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Pathophys Semester II > Exam IV Skin > Flashcards

Exam IV Skin Flashcards

1
Q

The three layers of the skin

A

The Epidermis provides a waterproof barrier and creates the skin tone

The Dermis contains tough connective tissue, hair follicles, and sweat glands

The Hypodermis is made of fat and connective tissue

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2
Q

Primary Skin Lesions: Macule and Patch

A

Macule:

A flat circumscribed area that is a change in color of skin; less than 1 cm in diameter

Examples” Freckles, flat moles (nevi), petechiae, measles, scarlet fever

Patch:

Bigger Macule

Example: Vitiligo

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3
Q

Primary Skin Lesions: Papule and Nodule

A

Papule:

An elevated, firm, circumscribed area less than 1 cm in diameter

Examples” Wart, elevated moles, lichen planus, fibroma, insect bite

Nodule:

A bigger version of a papule

Example: lipomas

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4
Q

Primary Skin Lesions: Plaque and Wheal

A

Plaque:

Elevated, firm. and rough lesion with flat top surface greater than 1 cm in diameter

Example: Psoriasis, seborrheic and actinic keratoses

Wheal:

Elevated, irregular-shaped area of cutaneous edema; solid, transient; variable diameter

Examples: Insect bites, urticaria, allergic reaction

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5
Q

Primary Skin Lesions: Vesicle and Bulla

A

Vesicle:

Elevated, circumscribed, superficial; does not extend into dermis; filled with serous fluid; less than 1 cm in diameter

Examples: Varicella (chicken pox), herpes zoster (shingles), herpes simplex

Bulla:

A bigger Vesicle

Examples: Blister, pemphigus vulgaris

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6
Q

Primary Skin Lesions: Pustule and Cyst

A

Pustule:

Elevated, superficial lesion; similar to a vesicle, but filled with purulent fluid

Example: Impetigo, acne

Cyst:

Elevated, circumscribed, encapsulated lesion; in dermis or subcutaneous layer; filled with fluid or semisolid material

Example: Sebaceous Cyst, cystic acne

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7
Q

Primary Skin Lesions: Telangiectasia and Tumor

A

Telangiectasia :

Fine (0.5-1 mm), irregular, red lines produced by capillary dilation; can be associated with acne rosacea (face), venous HTN (spider veins in legs), systemic sclerosis, or developmental abnormalities (port wine birthmarks)

Example: Telangiectasia in rosecea

Tumor:

Elevated, solid lesion; may be clearly demarcated; deeper in dermis; more than 2 cm in diameter

Example: Neoplasms, benign tumor, lipoma, neurofibroma, hemangioma

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8
Q

Scale

A

Heaped-up. keratinized cells; flaky skin; irregular-shape; thick or thin; dry or oily; variations in size.

Ex. Think flaking skin

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9
Q

Lichenification

A

Rough THickened epidermis secondary to persistant rubbing, itching, or skin irritation; often involves flexor surface extremity.

Ex - Chronic dermatitis

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10
Q

Excoriation

A

Loss of epidermis; linear, hollowed out crusted area

Ex - Abrasion/scratch/scabies

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11
Q

Fissure

A

Linear crack or break

ex - athletes foot, anal fissure

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12
Q

Erosion

A

Loss of a part of the epidermis

ex - think remains after a ruptured blister

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13
Q

Ulcer

A

Loss of epidermis and dermis; concave; varies in size.

ex - larger version of eroision / pressure ulcer

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14
Q

Steven-Johnson Syndrome/Toxic Epidermal Necrolysis

A

Severe mucocutaneous reactions to certain drugs (oral, ocular, genital) –> keratinocyte necrosis

  • apoptotic pathway
  • drug-specific CD8+ cytotoxic T cells release perforin, granzyme B and granulysin to kill keratinocytes
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15
Q

Psoriasis

A

Autoimmune inflammatory, a hyperproliferative state of epidermal cells

Most common clinical presentation: erythematous plaques with silver scale

Pre-psoriasis skin:

  • dendritic cells, T cells
  • Differentiation of T cells is stimulated by IL-23

Psoriasis skin:

  • activated dendritic cells mainly produce TNFα
  • The clinical success of TNF-blocking agents is therefore not surprising
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16
Q

Acne Vulgaris

A
  • disease of pilosebaceous follicles
  • Follicular hyperkeratinization
  • Increased sebum production
  • Cutibacterium (formerly known P. acnes) within the follicle
  • Inflammation
  • microcomedo (a precursor) might lead to closed comedos by accumulation of sebum and keratinous material
  • Androgens stimulates the growth and secretory function of sebaceous glands
  • all women with the combination of acne and oligomenorrhea should be evaluated for PCOS
17
Q

Rosacea

A
  • chronic inflammatory skin condition

Four main clinical manifestations:

  • Erythematotelangiectatic
  • Papulopustular
  • Phymatous
  • Ocular

Pathogenesis:

  • Immune dysfunction
  • Ultraviolet radiation
  • Vascular hyperreactivity
18
Q

Melanocytic Nevus

A

benign proliferations of a type of melanocyte known as a “nevus cell” that cluster as nests

  • types:
    congenital (CMN)
    acquired types:
    common (not mentioned in the lecture)
    atypical
  • terminology of acquired nevi:
    junctional
    intradermal
    compound
19
Q

Congenital Melanocytic Nevi

A

Pathogenesis:
- Cellular proliferation by mitogen-activated protein kinase (MAPK)

Clinical Features:
- Present at birth or within the first few months of life

20
Q

Atypical Acquired Nevi

A

  • nevi with an architectural disorder such as eclipse nevus
  • Benign acquired melanocytic nevi that share, to a lesser extent, some of the clinical features of melanoma
21
Q

Melanoma

A
  • The mitogen activated protein kinase (MAPK) pathway is activated in almost all melanomas (much more than in CMN).

Clinical Features:
BRAF inhibitors -> tumor regression and prolonged overall survival

  • UV causes p53 mutation & POMC increased expression -> secretion of MSH -> stimulation of MC1R -> expression of MITF
  • growth phases of melanoma melanocytic nevus pathogenesis): benign nevus -> atypical nevus -> radial/horizontal growth phase (curable by excision) -> vertical growth phase (have metastatic potential) -> melanoma
22
Q

Basal Cell Carcinoma (BCC)

A
  • cancer in Basel layer of epidermis
  • called epithelioma

Pathogenesis:

  • UV-induced inflammation
  • PTCH1 gene
  • UVB: intense & intermittent (sunburn/childhood exposure) –> BCC & melanoma
23
Q

Cutaneous Squamous Cell Carcinoma (cSCC)

A
  • malignant proliferation of keratinocytes

Pathophysiology:

  • UV-induced mutations in the p53 gene
  • Mutation of RAS pathway

UVB exposure: cumulative/occupational –> cSCC

24
Q

Impetigo

A
  • contagious S. aureus infection

Clinical Features:

  • Non-bullous impetigo:
  • Lesions begin as papules -> vesicles surrounded by erythema -> thick crusts with a golden appearance
25
Q

Acanthosis Nigricans

A

  • hyperkeratosis associated with hyperinsulinemia
  • clinical feature: velvety hyperpigmented plaques

Clinical significance:
- Mainly associated with insulin resistance, diabetes, obesity
Pathophysiology:
- Abnormalities involving three types of receptors:
IGFR1
FGFR
EGFR

26
Q

Vitiligo

A

acquired pigmentory disorder

Clinical Features:
- The development of white macules (no clinical signs of inflammation) due to the loss of functioning melanocytes in the skin or hair, or both

Pathogenesis:(convergence theory)
- Depigmentation caused by a hyperactive response of the immune system against melanocytes

associated with Koebner phenomenon caused repeated mechanical trauma

27
Q

ABCDEs of melanoma

A

benign vs malignant features for ABCDEs

Pathophys Semester II (14 decks)

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