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Pruritus and Lesion Identification
1. Pruritus Pruritus is defined at the unpleasant sensation that elicits the desire or reflex to scratch (rub, lick, chew). Pruriceptive pruritus is due to stimulation of peripheral receptors in the skin in the presence of a healthy nervous system. This is usually due to skin disease. Neuropathic pruritus is generated in the CNS as a response to circulating pruritogens, pharmacological mediators or due to an anatomical lesion of the PNS or CNS. Pruritus is a physiological mechanism designed to move the agent causing sensation. However, there are consequences of pruritus if the agent is not promptly removed. Somato-sensory activity of the skin involves mechanoreceptors, thermoreceptors and nociceptors. Nociceptors are responsible for detecting itch and pain. They transmit information mainly via unmyelinated slow conducting C-fibres. Some of these fibres are dedicated solely to the sensation of itch. Alpha delta fibres also transmit some itch information. There is complex interaction between itch and pain. Painful stimuli can inhibit itch. Inhibition of pain with delta receptor agonists results in pruritus, and blocking of spinal K-opioid receptors reduced pruritus. Keratinocytes in the skin express a range of neuropeptide mediators and receptors involved in pruritus, such as opioids, nerve growth factor, substance P, vanilloid receptors and voltage gated ATP channels. Sensory fibres that detect itch from the head are carried in the trigmeninal (CN V), facial, (CN VII), glossopharyngeal (CN IX) and vagus (CN X) nerves. Pro-inflammatory mediators may stimulate itch via a direct pruritogenic effect, stimulation of mast cells and release of pruritogens or potentiation of other pro-inflammatory mediators. Peripheral sensitisation occurs in chronic pruritus when scratching increases local inflammation, resulting in the production of pruritogens by inflammatory cells. This increases C-fibre responsiveness. Central sensitisation may also occur when inflammation of the skin results in an altered perception of gentle mechanical or other stimuli, and this is perceived at pruritus. This condition is called allokinesis. In the chronically pruritic animal, marked pruritus may therefore be incited by only minor stimuli - hyperkinesis. When the sensation of pruritus is taken over the pruritic threshold, clinical pruritus results. This may be due to the combined effects of pruritus from multiple sources, such as allergen concentrations, heat, ectoparasites and stress factors. Therapeutic interventions for pruritus include: the reduction of skin inflammation by the administration of corticosteroids or cyclosporine; blockage of peripheral inflammatory mediators, for example antihistamines block H1 receptors of C-neurons; application of moisturisers and topical cooling preparations such as calamine or menthol.
2. Dermatological response to damage Epidermal responses to damage include hyperkeratosis, acanthosis, lichenification, vesicle/pustule formation, crusting and hyper or hypo pigmentation. Dermal responses to damage include erythema, oedema, thickening and alopecia. a) Hyperkeratosis Hyperkeratosis is increased depth of the cornified layer of the epithelium. It can result in scaling and crusting. Excessive scaling is also known as seborrhoea, and can be primary (inherited) or secondary. Crusting is the formation of a dried exudate that may contain microorganisms. Crusting is always secondary to hyperkeratosis.
Follicular hyperkeratosis occurs when keratinaceous plugs form in the infundibulum of hair follicles in the absence of hair. These plugs are called comedones.
Follicular casts form from an accumulation of keratinous debris around the hair shaft seen protruding from the follicular ostium or present when hairs are plucked and examined.
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