Quiz 1 - Smith - AMDs Flashcards

1
Q

What is an antibiotic?

A

Low molecular substance produced by a microorganism that inhibits or kills other microorganisms while causing little or no damage to itself

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2
Q

What is an antimicrobial?

A

A natural, semisynthetic, or synthetic origin that kills or inhibits the growth of microorganisms while causing little or no damage to the host

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3
Q

All antibiotics are ____________, but not all antimicrobials are ___________.

A

Antimicrobials

Antibiotics

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4
Q

Antifungals are also called what?

A

Antimycotics

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5
Q

Bacterocidal does what?

A

Kills

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6
Q

Bacteriostatic does what?

A

Stops growth

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7
Q

Broad spec is what?

A

Drugs that are active against a wide range of microorganisms

*Tetracyclines

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8
Q

Narrow spec does what?

A

Limited activity and are used against particular species of microorganisms

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9
Q

No _______ is effective against all microbes.

A

Antimicrobial

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10
Q

With AIDS patients, only use what type of anticmicrobial?

A

BACTERIOCIDAL

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11
Q

What is the MIC and what does it mean?

A

Minimal inhibitory concentration - based on the diameter of the zone of inhibition

*The minimum lowest conc of an antimicrobial drug that inhibits the growth of the bacterial strain plated

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12
Q

What does MBC mean?

A

Minimum bactericidal concentration

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13
Q

What phase of bacterial growth is most sensitivity to antimicrobial intervention?

A

Log phase - Period of most rapid growth

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14
Q

Empiric vs definitive AMT

A

Empiric - After symptoms, but before pathogen has been identified.

Definitive - When we know what bug it is

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15
Q

Pharmacokinetics vs pharmacodynamics?

A

PK - What the body does to the drug (ADME)

PD - What the drug does to the body

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16
Q

What does ADME stand for?

A

Absorption - Route of administration and determines the compound’s bioavailability

Distribution - Lipid or H2O soluble, bbb crossing?

Metabolism - Usual routes of clearance are thru liver and kidneys. Cytochrome P450 enzymes

Excretion - Low potency drugs are often used for UTI’s since they concentrate in urine b/c their resorption is so low

17
Q

Although MIC is often compared to plasma concentrations, these concentrations may NOT reflect ______ concentrations at the infection site.

A

Drug

18
Q

Ideally, antimicrobial therapy will be dosed to provide overkill w/o causing what in the host?

A

Toxicity

19
Q

What distinguishes antimicrobials from disinfectants?

A

Selective toxicity

*When selectivity is high, the risk of adverse effects are reduced

20
Q

The ideal AMT is defined by what?

A

It’s specificity of action in host vs bacteria

21
Q

Not all, but many, adverse effects are dependent upon what?

A

Dosage

22
Q

Therapeutic index is calculated how?

A

TD50/ED50

Toxic dose / effective dose

*Higher or wider the therapeutic index, the better/safer the antibiotic

23
Q

Adverse effects of AMTs can be __________ to antimicrobial action.

A

Analogous

24
Q

Adverse effect of AMTs may be ____________ of antimicrobial action.

A

Independent

*There may be an irritation or an allergy that the patient has

25
Q

AMDs target all essential microbial processes which include what 4 things?

A

Cell wall synthesis and cell membrane function/permeability

Protein synthesis - inhibits the 50s and/or 30s ribosomal subunits

Inhibition of metabolic pathways

Nucleic Acid synthesis of DNA and/or RNA

26
Q

What are 4 reasons to use combination therapy?

A

Treat inherently mixed infections - Antimicrobial combos broaden spectrum of coverage

Improve efficacy - However, NOT ALL COMBOS INCREASE EFFICACY

Initial empiric therapy of uncharacterized serious infection

Prevent emergence of resistance - lowers probability of selection of naturally occurring drug-resistant mutants

27
Q

What is a superinfection?

A

An overgrowth of pathogenic bacteria

28
Q

How are superinfections caused?

A

Use of broad-spec antimicrobial agents

Use of higher than normal concentrations of even narrow-spec antimicrobial agents

29
Q

What is antimicrobial resistance (AMR)?

A

Natural process by which microbes evolve to resist the effects of the medications used to treat them

30
Q

Bacteria can mutate in 3 main ways. Name them.

A

By chance

By horizontal gene transfer

By strong selective evolutionary pressures (like the increased use of antibiotics in both clinical and agricultural settings)

31
Q

What is horizontal gene transfer (HGT)?

A

Process whereby genetic material in small packets of bacterial DNA are t-ferred b/t individual bacteria of either the same or different species.

This material often conveys antimicrobial resistance b/t bacteria.

32
Q

HGT has three mechanisms. Name them.

A

Conjugation - MAIN MECHANISM FOR HGT - Plasmid transfer (bacterial sex)

Transformation - Resistant gene can be taken up from a dead bacteria

Transduction - Viral route via bacteriophage

33
Q

What are the major mechanisms of resistance?

A

Restrict AMD access - Prevent entry, or to pump in back out of the bacterial cell before the desired effect (efflux pumps)

Modify AMD’s target - Alter target protein or overexpress target protein requiring more drug

Modification of the AMD - Inactivate the AMD before affecting its target
or Prevent AMD activation - changing expression of bacterial factors/enzymes needed to activate the precursor

34
Q

Antibiotics fit in to their target proteins like a key in a lock, so how do bacteria modify the target?

A

Change protein sequence

Add chemical groups (Methylation, etc.)

*Change the key and/or change the lock

35
Q

How are beta-lactams inactivated?

A

Beta-lactams target PBP (penicillin-binding proteins) by binding them and inactivating them.

Bacteria alter the PBP site to prevent binding and normal bacterial function is restored

36
Q

What do beta-lactamase enzymes do?

A

Destroy the antibiotic by breaking open the beta-lactam ring

*The more beta-lactamase produced, the higher the level of resistance

37
Q

Resistance by modifying expression of bacterial factors needed to activate the antibiotic - prodrug

A

This renders the pro-drug inactive

38
Q

Antimicrobial effects may be classified based on three types. Name and describe them.

A

Type I - Conc-dependent - Goal maximize concentrations

Type II - Time-dependent - Maximize duration of exposure

Type III - Time-dependent with persistent effects - Maximize amount of drug