Anatomy of Skin and Basic Skin Lesions

Nutritional DermatosesStages of nutritional deficiency syndromeStage I Intake falls below daily requirement but the reserves maintain normal blood valuesStage II Blood levels decrease but patient is asymptomaticStage III Development of clinical signs and symptomsCauses of deficienciesDecreased intake Poverty Food faddismCrash diets Anorexia/Bulimia nervosa AlcoholismIncreased requirmentPregnancyLactation FeverHyperthyroidismMalignancy

CausesDecreased absorption and utilizationGI - mucosal disturbances: Malabsorption syndromeDietary factors: High dietary phytate, TPN, alcoholism Trauma: Burns , Post surgical proceduresMalignancyRenal disorders Infections: Parasitic, bacterial, viralCollagen vascular disease, HIVNutritional deficienciesFat soluble vitamins (A,D,E,K)Water soluble vitamins (B-complex, Niacin, Pantothenic acid, Biotin, Vit C)Minerals Trace elements (Zinc, Iron)Essential fatty acids (EFA) PEM (Protein energy malnutrition)Important Points1. Water soluble vitamins Not stored in body Excessive consumption will not lead to toxicity

2. Fat soluble vitamins (A, D, E, K)Stored in liver Excessive consumption toxicity

Vitamin A (Retinol) deficiencySourcefish liver oils, milk, butter, eggs, liver , kidneys

Provitamin A (Beta carotene)Green and yellow parts of plants (spinach, drum sticks, spring onions, cabbage, pumpkin, carrots, tomato)Fruits mango, papayaClinical featuresSkin manifestations: Infants, very young children Extensive xerosis Phrynoderma (Toad skin)-Follicular hyperkeratosis

Sites: extensor extremities, back , buttocks. Mixed deficiencies of Vit A, B, C and EFA

Clinical featuresEye Manifestations:Common cause of blindness in developing countriesEarliest symptoms: Nyctalopia (night blindness) Hemeralopia (inability to see bright light)

Xerophthalmia:Bitots spotKeratomalacia Conjunctival and corneal xerosisCorneal ulceration Scarring, blindness TreatmentDose :1-3 lac IU for 1-3 days (Stop in case of headaches)Supplements: Vit. B complex and EFAsTreatmentProphylactic Treatment:Vit. A (2 lacs IU) every 6 months to pre-school children Good quality protein diet + vitaminsEducation of local community

Vitamin DVitamin D is sterol considered as a hormoneSkin: Role in synthesis, storage and release of Vitamin D Active form: 1, 25 di-hydroxy cholecalciferol (Calcitriol) Absorbtion and metabolism of calciumClinical features and treatmentChildren: Rickets, TetanyAdults: OsteomalaciaType I Vit.D dependent rickets : No skin lesionsType II Vit.D resistant rickets : Progressive alopeciaTreatment:Normal daily requirement: 400 IUIn rickets : 5000 IU oral Vit D for 3 to 5 weeksExposure to sunlightVitamin B ComplexUsually occur in combination with proteins and mineral deficiencyVitamin B1 (Thiamine, Aneurin)Dry beriberi Peripheral neurologic syndrome, Korsakoff's psychosis, Wernicke's encephalopathyDry skin, red burning tongue Wet beriberiHigh output cardiac failureRiboflavin (B12) deficiency

Oro - Oculo - Genital syndrome

Oral manifestations: Angular stomatitis (perleche) with candidiasis Cheilosis : lip involvement with vertical fissuring Glossitis : magenta coloured tongue atrophic filiform papillae enlarged fungiform papillae

Skin manifestations:

Seborrheic dermatitis like rashFollicular papules Patchy alopecia with scaling on scalp and eyebrows

Clinical featuresGenitals: scrotum, vulva Early - Patchy redness, fine powdery desquamation Late - Lichenification Severe - Raw areas over shaft of penis, inner thighsEyes: Photophobia, lacrimation, conjunctivitis, decrease in visual acuity, corneal vascularizationCNS: Psychomotor, intellectual development impaired in childrenTreatment Infants : 1-3 mg Adults : 10-30 mg

Vitamin B3 (Nicotinic acid, Nicotinamide, Niacin )Pellagra Pelle - skin, agra roughNiacinamide is active form and is converted to coenzymes NAD, NADP Plays a vital role in cell, fatty acid, carbohydrate metabolismSourcesMeat, fish, eggsMilk, cheeseCereals, grains, legumesCoffee and teaEndogenous production 60 mg of tryptophan 1mg of niacinEtiology Maize and jowar as a staple diet Maize - poor source of nicotinic acid and tryptophan - niacin is present but not bio-availableJowar - high content of leucineChronic alcoholics - unbalanced diet Clinical featuresThis disease is characterized by 4 DsDermatitisDementiaDiarrheaDeathClinical featuresSkin:Photo exposed areas

Well demarcated erythematous patches develop into dry brownish scaly patchesClinical featuresPellagrins nose Dull erythema, butterfly rash with scaling on bridge of noseCasal's necklace Sharply demarcated lesion on upper central chest, neckCravat Anterior continuation of necklace on chestScrotal erythemaGlove or gauntlet

Clinical featuresMucous membrane Angular stomatitis, cheilitisScarlet glossitis with imprint of teethTongue is red, smooth, atrophy of filiform papillae, erosions, ulcerations, fissuresSwelling of parotid gland, increased salivationGIT: Anorexia, nausea, vomiting, abdominal pain, bloody diarrhoeaCNS: Depression, psychosisTreatmentTherapeutic dose: 300 - 500 mg niacinamide orally or intramuscular in divided doses (amide preferred because it does not precipitate flushing, itching, burning)Supplement with B complex, animal proteins eggs, milkBalanced dietReduce alcoholVit B12 deficiency (Cobalamin, Cyanocobalamin)Sources:Liver, kidney, heart - richestMeat, fish, cheese, eggs, milkVegetables, fruits, legumes - nil; but present if contaminated by bacteriaVit B12 is synthesized in colon (low bio-availability) Cause of deficiency of Vit.B12 Strict vegetarian dietintrinsic factor deficiency (pernicious anemia)Diphyllobothrium latum infestationMalabsorption syndromes (sprue, intestinal TB, Whipples disease)Clinical featuresSkinSymmetrical generalized hyperpigmentation (greyish - brown)Mucous membrane Hyperpigmentation, cheilitis, glossitis with beefy red tongue, glossodynia, aphthae like lesionsNails: Pigmented streaksHair: Premature graying, canitiesOther manifestations: Megaloblastic, pernicious anemia, peripheral neuritis, poor memoryDiagnosisSerum Vit. B12 7 yrs, adults : 16 mgPregnant and lactating mothers : 20 -25 mg Treatment Dose Oral zinc : 2mg/kg/day for 1- 2 weeks30 to 55 mg of elemental Zn for 1-2 weeks(220 mg ZnSo4 = 55 mg of elemental Zn)Hereditary type requires life long treatmentIron deficiencySources:Green leafy vegetables, pulses, meat productsVitamin C rich foods improve absorption; tea and tamarind inhibits absorptionClinical features:Generalized pruritus, increased hair loss, koilonychiaAngular stomatitis, cheilitis, glossitisHypochromic microcytic anemia

TreatmentTherapeutic dose:Ferrous sulphate or gluconate 300mg thrice dailyTreat underlying cause: chronic blood loss, parasitic infestations, malariaSupplementation with Vitamin CSupplementation during pregnancy

Protein Energy Malnutrition (PEM)PEM is most common form of malnutritionAge: 1-3 years, commonly seen during weaning and post weaning periodMarasmus: Patient with 60% of expected body weight without edema Kwashiorkor:Patient who weighs 60 - 80 % of expected body weight for that age with severe protein malnutrition with relative carbohydrate excessMarasmusSkinDry, thin, wrinkled and inelasticFollicular hyperkeratosis (adults)HairSparse, lustrelessGrowth of lanugo hair occurs Nails : FissuredFacies :Monkey facies- wrinkled skin with loss of buccal pad of padChild is alert- will crave for food

Kwashiorkor: Clinical featuresSkinExtensive peeling of skin with erosions - flaky paint or crazy pavement dermatosesEnamel paint dermatoses Sharply demarcated hyperpigmented plaques with burnt out appearance and waxy feel (spares feet and dorsa of hands)Clinical featuresMucosae:Cheilitis with fissuring on lipsAngular stomatitis, glossitisNails: Soft and thinHair :Sparse, thin, brittle, easy pluckableDyschromotrichia : golden, blonde, rust (red boy)Flag signEyelashes : broomstick appearanceEdematous, hepatomegaly, lethargic

Treatment High protein, high caloric dietTopical zinc paste, oral zinc supplementsCorrection of other associated deficiencyTreatment of infection and infestation Very common Poor feeding in children Alcoholism in males Combined deficiency is very common treat the underlying causeThank you