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Systemic Pathology I > Pathology of the Integumentary System, Pt. 2 > Flashcards

Pathology of the Integumentary System, Pt. 2 Flashcards

1
Q

What are the 5 major components of the skin?

A
  1. epidermis
  2. basement membrane zone
  3. dermis
  4. adnexal structures - hair follicles, apocrine glands, eccrine glands, sebaceous glands, arrector pili muscles
  5. subcutis
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2
Q

In what areas does the skin lack subcutis?

A
  • cheek
  • eyelid
  • anus
  • external ear
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3
Q

What are the 4 layers of the epidermis?

A
  1. stratum Corneum
  2. stratum Granulosum (purple granules)
  3. stratum Spinosum
  4. stratum Basale (adhered to BM)
    BM —> dermis

(come get some beer)

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4
Q

Skin histology:

A
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5
Q

What type of epithelium is the skin? What are the major 4 cell types?

A

keratinized stratified squamous epithelium

  1. keratinocytes (85%)
  2. Langerhans cells (3-8%) - communicates with T cells
  3. melanocytes (5%) - pigmentation
  4. Merkel cells (2%) - mechanoreceptors
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6
Q

What are 3 major functions of keratinocytes?

A
  1. permeability barrier - hydrophobic
  2. structural support
  3. immunoregulation - secretes cytokines to communicate with Langerhans cells
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7
Q

How do keratinocytes provide structural support?

A

contain keratin, which is an intermediate filament that is able to connect to desmosomes

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8
Q

How can intermediate filaments be used for diagnostic purposes? What do abnormalities in keratin lead to?

A

epithelial-derived neosplasm can be stained for keratin for diagnosis

cornification defects

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9
Q

How do the cells in the epidermis compare in each layer?

A

differentiates and loses nuclei from bottom to top (modified apoptosis), exfoliating the most differentiated keratinocytes about every 21 days

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10
Q

What are lamellar bodies?

A

secretory organelles in keratinocytes present between the stratum corneum and stratum granulosum that contain hydrolytic enzymes, phospholipids, ceramides, glycosyl ceramides, and sterols to form an impermeable, lipid-containing membrane that serves as a water barrier and is required for correct skin barrier function

(brick and mortar)

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11
Q

What is hyperkeratosis? What are 2 causes?

A

abnormality of cornification where there is excessive thickening (hyperplasia) of the stratum corneum

  1. PRIMARY: mutation in lipids, enzymes, or structural proteins (ichthyosis)
  2. SECONDARY: chronic irritation (allergic skin disease, endocrine disorders, parasitic/bacterial infections)
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12
Q

What is the difference between orthokeratosis and parakeratosis?

A

ORTHOKERATOSIS: keratinocytes undergo complete cornification and thus lose their nucleus

PARAKERATOSIS: keratinocytes undergo partial/incomplete cornification and retain their nucleus (nuclei Persist)

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13
Q

What is ichthyosis? Which breed of dog does it have a strong predilection for? What causes it in this breed?

A

congenital and/or hereditary defects in the formation of the stratum corneum

Golden retriever - ICH-1 and ICH-2 mutation

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14
Q

What is the symptom of Golden retriever ichthyosis? What is seen histologically?

A

generalized scaling of the trunk

lamellar orthokeratotic hyperkeratosis

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15
Q

What is primary seborrhea? Why is it controversial?

A

excessive scaling

NOT a diagnosis —> need to rule out other causes of scaling, like ectoparasitism, metabolic disease, endocrinopathies, allergic disease

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16
Q

What does primary seborrhea likely represent?

A

variety of conditions, such as pyoderma, Malassezia dermatitis, sebaceous adenitis, allergic dermatitis, vitamin A-responsive dermatosis

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17
Q

What is epidermal hyperplasia? What is it a common response of?

A

(acanthosis)
thickening due to an increased number of cells within the epidermis, especially of the stratum spinosum

chronic irritation, like inflammation, trauma, metabolic or nutritional disorders (acral lick dermatitis)

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18
Q

What is acral lick dermatitis? What causes it?

A

(acral lick granuloma)
multifactorial disorder of dogs often associated with underlying diseases, such as atopy, food allergy, trauma, endocrinopathy, bone pain, neuropathy, or behavioral causes

chronic focal trauma and/or secondary deep pyoderma

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19
Q

What is the presentation of acral lick dermatitis? What needs to be addressed?

A

focal alopecic, firm, raised plaque or nodule on the dorsal carpus or dorsolateral metatarsus

Why is the dog licking?
- food allergy, trauma, infection, behavior

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20
Q

What is the difference between apoptosis and necrosis?

A

APOPTOSIS: programmed cell death caused by physiologic processes and immune-mediated disease (erythema multiforme, cutaneous lupus)

NECROSIS: death of cells characterized by nuclear pyknosis, karyorrhexis, or karyolysis, caused by physical injury, chemical injury, or ischemia (photosensitization)

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21
Q

Apoptotic cell:

A
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22
Q

What is the difference between intercellular and intracellular edema? How does the position of the cells affect intracellular edema?

A

INTERCELLULAR: spongiosis, edema between cells, causing desmosomes to expand

INTRACELLULAR: edema within the cell
- SUPERFICIAL: ballooning degeneration (viral infection)
- BASAL: hydropic degeneration (cutaneous lupus erythematosus)

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23
Q

What is epidermal atrophy? What is the most common cause?

A

epidermis becomes thinner due to cellular shrinkage, which can cause underlying vessels seem superficial and dilated

hormonal imbalances —> hyperadrenocorticism (Cushings)

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24
Q

What is acantholysis? In what 2 conditions is it commonly seen?

A

disruption of intercellular junctions (desmosomes) between keratinocytes of the epidermis

  1. pemphigus foliaceus
  2. pemphigus vulgaris
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25
Q

What is seen clinically in acantholysis? How does it compare in pemphigus foliaceus and vulgaris?

A

vesicle and bullae

PF: subcorneal (under stratum corneum)
PV: suprabasal (only one layer of keratinocytes on BM)

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26
Q

What is exocytosis? Pustules? Crusts?

A

aggregation of migrating leukocytes in the epidermis

microabscesses; accumulations of inflammatory cells within the epidermis

dried fluid and cellular debris located on the epidermal surface

27
Q

What are Langerhans cells?

A

dendritic cells of bone marrow-derived monocyte-histiocyte lineage that process and present antigens to T cells (APC - immune system)

28
Q

What is contact hypersensitivity (allergic contact dermatitis)?

A

hapten-type delayed hypersensitivity (Type IV) where haptens bind to small toxins and present them to the immune system that would usually not respond to such small molecules —> first contact will not cause a response, but subsequent exposure will cause skin response

29
Q

What dermatological tests use the principle of hapten-type delayed hypersensitivities (Type IV)?

A
  • tuberculin test
  • patch test
30
Q

What do melanocytes do? Where are they found?

A

transfer melanin to keratinocytes (pigmentation)

basal cell layer of the epidermis and anagen hair follicle
- 1 melanocyte to 10-20 keratinocytes

31
Q

What 2 functions do melanocytes carry out?

A
  1. solar protection (protects and absorbs UV light)
  2. scavenge free radicals
32
Q

What 3 skin disorders are caused by abnormal melanization?

A
  1. HYPERPIGMENTATION: overproduction of melanin (lentigo simplex, post-inflammatory hyperpigmentation)
  2. HYPOPIGMENTATION: decreased production of melanin (vitiligo, copper deficiency)
  3. PIGMENTARY INCONTINENCE: loss of melanin pigment
33
Q

What is the pathogenesis of pigmentary incontinence? In what 2 disorders is this common?

A

damage to cells of the basal layer or follicular layer components leads to an accumulation of the pigment in macrophages in the upper dermis or perifollicular regions

  1. cutaneous lupus erythematosus
  2. uveodermatologic syndrome
34
Q

Post-inflammatory hyperpigmentation:

A
35
Q

Lentigo simplex:

A

common in ginger cats
- macules on nose, gingiva, lips

36
Q

Vitiligo:

A

thought to be autoimmune cells attacking melanocytes

37
Q

What is uveodermatologic syndrome? In what breeds is it most common?

A

autoimmune skin disease where melanocytes in the skin and eye are attacked, causing actue uveitis, photophobia, blepharospasm, and blindness, in addition to depigmentation of the nose, lips, eyelids, and hair

Akita, arctic breeds
(AKA Vogt-Koyanagi-Harada-like syndrome)

38
Q

How is uveodermatologic syndrome diagnosed?

A

biopsy + ophthalmic workup

39
Q

What are Merkel cells?

A

vacuolated cells that serve as mechanoreceptors in tylotrich pads and hair follicles

40
Q

What are 3 functions of the basement membrane zone? What pathological processes affect it?

A
  1. anchors epidermis to dermis
  2. protective barrier
  3. wound healing

subepidermal blistering diseases, like epidermolysis bullosa (injury beyond BM = scarring)

41
Q

What are the clinical and histological characteristics of subepidermal blistering disease?

A

vesicles —> ulcers

subepidermal clefts

42
Q

What are the 3 major proteins that make up the dermis? What 3 cells can be found here? What is its function?

A

collagen, elastin, proteoglycans

perivascular dendritic cells, lymphocytes, mast cells

tensile strength
support blood vessels, lymphatics, and nerves

43
Q

What is Ehlers-Danlos syndrome?

A

(collagen dysplasia, cutaneous asthenia, hyperelastic cutis, dermatosparaxis)

inherited congenital defect in dermal collagen, where an enzyme defect affects the synthesis and processing of collagen, which causes cutaneous hyperextensibility and laxity, and increased odds of tears, wounds, and scars

44
Q

How is Ehlers-Danlos syndrome diagnosed?

A

skin extensibility index
- histopathology tends to be inconclusive

45
Q

What is solar dermatitis? In what animals is it most common?

A

chronic exposure to sunlight causes altered fibroblast function

lightly skinned, short-coated breeds

46
Q

What is the common presentation of solar dermatitis? What is it commonly associated with?

A

erythema and scales on the flank, groin, and axilla that can lead to thick, firm and wrinkled skin with erosions, ulcers, and comedones

development of squamous cell carcinoma, hemangioma, and cutaneous hemangiosarcoma

47
Q

What is calcinosis cutis? What causes it? What gross lesions are commonly found?

A

dermal mineralization with granulomatous dermatitis due to hypercortisolemia

disease affecting cortisol production (Cushings) or iatrogenic (too much cortisol in allergy testing)

erythematous or white plaques with ulcers on the dorsal neck region, axilla, or groin

48
Q

What is seen on histology of a sample from calcinosis cutis?

A

multinucleated giant cells surrounding mineralized collagen fibers

49
Q

Responses of the dermis to injury:

A
50
Q

What are the 5 functions of hair follicles?

A
  1. physical and photoprotective barrier (much more hair to follicle compared to humans)
  2. thermoregulation
  3. social communication
  4. sensory perception
  5. wound healing
51
Q

How do hair follicles compare according to species?

A

SIMPLE: humans, cattle, horses, pigs
COMPOUND: dogs, cats, sheep, goats

52
Q

What are the 2 major hair growth stages?

A

ANAGEN: growing phase, long dermal papillae
TELOGEN: resting phase, dermal papillae retracts to epidermis

53
Q

Anagen vs telogen, histology:

A
54
Q

What are the 2 types of tactile hairs?

A
  1. SINUS HAIRS: whiskers, vibrissae; slow-adapting mechanoreceptors
  2. TYLOTRICH HAIRS: rapidly adapting mechanoreceptors scattered among normal hair with Merkel cells
55
Q

In what 4 ways does the adnexa respond to injury?

A
  1. atrophy - endocrine dermatopathy
  2. hair follicle dysplasia - color dilution alopecia
  3. hair cycling disorders
  4. inflammation - folliculitis, perifolliculitis, furunculosis
56
Q

What are 2 hormones that stimulate anagen? Inhibit anagen?

A
  1. thyroid hormone
  2. androgens
  3. glucocorticoids
  4. estrogen
57
Q

What is seen histologically in adnexal atrophy? What tends to cause this?

A

majority of hair follicles in telogen (contracted into epidermis)

endocrine dermatopathy

58
Q

What are sebaceous glands? What cells are found in them and what do they do?

A

holocrine glands that open into hair follicles

sebocytes degenerate to form sebum

59
Q

What are the 2 major functions of sebaceous glands? What does injury to these glands cause?

A
  1. provide moisture and water repellence to stratum corneum
  2. antibacterial and pheromone production

dry, scaling skin (sebaceous adenitis)

60
Q

What is sebaceous adenitis? What are breeds are commonly affected? How does it present?

A

inflammation of sebaceous glands that can lead to injury/destruction of the glands, with unknown cause

Poodles, Akitas, Samoyeds, Vizslas, Goldendoodles

scaling, thinning of hair coat or annular alopecia productin follicular casts, commonly found on the dorsum, head, and pinnae

61
Q

What is seen histologically in sebaceous adenitis? How is it diagnosed?

A

diffuse loss of sebaceous glands or granulomatous sebaceous adenitis

punch biopsy

62
Q

What are the 2 types of sweat glands found in the skin?

A

APOCRINE glands (epitrichial) that empty into hair follicles and have a single layer of cuboidal epithelium (larger lumen)

ECCRINE glands (atrichial) present in paw pads that empty directly into the skin surface; found deeper with stratified epithelium

63
Q

What is the subcutis? What is its function? What is inflammation in this layer called?

A

adipose tissue (panniculus) and loose connective tissue between the dermis and skeletal muscle

  • metabolic storage pool
  • protection of deeper structure

panniculitis

64
Q

What 2 vessels are found in the subcutis? What do they do?

A

BLOOD VESSELS
- skin metabolism
- temperature regulation
- microorganism defense

LYMPHATIC VESSELS
- supply and drain tissue fluid
- microorganism defense

Systemic Pathology I (25 decks)

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