skin signs of systemic disease Flashcards
in chronic renal failure the muddy hue i due to the
accumulation of the
carotenoid and nitrogenous pigments (urochromes)
in the dermis
occurs in states that produce low
arterial oxygen saturation
central cyanosis
develops when there is
normal arterial oxygen saturation but reduced blood
flow,
peripheral cyanosis
in secondary polycythemia there may be presence of
nail clubbing
melanosis is primarily seen n
primary biliary cirrhosis
Metallic gray or bronze-brown discoloration
Accentuated in sun exposed and traumatized skin,
occasionally there is buccal and conjunctival
pigmentation
Hemochromatosis
Vitamin B3 deficiency
pellagra
4Ds in pellagra
dermatitis, dementia, diarrhea, death
Casal’s necklace is a feature of
pellagra (niacin deficiency)
jaundic is most prominent in
xtra-hepatic
biliary obstruction and PBC
cholestatic pruritus is due to
retained cutaneous bile acids
management of cholestatic pruritus
oral nalmefene/
IV or oral naloxone for short term efficacy
Hyperpigmentation of the skin (brown-black) seen
usually on skin folds such as neck, axilla and groins
Manifested by diabetic and obese patient
acanthosis nigricans
Metastases at the umbilicus
Sister mary joseph nodule
cancer associated with MIGRATORY SUPERFICIAL THROMBOPHLEBITIS
pancreatic cancer
Nails are normal in their distal 50% (red/pink/brown) and
white in the proximal 50%, with sharp demarcations
LINDSEY OR HALF-AND-HALF NAILS
Are characteristic of cirrhosis
• The so-called watch-glass deformity may accompany
white nails.
TERRY’S WHITE NAILS
In hepatolenticular degeneration (Wilson’s disease)
• bluish discoloration of the lunular portion of nails
AZURE LUNULE
Clubbing is common in all forms of cirrhosis, especially
PBC and chronic active hepa
most
representative and classic vascular lesion of chronic
liver disease
SPIDER NEVUS
lipid deposits localized on the eyes
Xanthelasma
most common manifestation of subacute bacterial endocarditis
petechiae
conjunctival petechiae
Roth’s spots-
Erythematous or hemorrhagic papules, macules or
nodules
Painful, tender and located distally on the digital
units
Osler’s nodes:
non-tender, located proximally on the palms and
soles
Janeway lesions
Hyperkeratotic papules with central, crust-filled crater on
the trunk and extensor surface often in linear pattern
ACQUIRED PERFORATING DERMATOSES
Tightness and thickening of the skin and periarticular
connective tissue of the fingers, resulting in a painless
loss of joint mobility
DIABETIC LIMITED JOINT MOBILITY
CHEIROARTHROPATHY
Painless, symmetric induration and thickening of the
skin on the upper back and neck
SCLERODERMA DIABETICORUM
pathogenesis of scleredema diabeticorum
unregulated production of ECM mol by fibroblasts w/c leads to thick collagen bundles and deposition of GAGS
1- to 4-mm, reddish-yellow papules on the buttocks and
extensor surfaces of the extremities
• There is often underlying severe hypertriglyceridemia
ERUPTIVE XANTHOMAS
Sharply demarcated yellow-brown plaques on the
anterior pretibial area
NECROBIOSIS LIPOIDICA
Small (<1cm), atrophic, pink to brown, scar-like macules
on the pretibial areas
DIABETIC DERMOPATHY
Pruritic, keratotic papules on the extensor surfaces of
the extremities
ACQUIRED PERFORATING DISORDERS
Abrupt, spontaneous blisters on the lower extremities
• painless and non-pruritic
BULLOSIS DIABETICORUM
classic manifestation of hyperthyroidism and
Grave’s disease
pretibial myxedema/ pretibial thyroid dermopathy
Concave shape with distal onycholysis
• Plummer’s nails
Digital clubbing, soft-tissue of the hands and feet,
presence of characteristic periosteal reactions
Thyroid acropachy
cutaneous manifestations of hypothyroidism
myxedema
carotenemia
most classic finding associated with hypothyroidism
Myxedema
myxedema is due to
dermal accumulation of
mucopolysaccharides, namely, hyaluronic acid and
chondroitin sulfate.
Excessive production of endogenous cortisol
cushing’s syndrom
in cushing’s the pituitary secretes what in excess
corticotropin or excess production of cortisol
moon facies is associated with
cushing’s
Destruction of the adrenal glands and the resulting lifethreatening
deficiency of glucocorticoids,
mineralocorticoids, and adrenal androgens
addison’s disease
why is there longitudinal pigmented bands in the nails of a person with addison’s
it is a consewuence of low cortisol levels and the resulting loss of negative feedback on the hypothalamus and pituitary
why is there decreased axillary and pubic hair in women and not in men
it is due to the loss of adrenal androgens it doesn’t occur in men because adequate androgen levels
are maintained by the testes
addison’s disease presentation in men
Calcification of auricular cartilages
