Test 3: skin Flashcards
— prevents water loss and protect from environmental insults
enclosing barrier
stratum corneum
3 ways skin acts as barrier
continuously shed- desquamation
hydrophobic
inherent immune system= keratinocytes, langerhands, dendritic cells and lymphocytes
basal layer of skin attaches to basement membrane by —
hemidesmosomes
what do merkel cells do
sensory in skin, can tell if hair is moved
histiocytosis is cancer of —
langerhans cell- can spontaneously regress
melanocytes transfers melanin to —
keratinocytes
what causes hyperpigmentation after injury such as constant scratching
melanocyte
vitiligo is also called
depigmentation
leukoderma
loss of melanocytes
is this malignant?
no not melanoma
flat/macules of pigment
lentigo simplex
incidental finding
melanocytoma
raised black nodule on haired skin
melanoma- usually in oral cavity
merkel cells are mechanoreceptors in — and hair follicles
tylotrich pads
keratinization is also called
cornification
keratinocytes deposit keratin to form barrier
sarcoma has —intermediate filament
vimentin
carcinoma has — intermediate filament
keratin
— have hemidesmosomes that attach to basement membrane
stratum basale
stratum basale is the — layer with slow cycling stem cells
progenitor layer
stratum spinosum attaches by —
desmosomes
where can you find langerhans cells
stratum spinosum
what does filaggrin do?
takes keratin filaments and packs them together
contains keratohyalin granules
found in the stratum granulosum layer
— is the outermost layer of skin that is fully keratinized, anucleate and dead
stratum corneum
continuously shed
mortar and bricks
primary abnormalities of cornification are —
mutations in the enzymes, structural proteins or lipids that form the outer layer of skin
fish scale disease is called
ichthyosis
genetic condition of scaling due to faulty formation of stratum corneum
xerosis means
dry skin
how does cornification work
1) Cleavage of keratinocyte cytoplasmic contents
2) Compaction of keratinocytes
* Binding of keratin via Filaggrin
* Replacing cell membrane via Transglutaminase
3) Lipid bilayer formation
stratum corneum with retained nuclei
parakeratosis
how is lipid bilayer formed in skin
lamellar granules will unfurl and dump lipid into junction between granular and corneum layer
lipids hold corneocytes together and repels water- provides moisture and hydrophobic barrier
harlequin ichthyosis
defective lamellar bodies- no lipids in top layer
can’t slough stratum corneum
what happens with golden retriever ichthyosis
shedding/scaling
abnormal lipid
Epidermolytic ichthyosis Keratin mutation
Norfolk terrier
become very pigmented and scaly
cell membrane in corneum layer becomes— by —
cornified envelope
transglutaminases (TGM1)
jack russel
transglutaminases (TGM1) mutation
cells membrane is not changed into cornified envelope
what causes desquamation
sloughing/shedding of skin
enzymes
Epidermolysis bullosa
problem with basement membrane- skin falls off, hoof falls off
epidermis is not anchored to dermis
clear zone in the basement membrane seen on electron microscopy
lamina lucida
part of basement membrane that contains primarily type IV collagen
lamina densa
part of basement membrane that anchors fibrils and type VII collagen
sublamina densa
blisters
Epidermolysis Bullosa Acquista
problem with basement membrane- leads to blister and epidermis not attaching to dermis
what causes wrinkles in shar pei
excess hyaluronic acid- filler
can lead to vesicles
ehlers-danlos
problem with collagen
affects connective tissue, primarily the skin, joints, and blood vessel walls.
sebaceous gland in hair follicle is what type of secretion
holocrine
hair cycle
anagen- growing
telogen- arrested
furunculosis
rupture of hair follicle
leads to hair loss
can be secondary to inflammation in infundibulum of hair follicle →folliculitis
what hormones inhibit hair growth
Glucocorticoids
Estrogen
what hormones stimulate hair growth
thyroid hormone and androgens
Tylotrich hairs are —
mechanoreceptors that attach to merkel cells
sebaceous adenitis
problem with sebaceous gland, leads to decrease in lipids, corneum can’t slough, leads to scaling
eccrine sweat galnds (atrichial) are found —
paw pads
empty directly onto surface of skin
apocrine sweat glands (epitrichial) are found —
empty into hair follicle
papules- little raised lesions
demodex infestation
plaques- large flat lesion
eosinophilic granuloma complex
pustule → papule filled with pus
eosinophilic or neutrophilic
pustule and crust
crust vs scale
crust- ruptured pustule, cell debris, bacteria
scale- dandruff, stratum corneum
hemorrhagic crust
scale
hypothyroidism will do what to blood work?
hypercholesterol
mild anemia
eschar resulting from thermal burn
bullae
vesicles- smaller then bullae
wheal- hives- solid firm raised
macules- flat/even with skin surface
sertoli cell tumor producing estrogen
patches- flat/ even with skin surface
patches- flat/ even with skin surface
> 1 cm
erosion
above basement membrane
ulcer
below basement membrane
comedomes - blackheads
comedo can be caused by
demodex mites
or
filled with keratin
where are scabies and demodex found?
demodex- in hair follicle
scabies- on skin surface
hyperplastic change resulting from chronic friction or inflammation
Lichenification
epidermal collarette
rums of flaking scale and the erosion of the center
itching is also called
pruritus
caused by
epidermal collarette
superficial pyoderma- caused by Staph Pseudintermedius
what is the most common cause of pyoderma in dogs
staph pseudintermedius
name 4 chronic changes
Alopecia
lichenification
erythema
hyperpigmentation
with chronic skin trauma what will happen to the hair follicles, glands and dermis
hyperplasia and folliculitis
sebaceous glands- hyperplasia
apocrine gland- cystic dilation and inflammation
dermis- fibrosis
sub-epidermal vesicular pattern/ pustular dematitis
Perivascular Dermatitis
lichenoid Interface Dermatitis
Epidermal Vesicular and Pustular Dermatit
Nodular and Diffuse Dermatitis- panniculitis
Folliculitis/ perifolliculitis and furunculosis
Atrophic Dermatoses
Acantholysis is the hallmark of — which is driven by a Type II hypersensitivity reaction to intercellular adhesion molecules.
pemphigus foliaceus
antibodies attack adhesion molecule between keratinocytes
two differentials
superficial pyoderma
or
Pemphigus foliaceus- autoimmune type II reaction
three differentials for filliculitis
staph pseud
demodex
dermatophytosis (ring worm)
what can cause this
steroid- cause epidermal atrophy and hair loss/atrophy
Perivascular Dermatitis
Inflammatory cells
aggregate around
blood vessels
nonspecific
dermal edema/ space between epidermal cells
spongiosis
chronic perivascular will cause
Epidermal hyperplasia
Acanthosis
Spongiosis
Rete ridges
Orthokeratotic vs Parakeratotic hyperkeratosis
ortho- normal formation, just alot of keratin
para- abnormal, still has nucleus
type 1 hypersensitivity reaction
mast cell histamine
produce wheal/ hive
superficial perivascular dematitis can be caused by hypersensitivity disorders such as — or by —
flea bite hypersensitivity
atopy- the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema)
food allergy
ectoparasitism- sarcoptic mange
Pruritus vs Pruritic
- Pruritus = unpleasant sensation which provokes the desire to scratch
(itching)
*Pruritic = itchy
what three things can cause this
- Superficial trauma
*Bacterial
- Fungal- Malassezia
Lichenification: thickening of the skin associated with accentuation of the normal skin markings
hyperpigmentation
what does Malassezia look like
snow man or foot prints - fungus
flea bite hypersensitivity reaction
sarcoptic mange- ears, elbows, eyes
Notoedres cati - “feline scabies”
what causes parakeratosis
increased epidermal turnover or metabolic disease
can be caused by trauma, malassezia (fungi) infection
corneum with nucleus
Zinc Responsive Dermatosis with Pa rakeratosis
zinc is needed for epidermal differentiation
Arctic breeds but any breed possible if poor diet, scaly plaques on face and pressure points. Perivascular dermatitis with epidermal and follicular parakeratotic hyperkeratosis
Zinc-responsive dermatosis occurs in — and causes the formation of —-
Arctic breeds but any breed possible if poor diet, scaly plaques on face and pressure points. Perivascular dermatitis with epidermal and follicular parakeratotic hyperkeratosis
Superficial necrolytic dermatitis (SND)
(Hepatocutaneous syndrome)
causes parakeratosis
skin disorder in dogs caused either liver disease (hepatocutaneous syndrome) or less likely glucagonoma (glucagonoma syndrome). Characteristic low magnification features: parakeratotic hyperkeratosis (red), acanthosis with intracellular edema in spinous layer (pallor- white), hyperplasia of basal layer keratinocytes (blue); so-called “red, white, and blue” appearance. Poor prognosis
Superficial necrolytic dermatitis (SND) is caused by — and forms — in the skin
liver disease (hepatocutaneous syndrome) or less likely glucagonoma (glucagonoma syndrome),
faulty proteins- have very low animo acids
effects paw pads, lips and genitalia
Characteristic low magnification features: parakeratotic hyperkeratosis (red), acanthosis with intracellular edema in spinous layer (pallor- white), hyperplasia of basal layer keratinocytes (blue); so-called “red, white, and blue” appearance. Poor prognosis
Superficial necrolytic dermatitis (SND)
Pathologic events target basal keratinocytes and dermoepidermal
junction
Interface Dermatitis
three causes of Interface Dermatitis
Immune complex deposition
Type II hypersensitivity reaction
Autoreactive cytotoxic T cells
what are some differentials for interface dermatitis
drug reaction
lupus
german short hair pointer
Exfoliative Cutaneous lupus
form of interface dermatitis
Erythema multiforme can be caused by —. what happens to skin?
adverse drug reaction
Lymphocyte-mediated destruction of keratinocytes
— is Lymphocyte-mediated destruction of keratinocytes
Erythema multiforme
how does interface dermatitis differ from pericascular dermatitis
usually immune dysfunction
attacks basal keratinocytes and dermoepidermal junction
can be caused by immune complex, type II hypersensitivity, autoreactive cytotoxic T cells, drug reaction
example: lupus or erythema multiforme
vesicle vs bulla
blisters
vesicle smaller then bulla
— are keratinocytes which separate
completely from their neighbors, become round, with a round nucleus and eosinophilic cytoplasm
acantholytic cells
— is the loss of cohesion between epidermal cells or keratinocytes. Results in the formation of clefts, vesicles and pustules.
Acantholysis (loosening of the spines Gk .)
not the same as acanthosis- hyperplasia of the stratum spinosum
Acantholysis- (loosening of the spines Gk .) is the loss of cohesion between epidermal cells or keratinocytes. Results in the formation of clefts, vesicles and pustules.
most common cause of acantholysis
Autoimmune disease due to autoantibody production to cell
adhesion molecules
type II hypersensitivity reaction
other then autoimmune what else can cause acantholysis
bacterial infection with release of proteolytic enzymes and bacterial
toxins
(rare) dermatophytosis (Trichophyton sp.)
severe edema (spongiosis)
caused by autoantibody to —
desmocollin-1
Pemphigus Foliaceus
sterile pustules
Acantholysis, healthy neutrophils, no bacteria
Pemphigus vulgaris is caused by antibody to —
desmoglein-3
(lower in the skin then Pemphigus foliaceus)
found in the mouth
Acantholysis with suprabasilar clefting
— caused Acantholysis with suprabasilar clefting and is found in the mouth
Pemphigus vulgaris
Desmoglein-3 autoantibody
get tombstone effect
— causes tombstone effect basal cells stay cause disease does not attack hemidesmosomes
Pemphigus vulgaris
Acantholysis with suprabasilar clefting
mouth
Desmoglein-3 autoantibody
PF vs pyoderma
PF- no bacteria, healthy neutrophils
pyoderma- + bacteria, necrotic cells, smaller, minimal acantholysis
PF has autoantibody to –
intracellular molecule in the desomones that hold cells together
causes cells to break apart
PF= desmocollin-1 autoantibody
PV= Desmoglein-3 autoantibody (mouth)
blistering disorder of the basement membrane caused by autoantibody formation
epidermolysis bullosa aquisita
bullous pemphigoid
can peel off skin
Co ngenital Epidermolysis Bullosa
skin peeling off
Epidermolysis Bullosa
nodular/diffuse dermatitis will have infiltrate with —
(1) neutrophilic (e.g. bacterial)
(2) eosinophilic (e.g. parasitic or eosinophilic granuloma)
(3) histiocytic - chronic granulomatous or pyogranulomatous lesions (e.g. mycobacteria, fungal, foreign body)
acid fast stain showing mycobacteria what type of dermatitis?
infectious nodular/diffuse
what are two causes of noninfectious diffuse/nodular dermatitis?
Eosinophilic collagenolytic granuloma
Often associated with hypersensitivity disorder
what type of organism cause nodular/diffuse dermatitis?
mycobacteria, fungal
How does the character of the infiltrate of nodular/diffuse dermatitis give clues to cause?
epithelioid macrophages= granuloma =mycobacteria or fungus or foreign body
neutrophilic (e.g. bacterial)
(2) eosinophilic (e.g. parasitic or eosinophilic granuloma)
— forms scabs with oily exudate, in dogs often idiopathic and sterile
panniculitis
inflammation of the hair follicle
folliculitis
follicle rupture with inflammation;
Furunculosis
What are the three major causes of folliculitis?
bacteria infection- staph pseud
dermatophyte- ringworm
demodex mites
what kind of bacteria causes folliculitis?
Staph. pseud
ringworm is also called
dermatophytosis (fungi)
Dermatophytosis is a Specific group of fungal organisms that utilize — in hair
keratin
ringworm= Microsporum, trichophyton, epidermophyton
cause folliculitis and furunculosis
clinical presentation of folliculitis
alopecia
nodules
What inflammatory reaction occurs when the hair follicle ruptures?
granulomatous
atrophic dermatoses cause atrophy of skin and is caused by —
steroids
or
spontaneous Hyperadrenocorticism
caused by steroid use
calcinosis cutis
spontaneous Hyperadrenocorticism
or from steroid use
