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Antibiotics! Flashcards

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1
Q

How does the penicillin-family of antibiotics work? What structure do the antibiotics of this family contain?

A
  • penicillin-family antibiotics kill bacteria by binding to and inhibiting transpeptidase (this is the bacterial enzyme needed to cross-link the disaccharide units of the peptidoglycan cell wall) via competitive inhibition
  • these antibiotics are all bicyclic and contain a beta-lactam ring (exception: aztreonam is monocyclic with only the beta-lactam ring)
  • (this is why transpeptidase is AKA the penicillin-binding protein)
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2
Q

What are the major types of antibiotics in the penicillin family? What is each generally used for?

A
  • penicillin G: (the original penicillin) still effective for pneumonia via Strep. pneumoniae and strep throat via group A beta-hemolytic strep (Strep pyogenes)
  • aminopenicillins: enhanced Gram negative and Gram positive enterococcus killing power
  • penicillinase-resistant penicillins: enhanced Gram positive killing power (especially against Staph aureus)
  • anti-psuedomonal penicillins: expanded Gram positive and Gram negative killing (especially Pseudomonas aeruginosa!), also good for anaerobes
  • cephalosporins: penicillinase resistant, wide spectrum of activity depending on the generation of the drug
  • carbapenems: have the broadest antibacterial coverage!
  • aztreonam: kills ALL Gram negatives (including Pseudomonas aeruginosa)
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3
Q

What are the four mechanisms in which bacteria can become resistant to the penicillin?

A
  • 1) some Gram negatives can alter their porins (these are the channels in the outer layer that penicillin must pass through to gain entry to the cell wall)
  • 2) some bacteria have beta-lactamase (penicillinase) enzymes
  • 3) some bacteria can alter the structure of their transpeptidase (AKA penicillin-binding protein) to prevent penicillin from binding and inhibiting it
  • 4) some bacteria can actively pump out the penicillin via an efflux pump before it is able to bind to the transpeptidase
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4
Q

What are the major adverse reactions that can occur with the penicillins?

A
  • the penicillin antibiotics can cause anaphylactic reactions (these are IgE mediated): bronchospasm, hives, shock (these occur in minutes to hours); delayed rash (this occurs days to weeks later)
  • they can also cause diarrhea via opportunistic infections of the colon
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5
Q

Penicillin G

A
  • the original penicillin
  • available in IM, IV, and oral forms (IM and IV are more common)
  • extremely sensitive to beta-lactamases / penicillinases (many organisms have therefore developed resistance)
  • give for pneumonia via Strep pneumoniae
  • give for strep throat (pharyngitis) via Strep pyogenes (group A beta-hemolytic strep)
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6
Q

What are the aminopenicillins?

A
  • the aminopenicillins have enhanced killing power (some Gram negatives, especially the enterics, and the Gram positive Enterococcus) because of better penetration through the outer membranes and better transpeptidase binding
  • they are still inhibited by beta-lactamases / penicillinases
  • ampicillin and amoxicillin are the major types
  • ampicillin is better absorbed orally (so give for bronchitis, otitis media, sinusitis)
  • amoxicillin is commonly given IV in conjunction with other antibiotics for broad Gram negative coverage
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7
Q

What are the anti-pseudomonal penicillins?

A
  • these antibiotics have very expanded Gram negative coverage and are able to kill the difficult Pseudomonas aeruginosa; they are also effective against anaerobes and some Gram positives
  • there are two groups: the carboxypenicillins and the ureidopenicillins
  • however, these are sensitive to beta-lactamases / penicillinases
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8
Q

What are the penicillinase-resistant penicillins?

A
  • these antibiotics are resistant to beta-lactamases / penicillinases, making them very effective against Staph aureus and other Gram positives (but MRSA is becoming more and more apparent!)
  • methicillin, nafcillin, oxacillin are IV drugs
  • cloxacillin and dicloxacillin are oral
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9
Q

What are the cephalosporins?

A
  • these antibiotics are also resistant to beta-lactamases / penicillinases
  • they have an additional R-group side chain that allows for numerous different lab manipulations
  • there are 3 classic generations of this drug (1st generation drugs tend to be better against Gram positives, while 3rd generation drugs are more anti-Gram negatives)
  • MRSA and Enterococci are resistant to cephalosporins
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10
Q

1st Generation Cephalosporins

A
  • use these as an alternative to penicillin (in patients who are allergic to penicillin) for Staph and Strep infections
  • this group of cephalosporins is commonly used before/during surgery to prevent infection (most common: cephalexin)
  • only the 1st generation has a “-ph” in the name (cephalothin, cephapirin, cephradine, cephalexin)
  • others: cefazolin, cefadroxil
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11
Q

2nd Generation Cephalosporins

A
  • use these antibiotics for Strep pneumoniae and H. influenzae (especially cefuroxime)
  • use these for anaerobic coverage
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12
Q

3rd Generation Cephalosporins

A
  • use these antibiotics for community acquired pneumonia, meningitis, and pyelonephritis
  • most of these drugs have an “-ft” in their name (ceftriaxone, ceftazimide, ceftizoxime, ceftibuten)
  • ceftriaxone is the drug of choice for adult meningitis because it has excellent CSF penetration
  • cefotaxime is the drug of choice for neonatal and child meningitis because it also has excellent CSF penetration (and because ceftriaxone can interfere with bilirubin metabolism in neonates!)
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13
Q

What is cefepime?

A
  • cefepime is essentially a 4th generation cephalosporin that is good for both Gram positive and Gram negative organisms
  • cefepime can kill Pseudomonas aeruginosa
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14
Q

Which cephalosporins can kill Pseudomonas aeruginosa?

A
  • 1st generation: none
  • 2nd generation : none
  • 3rd generation: ceftazidime and cefoperazone
  • 4th generation: cefepime
  • “give Pseudomonas the TAZ, the FOP, and the FEP”
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15
Q

What can be given in combination with the penicillins to increase the antibiotic coverage? What are the major combos?

A
  • beta-lactamase inhibitors (clavulonic acid, sulbactam, tazobactam)
  • the combo will provide broad range coverage against beta-lactamase / penicillinase producing Gram positives (Staph aureus), Gram negatives (H. influenzae), and anaerobes (Bacteroides fragilis)
  • augmentin: amoxicillin (an aminopenicillin) and clavulonic acid
  • unasyn: ampicillin (an aminopenicillin) and sulbactam
  • zosyn: piperacillin (a ureidopenicillin, a type of anti-pseudomonad penicillin) and tazobactam
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16
Q

What are the carbapenems? What is a major side effect of these antibiotics that isn’t an issue with the other penicillin-family antibiotics?

A
  • these are a newer class of penicillins that have the BROADEST antibacterial activity (kills Gram positives, Gram negatives, and anaerobes)
  • (the carbapenem ertapenem does NOT cover Pseudomonas aeruginosa)
  • they are resistant to beta-lactamases / penicillinases
  • MRSA, Mycoplasma, and some Pseudomonas species remain resistant
  • these end in “-penem” and the main one is imipenem
  • major side effect: lowered threshold for seizures
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17
Q

What is given with the carbapenem imipenem? Why?

A
  • imipenem is rapidly broken down by the kidneys’ dihydropeptidase
  • to prevent this, the antibiotic is given with cilastatin, which inhibits the kidneys’ dihydropeptidase
  • (note that other carbapenems do not need cilastatin as they are not broken down by the enzyme)
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18
Q

What is aztreonam? What is unique about its structure?

A
  • this antibiotic covers ALL Gram negatives (including Pseudomonas aeruginosa)
  • it’s structure is unique compared to the other penicillin-family antibiotics in that it is only monocyclic (contains only the beta-lactam ring), while the others are all bicyclic
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19
Q

Which antibiotics kill Pseudomonas aeruginosa?

A
  • the anti-pseudomonal penicillins
  • 3rd generation cephalosporins (ceftazidime, cefoperazone) (penicillin family)
  • 4th generation cephalosporin (cefepime) (penicillin family)
  • the carbapenems (but NOT ertapenem) (penicillin family)
  • aztreonam (penicillin family)
  • ciprofloxacin (a fluoroquinolone)
  • the aminoglycosides ( nti-ribosomal antibiotics)
  • the polymixins
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20
Q

Which antibiotics kill anaerobic bacteria (mainly Bacterioides fragilis)?

A
  • the penicillins with a beta-lactamase inhibitor (augmentin, timentin, unasyn, zosyn)
  • 2nd generation cephalosporins (penicillin family)
  • the carbapenems (penicillin family)
  • chloramphenicol (an anti-ribosomal antibiotic)
  • clindamycin (an anti-ribosomal antibiotic)
  • metronidazole
  • moxifloxacin (a fluoroquinolone)
  • tigecycline (an anti-ribosomal antibiotic)
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21
Q

Which antibiotics kill the resistant Gram positives (MRSA, MRSE, VRE)?

A
  • MRSA (methicillin resistant S. aureus) and MRSE (methicillin resistant staph. epidermidis): vancomycin, linezolid (an anti-ribosomal antibiotic), daptomycin, tigecycline (an anti-ribosomal antibiotic)
  • VRE (vancomycin resistant Enterococcus): linezolid, daptomycin, tigecycline
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22
Q

How do the anti-ribosomal antibiotics work? Why don’t they also target human ribosomes?

A
  • this family of antibiotics inhibits bacterial ribosomes, preventing protein synthesis; inhibiting protein synthesis results in cell death
  • they don’t inhibit human ribosomes because we have the 80S ribosome, while bacteria have the 70S ribosome (has the large 50S and small 30S subunits)
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23
Q

Which drugs belong to the anti-ribosomal antibiotic family? Which bacterial ribosomal subunit does each inhibit?

A
  • “CLEan TAg”
  • chloramphenicol and clindamycin (large 50S)
  • linezolid (large 50S)
  • erythromycin (large 50S) (erythromycin is a macrolide)
  • tetracycline/doxycycline and tigecycline (small 30S)
  • aminoglycosides (small 30S)
  • others: quinupristin/dalfopristin (large 50S), spectomycin (small 30S)
24
Q

How is each anti-ribosomal antibiotic absorbed?

A
  • all are absorbed orally!

- EXCEPT for the aminoglycosides; these require IM or IV administration

25
Q

Chloramphenicol

A
  • this is an anti-ribosomal antibiotic that inhibits the large 50S ribosomal subunit
  • chloramphenicol has a very large spectrum of activity against Gram positives, Gram negatives, and anaerobes (it is very similar to the carbapenems in this sense)
  • treat bacterial meningitis when the organism is unknown and when the patient is allergic to penicillin and cephalosporin
  • treat Rocky Mountain Spotted Fever in young children and pregnant women (normally, RMSF is treated with tetracycline)
  • use only when there is no alternative antibiotic, as there are very severe potential side effects
26
Q

What are the major side effects of chloramphenicol?

A
  • (remember, this antibiotic should only be used when there are no alternatives because of the potential for these side effects) although rare, these are very serious
  • major adverse effects revolve around bone marrow depression (the drug can wipe out bone marrow!): an irreversible, usually fatal, aplastic anemia
  • also gray baby syndrome: neonates/premies can’t fully conjugate the drug in the liver or excrete it via the kidneys, resulting in toxicity, shock, and cyanosis (presents as a gray color)
27
Q

Clindamycin

A
  • this is an anti-ribosomal antibiotic that inhibits the large 50S ribosomal subunit
  • clindamycin is effective against Gram positives and anaerobes, but NOT against Gram negatives
  • can treat toxic shock syndrome when given with vancomycin or a penicillin
  • major adverse effect: large propensity to cause pseudomembranous colitis via clindamycin resistant Clostridium dificile
28
Q

Linezolid

A
  • this is an anti-ribosomal antibiotic that inhibits the large 50S ribosomal subunit
  • linezolid is very good against the resistant Gram positives (MRSA, MRSE, and VRE)
  • linezolid is very expensive and like chloramphenicol can also cause bone marrow suppression (although it tends to be less severe)
29
Q

Macrolides

A
  • this is a group of anti-ribosomal antibiotics that inhibits the large 50S ribosomal subunit
  • erythromycin (largely replaced by the other two), azithromycin (Z-pack!), clarithromycin
  • cover Gram positives, Gram negatives, and the atypicals (Legionella, Chlamydophilas, Mycoplasma), making them largely used for community-acquired pneumonia
  • very few side effects, making them among the safest antibiotics
30
Q

What is telithromycin? In which patients should it be avoided?

A
  • telithromycin is often grouped in with the macrolides (erythromycin, azithromycin, clarithromycin) because it also covers Gram positives, Gram negatives, and the atypicals
  • good for when the bug is macrolide resistant
  • it is actually a ketolide, not a macrolide
  • do not give to patients with myasthenia gravis, as they can develop an acute life-threatening respiratory failure
31
Q

Tetracycline and Doxycycline

A
  • these are anti-ribosomal antibiotics that inhibit the small 30S ribosomal subunit
  • they are largely used for venereal diseases caused by Chlamydia trachomiatis, walking pneumonia caused by Mycoplasma, diseases caused by Brucella and Rickettsia, and acne
  • these drugs chelate with many cations, and when chelated can not be absorbed in the gut (this is much worse with tetracycline)
  • major side effects: brown teeth and depressed bone growth (because of the chelation with calcium!), phototoxic dermatitis (skin inflammation with sunlight exposure)
32
Q

Tigecycline

A
  • this is an anti-ribosomal antibiotic that inhibits the small 30S ribosomal subunit
  • tigecycline is a tetracycline derivate
  • it is less likely to induce resistance than normal tetracycline and can kill MRSA and VRE
33
Q

The Aminoglycosides

A
  • this is a group of anti-ribosomal antibiotics that inhibits the small 30S ribosomal subunit
  • streptomycin, gentamicin, tobramycin, neomycin, netilmicin, amikacin
  • used against Gram negative aerobic enterics and Pseudomonas aeruginosa
  • this family of antibiotics must diffuse across the cell wall in order to work (thus, they are often given with penicillins, which break the wall to help this diffusion)
  • side effects: CN VIII toxicity (hearing loss, vertigo), renal toxicity, neuromuscular blockade (total paralysis; rare)
34
Q

What is each aminoglycoside used for?

A
  • the aminoglycosides are largely used for Gram negative aerobic enterics and Pseudomonas aeruginosa
  • streptomycin (the oldest one)
  • gentamicin (this is the most commonly used)
  • tobramycin (very good against Pseudomonas aeruginosa)
  • neomycin (used topically for skin infections only)
  • netilmicin (used pre-operatively to prevent )
  • amikacin (has the broadest spectrum, use for nosocomial infections)
35
Q

Which “-mycin”s are NOT aminoglycosides?

A
  • clindamycin (targets the large 50S subunit)
  • erythromycin, azithromycin, clarithromycin (the macrolides, which target the large 50S subunit)
  • telithromycin (a ketolide that is grouped in with the macrolides)
  • spectomycin (not an aminoglycoside, but also targets the small 30S subunit)
  • vancomycin (a miscellaneous antibiotic)
36
Q

Quinupristin and Dalfopristin

A
  • these are anti-ribosomal antibiotics that inhibit the large 50S ribosomal subunit
  • these drugs are effective against Gram positives
  • they are only used in life-threatening cases of VRE and MRSA because side effects are common
37
Q

Side effects of quinupristin and dalfopristin are quite common - what are they?

A
  • hyperbilirubinemia occurs in up to 35%
  • pain at infusion site occurs in 40%
  • arthralgia and myalgia occurs in 40%
38
Q

Which antibiotics are given as an alternative to penicillin and/or tetracycline/doxycycline?

A
  • ceftriaxone (a 3rd generation cephalosporin)
  • quinolones
  • spectinomycin (this inhibits the small 30S ribosomal unit, but it is NOT an aminoglycoside despite its name)
39
Q

What are the first line drugs used to treat tuberculosis? Which are the most common?

A
  • isoniazid
  • rifampin
  • pyrazinamide
  • ethambutol
  • streptomycin (an aminoglycoside anti-ribosomal antibiotic)
  • the first 3 are the most commonly used
40
Q

What are the most commonly used anti-tuberculosis antibiotics? What is a major side-effect that can occur from these?

A
  • isoniazid, rifampin, and pyrazinamide
  • all 3 can cause liver damage (they are hepatotoxic): 10-20% will develop elevated LSTs and 1 in 1000 will develop hepatitis
41
Q

Isoniazid

A
  • abbreviated INH
  • isoniazid is a common anti-TB antibiotic that interferes with Mycobacteria’s synthesis of the cell wall
  • side effects: it is the most hepatotoxic of the anti-TB drugs; it increases vitamin B6 excretion (B6 is important for nerve function, so these patients can develop peripheral neuropathy and rash), so give a vitamin B6 supplement with this drug
42
Q

Rifampin

A
  • rifampin is a common anti-TB antibiotic that inhibits Mycobacteria’s RNA polymerase
  • side effects: hepatotoxicity; turns body fluids (urine, saliva, feces, sweat, tears) a bright red-orange color (this is harmless); increases the cytochrome p450 enzyme system (this means it decreases the half-lives of other drugs such as anticoagulants, OCPs, and anticonvulsants)
43
Q

Pyrazinamide

A
  • pyrazinamide is a common anti-TB antibiotic that has an unknown method of action
  • side effects: hepatotoxicity; joint pain; gout flare-ups
44
Q

Ethambutol and Streptomycin

A
  • these are both anti-TB antibiotics, but are less commonly used
  • they are NOT hepatotoxic like the more common drugs, but ethambutol is oculartoxic, and streptomycin is ototoxic and nephrotoxic
  • (remember that streptomycin is an aminoglycoside antibiotic that inhibits the small 30S ribosomal subunit)
45
Q

What is rifamate? Rifater?

A
  • rifamate: a combo of isoniazid and rifampin to treat TB

- rifater: a combo of isoniazid, rifampin, and pyrazinamide to treat TB

46
Q

How do we treat active tuberculosis?

A
  • treat active TB with 6 months of a rifampin based regimen
  • rifampin, isoniazid, pyrazinamde, and ethambutol for 2 months followed by rifampin and isoniazid for 4 months
  • “4 for 2, 2 for 4”
47
Q

How do we treat latent tuberculosis?

A
  • (this means treating positive PPD reactions to prevent reactivation of TB; this treatment is prophylactic)
  • isoniazid for 9 months OR rifampin for 4 months
48
Q

How do we treat leprosy?

A
  • treat leprosy with dapsone (a sulfa drug), rifampin (an anti-TB drug), and/or clofazimine for a minimum of 2 years in severe cases
  • (in mild cases, 6 months is usually sufficient)
49
Q

Clofazimine

A
  • this is an anti-leprosy antibiotic that binds to the DNA of the Mycobacteria
  • it is red colored and will turn the areas it deposits in red
  • clofazimine also has anti-inflammatory actions and therefore helps to limit the common “leprosy reactions” that occur in patients being treated for leprosy
50
Q

50% of patients being treated for leprosy will develop what? How do we treat this complication?

A
  • 50% will develop “leprosy reactions,” which are due to the immune-mediated response to the accumulation of the dead Mycobacteria
  • these are systemic inflammatory reactions of the nerves, testes, eyes, joints, and skin
  • do NOT withdraw the anti-leprosy antibiotics!
  • treat the reaction with prednisone or clofazimine (clofazimine is an anti-leprosy drug that also has anti-inflammatory actions)
51
Q

Which five antibiotics are considered “miscellaneous” in that they don’t belong to any of the other families/groups of antibiotics?

A
  • the fluoroquinolones (“-floxacin”)
  • vancomycin (despite its name, it is not an aminoglycoside or a macrolide) and telavancin
  • trimethoprim (TMP) and sulfamethoxazole (SMX) (these are antimetabolites)
52
Q

Fluoroquinolones

A
  • these are a group of miscellaneous antibiotics
  • they end in “-floxacin” (ex: ciprofloxacin)
  • most useful against Gram negatives (including Pseudomonas aeruginosa)
  • inhibits bacterial DNA gyrase
  • safe, excellent oral absorption, and strong tissue penetration (especially for bone and prostate)
  • side effects: GI irritability, damage to cartilage, tendonitis and rupture (especially of Achilles tendon); ciprofloxacin also inhibits GABA, increasing the risk of seizures in patients with low renal clearance
53
Q

How are fluoroquinolones excreted?

A
  • these antibiotics undergo enterohepatic circulation; they are partially excreted in bile, partially reabsorbed in the intestine, and then partially excreted by the kidneys
  • this means fluorquinolones are highly concentrated in stool and urine (the latter makes them good for treating UTIs)
54
Q

Vancomycin

A
  • vancomycin is a miscellaneous antibiotic that is neither a macrolide nor an aminoglycoside despite the “-mycin” in its name
  • it is an IV antibiotic that covers ALL gram positives (including MRSA and MRSE), although VRE does exist; it is NOT orally absorbed (this makes it good for treating enteritis)
  • side effects: rapid infusion causes Red Man Syndrome (rapid infusion results in histamine release, causing a red rash of the torso and itchy skin); prevent with a slow infusion
55
Q

Telavancin

A
  • telavancin is a miscellaneous antibiotic that is the same as vancomycin (IV; covers all gram positives; can cause Red Man Syndrome)
  • however, it is effective against vancomycin resistant strains
56
Q

Trimethoprim and Sulfamethoxazole

A
  • trimethoprim (TMP) and sulfamethoxazole (SMX) are antimetabolites that belong to the miscellaneous group of antibiotics
  • these completely inhibit the production of TH4 (tetrahydrofolate), which is needed for DNA formation (sulfa drugs resemble the TH4 component PABA, while TMP resembles an enzyme needed)
  • effective against many Gram positives and Gram negatives, but not anaerobes
  • absorbed orally and excreted really (good for UTIs)
57
Q

Which patients are at risk of developing an adverse reaction to the antimetabolites? Which patients should they be avoided in?

A
  • antimetabolites: trimethoprim (TMP) and sulfamethoxazole (SMX)
  • 50% of AIDS patients will develop a rash and bone marrow suppression; however, the antimetabolites are effective at preventing PCP (Pneumocystis carinii pneumonia), which is a common complication of AIDS patients
  • avoid antimetabolites in patients on warfarin, as they increase warfarin levels and pose a large risk of bleeding

Microbiology (16 decks)

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