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MHD2 > Block 9 - L18, 19 > Flashcards

Block 9 - L18, 19 Flashcards

1
Q

How is a congenital melanocytic nevus different from a regular melanocytic nevus?

A

Infants are born with it, benign almost all of the time, tend to be larger

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2
Q

What are the two types of skin biopsy?

A
  1. Shave biopsy

2. Punch biopsy

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3
Q

What is chronic bullous disease of childhood?

A

Type of linear IgA bullous dermatosis

Presents with a crown of Jewels/string of pearls/annular rosette

Mucous membrane involved in 75% of cases

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4
Q

How does linear IgA bullous dermatosis present in adults?

A

Idiopathic or drug-induced, mucus membrane involved less frequently (50%)

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5
Q

What is the presentation of pemphigus vulgaris?

A

Flaccid bullae
+ Nikolsky sign - sloughing of the bullae with lateral pressure
+ Asboe Hansen sign - spreading out of bullae with vertical pressure
Life threatening

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6
Q

What are the auto-Ab attacking in pemphigus vulgaris?

A

Desmoglein 1 and 3

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7
Q

What is the presentation of dermatitis herpetiformis?

A

Papules, vesicles, or bullae on a red base; extensor surfaces, scalp, nuchal area, buttocks

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8
Q

What is seen on H&E in dermatitis herpetiformis?

A

IgA in the dermal papillae

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9
Q

What is dermatitis herpetiformis associated with?

A

Celiac disease

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10
Q

How does SJS present?

A

Fever and influenza-like symptoms, mucous membrane involvement, often-drug induced

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11
Q

What causes SJS in kids?

A

Mycoplasma

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12
Q

List the dermal diseases caused by HSV.

A
  1. Herpes labialis
  2. Gingivostomatitis (mouth)
  3. Herpetic whitlow (finger)
  4. Eczema herpeticum
  5. Genital HSV
  6. Disseminated disease in infants (congenital)
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13
Q

How does varicella (chicken pox) present?

A

Dewdrops on a rose petal, lesions in various stages

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14
Q

What is the most common complication of varicella?

A

Secondary infection with Staph or Strep

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15
Q

What causes SSSS?

A

Exfloiate toxin A, an active serine protease that cleaves proteins holding keratinocytes together

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16
Q

What can be cultured in SSSS to identify the source?

A

Mucus membrane (NOT the skin)

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17
Q

How does psoriasis present?

A 
Annular variant
Thick silvery/white scale
Auspitz sign - pinpoint bleding
Gluteal cleft, nails (onycholysis, pitting, thickening), scalp, conchal bowls, dorsal hands
Koebner phenomenon
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18
Q

___ is seen in 20% of children in the US and is associated with seasonal allergies, asthma, and eczema in families.

A

Atopic dermatitis

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19
Q

What are the important features of tinea corporis?

A

Caused by a merphatophyte infection, may be pruritic, leading edge of scale, KOH scrape would be positive

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20
Q

What are the important features of discoid lupus erythematosus?

A

Thin, violaceous, scaly plaque on the nasal dorsum, can scar; scaling, follicular plugging

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21
Q

What are the important features of pityriasis rosea and how is it treated?

A

Caused by HHV6 or 7
Herald patch
Follows skin tension lines
3-8 weeks, self-resolving

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22
Q

What are the important features of urticaria (hives)?

A

Lesions last <24 hours
Pruritic
Acute if <6 weeks, chronic if >6 weeks
Can be caused by infection, drugs, food

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23
Q

What are the important features of viral exanthem?

A

Difficult to distinguish from drug exanthem, children > adults, extremities > trunk

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24
Q

What are the important features of erythema nodosum?

A

Tender, indurated subcutaneous nodules, pretibial area, lateral shins, septal panniculitis

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25
Q

What can cause erythema nodosum?

A

Infection (strep), drugs (OCP, echinacea), infalmmatory

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26
Q

What are the features of cellulitis?

A

Warm, pink, red, tender, +/- fever/leukocytosis, Staph and Strep

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27
Q

What are the features of morbilliform drug exanthem?

A

Begin proximally and generalize

Trunk > extremities

Within first 2 weeks of treatment (antibiotics are most common)

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28
Q

What are the features of pyogenic granuloma?

A

Friable surfaces, bleeds, non-tender, spontaneous

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29
Q

What are the features of Kaposi’s sarcoma?

A

Classically presents on toes, plantar feet, face (including oral mucosa)

Often happens in immunocompromised patients

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30
Q

What is the most common vascular lesion and how does it present?

A

Cherry angioma, round, slightly elevated ruby red papule

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31
Q

What are the most common pathogens seen in SSTIs?

A

S. aureus
GAS (pyogenes)
GBS (agalactiae)

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32
Q

Discuss the genetic element of MRSA.

A

SCCmec is the mobile genetic element that contains mecA - this encodes PBP2a, an altered penicillin-binding protein with low affinity for binding beta-lactam antibiotics

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33
Q

What is Panton-Valentine Leukocidin (PVL)?

A

Cytotoxin associated with SCCmec IV and V (community-acquired strains), associated with skin infections and necrotizing pneumonias

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34
Q

What is cellulitis?

A

Diffuse superficial skin lesion (deeper dermis and subcutaneous fat)

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35
Q

What predisposes you to developing cellulitis?

A
  1. Edema, lymphedema
  2. Obesity
  3. Pre-existing skin breaks (ulcers, psoriasis, eczema)
  4. Skin infections (tinea pedia, varicella)
  5. Immunosupression
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36
Q

Discuss the clinical features of cellulitis.

A

Almost always unilateral, lower extremity most common; red, warm, swollen, painful

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37
Q

What is the most common cause of cellulitis?

A

Streptococci (Staph can also cause it)

38
Q

What is erysipelas?

A

Diffuse superficial skin infection of the upper dermis and superficial lymphatics

39
Q

Discuss the clinical features of erysipelas.

A

Face, extremities

Raised, tender, intense color, very well-circumscribed

40
Q

Discuss the clinical features of impetigo.

A

Localized lesion of the epidermis
Common in kids 2-5 y/o
Transmissible
Honey-colored crust

41
Q

What causes impetigo?

A

S. aureus > S. pyogenes

42
Q

What is a sequelae of impetigo?

A

Post-streptococcal GN

43
Q

Discuss the clinical features of ecthyma.

A

Ulcerations affecting the deep epidermis and dermis, +/- bacteremia

44
Q

What is a purulent collection in the dermis and subcutaneous tissue?

A

Cutaneous abscess

45
Q

What is an infection of the hair follicle that ruptures into the subcutaneous tissue to form an abscess?

A

Furuncle (boil)

46
Q

What is a coalescence of multiple furuncles?

A

Carbuncle

47
Q

What is a collection of pus in a muscle group, typically caused by hematogenous seeding, with localized pain +/- swelling?

A

Pyomyositis

48
Q

What causes purulent SSTIs?

A

S. aureus predominantly

49
Q

How are purulent SSTIs treated?

A

Drainage (mainstay), antibiotics if extensive, systemic signs of infection, poor response to therapy, immunocompromised

50
Q

What organisms are commonly seen in trauma with water exposure? Which progresses quickly?

A
  1. Aeromonas
  2. Edwardsiella tarda
  3. Erysipelothrix rhusiopathiae
  4. Vibrio vulnificus - quick progression
  5. Mycobacterium marinum
51
Q

What type of water is Aeromonas found in?

A

Freshwater

The guts of leeches are colonized by Aeromonas

52
Q

What type of water is Mycobacterium marinum found in?

A

Fish tank exposure

53
Q

What type of water is Vibrio vulnificus found in?

A

Salt or brackish water

54
Q

What type of water is Edwardsiella tarda found in?

A

Salt water

55
Q

What is associated with Erysipelothrix rhusiopathiae?

A

Fisherman with hook puncture, seafood packers

56
Q

What organisms are transmitted by human bite wounds?

A 
Eikenella corrodens
Fusobacterium
peptostreptococcus
Prevotella
Porphyromonas
57
Q

What organisms are transmitted by dog bite wounds?

A

Capnocytophagia canimorsus

Pasteurella multocida

58
Q

What organisms are transmitted by cat bite wounds?

A

Pasturella multocida

Bartonella henselae

59
Q

What are the features of diabetic foot ulcers?

A

Neuropathy and PVD predispose to ulceration; when infected, often polymicrobial

60
Q

What organisms are often seen in diabetic foot ulcers?

A

S. aureus, GBS, P. aeruginosa (GN rod, also seen in burns, immunocompromised)

61
Q

What is necrotizing fasciitis?

A

Infection involving the full thickness of the skin down to the superficial fascia

62
Q

What organisms may cause necrotizing fasciitis?

A

Monomicrobial - S. pyogenes, S. aureus, Aeromonas, V. vulnificus, Clostridial
Polymicrobial - seen in wounds, associated anaerobes

63
Q

What are the features of necrotizing fasciitis?

A

Pain out of proportion

Bullous lesions, necrotic tissue, “woody” edema, rapid spread, signs of shock, fever, etc.

64
Q

What causes myonecrosis/gas gangrene (trauma/vascular compromise vs. spontaneous)?

A

Contiguous spread via trauma/vascular compromise - C. perfringens

Spontaneous (hematogenous spread, from neutropenia, GI cancer) - C. septicum

Also Streptococci

65
Q

How are necrotizing skin infections treated?

A

DEBRIDEMENT

Broad-spectrum antibiotics + Clindamycin to suppress toxin production

66
Q

What causes Streptococcal TSS and what happens?

A

Invasive S. pyogenes (exotoxins A and b, M protein fragments) infection; often associated with a focus of necrotizing fasciitis, myonecrosis, hypotension and ogan failure, progressive pain at site of infection

67
Q

How is Streptococcal TSS treated?

A

Debridement

Penicillin + clindamycin

68
Q

What causes Staphylococcal TSS and what happens?

A

S. aureus ITSST-1); seen in menstruating women, non-menstrual cases related to wounds, burn injury, trauma, hypotension and organ failure

Erythroderma, maculopapular rash, late desquamation

69
Q

What are risk factors for osteomyelitis?

A
  1. Risk for bacteremia (remote site of infection, IV drug use, hemodialysis, central line/cardiac devices)
  2. Skin ulcers
  3. Peripheral artery disease
  4. Penetrating trauma
  5. Recent surgery
  6. Bites
70
Q

What are the three routes of infection leading to osteomyelitis?

A
  1. Hematogenous (most common in children - long bones; adults - vertebral bones) - monomicrobial
  2. Contiguous (diabetic or ischemic ulcers, decubitus ulcers) - polymicrobial
  3. Direct inoculation (trauma, bites, surgery) - polymicrobial
71
Q

Discuss the microbes involved in osteomyelitis.

A

Most common - S. aureus

  1. Coagulase-negative staph
  2. Strep (GBS in neonates)
  3. Enterococcus
  4. GN rods (Pseudomonas aeruginosa - puncture, H. influenzae - neonates, Slamonella species - sickle cell disease)
72
Q

How does contiguous osteomyleitis present?

A

Subacute to chronic, enlarging non-healing ulcer, increased drainage, erythema

73
Q

How does discontinuous inoculation osteomyelitis present?

A

Subacute to chronic, non-union, poor incisional healing/surgical site infection

74
Q

How does hematogenous osteomyelitis present?

A

Fevers and chills may be present with acute onset

Kids - often spread to skin, soft tissue, joints
Adults - often just pain with vertebral disease

75
Q

How is osteomyelitis diagnosed?

A

MRI is the modality of choice, good negative predictive value; probe to bone test (high positive predictive value)

Gold standard - bone biopsy

76
Q

Why are cultures not useful for osteomyelitis?

A

Poor correlation with bone biopsy culture result (exception - S. aureus)

77
Q

How is osteomyelitis treated?

A
  1. Debridement
  2. May need revascularization to heal
  3. IV anti-microbials (prolonged course, 6 weeks)
78
Q

Discuss TB osteomyelitis (Pott’s).

A

Usually hematogenous spread, long bones/vertebrae, usually solitary lesions, granulaomatous inflammation (caseous necrosis, bone destruction)

79
Q

What are the risk factors for septic arthritis?

A
  1. Elderly (>80 y/o)
  2. Prosthetic joint or other foreign material
  3. Recent joint surgery
  4. Intra-articular steroid injection
  5. IV drug use
  6. Alcohol use disorder
  7. Endocarditis
  8. Immunosuppression/chronic diseases (DM)
  9. Joint disease - RA, OA, gout
  10. Skin infection/ulcer
80
Q

Discuss the pathogenesis of septic arthritis.

A

Synovial cells have no basement membrane. bacteria and inflammatory cells enter, causing inflammation, synovial membrane hyperplasia, and synovial effusion. Cartilage damage occurs via cytokines and proteases. Pressure necrosis from large synovial effusions leads to cartilage and bone loss.

81
Q

Discuss what organisms cause septic arthritis.

A

Majority are bacterial (acute pyogenic process, usually monoarticular) - emergency

Viral (acute, systemic illness, polyarticular)

Fungal/mycobacterial (chronic, monoarticular, immunocompromised host)

82
Q

When is septic arthritis with S. aureus seen?

A

Native joints of adults and older kids
Early-onset and late prosthetic joint infection (PJI)
Bacteremia has high predilection for damaged joints

83
Q

When is septic arthritis with coag-negative staph seen?

A

Delayed-onset PJI

84
Q

When is septic arthritis with GN species seen?

A

More common in IV drug use, immunocompromised, elderly, Salmonella - sickle cell, H. influenzae - young children, late onset PJI

85
Q

How does septic arthritis present?

A

Acute onset of monoarticular symptoms (pain, swelling, decreased function)
Knee in >50%, axial skeleton in IVDU

Effusion, erythema, decreased range of motion on exam

Fever is common

86
Q

How is septic arthritis diagnosed?

A

Arthrocentesis - positive culture (WBC usually >50k, many >100k)

87
Q

How is septic arthritis treated?

A

Drainage
Empiric antibiotics
3-4 weeks for a native joint
6+ weeks for a proesthetic joint

88
Q

What is disseminated gonococcal infection (DGI)?

A

Most common in sexually active adolescents and young adults; asymptomatic mucosal infection goes untreated and disseminates

89
Q

What are risk factors for dGI?

A

Pregnancy/post-partum, menstruation, terminal complement deficiencies

90
Q

How does DGI manifest?

A

Occult bacteremia, classic triad, septic joint

91
Q

What is the classic triad of DGI?

A
  1. Dermatitis (numerous painless, non-pruritic macules, papules, pustular lesions)
  2. Tenosynovitis (hands and wrists)
  3. Migratory polyarthralgia or arthritis
92
Q

How is DGI diagnosed?

A

Arthrocentesis, NAAT testing of synovial fluid

MHD2 (34 decks)

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