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Therapeutics IV > Intro to ABX - Block 1 > Flashcards

Intro to ABX - Block 1 Flashcards

1
Q

What is prophylaxis?

A

ABX administered to prevent infection that hasn’t occurred (high risk patients)

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2
Q

What is empiric therapy?

A

ABX given to proven or suspected infection, but culprit has not been identified

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3
Q

What is definitive therapy?

A

Given after the cultur and sensitivity report

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4
Q

What are the approaches of ABX systemic approach therapy?

A
  1. Confirm presence of infection
  2. Identifying the pathogen
  3. Selection of empiric therapy
  4. Monitor therapeutic response
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5
Q

What is stage 1 of infection?

A
  1. Early, 1-3 days of illness
  2. Characterized by clinical instability, abnormal lab values
  3. Uncertainty surrounding the identity of culprit for suspected infection
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6
Q

What is stage 2 of infection?

A
  1. 4-6 days of suspected infection
  2. Appropriate therapy -> clinical stability begins
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7
Q

What is stage 3 of infection?

A
  1. 7 days of suspected infection
  2. Appropriate therapy -> resolution of abnormal vital sugns, WBC count, fever
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8
Q

How can body temp indicate infection?

A

> 38°C (100.4°F) or < 36°C (96.8°F) -> inflammation

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9
Q

Normal WBC range

A

4,000-10,000

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10
Q

What are results of an elevated WBC?

A

Bacterial infection:
1. Presence of band neutrophils (left shift) -> increased bone marrow response to infection
2. Leukocytosis is normal in infection

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11
Q

What is the most common granulocyte def?

A

Neutropenia

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12
Q

What are the local signs of infection?

A
  1. Swelling, erythema, tenderness, purulent discharge
  2. Neutrophils in CSF, lung secretion, urine -> infection
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13
Q

How do we identify pathogens by microbial studies?

A
  1. Blood cultures in acute, febrile patients (2 sites, 1 hr apart)
  2. Gram stain
    * Premature use of ABX -> false-negative cultures
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14
Q

What are the characteristics of G+?

A
  1. Thick cell wall
  2. Dark purple due to crystal violet
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15
Q

What are the characterisitcs of G-?

A
  1. Thin cell wall
  2. Pink/red due to safranin counterstain
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16
Q

Characterisitcs of atypical organisms?

A
  1. No cell wall
  2. Doesn’t stain well
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17
Q

Factors you need to consider when selecting empiric therapies?

A
  1. Severity of ID
  2. Local epidemiology trends
  3. Patient Hx
  4. Host factors
  5. Drug factors
  6. Necessity of combo therapy
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18
Q

What is an antibiogram?

A

Annual summary of antibiotic susceptibilities for organisms cultured from patients at a specific institution

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19
Q

What is the rule of thumb in patients with penicillin allergy?

A
  1. Avoid cephalosporins for patients with immediate/accelerated rx
  2. Use cephalosporins under close supervision for patients with history of delayed reactions
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20
Q

Use for gram-negative infections in patients with PCN allergy due to no β-lactam cross-sensitivity.

A

Aztreonam

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21
Q

Non-allergy rx to penicillin?

A

N/D, yeast vaginitis

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22
Q

Mild non-IgE mediated rx to penicillin?

A
  1. Maculopapular eruption
  2. Recorded to have penicillin allergy, but no recall of rx
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23
Q

IgE rx to penicillin

A
  1. Anaphylaxis
  2. Angioedema
  3. Breathing issues
  4. Hypotension
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24
Q

ABX that should be avoided in pregnancy?

A
  1. Fluoroquinolones
  2. Tetracyclines
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25
Q

Nephrotoxic ABX?

A

Aminoglycosides

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26
Q

What are the similar properties that don’t require renal dosing?

A

Lipophilic requiring liver metabolism

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27
Q

What are the drugs that don’t require renal dosing?

A

Penicillin V and G
Anti staph: Naficillin, oxacillin, dicloxacillin
Ceph+BLI: Cetriaxone
Macrolides: Azithromycin, Erythromycin
Fluoroquinolones: Moxifloxacin
Tetracyclines: Doxycycline, Minocycline, Tigecycline, Erovacycline, Omadacyclin
Pleuromutilins: Lefamulin
Lipoglycopeptides: Oritavancin
Oxazolidinones: Linezolid, Tedizolid
Lincosamide: Clindamycin
Folate Antagonists: Daysone, Pyremethamine
Streptogramins: Synercid
Nitrofurantoin and Fosfomycin
Nitromidazole: Metrinidazole, TInidazole
Polymyxins B
Anti-C diff: Vanc, Fidaxomicin
Anti TB: Rifampin, Isoniazind

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28
Q

What drugs can interact with AG?

A

Monitor renal function (nephro/ototoxins):
* Amphotericin B
* Cisplatin
* Cyclosporine
* Furosemide
* NSAIDs
* Radiocontrast dye
* Vancomycin

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29
Q

What do you need to do when combining AG with b-lactams?

A

Separate administration and flush line thoroughly between doses

30
Q

Drugs that interact with Amphotericicn B?

A

Nephrotoxins:
* AG
* Cyclosporine
* Foscarnet

31
Q

What happens when you combine isoniazids with anticonvulsants?

A

Monitor for signs and symptoms of phenytoin & carbamazepine toxicity:
* Decreased metabolism of carbamazepine and phenytoin -> increases serum drug concnetration

32
Q

What drug interacts with metrinidazole? Effect?

A

Ethanol causes a disulfiram like rx -> Avoid concomitant use with EtOH-containing products

33
Q

What are the effects of Rifampin?

A

Avoid concomitant use: Increased metabolism of interacting agent by CYP induction -> decrease serum concentrations

34
Q

Interacting agents with fluoroquinolones?

A

QTc prolonging agents
Multivalent cations -> decreased absorption -> separate for at least 2 hrs

35
Q

Interacting agent of sulfonamides?

A

Warfarin
* Decrease metabolism -> increase serum drug concnetration
* Monitor INR

36
Q

Interacting agents of doxycycline?

A

Multivalent cations -> decreased absorption -> separate by 2 hrs

37
Q

What is the difference between bactericidal and static?

A

Cidal: eliminates bacterial growth
Static: inhibits bacterial growth

38
Q

What are the hydrophilic meds?

A

B-lactams, AG, Glycopeptides, Daptamycin, Polymyxins

39
Q

What are the characterisitcs of hydrophillic meds?

A
  1. Poor tissue penetration
  2. Renal elimination
  3. No activity vs atypicals
  4. Consider LD and higher doses
  5. Low F -> IV:PO ration is NOT 1:1
40
Q

Examples of lipophilic meds?

A

Fluroquinolones, macrolides, linezolid, rifampin, tetracyclines

42
Q

Characterisitcs of lipophillic drugs?

A
  1. GOod tissue penetration
  2. Hepatic metabolism (DDI and hepatotoxicity)
  3. GOod activity vs atypicals
  4. No dose adjustment for sepsis
  5. Good F -> IV:PO ratio is 1:1
43
Q

What are the bactericidal agents?

A
  • Aminoglycosides
  • β-lactams
  • Colistin
  • Daptomycin
  • Fluoroquinolones
  • Metronidazole
  • Vancomycin
44
Q

What are the bacteriostatic agents?

A

Clindamycin
Linezolid
Macrolides
Sulfonamides
Tetracyclines
Tigecycline
Trimethoprim

45
Q

Time dependnet agents?

A

β-lactams
Vancomycin
Tigecycline
Linezolid
Macrolides
Clindamycin

46
Q

Concentration dependent agents?

A
  1. AG
  2. Fluoroquinolines
  3. Daptomycin
  4. Metrinidazole
  5. Colistin
  6. Bactrim
47
Q

What ABX demonstrates postABX effects?

A

AMinoglycosides

48
Q

PK/PD of AG?

A

Concentration dependent, bactericidal
* peak:MIC

49
Q

PK/PD of fluroquines?

A

Concnetration-dependent, bactericidal
* AUC:MIC

50
Q

PK/PD of beta-lactams?

A

Time dependent, bactericidal

51
Q

Due to tissue penetration, which ABX is not good for the lungs?

A

Daptomycin is not good for MRSA pneumonia -> inactivated by lung surfactant

52
Q

Why is nitrofurantoin not good for pyelonephritis?

A

Poor cocnetration in kidneys

53
Q

Why is moxifloxacin not good for UTIs?

A

Poor concentration in urine/bladder

54
Q

When do you use PO vs IV formulations?

A

PO: mild infection
IV: severe infection

55
Q

What is MIC?

A

Lowest concnetration of an antimicrobial agent that inhibits visible in-vitro bacterial growth

56
Q

What is MBC?

A

Lowest concnetration of antimicrobial that kills 99.9% of bacterial inoculum

57
Q

ABX with lowest MIC is the best therapy choice?

A

False: different ABX have different concentrations in different areas
* DOn’t select ABX by comparing MICs

58
Q

What is susceptible dose dependent?

A

Specific organisms are suspectible to higher doses

59
Q

What is susceptible?

A

Specific cutoff MIC (breakpoint)

60
Q

Drugs that target cell wall?

A
  1. Beta lactams (penicillins, cephalosporins, carbapenems, monobactams)
  2. Bacitracin
  3. Glycopeptids
61
Q

ABX that are 30S inhibitors?

A
  1. AG
  2. Tetras
  3. Tigecycline
62
Q

ABX that are 50S inhibitors?

A
  1. Chloramphenicol
  2. Clindamycin
  3. Linezolid
  4. Macrolides
  5. Streptogramins
63
Q

ABX that disrupt membrane integrity?

A
  1. Polymyxin B
  2. Daptomycin
64
Q

ABX that disrupt nucleic acid synthesis?

A
  1. Fluoroquinolones
  2. Metronidazole
  3. Rifamycins
65
Q

ABX that disrupt the folate metbolic pathway?

A
  1. Sulfonamides
  2. Trimethoprim
66
Q

What are the reasons to consider combo?

A
  1. Broaden spectrum of coverage
  2. Achieve synergistic activity against infection
  3. Reduce the emergece of antimicrobial resistance
67
Q

Origins of ABX resistance?

A
  1. Active eddlux
  2. Decreased permeability
  3. Enzymatic mods
  4. Target site changes
68
Q

What are the ESKAPE pathogens?

A

§Enterococcus faecium
§Staphylococcus aureus
§Klebsiella pneumoniae
§Acinetobacter baumannii
§Pseudomonas aeruginosa
§Enterobacter species

69
Q

How do we prevent resistance?

A
  1. Treatment guidelines
  2. Avoid antibiotics to treat colonization or contamination
  3. Utilize the most narrow-spectrum agent appropriate to treat the infection -> definitive therapy
  4. Utilize appropriate dosing & shortest effective duration of therapy
70
Q

ABX that require serum monitoring?

A

Vanc and aminoglycosides

71
Q

What type of ABX do you use for de escalation?

A

Narrowest SOA

Therapeutics IV (39 decks)

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