Kelainan Kulit di Wajah

Kelompok 4 PSPD Ilmu Penyakit Dalam

Fakultas Kedokteran Universitas Padjadjaran
Preseptor : Hendarsyah,dr.,Sp.PD
Skin Examination
 The skin is examined by inspection, including
compression and magnification,
supplemented by palpation to detect
nodularity and induration. A systematic
examination is essential noting especially the
anatomic distribution of lesions, the
configuration of grouped lesions, if present,
and the morphology of the individual lesions
Anatomic Distribution of Lesions

 Face
 Acne
 Actinic Keratosis
 Herpes Zoster (trigeminal nerve distribution)
 Secondary Syphilis
 Variola
acne herpes zoster syphilis

Small pox
Erythema Multiforme

 Target lesion palm,sole, and face

 Painful lesion and pruritic may progress to bullae
Scleroderma
 In scleroderma, skin and underlying tissue become contracted and fibrosed.
 Diffuse Cutaneous Scleroderma. Tight shiny skin is present on the distal
extremities and face and progresses to involve the more proximal extremities
and to a lesser extent the trunk
Lupus Erythematosus
 Acute Cutaneous Lupus: Several lesions occur: an acute malar or generalized
rash appears, precipitated by sunlight exposure
Dermatomyositis
 There is atrophy, edema, or fibrosis of the skin and nonsuppurative
inflammation of skin and striated muscle; the cause is unknown. Malaise,
weight loss,muscle stiffness, and dysphagia are presenting symptoms; pruritus
is especially characteristic. Heliotrope discoloration of the upper lids and
bridge of the nose and flat-topped violaceous papules (Gottron papules) over
the backs of the interphalangeal joints of the hands are classic signs. In
addition, erythematous rashes or exfoliative dermatitis may be seen
Telangiectasia. Dilated small blood vessels
that blanch with pressure
Spider Angiomata
The dilation, in turn, is caused by increased estrogen levels in the blood.
Many pregnant women, or women using hormonal contraception have spider
angiomas, due to high estrogen levels in their blood. Individuals with
significant hepatic disease also show many spider angiomas, as their liver
cannot metabolize circulating estrogens, specifically estrone, which derives
from the androgen androstenedion
Osler-Weber-Rendu disease (OWRD)
is a rare autosomal dominant disorder that affects blood vessels throughout the
body (causing vascular dysplasia) and results in a tendency for bleeding. (The
condition is also known as hereditary hemorrhagic telangiectasia (HHT)
Angioedema
 Localized interstitial edema in the dermis and subcutaneous tissues can be
caused by immunoglobulin (Ig) E-mediated allergy, complement activation, or
nonimmunologic mast cell activation, may be idiopathic.
 CLINICAL OCCURRENCE: IgE Mediated hymenoptera (bee) stings, drugs (e.g.,
penicillin and other antibiotics), food allergens (e.g.,peanuts, shellfish),
foreign proteins used therapeutically, many others; Non-IgE Mediated
angiotensin-converting enzymeinhibitors, radiologic contrast agents, cold
exposure; Complement Mediated hereditary angioedema (C1-esterase
deficiency), serum sickness, vasculitis.
Decreased Skin Elasticity

 Destruction or disruption of the elastic fibers in the skin results in decreased

elasticity. Decreased elasticity is evident as wrinkling and redundancy of the
skin. CLINICAL OCCURRENCE: Sun exposure (solar elastosis), actinic
cutaneous atrophy, excessive stretching of the skin (e.g., pregnancy, obesity),
glucocorticoid excess (Cushing syndrome), pseudoxanthoma elasticum.
Jaundice
 Unconjugated hyperbilirubinemia.
 This is usually caused by hemolysis producing unconjugated bilirubin at a rate exceeding the
maximal rate of liver uptake,conjugation and excretion. The stools are normal in color. The increase
in bilirubin excretion into the gut leads to an increase in urinary urobilinogen. The urine contains no
bilirubin because only water-soluble conjugated bilirubin is excreted in the urine. Tests for intrinsic
liver disorders are negative. Less often, unconjugated bilirubinemia is caused by diminished hepatic
uptake or a defect in hepatic conjugation.

 CLINICAL OCCURRENCE:
 Increased Production: Hemolysis of normal red cells autoimmune hemolytic anemia,
transfusion hemolysis, hemolysis from chemicals, drugs, or infections; Red cell defects sickle
cell disease, thalassemia, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, pyruvate
kinase deficiency, paroxysmal nocturnal hemoglobinuria;
 Ineffective erythropoiesis thalassemia major, folate, and vitamin B12 deficiency;
 Miscellaneous absorption of hematoma, pulmonary infarction.
 Deficient Hepatic Uptake: sepsis, fasting, hypotension, and drugs. DeficientHepatic
Conjugation: Congenital Gilbert syndrome,Crigler-Najjar syndromes; Acquired: advanced
hepatocellular
 Conjugated hyperbilirubinemia. This results from impaired excretion of conjugated
bilirubin from the hepatocyte into the bile canaliculi or obstruction of the biliary
flowthrough the canaliculi, intrahepatic, and extrahepatic bile ducts to the duodenum.
The feces may be acholic in which case the urine lacks urobilinogen but contains
bilirubin. The serum alkaline phosphatase is elevated out of proportion to the
transaminases. Clinically, it is important to distinguish mechanical extrahepatic
obstruction from intrahepatic obstruction that results from either mechanical
obstruction or altered hepatocyte and canalicular function (cholestasis). In most cases
of extrahepatic obstructive jaundice, dilatation of the bile ducts can be detected by
ultrasonography.

 CLINICAL OCCURRENCE:
 Intrahepatic Cholestasis: Congenital Dubin-Johnson syndrome, Rotor syndrome;
 Acquired hepatocellular disease, drugs (especially sex steroids), sepsis,
hypotension, primary biliary cirrhosis.
 Extrahepatic Obstruction: Intrinsic gallstones, biliary sludge, biliary carcinoma,
sclerosing cholangitis, stricture, parasites; Extrinsic pancreatic carcinoma,
portahepatis lymphadenopathy, pancreatitis, pancreatic pseudocyst.