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Pharmacology Final > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

what are the different types of penicillins?

A

natural penicillins (PCN G, PCN B, PCN G Procaine); aminopenicillins (amoxicillin, amp); penicillinase-resistance penicillins (oxacillin, cloxacillin, methacillin, nathacillin); extended spectrum penicillins (tigeracillin, piperacillin and azocillin)

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2
Q

what do all penicillins contain?

A

a nucleus which is composed of a b-lactam ring

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3
Q

what is the mechanism of action for natural penicillins?

A

exert bactericidal action against penicillin suscpetible microorganisms during the stage of active replication; interfere with bacterial cell wall synthesis by reacting to one or more PCN binding proteins

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4
Q

how many different types of binding proteins do bacteria produce?

A

4

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5
Q

what is the mechanism by which resistance is formed against natural PCNs by bacteria?

A

mediated mainly through production of B-lactamase, which covalently binds to the B-lactam bond to form an acyl enzyme intermediate, which destroys the activity of the drug

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6
Q

what is the method of metabolism and disposition of natural PCNs?

A

metabolism and disposition vary significantly among the various PCNs, also vary with the age of the patient

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7
Q

Most natural PCNs are not well absorbed by the GIT, with what exception?

A

PCN V

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8
Q

Which natural PCN is generally used parenterally?

A

PCN G

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9
Q

To what do natural PCNs bind?

A

serum proteins, mainly albumin

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10
Q

do natural PCNs penetrate the CSF?

A

No

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11
Q

what is the spectrum of activity of natural PCNs on gram positive cocci?

A

effective against most strains of streptococci and susceptible strains of staphococi, enterococci and pneumoncocci; tolerance to PCN from group B streptococci isolates have been reported; PCN acts synergistically with gent or tobramycin against many strains of enterococci

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12
Q

what is the spectrum of activity of natural PCNs on gram positive bacilli?

A

listerium

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13
Q

what is the spectrum of activity of natural PCNs on gram negative bacteriai?

A

H influenza, gonhorrhea, streptobacillis monolith forms

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14
Q

what is the spectrum of activity of natural PCNs on anaerobic bacteria and spirochetes?

A

covers spirochetes; anaerobic: clostrius species

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15
Q

what are the clinical uses of natural PCNs?

A

effective in the treatment of: group A step, group B strep, meningococci, actinomyces, T.pallidum, also susceptible streptococcus pneumoniae, enterococci and gonococci

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16
Q

what should be done in patients with poor compliance?

A

option of IM benzothulium PCN can be given Q3-4 wk

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17
Q

natural PCNs are the drug of choice in the treatment of what STI?

A

primary, secondary, tertiary syphilis (not neuro)

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18
Q

what treatment is recommended for patients with congenital syphilis?

A

PCN G or procaine PCN

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19
Q

what adverse reactions have been a/w administration of natural PCNs?

A

allergic reactions, hematologic toxicity (coombs positive hemolytic anemia, leukopenia and thromobocytopenia), Na overload, hyperkalemia and neurologic toxicity (sz reported following massive dose); severe even fatal anaphylaxis has occured

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20
Q

how frequently do anaphylaxis reactions occur in pts receiving natural PCNs?

A

estimated to occur in 0.01-0.05% of persons

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21
Q

what can occur in patients receiving cont IV tx with PCN G?

A

in high doseage may suffer severe and even fatal K poisoning, particularly if they have some degree of renal insufficiency

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22
Q

what is the interaction with natural PCNs and concurrent administration of bacteriostatic antibiotics?

A

may diminish the bactericidal effects of PCNs by slowing the rate of bacterial growth

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23
Q

What can prolong PCN blood levels?

A

concurrent administration of probenecid, which blocks the renal tubular secretions of PCNs

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24
Q

what is the composition of aminoPCNs?

A

contain a free amino group at the alpha position on the b-lactam ring of the PCN nucleus, increasing their ability to penetrate the outer membranes of the gram negative organisms

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25
Q

what is the mechanism of action of aminoPCNs?

A

exert bactericidal action against PCN-susceptible microorganisms during the stage of active replication

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26
Q

what is the mechanism by which resistance is formed against aminoPCNs by bacteria?

A

aminoPCNs are inactivated by the B-lactamases produced by either gram positive or gram negative bacteria

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27
Q

what is the preferred oral aminoPCN?

A

amoxicillin has the best absoprtion and bioavailability, absorption is impaired by food

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28
Q

where do aminoPCNs achieve therapeutic levels?

A

in most bodily fluids- CSF, peritoneal, joint and pleural

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29
Q

how are aminoPCNs cleared by the body?

A

kidneys

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30
Q

what is the spectrum of activity of aminoPCNs?

A

increased efficacy against most strains of enterococc, listeria, L. monocytogenes, H influenza, N gonorrhea; [some strains of E coli, shigella and salmonella are resistant]

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31
Q

what is the clinical use of amoxicillin?

A

drug of choice for acute otitis media, some clinical manifestations of Lyme dz

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32
Q

what is the clinical use of ampicillin?

A

widely ised in septic neonates partly because of its coverage against listeria

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33
Q

what are the adverse events a/w aminoPCNs?

A

hypersensitivity reactions

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34
Q

what are penicillinase-resistant PCNs?

A

semisynthetic PCN derivatives

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35
Q

what is the mechanism of action of penicillinase-resistant PCNs?

A

act by binding to PBPs and preventing cell wall synthesis; resistant to the action of bacterial penicillinases by steric hinderance of the acyl chain, thereby preventing opening of the b-lactam ring

36
Q

what is the spectrum of activity of penicillinase-resistant PCNs?

A

effective against b-lactamase producing isolates of staphylococcus aureus and coagulase-negative staphylococci

37
Q

what is the pharmacokinetics of penicillinase-resistant PCNs?

A

absorbed after oral administration, adversely affected by food; urinary/biliary excretion

38
Q

what are the clinical indications of penicillinase-resistant PCNs?

A

semi-synthetic PCNs are commonly used for the empiric tx of skin and skin structure infections and bone and joint infections when staphylococcus aureua is a likely pathogen

39
Q

how does interstitial nephritis manifest clinically?

A

fever, rash, eosinophilia, proteinurea and hematuria

40
Q

what are the adverse effects a/w methicillin use?

A

interstitial nephritis

41
Q

what are the adverse effects a/w oxacillin use?

A

cholestasis without jaundice; liver enzymes return WNL s/p tx cessation

42
Q

what is the spectrum of activity of extended-spectrum PCNs?

A

broader spectrum of activity than natural PCNs and aminoPCNs

43
Q

what is the pharmacokinetics of extended-spectrum PCNs?

A

serum and tissue levels are not adequate for the treatment of systemic infections, better suited for uncomplicated UTIs; minimal CSF penetration; primary elimination if renal

44
Q

what are the clinical indications of extended-spectrum PCNs?

A

effective against a variety of gram negative organisms; prescribed in combination with gentamicin to combat gram negative bacilli; generally used clinically in combination with a b-lactamase inhibitor

45
Q

what are the adverse effects of extended-spectrum PCNs?

A

hypersensitivity reactions, similar to the other types of PCNs, inhibition of platelet aggregation- platelet dysfx and prolonged bleeding times

46
Q

what is the interaction of extended-spectrum PCNs with warfarin?

A

decreased anticoagulation effect

47
Q

what is the interaction of extended-spectrum PCNs with piperacillin?

A

potentiate the action of non depolarizing blocking agents

48
Q

what is the interaction of extended-spectrum PCNs with aminoglycosides?

A

has been shown to degrade the aminoglycoside

49
Q

because of varied drug interactions with extended-spectrum PCNs, what is the recommendation for their parenteral administration?

A

this class of drugs should not be mixed in solutions and their administration be separated by 30-60 min

50
Q

what is the mechanism of action of cephalosporins?

A

possess a b-lactam ring; interfere with synthesis of peptidoglycan in the bacterial cell wall and binds to and inactivates PBPs, which are enzymes responsible for the synthesis of the bacterial cell wall

51
Q

how are cephalosporins classified?

A

classified into generations on the basis of their spectrum of microbiologic activity. this classification reflects increase in stability of higher generations to various bacterial b-lactamases,

52
Q

Given alone, none of the cephalosporins are effective against what organisms?

A

MRSA, listeria or clostridium species

53
Q

what is the spectrum of activity of first gen cephalosporins?

A

good activity against G+ cocci and relatively modest activity against many G-. most G+ cocci are susceptible (except MRSA, staph epidermis and entercocci).

54
Q

what is the spectrum of activity of second gen cephalosporins?

A

more active against G- although less than third gen; variable activity against G+ cocci, improved activity against H influenza, gonohrrea and Nisseria meningitis

55
Q

what is the spectrum of activity of third gen cephalosporins?

A

more active against enterbactors including b-lactamase producing strain, also against staph pneumonia.

56
Q

what is the spectrum of activity of fourth gen cephalosporins?

A

have a greater spectrum of activity than the third gen; effective against H influenza, nisseria species and pseudonomas. Also effective against G+ cocci: staph aureus, staph pneumonia and other streptococci

57
Q

what are the pharmacokinetics of cephalosporins?

A

good penetration into tissues and fluid compartments, including CSF

58
Q

what is the mechanism by which bacterial builds resistance to cephalosporins?

A

three mechanisms of resistance: 1) inactivation by bacterial B-lactamase, 2) alterations of PBPs, 3) alteration of bacterial permeability

59
Q

what is the clinical use of first and second gen cephalosporins?

A

skin and respiratory tract infections

60
Q

what is the clinical use of third gen cephalosporins?

A

empiric treatment

61
Q

what is the clinical use of fourth gen cephalosporins?

A

febrile neutropenia dn nosocomial infections

62
Q

what are the adverse reactions a/w cephalosporin administration?

A

maculopapular skin eruptions, drug fever and a positive Coombs test; frequency of anaphylactic reaction varies from 0.0001-0.1%; renal insufficiency may require doseage adjustments

63
Q

what are the advantages of aminoglycosides?

A

effective against G- organisms, synergism with b-lactam antibiotics, limited bacterial resistance and low cost

64
Q

what has compromised the successful use of aminoglycosides?

A

nephrotoxicity and ototoxicity in significant number

65
Q

what is the mechanism of action of aminoglycosides?

A

alter the integrity of the bacterial cell wall membrane in growing bacteria by way of disturbing protein synthesis; binding of the aminoglycosides to the bacterial cell membrane itself may play a role int he rapid bacterial cell death

66
Q

what are the clinical uses for aminoglycoside prescription?

A

mainly used for treating serious G- infections caused by enteric bacilli; act synergistically with cephalosporins and PCNs; used in combination with vanc for S. aureus, both methicillin- sensitive and methicillin-resistant

67
Q

what are the indications for aminoglycoside administration?

A

NEONATAL SEPSIS; G- bacteria (E coli, klebsiella species, enterobacter species and pseudomonas species); synergistic with b-lactam antibiotics in treating group B strep and coag neg staph infx; important role in the initial empiric treatment of neonatal septicemia; UTI

68
Q

how to aminoglycosides treat UTIs?

A

excreted by way of glomerular filtration and are partly actively reabsorbed, leading to high tissue and urine concentrations

69
Q

renal toxicity may be r/t what with aminoglycoside administration?

A

toxicity seems to be r/t high trough concentration, indicating that these concentrations are not low long enough to prevent renal accumulation

70
Q

what due most experts attribute ototoxicity to with aminoglycoside administration?

A

r/t total dose and duration of tx rather than to serum aminoglycoside concentration

71
Q

what are risk factors for neonatal hearing loss?

A

perinatal infection, meningitis, preterm birth, hyperbili, BW <1500g, RDS, asphyxia, mechanical ventilation, bx and diuretics

72
Q

how does nephrotoxicity occur with aminoglycoside administration?

A

proximal tubular injury leading to cell necrosis; occurs less frequently than in adults

73
Q

how does ototoxicity occur with aminoglycoside administration?

A

potentially cochleo- and vestibulotoxic; hearing loss if usually BL, symmetrical and permanent; can have a delayed onset of months

74
Q

what special circumstances would require adjustments made to how aminoglycosides are ordered?

A

renal compromise, s/p asphyxia, low apgar scores or is receiving other nephro/ototoxic drug (indomethacin or diuretics); doseges and intervals are dependent on GA and PNA

75
Q

how has recommendations concerning monitoring and doseage changed with aminioglycosides?

A

has been revised toward larger doses in extended intervals

76
Q

what is the frequency of complications with aminoglycosides in courses <7 days?

A

very rare

77
Q

when is TDM mandated in aminoglycoside administration?

A

3rd or 4th dose

78
Q

what is the most widely used glycopeptide antibiotic?

A

vanc; frequently used for G+ infections

79
Q

When is vanc at risk of being inactivated?

A

when administered simultaneously with heparin in high concentrations

80
Q

what is the mechanism of action of glycopeptides?

A

bacterialcidal activity of vanc is based on the inhibition of bacterial cell wall synthesis

81
Q

what is VIRSA?

A

vancyomycin intermediate resistant staph aureus; resistance is r/t aggregated and thickened cell walls. infx with VIRSA is a/w failure to tx with vanc

82
Q

how has resistance to vanc come about?

A

a mechanical factor in the clinical resistance of staph aureus infx to van is r/t a production of a bile film on the bacteria, which shields it from the abx

83
Q

where is clinically important resistance to glycopeptides seen?

A

in enterococci, s aureus and s epidermis

84
Q

what are the indications for glycopeptide use?

A

drugs of choice for methicillin-resistant strains of staphylococcal infections; widely used empirically for the treatment of CLABSI; late onset septicemia

85
Q

what are the pharmacokinetics r/t glycopeptides?

A

eliminated primarily by glomerular filtration; VANC CANNOT BE RELIED UPON TO ADEQUATELY TX G + MENINGITIS WHEN GIVEN ALONE; GA and PNA and post conceptual age all have the ability fo alter the pharmacokinetics of this drug, more so PCA

86
Q

what are the drug related adverse effects of glycopeptides?

A

thrombocytopenia, neutropenia, eosinopilia, chills, fever, rash, nephrotoxicity and ototoxicity

87
Q

what are infusion related adverse effects r/t vanc administration?

A

“red man” syndrome- a histamine mediated rash of the face, neck, upper trunk, back and arms; a/w puritius, tingling, flushing, tachycardia and shock; CAUSED BY THE RATE OF INFUSION

Pharmacology Final (5 decks)

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