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derm Flashcards

1
Q

skin anatomy 3 parts

A

3 parts:
-epidermis
-dermis
-subcutis (mostly adipose tissue)

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2
Q

epidermis structure 4 layers

A

-top to bottom
 Stratum Corneum
 Stratum Granulosum
 Stratum Spinosum
 Stratum Basale
 Stratum Lucidum (nonhaired skin only)

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3
Q

rete pegs/ rete ridges

A

the basement membrane is the scaffold of wound healing
-hold the epidermis to the subcutis, strengthens connection.
-calluses are thickening of epidermis with more rete pegs.

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4
Q

nerves in the skin

A

-motor nerves for hair follicle movement and skin contraction
-sensory: itchy, pain. touch, pressure, temperature

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5
Q

hair growth cycle

A

-humans and poodles anagen is the growing phase
-most mid hair dogs 20% in anagen
-large hair breeds Husky 9% in anagen takes along time for hair to grow back.

-anagen: growing
-catagen: transitional
-telogen: resting
-early anagen
-exogen

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6
Q

follicular growth anagen phase

A

 Anagen = growth stage

 Stimulated by:
 Thyroid and growth hormone
 Melatonin

 Suppressed by:
 Estrogen and glucocorticoids

-hair Needs protein, starving leads to weak, not growing hair.

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7
Q

functions of hair

A

-hair follicles: protection, thermal insulation, social communication, sensory perception

-tactile hairs: specialized mechanoreceptors

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8
Q

stratum corneaum function

A

-insoluable and impermeable, protection
-melanin protects from UV rays
-basement mambrane zone helps with achoring of skin and filering of chemicals
-collagen and elastin: resilience strength support

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9
Q

functions of skin

A

 Adnexal glandular secretions:
 Sebaceous = sebum (oil)
 Apocrine = sweat to protect skin
surface
 Eccrine = foot sweat

 Panniculus (subcutis):
 Padding and anchoring
 Facilitates movement
 Store fat, etc.

 Claws, hooves:
 Thick cornification for traction and
protection

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10
Q

alterations in epidermal growth in response to injury

A

-hyperkeratosis: increase in thickness of the stratum corneum. normal in some locations (paw pads, nasal planum). parakaratosis are cells with nucli present.

-hyperplasia: increase # of cells in the epidermis, common with inflammation

-Acanthosis: hyperplasia of the stratum spinosum

-hypoplasia: decrease in # of cells/ size (hyperadrenocorticism)

-aplasia: failure to develop (epitheliogenesis importfecta

-apoptosis: cell death, programed kertitination or pathological (Immune disease)

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11
Q

alterations in fluid balance and cell adhesion of the epidermis

A

-edema: spongiosis is inflammatory change, swelling with some viruses

-acantholysis and vesicles: loss of cohesion between epidermal cells. (pemphigus), pyoderma

-alterations in epidermal growth: atrophy (thin skin in cushing dogs)

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12
Q

inflammatory lesions of the epidermis in response to injury

A

-exocytosis of leukocytes into the epidermis, vesicles with inflammatory cells and crusts of dried ecaudate on epidermal surface.

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13
Q

epidermal pigmentation in response to epidermal injury

A

-leukoderma: hyperpigmetation
-lentigo (common) older orange cats, where they rub skin (anus, face, ears) dark pigments, normal.

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14
Q

response to injury dermis

A
  1. Alterations in dermal growth or differentiation
  2. Atrophy
  3. Fibrosis
  4. Solar elastosis
    -horses get exuberant granulation tissue
  5. Inflammatory lesions and depositions, fragmented collagen
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15
Q

follicular atrophy in response to injury

A

PHYSIOLOGIC ATROPHY
 Growth of hair is seasonal* and it
is controlled by environmental*
and genetic factors

PATHOLOGIC ATROPHY
 Hormonal abnormality*
 Inadequacy of vascular supply
 Inflammation*
 Systemic illness & Stress

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16
Q

panniculitis

A

-inflammation of SUBQ fat

causes:
primary: vit E deficiency, vaccination
secondary: bacterial foliculitis

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17
Q

folliculitis

A

-inflammation of the hairfollicle
-causes: parasites (demodex), bacteria (staph), dermatophytes

-furnucolosis: perforating folliculitis, has edema, hair follicle fully ruptures and invades tissue around it

-the progression of folliculitis is: perivascular, mural, luminal , rupture, drain

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18
Q

congenital or hereditary skin disorders

A

epitheliogenesis imperfecta:
1 complete failure of epithelium and adenxa to develop
2 small lesions animal will be fine
-bacteria can get in and lead to septicemia (e.coli)

ichthyosis fetalis:
1 FATAL, congenital and inherited disorder (calves, puppies)
-usually on feet and muzzle, on charlae cattle entire body. not common.

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19
Q

Temperature injuries cold

A

frostbite:
 Freezing of water in and around cells -> ice crystals pull water from cells -> increased osmotic pressure

-leads to vasoconstriction-> tissue anoxia
-endothelial damage-> decreased BP
-coagulation necrosis from blood clots

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20
Q

temperature injuries heat

A

burns
 Dry heat (hair dryer) -> desiccation + carbonization
 Moist heat (hot water) >coagulation of tissue

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21
Q

different degrees of burns

A

Partial thickness = 1 st (epidermis) and 2nd degree burns:
 Accelerated cellular metabolism
 Inactivation of enzymes
 Vascular injury
 Scarring, but adnexa are preserved, regeneration

 Full thickness = 3rd degree burns
 Coagulation of the epidermis and dermis
 4 th degree burns extend into the fascia and SQ
 Sloughing

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22
Q

temperature solar injury

A

-called Actinic dermatosis
 UVB is most damaging
 Acute = sunburn
 Chronic = solar dermatosis or neoplasia

-lesions develop in poorly haired or lighty pigmented sites (exp abdomen)

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23
Q

photosensitization

A

 Pathogenesis:
 UV light absorbed by photodynamic chemical in skin tissue -> reactive oxygen
(free radicals) -> mast cell degranulation

-erythema and edema–>blisters, excudation, necrosis, sloughing

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24
Q

photosensitization types

A

Primary photosensitization
type 1
 Ingestion of preformed photodynamic substances
 Administration of drugs (tetracycline, sulfonamides…)

type 2
 Abnormal porphyrin metabolism
(NB: Triple “I”: ingestion, injection and inheritance)

 Secondary photosensitization
-type III Hepatic diseases

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25
Q

plants and substances associated with photosensitazation

A

 Plants associated with hepatic photosensitization:
 Lantana
 Puncture vine
 Mycotoxins

 Plants with photodynamic substances:
 St. John’s wort
 Buckwheat
 Spring parsley

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26
Q

chemical injruy

A

 Contact Irritant Dermatitis
 Direct damage caused by caustic
chemicals
 Systemically distributed
chemicals:
 Arsenic, mercury, thallium, iodine,  Plants: selenium, mimosine,
trichothecenes

lesions: Hyperkeratosis, squamous
metaplasia

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27
Q

ergot poisoning

A

 Pathogenesis:
 Ingestion of grain/seeds infected by Claviceps purpurea -> produce ergotamin ->
arteriolar spasm and endothelial damage -> ischemia of distal extremities, tail etc.
 Appetite, cardiovascular function, endocrine activity, gastrointestinal motility, muscle
contraction, and temperature regulation (vasoconstriction)**

-gangrene feet or fescue foot

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28
Q

fescue foot

A

 Tall fescue is infected with the fungal endophyte Neotyphodium
coenophialum
 The endophyte produces Ergot Alkaloids

29
Q

injection site reactions

A

 Injection site reactions (rabies vax alopecia) 3-6 months after vaccination** then hair growns back
-ischemia and damage to hair follices, panniculitis

-usually self harm diseases from atopy or allergic reactions

30
Q

acral lick dermatitis

A

 Hyperkeratosis, acanthosis,
 lick granulation tissue and fibrosis
-common, usually has underying cause, food allergies or skin damage.
-lesions: circumscribed, hairless, erythamtous, ulcerated.

31
Q

hot spots (pyotraumatic dermatitis)

A

-moist crusty lesion
-common in dogs
 Occur secondary to licking and scratching
 Usu. Underlying diseases
-self inflicted trauma, biting, pain
gross: excudative, ulcerative, red egdes, alopecia.

32
Q

infectious skin diseases defense mechanisms

A

 Cutaneous infections develop when there is disruption of dermal
defense mechanisms

 Physical barrier (hair coat, pigment, desquamation of stratum corneum)
 Chemical and biochemical barrier (lipids, transferrin, antimicrobial substances)
 Biologic barrier (microbial flora)
 Innate immunity (transferrin, antimicrobial substances, defensins)
 Acquired immunity (antibodies, lymphocytes)

33
Q

contagios ecthyma ORF

A

 Parapoxvirus
 young sheep and goats
 High morbidity and low mortality
 Lesions: proliferative, crusting dermatitis
 Mouth -> oral mucosa, eyelids, and feet
 $$ weight loss in lambs
 Zoonosis possible (milkers nodules)

34
Q

papilomaviruses

A

 GAIN access through defects in epithelium
 ENTER basal layer

 3 outcomes:
1. Virus DNA replicates with cells.
2. Virus converts from latent to productive
3. Virus is integrated into the genome -> tumor
 Exophytic or endophytic papillary benign masses
 Sarcoids = fibropapillomas (particularly in equids)
 Bovine papillomavirus 1 and 2 infection of fibroblasts
 Frequently recur, may regress, locally aggressive (non-metastatic)

35
Q

exudative epidermitits

A

-greasy pig disease
-caused by staphlococcus hysius
-neutrophillic pustules that develop into crusts in pigs and dogs
-acute often FATAL dermatitis of neonatal piglets, mild in older piglets

36
Q

deep pyoderma

A

-deep bacterial infections involve the entire infundibular, isthmic and/or inferior portion of the hair follicles +/- surrounding dermis and subcutis.
 Less common than superficial pyoderma
causes:
 S. pseudointermedius folliculitis/furunculosis in dogs
 Cat fight abscesses
 Often secondary

37
Q

feline leprosy

A

-caused by Mycobacterium lepraemurium
 Cold, wet areas – PACIFIC NORTHWEST (USA/CA) BC and washington
 PCR test only
 Gross: Head, neck and limbs – SQ nodules and crusts

 Histo: two patterns
1. diffuse granulomatous w/o necrosis, many intrahistiocytic acid fast bacilli
2. granulomas with central necrosis, surrounded by lymphocytes, few
acid fast bacilli

38
Q

Erysepelas

A

 Secondary to systemic bacterial infections, usually in finisher pigs 12 weeks of age.
 Erysipelothrix rhusiopathiae (“diamond skin disease”) due to rhomboid shaped skin lesions
 Vasculitis, thrombosis and ischemia (infarction) central of single BV

morph: dermal and epidermal infarctions

39
Q

contagious foot rot

A

 Pathogenesis:
 Trauma & moisture + Bacteroides nodosus and Fusobacterium necrophorum
 B. nodosus produces potent proteolytic enzymes
 F. necrophorum is predominantly
responsible for necrosis resulting in
separation and sloughing of hooves

40
Q

dermatophilosis (rain rot)

A

-associated with prolonged wet skin, keep dry for treatment.
-ZOONOTIC on fingers
-horses and cattle, usually young.
sheep= lumpy wool

-lesions: crusts with matted hair over back and distal extremitires. paint brush on pulled hair

41
Q

mycotic skin disease ringworm

A

-RINGWORM: caused by mycrosporum canis/ trichophyton.
 Love the Stratum Corneum layer and
Hair Shafts
 DO NOT have to enter the living skin tissue to cause disease
 ZOONOTIC
 Asymptomatic cats – Toothbrush technique

42
Q

mycotic skin infection yeasts

A

-malassia pachydermatis
-lipophilic yeast normal in ear canal and skin
lesions: hyperpigmented, alopecic, scaly
 Microclimate or host defenses changed
 Mostly interdigital, otic, perianal, and intertriginous (spots that rub)

43
Q

ectoparasites mites

A

-demodex canis: demodectosis.
in juvenile dogs from the dam. they have underlying disease causing immune suppression.

-localized ( face or forlegs )or generalized scaling. not pruritic unless pyoderma.
-deep skin scraping

-sarcoptic mange (zoonosis) dogs and cats. extreme puritis
-cheyketiella (walking mange) looks like dandruff on fur
-chortoptic mange (cattle)

44
Q

lice skin diseases

A

-pediculosis
-from biting or sucking lice, whole cycle on host

45
Q

ectoparasites causing skin lesions myisasis

A

-larval infestation by dipterous flies
-blow flies and fresh flies
-eggs on wounds-> larve secrete enzymes-> holes and ulcerated skin.
-cuterebra sp. (kittens)
-screwworm in cattle $$

46
Q

screwworms

A

 New world = Cochliomyia hominivorax
 Old world = Chrysomyia bezziana
 Tropical climates
 Screwworm flies deposit eggs in
wounds or near mucocutaneous
junctions -> develop into L1 and feed on
tissue -> soon develop into L2

-regulatory pest

47
Q

cutaneous habronemiases

A

 Habronema or Draschia sp. larvae
 Skin that is traumatized or moist.
 Medial canthus of eye or prepuce.
 Unable to penetrate normal skin
-horse disease on mouth or penis

48
Q

immunological diseases rxn types

A
  • Hypersensitivity: reaction to normally harmless foreign substances.
    – Most are type I and IV reactions in skin
    – Common in dogs and horses
    – Less common in cats, uncommon in FA
  • Autoimmune: antibodies or T lymphocytes react against self-antigens.
    – Tend to be type II and III.**
    – Cutaneously manifested autoimmune diseases are uncommon in domestic
    animals.
49
Q

Urticatia and Angioedema

A
  • Urticaria = hives: edema of the
    superficial dermis
  • Angioedema: edema of the deep
    dermis and subcutis
  • Most common in dogs and horses
  • Causes:
    – Immunologic: foods, drugs, antisera,
    insects
    – Non-immunologic: heat, stress, exercise
50
Q

atopic dermatitis

A

-Genetically predisposed** inflammatory and pruritic allergic skin disease
* Type I hypersensitivity**
* Average age of onset is from 1 to 3 years
 Skin is the major target organ in dogs, cats, and horses
 Route of allergen exposure could be respiratory or skin
 It is suspected to be predominantly percutaneous absorption of allergens
-2nd most hypersens in dogs

-lesions: rubbing, PURITIS, alopecia. do allergen test

51
Q

flea bite hypersensitivity

A

Mixed type I and type IV: Cutaneous basophil hypersensitivity
* Dogs and cats
* Pruritic papular dermatitis -> self-inflicted trauma and chronic lichenification (thickening of skin)
* Fibropruritic nodules: core of collagen covered by a hyperplastic
epidermis

52
Q

mosquito bite hypersensitivity

A
  • Type I hypersensitivity
    – Intradermal skin tests
    – Prausnitz-Kustner tests
  • Primarily on the external nose -> nasal planum, periocular skin, pinnae and less commonly foot pads.
  • Erythematous papules ->crusts, ulcers, alopecia
  • Hypopigmentation or hyperpigmentation
53
Q

food allergies

A

-common and misdiagnosed
 Frequent skin and ear infections.
 May also present with vomiting and diarrhea.
 Similar presentation to Atopy, at any age
 Need to do a strict elimination trial to determine the foods animals are
allergic to diagnose
 (ELISA assay is not reliable predictor of these).

54
Q

contact dermatitis

A

Type IV reaction:**
– Haptens and cytotoxic T cells
– Eosinophils are variable
* Chemicals: aniline dyes in carpets, plant resins, chemicals in shampoos, plastic food dishes.**
* Pruritus with self-inflicted trauma
* Regions in contact with antigen.
* Spongiotic superficial perivascular
dermatitis, epidermal hyperplasia
with varying numbers of eosinophils

55
Q

pemphigus and 2 types

A

 Gross: Transient vesicles or bullae
 Histo: Acanthosis
 Type II reaction**
 Autoantibodies against proteins responsible for cell adhesion
(desmosomes)
 Damage to desmosomes ->acantholysis ->formation of bullae

pemphigus folaceous: when vesicles become pustules –> secondary crusts and scales
-dogs and cats: NOSE then ears, eyes, neck
* Horse: subcorneal pustules
* Dog: stratum spinosum

pemphigus vulgaris:  Basal cells attached to basement
membrane -> tombstoning
 Mucocutaneous junctions
 More severe than PF
-rare, oral skin.

56
Q

systemic lupus erythematosus

A

 Type III response**
 Defective T cell suppressor and cytokine disregulation
 Immune complexes formed and deposited in skin
 Basal cell or keratinocyte degeneration

-dogs, cats, horses: uncommon. look for in the nose. lichenoid inflammation

57
Q

hyperthyroidism clinical on skin

A

-cats
-self inflicted alopecia (forearms and bellys)
-rough appearance, thin

58
Q

hypothyroidism on skin

A

 The most common endocrine dermatosis in dogs
 Age: over 6 years
 Intolerance to cold
 Obesity
 Hair coat dry, dull, coarse, sparse
 Alopecia
 Adnexal atrophy
 Dermal edema
 Hyperpigmentation
 Scaling

59
Q

hyperadrenocorticism on skin

A

Cortisol excess:
 Adnexal atrophy ->alopecia
 Fibroblasts inhibited -> thin skin
 Hepatic glycogen -> hepatomegaly
 Collagen/elastin change -> dystrophic calcification (calcinosis cutis)
 Immunosuppression -> infections

Causes:
 Pituitary (85-90% of dogs)
 Adrenocortical (10-15% of dogs)
 Iatrogenic
 The second most common endocrine dermatosis in dogs

60
Q

hyperestronism on skin

A

 Males and females
 Sertoli cell tumor (cryptorchid)
 Ovarian cysts
 Atrophied hair follicles
-swollen vulva in females gross looks like hypothyroid skin

61
Q

alopecia X

A

 Dogs with normally PLUSH hair coats, 1-2 years old
 The head and distal extremities are often spared of alopecia
 Normal thyroid and glucocorticoid levels
 Skin biopsy samples with telogen follicles
(retained hair shafts and flame follicles)

-permanent disease, neutering may work. some dogs respond to melatonin

62
Q

seborrhi disease complex

A

-chronic disease complex secondary to abnormalities of the sebasceous glands associated with a change from bacteria to pathogenic.

 Seborrhea Sicca - Dry form
 Dry skin and white-gray scales.

 Seborrhea Oleosa - Greasy form
 Scaling and excessive brown to yellow lipids that adhere to the skin and hair.

-primary ideopathic is most common
-secondary with inflammation

63
Q

ichthyosis

A

 Cattle and dogs
 Scaly, cracked skin

-ichytosis fetalis - FATAL, congenital fetal disorder,

64
Q

zinc responsive dermatosis

A

 Dogs (pigs)
 Lesions: scaling and crusting with marked diffuse parakeratosis** eyes and nose

 Pathogenesis:
Inherited reduced ability to absorb Zn from the intestine (Alaskan
Malamute and Siberian husky)
Large breed, rapidly growing pups – low zinc diets. they need zinc supplaments

65
Q

esonophilic skin diseases

A

 Eosinophilic plaques:
 Common in cats
 Possible link to hypersensitivity reactions

 Eosinophilic granulomas:
 Horses, dogs and cats
 Flame figures, eosinophil degranulation
 Lesions: nodular dermatitis, indolent ulcers

66
Q

juvinille sterile granulatamous disease

A

 Puppy strangles
 No microorganism identified (sterile lesions)
 Secondary bacterial infections
 Lesions: pustular and nodular dermatitis with edema (facial mostly)

67
Q

tumors of the skin

A

-squamous cell carcinoma (cats* nose)
-histocytoma (common), regress on their own
-lipoma (cut open, hide Mast cell tumor. boxers**)
-injection site fibrosarcoma (FLV, rabies)
-basal cell tumors
-sebaceous gland hyperplasia

68
Q
A

sys path (13 decks)

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