Group 2, Column 1 Flashcards
1
Q
What other disorder does acute generalized exanthematous pustulosis mimic?
A
von Zumbusch pustular psoriasis
2
Q
What is the typical onset after drug exposure for AGEP to occur?
A
It occurs rapidly - within four days.
3
Q
Name the diagnosis.
- What vital sign abnormality is this associated with?
- What might this have that pustular psoriasis would not?
A
Acute Generalized Exanthematous Pustulosis (AGEP)
- High fever with small non-follicular, sterile pustules arising on background of edematous skin
- 50% of patients have purpuric or EM-like lesions, mucosal involvement, edema of hands/face, or bulla (pustular psoriasis WOULD NOT have these findings)
4
Q
What lab derangements are classically seen in acute generalized exanthematous pustulosis (AGEP)?
- What is a special test that can be used to identify the trigger?
A
- Leukocytosis with neutrophilia +/- eosinophilia
- Hypocalcemia
- Renal insufficiency
- Note patch test positive in majority of cases (50-60%)
5
Q
What are the most common offending agents associated with acute generalized exanthematous pustulosis (AGEP)?
A
- Beta-lactams
- Macrolide antibiotics
- Calcium channel blockers (diltiazem most common)
- Antimalarials
- Mercury exposure, radiocontrast and enterovirus are other known causes
6
Q
What is the histopathology of AGEP?
- What occurs in the epidermis? Dermis?
- Where is the infiltrate and what is it composed of?
A
- Subcorneal and intraepidermal spongiform pustules, prominent superficial dermal edema with eosinophils, and perivascular mixed inflammatory infiltrate with eosinophils
7
Q
What is the treatment for acute generalized exanthematos pustulosis (AGEP)?
A
- Stop offending drug
- Supportive therapy with topical steroids and antipyretics
8
Q
How would you discriminate between AGEP and pustular psoriasis?
- On clinical exam?
- On histology?
A
- 50% of patients with AGEP have purpuric or EM-like lesions, mucosal involvement, edema of hands and face, and bullae (not usually seen in pustular psoriasis)
- Presence of dermal edema and eosinophils and lack of significant acanthosis occurs in AGEP only
9
Q
Name the lesion and association we worry about in childhood.
- These lesions on the face can be associated with what TWO other diseases?
A
Angiofibromas
- Multiple angiofibromas with onset of childhood associated with tuberous sclerosis
- Lesions in this case are also called “adenoma sebaceum”
- Also associated with MEN1 and Birt-Hogg-Dubé syndrome
10
Q
Name the diagnosis.
A
Angiofibroma (specifically fibrous papule of the nose)
11
Q
What is the classic histopathology of angiofibroma?
- What cells are present in the dermis?
- What happens to the vessels?
A
- Stellate (dermal) stromal cells
- Concentric perivascular fibrosis
12
Q
Name the diagnosis.
A
Angiokeratoma of Mibelli
- Rare
- Several 1-5mm dark, red-grey papules over acral areas with verrucous surface
13
Q
Name three diseases associated with multiple facial angiofibromas.
A
- Tuberous sclerosis
- MEN1
- Birt-Hogg-Dubé
14
Q
What are the five types of angiokeratoma?
A
- Angiokeratoma of Mibelli
- Angiokeratoma of Fordyce
- Angiokeratoma corporis diffusum (associated with Fabry disease)
- Angiokeratoma circumscriptum
- Solitary and multiple angiokeratomas
15
Q
What is the classic histology of angiokeratoma?
- What occurs in the epidermis and to vessels?
A
- Dilated superficial dermal vessels
- Epidermal hyperplasia
- Rete hug vessels
16
Q
Name the diagnosis.
- When is the typical onset?
A
Angiokeratoma circumscriptum
- Large verrucous papules or plaques typically involving extremitiy/fingers/toes
- Onset in early childhood/infancy
17
Q
Name the diagnosis.
A
Angiokeratoma of Fordyce
- Seen in older men (scrotum) and females (vulva)
18
Q
Name the diagnosis.
- What is the typical distribution for this condition?
- What disorder is this condition classically seen in?
A
Angiokeratoma corporis diffusum
- Multiple lesions in childhood/adolescence
- Bathing suit distribution
- Seen in Fabry disease and other enzyme deficiencies
19
Q
Name the diagnosis.
A
Solitary angiokeratoma
- Single red to dark brown papule usually over lower extremity
20
Q
Name the diagnosis.
A
Arthropod bites
(Notice grouped lesions in an exposed area)
21
Q
Name the diagnosis.
A
Arthropod bite
22
Q
Name the clinical finding.
A
Beau’s lines
23
Q
Name the diagnosis.
- Onset?
- What syndrome may this be associated with?
- What is seen on histology? What other lesion is nearly identical on histology alone?
A
Becker’s nevus (aka Becker’s melanosis)
- Hyperpigmented, irregular plaque of upper torso
- Onset around puberty
- May have ipsilateral breast hypoplasia (Poland syndrome)
- Histology: increased basal melanocytes, acanthosis, elongated rete ridges, dermal smooth muscle hamartoma-like changes
- Hard to distinguish from smooth muscle hamartoma
24
Q
On histology alone, a Becker’s nevus is difficult to distinguish from what other lesion?
A
Smooth muscle hamartoma (see photo)
- A Becker’s nevus has dermal smooth muscle hamartoma-like changes
25
What are associations with Beau's lines?
* What causes Beau's lines?
**Temporal stoppage of growth at _proximal nail matrix_**
* **Chemotherapy**
* **Systemic illness**
* Mechanical trauma or skin diseases of proximal nail fold
* Stress on body (e.g. childbirth)
* Major injury
26
What are associations with **Becker's melanosis (Becker's nevus)**?
* Onset?
* What syndrome may this be associated with?
* Thought to be due to androgen-mediated hyperplasia
* More common in teenage and young adult males
* Onset around puberty
* Look for **ipsilateral breast hypoplasia** (Poland syndrome)
27
What is the classic histopathology of **Becker's melanosis (Becker's nevus)**?
* What happens in the epidermis? Dermis?
* What other lesion is nearly identical on histology alone?
* **Increased basal melanocytes**
* Acanthosis
* Elongation of rete ridges
* **Dermal smooth muscle hamartoma-like changes**
* Difficult to distinguish histologically from smooth muscle hamartoma
28
What activating mutations are seen in **blue nevi**?
* What other lesion has the same mutation?
* **GNAQ and GNA II** (seen in 83%), resulting in downstream MAPK pathway activation
* Also seen in **uveal melanoma**
29
Name the diagnosis.
**Blue nevus**
30
What disease is associated with **multiple blue nevi** or **epithelioid blue nevi**?
**Carney complex**
31
Name the four variants of **blue nevus**.
1. **Common blue nevus**
2. **Cellular blue nevus**
3. **Epithelioid blue nevus**
4. **Malignant blue nevus ( = melanoma)**
32
Name the diagnosis.
**Blue nevus**
33
What is the target of autoantibodies in **bullous pemphigoid**?
* What type of immunoglobulin (Ig) is involved?
* **IgG** autoantibodies bind to **hemidesmosomal** proteins
* **BP180** (a.k.a. BPAG2, primary mediator of BP)
* **BP230** (a.k.a. BPAG1)
34
Name the diagnosis.
**Bullous pemphigoid**
35
What is the classic histopathology for urticarial **phase bullous pemphigoid**?
* What occurs in the epidermis? DEJ?
* What special histologic finding may be seen at any phase of BP?
* **Eosinophilic spongiosis** with eosinophils lining up at DEJ and scattered in superficial dermis
* Vacuoles at DEJ (early blister formation)
* May see **flame figures (eosinophil granules of MBP)** at any phase
36
What is the classic histopathology for **_bullous phase_ bullous pemphigoid**?
* What occurs in the epidermis? What type of cells predominate the blister cavity?
* What composes the inflammatory infiltrate?
* What special histologic finding may be seen at any phase of BP?
* **Subepidermal split** with numerous **eosinophils in blister cavity**
* Dense dermal lymphoeosinophilic inflammation
* May see **flame figures (eosinophil granules of MBP)** at any phase
37
Name the diagnosis.
**Bullous pemphigoid**
38
What is the most sensitive skin test for **bullous pemphigoid**?
* What kind of pattern is seen and with what is it composed of?
* **DIF of perilesional skin**
* Look for **linear C3 (n-serrated pattern) and IgG** along DEJ
39
What are treatment options for **bullous pemphigoid**?
* First line?
* Second/third/last line?
* What can be used for mucosal-predominant disease?
* First line: **systemic steroids and steroid-sparing agents** (MMF, MTX, azathioprine, cyclophosphamide)
* Other options:
* Tetracyclines + nicotinamide (mild disease)
* Dapsone (mucosal-predominant disease)
* **Rituximab**
* IVIG, plasma exchange
40
Where do antibodies localize on salt-split skin DIF of perilesional skin with **BP** and **EBA**?
* Staining/pattern?
* **BP: "roof staining"** ( = **n-serrated** pattern on standard DIF)
* **EBA: "floor staining"** ( = **u-serrated** pattern on standard DIF)
41
Which IIF substrate is used in the following: **PV**, **PF** and **PNP**?
* **PV: monkey esophagus** ("Monkeys are so vulgar.")
* **PF: guinea pig esophagus** ("Guinea pigs eat foliage.")
* **PNP: rat bladder** ("Rats, I have cancer!")
42
What lab test correlates with **BP** disease activity, IIF or ELISA?
* What does it test for?
**ELISA levels** (IgG and IgE to BP180 and BP230)
43
Name the diagnosis.
**Calciphylaxis**
* Painful stellate or retiform purpuric plaques on legs
44
Name the diagnosis.
**Calciphylaxis**
* Painful stellate or retiform purpuric plaques on legs
45
What are notable associations with **calciphylaxis**?
* ESRD (increased calcium-phosphate product)
* Diabetes
* Hyperparathyroidism (i.e., partial parathyroidectomy may help treat calciphylaxis)
46
What is the treatment for **calciphylaxis**?
* Including procedures and medicines
* Treat underlying renal failure
* Partial parathyroidectomy
* Debridement
* **Sodium thiosulfate, pentoxifylline, apixaban** (and stop taking warfarin)
* Treat any infections
47
Name the diagnosis.
**Chondrodermatitis nodularis helicis**
48
What is the classic histopathology of **chondrodermatitis nodularis helicis** (CNH?)?
* Central ulceration with adjacent acanthosis overlying zone of fibrin
* Degenerating (eosinophilic) cartilage
49
Name the diagnosis.
* What is the source?
**Cutaneous larva migrans**
* Erythematous, serpiginous "tract" that is very itchy
* Typically occurs after walking barefoot in area contaminated by **animal feces** (eggs in animal feces --\> passed to soil and larvae hatch) --\> larvae **unable to penetrate basement membrane** of skin and die
50
What is the treatment of **cutaneous larva migrans**?
* **Topical/oral thiabendazole**
* Oral albendazole
* Oral ivermectin
* LN2
51
Name the diagnosis.
* What may be the only finding on exam?
* Classic distribution?
* What may be present on hands?
**Dermatitis herpetiformis**
* **Extremely itchy herpetiform vesicles arising on urticarial plaques**
* Vesicles rupture easily, so **excoriations usually only finding on clinical exam**
* Classically involves **symmetric extensor extremities, buttocks**, back/neck
* **Hemorrhagic palmoplantar lesions** may be present (see photo)
52
97% of those with dermatitis herpetiformis have which HLA II alleles?
* **HLA-DQ2 (90%)**
* HLA-DQ8 (7%)
53
**Dermatitis herpetiformis** is strongly associated with which other autoimmune diseases (3)?
* **Hashimoto's thyroiditis (****most common, \> 50%)**
* **Pernicious anemia**
* Type 1 diabetes
54
What are the autoantigens and antibodies involved in **dermatitis herpetiformis**?
* In the gut?
* In the skin? (2)
* Immunoglobulin (Ig) type?
Autoantigens:
* Epidermal transglutaminase
* Tissue transglutaminase (endomysial; a.k.a. TTG)
* **TTG2:** responsible for **gut** involvement
* **TTG3:** responsible for **skin** involvement
Antibody:
* IgA
55
Name the diagnosis.
* Most common cause in children? Adults?
**Erythema nodosum**
* Erythematous subcutaneous nodules commonly over pretibial areas
* Progress to bruise-like color, +/- fever, arthralgias, malaise
* Most common cause in children: streptococcal infection
* Most common causes in adults: sarcoidosis, IBD and medications (especially OCPs)
56
Name the diagnosis.
* Most common cause in children? Adults?
**Erythema nodosum**
* Erythematous subcutaneous nodules commonly over pretibial areas
* Progress to bruise-like color, +/- fever, arthralgias, malaise
* Most common cause in children: streptococcal infection
* Most common causes in adults: sarcoidosis, IBD and medications (especially OCPs)
57
What is the histopathology for **dermatitis herpetiformis**?
* In the epidermis? The dermal papillae?
* What other condition does this look like under the microscope?
* **Subepidermal** **bullae**
* **Neutrophilic papillitis** (neutrophils "stuffing" dermal papillae)
* Looks like linear IgA bullous dermatosis under the microscope
58
What do you see on DIF for **dermatitis herpetiformis**?
* What is the pattern, and what composes it?
**Granular IgA deposits** +/- C3 in dermis
59
What is the treatment for **dermatitis herpetiformis**?
* What can help with just skin disease? Both skin and GI disease?
* What compound can trigger a flare?
* **Dapsone** (check for G6PD deficiency before starting)
* No effect on GI disease/lymphoma risk
* Sulfapyridine can be used if dapsone cannot
* **Gluten-free diet** (controls both skin and GI disease, decreases risk of GI lymphoma)
* **Avoid iodide**, which may trigger flare
60
What is the most common **panniculitis**, and what is its type of immune response?
**Erythema nodosum**
* Delayed hypersensitivity response (Th1 cytokine pattern) to various antigens
61
What are the most common causes of **erythema nodosum**?
Think about:
* Infections
* Drugs
* Other conditions
* Idiopathic (most common)
* **Streptococcal infections (#1 identifiable cause)**
* Other infections (bacterial GI infections, viral URIs, TB, histoplasmosis, coccidioidomycosis)
* **OCPs, sulfonamides, NSAIDs**
* Sarcoidosis, IBD
62
What is **Löfgren's Syndrome**?
* What is its general prognosis?
Type of **sarcoidosis** that presents with:
* **Erythema nodosum**
* **Hilar lymphadenopathy**
* Fever
* Polyarthritis
* Uveitis
Associated with a _good prognosis_
63
What is the classic histopathology of **erythema nodosum**?
* What is found it the fat septae?
* What cells are present in early lesions?
* **Septal panniculitis** with **thickening/fibrosis of septae**
* **Neutrophils** seen in early lesions
* **Miescher's microgranulomas** (small histiocytic aggregates in subcutaneous fat septae)
* +/- thrombophlebitis
64
What are treatment options for **erythema nodosum**?
* What if it's Behcet's associated? IBD associated?
* Treat underlying medical issue (if present)
* Bed rest/elevation
* **NSAIDs**
* SSKI (potassium iodide)
* Colchicine (if Behcet's associated)
* Dapsone
* TNF-alpha inhibitors (if IBD associated)
65
Name the diagnosis.
* What should you look for to make the diagnosis?
**Factitial dermatitis (dermatitis artefacta)**
* Geographic excoriations/erosions/ulcers
* Look for acute angles
66
Name the diagnosis.
* What should you look for to make the diagnosis?
**Factitial dermatitis (dermatitis artefacta)**
* Geographic excoriations/erosions/ulcers
* Look for acute angles
67
What are the most common medications causing a **fixed drug eruption (FDE)**?
* Most common cause? Most common cause on genitalia?
* Classic cause of non-pigmented FDE?
* **Sulfonamides (75% of cases; #1 cause on genitalia)**
* NSAIDs (especially **naproxen**; predilection for lips)
* Tetracyclines
* **Phenolphthalein** (previously in laxatives)
* **Pseudoephedrine** (Sudafed; classic cause of **non-pigmented FDE**)
68
Name the diagnosis.
* Where is commonly affected?
* When is its onset?
**Fixed drug eruption**
* Most commonly affects oral and genital mucosa
* **Well-demarcated, edematous plaques with erythematous/violaceous hue**
* Commonly get **central dusky hue, bulla or erosion**
* Prominent post-inflammatory hyperpigmentation
* Onset is **1-2 weeks after initiating offending drug**
69
Name the diagnosis.
* Where is commonly affected?
* When is its onset?
**Fixed drug eruption**
* Most commonly affects oral and genital mucosa
* **Well-demarcated, edematous plaques with erythematous/violaceous hue**
* Commonly get **central dusky hue, bulla or erosion**
* Prominent post-inflammatory hyperpigmentation
* Onset is **1-2 weeks after initiating offending drug**
70
How long does a **fixed drug eruption** take to develop?
* Initial episode?
* Subsequent episodes?
* **Initial episode:** develops 1-2 weeks after administration of causative drug
* **Subsequent episodes:** eruption recurs at same site **very rapidly** after reexposure (30 min to 8 hrs)
71
What is the classic histopathology of **fixed drug eruption** (FDE)?
* What is the inflammatory pattern?
* What kind of infiltrate is present?
* How is the corneum affected?
* What may be present if it is not the first occurrence?
* **Vacuolar interface dermatitis**
* **Polymorphous infiltrate** (including eosinophils and neutrophils)
* **Acute (normal) stratum corneum**
* **Chronic dermal changes may be present** if not first occurrence
* Papillary dermal fibrosis
* **Melanin pigment incontinence in perivascular location**
72
What skin testing can be performed to help identify the culprit medication causing a **fixed drug eruption**?
**Patch testing within a site of prior involvement**
73
Name the diagnosis.
* What is this associated with?
* What other condition does this look like histologically?
**Geographic tongue**
* Well-demarcated patches of atrophy with surrounding erythema surrounded by white/yellow scalloped border on dorsal tongue
* **Associated with psoriasis and atopic dermatitis**
* Histologically looks like psoriasis
74
What is important to know about the virus ***Coxsackie A6***?
* What is it associated with?
* Causes more widespread and severe vesiculobullous eruptions
* Associated with atypical HFMD presentations, including **eczema coxsackium** (in atopics; see photo), **Gianotti-Crosti-like eruptions** and **onychomadesis** (nail matrix arrest at time of acute infection)
75
Name the diagnosis.
* Areas typically affected?
* Most common causes? (3)
**Hand-foot-and-mouth disease**
* Vesicular eruption most commonly involving palms/soles/buttocks/oral cavity
* Erythematous macules and oval, deep-seated erythematous vesicles and bulla with gray center
* Caused by ***Coxsackie A16 virus*** (\> *Coxsackie A6* and *Enterovirus*)
76
Name the diagnosis.
* Areas typically affected?
* Most common causes?
**Hand-foot-and-mouth disease**
* **Vesicular eruption** most commonly involving palms/soles/buttocks/oral cavity
* Erythematous macules and oval, deep-seated erythematous vesicles and bulla with **gray center**
* Caused by ***Coxsackie A16* virus** (\> *Coxsackie A6* and *Enterovirus*)
77
What virus causes **hand-foot-and-mouth disease**? (3)
* Which is most common?
***Coxsackie A16* virus (most common)** \> *Coxsackie A6* and *Enterovirus*
78
Name the diagnosis.
* Areas typically affected?
* Cause?
**Hand-foot-and-mouth disease**
* Vesicular eruption most commonly involving palsm/soles/buttocks/oral cavity
* Erythematous macules and oval, deep-seated erythematous vesicles and bulla with gray center
* Caused by ***Coxsackie A16* virus** (\> *Coxsackie A6* and *Enterovirus*)
79
Name the diagnosis.
* What glands are thought to be affected?
* How might sinus tracts present?
**Hidradenitis suppurativa**
* Affects **apocrine gland-bearing areas (axilla, inguinal, anogenital, inframammary)**
* Inflammatory nodules, sterile abscesses
* Can develop sinus tracts, hypertrophic scars, contractures
* Superficial sinus tracts present as **double-ended comedones**
80
What viral exanthem is this finding classically associated with?
**Hand-Foot-Mouth (HFM) disease** (caused by *Coxsackie A16* and *A6*) is associated with **onychomadesis**
81
Name the diagnosis.
* What glands are thought to be affected?
* How might sinus tracts present?
**Hidradenitis suppurativa**
* Affected **apocrine gland-bearing areas (axilla, inguinal, anogenital, inframammary)**
* Inflammatory nodules, **sterile abscesses**
* Can develop sinus tracts, hypertrophic scars, contractors
* Superficial sinus tracts present as **double-ended comedones**
82
What comprises the **follicular occlusion tetrad**?
1. **Hidradenitis suppurativa**
2. **Acne congoblata**
3. **Dissecting cellulitis of the scalp**
4. **Pilonidal cyst**
83
What are the associations seen in **hidradenitis suppurativa** patients?
* Obesity
* Smoking
* Metabolic syndrome
* Depression
84
What is the classic histopathology of **hidradenitis suppurativa**?
* What glands may be involved?
* Suppurative folliculitis with abscess formation
* Follicular plugging
* Granulation tissue
* Inflammation "spills over" to **apocrine glands**
85
Name the diagnosis.
* Onset?
* What is present on palms and soles?
* What areas are spared?
**Icthyosis vulgaris**
* Fine white scales on extensor surfaces
* **Flexures spared**
* Hyperlinearity palms/soles, atopic diathesis
* Presents few months after birth to early childhood
86
Name the diagnosis.
* Onset?
* What is present on palms and soles?
* What areas are spared?
**Ichthyosis vulgaris**
* Fine white scales on extensor surfaces
* **Flexures spared**
* Hyperlinear palms/soles, atopic diathesis
* Presents few months after birth to early childhood
87
What is the inheritance pattern pattern of **ichthyosis vulgaris**?
**Autosomal dominant**
88
What gene and gene product is involved in **ichthyosis vulgaris**?
***FLG*, which encodes profillagrin**
89
What are the histopathologic features of **ichthyosis vulgaris**?
* How is the epidermis and corneum affected?
* Attenuated/absent granular layer
* Orthohyperkeratosis
90
Name the diagnosis.
**Kaposi sarcoma**
91
What are the four clinical variants of **Kaposi sarcoma** (KS)?
* Who is classically affected with each type?
1. **Classic KS**: Mediterranean or Ashkenazi Jewish descent; elderly men; initially on distal extremities
2. **African endemic**: Young African males; fatal
3. **Iatrogenically immunocompromised**: transplant/cancer/autoimmune patients
4. **AIDS-associated**: gay men; initially on midface and trunk
92
Name the diagnosis.
**Kaposi sarcoma**
93
Name the diagnosis.
**Kaposi sarcoma**
94
What virus is associated with **Kaposi sarcoma**?
* What immunohistochemistry can be done to diagnose this on histology?
**HHV-8**
* Do immunohistochemistry for **LANA-1** of HHV-8 (latency-associated nuclear antigen); 100% sensitive and specific
95
What is the classic histopathology of **Kaposi sarcoma**?
* What immune cells are involved?
* What special sign may be seen?
* Infiltrative small vessels with bland endothelium associated with plasma cells
* RBC extravasation and hemosiderin
* Look for **promontory sign** (newly formed vessel projects into existing space)
96
Name the disorder.
**Lichen sclerosis**
* **Sclerotic, ivory-white,** atrophic and flat-topped papules and plaques
97
Name the disorder.
**Lichen sclerosis**
* **Sclerotic, ivory-white,** atrophic and flat-topped papules and plaques
98
Name the disorder.
**Lichen sclerosis**
* **Sclerotic, ivory-white,** atrophic and flat-topped papules and plaques
99
What is lichen sclerosus called when it involves the penis?
**Balanitis xerotica obliterans (BXO)**
* A common cause of phimosis
100
80% of patients with **lichen sclerosis** have which **autoantibodies**?
* What immunoglobulin (Ig) is involved?
**IgG autoantibodies against ECM-1** **(a BMZ glycoprotein)**
101
What is the most common autoimmune disease seen in association with **lichen sclerosis**?
* What are other less common disease associations?
**Autoimmune thyroid disease (15%)**
Can also see pernicious anemia, localized scleroderma/morphea, psoriasis and vitiligo but much less common
102
What is the classic histopathology of **lichen sclerosus**?
* Corneum?
* Dermis?
* What is the inflammatory pattern, and what composes it?
**"Red, white and blue sign"**
* Orthohyperkeratotic stratum corneum
* Hyalinized/edematous papillary dermis
* Band-like (lichenoid) lymphocytic infiltrate
103
Name the diagnosis.
**Lichen simplex chronicus**
* Well-defined plaques with **lichenification**, hyperpigmentation and varying erythema
104
What is the classic histopathology of **lichen simplex chronicus**?
* What happens in the epidermis? Corneum?
* What happens in the dermis?
* How does its histology compare with prurigo nodularis?
* Orthohyperkeratosis
* **Hypergranulosis**
* **Irregular acanthosis**
* Papillary dermal fibrosis (vertical collagen)
* Not as "dome-shaped" as prurigo nodularis
105
Name the diagnosis.
* What kind of distribution classically occurs?
**Lichen striatus**
* Asymptomatic 2-4mm pink or hypopigmented scaly papules, **linear/Blaschkoid** distribution
* Post-inflammatory hypopigmentation may persist for months to years
* Nail dystrophy may occur
106
Name the diagnosis.
* What kind of distribution classically occurs?
**Lichen striatus**
* Asymptomatic 2-4mm pink or hypopigmented scaly papules, **linear/Blaschkoid** distribution
* Post-inflammatory hypopigmentation may persist for months to years
* Nail dystrophy may occur
107
Name the diagnosis.
* What kind of distribution classically occurs?
**Lichen striatus**
* Asymptomatic 2-4mm pink or hypopigmented scaly papules, **linear/Blaschkoid** distribution
* Post-inflammatory hypopigmentation may persist for months to years
* Nail dystrophy may occur
108
Name the clinical finding.
* Where is the classic site for this condition?
* Buzzword?
**Lipodermatosclerosis**
* Acute: rubor, dolor, calor
* Chronic: well-defined induration, hyperpigmentation; **"inverted champagne bottle"** from sclerosis
* Common site: **medial lower leg**, superior to malleolus
109
Name the clinical finding.
* Where is the classic site for this condition?
* Clinical exam buzzword?
**Lipodermatosclerosis**
* Acute: rubor, dolor, calor
* Chronic: well-defined induration, hyperpigmentation; **"inverted champagne bottle"** from sclerosis
* Common site: **medial lower leg**, superior to malleolus
110
What is the classic histopathology of **lipodermatosclerosis**?
* What happens in the septae?
* What kind of change occurs to the fat?
* **Septal thickening and fibrosis**
* **Cystic fat necrosis**
* **Lipomembranous change** (cystic cavities lined by hyaline membranes in fat)
111
What is the treatment of **lipodermatosclerosis**?
* Leg compression and elevation
* **Danazole, pentoxifylline**
112
What are the common medication culprits of **lichenoid drug?**
* Name at least the first five most common.
1. **HCTZ**
2. **B-blockers**
3. **ACE inhibitors**
4. **Antimalarials**
5. **Gold salts**
6. TNF-alpha inhibitors
7. NSAIDs
8. Penicillamine
9. Quinidine
113
Name the diagnosis in this patient who took HCTZ (or a beta-blocker, or ACE inhibitor, or antimalarial, or gold...).
* What is the average latency period before this classically occurs?
**Lichenoid drug eruption (drug-induced LP)**
* Symmetric, flat-topped erythematous or violaceous papules, often grouped and confluent
* Favors trunk and extremities
* More eczematous or psoriasiform than classic LP
* Wickham's striae absent
* Spares mucous membranes
* Average latency period of 1 year
114
Name the diagnosis in this patient who took HCTZ (or a beta-blocker, or ACE inhibitor, or antimalarial, or gold...).
* What is the average latency period before this classically occurs?
**Lichenoid drug eruption (drug-induced LP)**
* Symmetric, flat-topped erythematous or violaceous papules, often grouped and confluent
* Favors trunk and extremities
* More eczematous or psoriasiform than classic LP
* Wickham's striae absent
* Spares mucous membranes
* Average latency period of 1 year
