Common Skin Complaints and Disorders

These flashcards cover essential vocabulary and definitions related to common skin complaints and disorders, aiding in exam preparation.

What is Alopecia?

An autoimmune disease causing hair loss which can be temporary or permanent.

What is the pathophysiology of Alopecia Areata?

T-cell mediated autoimmune attack on anagen hair follicles, leading to their premature entry into catagen and telogen phases.

What are the clinical presentations of Alopecia Areata?

Sudden onset of well-demarcated, smooth, non-scarring patches of hair loss; 'exclamation mark' hairs (hairs wider at the top than the base) may be present at the periphery of patches.

How is Alopecia Areata diagnosed?

Primarily clinical diagnosis based on characteristic appearance; dermoscopy may show 'exclamation mark' hairs and yellow dots; scalp biopsy (rarely needed) reveals peribulbar lymphocytic inflammation.

What are the management options for Alopecia Areata?

First-line: Intralesional corticosteroids for localized patches. Other options: Topical corticosteroids, topical minoxidil, oral corticosteroids (for severe acute cases), JAK inhibitors (for severe chronic cases).

What is Hyperpigmentation?

An increase in skin color due to excess melanin production and/or deposition.

What is the pathophysiology of Hyperpigmentation?

Increased activity of melanocytes or an increase in the number of melanocytes, leading to overproduction of melanin, often triggered by inflammation, sun exposure, or hormonal changes.

What is the clinical presentation of Hyperpigmentation?

Darkened patches or spots on the skin, which can range from light brown to black, varying in size and distribution depending on the cause.

How is Hyperpigmentation diagnosed?

Clinical examination; Wood's lamp examination can help distinguish epidermal from dermal melanin; skin biopsy may be considered for atypical lesions.

What are the management options for Hyperpigmentation?

Topical agents (hydroquinone, retinoids, azelaic acid, kojic acid), chemical peels, laser therapy, and strict sun protection.

What is Vitiligo?

A chronic autoimmune disorder causing total loss of pigment in patchy areas of the skin, hair, and mucous membranes.

What is the pathophysiology of Vitiligo?

Autoimmune destruction of melanocytes, leading to their absence in affected skin areas. Genetic predisposition and oxidative stress are contributing factors.

What is the clinical presentation of Vitiligo?

Well-demarcated, depigmented (milky white) macules and patches, often symmetric, found anywhere on the body but commonly affecting periorificial areas, extensor surfaces, and sites of trauma (Koebner phenomenon).

How is Vitiligo diagnosed?

Clinical examination; Wood's lamp examination accentuates depigmented areas; skin biopsy (rarely needed) shows absence of melanocytes.

What are the management options for Vitiligo?

Topical corticosteroids, topical calcineurin inhibitors, phototherapy (narrowband UVB), excimer laser, depigmentation therapy (for extensive cases), surgical grafting for stable localized patches.

What is Melasma?

A common acquired disorder of hyperpigmentation characterized by symmetric brown or gray-brown patches on sun-exposed areas of the face.

What is the pathophysiology of Melasma?

Increased melanin production by hyperactive melanocytes, triggered by UV radiation, hormonal influences (estrogen, progesterone), and genetic predisposition. Vascular proliferation and mast cells also play a role.

What is the clinical presentation of Melasma?

Symmetric, irregular, dark brown to gray-brown macules and patches primarily on the face (cheeks, forehead, upper lip, chin), often forming characteristic patterns (centrofacial, malar, mandibular).

How is Melasma diagnosed?

Clinical examination; Wood's lamp examination helps determine the depth of pigment (epidermal usually enhanced, dermal not).

What are the management options for Melasma?

Aggressive sun protection, topical agents (hydroquinone, Tretinoin, corticosteroids – often in triple combination therapy), chemical peels, laser and light therapies (used cautiously due to risk of worsening).

What is Chloasma?

A specific term for melasma that occurs during pregnancy, often referred to as 'the mask of pregnancy'.

What is the pathophysiology of Chloasma?

Similar to melasma, it's primarily driven by hormonal changes during pregnancy (increased estrogen and progesterone), combined with sun exposure, leading to melanocyte overactivity.

What is the clinical presentation of Chloasma?

Brownish patches on the face, typically symmetric, affecting areas like the forehead, cheeks, and upper lip, consistent with melasma patterns but occurring specifically during gestation.

How is Chloasma diagnosed?

Clinical examination, based on the typical presentation of melasma occurring specifically in a pregnant individual.

What are the management options for Chloasma?

Primarily sun protection. Topical treatments (e.g., azelaic acid, glycolic acid) can be used, but treatments like hydroquinone and retinoids are generally avoided during pregnancy. Often resolves spontaneously postpartum.

What is Drug-Induced Hyperpigmentation?

Skin discoloration or darkening caused by systemic medications, which can manifest in various patterns and colors.

What is the pathophysiology of Drug-Induced Hyperpigmentation?

Mechanisms vary by drug, including increased melanin production (e.g., psoralens), deposition of drug metabolites or complexes in the dermis (e.g., minocycline, amiodarone), and post-inflammatory hyperpigmentation.

What is the clinical presentation of Drug-Induced Hyperpigmentation?

Variable, ranging from diffuse grayish-blue discoloration (e.g., minocycline in sun-exposed areas) to blue-gray facial discoloration (amiodarone), or brown macules. Often symmetric and can involve mucous membranes.

How is Drug-Induced Hyperpigmentation diagnosed?

History taking to identify culprit medication; skin biopsy may show pigment deposition within macrophages or increased melanin in the epidermis.

What are the management options for Drug-Induced Hyperpigmentation?

Discontinuation of the offending drug (if possible), strict sun protection, and in some cases, laser therapy for persistent pigmentation.

What is Angioedema?

Localized, self-limiting edema of the deep dermis, subcutaneous, or submucosal tissues, often involving the face, lips, tongue, larynx, and genitalia.

What is the pathophysiology of Angioedema?

Mediated by bradykinin or histamine. Histamine-mediated angioedema is often allergic, causing mast cell degranulation. Bradykinin-mediated angioedema can be hereditary, acquired (C1 esterase inhibitor deficiency), or drug-induced (e.g., ACE inhibitors).

What is the clinical presentation of Angioedema?

Rapid onset of localized, non-pitting, often asymmetric swelling, without pruritus or erythema (especially bradykinin-mediated). Can involve mucous membranes, leading to airway obstruction (laryngeal angioedema is life-threatening).

How is Angioedema diagnosed?

Clinical picture; history of exposures or medications (ACE inhibitors); lab tests if hereditary/acquired suspected (C4, C1 esterase inhibitor levels/function for bradykinin-mediated).

What are the management options for Angioedema?

Histamine-mediated: Antihistamines, corticosteroids, epinephrine. Bradykinin-mediated: C1 esterase inhibitor concentrate, bradykinin receptor antagonists (icatibant), kallikrein inhibitors (ecallantide). Airway management is crucial for laryngeal involvement.

What is Pruritus?

An unpleasant sensation that provokes the desire to scratch; commonly known as itching.

What is the pathophysiology of Pruritus?

Complex and multifactorial. Involves activation of specific nerve fibers by pruritogens (histamine, opioids, cytokines, neuropeptides), mechanical stimulation, or central mechanisms. Can be dermatologic, systemic, neuropathic, or psychogenic.

What is the clinical presentation of Pruritus?

The primary symptom is itching, which can be localized or generalized, acute or chronic. Secondary skin lesions (excoriations, lichenification, prurigo nodules) often result from scratching.

How is Pruritus diagnosed?

Thorough history and physical examination to identify underlying causes (skin conditions, systemic diseases like renal failure, cholestasis, hematologic disorders, drug reactions, neurological conditions); relevant lab tests based on suspicion.

What are the management options for Pruritus?

Treating the underlying cause; symptomatic relief with emollients, topical corticosteroids, antihistamines (sedating ones for nocturnal pruritus), oral neuropathic agents (gabapentin, pregabalin), phototherapy. Avoid triggers like hot baths, harsh soaps.

What is Urticaria?

Also known as hives, it is a common skin condition characterized by the transient appearance of evanescent, itchy wheals (hives) or papules, with or without angioedema.

What is the pathophysiology of Urticaria?

Activation and degranulation of mast cells and basophils, releasing histamine and other mediators (leukotrienes, prostaglandins, cytokines). This leads to vasodilation, increased vascular permeability, and dermal edema.

What is the clinical presentation of Urticaria?

Erythematous, edematous, intensely pruritic wheals that blanch with pressure, often surrounded by a flare. Individual lesions typically resolve within 24 hours without scarring. Can be acute or chronic.

How is Urticaria diagnosed?

Clinical diagnosis based on the characteristic appearance and transient nature of wheals. Chronic urticaria requires investigation for underlying causes (e.g., autoimmune, infection, physical stimuli, drugs), though many cases are idiopathic.

What are the management options for Urticaria?

First-line: Second-generation H1 antihistamines (non-sedating), often at increased doses. For refractory cases: Omalizumab, H2 blockers, oral corticosteroids (short courses), leukotriene receptor antagonists, cyclosporine.

What is Scabies?

A highly contagious skin infestation caused by the mite Sarcoptes scabiei var. hominis, leading to intense pruritus.

What is the pathophysiology of Scabies?

Female mites burrow into the stratum corneum to lay eggs and deposit fecal matter. The intense itching, worst at night, is a hypersensitivity reaction (Type IV) to the mites, their eggs, and their waste products.

What is the clinical presentation of Scabies?

Severe, generalized pruritus (especially nocturnal) that spares the head and neck in adults. Characteristic lesions include erythematous papules, vesicles, and burrows (fine, wavy lines). Common sites: finger webs, wrists, elbows, axillae, breasts, umbilicus, belt line, genitalia.

How is Scabies diagnosed?

Clinical suspicion based on characteristic rash and pruritus. Definitive diagnosis by microscopic identification of mites, eggs, or fecal pellets from skin scrapings, or visual identification of burrows.

What are the management options for Scabies?

Topical permethrin 5% cream (applied head-to-toe, left on for 8-14 hours, repeated in 7-14 days). Oral ivermectin (for crusted scabies or widespread disease). Treat close contacts. Wash all bedding and clothing in hot water.

What is Pediculosis?

Infestation of lice, wingless insects that are obligate human parasites, affecting various parts of the body (head, body, pubic area).

What is the pathophysiology of Pediculosis?

Lice feed on human blood multiple times a day. Their saliva and fecal matter cause an allergic reaction in the host, leading to pruritus and local irritation. They transmit through close contact or contaminated fomites.

What is the clinical presentation of Pediculosis?

Intense pruritus, excoriations, and visible nits (lice eggs firmly attached to hair shafts) or adult lice. Pediculosis capitis (head lice): Itching of the scalp, particularly behind the ears and at the nape of the neck. Pediculosis corporis (body lice): Pruritus and characteristic linear excoriations on the trunk and neck. Pediculosis pubis (pubic lice/crabs): Itching in the pubic area; can involve eyelashes, eyebrows, beard.

How is Pediculosis diagnosed?

Visual identification of live lice or nits using a fine-toothed comb and magnifying lens during a clinical examination.

What are the management options for Pediculosis?

Head lice: Topical permethrin 1% lotion/cream rinse, malathion lotion, spinosad, ivermectin lotion. Manual removal of nits. Body lice: Improve hygiene, wash infested clothing/bedding in hot water. Pubic lice: Permethrin 1% cream rinse or pyrethrins with piperonyl butoxide. Treat sexual partners.

What is Candidiasis?

An opportunistic fungal infection caused by species of Candida (most commonly Candida albicans), which typically affects mucocutaneous surfaces but can become systemic.

What is the pathophysiology of Candidiasis?

Candida is part of normal flora but can become pathogenic under conditions that compromise host defenses (e.g., immunosuppression, broad-spectrum antibiotic use, uncontrolled diabetes, moisture, occlusion).

What is the clinical presentation of Candidiasis?

Oral (thrush): White, creamy patches on the tongue and oral mucosa, which can be scraped off to reveal erythematous, sometimes bleeding, tissue. Vulvovaginal: Intense pruritus, burning, erythema, and a thick, white, 'cottage cheese' discharge. Cutaneous (intertrigo): Erythematous patches with satellite lesions (papules and pustules) in skin folds (e.g., axillae, groin, inframammary folds).

How is Candidiasis diagnosed?

Clinical appearance; potassium hydroxide (KOH) microscopy revealing budding yeasts and pseudohyphae; fungal culture (less common for routine diagnosis).

What are the management options for Candidiasis?

Oral: Topical antifungals (nystatin swish and swallow, clotrimazole troches) or oral fluconazole. Vulvovaginal: Topical antifungals (clotrimazole, miconazole) or a single oral dose of fluconazole. Cutaneous: Topical antifungal creams (e.g., nystatin, miconazole, clotrimazole), ensuring dryness and aeration of affected areas.

What are Dermatophytoses?

Superficial fungal infections of the skin, hair, and nails caused by dermatophytes (e.g., Trichophyton, Microsporum, Epidermophyton), also known as tinea infections.

What is the pathophysiology of Dermatophytoses?

Dermatophytes thrive on keratin, invading the stratum corneum, hair, or nails. Transmission occurs through direct contact with infected individuals, animals, or contaminated surfaces. Warm, moist environments facilitate growth.

What is the clinical presentation of Dermatophytoses?

Varies by location: Tinea corporis (body): Annular, erythematous, scaling plaques with central clearing ('ringworm'). Tinea pedis (foot): Itching, scaling, erythema, maceration between toes ('athlete's foot'). Tinea cruris (groin): Erythematous, pruritic, scaling rash in the groin folds ('jock itch'). Tinea capitis (scalp): Scaling, hair loss, broken hairs, sometimes painful pustules (kerion). Tinea manuum (hand): Unilateral fine scaling of the palm, often described as 'two feet-one hand' disease.

How are Dermatophytoses diagnosed?

Clinical appearance; potassium hydroxide (KOH) microscopy of skin scrapings demonstrating hyphae; fungal culture (especially for tinea capitis or recalcitrant cases); Wood's lamp for Microsporum (fluoresces green).

What are the management options for Dermatophytoses?

Localized skin infections: Topical azole antifungals (e.g., miconazole, clotrimazole) or allylamines (e.g., terbinafine). Extensive skin infections, tinea capitis, tinea unguium (onychomycosis): Oral antifungals (terbinafine, griseofulvin, itraconazole, fluconazole).

What is Onychomycosis?

A chronic fungal infection of the toenails and/or fingernails, primarily caused by dermatophytes (tinea unguium) but also non-dermatophyte molds and yeast (Candida).

What is the pathophysiology of Onychomycosis?

Fungal organisms invade the nail plate, nail bed, or both. Common predisposing factors include trauma, tinea pedis, occlusive footwear, immunosuppression, and increasing age.

What is the clinical presentation of Onychomycosis?

Typical features include discoloration (yellow, white, brown, black), thickening (hyperkeratosis), crumbling, and lifting (onycholysis) of the nail plate. Subungual hyperkeratosis and dystrophic changes are common.

How is Onychomycosis diagnosed?

Clinical appearance; definitive diagnosis requires laboratory confirmation: KOH microscopy of nail clippings/scrapings to identify hyphae, and fungal culture or PCR to identify the specific pathogen (essential before starting oral antifungals).

What are the management options for Onychomycosis?

Topical antifungals: Ciclopirox lacquer, efinaconazole, tavaborole (for superficial or mild distal infections). Oral antifungals: Terbinafine (most effective for dermatophytes), itraconazole, fluconazole (preferred for extensive or severe infections, or when topical treatment fails). Laser therapy, debridement, or nail avulsion may be adjuncts.

What is Impetigo?

A highly contagious superficial bacterial skin infection, most commonly caused by Staphylococcus aureus or Streptococcus pyogenes, characterized by vesicular lesions and honey-colored crusts.

What is the pathophysiology of Impetigo?

Bacteria colonize the skin and produce toxins that cause epidermal breakdown, leading to vesicles and bullae. It often occurs in areas of minor skin trauma or pre-existing dermatitis.

What is the clinical presentation of Impetigo?

Non-bullous impetigo (most common): Small vesicles or pustules that rupture, forming characteristic adherent, golden-brown ('honey-colored') crusts. Often on the face (especially around the nose and mouth) and extremities. Bullous impetigo: Larger, fragile, flaccid bullae (blisters) that rupture to leave thin, varnish-like crusts. More commonly caused by S. aureus toxin and can affect intact skin.

How is Impetigo diagnosed?

Clinical appearance is usually sufficient. Bacterial culture of exudate from lesions can be done for atypical presentations, treatment failure, or outbreaks.

What are the management options for Impetigo?

Localized, mild cases: Topical antibiotics like mupirocin or retapamulin cream. Widespread or severe cases: Oral antibiotics such as penicillin (if strep suspected), cephalexin, dicloxacillin, or clindamycin (if MRSA suspected). Good hygiene is important to prevent spread.

What is Folliculitis?

Inflammation of hair follicles, typically caused by bacterial (most commonly Staphylococcus aureus) or fungal infection, but can also be non-infectious.

What is the pathophysiology of Folliculitis?

Hair follicles become infected or inflamed due to various factors. Bacterial invasion (e.g., Staphylococcus aureus) is common. Other causes include friction, occlusion, hot tub exposure (Pseudomonas folliculitis), or fungal infections (Pityrosporum folliculitis).

What is the clinical presentation of Folliculitis?

Small, erythematous papules or pustules centered on a hair follicle, often surrounded by a red halo. Can be pruritic or tender. Common sites include the scalp, face (beard area), neck, trunk, and buttocks.

How is Folliculitis diagnosed?

Clinical examination. Swab culture of pustule contents can confirm bacterial cause and guide antibiotic choice. KOH microscopy of pus/scales if fungal etiology suspected.

What are the management options for Folliculitis?

Mild bacterial: Topical antibiotics (mupirocin, clindamycin) or antibacterial washes (chlorhexidine, benzoyl peroxide). Severe/recurrent bacterial: Oral antibiotics (cephalexin, doxycycline). Pseudomonas ('hot tub') folliculitis: Usually self-limiting, but ciprofloxacin can be used in severe cases. Fungal (Pityrosporum): Topical or oral antifungals (ketoconazole, itraconazole).

What are Furuncles?

Deep bacterial infections of hair follicles and surrounding subcutaneous tissue, typically caused by Staphylococcus aureus, forming painful, erythematous, fluctuating lumps (boils).

What is the pathophysiology of Furuncles?

Extension of folliculitis deeper into the dermis and subcutaneous tissue, leading to a localized abscess formation. Often initiated by minor trauma or friction.

What is the clinical presentation of Furuncles?

A painful, tender, red, firm nodule that gradually enlarges and becomes fluctuant (pus-filled). A central core of necrotic tissue often develops, which may spontaneously drain. Common sites include the neck, face, axillae, buttocks, and thighs.

How are Furuncles diagnosed?

Clinical diagnosis. Culture of pus may be done, especially for recurrent lesions or to rule out MRSA.

What are the management options for Furuncles?

Warm compresses to promote drainage. Incision and drainage (I&D) is usually required once fluctuant. Oral antibiotics (e.g., cephalexin, dicloxacillin; clindamycin or trimethoprim-sulfamethoxazole for MRSA) may be used for large lesions, surrounding cellulitis, or immunocompromised patients.

What is Cellulitis?

An acute bacterial infection involving the dermis and subcutaneous tissue, characterized by localized redness, warmth, swelling, and pain.

What is the pathophysiology of Cellulitis?

Bacteria (Streptococcus pyogenes or Staphylococcus aureus are most common) gain entry through a break in the skin barrier (e.g., wound, fungal infection, insect bite). They proliferate in the dermis and subcutaneous fat, triggering an inflammatory response.

What is the clinical presentation of Cellulitis?

Rapidly spreading area of erythema, edema, warmth, and tenderness, often with poorly defined borders. Fever, chills, and malaise may be present. Common sites: lower extremities, but can occur anywhere.

How is Cellulitis diagnosed?

Primarily clinical diagnosis. Blood cultures (low yield, usually for severe systemic symptoms). Wound culture (if open wound or purulent drainage). Imaging (CT, ultrasound) to rule out abscess or osteomyelitis in complicated cases.

What are the management options for Cellulitis?

Oral or intravenous antibiotics chosen based on suspected pathogen and severity. Non-purulent/mild: Penicillin, cephalexin, dicloxacillin. Purulent/concern for MRSA: Clindamycin, trimethoprim-sulfamethoxazole, doxycycline. Severe/systemic signs: IV antibiotics (e.g., ceftriaxone, vancomycin). Elevation of affected limb, pain control.

What are Warts?

Contagious, benign epidermal growths caused by infection with the human papillomavirus (HPV).

What is the pathophysiology of Warts?

HPV infects keratinocytes in the basal layer of the epidermis, stimulating them to proliferate, leading to epidermal hyperplasia and characteristic wart morphology. Transmitted by direct contact. Incubation period is weeks to months.

What is the clinical presentation of Warts?

Appearance varies by HPV type and location: Common warts (Verruca vulgaris): Rough, hyperkeratotic papules/nodules with punctate black dots (thrombosed capillaries), typically on hands and fingers. Plantar warts: Flat, endophytic (grow inward) lesions on the soles of feet, often painful, with black dots. Flat warts (Verruca plana): Smooth, flesh-colored, slightly elevated papules, often on the face, arms, and legs. Genital warts (Condyloma acuminata): Soft, fleshy, cauliflower-like lesions in the anogenital region.

How are Warts diagnosed?

Clinical examination; paring the surface may reveal thrombosed capillaries (black dots). Biopsy for atypical or persistent lesions.

What are the management options for Warts?

No single universally effective treatment. Options include: salicylic acid (topical), cryotherapy, cantharidin, imiquimod cream (for genital warts), excisional surgery, laser therapy. Treatment often requires multiple sessions.

What is Herpes Simplex Virus (HSV) infection?

A lifelong viral infection caused by HSV-1 (typically oral/orofacial) or HSV-2 (typically genital), characterized by recurrent episodes of vesicular lesions.

What is the pathophysiology of HSV infection?

HSV infects epithelial cells, causing characteristic lesions. It then establishes latency in sensory nerve ganglia. Reactivation (triggered by stress, fever, UV, trauma, immunosuppression) leads to recurrent outbreaks at or near the primary infection site.

What is the clinical presentation of HSV infection?

Primary infection: Often asymptomatic or more severe with fever, malaise, lymphadenopathy. Presents as painful vesicles on an erythematous base, which then ulcerate and crust. Recurrent infection: Prodromal symptoms (tingling, burning) followed by clusters of small, painful vesicles that progress to ulcers and crusts, typically healing in 7-10 days. HSV-1: Cold sores (herpes labialis). HSV-2: Genital herpes lesions.

How is HSV infection diagnosed?

Clinical appearance; Tzanck smear: Reveals multinucleated giant cells (non-specific, also seen in VZV). Viral culture: Gold standard, especially for active lesions. PCR: Highly sensitive, especially for CSF in CNS infections. Serology: Detects antibodies (IgG for past infection, IgM for recent primary infection), useful for asymptomatic cases.

What are the management options for HSV infection?

Antiviral medications (acyclovir, valacyclovir, famciclovir) for episodic treatment (to shorten duration/severity of outbreaks) or suppressive therapy (to reduce frequency of recurrences and transmission).