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Patho Phys Exam 1 > Skin > Flashcards

Skin Flashcards

1
Q

Define Macule or patch

A

Spot,flat lesion, red/pink

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2
Q

Define papule or nodule

A

a large, more raised macule/patch

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3
Q

Define plaque

A

Raised flat large patch

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4
Q

Define pustule

A

Raised and filled with pus

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5
Q

Define Scale

A

scaly skin, from layers of keratin sloughing off

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6
Q

Define vesicle and bulla

A

Vesicle is a blister, bulla is a large blister

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7
Q

Define Acanthosis

A

thickening of epidermal layer

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8
Q

Define hyperkeratosis

A

hyperplasia of stratum coreum

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9
Q

Define parakeratosis

A

cells retain nuclei in stratum corneum and the other layers

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10
Q

Define spongiosis

A

Intercellular edema in the epidermis

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11
Q

Explain and compare the pathophysiology of..

acute inflammatory dermatoses – urticaria,

acute eczematous dermatitis (limit this to allergic contact dermatitis),

and erythema multiforme

Just in general terms…
(think what causes it, rate, etc.)

A

hives– present as erythematous, edematous, often circular
plaques (wheals), pruritic (itchy)

These appear FAST, from allergens
**DERMIS ONLY

(ex: poison ivy, Ni)
* *THIS IS DELAYED TYPE 4/T CELLS
* *BLISTERING

– reaction to infections (herpes simplex,
pneumonia) and sometimes to drugs

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12
Q

Explain and compare the pathophysiology of..

acute inflammatory dermatoses – urticaria,

acute eczematous dermatitis (limit this to allergic contact dermatitis),

and erythema multiforme

Type of hypersensativity

A

is Type 1-Fast rxns which involve histamine and mast cells/dilated vessels and are superficial

is Type 4-DELAYED (2-4 days): T cell involvement where Th recruit macrophages and CD8 killers –> apoptosis which creates a blister forming space

EM is Type 4- (3-5 days)

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13
Q

Type 1 Sensitivity and cells?

Rate?

A

Mast cells release histamine –> creates immediate hypersensitivity
reaction (normally an allergy), involves vasodilation and is FAST; ONLY Epidermis

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14
Q

Delayed (Type IV) hypersensitivity reaction and cells?

Rate?

A

T-lymphocytes (T-cells):

i. Th (CD4) recruit other immune cells like macrophages –> inflammation
ii. Tc (CD8) cause target cells to undergo apoptosis

This is DELAYED

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15
Q

Explain and compare the pathophysiology of

acute inflammatory dermatoses – urticaria,

acute eczematous dermatitis (limit this to allergic contact dermatitis),

and erythema multiforme.

c. Appearance and type of skin lesion (gross level) –

A

urticaria: hives – present as erythematous, edematous, often circular
plaques (WHEALS), pruritic (itchy)-FAST

Acute eczematous dermatitis- If fluid continues to enter epidermis –> BLISTER
(vesicles/bulla or spongiosis)

Erythema multiforme-
HALLMARK TARGET
*These can burst

a. Bright red outer ring
b. Paler, raised area (edema)
c. Dusky or dark red central area with blister or crust
d. Appear over 3-5 days and resolve in 2 weeks

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16
Q

Erthythema multiforme minor vs EM major

A

minor skin

major skin with mucousal involvement

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17
Q

Appearance of EM (4 hallmarks)

**ONE BIG ONE

A

**TARGET LESION

a. Bright red outer ring
b. Paler, raised area (edema)
c. Dusky or dark red central area with blister or crust
d. Appear over 3-5 days and resolve in 2 weeks

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18
Q

Acute eczematous dermatitis appearance

A

If fluid continues to enter epidermis –> blister
(vesicles/bulla).

redness, edema in outermost layers of
dermis, itchy

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19
Q

Urticaria appearance

A

hives – present as erythematous, edematous, often circular

plaques (WHEALS), pruritic (itchy)-appear in minutes

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20
Q

Explain and compare the pathophysiology of

acute inflammatory dermatoses – urticaria,

acute eczematous dermatitis (limit this to allergic contact dermatitis),

and erythema multiforme.

d. Involvement of the oral mucosa

A

Seems to be that of these three acute hypersensativity rxns only Erythema multiforme involves
the oral mucosa

EM Major: with mucosal involvement
a. Mucosal lesions develop a few days after the skin rash
begins

b. Swelling, redness, blister formation -> breaks and
leaves painful ulcers

Disappear quickly

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21
Q

For chronic inflammatory dermatoses – psoriasis and lichen planus.

a. Explain involvement of T cells…

Autoimmune?

and their effect on…
basal cells, keratinocytes, the epidermis, blood vessels

A

T cell mediated autoimmune disease

i. Genetic and environmental factors –> antigens –> sensitized T
cells to the dermis and accumulate in the epidermis –> release
cytokines (IL 22) –> keratinocyte hyperproliferation in epidermis –>
excessive and rapid growth of epidermis… This leads to a delay in migration time from basal cells to surface and cells with retained nuclei at the surface (PARAKERATOSIS)

**does lead to DILATED, HYPERPLASTIC BLOOD VESSELS

___ is a disease of skin or mucous membrane that resembles lichen,
thought to be autoimmune but trigger is unknown

Antigen on cells in basal layer –> activation of CD8 –> KERATINOCYTE APOPTOSIS –> causes degeneration of basal layer and gives lesion a purple color, concentrated at the
epidermal-dermal interface this leads to SAW-TOOTH EPIDERMIS

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22
Q

Explain and compare the pathophysiology of chronic inflammatory dermatoses – psoriasis and lichen planus.

c. Appearance and type of skin and/or oral lesions (gross level) – why and how these occur?

Describe each epidermis, and what they look like grossly
-both have 2 unique things

A

thin area of epidermis becuase of parakeratosis

silver/white Scale…
When this scale is removed –> small bleeding = AUTZPITZ SIGN

Saw-tooth epidermis

  • Pink-purple, elevated polygonal papule
  • Wickham striae (white, lacelike markings)
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23
Q

pathophysiology of chronic inflammatory dermatoses – psoriasis and lichen planus.

d. Involvement of the oral mucosa

A

Psoriasis does not…

Lichen planus: wickman’s striae on tongue (white lace-like)

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24
Q

pathophysiology of chronic inflammatory dermatoses – psoriasis and lichen planus.

e. Possible precipitating events

2 for Psoriasis
2 for Lichen

A

–> –> keratinocyte hyperproliferation in epidermis –>
excessive and rapid growth of epidermis –>
–> (PARAKERTOSIS, where cells on surface have nuclei and epidermis is THIN)
—AUTZPITZ Sign

Pink-purple, elevated polygonal papule
Wickman striae (white, lacelike)
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25
Q

pathophysiology of chronic inflammatory dermatoses – psoriasis and lichen planus.

f. What are Auspitz signs and explain why they occur?

A

When the formed scale is removed or peeled off, it creates small bleeds due
to not a lot of room between blood vessels and epidermis = Autzpitz Sign

This is a result of hyperplasia of keratinocytes leading to PARAKERATOSIS and a THIN EPIDERMIS

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26
Q

pemphigus vulgaris and foliaceus

Target proteins or antigens involved – explain why the blisters develop in the different locations (i.e. cleft position)

A

Anti-desmoglein IgG-lose cell to cell adhesion between keratinocytes

Desmoglein 1 is concentrated in the upper epidermis…

Desmoglein 3 is in the lower epidermis and mucous membranes

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27
Q

Where are lesions of pemphigus vulgaris and foliaceus found?

A

Vulgaris has Abs to Desmoglein 1 and 3-so it is in the upper and lower epidermis, AND mucous membranes..

Foliaceus is ONLY in the upper epidermis and Skin only because desmoglein 1-NOT oral mucosa

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28
Q

bullae vs vessicle

A

bullae is a big blister, vessicle is smaller

29
Q

Skin layer of pemphigus vulgaris and foliaceus

A

intraepidermal and supra epidermal

30
Q

Skin layer of pemphigus vulgaris and foliaceus-where does it cause cleavage and where does it stain?

A

____ Stains intraepidermal
It causes cleavage supra-basal

___stains in the upper epidermis and cleaves subcorneal

31
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

pemphigus vulgaris and foliaceus,

bullous pemphigoid,

dermatitis herpetiformis.

a. Target proteins or antigens involved – explain why the blisters develop in the different locations (i.e. cleft position)

A

Vulgaris= Abs to desmoglein 1 and 3

Foliaceous= Abs to desmoglein 1

ii. More desmoglein 1 in upper part of epidermis
iii. Desmoglein 3 more concentrated in lower part of epidermis and
mucous membranes

—– targets proteins such as type XVII collagen in hemidesmosomes and BM and can affect skin and mucous membranes

Dermatitis Herpetiformis is caused by gluten and causes intact subepidermal blisters-Glutinamase

32
Q

A 45-year-old male presents to his dentist with difficulty eating and drinking. Erosions on his tongue and lips are noted, which apparently started a few months ago as a small blister, but has ‘spread’. The dentist also notes areas of erosions with a few flaccid bullae on his skin. The patient states that one time, when he pressed on his skin with a sliding motion, the outer layer of skin seemed to rub off.
There is high suspicion that he has:

A

Pemphigus vulgaris-the skin rubs off

33
Q

One reason why the lesions associated with acute eczematous dermatitis may not occur for a day or 2 after antigen exposure is because it takes a while for:
A. An allergen to bind to IgE on mast cells
B. Memory T cells to move to the site of
antigen exposure and be activated
C. IgE to be produced by plasma cells and
bind to mast cells in connective tissue
D. Langerhans cells to present antigen to a
naïve T cell in a lymph node

A

Probably B?

34
Q

Explain and compare the pathophysiology of blistering (bullous) disorders – pemphigus vulgaris and foliaceus,

bullous pemphigoid,

dermatitis herpetiformis

f. Possible precipitating events (is it erosive? Flacid?)

A

pemphigus vulgaris: skin erosion and broken blisters

foliaceus: less erosive.. tends to break

——–: hard to break blisters, can affect mucosa

——-: erode and become ulcerated

35
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

dermatitis herpetiformis.

a. Target proteins or antigens involved – explain why the blisters develop in the different locations (i.e. cleft position)

A

Autoimmune blistering disorder responding to a gluten-free diet (celiacs)

**NOT herpes

Subepidermal blister with intact epidermis-itchy

36
Q

A 44-year-old female presented to her primary care physician with a complaint of an itchy, red area on her neck. She states that she wore a new necklace for the last 2 days and then this started!

What does she have?

A

Allergic contact dermatitis

37
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

pemphigus vulgaris and foliaceus

b. Characteristic histological features – both with H&E staining and immunofluorescence

A

Suprabasal acantholysis (lysed layer of
ENTIRE EPITHELIAL CELL LAYER above
basal membrane)

antibodies to desmoglein 1; also has SUBCORNEAL-ONLY UPPER EPIDERMIS

38
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

bullous pemphigoid

b. Characteristic histological features – both with H&E staining and immunofluorescence

A

Subepidermal blister, very full and thick epidermis

Linear in Subepidermal basement membrane

39
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

dermatitis herpetiformis.

b. Characteristic histological features – both with H&E staining and immunofluorescence

A

Subepidermal….
intact epidermis

– blister with intact epidermis

iii. Grouped intact or eroded pustules and vacuoles

40
Q

A 25-year-old male with a nut allergy accidentally eats a cookie with nuts. About 15 minutes later he breaks out in an itchy rash.
Erythematous, edematous, often circular plaques (Wheals)
Pruritic
What does he have?

A

Uticaria

41
Q

A pathologists is looking at a skin biopsy and the first thing they note is hyperkeratosis. When starting to build their list of differential diagnoses, they are most likely considering a(n):

A. Acute inflammatory
dermatosis 
B. Chronic inflammatory
dermatosis 
C. Blistering disorder
A

B. Chronic inflammatory

42
Q 
A 25-year-old male is stung by a bee in his hand.  Within about 10 minutes, the area that was stung is beginning to get red and swollen. Which of the following would be most useful in reversing or treating his symptoms?
A. Blocking histamine receptors 
B. Blocking TNF receptors 
C. Inhibiting T cell activation 
D. Preventing IgE production 
E. Preventing mast cell degranulation
A

A. Blocking histamine receptors

Has uticaria

43
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

pemphigus vulgaris and foliaceus

d. Type of blister – how erosive and their tendency to break (flaccid or tense).

A

Pemphigus (vulgaris and foliaceous)
i. Vulgaris: antibodies to desmoglein 1 and 3

Blister tends to be more erosive and flacid, can break-SCRAPES OFF

Foliaceous:
Less erosive, tend to break also

44
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

bullous pemphigoid

d. Type of blister – how erosive and their tendency to break (flaccid or tense).

A

More erosive, difficult to break-THICK EPIDERMAL LAYER

45
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

dermatitis herpetiformis.

d. Type of blister – how erosive and their tendency to break (flaccid or tense).

A

More erosive, tends to break/ulcerate

46
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

pemphigus vulgaris and foliaceus

c. Appearance and type of skin and/or oral lesions (gross level)

A

Vulgaris:
blister that scrapes off and can be in mouth

Foliaceus: cutaneous blister, less likely to scrap off

47
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

bullous pemphigoid

c. Appearance and type of skin and/or oral lesions (gross level)

A

Subepidermal blister, very full and thick epidermis, harder for blister
to break
1. Tense bullae

48
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

dermatitis herpetiformis

c. Appearance and type of skin and/or oral lesions (gross level)

A

Subepidermal blister with intact epidermis

iii. Grouped intact or eroded pustules and vacuoles – very itchy, erode
- —> and become ulceration

49
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

pemphigus vulgaris

and foliaceus

e. Involvement of the oral mucosa or mucous membranes

A

Vulgaris=desmoglein 1 and 3 so it does involve mucous membranes

Foliaceus: Desmoglein 1 only, so NO MUCOSAL involvement just upper epidermis

50
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

bullous pemphigoid

e. Involvement of the oral mucosa or mucous membranes

A

Yes-via effecting hemidesmosomes

51
Q

Explain and compare the pathophysiology of blistering (bullous) disorders –

dermatitis herpetiformis

e. Involvement of the oral mucosa or mucous membranes

A

Subepidermal blister which does not have mucosal involvement

52
Q

Explain and compare the pathology of benign and premalignant epithelial lesions –

seborrheic keratosis

and actinic keratosis.

a. Involvement of UV radiation or sun damage

Cause/Risk Factors?

Dysplasia?

A

—- cause unkown, age related (over 50), many have a mutation in FGFR3 –> excessive production of keratin

—Sun, occurs on balding scalp, lateral neck,
distal upper or lower extremities

i. Sun related: UV –> DNA damage –> TP53 mutation –> proliferation of basal cells –> interpithelial DYSPLASIA

53
Q

Define dysplasia

A

Dysplasia is atypical cells in the epithelium with signs of malignant cells including the 5 keys:

(hyperchromatic nuclei, irregular nuclear membranes, increased nuclear to cytoplasmic ratio, mitotic figures, architectural anarchy)

This is NOT malignancy and is confined to epithelium, no metaplasia and well differentiated

54
Q

Where does dysplasia tend to occur/confined to where?

A

confined to the epithelium

55
Q

What are some of the characteristic cellular features of dysplasia?

(the 5)

A

The 5 signs…
hyperchromatic
nuclei, irregular nuclear membrane, increased nuclear to cytoplasmic ratio, mitotic figures, architectural anarchy

Cells do not change cell type, cells have some atypical cytology and are not
well differentiated

56
Q

Differentiate between dysplasia, malignancy and metaplasia

A

Dysplasia cells do not metastasize… BUT they can lead to Malignant cells which do metastasize…

Dysplasia cells are not metastatic (they do not change to different types of cells)

57
Q

Explain and compare the pathology of benign and premalignant epithelial lesions –

seborrheic keratosis

and actinic keratosis

Mutations involved??

A
  • – cause unkown, age-related (over 50),
  • **many have a mutation in FGFR3 –> excessive production of keratin

: occurs on balding scalp, lateral neck, distal upper or lower extremities

i. Sun related: UV –> DNA damage –> TP53 mutation –> proliferation of basal cells –> interpithelial dysplasia

58
Q
  1. Explain and compare the pathology of benign and premalignant epithelial lesions –

seborrheic keratosis (3 things here)

d. Characteristic histological features – why and how these occur.

A

Histological features

  1. Acanthosis: diffuse thickening of epidermal layer
  2. HORN CYSTS – filled with keratin
  3. No rete ridges

**Result of excess keratin production

59
Q
  1. Explain and compare the pathology of benign and premalignant epithelial lesions –

actinic keratosis (4)

d. Characteristic histological features – why and how these occur.

A

Histological features
1. Partial thickness dysplasia on bottom half of epidermis
2. Hyperchromasia (dark nuclei)
3. Varied nuclei and cell shape with loss of orientation
(pleomorphism)
4. Hyperkeratosis and parakeratosis

60
Q
  1. Explain and compare the pathology of benign and premalignant epithelial lesions –

and actinic keratosis (2)

e. Appearance and type of skin lesion (gross level) – why and how these occur.

A

On balding scalp, lateral neck, distal upper or lower extremities…

Gross morphology
1. Zone of redness (erythematous macule or patch)

  1. Rough/scaly (hyperkeratotic surface)
61
Q
  1. Explain and compare the pathology of benign and premalignant epithelial lesions –

seborrheic keratosis

and actinic keratosis.

f. Progression to skin cancer?

A

Causes scaly-keratinized skin but does not seem to progress to cancer

Can progress to….
squamous cell carcinoma in situ –> tends to grow slowly enlarging over the course of years and asymptomatic

OR SCC invasive which invades the dermis

62
Q

Compare actinic keratosis and squamous cell carcinoma in situ.

a. Which is the precursor lesion?
b. Histological and gross pathological differences.

A

– partial thickness epidermal dysplasia

– full thickness epidermal dysplasia but has not penetrated basement
membrane

Invasive SCC – full thickness epidermal dysplasia and has penetrated basement membrane
to involve dermis

63
Q

Oral SCC vs cutaneous?

A

Oral is more agressive

64
Q

Oral SCC commonly found where in mouth

A

Floor of mouth and lateral or ventral tongue

65
Q

Oral SCC histo

A

Histological features

  1. Full thickness dysplasia
  2. Carcinoma invaded dermis (should be mainly collagen) –> nuclear crowding and disorganization
  3. Keratin pearls: cells that make arrangements of keratin into swirls
66
Q

Compare the difference between actinic keratosis, squamous cell carcinoma in situ, and invasive squamous cell carcinoma – location of dysplasia and whether or not it has penetrated the basement membrane

A

Actinic keratosis – partial thickness epidermal dysplasia

SCC in situ – full thickness epidermal dysplasia but has not penetrated basement
membrane

Invasive SCC – full thickness epidermal dysplasia and has penetrated basement membrane
to involve dermis

67
Q

Explain and compare the pathophysiology of

acute inflammatory dermatoses – urticaria,

acute eczematous dermatitis (limit this to allergic contact dermatitis),

and erythema multiforme.

c. – why or how these occur?

A

Uriticaria: Caused by pollen, food, drugs, venom….

Just dilated vessels in the dermis really

Acute Eczematous dermatitis: apoptosis of keratinocytes caused by CD8 cells causes space between epidermis which can fill up and blister (spongiosis, bullae, vesicles)

Erythema multiforme is triggered by infectious diseases… These form similar to acute eczematous but these can burst.. :(

68
Q

Explain and compare the pathophysiology of chronic inflammatory dermatoses – psoriasis.

Migration time from basal layer to surface changed at all?

Blood vessels involved?

A
  1. Migration time from basal layer to surface increases to about
    4-7 days –> retained nuclei at skin surface because no time for
    keratinocytes (parakeratosis)
  2. Dilated, hyperplastic blood vessels

Patho Phys Exam 1 (14 decks)

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