This document discusses various cutaneous manifestations of internal diseases. It focuses on cutaneous findings in diabetes mellitus, thyroid disease, adrenal disease, and renal disease. Some of the key points discussed include:
1) Skin lesions occur in 30% of patients with diabetes mellitus, including necrobiosis lipoidica, granuloma annulare, diabetic bullae, and acanthosis nigricans. Skin infections are also more common.
2) Hyperthyroidism can cause pretibial myxedema, scleromyxedema, thyroid acropachy, and Graves' dermopathy. Hypothyroidism results in dry skin, hair changes, nail changes, and generalized
4. DIABETES MELLITUS
• approximately 30% of patients with DM develop
skin lesions at some point
• Overall prevalence of cutaneous disorders does
not differ between type I and type II diabetics
● Type I patients get more
autoimmune-type lesions
● Type II patients get more cutaneous
infections
5. DIABETES MELLITUS
• Cutaneous lesions usually appear after the
development of DM, but may be the first
presenting sign
• Four major groups of skin findings
1. Skin diseases associated with DM
2. Cutaneous infections
3. Cutaneous manifestions of diabetic complications
4. Skin reactions to diabetic treatment
6. NECROBIOSIS LIPOIDICA (NL)
• NL is 3x more common in
women.
• NL appears earlier (mean age
22) in Type I diabetics than
Type II (mean age 49.)
• Appearance
● Begins as an oval, violaceous patch
and expands slowly.
● Advancing border is red.
● Central area turns yellowish brown.
● Central area atrophies and
telangiectasia become evident.
● 13% of cases progress to ulceration
7. NECROBIOSIS LIPOIDICA (NL)
• Classically, NL occurs
bilaterally on the
pretibial or medial
malleolar areas.
• Not painful.
• Spontaneous resolution
occurs in 13-19% with
residual scarring.
8. GRANULOMA ANNULARE (GA)
• Appearance
● Ring of small, firm,
flesh-colored or red
papules
● If localized, most
frequently found on
lateral and dorsal
surfaces of hands and
feet
● Can spontaneously
regress without
scarring
9. DIABETIC BULLAE
• Approximately 0.5% of diabetics
• Two types have been described
● More frequent, non-scarring lesions with
a histologic intraepidermal split without
acantholysis
● Less common, occasionally hemorrhagic
bullae that heal with scarring, slight
atrophy, and have a histologic
subepidermal split
o Trauma and microvascular disease may
play a role
• Appearance
● Painless bullae on non-inflamed base
that appear suddenly
● Most common on the dorsa and sides of
lower legs and feet, sometimes with
similar lesions on the hands and forearms
● Bullae contain clear, sterile fluid
10. DIABETIC BULLAE
• Bullae tend to heal spontaneously in 2-5
weeks
• diagnosis of exclusion
● DDx: bullous pemphigoid, epidermolysis
bullosa acquisita, porphyria cutanea
tarda, bullous impetigo, erythema
multiforme
● May recur in the same or new locations
11. ACANTHOSIS NIGRICANS
• Seen in situations of insulin
resistance
• Besides in DM, also seen in the
following:
● Carcinomas, especially of the stomach
● Secondary to drugs (nicotinic acid,
estrogen, or corticosteroids)
● Pineal tumors
● Other endocrine syndromes (PCOS,
acromegaly, Cushing’s disease,
hypothyroidism)
● Obesity
• Pathogenesis
● it may be related to insulin binding
insulin-like growth factor receptors on
keratinocytes and dermal fibroblasts,
thus stimulating growth.
12. ACANTHOSIS NIGRICANS
• Appearance
● Hyperpigmented,
velvety plaques in
body folds, mostly
axillae and neck
● Can also present
on groin,
umbilicus, areolae,
submammary
areas, and on the
hands
13. SKIN INFECTIONS IN DM
• Occur in 20-50% of poorly controlled diabetics
• More common in Type II
• May be related to
➢ Abnormal microcirculation
➢ Hypohidrosis
➢ PVD
➢ Neuropathy
➢ Decreased phagocytosis and killing activity
➢ Impaired leukocyte adherence
➢ delayed chemotaxis
14. CANDIDIASIS IN DIABETICS
• Fungal infections- most
common
• Candida
● Candidial paronychia
● Inframammary candida
● Genital candida
• Oral candidiasis
• White, curdlike material
adherent to
erythematous, fissured
oral commisure;
• angular stomatitis
17. SKIN INFECTIONS IN DM
• Bacterial Infections- can
be more severe and
widespread in diabetics
• Malignant otitis externa
● Pseudomonas aeruginosa
● Fatal in over 50% patients
● Can progress to chondritis,
osteomyelitis, and
bacterial meningitis
18. SKIN INFECTIONS IN DM
• Bacterial infections in DM
• Erythrasma
● Sharply demarcated
erythematous patches
● upper inner thighs,
axillae, toe web spaces,
and inframammary
creases
● Gram positive
Corynebacterium
minutissimum
● Identified with Wood’s
light coral fluorescence
19. DIABETIC ERUPTIVE XANTHOMAS
• Seen in
uncontrolled
diabetes,
hypertriglyceride
mia
• Sudden crops on
firm, non-tender
yellow papules
with a red rim on
extensors
• Control of glucose
and lipid reduction
reduce the lesions
20. DIABETIC DERMOPATHY
➢ AKA “shin spots” or
pigmented pretibial
papules
➢ Most common
cutaneous
manifestation of
diabetes
➢ Benign asymptomatic
red brown macules on
shins
➢ No treatment needed
21. CUTANEOUS MANIFESTATIONS OF DIABETIC
COMPLICATIONS: FOOT ULCERS
• Peripheral neuropathy leads to unnoticed trauma
• Vascular complications may lead to ulcers and
complicate ulcer healing
• Risk of amputation goes up 8x once these develop
22. CUTANEOUS REACTIONS TO DIABETIC
TREATMENT
Insulin
● Allergy may be local or systemic and usually
occurs within the first month of therapy
• Erythematous or urticarial pruritic nodules
at the site of injection
● Lipoatrophy can also occur
• Circumscribed depressed areas of skin at the
insulin injection site 6-24 months after
starting insulin
• More common in women and children
● Lipohypertrophy can also occur
• Soft dermal nodules that resemble lipomas
at sites of frequent injection
• May be a response to the lipogenic action of
insulin
• Treat and prevent by rotating sites of
injection
23. CUTANEOUS REACTIONS TO DIABETIC TREATMENT-ORAL
HYPOGLYCEMICS
• Most rxns are associated with the first-generation
sulfonylureas (chlorpropamide and tolbutamide)
• 1-5% of patients on these drugs will develop skin rxns
during the first 2 months of treatment
• Most commonly, they present with maculopapular
eruptions that resolve despite continuation of the
drug.
25. THYROID HORMONE AND THE SKIN
• Thyroid hormone plays a pivotal role in the
growth and formation of hair and sebum
production.
• Thyroid hormone stimulates epidermal oxygen
consumption, protein synthesis, mitosis, and
determination of epidermal thickness.
• There is increased cutaneous blood flow and
peripheral vasodilation.
26. HYPERTHYROIDISM AND THE SKIN
• Skin is usually warm, moist, and smooth
(best assessed on the inner aspect of arm and over
the chest)
• Facial flushing
• Palmar erythema
• Hyperpigmentation, esp. creases of palms and soles
(buccal pigementation doesn’t occur)
• hair is fine and friable, hair loss may be excessive
• History of early graying
• Hyperhydrosis, particularly of palms and soles
27. PLUMMER’S NAIL IN HYPERTHYROIDISM
“Plummer’s nail”: concave contour and distal
onycholysis, esp. the ring finger (not specific- also seen
in hypothyroidism, psoriasis, after trauma, or in allergic
contact dermatitis)
28. SCLEROMYXEDEMA IN HYPERTHYROIDISM
• Numerous firm white, yellow, or
pink papules on face, trunk, axillae,
and extremities
● Lesions result from accumulation of
hyaluronic acid in the dermis,
accompanied by large fibrocytes
31. GRAVES’ DERMOPATHY
• Pretibial myxedema (0.5-4% of
patients)
• Late manifestation, accompanied by
ophthalmopathy in 99%.
● Presentation varies from “peau
d’orange” appearance to extensive
infiltration.
● Most often, bilateral, asymmetric,
raised, firm plaques or nodules
varying from pink to brown,
sometimes with woody induration
● Can appear anywhere (arms,
shoulders, head).
● Histologically, the process involves
dermal accumalation of hyaluronic
acid.
Pathogenesis :pretibial fibroblasts are
the target for antithyroid antibodies
T cells may be interacting with a
dermal antigen similar to a thyroid
autoantigen, with cytokines
subsequently activating fibroblasts to
secrete hyalouronic acid.
❖Can treat with topical steroids,
intralesional steroids, IV pulse
steroids, or IVIG
32. THYROID ACROPACHY IN GRAVES’
DISEASE
•Thyroid acropachy (1% of Graves’ patients).
•Triad of digital clubbing, soft tissue swelling of hands and feet, and periosteal
new bone formation
•Usually accomapanied by exophthalmos and dermopathy (diamond triad)
•May occur in hashimioto’s thyroiditis and hurtle cell adenocarcinoma.
33. HYPOTHYROIDISM AND THE SKIN
• Skin is cool, dry, and pale.
● Pallor results from cutaneous
vasoconstriction and increased
deposition of water and
mucopolysaccharides in the dermis,
which alter the refraction of light
• Hypohydrosis may lead to
palmoplantar keratoderma (possibly
along with reduced epidermal steroid
synthesis)
• Carotenemia (from decreased hepatic
conversion of beta carotene to Vit A)
gives skin yellowish hue (palms, soles,
+nasolabial folds)
• Hair: dry, brittle, coarse; partial
alopecia
• Loss of hair from lateral 1/3 of eyebrows
(lateral superciliary madarosis)
Hertog’s sign
• Hair growth slows down, the
proportion of telogen hair is increased.
• These changes normalise with
normalization of thyroid hormone
levels.
34. HYPOTHYROIDISM AND THE SKIN
• Nails are brittle, grow slowly, purpura
• Easy bruising
• Wound healing is impaired.
• Diminished levels of clotting factors may manifest as
purpura.
35. HYPOTHYROIDISM FACIES WITH GENERALIZED
MYXEDEMA
• Generalized myxedema
• Characteristic skin sign
● Occurs as a result of
deposition of PAS-positive
dermal acid
mucopolysaccharides (esp.
hyaluronic acid and
chondroitin sulfate) in the
skin
● Skin is non-pitting, with a
firm waxy appearance
● Characteristic facies: swollen
lips, broad nose, macroglossia,
and puffy eyelids
● Also apparent on the dorsa of
hands and feet and in the
supraclavicular fossa
● Carpal tunnel syndrome and
facila nerve palsy may occur
owing to nerve entrapment
36. CONGENITAL HYPOTHYROIDISM (CRETINISM)
• Myxodema
• Yellowing (carotenemia or prolonged jaundice)
• Pronounced clavicular fat pad
• Coarse, dry, brittle hair with patchy alopecia
• Persistent, long, lanugo hair on the upper back,
shoulders, and extremities
• Hypothermia
• Reflex peripheral vasoconstriction may
accentuate cutis marmorata
• Poor nail growth
• Delayed eruption of deciduous teeth
• Retardation of mental and physical development
• Delayed milestones
37. • Thyroid replacement therapy rapidly reverses
many of the cutaneous features of
hypothyroidism, with gradual disappeaarance of
excessive dermal mucopolysaccharides.
38. ASSOCIATION BETWEEN CUTANEOUS AND
THYROID DISEASE
• Vitiligo (higher levels of antithyroid
peroxidase, antithyroid microsome, anti-TSH)
• Connective tissue diseases
● Dermatomyositis, SLE, scleroderma,
polymyositis, sjogren’s syndrome.
● Generalised granuloma annulare,
● reticular erythematous mucinosis
● Chronic urticaria
● Melasma
● Chronic mucocutaneous candidiasis
● MEN syndromes
❖Patients with idiopathic chronic urticaria and/or angiodema should therefore
be screened for thyroid autoimmunity
39. ASSOCIATION BETWEEN CUTANEOUS AND
THYROID DISEASE CONTD.
➢ ALOPECIA
AREATA
● Rapid onset of
total hair loss in
a sharply
defined, usually
round, area
● Regrowth begins
in 1 to 3 months
and may be
followed by loss
in the same or
other areas
40. ASSOCIATION BETWEEN CUTANEOUS AND
THYROID DISEASE CONTD.
• Pemphigus foliaceus
Herpes gestationis
Bullous pemphigoid
Dermatitis herpetiformis
• Pemphigus vulgaris
42. ADRENAL INSUFFICIENCY
• Increased
stimulation of
melanocortin-2
receptor by ACTH
itself
• Pigmentation is
maximal over
photoexposed
areas, mucuos
membranes,
palmar creases,
areas subject to
friction, genitalia,
areola, axillae,
perineum as well as
in scars.
• Nails-longitudinal
melanonychia
43. HYPERCORTISM
• Truncal obesity
• Buffalo hump
• Moon facies
• Slender limbs
• Cutaneous atrophy and
telangiectasias
• Fragility with purpura
• Poor wound healing
• Acneform eruptions
• Hirsuitism
• Cigarette paper like
wrinkling of skin on
dorsum of hands(liddle’s
sign)
• Livid, purplish straie on
abdomen, breasts,
proximal part of limbs
44. RENAL DISEASES
➢ Signs of ESRD
➢ Signs associated with dialysis
➢ Signs in renal transplant patients
46. XEROSIS
• Most common cutaneous abnormality
• Is predominantly seen over the extensor surfaces of the forearms, legs and
thighs.
• The abdomen and chest may show fine scaling
• Hypervitaminosis A, reduction in size of eccrine sweat glands, high dose
diuretic regimens are some of the causes of xerosis
47. UREMIC PRURITUS
• Incidence is 50-90%
• Usually on forarms, back
• Cutaneous manifestations of pruritus
include excoriations, prurigo nodularis
and lichen simplex chronicus
● Decreased transepidermal
elimination of pruritogenic factors
● Hyperparathyroidism
● Hypercalcemia
● Hyperphosphatemia
● Elevated histamine levels
● Topical
➢ Moisturizing creams
➢ Capsaicin
o Physical treatments
➢ UVB light
➢ parathyroidectomy
o Systemic medications
➢ Sedating Antihistamines
➢ Cholestyramine
● Alternative strategies
➢ Acupuncture
➢ homeopathy
48. PIGMENTARY CHANGES PURPURA/ECHHYMOSIS
• Pallor – Anemia
• Yellow hue – Carotenoids and
nitrogenous pigments (urochromes) in
the skin.
• Brown-black Hyperpigmentation -
➢ Sunexposed areas
➢ can be attributed to retention of
chromogens and deposition of melanin in
the basal layer and superficial dermis due to
failure of kidney to excrete
beta-melanocyte stimulating
hormone
➢ Sunscreens, sun avoidance
measures and clothing are advised
for these pigmentary changes.
• Defects in primary
hemostasis like increased
vascular fragility
• Abnormal platelet function
• Use of heparin during
dialysis are the main causes
of abnormal bleeding in these
patients
• Dialysis treatment partially
corrects these changes
49. CALCIFIC UREMIC ARTERIOLOPATHY (CALCIPHYLAXIS)
• Metastatic skin calcification
• abnormally elevated level of
parathyroid hormone (PTH)
which may trigger the deposition of
crystalline calcium pyrophosphate
in the dermis, subcutaneous fat, or
arterial walls.
• papular or nodular cutaneous
lesions around large joints or
flexural sites
• acute thrombosis of calcified
vessels.
• This produces violaceous mottling
of the skin that are acutely painful
due to ischemia.Surrounding tissue
may be inflamed with cellulitis.
• Lesions often progress to necrosis
and gangrene.
• The condition is associated with a
high mortality, particularly when
the skin of the trunk is involved.
• Infectious complications – non
healing ulcers
50. ACQUIRED PERFORATING DERMATOSIS ( APD )
• Hyperpigmented papules, up
to 1 cm in diameter, with a
central keratinous plug in
patients of CRF.
• The exclusive feature of the
perforating disorders is the
trans-epidermal
elimination of altered
dermal substances.
• The changes are significantly
more prevalent in diabetic
patients
• Excessive scratching +
diabetic vasculopathy - dermal
necrosis- eliminated through
the epidermis
• The extensor surfaces of the
limbs are more commonly
affected but the trunk and face
may be involved.
oDistinct from primary perforating disorders
➢Kyrle’s disease
➢Elastosis Perforans serpiginosa
➢Perforating folliculitis
➢Reactive perforating collagenosis
51. BULLOUS DISEASE OF DIALYSIS
• Syndrome of cutaneous
fragility and blistering
• Sun-exposed skin, most
often on the dorsal
hands
• Resembles Porphyria
• Plasma porphyrin levels
are normal or only
minimally elevated
52. NEPHROGENIC FIBROSING DERMOPATHY (NFD)
• Scleroderma like fibrosing
skin condition
• Typically, symmetrical skin
plaques with a peau d’orange
surface and advancing
ameboid edges develop on
limbs and trunk sparing the
head and neck.
• Nodules and contractures
can be seen in patients with
disease of long duration.
• Skin biopsy-marked fibrosis
53. UREMIC FROST
➢ Was a frequent in the
pre-dialysis era
➢ blood urea nitrogen level of
more than 250-300 mg/dl.
➢ The concentration of urea in
sweat is increased and, after
evaporation, there is a
deposition of urea crystals on
the skin surface.
➢ The frost consists of a white or
yellowish coating of urea
crystals on the beard area and
other parts of the face, neck and
on the trunk.
54. NAIL CHANGES
• Lindsay's nails (half and half nails, prevalence 30-50 %)
• Others
● Koilonychia
● Subungual hyperkeratosis
● Onycholysis
● Mees’ lines
● Muehrcke’s lines
● Splinter hemorrhages
● Beaus lines
Proximal
half opaque
white
Normal to red
brown distal half
55.
56. Yellow nail syndrome (YNS) is triad of yellow nails,
lymphedema, and respiratory tract involvement
57. HAIR ABNORMALITIES
• Sparse body hair and diffuse alopecia with dry,
lusterless hair
• Decreased secretion of sebum
• Chronic telogen effluvium
• Drugs – Heparin / Statins / Antihypertensives
58. CUTANEOUS MANIFESTATIONS IN PTS
ON DIALYSIS
• Diffuse
hyperpigmentation
• Accelerated cutaneous
aging
➢ Actinic elastosis
➢ Excessive wrinkling of neck(
cutis rhomboidalis nuchae)
➢ Telangiectasias
o Skin infections common
59. DERMATOLOGIC DISORDERS ASSOCIATED WITH
RENAL TRANSPLANTATION.
❖ Drugs – Steroids, Immunosuppresants
❖ Infections
➢ Severe herpes zoster
➢ Viral warts and condylomata accuminata are more common later
➢ Pityriasis versicolor commonest fungal infection
➢ Candidal infections
❖ Malignancies
➢ Kaposi sarcoma- oral cavity, limbs, trunk; associated with edema
➢ SCC> BCC
✓ Younger age, multiple, extracephalic, HP features of HPV infection, spindle cell
morphology is more common
Transplant patients should be counselled on minimizing UV light
exposure, regular sunscreen use, self screening for skin lesions
61. CHRONIC LIVER DISEASES
• Jaundice
• Because of raised
levels of bilirubin
more than
2.5-3.0mg/dl
• Diffuse
hyperpigmentation
62. SPIDER ANGIOMAS/ SPIDER NEVUS/NEVUS ARANEUS
• Pinhead to upto 2mm
• Mostly on skin drained by
superior vena cava
• Central arteriole visible as a red,
flat or slightly elevated point
surrounded by multiple, small
and tortuous radiating capillaries
• Commoner in alcoholic cirrhosis
• Presence may indicate an
increased risk of bleeding from
oesophageal varices
• Abundant cutaneous spider
angiomata –clinical marker of
hepatopulmonary syndrome,
where circulatory and
gas-exchange abnormalities in
lungs occur secondary to
advanced CLD.
63. CHRONIC LIVER DISEASES
• Palmar erythema
• Exaggerated mottling or a well
defined hypothenar erythema
that later spreads to fingers
and rest of the palm
• gynaecomastia
(Because of hyperestrogenemia)
64. CHRONIC LIVER DISEASES
• Pruritus
• Recurrent purpura
• Xanthoma straitum
palmare
(Multiple xanthomas may
appear as yellowish plaques
covering large areas of skin
in palmar creases)
66. CHRONIC LIVER DISEASES
• 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 Terry’s nails
Muehrcke’s nails
clubbing
68. PORPHYRIA CUTANEA TARDA
• Vesicles and bullae
on sun-exposed
areas, scarring
with milia
• Hypertrichosis
• Fragile skin with
sclerodermoid
changes
• Anti HCV
antibodies found in
upto 2/3rd
of cases
of these patients
• HCV serology
should be a part
of routine
investigative
work up in
patients with
PCT
69. LICHEN PLANUS
• Variable association of
0.1% to 35%
• Associated with LP ,
especially in mucosal,
generalised or long
standing LP
• Purple, pruritic, polygonal
papules
70. NECROLYTIC ACRAL ERYTHEMA
• Starts as
erythematous papules
and sometimes
blisters that coalesce
into
well-circumscribed
dusky areas with
scaling and erosions.
• Hyperkeratotic
surface develops in
older lesions
• Mc site- drsal surface
of feet-great toes
• Spares periorificial
areas-d/f with other
necrolytic erythemas
such as necrolytic
migratory erythemas
and zinc deficiency
71. HEPATITIS B
• About 30% may
have Urticaria or
present a serum
sickness like picture
(because of
circulating immune
complexes)
• Associated with
5-7% cases of
Polyarteritis nodosa
➢ Classical PAN
➢ Renal vasculitis present
➢ ANCA negative
86. Major criteria:
Proximal Scleroderma :
Symmetrical thickening, tightening, induration of skin of digits
and
dorsal hands; may affect entire extremity and involve face and
torso
Minor criteria:
1. Sclerodactyly: skin changes (above) limited to
digits
2. Digital pitted scars or loss of finger pad soft
tissue
3. bibasilar pulmonary
fibrosis
Diagnosis requires 1 major or 2 minor
CRITERIA FOR DIAGNOSIS: SYSTEMIC
SCLEROSIS
92. HENOCH-SCHÖNLEIN PURPURA
•vasculitis with arthritis, abdominal pain, and
hematuria
• mainly affects children
• often follows streptococcal infection
• In the skin, the disease causes palpable purpura (small
hemorrhages)
• chronic kidney disease- loss of small amounts of blood
and protein in the urine
98. CYANOSIS
• Capillary concentration of
reduced Hb is more than
4g/Dl.
• Best observed in
fulorescent lightening
• Most prominent in areas
with thin vascular surfaces
➢ Oral mucosa
➢ Lips
➢ Earlobes
➢ Nail beds
➢ Palms and soles in children
99. CYANOSIS
• May be
• Central (decreased arterial oxygen saturation)
➢ Congenital heart disease
➢ Impaired pulmonary function
❖ Tongue is the most reliable site for detecting cyanosis.
• Peripheral (owing to poor blood flow)
➢ Cold exposure
➢ Peripheral vascular disease
➢ Congestive heart failure
➢ Polycytemia
❖ Oral mucosa is often spared in peripheral cyanosis
o Mixed
➢ Pulmonary odema
➢ Cardiogenic shock
100. CLUBBING
• Increase in the
angle between the
proximal nail fold
and the nail plate
(Lovibond’s angle)
• Due to connective
tissue proliferation
between the nail
matrix and the
underlying distal
phalanx
102. CUTANEOUS ASSOCIATIONS OF CORONARY
ARTERY DISEASE
• Xanthomas:
localized lipid
infiltrates in
the dermis or
tendons.
• Indicative of
abnormal
lipid profile
and risk of
coronary
artery disease
103. INFECTIVE ENDOCARDITIS
• Subungual splinter
hemorrhages
➢ 1-2mm brown streaks
under the finger/toe nails
➢ Proximal appearance has
more diagnostic value
➢ Petechiae
➢ Osler’s nodes
➢ tender purpuric nodules on
the finger pads and toes)
➢ Janeway lesions
➢ nontender purpuric macules
of the palms and soles
104. RHEUMATIC FEVER
• Subcutaneous
nodules:
➢ Extensor aspect of elbows and
knees
➢ Exclusively seen in pts of
rheumatic carditis
• Erythema marginatum
➢ Seen in 10% pts of
rheumatic fever
➢ Dull red ,flat or palpable,
discrete or confluent,
annular lesions on the
trunk, esp the abdomen
and proximal parts of the
extremities
105. CUTANEOUS SIGNS INDICATIVE OF
INTERNAL DISEASES
oErythema nodosum
oAcanthosis nigricans
oPyoderma gangrenosum
oAcquired ichthyosis
oGeneralised pruritus without an eruption
106. Erythema Nodosum
Due to panniculitis
(inflammation of the
subcutaneous fat)
deep, firm, and tender
reddish-blue nodules, 1-5 cm
diameter
Most commonly at calves
and shins
108. Acanthosis nigricans
Asymptomatic brown velvety plaques of coalescent papules
Affects flexures - neck, axillae, groin
Potential causes
obesity
endocrine disorders
(acromegaly, insulin-
resistant diabetes)
Inherited
GI malignancy
109.
110. Pyoderma Gangrenosum
rapidly expanding ulcer with purple
undermined border, start as pustules
Often affects legs
Causes
■
■
50% idiopathic;
10% associated with ulcerative colitis;
■ Other associations: Crohn’s, chronic
active hepatitis, rheumatoid arthritis,
HIV, leukemia, myeloma
111. ACQUIRED ICHTHYOSIS
➢ If develops in adulthood,
consider:
• underlying malignancy
(e.g. Hodgkin’s disease),
• essential fatty acid
deficiency (e.g. due to
malabsorption from
intestinal by-pass or from
lipid lowering drugs)
112. Generalized pruritus
without an eruption
Causes:
Idiopathic (‘senile’)
Iron deficiency
Liver disease
Malignancy (e.g. Hodgkin’s lymphoma)
Neurological disorders
Polycythemia
Renal failure
Thyroid dysfunction