Pathology of the Integumentary System Lecture 2people.upei.ca/hanna/skin2/skinL2-WebF17.pdf ·...

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Pathology of the Integumentary System Lecture 2 Histopathologic Pattern Analysis (Web review) Paul Hanna Fall 2017

Transcript of Pathology of the Integumentary System Lecture 2people.upei.ca/hanna/skin2/skinL2-WebF17.pdf ·...

Pathology of the

Integumentary System

Lecture 2

Histopathologic Pattern Analysis

(Web review)

Paul Hanna Fall 2017

[For Information Only]

In haired areas of normal dog and cat skin the nucleated layers

of the epidermis are only 2 to 4 cell layers thick. Note, It is much

thicker in animals with sparse hair coats (eg pigs, humans).

Hyperkeratosis - increased thickness of stratum corneum;

ortho- (anuclear) or parakeratotic (nucleated)

Epidermal Changes

severe orthokeratotic hyperkeratosis in an alpaca with

congenital ichthyosis JAVMA 2013; 243:1701-3

parakeratotic hyperkeratosis in a dog with zinc-responsive

dermatosis.

[For Information Only]

Epidermal hyperplasia (acanthosis) - increased thickness of the noncornified epidermis.

a) Regular epidermal hyperplasia [For Information Only]

b) Irregular epidermal hyperplasia [For Information Only]

c) Papillated epidermal hyperplasia [For Information Only]

d) Pseudocarcinomatous epidermal hyperplasia [For Information Only]

Epidermal atrophy - decreased thickness of the noncornified epidermis

[For Information Only]

Intracellular edema

a) Hydropic (vacuolar) degeneration

[For Information Only]

hydropic degeneration of keratinocytes is characterized by a zone of cytoplasmic vacuolation immediately around nucleus

Intracellular edema

b) Ballooning degeneration

[For Information Only]

Ballooning degeneration of epidermal cells in Orf (parapox virus) infection

Intercellular edema (spongiosis) - accumulation of edema in the intercellular spaces

Spongiosis is characterized by the keratinocytes

being separated (pushed apart) by clear zones of

edema; note the intercellular bridges / “spines”

(desmosomes) of keratinocytes are prominent.

[For Information Only]

Acantholysis - loss of cohesion between keratinocytes; leads to clefts / vesicles /

bullae or pustules

[For Information Only]

Exocytosis - migration of inflammatory cells into the epidermis

[For Information Only]

Pustule - microscopic or macroscopic cavity filled with inflammatory cells

dermatopathologymadesimple.blogspot.ca

[For Information Only]

Crust - surface accumulations of keratin, serum, inflammatory cells, debris, bacteria ...

[For Information Only]

Necrosis / apoptosis - microscopic forms of cell death

necrosis locally extensive area of cell death

apoptosis multifocal / single cell death

[For Information Only]

Epidermal necrosis can be seen in

conditions such as burns (thermal or

chemical), ischemia / infarction and

some immune-mediated disorders

www.skin-science.com

[For Information Only]

Apoptosis is often seen in immune-mediated disorders (above) and

sunburn (right). Regarding the latter, UV-B radiation can induce

apoptosis within 30 minutes of sun exposure.

Necrosis / apoptosis - microscopic forms of cell death

necrosis locally extensive area of cell death

apoptosis multifocal / single cell death

Hyper - / hypopigmentation - increased or decreased amounts of melanin in the epidermis

[For Information Only]

Dermal edema - see widened spaces between dermal collagen &/or lymphatic dilation

Dermal Changes [For Information Only]

Collagen changes - including hyalinization, “degeneration”, mineralization, etc

[For Information Only]

[For Information Only]

Fibroplasia / fibrosis - formation and maturation of fibrous tissue, leading to

scarring (sclerosis).

[For Information Only]

Pigmentary incontinence - melanin granules free in the dermis or in dermal macrophages

Follicular changes - atrophy, dilation, keratosis, dysplasia, inflammation, etc

Glandular changes - inflammation, atrophy, hyperplasia, cystic change, etc

Vascular changes - fibrinoid degeneration, vasculitis, thromboembolism, etc

[For Information Only]

SUBCUTANEOUS CHANGES

• a variety of reactions

(eg inflammation, necrosis, fibrosis, etc)

from direct extension of changes in the

overlying dermis

in isolation from changes in overlying dermis

[For Information Only]

• dermatitis is not particularly useful term without qualification, since the skin

becomes inflamed in response to a myriad of causes

• pattern-analysis, at low magnification, relates inflammatory patterns to various

types of skin diseases

• details at higher magnification often allow for a specific diagnosis

HISTOPATHOLOGIC PATTERN-ANALYSIS

Normal

Normal skin – in the diagram the uniform lighter grey

appearance of the dermis is used to represent the uniformity

of the closely packed collagen fibers, while the darker grey

represents the uniformity of the epidermal layer.

1) PERIVASCULAR (INTERSTITIAL) DERMATITIS

• inflammatory reaction centred on the superficial and/or deep dermal vessels.

[note: the term interstitial dermatitis is often used when the inflammatory cells

are more widely dispersed than just surrounding the dermal blood vessels]

Perivascular (interstitial) dermatitis

Spongiotic perivascular (interstitial) dermatitis

Hyperplastic perivascular (interstitial) dermatitis

Perivascular (interstitial) dermatitis

• esp hypersensitivities.

note edema in the superficial dermis (ie “washed

out” appearance) and perivascular accumulation

of inflammatory cells.

Spongiotic perivascular (interstitial) dermatitis

• esp HS’s, contact dermatitis, ectoparasitism, viral, dermatophytosis, Malasseziasis, etc

Note: similar to perivascular / interstitial dermatitis with the

addition of epidermal spongiosis (ie intercellular edema).

Hyperplastic perivascular (interstitial) dermatitis

• esp in chronic hypersensitivities, altered keratinization, lick dermatitis, etc

Note: similar to perivascular / interstitial dermatitis with the

addition of prominent epidermal hyperplasia.

2) INTERFACE DERMATITIS

• immune-mediated / autoimmune skin diseases, drug reactions, some viral infections, etc

Interface dermatitis – diagrams show obscuring of the dermoepidermal junction (ie interface) with hydropic

degeneration [left] and/or lichenoid infiltrate of inflammatory cells + hydropic degeneration [right]

3) VASCULITIS • seen with a variety of infections, immune mediated diseases, etc

Note, vasculitis denotes inflammation and damage of the

blood vessel wall; which is more obvious in the image above.

Nodular or multinodular dermatitis denotes discrete

cluster(s) of inflammatory cells within the dermis.

4) NODULAR AND DIFFUSE DERMATITIS

• esp traumatic implantation of foreign material / bacteria / fungi / protozoa

Diffuse dermatitis denotes a dense diffuse (within the

confines of the biopsy) inflammatory cell infiltrate with

effacement of the normal dermal architecture.

Note - some might think this is a form of interstitial dermatitis

but the density of the inflammatory cell infiltrate is much

greater in diffuse dermatitis

5) VESICULAR & PUSTULAR DERMATITIS

Intraepidermal vesicles / pustules:

Note: vesicular if cavity is empty (left) and pustular

if contains inflammatory cells (right).

a) acantholysis (eg neutrophilic enzymes, pemphigus Ab)

Normal Epidermis Leakage of neutrophil enzymes in

bacterial infections or Auto Ab’s (eg

pemphigus) damage desmosomal

adhesion molecules

Loss of cohesion between keratinocytes

results in intraepidermal vesicle /

pustule formation

Intraepidermal vesicles / pustules due to:

Normal Epidermis Ballooning degeneration of

keratinocytes due to viral

infection

Vesicle results from rupture &

coalescence of virally infected

(ballooning degenerate) cells

Intraepidermal vesicles / pustules due to:

b) coalescing ballooning degeneration in viral dermatitis

Intraepidermal vesicles / pustules due to:

c) intense intra- &/or intercellular edema of the epidermis

Severe intercellular (spongiosis) as seen in the photomicrograph above, can push the

keratinocytes apart resulting in breaking down of intercellular adhesion to form vesicles.

Early developing vesicle (above right) and well developed vesicle (below right)

5) VESICULAR & PUSTULAR DERMATITIS

Subepidermal vesicles / pustules

Note: vesicular if cavity is empty and pustular if

contains inflammatory cells.

Bullous pemphigoid showing subepidermal vesicle

a) genetic or autoimmune damage of hemidesmosome adhesion molecules

b) severe subepidermal edema and/or cellular infiltration damaging D/E junction

5) VESICULAR & PUSTULAR DERMATITIS

Subepidermal vesicles / pustules due to:

Normal dermoepidermal junction Genetically defective or

autoimmune attack of adhesion

molecules in hemidesmosomes

Loss of cohesion of basal keratinocytes to

dermis, resulting in subepidermal vesicle

or pustule formation

6) PERIFOLLICULITIS, FOLLICULITIS, FURUNCULOSIS

• especially due to bacteria (staph) or fungi (ringworm) or parasites (demodex)

Perifolliculitis – accumulation of

inflammatory cells surrounding hair

follicle.

Furunculosis – effacement / rupture of

the hair follicle due to intense

inflammation.

Folliculitis – accumulation of

inflammatory cells within the wall

&/or lumen of the hair follicle.

folliculitis furunculosis

7) PANNICULITIS

• often extension from nodular or diffuse dermatitis; nutritional, injection, idiopathic

Note: the inflammation in the subcutis can be lobular (in

fat) or septal (in connective tissue separating lobules),

but is mostly diffuse (ie involving both septa and lobules)

8) ATROPHIC DERMATOSIS

• usually due to endocrine disorders; less nutritional or developmental dermatoses

Note: with atrophic dermatosis see varying combinations of:

- orthokeratotic hyperkeratosis

- epidermal melanosis

- sebaceous gland atrophy

- changes indicating hair cycle arrest:

• telogen predominance (± hair shafts)

• follicle dilation & keratin plugging

• follicular atrophy

Hyperkeratosis with

increased melanin

Dilated, atrophic follicle

filled with keratin Atrophic sebaceous gland