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Clinical Pharmacology Year V NIŠ > Antibiotics > Flashcards

Antibiotics Flashcards

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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
Which ABs groups cause Neurotoxicity as an AE?
- PCN - Cephalosporins - Carbapenems - Polymixins - Linezolid (risk of 5 HT syndrome and peripheral neuropathy)
26
Which ABs groups cause Nephrotoxicity as an AE?
Indirect Nephrotoxicity: - PCN - Cephalosporin - TMP SMX Direct Nephrotoxicity: - AG's - Vancomycin
27
Which ABs groups cause Pancytopenia as an AE?
- PCN - Cephalosporins - TMP SMX - Chloramphenicol - Linezolid
28
Which ABs groups cause Respiratory Distress as an AE?
- Polymixins - Nitroforantoin (causes pulmonary fibrosis)
29
Which ABs groups cause Myasthenia Gravis worsening as an AE?
- Macrolides - FQ's - AG's - Clindamycin
30
Which ABs groups cause ototoxicity as an AE?
- AG's - Vancomycin
31
Which ABs have teratogenic AE?
- TMP SMX - FQ's - Chloramphenicol - Doxycycline
32
Which ABs increase QT interval?
- FQ's - Macrolides
33
Which AB groups cause hemolytic anemia?
(+) Coombs test: - PCN - Cephalosporins Worsen G6PDH Deficiency: - TMP SMX - FQ's - Nitroforantoin
34
Which AB groups inhibit CYP450?
- FQ's - Macrolides - TMP SMX
35
Which ABs cause phototoxicity?
- Doxycycline - TMP SMX
36
What are specific AE of PCNs?
- hypersensitivity (IgE)
37
What are specific AE of Cephalosporins?
- vitamin K decrease therefore risk of bleeding - Cholecystitis - Biliary sludge - In combo with AG's = increased nephrotoxicity
38
What are specific AE of Vancomycin?
- phlebitis (when drug is pushed in too quickly) - red man syndrome: muscle spasm, redness, itchiness - Drug Related Eosinophilic Systemic Symptoms (DRESS)
39
What are specific AE of Daptomycin?
- rhabdomyolysis
40
What are specific AE of Doxycycline?
- Pill induced esophagitis: when not enough water taken with pill or not standing upright when swallowing - binds to Ca2+ on teeth = teeth staining
41
What are specific AE of Macrolides?
MACRO -Motility dysfunction in GI -Arrhythmia -Cholestasis -Rash -eOsinophilia
42
What are specific AE of Clindamycin?
- increased risk of C.diff infection - symptoms e.g. diarrhea
43
What are specific AE of Linezolid?
- Lactic acidosis
44
What are specific AE of FQ's?
- hypo/ hyperglycemia - destruction of cartilaginous tissue - tendon rupture, avoid in > 60 years of age
45
What are specific AE of bactams (TMP SMX)?
- hyperkalemia
46
Which ABs are most suitable for MSSA?
- FQ's - Cephalosporins 1st Gen - Anti-staph PCN
47
Which ABs are most suitable for MRSA?
- vancomycin - 5th gen Cephalosporin - TMP SMX - Clindamycin - Doxycycline
48
Which ABs are most suitable for Strep. Pneu?
- Penicillin G - Amino PCN - Cephalosporin 3rd gen
49
Which ABs are most suitable for Strep A & B?
- Amino PCN - Cephalosporin 1st gen - TMP SMX - Macrolides - Clindamycin
50
Which ABs are most suitable for Enterococcus?
- PCN - Amino PCN
51
Which ABs are most suitable for Listeria?
- Amino PCN - TMP SMX
52
What are the Gram (+) batceria?
- MSSA - MRSA - Enterococcus - Listeria - Strep Pneumoniae - Strep A & B
53
What does HENS PEcK stand for?
2nd Generation Cephalosporins: - H. Influenza - Enterobacteria - Neisseria Gonorrhoea/ Meningitis - Serratia 1st Generation Cephalosporins: - Proteus - E.coli - Klebsiella
54
Which ABs are most suitable for HENS PEcK?
- PEcK: 1st gen Cephalosporins - HENS: 2nd gen Cephalosporins - Antipseudo PCN - Carbapenems - Monobactams - FQ's (but not N) - AG's (but not N)
55
How does bacterial resistance occur?
- 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
What is the rational approach for AB therapy?
- AB choice - Dosage - Duration - Interactions & SE - Combination 4D's: - right drug - right dosage - right duration - de-escalation
57
What are the basic principles of rational AB therapy?
- 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
How are AB treatment decisions made? What Q's to ask?
- 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
What is Empirical AB therapy?
- 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
What is the 4 step process to Empirical Therapy?
1) Make a clinical Dx of Microbial Infection 2) Obtain specimens for lab exams 3) Formulate microbiological Dx 4) Determine necessary empirical therapy
61
What factors decide the AB agent choice?
- age - comorbidities - pregnancy status - prior adverse effects - impaired ability to detoxify or eliminate drug
62
How may AB therapy be monitored?
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
Which ABs are bacteriostatic?
- Macrolides - Tetracyclines - Folic Acid Pathway Alters - Nitroforantoin
64
Which ABs are bactericidal?
- Daptomycin, Polymixins - PCN - Cephalosporins - Carbapenems - Monobactam - AG's - FQ's - Metronidazole - Vancomycin
65
What is the rational approach for combination AB therapy?
- 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
What is the AB resistance cycle?
- 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
How can we reduce bacterial resistance?
- 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
What are the pharmacokinetic changes in severe sepsis?
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
What are some common side effects of ABs in adults?
- nausea - vomiting - somnolence - measles on skin - arrhythmias - itchy skin - hyperkalemia - site of drug application reaction
70
What are the drug interactions of FQ's?
FQ's susceptible to inhibition of GI absorption - caffeine - sucralfate - theophylline
71
What are the drug interactions of macrolides
Clarithromycin and erythromycin inhibit CYP3A-4 and P-glycoprotein - quinidine - pimozide - theophylline
72
What changes are undergone by bacteria when developing resistance?
- enzyme degradation - target protein changes - bacterial membrane permeability - change in ribosome structure - changes in metabolic pathways
73
What are URTI and LRTI?
URTI: - rhinitis - tonsillopharyngitis - acute otitis media (AOM) - acute bacterial rhinosinusitis LRTI: - acute bronchitis - pneumonia - acute exacerbation of chronic bronchitis
74
Drug of choice for AOM?
- ABs not always necessary unless infection severe or infection lasts 2-3 days - amoxicillin - cephalosporin 2nd or 3rd gen - Azithromycin
75
Drug of choice for tonsillopharyngitis?
Children drug of choice: - PCN V - Amoxicillin - 2nd gen cephalosporin - or clindamycin, macrolides
76
Drug choice for acute bacterial rhinosinusitis?
- 2nd gen cephalosporins - amoxicillin - azithromycin
77
AB drug choice of acute bronchitis?
- psych you bitch! - acute bronchitis is predominantly caused by viruses - AB only if bacterial reinfection
78
AB drug of choice for exacerbation of chronic bronchitis?
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
What classes of ABs are there? Give examples.
*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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