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Clinical Pharmacology Year V NIŠ > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What are the different MOA of ABs?

A

Affect Cell Wall:
1) Inhibition of peptidoglycan (PG) synthesis
2) Inhibition of PG cross-linking

  • DNA gyrase function inhibition
  • DNA integrity alteration
  • mRNA synthesis inhibition
  • Cell membrane integrity alteration
  • Folic acid pathway alteration
  • 30s & 50s inhibition
  • beta lactamase inhibitors
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2
Q

Which ABs prevent PG synthesis?

A
  • Vancomycin
  • Fosfomycin
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3
Q

What ABs groups affect the cross-linking of PG and are b-lactams?

A

4 groups of ABs
- Penicillin (PCN)
- Cephalosporins
- Carbapenems
- Monobactam

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4
Q

Which ABs are part of PCN’s?

A
  • Natural: PCN G & V
  • Amino: Amoxicillin & Ampicillin
  • Anti staph: Oxacillin & Dioxacillin
  • Anti-pseudo: Piperacillin
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5
Q

Which ABs are part of Cephalosporins?

A

1st generation: cefezolin, cepharaxin

2nd generation: not common

3rd generation: ceftriaxone, ceftazaline, ceflataxine

4th generation: cefepine

5th generation: ceftaroline

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6
Q

Which ABs are part of Carbapenams?

A
  • Remember DIME
  • Doripenem
  • Imipenem
  • Meropenem
  • Etrapenem
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7
Q

Which AB are part of monobactams?

A
  • Aztranem
  • great for PCN allergic patient plus very broad use
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8
Q

Which drugs are part of beta lactamase inhibitors? Which ABs are they combined with?

A
  • Remember “CAST is A CAP”
  • Clavabactam –> amoxicillin
  • Arvibactam –> ceftazidine
  • Sulbactam –> ampicillin
  • Tazobactam –> piperacillin
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9
Q

What is the MOA of beta lactamase inhibitors?

A
  • Penicillin binding protein (PBP, a transpeptidase) help cross link PGs in cell wall
  • ABs inhibit PBP to form cross-linking of PG in cell wall
  • Resistance formed against these ABs
  • Bacteria produced an enzyme, beta lactamase
  • Beta Lactamase break down beta lactam ring in ABs which prevents AB to bind to PBP

*Beta-lactamase inhibitors block the enzymatic degradation of beta lactam rings in the ABs

  • therefore ABs can still have their bactericidal effect on bacteria
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10
Q

Which ABs alter bacterial cell membrane integrity? MOA?

A
  • Bacteriocidal
  • Daptomycin
  • Polymixin

*introduce efflux pumps to bacterial cell to make it more permeable- leaks out ions etc and therefore lysis of cell

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11
Q

Which ABs alter the folic acid pathways of bacteria? MOA

A

-Bacteriostatic

AKA Co-trimoxazole

  • Trimethoprim / Sulfamethoxazole
  • often used in combo TMP-SMX
  • Sulfamethoxazole: prevent conversion from PABA (para-aminobenzoic acid) to DHF (dihyrodrofolate)
  • inhibition of 1st step of folic acid pathway
  • Trimethoprim: decrease DHF therefore unable to convert to tetrahydrofolate (THF)
  • inhibition of 2nd step of folic acid pathway
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12
Q

Which ABs alter Bacterial DNA integrity? MOA?

A
  • Bacteriocidal
  • Metronidazole: increase production of free radicals which break DNA strands
  • Nitrofurantoin: same as above, plus causes protein damage
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13
Q

Which AB is inhibits the synthesis of mRNA? MOA?

A
  • Rifampin
  • MOA: inhibition of RNA polymerase enzyme
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14
Q

Which ABs alter DNA gyrase function? MOA?

A
  • inhibition of DNA gyrase (aka topoisomerase type 4) enzyme
  • therefore unable to cut up and re-ligate DNA leading to DNA fragmenation
  • Fluroquinolones:
    1st Generation: Ciprofloxacin
    2nd Generation: Levofloxacin, Gemifloxacin, Moxifloxacin

*2nd Gen FQ’s are aka respiratory FQ’s

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15
Q

Which ABs are 50s Ribosomal inhibitors? MOA?

A

Bacteriostatic

MOA: inhibition of translation stage of protein synthesis on 50s subunit

Macrolides:
- Azithromycin
- Erythromycin
- Clarithromycin
- Clindamycin
- Chloramphenicol (only developing countries)
- Linezolid

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16
Q

Which ABs are 30s Ribosomal Inhibitors? MOA?

A

Bacteriostatic & Bacteriocidal

MOA: inhibition of translation stage of protein synthesis on 30s subunit

Aminoglycosides (GAT): Bacteriocidal
- gentamycin, Amikacin, tobramycin

Tetracyclines: baceriostatic
-tetracycline, doxycycline

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17
Q

Empiric AB therapy for pneumonia?

A

CAP: Strep Pne. H. Influ. Atypical
- FQ’s e.g. ciprofloxacin
- Ceftriaxone (+/- doxycycline)
- Azithromycin
- Cefuroxime

HAP: (after 48 hours admission)- MRSA, Pseudomonas, E.coli
- Vancomycin
- Anti Pseudo PCN e.g. Piperacillin
- Ceftriaxone
- AG’s e.g. gentamycin

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18
Q

Empiric AB therapy for GI infections?

A

-Anti-pseudo PCN e.g. Piperacillin
- Carbapenems e.g. doripenem, imipenem
- MTZ + FQ’s
- MTZ + ceftriaxone
- MTZ + cefepine

  • MTZ = Metronidazole
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19
Q

Empiric AB therapy for urinary tract infections?

A

Pyelonephritis:
- ceftriaxone
- FQ’s e.g. ciprofloxacin
- Amino PCN e.g. amoxicillin

Acute Cystitis:
- TMP SMX
- Nitroforantoin
- Fosfomycin
- Ciprofloxacin (2nd line)

Complicated UTI:
- Vancomycin
- Amoxicillin/ Ampicillin
- Pipracillin, Cefepine’s
- Gentamycin

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20
Q

Empiric AB therapy for skin/soft tissue infection?

A

Strep A & MSSA:

PO form: Dicloxacin or Cephalexin
IV form: naficillin or oxacillin or cefezolin

Strep A & MRSA:
PO form: TMP SMX or doxycycline or Clindamycin

IV form: Vancomycin

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21
Q

Empiric AB therapy for bone/joint infections?

A
  • MRSA: Vancomycin
  • Neisseria: Ceftriaxone
  • Pseudomonas: Cefepine, Ceftazedine
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22
Q

Empiric AB therapy for Sepsis?

A

-MRSA: vancomycin
-Gram (-) + Anaerobe: Piperacillin or carbapenems

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23
Q

Empiric AB therapy for CNS infection e.g. meningitis?

A

CAM:
- Vancomycin
- Ceftriaxone (best for CNS penetration)

+/- ampicillin if patient suspected with Listeria

HAM:
- Vancomycin
- Cefepine

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24
Q

Empiric AB therapy for blood stream infections?

A
  • Vancomycin

*if any gram (-) add piperacillin or Tazobactam

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25
Q

Which ABs groups cause Neurotoxicity as an AE?

A
  • PCN
  • Cephalosporins
  • Carbapenems
  • Polymixins
  • Linezolid (risk of 5 HT syndrome and peripheral neuropathy)
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26
Q

Which ABs groups cause Nephrotoxicity as an AE?

A

Indirect Nephrotoxicity:
- PCN
- Cephalosporin
- TMP SMX

Direct Nephrotoxicity:
- AG’s
- Vancomycin

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27
Q

Which ABs groups cause Pancytopenia as an AE?

A
  • PCN
  • Cephalosporins
  • TMP SMX
  • Chloramphenicol
  • Linezolid
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28
Q

Which ABs groups cause Respiratory Distress as an AE?

A
  • Polymixins
  • Nitroforantoin (causes pulmonary fibrosis)
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29
Q

Which ABs groups cause Myasthenia Gravis worsening as an AE?

A
  • Macrolides
  • FQ’s
  • AG’s
  • Clindamycin
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30
Q

Which ABs groups cause ototoxicity as an AE?

A
  • AG’s
  • Vancomycin
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31
Q

Which ABs have teratogenic AE?

A
  • TMP SMX
  • FQ’s
  • Chloramphenicol
  • Doxycycline
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32
Q

Which ABs increase QT interval?

A
  • FQ’s
  • Macrolides
33
Q

Which AB groups cause hemolytic anemia?

A

(+) Coombs test:

  • PCN
  • Cephalosporins

Worsen G6PDH Deficiency:

  • TMP SMX
  • FQ’s
  • Nitroforantoin
34
Q

Which AB groups inhibit CYP450?

A
  • FQ’s
  • Macrolides
  • TMP SMX
35
Q

Which ABs cause phototoxicity?

A
  • Doxycycline
  • TMP SMX
36
Q

What are specific AE of PCNs?

A
  • hypersensitivity (IgE)
37
Q

What are specific AE of Cephalosporins?

A
  • vitamin K decrease therefore risk of bleeding
  • Cholecystitis
  • Biliary sludge
  • In combo with AG’s = increased nephrotoxicity
38
Q

What are specific AE of Vancomycin?

A
  • phlebitis (when drug is pushed in too quickly)
  • red man syndrome: muscle spasm, redness, itchiness
  • Drug Related Eosinophilic Systemic Symptoms (DRESS)
39
Q

What are specific AE of Daptomycin?

A
  • rhabdomyolysis
40
Q

What are specific AE of Doxycycline?

A
  • Pill induced esophagitis: when not enough water taken with pill or not standing upright when swallowing
  • binds to Ca2+ on teeth = teeth staining
41
Q

What are specific AE of Macrolides?

A

MACRO

-Motility dysfunction in GI
-Arrhythmia
-Cholestasis
-Rash
-eOsinophilia

42
Q

What are specific AE of Clindamycin?

A
  • increased risk of C.diff infection
  • symptoms e.g. diarrhea
43
Q

What are specific AE of Linezolid?

A
  • Lactic acidosis
44
Q

What are specific AE of FQ’s?

A
  • hypo/ hyperglycemia
  • destruction of cartilaginous tissue
  • tendon rupture, avoid in > 60 years of age
45
Q

What are specific AE of bactams (TMP SMX)?

A
  • hyperkalemia
46
Q

Which ABs are most suitable for MSSA?

A
  • FQ’s
  • Cephalosporins 1st Gen
  • Anti-staph PCN
47
Q

Which ABs are most suitable for MRSA?

A
  • vancomycin
  • 5th gen Cephalosporin
  • TMP SMX
  • Clindamycin
  • Doxycycline
48
Q

Which ABs are most suitable for Strep. Pneu?

A
  • Penicillin G
  • Amino PCN
  • Cephalosporin 3rd gen
49
Q

Which ABs are most suitable for Strep A & B?

A
  • Amino PCN
  • Cephalosporin 1st gen
  • TMP SMX
  • Macrolides
  • Clindamycin
50
Q

Which ABs are most suitable for Enterococcus?

A
  • PCN
  • Amino PCN
51
Q

Which ABs are most suitable for Listeria?

A
  • Amino PCN
  • TMP SMX
52
Q

What are the Gram (+) batceria?

A
  • MSSA
  • MRSA
  • Enterococcus
  • Listeria
  • Strep Pneumoniae
  • Strep A & B
53
Q

What does HENS PEcK stand for?

A

2nd Generation Cephalosporins:

  • H. Influenza
  • Enterobacteria
  • Neisseria Gonorrhoea/ Meningitis
  • Serratia

1st Generation Cephalosporins:

  • Proteus
  • E.coli
  • Klebsiella
54
Q

Which ABs are most suitable for HENS PEcK?

A
  • PEcK: 1st gen Cephalosporins
  • HENS: 2nd gen Cephalosporins
  • Antipseudo PCN
  • Carbapenems
  • Monobactams
  • FQ’s (but not N)
  • AG’s (but not N)
55
Q

How does bacterial resistance occur?

A
  • AB given without any indication
  • AB given for viral infection
  • Duration too short or long
  • AB not adapted to microbiological finding
  • Inadequate dosing
  • XS use of broad spectrum ABs
56
Q

What is the rational approach for AB therapy?

A
  • AB choice
  • Dosage
  • Duration
  • Interactions & SE
  • Combination

4D’s:
- right drug
- right dosage
- right duration
- de-escalation

57
Q

What are the basic principles of rational AB therapy?

A
  • Apply AB with narrowest spectrum of action to the most likely cause of action
  • Choose AB with lowest toxicity, price and convenient mode of administration
  • Monotherapy, combo justified for better efficacy, broad action, less toxicity and prevention of resistance
  • Take a suitable sample before applying ABs
  • Bacteriostatic with bactericidal is
    contraindicated
  • Evaluation of therapy 48-72 hrs
58
Q

How are AB treatment decisions made? What Q’s to ask?

A
  • Once pathogen identified, is there a more narrower spectrum agent that can be used?
  • One agent or combo?
  • Optimal dose? Route? Duration?
  • any susceptibility tests for any patients who don’t respond?
  • any adjunctive measures to eradicate infection? e.g. abscess drainage
59
Q

What is Empirical AB therapy?

A
  • AB are used initially before having identified the specific pathogen causing the infection
  • This use of AB is known as Empirical AB Therapy
  • the hope of EABT is that early intervention will improve the outcome
60
Q

What is the 4 step process to Empirical Therapy?

A

1) Make a clinical Dx of Microbial Infection

2) Obtain specimens for lab exams

3) Formulate microbiological Dx

4) Determine necessary empirical therapy

61
Q

What factors decide the AB agent choice?

A
  • age
  • comorbidities
  • pregnancy status
  • prior adverse effects
  • impaired ability to detoxify or eliminate drug
62
Q

How may AB therapy be monitored?

A

Clinically:
- improvement of symptoms e.g. fever, malaise

Microbiologically:
- culture of specimens showing eradication of bacteria
- useful to document reoccurrence or relapse
- follow up cultures to assess for superinfections or resistance

63
Q

Which ABs are bacteriostatic?

A
  • Macrolides
  • Tetracyclines
  • Folic Acid Pathway Alters
  • Nitroforantoin
64
Q

Which ABs are bactericidal?

A
  • Daptomycin, Polymixins
  • PCN
  • Cephalosporins
  • Carbapenems
  • Monobactam
  • AG’s
  • FQ’s
  • Metronidazole
  • Vancomycin
65
Q

What is the rational approach for combination AB therapy?

A
  • provide broad spectrum empiric therapy for seriously ill patients
  • treat polymicrobial infections e.g. abdominal abscess
  • decrease emergence of resistant strains
  • decrease dose-related toxicity by reducing dose of 1 or more components
  • enhance inhibition or killing
66
Q

What is the AB resistance cycle?

A
  • Increased AB use
  • Increase in resistant strain
  • Ineffective empiric therapy: increased morbidity and more ABs use
  • Increased hospitalisation : more AB use
  • increased healthcare resource use
  • limited alternatives: more AB use and increased Mortality
67
Q

How can we reduce bacterial resistance?

A
  • use appropriate sample whenever possible
  • monitor and evaluate AB therapy 48-72 hours
  • Education about rational use
  • Infection prevention and control measures
  • AB prescribing control
  • Improve microbiological diagnostics
68
Q

What are the pharmacokinetic changes in severe sepsis?

A

Phase 1- Lowered drug concentration due to:
- increase CO
- increased clearance extravasation
- increased volume of distribution
- CrCL > 130ml/min

Phase 2- Increased serum drug concentration:
- Organ dysfunction (liver, kidney), therefore decreased clearance
- renal failure

69
Q

What are some common side effects of ABs in adults?

A
  • nausea
  • vomiting
  • somnolence
  • measles on skin
  • arrhythmias
  • itchy skin
  • hyperkalemia
  • site of drug application reaction
70
Q

What are the drug interactions of FQ’s?

A

FQ’s susceptible to inhibition of GI absorption

  • caffeine
  • sucralfate
  • theophylline
71
Q

What are the drug interactions of macrolides

A

Clarithromycin and erythromycin inhibit CYP3A-4 and P-glycoprotein

  • quinidine
  • pimozide
  • theophylline
72
Q

What changes are undergone by bacteria when developing resistance?

A
  • enzyme degradation
  • target protein changes
  • bacterial membrane permeability
  • change in ribosome structure
  • changes in metabolic pathways
73
Q

What are URTI and LRTI?

A

URTI:
- rhinitis
- tonsillopharyngitis
- acute otitis media (AOM)
- acute bacterial rhinosinusitis

LRTI:
- acute bronchitis
- pneumonia
- acute exacerbation of chronic bronchitis

74
Q

Drug of choice for AOM?

A
  • ABs not always necessary unless infection severe or infection lasts 2-3 days
  • amoxicillin
  • cephalosporin 2nd or 3rd gen
  • Azithromycin
75
Q

Drug of choice for tonsillopharyngitis?

A

Children drug of choice:

  • PCN V
  • Amoxicillin
  • 2nd gen cephalosporin
  • or clindamycin, macrolides
76
Q

Drug choice for acute bacterial rhinosinusitis?

A
  • 2nd gen cephalosporins
  • amoxicillin
  • azithromycin
77
Q

AB drug choice of acute bronchitis?

A
  • psych you bitch!
  • acute bronchitis is predominantly caused by viruses
  • AB only if bacterial reinfection
78
Q

AB drug of choice for exacerbation of chronic bronchitis?

A

First line:
- Amoxicillin
- 2nd or 3rd gen cephalosporins

alternatives: azithromycin or doxycycline

*considering causes and resistance to beta-lactamase ABs- cefuroxime can be used

79
Q

What classes of ABs are there? Give examples.

A

*ABs Can Protect The Queens Men, Servants & Guards

  • AG’s e.g. Gentamycin
  • Cephalsporins e.g. ceftriaxone
  • PCN’s e.g. PCN G or amoxicillin
  • Tetracycline e.g. doxycycline
  • Quinolones/ FQ’s e.g. ciprofloxacin
  • Macrolides e.g. erythromycin
  • Sulfonamides e.g. sulfamethoxazole
  • Glycopeptides e.g. Vancomycin

Clinical Pharmacology Year V NIŠ (9 decks)

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