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DWT Exam 3 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What do 50s drugs have in common?

A

plasma concentration is not predictive of treatment success
concentrate intracellularly and reach high concentrations in abscesses
pharmacokinetic-pharmacodynamic parameters are not well defined

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2
Q

Should you co-administer 50s drugs?

A

No, they may competitively inhibit each other at the site of action and may decrease the effectiveness

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3
Q

What are the 3 types of 50s drugs?

A

Phenicols
Macrolides
Lincosamides

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4
Q

What is the spectrum of activity of phenicols?

A

Broad spectrum with activity against
-gram positive and gram negative aerobes and anaerobes
-rickettsia
-chlamydia
-mycoplasma

UNPREDICTABLE against gram negative enteric bacteria

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5
Q

How does chloramphenicol distribute in the body?

A

It is absorbed moderately well following oral absorption, but formulation matters!

Distributes very well to most tissues of the body and concentrations persist longer in tissues and distribute well to protected sites and abscesses

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6
Q

How is chloramphenicol metabolized?

A

It is metabolized extensively by the liver, but is deficient in cats and young animals

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7
Q

What are potential adverse effects of chloramphenicol administration?

A

Potential for dose-dependent hematologic toxicity
-Inhibition of mitochondrial protein synthesis in the bone marrow
CATS ARE MOST SUSCEPTIBLE
Anorexia, V/D, depression

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8
Q

What can chloramphenicol cause in people?

A

It can cause idiosyncratic and irreversible aplastic anemia in 1 in 10,000-30,000 people
This makes it prohibited for use in food animals and clients must wear gloves and be careful when administering

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9
Q

What drug interactions does chloramphenicol cause?

A

It is an inhibitor of hepatic microsomal enzyme inhibitor, so it may decrease clearance/metabolism of some drugs such as phenobarbital, phenytoin, and propofol

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10
Q

What are potential adverse effects of Florfenicol?

A

Does NOT have the para-nitro group that causes bone marrow toxicity

Horses: D+, injection site reactions

Less drug interactions

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11
Q

What are mechanisms of resistance to phenicols?

A

Acetylation and inactivation by bacterial enzymes, but cross-resistance does not always occur

Florfenicol is more resistant to bacterial enzymes

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12
Q

What do macrolide drugs all have in common?

A

They all end in “mycin”
ex. erythomycin, azithromycin, tulathromycin etc..

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13
Q

What is the spectrum of action of macrolides?

A

Gram positive aerobes such as R. equi, strep, and staph
Some activity against anaerobes (azithromycin)
Gram-Negative activity limited to BRd pathogens
Mycoplasma

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14
Q

What are the common pharmacokinetics of macrolides?

A

Differ between individual drugs, but in general most have moderate oral absorption and a wide volume of distribution

Macrolides are commonly metabolized in the liver and eliminated by the liver

They are detectable in cells 4 days longer due to their Cmax in cells being so high

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15
Q

What are potential adverse effects of macrolides?

A

GI:
V/D -> dogs/cats
Severe colitis -> rabbits/horses
Erythromycin is most common

Hyperthermia -> foals

Injection site rxns

Cardiotoxicity from IV injections of tilmicosin -> DONT use in cats, dogs, horses

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16
Q

What drug are macrolides commonly co-administered with due to the potential synergism?

A

Rifampin, despite decreasing the bioavailability of macrolides

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17
Q

What are potential drug-drug interactions of macrolides?

A

Inhibition of CYP-450 enzymes (erythromycin) leading to an increase in the plasma concentration and toxicity of other drugs

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18
Q

What is the spectrum of activity of Lincosamides and what are they most commonly used to treat?

A

Lincomycin, Clindamycin
Spectrum of Activity: gram positive organisms, anaerobes

Used to treat: wounds, abscesses, deep abscesses, dental disease, osteomyelitis

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19
Q

What is the distribution of lincosamides?

A

They are well absorbed orally in dogs and cats and distribute widely, working well for pyothorax and lung abscesses

Reach high concentrations in abscesses and accumulate in leukocytes, but penetrate poorly into the CNS

Hepatic metabolism and elimination

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20
Q

What are potential adverse effects of lincosamides?

A

Fatal diarrhea in horses and rabbits
Anorexia and vomiting in dogs
Pain/Irritation at IM/SQ injection site

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21
Q

What mechanism do Fluoroquinolones work through?

A

They are DNA Gyrase inhibitors, which means they alter the ability of bacteria to replicate their DNA and undergo transcription, repair, and recombination

Newer generations inhibit topoisomerase IV

They are bacterioCIDAL drugs and have a post antibiotic effects

22
Q

What are common drug names of Fluoroquinolones?

A

Dogs: Enrofloxacin, marbofloxacin, orbifloxacin, difloxacin

Cats: marbofloxacin, pradofloxacin

Ciprofloxacin off label

Extralabel use prohibited in food animals!!

23
Q

What are common uses of fluoroquinolones?

A

Treatment of gram negative aerobic infections (enteric/BRDC), staphylococci
similar to aminogylcosides, but safer for azotemic patients
May be used for pseudomonas, but require high doses and may develop resistance
Brucella, lehionella, chlamydia, leptospira, sometimes mycobacteria

Poor action against strep and no activity against enterococci

24
Q

What is the distribution of fluorquinolones?

A

Well absorbed in monogastrics except for Ciprofloxacin (poor absorption in cats and horses) and enrofloxacin in kittens (chelation from milk diet)

Distribute well to tissues!

25
Q

Do fluorquinolones penetrate intracellularly?

A

Yes, they penetrate intracellularly very well, with enrofloxacin reaching the highest concentration

Enrofloxacin is metabolized in vivo to ciprofloxacin

26
Q

How are fluoroquinolones eliminated?

A

Primarily the kidney, and highly effective in treating resistant UTIOs, but activity is pH dependent and is reduced in acidic environments

Typically does once daily

27
Q

What are potential adverse effects of fluoroquinolone administration?

A

Rare V/D and abdominal pain in dogs and cats

Rapid IV administration may cause CNS excitement, confusion, seizures, by inhibiting GABA and should not be used in epileptic patients

CIPRO causes fatal colitis in horses when given PO or IV

28
Q

What affect can fluorquinolones have on the cartilage?

A

They cause severe cartilage toxicity due to the chelation of Mg++ in cartilage, decreasing adherance of chondrocytes

Age, weight, and species matter -> dogs and FOALS are most susceptible, while cats and calves are more resistant

29
Q

In what species can ocular toxicity occur from fluoroquinolone (enrofloxacin) administration occur?

A

Cats, can cause retinal degeneration and blindness due to a functional defect in the ABCG2 transport protein in cats leading to an accumulation of photo reactive fluoroquinolones in the retina

30
Q

What are potential drug interactions of Fluoroquinolones?

A

They may inhibit the clearance of some drugs and cause chelation and must be given at different times than antacids, sucralfate, and iron containing vitamins

31
Q

What is the mechanism of resistance to fluorquinolones?

A

Bacteria alter the target enzyme (DNA gyrase), which is not plasmid mediated

Reduce access through altered porins (pseudomonas)

Resistance may develop during treatment and is not recommended as a systemic treatment but topical is ok

32
Q

What animals are sulfonamides typically used for?

A

Food animals, but extralabel use is prohibited in adult dairy cattle

Ruminants don’t absorb DHFRI (what makes it “potentiated”

33
Q

What species are potentiated sulfonamides commonly used for?

A

Commonly used for companion animals (extralabel for swine)

Dogs, cats, horses

34
Q

What makes a sulfa drug potentiated?

A

The addition of DHFRI
Sulfas -> bacteriostatic
DHFRIs -> bacteriostatic
Combo = CIDAL
Synergism!!

35
Q

What is the mechanism of action of sulfa drugs?

A

Inhibit folic acid synthesis
Sulfas: Inhibit Dihydropteroate synthase
DHFRI: Inhibit Dihydrofolate reductase
Bacteria cannot synthesize thymidine and cannot make DNA

36
Q

Why do sulfa drugs not affect mammals?

A

Mammals utilize dietary folate to synthesize dihydrofolic acid

37
Q

What is the spectrum of action of potentiated sulfonamides?

A

Broad spectrum reaching all 4 quadrants
First line choice for pyodermas, UTIs and soft tissue infectios
Effective against protozoa

38
Q

What is the absorption and distribution of potentiated sulfonamides?

A

They are well absorbed orally
Have good tissue distribution -> extracellular and intracellular that can reach the CNS and prostate

39
Q

Where are potentiated sulfonamides metabolized and eliminated?

A

Extensively metabolized in the liver and can be dosed once or twice daily

Primarily eliminated by the kidneys

40
Q

What are potential adverse effects of potentiated sulfonamides?

A

Horses: minimal, occasional diarrhea
Cats: taste, slobbering, difficulty pilling

41
Q

What are adverse effects of potentiated sulfonamides in DOGS

A

Dogs: some breeds lack N-acetyltransferase that leads to toxic metabolism production (dobermans, rottweilers, samoyeds, mini schnauzers) allergic/autoimmune reactions, cutaneous rxns and toxic epidermal necrolysis, hepatopathy and thrombocytopenia, keratoconjunctivitis sicca, reversible hypothyroidism, bone marrow suppression (rare), urinary crystal formation

42
Q

What are mechanisms of resistance against potentiated sulfonamides?

A

Increased synthesis of PABA -> low affinity or resistant DHP synthetase (plasmid)

DHFRIs -> increased production of normal DHFR, low affinity or resistant DHFR synthetase (plasmid)

43
Q

What drugs compose the Nitroimidazoles?

A

metronidazole, ronidazole, tinidazole

44
Q

What is the mechanism of action of Nitroimidazoles?

A

They are absorbed into bacterial cell and the antibiotic is reduced by nitroreductases forming highly reactive metabolites that disrupt bacterial DNA, leading to bacterial cell death

45
Q

What conditions are nitroimidazoles active in?

A

Only in ANAEROBIC conditions, oxygen competes with the antibiotic for electrons necessary for the nitroreductase rxn

Spectrum: ANAEROBES and some protozoa

46
Q

What is the distribution of metronidazole?

A

It is well absorbed orally and well distributed into tissues (CNS and abscesses) and works rapidly and is bactericidal

47
Q

What pathogens does metronidazole work best against?

A

Bacteroides, clostridium
Anaerobes, some protozoa
Most common -> “giardia”
Less active against actinomyces and proprionobacterium

48
Q

What are potential adverse effects of Nitroimidazoles?

A

Neurotoxicity -> severe ataxia, nystagmus, seizures, often preceded by anorexia and vomiting

Typically reversible, but signs may persist for up to 2 weeks

49
Q

What is the spectrum of Rifampin?

A

Spectrum: gram positive and gram negative bacteria

Inhibits bacterial DNA-dependent RNA polymerase and is mostly bacteriostatic

Good for abscesses, but can create resistance DURING treatment

50
Q

In what instance would Rimapin be used as a monotherapy?

A

Culture dependent MRSP pyoderma

DWT Exam 3 (6 decks)

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