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By :Dr.Pawana Kayastha. SKIN CHANGES IN OLD AGE Typical changes: include atrophy, laxity, wrinkling, dryness, irregular pigmentation and sparse grey hair.

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Presentation on theme: "By :Dr.Pawana Kayastha. SKIN CHANGES IN OLD AGE Typical changes: include atrophy, laxity, wrinkling, dryness, irregular pigmentation and sparse grey hair."— Presentation transcript:

1 By :Dr.Pawana Kayastha

2 SKIN CHANGES IN OLD AGE Typical changes: include atrophy, laxity, wrinkling, dryness, irregular pigmentation and sparse grey hair. changes are brought about by: age-related alterations in structure and function of the skin cumulative effects of environmental insults, especially ultraviolet radiation cutaneous consequences of disease in other organ systems

3 Immunity: alterations in immune surveillance and antigen presentation, and reduced cutaneous vascular supply which lead to decreases in the inflammatory response, absorption and cutaneous clearance of topical medications. Consequences: these changes make the skin less durable, slower to heal, and more susceptible to damage and disease.

4 COMMON SKIN DISEASES IN OLD AGE Prevalence: about 40% of individuals over the age of 60 years have significant dermatological problems. Diseases: the most common in this age group are: skin cancers leg ulcers, a major cause of morbidity in the elderly blistering disorders herpes zoster (shingles) and post-herpetic neuralgia

5 .  inflammatory skin diseases, e.g. asteatotic, gravitational and seborrhoeic eczema, psoriasis  lichen sclerosus et atrophicus  scabies  lymphoedema  pruritus of old age  drug-related rashes

6  Long standing pigmented spot.  The principal clinical concern is to distinguish correctly between benign pigmented lesions and melanoma.  The situation is complicated by the fact that any one of a number of changes in a pigmented lesion is highly sensitive as a marker of melanoma, specificity is low.

7 ABCDE FEATURES OF MALIGNANT MELANOMA  Asymmetry  Border irregular  Colour irregular  Diameter often greater than 0.5 cm  Elevation irregular (+ Loss of skin markings)

8  Determine the precise nature of the change. Is it due to the development of itch, inflammation, bleeding or ulceration, or does it relate to the colour, size, shape or surface of the lesion?  Subtle changes:plucking hair,shaving,irritants  Is the patient worried about change in one or many moles?  Positive family history of melanoma. Fewer than 10% of melanomas occur in individuals with a strong family history but in some of these families up to 50% of individuals may develop melanoma.

9  Examine the pigmented lesion carefully.  Look at the morphology of the melanocytic naevi at other sites.  magnifying glass or dermatoscope  whether the lesion is a benign melanocytic naevus or a malignant melanoma  Before trying to answer this, the clinician needs to exclude the possibility that it is another type of pigmented lesion:  Lentigo (a benign proliferation of melanocytes)  Freckle (ephelis, a focal overproduction of melanin,)

10  Seborrhoeic wart (basal cell papilloma, a benign keratinocyte tumour)  Dermatofibroma. This lightly pigmented firm dermal nodule is common on extremities in young adults. It feels larger than it looks. There is dimpling when the skin is squeezed on both sides (positive Fitzpatrick sign).  Pigmented basal cell carcinoma : This lesion is usually found on the face of the elderly and is slow-growing. It has a blue-brown hue with an opalescent look. There may be a rolled edge around an ulcer.  Subungual haematoma

11  Any changing lesion which is suspected of being a malignant melanoma should be excised without delay, with a clear margin.  If there is even a low index of suspicion of a malignant melanoma,then the lesion should be reviewed 1 month and may be 3mths later. Continuing change demands excision.  If benign then reassurance but advised to report back without delay if the change and concern continue  If in doubt cut out and then check the histology

12 An unpleasant localized or generalized sensation on the skin, mucus membranes or conjunctivae which the patient instinctively attempts to relieve by scratching or rubbing

13 Many Causes, Many Treatments to Trivial to Life threatening (mosquito bite) (malignancy) 10-50% of cases with generalized itching have systemic disease

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15 Skin diseases associated with generalised pruritus Eczema Scabies Urticaria/dermographism Pruritus of old age and xeroderma Skin diseases associated with localised pruritus Eczema Lichen planus Dermatitis herpetiformis Pediculosis

16 CAUSES OF PRURITUS iin IN PREGNANCY Condition Gestation and featuresTreatment Obstetric cholestasis 3rd trimester Associated with abnormal liver function tests Emollients Chlorphenamine Colestyramine Early delivery Pemphigoid gestationis 3rd trimester Pruritus followed by blistering Starts around the umbilicus Topical or oral corticosteroids Polymorphic eruption (urticarialpapules ) of pregnancy 3rd trimester, after delivery Polymorphic lesions with urticaria Chlorphenamine IN PREGNANCY

17 Prurigo gestationis 2nd trimester Excoriated papules Emollients Topical corticosteroids Chlorphenamine Pruritic folliculitis3rd trimester Aseptic pustules on trunk Topical corticosteroids

18  Chronic Renal Failure: 25-86% itching (not in acute renal failure)  Attrib to accumulation of pruritogens:  histamine (  mast cells), serotonin   Ca, Phos, Mg, Al, vit A also implicated  1/3 uremic patients not on dialysis  Maintenance hemodialysis: 70-80%

19  20-25% janudiced patients with hepatobiliary disease associated with cholestasis  100% primary biliary cirrhosis  Viral hepatitis  Attrib to bile salts in serum and tissues  Begins palms and soles & spreads inward

20  Polycythemia vera (50%)  iron def anemia,  lymphomas  Hodgkins – 30%  T-cell: almost all  leukemias, plasma cell dyscrasias, mastocytosis

21  Central: CNS abscess, spinal and cerebral tumors (17%), CVAs  Attrib to effects on descending pathways which  itching  Neurogenic  Shingles (10-15% in US)  Notalgia paresthetica: sensory entrapment syndrome causing neuropathy of T2-6 dorsal spinal nerves

22  Diabetes Thyrotoxicosis,Hypothyroidism Generalised due to dry skin Localised may be due to Candida  Myxodema  Postmenopausal syndrome  Most common trigger: mucocutanious candidiasis

23 HIV infectionInfection, infestation Eosinophilic folliculitis Unknown MalignancyUnknown PsychogenicUnknown

24  opioids commonly  Direct action on medullary dorsal horn and trigeminal nucleus of medulla – not t/histamine release  Spinal anesthesia with lidocaine: 30-100% pruritis

25  Fentanyl:  Intrathecal 67-100%  Epidural 67%  Morphine  Intrathecal 62-82%  Epidural 65-70%

26  Penicillin: immediate type I hypersensitivity reaction  Vancomycin: massive nonimmunologic release of histamine  “Red Man Syndrome”  (flushing CP, pruritis, muscle spasms, hypotension)  Related to rate of infusion  Potentiated by muscle relaxants and opioids  Attenuated by H1 blockers  Rifampin

27  Fentanyl: itching decreased when mixed with bupivicane, increased when mixed with procaine  Drug induced cholestasis  esp phenothiazenes, estrogens, tolbutamide, anabolic steroids

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31  Pressure  Low-intensity electrical  Histamine: acts directly on free nerve endings in skin

32  Histamine  Prostaglandins  Leukotrienes  Serotonin  Acetylcholine  Substance P  Proteases  Peptides  Enzymes  Cytokines

33  Cutaneous (pruritoceptive)  Neurogenic  Neuropathic  Mixed Psychogenic

34  C-Fibers originate @ dermal/epidermal jxn   Thin unmyelinated axons, lots of branching   Ipsilateral dorsal horn of spinal cord   Synapse with itch-specific secondary neurons  Cross to opposite anterolateral spinothalamic tract to thalamus   Somatosensory cortex of postcentral gyrus  SLOW transmission and BROAD receptor field

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36  Scratching stimulates large fast-conducting A-fibers adjacent to slow unmyelinated C fibers  A-fibers synapse with inhibitory interneurons and inhibit C-fibers  Scratching may either–stimulating ascending sensory pathway-inhibit itch at the spinal cord Or,may damage itch fibers directly

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38  Painful stimuli (thermal, mechanical, chemical) can inhibit itching  Inhibition of pain (opioids) may enhance itching

39  Inhibit mediators of itch: histamine, prostaglandins, substance P, serotonin, cytokines  Block chemicals that induce pruritis: opioids, antimicrobials  Treat effects of diseases which induce itching: eczema, CRF, LF, heme, neuro, endo

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41  cool compresses  emollients  topical steroids  antidepressants  anxiolytics  antibiotics

42  Tx for uremic itching: renal transplant  Effective even when transplant is failing as long as immunosuppresants are given  Antihistamines not effective  Also effective: moisturizers, UV-B tx (  vit A in skin), oral activated charcoal, cholstyramine, naltrexone, ondansterone, topical capsaicin, azelastin, thalidomide, IV lidocaine, erythropoetin, electric needle stim

43  Tx: reverse cholestatis, liver transplant  Also helpful: oral guar gum (dietary fiber) binds bile acids; cholestyramine; rifampin! (inhibits bile uptake), opioid antagonists, codeine, propofol, ondansetron, Naltrexone UVB  Not helpful: scratching

44  ThyrotoxicosisEmollients  LymphomaCimetidine  Iron defnIron supplement  HIV  Treatment of opportunistic infection Local corticosteroids, UVB UVB  PshychogenicPsychotherapy Anxiolytics Antidepressives

45 opioid related pruritis :  Diphenhydramine – for systemic opioids  For Neuraxial Opioids:  Ondansteron  Naloxone (1-2mcg/kg/hr)  Nalbuphine (10-20 mcg/kg/hr)  Propofol (.5-1mg/kg/hr)  Lidocaine (2mg/kg/hr)  NSAIDs (diclofenac, tenoxicam)  Droperidol  Penicillin Reaction Diphenhydramine


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