1. 5) Corticosteroids – systemic therapy, indications, contraindications, side effects)
Systemic steroids are also called corticosteroids, glucocorticoids or cortisones. They are synthetic
derivatives of the natural steroid, cortisol, which is produced by the adrenal glands. They are called
systemic if the steroids are taken by mouth or given by injection, whereas topical steroids are
applied directly to the skin.
Systemic steroids include prednisone, prednisolone, methylprednisolone, beclamethasone,
betamethasone, dexamethasone, fludrocortisone, hydrocortisone and triamcinolone.
Systemic steroids vary in strength. The beneficial effects as well as the side effects are
proportional to the dose taken. Steroid dose is commonly characterised into:
• Low dose (e.g. <10mg/day of prednisone)
• Medium dose (e.g. 10-20 mg/day of prednisone)
• High dose (e.g. >20mg/day of prednisone, sometimes more than 100mg/day).
Treatment for less than one month is considered short term treatment. Treatment continuing for
more than 3 months is regarded as long term, and results in the majority of undesirable side
effects.
Corticosteroids for a few days or weeks are relatively safe, e.g. for acute dermatitis.
One must always carefully assess the severity of the underlying disorder, the gains that can be
expected from corticosteroid therapy, and the risks. Excessive corticosteroid use is one of the
causes of Cushing syndrome.
Systemic corticosteroids
Steroids are required systemically for:
– acute and chronic disabling bullous disorders including pemphigus vulgaris, bullous pemphigoid,
pemphigoid gestationis
– connective tissue diseases - systemic lupus erythematosus, dermatomyositis, Wegener's
granulomatosis, relapsing polychondritis
– acute steroid sensitive disorders, e.g. severe acute allergic contact dermatitis where the allergen
is known and can be avoided to prevent relapse on cessation of steroids
– severe, widespread, inflammatory atopic eczema where acute control is required (care is
necessary on cessation of the oral steroids to prevent a widespread severe relapse)
– others - severe lichen planus, urticaria, pyoderma gangrenosum, Sweet's disease, Behcet's and
severe vasculitis
Oral steroids are perfectly satisfactory in the majority of dermatology patients who are rarely ill
enough to require either intramuscular or intravenous administration.
The skin is prone to the following adverse effects from prolonged courses or high doses of
systemic steroids. These may include:
• Increased risk of skin infections such as bacterial infections (e.g. cellulitis) and fungal
infections (e.g. tinea, candida)
• Skin thinning resulting in easy bruising (purpura), skin tearing after minor injury, slow
healing, and stretch marks (striae).
• Seroid acne: clusters of small spots on face, chest and upper back.
• Subcutaneous lipoatrophy (loss of fat under the skin surface) from injected steroid that does
not go deep enough into the muscle.

2. Nearly everyone on systemic steroids for more than a month suffers from some adverse effects.
These may include any of the following problems, which are not listed in any particular order of
importance.
• Reduction of cortisol production. During and after steroid treatment, the adrenal gland
produces less of its own cortisol, resulting from hypopituitary-pituitary-adrenal (HPA) axis
suppression. For up to twelve months after the steroids are stopped, the lack of steroid
response to stress such as infection or trauma could result in severe illness.
• Osteoporosis (thinning of the bones) particularly in smokers, postmenopausal women, the
elderly, those who are underweight or immobile, and patients with diabetes or lung
problems. Osteoporosis may result in fractures of the spine, ribs or hip joint with minimal
trauma. These occur after the first year in 10-20% of patients treated with more than 7.5mg
prednisone daily. It is estimated that up to 50% of patients on long term oral corticosteroids
will develop bone fractures.
• Reduction in growth in children, which may not catch up when the steroids are discontinued
(but it usually does).
• Muscle weakness, especially of the shoulder muscles and thighs.
• Rarely, avascular necrosis of the femoral head (destruction of the hip joint).
• Precipitation or aggravation of diabetes mellitus (high blood sugar).
• Increase in circulating blood fat (triglycerides).
• Redistribution of body fat: moon face, buffalo hump and truncal obesity.
• Salt retention: leg swelling, raised blood pressure, weight increase and heart failure.
• Shakiness and tremor.
• Eye disease, particularly glaucoma (increased intraocular pressure) and posterior
subcapsular cataracts.
• Psychological effects including insomnia, mood changes, increased energy, excitement,
delirium or depression.
• Headaches and raised intracranial pressure.
• Increased susceptibility to internal infections, especially when high doses are prescribed
(e.g. tuberculosis).
• Peptic ulceration, especially common in those also taking anti-inflammatory medications.
• There are also side effects from reducing the dose; these include tiredness, headaches,
muscle and joint aches and depression.
Monitoring during steroid treatment
If you have been prescribed systemic steroids, make sure you understand how to take the
medicine safely. Regular monitoring during treatment may include:
• Blood pressure
• Body weight
• Blood sugar
Avoid oral live polio vaccination. It is safe and advisable to have other routine immunisations such
as annual influenza vaccination.
Discuss any side effects you may experience with your doctor.

3. Prevention of osteoporosis
Specific measures to reduce the chance of steroid-induced osteoporosis should be considered for
patients that have taken or are expected to take 10 mg or more of prednisone or prednisolone
each day for a period of three months or longer.
A DEXA bone scan measures bone density. Bone density gives an indication of the risk of fracture
due to bone loss. Arrange to have a scan as you start systemic steroids, and it should be repeated
every year or as recommended by your physician.
Preventative treatment includes the following medications:
• Calcium tablets 500 to 1000 mg per day
• Vitamin D in various forms including monthly cholecalciferol 50,000 units (1.25 mg)
• Oestrogen i.e. hormone replacement tablets in females that have had early menopause
• Bisphosphonates (alendronate, etidronate); these are prescribed for patients at especially
high risk of fracture.
Some patients are poor candidates for corticosteroid systemic or locally injected corticosteroid
therapy because of conditions that may be made worse by the drugs. The most common of these
are discussed in this article:
• Diabetes: These drugs are called glucocorticoids because of their effect on blood sugar.
Use of systemic or locally injected glucocorticoids like prednisone causes a rise in blood
sugar levels. This can be in patients with known diabetes or in patients with pre-diabetes. It
is not uncommon in hospitalized patients to find quite high blood sugars in people not
previously diagnosed with diabetes when they are getting high dose prednisone as therapy.
This can sometimes require insulin therapy. In general physicians tend to try to avoid
systemic use of glucocorticoids in patients with diabetes.
• Tuberculosis: Latent TB, namely a positive skin test for TB, even in patients who have
received a course of therapy with anti-tubercular drugs, can lead to reactivation of the TB,
and is a strong contraindication to systemic therapy.
• Psychiatric disease: A common side effect of high dose systemic corticosteroid therapy is
some degree of anxiety, insomnia and in children hyperactivity. More serious psychosis and
severe depression are less common but do occur more often in patients with prior serious
psychiatric problems.

4. 8)Configuration of skin lesions
http://www.merckmanuals.com/professional/sec10/ch109/ch109b.ht
ml#sec10-ch109-ch109b-26
9) Simple diagnostic tests (Auspitz phenomenon, dermographism, Nikolski test,
Darrier’s sign, Koebner’s phenomenon, Tzanck’s test etc)
Dermatographism is the appearance of an urticarial wheal after focal pressure (eg, stroking or
scratching the skin) in the distribution of the pressure. Up to 5% of normal patients may exhibit this
sign, which is a form of physical urticaria.
Darier's sign refers to rapid swelling of a lesion when stroked. It occurs in patients with urticaria
pigmentosa or mastocytosis.
Nikolsky's sign is epidermal shearing that occurs with gentle lateral pressure on seemingly
uninvolved skin in patients with toxic epidermal necrolysis and some autoimmune bullous
diseases.
Auspitz sign is the appearance of pinpoint bleeding after scale is removed from plaques in
psoriasis.
Koebner phenomenon describes the development of lesions within areas of trauma (eg, caused
by scratching, rubbing, injury). Psoriasis frequently exhibits this phenomenon, as may lichen
planus.
the Tzanck test, is scraping of an ulcer base to look for Tzanck cells.
Tzanck cells (multinucleated giant cells) are found in:
• Herpes simplex[1]
• Varicella and herpes zoster
• Pemphigus vulgaris
• Cytomegalovirus
It is named after Arnault Tzanck (1886-1954), a French dermatologist.

5. 10) Anaphylactic shock, Hoigne syndrome
Anaphylaxis is an acute multi-system severe type I hypersensitivity reaction.
Skin involvement may include generalized hives, itchiness, flushing, and swelling of the lips,
tongue or throat
Respiratory symptoms may include shortness of breath, wheezes or stridor, and low oxygen
Gastrointestinal symptoms may include crampy abdominal pain, diarrhea, and vomiting
Due to the presence of histamine releasing cells in the heart, coronary artery spasm may occur
with subsequent myocardial infarction or dysrhythmia
A drop in blood pressure may result in a feeling of lightheadedness and loss of consciousness.
There may be a loss of bladder control and muscle tone
Anaphylaxis can occur in response to any allergen. Common triggers include insect bites or stings,
foods (peanut, fish, milk), medication and latex rubber
Any medication may potentially trigger anaphylaxis. The most common to do so include antibiotics
(β-lactam antibiotics in particular), aspirin, ibuprofen, and other analgesics
Anaphylaxis is a severe, whole-body allergic reaction. After an initial exposure "sensitizing dose" to
a substance like bee sting toxin, the person's immune system becomes sensitized to that allergen.
On a subsequent exposure "shocking dose", an allergic reaction occurs. This reaction is sudden,
severe, and involves the whole body.
Classified as a type I hypersensitivity, anaphylaxis is triggered when an antigen binds to IgE
antibodies on mast cells based in connective tissue throughout the body, which leads
to degranulation of the mast cells (the release of inflammatory mediators).[19] These immune
mediators cause many symptoms, including common symptoms of allergic reactions, such as
itching, hives, and swelling. Anaphylactic shock is an allergic reaction to an antigen that
causes circulatory collapse and suffocation due to bronchial and tracheal swelling.
Different classes of antibodies are produced by B cells to bind and destroy substances that the
immune system has identified as potentially dangerous pathogens. Each B cell produces
thousands of identical antibodies that can attack a single, small part of a pathogen. In susceptible
individuals, antibodies may be produced against innocuous antigens or allergens, such as
components of common foods or plants. One class, the IgE antibodies, can trigger anaphylaxis.
Production of IgE antibodies may persist for months, even in the complete absence of the allergen.
These IgE antibodies associate with a receptor on the surface of mast cells. If the antibody binds to
its specific antigen, then the antibody triggers degranulation of the mast cell.
Mast cells become the major effector cells for immediate hypersensitivity and chronic allergic
reactions
Anaphylaxis is diagnosed with high likelihood based on clinical criteria. These criteria are fulfilled
when any one of the following three is true:[14]
1. Symptom onset within minutes to several hours of allergen exposure with involvement of
the skin or mucosal tissue and any of the following: hives, itchiness, or swelling of the
airway; plus either respiratory difficulty or a low blood pressure.
2. Any two or more of the following symptoms within minutes to several hours of allergen
exposure: a. Involvement of the skin or mucosa b. Respiratory difficulties c. Low blood
pressure d. Gastrointestinal symptoms
3. Low blood pressure within minutes to several hours after exposure to known allergen

6. Apart from its clinical features, blood tests for tryptase (released from mast cells) might be useful in
diagnosing anaphylaxis.
Allergy testing may help in determining what triggered the anaphylaxis. In this setting, skin allergy
testing (with or without patch testing)
Anaphylaxis is a medical emergency which may require resuscitation measures such as airway
management, supplemental oxygen, large volumes of intravenous fluids, and close monitoring.
[9] Administration of epinephrine is the treatment of choice with antihistamines and steroids often
used as adjuncts.
Hoigne's syndrome
Hoigne's syndrome is a pseudoanaphylactic or pseudoallergic reaction that occurs after
intramuscular administration of penicillin G procaine or benzathine. These are usually embolic toxic
reactions possibly due to vascular occlusion by large crystals of the penicillin salts.
CASE REPORT: A 44-year-old woman received 1,200,000 U.I. of intramuscular procaine penicillin
once daily for treatment of acute amygdalitis. Immediately after the second dose the patient
developed mental confusion, visual and auditory hallucinations, perceived changes of body shape,
swelling of the tongue and a fear of impending death. Penicillin allergy study (serum-specific IgE
levels, skin tests and provocation test) was performed. The diagnosis of Hoigne's syndrome was
confirmed by negative oral challenge test with penicillin.
CONCLUSIONS: Hoigne's syndrome is a pseudoanaphylactic reaction that must be differentiated
from authentic anaphylactic shock due to penicillin. This distinction allows treatment to be
continued in Hoigne's syndrome, whereas it is contraindicated in anaphylactic shock.

7. 11) Basic types of immunologic reaction
Coombs and Gell classification
Comparison of hypersensitivity types
Type Alternative names Often mentioned disorders Mediators
• Atopy
• Anaphylaxis • IgE
I Allergy (immediate)
• Asthma
• Autoimmune hemolytic
anemia
• Thrombocytopenia
• Erythroblastosis fetalis
• Goodpasture's • IgM or IgG
syndrome
II Cytotoxic, antibody-dependent • (Complement
• Graves' disease *see )
type V explanation
below
• Myasthenia Gravis *see
type V explanation
below
• Serum sickness
• IgG
• Arthus reaction
III Immune complex disease • (Complement
• Systemic lupus )
erythematosus (SLE)
• Contact dermatitis
Delayed-type • Mantoux test
hypersensitivity (DTH), cell-mediated • Chronic transplant • T-cells
IV
immune memory response, antibody- rejection
independent • Multiple sclerosis

8. 12) Phototherapy – principles
phototherapy is a treatment that uses artificial light wavelengths to treat skin conditions. It utilizes
wavelengths from the ultraviolet part of the light spectrum at a higher intensity while leaving out the
other wavelengths in light.
Skin Conditions
• Phototherapy is used to treat skin conditions such as psoriasis, eczema, vitiligo and itchy
skin. Phototherapy is not designed to treat all forms of psoriasis and eczema.
Acne vulgaris
Sunlight was long known to improve acne, and this was thought to be due to antibacterial and
other effects of the ultraviolet spectrum which cannot be used as a long-term treatment due to the
likelihood of skin damage.[2]
It was found that some of the visible violet light present in sunlight (in the range 415–430 nm)
activates a porphyrin (Coproporphyrin III) in Propionibacterium acnes which damages and
ultimately kills the bacteria by releasing singlet oxygen. A total of 320 J/cm2 of light within this
range renders the bacteria non-viable.[3]
The use of light therapy for three consecutive days has been shown to reduce the bacteria in the
pores by 99.9%.[citation needed] Since there are few porphyrins naturally found in the skin, the
treatment is believed safe except in patients with porphyria;[4] although eye protection is used due
to light-sensitive chemicals in the retina. The light is usually created by superluminous LEDs.
Psoriasis and eczema
A feature of psoriasis is localized inflammation mediated by the immune system. UV radiation is
known to suppress the immune system and reduce inflammatory responses. Light therapy for skin
conditions likepsoriasis or eczema use UV-A (315–400 nm wavelength) or UV-B (280–315 nm
wavelength) light waves. UV-A, combined with a drug taken orally, is known as PUVA treatment.
Narrow band UV-B is the 310 nm wavelength and is given as a light therapy treatment rather than
full spectrum UV-B.
Tanning
Tanning is caused by the effects of two different spectrums of ultraviolet radiation: UV-A and UV-B.
Photodynamic therapy
Visible blue light is used with aminolevulinic acid for the treatment of actinic keratosis.
PUVA is a psoralen + UVA treatment for eczema, psoriasis, graft-versus-host disease and vitiligo,
and mycosis fungoides
The psoralen is applied or taken orally to sensitize the skin, then the skin is exposed to UVA. Long
term use has been associated with higher rates of skin cancer
Psoralens are photosensitizing agents found in plants.
Psoralens are taken systemically or can be applied directly to the skin. The psoralens allow a
relatively lower dose of UVA to be used. When they are combined with exposure to UVA in PUVA,
they are highly effective at clearing psoriasis.

9. 13) Advantages and dangers of topical corticosteroid treatment
Dermatology is one of the few disciplines in which we are able to apply therapy directly to
the target site. The concentration, the vehicle and the frequency of application can all be
altered according to the response, which can easily be monitored.
Corticosteroids have an important role because of their anti- inflammatory and immunosuppressive
effects and also their anti-proliferative effects on keratinocytes. They can suppress collagen
synthesis by fibroblasts, but this may lead to adverse effects. Conversely, this effect can help in the
treatment of keloid scars.
Skin disease
In general, acute inflammatory eruptions respond well to mild/moderate strength topical steroids
(Class I and II). Chronic, thickened or hyperkeratotic dermatoses may require potent or very potent
steroids (Class III and IV). Table 2 lists the corticosteroid-responsive skin diseases according to
likely response. The less responsive the disease, the greater the potency of the corticosteroid that
may be required.
Vehicle
For a given strength of the same steroid, ointments are more potent than creams. The occlusive
nature of ointment enhances steroid penetration. Ointment is often used for dry, fissured and
lichenified skin disease because of its moisturising effect.
Creams (oil in water emulsions) may be drying and thus more suitable for acute and subacute
weeping lesions. They are the most suitable vehicle for the moist and intertriginous (flexural) areas.
Creams require the addition of emulsifiers and preservatives that have the potential to sensitise
and cause allergic reactions.
For the scalp, steroids are often delivered in a lotion or gel. These vehicles lack the moisturising
benefit of either creams or ointments. Propylene glycol can act as a penetration enhancer. By
using it in a vehicle, the delivery of the topical steroid can be increased.
Occlusion
The efficacy of steroids can be increased by application under occlusion. This increases hydration
of the skin and enhances penetration. However, there is an increased risk of adverse effects if the
use of steroid under occlusion is prolonged. The occluding materials can include polythene gloves,
plastic film (such as `Gladwrap') and bio-occlusive dressings e.g. hydrocolloid.
Region or sites
The thickness of the stratum corneum, local occlusive factors, warmth and moisture are among the
factors that can increase corticosteroid penetration and also the risk of adverse effects. In
descending order of ease of penetration are mucous membrane, scrotum, submammary, axillary
and perineal flexures, eyelids, face, chest and back, upper arms and legs, lower arms and legs,
dorsum of hands and feet, palmar and plantar skin and nails.1
As a rule, Class I steroids are preferred for the face and flexures. If a stronger corticosteroid is
required, short-term (1-2 weeks) use is recommended. In contrast, palms and soles tend to require
Class III or IV steroids as there is a thick stratum corneum and frequent accidental removal of the
steroid may occur. On occasion, two or more different formulations may be required for different
regions of the body.
Age
Infants have an increased body surface to weight ratio. Premature babies and the elderly have
relatively thin skin so steroid penetration is enhanced. The lower potency steroids are used first in
this group. Particular care should be given when steroids are used in the nappy area.
If treatment involves application to a large proportion of the body surface area, low- to medium-
strength steroids are preferred because of the risk of extensive absorption.

10. Other guidelines
1. Topical steroids should be stopped when the skin disease has resolved. They are not used for
prevention of disease.
2. If possible, intermittent therapy is preferred to continuous application for long-term use. This is to
reduce both tachyphylaxis and the risk of adverse effects.
3. Prolonged use should be avoided, where possible, on the face and the flexures.
4. Some people benefit from using a more potent steroid first and then changing to a lower potency
as the condition improves.
Adverse effects
In general, the greater the potency, the greater the risk of adverse effects (Table 3).
Systemic adverse effects may occur with the use of topical steroids. The risk factors include use in
infants and children, prolonged and extensive use, use of high-potency steroids, use over large
areas and use under occlusion. The adverse effects include the standard ones of adrenal
suppression, growth retardation, Cushing's syndrome and hypertension. Cataracts and glaucoma
have been reported with periorbital use.
Intralesional therapy
The steroid is injected directly into the lesion. The common indications include recalcitrant lesions
of nodular prurigo, keloid scars, acne cysts, discoid lupus erythematosus, hypertrophic lichen
planus, alopecia areata and granuloma annulare.
Adverse effects related to topical corticosteroids
Skin atrophy, stellate scar and striae
Purpura and haemorrhage
Telangiectasia
Periocular, perioral dermatitis of the face
Folliculitis
Acneiform eruptions
Masking and aggravating fungal infections
Delayed wound healing
Hypertrichosis
Secondary infection and aggravating existing bacterial infections
Contact dermatitis
- preservatives
- other ingredients in vehicles
- corticosteroid itself

11. 16) Basic histologic terms (orthokeratosis, hyperkeratosis, akanthosis, akantholysis,
granuloma, dyskeratosis, blisters)
Orthokeratosis
Formation of an anuclear keratin layer, as in the normal epidermis
Hyperkeratosis is thickening of the stratum corneum, often associated with a qualitative
abnormality of the keratin.
It can be caused by vitamin A deficiency or chronic exposure to arsenic.
Hyperkeratosis is a thickening of the horny layer, usually accompanied by an increase also in the
granular layer. As the horny layer normally varies greatly in thickness in different sites, some
experience is needed to assess minor degrees of hyperkeratosis.
Acanthosis is diffuse epidermal hyperplasia. Acanthosis implies increased thickness of stratum
spinosum.
Acantholysis is the loss of intercellular connections, such as desmosomes, resulting in loss of
cohesion between keratinocytes[1], seen in diseases such as pemphigus vulgaris. It is absent
in bullous pemphigoid, making it useful for differential diagnosis.
This histological feature is also seen in herpes simplex infections (HSV 1 and 2).
Granuloma is a medical term for a roughly spherical mass of chronic immune cells that forms
when the immune system attempts to wall off substances perceived as foreign but unable to
eliminate. Such substances include infectious organisms such as bacteria and fungi, as well as
other materials such as keratin and suturefragments
Doctors occasionally use the term "granuloma" loosely to mean "a small nodule". Since a small
nodule can represent anything from a harmless nevus to a malignant tumor, this usage is non-
specific. Correct use of "granuloma" requires a pathologist to examine surgically removed and
specially colored (stained) tissue under a microscope. The following is a more technical definition
of a granuloma.
In pathology, a granuloma (classical Greek plural granulomata; modern anglicized
plural granulomas) is an organized collection of macrophages.[4]
Macrophages (also known as histiocytes) define a granuloma. They often, but not invariably, fuse
to form multinucleated giant cells.[5] The macrophages in granulomas are often referred to as
"epithelioid".
All granulomas, regardless of cause, may contain additional cells and matrix. These
include lymphocytes, neutrophils, eosinophils, multinucleated giant
cells, fibroblasts and collagen (fibrosis). The additional cells are sometimes a clue to the cause of
the granuloma.
Granulomas are seen in a wide variety of diseases, both infectious and non-infectious.[1] Infections
that are characterized by granulomas
include tuberculosis, leprosy, histoplasmosis, cryptococcosis,coccidioidomycosis, blastomycosis an
d cat scratch disease. Examples of non-infectious granulomatous diseases
are sarcoidosis, Crohn's disease, berylliosis, Wegener's granulomatosis, Churg-Strauss syndrome,
pulmonary rheumatoid nodules and aspiration of food and other particulate material into the lung.
An important feature of granulomas is whether or not they contain necrosis. Necrosis refers to
dead cells that, under the microscope, appear as a mass of formless debris with no nuclei present.
A related term, "caseation" (literally: turning to cheese) refers to a form of necrosis that, to the
unaided eye (i.e., without a microscope), appears cheese-like ("caseous"), and is typically (but not
uniquely) a feature of the granulomas of tuberculosis. The identification of necrosis in granulomas
is important because granulomas with necrosis tend to have infectious causes. There are several

12. exceptions to this general rule, but it nevertheless remains useful in day-to-day diagnostic
pathology.
Dyskeratosis it is abnormal keratinization occurring prematurely within individual cells or groups of
cells below the stratum corneum.
A blister is a small pocket of fluid within the upper layers of the skin, typically caused by forceful
rubbing (friction), burning, freezing, chemical exposure or infection. Most blisters are filled with a
clear fluid called serum or plasma[1] (aka, "blister water"). However, blisters can be filled
with blood (known as blood blisters) or with pus (if they become infected).

13. 17) Pigment cells, their function, pigments in the skin
Melanocytes
are melanin-producing cells located in the bottom layer (the stratum basale) of the skin'sepidermis,
the middle layer of the eye (the uvea),[1] the inner ear,[2] meninges,[3] bones,[4] and heart.
[5] Melanin is a pigment which is primarily responsible for the color of skin.
Melanin
melanin pigments are derivatives of the amino acid tyrosine. The most common form
of biological melanin iseumelanin, a brown-black polymer of dihydroxyindole carboxylic acids, and
their reduced forms.
There are two different types of eumelanin. The two types are black eumelanin and brown
eumelanin, with black melanin being darker than brown. Black eumelanin is mostly in non-
Europeans and aged Europeans, while brown eumelanin is in mostly young Europeans.
Another common form of melanin is pheomelanin, a red-brown polymerof benzothiazine units
largely responsible for red hair and freckles. Pheomelanin is also found in hair and skin and is both
in lighter skinned humans and darker skinned humans. Pheomelanin imparts a pink to red hue
and, thus, is found in particularly large quantities in red hair. Pheomelanin is particularly
concentrated in the lips, areola, nipples, glans of the penis.
Neuromelanin is the dark pigment present in pigment bearing neurons of four deep brain nuclei:
the substantia nigra (in Latin, literally "black substance") - Pars Compacta part, the locus
coeruleus ("blue spot"), the dorsal motor nucleus of the vagus nerve (cranial nerve X), and the
median raphe nucleus of the pons. Both the substantia nigra and locus coeruleus can be easily
identified grossly at the time of autopsy because of their dark pigmentation.
The increased production of melanin in human skin is called melanogenesis. Production of melanin
is stimulated by DNA damage induced by UVB-radiation,[1] and it leads to a delayed development
of a tan. This melanogenesis-based tan takes more time to develop, but it is long lasting
In humans, melanin is the primary determinant of skin color. It is also found in hair, the pigmented
tissue underlying the iris of the eye, and the stria vascularis of the inner ear. In the brain, tissues
with melanin include the medulla and zona reticularis of the adrenal gland, and pigment-bearing
neurons within areas of the brainstem, such as the locus coeruleus and the substantia nigra.

14. 20) Basic examination in phlebology
A Phlebologist is a medical specialist in the diagnosis and treatment of disorders of venous origin.
The specialty of Phlebology has developed to enable physicians sharing an interest in venous
disease but with a variety of backgrounds such as dermatology, vascular surgery, haematology, or
general medicine, to share knowledge and experience. Diagnostic techniques used include the
history and physical examination, venous imaging techniques and laboratory evaluation related to
venous thromboembolism. The American Medical Association has added phlebology to their list of
self-designated practice specialties.
A significant part of a phlebologist's work is involved with the treatment of superficial venous
disease, frequently of the leg. Conditions often treated include varicose veins and spider veins
(telangiectasia). Other conditions managed by Phlebologists include deep venous thrombosis
(DVT), superficial thrombophlebitis, chronic leg ulceration, and venous malformations.
Venography (also called phlebography) is a procedure in which an x-ray of the veins, a
venogram, is taken after a special dye is injected into the bone marrow or veins. The dye has to be
injected constantly via a catheter. Therefore a venography is an invasive procedure. Normally the
catheter is entered by the groin and the doctor moves it to the required place navigating through
the vascular system.
It is the Gold standard for diagnosing acute deep venous thrombosis and chronic cerebrospinal
venous insufficiency although its use has been largely supplanted by the less invasive duplex
ultrasonography.
Venography can also be used to distinguish blood clots from obstructions in the veins, to evaluate
congenital vein problems, to see how the deep leg vein valves are working, or to identify a vein for
arterial bypass grafting.
Areas of the venous system performed include lower extremities, [Inferior vena cava], upper
extremities.
A Doppler ultrasound is often the procedure of choice for detecting deep vein thrombosis (DVT).
This test uses reflected sound waves to show doctors how blood is flowing through veins and
arteries. It is very effective in detecting clots.
DVT is extremely difficult to detect because its symptoms are similar to those of many other
physical conditions. Doppler ultrasounds allow doctors to see how fast blood is flowing in veins and
arteries, thus helping them to determine if a patient actually has DVT.
Venous duplex ultrasound uses high-frequency ultrasound to analyze blood flow inside veins in the
arms and legs.