Disorders, Drug Reactions, Cancer Flashcards

(100 cards)

1
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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2
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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3
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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4
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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5
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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6
Q

Actinic Keratosis

A
  1. Dysplastic condition
  2. Can regress, small percentage become malignant
  3. UV-induced
  4. Rough, erythematous, yellow brown and scaly
  5. Middle Aged or elderly
  6. Men at risk
  7. Fair skin at risk

Destroy with surgery

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7
Q

Squamous Cell Carcinoma

A

Common tumor

  1. Elderly
  2. UV-induced usually
  3. Ulcers, burns, arsenic, radiation, HPV, carcinogens can contribute

Note that UV-induced SCC tends to be less aggressive

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8
Q

SCC in situ

A

Irregular shape
Erythematous
Scaly, crusted plaques

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9
Q

SCC invasive lesions

A

Nodular
Variable scaling
May ulcerate

Risk factors for metastasis: thickness of the lesion, degree of subcutis penetration

Can be well differentiated orderly lobules with keratinization zones, but can also be highly anaplastic with only abortive single-cell keratinization or anaplastic.

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10
Q

Keratoacanthoma

A
  1. SCC variation
  2. Solitary, pink/flesh colored dome shaped nodule
  3. Keratin plug in the middle (exophytic or endophytic lesions)
  4. Sun exposure
  5. Elderly people

Can involute (curl up) spontaneously, but may persist

Can cause local tissue destruction, so treat even though they are not metastatic

Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm

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11
Q

Basal Cell Carcinoma

A
  1. Cutaneous malignant neoplasm
  2. Elderly males
  3. Sun-exposed skin, face usually
  4. PTCH1 mutations (patched/hedgehog)
  5. Papule
  6. Pearly, translucent edge with telangiectasia

Grow slow, rarely become aggressive
Nodular lesions that grow downward into the dermis, basophilic

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12
Q

Dysplastic Nevi

A

Sporadic or familial. Risk for melanoma if there are many; however, most melanomas even in these patients will be de novo rather than from preexisting nevus.

  1. Irregular shape
  2. Uneven color
  3. Dark Brown Centers
  4. Can occur in places with minimal sun exposure

Dysplastic nevi are either junctional or compound; they are never intradermal. May also exhibit fusion of adjacent nests (bridging).

Will also replace the normal basal layer to form a lentiginous hyperplasia. May also create lateral borders penetrating adjacent dermal nevus cells (shoulder phenomenon)

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13
Q

Junctional Nevi

A

Nuclei are round, little mitosis. Nests in dermal/epidermal junction

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14
Q

Compound Nevi

A

Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells

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15
Q

Intradermal nevi

A

Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.

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16
Q

Actinic Keratosis

A
  1. Dysplastic condition
  2. Can regress, small percentage become malignant
  3. UV-induced
  4. Rough, erythematous, yellow brown and scaly
  5. Middle Aged or elderly
  6. Men at risk
  7. Fair skin at risk

Destroy with surgery

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17
Q

BRAF V600E inhibitor

A

Vemurafenib

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18
Q

SCC in situ

A

Irregular shape
Erythematous
Scaly, crusted plaques

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19
Q

SCC invasive lesions

A

Nodular
Variable scaling
May ulcerate

Risk factors for metastasis: thickness of the lesion, degree of subcutis penetration

Can be well differentiated orderly lobules with keratinization zones, but can also be highly anaplastic with only abortive single-cell keratinization or anaplastic.

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20
Q

Keratoacanthoma

A
  1. SCC variation
  2. Solitary, pink/flesh colored dome shaped nodule
  3. Keratin plug in the middle (exophytic or endophytic lesions)
  4. Sun exposure
  5. Elderly people

Can involute (curl up) spontaneously, but may persist

Can cause local tissue destruction, so treat even though they are not metastatic

Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm

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21
Q

Basal Cell Carcinoma

A
  1. Cutaneous malignant neoplasm
  2. Elderly males
  3. Sun-exposed skin, face usually
  4. PTCH1 mutations (patched/hedgehog)
  5. Papule
  6. Pearly, translucent edge with telangiectasia

Grow slow, rarely become aggressive
Nodular lesions that grow downward into the dermis, basophilic

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22
Q

Melanocytic Nevi

A

Well circumscribed, regular bordered uniformly pigmented areas

Superficial nevus cells larger, pigmented, grow in nests
Deeper nevus cells smaller/mature, less/no pigment, grow in cords

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23
Q

Junctional Nevi

A

Nuclei are round, little mitosis. Nests in dermal/epidermal junction

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24
Q

Compound Nevi

A

Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells

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25
Intradermal nevi
Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.
26
Mycosis Fungoides
T cell lymphoma, generally CD4 1. Male dominant 2. African American dominant 3. 30-40 years old Epidermotrophism, with T cells transiting to lymph node, undergoing antigenic stimulation, and forming plaques and patches and tumors in the epidermis. Form an infiltrate of mycosis cells and form intraepidermal vesicles known as Pautrier microabscesses. The cells themselves will initially be irregular, convoluted... as they transform more will lose their epidermotropism Variable prognosis
27
3 stages of mycosis fungoides
Patch phase: many years. First stage, and may be perceived as nonspecific dermatitis. Lower trunk and buttocks. Irregular size and random distribution. Plaque phase: Well-demarcated lesions, annular and violaceous. May or may not be scaly. Can be de novo or from patches. Get more widespread with disease progression Tumor stage: From pre-existing lesions. Red, tense and shiny. Ulceration may occur. Over 1 cm diameter.
28
SCC in situ
Irregular shape Erythematous Scaly, crusted plaques
29
Impetigo
Skin infection, highly infectious. 1. Children or immunocompromised adults 2. Staph usually, sometimes strep 3. Superficial vesicles that rapidly burst and replaced with thick yellowish dirty crust and erthema margin (honey-colored crust). Mouth, nose, extremities Warm, humid conditions Can form bullous, usually group II staph Can mimic autoimmune blistering. Treat with topical antibiotics or orals if severe.
30
Keratoacanthoma
1. SCC variation 2. Solitary, pink/flesh colored dome shaped nodule 3. Keratin plug in the middle (exophytic or endophytic lesions) 4. Sun exposure 5. Elderly people Can involute (curl up) spontaneously, but may persist Can cause local tissue destruction, so treat even though they are not metastatic Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm
31
Basal Cell Carcinoma
1. Cutaneous malignant neoplasm 2. Elderly males 3. Sun-exposed skin, face usually 4. PTCH1 mutations (patched/hedgehog) 5. Papule 6. Pearly, translucent edge with telangiectasia Grow slow, rarely become aggressive Nodular lesions that grow downward into the dermis, basophilic
32
Melanocytic Nevi
Well circumscribed, regular bordered uniformly pigmented areas Superficial nevus cells larger, pigmented, grow in nests Deeper nevus cells smaller/mature, less/no pigment, grow in cords
33
Junctional Nevi
Nuclei are round, little mitosis. Nests in dermal/epidermal junction
34
Compound Nevi
Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells
35
Intradermal nevi
Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.
36
Actinic Keratosis
1. Dysplastic condition 2. Can regress, small percentage become malignant 3. UV-induced 4. Rough, erythematous, yellow brown and scaly 5. Middle Aged or elderly 6. Men at risk 7. Fair skin at risk Destroy with surgery
37
Squamous Cell Carcinoma
Common tumor 1. Elderly 2. UV-induced usually 3. Ulcers, burns, arsenic, radiation, HPV, carcinogens can contribute Note that UV-induced SCC tends to be less aggressive
38
SCC in situ
Irregular shape Erythematous Scaly, crusted plaques
39
Wart histo
Papillomatous hyperplasia Prominent granular layer. Clumping of large irregular keratohyaline granules
40
Keratoacanthoma
1. SCC variation 2. Solitary, pink/flesh colored dome shaped nodule 3. Keratin plug in the middle (exophytic or endophytic lesions) 4. Sun exposure 5. Elderly people Can involute (curl up) spontaneously, but may persist Can cause local tissue destruction, so treat even though they are not metastatic Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm
41
Basal Cell Carcinoma
1. Cutaneous malignant neoplasm 2. Elderly males 3. Sun-exposed skin, face usually 4. PTCH1 mutations (patched/hedgehog) 5. Papule 6. Pearly, translucent edge with telangiectasia Grow slow, rarely become aggressive Nodular lesions that grow downward into the dermis, basophilic
42
Melanocytic Nevi
Well circumscribed, regular bordered uniformly pigmented areas Superficial nevus cells larger, pigmented, grow in nests Deeper nevus cells smaller/mature, less/no pigment, grow in cords
43
Junctional Nevi
Nuclei are round, little mitosis. Nests in dermal/epidermal junction
44
Compound Nevi
Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells
45
Intradermal nevi
Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.
46
Actinic Keratosis
1. Dysplastic condition 2. Can regress, small percentage become malignant 3. UV-induced 4. Rough, erythematous, yellow brown and scaly 5. Middle Aged or elderly 6. Men at risk 7. Fair skin at risk Destroy with surgery
47
Squamous Cell Carcinoma
Common tumor 1. Elderly 2. UV-induced usually 3. Ulcers, burns, arsenic, radiation, HPV, carcinogens can contribute Note that UV-induced SCC tends to be less aggressive
48
SCC in situ
Irregular shape Erythematous Scaly, crusted plaques
49
SCC invasive lesions
Nodular Variable scaling May ulcerate Risk factors for metastasis: thickness of the lesion, degree of subcutis penetration Can be well differentiated orderly lobules with keratinization zones, but can also be highly anaplastic with only abortive single-cell keratinization or anaplastic.
50
Keratoacanthoma
1. SCC variation 2. Solitary, pink/flesh colored dome shaped nodule 3. Keratin plug in the middle (exophytic or endophytic lesions) 4. Sun exposure 5. Elderly people Can involute (curl up) spontaneously, but may persist Can cause local tissue destruction, so treat even though they are not metastatic Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm
51
Basal Cell Carcinoma
1. Cutaneous malignant neoplasm 2. Elderly males 3. Sun-exposed skin, face usually 4. PTCH1 mutations (patched/hedgehog) 5. Papule 6. Pearly, translucent edge with telangiectasia Grow slow, rarely become aggressive Nodular lesions that grow downward into the dermis, basophilic
52
Melanocytic Nevi
Well circumscribed, regular bordered uniformly pigmented areas Superficial nevus cells larger, pigmented, grow in nests Deeper nevus cells smaller/mature, less/no pigment, grow in cords
53
Junctional Nevi
Nuclei are round, little mitosis. Nests in dermal/epidermal junction
54
Compound Nevi
Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells
55
Intradermal nevi
Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.
56
Dysplastic nevus syndrome
``` Familial or sporadic. 80 or more dysplastic nevi Autosomal dominant (incomplete penetration) with mutations of CDKN2A. ``` High risk for melanoma and pancreatic cancer
57
Melanoma
Most dangerous skin cancer Adults 1. UV exposure biggest risk factor, also consider sunburns, fair complexion, dysplastic nevi, family history, old age. 2. Xeroderma pigmentosum, familial dysplastic nevus syndrome, immunosuppression are also risks 1, Most cases are de novo 2. Most important clinic sign: CHANGE IN COLOR OR SIGN OF A PIGMENTED LESION 3. Striking color variation within a lesion
58
Melanoma ABCDE's
``` Asymmetry (dangerous) Border (irregularity is dangerous) Color (variation is dangerous) Diameter (larger is dangerous) Evolution (changing phenotype is dangerous) ```
59
Genetic basis for familial melanoma?
CDKN2A mutations or oncogene BRAF (V600E activating mutation) BRAF mutations correspond to poor prognosis.
60
BRAF V600E inhibitor
Vemurafenib
61
Radial growth phase melanoma
Epidermis in situ. Can be prolonged in this stage. Cannot metastasize
62
Vertical phase melanoma
Can expand into deeper layers of tissue. Will initially spread via lymphatics, but can later spread hematogenously. Depth of invasion (Breslow Thickness) from the nodule is the STRONGEST prognostic indicator! (lymph invasion, mitotic rate and overlying ulceration all are also somewhat prognostic)
63
Lentigo maligna melanoma
Sun damaged areas in elderly. | 10-15 years before tumor development. In situ during this period
64
Superficial spreading melanoma
Most common type of melanoma Found in trunk in men and legs in women
65
Nodular melanoma
Very high growth phase, no radial growth phase. Bad prognosis. Male more than women. Trunk and legs common
66
Acral lentiginous melanoma
Not common in caucasians, but common in people of color. Palmar, plantar, sublingual, and even mucosal surface melanomas. Older women most susceptible.
67
Melanoma in situ histology
Asymmetric population in epidermis. Clusters throughout all levels of epidermis, and known as pagetoid cells Large cytoplasm, with dusty melanin
68
Invasive melanoma histology
Poorly formed nests in the dermis
69
Mycosis Fungoides
T cell lymphoma 1. Male dominant 2. African American dominant 3. 30-40 years old Epidermotrophism, with T cells transiting to lymph node, undergoing antigenic stimulation, and forming plaques and patches and tumors in the epidermis. Form an infiltrate of mycosis cells and form intraepidermal vesicles known as Pautrier microabscesses
70
3 stages of mycosis fungoides
Patch phase: many years. First stage, and may be perceived as nonspecific dermatitis. Lower trunk and buttocks. Irregular size and random distribution. Plaque phase: Well-demarcated lesions, annular and violaceous. May or may not be scaly. Can be de novo or from patches. Get more widespread with disease progression Tumor stage: From pre-existing lesions. Red, tense and shiny. Ulceration may occur. Over 1 cm diameter.
71
Sezary syndrome
Rare variant of T cell lymphoma 1. Erythroderma 2. Blood Involvement 3. Poor Prognosis Generalized exfoliative erythroderma Tumor cells (Sezary cells) in the peripheral blood. 1-3 median survival
72
Impetigo
Skin infection, highly infectious. 1. Children or immunocompromised adults 2. Staph usually, sometimes strep 3. Superficial vesicles that rapidly burst and replaced with thick yellowish dirty crust and erthema margin (honey-colored crust) Warm, humid conditions Can form bullous, usually group II staph Can mimic autoimmune blistering. Treat with topical antibiotics or orals if severe.
73
Staph Scalded Skin Syndrome (SSSS)
Exfoliative dermatitis. Epidermolytic toxins A and B (ET-A, ET-B) from group II staph, type 71. Cause splitting at the granular layer in children and infants. Sudden skin tenderness, then macular eruption, then easily rupturable, flaccid bullae. This is followed with desquamation of the skin in sheets. Face, neck, trunk, axillae, groins. Can also hit mucus membranes In renal insufficient adults, can also see this (Can't clear ET-A or ET-B)
74
Cellulitis
Diffuse inflammation of connective tissue and deep tissues. Expanding Erythema, edematous and tender Beta-hemolytic strep or coagulase positive staph (staph aureus)
75
Erysipelas
Distinctive cellulitis with an elevated border and rapid spreading. Men over 65, commonly in lower extremities. Treat with oral or IV antibiotics
76
HPV clearance of warts
6 months to 2-3 years. Self limited
77
Verruca Vulgaris
Most common wart type. On the hands.
78
Verruca plana
Flat warts. Face and dorsal hand
79
Verruca plantaris
Wart of foot
80
Verruca Palmaris
Wart of palm
81
Imiquimod
TLR7 activator in immune cells. Boosts response to warts
82
Wart histo
Papillomatous hyperplasia Prominent granular layer. Clumping of large irregular keratohyaline granules
83
Condyloma Accuimatum
HPV 6 and 11 most common causes of condylomata High risk cancer HPV is 16, 18, 31, 33 Cauliflower, plaquelike. Can be pearly Smooth, verrucous, lobulated Treat liek oher warts Ecophytic growths that are hyperkeratotic or parakeratotic Contain vacuolated keratinocytes
84
Herpes Simplex
Prodrome includes painful tingling and vescle clusters and erosions after rupture Travel along sensory nerves. Can cause recurrent disease in sensory ganglia due to UV light, trauma, fever, HIV, menstruation, stress Best diagnosed by PCR Self resolve, but you got it forever
85
VAricella Zoster
11-20 day incubation Success crops of pocks at different stages Because asynchronous, will see vesicles, pustules, crusted lesions, healing all simultaneousl Children more than adults
86
Shingles (Herpes Zoster)
Girdle like vesicular eruptions in thoraacic or lumbar distributions. May be facial at Trigeminal nerve. Parasethsia and pain precede it in the same dermatome Sequlae can be avoided with early antivirals Less inflammatory than herpes
87
Molluscum Contagiosum
``` Cutaneous infection Poxvirus Skin contact Solitary or dome-shaped, small waxy papules (resemble skin tags) Adults, think sexual transmission. Usually in kids ``` Spontaneous resolution Eosinophilic inclusion bodies
88
Scabies
Contagious, close personal or sexual contact Hands and feet Papules and burrows between fingers and sides of fingers Papular eruption that is excoriated, potentially infected Treat with permethrin Decomantimate home For burrows, deposit eggs in stratum corneum
89
Epidermophyton
Dermatophyte that only acts on epidermal keratin
90
Microsporum
Dermatophyte that acts on skin and hair
91
Trichophyton
Dermatophyte that acts on skin and hair
92
Dermatophytoses
Sandwich sign, with hyphae sandwiched betwweeen basket weave of normal corneal layer Variable appearance, often annular rings (tinea or ring worm) Manuum is on the hand, pedis is on the foot Cruris is on genitals Corporis is on body
93
Tinea Versicolor
Patches of hypo or hyperpigmentation Think young adults and usually female Warm climates Malassezia globosa, but also m fur fur Circular and macular spots Spaghetti and meatballs on his to
94
Urticaria
Hives Pink, edematous papules or plaques They can move Last less than 24 hours Sometimes, rarely, associated with Angioedema IgE mediated hypersensitivity (worry about anaphylaxis) Treat with oral antihistamines Topical Steroids ineffective
95
Exanthematous Drug Eruptions (Morbilliform rashes)
Type 4 Sensitivty Most common cutaneous drug eruption Monomorphic macule and papule lesions All over body, itchy. 2-14 days after the drug was started. Even if the drug was discontinued already! 1-2 week resolution, even if still on drug usually Corticosteroids or antihistamines help with itching
96
Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
Resembles morbilliform, but also is associated with facial edema, lymphadenapathy, fever and hepatic enzyme elevation Arthralgia also common. Eosinophilia not always present, but does not exclude diagnosis if absent. Can get other itis's (nephritis, myocarditis, thyroiditis, brain involvement) Can be fatal. Important to discontinue drug, find the source. Put on systemic corticosteroids
97
Eryhema multiforme
Common hands and feet. 3 or more color zones (targetoid lesions) Acral areas. Center is usually red or purple. 2 week before resolution. Triggered by infection mostly (herpes virus), but sometimes drugs. Self-resolves in a few weaks, and treat with corticosteroids if severe, otherwise just treat itchiness with antihistamines Giving antivirals will not help; the herpes has likely already resolved by the time this sequelae appears
98
Stevens Johnson Syndrome/Toxic Epidermal Necrolysis
SJS is less severe (10% body coverage) than TEN (30%+ body coverage) Starts with painful rash (rashes are usually itchy, not painful!) that has pretty generalized coverage, accompanied with fever, malaise, respiratory symptoms. Patches become bullae and necrotic, and epidermal detachment will occur Commonly induced by medications: Allopurinol, NSAIDs, Sulfa drugs, Anticonvulsants, Antibiotics Can cause sepsis, blindness with ocular involvement. Also has lip involvement commonly Remove the causal drug! IVIG acts to prevent apoptosis in these patients by blocking Fas ligand.
99
Leukocytoclastic vasculitis
Histologic diagnosis Small vessel vasculitis, neutrophil mediated 50% idiopathic Can be caused by infection (strep, Hep B or C, HIV) Can be a hypersentivitiy (antibiotics usually) Palpable purpora are a hallmark, especially on the legs. Urticarial lesions also possible, but not truly utricaria as they last for over 24 hours Nodules, ulceration and livedo reticularis are common (purple, lacy net-pattern on legs)
100
Henoch-Schonlein Purpose
Small vessel vasculitis In children more common IgA mediated DIF is used to diagnosse Triggered by strep infection or other respiratory infections Palpable purpura Buttocks and lower extremity Arthritis, abdominal pain, GI bleed, nephritis. Resolves 2-4 weeks.