SKIN 2 Flashcards by Quennie Ann Silverio

part of the epidermis that extends downward going to the dermis

Rete ridges

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part of the dermis that

extends upward to the epidermis

Dermal papillae/papilla

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• Composed of either 4 or 5 layers depending on the
location
• For areas with thick skin, composed of 5 layers. For
thin skin, 4 layers

Epidermis

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Single layer of cuboidal cells which are mitotically
active which actively divides and migrate toward the
upper surfaces to give rise to keratinocytes

Stratum Basale or Stratum Germinativum

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• Spinous layer
• Composed of more mature keratinocytes
• Keratinocytes- polygonal shaped cells in the
epidermis and attached to one another through
intercellular bridges called DESMOSOMES

Stratum Spinosum

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• Also made up with keratinocytes but with
characteristic cytoplasmic granules called
KERATOHYALINE GRANULES

Stratum Granulosum

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• 4th layer, that is present only on thick skin including
the palms and soles
• Made up of clear cells, flattened keratinocytes

Stratum Lucidum

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• The outermost layer, cornified or horny-cell layer
• Composed of dead skin cells which are usually
sloughed off

Stratum Corneum

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• Thickening of the spinous layer

Acanthosis

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• Separation of keratinocytes because of disruption of
desmosomes (or what we call the intercellular bridges)
• Clinical manifestation: BLISTERS

Acantholysis

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• Thickening of cornified layer or stratum corneum

Hyperkeratosis

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• Vacuolar change of the basal layer with lymphocytic infiltrate at the DEJ

Interface Dermatitis:

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• Separation of spinous layer because of increased

(edema) fluid in epidermis

Spongiosis

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There is a defective desquamation resulting to
accumulation of dead skin cells or dead keratinocytes
with in the stratum corneum

Ichthyosis

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Four types of Ichthyosis

Congenital Ichthyosiform Erythroderma
Lamellar Ichthyosis
X-linked Ichthyosis
Ichthyosis Vulgaris

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Main pathology for Ichthyosis

HYPERKERATOSIS

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ACUTE INFLAMMATORY DERMATOSES

Urticaria
Acute eczematous dermatitis
Erythema multiforme

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ACUTE INFLAMMATORY DERMATOSES common microscopic findings

neutrophilic

infiltration and edema

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A.K.A. Hives/wheals (when confluent)
(disorder of a) Localized mast cell degranulation
(results in) Increased vascular permeability

Urticaria

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Individual lesions develop and fade within hours

(usually less than 24 hours), and episodes may last for days or persist for months

Urticaria

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Urticaria main pathology:

Antigen-induced release of vasoactive mediators from mast cells

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• Types of Mechanism for Urticaria:

o Mast Cell-dependent, (IgE)-Dependent
o Mast Cell-dependent, (IgE)-independent
o Mast cell-independent, (IgE)-independent

Type I hypersensitivity

o Mast Cell-dependent, (IgE)-Dependent

§ Direct cell
§ From direct effect of the substances
that we have contact with
§ Instead of the antigen being 
presented with the IgE, this type of 
mechanism DOES NOT INVOLVE 
IgE

o Mast Cell-dependent, (IgE)-independent

Mast Cell-dependent, (IgE)-independent examples

Opiate Analgesics and some | antibiotics

§ Local Factors § Rare, less well-understood § Hypothesis: due to the release of local factors one example is exposure to ASPIRIN but he mechanism of Aspirin-induced urticarial is not very much understood

o Mast cell-independent, (IgE)-independent

gross appearance of urticaria

* Erythematous, edematous plaques | * Annular, linear or arciform

microscopic appearance of urticaria

• Perivenular infiltrate consisting of mononuclear cells (lymphocytes surrounds the vessels) and rare PMNs • Eos (eosinophil) may also be present • Aside from the epidermal involvement, Perivascular Edema

Urticaria Treatment

* Take oral anti-histamines * Localized: topical steroids * Sever and more wide spread: IV anti-histamines and corticosteroids

meaning “to boil over,”

eczema

Acute Eczematous Dermatitis is Group of disorders that presents with _________ PATTERN

SPONGIOTIC

AED main/common histologic appearance

Edema

Types of dermatitis

``` o Allergic contact dermatitis o Atopic dermatitis o Drug related eczematous dermatitis o Photo eczematous dermatitis o Primary irritant dermatitis ```

AED causes:

o disease resulting from external application of an antigen (e.g., poison ivy) o reaction to an internal circulating antigen (which may be derived from ingested food or a drug).

AED Treatment:

o search for offending substances that can be removed from the environment o topical steroids (corticosteroids) and moisturizers can be used to block the inflammatory response

AED hypersensitivity Type?

Focally, crusted, thickened, plaques and papules with some areas of erythema and redness. The crusts are dried up yellowish exudates

atopic dermatitis

Gross morpho AED

Red, papulovesicular, crusted

Characterized by pruritic, edematous, oozing plaques that often contain small and large blisters (vesicles and bullae) that are prone to bacterial superinfection, which produces a yellow crust (impetiginization)

Allergic contact dermatitis

o Characterizes acute eczematous dermatitis o Edema seeps into the intercellular spaces of the epidermis, splaying apart keratinocytes, particularly in the stratum spinosum

spongiosis

Initial manifestation of AED

papillary dermal edema and mast cell degranulation manifested by whites’ spaces with concomitant superficial,perivascular, lymphocytic infiltrate

perivascular infiltrates that often contain eosinophils in the superficial and deep dermis

Certain ingested drugs

produce a mononuclear inflammatory reaction without eosinophils that preferentially affects the superficial dermis.

Contact antigens

``` o body surface involved is <10% o febrile form; extensive involvement of the skin o often seen in children o skin, lips and oral mucosa, conjunctiva, urethra, and genital and perianal areas o Loss of skin integrity -> Secondary infection -> sepsis ```

Steven-Johnson Syndrome

o body surface area involved is >30% | o diffuse necrosis and sloughing of cutaneous and mucosal epithelial surfaces

Toxic Epidermal Necrolysis

between 10% to 30%

SJS-TEN overlap

``` ERYTHEMA MULTIFORME • Keratinocyte injury mediated by skin-homing CD8+ cytotoxic T lymphocytes o _______ - central portion of the lesions o ___________ - peripheral portions ```

CD8+ cytotoxic T cells; CD4+ helper T cells and Langerhans cells

* Macules, papules, vesicles, bullae | * Characteristic targetoid (target-like) lesions

Erythema multiforme

micro morpho Erythema multiforme

• Interface dermatitis

CHRONIC INFLAMMATORY DERMATOSES

Psoriasis Seborrheic dermatitis Lichen planus

• Chronic inflammation that appears to have an autoimmune basis. • Koebner phenomenon • Auspitz sign

Psoriasis

Psoriasis pathogenesis

* CD4+Th1 and Th17 cells | * CD8+ cytotoxic effector T cells

most frequently affects the skin of the elbows, knees, scalp, lumbosacral areas, intergluteal cleft, and glans penis.

psoriasis

is defined if one person to | develop psoriasis and experience local trauma they can trigger the formation of your plaques and papules.

Koebner Phenomenon