·
Extended-spectrum penicillin: certain gram-positivebacteria and gram-negative
rods (Haemophilus influenzae, Escherichia
coli, Listeria monocytogenes, Proteus mirabilis, Salmonella,
enterococci). HELPS
CEPHALOSPORIN
EXCLUSIVE:
First generation: gram-positive cocci, Proteus
mirabilis, E. coli, Klebsiella pneumoniae.PEcK
Second generation: gram-positive cocci, Haemophilus
influenzae, Enterobacter aerogenes, Neisseria
species,Proteus mirabilis, E. coli, K.
pneumoniae, Serratia marcescens.HENPEcK
Third generation: serious gram-negative
infections resistant to other beta-lactams; meningitis (most penetrate the
blood–brain barrier).
Examples:
ceftazidime for Pseudomonas; ceftriaxone for gonorrhea.
4th Gen: have PI in name
3rd Gen: have CEF/CEFT f/by AEIOU
1st GEN: have standalone L in nale (not CEFACLOR-
it does not have standalone L)
Acting
on pseudomonAZ: cefoperAZone, ceftAZidime
This
ONE having bile excretion, safe in renal failure: cefoperazONE, ceftriaxONE
C/I
in renal failure: cephaLOthin, cephaLOridine
Acting on Anaerobe: cefOTetan, cefOxiTin, cefOmeTazole, cefTizOxime (i.e. having –O- & -T- excluding other
mnemonics)
Cefoperazone, cefotetan, Cefmetazole:
inhibit aldehyde dehydrogenase, also the ones that are associated with vitamin
K–related bleeding problems
·
TETRACYCLINES:
Vibrio
cholerae, Acne, Chlamydia, Ureaplasma Urealyticum,
Mycoplasma pneumoniae, Borrelia burgdorferi (Lyme disease), Rickettsia,
tularemia. VACUUM your Bed Room
·
Foscarnet = pyroFosphate analogue
·
“Buy AT 30, CELL at 50”
30S inhibitors:
A = Aminoglycosides
(streptomycin, gentamicin, tobramycin, amikacin) [bactericidal]
T = Tetracyclines
[bacteriostatic]
50S inhibitors:
C = Chloramphenicol
[bacteriostatic]
E = Erythromycin
[bacteriostatic]
L = Lincomycin
[bacteriostatic]
L = cLindamycin
[bacteriostatic]
·
GET on the Metro!
Giardia, Entamoeba, Trichomonas,
Gardnerella vaginalis, anaerobes (Bacteroides,Clostridium)
·
INH: Injures Neurons & Hepatocytes
·
Amphotericin “tears” holes in the fungal
membrane.
·
Amantadine blocks influenza A and
rubellA and causes problems with the cerebellA.
·
Shake and Bake syndrome: with AMPHOTERICIN B, rigors
and fever, hypotension because of histamine release- test dose is advisable or do pretreatment with
NSAIDS, antihistamines, meperidine, adrenal steroids.
·
Amphotericin B
and fluconazole enter the CSF adequately. Ketoconazole has poor penetration.
·
Serum sickness reactions: Sulfonamides,
cephalosporins (especially cefaclor), minocycline, hydantoins, and penicillins.
·
Anidulafungin (Anti Fungal) and moxifloxacin (Anti
Biotic) are not effective agents for urinary tract infections.
·
AZTREONAM is the most appropriate antibiotic to prescribe
for gram negative coverage in a patient who is anaphylactic to penicillin.
·
Linezolid is not a bactericidal agent; it is a static
drug. Additionally, the drug requires monitoring of platelet counts due to the
risk of thrombocytopenia.
·
No single agent is bactericidal against enterococci.
Usually penicillin has high MICs and intrinsic resistance occurs with all
cephalosporins. Therefore, combination therapy with a cell wall active agent
along with an aminoglycoside is necessary.
·
Acute tubular necrosis from aminoglycoside therapy
typically occur Usually after 7 to 10 days of therapy.
·
Patient with recent kidney transplant is on cyclosporine
for immunosuppression. Requires antifungal agent for candidiasis → what
drug would result in cyclosporine toxicity?
→ ketoconazole.
·
CLINDAMYCIN
is not of Aminoglycoside group.
LINCOMYCIN is not of Macrolide group.
Both these are LINCOSAMIDE
group. Esp for Anaerobes & GN.
VANCOMYCIN only against GPC.
·
Sulfonamide potency is decreased in case of
co-administration with Local anesthetics – derivatives of paraaminobenzoic
acid.
·
There
are several main reasons for the greater propensity for
cardiovascular and bleeding problems with ticarcillin. The drug is available as a disodium salt and
we often need to administer large doses of the drug. The added sodium load can
increase blood volume and blood pressure. In addition, ticarcillin seems to
have antiplatelet activity. This, alone, can cause a slight increase in the risk
of spontaneous or excessive bleeding, and it appears that the risks are much
greater if the ticarcillin is given to a patient already taking antiplatelet
drugs or drugs that impair coagulation or platelet function by other
mechanisms.
·
·
INH:
mycolic acid synthesis inhibitor
·
Balantidiasis Rx: Tetracyclines
·
piperAChine:
blocking acetylcholine
transmission at the myoneural junction of helminthes
·
niclOXamide: Inhibiting oxidative
phosphorylation in some species of helminthes
·
PraziCantel: Increasing cell membrane permeability for calcium, resulting in paralysis,
dislodgement and death of helminthes
·
Pyrantel
pamoate: neuromuscular blocking agent
that causes release of acetylcholine and inhibition of cholinesterase, persistent
activation of the parasite's nicotinic
receptor
·
·
·
Atovaquone
possesses a novel mode of action against Plasmodium spp., inhibiting the electron transport system at the level of the
cytochrome bc1 complex. The drug is active against both the
erythrocytic and the exoerythrocytic stages of Plasmodium spp.; however,
because it does not eradicate hypnozoites from the liver, patients with
Plasmodium vivax or Plasmodium ovale infections must be given radical
prophylaxis.
·
About 3% of patients treated with abacavir have
an allergic reaction to it. These reactions usually include rash and nausea and
sometimes include fever. If a patient with a previous reaction to abacavir is
rechallenged with the medicine, he or she can develop a much more severe
life-threatening reaction with marked hypotension.
·
Ritonavir is a
powerful inhibitor of the liver’s P450 system. Ritonavir is used
in combination with saquinavir solely to inhibit saquinavir’s metabolism, thereby
keeping serum concentrations in a therapeutic range longer. Ritonavir does have
protease inhibitory activation, but in this combination it is the saquinavir
that is causing the main therapeutic effect.
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