5) Corticosteroids – systemic therapy, indications, contraindications, side effects)Systemic steroids are also called cort...
Nearly everyone on systemic steroids for more than a month suffers from some adverse effects.These may include any of the ...
Prevention of osteoporosisSpecific measures to reduce the chance of steroid-induced osteoporosis should be considered forp...
8)Configuration of skin lesionshttp://www.merckmanuals.com/professional/sec10/ch109/ch109b.html#sec10-ch109-ch109b-26   9)...
10) Anaphylactic shock, Hoigne syndromeAnaphylaxis is an acute multi-system severe type I hypersensitivity reaction.Skin i...
Apart from its clinical features, blood tests for tryptase (released from mast cells) might be useful indiagnosing anaphyl...
11) Basic types of immunologic reactionCoombs and Gell classification                             Comparison of hypersensi...
12) Phototherapy – principlesphototherapy is a treatment that uses artificial light wavelengths to treat skin conditions. ...
13) Advantages and dangers of topical corticosteroid treatment       Dermatology is one of the few disciplines in which we...
Other guidelines1. Topical steroids should be stopped when the skin disease has resolved. They are not used forprevention ...
16) Basic histologic terms (orthokeratosis, hyperkeratosis, akanthosis, akantholysis,   granuloma, dyskeratosis, blisters)...
exceptions to this general rule, but it nevertheless remains useful in day-to-day diagnosticpathology.Dyskeratosis it is a...
17) Pigment cells, their function, pigments in the skinMelanocytesare melanin-producing cells located in the bottom layer ...
20) Basic examination in phlebologyA Phlebologist is a medical specialist in the diagnosis and treatment of disorders of v...
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  1. 1. 5) Corticosteroids – systemic therapy, indications, contraindications, side effects)Systemic steroids are also called corticosteroids, glucocorticoids or cortisones. They are syntheticderivatives of the natural steroid, cortisol, which is produced by the adrenal glands. They are calledsystemic if the steroids are taken by mouth or given by injection, whereas topical steroids areapplied 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 areproportional 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 formore than 3 months is regarded as long term, and results in the majority of undesirable sideeffects.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 beexpected from corticosteroid therapy, and the risks. Excessive corticosteroid use is one of thecauses of Cushing syndrome.Systemic corticosteroidsSteroids are required systemically for:– acute and chronic disabling bullous disorders including pemphigus vulgaris, bullous pemphigoid,pemphigoid gestationis– connective tissue diseases - systemic lupus erythematosus, dermatomyositis, Wegenersgranulomatosis, relapsing polychondritis– acute steroid sensitive disorders, e.g. severe acute allergic contact dermatitis where the allergenis known and can be avoided to prevent relapse on cessation of steroids– severe, widespread, inflammatory atopic eczema where acute control is required (care isnecessary on cessation of the oral steroids to prevent a widespread severe relapse)– others - severe lichen planus, urticaria, pyoderma gangrenosum, Sweets disease, Behcets andsevere vasculitisOral steroids are perfectly satisfactory in the majority of dermatology patients who are rarely illenough to require either intramuscular or intravenous administration.The skin is prone to the following adverse effects from prolonged courses or high doses ofsystemic 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. 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 ofimportance. • 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 treatmentIf you have been prescribed systemic steroids, make sure you understand how to take themedicine safely. Regular monitoring during treatment may include: • Blood pressure • Body weight • Blood sugarAvoid oral live polio vaccination. It is safe and advisable to have other routine immunisations suchas annual influenza vaccination.Discuss any side effects you may experience with your doctor.
  3. 3. Prevention of osteoporosisSpecific measures to reduce the chance of steroid-induced osteoporosis should be considered forpatients that have taken or are expected to take 10 mg or more of prednisone or prednisoloneeach 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 fracturedue to bone loss. Arrange to have a scan as you start systemic steroids, and it should be repeatedevery 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 corticosteroidtherapy because of conditions that may be made worse by the drugs. The most common of theseare 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. 4. 8)Configuration of skin lesionshttp://www.merckmanuals.com/professional/sec10/ch109/ch109b.html#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 orscratching the skin) in the distribution of the pressure. Up to 5% of normal patients may exhibit thissign, which is a form of physical urticaria.Dariers sign refers to rapid swelling of a lesion when stroked. It occurs in patients with urticariapigmentosa or mastocytosis.Nikolskys sign is epidermal shearing that occurs with gentle lateral pressure on seeminglyuninvolved skin in patients with toxic epidermal necrolysis and some autoimmune bullousdiseases.Auspitz sign is the appearance of pinpoint bleeding after scale is removed from plaques inpsoriasis.Koebner phenomenon describes the development of lesions within areas of trauma (eg, causedby scratching, rubbing, injury). Psoriasis frequently exhibits this phenomenon, as may lichenplanus.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 • CytomegalovirusIt is named after Arnault Tzanck (1886-1954), a French dermatologist.
  5. 5. 10) Anaphylactic shock, Hoigne syndromeAnaphylaxis 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 throatRespiratory symptoms may include shortness of breath, wheezes or stridor, and low oxygenGastrointestinal symptoms may include crampy abdominal pain, diarrhea, and vomitingDue to the presence of histamine releasing cells in the heart, coronary artery spasm may occurwith subsequent myocardial infarction or dysrhythmiaA 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 toneAnaphylaxis can occur in response to any allergen. Common triggers include insect bites or stings,foods (peanut, fish, milk), medication and latex rubberAny medication may potentially trigger anaphylaxis. The most common to do so include antibiotics(β-lactam antibiotics in particular), aspirin, ibuprofen, and other analgesicsAnaphylaxis is a severe, whole-body allergic reaction. After an initial exposure "sensitizing dose" toa substance like bee sting toxin, the persons 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 IgEantibodies on mast cells based in connective tissue throughout the body, which leadsto degranulation of the mast cells (the release of inflammatory mediators).[19] These immunemediators cause many symptoms, including common symptoms of allergic reactions, such asitching, hives, and swelling. Anaphylactic shock is an allergic reaction to an antigen thatcauses 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 theimmune system has identified as potentially dangerous pathogens. Each B cell producesthousands of identical antibodies that can attack a single, small part of a pathogen. In susceptibleindividuals, antibodies may be produced against innocuous antigens or allergens, such ascomponents 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 toits specific antigen, then the antibody triggers degranulation of the mast cell.Mast cells become the major effector cells for immediate hypersensitivity and chronic allergicreactionsAnaphylaxis is diagnosed with high likelihood based on clinical criteria. These criteria are fulfilledwhen 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. 6. Apart from its clinical features, blood tests for tryptase (released from mast cells) might be useful indiagnosing anaphylaxis.Allergy testing may help in determining what triggered the anaphylaxis. In this setting, skin allergytesting (with or without patch testing)Anaphylaxis is a medical emergency which may require resuscitation measures such as airwaymanagement, supplemental oxygen, large volumes of intravenous fluids, and close monitoring.[9] Administration of epinephrine is the treatment of choice with antihistamines and steroids oftenused as adjuncts.Hoignes syndromeHoignes syndrome is a pseudoanaphylactic or pseudoallergic reaction that occurs afterintramuscular administration of penicillin G procaine or benzathine. These are usually embolic toxicreactions 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 penicillinonce daily for treatment of acute amygdalitis. Immediately after the second dose the patientdeveloped 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 IgElevels, skin tests and provocation test) was performed. The diagnosis of Hoignes syndrome wasconfirmed by negative oral challenge test with penicillin.CONCLUSIONS: Hoignes syndrome is a pseudoanaphylactic reaction that must be differentiatedfrom authentic anaphylactic shock due to penicillin. This distinction allows treatment to becontinued in Hoignes syndrome, whereas it is contraindicated in anaphylactic shock.
  7. 7. 11) Basic types of immunologic reactionCoombs and Gell classification Comparison of hypersensitivity typesType Alternative names Often mentioned disorders Mediators • Atopy • Anaphylaxis • IgE I Allergy (immediate) • Asthma • Autoimmune hemolytic anemia • Thrombocytopenia • Erythroblastosis fetalis • Goodpastures • 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. 8. 12) Phototherapy – principlesphototherapy is a treatment that uses artificial light wavelengths to treat skin conditions. It utilizeswavelengths from the ultraviolet part of the light spectrum at a higher intensity while leaving out theother 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 vulgarisSunlight was long known to improve acne, and this was thought to be due to antibacterial andother effects of the ultraviolet spectrum which cannot be used as a long-term treatment due to thelikelihood 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 andultimately kills the bacteria by releasing singlet oxygen. A total of 320 J/cm2 of light within thisrange renders the bacteria non-viable.[3]The use of light therapy for three consecutive days has been shown to reduce the bacteria in thepores by 99.9%.[citation needed] Since there are few porphyrins naturally found in the skin, thetreatment is believed safe except in patients with porphyria;[4] although eye protection is used dueto light-sensitive chemicals in the retina. The light is usually created by superluminous LEDs.Psoriasis and eczemaA feature of psoriasis is localized inflammation mediated by the immune system. UV radiation isknown to suppress the immune system and reduce inflammatory responses. Light therapy for skinconditions likepsoriasis or eczema use UV-A (315–400 nm wavelength) or UV-B (280–315 nmwavelength) 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 thanfull spectrum UV-B.TanningTanning is caused by the effects of two different spectrums of ultraviolet radiation: UV-A and UV-B.Photodynamic therapyVisible 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. Longterm use has been associated with higher rates of skin cancerPsoralens are photosensitizing agents found in plants.Psoralens are taken systemically or can be applied directly to the skin. The psoralens allow arelatively 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. 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 immunosuppressiveeffects and also their anti-proliferative effects on keratinocytes. They can suppress collagensynthesis by fibroblasts, but this may lead to adverse effects. Conversely, this effect can help in thetreatment of keloid scars.Skin diseaseIn 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 potentsteroids (Class III and IV). Table 2 lists the corticosteroid-responsive skin diseases according tolikely response. The less responsive the disease, the greater the potency of the corticosteroid thatmay be required.VehicleFor a given strength of the same steroid, ointments are more potent than creams. The occlusivenature of ointment enhances steroid penetration. Ointment is often used for dry, fissured andlichenified skin disease because of its moisturising effect.Creams (oil in water emulsions) may be drying and thus more suitable for acute and subacuteweeping 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 sensitiseand cause allergic reactions.For the scalp, steroids are often delivered in a lotion or gel. These vehicles lack the moisturisingbenefit of either creams or ointments. Propylene glycol can act as a penetration enhancer. Byusing it in a vehicle, the delivery of the topical steroid can be increased.OcclusionThe efficacy of steroids can be increased by application under occlusion. This increases hydrationof the skin and enhances penetration. However, there is an increased risk of adverse effects if theuse 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 sitesThe thickness of the stratum corneum, local occlusive factors, warmth and moisture are among thefactors that can increase corticosteroid penetration and also the risk of adverse effects. Indescending order of ease of penetration are mucous membrane, scrotum, submammary, axillaryand 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.1As a rule, Class I steroids are preferred for the face and flexures. If a stronger corticosteroid isrequired, short-term (1-2 weeks) use is recommended. In contrast, palms and soles tend to requireClass III or IV steroids as there is a thick stratum corneum and frequent accidental removal of thesteroid may occur. On occasion, two or more different formulations may be required for differentregions of the body.AgeInfants have an increased body surface to weight ratio. Premature babies and the elderly haverelatively thin skin so steroid penetration is enhanced. The lower potency steroids are used first inthis 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. 10. Other guidelines1. Topical steroids should be stopped when the skin disease has resolved. They are not used forprevention of disease.2. If possible, intermittent therapy is preferred to continuous application for long-term use. This is toreduce 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 potencyas the condition improves.Adverse effectsIn 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 ininfants and children, prolonged and extensive use, use of high-potency steroids, use over largeareas and use under occlusion. The adverse effects include the standard ones of adrenalsuppression, growth retardation, Cushings syndrome and hypertension. Cataracts and glaucomahave been reported with periorbital use.Intralesional therapyThe steroid is injected directly into the lesion. The common indications include recalcitrant lesionsof nodular prurigo, keloid scars, acne cysts, discoid lupus erythematosus, hypertrophic lichenplanus, alopecia areata and granuloma annulare.Adverse effects related to topical corticosteroidsSkin atrophy, stellate scar and striaePurpura and haemorrhageTelangiectasiaPeriocular, perioral dermatitis of the faceFolliculitisAcneiform eruptionsMasking and aggravating fungal infectionsDelayed wound healingHypertrichosisSecondary infection and aggravating existing bacterial infectionsContact dermatitis- preservatives- other ingredients in vehicles- corticosteroid itself
  11. 11. 16) Basic histologic terms (orthokeratosis, hyperkeratosis, akanthosis, akantholysis, granuloma, dyskeratosis, blisters)OrthokeratosisFormation of an anuclear keratin layer, as in the normal epidermisHyperkeratosis is thickening of the stratum corneum, often associated with a qualitativeabnormality 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 thegranular layer. As the horny layer normally varies greatly in thickness in different sites, someexperience is needed to assess minor degrees of hyperkeratosis.Acanthosis is diffuse epidermal hyperplasia. Acanthosis implies increased thickness of stratumspinosum.Acantholysis is the loss of intercellular connections, such as desmosomes, resulting in loss ofcohesion between keratinocytes[1], seen in diseases such as pemphigus vulgaris. It is absentin 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 formswhen the immune system attempts to wall off substances perceived as foreign but unable toeliminate. Such substances include infectious organisms such as bacteria and fungi, as well asother materials such as keratin and suturefragmentsDoctors occasionally use the term "granuloma" loosely to mean "a small nodule". Since a smallnodule 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 andspecially colored (stained) tissue under a microscope. The following is a more technical definitionof a granuloma.In pathology, a granuloma (classical Greek plural granulomata; modern anglicizedplural granulomas) is an organized collection of macrophages.[4]Macrophages (also known as histiocytes) define a granuloma. They often, but not invariably, fuseto 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. Theseinclude lymphocytes, neutrophils, eosinophils, multinucleated giantcells, fibroblasts and collagen (fibrosis). The additional cells are sometimes a clue to the cause ofthe granuloma.Granulomas are seen in a wide variety of diseases, both infectious and non-infectious.[1] Infectionsthat are characterized by granulomasinclude tuberculosis, leprosy, histoplasmosis, cryptococcosis,coccidioidomycosis, blastomycosis and cat scratch disease. Examples of non-infectious granulomatous diseasesare sarcoidosis, Crohns disease, berylliosis, Wegeners 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 todead 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 theunaided eye (i.e., without a microscope), appears cheese-like ("caseous"), and is typically (but notuniquely) a feature of the granulomas of tuberculosis. The identification of necrosis in granulomasis important because granulomas with necrosis tend to have infectious causes. There are several
  12. 12. exceptions to this general rule, but it nevertheless remains useful in day-to-day diagnosticpathology.Dyskeratosis it is abnormal keratinization occurring prematurely within individual cells or groups ofcells below the stratum corneum.A blister is a small pocket of fluid within the upper layers of the skin, typically caused by forcefulrubbing (friction), burning, freezing, chemical exposure or infection. Most blisters are filled with aclear fluid called serum or plasma[1] (aka, "blister water"). However, blisters can be filledwith blood (known as blood blisters) or with pus (if they become infected).
  13. 13. 17) Pigment cells, their function, pigments in the skinMelanocytesare melanin-producing cells located in the bottom layer (the stratum basale) of the skinsepidermis,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.Melaninmelanin pigments are derivatives of the amino acid tyrosine. The most common formof biological melanin iseumelanin, a brown-black polymer of dihydroxyindole carboxylic acids, andtheir reduced forms.There are two different types of eumelanin. The two types are black eumelanin and browneumelanin, 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 unitslargely responsible for red hair and freckles. Pheomelanin is also found in hair and skin and is bothin lighter skinned humans and darker skinned humans. Pheomelanin imparts a pink to red hueand, thus, is found in particularly large quantities in red hair. Pheomelanin is particularlyconcentrated 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 locuscoeruleus ("blue spot"), the dorsal motor nucleus of the vagus nerve (cranial nerve X), and themedian raphe nucleus of the pons. Both the substantia nigra and locus coeruleus can be easilyidentified grossly at the time of autopsy because of their dark pigmentation.The increased production of melanin in human skin is called melanogenesis. Production of melaninis stimulated by DNA damage induced by UVB-radiation,[1] and it leads to a delayed developmentof a tan. This melanogenesis-based tan takes more time to develop, but it is long lastingIn humans, melanin is the primary determinant of skin color. It is also found in hair, the pigmentedtissue underlying the iris of the eye, and the stria vascularis of the inner ear. In the brain, tissueswith melanin include the medulla and zona reticularis of the adrenal gland, and pigment-bearingneurons within areas of the brainstem, such as the locus coeruleus and the substantia nigra.
  14. 14. 20) Basic examination in phlebologyA 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 venousdisease but with a variety of backgrounds such as dermatology, vascular surgery, haematology, orgeneral medicine, to share knowledge and experience. Diagnostic techniques used include thehistory and physical examination, venous imaging techniques and laboratory evaluation related tovenous thromboembolism. The American Medical Association has added phlebology to their list ofself-designated practice specialties.A significant part of a phlebologists work is involved with the treatment of superficial venousdisease, 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, avenogram, is taken after a special dye is injected into the bone marrow or veins. The dye has to beinjected constantly via a catheter. Therefore a venography is an invasive procedure. Normally thecatheter is entered by the groin and the doctor moves it to the required place navigating throughthe vascular system.It is the Gold standard for diagnosing acute deep venous thrombosis and chronic cerebrospinalvenous insufficiency although its use has been largely supplanted by the less invasive duplexultrasonography.Venography can also be used to distinguish blood clots from obstructions in the veins, to evaluatecongenital vein problems, to see how the deep leg vein valves are working, or to identify a vein forarterial bypass grafting.Areas of the venous system performed include lower extremities, [Inferior vena cava], upperextremities.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 andarteries. It is very effective in detecting clots.DVT is extremely difficult to detect because its symptoms are similar to those of many otherphysical conditions. Doppler ultrasounds allow doctors to see how fast blood is flowing in veins andarteries, 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 thearms and legs.