Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

What are the two types of skin biopsy?

A
  1. Shave biopsy

2. Punch biopsy

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

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

How does linear IgA bullous dermatosis present in adults?

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the auto-Ab attacking in pemphigus vulgaris?

A

Desmoglein 1 and 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the presentation of dermatitis herpetiformis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is seen on H&E in dermatitis herpetiformis?

A

IgA in the dermal papillae

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

What is dermatitis herpetiformis associated with?

A

Celiac disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does SJS present?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes SJS in kids?

A

Mycoplasma

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

How does varicella (chicken pox) present?

A

Dewdrops on a rose petal, lesions in various stages

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

What is the most common complication of varicella?

A

Secondary infection with Staph or Strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes SSSS?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can be cultured in SSSS to identify the source?

A

Mucus membrane (NOT the skin)

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the important features of viral exanthem?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the important features of erythema nodosum?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What can cause erythema nodosum?
Infection (strep), drugs (OCP, echinacea), infalmmatory
26
What are the features of cellulitis?
Warm, pink, red, tender, +/- fever/leukocytosis, Staph and Strep
27
What are the features of morbilliform drug exanthem?
Begin proximally and generalize Trunk > extremities Within first 2 weeks of treatment (antibiotics are most common)
28
What are the features of pyogenic granuloma?
Friable surfaces, bleeds, non-tender, spontaneous
29
What are the features of Kaposi's sarcoma?
Classically presents on toes, plantar feet, face (including oral mucosa) Often happens in immunocompromised patients
30
What is the most common vascular lesion and how does it present?
Cherry angioma, round, slightly elevated ruby red papule
31
What are the most common pathogens seen in SSTIs?
S. aureus GAS (pyogenes) GBS (agalactiae)
32
Discuss the genetic element of MRSA.
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
33
What is Panton-Valentine Leukocidin (PVL)?
Cytotoxin associated with SCCmec IV and V (community-acquired strains), associated with skin infections and necrotizing pneumonias
34
What is cellulitis?
Diffuse superficial skin lesion (deeper dermis and subcutaneous fat)
35
What predisposes you to developing cellulitis?
1. Edema, lymphedema 2. Obesity 3. Pre-existing skin breaks (ulcers, psoriasis, eczema) 4. Skin infections (tinea pedia, varicella) 5. Immunosupression
36
Discuss the clinical features of cellulitis.
Almost always unilateral, lower extremity most common; red, warm, swollen, painful
37
What is the most common cause of cellulitis?
Streptococci (Staph can also cause it)
38
What is erysipelas?
Diffuse superficial skin infection of the upper dermis and superficial lymphatics
39
Discuss the clinical features of erysipelas.
Face, extremities | Raised, tender, intense color, very well-circumscribed
40
Discuss the clinical features of impetigo.
Localized lesion of the epidermis Common in kids 2-5 y/o Transmissible Honey-colored crust
41
What causes impetigo?
S. aureus > S. pyogenes
42
What is a sequelae of impetigo?
Post-streptococcal GN
43
Discuss the clinical features of ecthyma.
Ulcerations affecting the deep epidermis and dermis, +/- bacteremia
44
What is a purulent collection in the dermis and subcutaneous tissue?
Cutaneous abscess
45
What is an infection of the hair follicle that ruptures into the subcutaneous tissue to form an abscess?
Furuncle (boil)
46
What is a coalescence of multiple furuncles?
Carbuncle
47
What is a collection of pus in a muscle group, typically caused by hematogenous seeding, with localized pain +/- swelling?
Pyomyositis
48
What causes purulent SSTIs?
S. aureus predominantly
49
How are purulent SSTIs treated?
Drainage (mainstay), antibiotics if extensive, systemic signs of infection, poor response to therapy, immunocompromised
50
What organisms are commonly seen in trauma with water exposure? Which progresses quickly?
1. Aeromonas 2. Edwardsiella tarda 3. Erysipelothrix rhusiopathiae 4. Vibrio vulnificus - quick progression 5. Mycobacterium marinum
51
What type of water is Aeromonas found in?
Freshwater The guts of leeches are colonized by Aeromonas
52
What type of water is Mycobacterium marinum found in?
Fish tank exposure
53
What type of water is Vibrio vulnificus found in?
Salt or brackish water
54
What type of water is Edwardsiella tarda found in?
Salt water
55
What is associated with Erysipelothrix rhusiopathiae?
Fisherman with hook puncture, seafood packers
56
What organisms are transmitted by human bite wounds?
``` Eikenella corrodens Fusobacterium peptostreptococcus Prevotella Porphyromonas ```
57
What organisms are transmitted by dog bite wounds?
Capnocytophagia canimorsus | Pasteurella multocida
58
What organisms are transmitted by cat bite wounds?
Pasturella multocida | Bartonella henselae
59
What are the features of diabetic foot ulcers?
Neuropathy and PVD predispose to ulceration; when infected, often polymicrobial
60
What organisms are often seen in diabetic foot ulcers?
S. aureus, GBS, P. aeruginosa (GN rod, also seen in burns, immunocompromised)
61
What is necrotizing fasciitis?
Infection involving the full thickness of the skin down to the superficial fascia
62
What organisms may cause necrotizing fasciitis?
Monomicrobial - S. pyogenes, S. aureus, Aeromonas, V. vulnificus, Clostridial Polymicrobial - seen in wounds, associated anaerobes
63
What are the features of necrotizing fasciitis?
Pain out of proportion | Bullous lesions, necrotic tissue, "woody" edema, rapid spread, signs of shock, fever, etc.
64
What causes myonecrosis/gas gangrene (trauma/vascular compromise vs. spontaneous)?
Contiguous spread via trauma/vascular compromise - C. perfringens Spontaneous (hematogenous spread, from neutropenia, GI cancer) - C. septicum Also Streptococci
65
How are necrotizing skin infections treated?
DEBRIDEMENT Broad-spectrum antibiotics + Clindamycin to suppress toxin production
66
What causes Streptococcal TSS and what happens?
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
How is Streptococcal TSS treated?
Debridement Penicillin + clindamycin
68
What causes Staphylococcal TSS and what happens?
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
What are risk factors for osteomyelitis?
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
What are the three routes of infection leading to osteomyelitis?
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
Discuss the microbes involved in osteomyelitis.
Most common - S. aureus 2. Coagulase-negative staph 3. Strep (GBS in neonates) 4. Enterococcus 5. GN rods (Pseudomonas aeruginosa - puncture, H. influenzae - neonates, Slamonella species - sickle cell disease)
72
How does contiguous osteomyleitis present?
Subacute to chronic, enlarging non-healing ulcer, increased drainage, erythema
73
How does discontinuous inoculation osteomyelitis present?
Subacute to chronic, non-union, poor incisional healing/surgical site infection
74
How does hematogenous osteomyelitis present?
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
How is osteomyelitis diagnosed?
MRI is the modality of choice, good negative predictive value; probe to bone test (high positive predictive value) Gold standard - bone biopsy
76
Why are cultures not useful for osteomyelitis?
Poor correlation with bone biopsy culture result (exception - S. aureus)
77
How is osteomyelitis treated?
1. Debridement 2. May need revascularization to heal 3. IV anti-microbials (prolonged course, 6 weeks)
78
Discuss TB osteomyelitis (Pott's).
Usually hematogenous spread, long bones/vertebrae, usually solitary lesions, granulaomatous inflammation (caseous necrosis, bone destruction)
79
What are the risk factors for septic arthritis?
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
Discuss the pathogenesis of septic arthritis.
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
Discuss what organisms cause septic arthritis.
Majority are bacterial (acute pyogenic process, usually monoarticular) - emergency Viral (acute, systemic illness, polyarticular) Fungal/mycobacterial (chronic, monoarticular, immunocompromised host)
82
When is septic arthritis with S. aureus seen?
Native joints of adults and older kids Early-onset and late prosthetic joint infection (PJI) Bacteremia has high predilection for damaged joints
83
When is septic arthritis with coag-negative staph seen?
Delayed-onset PJI
84
When is septic arthritis with GN species seen?
More common in IV drug use, immunocompromised, elderly, Salmonella - sickle cell, H. influenzae - young children, late onset PJI
85
How does septic arthritis present?
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
How is septic arthritis diagnosed?
Arthrocentesis - positive culture (WBC usually >50k, many >100k)
87
How is septic arthritis treated?
Drainage Empiric antibiotics 3-4 weeks for a native joint 6+ weeks for a proesthetic joint
88
What is disseminated gonococcal infection (DGI)?
Most common in sexually active adolescents and young adults; asymptomatic mucosal infection goes untreated and disseminates
89
What are risk factors for dGI?
Pregnancy/post-partum, menstruation, terminal complement deficiencies
90
How does DGI manifest?
Occult bacteremia, classic triad, septic joint
91
What is the classic triad of DGI?
1. Dermatitis (numerous painless, non-pruritic macules, papules, pustular lesions) 2. Tenosynovitis (hands and wrists) 3. Migratory polyarthralgia or arthritis
92
How is DGI diagnosed?
Arthrocentesis, NAAT testing of synovial fluid

MHD2 (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions