Block 3 material skin Flashcards
INFLAMMATORY DERMATOSES
A type 1 hypersensitivity reaction that is associated with asthma & allergic rhinitis that presents as a pruritic & erythematous oozing rash with vesicles & edema of the face & flexor surfaces
Atopic (Eczematous) Dermatitis
Atopic (Eczematous) Dermatitis
What is it:
INFLAMMATORY DERMATOSES
A type 1 hypersensitivity reaction that is associated with asthma & allergic rhinitis that presents as a pruritic & erythematous oozing rash with vesicles & edema of the face & flexor surfaces
INFLAMMATORY DERMATOSES
A pruritic, erythematous, oozing rash with vesicles & edema due to exposure to allergens like poison ivy/Nickle jewelry (IV hypersensitivity), Irritants (chemicals), & Drugs (penicillin)
Treatment:
Removing the agent & Topical Glucocorticoids
Contact dermatitis
Contact dermatitis
What is it:
What are the treatment options:
INFLAMMATORY DERMATOSES
A pruritic, erythematous, oozing rash with vesicles & edema due to exposure to allergens like poison ivy/Nickle jewelry (IV hypersensitivity), Irritants (chemicals), & Drugs (penicillin)
Treatment:
Removing the agent & Topical Glucocorticoids
INFLAMMATORY DERMATOSES
Hormone associated excess of sebum/keratin which plug pores to form comodones
&
Chronic inflammation from P. bacterium which produces lipases that break down sebum & release proinflammatory fatty acids forming pustules/nodules
Treatments:
Benzoyl peroxide
Vitamin A derivatives (Isotretinoin)
Acne vulgaris
Acne vulgaris
What is it:
What are the treatment options:
INFLAMMATORY DERMATOSES
Hormone associated excess of sebum/keratin which plug pores to form comodones
&
Chronic inflammation from P. bacterium which produces lipases that break down sebum & release proinflammatory fatty acids forming pustules/nodules
Treatments:
Benzoyl peroxide
Vitamin A derivatives (Isotretinoin)
INFLAMMATORY DERMATOSES
Excessive keratinocyte proliferation leads to the formation of well circumscribed/salmon-colored plaques with silver scaling on the scalp, trunk, elbows, and knees (extensor surfaces) & sometimes pitting nails.
Causes:
Autoimmune condition associated with HLA-C genotype & environmental triggers (plaques arise in areas of trauma)
Histology:
1) Acanthosis (thickened epidermis aka hyperplasia)
2) Parakeratosis (retention of nucleated keratinocytes in the stratum corneum)
3) Munro micro-abscesses (neutrophils in corneum stratum)
4) Auspitz sign (thinned epidermis above elongated dermal papillae; results in bleeding when scale is picked off)
Psoriasis
Psoriasis
What is it:
What causes it:
What are the histological findings:
MAAP
INFLAMMATORY DERMATOSES
Excessive keratinocyte proliferation leads to the formation of well circumscribed/salmon-colored plaques with silver scaling on the scalp, trunk, elbows, and knees (extensor surfaces) & sometimes pitting nails.
Causes:
Autoimmune condition associated with HLA-C genotype & environmental triggers (plaques arise in areas of trauma)
Histology:
1) Acanthosis (thickened epidermis aka hyperplasia)
2) Parakeratosis (retention of nucleated keratinocytes in the stratum corneum)
3) Munro micro-abscesses (neutrophils in corneum stratum)
4) Auspitz sign (thinned epidermis above elongated dermal papillae; results in bleeding when scale is picked off)
INFLAMMATORY DERMATOSES
Pruritic, planar/polygonal, purple papules with Wickham striae (white reticular lines on the surface) on the wrists, elbow, & mouth
Histology:
1) Inflamed 9dermal epidermal junction with a sawtooth appearance
Causes:
It’s associated with Hep C infection
Lichen planus
Lichen planus
INFLAMMATORY DERMATOSES
Pruritic, planar/polygonal, purple papules with Wickham striae (white reticular lines on the surface) on the wrists, elbow, & mouth
Histology:
1) Inflamed 9dermal epidermal junction with a sawtooth appearance
Causes:
It’s associated with Hep C infection
Autoimmune destruction of desmosomes between the keratinocytes causing skin & mouth Bullae
Causes:
IgG antibodies against desmoglein (II hypersensitivity)
Histology:
1) Acantholysis (Separation of the stratum spinosum keratinocytes causing suprabasal blisters)
2) Nikolsky sign (Thin-walled bullae that rupture easily causing shallow erosions with dried crusts)
3) Fish-net appearance due to IgG’s surrounding keratinocytes (immunofluorescence)
4) Tombstone appearance of the basal layer (because it’s still attached to the basement membrane by hemidesmosomes)
Pemphigus vulgaris
Pemphigus vulgaris
Autoimmune destruction of desmosomes between the keratinocytes causing skin & mouth Bullae
Causes:
IgG antibodies against desmoglein (II hypersensitivity)
Histology:
1) Acantholysis (Separation of the stratum spinosum keratinocytes causing suprabasal blisters)
2) Nikolsky sign (Thin-walled bullae that rupture easily causing shallow erosions with dried crusts)
3) Fish-net appearance due to IgG’s surrounding keratinocytes (immunofluorescence)
4) Tombstone appearance of the basal layer (because it’s still attached to the basement membrane by hemidesmosomes)
Autoimmune destruction of hemidesmosomes between the basal cells & the basement membrane (milder than pemphigus vulgaris), it only causes skin blisters ONLY***
Causes:
IgG antibodies against the basement membrane collagen
Histology:
1) Basal layer detached from basement membrane
2) Tense bullae that DO NOT rupture easily
3) IgG along the basement in a linear pattern (immunofluorescence)
Bullous pemphigoid
Bullous pemphigoid
What is it:
What causes it:
What are the histological findings:
Autoimmune destruction of hemidesmosomes between the basal cells & the basement membrane (milder than pemphigus vulgaris), it only causes skin blisters ONLY***
Causes:
IgG antibodies against the basement membrane collagen
Histology:
1) Basal layer detached from basement membrane
2) Tense bullae that DO NOT rupture easily
3) IgG along the basement in a linear pattern (immunofluorescence)
A hypersensitivity reaction with central epidermal necrosis surrounded by erythema that causes targetoid rash & bullae
Causes:
Most common is HSV***
Others are mycoplasma, drugs (penicillin & sulfonamides), Autoimmune (SLE), & Malignancy
Complication:
If It involves the oral mucosa/lips it is considered Steven-Johnson-Syndrome
(Toxic epidermal necrolysis characterized by diffuse sloughing of the skin that looks like a large burn typically caused by an adverse drug reaction)
Erythema Multiforme
Erythema Multiforme
What is it:
What causes it: main vs other
What is a complication of this condition:
A hypersensitivity reaction with central epidermal necrosis surrounded by erythema that causes targetoid rash & bullae
Causes:
Most common is HSV***
Others are mycoplasma, drugs (penicillin & sulfonamides), Autoimmune (SLE), & Malignancy
Complication:
If It involves the oral mucosa/lips it is considered Steven-Johnson-Syndrome
(Toxic epidermal necrolysis characterized by diffuse sloughing of the skin that looks like a large burn typically caused by an adverse drug reaction)
Autoimmune IgA deposition into the tips of the dermal papillae that cause pruritic vesicles & bullae that are grouped together.
Causes:
Strong association with Celiacs
Treatment:
Gluten-free diet
Dermatitis herpetiformis
Dermatitis herpetiformis
What is it:
What causes it/is strongly associated with it:
What is the treatment option:
Autoimmune IgA deposition into the tips of the dermal papillae that cause pruritic vesicles & bullae that are grouped together.
Causes:
Strong association with Celiacs
Treatment:
Gluten-free diet
A benign tumor made of squamous proliferation that is common in the elderly. It is a raised, discolored plaque with a coin-like waxy stuck on appearance on the face.
Histology:
1) Keratin pseudocysts
Complication:
Leser-Trelat sign (the sudden onset of multiple seborrheic keratoses that suggests an underlying Gi carcinoma)
Seborrheic Keratosis
Seborrheic Keratosis
What is it:
What does the histology show:
What is a complication of the condition:
A benign raised, discolored plaque with a coin-like waxy stuck on appearance on the face.
Histology:
1) Keratin pseudocysts
Complication:
Leser-Trelat sign (the sudden onset of multiple seborrheic keratoses that suggests an underlying Gi carcinoma)
Darkening epidermal hyperplasia (velvet-like skin) in the axilla or groin
Causes:
1) Associated with insulin resistance (non-insulin dependent Diabetes)
2) Malignancy (Gi carcinoma)
Acanthosis Nigricans
Acanthosis Nigricans
What is it:
What causes it:
Darkening epidermal hyperplasia (velvet-like skin) in the axilla or groin
Causes:
1) Associated with insulin resistance (non-insulin dependent Diabetes)
2) Malignancy (Gi carcinoma)
Localized loss of skin pigmentation due to autoimmune destruction of melanocytes
Vitiligo
Vitiligo
What is it:
Localized loss of skin pigmentation due to autoimmune destruction of melanocytes
Congenital lack of pigment due to an enzyme deficiency (Tyrosinase) that impairs melanin production it can be ocular or oculocutaneous
Complications:
Risk of SCC, BCC, Melanoma (increased UVB-DNA damage from sun exposure)
Albinism
Albinism
What is it:
What are the complications of this condition:
Congenital lack of pigment due to an enzyme deficiency (Tyrosinase) that impairs melanin production it can be ocular or oculocutaneous
Complications:
Risk of SCC, BCC, Melanoma (increased UVB-DNA damage from sun exposure)
A mask-like hyperpigmentation of the cheeks
Causes:
Associated with preggos or oral contraceptives
Melasma
Melasma
What is it:
What causes it:
A mask-like hyperpigmentation of the cheeks
Causes:
Associated with preggos or oral contraceptives
A benign neoplasm of melanocytes that can be a flat or raised papule with symmetry, sharp borders, & even color throughout. Different forms:
1) Congenital has hair (at birth)
2) Acquired
- Junctional nevus (nests of melanocytes at dermal-epidermal junctions most common in children)
- Compound nevus (grows extensions into the dermis)
- Intraepidermal nevus (junctional nevus disappears, most common in adults)
Complication:
Nevus dysplasia that is a precursor to melanoma
Nevus
Nevus
What is it: Congenital vs Acquired
What is a complication:
A benign neoplasm of melanocytes that can be a flat or raised papule with symmetry, sharp borders, & even color throughout. Different forms:
1) Congenital has hair (at birth)
2) Acquired
- Junctional nevus (nests of melanocytes at dermal-epidermal junctions most common in children)
- Compound nevus (grows extensions into the dermis)
- Intraepidermal nevus (junctional nevus disappears, most common in adults)
Complication:
Nevus dysplasia that is a precursor to melanoma
A malignant neoplasm of melanocytes that presents as a mole-like growth with “ABCD”
-Asymmetrical
-Borders are irregular
-Color is NOT uniform
-Diameter over 6mm
It grows in 2 phases:
1) Radial growth horizontally along the epidermis & superficial dermis (low risk of metastasis)
2) Vertical growth into the deep dermis with Breslow thickness (best diagnostic factor & it has a high risk of metastasis)
Risk factors:
1) UVB-induced DNA damage (Sunlight, Albinism, Xeroderma pigmentosum)
2) Dysplastic nevus syndrome (auto dom)
Subtypes:
1) Superficial spreading (most common with early dominant radial growth & a good prognosis)
2) Lentigo maligna (Lentiginous proliferation & radial growth & a good prognosis)
3) Nodular (Early vertical growth & a poor prognosis)
4) Acral Lentiginous (arise on the palm/soles of dark skinned patients not ass with sunlight)
Melanoma
Melanoma
What is it:
What are it’s growth phases:
What are the risk factors:
What are the subtypes:
A malignant neoplasm of melanocytes that presents as a mole-like growth with “ABCD”
-Asymmetrical
-Borders are irregular
-Color is NOT uniform
-Diameter over 6mm
It grows in 2 phases:
1) Radial growth horizontally along the epidermis & superficial dermis (low risk of metastasis)
2) Vertical growth into the deep dermis with Breslow thickness (best diagnostic factor & it has a high risk of metastasis)
Risk factors:
1) UVB-induced DNA damage (Sunlight, Albinism, Xeroderma pigmentosum)
2) Dysplastic nevus syndrome (auto dom)
Subtypes:
1) Superficial spreading (most common with early dominant radial growth & a good prognosis)
2) Lentigo maligna (Lentiginous proliferation & radial growth & a good prognosis)
3) Nodular (Early vertical growth & a poor prognosis)
4) Acral Lentiginous (arise on the palm/soles of dark skinned patients not ass with sunlight)
A superficial bacterial skin infection (S. aureus or S. epidermidis) usually in children that presents as erythematous macules that progresses to pustules on the face which rupture leaving honey crusted lesions
Impetigo
Impetigo
What is it:
A superficial bacterial skin infection (S. aureus or S. epidermidis) usually in children that presents as erythematous macules that progresses to pustules on the face which rupture leaving honey crusted lesions
Flesh-colored papules with a rough surface & characterized by koilocytic change in the hands/feet
Causes:
HPV skin infection
Verruca (warts)
Verruca (warts)
Flesh-colored papules with a rough surface & characterized by koilocytic change in the hands/feet
Causes:
HPV skin infection
Firm, pink & umbilicated papules typically seen in children, sexually active adults, or immunocompromised patients
Causes:
Poxvirus
Histology:
Molluscum bodies
Molluscum contagiosum
Molluscum contagiosum
What is it:
What causes it:
What are the histological findings:
Firm, pink & umbilicated papules typically seen in children, sexually active adults, or immunocompromised patients
Causes:
Poxvirus
Histology:
Molluscum bodies
