Antibiotics Flashcards

1
Q

T/F: Tetracycline works by killing bacteria.

A

F

Bacteriostatic; they work by inhibition of protein synthesis through reversible binding to bacterial 30S ribosomal subunits

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2
Q

T/F: Penicillins work by inhibition of cell wall synthesis.

A

T

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3
Q

T/F: Antimicrobials that affect the cell wall (ie penicillin, cephalosporin) or the cell membrane (polymixin B, colostin) are bactericidal.

A

T

They affect the integrity of the barrier of the cell to the environment. Without the integrity of the cell wall, the cell cannot survive.

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4
Q

T/F: Ketoconazole works by inhibition of metabolic processes.

A

F

It inhibits nucleic acid synthesis

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5
Q

T/F: A superinfection is more common following treatment with a narrow-spectrum antibiotic.

A

False

Superinfections are unrelated to the first infection which the antibiotic was originally taken for. The original antibiotic makes superinfection possible because it disrupts the normal bacterial microbiome of the body. Broad spectrum antibiotics disrupt the normal microbiome more than narrow spectrum antibiotics.

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6
Q

For an antibiotic to be successful, it must accomplish these 3 things.

A
  1. The pathogen must be susceptible to the drug.
  2. The drug must reach the site of infection at a high enough concentration to inhibit/kill the pathogen.
  3. The animal must be able to tolerate the concentration of drug needed to inhibit/kill the pathogen.
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7
Q

What are the 3 ways bacteria become resistant?

A
  1. Inherited a genetic mutation
  2. Acquired from transfer of DNA from resistant bacteria
  3. Picked up DNA from environment
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8
Q

5 Steps to reduce selection pressure

A
  1. use appropriate doses
  2. administer drug for long enough period of time
  3. educate clients to treat for entire dosage regimen
  4. don’t use antibiotics to treat non-bacterial infections such as a virus
  5. be aware of your patient’s immune status
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9
Q

What are the 5 areas that an antibiotic can target?

A
cell wall
cell membrane 
protein synthesis
nucleic acids
folic acid pathways
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10
Q

Targeting the bacterial cell wall usually results in __________.

A

-cidal

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11
Q

What are drug classes that target the bacterial cell wall?

A

penicillins

cephalosporins

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12
Q

Targeting the cell membrane usually results in bacterial cell _________.

A

-cidal

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13
Q

What drugs target the cell membrane?

A

polymycins

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14
Q

What route of admin are polymycins?

A

topical

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15
Q

Antibiotics that target bacterial protein synthesis are __________

A

cidal or static

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16
Q

Name the antibitoic(s) that target protein synthesis and are cidal

A

aminoglycosides

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17
Q

Name the antibiotics that target protein synthesis and are static

A

tetracyclines

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18
Q

Drugs that target nucleic acid synthesis are usually ___________

A

-cidal

19
Q

What antibiotic targets bacterial nucleic acids?

A

quinolones

20
Q

What antibiotic targets the folic acid pathway? When is it cidal vs static?

A

Sulfonamides
unpotentiated are static
potentialted are cidal

21
Q

What are the groups of penicillins?

A

Pen-G (natural)
Amoxicillin & ampicillin (upgraded from natural penicillins)
pencillinase-resistant penicillins (very narrow spectrum of activity)
Exteded spectrum (held in reserve)

22
Q

How can you identify a drug as a cephalosporin?

A

starts with “cef” or “ceph”

23
Q

How do you identify tetracycline antibiotics?

A

end in -cycline

24
Q

What are the 2 groups of tetracyclines?

A

Old: Tetra- & oxytetracycline
New: Mino- & doxycycline

25
Q

What is the difference between new vs old tetracyclines?

A

older bind to ions and cant diffuse through membranes; newer are less likely to bind ions and can diffuse through membranes

26
Q

What drugs should tetracyclines not be given with and why?

A
  • Sucralfate, iron, kaopectate, peptobismol (b/c tetracyclines will bind to it)
  • penicillins & cephalosporins (-cyclines are bacteriostatic)
27
Q

What species should doxy not be given via IV route?

A

Horses

causes sudden collapse, death

28
Q

How can you identify an antibiotic as an aminoglycoside?

A

ends in “mycin” or “micin”

29
Q

Why is it important to form a gradient with aminoglycosides?

A

If no gradient is formed, there drug will accumulate in the tissues and you will get a toxicity.

30
Q

What are macrolides typically used for?

A

respiratory infections

31
Q

List some examples of macrolides

A

azithromycin
erythromycin
tilmicosin
tylosin

32
Q

Similarities between chloramphenicol and floriphenicol

A
  • excesllent at tissue penetration

- target protein synthesis

33
Q

Differences between chloramphenicol and floriphenicol

A
  • Chloram. is banned from food animals b/c it causes aplastic anemia, whereas flori does not cause that and is FDA approved in cattle
  • Chloram is either -static or -cidal based on amount, whereas flori. is only -static
34
Q

How can you identify an antibiotic as a fluroquinolone?

A

-ends in “floxacin”

35
Q

Why are fluoroquinolones good for treating UTIs?

A

they accumulate in higher concentrations in the urine

36
Q

What drugs should not be given at the same time as a fluroquinolone? Why?

A
  • antacids (drug precipitates out)
  • sucralfate (drug will stick to it)

If you must give together, give the fluroquinolone 4hrs after the other drug

37
Q

What is the special sulfonamide? How does it work?

A

Sulfasalazine

  • gets broken down by bacteria in colon into azulfidie and mesalamine
  • mesalamine is used for antiinflammatory properties in colon
38
Q

How do you identify a sulfonamide antibiotic?

A

starts with “sulfa”

39
Q

What do potentiated sulfonamides end in?

A

“prim”

40
Q

List Lincosamide drugs

A

lincomycin
clincamycin
pirlimycin

41
Q

What are lincosamdies good at?

What species are they toxic to?

A

Tx anaerobic bacteria

Toxic to rabbits, GPs, horses, ruminants

42
Q

What is metronidazole used for?

A

kill giardia

43
Q

Can metronidazole be used in calves?

A

NO