Painful Skin Lesions Flashcards
1
Q
Impetigo
A
- Common inf. of the superficial layer of the epidermis
- Most often Gram + (Strep pyogenes/ Staph aureus)
- Highly contagious
- Bullous/ non-bullous (blisters)
- Outbreaks kindergarten
2
Q
Impetigo Pathophysiology
A
Need a break in skin barrier:
- Scratching
- Dermatophytosis (highly contagious, fungal, red/silvery ring-like rash on skin/scalp)
- Varicella
- HSV (blister pops = infection)
- Thermal burns
- Surgery
- Trauma
3
Q
S Aureus & GABHS colonization
A
- Group A beta haemolytic Strep from other individuals
- S Aureus part of commensal Flora (can become pathological or get from other carriers)
4
Q
Bullous impetigo
A
- Exfoliative toxins of S. aureus = exfoliatins A & B
- These toxins cause loss of adhesion btwn keratinocytes (skin cells) in epidermis
- Specifically target Desmoglein I protein (chain keeping skin cells tog.)= adhesion molecule linking keratinocytes
5
Q
Folliculitis
A
- Inflammation of hair follicle
- Infectious/ non-infectious
6
Q
Infectious Folliculitis
A
- Bacteria (most common)
- Staph Aureus
- pseudomonas aeruginosa (hot tub Folliculitis) - Virus
- HSV > H zoster
- Molluscum contagiosum - Fungi & yeasts
- Malassezia
- Candida
- Dermatophytes (Trichophyton tonsurans) - Parasites (least common)
- demodex
- scabies
7
Q
Non-infectious Folliculitis
A
- irritation from regrowing hairs (shaving, waxing)
- occlusion eg: moisturizers (thick)
- chemicals
- drugs
= corticosteroids (prednisone), androgens (male hormones, testosterone), adrenocorticotrophic hormone (ACTH), lithium, isoniazid (INH - TB treatment), phenytoin & B-complex vitamins
8
Q
Boils (Furuncle)
A
- localized deep suppurative necrotic form of Folliculitis = dermis & subcutaneous tissue (inflammation)
- S. Aureus most common
- access through skin & invade hair follicle
- develops in moist/ sweaty areas = scalp, face, buttocks, axillae & areas with friction & perspirations
- group = carbuncle
9
Q
Abscess
A
- manifestations of S. Aureus skin & soft tissue infections, formed to contain the nidus of inf.
- PMNs (neutrophils) = primary cellular host defense against S. Aureus inf. & major component of S. Aureus abscesses
- S. Aureus = several molecules that contribute to formation
10
Q
Process of formation of mature abscess
A
- 0-2 hrs (infection)
- need break in skin for S. Aureus = epidermis, dermis into subcutis - 2-24 hrs (inflammatory response)
- polymorphic nucleocytes = neutrophils to fight off inf. - 2-6 days (abscess formation)
- leucocytes = liquefaction & coagulative necrosis - 6-14 days (mature abscess)
- fibrous capsule = keep inf. from infiltrating rest of tissue
11
Q
Cellulitis
A
- non-necrotizing inflammation of the skin & subcutaneous tissue, acute infection
- breach in the skin, portal of entry may not be obvious
- organisms on skin & appendages = cellulitis & multiply
- Strep pyogenes, lesser S. Aureus
- Group A Strep = most common, produce virulence factors eg: pyrogenic exotoxins (A, B, C & F) & Strep superantigen
- rare cases = occur from hematogenous spread from S. Pneumoniae & marine vibrio species
Neisseria meningitidis, pseudomonas aeruginosa, brucella species & legionella species
12
Q
Clinical features of cellulitis
A
- erythema, warmth, edema, tenderness = cytokine & neutrophil response from bacteria breaching epidermis
13
Q
Risk factors for cellulitis
A
- culprit = breakdown in skin barrier eg: skin injuries, surgical incisions, intravenous site punctures, fissures btwn toes, insect bites, animal bites & other skin infections
- patients with comorbidities eg: DM, venous insufficiency, peripheral arterial disease & lymphedema
14
Q
Herpes virus
A
More than 100 types
- HSV 1 & 2 (cold sores/ genital herpes)
- VZV (chicken pox/ shingles)
- CMV
- EBV
- human HSV 6, 7 & 8
15
Q
HSV pathophysiology
A
- dissemination of HSV inf. = people with impaired T-cell immunity (eg: organ transplant receipts & AIDS patients)
- HSV inf. complicate burn wounds/ damaged skin eg: atopic dermatitis
- close personal contact, inoculation of virus in susceptible mucosal surfaces
