Pruritis, Eczematous Dermatitis, and Topical Corticosteroids
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
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?
Endocrinologic (thyroid disease, diabetes)
Uremia Þ renal failure
Hematological (polycythemia Vera)
Psychiatric (delusions of parasitosis)
Eczematous dermatitis; Psoriasis
Infection (tinea, folliculitus)
Autoimmune blistering disease
Xerosis (dry skin)
- In urticaria (hives) inhib of histamine release stops itch but not erythema/edema.
- Treatment: antihistamines, mast cell stabilizers.
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
Principles of Percutaneous Absorption
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