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Infectious Diseases > Therapeutics - SSTIs > Flashcards

Therapeutics - SSTIs Flashcards

1
Q

What is retapamulin 1% oint good against? MoA? Indicated in?

A

S. aureus and S. pyogenes
Binds to 50S ribosome
Indicated in uncomplicated skin infections >9months of age: primarily impetigo

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2
Q

What is impetigo?
What is it mostly caused by?
Peak incidence is in what population group?

A

Well-localized multiple purulent lesions, usually on exposed areas (face and extremities)
S. auerus or S. pyogenes are the primarly cause
Mostly in children 2-5 years old

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3
Q

How does impetigo occur?

A

Microorganisms colonize unbroken skin (streptococci precedes lesions by around 10 days due to poor hygiene)
Organisms inoculate into skin by abrasions, minor skin trauma
During 2-3 weeks streptococcal strains may also be transferred to URT
In staphylococcal disease, present in nose first

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4
Q

Nonbullus Impetigo

  • primarily caused by?
  • Pathophysiology
A
  • S. pyogenes
  • Begins as papules that evolve into vesicles, then become pustules. Gradually enlarge, pop and form thick crusts. Lesions heal and leave hypo-pigmented areas
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5
Q

Bullous Impetigo

  • primarily caused by?
  • pathophys
A
  • S. aureus that produces toxin
  • initially appear as superficial vesicles that enlarge to form flaccid bullae filled with clear yellow fluid. Later become darker or purulent, may rupture to form brown crust
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6
Q

First line treatment for Bullous and Nonbullous Impetigo

If numerous lesions or unresponsive to first line

Why should systemic antimicrobials be used for impetigo infections during outbreaks of post-strep nephritis?

A

-topical mupirocin or retapamulin bid x5 days

-PO tx:
MSSA: Cloxacillin or cephalexin
MRSA: doxycycline, TMP/SMX, or clindamycin

Want to eliminate nephritogenic strains of S. pyogenes from community

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7
Q

Presentation of cutaneous abscesses: folliculitis, furuncles and carbuncles

What pathogens often cause this?

A

Collections of pus within dermis and deeper tissue
Painful, tender, fluctuant red nodules often surmounted by pustule with an erythematous rim

S. aureus is a single pathogen in most patients, often polymicrobial from skin flora

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8
Q

How to treat cutaneous abscesses?

What role does abx have in this?

A
  • Incision and drainage with probing
  • Cover site with dry dressing

Topical abx does not improve cure rates (even with MRSA)
Systemic abx only in immunocompromised or signs of systemic infection

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9
Q

What is folliculitis?
What is a furuncle?
Outbreaks caused by which pathogen?
What is often a predisposing factor?

A

Folliculitis: superficial infection of hair follicle with pus limited to epidermis
Furuncle (boil): infectious of hair follicle which extends through the dermis to SC tissue where a small abscess forms
MSSA or MRSA
Poor hygiene

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10
Q

What is a carbuncle?

In which patient population is it most common?

A

Carbuncle: infection extends to involve several adjacent follicles producing an inflammatory mass with pus draining from multiple follicular orifices
Common in diabetics

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11
Q

Which abx are used in treatment of carbuncles?

A
  • Cloxacillin or cephalexin, only is hot compresses don’t owrk
  • Severe beta-lactam allergy: Doxycycline or clindamycin
  • MRSA: TMP/SMX or clindamycin
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12
Q

What are cellulitis and erysipelas?

What are the signs of these infections?

What feature do these infections NOT contain, helping distinguish it from other SSTIs?

Presentation (superficial and systemic)

A

Rapidly spreading, diffuse skin infection including dermis and SC tissues

Signs: erythema, edema and head, occasionally accompanied by lymphangitis and lymph node inflammation

NO PUS

Skin surface looks like orange peel
Systemic sx: fever, tachycardia, confusion, hypotension, leukocytosis

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13
Q

Predisposing factors of cellulitis/erysipelas

A

Factors that make skin more fragile or local host defences ineffective:

  • edema from venous insufficiency or lymphatic obstruction
  • cutaneous damage
  • Pre-existing skin infections (ex. fissured toe webs)
  • obesity
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14
Q

What is cellulitis?

What is erysipelas?. Name 2 distinguishing factors

A

Cellulitis: deeper dermis and SC fat infection

Erysipelas: upper dermis including superficial lymphatics

  1. lesions raised above level of surrounding skin
  2. clear demarcation between involved and uninvolved tissue
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15
Q

Which pathogens often cause cellulitis/erysipelas?

In what patient population group is it most common?

Prognosis?

A

Also always S. pyogenes. Rarely S. aureus.

Infants, young children, older adults

Excellent with early diagnosis and treatment

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16
Q

CA-MRSA:
What strain is now commonly found in Canada?
How does it confer resistance?

A

CMRSA10

Altered PBP 2a encoded by mecA gene

17
Q

What are some clincal manifestations of CA-MRSA?

A
  • folliculitis
  • furuncles
  • carbuncles
  • mastitis
  • cellulitis
  • occasionally, severe necrotizing pneumonia
18
Q

What abx can be used to treat MRSA?

A
  • Tetracycline (95%S)
  • TMP/SMX (95%S)
  • Clindamycin (72%S)
  • Vanco and linezolid (100%S)
19
Q

Principles of treating MRSA

A
  1. Incision and drainage are most important
  2. Abx not used routinely unless large and complicated in patients with comorbidities
  3. Covering wound and hand hygiene important
  4. recurrent infections: decolonization with chlorhexidene washes, mupirocin oint intranasally with rifampin or doxycycline x7 days
20
Q

First line treatment in:

  • In mild CA-MRSA skin infection
  • in moderate infection
A

Mild:
-Cover draining lesions, no abx necessary unless otherwise specified

Mod:
-drainage, po therapy in older child/adult: clinda, TMP/SMX, doxycycline (parenteral in young)

Severe:

  • vanco and/or cloxacillin/1st gen cephalosporin
  • add clindamycin if toxin mediated syndrome
21
Q

What is Necrotizing Fasciitis?

A

-Rare SC infection that tracks along fascial planes (superficial fascia: all tissue b/t skin and underlying muscle) and extends much beyond superficial signs of infection

22
Q

How does necrotizing fasciitis start? What is a telltale sign that it’s not just a simple infection?

A
  • Extension from a simple skin infection- may not even have a lesion involved
  • pain is out of proportion to the apparent skin lesion
23
Q

What is the presentation of necrotizing fasciitis?

A
  • initial presentation: cellulitis
  • progression: high fevers, disorientation, lethargy (often septic shock)
  • SC have wooden-hard feel
24
Q

What is the most common pathogen causing Necrotizing Fasciitis?

A

-S. pyogenes and S. aureus

25
Q

Treatment for Necrotizing Fasciitis

Prophylaxis for contacts

A
  • Surgery and debridement necessary
  • Vanco + Piptazo (empiric therapy) to cover possible broad polymicrobial infection
  • Directed therapy: S. pyogenes causing TSS -> Penicillin + clindamycin (clinda inhibits toxin production)

Prophylaxis: Cephalexin

Infectious Diseases (9 decks)

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