skin manifestation liver disease.pptx

skin manifestation liver disease

1. Skin manifestation of liver diseases

2. PIGMENTARY CHANGES VASCULAR CHANGES 3.COAGULATIO N DEFECTS 4 .PRURITIS 5.NAILCHANGES CUTANEOUS MANIFESTATIONS OF HEPATIC DISEASES

3. PIGMENTARY CHANGES JAUNDICE/ICTERUS: generalized yellowish coloration of the skin and mucosae serum bilirubin levels greater than 2.5–3.0 mg/dL HYPERMELANOSIS diffuse hyperpigmentation – long standing cirrhosis over exposed sites or palmoplantar creases, or in a perioral and periorbital distribution

4. VASCULAR CHANGES SPIDER ANGIOMA (NEVUS ARANEUS, SPIDER NEVUS) Seen in chronic liver disease central arteriole visible as a red, flat or slightly elevated point surrounded by multiple, small, and tortuous radiating capillaries Pinhead-sized to up to 2 cm in diameter Blanchable lesions Larger lesions may pulsate lesions are commoner in alcoholic cirrhosis presence may indicate an increased risk of bleeding from esophageal varices in such patients

5. PALMAR ERYTHEMA/ LIVER PALMS: Exaggerated mottling or a well defined hypothenar erythema that later spreads to fingers and rest of the palm. UNILATERAL NEVOID TELENGIECTASIA : Fine thread like telengiectasia present mostly over C3, C4 dermatome

6. PAPER MONEY SKIN Presence of numerous threadlike small blood vessels scattered randomly throughout the skin CAPUT MEDUSAE dialated & radiating veins seen around the umblicus due to portal hypertension

7. COAGULATION DEFECTS Bruising, petechiae, purpura, and ecchymosis. Mucosal bleeding (epistaxis or gingival bleeding).

8. PRURITUS Mostly seen in cholestasis presenting complaint in more than half of the patients of primary biliary cirrhosis Itch is usually more pronounced on the extremities , although the trunk may be equally affected and multiple excoriations may be found. Due to- Retained cutaneous bile acids . The endogenous opioid system also play a major role Severe pruritus in primary biliary cirrhosis may be accompanied by a diffuse hyperpigmentation , often sparing a “butterfly” area on the upper back

9. Treatment: Bile acid sequestrants like cholestyramine drugs relieving cholestasis like ursodeoxycholic acid Opiod antagonists – Naltrexone Naloxone Nalmefene Sedating antihistaminics Phototherapy Hepatic enzyme inducers (rifampicin, phenobarbital . )

10. NAIL CHANGES Clubbing Longitudinal ridging Thickening Brittleness Total leuconychia Terry’s nails (whitening of the entire nail plate except for a narrow pink band distally) Muehrcke’s nails (multiple parallel transverse white bands)

11. PRIMARY BILIARY CIRRHOSIS Jaundice & pruritis CREST syndrome - Reynolds’ syndrome Xanthomas - yellowish plaques covering large areas of skin in palmar creases (xanthoma striatum palmare ) and in scars

12. Hepatitis B infection Urticaria serum sickness-like picture resulting from the deposition of circulating immune complexes Angioedema, erythema nodosum, or erythema multiforme may also be associated Gianotti – Crosti syndrome papular acrodermatitis. Multiple, monomorphic, erythematous papules occurring on the acral areas and the face are characteristic of this condition. Skin lesions typically last at least 10 days. GCS is thought to be a hypersensitive response to the underlying infection.

13. Hepatitis C Mixed cryoglobulinemia Due to chronic stimulation of the immune system by HCV. Characterized by the presence of cryoglobulins in the blood. Cryoglobulins are abnormal proteins that thicken and clump together at cold temperature resulting in palpable purpura, livedo reticularis, acrocyanosis, urticated plaques, hemorrhagic bullae, or ulcers. Interferon alfa (IFN-α) can improve skin, kidney, and/or joint involvement, and may be the drug of choice for HCV-related cryoglobulinemia

14. porphyria cutanea tarda painful, blistering skin lesions that develop on sun-exposed skin (photosensitivity). Affected skin is fragile and may peel or blister after minor trauma Pathogenesis - oxidative stresses due to intracellular glutathione depletion, elevation of hepatic iron levels, and reduced activity of hepatic uroporphyrinogen decarboxylase due to autoantibodies

15. NECROLYTI C ACRA L ERYTHEMA occur almost exclusively in individuals with HCV infection Starts as erythematous papules that coalesce into well-circumscribed dusky areas with scaling and erosions. Older lesions- hyperkeratotic surfac e. Mc site- dorsal surface of feet-great toes. Periorificial areas are not involved Zinc deficiency play a role in the pathogenesis RED FINGERS SYNDROME HCV-associated dermatosis. It is characterized by well defined telangiectatic erythema of the fingers and toes

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