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Post-Midterm Micro > Skin & MSK > Flashcards

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
Q

Wheal

A

Localized area of edema, often irregular and of variable size and color
Ex: hive, insect bite

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26
Q

Plaque

A

Large, flat, elevated, solid surface
Ex: psoriasis
Pathogen: tineas

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27
Q

Scale

A

Think or thick flake of skin varying in color, usually secondary to desquamated, dead epithelium
Ex: dandruff

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28
Q

Crust

A

Dried residue of exudates

Ex: residue of impetigo

29
Q

Fissure

A

Linear crack in the skin

Ex: Athlete’s foot

30
Q

Ulcer

A

Opening in the skin caused by sloughing of necrotic tissue, extending past the epidermis
Ex: pressure ulcer, stasis ulcer

31
Q

Most common bacterial skin pathogens

A

S. aureus

Group A, B-hemolytic streptococci

32
Q

Most common viral skin infection

A

Herpes simplex

33
Q

Most common fungal skin pathogen

A

Trichophyton rubrum

often infects nails

34
Q

Most common parasitic skin infections

A

Cutaneous larva migrans

lice, bedbugs, scabies

35
Q

Top 5 common causes of skin infections

A 
S. aureus
GAS
Herpes simplex
Trichophyton rubrum
cutaneous larva migrans
36
Q

PYR test

A

Pyrrolidonyl Arylamidase rapid test–> used to identify GAS and enterococci.
These are both PYR positive and differentiated from the rest of the population

37
Q

Substrate for the PYR test

A

L-naphthylamide-B-naphthylamide

It’s hydrolyzed by a pyroglutamate aminopeptidase enzyme

38
Q

Coagulase positive spp.

A

S. aureus

S. intermedius

39
Q

Coagulase negative spp.

A

S. saprophyticus
S. epidermidis (icaA, mecA, and IS256)
S. lugdunensis

40
Q

Staphylococcus features

A 
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
Q

Inflammatory diseases caused by S. aureus

A 
Skin infections
Osteomyelitis
Arthritis
Septicemia
Endocarditis
Pneumonia
42
Q

Toxin-mediated S. aureus infections

A

Scalded skin syndrome
Gastroenteritis
TSS

43
Q

Virulence factors of S. aureus: Structural components

A

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
Q

Virulence factors of S. aureus: Toxins

A

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
Q

Virulence factors of S. aureus: Enzymes

A 
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
Q

Virulence factors of S. epidermidis

A

Lipase

Polysacc slime layer

47
Q

Protein A

A

On S. aureus surface–> attached Fc portion of IgG Ab and makes it unavailable to be recognized/taken up by the phagocytes

48
Q

Exfoliative toxin

A

Targets Desmoglein-1

toxin cuts Dsg1 in the stratum corneum and allows S. aureus to open the skin itself and then invade

49
Q

How to differentiate Strep from Staph

A

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
Q

MRSA and VRSA/VISA genes

A

MRSA staph have mecA gene

and vancomycin resistant have vanA gene

51
Q

MRSA

A

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
Q

Vancomycin

A

standard for systemic Staph infections.
Must be hospitalized to use–IV
Vvv. toxic and expensive, avoid using it

53
Q

spa gene

A

encodes Protein A for S. aureus

54
Q

mecA gene

A

encodes PBP2A

55
Q

SCCmec gene

A

codes for the staphylococcal cassette where chromosome mecA is located

56
Q

Types of MRSA

A 
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
Q

At risk ethnic group for MRSA

A

Alaskan-natives

Native Americans

58
Q

Infections of the epidermis

A

Impetigo

Folliculitis

59
Q

Infections of the dermis

A 
Ecthyma
Erysipelas
Furunculosis
Carbunculosis
Cellulitis
60
Q

Infections of the Hypoderm

A

Necrotizing fasciitis

61
Q

Infections of the muscle

A

Myonecrosis

62
Q

Impetigo

A

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
Q

Nonbullous impetigo

A 
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
Q

Bullous impetigo

A

> 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
Q

Ecthyma

A

Impetigo spread to dermis

Cause: B-hemolytic strep.

66
Q

Most common pathogens of Cellulitis and Erysipelas

A

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
Q

Erysipelas

A 
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
Q

Cellulitis

A 
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

Post-Midterm Micro (1 decks)

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