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Module 6 Week 2 > Antibiotics For UTI > Flashcards

Antibiotics For UTI Flashcards

1
Q

What does MIC stand for and what is it?

A

Minimum inhibitory concentration
-conc of drug that will inhibit growth of bacteria at site of infection

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2
Q

Features that affect which type of antimicrobial/antibiotic treatment is used for UIT

A

-Type of infection; simple (cystitis), complicated (pregnancy, immunocompromised)
-type of organism eg streptococci, enterococci, P. aeruginosa, Staph. pseudintermedius, Proteus, Streptococcus, Klebsiella

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3
Q

Most antibiotics for UTI are known as…

A

Imperical—> based on observation you give antibiotics for UTI and don’t send sample to lab (if its a first time infection) (recurrent infection sample would want to be sent to lab)

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4
Q

Pharmacokinetic properties of an antimicrobial (what body does to drug)

A

Metabolism (via liver)

Excretion – via kidney (e.g., glomerular filtration of small molecules)

Dose and frequency depending on how fast drug is eliminated out of body

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5
Q

Since e reaction occurs via kidney, if animal has renal impairment what may you need to do to drug?

A

^ dose

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6
Q

% of
dogs
Cats
who will get a UTI in lifetime

A

14%
5%

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7
Q

UTI in ruminants particularly associated with what?

A

Pregnancy and catheterisation and kidney stones

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8
Q

Lots of antibiotics are excreted normally via

A

Kidney (good to treat UTI)

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9
Q

Disadvantage with many antibiotics we use

A

Don’t penetrate cells so persistence can occur

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10
Q

Recommended no. Of days to treat UTI with antibiotics
-simple
-complicated

A

7days
7-10+days

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11
Q

For simple UTI (cystitis), do we want antibiotic conc higher in urine or serum?
For complicated UTI pyelonephritis, do we want antibiotic conc higher in urine or serum?

A
  1. > urine conc
  2. > serum conc as we want antibiotics to penetrate kidney tissue
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12
Q

Urine concentration how many times or greater than MIC of infecting organism to be most effective

A

4x

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13
Q

2 types of antibiotics

A

-Bactericidal—> kill bacteria
-bacteriostatic antibiotics—> inhibit its growth and allow immune response to clear out rest of bacteria

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14
Q

Effectiveness of antibiotics falls into 2 classes

A

Concentration dependant killing-> high levels of drug
Time dependant killing-> how long you give drug for

I.e some drugs work best when you give very high doses or some work (reaching peak produces best effect) if you give drug for longer period of time (reaching >MIC produces best effect)

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15
Q

Pharmacokinetics of Penicillins (in general)
-routes of infection
-what are not very good for/good at

A

-Mostly intravenous or intramuscular, not good orally
-don’t get into cells very well so wont be good for persistent infections
-not good at penetrating specific cellular barriers except in inflammation
-poor lipid solubility

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16
Q

General pharmacokinetics of b-lactams
-half life
-advantages
-disadvantages

A

• Short half-lives (0.5-1.2 hour)
• Little or no post-antibiotic effect (PAE)

• Minimal hepatic metabolism
• Eliminated largely by kidney
• 60-100% excreted unchanged in urine
• Relatively cheap drugs, widely used

17
Q

What are the Limitations in the use of narrow spectrum
penicillins

A

• Susceptible to b-lactamases which breaks down penecillin
• Pen G inactivated by stomach acid (not oral)
• Pen V less active but more acid stable
• May cause super-infections in certain species (small furrries) causes death
• Rapid excretion so delayed absorption forms developed e.g. procaine and benzathine penicillins
• Procaine is a banned substance in racing horses and greyhounds

18
Q

Since penicillin has a narrow spectrum what is done to it? This produces what 2 drugs?

A

Spectrum is increased by adding side chains to it which makes ampicillin and amoxicillin

19
Q

Ampicillin and amoxicillin properties
-stable or not?
-which is better orally absorbed
-which is good for biliary tract infections
-both have good activity against what type of bacteria?
-both susceptible to what?

A

-relatively acid stable
-amoxycillin
-ampicillin
-gram negative (especially E. coli, Proteus, Salmonella)
- b-lactamases

20
Q

What is added to drugs to overcome b-lactamase action

A

Synulox

21
Q

Cephalosporins- properties

A

Has many generations
Each generation going up has better Gram negative coverage
Excreted by kidneys
Long term cephalosporins like cefovecin reserved for cases showing resistance to the usually used antibiotics

22
Q

Sulfonamides
-what is it
-mechanism of action

A

1st antibiotic ever developed
Synthetic antimicrobials
-inhibits folic acid biosynthesis

23
Q

Describe sulfonamides mechanism of action works

A

Inhibit enzyme dihydropteroate synthase (DHPS) in the folic acid pathway, meaning folic acid can’t be formed. This results in bacteria’s death

24
Q

Potentiated sulfonamides
-what is it

A

Sulfonamides + another drug

25
Q

Name common drugs combined with sulfonamide to form potentially sulfonamide

A

-Diaminopyrimidines
-Sulfadiazine and trimethoprim
-Trimethoprim (TMP)
-Ormetoprim
-Baquiloprim

26
Q

What is the advantage of combined drugs i.e potentiated sulfonamides

A

Both drugs will work together to inhibit pathway at different steps

27
Q

Sulfonamide
-bacteriostatic or bactericidal?

A

-bacteriostatic

28
Q

Potentiated Sulfonamide spectrum of activity
-bacteriostatic or bactericidal?
-inhibit what organisms?
-well absorbed orally or not?
-advantage
-problem

A

-thought to be bactericidal
-gram negative bacteria, gram positive bacteria, some Protozoa, some anaerobic bacteria
-well absorbed orally
-Distribution is wide in tissues and body fluids so can be used for tricky infections
-problem; lots of bacteria resistant to them

29
Q

Pharmacokinetics of sulfonamides

A

weak acids, well absorbed from gut and can be ion trapped in urine
• Diaminopyrimidines - weak bases
• Well distributed in the body; cross cellular barriers including BBB, CSF, synovial fluid, prostate and eye
• Can reach high concentrations tissues - in the lungs and the kidney
• Metabolism: acetylation in most species, glucuronide conjugation (dogs; highly water
soluble)
• Excreted in urine as parent compound or in conjugated metabolites

30
Q

Adverse effects on sulfonamides used on their own

A

They have lots of side effects-

Renal crystalluria (crystallisation in urine and kidney)
Urine solubility exceeded (acetylated compounds)

Hypersensitivity reactions rare but particularly in certain breeds, e.g. Doberman, pinscher, Scottish terrier, German shepherd

skin eruptions, hepatitis, fever, arthropathy

Haemorrhagic syndrome (poultry)
Soft shelled egg

Dry eye (keratoconjunctivitis sicca, prolonged use of certain sulphonamides)

31
Q

Advantages of potentiated sulfonamides

A

Ratio between sulfonamide and other drug is made bigger so less sulphonamide used so less side effects

Synergistic and bactericidal – high concentrations in urine not achievable in other tissues
Sulfonamide can be reduced to about 1/8 normal dose (reduces side effects and toxicity)
Bacterial Resistance to combinations is low

32
Q

What is the ratio between sulfonamide to diaminopyrimidine in potentiated sulphonmide?

A

5:1

33
Q

Name some examples of potentiated sulfonamides

A

Trimethoprim and sulfadoxine (Borgal, Trivetrin) Trimethoprim and Sulfadiazine (Co-trimizin) Trimethoprim and Sulfamethoxazole (Co-trimoxazole) Baquiloprim and Sulfadimethoxine (Zaquilan)

34
Q

Fluoroquinolones
-what do they do
-advantages

A

• Inhibit DNA gyrase and topoisomerase IV • Well absorbed
• Renal and non renal excretion
• Get into prostate for treatment of prostatitis • Dosage adjustment in renal or liver disease • Reserved for resistant organisms

Module 6 Week 2 (10 decks)

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