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Terms in this set (43)
Common metabolic products of bacteria and fungi.
KILL bacteria. Used when host function is compromised. (If patient is losing battle)
Inhibit bacteria. Knock them down a little. Used when host cell function is good.
"good" help keep the "bad" in check with natural sources of antibiotics and growth restrictions. BUT they have the same basic structures.
Target of antibiotics
They kill anything that has a target. Antibiotics and your body are not friends. Your body wants the antibiotics out!
Minimum Inhibitory concentration (MIC)
Lowest concentration of antibiotic use to slow bacterial growth. Lowest amount of antibiotic someone can use.
Minimum bacteriocidal concentration (MBC)
Lowest concentration of antibiotic to kill bacteria.
Immune system recognizing antibiotics has "foreign" and stimulates a response against it. Can be mild or severe. Body just kills it all. 25% claim they are allergic but one 1% really are.
4 major mechanisms of Bacterial Antibiotics
1.Inhibition at Cell wall level
2.Inhibition of protein synthesis
3.Inhibition of metabolic synthesis (antimetabolites)
4.Inhibition of nucleic acid structure and function
Mechanism I Cell Wall Synthesis Inhibitors (Family I)
Beta-lactam antibiotics. β-lactam ring functional group ("garage and house") "-Cillin" compounds-penicillin, amoxicillin.
Inhibits peptidoglycan synthesis-Prevents cross-linking of NAM/NAG subunits by inhibiting bacterial transpeptidase enzymes.
Effective only when bacterial cells are growing.
"-Cillins" Best effective against Gram (+)!
Adverse effects: Allergic reactions(low) anaphylactic shock(varying degrees
Nephritis (especially for methicillin)
Platelet dysfunction-from giving too much
β-Lactam Antibiotics Examples
*Ampicillin(Unasyn) and Amoxicillin (Amoxil, Trimax)-"Extended spectra" can be used in many infections.
*Carbeni/pipera/mezlo-anti-pseudomonals or resistant Gram (+)
Cell Wall synthesis Inhibitors (Family II)
"PEN like" antibiotics. Similar targets, slightly different mechanisms.
Isoniazid and Ethambutol
Vancomycin (Family II Cell Wall)
Most powerful antibiotic. Better then β-lactam's against Gram (+). If you can't get rid of it with this then your patient is in trouble.
--Interferes with alanine-alanine bridges in PPG.
Works against almost all Gram (+) but not Gram (-)
Imipenem (Family II Cell Wall)
Same mechanisms as PEN but resistant to β-lactamase.
"Carbepenem" Family. Very broad, "β-lac of choice" for Gram (-)
GREAT for Gram (-)
Isoniazid and Ethambutol (Family II Cell Wall)
Disrupt formation of arabinogalactan-mycolic acid (Equivalent to PPG) in myobacterial and other Gram NA
Cell Wall Synthesis Inhibitors (Family III)
Cephalosporin Antibiotics-Better targeted.
Still has β-Lactam ring functional group but added a "basement"
Also prevents cross-linkage of NAM/NAG subunits by inhibiting transpeptidases.
"Generations" allow for specialization of treatment.
1st generation cephalosporins
Gram (+) and HEN
2nd generation cephalosporins
Fewer Gram (+) and HEN PEcK
3rd generation cephalosporins
Ceftazidime (Fortaz), Ceftriaxone (Rocephin)
3rd Generation and up can cross the blood-brain barrier due to lipid solubility.
Fewer Gram (+) and HEN PEcK
4th generation cephalosporins
Fewer Gram (+) and PPEcK
Other bacterial membrane disruption antibiotics
Not classic PPG attackers but still at level of membrane.
Antibiotics incorporated into cytoplasmic membrane and damage integrity.
--Bacitracin + Polymyxin B
Bacitracin + Polymyxin B
Simple Gram +/- organisms.
"pore forming" rather than attack PPG
Nephrotoxic, so TOPICAL use only
β-lactam not fused to another ring.
Works for patients allergic to PEN
Very narrow activity, not very active against Gram (+)
Mechanism II Protein Synthesis Inhibitors
Prokaryotic Ribosomes are 70S (30S and 50S subunits)
Eukaryotic Ribosomes are 80S (40S and 60S subunits)
"Universal" (broad) target because all bacteria cells require ribosomes
Ribosomes essential for translation of mRNA→proteins
-Can attack either ribosomal subunits to shut down
No translation→No protein synthesis→NO GROWTH
CLEAn TAG Mnemonic
Home plate-Top of plate is 50S (big subunit) so big word (CLEAn) attacks the 50S subunit
Bottom of Plate-30S subunit. Small bottom part of home plate attacks 30S (small subunit) and small word (TAG)
VERY broad spectrum antibacterial, high side effects.
Restricted to life-threatening infections with NO ALTERNATIVES
Adverse effects-Bone marrow suppression, aplastic anemia, grey baby syndrome, leukemia.
L-Lincomycin and CL-Clindamycin
Used for anaerobic and severe aerobic infections (Streptococcal toxic shock syndrome)
Adverse effects-Pseudomembranous colitis (Clostridium Difficile)
-Wipes out normal flora
E-Erythromycin and A-Azithromycin
Very good antibiotics. Safe and work on a huge amount of stuff. Didn't work on what it was planned for.
Azithromycin(Zithromax, Z-pak, Zmax) and Clarithromycin (Biaxin)
Gram (+) and Gram NA-Chlamydia,Syphilis, intracellular bacteria.
Good choice for PEN allergies.
Adverse effects-Disrupt normal GI flora, nausea, vomiting, abdominal pain, diarrhea
Brand name-Doxycycline. Discovered at MU in 1948
VERY broad spectrum-Gram NA, many Gram (+/-)
Low cost but high adverse effects.
Gastric discomfort but inactivated by Calcium
May be teratogenic for fetuses, may effect bone/teeth/growth development.
Not for kids under 8
Mostly for serious Gram (-)
Can't be taken orally
Only good for really serious issues, giving too much will attack kidneys quick.
Adverse Effects-Nephrotoxicity (kidney failure), Ototoxicity (Hearing loss), will cross placenta.
Inhibits the 50S ribosome, inhibiting translation.
Effective against staphylococcus and Enterococcus species and against resistant strains of Streptococcus.
Inhibit the 50S ribosome for protein synthesis initiation.
NEVER prescribed outside of the hospital-Last attempt for Gram (+)
All we have left for MRSA
Used to treat infections caused by two of the most difficult pathogens: MRSA and Vancomycin-Resistant Enterococcus (VRE)
Mechanism III Antimetabolite Antibiotics
Exploited when differences exist between metabolic processes of host and pathogen
Most are anti-bacterials (Include antivirals)
Often "mimics" a natural compound, aka "competitive inhibition" or shuts down a natural process, aka "noncompetitive inhibition"
-Bacterial synthesis of folic acid is necessary for DNA replication. (Humans obtain folic acid from diet)
Bacterial Antimetabolite Antibiotics
"Sulfa drugs" very first modern antimicrobials
Mimic of PABA, necessary for making folate.
Gram (-), Enteric Bacteria, Shigellosis, Acute UTI.
*Never works alone. Paired with Trimethoprim.
*Good for UTI because body wants to pee it out
Inhibits an enzymatic step immediately after the step inhibited by sulfonamides is the synthesis of folic acid.
SPoA-Otitis media, UTI. One of the primary treatments of Pneumocytis(carinii) Jroveci pneumonia (PCP) in AIDS patients.
Brand names-Bactrim (Sulfa and trimeth combined), Cotrim, Septra
Mechanism IIII-Antibiotic Inhibitors or Bacterial Nucleic Acid Synthesis
Last place to stop bacteria is at the replication.
Shut down Gyrase, stopping replication
-Quinolones/Fluoroquinolones ("-flox" antibiotics)
Quinolones/Fluoroquinolones ("-flox" antibiotics)
Inhibit prokaryote DNA gyrase (unwinding) Stopping replication.
-Ciprofloxacin (Cipro)-Prophylaxis, anthrax. Pre and post operation
-Norofloxacin (Noroxin)-Gram (+/-), Pseudomonas, UTI's-quickly cleared in urine.
-Levofloxacin (Levaquin)-Many STD organisms, skin infections, systemic infections-reactive. Stop already growing bacteria
Inhibit action of bacteria RNA polymerase during transcription
Gram (+/-), mycobaterium tuberculosis
-Used in treatment of pneumonia, UTI, Gastroenteritis, and atypical pneumonia.
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