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Infeksjonsmedisin > Antibiotika - Amboss > Flashcards

Antibiotika - Amboss Flashcards

1
Q

Hva er antibiotika?

A

Antibiotics:

Antimicrobial drugs effective against bacteria

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2
Q

Hvilken egenskap har bakteriocide ab.?

A
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3
Q

Hvilken egenskap har bakteriostatiske ab.?

A
Dapsone is only weakly bactericidal.
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4
Q

Som en generell regel, hvilke ab.-typer kan man si er bakteriocide/bakteriostatiske?

A
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5
Q

Hvilke typer ab. inhiberer bakterienes celleveggsyntese?

A

𝛽-laktam

Penicilliner

Cefalosporiner

Karbapenemer

Monobaktamer

Glykopeptider

Epoksider

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6
Q

Om betalaktamer, gi hhv.:
- Noen eksempler på ab.
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
PBP; Penicillin-binding proteins.
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7
Q

Av glykopeptider, gi hhv.:
- Eksempler på ab.
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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8
Q

Av epoksider, gi hhv.:
- Eksempler på medikament
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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9
Q

Hvilke typer ab. forstyrrer bakterienes cellemembran integritet?

A

Lipopeptider

Polymyksin

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10
Q

Av lipopeptider, gi hhv:
- Eks. på medikament
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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11
Q

Av polymyksiner, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriosid/bakteriostatisk
- Resistensmekanisme

A
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12
Q

Hvilke ab.typer inhiberer proteinssyntesen?

30S ribosomal subenheten

A

Aminoglykosider

Tetrasykliner

Glycylsykliner

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13
Q

Av aminoglykosider, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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14
Q

Av tetrasykliner og glycylsykliner, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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15
Q

Hvilke ab. typer inhiberer proteinssyntesen?

50S ribosomale subenheten

A

Makrolider og ketolider

Linkosamider

Streptogramins

Oxazolidioner

Amfenikoler

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16
Q

Av makrolider og ketolider, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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17
Q

Av linkosamider, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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18
Q

Av streptograminer, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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19
Q

Av oxazolidioner, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
A part of the bacterial 50S subunit of the bacterial ribosome
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20
Q

Av amfenikoler, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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21
Q

Hvilke ab. typer inhiberer bakterienes DNA gyrase?

A

Fluorokinoloner/kinoloner

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22
Q

Av fluorokinoloner, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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23
Q

Hvilke ab. typer gir forstyrret DNA integritet?

A

Nitromidazoler

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24
Q

Av nitromidazoler, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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25
Q

Hvilke ab. typer inhiberer folinsyresyntesen hos bakterier?

A

Sulfonamider og diaminopyrimidiner

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26
Q

Av sulfonamider og diaminopyrimidiner, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
The active form of folic acid.
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27
Q

Hvilke antimykobakterielle ab. har man?

A

Rifamyciner

Hydrasider

Nikotinamider

Etylendiamin derivater

Sulfoner

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28
Q

Av rifamyciner, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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29
Q

Av hydrazider, nikotinamider, etylendiamid derviater og sulfoner, gi hhv.:
- Eks. på medikamenter
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
The mechanism through which the mutation leads to the resistance to pyrazinamide is unknown.
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30
Q

Ved nitrofuraner, gi hhv.:
- Eks. på medikament
- Virkningsmekanisme
- Bakteriocid/bakteriostatisk
- Resistensmekanisme

A
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31
Q

Fyll inn figruen

A

Mechanism of action: antibiotics

A. Bacterial cell envelope

Polymyxins disrupt the outer membrane that is present in gram-negative bacteria.

Beta-lactams, glycopeptides, and epoxides inhibit cell wall synthesis.

Daptomycin forms ion channels on the cell membrane that lead to membrane depolarization and disruption.

B. Nucleic acids and related enzymes

Nitroimidazoles disrupt DNA strands by creating free radicals.

Fluoroquinolones interrupt DNA replication by inhibiting prokaryotic DNA gyrase.

Rifamycin prevents transcription by inhibiting RNA polymerase.

C. Bacterial ribosomes

Macrolides, amphenicols, lincosamides, and oxazolidinones inhibit protein synthesis by binding to the 50s subunit of the bacterial ribosome.

Aminoglycosides, tetracyclines, and glycylcyclines inhibit protein synthesis by binding to the 30s subunit of the bacterial ribosome.

D. Folic acid metabolism (required for DNA synthesis)

Sulfamethoxazole inhibits bacterial purine synthesis by inhibiting dihydropteroate synthetase, which converts para-aminobenzoate (PABA) into dihydrofolate (DHF).

Trimethoprim, a diaminopyrimidine, inhibits bacterial purine synthesis by inhibiting dihydrofolate reductase, which converts DHF into tetrahydrofolate (THF).

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32
Q

Fyll inn figuren

A

Mechanisms of action of antibiotics on the bacterial ribosome

Schematic indicating how various antibiotics inhibit the protein synthesis activity of the bacterial ribosome by their actions during the initiation phase (left) and the elongation phase (right).

Note that the details of some of these interactions vary across the literature.

Interactions at the 50S bacterial ribosome subunit:

Oxazolidinones block the formation of the initiation complex.

Macrolides and lincosamides primarily act by blocking translocation (solid markers) but also block the formation of the initiation complex (dotted markers indicate that this is not their main mechanism of action).

Amphenicols block the enzyme peptidyl transferase

Interaction at the 30S bacterial ribosome subunit:

Aminoglycosides block the formation of the initiation complex, cause codon misreading, or inhibit translocation.

Tetracyclines and glycylcyclines block aminoacyl-tRNA from binding to the ribosome acceptor site

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33
Q

Fyll inn figuren

A

Antibiotics interfering with folate/tetrahydrofolate synthesis

Sulfonamides and dapsone inhibit dihydropteroate synthase (present in bacteria).

Trimethoprim and pyrimethamine inhibit the dihydrofolate reductase (present in bacteria and humans).

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34
Q

Hva er definisjonen på beta-laktam ab.?

A

Definition:

A group of antibiotics that contains beta-lactam ring in their molecular structure and includes penicillins, carbapenems, monobactams, and cephalosporins

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35
Q

Hvordan virker betalaktamab.?

A
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36
Q

Hvordan er penetrasjonen av betalaktamab. av CNS?

A
Due to disruption of the blood-brain barrier.
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37
Q

Hvordan elimineres betalaktamab.?

A
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38
Q

Hva er generelle bivirkninger ved betalaktamab.?

A
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39
Q

Hvilke bakterier produserer betalaktamase?

A
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40
Q

Hva er betalaktamaseinhibitorer?
Hvilke medikamenter er dette?

A
The combination of amoxicillin with clavulanate is called co-amoxiclav.
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41
Q

Nevn noen eks. på naturlige penicilliner?

Prototype betalaktam ab.

A
Naturlige penicilliner = betalaktamasefølsomme penicilliner.
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42
Q

Ved hvilke mikroorganismer bruker man naturlige penicilliner?

A
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43
Q

Hvilke bivirkninger har naturlige penicilliner?

A
Penicillins bind to the bacterial breakdown products that form haptens, thereby eliciting the formation of antibodies (anti-IgG) that trigger hemolysis with a positive direct Coombs test.
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44
Q

Hvilke mekanismer gir resistensutviklingen av naturlige penicilliner?

A
Penicillins cannot bind to the mutant proteins.
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45
Q

Hvilke penicilliner regnes som betalaktamasestabile?

A
No longer administered due to high rates of side effects.
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46
Q

Hva er det som gjør betalaktamasestabile penicilliner virksomme mot bakterier som produserer dette?

A
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47
Q

Hvordan bruker man betalaktamasestabile penicilliner i klinikken?

A
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48
Q

Hvilke bivirkninger kan betalaktamasestabile penicilliner gi?

A
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49
Q

Hvilken mekanisme gjør bakterier resistente mot betalaktamasestabile penicilliner?

A
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50
Q

Gi noen eks. på bredspektrede penicilliner?

A
Clavulanate is a β-lactamase inhibitor which prevents the destruction of the β-lactam ring by β-lactamase.
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51
Q

Hvilke spesielle karakteristikker har bredspektrede penicilliner?

A
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52
Q

Hvilke mikroorganismer bruker man bredspektrede penicilliner mot?

A
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53
Q

Hvilke bivirkninger har bredspektrede penicilliner?

A
Almost all antibiotics can cause pseudomembranous colitis, but the use of aminopenicillins is associated with the highest risk of this complication. This side effect commonly occurs in cases in which aminopenicillins are used in patients with infectious mononucleosis that has been misdiagnosed as bacterial tonsillitis.
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54
Q

Hvilken mekanisme driver resistensutviklingen av bredspektret ab.?

A

Mechanisms of resistance:

Cleavage of the β-lactam ring by penicillinases

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55
Q

Hva viser bildet?

A
Aminopenicillin-related exanthem in infectious mononucleosis: Ventral upper body of a patient with a pruritic rash associated with the administration of an aminopenicillin in a patient erroneously diagnosed with bacterial tonsillitis. There is a erythematous, patchy, partly confluent, and pruritic exanthema. This appearance is typical of an aminopenicillin-related exanthema as a drug reaction in infectious mononucleosis.
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56
Q

Hvilke penicilliner er antipseudomonale?

A
Antipseudomonal penicillins are sensitive to β-lactamase and should be used with β-lactamase inhibitors.
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57
Q

Hvordan er den kliniske bruken av antipseudomonale penicillinene?

A
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58
Q

Hvilken bivirkningen forekommer ved antipsudomonal ab.?

A

Hypersensivitetsreaksjoner

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59
Q

Hvilke medikamenter er antipseudomonale ab.?

A

“The PIPER in his CAR full of TICks ran over *pseudomonas *”

Piperacillin

Carbenicillin

Tiaarcillin

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60
Q

Nevn noen medikamenter som er karbapenemer?

A
don't DIe on ME: Doripenem, lmipenem, Meropenem, and Ertapenem are carbapenems and used in life-threatening infections.
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61
Q

Hvilken spesiell karakterisitikk har karbapenemer?

A
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62
Q

Hvordan bruker man karbapenemer i klinikken?

A
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63
Q

Hvilke bivirkninger har karbapenemer?

A
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64
Q

Hvilken mekanisme gjøre bakterier resistente mot karbapenemer?

A
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65
Q

Nevn et medikament som er et monobaktam?

A

Aztreonam

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66
Q

Hvilke karakteristikker har monobaktamer?

A
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67
Q

Hvordan bruker man monobaktamer i klinikken?

A
The opposite of vancomycin.
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68
Q

Hvilke bivirkninger har monobaktamer?

A
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69
Q

Nevn eks. på alle generasjoner cefalosporiner?

A
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70
Q

Ved 1. generasjon cefalosporiner, hva er hhv.:
- Aktiviteten ved gram-positive bakterier
- Aktivitet ved gram-negative bakterier
- MRSA
- Listeria
- Pseudomonas
- Enterokokker
- Klamydia, mykoplasma, legionella
- Speiselle kliniske betraktninger

A
1 PEcK: 1st generation cephalosporins cover Proteus mirabilis, E. coli, Klebsiella pneumoniae.
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71
Q

Ved 2. generasjon cefalosporiner, hva er hhv.:
- Aktiviteten ved gram-positive bakterier
- Aktivitet ved gram-negative bakterier
- MRSA
- Listeria
- Pseudomonas
- Enterokokker
- Klamydia, mykoplasma, legionella
- Speiselle kliniske betraktninger

A
2 HENS PEcK: 2nd generation cephalosporins cover H. influenzae, Enterobacter aerogenes (now Klebsiella aerogenes), Neisseria, Serratia marcescens, Proteus mirabilis, E. coli, Klebsiella pneumoniae. 2nd graders wear fake fox fur to tea parties: 2nd generation cephalosporins include cefaclor, cefoxitin, cefuroxime, and cefotetan.
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72
Q

Ved 3. generasjon cefalosporiner, hva er hhv.:
- Aktiviteten ved gram-positive bakterier
- Aktivitet ved gram-negative bakterier
- MRSA
- Listeria
- Pseudomonas
- Enterokokker
- Klamydia, mykoplasma, legionella
- Speiselle kliniske betraktninger

A
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73
Q

Ved 4. generasjon cefalosporiner, hva er hhv.:
- Aktiviteten ved gram-positive bakterier
- Aktivitet ved gram-negative bakterier
- MRSA
- Listeria
- Pseudomonas
- Enterokokker
- Klamydia, mykoplasma, legionella
- Speiselle kliniske betraktninger

A
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74
Q

Ved 5. generasjon cefalosporiner, hva er hhv.:
- Aktiviteten ved gram-positive bakterier
- Aktivitet ved gram-negative bakterier
- MRSA
- Listeria
- Pseudomonas
- Enterokokker
- Klamydia, mykoplasma, legionella
- Speiselle kliniske betraktninger

A
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75
Q

Hvilke spesielle karakteristikker har cefalosporiner?

A

Special characteristics:

Less susceptible to penicillinases

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76
Q

Hvilke bivirkninger har cefalosporiner?

A
Drug-induced AIHA is most commonly caused by cefotetan, ceftriaxone, or piperacillin, which stimulate the production of anti-drug antibodies (usually IgG). When these drugs are administered, they bind to RBC membrane proteins. The preformed antibodies then bind to the drug-coated RBCs, which are subsequently hemolyzed in the spleen. The mechanism through which cephalosporins cause hypoprothrombinemia is not fully understood. Either cephalosporins inhibit the growth of vitamin K-producing intestinal bacteria (e.g., Bacteroides, Enterobacteriaceae, Enterococci) or they inhibit enzymes of vitamin K metabolism (e.g., vitamin K epoxide reductase).
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77
Q

Gi noen eks. på glykopeptidab.

A
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78
Q

Hva er virkningsmekanismen til glykopeptider?

A
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79
Q

Hvordan er glykopeptidab. sin penetrasjon til CNS?

A
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80
Q

Hvordan kvitter kroppen seg med glykopeptider?

A

Renal eliminasjon via glomerulær filtrasjon

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81
Q

Ved hvilken klinikk bruker man glykopeptider?

A
Vancomycin passes through the GI tract without being absorbed, so it has high concentration in the colon.
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82
Q

Hvilke bivirkninger har glykopeptider?

Intravenøs adm.

A

The vancomycin van carries a TON of flashy DRESSes: the side effects of vancomycin are Thrombophlebitis, Ototoxicity, Nephrotoxicity, vancomycin flushing reaction, and DRESS syndrome.

In contrast to aminoglycosides, nephrotoxicity is rare in glycopeptides on their own. However, there is a high risk of nephrotoxicity with concomitant use of other nephrotoxic drugs. Therefore, glycopeptide antibiotics should not be combined with NSAIDS, aminoglycosides, and/or furosemide. In contrast to aminoglycosides, ototoxicity and vestibular toxicity are rare for glycopeptides. Prolonged vancomycin therapy (> 7 days) is associated with neutropenia.
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83
Q

Hvilke kontraindikasjoner har man for bruk av glykopeptider?

A

Consider use in pregnant women only if the benefits outweigh the risks.

The safety of vancomycin during pregnancy has not yet been sufficiently established.

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84
Q

Hva er det som gjør bakterier resistente for glykopeptider?

A

“The fine for VAMdalism in one DALiAr in LACjac”

VANcomycin resistance is caused by amino acid modification (D-Ala-D-Ala to D-Ala-D-Lac)

Vancomycin is not a beta-lactam antibiotic.
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85
Q

Hva viser bildet?

A
Vancomycin flushing reaction; Erythema of the skin is visible, especially on the patient's cheeks and nose. This symptom usually resolves within minutes after treatment. Vancomycin flushing reaction is not a true allergic reaction, but rather a rate-dependent hypersensitivity reaction. It can be avoided by slow infusion.
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86
Q

Gi et eks. på et epoksid (epoxides) medikament?

A

Oral eller iv. Fosfomycin

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87
Q

Hvordan virker epoksider?

A
Fosfomycin is not active against aneroebes.
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88
Q

Hvordan kvitter kroppen seg med epoksider?

A

Renal eliminasjon

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89
Q

Ved hvilke kliniske problemstillinger bruker man fosfomycin?

A
Although fosfomycin is a broad-spectrum antibiotic that is effective against many gram-negative bacteria (e.g., E. coli, Enterobacter species, Pseudomonas, and Klebsiella) and gram-positive bacteria (e.g., S. aureus, MRSA, and VRE), in the US it is only approved and available for uncomplicated UTIs in women. Moreover, only oral salt is available in US (not the IV form).
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90
Q

Hvilke bivirkninger kan epoksider gi?

A
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91
Q

Hva er kontraindikasjoner for epoksider, og hvilken bakteriemekanisme gjør de resistente?

A
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92
Q

Gi et eks. på et lipopeptid?

A

Daptomycin

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93
Q

Hvilken virkningsmekanisme har lipopeptidene?

A
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94
Q

Hvordan kvitter kroppen seg med lipopetider?

A

Renal eliminasjon

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95
Q

Ved hvilke klinikk bruker man lipopeptider?

A

Dap-to-my-cin is good to my skin

Daptomycin is used to treat skin infections

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96
Q

Hvilke bivirkninger har lipopeptider, og ved hvilke tilstander er de kontraindisert?

A
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97
Q

Hva gjør bakterier resistente mot lipopeptider?

A
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98
Q

Gi noen eks. på medikamenter som er polymyksiner?

A
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99
Q

Hvilken virkningsmekanisme har polymyksiner?

A
Colistin binds to the lipopolysaccharide on the cell membrane (i.e., endotoxin), thereby neutralizing LPS.
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100
Q

Hvordan penetrerer polymyksiner CNS, og hvordan kvitter kroppen seg med medikamenter?

A
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101
Q

Ved hvilke tilfeller bruker man polymyksiner?

A
Proteus, Neisseria, and Serratia spp. are resistant to polymyxins. Because gram-positive bacteria do not have an outer membrane. Polymyxins have a poor oral absorption.
102
Q

Hvilke bivirkninger har polymyksiner?

A
103
Q

Hvilke kontraindikasjoner har man for bruk av polymyksiner?

A
104
Q

Nevn noen aminoglykosider?

A
105
Q

Hvilken virkningsmekanisme har aminoglykosider?

A
Depending on the aminoglycoside, translocation or the formation of the initiation complex is either inhibited or results in codon misreading.
106
Q

Hvordan er penetransen av aminoglykosider til CNS, og hvordan kvitter kroppen seg med medikamentet?

A
107
Q

Ved hvilken klinikk bruker man aminoglykosider?

A

“Me and my NEw AMIgA are taking GENeral STEPs to AMeliorate our TOBacco intake but are still unsuccessful”

NEomycin, AMIkAcin, GENtamicin, STrEPtomycin AMInoglycosides and TOBramycin are unsuccsessful in killing anaerobes.

108
Q

Hvilke bivirkninger har aminoglykosider?

A

“Ah, MI(y) NEPHew´s OTter keeps TERrorizing our block”

Side effects of AMInoglycosides include NEPHrotoxicity, OTotoxicity, TERatogenicity and neuromuscular blockade.

Aminoglycosides should not be combined with other nephrotoxic drugs (e.g., NSAIDS, vancomycin, furosemide). The risk of neuromuscular blockade increases in the event of hypomagnesemia or myasthenia gravis, and in patients who use calcium channel blockers.
109
Q

Ved hvilke tilstander er aminoglykosider kontraindisert?

A
110
Q

Hvilke mekanismer gjør bakterier resistente mot aminoglykosider?

A
111
Q

Fyll inn figuren

A

Mechanisms of action of antibiotics on the bacterial ribosome

Schematic indicating how various antibiotics inhibit the protein synthesis activity of the bacterial ribosome by their actions during the initiation phase (left) and the elongation phase (right). Note that the details of some of these interactions vary across the literature.

Interactions at the 50S bacterial ribosome subunit:

Oxazolidinones block the formation of the initiation complex.

Macrolides and lincosamides primarily act by blocking translocation (solid markers) but also block the formation of the initiation complex (dotted markers indicate that this is not their main mechanism of action).

Amphenicols block the enzyme peptidyl transferase
**
Interaction at the 30S bacterial ribosome subunit:**

Aminoglycosides block the formation of the initiation complex, cause codon misreading, or inhibit translocation.

Tetracyclines and glycylcyclines block aminoacyl-tRNA from binding to the ribosome acceptor site

112
Q

Nevn noen tetrasykliner?

A
May be used as a diuretic for SIADH because it is an ADH antagonist.
113
Q

Hva er virkningsmekanismen til tetrasykliner?

A
114
Q

Hvordan er penetransen av tetrasykliner, og hvordan kvitter kroppen seg med det?

A
115
Q

Ved hvilken klinikk bruker man tetrasykliner?

A
116
Q

Hvilke spesielle betraktninger bør man ha i mente ved bruk av tetrasykliner?

A
117
Q

Hvilke bivirkninger har tetrasykliner?

A

Teethracyclines

Teeth discoloration is a side effect of tetracyclines

Tetracyclines can form complexes with calcium ions.
118
Q

Hvilke kontraindikasjoner har man for bruk av tetrasykliner?

A
This contraindication is based on a high risk of teeth discoloration with the use of tetracycline. Recent studies, however, suggest that the risk of disrupted odontogenesis is much lower with doxycycline. Currently, short (< 21 days) use of doxycycline is allowed in children below 8 years of age for the treatment of diseases caused by Rickettsia spp. Except for doxycycline which is only allowed in pregnant women for the treatment of diseases caused by Rickettsia spp. Tetracyclines can be hepatotoxic.
119
Q

Hva gjør bakterier resistente mot tetrasykliner?

A
120
Q

Nevn et medikament som er et glycylsyklin?

A

Tigecyklin

121
Q

Hva er virkningsmekanismen til glycylsykliner?

A
Glycylcycline was designed to have a mechanism of action similar to tetracycline but to overcome tetracycline's mechanisms of resistance (e.g., efflux by pumps).
122
Q

Hvordan er CNS perforasjonen til glycylsykliner, og hvordan elimeneres det fra kroppen?

A
123
Q

Hvordan bruker man glycylsykliner i klinikken?

A
124
Q

Hvilke spesielle betraktninger om glycylsykliner må man ha i mente ved bruk?

A
125
Q

Hvilke bivirkninger har glycylsykliner?

A
Glycylcyclines share many side effects and contraindications with tetracyclines. Like tetracyclines, glycylcycline can form complexes with calcium ions.
126
Q

Hvilke kontraindikasjoner gjelder for glycylsykliner?

A
127
Q

Gi noen eks. på makrolider?

A
Roxithromycin is not available in the US.
128
Q

Hvordan er virkningsmekanismen til makrolider?

A

Macroslides

Macrolides inhibit translocation during protein synthesis, in which ribosomes slide along mRNA

Binding to the 50S subunit causes peptidyl-tRNA to dislocate from the ribosome during the elongation phase, resulting in inhibited protein synthesis.
129
Q

Hvordan er penetransen av makrolider til CNS, og hvordan eliminerer kroppen medikamentet?

A
130
Q

Ved hvilken klinikk bruker man makrolider?

A
Azithromycin is used to cover C. trachomatis, which often co-exists with N. gonorrhoeae. Azithromycin itself is also active against N. gonorrhoeae, but it is rarely used as a monotherapy for gonorrhea because of a high rate of resistance to it in N. gonorrhoeae. PPI combined with clarithromycin and amoxicillin or metronidazole
131
Q

Hvilke bivirkninger har makrolider?

A

The adverse effects of MACROlides include:

Gastrointestinal Motility issues

Arrythmia (due to prolonged QT interval)

Acute Cholestatic hepatitis

Rash

EOsinophilia

Especially with erythromycin. Especially if the exposure occurs within 2 weeks after birth.
132
Q

Hvilke medikamenter kan makrolider interagere med?

A
133
Q

Hvilke spesielle betraktninger må man ha i mente ved bruk av makrolider?

A
134
Q

Hvilke kontraindikasjoner har makrolider?

A
135
Q

Hva driver driver resistensutviklingen av makrolider?

A
136
Q

Gi et eks. på et linkosamid?

A

Klindamycin

137
Q

Hvilken virkningsmekanisme har linkosamider?

A
138
Q

Hvordan er CNS penetransen til linkosamider, og hvordan elimineres det fra kroppen?

A
139
Q

Ved hvilken klinikk bruker man linkosamider?

140
Q

Hvilke spesielle betrakninger må man ha i mente ved bruk av linkosamider?

A
141
Q

Hvilke bivirkninger har linkosamider?

A
Clindamycin, along with fluoroquinolones and 3rd and 4th generation cephalosporins, is one of the antibiotics most frequently associated with pseudomembranous colitis.
142
Q

Hvilke kontraindikasjoner har linkosamider?

A
While there is sufficient data to support the safety of clindamycin use during the 2nd and 3rd trimester, evidence regarding its safety during the 1st trimester is insufficient. Clindamycin is secreted into the breast milk and may cause adverse effects on the gastrointestinal flora of the infant.
143
Q

Gi et eks. på et streptogramin?

A

IV quinupristin-dalfopristin

144
Q

Hva er virkningsmekanismen til streptogramin?

A
145
Q

Hvordan elimineres streptograminer fra kroppen?

A

Biliært og renalt

146
Q

Ved hvilken klinikk bruker man streptogramin?

A
147
Q

Hvilke spesielle betraktninger må man ha i mente ved bruk av streptograminer?

A

Inhiberer CYP3A4

148
Q

Hvilke bivirkninger har streptograminer?

A
149
Q

Hvilke kontraindikasjoner har man for streptograminer?

A
150
Q

Hvilken bakteriemekanisme fører til resistens mot streptograminer?

A
Crossresistance with clindamycin and macrolides.
151
Q

Nevn et oxazolidinon?

A

Linezolid

152
Q

Hvilken virkningsmekanisme har oxazolidinoner?

A
Specifically, it binds to the bacterial 23S ribosomal RNA of the 50S subunit. Unlike other antibiotics that inhibit later stages of bacterial protein synthesis (e.g., elongation), linezolid inhibits protein synthesis at the very first step of translation.
153
Q

Hvordan er penetransen til CNS, og hvordan elimineres oxazolidinoner?

A
154
Q

Ved hvilken klinikk bruker man oxazolidinoner?

A
155
Q

Hvilke bivirkninger har oxazolidinoner?

A
156
Q

Hvilke kontraindikasjoner har man for bruk av oxazolidinoner?

A
157
Q

Hvilken bakteriemekanisme gir resistens mot oxazolidinoner?

A
158
Q

Nevn et amfenikol

A

Kloramfenikol

159
Q

Hvilken virkningsmekanisme har amfenikoler?

A
May be bactericidal in high concentrations.
160
Q

Hvordan er penetrasjonen av CNS, og hvordan eliminerer kroppen amfenikoler?

A
Dose adjustment is not required in the case of renal failure, but is required in the case of hepatic dysfunction.
161
Q

Ved hvilken klinikk bruker man amfenikoler?

A

Konjunktivitt

Chloramphenicol is rarely used in the US because it has severe adverse effects. However, it is still often used in developing countries because of its low cost.
162
Q

Hvilke spesielle betrakninger må man ha i mente ved bruk av amfenikoler?

A

Potent inhibitorisk effekt av cytokrom P450 isoformene CYP2C19 og CYP3A4

163
Q

Hvilke bivirkninger har amfenikoler?

A
164
Q

Hvilke kontraindikasjoner har man for amfenikoler?

A
Except for the treatment of diseases caused by Rickettsia spp. Caution should be used when administering during the third trimester of pregnancy due to the risk of development of gray baby syndrome.
165
Q

Hvilke mekanismer driver resistensen av amfenikoler?

A
166
Q

Gi noen eks. på fluorokinoloner/kinoloner

A
167
Q

Hvilken virkningsmekanisme har fluorokinoloner?

A
168
Q

Hvordan penetrerer fluorokinoloner CNS, og hvordan elimineres medikamentet?

A
169
Q

Ved hvilken klinikk bruker man norfloxacin, ciprofloxacin og ofloxacin?

A
170
Q

Ved hvilken klinikk bruker levofloxacin, moxifloxacin og gemifloxacin?

A
171
Q

Hvilke bivirkninger har fluorokinoloner?

A

Fluoroquinolones hurt the attachments to your bones

NSAIDs increase the displacement of GABA from its receptor caused by quinolones. Especially with gatifloxacin, which has been removed from the US market for this reason. Common with newer fluoroquinolones.
172
Q

Hvilke spesielle betrakninger må man ha i mente vba. fluorokinoloner?

A
173
Q

Hvilke kontraindikasjoner har man for bruk av fluorokinoloner?

A
The only exception is ciprofloxacin which can be used in this cohort for complicated UTI including pyelonephritis and anthrax. Potentially life-threatening exacerbations. Aluminum- and magnesium-containing antacids decrease the absorption of fluoroquinolones.
174
Q

Hvilken mekanisme er det som gir resistens mot fluorokinoloner?

A
175
Q

Gi eks. på nitromidazoler?

A
176
Q

Hvilken virkningsmekanisme har nitromidazoler?

A
The reduced nitro groups of the active drug lead to complex formation and introduction of strand breaks within DNA.
177
Q

Hvordan er CNS penetrasjonen, og hvordan elimineres nitromidazoler?

A
178
Q

Ved hvilken klinikk bruker man nitromidazoler?

A

Take the Metro To lonG BEaCH

Metronidazoles treats Trichomonas, Giardia/ Gardnerella, Bacteroides, Entamoeba, Clostridium, and H.pylori

In anaerobes, metronidazole is reduced to its active metabolite. In aerobes, the presence of oxygen, which increases electron acceptance, prevents the reduction of metronidazole and its consequent formation into an active metabolite.
179
Q

Hvilke bivirkninger har nitromidazoler?

A
In the majority of these reported cases, other potential causes for this reaction have not been explored.
180
Q

Hvilke kontraindikasjoner har man for bruk av nitromidazoler?

A
181
Q

Hvilken medikamentklasse tilhører sulfonamider og diaminopyrimidiner?

A
Many classes of drugs contain a sulfonamide structure.
182
Q

Gi noen eks. på sulfonamider og diaminopyrimidiner

A
Diaminopyrimidine derivative.
183
Q

Hvilken virkningsmekanisme har sulfonamider og diaminopyrimidiner?

A
TMP shares this mechanism of action with other drugs such as methotrexate (an antirheumatic) and pyrimethamine (an antimalarial). The combination of TMP and SMX also prevents antibiotic resistance.
184
Q

Hvordan er penetransen av sulfonamider og diaminopyrimidiner, og hvordan eliminerer kroppen medikamentene?

A
Only a small amount is excreted with bile.
185
Q

Hva er den vanligste indikasjoen for sulfonamider og diaminopyrimidiner?

A

Vanlige indikasjoner er UVI´er og akutt otitis media

186
Q

Ved hvilken klinikk bruker man sulfisoxazole?

A
187
Q

Ved hvilken klinikk bruker man trimetoprim-sulfametoksazol (TMP/SMX)?

A
188
Q

Hvilke bivirkninger har sulfonamider?

A
Because SMX has a higher binding affinity to albumin, it can displace drugs such as warfarin and increase their free plasma concentration. After β-lactams, sulfonamides are the second most common antibacterial drugs to cause hypersensitivity reactions.
189
Q

Hvilke bivirkninger har diaminopyrimidin derivater?

A

TMP Treats Marrow Poorly

190
Q

Hvilke kontraindikasjoner har man for bruk av sulfonamider og diaminopyrimidiner?

A
191
Q

Hvilken mekansime fører til resistens mot sulfonamider?

A
PABA is a substrate of dihydropteroate synthase and a precursor of folic acid.
192
Q

Fyll inn figuren

A
Antibiotics interfering with folate/tetrahydrofolate synthesis: Sulfonamides and dapsone inhibit dihydropteroate synthase (present in bacteria). Trimethoprim and pyrimethamine inhibit the dihydrofolate reductase (present in bacteria and humans).
193
Q

Nevn et nitrofuran

A

Nitrofurantoin

194
Q

Hva er virkningsmekanismen til nitrofuraner?

A
195
Q

Hvordan elimineres nitrofuraner?

A
Nitrofurantoin is rapidly excreted after absorption.
196
Q

Ved hvilken klinikk bruker man nitrofuraner?

A
197
Q

Hva er NILD?

A
Chest pain, arthralgia, tachycardia, and tachypnea may also be present. Chest pain, fatigue, myalgia, and weight loss may also be present. Improvement of symptoms after nitrofurantoin discontinuation confirms the diagnosis. Consider in patients who do not improve after cessation of nitrofurantoin. Most patients with acute NILD improve rapidly upon cessation, whereas recovery in patients with chronic NILD may take several months.
198
Q

Hvilke bivirkninger forekommer ved bruk av nitrofuraner?

A

Pulmonal fibrose

Hemolytisk anemi hos pas. med G6PD mangel

GI symptomer

Reversibel perifer nevropati

199
Q

Hvilke kontraindikasjoner har man mot nitrofuraner?

A
Because of the risk of hemolytic anemia in an infant due to the lack of erythrocyte glutathione peroxidase. In renal failure, urinary drug levels do not reach concentrations required to treat UTIs, and the retention of nitrofurantoin in systemic circulation increases the risk of adverse effects.
200
Q

Hvilke antimykobakterielle medikamenter har man?

A

Rifamycin

Isoniazid

Pyrazinamid

Etambutol

Dapson

201
Q

Fyll inn figuren

A

Mechanism of action: antimycobacterial drugs

Rifamycin and streptomycin: inhibit RNA polymerase → reduction in protein synthesis

Dapsone: inhibits bacterial synthesis of dihydrofolic acid, via competition with para-aminobenzoate → reduced nucleic acid synthesis

Isoniazid: a prodrug converted into the active form isoniazid by catalase-peroxidase (KatG), which prevents cell wall synthesis via inhibition of mycolic acid production

Pyrazinamide: mechanism unknown

Ethambutol: inhibits arabinosyltransferase → prevention of mycobacterial cell wall synthesis (bacteriostatic effect)

202
Q

Gi noen eks. på rifamyciner?

A
Rifaximin is not absorbed systemically and is therefore used as a gut antibiotic.
203
Q

Hva er virkningsmekanismen til rifamyciner?

A
204
Q

Hvordan elimineres rifamyciner fra kroppen?

A

Biliært

205
Q

Ved hvilken klinikk kan man bruke rifamyciner?

A
The exact treatment scheme depends on the form of the disease. Treatment of the most dangerous form, disseminated, consists of clarithromycin combined with ethambutol with a possible addition of rifabutin. Rifaximin can be added to nonabsorbable disaccharides (e.g., lactulose, lactitol) to decrease ammonia production by reducing the amount of urease-producing colonic bacteria.
206
Q

Hvilke bivirkninger har rifamyciner?

A

“The 6Rs of Rifampin”

Red or orange urine

RNA polymerase Repression

Ramping up of cytochrome P450 activity

Rapid Resistance development if used alone

Rifampin really amplifies (induces) cythochrome P450, but rifabutin does not

Protease inhibitors and NNRTIs (e.g., efavirenz) are also cytochrome P450 substrates.
207
Q

Hvilke kontraindikasjoner har rifamyciner?

A
Because the safety in this population has not been established.
208
Q

Hvilken mekanisme driver resitensen av rifamyciner?

A
Mutations in the β subunit of the bacterial RNA polymerase confer near-complete resistance to the drug.
209
Q

Hvilken virkningsmekanisme har isoniazid?

A
Mycolic acid is a component of the cell wall of Mycobacteria.
210
Q

Hvordan er CNS penetransen til isoniazid?

A

Variabel

211
Q

Hvordan er metabolismen til isoniazid?

A
212
Q

Hvordan elimineres isoniazid ut av kroppen?

A

Renal eliminasjon etter hepatisk metabolisme

Dose adjustment is not required in the case of renal failure.

213
Q

Ved hvilken klinikk bruker man isoniazid?

A
214
Q

Hvilke bivirkninger har isoniazid?

A

INH Is Not Healthy In Neurons and Hepatocytes

Pellagra; A deficiency of niacin (vitamin B3).
215
Q

Hvilke kontraindikasjoner har isoniazid?

A
Because the safety in this population has not been established.
216
Q

Hvilken mekanisme driver resistensen av isoniazid?

A
217
Q

Hva er virkningsmekanismen til pyrazinamid?

A
218
Q

Hvordan er penetrasjonen av CNS ved bruk av pyrazinamid, og hvordan elimineres medikamentet?

A
Due to disruption of the blood-brain barrier.
219
Q

Ved hvilken klinikk bruker man pyrazinamid?

A

Mycobacterium tuberculosis

Together with isoniazid, rifampin, and ethambutol

220
Q

Hvilke bivirkninger og kontraindikasjoner har pyrazinamid?

A
Because the safety in these populations has not been established.
221
Q

Hva driver resistensen av pyrazinamid?

A
The mechanism through which the mutation leads to the resistance to pyrazinamide is unknown.
222
Q

Hvilken virkningsmekanisme har etambutol?

A
Arabinosyltransferase catalyzes the production of arabinogalactan, a constituent of the cell wall of Mycobacteria.
223
Q

Hvordan er etambutol sin penetrasjon av CNS, og hvordan skilles det ut av kroppen?

A
Due to disruption of the blood-brain barrier.
224
Q

Ved hvilken klinikk bruker man etambutol?

A
225
Q

Hvilke bivirkninger har etambutol?

A

“EYEthambutol”

Ethambutol causes optic neuropathy

226
Q

Hvilke kontraindikasjoner har etambutol?

A
The safety of ethambutol use in children has not yet been sufficiently established.
227
Q

Hvilken mekanisme gir resistensen av etambutol?

A
228
Q

Hvilken virkningsmekanisme har dapson?

A
229
Q

Hvordan kvitter kroppen seg med dapson?

A

Hovedsakelig renalt

230
Q

Ved hvilken klinikk kan man bruke dapson?

A
231
Q

Hvilke bivirkninger har dapson?

A
232
Q

Hvilke kontraindikasjoner har man ved bruk av dapson?

A
Because the safety in these populations has not been established.
233
Q

Hva er det som driver resistensen mot dapson?

A
234
Q

Ved ab. bruk hos barn, hva er hhv:
- Absolutt kontraindisert
- Relativt kontraindisert
- Trygt å bruke

A
May cause gray baby syndrome.
235
Q

Ved bruk av ab. hos gravide, hva er hhv.:
- Absolutt kontraindisert
- Relativt kontraindisert
- Trygt å bruke

A
The rate of hepatotoxicity is higher in pregnant women if using erythromycin estolate. Except erythromycin estolate.
236
Q

Ved bruk av ab. hos kvinner som ammer, hva er hhv.:
- Absolutt kontraindisert
- Relativt kontraindisert
- Trygt å bruke

A
237
Q

Ved bruk av ab. hos individer med nyresvikt, hva er hhv.:
- Absolutt kontraindisert
- Relativt kontraindisert
- Trygt å bruke

A
Nephrotoxicity is rare in glycopeptide use. However, there is a high risk of nephrotoxicity with concomitant use of other nephrotoxic drugs (e.g., NSAIDS, aminoglycosides). Rifamycins should be administered daily because intermittent therapy is associated with an increased risk of renal failure.
238
Q

Ved bruk av ab. hos pas. med leversvikt, hva er hhv.:

A
Due to hepatotoxicity. Due to hepatotoxicity. Due to hepatotoxicity.
239
Q

Hva mener man med empirisk ab. behandling?

A

Empiric antibiotic therapy covers the most probable causative organism(s) before the pattern of resistance and/or causative organism are known.

240
Q

Ved hvilke indikasjoner bruker man ab. behandling empirisk?

A
241
Q

Hvilke faktorer hjelper oss når man må gi ab. empirisk?

Vert faktorer

A

Bakgrunn for infeksjonen

Infeksjonsfokus

Relative kontraindikasjoner

Tidligere ab. behandling:
- Infections in which previous antibiotic therapy has been unsuccessful may have resistant pathogens.

242
Q

Ved empirisk ab. bruk, hvordan hjelper infeksjonsbakgrunnen oss til å velge riktig ab.?

A
The causative pathogen and its resistance pattern may vary depending on where the infection was acquired. Community-acquired infections are less likely to be resistant, while nosocomial infections are more likely to be caused by antibiotic-resistant organisms (e.g., MRSA, Pseudomonas). Certain procedures such as intubation and/or the placement of a central line are associated with a greater risk of infection with certain pathogens. For example, the incidence of tuberculosis is much higher in India than in the US. The policies for antibiotic therapy vary between hospitals depending on the resistance pattern of an organism.
243
Q

Hvordan hjelper infeksjonsfokuset oss til å velge ab. ved empirisk behandling?

A
Due to the proximity of the anal and genital regions.
244
Q

Hvorfor er kontraindikasjoner viktig ved velg av empirisk ab. behandling?

A
For infections in immunosuppressed individuals, bactericidal antibiotics should be chosen over bacteriostatic ones.
245
Q

Hvilke faktorer ved medikamentet styrer den empiriske ab. behandlingen?

A
In addition to pharmacokinetic properties, the route of drug administration is influenced by the site and severity of the infection. For example, IV drug administration might be preferred in a patient who cannot take oral medications (e.g., an unconscious patient) or when an immediate effect is required because IV administration is the fastest way to deliver a drug to the systemic circulation. Some antibiotics should only be used if the benefit clearly outweighs the risk. For example, if a pregnant woman has a severe infection with a multiresistant pathogen that after testing turns out to be sensitive only to aminoglycosides, aminoglycoside should be used despite the possible teratogenic effect. E.g., chloramphenicol is rarely used in the US because of its severe adverse effects, but it is still frequently used in resource-limited countries because it is relatively inexpensive.
246
Q

Hvordan kan man eskalere den empiriske ab. behandlingen?

A
247
Q

Når velger man å deeskalerer den empiriske ab. behandlingen?

A
De-escalation of antibiotic therapy should be avoided if the infection is likely polymicrobial.
248
Q

Hvilket prinsipp må man alltid følge (hvis mulig) hvis det er nødvendig med empirisk ab. behandling?

A

Blood cultures should be taken before initiating empiric antibiotic therapy.

249
Q

Hva er målrettet ab. behandling?

A
250
Q

Når er det akt. med ab. profylakse?

A

Infeksjonsmedisin (14 decks)

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