Antimicrobials - UGHHHHH Flashcards
what do Beta Lactams do?
destroy cell wall via interfering with transpeptidase enzymes (responsible for cross-links between peptidoglycan strange)
what are some restrictions of beta-lactams (the MUST haves?)
MUST have cell walls and/r growing (most effective during log phase of growth)
What organisms may persist with beta lactase?
static
leta-lactams have synergism with ________ thus help prevent relapse and failures in serious infections with tolerant microorganisms
Aminglycosides
what is penicillin effective against?
many G+ (FEW G- [inactive at normal dose])
BOTH anaerobic and aerobic bacteria
What is the exception of anaerobic and aerobic penicillin efficacy?
Bacteroides
3rd generation cephalosporins are a class of _______?
B-lactams
How are 3rd generation cephalosporins different than normal?
WIDER spectrum f activity (tx resistant G- infections in very compromised cases)
3rd generation cephalosporins have properties like _________?
penicillins (BUT are more stable and temp changes)
T/F 3rd generation cephalosporins are toxic?
FALSE/NOPE, relatively non-toxic (BUT repeated IV administration may cause local phlebitis)
T/F 3rd generation cephalosporins HURT when they are injected.
T
Carbapenems are a class of what?
New class of 3rd generation cephalosporins
______ & ______ are among the most active drugs against a wide variety of bacteria (resistant to B-lactamase destruction) - What are they effective against?
imipenem and meropenem
anaerobic and aerobic microorganisms
Anaerbes are highly susceptible (Bacteroides fragilis)
T/F toxicity is common with B-lactams?
What are some effects?
F (toxicity is rare)
Hypersensitivity reactions = skin reactions, angioedema, drug fever, serum sickness, vasculitis, eosinophilic, anaphylaxis
What should be administered IV with caution esp. if hyperkalemia is present?
Potassium Penicillin
What are 3 common examples of aminoglycosides?
Gentamycin, toramycin, amikacin
what do aminglycosides interfere with? Are they most effective against G+ or G-
membrane associated bacterial ribosomes
susceptible aerobic bacteria
Mostly G- (bacilli) - ex. pseudomonas
What facilitates the movement of Aminoglycosides across cell wall?
What decreases the movement?
passive movement facilitated by ALKALINE ph!
low PH increases resistance more >100x
decreased passage also with low O2 tension (hypoxic tissues) - caution with treating anaerobes in low O2 environments (NOT effective against obligate anaerobes & fungi)
What is hella important to remember with regards to administering Beta-lactams and any drugs given after?
Cell wall injury from B-lactams will increase uptake of aminoglycosides
Are aminoglycosides effective against streptococci?
NOT really (moderately sensitive - quite resistant)
What is a major negative effect of animoglycosides?
what are 2 others?
filtered and absorbed into brush border of proximal tubule & LOH via ionization = transported into cells= sequestered in lysosomes = lysosomes rupture = accessive accumulation (mainly in renal cortex) = tubular necrosis = MONITOR renal function (evidence in 3-5d)
ototoxicity, NM blockage
what is an example of fluoroquinolone?
enrofloxacin
What does fluoroquinolone do?
inhibits DNA/RNA enzyme synthesis
what is fluoroquinolone effective against?
aerobic G- (genitourinary, GI tract, bone inf, soft tissues/skin infections) & G+
What are fluoroquinolone not effective against?
anaerobic
what are examples of macrlids?
Erythromycin, azithromycin, clarithromycin
What do macrolids do?
What is is confined to?
interfere with protein synthesis (reversibly bind to 50s subunit of ribosome) - confined to rapidly dividing bacteria and mycoplasmas
What are macrolids affective against?
G+ > G-
Are macrolids bacteriostatic r bacteriocydal?
static
T/F macrolides are concentration dependent?
F (they are time dependent)
What are macrolids syngergicstic with?
rifampin (Rhodococcus equi)
macrolids can be used to tx _______ infections.
respiratory
_____ are sensitive to macrolid-indiced GI disturbances.
Horses (can be fatal)
what do sulfonamides do?
blocks several enzymes needed for biogenesis and other metabolic reactions necessary for formation of RNa
______ is great against external auditory canal infections.
fluoroquinolone
are sulfonamides static or cidal?
static
high concentrations of sulfonamides are found in the _____.
urine
what are some potentiated sulfonamides? What do they do?
trimethoprim, pyrimethamine
inhibit dihydrofolate reductase in bacteria and protozoa (not effective if used alone)
what is critical in defense mechanism for bacteriostatic Abs?
adequate cellular and humoral defense mechanisms
When are sulfonamides most effective?
early stages of acute infections (when organisms are rapidly multiplying)
What do sulfonamides effective against?
G+, G-, some protozoa
what is combined to tx protozoal disease
sulfonamides + pyrimethamine
what is used to tx burns to prevent gram + & G- organisms?
SSD
Concentrations of sulfonamides in _______ exceed concentrations in _________..
kidneys, plasma
skin, liver, lungs, are slightly less than corresponding plasma concentrations
how are sulfonamides excreted?
urine primarily; also in feces, milk (1-3.5x higher than plasma)
what do tetracyclines do?
reversible binding of 30s subunit (prevention ribosomal translation)
How are tetracyclines further classified (include examples)
short acting - oxytetracycline,
intermediate acting - de-methyl-choro-tetracycline
long acting = doxy
Are tetracyclines static or cidal?
Are they concentration or time dependent?
static
time
Where are tetracyclines found in high concentrations in the body?
kidneys, liver, bile, spleen, lungs, bone
tetracyclines are the drug of choice to tx ____ & ____.
rickettsia & mycoplasma
what are tetracyclines effective against?
G +, G-, anaerobe, aerob., even some protozoa
What is a SE of tetracyclines?
D in horses (esp, of animal is critically ill or stressed)
chelate Ca in teeth & bones (yellow-brownish discoloration, impairs healing)
rapid Iv injection = hypotension
nephrotocic
WBC chemotactic/phagocytosisi
What is an examples of a phenol?
chloremphenicol
What are phenols effective against?
G+, G-, anaerobes (bactericides fragilis)
phenols are known to be…
highly effective well tolerated broad spec Abs
what do phenols do?
inhibit microbial protein synthesis by binding to 50s bubonic of 70s ribosome (IMPAIRS peptide transferred activity)
are phenols static or cidal?
static (can be Cidal in high concentrations)
Where are phenols absorbed?
upper GI
T/F chloramphenicol doesn’t undergo hepatic metabolism?
FALSE - it undergoes extensive haptic metabolism (liver dz prevents normal metabolic degradation and active Ab accumulates in body)
What is an example of glycopeptide?
vancomycin
what do glycopeptides do?
prevents cell wall synthesis and produces rapid bactericidal effect in DIVIDING bacteria
What are glycopeptides effective against?
G+ (NOT against G-)
where are glycopeptide excreted?
kidneys (in ACTIVE form)
what are some hypersensitivity reactions related to glycopeptides?
ototoxicity
nephrotoxicity
what are Nitroimidazles used to tx?
protozoa ABs
anaerobic
what is an examples of Nitroimidazle?
metronidazole
T/F Nitroimidazles can be used off label in feed animals?
FUCK NO!
this is prohibited
metronidazole is effective against what?
ptotozoa + obligate anaerobic bacteria (Bacteriodes fragilis, B. melanogenicus, Fusobacterium, C. perfringens, other clostridial inf)
metronidazole is NOT effective against what?
facultative anaerobes, obligate aerobes, microaerophilic bacteria
how is metronidazole absorbed?
in GI (bioavailability = 60=100%)
- serum concentrations in 1-2h (widely distributed to all tissues) - penetrates BBB - attains tx concentrations in abscesses & empyema fluid
What is a weird thing that metronidazole is also effective against?
adjunct to tx solid tumors (radiosensitizors)
How do NSAIDS work?
reduce biosynthesis of Prostaglandins via inhibiting COX (converts arachidonic acid into prostaglandins) = impairs inflammatory process
where is Cox 1 found?
what is it classified as?
all tissues
constitutive
Where is cox 2 found?
what is it classified as?
damaged or inflamed tissues
non-constitutive (also involved in thermoregulation and pain response)
What are the bodies NORMAL protective mechanisms?
D ulcers colic protein less right dorsal colitis renal papillary necrosis toxicity
What do most NSAIDS on the market tx?
cox 1 & cox 2
what is the cox 2 inhibitor on the market?
firocoxib
what is flunixin meglamine commonly used to tx?
pain & enodtoxemia associated with colic (helps with arterial hypoxemia, vasdilation, CV shock, D)
what can be used with lameness exams?
lidocaine (30-45 mins), bupivicane (90-120mins), mepivicaine HCL (4-6hrs)
complications of nerve blocks
broken needle shaft
SC infection
synovial infection
