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MSK Week 4 > ICL 1.3: Dermatopathology > Flashcards

ICL 1.3: Dermatopathology Flashcards

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1
Q

what are the types of inflammatory dermatoses?

A
  1. acute
  2. chronic
  3. blistering diseases
  4. disease of appendages
  5. fibrosing dermopathy
  6. panniculitis
  7. vasculitis
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2
Q

which inflammatory dermatoses are acute?

A
  1. urticaria
  2. spongiotic dermatitis
  3. erythema multiform
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3
Q

which inflammatory dermatoses are chronic?

A
  1. lichen planus
  2. lupus
  3. psoriasis vulgaris
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4
Q

which inflammatory dermatoses are blistering diseases?

A
  1. pemphigus vulgaris
  2. bullous pemphigoid
  3. dermatitis herpetiformis
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5
Q

which inflammatory dermatoses are diseases of cutaneous appendages?

A

acne vulgaris

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6
Q

which inflammatory dermatoses are fibrosing dermopathy?

A

scleroderma

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7
Q

which inflammatory dermatoses are panniculitis?

A

erythema nodosum

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8
Q

which inflammatory dermatoses are vasculitis?

A

leukocytoclastic vasculitis

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9
Q

what is urticaria?

A

an acute dermatoses that is a type I hypersensitivity reaction

so most of it is IgE mediated but others can cause direct mast cell degranulation

what happens is that an allergen binds to a cell that has been sensitized by IgE which then leads to mast cell degranulation –> histamine release –> vasodilation –> edema

hallmark = wheal!! aka hive! –> individual wheals persist less than 24 hours, but new lesions develop

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10
Q

what histological findings are consistent with urticaria?

A
  1. dermal edema
  2. EOSINOHPILS
  3. PMNs in capillaries
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11
Q

what is spongiotic (eczematous) dermatitis?

A

it’s an acute dermatoses that is the most common dermatitis!!

  1. atopic, contact, nummular eczema
  2. pityriasis rosea
  3. seborrheic dermatitis
  4. drug eruption

**it is a cause of erythroderma = total body erythema and scaling

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12
Q

where can spongiotic dermatitis be observed on the body? what will it look like?

A

the site depends on the type of of spongiotic dermatitis

  1. atopic –> flexural surfaces: elbow, knees, etc.
  2. seborrheic –> scalp, T-zone, intermammary, axilla
  3. irritant/contact –> at the site of contact

the clinical appearance then depends on the age of the lesion

  1. acute = erythematous, moist papules/vesicles
  2. subacute = erythematous, scaly papules/plaques
  3. chronic = lichenified plaques
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13
Q

what are some examples of spongiotic dermatitis?

A

contact dermatitis = poison ivy, allergy to soaps, detergents, deodorants, etc.

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14
Q

which three dermatoses can cause erythroderma?

A
  1. psoriasis vulgaris
  2. spongiotic dermatitis

erythroderma = total body erythema and scaling

  1. cutaneous T-cell lymphoma
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15
Q

what is the pathology of spongiotic dermatitis?

A
  1. Ag contacts epidermis
  2. Ag picked up by LC
  3. LC/Ag migrates to LN
  4. LC presents Ag to CD4+ T cell
  5. sensitized T cells go to affected area and do cytokine release, more inflammation, edema into epidermis

this all leads to spongiosis +/- vesicles

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16
Q

what histological findings are consistent with spongiotic dermatitis?

A
  1. extensive spongiosis = increased intercellular edema

2. epidermal acanthosis = increased thickness of the spinous layer of the epithelium

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17
Q

what is erythema multiforme?

A

it’s an acute dermatoses that is a hypersensitivity reaction

it’s an interface injury so there is damage to the basal layer and you will see necrotic keratinocytes

the epidermal injury will be out of proportion to the amount of inflammation seen!

usually skin involvement only; no systemic symptoms and caused by HSV

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18
Q

what are the stages of erythema multiforme?

A
  1. erythema multiforme
  2. stevens-johnson syndrome
  3. toxic epidermal necrolysis (TEN)
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19
Q

what is stevens-johnson syndrome?

A

a progression of erythema multiforme that involves the skin AND mucous membranes

usually due to medications or mycoplasma

looks like vampire child lips…

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20
Q

what is toxic epidermal necrolysis?

A

a progression of erythema multiforme that is the most severe end of the spectrum and involves TOTAL skin sloughage; they literally look like burn patients…

usually due to medications

histologically, the epidermis is literally peeling off and totally disattached from the dermis underneath

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21
Q

what are some of the causes of erythema multiforme?

A
  1. medication
  2. herpes simplex virus
  3. mycoplasma
  4. collagen vascular diseases
  5. malignancies (lymphoma, carcinoma)
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22
Q

what are lichenoid dermatoses? which diseases are lichenoid dermatoses?

A

a chronic dermatoses that involves:

  1. vacuolar basal layer damage
  2. eosinophilic necrosis of keratinocytes
  3. band-like lymphocytic infiltrate**
    ex. lichen planus and lupus erythematosus
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23
Q

what is lichen planus?

A

a lechenoid dermatoses which means it’s chronic and there is vacuolar basal layer damage, eosinophilic necrosis of keratinocytes and *band-like lymphocytic infiltrate

the sites effected are skin or mucous membranes often on extensor surfaces, oral mucosa, genitalia +/- scalp

the lesions are usually symmetrical = on BOTH elbows, wrist, knees, etc.

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24
Q

what is the appearance of lichen planus?

A

5 Ps = pruritic, polygonal, purple, papules AND plaques*

the lesions will heal with hyperpigmentation because of destruction of the basal layer which is what houses melanocytes!

Koebner phenomenon = new lesions develop at sites of injury

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25
Q

what is Koebner phenomenon?

A

when new lesions develop at sites of injury

seen in lichen planus

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26
Q

what is the pathology of lichen planus?

A

possibly a delayed hypersensitivity reaction but we don’t really know….

so maybe there is an unknown antigen in basal cells that causes the lymphs to destroy the basal cells and leads to vacuolar/dropic degeneration = intracytoplasmic accumulation of water

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27
Q

what are the histological findings consistent with lichen plus?

A
  1. colloid/Civatte bodies (swollen cells)
  2. squamatization of basal layer
  3. pigment incontenence = loss of melanin into dermis which leads to hyperpigmentation
  4. hyperkeratosis, hypergranulosis and acanthosis following injury of the epidermis
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28
Q

what are the 3 subtypes of lupus erythematosus?

A
  1. systemic LE = skin + other organs
  2. subacute LE = skin +/- other organs
  3. discoid LE = skin only
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29
Q

what’s the hallmark symptom of systemic lupus erythematosus?

A

malar rash = butterfly rash

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30
Q

what’s the hallmark symptom of subacute lupus erythematosus?

A

annular plaques

they have build up borders with scales

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31
Q

what are the hallmark symptoms of discoid lupus erythematosus?

A
  1. follicular plugging = yellow looking dots which are hyperkeratosis at the follicular opening
  2. erythematous plaques
  3. hypo and hyperpigmentation

scarring happens open and discoid LE especially effects the head and neck

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32
Q

what is the pathogenesis of lupus erythematosus?

A

it’s an autoimmune reaction to basal keratinocytes (as well as other end organ targets) which leads to:

  1. hydropic degeneration
  2. keratinocyte necrosis
  3. BM thickening
  4. pigment incontinence –> hyperpigmentation because the basal membrane is being destroyed and it houses melanocytes
  5. dermis develops vasodilation and edema (lots of while on LM)
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33
Q

what is follicular plugging?

A

a symptom of discoid lupus erythematosus

it’s when initial injuries cause reactive hyperkeratosis, especially in the follicles which leads to follicular plugging

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34
Q

what immunofluorescence findings are consistent with lupus?

A

granular IgG and C3 along DE junction (BM) = lupus band test!

with discoid LE, the lupus band test will only be positive in lesional skin only!!

with systemic and subacute LE, the lupus band test will be positive in both lesional and non-lesional skin

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35
Q

what is psoriasiform?

A

a chronic dermatoses with regular elongation and widening of the rete ridges

ex. psoriasis

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36
Q

what is psoriasis vulgaris? what patient population does it effect?

A

a type of psoriasiform = chronic dermatoses with regular elongation and widening of the rete ridges

onset is in early adulthood and there is an HLA association

may be associated with arthritis

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37
Q

what are the symptoms and lesions associated with psoriasis vulgaris?

A
  1. erythematous, well-demarcated plaques with silver scale often on extensor surfaces and symmetrical
  2. nails have pitting and oil-spots
  3. Koebner phenomenon = new lesions develop at sites of injury
  4. can cause erythroderma =
    total body erythema and scaling
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38
Q

which two dermatoses can cause Koebner phenomenon?

A
  1. psoriasis vulgaris

2. lichen planus

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39
Q

what is the pathogenesis of psoriasis vulgaris?

A

it’s unknown, we have no idea why it happens but it’s probably an immune related response that causes keratinocytes to proliferate extremely fast

this causes you to lose the normal appearance of the stratum corneum since the cells retain their nuclei since they’re proliferating so fast

there is regular acanthosis and elongation and widening of rete ridges and dermal papillae

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40
Q

what histologic findings are consistent with psoriasis vulgaris?

A
  1. parakeratosis = retained nuclei in the stratum corneum
  2. hypogranulosis = basically no granular cell layer
  3. supra papillary plate thinning
  4. PMNs migrate into the epidermis and stratum corneum = Munro’s microabscesses
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41
Q

what is the hallmark sign of psoriasis vulgaris?

A

Auspitz sign

this is pinpoint bleeding if the skin is scratched

it happens because of suprapappillary plate thinning – so the dermal papilla are delegated and the epidermis is so thin so when you scratch the capillaries in the papilla just bleed

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42
Q

how are blistering diseases classified?

A

they are classified according to histologic level of the split

so where in the epidermis do they split down to?

ex. sub corneal, supra basal, subepidermal etc.

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43
Q

what is a routine biopsy vs. an immunofluorescence biopsy?

A

routine biopsy needs to be from lesional skin – but take it from the edge of the blister not the center (duh)

biopsies for immunofluorescence should be taken from perilesional skin so not the actual blister but right next to it

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44
Q

what is pemphigus vulgaris? what patient population does it effect?

A

a blistering dermatoses that effects middle aged people

the blisters are often at sites of pressure and oral lesions are also common!!

the blisters are *flaccid vesicles/bullae so they rupture easily and can therefore lead to superficial erosions

since the blisters rupture so easily and exposure the skin, this skin condition could be potentially fatal due to the high risk of infection

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45
Q

what is the hallmark sign o pemphigus vulgaris?

A

Nikolsky sign

pressure on edge of blister causes blister to expand in the direction of where you put pressure

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46
Q

what’s the pathogenesis of pemphigus vulgaris?

A

it’s an autoimmune disease where IgG targets desmoglein 3, an intercellular cadherin

desmogleins are the transmembrane proteins in macula adherens junctions aka desmosomes!!

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47
Q

what histological findings are consistent with pemphigus vulgaris?

A
  1. acantholysis = loss of intercellular connections in spinous layer
  2. suprabasilar vescile
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48
Q

what immunofluorescence findings are consistent with pemphigus vulgaris?

A

intercellular IgG between spinous keratinocytes

it’s a net-like pattern (really does look like a net)

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49
Q

what is bullous pemphigoid? what patient population does it effect?

A

a blistering dermatoses that is usually self-limited and effects middle aged to elderly people

it effects the skin and mucous membranes just like pemphigus vulgaris but it tends to effect mucous membranes less than PV

effects sites of friction = inner thighs, AC fossa, axillae, groin, etc.

the blisters are tense bull (tight), sub epidermal, filled with clear fluid and heal without scarring

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50
Q

what’s the pathogenesis of bulls pemphigoid?

A

IgG+C3 bind to hemidesmosomes (DE jxn)

since the basal layer is the only thing attached via hemidesmosomes these are sub epidermal vesicles

the blister cavity is filled with lymphs, PMNs, and TONS of eosinophils!!

51
Q

what are the immunofluorescence findings consistent with bullous pemphigoid?

A

linear IgG and C3 along the DE junction

so not net-like like pemphigus vulgaris

52
Q

what is dermatitis herpetiformis? what patient population does it effect?

A

a blistering dermatoses that usually effects young adults

it’s associated with gluten-sensitivity enteropathy like celiac disease

grouped vessies on an erythematous base at extensor surfaces like elbows, shoulders, lower back etc. are what you will see

53
Q

what’s the pathogenesis of dermatitis herpetiformis?

A

IgA autoantibodies against anchoring fibrils in BM – this makes sense because IgA is the antibody predominantly in the GI tract!

54
Q

what histological findings are consistent with dermatitis herpetiformis?

A
  1. sub epidermal vesicle at the tips of the dermal papillae

2. PMNs in the blister cavity and the tips of the dermal papilla

55
Q

what immunofluorescence findings are consistent with dermatitis herpetiformis?

A

granular IgA deposits along the tips of the dermal papillae

56
Q

what are the steps in a pimple forming? aka acne vulgaris

A

a disorder of cutaneous appendages

  1. androgen stimulation of sebum secretion
  2. accumulation of shed keratin and sebum plug up the follicle
  3. inflammation and bacteria in the follicle
  4. follicle ruptures and even more inflammation!!

this is a pimple (:

57
Q

what is the difference between a whitehead and a blackhead?

A

blackhead = open comedones –> the lesion is open to the outside environment and oxidation is what makes it black

whitehead = closed comedones –> the lesion is covered by epithelium

58
Q

what is acne vulgaris? what patient population does it effect?

A

it effects the pubertal age group or people in hyperandrogenic states

patients will present with erythematous papules/pustules/cysts = wide variety!

larger lesions may heal with scarring, particularly when they rupture (aka don’t pop your pimples)

59
Q

what is scleroderma? what patient population does it effect?

A

it usually effects F > M that are 50-60 years old

it causes the skin to have tightening, induration, ulceration, autoamputation of digits (because skin is so tight)

it can also effect blood vessels, lungs, GI tract, kidneys which could lead to Raynaud’s phenomenon, dysphagia, respiratory insufficiency, proteinuria, hypertension

60
Q

what are the types of scleroderma?

A
  1. diffuse scleroderma

2. limited scleroderma

61
Q

what is diffuse scleroderma? which antibody is associated with it?

A
  1. Systemic involvement
  2. Skin and visceral organs involved
  3. Rapid progression
  4. Anti-SCL70 Ab***
62
Q

what is limited scleroderma?which antibody is associated with it?

A
  1. morphea = skin and subcutaneous involvement only (no organs) –> the deep dermis contracts and pulls down everything making the skin look scarred
  2. anti-centromere antibody
  3. CREST

Calcinosis

Raynaud’s

Esophageal dysmotiligy

Sclerodactyly

Telangiectasia

63
Q

which histological findings are consistent with scleroderma?

A
  1. sclerosis and hyalinization of collagen bundles (doesn’t even look like collagen bundles anymore)
  2. loss of perieccrine fat around the eccrine coils
  3. inflammation = lymphs, histiocytes, plasma cells
  4. blood vessel involvement which inhibits blood flow
64
Q

what is panniculitis?

A

inflammation of the subcutaneous layer of fat

it’s a syndrome characterized by recurring fever and usually painful inflammatory and necrotic nodules in the subcutaneous tissues especially of the thighs, abdomen, or buttocks

65
Q

what is erythema nodosum?

A

a type of panniculitis that effects F>M in their 20s-40s

patients will present with painful, indurated subcutaneous nodules in their anterior lower legs

66
Q

which conditions are associated with erythema nodosum?

A
  1. strep throat
  2. inflammatory bowel disease
  3. TB
  4. fungi
  5. drugs
  6. sarcoidosis
  7. malignancy

so all these conditions predispose you to developing erythema nodosum!

67
Q

what histological findings are consistent with erythema nodosum?

A
  1. subcutaneous involvement
  2. septal widening
  3. inflammation within the septae

early on you’ll see PMNs and edema

later on you’ll see giant cells and fibrosis

68
Q

what is leukocytoclastic vasculitis? what patient population does it effect?

A

it effects any age!!

patients present with palpable purpura usually in gravity-dependent areas aka lower extremities

it effects small arteries, capillaries and veins

69
Q

what is the pathogenesis of leukocytoclastic vasculitis? what are some of the possible causes?

A

type III immune complex reaction where immune-complexes deposit in vessel walls of the capillaries of the skin

it’s possible caused byL

  1. infections (strep, TB, HIV, CMV, HBV/HCV, etc.)
  2. drugs (ASA, PCN, etc.)
70
Q

which conditions are associated with leukocytoclastic vasculitis?

A
  1. AI: SLE, IBD, RA, MCTD, etc
  2. IC: cryoglobulinemia, HSP, PAN, Wegener’s, Churg-Strauss
  3. sarcoidosis
  4. malignancies
71
Q

which histological findings are consistent with leukocytoclastic vasculitis?

A
  1. perivascular PMNs
  2. leukocytoclasis = fragmentation of PMNs
  3. small vessel destruction
  4. extravasated RBCs
  5. fibrin deposition within vessel walls which prevents blood flow and causes the purple lesions that patients present with(dark pink on historic slide)
72
Q

which neoplasias effect the epidermis?

A
  1. inclusion cysts
  2. seborrheic keratosis
  3. actinic keratosis
  4. squamous cell carcinoma in situ
  5. invasive squamous cell carcinoma
  6. basal cell carcinoma
73
Q

which neoplasias are melanocytic?

A
  1. lentigo
  2. nevus
  3. dysplastic nevus
  4. melanoma in situ
  5. invasive melanoma
74
Q

which neoplasias effect the dermis?

A
  1. vascular

hemangioma, pyogenic granuloma, kaposi’s sarcoma, angiosarcoma

  1. neural

neurofibroma

  1. hematolymphoid

mycosis fungoides

75
Q

what are inclusion cysts?

A

a type of neoplasia that effects the epidermis

usually due to dilated or plugged follicles

patients present with a mobile, dermal nodule +/- overlying dilated pore

  1. epidermal = epidermal inclusion cyst
  2. follicular = pilar or trichilemmal cyst
76
Q

what is seborrheic keratosis? what patient population is effected?

A

a type of neoplasia that effects the epidermis

it usually effects middle-aged to elderly

patients present with exophytic, waxy papule/plaque on their trunk, back or face (literally anywhere)

77
Q

what is the sign associated with seborrheic keratosis?

A

Leser-Trelat sign

it’s a sudden appearance of seborrheic keratosis

it could be a sign up underlying malignancy especially in older patients

however, alone they are totally benign and you probably should worry unless there’s a ton of them

78
Q

what is actinic keratosis?

A

a type of neoplasia that effects the epidermis

it results from UV damage to keratinocytes

patients will present with scaly, erythematous papules/plaques
that arise on sun-damaged/exposed skin –> the papules will have a sandpaper texture**

can literally grow a cutaneous horn that’s a stratum corneum build up….

overtime, 1% transform into squamous cell carcinoma

79
Q

what is squamous cell carcinoma in situ?

A

a type of neoplasia that effects the epidermis –> aka Bowen’s disease

patients will present with larger erythematous, scaly plaques that are SLOW to develop invasion

certain sites are at an increased risk for invasion like the lips

80
Q

which histological findings are consistent with squamous cell carcinoma in situ?

A
  1. full-thickness dysplasia of keratinocytes
  2. no invasion; the dysplasia is retained within the basement membrane
  3. BM is intact = “eyeliner sign”
81
Q

what is squamous cell carcinoma?

A

a type of neoplasia that effects the epidermis

patients present with keratotic nodule with dermal induration which indicates invasion!

nodule will be erythematous with irregular borders

low risk of metastasis to lymph nodes but lips or other mucosal sites have an increased risk of recurrence or metastasis

82
Q

how do you treat squamous cell carcinoma?

A

surgical excision

83
Q

which histological findings are consistent with squamous cell carcinoma?

A

nests and islands of atypical keratinocytes which indicate invasion into the dermis

the neoplasia can wrap around nerves or invade into blood vessels and other adjacent structures

84
Q

what is basal cell carcinoma?

A

A type of neoplasia that effects the epidermis

it’s the MOST common non-melanoma skin cancer

metastasis is rare but local recurrence is common = spreading around where it’s happening

risks include age, UV exposure, skin type

85
Q

what are the different types of lesions seen with basal cell carcinoma?

A
  1. nodular: pearly papule with telangiectasia
  2. superficial: scaly erythematous plaque
  3. morpheaform: indurated plaque with indistinct borders
86
Q

which histological findings are consistent with basal cell carcinoma?

A
  1. nodules or nests of basaloid keratinocytes –> the nests are really blue because the cells have a HUGE nucleus with little cytoplasm
  2. mitoses and apoptotic bodies in the nests are common
  3. tumor-stromal clefting
87
Q

how do you treat a basal cell carcinoma?

A
  1. surgical excision

Moh’s surgery

  1. topical immune modulators, destructive cryo or electrocautery
  2. radiation if not operable
88
Q

what is lentigo?

A

a benign neoplasia effecting melanocytes

patients present with dark brown macules

two types:
1. solar (due to UV exposure; usually in older individuals)

  1. simplex
89
Q

what histological findings are consistent with lentigo?

A
  1. increased single melanocytes
  2. linear patient along the basal layer that looks like “muddy boots”

the rate ridges are elongated and bulbous and dark due to increased melanin

90
Q

what is nevi?

A

a benign neoplasia effecting melanocytes

91
Q

what are the 3 types of nevi?

A
  1. junctional nevus
  2. compound nevus
  3. intradermal nevus
92
Q

what is a junctional nevus?

A

a benign neoplasia effecting melanocytes

specifically it’s nests of melanocytes at DE junction - at the tips of the rete ridges

patients will present with brown macule

93
Q

what is a compound nevus?

A

a benign neoplasia effecting melanocytes

specifically it’s nests of melanocytes at the DE junction AND in the dermis

patients will present with brown to tan papules

94
Q

what is an intradermal nevus?

A

a benign neoplasia effecting melanocytes

specifically it’s nests of melanocytes in dermis –> there is no longer a junctional components

patients present with tan to flesh-colored papules

95
Q

what is a dysplastic nevi? which patient population does it effect?

A

aka atypical nevus or Clark’s nevus

it’s a neoplasia effecting melanocytes in teens and adults

may have some but not all ABCDE criteria of melanoma

*fried egg appearance clinically

96
Q

what are the two types of dysplastic nevi?

A
  1. dysplastic nevus syndrome

hereditary, hundreds of lesions, high risk of melanoma

  1. sporadic nevi
97
Q

which histological findings are consistent with a dysplastic nevi?

A
  1. shoulder = aka the egg white part –> it’s the junctional component that extends lateral beyond the dermal component
  2. elongation of rete ridges
  3. bridging of nests between rete ridges
98
Q

what is melanoma in situ?

A

it’s a neoplasia effecting melanocytes and usually effects older patients

lesions will adhere to ABCDE criteria

99
Q

what are the risk factors of melanoma in situ?

A
  1. fair complexion
  2. severe childhood sunburns
  3. history of dysplastic nevi
  4. history of melanoma in 1º relative
100
Q

which histological findings are consistent with melanoma in situ?

A
  1. melanocyte hyperplasia

2. intraepidermal** = melanocytes do NOT break through the basement membrane of the epidermis; no invasion

101
Q

what is a malignant melanoma? what patient population does it effect?

A

it’s a neoplasia effecting melanocytes effecting any age (but rare in kids)

ABCDE criteria apply

lesions will usually bleed and itch

102
Q

what are the ABCDE criteria of melanoma?

A

Asymmetry

Borders (irregular)

Color (variegated)

Diameter (>6mm)

Evolution

103
Q

what are the clinical subtypes of malignant melanoma?

A
  1. lentigo maligna
  2. superficial spreading melanoma
  3. nodular melanoma
  4. acral melanoma
104
Q

what is lentigo maligna?

A

a clinical subtype of malignant melanoma

usually effects the elderly

lesions on the head, neck, face

more indolent = grow slower

105
Q

what is superficial spreading melanoma?

A

a clinical subtype of malignant melanoma

lesions are in sun-exposed areas

lesions have horizontal THEN vertical growth

106
Q

what is nodular melanoma?

A

a clinical subtype of malignant melanoma

thought to be more aggressive but this term really isn’t used as much anymore

107
Q

what is acral melanoma?

A

a clinical subtype of malignant melanoma

lesions present on acral sites = palms, soles of the feet

it’s the most common melanoma subtype in african americans

108
Q

what prognostic information is used to determine the severity of a malignant melanoma?

A
  1. breslow thickness = depth of invasion

the MOST important

  1. ulceration presence or absence

SECOND most important

  1. Clark level = histologic level of invasion (hand in hand with Breslow thickness)
  2. gender = males have worse outcome
  3. site = proximal sites have worse prognosis
109
Q

what is a sentinel lymph node?

A

it’s the first lymph node to drain the primary site of a malignant melanoma

110
Q

which genetic mutation is directly linked to malignant melanoma?

A

BRAF V600E

so BRAF is part of the RAS-RAF pathway that eventually leads to normal cell proliferation when stimulated by outside growth factors

however, the BRAF V600E mutation doesn’t need an outside stimulus and it’s just always active which leads to increased cell proliferation and eventually melanoma

111
Q

what are hemangiomas?

A

benign vascular neoplasms

they are red papules that batch with pressure

they are acquired with age

112
Q

what histology is consistent with a hemangioma?

A

increased small blood vessels in the dermis

113
Q

what is a pyogenic granuloma?

A

a specific type of hemangioma which is a benign vascular neoplasms

aka lobular capillary hemangioma

these are red papules +/- ulcerations (gross looking but totally benign)

they tend to be associated with trauma and pregnancy

114
Q

which histological findings are consistent with pyogenic granuloma?

A
  1. exophytic = they bulge out of the skin
  2. collarette
  3. increased small blood vessels
  4. lobular growth pattern
115
Q

what is a Kaposi’s sarcoma?

A

a malignant vascular neoplasm

tend to occur in immunocompromised patients like HIV, or elderly

lesions tend to be on the skin, oral cavity, GI, tract, pulmonary tract

lesions are deep red/purple because they’re filled with blood so that makes sense

116
Q

which virus causes Kaposi’s sarcoma?

A

herpes virus 8

QUIZ QUESTION

117
Q

which histological findings are consistent with Kaposi’s sarcoma?

A
  1. spindle cell endothelial proliferation with hemorrhage (extravasated RBCs)
  2. promontory sign (vascular vessels extending out into other vascular space)
118
Q

what is an angiosarcoma?

A

a malignant vascular neoplasm

it’s rare but highly aggressive

119
Q

what are the two types of angiosarcoma?

A
  1. primary

effects the elderly

lesions will appear on sun-exposed areas-head and neck

  1. post-therapy

Radiation

Chronic
lymphedema

Breast- most common

120
Q

what histological findings are consistent with angiosarcoma?

A
  1. malignant endothelial cells that are pleomorphic, hyperchromatic and mitoses

looks like a “school of fish”

121
Q

what is a neurofibroma?

A

a benign neural neoplasm

it’s a growth of spindled peripheral nerve fibers which grow in fascicles

most are sporadic but there is a syndromic where you get a lot of them all at once (NF-1 gene mutation can lead to von Recklinghausen’s)‏

syndromic form can have malignant degeneration

122
Q

what is the most common hematolymphoid tumors?

A

leukemias or lymphomas

specifically cutaneous T-cell lymphoma

123
Q

what is cutaneous T-cell lymphoma?

A

a type of hematolymphoid disease that has malignant CD4+ cells

slow, indolent clinical course

lesions are red-purple patches/plaques/nodules – lesions usually occur in double covered areas like trunk, back, groin (but can spread to extremities)

this is one cause of erythroderma

Sezary syndrome = blood involvement by CTCL = systemic involvement

124
Q

which histological findings are consistent with cutaneous T-cell lymphoma?

A

early on it often mimics a spongiotic dermatitis

but later on you get malignant T-cells

  1. epidermotropism = lymphocytes infiltrate epidermis
  2. Pautrier microabscesses = collections of malignant T-cells in the epidermis
  3. malignant T-cells in dermis sometimes too

MSK Week 4 (11 decks)

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