Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Gen Path Final > Skin > Flashcards

Skin Flashcards

1
Q

Macule:

A

flat, circumscribed area <5 mm • Patch: flat, circumscribed area >5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

• Papule:

A

elevated lesion <5 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • Plaque: elevated lesion > 5 mm

* Pustule:

A

discrete pus-filled lesion •

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vesicle:

A

fluid-filled lesion <5 mm •

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bulla:

A

fluid-filled lesion >5 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Urticaria: Hives

A

CLINICAL FEATURES
• Erythematous, edematous, and pruritic papules and plaques (wheals)
• Individual hives last <24 hours (just a few hours), but episodes can continue for weeks
• Localized or generalized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute Urticaria PATHOGENESIS

A

Mast cell degranulation
increased dermal vascular permeability
dermal edema
• Immediate Type I (IgE) hypersensitivity rxn
• Inciting factor: medications (opiates, abx)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute Urticaria treatment

TREATMENT

A

• Antihistamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute Eczema CLINICAL FEATURES

A
  • Pruritic inflammatory erythematous papules and scaly plaques
  • Can become vesicular and crusted
  • over time, skin thickens due to acanthosis
  • Spongiotic dermatitis on histo: epidermal edema, perivascular lymphocytic infiltrate, and mast cell degranulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Types of Eczema

A

Atopic :
• Allergic contact:
• Photoeczematous:
Irritant dermatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Eczema

Atopic :

A

autoimmune related
– Genetic predisposition
– Atopic triad of asthma, allergies, and eczema – More common in childhood, outgrow as adult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Eczema

• Allergic contact:

A

contact exposure to an allergen

– Type IV hypersensitivity rxn: CD4+T lymphocyte mediated – Poison ivy, neosporin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Eczema

• Photoeczematous:

A

abnl reaction to ultraviolet light •

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Eczema

Irritant dermatitis:

A

contact exposure to irritant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Erythema Multiforme

A

Hypersensitivity reaction most often due to medication/drug and certain infections
•
– Common meds: sulfonamides, PCN, NSAIDs, hydroquinone
– Infections: HSV and mycoplasma
On spectrum of Stevens Johnson (more mucosal involvement and wider surface area) and toxic epidermal necrolysis (TEN- full thickness epidermal necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Erythema Multiforme

CLINICAL FEATURES

A
  • “targetoid” lesions
  • Multiple features with macules, papules, vesicles with central pallor
  • Can lead to epidermal desquamation if progresses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chronic Inflammatory Dermatosis: PSORIASIS

• Chronic inflammatory dermatosis in

A

1-2% of US population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Chronic Inflammatory Dermatosis: PSORIASIS

• Associated with

A

heart disease and 10% can develop psoriatic arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Chronic Inflammatory Dermatosis: PSORIASIS

————- mediated rxn

A

• Autoimmune, T-cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Chronic Inflammatory Dermatosis: PSORIASIS

• Can be localized to

A

specific areas or generalized and severe (erythroderma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Chronic Inflammatory Dermatosis: PSORIASIS

CLINICAL FEATURES

A

• erythematous salmon-pink colored plaques with silvery scale
– extensor elbows, knees, scalp, gluteal cleft
– nail thickening and dystrophy
• Koebner: induce lesion by local trauma
• Auspitz sign: punctate bleeding when overlying scale is removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Psoriasis Histopathology:

A

• Epidermal thickening (acanthosis) with incr epidermal cell turnover but lack of maturation
– Epidermal hyperplasia
– Downward extension of rete ridges
– Parakeratotic scale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Chronic Inflammatory Dermatosis: Lichen Planus

A
  • Pruritic
  • Purple
  • Polygonal
  • Planar papules and plaques
  • Covered in Oral Pathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Infectious Dermatoses
Bacterial Infection • Impetigo

– ———-, can be Strep pyogenes

A

Staph Aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Infectious Dermatoses Bacterial Infection • Impetigo – Contagious, more commonly
in kids, spread through direct contact
26
Infectious Dermatoses Bacterial Infection • Impetigo – Starts as small
macule often perioral/perinasal
27
Infectious Dermatoses Bacterial Infection • Impetigo – Enlarges with
honey-colored crust (dried serum)
28
Infectious Dermatoses Bacterial Infection • Impetigo – Treat with
antibiotics with good Staph coverage
29
Blistering Dermatoses | Blistering disease where
vesicles and bullae are primary skin finding | Blisters occur at different levels within epidermis Distinguished clinically and histopathologically
30
– Direct immunofluorescence (DIF) can help diagnose
Blistering dermatoses
31
Blistering dermatoses examples
* Pemphigus Vulgaris | * Pemphigus Foliaceus • Bullous Pemphigoid
32
Acantholysis:
lysis of intercellular junctions between squamous cells
33
• Subcorneal
(superficial epidermis at stratum granulosum): pemphigus foliaceus
34
• Suprabasal (above basal cell):
pemphigus vulgaris | Nonacantholysis
35
• Subepidermal (below DEJ):
bullous pemphigoid with intact intercellular junctions
36
Pemphigus • Type ----- hypersensitivity reaction
II
37
Pemphigus | • IgG autoantibodies bind to
desmoglein type I and type 3 intercellular desmosomal proteins
38
Pemphigus | – Disrupted intercellular adhesion causes
blistering
39
Pemphigus | • DIF:
``` intercellular IgG deposition along keratinocyte cell membranes (fish-net) ```
40
– Pemphigus vulgaris:
IgG deposits throughout epidermis
41
– Pemphigus foliaceus:
IgG deposits in superficial layers of | epidermis
42
Pemphigus Vulgaris
• Rare disease of elderly • women>men • Mucosal and skin involvement – Pressure points on trunk, groin, axillae, face – Intraoral involvement • Flaccid blisters that easily rupture leaving denuded skin with extensive erosions and crusting • Treatment: immunosuppressants +/- systemic steroids
43
Pemphigus Vulgaris DIF:
fishnet pattern with intercellular IgG deposition around keratinocyte cell membranes throughout epidermis
44
Actinic Keratosis/Cheilitis | Red, rough patches on
chronically sun exposed skin (mainly head/neck, lips, dorsal hands)
45
Actinic Keratosis/Cheilitis | • More common in
fair-skinned and blond/red heads
46
Actinic Keratosis/Cheilitis | • Histo:
cytologic atypia with hyperplasia of basal cells with overall epidermal thinning
47
Actinic Keratosis/Cheilitis | • Can rarely evolve into
squamous cell carcinoma, particularly with TP53 mutation from UV DNA damage
48
Actinic Keratosis/Cheilitis | • Treatment:
cryotherapy (liquid nitrogen), topical chemotherapy agents
49
Squamous Cell Carcinoma
``` • Forms in basal layer of epidermis • 2nd most common type of skin cancer • UV light exposureDNA mutations, loss of DNA repair, leading to cell damage • TP53 mutation • HRAS and Notch receptor mutations ```
50
Squamous Cell Carcinoma-in-situ:
red scaly plaque with squamous atypia throughout epidermis • Over time, become invasive, nodular, and ulcerate • Men>women • Squamous atypia through epidermis • Invasive when penetrates through BM
51
SCC metastasis
* Mucosal>cutaneous * Thickness of lesion and depth of invasion into dermis * Size >2 cm * Ulceration * High risk locations such as head/neck, particularly lips, ears, around eyes
52
SCC Treatment | • Treatment of choice is
tumor resection – If detected early, simple excision – If more aggressive, can be done by Mohs surgical technique (tumor removed layer by layer, evaluated histopathologically in real time, with additional layers taken for residual tumor; repair of defect)
53
Basal Cell Carcinoma
• Most common type of skin cancer • Pearly pink, translucent papules with telangiectasias; can become nodular and ulcerate • Superficial: multifocal growth in epidermis • Nodular: downward invasion to dermis – Can be locally aggressive but rarely metastasizes
54
Basal Cell Carcinoma | Histopathology
* Arise in basal layer of epidermis | * Palisading nests of basaloid cells with hyperchromatic nuclei surrounded by fibrotic stroma
55
• Genetic disorder: Basal Cell Nevus Syndrome (Gorlin Syndrome) with
PTCH gene mutation in Hedgehog tumor suppressor pathway
56
Nodular BCC
Frequently on nasaolabial folds or above upper lip | Pearly translucent nodule with telangiectasias
57
``` Melanocytic Nevi (Moles) • benign neoplasm of melanocytes ```
Congenital or acquired • BRAF mutation as common factor in nevi • Cellular senescence: migration of nevi from DEJ into dermis – Superficial nevi: produce melanin, grow in nests – Deeper nevi: minimal to no pigment, grow in cords or single cells
58
Growth pattern of Nevi | • Junctional
– Nests at dermal-epidermal junction
59
Growth pattern of Nevi | • Compound
– Nests at DEJ and dermis
60
Growth pattern of Nevi | • Intradermal +/- cellular senescence
– Nests primarily dermal (intradermal)
61
Dysplastic Nevi
• Marker for melanoma, not precursor • Vast majority will not transform into melanoma • BRAF mutation common, NRAS mutation • Size>5mminsize • Pigment variegation • Border irregularity • Familial Dysplastic Nevus Syndrome – Dysplastic nevi >100s with strong melanoma risk • Cytologic atypia of melanocytes on histopath
62
Melanoma
* Skin cancer derived from melanocytes * 3rd most common type of skin cancer after BCC and SCCs, but can be highly aggressive and more likely to metastasize if untreated * Early detection critical and can be curative * Delayed detection can lead to metastasis and poor prognosis
63
Clinical Signs of Melanoma
* Rapid change in size of prior nevus with asymmetry * Color change and/or variability * Itching/pain associated in a lesion * New onset pigmented lesion esp in adults * Irregular borders
64
Melanoma | ABCDEs
(Asymmetry, Border irregularity, Color change, Diameter, Evolution)
65
• Vertical growth phase is the key factor in nature of
melanomas
66
Melanoma Histopathology
* Melanocytes are irregular in size and shape with prominent nucleoli * Radial and vertical growth seen histologically * Atypical mitoses common * Specific special stains, such as HMB-45, can help detect melanocytes
67
Risk Factors for Metastasis
• Depth of invasion (Breslow thickness in mm) – In-situ: intraepithelial – Dermal/Invasive: through epidermis into dermis • Tumor Size • Ulceration • Mitoses • Lymph node involvement

Gen Path Final (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions