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Antibiotics TY Flashcards

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1
Q

Compare the differences between ribosomal subunits in bacteria vs eukaryotes.

A

Bacteria: 70s ribosome; 30s and 50s subunits

Eukaryotes: 80s ribosome; 40s and 60s subunits

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2
Q

Define time dependent antibiotic and list examples.

A

Time dependent: Serum concentrations remain above MIC during dosing interval (t>MIC)

Greater concentrations do not result in greater effectiveness

Minimal to no post-antibiotic effect (PAE)

Examples: β-Lactams, clindamycin, macrolides

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3
Q

Define concentration dependent antibiotic and list examples.

A

High concentrations at the binding site eradicates microorganism (peak/MIC ratio).

Greater concentrations do result in more bacterial killing.

Associated concentration-dependent PAE; bactericidal action continues for a period of time after antibiotic level falls below MIC.

Examples: aminoglycosides, fluoroquinolones, tetracyclines

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4
Q

Which antibiotic classes are bacteriCIDAL?

A

B-lactams

Fluoroquinolones

Aminoglycosides

Rifampin

Topicals: Mupirocin, silver sulfadiazine, nitroimidazoles

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5
Q

Which antibiotic classes are bacterioSTATIC?

A

Tetracyclines

Chloramphenicols

Macrolides

Lincosamides

Sulfonamides

Trimethoprims

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6
Q

Define post antibiotic effect (PAE). Do time or concentration dependent antibiotics have a greater PAE?

A

PAE= Bactericidal action continues for a period of time after antibiotic level falls below MIC Concentration dependent drugs have increased PAE

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7
Q

Give examples of antibiotic synergism.

A

Drug combination generates an effect greater than the sum of the effects of each component alone

  • Aminoglycosides and β-lactams
    • Aminoglycosides increase access to the cell wall
  • Polymyxin B and miconazole
    • Polymyxin B increases penetration of hydrophobic drugs and allows access to IC space
  • Trimethoprim and sulfonamides
    • Inhibit sequential steps in folic acid pathway
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8
Q

What is antibiotic antagonism? Give examples.

A

Two drugs given together have an opposite effect of one another

  • Penicillin and tetracycline: tetracyclines are bacteriostatic and penicillins require cell growth to be effective
  • Erythromycin and chloramphenicol: Compete for binding site
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9
Q

Define mutant prevention concentration

A

Antibiotic’s ability to minimize or limit the development of resistant organisms

MIC of least susceptible single-step mutation

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10
Q

What is the significance if bacterial growth occurs when antibiotic concentration is greater than MPC?

A

Bacteria has developed two or more resistance-causing spontaneous chromosomal point mutations

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11
Q

What is the area between the MIC and MPC called?

A

Mutant selection window

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12
Q

Give examples of antibiotics that are cell wall synthesis inhibitors.

A

Penicillin

Cephalosporins

Carbapenem

Vancomycin

Bacitracin

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13
Q

What is the b-lactam ring composed of?

A

Cyclic amide- contains 3 carbon and 1 nitrogen atom

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14
Q

Name 3 b-lactamase inhibitors

A

Clavulanate Sulbactam Tazobactam

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15
Q

What are the classes of penicillins and give examples of each

A

a. Natural penicillins: penicillin G, penicillin V
b. β-lactamase-resistant penicillins: methicillin, naficillin, oxacillin
c. Aminopenicillins: ampicillin, amoxicillin, talampicillin, bacampicillin, pivampicillin, talampicillin
d. Carboxypenicillins: carindacillin, carfecillin, carbenicillin, ticarcillin
e. Ureidopenicillins: azlocillin, mezlocillin, piperacillin

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16
Q

What are the generations of cephalosporins and give examples of each.

A

a. 1st generation: cephalothin, cephaloridine, cephapirin, cefazolin, cephalexin, cephradine, cefadroxil b. 2nd generation: cefamandole, cefoxitin, cefotiam, cefachlor, cefuroxime, ceforanide c. 3rd generation: cefpodoxime, ceftiofur, ceftriaxone, cefsulodin, cefotaxime, cefoperazone d. 4th generation: cefixime, cefclidine, cefluprenam, cefoselis, cefozopran e. 5th generation (not in vet med): ceftobiprole, ceftaroline

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17
Q

What is the MOA of b-lactam antibiotics?

A

Interfere w synthesis of cell wall

  • PBPs catalyze transpeptidase reaction that removes terminal alanine to form crosslink with neighboring peptide
  • B-lactam antibiotics attach to penicillin binding protein (PBP) and inhibit this step
  • Cell wall synthesis is blocked , cell dies
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18
Q

What are the resistance mechanisms of b-lactam antibiotics?

A

1) Inactivation of Abx by b-lactamase- **most common**, plasmid encoded
2) Modification of PBPs- resistant organisms produce PBPs with low affinity for binding, chromosomal (i.e MecA)
3) Impaired penetration of drug to target PBP- occurs in Gram- only

4) Presence of efflux pump

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19
Q

How are b-lactam antibiotics excreted?

A

Renal. Plasma levels can be increased in renal insuff patients

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20
Q

What are the AE of penicillins?

A

Hypersensitivity to penicilloyl group- immediated and delayed HS;

anaphylaxis, drug eruption, EM, TEN/SJS, vasculitis, PF

Dogs, cats: hives, fever, joint pain

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21
Q

What are the AE of cephalosporins?

A

Similar to penicillins (HS) but not as common. GI upset, renal toxicity can occur

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22
Q

What enzyme breaks down imipenem into nephrotoxic metabolites?

A

Dehydropeptidase-1

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23
Q

What drug inhibits dehydropeptidase-1 and is usually incorporated with imipenem?

A

Cilastatin

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24
Q

What is the specific MOA of bacitracin?

A

Forms complex with bactroprenol pyrophosphate which interferes with dephosphorylation Peptidoglycan cross links fail to form and osmotic pressure lysis bacteria

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25
What is specific MOA of vancomycin?
Modification of D-Ala-D-Ala binding site of PG cell wall; D-Ala terminal is replaced with D-lactate which blocks synthesis Also interferes with RNA synthesis
26
What are the AE of vancomycin?
Humans- fever, chills, phlebitis with injection, erythroderma (Red Man Syndrome- caused by non specific mast cell degranulation)
27
Describe bacterial protein synthesis.
a. Initiation: ribosome assembled on mRNA b. Elongation: AA brought to ribosome by tRNA, joins immature polypeptide chain and entire assembly moves one position along mRNA c. Termination: reach a stop codon and entire assembly separates
28
Which antibiotics inhibit at the 30s ribosomal unit?
Tetracyclines Aminoglycosides
29
Which antibiotics inhibit at the 50s ribosomal unit?
Macrolides Lincosamides Chloramphenicol
30
What is the MOA of tetracyclines?
a. Reversibly bind to 30s ribosome subunit b. Inhibits binding of tRNA to mRNA during translation c. Amino acids can’t attach to peptide strand
31
How are tetracyclines generally excreted? What is the exception?
Generally kidney and liver excretion. Doxycycline is excreted via intestines
32
What are the mechanisms of resistance to tetracyclines?
Active efflux, plasmid encoded TetK or TetL Ribosomal protection, chromosomal TetO or TetM
33
What are the anti-inflammatory effects of tetracyclines?
Inhibit metalloproteinase enzyme inhibitors (MMP 8/9), IL-1B Inhibit neutrophil chemotaxis Inhibit mast cell degranulation
34
What are the AEs for tetracyclines?
GI upset- esophagitis and esophageal stricture in cats Hepatotoxicity-Inhibit hepatic microsomal enzymes Nephrotoxicity- Acute **tubular** necrosis IV Doxy- cardiac arrhythmia, collapse, death in horses Teeth discoloration, enamel hypoplasia; can affect growing cartilage
35
What is the MOA of aminoglycoside drugs?
a. Irreversibly bind to 30s ribosome and freeze initiation complex b. Induces misreading of mRNA and can slow initiated protein synthesis c. Mistranslation of elongating peptide strands causing misfolded proteins
36
List examples of aminoglycoside drugs.
Neomycin, gentamicin, amikacin, streptomycin, kanamycin and tobramycin
37
What is the first impending sign of renal toxicity associated with aminoglycosides? What is the location of the kidney most commonly affected?
Nephrotoxicity is due to update of aminoglycosides by proximal renal tubular cells & drug retention in lysosomes of these cells in the renal cortex. Above a cerntain concentration cell necrosis occurs leading to renal proximal tubular dysfunction. Casts: 1st sign of impending renal toxicity, monitor for proteinuria
38
In terms of ototoxicity, where to AGs specifically target?
a. Vestibulotoxic: streptomycin and gentamicin b. Cochleotoxic: amikacin, neomycin and kanamicin
39
What is the MOA for macrolide antibiotics?
Erythromycin, tylosin, azithro, clarithro Binds to 50s ribosomal 23S rRNA i. Peptidyltransferase is located here ii. Prevents amino acid from attaching to peptide chain iii. Premature dissociation of tRNA/amino acid complex from ribosome
40
Macrolides accumulate \_\_\_\_\_\_\_
In neutrophils and macrophages
41
Which two other drug classes have similar MOAs and compete with macrolides for binding sites?
Lincosamides, chloramphenicol
42
Why is chloramphenicol poorly absorbed in cats?
Poor hepatic glucuronidation capacity
43
Is resistance to chloramphenicol common? What is the mechanism?
Resistance is rare. Bacteria produce enzyme **chloramphenicol acetyltransferase** i. Covalently attaches acetyl group from acetyl-CoA ii. Prevents drug from binding to ribosomes
44
What are the AE of chloramphenicol?
Bone marrow suppression Aplastic anemia (irreversible) in humans Paraparesis (reversible)
45
What is the specific MOA of lincosamides?
Premature dissociation of tRNA from the ribosome
46
What are the two genes associated with clindamycin resistance
Erm gene- Confers inducible or constitutive resistance to MLS-B Msr A gene- codes for efflux mechanism against macrolides
47
What test can be used to identify inducible clindamycin resistance?
D-zone test: place erythromycin testing disc in close proximity to clindamycin testing disc
48
Describe the D-zone test for inducible clindamycin resistance and its importance.
Bacterial suspensions are plated on Mueller-Hinton agar to evenly cover the surface. Clindamycin & erythromycin disks are placed on the center separated by 15 mm between. After incubation, examine for any blunting or flattening of one side of the clindamcyine zone - indicates inducible resistance; this is most often seen with HA-MRSA.
49
What molecule uncoils the DNA double helix during synthesis?
DNA topoisomerase (subunit of gyrase)
50
What molecule unzips the DNA strands apart?
Helicase
51
What is the specific MOA of fluoroquinolones?
Inhibit bacterial topoisomerase i. TP-II in gram negative organisms ii. TP-IV in gram positive organisms
52
What is enrofloxacin converted to in the liver?
Ciprofloxacin
53
How do fluoroquinolones affect cartilage in young dogs?
Inhibit mitochondrial dehydrogenase activity and proteolglycan synthesis (creates bubbling of cartilage)
54
What AE do fluoroquinolones have in cats?
Mydriasis and retinal degeneration
55
What is the specific MOA of rifampin?
Inhibits RNA polymerase
56
Why is folate necessary for DNA and RNA synthesis?
Carries carbon groups for methylation and nucleic acid synthesis (esp. thymine)
57
What is specific MOA of sulfonamides?
False-substrate inhibitor of dihydropteroate reductase Inhibits production of tetrahydrofolic acid
58
What bacteria is resistant to trimethoprim-sulfonamides since it is able to utilize preformed folates?
Enterococcus
59
What breed of dog is especially sensitive to reactions with trimethoprim-sulfonamides?
Doberman
60
What is specific MOA of trimethoprims?
a. Analogues of p-aminobenzoic acid (PABA) b. Competitive inhibitor of pteridine synthetase i. Inhibits production of dihydropteroic acid
61
What is the known MOA of mupirocin?
Inhibit protein and RNA synthesis
62
How are bacteria becoming resistant to mupriocin?
n in wild type isoleucine tRNA synthetase
63
Which antibiotics are synergistic with EDTA
Aminoglycosides and fluoroquinolones
64
What antibiotics have been implicated in causing false glucosuria?
Tetracyclines Enrofloxacin Nitroflurane
65
In relation to antibiotic therapy, define antagonism.
Two antibacterial classes work against each other ie "bacteriostatic" drugs that inhibit ribosomes and thus microbial growth should not be combined with drugs whose MOA depends on protein synthesis such as growth of the organism (β lactams) or formation of a target protein Can also have chemical antagonisms - ie Aminoglycosides & quinolones are chemically inactivated by penicillins at sufficient concentration
66
In relation to antibiotic therapy, define additive.
Drug that have the same MOA would act in an additive fashion ie: tetracycline with chloramphenicol Additive effects probably occur when active metabolites are produced from an active parent compound (ie Enrofloxacin & Ciprofloxacin)
67
In relation to antibiotic therapy, define synergism.
might occur if the antimicrobial targets are subtly different; can occur if the 2 antimicrobials kill bacteria through independent mechanisms or through sequential pathways toward the same target (ie Sulfonamide & trimethoprim; β-lactams & aminoglycosides)
68
For cephalosporins, what are the differences in antibacterial spectrum with higher generation drugs?
Increasing Gram- spectrum (decr Gram+) Increasing b-lactamase activity
69
What is the most common side effect of clofazimine and what is this drug used to treat?
Common side effects: discoloration of skin - pink to brownish skin pigmentation Clofazimine is a fat-soluble riminophenazine dye used in combination with rifampicin and dapsone as multidrug therapy (MDT) for the treatment of **leprosy**.
70
What are the antiinflammatory effects of tetracyclines?
Inhibit metalloproteinase enzyme inhibitors Inhibit neutrophil chemotaxis Inhibit mast cell degranulation
71
Give examples of antibiotics that are protein synthesis inhibitors.
**_30s ribosomal unit_** Tetracyclines Aminoglycosides **_50s ribosomal unit_** Macrolides Chloramphenicol Lincosamides Sulfonamides
72
Give examples of antibiotics that are DNA/RNA synthesis inhibitors.
**_DNA gyrase inhibitors_** Fluoroquinolones **_RNA inhibitors_** Rifamycin **_Inhibit folic acid (and thereby DNA synthesis)_** Sulfonamides Potentiated sulfonamides Sulfones Trimethoprims
73
Describe the structure of the peptidoglycan cell wall
Peptidoglycan: Polymer that consists of sugars + amino acids (N-acetylglucosamine + N-acetylmuramic acids+ oligopeptide (binding) OUTSIDE the plasma membrane for structural strength Counteracts osmotic pressure of cytoplasm
74
How to b-lactamases cause resistance to b-lactam antibiotics? How is this resistance circumvented?
Hydrolyzes ring and inactivates antibiotic Encoded on chromosomes or plasmids Modified penicillin-binding protein in cell wall eg methicillin-resistance B-lactamase resistant penicillins: methicillin, oxacillin, cloxacillin, etc Add B lactamase inhibitor: clavulanate, sulbactam, tazobactam
75
What are the
76
77
T/F. Aminoglycosides have excellent activity against anaerobic bacteria.
FALSE. Aminoglycosides require O2 for cell membrane uptake, therefore they are ineffective against anaerobes
78
What are the resistance mechanisms of aminoglycosides
1) Ribosomes alter ribosome receptors 2) Decreased bacterial cell penetrability 3) Enzymes produced that inactivate drug
79
How are azithromycin and clindamycin different than parent molecule erythromycin?
More GI stable Azithromycin may have immunomodulatory effects

Pharmacology TY (2 decks)

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