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Pharm Exam 1 > Abx 4 > Flashcards

Abx 4 Flashcards

1
Q

What are the 5 veterinary fluoroquinolone drugs most commonly used in veterinary medicine?

What is the human fluoroquinolone drug used in veterinary medicine?

Which of the five veterinary drugs is exclusively for large animal only?

A 
Enrofloxacin – Baytril®
Orbofloxacin – Orbax®
Marbofloxacin - Zeniquin®
Difloxacin – Dicural®
Danofloxcin  -- Cattle ONLY
Sarafloxacin  -- poultry (not anymore)
Ciprofloxacin
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2
Q

What is the fluoroquinolone that was approved for poultry use but then pulled because of concerns over developing resistant bacteria?

A

Sarafloxacin

- because of concerns about Campylobacter resistance

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3
Q

• How can you recognize a quinolone drug by its generic name?

A

o -floxacin

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4
Q

• Are quinolones bactericidal/bacteriostatic? Gram negative activity or Gram positive activity? Aerobic or anaerobic? Concentration dependent or time dependent?

A

o Rapidly bactericidal
o Good against gram (-) aerobes
o Concentration dependent

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5
Q

• What is the mechanism of action of the fluoroquinolones against bacteria? What are the two target sites for the drug?

A

o Bactericidal → Inhibit bacterial DNA replication and transcription
• Bacterial DNA must be coiled by an enzyme – DNA gyrase
• Quinolones target Subunit A of DNA gyrase → inhibits its function → inhibits supercoiling

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6
Q

• Why are mammalian cells not affected by quinolones like bacteria are?

A

o Quinolones target Subunit A of DNA gyrase and inhibits its function – inhibits supercoiling
o Mammalian cells have topoisomerase like DNA gyrase but it’s only inhibited at concentrations 1000x above inhibition of bacterial DNA gyrase

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7
Q

• What is the relationship between quinolones and Streptococcus that wasn’t mentioned with any other antimicrobial drug group?

A

o Quinolones secondary target is bacterial Topoisomerase IV which unwinds the double stranded bacterial DNA
o Topoisomerase IV isn’t a quinolone target in Gram (-) bacteria but may be a target in Gram (+)’s: Staph and Streptococci

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8
Q

• What is the post antibiotic effect seen in quinolones? What other antimicrobial drugs discussed in this lecture series also has a significant post-antibiotic effect?

A

o They still work after their concentration decreases from its peak (concentration dependent). Aminoglycosides also have a post-antibiotic effect.

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9
Q

• Besides anaerobic bacteria, what three other groups of bacteria are considered to be pretty resistant to quinolones? Why is the resistance to Pseudomonas to quinolones of particular concern in the practice of veterinary medicine?

A

o Staph – MRSA
o Streptococcus
o Pseudomonas
• Quinolones are the ONLY antibiotic we still can use against Pseudomonas

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10
Q

• There are 4 mechanisms by which bacteria are resistant to quinolones. What are they?

A

o Mutation of gryA gene that codes for subunit A of DNA gyrase; this mutation allows the enzyme to function without having a binding site for the quinolones to bind and inhibit it
o Coding mutation for Topoisomerase IV – Gram (+) bacterial resistance
o Efflux pumps that remove quinolones (multidrug resistant)
o Change in Gram (-) outer membrane porin: reduces the entrance of the quinolones into the bacterial cell
o One resistance mechanism can produce some increased resistance within a bacteria, but resistance is additive with each additional resistance mechanism!

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11
Q

• How did the use of quinolones in drinking water of chickens result in a concern about veterinary drug use causing human bacterial resistance to drugs? What bacteria were involved in this chicken problem?

A

o All use of quinolones in poultry is prohibited because resistance was seen in Campylobacter
• In 1997 (2 years after approved for use in poultry), quinolone resistant Campylobacter infected chicken caused outbreak of food poisoning in humans.

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12
Q

• Can quinolones be used extra label in food animals? Can they be used in poultry at all?

A

o No, it is prohibited, you CANNOT use in poultry or lactating dairy.

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13
Q

• Generally speaking, how well are quinolones absorbed in dogs and cats when given PO? By injection? In what species is absorption much more variable than dogs and cats?

A

o PO in dogs, cats, and swine → absorption is close to 100%
o IM injection → close to 100%
o PO in horses and ruminants → highly variable (10-90%)

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14
Q

• Why do inflamed tissues achieve higher fluoroquinolone concentrations than the same type of normal tissues?

A

o . Concentrate in high levels inside macrophages and neutrophils → 4-10x HIGHER than plasma concentrations
• Leukocyte migration into inflamed tissue accounts for higher concentration of quinolones in infected inflamed tissue than normal tissue

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15
Q

• What are quinolones a good drug of choice for use in pyodermas?

A

o Concentrate in high levels inside macrophages and neutrophils → 4-10x HIGHER than plasma concentrations
• Leukocyte migration into inflamed tissue accounts for higher concentration of quinolones in infected inflamed tissue than normal tissue
• Pyoderma concentrates quinolones in the skin by this mechanisms

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16
Q

• Why are quinolones pretty effective in treatment of bacterial urinary tract infections? Which quinolone is NOT very effective for urinary tract infections — and why?

A

o Quinolones are effective for UTIs because they are excreted by passive diffusion (GFR) and active secretion (PCTs) which allows for a high concentration of the drug in the urine
o EXCEPTION: difloxacin because it is eliminated by the liver and will have a low concentration in the urine

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17
Q

• Typically are quinolones more likely to be administered s.i.d. or t.i.d.? Why?

A

o Enrofloxacin is concentration dependent. You want the peak at 8-10x MIC, so there is no advantage to frequent dosing as long as high Cmax:MIC ratio is maintained.
o Quinolones are typically given SID

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18
Q

• What rickettsial disease are quinolones used for treatment?

A

o Rickettsia rickettsia = Rocky Mountain Fever

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19
Q

• Do quinolones have any FDA approved uses in horses? Are quinolones used in horses?

A

o No, but extra label doses do exist.
o It is considered useful in horses because
• It can be given PO, IV, or IM
• Effective against gram (-) aerobes
• PO administration is less likely to allow GI overgrowth since “good” anaerobic gut flora are not affected by the drug.

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20
Q

• Why might quinolones be useful in treating bacterial infections in reptiles?

A

o Quinolones are commonly used in reptiles because they are effective against serious gram (-) infection including Salmonella and Pseudomonas.
• Good absorption IM, variable PO

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21
Q

• Can enrofloxacin (Baytril®) be used in any food animals? If so, which ones? Can enrofloxacin be used extra-label in any food animal specie?

A

o Enrofloxacin has LIMITED use in food animals
• NOT able to use in dairy or veal calves
o NO EXTRA LABEL USE IN FOOD ANIMALS

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22
Q

• Why are enrofloxacin and ciprofloxacin generally considered to be synonymous drugs as far as culture and sensitivity testing and results?

A

o Because 10-40% of enrofloxacin is metabolized into ciprofloxacin

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23
Q

• By what route of administration is enrofloxacin primarily excreted? Why is it, then, that we can still use enrofloxacin in animals with compromised renal function?

A

o Enrofloxacin is primarily excreted through the KIDNEY → glomerular secretion → active secretion into the renal tubules
o Small amount is eliminated by the liver → biliary excretion

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24
Q

• In what dogs is the use of enrofloxacin contraindicated? Why is this?

A

o It is contraindicated in dogs because you see bubble like changes in articular cartilage during periods of rapid bone growth with doses 2-5x normal dose for 30 days
o BUT use it in life or death situations as long as you have explained the contraindication properly to the owners

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25
Q

• How do bubbles form in the articular cartilage in animals receiving 5x the normal dose for 30 days?

A

o Quinolones concentrate in articular cartilage → cause complexes with magnesium → interferes cell metabolism → apoptosis → cartilage defects → arthritis in old age

26
Q

• Why enrofloxacin considered to be contraindicated in larger dogs for longer than small or medium dogs?

A

o Small and medium breed dogs 2-8 months old
o Larger dogs are not considered full grown until 1.5 to 2 years
• it is not technically a contraindication

27
Q

• How does the higher dose or IV dose of quinolone increase frequency of seizure activity in animals that have a history of seizures? Do quinolones typically cause seizures in animals without a previous history of seizures?

A

o High doses or IV doses can cause CNS excitation → GABA neurotransmitter inhibition → causes increased activity of the CNS
o Can cause increased frequency of duration of epileptic seizure activity → does NOT typically cause seizures in animals that do not previously have seizures

28
Q

• What is the problem about enrofloxacin and cats? Has this been seen in other veterinary quinolones? Why hasn’t it been seen in difloxacin?

A

o Idiopathic blindness with doses <5mg/kg

o Difloxacin is not approved for use in cats so it has not been documented to cause

29
Q

• Why shouldn’t you crush or split film-coated quinolone tablets?

A

very bitter taste

30
Q

• What is the interaction between antacid drugs, sucralfate, and enrofloxacin?

A

o Orbax will chelate with sucralfate and antacids

31
Q

• How does the spectrum vary among enrofloxacin, orbafloxacin, marbofloxacin, difloxacin?

A

o Orbafloxacin = enrofloxacin = marbofloxacin = difloxacin

o The quinolones are quite similar

32
Q

• Which quinolone of the four quinolones used in small animal medicine is eliminated far more by the liver than the kidney?

A

o Difloxacin

33
Q

• What’s the difference between a sulfonamide drug and a potentiated sulfonamide drug? What are the two potentiated sulfonamide drugs used most in veterinary medicine?

A

o Potentiated sulfonamides = old sulfa drugs + trimethoprim or ormetoprim
• Trimethoprim + sulfadiazine = Tribrissen®
• Ormetoprim + sulfadimethoxin = Primor®

34
Q

• Single sulfas (unpotentiated) are still used for what purpose in food animal medicine? What is the single sulfa compound used in veterinary medicine?

A

o Single sulfas are used for coccidian and other protozoa in POULTRY (sulfadimethoxine = albon)
o Sulfasalazine is used for its anti-inflammatory effect on the colon

35
Q

• What is sulfasalazine not used for its antimicrobial effect?

A

o Sulfasalazine is a GI tract drug used more for its anti-inflammatory effect in the colon more than for its antimicrobial effect (doesn’t really say why)

36
Q

• What is the mechanism for action of sulfonamide drugs?

A

o Sulfonamide drugs inhibit the formation of folic acid by disrupting the bacteria’s enzymatic processes
o Sulfas by themselves are bacteriostatic because they only block folic acid synthesis at one step. This mechanism of action is very safe for mammalian cells because we do not make folic acid, we get it from our diet.

37
Q

• What is the mechanism for action of the potentiating agents (trimethoprim and ormetoprim)

A

o Potentiating compounds block formation of THFA. This combined effect is bactericidal.

38
Q

• Why is it said that PABA and sulfa are competitive antagonists?

A

o PABA is the actual target of the enzyme and sulfonamide is an introduced target (the sulfonamide keeps the enzyme busy so that PABA does not get utilized to make folic acid).
o If there is an overwhelming production of PABA, the bacteria can be resistant to the sulfonamide (folic acid will still be made)

39
Q

• Are sulfonamides bactericidal or bacteriostatic? What about potentiated sulfa drugs?

A

o Sulfas by themselves → bacteriostatic

o Potentiated sulfa drugs → bactericidal

40
Q

• What are the three mechanisms by which bacteria become resistant to sulfonamides?

A

o Alteration of the enzyme: then sulfa cannot bind to the enzyme
o Reduced penetration of the bacterial cell: preventing th esulfa from entering the site of folic acid synthesis (can only work at the site of action)
o If the bacteria is resistant to 1, it is resistant to ALL

41
Q

• What is the problem with distribution patterns of sulfonamide antibiotics when they are used with trimethoprim or ormetoprim? How does this affect the concentrations achieved in the prostate?

A

o Great distribution, but sulfa and trimethoprim are chemically dissimilar – slightly different patterns of distribution. If the drugs are not both in the tissue at the same time, the result is only bacteriostatic
o In the prostate → trimethoprim concentration is 380% > than plasma vs. Sulfadiazine is only 11% > than plasma → results in a static effect

42
Q

• How does some equine food stuff interfere with sulfonamides?

A

o Sulfas combine with plant carbohydrates and could be stuck with the material until it is digested in the colon (it won’t get absorbed)

43
Q

• Why are sulfonamides not generally used in dairy cattle?

A

o Penetration into milk is not high enough to be therapeutic, but still high enough to contaminate the milk → DON’T use in dairy cattle

44
Q

• Why do we tend to avoid sulfonamide use in food animals in general?

A

o Sulfas contaminate milk and generally the drug residues from sulfa drugs last for a while. Systemic use in food animals is avoided.

45
Q

• If sulfonamides undergo filtration, active secretion, and reabsorption in the kidney, which of these processes accounts for the higher concentrations in the urine than in the plasma? Which of these processes can account for a longer half life for some sulfonamides?

A

o Primarily by GFR → some degree of active secretion so high concentrations can be achieved in the urine → reabsorption from renal tubules does occur, especially if urine pH is acidic
o The long half-life of some sulfas is due to significant passive diffusion reabsorption of sulfa from renal tubule to peritubular caps.

46
Q

• How are KCS and sulfas linked? What is used to treat KCS if it is irreversible?

A

o KCS = keratoconjuctivitis sicca (dry eye): lack of adequate tear production, the eye becomes inflamed with mucoid discharge
o Sulfa causes a direct toxic effect on the lacrimal acinar cells that produce tears.
o It may or may not be reversible
o Can use cyclosporine to stimulate tear production (usually have to stay on for life)

47
Q

• If the sulfa causes KCS, then how is it treated? (what drug?)

A

o KCS is dry eye → use cyclosporine to stimulate tear production

48
Q

• How would a hypersensitivity reaction to sulfa drugs appear clinically?

A

o The hypersensitivity reaction in dogs is delayed and causes renal disease signs, lameness, skin rash, redness, itching, hepatopathy, and blood dyscrasia: thrombocytopenia, neutropenia, anemia

49
Q

• How is it that sulfonamides might decrease levels of T3 and T4 in the dog?

A

o Interferes with normal thyroid hormone synthesis (controversial as to whether this is a true phenomenon or not)
o Thought that they interfere with thyroid peroxidase that produces T3 and T4
o Reversible within 3 weeks of discontinuing sulfa drug

50
Q

• What are the four major indications for potentiated sulfonamides in the dog?

A

o Pyoderma
o UTI
o Respiratory infections
o Protozoal infections (coccidian, toxoplasma)

51
Q

• Which sulfa drug is FDA approved for control of coccidiosis in poultry?

A

o Primor® → sulfadimethoxine + ormetoprim
• Second most commonly used sulfa in vet med
• Available as medicated feed supplement for use in poultry to decrease coccidiosis

52
Q

• Which of the four sulfa drugs is an enteric sulfa? What is it used for? How does it produce its anti-inflammatory effect? What is 5-ASA and how is it related to Azulfidine®?

A

o Sulfasalazine (Azulfidine®) = sulfa + 5-aminosalicylic acid (5-ASA)
• produces a local anti-inflammatory effect
• in the colon, the bond is cleaved by colonic bacteria and 5-ASA is released – blocks prostaglandins like other NSAIDs

53
Q

• What are three macrolides?

A

o Erythromycin
o Tylosin – Tylan ®
o Tilmicosin – Micotil ®

54
Q

• How do macrolides work? Concentration dependent or time dependent? Bactericidal or bacteriostatic?

A

o Macrolides target the 50S ribosome and disrupt bacterial protein synthesis
o Time dependent
o bacteriostatic

55
Q

• Which macrolide is used to treat pink eye in cattle? What macrolide is used as a growth promotant?

A

o Tylosin – Tylan ® → used to treat cattle “pink eye” – Moraxella bovis
o Major use → feed additive for cattle, swine, chicken → growth promotant

56
Q

• What is “tylosin responsive chronic diarrhea in dogs”?

A

o Dogs that respond to Tylosin with or without having identified a causative organism

57
Q

• What is the FDA approved use of tilmicosin in cattle?

A

o Tilmicosin → FDA approved & indicated for Bovine Respiratory Disease (BRD)

58
Q

• What is the precaution about using tilmicosin? What is the actual detrimental effect on people? Is there an antidote?

A

o The injectable form has caused cardiac arrhythmias in primates
o Could cause death in farm workers/veterinarians accidentally injected with the drug – NO antidote!

59
Q

• Why has tilmicosin been called a suicide drug?

A

o Could be stolen from a large animal truck/mobile clinic and used for suicide
o Injectable form has caused cardiac arrhythmias in primates → linked to possible deaths in farm workers accidentally injected

60
Q

• What are the two lincosamide drugs? What is their particular therapeutic advantage over a lot of other antimicrobial drugs? What kind of infections would clindamycin be used for?

A

o Lincomycin and clindamycin
o They work in anaerobic environments on anaerobes!!
o Used for dental infections, abscesses, osteomyelitis

61
Q

• In what species are lincosamides contraindicated for use? Why?

A

o Lincosamides are contraindicated in horses, cattle, hamsters, rabbits, chinchillas, and Guinea pigs
• SEVERE alterations to GI flora
• Severe and sometimes fatal enteritis

62
Q

• What is florfenicol known for? What is its relationship to chloramphenicol? Why is chloramphenicol absolutely contraindicated for use in food animals even though florfenicol is FDA approved for use in cattle and swine?

A

o Florfenicol has excellent penetration into tissues and the CNS
o Flofenicol is related to chloramphenicol, BUT its not used because it causes aplastic anemia

Pharm Exam 1 (6 decks)

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