Pigment

Pigment - colored substance inorganic and organic, intra i extracellular , soluble or corpuscular.

The main one pigment surface human of the organism is melanin contained in  skin ,  hair  and '' eye .' ' bodies then hem and from it emerging bilirubin, both related to the most widespread pigment in nature - chlorophyll - green leafy.

Melanin


Melanin is a polymer of metabolites tyrosine or dopamine ( polyindolequinone bound on protein ). It is usually " yellow -brown " to " black ". It is stored intracellularly in melanosomes ( derived from Golgi complex ) or in lysosomes, is decolorized by oxidizing agents reagents (H2O2), is argentaffine ( reduces ammoniacal solution silver – Masson's reaction ).


 * Disorders in melanin pigmentation :
 * 1)  Hyperpigmentation  ( diffuse - Addison, focal - chloasma, melanoderma, melanoma ):
 * 2) *  Addison's disease  ( peripheral type ) – panhypocorticalism ( insufficiency bark adrenal glands ) from adrenal causes, as a result decline blood concentration cortisol is elevated production of ACTH and MSH ( have common POMC precursor – proopiomelanocortin ), as a result it is generalized hyperpigmentation skin especially highlighted in places with physiological increased pigmentation ( linea alba, perianal and perigenital area), exposed solar radiation ( hands , face ) and in place skin scar , on bearing occurs _ melanin pigmentation buccal mucous membrane in the place of 1. upper molars ( graphite spots );
 * 3) *  hyperfunction pituitary glands ;
 * 4) * Peutz-Jeghers syndrome ;
 * 5) * ' transient diffuse " hyperpigmentation " after radiation ( sunbathing ), in people with sensitive skin skin arise freckles (ephelides'') which they can be permanent ;
 * 6) * chloasma - yellow-brown spot emerging especially hormonal influences, in pregnancy (chloasma uterinum ) or at usage hormonal contraception ;
 * 7) *  melanodermia  - hyperpigmentation leather from different causes, e.g. _ by radiation , chemicals , traumatization , inflammation ;
 * 8) *  melanosis smokers  - oral hyperpigmentation cavity and on by hand strong smokers ;
 * 9) *  neurofibromatosis  - spots colors white coffee on skin _
 * 10) *  melanoma  - tumor from melanocytes ( tumor cells are labeled like melanoblasts );
 * 11) *  hemochromatosis  - general hyperpigmentation skin ;
 * 12)  Depigmentation  ( congenital – albinism, acquired – vitiligo, leukoderma);
 * 13) * vitiligo - postnatally emerging speckled depigmentation skin, stains they are keen bordered , hair they are white , apparently it is a given autoimmune blockade function melanocytes ( melanosomes they are not changed , but contain little pigment );
 * 14) * leukoderma - focal loss pigment ( pale stains they don't have keen border ) after the pre -existing skin inflammation, is given destruction melanocytes ;
 * 15) *  albinism  - Hereditary (AR) disorder metabolism, which leads to a partial whose complete absence melanin.

For pathology pigments is important also  alkaptonuria  ( homogentisate-1,2-dioxygenase defect which catalyzes transformation homogentisate on maleinyl acetate, resulting in accumulation vinegar . homogentis - excretion in urine , dark urine ), ochronosis  ( oxidation and polymerization homogentisate and binding on proteins binder - disability joints , especially spine ).

Lipopigments
Lipopigments are  yellow-brown  to ' brown ' ' ' pigments which they arise in autophagic  lysosomes '' by polymerization products peroxidation unsaturated greasy acids.


 * 1) Ceroid + lipofuscin' - brown pigments insoluble in fats, stains with Sudan , PAS+, fluoresce in UV, are argentaffine (ceroid is considered a precursor lipofuscin - there are more Sudanophile and less reduces solution silver than lipofuscin) – formation these of pigments is generally influenced by the ratio for – ( mainly heavy metals as Fe) and antioxidant ( mainly vitamin E) factors , peroxidation affects especially pathologically cumulative lipids ( steatosis ,  lipidosis ) or direct cellular membranes.
 * 2)  Lipochrome  (lutein) – an exogenous pigment arising from carotenoids ( obtained alimentary ), fat - soluble, his presence in the body is however constant , occurs dissolved ( non-corpuscular pigment ) in fat tissue whose _ yellow-orange color conditions.


 * Ceroid ( occurrence ) – macrophages around hematomas ( mix ceroid with hemosiderin is indicated such as  hemofuscin ), lysosomal accumulation lipids ( e.g. in macrophages at steatoses and lipidoses ), in muscle ( thin gut, myocardium etc. ) at avitaminosis E, in mucosa thick intestines ( permeated pigmentophages , unclear pathogenesis ) – melanosis coli ( na difference from the so- called pseudomelanosy , which is greenish coloring abdominal wall and abdominal organs given posthumously diffusion gases – H2S from the intestines acts on hemoglobin in blood vessels and changes him in verdohemoglobin ).
 * Melanosis coli – benign pigmentation, appears at chronic use of laxatives ( by storing anthraquinones pigments released from the drug ).


 * Lipofuscin - the so- called pigment from wear ( proliferates in old age, especially in cells with small mitotic activity - the so- called Brown atrophy –  atrophy fusca ), occurs in these organs : liver ( hepatocytes mainly in the center liver lobules ), myocardium ( forms caps over cores cardiomyocytes ), adrenal glands (zona reticularis), nervous cells , skeletal muscles.


 *  Lipochrome  ' - normally found in fat tissues, pathologically is multiplied by increased income of carotenoids in food ( e.g. at diabetes ), when it is increased yellow fat subcutaneous , palms and soles ( xanthosis ) and skull base , differentially diagnostically necessary _ distinguish carotenemia from icterus – with  carotenemia it isn't yellowish  coloring  sclera '.

Hematogenous pigments
These pigments arise degradation hemoglobin. To breakdowns hematogenous pigmentation belongs however disorders ''' own hematogenous of pigments ( hemosiderosis ), on the one hand disorders of " biosynthesis " ( porphyria ) or " degradation " ( icterus ) of heme. Hemoglobin is released at decay erythrocytes, hemolysis. She can be intravascular or extravascular. Hemoglobin is here is falling apart to globin, biliverdin and Fe3+.


 * Hemosiderin - complex compound containing hydroxide ferrous with proteins, polysaccharides and lipids , form grains rusty Brown colors in HE ( identification card from lipofuscin – Perlsova reaction – Fe in hemosiderin forms with ferrocyanide potassium ( Berlin blue ) in acid environment blue coloring ), is almost always  intracellular  inside macrophages ( siderophages ).
 * Hematoidin - chemically identical to bilirubin, forms red yellow rhombic until needle-like crystals in older ones hematomech , is almost exclusively  extracellular , does not contain Fe ( Perls reaction negative ).
 *  Hemofuscin  – mixture of hemosiderin with ceroid in hematomas ( intracellularly in histiocytes ).
 * 'Hematin' - brown pigment similar hemosiderin, but Fe is fixed bound ( Perls ) , occurs in scum acute gastric ulcer ( where arises by the effect of HCl on hemoglobin ), is the cause colors dry gangrene.
 * Stocks with excess hematogenous pigments
 *  Hemosiderosis  - excessive saving hemosiderin in RES ( mainly The Kupffers cells liver in periportal areas, spleen , nodes - pigmentation endothelium rafts ), storage leads to a small multiplication ligaments , blood along the way , hemosiderin reaches the kidneys and is stored in the cells there proximal tubules . Hemosiderosis it isn't sickly unit , but only raised by the  flag hemolysis , accompanies also repeatedly transfusion in anemias ( changes reminiscent rather hemochromatosis – secondary hemochromatosis ) or in alcoholics , where it is increased absorption iron from the GIT due to alcohol - accumulation ferrous pigment in hepatocytes ( siderosis ).


 *  Hemochromatosis  - conditional increased absorption of iron in the duodenum ( iron taken in food is in in the form of Fe3+, it is reduced in the stomach on Fe2+ and in this form is also resorbed, it is again in the enterocytes oxidized to Fe3+ and either is deposited in form ferritin or is transported transferrin ), excess iron is deposited similarly as hemosiderin in RES cells (but the spleen is affected less , in the kidneys it is stored in cells distal tubules ), is accompanied prominent fibroproduction (in the liver can lead up to the so- called pigmented cirrhosis ), at the same time it happens proliferated ceroid , affects and other organs ( pancreas + pigmentation skin – bronze diabetes, salivary glands , bile pathways , plexus chorioideus ).


 *  Hemoglobinemia  - accompanies sharp hemolysis ( e.g. at _ transfusions incompatible blood ) when haptoglobin is depleted and RES is not enough process all hemoglobin . Hemoglobin enters the kidney _ tubules – hemoglobinuria, hemoglobinuric nephrosis.
 *  Icterus  - jaundice, causes yellow skin , sclera , mucous membrane.

Exogenous pigments
way exogenous pigmentation is threefold :
 * 1)  Pigmentation by injury  - affect most often the skin and eye, mostly at injury ( entrapment sand , fire wounds and intrusions iron shrapnel into the skin - siderosis , particles copper or their alloy ( brass ) – chalcose , decorative tattoo - pigmentation joints ).
 * 2)  Pigmentation digestive tract and blood by way of  - arise by some metals and their salts that are absorbed _ mucous membrane GIT and they are divorced blood into different tissue.
 * 3) *  Argyrosis  - gray pigmentation silver, accumulates mainly in the basal membranes sweat gland or in conjunctivae at long term administration eye drops with AgNO 3.
 * 4) *  Chrysocyanosis  - bluish discoloration after administration colloidal of gold  iv  ( rheumatic arthritis ).
 * 5) *  Leaden hem gum  – formed PbS ( influence bacterial sulfane ) at chronic Pb intoxication and others heavy ones metals (Bi, Sb...).
 * 6)  Pigmentation by inhalation  – inhaled particle larger than 10 μm is trapped in the nose and nasopharynx, between 5 and 10 μm is trapped in the mucus bronchi and bronchioles and are coughed up or taken away ciliary by transport , particles smaller than 5 μm are obtained up to the alveoli , where they are absorbed alveolar macrophages ( coniophages ) and they are with the engulfed pigment either coughed up , or they pass to the fibrous one interstitium alveoli and from it they can get lymphatic vessels to the lymphatics nodes ( example lymogenic metastasis pigment ).
 * 7) *  Pigmentation simple  - particles pigment they are inert ( anthracosis, tobacco , stannosis ).
 * 8) *  Pneumoconiosis  - particles they evoke fibroproduction ( silicosis, asbestosis , berylliosis , talcosis , aluminosis ).

Simple pigmentation amorphous carbon ( soot ), to lung the tissue behaves inertly ( does not act fibroproduction ), but it is increasingly stored in the bearings fibrosis ( e.g. tuberculosis _ bearings ) – so- called shale induration ( induratio nigra).
 * Anthracosis

Brown coloring lungs tobacco dust, does not work strange disorders. Dustiness lungs oxide tin ( SnO 2), does not work clinical disorders. Damage lungs caused by inhalation inorganic of material – in this the case fibrogenic particles oxide siliceous SiO 2.
 * Tobacco
 * Stannosis
 * Silicosis

Dustiness lungs fibers asbestos ( silicate magnesium ).
 * Asbestosis

Creation tuberculoid granulomas. Pneumonitis emerging on hypersensitive based on, arises at inhalation of dust from damp hay which contains microorganism ' Micropolyspora faeni '.
 * Berylliosis
 * Farmer lung

Related articles

 * Phototypes
 * Faults pigmentation
 * Melanoma
 * Anatomy skin
 * Physiology skin

Source
}
 * {{ Citation
 * type = web
 * lastname1 = Pastor
 * name1 = Jan
 * url = https://langenbeck.webs.com/
 * name = Langenbeck's medical web page
 * year = 2005
 * cited = 2011-03-08

Used literature
Category:Histology Category:Dermatovenerology Category:Pathology 