Pruritus – sensation which leads to a desire to scratch, scratching in response to an itch is a spinal reflex

• Repeated scratching induces thickened skin with accentuated markings - lichenification
• Anatomic factors: itch receptors/pain receptors are free nerve endings at dermal-epidermal junction (DEJ), transmitted through same neural pathways.
• Non-anatomic factors:
• Histamine – from mast cells, low conc at DEJ activates H1 receptors Þ itch.
• In urticaria (hives) inhib of histamine release stops itch but not erythema/edema.
• Treatment: antihistamines, mast cell stabilizers.
• Prostaglandins - lowers the threshold of skin to histamine-provoked itching.
• Opioid peptides – involved in itch perception. Naloxone – selective opiate antagonist, may relieve pruritus if its secondary to cholestasis.
• Causes of pruritus: Systemic or Dermatologic?
• Systemic
• Endocrinologic (thyroid disease, diabetes)
• Neoplastic (lymphoma)
• Drugs (narcotics)
• Uremia Þ renal failure
• Hematological (polycythemia Vera)
• Hepatic (Cholelithiasis)
• Psychiatric (delusions of parasitosis)
• Dermatologic
• Eczematous dermatitis; Psoriasis
• Infection (tinea, folliculitus)
• Infestations (scabies)
• Dermatitis Herpetiformis
• Autoimmune blistering disease
• Urticaria
• Xerosis (dry skin)

• non specific diagnosis, refers to broad group of skin eruptions, result from some exogenous or endogenous agent
• Usually respond to corticosteroids
• Common histology: Spongiosis.
• Acute Eczematous Dermatitis – red plaque, pebbly surface, often with vesicles, bullae, scale (eg. poison ivy).
• Subacute Eczematous Dermatitis – less prominent vesicle, secondary changes: scratching Þ erosions, infectionÞ crusting
• Chronic Eczematous Dermatitis – inflamed, thickened plaques. Secondary changes: lichenification.
• Etiologies of Eczematous Dermatitis: Contact dermatitis (allergic vs. irritant), atopic, stasis (slowed blood flow), asteatotic/xerisos (loss of moisture), seborrheic (eg dandruff), idiopathic (eg nummular), tinea infections.
• Treatment: remove etiology if possible, if acute (blistering) – apply drying agent, if subacute/chronic – lubricate, corticosteroids (topical).

• Potency of cortisol/hydrocortisone increases via enhanced lipid solubility and substitution of fluorine at 9a position
• Potency measured by vasoconstrictor assay of McKenzie-Stoughton.
• Degree of visible blanching at sites of application correlates with anti-inflammatory potency.
• Classes 1 (most potent) to 7 (least potent).
• Pharmacological actions: bind cytoplasmic receptors Þ goto nucleus Þ steroid:receptor binds DNA Þ protein synthesis altered with following actions: anti-inflammatory, immunosuppressive, and catabolic effects on skin.
• Choice depends upon potency required and cost. Higher potency used for severe eruptions and thick skin; lower potency used for milder eruptions, on face, intertriginous areas, and for kids.
• Potency: ointment (best for dry areas) > cream > lotion
• Occlusion increases potency (i.e. wrap saran-wrap around treated area, will ‘force’ the drug into skin).
• Toxicities of Topical Steroids:
• Systemic – Cushing’s Syndrome
• Local – Atrophy, glaucoma/cataracts, acne, persistence of infection

• Rate of diffusion of a compound across the skin is related to:
• (1) concentration of drug
• (2) surface area to which applied
• (3) mobility through skin (diffusion coefficient)
• (4) relative tenacity with which it binds to its vehicle compared to the epidermis (partition coefficient)
• (5) thickness of stratum corneum
• Practical Considerations for topical drug therapy:
• (1) Dosage/Surface area relationships – Hand (2gm), arm (3gm), leg (4gm), entire body (30-60 gm)
• (2) Hydration of stratum corneum – Enhances drug’s mobility through skin
• (3) Vehicle – Enhances drug’s penetration into skin, though can be irritant/allergen
• (4) Site – Permeability greater where skin is thinner (face, groin)
• (5) Inflammation – Permeability greater if skin is inflamed
• (6) Age of patient – Kids have increased risk of systemic toxicity