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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
Nephrotoxic ABX?
Aminoglycosides
26
What are the similar properties that don't require renal dosing?
Lipophilic requiring liver metabolism
27
What are the drugs that don't require renal dosing?
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
28
What drugs can interact with AG?
Monitor renal function (nephro/ototoxins): * Amphotericin B * Cisplatin * Cyclosporine * Furosemide * NSAIDs * Radiocontrast dye * Vancomycin
29
What do you need to do when combining AG with b-lactams?
Separate administration and flush line thoroughly between doses
30
Drugs that interact with Amphotericicn B?
Nephrotoxins: * AG * Cyclosporine * Foscarnet
31
What happens when you combine isoniazids with anticonvulsants?
Monitor for signs and symptoms of phenytoin & carbamazepine toxicity: * Decreased metabolism of carbamazepine and phenytoin -> increases serum drug concnetration
32
What drug interacts with metrinidazole? Effect?
Ethanol causes a disulfiram like rx -> Avoid concomitant use with EtOH-containing products
33
What are the effects of Rifampin?
Avoid concomitant use: Increased metabolism of interacting agent by CYP induction -> decrease serum concentrations
34
Interacting agents with fluoroquinolones?
QTc prolonging agents Multivalent cations -> decreased absorption -> separate for at least 2 hrs
35
Interacting agent of sulfonamides?
Warfarin * Decrease metabolism -> increase serum drug concnetration * Monitor INR
36
Interacting agents of doxycycline?
Multivalent cations -> decreased absorption -> separate by 2 hrs
37
What is the difference between bactericidal and static?
**Cidal:** eliminates bacterial growth **Static:** inhibits bacterial growth
38
What are the hydrophilic meds?
B-lactams, AG, Glycopeptides, Daptamycin, Polymyxins
39
What are the characterisitcs of hydrophillic meds?
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
Examples of lipophilic meds?
Fluroquinolones, macrolides, linezolid, rifampin, tetracyclines
41
42
Characterisitcs of lipophillic drugs?
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
What are the bactericidal agents?
* Aminoglycosides * β-lactams * Colistin * Daptomycin * Fluoroquinolones * Metronidazole * Vancomycin
44
What are the bacteriostatic agents?
Clindamycin Linezolid Macrolides Sulfonamides Tetracyclines Tigecycline Trimethoprim
45
Time dependnet agents?
β-lactams Vancomycin Tigecycline Linezolid Macrolides Clindamycin
46
Concentration dependent agents?
1. AG 2. Fluoroquinolines 3. Daptomycin 4. Metrinidazole 5. Colistin 6. Bactrim
47
What ABX demonstrates postABX effects?
AMinoglycosides
48
PK/PD of AG?
Concentration dependent, bactericidal * peak:MIC
49
PK/PD of fluroquines?
Concnetration-dependent, bactericidal * AUC:MIC
50
PK/PD of beta-lactams?
Time dependent, bactericidal
51
Due to tissue penetration, which ABX is not good for the lungs?
Daptomycin is not good for MRSA pneumonia -> inactivated by lung surfactant
52
Why is nitrofurantoin not good for pyelonephritis?
Poor cocnetration in kidneys
53
Why is moxifloxacin not good for UTIs?
Poor concentration in urine/bladder
54
When do you use PO vs IV formulations?
PO: mild infection IV: severe infection
55
What is MIC?
Lowest concnetration of an antimicrobial agent that inhibits visible in-vitro bacterial growth
56
What is MBC?
Lowest concnetration of antimicrobial that kills 99.9% of bacterial inoculum
57
ABX with lowest MIC is the best therapy choice?
False: different ABX have different concentrations in different areas * DOn't select ABX by comparing MICs
58
What is susceptible dose dependent?
Specific organisms are suspectible to higher doses
59
What is susceptible?
Specific cutoff MIC (breakpoint)
60
Drugs that target cell wall?
1. Beta lactams (penicillins, cephalosporins, carbapenems, monobactams) 2. Bacitracin 3. Glycopeptids
61
ABX that are 30S inhibitors?
1. AG 2. Tetras 3. Tigecycline
62
ABX that are 50S inhibitors?
1. Chloramphenicol 2. Clindamycin 3. Linezolid 4. Macrolides 5. Streptogramins
63
ABX that disrupt membrane integrity?
1. Polymyxin B 2. Daptomycin
64
ABX that disrupt nucleic acid synthesis?
1. Fluoroquinolones 2. Metronidazole 3. Rifamycins
65
ABX that disrupt the folate metbolic pathway?
1. Sulfonamides 2. Trimethoprim
66
What are the reasons to consider combo?
1. Broaden spectrum of coverage 2. Achieve synergistic activity against infection 3. Reduce the emergece of antimicrobial resistance
67
Origins of ABX resistance?
1. Active eddlux 2. Decreased permeability 3. Enzymatic mods 4. Target site changes
68
What are the ESKAPE pathogens?
§Enterococcus faecium §Staphylococcus aureus §Klebsiella pneumoniae §Acinetobacter baumannii §Pseudomonas aeruginosa §Enterobacter species
69
How do we prevent resistance?
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
ABX that require serum monitoring?
Vanc and aminoglycosides
71
What type of ABX do you use for de escalation?
Narrowest SOA

Therapeutics IV (39 decks)

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