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Bloc F - Defense > Dermatology > Flashcards

Dermatology Flashcards

1
Q
A

Macule (vitilgo)

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2
Q
A

Patch (café au lat macule)

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3
Q
A

Papule (MOLLUSCUM CONTAGIOSUM)

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4
Q
A

Plaque (PSORIASIS)

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5
Q
A

Nodule (BASAL CELL CARCINOMA)

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6
Q
A

Tumour (BASAL CELL CARCINOMA)

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7
Q
A

Vesicle (HERPES ZOSTER)

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8
Q
A

Bulla (BULLOUS PEMPHIGOID)

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9
Q
A

URTICARIA

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10
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A

Cyst (EPIDERMOID CYST)

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11
Q
A

Pustule (acne)

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12
Q
A

Scale (Tinea pedis)

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13
Q
A

Crust (IMPETIGO)

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14
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A

Atrophy (STRIAE)

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15
Q
A

Erosion (PEMPHIGUS VULGARIS: MORTEL ET URGENT)

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16
Q
A

Ulcer (diabetic ulcer)

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17
Q

Redness and scaling of more than 90% of the skin, caused by dermatitis, psoriasis, drug reactions, cutaneous T cell lymphoma or idiopathic.

What’s your diagnosis?

A

Erythroderma, EMERGENCY –> biopsy, supportive and symptomatic treatment to relief pain and itching

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18
Q
  • Pain out of proportion
  • Skin is shiny and tense
  • Does not respond to antibiotics
  • Progresses at an alarming rate
  • Characteristic gray–blue color within 36 hours of onset due to vessel thrombosis
  • Thin, watery, malodorous fluid
  • Sick and septic

What’s your diagnosis?

A

Necrotizing fasciitis EMERGENCY

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19
Q

Massive immune reaction, presents as Stevens-Johnson syndrome, SKIN DETACHMENT, high complications and mortality.

What’s your diagnosis?

A

Severe trug reaction –> caused by drug (allopurinol ++, antibiotics, NSAIDS, anticonvulsants) EMERGENCY –> STOP causative drug, aggressive supportive care

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20
Q

Reaction to a drug 2-6 weeks later?

A

Dress syndrome EMERGENCY –> steroids for months

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21
Q

Pathogenesis of atopic dermatitis?

A
  1. Lack of filaggrin protein and other proteins, oil and moisture
  2. Hyperreaction of TH2
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22
Q
  • Pruritus
  • Redness
  • Texture
  • Typical morphology and distribution: depends on the age: starts on the extensors and on the face (baby) and ends on the flexors (adults)
  • Chronic or chronically-relapsing
  • Personal or family history
  • Increased sensitivity to irritants and environmental stimuli
  • Increased rates of infections
  • Associated with atopic features (allergy, asthma, allergic rhinitis)

What’s your diagnosis?

A

Atopic dermatitis

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23
Q

Investigation rules of a skin lump/bump?

A

ABCDE Rule

  • Asymmetry (color or bordr)
  • Border (irregular)
  • Colour (more than 2)
  • Diameter (> 6mm)
  • Evolution (wks-months)

EFG Rule (nodular or amelanotic subtypes)

  • Elevated
  • Firm
  • Growing
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24
Q

Most important prognosis factor of skin lump/bump?

A

depth/thickness

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25
Q

Types of Non-melanoma skin cancer (NMSC)?

A
  1. Basal cell carcinoma
  2. Squamous cell carcinoma
26
Q

Malignant lesions of skin?

A
  1. Acquired melanocytic nevus
  2. Congenital melanocyte nevus
  3. Dysplastic nevus
  4. Melanomas
27
Q

What is a Papulosquamous lesion?

A

Consists of papules = elevated primary skin lesions < 1.0 cm AND scale = surface change/laminated masses of keratin from stratum corneum

28
Q

Pathogenesis of psoriasis?

A

DCs, T-cells, keratinocytes + endothelial cells (complicated)

  • Triggers: stress, infection (strep, HIV), meds (β-blockers, TNF-α inhibitors), trauma (linear)
  • Often in extensor elbows + knees, lumbo-sacral, scalp
  • Psoriasis is NOT mediated by Th2 helper CD4+ T-lymphocytes
29
Q

Treatment of psoriasis?

A
  • General measures: emollients for moisturizing + avoid trauma
  • Topicals: steroids, vitamin D, calcineurin inh.
  • Systemics: PO meds, biologics
30
Q

Pathogenesis of Lichen planus?

A
  • T-cell mediated autoimmune damage to skin keratinocytes expressing altered self-Ags at cell surface
  • Activation from self-expressed Ags attract dendritic cells = affects T-cells + get necrosis at basal layer (dermal epidermal junction of keratinocytes)
31
Q

Types of Lichen planus?

A
  • Drug-induced: onset = few mths to > 1 yr (ACE-I, diuretics, anti-malarials, NSAIDs, β-blockers)
  • Classic type: multiple P’s = purple, pruritic, polygonal, planar (flat) + papules/plaques
  • Oral: multiple variants; most common = white lacy reticulated (buccal mucosa, tongue)
  • Genital: most common = white lacy reticulated; erosive = risk of SCC
  • Nail: often isolated finding including nail thinning, longitudinal ridging + fissuring, oncholysis
  • Scalp: scarring alopecia + red perifollicular papules that are scaly when active
32
Q

Treatment of Lichen planus?

A
  • General measures: emollients for moisturizing, avoid trauma, stop meds if drug induced
  • Depends on: extent, location, variant, pt charact, nail disease, prior Rx + presence of Hep C
  • Topics: steroids, calcineurin inhibitors, retinoids ; systemics Þ retinoids, immunosupp. meds
33
Q

What is Pityriasis rosea?

A

Red patches common among teens + young adults

  • Occurs often in spring + fall, some clustering in close contacts ; maybe linked with viral activat.
  • Trauma is NOT assoc.; syphilis looks like PR + can be mistaken so WEAR GLOVES during PE!!
34
Q

Pityriasis rosea treatment?

A

General measures = stop meds if drug-induced + emollients for moisturizing + topical steroids

35
Q

What are the growth phases of the hair?

A
  1. Anagen: matrix cells grow, divide and become keratinized to form the growing hair
  2. Catagen: matrix proliferating cells abruptly cease proliferating so that hair bulb involutes and regresses
  3. Telogen: hair falls (100 days)
36
Q

What is Tinea Capitis?

A
  • Infection of the scalp by fungi
  • Diagnosis: Scraping, KOH, Culture
  • Treatment is oral antifungal; and topical therapy to reduce infectivity
37
Q

What is Trichotillomania?

A
  • Habitual, compulsive plucking of hair
  • A well-defined area of hair loss with shortened, broken-off hairs of different lengths (frontoptemporal or parietotemporal)
  • Treatment: stop + psychiatric evaluation
38
Q

What is Androgenetic alopecia?

A

De la calvitie

39
Q

What are the causes of Telogen effluvium Alopecia?

A
  • Stress: any sever systemic disease, surgery, fever, psychological stress
  • Endocrine: Hypo/hyperthyroidism…
  • Nutrotional: Iron deficiency….
  • Drug: Acitretin, Anticoagulant, Allopurinol…
40
Q

Structures of the nail?

A
  • Nail plate: keratinized structure which continues growing throughout life
  • Lateral nail folds: cutaneous folds providing lateral borders to the nail
  • Nail bed: the bed upon which the nail rests, extending from the lunula to the hyponychium
  • Hyponychium: cutaneous margin underlying free nail
41
Q

What is Onychomadesis?

A

Complete separation of the nail plate from the bed, full but temporary arrest of growth of nail matrix, caused by trauma, dermatoligic disease (eczema), fever, viral illness, hand-foot-mouth disease

42
Q

What causes Nail pitting?

A

holes in the plate because of matrix problem

43
Q

What usually causes Acute Paronychia?

A

staph aureus

44
Q

What usually causes Chronic paronychia?

A

Non purulent, glistening erythema with nail dystrophy, candida and irritation caused by saliva

45
Q

What is Melanonychia?

A
  • brown or black pigmented band along the length of nail, nail matrix nevus or lentigo, MAY BE subungual melanoma
46
Q

What is Racial melanonychia?

A

Nail problem with darker skin phototypes, benign

47
Q

What is Onychomycosis?

A

Fungal infection of nail unit, look at interdigital space

48
Q

What are the 2 main players of urticaria?

A
  • Mast cell: primary effector cell of urticaria
  • Histamine released from the mast cells is the most probable mediator
49
Q

What are the 2 Immunologic pathogenesis mechanisms of urticaria?

A
  1. IgE mediated (Type I hypersensitivity): no allergic reaction to the first exposure Þ antibody Þ reaction SECOND exposure
  2. Complement mediated:
  3. Infections: viral infection (+++), potentially in bacterial and parasitic infections
  4. Auto-immune/systemic disease: thyroid, collagen vascular
50
Q

What are the Non-immunologic pathogenesis of urticaria?

A
  1. Chemical histamine liberators: opiates, polymyxin, thiamine in cheese, egg white, muscle relaxant, narcotics
  2. Physical agents: cold, heat, sunlight
51
Q

What drug is important to avoid when you have an urticaria crisis?

A

Aspirin, NSAID

52
Q

What are the possible treatment of urticaria?

A
  • Identification and elimination or reduction of its cause
  • Symptomatic relief if not able to detect or avoid cause
  • Block the effect of already released histamine
  • Block the release of histamine (anti-histamine type 1 and 2)
  • Block mediator other than histamine (mast cell stabilizer such as Ketotifen, Leukotrine antagonists, Omalizumab)
  • Modulate inflammatory, cellular and immunological component of urticaria
53
Q

What is Angioedema?

A
  • Well-demarcated non-pitting edema that occurs deeper in the dermis and subcutaneous tissue, specially in area of loose connective tissue such as the face, eyelids or mucous membrane involving the lips and tongue
  • Often caused by the same pathological factors involved in urticarial
  • Not itchy but painful, last 72 hours
54
Q

Factors that contribute to acne?

A
  • ↑ Sebum production
  • Follicular Hyperkeratinization
  • Proprionibacterium acnes
  • Inflammatory response
55
Q

Types of acne?

A
  1. Acne vulgaris (Adolescent acne)
  2. Adult acne (post- Adolescent)
  3. Infantile and neonatal acne
  4. Acne excoriée (jeunes filles, rose)
  5. Acne conglobate & acne fulminans (systemic manifestations)
56
Q

Types of Acneiform eruptions?

A
  1. Drug-induced acne
  2. Occupational acne & acne cosmetica
  3. Acne mechanica
57
Q

Treatement of acne?

A
58
Q

What distinguishes rosacea from acne?

A

comedones

59
Q

Rosacea subtypes?

A
  1. Erythematotelangiectatic
  2. Papulopustular
  3. Phymatous
  4. Ocular
60
Q

What is Hidradenitis SUPPURATIVA?

A

Hidradenitis Suppurativa (HS) is a chronic inflammatory skin disease characterized by persistent or recurrent flares of inflamed painful nodules, sinuses and scars in the axilla, groin, or both.

Bloc F - Defense (7 decks)

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