Pharmacology Exam 3-Antibiotics 1

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a chemical substance produced by one organism that is destructive to another

property of drug action achieved by blocking a reaction vital to bacterial cells but not a patient’s cells, or by inhibiting an enzyme present in bacteria and humans but binding to the bacterial enzyme with greater affinity

agents that inhibit bacterial growth but do not kill bacteria

agents that causes lysis (death) of bacteria

narrow spectrum
selective for gram positive or gram negative, aerobic or anaerobic bacteria

broad spectrum
target many types of bacteria

gut flora
generally nonpathogenic bacteria normally living in our gut that help produce vitamins (biotin and K), aid in digestion of certain foods, and prevent harmful pathogenic bacteria from overgrowing and causing disease

pseudomembranous colitis
antibiotic-induced colitis characterized by sever inflammation of the inner lining of the colon, severe abdominal pain, bloody diarrhea, fever, fatigue, and loss of appetite

clostridium difficile
spore-forming anaerobic gram positive bacillus causing pseudomembranous colitis and existing as part of the normal flora in 3% of individuals

antibiotics causing p.c.
amoxicillin, cephalosporins (3rd gen)., clindamycin, macrolides, fluoroquinolones, tetracyclines

p.c. treatments
metronidazole, oral vancomycin as last resort, fecal microbiota transplant

B-lactam antibiotics
bactericidal cell wall biosynthesis inhibitors; penicillins, cephalosporins, carbapenems

rigid, impermeable bacterial cell walls built by two amino sugars with an extending pentapeptide

antibiotic degrading enzyme that cleaves B-lactam rings, inactivating the drug and causing acquired resistance to penicilins

penicillin prototypes
Penicillin V and Amoxicillin

penicillin V
natural penicillin prototype administered orally, not penicillinase resistant, acid stable

aminopenicillin administered orally, not penicillinase resistant, acid stable

clavulanic acid
irreversible, “suicide” inhibitor of many bacterial B-lactamases

amoxicillin plus clavulanic acid

adverse reactions to penicilins
hypersensitivity (degradation products combining with host proteins and becoming antigenic), anaphylaxis

penicillin contraindications
history of severe allergic reactions to penicillin, cephalosporins, or imipenem

one of the largest and most prescribed classes of antibiotics, sharing the same basic structure and mechanism of action as penicilins

1st generation cephalosporins
mainly gram positive activity and B-lacamase sensitive but penicillinase resistant

2nd generation cephalosporins
moderate gram positive and gram negative activity, improved B-lactamase resistance

3rd generation cephalosporins
mainly gram negative activity, penetrating CNS, B-lactamase resistant

4th generation cephalosporins
true broad spectrum activity towards both gram positive and negative bacteria, even more resistant to B-lactamases, administered only through IV

1st generation cephalosporin widely used for pre-surgical prophylaxis where gram positive skin microbes are likely pathogens

most frequently prescribed 1st generation cephalosporin, penicillin substitute for gram + cocci

cefdinir (omnicef)
most frequently prescribed 3rd generation cephalosporin

adverse effects of cephalosporins
5-15% of penicillin-allergic pts are also allergic, but 3rd generation are alternative for pts with mild allergic rxns to penicillins

adverse reactions to penicillins and cephalosporins
diarrhea (disruption of the normal balance of GI bacteria), more common with extended spectrum versions

used as a last resort to treat infections caused by G(-) which are resistant to other available drugs or for treatment of mixed aerobic and anaerobic infections

carbapenem prototype; B-lactam antibiotic, resistant to almost all B-lactamases, broad spectrum

adverse reactions to carbapenems
nausea, vomiting, diarrhea, superinfections with bacteria or fungi due to broad spectrum of activity, pseudomembranous colitis

carbapenem-resistant enterobacteriaceae (CRE)
gram negative, normal human gut bacteria that have become resistant by acquiring new, potent B-lactamases; occur among pts receiving treatment for other conditions in the hospital; 50% mortality rate

methcillin-resistant staphylococcus aureus (MRSA)
infections which have acquired a new PBP (transpeptidase) that is resistant to all B-lactam antibiotics; exists in hospital acquired and community acquired forms

antibiotic of “last resort”; used for serious infections in pts with severe penicillin allergies and serious infections caused by multidrug resistant G+ bacteria, as well as prophylaxis in hospitals with established MRSA colonization

vancomycin mechanism of action
bactericidal, interferes with peptide crosslinking during cell wall synthesis, does NOT inhibit transpeptidase (like the B-lactams)

vancomycin spectrum of activity
only effective against G+ bacteria; cannot penetrate Gram – outer membrane or porins

spectrum of activity
dictated by the ability for the drug to reach the transpeptidase (penicillin binding protein)

vancomycin absorption
not absorbed orally, administered slowly by IV

vancomycin distribution
well-distributed to tissues, body fluids, but not CNS

vancomycin excretion
renal excretion–dosage should be adjusted in pts with poor renal function

vancomycin adverse effects
fever and chills following infusion, needs to be given slowly (over at least 60 minutes), rapid infusion can->thrombophlebitis and skin reddening, rare effects include neutropenia, anaphylaxis, ototoxicity and nephrotoxicity

red man syndrome
vancomycin side effect characterized by widespread skin reddening due to histamine release (erythroderma)

bacterial protein synthesis inhibitors
antibiotics that bind to bacterial ribosomes and block protein synthesis; macrolides, clindamycin, tetracyclines, aminoglycosides

macrolide mechanism of action
bacteriostatic; reversibly bind the large subunit of the bacterial ribosome and inhibit protein synthesis, low affinity for the human ribosome subunit

erythromycin and clarithromycin
macrolides effective against many of the same organisms as penicillin V, former is unstable in acid (must be coated), latter is more acid stable and more bioavailable

macrolides, one of the world’s best selling antibiotics, similar spectrum as penicillin V, has unique slow tissue distribution and long half-life, more acid stable than erythromycin

adverse effects of macrolides
GI distress (more so for erythromycin), diarrhea and superinfections, cholestatic hepatitis and jaundice

macrolide DDIs
carbamazapine, digoxin, benzos, warfarin, Ca++ channel blockers, statins, viagra

macrolide CIs
heart disease (rhythm disorders)

bacteriostatic bpsi binding to the same site as macrolides and blocking protein synthesis

clindamycin spectrum of activity
narrow spectrum: excellent anaerobic Gram+ and Gram – activity but poor Gram – aerobic activity, very effective for streptoccus and staphylococcus gram +

clindamycin adverse effects
abdominal pain, nausea, vomiting, diarrhea, skin rashes, most associated with pseudomembranous colitus

bacteriostatic bpsis binding the small ribosomal unity and inhibiting protein synthesis

tetracycline spectrum of activity
broad spectrum, but resistance now limits, most common current use is in acne and rosacia

tetracycline DDIs/FDIs
dairy, calcium, iron, Mg and Al-containing antacids prevent oral absorption

tetracycline adverse effects
GI distressk photosensitivity (increased risk of sunburn, superinfections like p.c.

tetracycline CIs
pregnancy, nursing, children under 8 because of formation of stable complex with calcium in any bone-forming tissue, thereby staining teeth and preventing bone growth in utero and in young children

bactericidal bpsis binding to the small ribosomal subunit and blocking protein synthesis; ineffective anaerobically, given parenterally due to poor GI absorption, reserved for use in serious cases

aminoglycoside prototype

aminoglycoside adverse effects
nephrotoxicity; dose adjustments are absolutely necessary in pts with kidney disease, ototoxicity

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Name 5 mechanisms for antibiotics. 1) inhibit cell wall synthesis 2) inhibit protein synthesis 3) inhibit folic acid synthesis …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy MOA: PCN cell wall biosynthesis MOA: cephalosporins cell wall biosynthesis WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY …

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We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy What MOA class is vancomycin? Cell Wall Synthesis Inhibitor Is vancomycin bactericidal or bacteriostatic? Bactericidal WE WILL WRITE A …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Mycobacterium Waxy cell wall (hard to kill) Most common mycobacterium Tuberculosis Viruses Invade cells of host (intracellular parasites) Reproduce …

We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy Prokaryotes known as bacteria Prokaryotes are single celled organisms lacking a true nucleus and nuclear membrane WE WILL WRITE …

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