Hair, Autoimmune, skin (Clin Med I)

Urticaria definition

Multiple erythematous wheals associated with pruritus.

Pathophysiology of urticaria

Release of chemical mediators, especially histamine from mast cells.

Relationship between angioedema and urticaria

Angioedema is a deeper dermal/mucosal form of the same process.

Inducible causes of urticaria

Heat, cholinergic, aquagenic, vibratory, solar, contact, and dermatographism.

Chronic urticaria timeframe

Duration of greater than 6 weeks.

Common triggers of acute urticaria

Viral, bacterial, drugs, food, and insect bites.

Chronic spontaneous urticaria (CSU)

Chronic urticaria with unknown cause; often autoimmune.

Autoantibody target in CSU

Approximately 50% carry autoantibodies to IgE.

Treatment options for chronic urticaria

Cetirizine taper, dupilumab, or remibrutinib.

Angioedema presentation

Acute swelling of the deep dermal layer and mucosal tissue.

Mechanism of angioedema

Mast cell histamine release causing increased capillary permeability and extravasation.

Major life-threatening concern in angioedema

Airway compromise; must rule out associated anaphylaxis.

Treatment of angioedema

High-dose antihistamines, steroids, ± EpiPen.

Alopecia areata etiology

Autoimmune condition where T-cells attack hair follicles.

Alopecia areata scalp biopsy finding

Peribulbar lymphocytic infiltrate.

Risk factors for alopecia areata

Down syndrome, family history, thyroid disease, and vitiligo.

First-line treatment for alopecia areata

Topical and intralesional/injectable corticosteroids.

Treatment for severe alopecia areata

Systemic/oral steroids or JAK inhibitors.

Traction alopecia etiology

Acquired hair loss caused by repetitive hair tension (e.g., tight braids, extensions).

Typical site and symptoms of traction alopecia

Temporal region; causes itching, erythema, folliculitis, and pain.

Treatment for traction alopecia

Avoidance or modification of the causative tight hairstyle.

Scarring alopecia mechanism

Chronic inflammation causing follicle scarring and permanent hair loss.

Central Centrifugal Cicatricial Alopecia (CCCA)

Scarring alopecia at vertex scalp, primarily in African American women.

Treatment for CCCA

Corticosteroids, doxycycline, and Plaquenil (hydroxychloroquine).

Frontal fibrosing alopecia / Lichen planopilaris

Marked inflammation and fibrosis around hair follicles, primarily in frontal hairline.

Most common overall type of hair loss

Androgenetic alopecia.

Mechanism of male androgenetic alopecia

Increased sensitivity to DHT leading to a shortened anagen phase.

Enzyme involved in DHT conversion

5-alpha reductase.

Distribution difference: Male vs. Female pattern hair loss

Male: frontal hairline recession; Female: crown sparing frontal line.

Workup for female-pattern hair loss

CBC, iron studies, thyroid panel, hormone levels, and vitamin D.

Pharmacologic treatments for androgenetic alopecia

Topical/oral minoxidil, and 5-alpha reductase inhibitors (finasteride, dutasteride).

Pregnancy precaution for 5-alpha reductase inhibitors

Pregnant women must not touch crushed/broken pills due to teratogenicity.

Telogen effluvium etiology and timeline

Temporary hair loss 2-4 months after major physiological stress/shock.

Resolution and hair pull test in telogen effluvium

Resolves in 6-9 months; pull test shows intact hair bulbs.

Alopecia quick differentiation: Patchy vs Temporal vs Vertex

Patchy = Areata; Temporal = Traction; Vertex (African American women) = CCCA.

Discoid lupus lesion presentation

Atrophic erythematous plaques, commonly on scalp, face, and ears.

Workup for discoid lupus diagnosis

Skin biopsy, CBC, renal function tests, and ANA.

Systemic involvement in discoid lupus

Most patients with discoid lupus do NOT have SLE.

First-line oral systemic treatment for discoid lupus

Plaquenil (hydroxychloroquine).

Acanthosis nigricans physical appearance

Hyperpigmented, thickened, velvety plaques in intertriginous areas.

Clinical significance of acanthosis nigricans

Indicates underlying metabolic disease like Type 2 diabetes or PCOS.

Recommended lab screening for acanthosis nigricans

Hemoglobin A1c (HbA1c).

Erythema nodosum presentation

Panniculitis presenting as tender red nodules on the anterior shins.

Systemic symptoms accompanying erythema nodosum

Fever and arthralgias (joint pain).

Infectious and non-infectious causes of erythema nodosum

Infectious: Strep, TB, Chlamydia; Non-infectious: IBD, drugs, pregnancy, sarcoidosis.

Erythema nodosum management

NSAIDs for pain; systemic steroids only after ruling out infection.

Necrobiosis lipoidica clinical features

Atrophic plaques with telangiectasias on shins; high association with diabetes.

Major complication of necrobiosis lipoidica

Ulceration.

Granuloma annulare morphology

Circular, smooth, raised papules or plaques with central clearing.

Treatment options for granuloma annulare

Topical/intralesional steroids, cryotherapy, or systemic agents (dapsone, Plaquenil).

Xanthelasma vs. Eruptive Xanthomas

Xanthelasma: periorbital cholesterol deposits; Eruptive: pruritic yellow papules (high triglycerides).

Livedo reticularis appearance and trigger

Mottled, lace-like vascular pattern triggered by cold exposure.

Pathologic concern with livedo reticularis

Antiphospholipid syndrome or other hypercoagulable thrombotic states.

Tophi definition and etiology

Uric acid crystal deposits around joints from untreated chronic gout (~10 yrs post-onset).

Dermatomyositis temporal pattern of onset

Skin manifestations typically precede muscle weakness.

Classic skin signs of dermatomyositis

Heliotrope rash (eyelids), Shawl sign (upper back), Gottron's papules (hand joints).

Biopsy and lab findings in dermatomyositis

Interface dermatitis on biopsy; elevated CK, positive anti-Jo-1, anti-Mi-2.

Later-onset dermatomyositis risk factor

Strong association with underlying internal malignancy.

Stasis dermatitis etiology and presentation

Venous insufficiency leading to edema, pruritic purple plaques, and hemosiderin staining.

Treatment for stasis dermatitis

High-potency topical steroids, compression therapy, and leg elevation.

Clubbing association and diagnostic sign

80% linked to pulmonary malignancy/disease; tested via Schamroth's sign.

Systemic associations of Mees lines, Lindsay nails, and Terry nails

Mees: drugs; Lindsay: renal/liver/heart disease; Terry: CKD/psoriasis.

Splinter hemorrhages diagnostic concern

Trauma (most common) or infective endocarditis (up to 30%).

Arterial vs. Venous Ulcer: Primary pathology

Arterial = lack of blood FLOW; Venous = improper valves causing POOLING.

Arterial vs. Venous Ulcer: Anatomical location

Arterial = toes and bottom of feet; Venous = medial and lateral malleoli.

Arterial vs. Venous Ulcer: Pain and positional relief

Arterial: sharp pain, relieved by dangling leg; Venous: dull ache, relieved by elevation.

Arterial vs. Venous Ulcer: Physical Exam findings

Arterial: no edema, potential necrosis; Venous: lower extremity edema present.