A site for medical students - Practical,Theory,Osce Notes

Showing posts with label dermatology. Show all posts
Showing posts with label dermatology. Show all posts

Examination of skin lesions an OSCE guide

1. Use good lighting: preferably natural lighting.
2. Patient is adequately exposed.
3. Comment on:              
  • Type of the lesion—primary and sequential: colour.
  • Shape of the lesions.
  • Arrangement of two or more lesions.
  • Distribution of the lesions—examine specifically the hair, nails and mucous membranes.
4. Do palpation to confirm findings.
5 Tell the probable diagnosis.
6. Do or tell one specific test to clinch the diagnosis.
1. Primary lesions They could lie
  • Flat (in the plane of the skin): Macule.
  • Elevated (above the plane of the skin): Papule, plaque, vesicle, bullae, pustule, cyst, wheal.
  • Depressed (below the plane of the skin): Ulcer, erosion.
2. Sequential lesions (occur over a primary lesion) Scaling, dry or wet exudation or llchenification.
3. Shape Round, oval, annular, iris, serpiginous, umbillicated. polygonal or polycyclic.
4. Arrangement herpctiform. zosteriform. reticular, linear or serpiginous.             '
5. Distribution Symmetrical or asymmetrical, exposed areas, intertriginous areas, sites of pressure, local or generalised.
6. Specific tests Include microscopic examination of the scales, crusts or exudate. Tzanck test. Auspltz sign. Nikolsky's sign. Koebner's phenomenon, patch test. etc.
7. The manifestations of a few common diseases are:
  • Iris lesion or target lesion: Erythema multlforme.
  • Annular lesions with scaling: Dermatophytosts. psoriasis and pityriasis rosea.
  • Annular lesions without scaling: SLE. Secondary syphilis.
  • Bilateral symmetrical eruptions: Drug or endogenous  hypersensitivity
  • On exposed areas: Pellagra, photosensitivity.
  • On interlriginous areas: Candidiasis.
  • On sites of pressure: Psoriasis.
  • Velvety brown pigmentation of the axilla and groins: Acanthosis nigricans.

This is very important for students preparing for USMLE and MRCP

How to examine an erythematous lesions the OSCE guide

1. Expose the skin adequately.
2. Use natural lighting.
3. Examine lor blanching on compression with a glass slide.
4. Comment on site, number, size and blanching on compression.
5. Tell the probable diagnosis.
1. Blanching on compression occurs in erythema, telangiectasia, spider naevi and partially in senile
angiomas. Blanching does not occur in purpura.
2. Purpura is a term used for collection of blood in the skin.
  • Petechiae are pin-point haemorrhages in the dermis.
  • Ecchymosis is a large subcutaneous collection of blood.
  • Haematoma is deeper and forms a palpable swelling.

These steps are very important for students preparing for USMLE and MRCP

How to examine exanthematous (rash) lesions-OSCE guide

Examination of exanthematous (rash) lesions
Elicit History
a. Duration of prodromal symptoms (including fever).
b. Onset and progression.
c. History of an epidemic in the locality.
Inspection and Palpation
1. Expose the patient adequately.
2. Ensure good lighting.
3. Observe and note down:
  • Involvement of oral mucosa, conjunctiva and external genitalia.
  • Distribution: centripetal, centrifugal, segmental.
  • Stage of the lesions: macule, papule, vesicle, pustule, scabs, combined or crops.
  • Regional lymphadenopathy.
Comment on:
Probable diagnosis.
Specific test to confirm diagnosis.

These steps are very imporatant for students who prepare for USMLE and  MRCP examinations

How to examine a patch lesion- OSCE guide

1 Elicit history of Itching, numbness, course of the lession.
2. Inspect and note: site. size, shape, number, margins (ill or well-defined).surface (flat or raised), pigmentation,scaling, central clearing.
3. Examine for sensory loss and regional nerve thickening (if relevant).
4. Comment on the possible diagnosis.
5. Do one specific test to confirm the diagnosis, e.g. sensory loss in Hansen's patch.
1. Patch refers to a flat lesion with a colour different from the surrounding skin. It is large and > 2 cm in diameter. It is called a macule,  it is < 2 cm.
2.. Common causes of patch lesions are dermatophytosis. leprosy and psoriasis.

Examination of hair

The scalp contains approximately 1,00,000 hairs.Each hair grows for about 1,000 days.
Rate of hair loss per day is approximately 100 normally.
Examination of hair consists of:
  • Distribution-normal or abnormal
  • Color of hair
  • Alopecia
  • Hypertrichosis
  • Hirsutism

Causes of hypertrichosis

Hypertrichosis is a condition where there is excessive growth of hair in generalized or localized pattern but this is not of male pattern of distribution.
Congenital hypertrichosis is seen in porphyria cutanea tarda, Hurler's syndrome, giant pigmented naevus also called as [bathing suit naevus]
Acquired hypertrichosis is seen in the following conditions
Malignancy-bronchogenic carcinoma
Drugs-phenytoin, steroids,minoxidil, diazoxide, streptomycin.
Endocrine causes
  • Sexual precocity
  • Hypothyroidism
  • Adrenal hyperplasia or neoplasm
Increased growth of terminal hair in women similar to  male secondary sexual pattern.
Causes of hirsuitism are 
  1. Idiopathic
  2. Virilization in adrenal and ovarian tumors
  3. Corticosteroid therapy

Causes of Greying of hair

Graying of hair can be seen as part of  Aging process
Starts at an age >20 in whites and at an age > 30 in black
Poliosis is the presence of grey hair in circumscribed pattern
What are the causes of premature graying of hair?
  • Megalobastic anemia
  • Diabetes mellitus
  • Hyperthyroidism
  • Dystrophia myotonica
  • Rare syndromes like Werners syndrome ,Vogt Koyanagi syndrome, Waardenbure syndrome, Chediak-Higashi syndrome.
Flag sign is the brownish discolouration of hair, with interspersed normal colour of hair, is seen
in protein energy malnutrition

What are the causes of alopecia?

Alopecia is the loss of hair from skin. It is of 2 types
Non-cicatrical alopecia and Cicatrical alopecia 
Causes of Non-cicatrical alopecia 
Physiological alopecia also called as male pattern of alopecia
Physiologic androgenic alopecia is an autosomal dominant male pattern of baldness,there is bitateral pattern of hair loss and is usually familial. 5-alpha reductase inhibitor finasteride is useful in the treatment. Other causes are puberty, pregnancy and neonatal period.
Alopecia areata is the most common type of noncicatricial alopecia.It is a autoimmune disease characterised by single or multiple areas of alopecia without any inflammation.
If it involves the whole of the scalp it is called atopecia totatis 
If it involves the whole of the body it is called atopecia universalis
It is associated with other auto immune disease like  SLE, vitiligo, autoimmune haemolytic anemia
Systemic diseases that produce alopecia are 
  • SLE
  • Hyperthyroidism
  • Hypothyroidism
  • Acrodermatitis enteropathica
  • Pernicious anemia 
  • Down's syndrome.
Infection: Moth eaten type of alopecia is seen  in syphilis and fungal infections.
Drugs: Antimetabolites, Cytotoxic agents, Carbimazole, Iodine, Bismuth, Vitamin A and Amphetamines. 
Telogen effluvium: is the hair loss following systemic illness (typhoid, measles, pneumonia) postpartum and postsurgical cases.
Alopecia in females  seen in virilising tumor of ovary or adrenal
Causes of cicatricial Alopecia
It is due to primary dermatological conditions
  • Trauma
  • Burns
  • Folliculitis, gumma, lupusvulgaris and herpes zoster
  • Morphea, lichen planus, saroidosos and DLE
  • Drugs-Mepacrine.
Decreased Body Hair Distribution (Loss of Secondary Sexual Character)
This is seen in the following conditions:
  • Decompensated liver disease
  • Klinefelter's syndrome
  • Bilateral testicular atrophy as seen in Hansen's disease.

What are the cardinal manifestations of hemochromatosis?

What is haemochromatosis ?
It is an iron storage disease that is characterised by increased Intestinal iron absorption.There is deposition of iron in parenchymal cels with tissue damage -The disease is clinically manifested as the following
  • Excessive skin pigmentation (due to increased melanin and iron .Melanin is responsible for bronzing of skin
  • Diabetes mellitus (bronze diabetes)
  • Arthropathy
  • Cardiac involvement- Congestive cardia faiure or cardiomyopathy
  • Hepatic involvement - Cirrhosis or hepatocellular carcinoma with hepatocellular failure
  • Loss of libido and testicular atrophy.
What are the cause of death in Hemochromatosis
  • CCF
  • Hepatocellular failure
  • Hepatocellular carcinoma
What is the treatment of hemochromatosis
  • Phlebotomy.
  • Iron chelation by desferrioxamme.
  • Treatment of CCF. hepato-cellular failure .diabetes mellilus etc.

What are the functions of the Skin ?

  • Protection:Skin provide protection from  Physical, Chemical, Infections agents
  • Thermoregulation: Blood vessels and Eccrine sweat glands are involved in thermoregulation
  • Homeostasis of water, electrolytes and protein
  • Lubrication and waterproofing: Sebum secreted by sebaceous glands
  • Sensations - specialized nerve endings act as sensory organs
  • Immunological: Lymphocytes, macrophages, Langerhans cells are involved in immunity
  • Synthesis of vitamin D by keratinocyte
  • Body odour: Apocrine glands produce body odour
  • Protection and prising: Nails are involved in this function
  • Calorie reserve: Subcutaneous fat preserve body heat
  • Psychosocial: Cosmetic functions -skin, lips, hair, nails.

What is melasma or chloasma ?

This is a frequently seen hyperpigmentation in young females
It is rare in males
Chloasma may be frequently precipitated by pregnancy also called as Chloasma gravidarum or mask of pregnancy
They may be precipitated by oral contraceptive pills
The pigmentation is generally seen on the malar prominence and bridge of nose
They are frequently symmetrical

Cardinal features of addisons disease

Following are the cardinal features of Addison s disease
Commonly the patient is female and suffers from :
  • Asthenia,hypotenstion.hyperpigmentation are the major manifestations
The minor manifestations are
  • Anorexia, malaise, weight loss.
  • Decreased body hairs
  • Hyperkalaemia.
  • Hvpoglycaemia
  • Nausea, vomiting.
  • Chronic fatigue syndrome.
  • Acute adrenal crisis.
Pigmentation in addison's disease .
  • Pigmentation in addisons disease is due to increased pituitary MSH andACTH secretions
  • Initially there is tanning after exposure to the sun.
  • Later there is tanning noticed pressure points (elbow).
  • Normally  pigmented areas like areola ,knuckles palmar creases and scars become more pigmented
  • Mucous membrane pigmentation can occur (genitals and oral cavity)
  • There may be areas of vililigo
Differentiation between primary and secondary adrenocortical insufficiency
In primary (Addison s disease) cases, there are features of.
  • Absence of hypothyroidism and hypogonadism
  • High plasma ACTH level.
In secondary hypofunction, there are :
  • Absence of pigmentation.
  • Presence of hypothyroidism and hypogonadism
  • Low plasma ACTH level.

What are the systemic diseases with Pruritus?

Pruritus is a prominent symptom in the following illness
  • Obstructive jaundice
  • CRF
  • Diabetes mellitus
  • Hypothyroidism
  • Hyperthyroidism
  • Polycythemia vera
  • Internal malignancy-lymphoma, myeloma
  • Carcinoid syndrome
  • Psychosis

Skin lesions that give clue to the underlying diagnosis

Certain skin lesions are important as they give clue to some underlying illness
Purplish striae is seen over the lower, anterior abdominal wall in Cushing's syndrome.
Erythema marginatum is a cutaneous sign in rheumatic fever.

Purpuras, ecchymosis are seen in ITP, Henoch-Schonlein purpura, coagulation defects, Leukemias.
Adenoma sebaceum ,Shagreen patch and  Ash leaf macules are seen in Tuberous sclerosis
Hemangiomas present externally may also be present in the CNS.
Telangiectasia are seen in ataxia telangiectasia .Multiple telangiectasias are seen in Osler-Rendu Weber syndrome.
 Osler-Rendu Weber syndrome there is AV malformations  found in
  • Lung
  • Liver
  • CNS 
  • Mucous membranes.
Spider naevi indicate decompensated liver disease ,SVC obstruction.
Palmar erythema is seen in
  • Decompensated liver disease
  • Chronic febrile illness
  • Chronic leukemias
  • Polycythemia 
  • Rheumatoid arthritis  
  • Thyrotoxicosis
  • Chronic alcohol intake 
  • Physiological states like pregnancy.
Erythema nodosum  is a nonspecific skin marker and it may be seen in conditions like primary complex, sarcoidosis and with certain drugs

Multiple neurofibromas are seen in von Recklinghausen's disease

Xanthomas indicate underlying Hyperlipidemia

Malignant tumours of the skin are Squamous cell carcinoma, basal cell carcinoma, malignant melanoma.
Pigmentation of the mucous membrane of the oral cavity is seen in

Addison's disease, and in Peutz-Jeghers syndrome which is associated with perioral pigmentation and polyposis of colon.
A tuft of hair or a lipoma over the lower lumbar region in the back may give clue to the presence of spina bifida.

Cutaneous manifesation of gastrointestinal disease

  • Pigmentation of peri oral lips and hand is seen in Peute Jegher s syndrome
  • Derma1 cyst-Gardener's syndrome
  • Pyoderma gangrenosum-ulcerative colitis
  • Dematitis herpetiformis –Gluten sensitive enteropathy
  • Eczematous lesion of acral parts-acrodermatitis enteropathica
  • Cirrhosis liver is characterised by pruritus ,Palmar erythema, purpura and jaundice
  • Migratory thrombophlebitis-Ca head of pancreas-Trousseau's syndrome
  • Dermatomyositis-GI malignancy
  • Pityriasis rotunda-Hepatocellular carcinoma, hyperpigmented scaly lesions over trunk and thighs.
  • Palmar tylosis-Ca esophagus'
  • Necrolytic migratory erythema-glugonoma
  • Flushing of skin-carcinoid syndrome.

Cutaneous manifestations of Cardiovascular Diseases

Infective endocarditis is characterised by 
  • Osier's nodes
  • Janeway lesions
Rheumatic fever has the following cutaneous manifestations
  • Erythema marginatum
  • Erythema nodosum
  • Subcutaneous nodules

What are Neurocutaneous diseases?

Cutaneous manifestations that are characteristic of certain neurological disease are described here
Tuberous sclerosis  is characterised by the following lesions
  • Adenoma sebaceum/Angiofibroma of face 
  • Subungual  fibroma
  • Shagreen patch
  • Leafy macule
Von Recklinghausen's disease
  • Multiple cutaneous and subcutaneous neurofibroma
  • Cafe-au-lait spots > 6 in no: >1.5 cm in size
  • Axillary freckles
Sturge Weber syndrome
Capillary hemangioma in trigeminal nerve distribution is seen in Encephalo-trigeminal angiomatosis
Hereditary hemorrhagic telangiectasia
There is multiple telangiectasia of skin, mucosa, and pulmonary system

Hypopigmentation of skin

Generalised absence of skin pigmentation is seen in Albinism 
Following are the syndromes with albinism
Chediac higashi syndrome also called as phagocytic deficiency disease
Phenylketonuria a condition characterised by inborn error of metabolism
Patchy absence of skin pigmentation may be due to Vitiligo which is seen in 
  • Idiopathic cases
  • Autoimmune disease
  • Thyroid disease
  • Pernicious anemia
In the presence of vitiligo always rule out immune causes in that patient
What are the causes of Hypopigmented Lesions
  • Early vitiligo
  • Leukoderma-early
  • Hansen's disease
  • Nevus anemicus
  • Leafy macules-tuberous sclerosis
  • Tinea versicolor
  • Pityriasis alba
Circumscribed hypopigmented lesions of the skin may be seen in Hansens disease ( Tuberculoid or Borderline Tuberculoid types) and Tinea versicoior.

Causes of cutaneous hyperpigmentation

Patchy hyperpigmentation of the skin is seen in 
  • Pellagra on exposed part to sunlight
  • Porphyria cutanea tarda
  • Scleroderma
  • Chloasma
  • Butterfly rash on face of sle
  • Acanthosis nigricans
  • Fixed drug eruptions
  • Drugs like Chlorpromazine, crofazimine,heavymetals like bismuth and gold
Acanthosis nigricans is a pigmented velvety thickening of skin
Types of Acanthosis nigricans
  • Benign type is seen in - Obesity, Cushing's syndrome, drugs-OCP, nicotinic acid, protease inhibitors
  • Malignant type seen in Internal malignancy
Megaloblastic anemia-hyperpigmentation of hands and face can be seen
Endocrine disorders
  • Addison's disease
  • Cushing's syndrome
  • Ectopic ACTH production.
  • Nelson's syndrome is seen in post adrenelectomy cases
Arsenic poisoning
Common causes of hyperpigmentation are
  • Familial, racial.
  • Sunburn. 
  • Addison'sdisease
  • Hemochromatosis
  • Peutz-Jeghcrs syndrome.
  • Chronic kala-azar.
  • clofazimine (red), busulphan.
  • Pellagra.
  • Chronic arsenical poisoning.
  • Facial pigmentation in chloasma or melasma. SLE
  • Porphyria (cutanea tarda) 
What are the sites examined for increased pigmentation :
  • Face.
  • Inside the oral cavity, specially cheeks and palate 
  • Palmar creases
  • General skin surface 
  • Pressure points
  • Normally pigmented area like areola
  • Sun exposed area
  • Recent scars
  • Palms and sole