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Step 1 Miscellanous > Pathoma Skin Pathology > Flashcards

Pathoma Skin Pathology Flashcards

1
Q

What type of allergic reaction is eczema vs allergic contact dermatitis?

A

Eczema = Atopic dermatitis - Type I hypersensitivity, associated with asthma and allergic rhinitis

Allergic contact dermatitis - Type IV hypersensitivity

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2
Q

What are some typical causes of allergic contact dermatitis?

A

Poison ivy
Nickel Jewelry
Drugs i.e. Penicillin, Neomycin

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3
Q

What is a blackhead vs a whitehead?

A

These are NON-inflammatory processes
1. Open comedone - blackhead - where pore is plugged with keratin debris and oxidation turns it black

  1. Closed comedone - whitehead - the black part becomes hidden and skin grows overtop. Note, NOT a pustule.
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4
Q

What is the progression of acne after whitehead? How will scarring occur?

A

Closed comedone ->
Inflammation begins:
papule -> pustule (with marked inflammatory infiltrate) = pimple -> nodule / cyst, when the pimple bursts and inflammatory infiltrate is let into the epidermis -> will lead to a scar

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5
Q

What are some OTC topic agents used for acne treatment? How do they work?

A

Benzoyl peroxide - Antibacterial, anti-inflammatory, and anticomedonal -> opens up pores for more effectiveness

Topical retinoids - apadelene, tazoretene - reduce keratin production and should be used with benzoyl peroxide
-> best anticomedonal

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6
Q

How does P. acnes contribute to acne?

A

Produces lipases which break down the sebum -> causes inflammation and growing of the comedone below til it becomes a pustule.

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7
Q

What is the pathogenesis of psoriasis?

A

Overproduction of Th1 cytokines leads to immune-mediated proliferation of basal cell keratinocytes -> hyperproliferation and rapid turnover

Happens in response to trauma on extensor surfaces, as an autoimmune process in genetically susceptible individuals.

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8
Q

What are classical findings on skin biopsy of psoriasis?

A
  1. Acanthosis - epidermal hyperplasia of spinosum layer
  2. Parakeratosis - hyperkeratosis with retention of keratinocyte nuclei in stratum corneum - (leads to silvery scaling)
  3. Neutrophils in stratum corneum - Monro microabscesses
  4. Thinning of epidermis above elongated dermal papillae - Auspitz sign
  5. Thinning of stratum granulosum.
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9
Q

What are the general treatments for psoriasis?

A
  1. Topical corticosteroids
  2. Phototherapy, especially psoralen + UVA therapy to immunosuppress = PUVA. Psoralen = Psoriasis.
  3. Immunomodulating therapy -> methotrexate, TNF inhibitors, etc
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10
Q

What does psoralen do?

A

It intercalates into DNA and sensitizes the skin to UV light.
-> used on areas of hyperkeratosis to sensitize skin for treatment.

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11
Q

What are the 5 P’s of lichen Planus?

A

Pruritic, planar (flat-topped), polygonal, purple papules

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12
Q

What will close inspection of the surface of Lichen Planus show? What is seen under the microscope?

A

Wickham’s striae - Lacy, reticular pattern of crisscrossed, whitish lines

Sawtooth infiltrate of lymphocytes at the dermal-epidermal junction (base of epidermis)

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13
Q

Where do Lichen Planus lesions occur?

A

Flexor surfaces of wrists and forearms (elbows), oral mucosa

Can involve mucuous membranes, especially buccal mucosa of mouth

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14
Q

Lichen planus is itchy like Dermatitis Herpetiformis. Will the lesions be excoriated?

A

Patient will say the itching is very severe, but there will be minimal excoriation of the lesions since they are very tender

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15
Q

What is thought to be the cause of Lichen Planus / what is associated? Give a major risk factor.

A

Etiology is unknown, but there is a genetic component and it is associated with Koebnerization (i.e. scratching could cause an eruption).

Chronic HEPATITIS C is a major risk factor.

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16
Q

What type of lesions does pemphigus vulgaris cause and will there be scarring?

A

Causes flaccid blisters that rupture easily leaving superficial erosions

  • > this is due to loss of intraepidermal integrity
  • > erosions last for weeks but heal WITHOUT scarring (defect is very superficial).

(IgG antibodies against desmogleins)

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17
Q

Where will lesions appear, and what two signs are characteristically positive in pemphigus vulgaris?

A

Lesions appear anywhere where there’s skin, as well as in ORAL MUCOSA (vs BP)

  1. Nikolsky’s sign + - firm pressure / rubbing on normal skin will induce a blister. Think Nikolsky = Normal.
  2. Asboe-Hansen sign+ - Lateral pressure on intact bullae causes the fluid to dissect laterally into adjacent normal appearing skin
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18
Q

What will DIF and H&E show for pemphigus vulgaris?

A

DIF - reticular pattern of immune complex deposition around keratinocytes (affecting stratum spinosum)

H&E - “tombstone appearance”, as basal cells remain attached to basement membrane by hemidesmosomes, but rest of epidermis is lifted off. Epithelium shows acantholysis.

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19
Q

What are the autoantibodies of bullous pemphigoid and how do you remember their location?

A

Anti BP180 (BPA2) and anti BP230 (BPA1)

  • > subepidermal because they are “bullow” the epidermis
  • > hooks basal epithelial cells into basement membrane
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20
Q

What will skin biopsy show by direct immunofluoresence and H&E?

A

H&E: Subepidermal bulla with infiltrate of EOSINOPHILS

DIF: Linear IgG deposition alone epidermal basement membrane zone

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21
Q

What is the Nikolsky sign for Bullous pemphigoid?

A

Negative. That is, firm pressure on normal skin will not induce a blister
-> skin still has good structural integrity

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22
Q

What will skin biopsy of Dermatitis Herpitiformis show via H&E and direct immunofluorescence?

A

H&E - neutrophilic infiltrate of papillary dermal tips (vs. psoriasis which shows neutrophils in the stratum corneum).

DIF - granular IgA deposition
-> strong association with celiac disease

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23
Q

How does dermatitis herpetiformis (DH) appear? Are they itchy? Where are the lesions most often found?

A

Intensely pruritic clusters of vesicles or excoriations (often hard to find vesicles since they are so itchy)
-> grouped together like herpes “herpetiform”

Lesions often found on extensor surfaces such as elbows and knees

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24
Q

What are the two treatments for dermatitis herpetiformis and their mechanisms of action in this disease?

A
  1. Strict gluten free diet

2. Oral dapsone -> inhibits myeloperoxidase

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25
Q

What is the typical appearance of lesions in erythema multiforme and what is the cause of the disease broadly?

A

It is a hypersensitivity reaction mediated by antigens depositing in the skin -> Systemic immune response to a localized process. #11662

Lesions will appear targetoid with bullae, due to central epidermal necrosis surrounded by erythema

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26
Q

What is the most common cause of EM and some other causes?

A
  1. HSV infection*
  2. Mycoplasma
  3. Drugs - i.e. penicillin, sulfonamides
  4. Autoimmune disease like SLE
  5. Cancer
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27
Q

What do the lesions of SJS/TEN look like / how do they form?

A

They are flaccid blisters which are formed when the necrotic epidermis detaches from dermis, and edema fluid fills the space

Mucosal eruptions are also very painful, can interfere with vision, voiding, etc

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28
Q

What are the clinical symptoms of SJS / TEN? Does it involve mucosal surfaces?

A

Prodrome of fever and generally feeling bad

Rash starts on trunk, the spread to face and upper extremities

It ultimately involves the buccal, ocular (including conjunctiva), and genital mucosa in 90% of cases

SJS: <10% of body surface involved
SJS-TEN: 10-30% of body surface involved
TEN: >30% of body surface involved

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29
Q

What lesion is a benign squamous proliferation which is a very common tumor in the elderly? How does it appear?

A

Seborrheic keratosis

-Raised, pigmented plaque filled with horn cysts or pseudo-horn cysts (keratin proliferations plugged up invaginations in the skin)

Histology shows pseudocysts with abundant pink keratin.

30
Q

What is the sign of Leser-Trelat?

A

Sudden appearance of multiple seborrheic keratoses

-> indicates underlying GI malignancies

31
Q

What is acanthosis nigricans and where does it appear?

A

Epidermal hyperplasia causing elevated, hyperpigmented skin thickening (‘velvet-like’ skin). Appears especially in neck, axilla, and groin

32
Q

What conditions are associated with acanthosis nigricans and how is their onset different?

A

Insulin resistance - i.e. diabetes, obesity, Cushing syndrome

Visceral malignancy - i.e. gastric adenocarcinoma -> much more rapid onset than insulin-resistance related

33
Q

How do basal cell carcinomas appear grossly and what are the major risk factors?

A

Generally appears as pink or pearly-white nodules with overlying telangiectasias. Can bleed, become erosive, and ulcerate in the center. May develop a raised, rolled border.

Risk factor: cumulative UVB exposure (i.e. prolonged sunlight exposure, albinism, or xeroderma pigmentosum)

34
Q

What will histology show for a basal cell carcinoma?

A

Nodules of basal cells with peripheral palisading -> lining up around the periphery of nodules

35
Q

What are risk factors for squamous cell carcinoma?

A
  1. Ultraviolet light exposure
  2. Immunosuppression (i.e. transplants)
  3. Chronic inflammation, i.e. due to chronically draining sinus tracts (i.e. from osteomyelitis) or scars from burns
  4. Arsenic exposure -> causes hyperkeratosis
36
Q

What are the histological findings for actinic keratosis / what is it? What typically causes these lesions?

A

Intraepidermal, partial thickness atypia of epidermis

  • > dysplasia which is the precursor to SqCC
  • > caused by sun damage, can be prevented by avoiding sun / using sunscreen
37
Q

What is a Keratoacanthoma? What does it look like / what is the prognosis?

A

Invasive squamous cell carcinoma variant with cup-like shape and keratotic debris in the middle (central keratotic core)

Prognosis - Rapidly progresses for 4-6 weeks, then often spontaneously regresses over months

38
Q

What enzyme is important for the beginning of melanin synthesis?

A

Tyrosinase -> converts tyrosine to DOPA quinone

39
Q

What causes vitiligo and how will you generally pick this up in a white person on a board exam?

A

Localized autoimmune destruction of melanocytes

-> generally will only see in a white person when they go to tan and are unable to darken some areas of skin

40
Q

What is the defect in albinism?

A

Normal melanocyte number but decreased melanin production due to decreased tyrosinase activity

41
Q

What are the two forms of albinism?

A
  1. Ocular form - involves pigmentation of eyes

2. Oculocutaneous form - involves both the eyes and skin

42
Q

What are the risks associated with albinism?

A

Increased risk of skin cancer, including SqCC, BCC, and melanoma, due to reduced protection against UVB

43
Q

What is an ephelis and what causes it?

A

Freckle - a tan-brown macule which darkens with sunlight

Due to increased number of melanoSOMES, but the melanoCYTES are NOT increased.

44
Q

What is melasma? What causes it / what does it look like / where is it?

A

“Mask of pregnancy” - hyperpigmentated poorly demarcated patches, typically on the face. Can also be associated with oral contraceptive use.
-> estrogen-sensitive

45
Q

What is a congenital nevus / how does it appear? What does it have in it? Why can it be worrisome?

A

Nevus present at birth, generally slightly raised / pebbly. Often has hair in it (not destructive like a melanoma).

Variability in color is common, with irregular margins -> can be worrisome for melanoma

46
Q

What is the typical progression of an acquired nevus on the microscopic level?

A
  1. Junctional nevus - melanocyte nests grow at the dermal-epidermal JUNCTION, childhood
  2. Compound - Nevus cells grow at DEJ and inward into the dermis
  3. Intradermal nevus - nevus nests lose their junctional component and grow directly into the dermis, adulthood
47
Q

What is the typical progression of an acquired nevus on the macroscopic level?

A
  1. Junctional nevus - flat brown MACULE will well defined borders
  2. Compound nevus - light BROWN PAPULE
  3. Intradermal nevus - verrucous (wartlike) tan / FLESH-colored PAPULE.

flat brown -> raised brown -> raised fleshy.

48
Q

What should you do if you see many dysplastic nevi on a patient?

A

Biopsy the “ugly duckling” of the bunch to confirm it’s benign. Take many photos and look for progression.

Keep in mind removing them does not necessarily change the cancer risk since the mutation causing these is germline in these patients
-> “Dysplastic Nevus syndrome”

49
Q

What signs should you look for to differentiate nevus from melanoma?

A

ABCDE’s

Asymmetry
Border irregularity
Color variation
Diameter >6mm
Evolution - change, i.e. bleeding, growth, crusting, symptoms, oozing erosion, scaling, itchiness, swelling etc
50
Q

What are the four core types of melanoma? Which is most common?

A
  1. Superficial spreading - most common
  2. Nodular
  3. Lentigo maligna
  4. Acral lentiginous
51
Q

How do you stage a melanoma and how much should you remove when staging / confirming diagnosis?

A

Breslow’s thickness -> depth of tumor, most important for prognosis

Should biopsy and remove the entire lesion to prevent sampling error

52
Q

What does superficial spreading mean? Prognosis?

A

Dominant early radial growth pattern -> good prognosis because they grow laterally before they grow down, (tends to stay in situ)

53
Q

What is lentigo maligna melanoma and where does it appear? Who gets it?

A

Lentigo = freckle
Lentigo maligna = malignant freckle

Appears over sun-exposed areas of face (cheek / nose), usually related to chronic sun damage
-> happens more in the elderly

Radial growth like superficial spreading gives it a good prognosis.

54
Q

What is a nodular melanoma and the prognosis?

A

Subtype with early vertical growth, poor prognosis. (Creates a nodule because they grow into the dermis and push the epidermis up).

Can be any color and rapidly evolving / bloody.

55
Q

What is the least common subtype of melanoma and who is it actually common in? Where does it grow? Is it related to sun exposure?

A

Acral lentiginous melanoma
-> A freckle-like melanoma of the palms, soles, and nails

Most common type of melanoma in African Americans!! - not related to UV exposure (unlike lentigo maligna)

56
Q

What is impetigo and what is its classic appearance?

A

A very superficial skin infection which is limited to the epidermis

Classical appearance: erosion with honey-colored crust (from pustular exudate following pustule bursting)

57
Q

What organisms typically cause impetigo?

A

S. aureus more commonly than S. pyogenes

Bullous impetigo in particular is caused by S. aureus
-> localized SSSS via exfoliative toxins

58
Q

What is cellulitis and what agents typically cause it? What can this progress to?

A

Acute, painful, spreading infection of the deep dermis and subcutaneous tissues

Usually caused by S. pyogenes or S. aureus
-> can progress to necrotizing fasciitis

59
Q

What are risk factors for development of cellulitis?

A

Skin trauma, animal / insect bites (think Harrisonlift), or recent surgery

60
Q

What typically causes crepitant vs necrotizing fasciitis? What physical exam finding is characteristic of the latter?

A

Crepitant - gas gangrene: Clostridium perfringens

Necrotizing fasciitis - Group A strept, MRSA, or polymicrobial

Necrotizing fasciitis is due to deep tissue injury. Pain will be OUT OF PROPORTION to physical exam findings.

61
Q

What is bullous impetigo, and what is the cause of the systemic form of this disease?

A

Bullous impetigo is the localized form of SSSS, which in this case you would be able to culture S. aureus locally

Systemic form is SSSS, and is caused by toxins circulating throughout body distant from site of infection.
-> Staphylococcal exfoliative toxins cause INTRAepidermal splitting by cleaveage of desmoglein 1 in desmosomes

62
Q

What pathology does SSSS cause? Is Nikolsky sign positive or negative?

A

Causes flaccid bullae since it’s intraepidermal. Nikolsky sign will by positive, like pemphigus vulgaris (pressing on the skin can create blisters due to circulating toxin which cleaves desmosomes)

63
Q

How is SSSS distinct from SJS-TEN?

A

Basically SJS-TEN is the SSSS of bullous pemphigoid -> the separation is at the DEJ in SJS-TEN (deeper than SSSS).

64
Q

What causes verruca vulgaris and where is it typically found?

A

HPV (6,11), typically found on the hands and feet as hyperkeratotic, cauliflower-like papules.

65
Q

What do Molluscum Contagiosum lesions look like and how are they spread?

A

Pearly-pink dome-shaped papules with central “umbilication” which is dimpled, seen on trunk, face, and groin

Spread sexually typically, but can also be spread in children by direct contact and then hand to groin transmission elsewhere in the body

66
Q

What are the four major subtypes of rosacea?

A
  1. Erythematotelangiectatic
  2. Papulopustular
  3. Phymatous
  4. Ocular
67
Q

What is erythematotelangiectatic rosacea characterized by?

A

Flushing, usually triggered by emotion, hot beverages, caffeine, alcohol etc, as well as persistent facial erythema with or without telangiectasia.

68
Q

What is papulopustular rosacea characterized by? What is notably absent?

A

Persistent facial erythema with transient papules / pustules
-> inflammatory type rosacea
“adult acne”

Notably absent: comedones (the precursor to papules / pustules which are NON-inflammatory)

69
Q

What is phymatous rosacea characterized by? Why does it occur?

A

Phyma = growth. This is characterized by thickened skin, irregular surface nodularities, and enlargement.

Frequently associated with rhinophyma (irreversible hypertrophy of the nose).
-> occurs due to sebaceous gland enlargement + scar tissue formation

70
Q

What characterizes ocular rosacea? Why does it occur?

A

Ocular photosensitivity, blurred vision, telangiectasia of the sclera, foreign body sensation in the eye
-> occurs because oil glands and tear ducts get blocked

71
Q

What is the effect of vitamin D analogs in the treatment of psoriasis?

A

Inhibits keratinocyte proliferation and stimulates keratinocyte differentiation #8569

Step 1 Miscellanous (40 decks)

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