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Year 5 Path Charis > Histopathology - Skin > Flashcards

Histopathology - Skin Flashcards

1
Q

Haematoxylin + Eosin stain

A
  • Haematoxylin  Blue/purple stain – stains RNA + DNA (nucleus)
  • Eosin stain  cytoplasma, collagen
  • Nuclei > cytoplasm – tissue looks more blue/purple
  • Cytoplasma/collagen > nuclei – tissue looks more pink
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2
Q

Layers of the epidermis

A

“come, lets get some beers”

o Stratum basale – blue (little cytoplasm, more nuclei), where the keratinocytes are born (there are stem cells within the basal epidermis which divide to produce the rest of the epidermis) (most deep) - melanocytes usually seen here
o Stratum spinosum – thickest layer, desmosomes/spines connect keratinocytes to each other, this gives strength to the epidermis
o Stratum granulosum – purple granules in cytoplasm
o After this, the cells die and lose their nuclei – left with keratin shells
o Stratum lucidum
o stratum corneum (most superficial)

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3
Q

Eczema under the microscope

A

Defect in epidermis

Spongiosis/ intercellular oedema (white spaces bn cells)

Exocytosis of lymphocytes into the epidermis

Blisters/Vesicles containing oedema, lymphocytes, Langerhans cells

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4
Q

What is acanthosis?

A

Increase in stratum spinosum

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5
Q

Acute and chronic histology of atopic and contact dermatitis

A

Acute

  • Spongiosis
  • Inflammatory infiltrate in the dermis
  • Dilated dermal capillaries

Chronic

  • Acanthosis
  • Crusting, scaling
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6
Q

What are Wickham striae?

A

• White striations over the surface of the lichenification

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7
Q

Lichen planus pathophysiology

A

• Autoimmune disease

o T-cell mediated, T lymphocytes start attacking the base of the epidermis
• Liquefaction degeneration of the basal layer of the epidermis

o T-lymphocytes have destroyed bottom keratinocytes

o Creates band-like inflammation
• Band of lymphocytes at the dermal-epidermal interface

o Cannot see where dermis finished, and epidermis starts

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8
Q

Give examples of spongiotic reaction

A

Eczema
Discoid eczema
Contact dermatitis

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9
Q

Give examples of lichenoid inflammation

A

Lichen planus

Erythema multiforme
Steven Johnson syndrome
Toxic epidermal necrolysis

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10
Q

Lichenoid inflammation pathophysiology

A

Lymphocytes attacking the base of the epidermis

Band of lymphocytes, dead keratinocytes, basal vacuolation

Liquefaction degenerating of the basal layer of the epidermis

Band of inflammatory cells beneath epidermis

Melanin beneath the epidermis

Irregularly thickened epidermis

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11
Q

TEN vs SJS

A
  • TEN  widespread process, sloughing off of the skin
  • SJS mucus membranes are also affected

Skin detachment
 <10% body surface area in SJS
 >30% in TEN

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12
Q

Erythema multiforme causes causes

A

 Infections – HSV, mycoplasma

 Drugs – SNAPP – Sulphonamides, NSAIDs, Allopurinol, Penicillin, Phenytoin

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13
Q

What is

  • Auspitz’s sign
  • Koebner phenomenon
A

Signs of psoriatic arthritis

  • Auspitz’s sign – rubbing them causes pin point bleeding
  • Koebner phenomenon – lesions form at sites of trauma
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14
Q

Hallmarks of psoriasis under microscope

A

Acanthosis = increase in stratum spinosum

Parakeratosis = nuclei in s. corneum

o Histo – parakeratosis, acanthosis, loss of granular layer, clubbing of rete ridges giving “test tubes in a rack” appearance, Munro’s microabscesses

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15
Q

Psoriasis pathophysiology

A

Defect in epidermis

o Normal keratinocyte turnover time = 56 days
o Psoriasis keratinocyte turnover time = 7 days – increased proliferation rate

o Rapid turnover  thicker epidermis = acanthosis
o Hypogranulosis No time for a granular layer to form  stratum granulosum disappears
o Parakeratosis = Keratinocytes carry their nuclei into the stratum corneum (no time for nuclei to be lost)

o Inflammatory cells/lymphocytes attract neutrophils – Neutrophils in stratum corneum
o Munro’s microabscesses form (recruitment of neutrophils)

o Dilated vessels form

o Pathophysiology – Type IV T cell hypersensitivity reaction

• accumulation of thick scale over sites of frequent trauma or irritation

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16
Q

Give examples of vesiculobullous reaction pattern

A

• Antibodies attacking the epidermis

Dermatitis herpetiformis
Bullous Pemphigoid
Pemphigus vulgaris
Pemphigus foliaceus

17
Q

Pemphigoid vs pemphigus

A

• Different forms based on which part of the epidermis these antibodies attack
o Pemphigoid – antibodies attack the BM (SUBepidermal blisters)

o Pemphigus – antibodies against the desmosomes (INTRAepidermal blisters)
 Pemphigus foliaceous – superficial form
 Pemphigus vulgaris – deep form

18
Q

Pathophysiology + histology of dermatitis herpetiformis

A

coeliac disease, itchy vesicles on elbows + buttocks

IgA ab bind to BM - subepidermal blisters

Histo
Microabscesses coalesce together forming subepidermal blisters
IgA +neutrophil deposits at tips of dermal pappilae

19
Q

Bullous pemphigoid what is affected?

A

Dermo epidermal junction

IgG antibodies + C3 bind to hemidesmosomes of BM –> elastase released by oesinophils destroys anchoring proteins –> fluid fills space between epitheliumand BM –> subepidermal bullae

Bullae

  • SUBepidermal
  • Deep
  • Tense
  • Do not rupture as easily as in pemphigus

Histo

  • Linear deposition of IgG along BM (IgG antihemidesmosome)
  • Subepidermal bulla with oesinophils
20
Q

What is pemphigus foliaceous

A
  • Epidermis
  • Superficial form
  • Top layer is very thin – never blisters

• Pathophysiology
o IgG-mediated
o Outer layer of striatum corneum shears off

• Diagnose with immunofluorescence

21
Q

Pemphigus vulgaris pathophysiology + histology

A

Epidermis

IgG antibodies against desmoglein 1 + 3

  • INTRAepidermal bullae
  • Acantholysis (keratinocytes in stratum spinosum fall apart bc f antibodies)
  • Flaccid blisters, rupture easily - red raw surface
  • Nikolsky’s sign +ve

Histology

  • INTRAepidermal bulla
  • Acantholysis
  • Intracellular IgG deposition in a netlike/chickenwire pattern around the keratinocytes
22
Q

What is pyoderma gangrenosum?

A
  • Vasculitis
  • Non-healing ulcer
  • Often first manifestation of a systemic disease – colitis, hepatitis, leukaemia
23
Q

Seborrhoeic keratosis buzzwords

A

Cauliflower appearance
stuck on appearance
benign

Histology
horn pseudocyst 
acanthosis 
ordered and benign growth of epidermis
http://mohs-md.com/wp-content/uploads/2018/05/seborrheic-keratosis.jpg
24
Q

Histology of actinic keratosis

A

Pre-malignant cells are proliferating at the base of the epidermis

BM is not lost

SPAIN
Solar elastosis
Parakeratosis
Atypia/Dysplasia
Inflammation 
Not full thickness
25
Q

general structure of skin

A

Epidermis
Basement membrane
Dermis

26
Q

What is a keratoacanthoma

A
  • Rapidly growing dome shaped nodule
  • May develop a necrotic, crusted centre
  • Grows over 2-3 weeks + clears spontaneously
  • Similar histology to SCC – hard to differentiate
27
Q

What is Bowen’s disease

A

• intra-epidermal Squamous cell carcinoma in situ (i.e. pre-cancerous)

o Full thickness dysplasia (whole thickness of the epidermis)
o BM is still intact i.e. not invading the dermis

  • Hasn’t yet become invasive
  • Flat, red, scaly patches on sun exposed areas
  • Not always in the context of sun exposure
28
Q

SCC buzzwords

squamous cell carcinoma

A

When Bowen’s disease invades the BM –> atypia/ dysplasia throughout the epidermis, nuclear crowding and spreading through BM into dermis

Similar to Bowen’s disease but may ulcerate

Pink under the microscope
Peri-neural invasion
Can metastasise through blood vessels

Keratin pearls
Keratinocytes in dermis

29
Q

Basal cell carcinoma buzzwords

A

Commonest form of skin cancer

PTCH mutation

Arises from stratum Basale - mass of basal cells (cancer from keratinocytes at the bottom of the epidermis)
nuclei > cytoplasm = blue tumour
Palisading
Does not invade the BM –> does not metastasise

30
Q

Where do melanocytes normally exist?

A

Basal layer of epidermis

Dermis as single cells

31
Q
  • Junctional naevus
  • Compound naevus
  • Intradermal naevus
A

• Junctional naevus
o Melanocytes nest in the epidermis
o Flat and coloured

• Compound naevus
o Melanocytes nest in the epidermis and dermis
o Raised area
o Surrounded by flat pigmented area

• Intradermal naevus
o Melanocytes nest in the dermis
o Raised area
o Skin-coloured or pigmented

32
Q

Mutations associated with malignant melanoma

A

BRAF V600E mutation

33
Q

How do melanocytes grow in malignant melanoma?

A

Initially grow horizontally (radial growth phase)

then vertically (vertical growth phase)

vertical growth phase produces “buckshot appearance” - pagetoid spread (upward spreading of abnormal melanocytes in the epidermis (these cells are normally found along the base of the epidermis))

34
Q

what is pagetoid spread

A

pagetoid spread (upward spreading of abnormal melanocytes in the epidermis (these cells are normally found along the base of the epidermis))

seen in malignant melanoma

35
Q

Most important prognostic factor for malignant melanoma

A

Breslow thickness

<0.8mm good prognosis
>4mm >50% mortality

measured for granular layer of epidermis to last abnormal melanocyte

36
Q

Behaviour of melanocytes in the dermis in malignant melanoma

A

large melanocytes with mitotic activity in the dermis

Normal physiology

  • Bigger melanocytes between the dermal/epidermal junction and then they get smaller as they go down into the dermis
  • You shouldn’t be seeing mitotic activity in the dermis

 The junctional melanocytes are no longer maturing + dropping out of the dermis
 They are moving up through the dermis instead = pagetoid spread
 This is not normal

37
Q

o Melanocyte immunomarkers that can be stained using immunohistochemistry

A

 Melanin A
 S100
 HMB45

38
Q

What is Pityriasis Rosea

A

o Salmon pink rash appears first (= herald patch)
o Followed by oval macules in Christmas tree distribution

o Appears after viral illness
o Remits spontaneously

Year 5 Path Charis (44 decks)

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