Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Micro final > Lect 23 > Flashcards

Lect 23 Flashcards

1
Q

If foreign body is present (splinter, stitches), what happens to the infection dose

A

infection dose drops dramatically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is acne vulgaris

A
  • disease of sebaceous follicles
  • a noninfectious form of folliculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acne vulgaris affects what patient population? what may be initial trigger?

A
  • teens and young adults
  • androgen hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

acne vulgaris is caused by what pathogen

A

propionibacterium acnes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

propionibacterium acnes

  • gram status
  • shape
  • oxygen requirement
  • where is it normally found
A
  • gram +
  • anaerobic
  • rod
  • normal skin flora, colonizes in sebaceous glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do inflammatory acne vulgaris develop

A
  • when follicular contents rupture into the dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

stages of inflammatory acne vulgaris

A
  1. papules
  2. pustule
  3. nodule: most severe form of acne
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

multiple small papules and pustules on erythematous base pierced by central hair

A

superficial folliculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

two primary pathogens of superficial folliculitis is

A
  • staph aureus: majority of abscess-type infection
    • gram +
  • pseudomonas aeruginosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pseudomonas aeruginosa

  • gram status
  • shape
  • interesting feature
A
  • gram -
  • rod
  • pyocyanin/pyoverdin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

hot tub folliculitis is caused by what pathogen

A

pseudomonas aeruginosa

  • appars 8-48 hrs after exposure in contaminated water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

abscess caused by S. aureus involving a hair follicle and surrounding tissue, often on neck, thichs, buttocks, and face

A

furuncles (boils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

clusters of furuncles with subcutaneous connections, extend into dermis and subcutaneous tissue. may be accompanied by fever. common locations: back of neck, back, and thighs

A

Carbuncles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Carbuncles and furuncles may affect healthy young persons but are much more common in

A
  • obese
  • immunocompromised
  • diabetic
  • eldery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when are abx given for furuncles and carbuncles

A
  • lesions > 5 mm
  • do not resolve with drainage
  • evidence of spreading
  • occur in immunocompromised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

impetigo is a superficial skin infection with crusting or bullae and caused by

A
  • staphylococci
  • streptococci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is ecthyma

A

ulcerative form of impetigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

risk factors for impetigo and ecthyma

A
  • moist environment
  • poor hygiene
  • chronic nasopharyngeal carriage of agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is nonbullous impetigo? cause of nonbullous impetigo?

A
  • clusters of vesicles that rupture and crust
  • S. aureus
    • MRSA 20%
    • possible co-infection with strep pyogenes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is bullous impetigo

A
  • vesicles enlarge to form bacteria-colonized fluid-filled bullae created by exfoliative toxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cause of bullous impetigo

A

specific strains of S. aureus exclusively

22
Q

What is staphylococcal scaleded skin syndrome (Ritter’s disease)

A
  • acute and extensive epidermolysis due to action of staphylococcal toxin (Exfoliatin) that splits the skin just beneath the granule cell layer
23
Q

do bullae in staphylococcal scaleded skin syndrome (Ritter’s disease) have bacteria or leukocytes?

A
  • no, Bullae are sterile
  • due to toxin
24
Q

what sign is positive in staphylococcal scaleded skin syndrome (Ritter’s disease)

A

Nikolsky’s sign: skin peels easily

25
Q

what patient population is most affected with staphylococcal scaleded skin syndrome (Ritter’s disease)

A
  • infants
  • children < 6
26
Q

mortality rate for staphylococcal scaleded skin syndrome (Ritter’s disease)

A
  • low
  • often due to secondary infections
27
Q

if affected area of skin is extensive in staphylococcal scaleded skin syndrome (Ritter’s disease), treat as if for

A

burns

28
Q

how is staphylococcal scaleded skin syndrome (Ritter’s disease) diagnosed

A

biopsy

29
Q

what is erysipelas

A
  • superficial cellulitis with focal dermal lymphatic involvement
30
Q

erysipelas is usually caused by

A

group A streptococci

31
Q

pathogens that cause cellulitis

A
  • S aureus
  • S. pyogens (GAS)
    • more likely to create diffuse swiftly spreading infections
32
Q

hallmarks of cellulitis

A
  • HEET
    • heat
    • erythema
    • edema
    • tenderness
33
Q

symptoms of cellulitis are due to

A
  • bacterial toxins
  • inflammatory response
34
Q

how is cellulitis diagnosed

A
  • clinical exam
  • be aware infections may be mixed etiology
35
Q

what medications should be avoided in the tx of cellulitis

A

NSAIDs

  • may mask pain of developing myonecrosis and interfere with response to agent
36
Q

What are classic signs of necrotizing fasciitis

A
  1. infection of deeper tissues
  2. spreads along muscle fascia, muscle tissue spared
  3. pain out of proportion to clinical signs
37
Q

type 1 or polymicrobic necrotizing fasciitis is caused by

A
  • Group A strep and
  • anaerobes
38
Q

risk factors for type 1 or polymicrobic necrotizing fasciitis

A
  • diabetes
  • surgery
  • immunocompromised
39
Q

type 2-“flesh eating bacteria” necrotizing fasciitis is caused by

A
  • Group A streptococcus pyogens: monomicrobic)
40
Q

clinical presentation

  • skin breakdown with bullae
  • thick pink/purple fluid
  • cutaneous gangrene visible
  • no longer tender - cutaneous anesthesia
A

necrotizing fasciitis

41
Q

which responds to antibiotic therapy: necrotizing fasciitis or cellulitis

A

cellulitis

42
Q

Myonecrosis of gas gangrene is caused by

A

clostridium perfringens type A

43
Q

clostridium perfringens type A

  • gram status
  • spore?
  • oxygen?
  • shape
A
  • gram +
  • anaerobic bacillus
  • spore forming
44
Q

pathogenesis of gas gangrene

A
  1. introduction of anaerobic cells or spores
  2. reduced oxygen tension: trauma or other bacteria
  3. production of exotoxins and insoluble H2 gas
    • promotes split and invasion of nearby tissue
45
Q

clinical presentation

  • rapid onset
    • < 24 hrs
  • sudden onset of pain
  • skin: bronze appearance
  • skin becomes tense, crepitant
  • overlying bullae
A

gas gangrene

  • crepitant due to H2 gas
46
Q

how is gas gangrene diagnosed

A

tissue biopsy

47
Q

toxic shock syndrome is caused by

A
  • staph aureus
  • strep pyogenes
48
Q

streptococcal toxic shock syndrome begins as

A
  • soft tissue inflammation at site of skin infection
  • patients are usually bacteremic and have necrotizing fasciitis
49
Q

antigens of streptococcal causing toxic shock syndrome

A

superantigens SpeA and SpeC

50
Q

antigen causing toxic shock syndrome by staph aureus

A

enterotoxin type B superantigen

51
Q

staph aureus toxic shock syndrome is associated with

A

tampon use and surgery

Micro final (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions