Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

199 Cards in this Set

  • Front
  • Back
what is the difference between bacteristatic and bactericidal?
bacteristatic antibiotics do not kill the organism, rather they inhibit a metabolic pathway required for growth making it more susceptible to the immune system. bactericidal antibs kill the organism outright via lysis.
can an antibiotic cause resistance? why or why not?
NO, antib resistance is due to a mutation in the bacteria the antib is targeting. this mutation would have occured no matter what. the bacteria's mutation may create an enzyme which metabolizes the antib.
why is antib resistance dangerous? what should the course of drug treatment be?
if the antib has selective resistance, it will only kill the bacteria which are still susceptible to it. the bacteria that resisted the antib will overgrow in population. begin tx with a broad spectrum antib then choose a more specific rx once the pathogen is known.
define synergism in regards to antibiotics.
using two drugs in conjunction will give a greater effect than using each separately.
how are frequencies of resistance related?
they are additive.
is fever always related to an infection?
no, it can be due to a pyrogen (foreign substance altering the thermoregulatory system).
what types of drugs are sulfonamides, generally?
broad spectrum STATIC against g+/g-
what is the mechanism for sulfonamides?
inhibit dihydropteroate synthase, the first step of folic acid synthesis.
name the enzyme required for this rxn:

PABA + pteridine -> dihydropteroic acid
dihydropteroate synthase
what is N5, N10 methylene THF?
the 1 carbon carrier which transfers a methyl group to dUMP in the synthesis of thymidine.
at what stage is glutamate involved in folic acid synthesis?
it is added to dihydropteroic acid to form FH2 which is reduced by DHFR to FH4.
why are sulfonamides ultimately succesful?
they are able to inhibit DNA synthesis.
why don't the sulfonamides affect human DNA synthesis?
b/c humans don't make folic acid, they take it in pre-formed as green veggies, etc.
what are DHFR inhibitors used with? why?
they are used with sulfa drugs for a synergistic affect.
what is the function of DHFR?
it reduces FH2 to FH4 to be reused in thymidine synthesis.
why does a DHFR inhibitor provide synergism with a sulfonamide?
because together they inhibit two steps in the synthesis of TH4.
name three DHFRIs
which DHFRI is antimalarial? which DHFR does it inhibit?
it inhibits protozoal DHFR
which DHFRI inhibits mammalian, bacterial and protozoal DHFR? what else is it used to treat?
methotrexate. it's also used for psoriasis and various cancers.
which DHFRI may cause blood dyscrasius? which DHFR does it inhibit?
trimethoprim. it inhibits bacterial DHFR.
what must you consider when treating women with sulfonamides?
pregnancy. sulfonamides can cross the placenta and cause unwanted side effects in fetus and antibacterial effects. it is pregnancy category B (animals = no risk)
what are two common oral sulfonamides?
sulfisoxazole and sulfamethoxazole
what antib should be used in kids with acute otitis media? recurrent?
acute: amoxicillin or an 2nd/3rd generation cephalosporin.
recurrent: sulfisoxazole
what are the main causes of UTIs in community? in hospitals?
e.coli 80%
s.saph. 10%

e.coli 50%
klebsiella, proteus,enterobacter, serratia 40%
enterococcus faecalis, s.saph & s.aures 10%
what is an alternative antib for an uncomplicated UTI?
what is sulfamethoxazole often offered with? why?
it's often available with trimethoprim, aka Co-trimoxazole. it's a DHFRI, which provides synergism.
how is co-trimoxazole given? what is another name for it?
oral and IV
what are some uses for trimethoprim-sulfamethoxazole?
1.UTI if local e.coli rez to TMP-SMZ is < 20%.
2. respiratory and GI infections
3. high doses for pneumocystis carinii in AIDS
if resistance to e.coli is greater than 20%, what can be used to treat a UTI?
nitrofurantoin or phosphomycin
a flouroquinalone (ie ciproflaxin)
what are some topical sulfonamides?
silver sulfadiazine
why is sulfacetamide given with phenylephrine? what is this combination called?
sulfacetamide is given in eye infections. the phenylephrine is a vasoconstrictor and helps with bloodshot eyes. VASOSULF
how do vasopressers work? give an example of one.
vasopressers stimulate the alpha 1 adrenergic receptors on vasculature. this constricts the smooth muscle.
what is glucocorticoid given with a sulfonamide? what is the fxn of this combination?
sulfacetamide + prednisolone = BLEPHAMIDE
it treats a bacterial eye infection, the glucocorticoid is anti-inflammatory.
what does a drug like blephamide treat?
it is for bacterial eye infections, but it also treats the inflammatory component of the infection.
what is blephamide an alternate for? what would be a better/preferable choice?
it's an alt. for ulcerative blepharitis, an inflammatory condition cause by bacteria.

ideally it would be treated with polysporin ointment.
what are common bacterial causes of ulcerative blepharitis?
s.aureus and s.epidermidis
what is polysporin ointment composed of? what sort of coverage does it offer? is it rx?
it's composed of bacitracin and polymyxin B. bacitracin gives g+ coverage, plymyxin B gives g- coverage. it is an OTC ointment.
how would you 'up' your gram negative coverage in the case of ulcerative blepharitis.
use the aminoglycoside antibiotic GENTAMICIN ophthalmic ointment.
what are the most common bacterial culprits of bacterial conjunctivitis?
strep pneumonia
moraxella catarrhalis
when suffering from bacterial conjunctivitis, which drug is preferrable? why?
vasosulf (sulfacetamide + phenylephrine). vasodilation is common in bacterial conjunctivitis, causing red sclera. this rx will remove the infxn and the redness.
in the case of bacterial conjunctivitis with NO VASODILATION, what is the drug of choice?
polysporin (bacitracin + polymyxin B).
what provides better gram negative coverage for a bacterial conjunctivits? (than polysporin)
ophthalmic form of flouroquinolone ciprofloxacin
if a newborn presents with bacterial conjunctivitis, how will you proceed?
it is important to know how soon after birth the symptoms appeared, this will determine the causative organisms and tx.
what are two sulfonamides used for burn tx? what is specific about them?
silver sulfadiazine
which sulfonamide helps prevent sepsis in burn victims? how does it work?what caution must be taken?
silver sufadiazine. the silver released is toxic to microorganisms. caution must be taken not to use the drug over too large a surface area, or the sulfa can be absorbed.
what are the general side effects of sulfonamide drugs?
3.blood dyscrasias
which side effect of sulfonamides is preventable with drinking lots of water with oral dose?
which side effect demands that sulfonamides not be given to newborns and infants under 2 mos old?
which side effect of sulfonamides causes generalized CNS depression and neonatal jaundice? how does it happen?
it's a form of jaundice where the bilirubin gets displaced from plasma proteins. free bilirubin then enters the CNS and deposits in the basal ganglia and other areas.
what is a rare but potentially fatal side effect of sulfonamides? what does it cause?
blood dyscrasius. acute hemolytic anemia, agranulocytosis, aplastic anemia.
what is stevens-johnson syndrome?
a form of hypersensitivity and a side effect to sulfonamides. 'erythema multiforme major'. it's characterized by bullous eruptions on the skin and mucous membranes. ****can cause suffocation***
what is rx fever?
another sensitivity side effect to sulfonamides.
name a group of broad spectrum cidal agents used mostly for gram negative (SOME gram positives).
what is the fq g- mechanism? g+?
g-: inhibit DNA gyrase (cuts and reanneals DNA). get ds DNA fragmentation.

g+: inhibits topoisomerase IV which is involved in separation of daughter cells during replication.
list 9 flouroquinolones
which flouroquinalones are for ophthalmic use?
ciprofloxacin = ciloxan
gatifloxacin = zymar (oral + ophthalmic)
moxifloxacin = vigamox
what flouroquinalone has an otic version?
ciprofloxacin = cipro hydrocortisone otic
which flouroquinalone is for mild comm.acquired pneumonia and exacerbations of chronic bronchitis?
which flouroquinalone is for UTIs and lower RTIs?
which flouroquinalone is NOT good for systemic infxn? what is it used for?
norfloxacin. use for UTI.
what is ciprofloxacin known for?
it has the best gram negative activity. (and a ophthalmic and otic version)
a patient suffers peritonitis in a perforated colon. what is the most likely bacteria and some of it's characteristics? what is the first choice tx?
b.fragilis, a gram negative rod (part of colon's normal flora). weak endotoxic activity.
1st choice tx:
ampicillin and sulbactam
what is an alternative rx for b.fragilis?
which potential rx for b.fragilis has increased gram negative activity?
ampicillin + sulbactam = an aminoPCN with a beta-lactamase inhibitor.
how do piperacillin and tazobactam work? what other bacteria, besides b.fragilis are they helpful towards?
you have an antipseudomonas PCN with a beta lactamase inhibitor. P.aeruginosa is another common pathogen in peritonitis. it's gram positive spectrum is similar to PCN.
what are the major side effects of flouroquinalones? what bacterial infxn are they often responsible for?
nausea, vomiting and diarrhea. they cause c.difficle-induced diarrhea and psuedomembranous colitis.
what is the pathogenesis of c.difficile?
it survives as spores until the antib is discontinued. it then grows w/o competition for nutrients. it makes toxin A and B, which cause fluid production and cell lysis. it causes psuedomembranous plaques to form on the colon wall.
how do flouroquinolones cause c.difficile?
they disrupt normal bowel flora.
how can c.difficile be treated?
1st choice: metronidazole (forms reactive anion which damages bacterial DNA, kills c.difficile)

2nd: vancomycin
name five side effects of flouroquinolones.
1.phototoxicity (red rash)
2.increased QTc (conduction)
3.arthropathy (cartilage dmg)
4.tendon rupture
5.CNS stimulation (convulsions, psychoses)
a patient suffering an ear infxn is carrying an rx for moxifloxacin/gatifloxacin/ sparfloxacin AND one for altered cardiac conduction. what do you do?
take them OFF flouroquinolones! they can cause increased QTc.
which part of the PCN structure is required for activity? which part determines the property/spectrum?
thiozolidine and beta-lactam rings make the nucleus and are required for activity. side chains determine property and spectrum.
what are two beta-lactamase inhibitors?
sulbactam and tazobactam.
what do gram positive bacterial cell walls contain? how does PCN work on this?
the walls are made of pep-g, made of two alternating sugars, NAG & NAM. they are CROSS-LINKED. NAM has a D-aa which has to be removed by transpeptidase before this cross-linking can occur. PCN INHIBITS THE TRANSPEPTIDASE.
what does inhibition of the transpeptidase by PCN cause? what sort of antibiotic are PCNs?
inhibition of cell wall synthesis and, ultimately, lysis. therefore PCNs are CIDAL.
what is the main mechanism of resistance to PCN?
development of beta-lactamases.
why is PCN-G given paraenterally? in which case will it distribute to the the CNS?
it's given via IV/IM b/c it is unstable in the stomach. it'll distribute to the CNS only if the meninges are inflamed.
how is the activity of PCN expressed?
UNITS. 1 unit = 0.6 micrograms
what are the three forms of PCN G?
1.aqueous (IV/IM) Na+/K+ salts

2.procaine (suspension IM only) + anasthetic

3.benzathine (suspension IM)
which PCN G is the longest acting?
the g+ spirochete treponema pallidum causes what dz? what is the rx? what is an alternative if allergic?
syphilis. benzathine is given ideally.
if allergic:
doxycycline or tetracycline (orally)
or 3rd gen.cephalosporin ceftriaxone (IV/IM)
what is another name for PCN G?
benzyl PCN
what is the difference between PCN G and PCN V?
V is an acid stable form for oral use. G is not stable in the stomach. V is dosed in mgs, G is dosed in units.
what is PCN V also knowns as? how is it prescribed?
phenoxymethyl PCN. food interferes with it's absorption, so give 1hr pre meals a.c. or 1hr p.c.
what are three drugs only to be used against resistant staph (not against microbes sensitive to PCN G or V)?

what is another name for them?
1.dicloxacillin (oral)
2.oxacillin (oral sol & inject)
3.nafcillin (injection)

penicillinase resistant PCNs
what does MRSA mean?
methicillin resistant staph aureus.
how are dicloxacillin, oxacilin, and nafcillin eliminated? when is this an advantage?
50% biliary and 50% renal excretion. this is an advantage in liver or kidney dz.
what are 'extended spectrum PCNs?' how are they similar to PCN? different?
aminopenicillins. they are still susceptible to PCNases and strains that resist PCN resist aminoPCNs. BUT they have MORE gram negative coverage.
what are some aminopenicillins?
ampicillin & amoxicillin
what is ampicillin often given with? what is it given for? how is it administered?
it's often given with sulbactam/unasyn for peritonitis due to b.fragilis. it's administered IV/IM.
what is sulbactam?
it's a beta lactamase inhibitor.
what is augmentin? what are it's uses?
clavulanate (beta lactamase inhibitor) + amoxicillin.

1.alt for UTI if TMP/SMZ or fq fails.
2.otitis media **
3.prophylaxis pre dental procedure if mitral valve prolapse.
why isn't amoxicillin available for peritonitis? how is it administered?
it's not available paraenterally.
it's administered with oral caps and pediatric drops.
what are the major causes of otitis media? what guidelines must be kept in mind when prescribing?
strep pneumonia (g+) causes 50%
h.influenza(g-) causes 25%

rule: NO antib in past month use amoxicillin
YES antib in past month, augmentin.
a child suffering from otitis media is allergic to PCN. what's the rx? for his mom with the same problem?
pediazole (sulfisoxizole + macrolide erythromycin)

macrolide (clarithromycin)
an RTI from s.pyogenes, s.pneumonia (g+) and h.flu (g-rod) can all be treated with what aminopenicillin?
either ampicillin and amoxicillin.
what forms of sinusitis can either aminopenicillin treat?

what are other first line agents for these infections?
from strep pneumoniae, h.influenzae and moraxella catarrhalis.

other agents: 3rd generation cephalosporins, cefdinir, cefpodoxime.
what is unique about antipseudomonas PCNs? name two.
they are active against some pseudomonas (modest v. P.aeruginosa) and some resistant proteus but still susceptible to PCNases.

2.piperacillin (+tazobactam always)
what is ticarcillin available with? what is this combination active against?
clavulanate (beta lactamase inhibitor) as timetin. it's active vs some pseudomonas and some resistant proteus. still susceptibile to PCNases!
what are the general side effects of PCNs as a group?
4.increase seizure risk
what is an example of 'superinfection'?
overgrowth of c.difficile produces toxins which cause psuedomembranous colitis.
what is the hypersensitivity to PCNs due to?
it's from metabolites acting as haptens and is IgE mediated. it's characterized by rashes, fever, bronchospasms, serum sickness, steven-johnson syndrome, anaphylaxis.
which PCN side effect does decreased renal function adversely affect?
it increases the chance that the PCN will cross the BBB, increasing seizure likelihood.
what is the structure of cephalosporins? what is the mechanism?
beta lactam + dihydrothiazine ring with side chains. they act by the same mech as PCNs (inhibits transpeptidase enzyme).
what is the advantage to using a cephalosporin?
they resist many beta lactamases.
what organisms do the 1st generation cephalosporins work on?
proteus mirabilis (enteric)
e.coli (enteric)
klebsiella pneumoniae (RTI/UTI)
which organism, which can be treated by 1st generation cephalosporins, is urease +, promoting stones?
proteus mirabilis
when does proteus mirabilis infect? what does it generally cause?
it infects when it leaves the intestinal tract. it generally causes UTIs.
what are two 1st gen. cephalosporins? how are they given?
cephalexin and cefadroxil. both given orally.
what coverage do first generation cephalosporins have? what kind of PCNase do they resist?
they have good g+ coverage and PEcK g-. they resist staph PCNases.
what kind of coverage do second generation cephalosporins have?
less g+ but more g-.
Proteus mirabilis
Klebsiella pneumoniae
what are some 2nd generation cephalosporins? include dosage.
1.cefaclor (oral q.8hrs) *serum sickness*
2.loracarbef (oral q.12h)
3.cefuroxime q.12hr (oral = ceftin, IV = zinacef)
what is a 2nd generation cephalosporin active against bacteroides fragilis?
the cephamycins, specifically cefoxitin (IV/IM)
what differentiates the 3rd generation cephalosporins? name four.
they have much less g+ and much MORE gram negative coverage. also best v. meningitis.

1.ceftriaxone (IV/IM)
2.cefotaxime (IV/IM)
3.cefpodoxime (oral)
4.cefdinir (oral)
which 3rd generation cephalosporin should not be given to children under 3 mos due to kernicterus risk? what is the exception to this?
ceftriaxone should not be given (it's HIGHLY protein bound, can displace bilirubin easily) UNLESS as single does for gonorrheal conjunctivitis.
how is ceftriaxone a good drug in case of renal failure?
1/2 is excreted in bile, 1/2 in kidneys.
what is the best 3rd generation cephalosporin aganist n.gonorrhea?
which 3rd generation cephalosporin will also cover bacteroides?
cefotaxime (IV/IM)
an infant develops reddened feces after meningitis tx. what is the cause?
an rx of cefdinir. it binds Fe and decreases it's absorption of Fe. infants fed formula high in Fe can suffer reddened feces.
name two 4th generation cephalosporins.
cefepime & cefditoren
how is cefepime administered? what is it effective against? what are it's side effects?
it's good for gram negative rods resistant to 3rd generation cephalosporins. it has good CNS penetration, but neurological side effects:
EEG changes with increase risk if epileptic.
what is the most common side effect of cephalosporins? what other abnormalities may present?
hypersensitivity is most common.

coagulation abnormalities may result due to interference with vitamin K, which increases prothrombin time. caution with warfarin/heparin or bleeding disorder.
with which drug must you use caution with a patient on warfarin or with a bleeding disorder?
what are carbapenems?
name 3.
they are the broadest spectrum beta lactams available. includes anaerobes and some MRSA.
what is cilastatin?
what is it given with?
Cilastatin is a chemical compound which inhibits the human enzyme dihydropeptidase. Dihydropeptidase is found in the kidney and is responsible for degrading the antibiotic imipenem.

it's given with imipenem.
which carbapenem causes fewer seizures? what is it not metabolized by?
meropenem. it's not metabolized by dipeptidase.
which carbapenem is only dosed once a day?
what are common uses of carbapenems?
2.lower RTIs (s.aureus, e.coli, klebsiella, enterobacter, h.influenzae)
3.intra-ab & gyn infxns, bacterial septicemia.
4.bone, joint & skin infxns(enterococcus faecalis, s.aureus & epidermidis, p.aeruginosa)
what is vancomycin used for?
IV for MRSA or for nonresistant staph if allergic to beta lactams. the oral form is not absorbed but is an alternate for psuedomembranous colitis.
what causes psuedomembranous colitis? how does it become a problem?
it makes 2 toxins, one causes fluid production and the other lyses epithelium to form plaques.
what is the first drug of choice for c.difficile?
metronidizone b/c it produces an anion which ruins the DNA of c.difficile
b.cereus is a spore forming g+rod which causes food poisoning. what is a good rx for it?
what is red man syndrome? what causes it?
due to IV of vancomycin. get flushed upper body, hypotension, tachycardia and shock. it's caused by the release of histamine from basophils and mast cells.
what are some other vancomycin side effects?
ototoxicity and nephrotoxicity.
what drug is not a beta lactam antibiotic, but still inhibits cell wall synthesis? it is useful against UTIs from e.coli and enterococcus faecalis in women.
what is it's mechanism?
fosfomycin. it inhibits enolpyruvate transferase.
how does fosfomycin inhibit cell wall synthesis?
it blocks addition of phosphoenolpyruvate to UDP-N-acetylglucosamine (2nd step in park peptide synthesis).
what is an injectable lipopeptide for skin infxns from g+ and MRSA organisms? what is it's side effect?
daptomycin. it's side effect is increased creatine kinase.
what type of anti-b is bacitracin? what is it's mechanism?
it's cidal vs. various g+ cocci and bacilli.

bactoprenol transports NAG/NAM outside cell, where it can be attached to pep-g. the bactoprenol must be de-pho'd before combining with NAM.
bacitracin + pho, preventing de-pho of bactoprenol. NO CELL WALL SYNTHESIS.
what is bactoprenol? how does bacitracin affect it?
it's a lipid carrier molecule involved in cell wall synthesis. bacitracin prevents it from being de-phosphorylated and therefore keeps it inactive.
what staph infxn is bacitracin useful for?
ulcerative blepharitis from s.aureus and s.epidermidis
what causes bacterial conjunctivitis?
strep pneumonia
moraxella catarrhalis
what is the structure of aminoglycosides? how are they used synergistically?
amino sugars attached in glycosidic links to an aminocyclitol ring. mostly for g- organisms. used with beta lactams for synergistic effect for g+ coverage.
what drugs are aminoglycosides used with in synergy?
carbapenems: broadest spectrum of all beta lactams. no nephro or ototoxicity.

cephalosporins: 3rd and 4th gen. give best g- coverage

flouroquinalones: no nephrotox.
how are aminoglycosides usually given? what is an exception to this?
they are polycations, v.polar and usually given by IV. sometimes they are given orally to clean out the bowel.
what are side effects to aminoglycosides?
they are nephrotoxic and ototoxic. all are excreted by kidney!
what is the antibiotic mechanism of aminoglycosides?
they enter the periplasmic space of G-bacteria thru porin channels. they pass thru inner membrane by flowing down the electrochemical gradient.
what are the static effects of aminoglycosides? how is this altered by does?
at low levels: mRNA is misread, giving faulty proteins. some insert into membrane = lysis.

at high levels: inhibit initiation of pr- synthesis.
at which levels are aminoglycosides cidal?
at LOW levels. the faulty proteins produced cause leaky membranes.
where can aminoglycosides attain their highest levels?
renal cortex = nephrotoxicity
(in proximal tubules the drug accumulates in lysosomes, ruptures)

endolymph = ototoxicity
what is the ultimate effect of ototoxicity?
irreversible damage b/c sensory hair cells cannot regenerate.
what can cause ototoxicity in neonates? why?
aminoglycosides, b/c the drugs accumulate in the fetal plasma.
name three IV administered aminoglycosides:
what aminoglycoside is topical, used for burns, wounds; ophthalmic prep. AND is interchangeable with tobramycin?
what is an ophthalmic rx for conjunctivitis and blepharitis with g- organisms?
tobradex (tobramycin + dexamethasone *glucocorticoid*)
what is a nosocomial "big gun" aminoglycoside?
name three oral aminoglycosides.
what are kanamycin and neomycin both used for? which is also a topical disinfectant?
both are oral for bowel prep. neomycin is also a topical antiinfectant.
what is the number one choice for amoebic dysentary (entamoeba histolytica)?
which aminoglycoside can be given orally and by IV?
name two ways to adjust dose for renal fxn.
1.change dose amt.
2.manipulate dose interval
what is the formula for creatine clearance?
(140-age)x(lean wt in kg)/
72 x serum creatine (mg/dl)

women: x 0.85
where do aminoglycosides distribute? why?
in lean body mass b/c they are polycations.
how is lbw calcuated for men? women?
men: 50 kg + 2.3kg for each inch over 5ft

women: 45.5kg + 2.3kg for each inch over 5ft
what is the aminoglycoside dose formula?
max daily dose x est CLcr/normal CLcr
what is normal CLcr for a typical 70kg male?
120-125 ml/min
when should peak levels be drawn after the dose?
30-60 minutes
what are some other side effects of aminoglycosides? what is the mechanism?
neuromuscular block causing respiratory paralysis. Ach release is blocked.
how can you treat Ach inhibition?
IV of Ca2+ or neostigmine
what kind of rx is neostigmine?
it's a cholinesterase inhibitor. it metabolizes Ach, so if inhibited, Ach levels rise.
what is the mechanism of tetracyclines?
they inhibit the binding of aminoacyl tRNA to acceptor site of ribosome. STATIC. inhibit protein synthesis.
why can levels of tetracycline persist?
they undergo enterohepatic recycling.
what type of tetracycline is tetracylcine? what is it given for? what might be better?
it's a short acting (6-8hr t1/2). it's an alternate oral or topical for inflammatory acne.

1st choice: topical erythromcin (a macrolide) + benzoyl peroxide w or w/o oral antib
what symptom of syndrome of inappropriate ADH secretion can be treated by this sort of tetracycline?
chronic dilutional hyponatremia. tx with demeclocycline, an intermediate acting tetracycline (t1/2 = 12hrs)
this tetracycline can tx rickettsia, chlamydia trachomatis and lyme dz. how is it administered?
doxycycline. oral and IV.
what can rickettsia cause? what does chlamydia trachomatis cause?
rocky mountain spotted fever.
nongonococcal urethritis and most nongonococcal cervicitis.
the spirochete borrelia burgdorferi causes this dz which results in skin lesions, joint pain, maybe cardiac and neuro issues. what drug can treat it?
lyme dz. doxycycline.
a pt with syphilis AND vibrio cholerae is allergic to PCN. what should you give them?
what would be the first choice drug for the pt with cholera?
flouroquinalone b/c better g- coverage.
what decreases absorption of tetracyclines? by what mechanism?
dairy products and antacids.
via chelation
what are side affects to tetracyclines?
1.GI upset (take with food)
2.photosensitivity (esp demeclocycline)
3.brown discoloration of teeth.
what rx is structurally similar to tetracyclines? what is it's mechanism?
tigecycline. it inhibits pr- synthesis by blocking entry of aminoacyl t-RNA to the acceptor site.
what is tigecycline good for?
it's active v.tetracycline sensitive g+/g- organisms and MRSA. it's used for complicated skin and intraabdominal infections.
what is the structure of the macrolides? what are they effective against?
lactone ring + 1 or more deoxy-sugars. effective against methicillin sensitive s.aureus, moraxella catarrhalis, h.influenzae
what is the macrolide mechanism?
they inhibit translocation from acceptor site to donor site (near where tetracycline acts)
what is an example of a macrolide? what was it historically effective against? is it still used for that?
erythromycin (enteric coated). it was first used against legionanaire's dz, now azithromycin is preferred b/c of better lung penetration. paraenteral flouroquinalone is also useful.
what sort of macrolide is used for otitis media?
erythromycin + sulfisoxazole = pediazole! *RECURRENT*
how is erythromycin coated?
with estolate salt (causes cholestatic hepatitis, but best absorbed)
what is erythromycin first choice for?
1.pneumonia by various organisms
2.camyplobacter jejuni
3.corynebacterium diptheriae
4.bordetella pertussis
what does campylobacter cause? what does it look like?
a comma shaped g- rod which causes diarrhea.
what is a g+ rod which produces exotoxin to damage respiratory mucosa? it is treated with erythromycin.
what bacteria causes whooping cough? what does it allow for?
bordetella pertussis. a g- organism, makes pertussis toxin. the coughing and necrosis can allow for staph or influenza invasion.
how does erythromycin inhibit it's own metabolism?
it's metabolites complex with cytochrome heme Fe2+ and inhibit CYP3A (the P450 which metab. erythromycin).
what is torsades? how can it be caused by erythromycin?
torsades is an arrhythmia. erythromycin can prolong repolarization. the risk is increased with any other rx that inhibits cyp3a b/c that increases your levels of erythromycin.
what are diltiazem and verapamil? how are they related to erythromycin?
they are also metabolized by CYP3A. taking one of these with erythromycin increases risk of sudden death five-fold. (they are Ca2+ channel blockers)
what are the uses of azithromycin? acquired pneumonia
3.chlamydia trachomitis
4.bordetella pertussis
5.mycobacterium avium complex
how is azithromycin metabolized?
it's t1/2 is 70 hrs and it concentrates intracellularly. it does NOT inhibit P450 and is excreted unchanged in the bile.
what rx can cause hypoglycemia (a macrolide)? what is it used for?
clarithromycin. it's used for community acquired pneumonia and mycobacterium avium complex. it does inhibit CYP3A.
what is a macrolide derivative with increased gram positive activity?
which macrolide concentrates in pulmonary tissue and WBCs? what is it for?
it's for community acquired respiratory infections. it's active v.beta lactam and macrolide rez organisms.