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Pathology II (Kiva) > Topic 108-111: Skin > Flashcards

Topic 108-111: Skin Flashcards

1
Q

What are the three types of primary blistering disease? what are the locations that blistering can occur in the skin? in general what are blistering skin diseases caused by?

A
  • Pemphigus
  • bullous pemphigus
  • dermatitis herpetiformis

remember that blisters can form at multiple levels within the skin at:

  • subcorneal
  • suprabasal
  • subepidermal

they are all autoimmune mediated

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2
Q

pemphigus skin blisters are caused by what? what is the autoimmune target? what are the major types and their general location of pathology?

A

-type 2 hypersensitivity rxn with IgG against desmoglein 1 - 3 (proteins that keep cells attached, a desmosome)

  • pemphigus vulgaris - suprabasal location, oral mucosa and skin typically
  • pemphigus foliaceus - subcorneal, skin
  • paraneoplastic pemphigus - associated with internal malignancy
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3
Q

bullous pemphigoid skin blisters are caused by what? what is the autoimmune target? what is the general location of pathology?

A

typically in elderly people, there is a linear IgG deposition on the BM (subepidermal)
-target is the bullous pemphigoid antigen (BPAG)

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4
Q

dermatitis herpetiformis skin blisters are caused by what? what is the autoimmune target? what is the general location of pathology?

A
  • associated with celiac disease and urticaria
  • there is an IgA reaction to gluten and these antibodies cross react with reticulin (anchoring fibrils)
  • cause subepidermal blister
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5
Q

What are the 4 inflammatory skin diseases?

A
  • urticaria
  • acute eczematous dermatitis
  • erythema multiforme
  • acne vulgaris
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6
Q

urticaria is what? it is typically mediated by what? what is the target?

A

urticaria or hives are caused by mast cell degranulation that causes microvascular hyperpermeability

it can be IgE dependant or independant:

  • -IgE dependant (Hypersensitivity type 1, most common) induced by an antigen of any types
  • -IgE independent can be caused by opioids or antibiotics
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7
Q

acute eczematous dermatitis is described as what? what are the causes? what is the mechanism of the most common types?

A
  • red, papulovesicular crusted lesions (can be raised or scaling)
  • allergic
  • atopic (defective keratinocyte barrier)
  • drug-related
  • photoeczematous
  • primary irritant

-allergic contact dermatitis is the most common
it is not a HSR1 but and initial exposure followed by the production of CD4 educated t lymphocytes that will cause dermal damage upon re-exposure

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8
Q

erythema multiforme is what? what is is it typically caused by? what is the location of pathology?

A
  • self-limiting skin disorder caused by a hypersensitivity rxn to drugs and infections (mycoplasma, fungi)
  • T cell mediated response that occurs as the cells target cross-reactive antigens at the basal cell layer of the skin
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9
Q

what are 3 chronic inflammatory skin diseases?

A
  • psoriasis
  • lichen planus
  • lichen simplex chronicus
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10
Q

psoriasis is what? what kind of reaction is it?

A
  • salmon colored with silvery scales, affects 1-2% of people
  • it’s a immune mediated response to an unknown antigen (can be genetic, environmental trauma - koebner phenomena)
  • sensitized T cells enter the skin, secrete GF and cause hyperproliferation of the keratinocyte
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11
Q

lichen planus is characterized by 5 Ps. what is the pathogenesis?

A
  • purple
  • pruritic
  • polygonal
  • planar papules
  • plaques

-unknown pathogenesis, can be due to altered antigens at the basal cell layer that elicit a CD8 response

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12
Q

lichen simplex chronicus looks how? how is it induced?

A
  • looks like lichen on a tree, can be localized to nodules

- it can occur in response to rubbing/scratching/repetitive trauma

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13
Q

melanocytic tumors can be either benign or malignant. what are the two benign types? they are all derived from which cells?

A

all are from melanocytes

-common nevi (mole)
-dysplastic nevi
vs
-malignant melanoma

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14
Q

melanocytic nevi are classified into 3 types based on location and maturation. the majority of them have what mutation?

A
  • junctional - nests of melanocytes at the dermal/epidermal junction. young/not matured
  • compound - when these junctional nest grow downward with age
  • intradermal - even older, less pigment, deeper in the dermis until they are gone

transformed melanocytes turn into nevi. the majority of nevi have the BRAF mutation (downstream of RAS) or even a RAS mutation.

    • it is UV induced
  • –these two mutations are mutually exclusive!
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15
Q

dysplastic nevi are what? they can be two categories:

A

dysplastic nevi are just atypical nevi

they can be

  • sporadic (low risk)
  • familial (almost 100% chance of developing melanoma during lifetime)
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16
Q

malignant melanoma forms from what?how does it always initially spread? what are the 4 subtypes

A
  • more commonly de novo but can also be from preexisting nevi
  • initially spread via lymphatics and through the blood later (and when it’s impossible to stop)

-lentigo maligna - spreads radially, typically from sun damaged skin!
-superficial spread - also spreads radially but the most common type! also more multicolored than the lentigo maligna
-nodular - vertical growth upwards
acral lentiginous - on palms and feet soles, typically not related to sun exposure

17
Q

what kind of growth can occur in melanoma?

A
  • radial growth:growth horizontal in epidermis. no ability to metastasize here
  • vertical growth - growth downward into the dermal layer. dangerous
18
Q

What are the two scales used to measure melanoma?

A

–Breslow measures the thickness in mm (to the 1/10th of a mm)

–clark uses depth measurement in comparison to levels of the skin (is it at the epithelial layer, junction, papillary, level of sweat glands, subcutaneous invasion, etc).

Both of these scales need to be used because if you have a melanoma protruding out of the skin by 3 mm and 1 mm deep in the skin, it is a 4 mm melanoma but only at the level of the upper epithelium. But if you have a melanoma that is 4 mm deep into the skin at the subcutaneous level or something, that changes prognosis a lot.

19
Q

what is the ABCDE?

A

A- asymmetry
B- border is irregular
C- color is also irregular with several variations in pigment
D- diameter (larger than 6mm)
E- evolving -any change in color, size, border

20
Q

what is the common hereditary mutation?

what is the Non-UV related mutation in melanoma?

A
  • hereditary is the CDKN2A oncosuppressor mutation on p16

- non-UV mutation is c-KIT

21
Q

non-melanocytic skin tumors can be benign or malignant. what types are in either category?

A

benign

  • seborrheic keratosis
  • sebaceous adenoma
  • actinic keratosis

malignant

  • squamous cell carcinoma
  • basal cell carcinoma
22
Q

what is the most common type of cancer? what are the mutations involved?

A

basal cell carcinoma is #1 (UV induced)
called krompecher bc he was hungarian

PTCH loss (sonic hedgehog pathway signaling)
p53 later

think baseball terms: at 1st base, PiTCH the ball

23
Q

basal cell carcinoma arises commonly due to? can it metastasize?

what is a stupid histological feature?

A

sun exposure is a huge risk

yes, but not frequently

palisading on the edge of the nest. also it has a rodent like tunneling pattern under the epidermis but still radially

24
Q

squamous cell carcinoma risk factors? what are the mutations?

A
  • immune suppression
  • sun exposure
  • ionizing radiation
  • arsenic poisoning
  • xeroderma pigmentosum

HRAS and loss of function in the notch receptor and p53 due to UV

25
Q

what is a seborrheic keratosis? what could be the mutation involved?

A

proliferation of basal cells to create a warty lesion

-fibroblast growth factor receptor 3 mutations

26
Q

what is a sebaceous adenoma? what might be the pathomech?

A

proliferation of sebaceous glands, occur at head and neck. rare.

loss of DNA mismatch repair protein causing chromosomal instability

27
Q

actinic keratosis is what? what is is caused by? what mutations are associated?

A
  • premalignant lesion that is tan-brown or reddish with sandpaper consistency
  • UV exposure is a big risk factor
  • p53 mutations

Pathology II (Kiva) (23 decks)

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