The Source Material

NB UNDER CONSTRUCTION. PLEASE DO NOT PURCHASE ACCESS AT THIS STAGE

Aspects of Dermatopathology will be taught using the two illustrated resources. The book Requisites in Dermatopathology has excellent illustrations and a series of very good lectures. It costs about $125 AUS including the website access. It can be purchased from Amazon

The second resource is the Derm101 website. It has a remarkable selection of dermpath cases and books available online. You can access it here and pay for it monthly for about $12 AUS.

This course will be delivered through a series of podcasts which you purchase via Pay Pal but you initially need to organise access to these two resources. 
Using this method you can pay only for the elements of this course that best suit your needs. eg If you are mainly in GP Skin Cancer work and require some directed instruction in tumour pathology then you would only select and pay for those podcasts relevant to Skin Cancer. 
Following completion of the course you can opt to sit an online examination and if you pass be awarded a Certificate in Skin Cancer Histology or the Certificate in Dermatopathology from the Australian Institute of Dermatology. Details of these exams can be found here.

If you are working in the skin cancer field then you need to have some idea of the histology of the lesions you are biopsying. You need to know the terms used in dermatopathology reports to assess their significance. It is not enough to look at the diagnosis at the end. BCCs are managed on the nature of their histological pattern. There is a big difference in management options between a superficial multifocal BCC and an infiltrating or morphoeic BCC. Similarly with SCC and whether they are well differentiated, moderately differentiated or poorly differentiated.

Melanocytic lesions present other difficulties because of the way lesions are sampled for examination and the problems the pathologist has in differentiating between dysplastic nevi and early melanoma.

You also have to understand the indications for and the limitatations of different types of biopsy of pigmented lesions eg punch, shave, incisional and excisional biopsies.

The resources on which this course is based go only so far. You will benefit from being led through these resources by an expert trained in both dermatology and dermatopathology, pointing out what is important and why and at the same time directing you through the pitfalls, using podcasts and videoconferences.

This method is the most economical I could come up with to deliver this educational experience. Should you wish to take an online examination at the end of the course then the Australian Institute of Dermatology will organise this and will issue you with a Certificate should you reach the required standard.
Beginning the Course    You can start this course whenever you want. The first step is to purchase the resource material above and then look at the posts starting with number 1 and working methodically through. The Skin Cancer Pathology course is numbers 1-8 and the full dermatopathology course includes the rest of the posts. I hope you enjoy it. If you have any questions email me at imccoll@ozemail.com.au 
Best wishes
Dr Ian McColl FACD
Dermatologist.

GP Histopathology course for Skin Cancers

Below is an overview of the GP histopathology course. Each of the topics will have a separate illustrated post. The GP Histopathology course is made up of Modules 1 thru 7B


View the video telecast for this topic (not active at present)

Here we will deal with the histopathology of the common tumours you will see in skin cancer practice. We will concentrate on those histological features that have a crucial impact in determining how you treat the lesion.
eg BCCs- Pathology relates to the treatments used
Superficial bcc V Nodular bcc V Infiltrating or Morphoeic
Thickness - penetration of creams eg Aldara and red light in PDT
Significance of Infiltrating BCC with these modalities
Basisquamous BCC
BCC with perineural spread
BCC in vessels- very rare

eg SCCs-   SCC in situ- confined to epidermis
Compare and contrast clonal Seb K V SCC in situ
Invasive SCC can be well differentiated through to poorly differentiated -Significance for treatment?
SCC with perineural spread
Spindle cell tumours- Need for special stains to sort them out

Pigmented Lesions
Solar lentigo V Lentigo maligna V flat dark Seb K
Clinical V dermatoscopic V histology V Confocal microscopy
Different types of melanoma
Dysplastic nevus V Melanoma
Important clinical features- Age, other dysplastic nevi, dermatoscopic view
When to ask for further cuts
Importance of the type of biopsy used to sample the pigmented lesion.
Why partial punch biopsies are a potential death trap.
What cytological features make a melanocyte histologically atypical?

Nevi
Types of nevi- junctional, compound, dermal, congenital, dysplastic, Spitz, combined , blue
The difficulties with Spitz nevi

Pigmented non melanocytic tumours
Pigmented BCC
Pigmented SCC in situ Bowen's disease

Other Tumours- Benign and Malignant
Malignant
Merkel cell- histology, special stains, wide excision, refer, radiotherapy
AFX- Atypical fibroxanthoma, like a poorly differentiated SCC,
MFH- Malignant fibrous histiocytoma- goes deep, wide excision 10 mms.
DFX- dermtofibrosarcoma protuberans- very wide excision 3-5 cms- refer.
Recurrent SCCs- refer early, wide excision, often perineural or lymphatic spread.
Angiosarcoma- looks like a big bruise
T and B cell lymphomas

Benign
Often face- Adnexal tumours
Eccrine glands- syringomas, hidradenomas
Hair follicles- Trichoepitheliomas, desmoplastic variant, Cylindromas
Sebaceous glands- Seb adenoma, Sebaceous carcinoma
Vascular- Pyogenic granuloma, Kaposi's sarcoma
Epidermal nevi- Sebaceous nevi- Syringocystadenoma papilliferum, Trichoblastoma, form fruste BCC
Clear cell acanthoma
LPLK
Porokeratosis
Actinic keratosis
Viral wart

Medical Conditions confused with Skin Cancer
Prurigo nodules- pseudoepitheliomatous hyperplasia
Discoid lupus erythematosus
Deep fungal and Atypical mycobacterial infections
Early T cell lymphoma
Angiolymphoid hyperplasia
Granuloma faciale
Lymphocytoma cutis
Post scabetic nodule
Persistent insect bite reaction
Sweet's syndrome
Erythema elevatum diutinum
Tumoral calcinosis
granuloma annulare and NLD
Sarcoidosis
Xanthomas

Introduction to Skin Structure and Cells

You are welcome to listen to this podcast for free. It will introduce you to the way this course will be taught. If you find it to your liking then you can purchase subsequent module podcasts as you progress through the course. Each podcast will cost $25 AUS. You can purchase them either through your own Pay Pal account if you have one, or using your credit card through Pay Pal by clicking the Buy Now button at the bottom of each module introduction.

When you have completed all the podcasts in the course you may take the Australian Institute of Dermatology Certificate in Skin Cancer Histology.

To listen to this podcast please  first of all download a Powerpoint of the images used in the podcast and minimise it. Then Click this Link  to download the podcast. Start the podcast by clicking on the arrow. If you run a PC you will need Quicktime installed on your computer.  See this link if you need to download Quicktime. The podcast will run directly on a Mac.  


Each podcast will run for about one hour. It will contain audio and images plus instructions on which sections of the resource material to read with comments on the significance of that material as you work your way through it.
This first podcast though will use other online resources for illustrative purposes rather than the two recommended resources because I am assuming you will not already own them if you are just contemplating taking the course!

Try this uTube video on skin structure

1. BCCs

If you are doing skin cancer work then you need to have some idea of the histology of the lesions you are biopsying. You need to know the terms used in dermatopathology reports to assess their significance. It is not enough to look at the diagnosis at the end. BCCs are managed on the nature of their histological pattern. There is a big difference in management options between a superficial multifocal BCC and an infiltrating or morphoeic BCC.

 BCCs- Pathology relates to the treatments used

Superficial bcc V Nodular bcc V Infiltrating or Morphoeic

Thickness - penetration of creams eg Aldara and red light in PDT

Significance of Infiltrating BCC with these modalities

Basisquamous BCC

BCC with perineural spread

BCC in vessels- very rare

You can purchase a year's access to Modules 1 and 2 on BCCs and SCCs for $50. When you have completed Modules 1-7B you can sit the Certificate Examination on Skin Cancer Pathology of the Australian Institute of Dermatology and Skin Cancer College of Australia and New Zealand.

2. SCCs

SCCs-   SCC in situ- confined to epidermis

Compare and contrast clonal Seb K V SCC in situ

Invasive SCC can be well differentiated through to poorly differentiated -Significance for treatment?

SCC with perineural spread

Spindle cell tumours- Need for special stains to sort them out

3. Pigmented Tumours Malignant

Pigmented Lesions
Solar lentigo V Lentigo maligna V flat dark Seb K
Clinical V dermatoscopic V histology V Confocal microscopy
Different types of melanoma
Dysplastic nevus V Melanoma
Important clinical features- Age, other dysplastic nevi, dermatoscopic view
When to ask for further cuts
Importance of the type of biopsy used to sample the pigmented lesion.
Why partial punch biopsies are a potential death trap.
What cytological features make a melanocyte histologically atypical?

4. Pigmented tumours benign

Nevi

Types of nevi- junctional, compound, dermal, congenital, dysplastic, Spitz, combined , blue

The difficulties with Spitz nevi

Pigmented non melanocytic tumours

Pigmented BCC

Pigmented SCC in situ Bowen's disease

5. Other Malignant tumours

Malignant

Merkel cell- histology, special stains, wide excision, refer, radiotherapy

AFX- Atypical fibroxanthoma, like a poorly differentiated SCC,

MFH- Malignant fibrous histiocytoma- goes deep, wide excision 10 mms.

DFX- dermtofibrosarcoma protuberans- very wide excision 3-5 cms- refer.

Recurrent SCCs- refer early, wide excision, often perineural or lymphatic spread.

Angiosarcoma- looks like a big bruise
B and T cell lymphomas

6. Other Benign Tumours

Below is an overview of the GP histopathology course. Each of the topics will have a separate illustrated post.

Here we will deal with the histopathology of the common tumours you will see in skin cancer practice. We will concentrate on those histological features that have a crucial impact in determining how you treat the lesion.

eg BCCs- Pathology relates to the treatments used

Superficial bcc V Nodular bcc V Infiltrating or Morphoeic

Thickness - penetration of creams eg Aldara and red light in PDT

Significance of Infiltrating BCC with these modalities

Basisquamous BCC

BCC with perineural spread

BCC in vessels- very rare

eg SCCs-   SCC in situ- confined to epidermis

Compare and contrast clonal Seb K V SCC in situ

Invasive SCC can be well differentiated through to poorly differentiated -Significance for treatment?

SCC with perineural spread

Spindle cell tumours- Need for special stains to sort them out

Pigmented Lesions

Solar lentigo V Lentigo maligna V flat dark Seb K

Clinical V dermatoscopic V histology V Confocal microscopy

Different types of melanoma

Dysplastic nevus V Melanoma

Important clinical features- Age, other dysplastic nevi, dermatoscopic view

When to ask for further cuts

Importance of the type of biopsy used to sample the pigmented lesion.

Why partial punch biopsies are a potential death trap.

What cytological features make a melanocyte histologically atypical?

Nevi

Types of nevi- junctional, compound, dermal, congenital, dysplastic, Spitz, combined , blue

The difficulties with Spitz nevi

Pigmented non melanocytic tumours

Pigmented BCC

Pigmented SCC in situ Bowen's disease

Other Tumours- Benign and Malignant

Malignant

Merkel cell- histology, special stains, wide excision, refer, radiotherapy

AFX- Atypical fibroxanthoma, like a poorly differentiated SCC,

MFH- Malignant fibrous histiocytoma- goes deep, wide excision 10 mms.

DFX- dermtofibrosarcoma protuberans- very wide excision 3-5 cms- refer.

Recurrent SCCs- refer early, wide excision, often perineural or lymphatic spread.

Angiosarcoma- looks like a big bruise

Benign

Often face- Adnexal tumours

Eccrine glands- syringomas, hidradenomas

Hair follicles- Trichoepitheliomas, desmoplastic variant, Cylindromas

Sebaceous glands- Seb adenoma, Sebaceous carcinoma

Vascular- Pyogenic granuloma, Kaposi's sarcoma

Epidermal nevi- Sebaceous nevi- Syringocystadenoma papilliferum, Trichoblastoma, form fruste BCC

Clear cell acanthoma

LPLK

Porokeratosis

Actinic keratosis

Viral wart

7A Medical conditions confused with skin cancer1

Medical Conditions confused with Skin Cancer

Prurigo nodules- pseudoepitheliomatous hyperplasia

Discoid lupus erythematosus

Deep fungal and Atypical mycobacterial infections

Early T cell lymphoma

Angiolymphoid hyperplasia

Granuloma faciale

Lymphocytoma cutis

Post scabetic nodule

Persistent insect bite reaction

7B Medical conditions confused with skin cancer2

Sweet's syndrome

Erythema elevatum diutinum

Tumoral calcinosis

granuloma annulare and NLD

Sarcoidosis

Xanthomas

8. Inflammatory Skin Diseases- Reaction patterns

Skin histopathology can be divided into 7 patterns. The red scaly diseases PMs PET (AL) clinically correspond with the 2 epidermal histological patterns, namely Psoriatic or Spongiotic.
The red nonscaly diseases CUL DVA EVIE have essentially dermal histological patterns and they are Superficial and deep perivascular, Granulomatous, Interface, Lichenoid and Vesiculobullous. The Interface pattern may show epidermal features as it occurs at the level of the basement membrane eg Discoid lupus and the Vesiculobullous pattern may also show epidermal features if the vesicles or bullae are in the epidermis which is the case in herpes virus and bullous impetigo.
An 8th deep reaction pattern is Panniculitis when inflammation is in the fat layer in either the septae between the fat lobules or in the lobules themselves.


To diagnose an inflammatory skin disease you look at the Epidermis and then the Dermis and see which reaction pattern predominates. You may have more than one reaction pattern. When you have decided, consider the diagnostic possibilities and look for features which justify your choice. Alternatively look for other features on the slide before making a definite diagnosis and avoid biasing yourself!

9. Epidermal Patterns- Psoriasiform

A Psoriatic pattern does not just apply to psoriasis. Most of the red scaly diseases will show some features of a Psoriatic pattern, particularly acanthosis (thickening of the epidermis) and hyperkeratosis ( thickening of the stratum corneum). Remember the red scaly diseases are the PMs PET so Psoriasis, some types of eczema with lichenification (scratch induced epidermal thickening) and Tinea, plus Pityriasis rosea, Pityriasis versicolor and Pityriasis rubra pilaris plus Mycosis fungoides and s for Solar damage (Solar keratoses, Bowen's disease) will all exhibit some features that we classify as psoriasiform!

10. Epidermal Patterns- Spongiotic

Spongiotic This is the second Epidermal reaction pattern and is the hallmark of the Eczemas, especially the acute forms such as pompholyx and weeping atopic or contact eczema but also to a lesser degree in discoid eczema and lichen simplex chronicus.
Spongiosis refers to separation of the keratinocytes in the epidermis by fluid between them highlighting the desmosomes or spines in the spinous layer that hold the cells together. If some of these intercellular bonds break down you get little collections of fluid between the cells in the epidermis and these are called vesicles.(remember pompholyx eczema).

11. Dermal Interphase pattern

Working your way down from the epidermis the next reaction pattern you will meet will be what is called an Interphase pattern. This means the action is centred on the dermoepidermal junction and involves the basal cells including melanocytes and has some inflammatory cells , usually lymphocytes and histiocytic (scavenger) cells abutting the basement membrane and also passing through into the basal layers of the epidermis. The basement membrane may well be damaged and keratinocytes may shrivel up and become eosinophilic apoptotic cells. Because of damage to these basal layers the epidermis will look thinner. It is also useful to see if this process involves the walls of the hair follicles because if it does it suggests lupus erythematosus.

The diagnoses that mainly show this Interphase pattern are in the red nonscaly ballpark CUL DVA EVIE namely Lupus erythematosus, Drug reactions, some Viral exanthems and Erythema multiforme.

Lichenoid pattern we will deal with in the next section but it is characterised by a wide band of lymphocytes and histiocytic cells in the upper dermis, much wider than you see with an Interphase picture, although it also can show basal layrer damage. As the name suggests this pattern is mainly seen with lichen planus and its variant forms.

12. Dermal Lichenoid pattern

Next you come to the true Lichenoid pattern with a much denser infiltrate of lymphohistiocytic cells hugging the undersurface of the basement membrane. The degree of damage to the basal layer epidermal cells is often less in this reaction pattern than in the Interphase pattern but there can still be extensive damage to the basement membrane itself. Damage to basal layer melanocytes in this reaction pattern leads to pigment incontinence where melanin pigment is found in macrophages in the dermis. Hence clinically, diseases showing a lichenoid reaction pattern histologically, will show post inflammatory pigmentation clinically. The classic examples are Lichen planus and lupus erythematosus (discoid type). Although the cellular infiltrate in the band is usually lymphocytic you can see a plasma cell infiltrate in Syphillis and some eosinophils in a lichenoid drug reaction. Again note that most of the action is in the dermis so these will be mainly red nonscaly diseases but lichen planus does have Wickham's striae on the surface of the papules and pityriasis lichenoides as it's name suggests also has a scaly component. In T cell lymphoma, if the atypical lymphocytes invade the epidermis, you will also get a bit of scale.

Lupus erythematosus can also show a lichenoid pattern but it is usually not as extensive as lichen planus and it is more likely to involve the walls of the hair follicles. Unlike lichen planus it also causes a thickening of the basement membrane despite cells crossing this membrane and causing some gamage to the basal layer of cells. It can also cause melanin incontinence in macrophages in the dermis contributing to the post inflammatory hyperpigmentation seen in discoid lupus.

13. Dermal Perivascular vasculitic pattern

The next reaction pattern you should look for is the Superficial and Deep Perivascular infiltrate. Sometimes it is mild and sometimes florid with associated vascular damage with fibrin deposition in a vessel lumen clinically giving a frank vasculitis with palpable purpura. Again the diseases presenting with this reaction pattern will be dermal diseases, usually covered by the red nonscaly mnemonic, CUL DVA EVIE

The annular erythemas classically give this superficial and deep perivascular infiltrate with a tight cuff of lymphocytes around the vessels of the superficial and deep dermal plexus. This reaction pattern is in it's purest form in the annular erythemas(EAC, Erythema chronicum migrans, Erythema gyratum repens etc)but it is seen in a more non specific way in other reaction patterns involving lymphocytes and other inflammatory cells which initially have to make their way out of the blood vessels into the tissues! So do not call this the main reaction pattern unless it is all you have!

This reaction pattern is also seen in lupus erythematosus and dermatomyositis but you need a bit of Interphase damage as well to call either of those two diagnoses. Some measles like viral exanthems show it and some mild drug reactions where the addition of a few eosinophils to the perivascular lymphocytes help to point you in that direction.
A superficial and deep perivascular reaction pattern plus extravasated red cells is typically seen with the pigmented purpuric dermatoses found around the ankles.
A true vasculitis is characterized by neutrophils or lymphocytes infiltrating a vessel wall, plus pinkish fibrin being laid down in the wall or having nuclear dust from fragmented neutrophils within and around a vessel plus some extravasated red blood cells. These vasculitides can be classified histologically as leukocytoclastic when neutrophils are the predominant cell seen and lymphocytic when lymphocytes are predominant but the later a lesion is biopsied the more likely you are to see lymphocytes rather than neutrophils! Remember true vasculitis gives rise to palpable purpura clinically.
Large vessel vasculitis is seen deep in the reticular dermis with fibrin deposition in the thickened swollen walls. When one of these vessels is involved you get frank necrosis of the skin eg in Polyarteritis nodosa (See part 4 of Module) or Temporal arteritis or in some cases of Wegener's granulomatous vasculitis.

14. Dermal Granulomatous pattern

The next reaction pattern to look for in the dermis is the Granulomatous pattern. Granulomas are collections of histiocytic (macrophage) cells and lymphocytes (T cells) surrounding a central focus of infection or altered collagen or elastin or ocassionally other foreign bodies. The lymphocytes represent the T cell response of the acquired immune system trying to localise or remove a foreign antigen partly taken up by the macrophages. Nontheless the commonest cause of granulomas in the skin is the body's response to ruptured cysts or infected follicles or foreign body reactions to gout crystals or retained sutures or suture material.

Certain features of granulomas suggest certain diseases but there is significant overlap and some are not true to type. eg Palisading granulomas have the lymphohistiocytic cells surrounding degenerated collagen, elastin or mucin or fibrin. The main examples are Granuloma annulare, Necrobiosis lipoidica and Rheumatoid nodule. Because these are all dermalhistological changes they present as smoothe surfaced plaques or nodules generally skin coloured.
Caseating granuloma is characteristic of TB with necrosis developing in the centre of the granuloma.
Tuberculoid granulomas are described as naked granulomas because they are mainly made up of macrophages with very few surrounding lymphocytes. The main conditions showing this histological feature are Sarcoidosis, non caseating forms of TB and Leprosy where there is a highly developed immune response and few remaining organisms.

15. Dermal Epidermal Vesiculobullous pattern

Vesiculobullous Reaction Pattern This reaction pattern can involve both the epidermis and the dermis but essentially it is only the upper dermis and the undersurface of the dermo epidermal junction.Vesicles can form in the epidermis from severe spongiosis in eczema or because of epidermal cell necrosis from blistering viral infections such as herpes simplex or zoster or chickenpox. Bacteria can also cause blisters in the upper epidermis by lifting the stratum corneum from toxin damage or antibodies can break down the desmosomes between epidermal cells causing blisters or erosions as in pemphigus vulgaris.

However the classical blistering diseases occur because of damage at the basement membrane or the dermoepidermal junctional complex holding the two areas together.

16. Dermal infiltrates of cells or substances

Infiltrates of cells or substances is not a classical reaction pattern but it helps to include it to describe those dermal conditions not covered by the other reaction patterns. The cellular infiltrates can be neutrophils in cellulitis and Sweet's syndrome, eosinophils in allergic reactions such as insect bites or Well's syndrome or lymphocytes in follicles as in lymphocytoma or lymphoma and plasma cells in syphillis and some mucosal diseases.. Substances in the dermis include mucin in the mucinoses and other disorders including lupus and necrobiosis lipoidica, calcium in ectopic calcification, some drugs such as minocycline, tatoo pigments, uric acid in gouty tophi and cholesterol and triglycerides in the xanthomas etc!

17. Dermal Panniculitis pattern

The last reaction pattern I want you to look at is the Panniculitic pattern where you have damage to the fat layer either as a septal panniculitis with inflammation centred on the vessels in the septae between the fat lobules or a lobular panniculitis where most of the inflammation is centred on the fat lobules themselves. In reality there is often a bit of an overlap!