ICL 1.3: Dermatopathology Flashcards
1
Q
what are the types of inflammatory dermatoses?
A
- acute
- chronic
- blistering diseases
- disease of appendages
- fibrosing dermopathy
- panniculitis
- vasculitis
2
Q
which inflammatory dermatoses are acute?
A
- urticaria
- spongiotic dermatitis
- erythema multiform
3
Q
which inflammatory dermatoses are chronic?
A
- lichen planus
- lupus
- psoriasis vulgaris
4
Q
which inflammatory dermatoses are blistering diseases?
A
- pemphigus vulgaris
- bullous pemphigoid
- dermatitis herpetiformis
5
Q
which inflammatory dermatoses are diseases of cutaneous appendages?
A
acne vulgaris
6
Q
which inflammatory dermatoses are fibrosing dermopathy?
A
scleroderma
7
Q
which inflammatory dermatoses are panniculitis?
A
erythema nodosum
8
Q
which inflammatory dermatoses are vasculitis?
A
leukocytoclastic vasculitis
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
10
Q
what histological findings are consistent with urticaria?
A
- dermal edema
- EOSINOHPILS
- PMNs in capillaries
11
Q
what is spongiotic (eczematous) dermatitis?
A
it’s an acute dermatoses that is the most common dermatitis!!
- atopic, contact, nummular eczema
- pityriasis rosea
- seborrheic dermatitis
- drug eruption
**it is a cause of erythroderma = total body erythema and scaling
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
- atopic –> flexural surfaces: elbow, knees, etc.
- seborrheic –> scalp, T-zone, intermammary, axilla
- irritant/contact –> at the site of contact
the clinical appearance then depends on the age of the lesion
- acute = erythematous, moist papules/vesicles
- subacute = erythematous, scaly papules/plaques
- chronic = lichenified plaques
13
Q
what are some examples of spongiotic dermatitis?
A
contact dermatitis = poison ivy, allergy to soaps, detergents, deodorants, etc.
14
Q
which three dermatoses can cause erythroderma?
A
- psoriasis vulgaris
- spongiotic dermatitis
erythroderma = total body erythema and scaling
- cutaneous T-cell lymphoma
15
Q
what is the pathology of spongiotic dermatitis?
A
- Ag contacts epidermis
- Ag picked up by LC
- LC/Ag migrates to LN
- LC presents Ag to CD4+ T cell
- sensitized T cells go to affected area and do cytokine release, more inflammation, edema into epidermis
this all leads to spongiosis +/- vesicles
16
Q
what histological findings are consistent with spongiotic dermatitis?
A
- extensive spongiosis = increased intercellular edema
2. epidermal acanthosis = increased thickness of the spinous layer of the epithelium
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
18
Q
what are the stages of erythema multiforme?
A
- erythema multiforme
- stevens-johnson syndrome
- toxic epidermal necrolysis (TEN)
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…
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
21
Q
what are some of the causes of erythema multiforme?
A
- medication
- herpes simplex virus
- mycoplasma
- collagen vascular diseases
- malignancies (lymphoma, carcinoma)
22
Q
what are lichenoid dermatoses? which diseases are lichenoid dermatoses?
A
a chronic dermatoses that involves:
- vacuolar basal layer damage
- eosinophilic necrosis of keratinocytes
- band-like lymphocytic infiltrate**
ex. lichen planus and lupus erythematosus
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.
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
25
what is Koebner phenomenon?
when new lesions develop at sites of injury
seen in lichen planus
26
what is the pathology of lichen planus?
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
27
what are the histological findings consistent with lichen plus?
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
28
what are the 3 subtypes of lupus erythematosus?
1. systemic LE = skin + other organs
2. subacute LE = skin +/- other organs
3. discoid LE = skin only
29
what's the hallmark symptom of systemic lupus erythematosus?
malar rash = butterfly rash
30
what's the hallmark symptom of subacute lupus erythematosus?
annular plaques
they have build up borders with scales
31
what are the hallmark symptoms of discoid lupus erythematosus?
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
32
what is the pathogenesis of lupus erythematosus?
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)
33
what is follicular plugging?
a symptom of discoid lupus erythematosus
it's when initial injuries cause reactive hyperkeratosis, especially in the follicles which leads to follicular plugging
34
what immunofluorescence findings are consistent with lupus?
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
35
what is psoriasiform?
a chronic dermatoses with regular elongation and widening of the rete ridges
ex. psoriasis
36
what is psoriasis vulgaris? what patient population does it effect?
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
37
what are the symptoms and lesions associated with psoriasis vulgaris?
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
38
which two dermatoses can cause Koebner phenomenon?
1. psoriasis vulgaris
| 2. lichen planus
39
what is the pathogenesis of psoriasis vulgaris?
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
40
what histologic findings are consistent with psoriasis vulgaris?
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
41
what is the hallmark sign of psoriasis vulgaris?
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
42
how are blistering diseases classified?
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.
43
what is a routine biopsy vs. an immunofluorescence biopsy?
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
44
what is pemphigus vulgaris? what patient population does it effect?
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
45
what is the hallmark sign o pemphigus vulgaris?
Nikolsky sign
pressure on edge of blister causes blister to expand in the direction of where you put pressure
46
what's the pathogenesis of pemphigus vulgaris?
it's an autoimmune disease where IgG targets desmoglein 3, an intercellular cadherin
desmogleins are the transmembrane proteins in macula adherens junctions aka desmosomes!!
47
what histological findings are consistent with pemphigus vulgaris?
1. acantholysis = loss of intercellular connections in spinous layer
2. suprabasilar vescile
48
what immunofluorescence findings are consistent with pemphigus vulgaris?
intercellular IgG between spinous keratinocytes
it's a net-like pattern (really does look like a net)
49
what is bullous pemphigoid? what patient population does it effect?
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*
50
what's the pathogenesis of bulls pemphigoid?
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
what are the immunofluorescence findings consistent with bullous pemphigoid?
linear IgG and C3 along the DE junction
so not net-like like pemphigus vulgaris
52
what is dermatitis herpetiformis? what patient population does it effect?
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
what's the pathogenesis of dermatitis herpetiformis?
IgA autoantibodies against anchoring fibrils in BM -- this makes sense because IgA is the antibody predominantly in the GI tract!
54
what histological findings are consistent with dermatitis herpetiformis?
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
what immunofluorescence findings are consistent with dermatitis herpetiformis?
*granular* IgA deposits along the tips of the dermal papillae
56
what are the steps in a pimple forming? aka acne vulgaris
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
what is the difference between a whitehead and a blackhead?
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
what is acne vulgaris? what patient population does it effect?
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
what is scleroderma? what patient population does it effect?
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
what are the types of scleroderma?
1. diffuse scleroderma
| 2. limited scleroderma
61
what is diffuse scleroderma? which antibody is associated with it?
1. Systemic involvement
2. Skin and visceral organs involved
3. Rapid progression
4. Anti-SCL70 Ab***
62
what is limited scleroderma?which antibody is associated with it?
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
which histological findings are consistent with scleroderma?
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
what is panniculitis?
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
what is erythema nodosum?
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
which conditions are associated with erythema nodosum?
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
what histological findings are consistent with erythema nodosum?
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
what is leukocytoclastic vasculitis? what patient population does it effect?
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
what is the pathogenesis of leukocytoclastic vasculitis? what are some of the possible causes?
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
which conditions are associated with leukocytoclastic vasculitis?
1. AI: SLE, IBD, RA, MCTD, etc
2. IC: cryoglobulinemia, HSP, PAN, Wegener’s, Churg-Strauss
3. sarcoidosis
4. malignancies
71
which histological findings are consistent with leukocytoclastic vasculitis?
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
which neoplasias effect the epidermis?
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
which neoplasias are melanocytic?
1. lentigo
2. nevus
3. dysplastic nevus
4. melanoma in situ
5. invasive melanoma
74
which neoplasias effect the dermis?
1. vascular
hemangioma, pyogenic granuloma, kaposi's sarcoma, angiosarcoma
2. neural
neurofibroma
3. hematolymphoid
mycosis fungoides
75
what are inclusion cysts?
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
what is seborrheic keratosis? what patient population is effected?
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
what is the sign associated with seborrheic keratosis?
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
what is actinic keratosis?
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
what is squamous cell carcinoma in situ?
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
which histological findings are consistent with squamous cell carcinoma in situ?
1. *full-thickness* dysplasia of keratinocytes
2. no invasion; the dysplasia is retained within the basement membrane
3. BM is intact = "eyeliner sign"
81
what is squamous cell carcinoma?
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
how do you treat squamous cell carcinoma?
surgical excision
83
which histological findings are consistent with squamous cell carcinoma?
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
what is basal cell carcinoma?
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
what are the different types of lesions seen with basal cell carcinoma?
1. nodular: pearly papule with telangiectasia
2. superficial: scaly erythematous plaque
3. morpheaform: indurated plaque with indistinct borders
86
which histological findings are consistent with basal cell carcinoma?
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
how do you treat a basal cell carcinoma?
1. surgical excision
Moh’s surgery
2. topical immune modulators, destructive cryo or electrocautery
3. radiation if not operable
88
what is lentigo?
a benign neoplasia effecting melanocytes
patients present with dark brown macules
two types:
1. solar (due to UV exposure; usually in older individuals)
2. simplex
89
what histological findings are consistent with lentigo?
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
what is nevi?
a benign neoplasia effecting melanocytes
91
what are the 3 types of nevi?
1. junctional nevus
2. compound nevus
3. intradermal nevus
92
what is a junctional nevus?
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
what is a compound nevus?
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
what is an intradermal nevus?
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
what is a dysplastic nevi? which patient population does it effect?
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
what are the two types of dysplastic nevi?
1. dysplastic nevus syndrome
hereditary, hundreds of lesions, high risk of melanoma
2. sporadic nevi
97
which histological findings are consistent with a dysplastic nevi?
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
what is melanoma in situ?
it's a neoplasia effecting melanocytes and usually effects older patients
lesions will adhere to ABCDE criteria
99
what are the risk factors of melanoma in situ?
1. fair complexion
2. severe childhood sunburns
3. history of dysplastic nevi
4. history of melanoma in 1º relative
100
which histological findings are consistent with melanoma in situ?
1. melanocyte hyperplasia
| 2. intraepidermal** = melanocytes do NOT break through the basement membrane of the epidermis; no invasion
101
what is a malignant melanoma? what patient population does it effect?
it's a neoplasia effecting melanocytes effecting any age (but rare in kids)
ABCDE criteria apply
lesions will usually bleed and itch
102
what are the ABCDE criteria of melanoma?
Asymmetry
Borders (irregular)
Color (variegated)
Diameter (>6mm)
Evolution
103
what are the clinical subtypes of malignant melanoma?
1. lentigo maligna
2. superficial spreading melanoma
3. nodular melanoma
4. acral melanoma
104
what is lentigo maligna?
a clinical subtype of malignant melanoma
usually effects the elderly
lesions on the head, neck, face
more indolent = grow slower
105
what is superficial spreading melanoma?
a clinical subtype of malignant melanoma
lesions are in sun-exposed areas
lesions have horizontal THEN vertical growth
106
what is nodular melanoma?
a clinical subtype of malignant melanoma
thought to be more aggressive but this term really isn't used as much anymore
107
what is acral melanoma?
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
what prognostic information is used to determine the severity of a malignant melanoma?
1. breslow thickness = depth of invasion
the MOST important
2. ulceration presence or absence
SECOND most important
3. Clark level = histologic level of invasion (hand in hand with Breslow thickness)
4. gender = males have worse outcome
5. site = proximal sites have worse prognosis
109
what is a sentinel lymph node?
it's the first lymph node to drain the primary site of a malignant melanoma
110
which genetic mutation is directly linked to malignant melanoma?
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
what are hemangiomas?
benign vascular neoplasms
they are red papules that batch with pressure
they are acquired with age
112
what histology is consistent with a hemangioma?
increased small blood vessels in the dermis
113
what is a pyogenic granuloma?
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
which histological findings are consistent with pyogenic granuloma?
1. exophytic = they bulge out of the skin
2. collarette
3. increased small blood vessels
4. lobular growth pattern
115
what is a Kaposi's sarcoma?
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
which virus causes Kaposi's sarcoma?
herpes virus 8
QUIZ QUESTION
117
which histological findings are consistent with Kaposi's sarcoma?
1. spindle cell endothelial proliferation with hemorrhage (extravasated RBCs)
2. promontory sign (vascular vessels extending out into other vascular space)
118
what is an angiosarcoma?
a malignant vascular neoplasm
it's rare but highly aggressive
119
what are the two types of angiosarcoma?
1. primary
effects the elderly
lesions will appear on sun-exposed areas-head and neck
2. post-therapy
Radiation
Chronic
lymphedema
Breast- most common
120
what histological findings are consistent with angiosarcoma?
1. malignant endothelial cells that are pleomorphic, hyperchromatic and mitoses
looks like a "school of fish"
121
what is a neurofibroma?
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
what is the most common hematolymphoid tumors?
leukemias or lymphomas
specifically cutaneous T-cell lymphoma
123
what is cutaneous T-cell lymphoma?
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
which histological findings are consistent with cutaneous T-cell lymphoma?
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
