Part three Flashcards

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1
Q

What is selective drug?

A

A drug that causes no harm to patients; stops and destroys the bacteria without affecting the host.

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2
Q

Explain selectivity

A

key to sucess of of a drug
- any harmful pathogen can be a target however a drug must be more harmful to the pathogen cells then toxic to the hosts cells.

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3
Q

Differentiate between toxicity and effectivity?

A

toxicity: damage to host
effectivity: damage to pathogen

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4
Q

How do you figure out the therapeutic index?

A

toxicity/effectivity = therapeutic index

bigger the better

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5
Q

Spectrum of action

A

refers to the spectrum of actions

drugs can be specific to pathogen to wide range ( responds to everything

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6
Q

May allow for secondary or super infections to develop due to killing of normal flora because it decreases microbial antagonism.. what is this?

A

Broad spectrum antimicrobials

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7
Q

What does antimicrobial antagonism do for the body?

A

reinforces defence by limiting the ability of pathogen to colonize on skin and mucous membrane

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8
Q

What are the three ways efficacy is measured

A

diffusion susceptibility test
minimum inhibitory concentration (MIC)
minimum bactericidal concentration (MBC)

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9
Q

Whats the process of the diffusion susceptibility test:

A

you put the pathogen on a petrie disc, then small paper discs throughout with the drug on them … susceptible bacteria will decrease growth, and unsusceptible will continue to grow
-zone of inhibition is evaluated.

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10
Q

what is the process of MIC

A

lowest concentration of antibiotics that result in inhibition of visible growth. Once affective antimicrobial agent is identified, MIC is the smallest amount of drug that will inhibit growth of the pathogen
Results:
turbidity: pathogen is still present and bacterial growth
low turbidity: bacteria was killed

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11
Q

what is the process of MBC

A

lowest concentration of antibiotics that kills 99.9% of the original inoculum.
Samples are taken from clear MIC tube, transfered to plates + appearance of bacteria growth after incubation indicates that at least some bacteria survived

  • if MBC is higher then MIC = it is not killing on impact but stopping them from growing (bacteriostatic)
    if MBC = MIC — bacteriocidal
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12
Q

Routes of administration:

A

PO- takes long time to peak but it is safer for patients
IM: cant maintain serum levels
IV: best practice for immediate results

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13
Q

Selective Cell wall damage caused by:

A

beta lactam antibiotics (penicillin) = prevents peptide bridges formation, doesn’t break the chain but prevents new ones from forming and growing

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14
Q

Beta Lactam Antibiotics:

A

inhibits enzymes by binding to them that are responsible for cross linking NAM and NAG chains
Prevents bacteria from increasing amount of peptidoglycan
-weakens the cell and eventually lyse.

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15
Q

What drug inhibits the cell wall synthesis by binding to the D-alanine amino acids at the end of the chain

A

VANCOMYSIN- covers the end of the chain so it cant bind to the l-lysine .. therefore preventing the formation of peptidoglycan

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16
Q

How does vancomycin resistance work?

A

changes the last D-alanine amino acid to lactic acid - so it prevents the vancomycin from covering it = doesnt work

17
Q

What three antibiotics fall under the “inhibit protein synthesis” category?

A

Aminoglycosides,Chloramphenicol, Tetracyclines

Animal Crackers Talks

18
Q

What is the mode of action of an aminoglyoside?

A

Irreversible binds to the 30S ribosomal sub unit - doing so freezes the 30S inhibition complex (30S–>mRNA–>tRNA)
50S cannot bind to this complex
-causes changes in 30S shape, leading to mRNA not reading the ribosomes right.
examples: steptomycin.gentomycin

19
Q

Aminoglycosides are Bactericidal or Bacteriostatic?

A

Bacteriocidal

20
Q

Define synergy in aminoglycodsides:

A

Aminoglycoside synergize with beta lactam antibiotics - which inhibit cell wall synthesis and increase the permeability for the aminoglycosides (help the drug get in the cell)

21
Q

What is the mode of action for tetracyclines

A

reversibly binds to the 30S ribosome and inhibit the binding of tRNA to the acceptor site on 70S ribosomes - BLOCKS THE DOCKING SITE FOR tRNA!

22
Q

are tetracyclines bacteriostatic or bactericidal?

A

bacteriostatic

23
Q

adverse affects of tetracyclines?

A
  • destruction of intestinal normal flora
    increased 2ndary infections = c-diff
    staining and impairment of structures such as bone and teeth (yellow) - not recommended for pregnant or young females.
24
Q

Is chloramphenicol bacteriostatic or bactericidal?

A

bacteriostatic!

25
Q

Mode of action of chloramphenicol:

A

binds to 50S and inhibits peptidyl transferase activity

26
Q

What is the most concern/adverse affect of chloramphenicol?

A

TOXCITY!!
bone marrow supression
-it is used in bacterial meningitis tx

27
Q

What drugs fall under the “inhibitors of RNA synthesis” category?

A

Rifamycin

28
Q

Mode of action for rifamycin

A

binds to dna dependent RNA polymerase - inhibits the initiation of mRNA synthesis

29
Q

Rifamycin is bacteriocidal : True or fale

A

true

30
Q

When is rifamycin used?

A

in first line defenses against TB

31
Q

What drug causes a Disruption of cytoplasmic membrane

A

Polymixins: disrupts outer membrane of gram negative bacteria after binding to LPS
very toxic!
puts holes in our cells too - so it has a limited selectivity

32
Q

What two drugs are considered anti-metabolic antibiotics?

A

Sulfonamides and Trimethoprim

33
Q

Sulfonamides mode of action and type of drug:

A

analogues PABA and competetivley inhibits the formation of dihydropteroic acid
its BACTERIOSTATIC

34
Q

Trimethoprim mode of action and type of drug:

A

antimicrobial binds to second enzyme of this pathiway and inhibits formation of THF
bacteriostatic