Histopathology - Skin pathology Flashcards
Normal Skin is made up of what Three Layers?
- Epidermis
- Dermis
- SC fat
Epidermis what cells does it consist of and whats it’s function?
Made up of keratinocytes (squamous epithelial cells)
This functions as the barrier
Dermis - ft and made up of what?
Supporting structure to epidemis
Made up of collagen, elastin fibres, adnexal structures, eccrine glands, sebaceous glands and hair follicles
Skin differ throiughout the body:
Face vs torso and arms?
How does palms and soles differ?
On your face, you will have more sebaceous glands than on your torso and arms (left)
The palms of hands and soles of the feet have no hair follicles but have sweat glands (right)
There is much thicker stratum corneum (thick layer at the top) – which correspond to callouses on hands and feet
Skin Changes with Ageing?
Epidermis is much thinner
Much more fragile dermis- poorer quality collagen bundles and elastic fibres
Layers of the epidemis and what cell types found in each layer?
List the 6 diferent Inflammatory Reaction Patterns?
- Vesiculobullous- forms bullae
- Spongiotic- becomes oedematous
- Psoriaform- becomes thickened
- Lichenoid- forms a sheeny plaque
- Vasculitis- associated with vasculitis
- Granulomatous- associated with granulomas
What is this condition, it’s Presentation, it’s Pathophysiology?
BULLOUS PEMPHIGOID
- Presentation: Present with tense bullae which occur in flexural surfaces (behind knees or in elbows)
- Pathophysiology:
Autoimmune disorder driven by IgG and C3, which attack the keratinocytes (epithelial cells) sitting on the basement membrane
- IgG binds to hemidesmosomes on the basement membrane
- Complement attracts eosinophils and these release a protein called elastase which causes more damage to anchoring proteins (anchoring lower keratinocytes to the basement membrane).
- This leads to fluid production and the whole epidermis then lifts up to produce tense bullae
E.g. a house is made out of bricks and the bricks are the keratinocytes, house sits on a concrete foundation. Damage occurs to the bottom layer of bricks which leads to the whole house being lifted up.
There are a number of different disorders which lead to these tense bullae e.g. drug reaction
How to dx Bullous Pemphigoid and what will u see?
TX?
Immunofluorescence IgG and C3-dermoepidermal junction Of the specimen directly or of the serum
See a band along the basement membrane zone
TX If it is bullous pemphigoid, need to give some immunotherapy
Dx + Describe appearance, pathophysiology, how u would diagnose?
Appearance: Flaccid-looking blisters, these rupture easily leaving a raw, red surface underneath
Pathophysiology:
autoimmune IgG Disorder directed against epidermal cadherins (desmosomes) [proteins which keep the keratinocytes stuck together] = acantholysis (loss of intercellular connections leading to loss of cohesion between keratinocytes) ∴ The bottom layer is attached but the breakage causes the layer above to free float
E.g. Abs directed vs the cement that keeps the bricks together which is being destroyed
_Diagnosis:_Immunofluorescence to show IgG around these individual keratinocytes
What is the diagnosis, describe appearance
PEMPHIGUS FOLIACEUS
Appearance:
- You don’t see the intact bullae because these are so thin that they come off easily
- Looks excoriated, the stratum corneum has lifted off [This is the roof that has come off (the top layer)]
Pathophysiology:
- This is against the pemphigus antibody and is also IgG mediated (IgG-mediated attack on the outer layer of the keratinocytes (where stratum corneum is found)
BULLOUS PEMPHIGOID + PEMPHIGUS VULGARIS + PEMPHIGUS FOLIACEUS are an example of what inflammatory reaction pattern and how do you distingush between them?
Inflammatory Reaction Patterns [Vesiculobullous- forms bullae]
All conditions caused by pemphigus antibody (IgG mediated) however directed at different layers of the epidemis. Immunofluorescence is KEY in diagnosis
dx?
Eczema
Eczema - different causes, typical presentation + distribution?
- Causes - Can occur from contact, atopy, allergy
- Can get it from contact e.g. nickel, latex gloves, watch bands
- Presentation
- Typically producing white plaques on flexural surfaces e.g. antecubital fossa, behind the knees
- Can be so itchy that the person looks erythematous as a result
Explain what this Histology of Eczema shows and what is respobsle for such changes?
- Shows hyperparakeratosis (thickening of the skin on the surface where you’ve been scratching - epidemis gets thicker w/ time as you scratch more) and spongiosis (oedema between the keratinocytes - ass w/ lots of eosinophils = oedema)
- E.g. the cement between the bricks is soggy and wet
What is responsble for skin changes observed?
- This is T cell mediated and eosinophils are recruited
List another differential for an eczematous skin pattern?
A differential for an eczematous pattern can be a drug reaction
Whats the dx, commmon distribution + describe appearance?
- This occurs on EXTENSOR surfaces e.g. knuckles, knees
- This tends to produce classical silvery plaques
- NOTE: the skin always sheds
Pathophysiology and explain the histology of plaque psoriasis?
Pathophysiology:
- Normally the transit time from a stem cell differentiating into a fully formed keratinocyte is around 56 days (to go from bottom to top)
- The skin SHEDS RAPIDLY with psoriasis, whereby this occurs every 7 days
Histology:
- Because of the rapid turnover, the epidermis gets thicker = parakeratosis at the top + The granular cell layer (stratum granulosum) disappears in this condition because there is NOT enough time to form it
- You also see the recruitment of neutrophils (forms Munro’s microabscesses) + Also get dilated blood vessels (= inflmmatory sx - hot and itchy plaques)
Dx, Typical presentation, what is a hallmark sign of this condition?
- This is an example of a lichenoid reaction pattern
- These patients present with itchy purply red patches and plaques on the distal extensor surfaces e.g. around the wrists and arms
- There are classic white lines in the mouth (Wickham’s striae)
Explain Histology of Lichen planus and in what other condition can a similar histology be seen?
- T lymphocytes are attacking the bottom layer of keratinocytes at the epidermis
- The keratinocytes become damaged and die and so there is then band-like inflammation (right image) underneath the epidermis (e.g. house is being attacked by ants underneath)
- You can barely see where the dermis finishes and the epidermis starts
- This can also be seen in mycosis fungoides [cutaneous T-cell lymphoma]
Whats the dx, what is this a form of, how does it poresent, what is it a sign of ?
Pyoderma Gangrenosum
- This is a form of vasculitis
- This is NOT actually gangrenous
- It presents as an ulcer
- It is often the first manifestation of an underlying systemic disease (e.g. IBD, sclerosing cholangitis, hepatitis, leukaemia etc.)
dx, describe appearance, prognosis
Seborrhoeic Keratosis
- Pigmented, have a ‘stuck on’ appearance [“cauliflower-ish” and can get caught up in clothing]
- These are completely harmless and very common in the elderly
- The keratinocytes in the epidermis start to proliferate in an orderly way ( E.g. start to build a skyscraper)
What is a keratin horn and what base can it form on ?
keratin horn (aka cutaneous horn)
= entrapped keratin surrounded by a proliferating epidermis)
- resemble an animal’s horn ∴cutaneous horn
can form on a on Seborrhoeic Keratosis base, SCC base
dx, presentation, complications, histology
Sebaceous cyst
- Smooth, round
- They are non-mobile and tend to have a central punctum
Complications: They can get infected, inflamed and rupture
Histology
- Epidermis has invaginated into the dermis and produces the keratin
- There is squamous epithelium along the lining
- The keratin that comes out can look caseous and smell
dx, describe lesion, distribution on skin, prognosis
Basal Cell Carcinoma
Appearance: Has ulcerated, pearly rolled edge which is raised with a central ulcer and telangiectasia
Distribution: Occurs in sun-exposed areas in the elderly
Prognosis:
- Causes disfigurement but not death
- Can get deep and ulcerate/ erode away
Explain Histology of BCC - appearance, what does cancer arise from, ?
- Large islands of tumour arises from the keratinocytes/ epithelial cells along the bottom of the epidermis, these cells break through the basement membrane and go into the underlying submucosa/ dermis
- BCCs do NOT metastasise, they are locally invasive
- They can spread via the nerves and lymphovascular system or they can cause local infiltration????
dx?
Bowen’s Disease
Dx + classification + Prognois?
Squamous Cell Carcinoma
This can be divided into well differentiated, moderately differentiated and poorly differentiated
Metastasis occurs, prognosis is poor
Dx?
Benign Junctional Naevus - what age range affected, how is to formed, macule or papule?
Dx + how is it formed?
Compound naevus - nests within the epidermis and dermis
- Note: As the melanocytes mature, they will become smaller and go deeper down (so seeing melanocytes in the dermis is not a problem)
Dx, how do you asess this lesion clinically and describe worrying sx?
Malignant melanoma
- Think of ABCDE: asymmetry, border irregularity, colours, diameter, evolution
- There is an irregular outline in image- should be nice and symmetrical
- Worrying symptoms: bleeding, itchy, growing
Pathophysiology of malignant melanoma?
- In the dermis, the melanocytes are the same size at the top of the dermis and at the bottom (normally, melanocytes should get smaller and smaller the deeper down the dermis they go, instead the melanocytes get BIGGER and move up through the epidermis – Pagetoid spread. )
- Thus, they are lacking maturation and start to get mitotically active
- Should not see mitotic figures in the dermal component of a melanocytic lesion
How might a Metastatic Renal Cell Carcinoma present?
Can appear like with smooth papule
