Flashcards in Anti-Microbials Deck (135):
What is the general goal of antimicrobial therapy in anesthesia?
Inhibit microorganisms at concentrations that are tolerated by the host.
Name two general rules of antimicrobial therapy in anesthesia.
1. For seriously ill/immunocompromised patients select bactericidal.
2. Narrow spectrum before broad spectrum or combination therapy to preserve normal flora.
When we kill a patients normal flora we introduce them to what? Why?
Super infections because the normal flora can secrete "things" that kill opportunistic bacteria.
Name 5 considerations for antimicrobials used for surgical prophylaxis.
1. Weigh the risks/benefits.
2. select cost effective broad spectrum antibiotics
3. Prophylactic antibiotics should be given no more than 1 hour before incision.
4. Usually a single dose but may be continued for 48 hours.
5. No proof that a brief course of antibiotics results in emergence of resistant organisms.
How do we select an antimicrobial? (6)
1. Identify the causative organism.
2. Efficacy depends on drug delivery to site.
3. Usually treat with a single drug
4. Route of administration
5. Duration of treatment
Name two considerations that may interfere with the efficacy of a drug to a particular site.
1. transport across the BBB varies greatly
2. More effective if infected material is removed..
Are hypersensitivity reactions dependent or independent of the dose?
Are drug toxicities dependent or independent of the dose.
Dependent (dose related)
What special considerations must be made with a parturient when determining the proper antimicrobial? (2).
1. Most antimicrobials cross the placenta and enter into maternal milk. Fetus's liver is immature and they can't metabolize or excrete that drug and could end up with toxicity. For milk mom should discard the first couple rounds.
2. Teratogenecity- the malformation of an embryo or fetus that we worry about with any drug.
What special considerations must be made with an elderly person when determining the proper antimicrobial? (4).
1. Renal impairment
2. Deceased plasma proteins
3. Reduced gastric motility and acidity
4. Increased body fat.
Killing the bacteria
Preventing the bacterium from reproducing, does not necessarily kill/damage the bacteria.
Is PCN bacteriostatic or bactericidal?
How does PCN kill the bacteria?
By interfering with the cell wall. Doesn't allow the cell wall to join correctly and interferes with an enzyme that keeps the cell wall stable.
What three organisms (did Denise mention) that PCN is effective against?
How is PCN excreted?
PCN is part of what family of antimicrobials?
What is the big difference between PCN and ampicillin?
Ampicillin has a wider range of activity including gram negative bacilli (H. influenzae and E coli)
Of the PCN class which has the highest incidence of a skin rash?
What is the main difference between amoxicillin and ampicillin?
Amoxicillin is more efficiently absorbed from the GI tract than ampicillin.
What is the most common side effect of the PCN class? What symptoms can be seen?
Rash and or fever, immediate anaphylactic reaction and rarely hemolytic anemia
How long can the hypersensitivity reaction from PCNs be delayed?
up to 24 hours.
Of all the microbials which is the most allergenic?
The PCN family.
Which class of drugs exhibits cross-sensitively with PCNs?
Are cephalosporins bactericidal or bacteriostatic?
How do cephalosporins kill the bacterium?
Inhibits cell wall synthesis.
What larger family are the cephalosporins a part of?
What kind of spectrum of action do cephalosporins exhibit?
How are cephalosporins excreted?
60% through the kidneys
40% through the bile
What type of adverse reactions are associated with cephalosporins?
Allergic reactions causing a rash
Anaphylactic reaction in 0.02% of treated patients
What were cephalosporins cross sensitive with again?
How many generations (per Denise, not any of the books) are there of cephalosporins? What does the classification depend on?
Classification depends on the antimicrobial spectrum.
Name a first generation cephalosporin and an advantage to using it.
Cefazolin, because it is the least expensive
What is the most commonly used antimicrobial in surgical prophylaxis?
Name a second generation cephalosporin.
Name a third generation cephalosporin.
P.S. we should get credit for merely spelling all this shit correctly
Which cephalosporins penetrate into joints?
All of them.
As you go up the generations of cephalosporins (1 to 2 to 3) they are more effective against what?
Gram negative bacteria
Are aminoglycosides bactericidal or bacteriostatic? Generally, how do they exert their effect?
2. Act on protein synthesis within the cell wall of the bacteria.
What class of bacteria is the aminoglycoside family of antimicrobials affect againts?
Aerobic gram negative bacteria.
How are aminoglycosdies excreted?
Extensively renal excretion.
What is the elimination half time of the aminoglycosides? How much does it increase with renal failure?
1. 2-3 hour elimination half time
2. Increased 20-40 fold with renal failure.
Name four adverse reactions that are associated with aminoglycosides.
3. Skeletal muscle weakness
4. Prolongs neuromuscular blockade.
Define ototoxicity, explain how an aminoglycoside causes it, state what it is usually dependent on and whether or not it is reversible.
1. Ototoxicity is vestibular/auditory dysfunction
2. Is caused by drug induced destruction of vestibular or cochlear sensory hairs.
3. It is dose dependent- usually occurs with chronic therapy.
4. Usually irreversible
Explain how aminoglycosides can cause nephrotoxcicity.
State what this nephrotoxicty results in.
State whether this nephrotoxicity is reversible or not.
Name the most nephrotoxic of the aminoglycosides.
1. Drug accumulates in the renal cortex causing tubular necrosis
2. Results in the inability to concentrate the urine (first sign), proteinuria and RBC casts.
Explain two ways which aminoglycosides can result in skeletal muscle weakness, name a disease that is uniquely sensitive to weakness, state whether a single dose in a healthy patient is or isn't a problem and name two classes of drugs that's actions are prolonged by this class of antimicrobials.
1. Can inhibit pre-junctional release of acetylcholine and decerse the post synaptic sensitivity to the neurotransmitter.
2. Myasthenia Gravis.
3. A single dose in a healthy patient is not usually a problem.
4. Non-depolarizing and depolarizing muscle relaxants.
Explain when aminoglycosides can result in a potentiation of neuromuscular blockade (two), could this happen outside of the OR, name a drug that is enhanced and considerations that must be made when reversing a patient.
1. Potentiation of NM blockade can result from high plasma concentration when given IV and from systemic absorption from large volumes of irrigation.
2. The reappearance of NM blockade can reappear outside the OR, maybe in the PACU
3. NM blocking properties of lidocaine are enhanced.
4. Neostigmine or calcium induced antagonism may be incomplete or transient (use your clinical judgement even if you have a decent train of four).
Steptomycin and Kanamycin (aminoglycosides) have what type of use? What is the most frequent adverse reaction associated with them?
1. Limited use.
2. Vestibular Damage
Gentamicin (aminogylcoside) has what type of spectrum when compared to other drugs in this family? What does this drug require? What is the toxic level?
1. Broader spectrum
2. Monitoring drug levels because of it's high toxic profile
3. Over 9mcg/ml
Amikacin (aminogylcoside) is a derivative of which drug?
Neomycin (aminoglycoside) is used as an adjunct therapy for what condition? Why?
1. Hepatic Coma
2. To decrease plasma ammonia levels.
Are tetracyclines bactericidal or bacteriostatic? How do they act?
2. Inhibits bacterial protein synthesis.
What type of spectrum do the tetracyclines have?
What are the tetracyclines usually used for? Why?
1. Treatment of acne
2. Because they decrease the fatty acid content of the sebum.
How are tetracyclines excreted?
Urine and the bile.
Name two side effects of tetracyclines, two patient populations we wouldn't give them too and describe why.
1. Permanent discoloration of the teeth and photo-sensitivity.
2. Parturients and children.
3. Deposits in teeth and bones by forming a tetracycline-orthophosphate-calcium complex.
How is tetracycline (the drug not the class) prepared and what is the route of administration?
1. Standard preparation
2. PO only.
How is doxycyline (tetracycline family) prepared and what is the route of administration. Also, name the one group of infections Denise mentioned they are used to treat.
1. Long acting preparation
2. IV or PO
3. GYN infections.
What class of antimicrobials does erythomycin fall under?
Is erythromycin bacteriostatic or bactericidal? How does it work?
1. It can be BOTH
2. inhibits bacterial protein synthesis.
What kind of spectrum does erythromycin have?
Narrow spectrum mostly gram positive bacteria.
How is erythromycin metabolized and why is this important?
Metabolized by the Cytochrome P-450 system so it can prolong any drug that is broken down by the P-450 system because it is using up the enzymes.
How is erythromycin excreted?
Mostly in the bile.
Name four adverse reactions associated with erythromycin. Which is the most common?
1. GI intolerance (which is the most common side effect) which can include severe N/V with IV infusion.
2. Gastric emptying
3. QT effects including prolonged cardiac re-polarization and incidences of torsades.
4. Thrombophlebitis which is common with prolonged IV use.
Which class includes clindamycin?
Is clindamycin bacteriostatic or bactericidal?
Which drug is it similar to Clindomycin in antimicrobial activity? Meaning that it is what?
2. Narrow spectrum mostly gram positive bacteria.
What is clindamycin more active against than erthryomycin?
When is clindamycin used (two)? When would we decrease the dose?
1. Would use with serious gastrointestinal infections and infections of the female genital tract.
2. Would decrease the dose with severe liver disease.
Name two side effects associated with clindamycin.
Pseudomembranous colitis (severe diarrhea)
Pre and post junctional effects at the NM junction.
What should be done if a patient ends up with a pseudomembranous colitis with clindamycin administration?
1 Stop clindamycin immediately and treat with another antibiotic.
Name the two considerations regarding the pre and post junctional effects that clindamycin can have at the NM junction. Is this effect dependent or independent of the NM blocker we gave?
1. The effects at the NM junction caused by clindamycin are not antagonized with anticholinersterases or calcium and large doses can produce long lasting, profound NM blockade.
2. This side effect is completely INDEPENDENT of what we gave, so in and of itself clindamycin can cause severe weakness.
Vancomycin is a derivative of what?
Is vancomycin bacteriostatic or bactericidal? How does it work?
2. Impairs cell wall synthesis.
Against what type of bacteria is vanc effective?
Gram positive (including severe staph infectios, streptococcal, enterococcal endocarditits, MRSA, and with PCN and Ceph allergies)
*She said she wouldn't ask us about specific organisms but I put them on here anyway just in case to be safe.
How is vanc excreted? What is the elimination half time and when and by how much can it be prolonged?
2. 6 hours
3. Can be up to 9 days in renal failure patients.
Name two procedures and one type of related infection where vanc is commonly used.
2. Ortho procedures using prosthetic devices
3. CSF and shunt related infections
What is the dose of Vancomycin, how long is it normally given over and how is it normally mixed?
10-15mg/kg over 60 minutes
1 gm is normally mixed in 250ml.
A rapid infusion of vancomycin will result in what?
What other four adverse reactions could occur with vanc?
1. Red man syndrome (even with a slow infusion)
4. Return of NM blockade
What is happening in the body to cause red man syndrome?
Intense facial and truncal erythema from histamine release.
Are sulfonamides bactericidal or bacteriostatic How do they work?
2. Inhibit microbial synthesis of folic acid. (remember this one she thought it was "neat" haha)
When are sulfonamides used?
How are sulfonamides metabolized and excreted?
Metabolized by the liver and renally excreted.
Name five side effects of sulfonamides.
1. Skin rash to anaphylaxis
2. Drug fever
4. Acute hemolytic anemia (rare)
5. increased effect of PO anticoagulants.
Are polymyxin B and colistimethate bactericidal or bacterostatic? How do they work?
Effect bacterial cell wall membrane phospholipids.
When are polymyxin B and colistimethate effective?
Gram negative bacteria (severe UTIs, infections of the skin, mucous membranes, eyes and ears)
How are polymyxin B and colistimethate eliminated?
Name two side effects associated with polymyxin B and colistimethate.
1. Most potent of all antimicrobials in their action at the NM junction.
2. Highly nephrotoxic
Describe the effect that polymyxin B and colistimethate can have on the NM junction (four).
1. Predominately pre junctional
2. Can produce skeletal muscle weakness resembling nondepolarizing NM blockade.
3. Marked potentiation of non depolarizing NM blocking drugs
4. Neostigmine and calcium do NOT reliably antagonize this drug effect at the NM junction
Is metronidazole bactericidal or bacteriostatic?
What class of bacteria is metronidazole effective against?
Anaerobic gram negative bacilli
What type of infections is metronidazole used to treat?
Wide variety, CNS infections, Abdominal and pelvic sepsis and pseudomembranous colitis
Are fluoroquinolones bacteriostatic or bactericidal? How do they work? What kind of spectrum do they have?
2. Inhibit the part responsible for holding together the helical structure of bacterial DNA.
3.. Broad spectrum
What type of bacteria are fluoroquinolones effective against?
Gram negative bacilli
What is the elimination half time of the fluoroquinolones? How are they excreted?
1. 3-8 hours.
2. Mostly renal through glomerular filtration and tubular secretion.
What important set of enzymes can the fluoroquinolones inhibit?
What side effects are associated with the fluoroquinolones?
Mild GI disturbances (minimal side effects)
But can inhibit Cytochrome P450
When are fluoroquinolones useful?
Complicated GI and GU infections.
Ciprofloxacin (a fluroquinolone) is useful in the treatment of a variety of systemic infections including? (3).
Bone, soft tissue and the respiratory tract.
Rifampin is a drug used for?
Is Rifamipin bacteriostatic or bactericidal? Against what type of bacteria?
Bactericidal against mycobacteria. Inhibits growth of most gram positive and many gram negative bacteria (by acting on the DNA dependent RNA polymerase)
Fat solubility of rifampin allows what?
Penetration of tissues including the CNS.
How is rifampin administered?
Oral or parenteral.
How is rifamipin excreted?
Renal and biliary
What develops quickly with rifamipin?
What side effects are associated with rifampin? What does it potently induce?
Usually infrequent but with high doses we can see thrombocytopenia, anemia, hepatitis, fatigue, numbness, skeletal muscle weakness.
Potent inducer of the Cytochrome P-450 system (accelerated metabolism of opoids, NM blockers and warfarin.
Amphotericin B is what kind of a drug? When is it given? How is it given? And what kind of excretion?
2. Yeasts and fungi
3. Poor PO absorption so it is given IV
4. Slow renal excretion.
What is impaired in 80% of people taking amphotericin B? Is this reversible? What should be monitored?
1. Renal function
2. Most recover after this drug is stopped but some resulting permanent decrease in GFR may remain
3. Monitor plasma creatinine levels
What side effects are associated with amphotericin B during infusion (4)? What other side effects are also associated? (6).
During infusion- fever, chills, dyspnea and hypotension
General side effects- impaired hepatic function, hypokalemia, allergic reactions, seizure, anemia, thrombocytopenia
Viruses are what kind of parasites? What do they use to replicate?
1. Intracellular- can't reproduce outside of host cells.
2. Use many biochemical mechanisms of the host's cells.
Development of antivirals is?
What kind of alternatives are there out there to antiviral drugs? Name 3 of them.
Vaccines: Hepatitis A and B, HPV and Herpes Zoster.
Viruses are composed of what? How are they classified?
Composed of a nucleic acid core surrounded by a protein containing outer coat. Genome either contains RNA or DNA but NEVER both (classified on this part).
Acyclovir and Valacyclovir (antivirals) act against what virus and are excreted how?
1. Herpes viruses
2. Excreted by the kidneys.
Vidarabine (antiviral) is used for what two kinds of viruses? What two adverse properties does vidarabine include?
1. Cytomegalic inclusion disease and Herpes simplex encephalitis
2. It is Mutagenic and Carcinogenic
Famciclovir (antiviral) is used against what?
Acute herpes zoster.
Ganciclovir is used against what one virus and results in which one type of toxicity?
2. Hematologic toxicity
Amantadine is used to treat which virus and how is it excreted?
Influenza A and renal excretion.
What is an interferon? How does it work? What does it enhance?
Interferon is the term used to designate glycoproteins produced in response to viral infections (we make these). They bind to receptors on host cell membranes and induce the production of enzymes that inhibit viral replication and degradation of the viral mRNA. Enhances tumoricidal activities of macrophages.
Name 3 uses for interferons?
Chronic Hep B
Nasal sprays for rhinal virus
Name some side effects of interferons (there are 11 listed).
1. Flu like symptoms
2. Hematologic toxicity
5. Decreased mental concentration
6. Development of autoimmune conditions
9. Changes in CV function
10. Changes in thyroid function
11. Changes in hepatic function.
Antivirals for AIDs include nucleoside reverse transcriptase inhibitors (NRTIs) which Denise refers to as?
Imposters. Looks like a fake human cell to the virus. Once the virus incorporates it it can't elongate it's chain or replicate.
Nonnucleoside reverse transcriptase inhibitors (NNRTIs) inhibit what?
Inhibit function of an enzyme used by the AIDs virus.
Protease inhibitors work by?
Binding to the HIV protease.
What type of therapy is commonly used in HIV treatment?
What side effects are associated with antivirals for AIDs?
Pancreatitis, hepatoxicity, lactic acidosis, fat redistribution, increases in serum cholesterol and triglycerides, hypersensitivity.
What side effects are associated mainly with protease inhibitors? (aside from the side effects of all antivirals for AIDs)
Most all of them inhibit the cytochrome P-450 system. Ritonavir ir the most potent.
Because of the inhibition of the CYP450 system large plasma increases of many drugs including analgesics, lidocaine, antimicrobials, anticonvulsants, anticoagulants, antiemetics, CCBs.
Name the 9 bactericidal drug classes Denise mentioned.
5. polymyxin B
Name the 3 bacteriostatic drug classes that Denise mentioned.
Which one drug did Denise mention that could be either bactericidal or bacteriostatic?
What two medications did Denise mention are useful only against gram positive bacteria?
Erythromycin and Vanc
Which one antimicrobial did Denise mention is effective against both gram positive and gram negative bacteria?
Which six antimicrobials did Denise mention are effective only against gram negative bacteria?
3. Polymyxin B