Antimicrobials 1 and 2 Flashcards

1
Q

Define antibiotic and antimicrobial

A

Antibiotic: technically a naturally produced chemical from a microorganism. Antibacterial: drugs to treat bacterial infections

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2
Q

Define bacteriostatic and bactericidal

A

Static stops growth so immune system can catch up. Cidal kill bacteria. Best for life-threatening or when immune systems broken.

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3
Q

Principles of Antimicrobial Therapy Flowchart.

A

Insert chart.

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4
Q

Betalactams

A

Only work when the cells are actively dividing

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5
Q

Penicillin pyramid

A

Penicillin most narrow, amoxicillin/ampicillin more, pipercillin most. Cloxacillin on the side only fights staph, some strep. Tunnels = add another drug to amoxicillin/pipercillin. Insert Picture.

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6
Q

General facts Cephalosporins

A

From mold. Blocks cross linking of peptidoglycan, activate autolytic enzymes. Gram -ve coverage increases with generation, gram +ve decreases. No Listeria, no Enterococcus, no coagulase negative staphylococci

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7
Q

Generations of cephalosporins

A
  1. Good gram +ve cocci, some gram -ve rod; 2. Good gram +ve cocci, more gram -ve; 3. Not great staph, good strep, even more gram -ve; 4. Good gram +ve, most gram -ve
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8
Q

Names of drugs in the generations of cephalosporins

A

1st: Cefazolin, cephalexin (po). 2nd: Cefuroxime, cefprozil. 3rd: (all T’s) Cefotaxime, ceftazidime, ceftriaxone, cefixime (po). 4th: cefepime

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9
Q

Monobactams

A

Aztreonams. No anaerobes covered.

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10
Q

Carbapenems

A

Imipenem and meropenem (fewer side effects) - cover almost all diseases.

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11
Q

Vancomycin

A

NOT A BETA LACTAM. Acts on early peptidoglycan wall synthesis

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12
Q

Bacitracin

A

NOT A BETA LACTAM. Acts by inhibiting the precursors from getting to the site of peptidoglycan wall synthesis. Only used as a cream/topical agent because of side effects

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13
Q

Summary of the drugs that affect cell wall

A

The cell wall active agents are the penicillins, the cephalosporins, the carbapenems, aztreonam and vancomycin. Penicillins – penicillin tree. Cephalosporins – ceph cycle. Aztreonam only gram negs. Carbapenems - gorillacillin. Vancomycin and bacitracin– only gram pos

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14
Q

Protein inhibitors

A

Need to be actively transported into cell - therefore don’t work well on anaerobes.

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15
Q

Aminoglycosides

A

Protein inhibitor. Gut gram negatives, bacteriocidal.

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16
Q

Macrolides/Erythromycins

A

Protein inhibitor. Mycoplama, chamydia, gram +ve, and respiratory gram -ve . Bacteriostatic.

17
Q

Clindamycin

A

Protein inhibitor. Bacteriostatic. Common for dental and gyne. Gram positive aerobe and anaerobe

18
Q

Chloramphenicol

A

Protein inhibitor. Bacteriostatic. Rarely used due to side effects - affect bone marrow and mitochondria.

19
Q

Tetracycline, doxycycline, tigecyclin

A

Protein inhibitor. Bacteriostatic. Good coverage. Deposit on bones and teeth, can stain.

20
Q

Linezolid

A

Protein inhibitor. Bacteriostatic. Acts on ribosome. Good for highly resistant gram +ve infections (superbugs)

21
Q

Drugs that affect nucleic acid synthesis.

A

Work on proteins that affect nucleic acids ie ribosomes, gyrase, other enzymes, etc.

22
Q

Quinolones

A

Inhibit enzymes for supercoiling (gyrase, etc). 1: rare. 2. Ciprofloxacin (urinary, diarrhea, gram +ve). 3. Levofloxain (pneumonia from community, mostly gram +, some gram -). 4. Gemifloxacin (powerful).

23
Q

Metronidazole

A

Affect nucleic acid synthesis. Converted to active form by anaerobic or parasites. May be cancerous.

24
Q

Rifampin

A

Inhibits RNA polymerase. Used in combination for mycobacteria. Prophylaxis against N meningitidis.

25
Q

Antimetabolites

A

Binary fission requires cofactors like THF and folic acid. Antimetabolites block these.

26
Q

TMP/SMX

A

Antimetabolites. No anaerobes. coverage good

27
Q

Cytoplasmic membrane agents

A

Polymyxin - alters permeability; Good for gram -ve rods. Daptomycin - distrupts CM; reserved for highly resistant gram +ve cocci

28
Q

How can bacteria become resistant?

A

Acquire genes via 3 mechanisms: Conjugation (plasmid). Bacteriophage transduction. Transformation (extracellular DNA)

29
Q

What are the resistance mechanisms?

A

Block target, change target, fake (different metabolic pathway), attack (breakdown before it can bind), efflux pump