma pneumoniae, chlamydiae, rickettsiae also H pylori, acne, AECB, CAP
28
Tetracylines AE
- GI (N/V, diarrhea) most common reasons for D/C - teeth and bones: tetracyclines bind Ca+ in new bones leading to tooth discoloration or bone deformation/growth inhibition - Photosensitivity
29
Tetracycline Resistance
1. Efflux by active transport protein pump encoded on plasmid 2. Ribosome protection by proteins that interfere with tetracycline binding 3. Enzymatic inactivation
30
Macrolides drugs/use
- mainly BACTERIOSTATIC; -cidal in high concentrations - Erythromycin - Azithromycin - Clarithromycin - DOC in diphtheria, all Chlamydial infections, CAP; mainly against gram +
31
Macrolides AE
- GI: anorexia, nausea, vomiting and diarrhea most common reason for D/C - acute hepatitis as hypersensitivity - drug interactions: inhibitor of CYP3A4 (Erythromycin and Clarithromycin ONLY); can prolong QT interval & increase risk for sudden cardiac death
32
Clindamycin moa/AEs/use
penicillin alternative, anaerobes; BACTERIOSTATIC MOA: Penetrates saliva, sputum, pleural fluid and bone but not CSF AE: psedomembranous colitis (suprainfection) Clinical Use: head and neck infections
33
Linezolid moa/use
MOA: also inhibits protein synthesis by preventing formation of the ribosome complex; BACTERIOSTATIC Clinical Use: Vancomycin resist. enterobacteria; multiple-drug resistant organisms
34
Aminoglycosides drugs/moa/use
- gentamicin, streptomycin, tobramycin - MOA: BACTERICIDAL inhibitors of protein synthesis, against gram - enteric bacteria - Clinical Use: bacteriemia and sepsis
35
Aminoglycosides AE
- ototoxicity and nephrotoxicity
36
aminoglycosides dosing
- concentration dependent killing; greater conc. kill more bacteria at faster rate (once daily dosing) - killing also occurs for several hours after med cleared from body
37
Antimetabolites MOA/spectrum
MOA: analogs of PABA that compete for a synthetic enzyme and block folic acid synthesis needed for DNA; BACTERIOSTATIC - targets both gram + & -, chlamydia, inhibits some enterics
38
Trimethropim- sulfamethoxazole (Bactrim) use/AEs
- anti-metabolite - P carinii pneumonia, shigellosis, salmonella (traveler's diarrhea), UTI's, prostatitis, otitis and upper resp tract infections, CAP - AE: frequent hypersensitivity reactions and rashes, photosensitivity, GI (N&V), hemolytic anemia, bone marrow depression
39
Fluoroquinolones drugs/moa
- Fluoroquinolones (anything ending in -floxacin, ex. ciprofloxacin) - MoA: block bacterial DNA synthesis by inhibiting DNA gyrase (required for DNA replication) Also inhibits topoisomerase. BACTERICIDAL
40
Fluoroquinolones use/ AEs
- resp., UTI's, soft tissue bone and joint infections, gonococcal infections; newer versions better for gram +'s - N/V, diarrhea, may prolong QT interval, tendonitis, cipro inhibits CYP1A2- increase levels, increase toxicity, hypoglycemia (most likely to occur in pts with DM)
41
Metronidalzole (Flagyl) moa/use/AEs
MOA: BACTERICIDAL, antiprotozoal with potent activity against anaerobes Clinical Use: intra-abdominal infections, antibiotic associated enterocolitis, trichomonas vaginitis, giardiasis, triple therapy for H.pylori ulcer disease AE: GI (N/V, metallic taste), CNS rxns -> seizures, peripheral neuropathy
42
-Azole Antifungals moa/use/drugs
MOA: reduce ergosterol synthesis by inhibiting fungal CYP enzymes Clinical Use: antifungal drugs are anything ending in -azole, ex. fuconazole, ketoconazole
43
Antimicrobials in Pregnancy
Avoid if possible: chloramphenicol metronidazole trimethoprim sulfonamides (last trimester) Contraindicated: fluoroqinolones tetracyclines