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
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
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
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