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Dermatology Drugs > Antibiotic Principles > Flashcards

Antibiotic Principles Flashcards

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Dermatology Board Prep flashcards
1
Q

Describe differences between the ways we use ABX

A

Prophylactic Tx - the Pt has a condition that warrants the use of ABX to prevent an infection.

Empiric Therapy - We suspect and infection but do not know what the pathogen is

Definitive Tx - We know there is an infection and have a better idea of what the pathogen is

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2
Q

Standard approach for selecting an ABX therapy

A

Confirming the presence of an infection

determining the likeliest pathogen

Selecting an Empiric Tx

Monitoring the Response

Modifying or Deescalating the Tx

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3
Q

Confirming the Infection

A

Important to reduce the unnecessary use of ABX

Resistance, Altering Micro flora, Cost Burden, Nephro/hepatotoxic

Threshold for empiric use is cases by case, for example, a Pt who is immunocompromised.

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4
Q

What are some S/S of infection

A

Fever, Leukocytosis (>10000), Clinical local or systemic signs (UTI, confusion)

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5
Q

Fever is not always a Reliable Sign of infections

A

Drug induced - beta-lactams, convulsants, allopurinol, hydralazine, nitrofurantoin, sulfonamides, phenothiazines, and methyldopa

disease induced - collagen-vascular (autoimmune d/o) acute thrombosis, malignancies, fever of unknown origin.

Other drugs can mask a fever - NSAIDS, Tylenol, corticosteroids

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6
Q

WBCs

A

During infection

WBCs may be as high as 40,000cells/mL, with lots of immature band cells

may remain normal

May be increased due to underlying conditions - MI, Trauma, leukemia, coorticosteroids

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7
Q

S/S may help us to hone in on the source of the infection

A

Superficial or bone/joint infections - pain, inflammation, swellin, erythema, tenderness, purulent d/c

Deep seated infections -pneumonia, meningitis, endocarditis, UTI; May require examination of local tissue fluids

S/S may be referred to an organ -

Cough and sputum productions: Pneumonia
Flank Pain: Pyelonephritis
Fevers with no other Sx: may require a lengthy differential.

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8
Q

Determining the most likely of pathogens

A

Requires labs and diagnostics

Can include Gram stains, blood cultures, cultures from the infected site.

Try to get samples before ABX as these will alter the samples; but sometimes the Pt life is more important.

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9
Q

Gram Stains

A

Gram stains give first clues

Gram positive v negative

Shape of the organism - rods vs cocci

Growth Patterns - Clusters, chains, and pairs

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10
Q

Aerobic Gram Positives Examples

A

Cocci - Streptococci pnuemoniae, viridans, Strep A group; Enterococcus, Staphylococcus

Bacilli - Corynebacterium, Listeria

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11
Q

Anaerobic Gram Positive Examples

A

Cocci - Peptococcus, Peptostreptococcus

Bacilli - Clostridia, C. Acnes

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12
Q

Aerobic Gram Negative Examples

A

Cocci Neisseria, Moraxella

Bacilli - Enterobacteriaceae (E. colli, klebsiella, enterobacter, citrobacter, proteus, salmonella, shingella, etc), Campulobacter jejuni, P aeruginosa, H. pylori, H. influenzae

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13
Q

Anaerobic Gram Negative Examples

A

Bacilli- Baceroides (fragilis)

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14
Q

Atypical Bacteria

A

Chlamydia pneumoniae, Mycoplasma pneumoniae, Legionella pneumophilia

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15
Q

In an acutely ill and febrile patient

A

Always obtain blood samples, and try to coincide with fever spikes if possible.

Obtain two sets from two different peripheral sites; an aerobic bottle and an anaerobic bottle; obtain 1 hr apart.

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16
Q

Cultures and sensitivities

A

Provide identification and susceptibility to ABX

but can take 24 to 48 hours or more for sensitivities

Reported as susceptible S, Intermediate I, or Resistant R

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17
Q

Positive cultures dont always confirm the presence of an infection.

A

An infection refers to the bacteria that is present and causing the Sx

There are bacteria that colonize and are normal flora and not the cause of the Sx

Contamination of the sample due to improper technique.

18
Q

The site of infection helps

A

Pneumonia can be indicative of SA, P. Aeruginosa, Klebsiella pneumoniae, Acinetobacter

Intr-abd infection may indicate B, fragilis, E. coli, Enterococcus faecalis/faecium.

UTI - E coli, klebsiella pneumoniae, proteus, SA, S. epidermis, enterococci, PA

IV site - SA, SE

19
Q

When choosing an empiric ABX

A

Consider the type of infection

The Pt - MH, allergies, organ function

The ABX - Characteristics, relative toxicity, $$$, IV v Oral

20
Q

Can consult

A

Infectious Disease Society of America

John Hopkins, ABX guideline

Sanford Guide to ABX therapy

21
Q

General Considerations for selecting the empiric regimen

A

Is the infections Community acquired or is it nosocomial; nosocomial tend to be more resistant to ABX

Is the infections Mild v Severe; severe mean more aggressive.

Is this the first infection? Recurrent?

Infections from a removable source? - Is there a drain-able abscess? Remove a contaminated line.

22
Q

Antibiotic Susceptibility

A

MIC - lowest concentration at which visible growth is prevented.

Susceptible - suggest high likelihood of clinical success at therapuetic concentrations

Intermediate - questionable likelihood of success; Would require aggressive dosing.

Resistant - high likelihood of therapeutic failure.

23
Q

Antibiograms

A

Help ID and track local resistance patterns

Cultures from community on annual basis + susceptibility profile.

24
Q

Pt factors

A

Age, Allergies and drug interactions, PMH, Pregnancy, Organ Function, metabolic and Genetics, costs and preferences, concomitant drugs(linezolid + ssris), Disease states

25
Q

Pt Hx can be used to guide empiric ABX decisions

A

Sick contacts at home, work, social stiuation?

Pets like bird

Employment based exposures

recent travel to an area where the pathogen is endemic

Vaccination status?

26
Q

Drug Factors

A

Pharmacokinetics and pharmacodynamics - does it get to the site of action; needs to touch the bacteria to work!

Tissue Penetration

Drug toxicity - may need to sacrifice efficacy to use

27
Q

Pharmaco kinetic Considerations

A

Available routes of administration (A)

Tissue Penetration (Vd)

Drug-Drug interactions (metabolism)

Safety in renal/hepatic dysfunction (E)

28
Q

Pharmacodynamic considerations

A

Bactericidal v bacteriostatic

Time-dependent vs concentration dependent

29
Q

Will the drug get to the site of the infection

A

Adequate blood supply - is it an abscess, osteromyelitis, a deep Cellulitis

Is the infection in the CNS - can it cross the BBB

Volume of distribution - Tigecycline cannot Tx blood borne infections b/c it has a high Vd

Special Circumstance - daptomycin gets inactivated by pulmonary surfactant.

30
Q

Dosing Strategies Based on how a medication will exert its effect - Time-Dependent Killers

A

Time-Dependent killers - Max Bactericidal activity is based on the medication being above the MIC for at least 40-50% of the dosing interval.

Therefore continuous or prolonged infusions can lead to therapeutic success, by maximizing T> MIC

*The duration of time @ [] leads to killing more dead

Ex are Beta-lactams, cephalosporins, carbapenems, and vanco

31
Q

Dosing Strategies Based on how a medication will exert its effect - Concentrations-Dependent Killers

A

The higher the drug concentrations the greater the killing power.

Fluoroquinolones: Maximize the AUC/MIC ratio

Aminoglycosides: Maximize the Peak:MIC Ratio

32
Q

Combination Therapy should be carefully considered, not universally applied

A

Can broaden the spectrum of coverage - increasing the chance of success; increases costs and risks, and resistance

May yield synergistic effects - B-Lactams + Aminoglycosides work well for endocarditis; But may increase the risk of superinfection with more resistant organisms

My prevent resistance - for example: Tb has multiple drugs as part of the course

33
Q

Failure of antimicrobal Therapy

A

Need to consider the drug, host, and the pathogen

34
Q

Selection and dosing of the ABX can influence Tx success

A

Empiric regimen may not cover the infecting organism- may have wrong Dx, empiric choice, or have a completely unexpected organism

*why monitoring the Pt is important

The concentration of the Antibiotic may be too low at the the infected site - b/c of poor absorption or distribution, drug-drug interactions, or drug-inactivation

*could have the correct ABX but it cant reach the site

35
Q

Host Factors

A

May Render ABX less effective

Immunosuppression - such as from HIV, DM, COPD, Lack of natural defense from a burn or asplenia

Or from Chemo induced neurtopenia, chronic corticosteroid use, transplant anti rejection Tx, Drugs for autoimmune d/o

*May require a prolonged or increased dose.

36
Q

Pathogens May be Resistant to the ABX Tx

A

Intrinsic Resistance - Naturally occuring; IE gram neg are unaffected by vancomycin which cannot penetrate their outer cell membrane

Acquired - a normally sensitive organism develops resistance through genetic mutation which can be shared in plasmids.

37
Q

4 categories of acquired antimicrobial resistance

A

Alteration in the target site (binding site)

Reduced intracellular antimicrobial exposure - more difficult to penetrate or efflux pumps spit it back out.

Bypass of natural metabolic processes - pathogen finds a new metabolic pathway

Drug inactivation - Enzyme degrades antimicrobials.

38
Q

Resistance Patterns

A

Staphylococcus - B-lactamases - affects all pcn

MRSA - Alter PBP - affects pcn cephalosporins, some fluoroquinolones

Streptococcus - Alter binding sites - pcn, macrolides

Enterococcus - alterations to target site - vancomycin

Pseudomonas - reduced permeability - pcn, cephalosporins, carbapenems, aminoglycosides, fluoroquinolones

Pseudomonas - B-Lactamase production - pcn

Enterobacteriaceae - b-lactamase production - pcn

39
Q

When Discussing with a Pt

A

Allergies?

Other Medications?

counsel on taking full course.

Women on OCP may need a back up for up to 7 D after the Course.

Come back if not getting better, or ADR

Probiotics

40
Q

ABX stewardship

A

Slows resistance

Saves Money

Avoids Adverse events

Dermatology Drugs (3 decks)

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