Skin & MSK Flashcards

1
Q

Stratum corneum

A

top layer of skin

composed of terminally differentiated dead keratinocytes (squames/corneocytes)

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2
Q

Natural defenses of the skin

A
Keratin
Antimicrobial peptides (AMPs)
Skin sloughing
Sebum: low pH, lipid (sphingoid bases)
Sweat: low pH, high salt, lysozyme (digests PDG)
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3
Q

Bacteria that typically controls the normal skin flora

A

S. epidermidis

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4
Q

Role of pheromones in assoc w/S. epidermidis

A

Pheromones inhibit colonization of other microbes in areas where S. epidermidis is already colonized.

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5
Q

Cellular priming

A

enables keratinocytes to respond more effectively and efficiently to pathogenic insults.

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6
Q

Skin microbiome

A

Predominate species:

  • In sebaceous areas: Propionibacterium
  • In moist areas: carynebacterium and staphylococcus spp.
  • dry areas: have the most diversity and lower load (less selective force)
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7
Q

Filaggrin

A

susceptibility protein. Responsible for maintaining normal epidermal homeostasis

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8
Q

Normal skin flora that are normally pathogenic

A

S. aureus

S. pyogenes

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9
Q

Main resident of skin flora

A

S. epidermidis
>90% flora
occasionally pathogenic

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10
Q

Common skin flora (other than S. epidermidis)

A
All are occasionally pathogenic
Staph warneri
Strep mitis
Propionibacterium acnes
Carynebacterium spp.
Acinetobacter johnsonii
P. aeruginosa
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11
Q

Primary skin infections

A

caused by a single pathogen
Affects normal skin
Ex: impetigo, folliculitis

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12
Q

Most common primary skin infection pathogens

A

S. aureus
B-hemolytic strep
Coryneform bacteria
Dermatophytes

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13
Q

Secondary skin infections

A

Occur in skin that is already diseased
Skin lesions that can become secondarily infected: scabies, psoriasis, poison ivy, atopic dermatitis, eczema, herpeticum, kerion

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14
Q

Athlete’s foot

A

Dermatophytes first cause skin damage–> allows bacterial overgrowth of coryneform bacteria and Brevibacterium.

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15
Q

Common pathogens of secondary infections

A

S. aureus

P. aeruginosa

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16
Q

Nerve infections manifesting as skin lesions

A

Herpesvirus- varicella zoster

Shingles

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17
Q

Types of Primary lesions

A
Macule
Papule
Nodule tumor
Vesicle
Bulla
Pustule
Wheal
Plaque
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18
Q

Types of secondary lesions

A

Scale
Crust
Fissure
Ulcer

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19
Q

Macule

A

Flat, discolored spot on skin w/sharp borders
Ex: freckle
Pathogen: Tinea versicolor

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20
Q

Papule

A

Solid elevations w/out fluid w/sharp borders
Ex: mole
Pathogen: Cutaneous leshmaniasis

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21
Q

Nodule, tumor

A

Palpable, solid, elevated mass nodules w distinct borders. Tumors extending deep into the dermis
Ex: wart (nodule) large lipoma (tumor)

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22
Q

Vesicle

A

Small distinct elevation w fluid
Ex: blister from HSV
Chickenpox

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23
Q

Bulla

A

Large distinct elevation w fluid
Ex: large friction or burn blister
Gangrene

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24
Q

Pustule

A

Vesicle or bulla filled w purulent fluid
Ex: acne, carbuncles
Smallpox, cutaneous anthrax

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25
Wheal
Localized area of edema, often irregular and of variable size and color Ex: hive, insect bite
26
Plaque
Large, flat, elevated, solid surface Ex: psoriasis Pathogen: tineas
27
Scale
Think or thick flake of skin varying in color, usually secondary to desquamated, dead epithelium Ex: dandruff
28
Crust
Dried residue of exudates | Ex: residue of impetigo
29
Fissure
Linear crack in the skin | Ex: Athlete's foot
30
Ulcer
Opening in the skin caused by sloughing of necrotic tissue, extending past the epidermis Ex: pressure ulcer, stasis ulcer
31
Most common bacterial skin pathogens
S. aureus | Group A, B-hemolytic streptococci
32
Most common viral skin infection
Herpes simplex
33
Most common fungal skin pathogen
Trichophyton rubrum | often infects nails
34
Most common parasitic skin infections
Cutaneous larva migrans | lice, bedbugs, scabies
35
Top 5 common causes of skin infections
``` S. aureus GAS Herpes simplex Trichophyton rubrum cutaneous larva migrans ```
36
PYR test
Pyrrolidonyl Arylamidase rapid test--> used to identify GAS and enterococci. These are both PYR positive and differentiated from the rest of the population
37
Substrate for the PYR test
L-naphthylamide-B-naphthylamide | It's hydrolyzed by a pyroglutamate aminopeptidase enzyme
38
Coagulase positive spp.
S. aureus | S. intermedius
39
Coagulase negative spp.
S. saprophyticus S. epidermidis (icaA, mecA, and IS256) S. lugdunensis
40
Staphylococcus features
``` G+ clusters non-motile non-spore forming Catalase +, Oxidase - Mannitol salt + Glucose fermenters High tolerance to salt Primarily aerobic, some are facultative anaerobes Colonies look buttery, cream or white colored ```
41
Inflammatory diseases caused by S. aureus
``` Skin infections Osteomyelitis Arthritis Septicemia Endocarditis Pneumonia ```
42
Toxin-mediated S. aureus infections
Scalded skin syndrome Gastroenteritis TSS
43
Virulence factors of S. aureus: Structural components
Capsule- inhibits chemotaxis and phagocytosis PDG- provides osmotic stability Teichoic acid- binds to fibronectin Protein A- Inhibits Ab-mediated clearance by binding IgG Fc receptors, is a leukocyte chemoattractant and is anticomplementary Cytoplasmic membrane- osmotic barrier Polysaccharide slime layer
44
Virulence factors of S. aureus: Toxins
Cytotoxins: toxic for many cells (Leukos, RBCs, MPs, platelets and fibroblasts) Exfoliative toxins (ETA and ETB): Serine proteases-split intercellular bridges in the stratum granulosum epidermis Enterotoxins: SuperAg--> cytokine storm, increases intestinal peristalsis and fluid loss TSS: Toxin-I, SuperAg--> cytokine storm, produces leakage/destruction of endothelial cells. Leukocidin
45
Virulence factors of S. aureus: Enzymes
``` Coagulase- converts fibrinogen to fibrin Catalase: removes H2O2 Hyaluronidase: hydrolyzes HA in connective tissue--> promotes spread of staph. Fibrinolysin: dissolves fibrin clot Lipases: hydrolyzes lipids Nucleases: Hydrolyzes DNA Penicillinase: hydrolyzes penicillins B-lactamase Staphylokinase ```
46
Virulence factors of S. epidermidis
Lipase | Polysacc slime layer
47
Protein A
On S. aureus surface--> attached Fc portion of IgG Ab and makes it unavailable to be recognized/taken up by the phagocytes
48
Exfoliative toxin
Targets Desmoglein-1 | toxin cuts Dsg1 in the stratum corneum and allows S. aureus to open the skin itself and then invade
49
How to differentiate Strep from Staph
Gram stain: - staph are in clusters - strep are in chains Catalase test: - staph is catalse + and is yellow on blood agar - strep is catalase - and doesnt produce a pigment Both can be B-hemolytic Staph is resistant to penicillin G
50
MRSA and VRSA/VISA genes
MRSA staph have mecA gene | and vancomycin resistant have vanA gene
51
MRSA
Methicillin and nafcillin arent broken down by normal penicillinase. MRSA staph have acquired mecA gene which encodes a new penicillin binding protein 2A--> allows the bacteria to cleave the drugs
52
Vancomycin
standard for systemic Staph infections. Must be hospitalized to use--IV Vvv. toxic and expensive, avoid using it
53
spa gene
encodes Protein A for S. aureus
54
mecA gene
encodes PBP2A
55
SCCmec gene
codes for the staphylococcal cassette where chromosome mecA is located
56
Types of MRSA
``` CA-MRSA- community acquired HCA-MRSA- healthcare associated HA-MRSA- hospital acquired LA-MRSA- livestock-associated (pork) Nosocomial- infection 48hrs+ after admission SSTI- skin and soft tissue infection ```
57
At risk ethnic group for MRSA
Alaskan-natives | Native Americans
58
Infections of the epidermis
Impetigo | Folliculitis
59
Infections of the dermis
``` Ecthyma Erysipelas Furunculosis Carbunculosis Cellulitis ```
60
Infections of the Hypoderm
Necrotizing fasciitis
61
Infections of the muscle
Myonecrosis
62
Impetigo
Bac infection of the epidermis S. aureus 80% Sometimes S. pyogenes Potential complication of strep infection: Post-strep glomerulonephritis, Rheumatic fever (way less common) Risks: injury to skin, children v. contagious Incubation: 1-3 days for strep 4-10 for staph
63
Nonbullous impetigo
``` Most common (<0.5cm) Teichoic acid adhesion (FnBPs) require epithelial cell receptor component fibronectin for colonization, but the receptors are unavailable on intact skin ```
64
Bullous impetigo
>0.5 cm Group II S. aureus-often phage type 71 Cause: exfoliating toxin-->degrades Desmoglein-1 and results in loss of adhesion of superficial epidermis. Lesions occur on INTACT skin (unlike non-bullous) Bullous lesions can invade and cause septicemia
65
Ecthyma
Impetigo spread to dermis | Cause: B-hemolytic strep.
66
Most common pathogens of Cellulitis and Erysipelas
B-hemolytic: - S. pyogenes - S. agalactiae S. aureus less common other less commons: - H. influ in <6yrs - Pasteurella multocida from dog/cat scratch - Aeromonas hydrophilia, V. vulnificus from seawater - P. aeruginosa from puncture wound or in IMCPs
67
Erysipelas
``` aka St. Anthony's fire Clinical: tender, well-defined borders, raised plaques, erythematous Indurated plaque on face or legs (assoc w nasopharyngeal infections) Involves dermis and superficial lymph Pain in affected region +/- fever Prodromal sxs 48hrs before rash ```
68
Cellulitis
``` Clinical: warm tender erythematous ill-defined borders expanding rapidly lymphangitis (affecting the vessels of the lymph) Bacteremia Presents mainly on legs Involves deeper dermis and subQ fat Pain in affected region +/- fever ```