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1.PIGMENTARY CHANGES
2.VASCULAR CHANGES
3.COAGULATION DEFECTS
4.PRURITIS
5.NAILCHANGES
CUTANEOUS MANIFESTATIONS OF HEPATIC DISEASES
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
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
 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
 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
COAGULATION DEFECTS
• Bruising, petechiae, purpura, and ecchymosis.
• Mucosal bleeding (epistaxis or gingival bleeding).
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
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.)
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)
PRIMARY BILIARY
CIRRHOSIS
1.Jaundice & pruritis
2.CREST syndrome - Reynolds’
syndrome
3.Xanthomas - yellowish
plaques covering large areas of
skin in palmar creases
(xanthoma striatum palmare)
and in scars
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.
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
 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
 NECROLYTIC ACRAL 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 surface.
• 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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skin manifestation liver disease.pptx

  • 1.
  • 2. 1.PIGMENTARY CHANGES 2.VASCULAR CHANGES 3.COAGULATION 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 1.Jaundice & pruritis 2.CREST syndrome - Reynolds’ syndrome 3.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.  NECROLYTIC ACRAL 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 surface. • 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

Notas do Editor

  1. pathogenetic mechanisms include oxidative stresses due to intracellular glutathione depletion, elevation of hepatic iron levels, and reduced activity of hepatic uroporphyrinogen decarboxylase due to autoantibodies