Ch. 9 - Inhibiting Growth of Pathogens in Vivo Using Antimicrobial Agents Flashcards

1
Q

Chemotherapy

A

The use of any chemicals (drug) to treat any disease/condition

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2
Q

Antimicrobial agents

A

The use of any chemical (drug) to treat an infectious disease either by inhibiting or killing the pathogen

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3
Q

Antibiotics

A

Substance produced by a microorganism that kills or inhibits the growth of other microorganisms

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4
Q

Semisynthetic antibiotic

A

Antibiotics chemically modified to kill a wider variety of pathogens or reduce side effects

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5
Q

Alexander Fleming

A

Discovered penicillin

-noticed that the farther away the bacteria were from the mould (which was creating penicillin), the better they grew

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6
Q

Staphylococcus aureus

A

Gram ( + )
Found in our microbiota, often found in our nose
=> staph infections
MRSA is most common

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7
Q

MRSA

A

Resistant to beta-lactams antibiotics.
- methicillin, oxacillin, penicillin, and amoxicillin.
Most MRSA infections are skin infections that often appear as a bump, a boil, or area that is red, tender and swollen, and is sometimes confused with a spider bite.

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8
Q

Bactericidal drugs

A

Agents that kill microbes

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9
Q

Bacteriostatic drugs

A

Agents that inhibit/slow the growth of microbes, but never actually kills it

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10
Q

How do antimicrobial agents work? (5)

A
  1. Inhibition of cell wall synthesis (Bactericidal)
  2. Damage to cell membrane (Bactericidal)
  3. Inhibition of nucleic acid synthesis (Bactericidal)
  4. Inhibition of protein synthesis (Bactericidal or Bacteriostatic)
  5. Inhibition of enzyme activity (Bacteriostatic)
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11
Q

Sulfonamide drugs

A

Competitive inhibitors, Bacteriostatic
Inhibit production of follic acid in bacteria that need p-aminobenzoic (PABA) to synthesis it
Without follic acid, bacteria cant produce certain essential proteins, so they die

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12
Q

Penicillin

A

Bactericidal,
Acts on mostly gram ( + )
Interferes with the synthesis and cross linking of peptidoglycan
Inhibits cell wall synthesis => destroy bacteria

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13
Q

narrow spectrum antibiotic

A

Use when we know specifically if we have gram ( - ) or ( + ) bacteria
ex: colistin

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14
Q

Broad spectrum antibiotics

A

Use when we arent sure if the bacteria is gram pos or neg

ex: ampicillin

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15
Q

Multi drug therapy

A

2+ drugs used simultaneously

ex: Tx tuberculosis

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16
Q

Synergism (drug related)

A

2 anitmicrobial agents are used together to produce a degree of pathogen killing greater than what just one of the drugs alone could do

17
Q

Antagonism (drug related)

A

The 2 drugs work against each other. The extent of pathogen killing is less than what each drug could have reached alone

18
Q

Categories of antibacterial agents

A
  1. Cephalosporins (bactericial)
    • interefere with cell wall synthesis
  2. Tetracycline (bacteriostatic)
    • inhibit protei synthesis
  3. Aminoglycosides (bactericidal)
    • inhibit protein synthesis
  4. Macrolides (low does bacteriostatic; high dose bactericidal)
    • inhibit protein synthesis
  5. Fluoroquinolones (bactericidal)
    • inhibit DNA synthesis
19
Q

3 ways that anti-fungal agents work

A
  1. bind with cell membrane steroids
  2. interfere with sterol synthesis
  3. block mitosis or nucleic acid synthesis
20
Q

Why do antifungal and antiprotozoal tend to be more toxic to humans?

A

They are also eukaryotic, so it is hard to finda gents that will specifically target the microbes compared to those in our body

21
Q

2 ways antiprotozoal agents work

A
  1. Interfere with RNA/DNA synthesis

2. Interfere with protozoal metabolism

22
Q

How do antivirals work?

A

Inhibiting viral replication

23
Q

Superbug

A

Microbes (mainly bacteria) that have become resistant to one or more microbial agents

24
Q

Intrinsic resistance

A

Naturally resistant ebcause they lack the specific target site for the drug or the drug is unable to cross cell membrane, therefore cannot reach its site of action

25
Q

Acquired resistance

A

Bacteria were once susceptible, but they become resistant

26
Q

Mechanisms of acquired resistance

A
  1. chromosomal mutation => change shape of drug binding site
    effect: drug cant bind
  2. chromosomal mutation => change in cell membrane permeability
    effect: drug cant pass through membrane
  3. Acquisition of a gene that enables bacterium to produce an enzyme that destroys or inactivates the drug
    ex: penicillinase acquired during conjugation and chews up penicillin
  4. Acquisition of a gene that enables the bacteria to produce MDR pump
    effect: drug is pumped out of the cell before it can damage/kill the cell
27
Q

B-lactamases

A

Produced by some bacteria to derstoy the B-lactam ring of penicillin.
no ring= no drug function

28
Q

3 strategies against drug resistance

A
  1. educate health professionally and patients
  2. patients stop demanding antibiotics and professionals stop prescribing them when not needed
  3. Not used in a prophylactic way
29
Q

Empiric therapy

A

When drug therpay is started before the lab results are available.

  • time constraint
  • educated guess
  • consideration of medical Hx, site of infection, pt age..
30
Q

4 reasons why antimicrobial agents shouldn’t be used indiscriminately

A
  1. selecting for resistant organisms
  2. Allergies
  3. Toxicity
  4. Flora => superinfection