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MICI module 1 > Antibiotics And Anti microbials > Flashcards

Antibiotics And Anti microbials Flashcards

1
Q

Define differential toxicity

A

Based on the concept that the drug is more toxic to the infecting organism than the host

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2
Q

Define minimum inhibitory concentration

A

Minimum concentration of an antibiotic require to INHIBIT THE GROWTH of the test organism

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3
Q

Definite minimum bactericidal concentration

A

Minimum concentration of antibiotic required to KILL the test organisms

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4
Q

Describe concentration dependent killing

A

Goal is to maximize concentration

Host can be dosed less frequently

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5
Q

Describe time dependent killing

A

Goal is to maximize exposure of drug to host. Dosed more frequently

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6
Q

Define prophylaxis

A

Anti microbial agents are administered to PREVENT infection

Ex. Dose of antibiotics BEFORE surgery to reduce chance of infection

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7
Q

Describe empiric therapy

A

With rapidly acting diseases you must treat quickly. Make an educated guess based on the knowledge you already have to start treatment while waiting for lab results. Based on epidemiology

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8
Q

What are advantages of combination therapy

A

Testing polymicrobial infections, broad coverage empirical therapy, synergy (1+1=4) and may prevent the emergence of resistance

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9
Q

What are disadvantages of combination therapy?

A

Antagonism (drug drug reaction), cost, increased risk of side effects, usually not necessary for maximal efficacy

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10
Q

Define resistance

A

The inability to kill or inhibit the organism with clinically achievable drug concentrations. Resistance may be innate or acquired

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11
Q

What are the three mechanisms of resistance

A

Transformation
Conjugation
Transduction

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12
Q

What may accelerate the development of resistance

A 
Inadequate levels of antibiotics at site of infection 
Duration of treatment 
Overwhelming # of organisms 
Overuse/misuse of antibiotics 
Counterfeits 
Animal husbandry 
Over the counter medication 
Frequent exposure
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13
Q

Define anti microbial stewardship

A

Limit use of broad spectrum antibiotics to patients that absolutely require them
Proper administration of antibiotics !!! Not all bugs need drugs

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14
Q

Describe penicillin binding proteins (PBP)

A

Target of betalactam drugs, inhibits transpeptidases, the cross linking reaction of bacterial cell wall, weakened cell wall = cell death

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15
Q

Define transpeptidases

A

Involved in the stages of assembling the cell wall by cross linking the peptidoglycan lager and reshaping cell wall during division
Target of betalactan drugs is to inhibit this PBP

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16
Q

What causes beta lactam resistance

A

Production of beta lactamase (enzyme that destroys betalactam drugs)
Altered PBP
Novel PBP (MRSA)
Altered permeability (gram negative outer membrane=drug can’t get in)

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17
Q

What are the most common betalactamase inhibitors

A

Clavulanic acid and tazobactam

18
Q

Define glycopeptides

A

Cell wall active agents
Only work on gram POSITIVE agents only
Bind to terminal D-ala of nascent cell wall peptides to prevent cross linking
Makes D-ala TOO big to fit and form cell wall

19
Q

Describe glucopeptide (vancomycin) resistance

A

D-ala target altered to d-lac therefore vancomycin can NOT bind and becomes resistant to drug

20
Q

When is vancomycin used? (Spectrum of activity)

A

Gram positive cocci & gram positive rods

C.difficile must be given ORALLY otherwise it is usually IV administered

21
Q

Describe Fosfomycin

A

Cell wall synthesis inhibitor. An old drug used to treat e.Coli induced UTI
Works in the cell wall and has less damage to kidney

22
Q

Describe the evolution of fluroquinolones

A

Gets more effective as generations increase
3rd generation uses in treating complicated respiratory diseases as it has enhanced gram positive -/+ anaerobic activity

23
Q

Describe floroquinolones mechanism of action

A

Inhibit 2 enzymes (topoisomerase & gyrase) involved in Bacterial dna synthesis enabling these agents to be specific and bactericidal

24
Q

Describe development of resistance for fluroquinolones

A

Spontaneous mutation of parC and gyrA (most common) produces reduced affinity
Over expression of Efflux pumps which leads to drug being pumped out of the cell
Down regulation of porin channels which leads to topoismerase protection

25
Q

What are some adverse events in fluoroquinolones

A

Hyper/hypo glycemia

Cartiledge toxicity/tendon rupture in pediatric useage

26
Q

What are some inhibitors of protein synthesis

A

Macrolides
Tetracyclines
Aminoglycosides
Linezolid

27
Q

Describe macrolides

A

Bind to 50s subunit of bacterial ribosomes to inhibit protein synthesis

28
Q

What are some mechanisms of resistance in macrolides?

A

Efflux pump and target site modification (erm site)

29
Q

When are macrolides typically used

A

Community acquired pneumonia
Pertussis (whooping cough)
Atypical pathogens (no cell wall)

30
Q

What are potential adverse reactions of macrolides

A

GI upset
Ventricular arrhythmia
Cyto p-450 interactions (drug drug interaction)

31
Q

Describe clindamycin

A

The antibiotic most commonly associated with C.diff colitis
Used in anaerobic infections
Gram positive infections

Binds to ribosomes to shut down proteins synthesis therefore shutting down toxin production

Usually avoided as a medication

32
Q

Describe tetracycline mechanism of action

A

Bind reversibly to 30s ribosomal unit

33
Q

Where is tetracyclines useful

A

Treating atypical bacteria, animal borne diseases and most gram positive infections and CA-MRSA

34
Q

What are potential adverse events of tetracyclines

A

Discolouration of teeth, photo sensitivity, depression of skeletal growth
Not prescribed to children under 8

35
Q

Describe Aminoglycosides

A

Natural/semi synthetic antibiotics with excellent gram NEGATIVE activity and good gram positive activity

36
Q

Describe Aminoglycosides mechanism of action

A

Binds IRREVERSIBLY to 30S ribosomal subunit, bacteria must actively transport drug into the cell. This step is rate limiting and blocked by divalenf cations and anaerobiosis

These drugs DO NOT work in anaerobic environments (abscess)

37
Q

What are mechanisms of resistance with Aminoglycosides

A

Enzymatic modification, modify the drug to render it inactive

38
Q

What are some adverse effects with Aminoglycosides

A

Ototoxic (affect hearing)
Nephrotoxic (kidney damage)
Long term use requires therapeutic drug monitoring

39
Q

Describe inhibitors of metabolic pathways

A

TMP/SMX prescribed together
Good gram NEGATIVE some gram positive
Block folic acid synthesis at 2 different points
Inhibits folic pathway

40
Q

Describe TMP/SMX

A

Resistance now high as often used for UTIs

Management of PCP pneumonia and GI infections

41
Q

Describe metronidazole (flagyl)

A

Inhibits nucleic acid synthesis by distrupting/damaging DNA
Go to for ANAEROBIC organisms
Very little resistance

42
Q

Describe adverse effects of Metronidazole

A

Antabuse effect (can not mix with alcohol)

MICI module 1 (4 decks)

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