By :Dr.Pawana Kayastha. SKIN CHANGES IN OLD AGE Typical changes: include atrophy, laxity, wrinkling,...

MAJOR MANIFESTATION OF SKIN DISEASE

By :Dr .Pawana Kayastha

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

•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.

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

.

inflammatory skin diseases, e.g. asteatotic, gravitational and seborrhoeic eczema, psoriasis

lichen sclerosus et atrophicus scabies lymphoedema pruritus of old age drug-related rashes

THE CHANGING MOLE

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.

'IS IT CANCER, DOCTOR?'

ABCDE FEATURES OF MALIGNANT MELANOMA

Asymmetry Border irregular Colour irregular Diameter often greater than 0.5 cm Elevation irregular

(+ Loss of skin markings)

HISTORY 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.

EXAMINATION 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,)

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

MANAGEMENT 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

PRURITISAn unpleasant localized or generalized

sensation on the skin, mucus membranes or conjunctivae which the patient instinctively attempts to relieve by scratching or rubbing

DIVERSITY OF CAUSES AND PRESENTATIONMany Causes, Many Treatments

Trivial to Life threatening

(mosquito bite) (malignancy)

10-50% of cases with generalized itching have systemic disease

DISEASES & ITCHING

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

CAUSES OF PRURITUS iin IN PREGNANCYCondition

Gestation and features Treatment

Obstetric cholestasis

3rd trimesterAssociated with abnormal liverfunction tests

EmollientsChlorphenamineColestyramineEarly delivery

Pemphigoid gestationis

3rd trimesterPruritus followed by blisteringStarts around the umbilicus

Topical or oral corticosteroids

Polymorphic eruption (urticarialpapules) of pregnancy

3rd trimester, after deliveryPolymorphic lesions with urticaria

Chlorphenamine

IN PREGNANCY

Prurigo gestationis

2nd trimesterExcoriated papules

EmollientsTopical corticosteroidsChlorphenamine

Pruritic folliculitis

3rd trimesterAseptic pustules on trunk

Topical corticosteroids

RENAL DISEASES AND ITCHING 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%

HEPATIC DISEASES & ITCHING 20-25% janudiced patients with

hepatobiliary disease associated with cholestasis100% primary biliary cirrhosisViral hepatitis

Attrib to bile salts in serum and tissues Begins palms and soles & spreads

inward

HEMATOLOGIC DISEASE & ITCHING Polycythemia vera (50%) iron def anemia, lymphomas

Hodgkins – 30% T-cell: almost all

leukemias, plasma cell dyscrasias, mastocytosis

NEUROLOGIC DISORDERS & ITCHING Central: CNS abscess, spinal and

cerebral tumors (17%), CVAsAttrib 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

ENDOCRINE D/O & ITCHING Diabetes Thyrotoxicosis,Hypothyroidism Generalised due to dry skin

Localised may be due to Candida Myxodema Postmenopausal syndrome

Most common trigger: mucocutanious candidiasis

HIV infection Infection, infestationEosinophilic folliculitisUnknown

Malignancy Unknown

Psychogenic Unknown

CHEMICALLY INDUCED ITCHING:

NEUROAXIAL opioids commonly

Direct action on medullary dorsal horn and trigeminal nucleus of medulla – not t/histamine release

Spinal anesthesia with lidocaine: 30-100% pruritis

Fentanyl: Intrathecal 67-100%Epidural 67%

Morphine Intrathecal 62-82%Epidural 65-70%

CHEMICALLY INDUCED ITCHING:ANTIBIOTICS 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 infusionPotentiated by muscle relaxants and opioidsAttenuated by H1 blockers

Rifampin

CHEMICALLY INDUCED ITCHING:OTHER DRUGS Fentanyl: itching decreased when mixed

with bupivicane, increased when mixed with procaine

Drug induced cholestasis esp phenothiazenes, estrogens,

tolbutamide, anabolic steroids

HISTORY & EXAMINATION

LOOK for skin changes If no skin disease identified then search for

systemic diseases by systemic examination

Investigation –as per systemic illness

PRURITOGENIC STIMULI Pressure Low-intensity electrical Histamine: acts directly on free nerve

endings in skin

ITCH MEDIATORS Histamine Prostaglandins Leukotrienes Serotonin Acetylcholine

Substance P Proteases Peptides Enzymes Cytokines

ITCH PATHWAYS Cutaneous (pruritoceptive) Neurogenic Neuropathic Mixed Psychogenic

ITCH PATHWAYS 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

LATERAL INHIBITION: “GATE THEORY” 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

PAIN & ITCH Painful stimuli (thermal, mechanical,

chemical) can inhibit itching Inhibition of pain (opioids) may enhance

itching

HOW TO TREAT AN ITCH(UNDERSTAND THE CAUSE!) 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

ECZEMA & ITCHING: TREATMENT cool compresses emollients topical steroids antidepressants anxiolytics antibiotics

RENAL DISEASES AND ITCHING 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

HEPATIC DISEASES & ITCHING 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,NaltrexoneUVB

Not helpful: scratching

OTHERS Thyrotoxicosis Emollients Lymphoma Cimetidine Iron defn Iron supplement HIV

Treatment of opportunistic infectionLocal corticosteroids, UVBUVB

Pshychogenic PsychotherapyAnxiolyticsAntidepressives

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 ReactionDiphenhydramine