Pigments Flashcards
Carbon + Other Dusts
Exogenous Pigmented Substances
coal mine dust lung dz (black lung) = pneumoconiosis
- major dust-inhalded = carbon (anthracosis)
- black discoloration in lung
many are not assoc. w/ clinical dz
- fine gray-black stippling to lungs + dark discoloration f tracheobronchial lymph nodes
carbon particles deposited in alveolar spaces phagocytized by macrophages
- transport to BALT + tracheobronchial ln.
histo:
- indigestible carbon particles + other dusts appears as fine black granular + crystalline material in macrophages adjacent to intrapulmonary airways + vasculature
usually incidental in older animals
- coal + other dusts (esp. silica) can elicit inflammatory response + promote progressive fibrosis
macrophages laden with carbon particles also have diminished capacity to phagocytize + destroy infectiuous agents
Carotenoid Pigments
Exogenous Pigmented Substances
abundant in leafy green plants + imparts yellow coloration to plasma, adipose tissue + other lipid-laden cells
- esp. in horses + dairy cattle of high milk fat breeds
not a lesion
- just a dietary indicator
- carotenoids stored in fat are source of antioxidants
carotenoids are fat soluble + removed during histo processing
Tetracycline
Exogenous Pigmented Substances
tetracycline binds to calcium phosphate in teeth + bones
if administered to animals during time of tooth mineralization, tetracycline results in permament discoloration
- initially yellow but after tooth errupts + gets exposed to light = oxidation changes color to brown
yellow discoloration (w/ bright yellow fluorescence under UV light) also observed in bone
Melanin
Non-hematogenous Endogenous Pigments
pigment responsible for color of hair, skin, iris
- also colors leptomeninges in black-faced sheep/cattle
- may be present multifocally in oral mucosa of various species
melanosis common on aortic intima in ruminants w/ pigmented coats + on lungs of red or black pigs
congenital melanosis = merely a color change, not lesion
Melanocytes = synthesize + secrete melanin
- derived from neural crest + mirage to site of pigment production during embryonic dev.
- melanin formed in melanosomes then transferred through dendritic cells to keratinocytes
in skin, melanocytes reside in stratum basale of epidermis + follicular epithelium
histo = melanin granules small, brown + non-refractile
can be diminished or excessive in disease
melanin synthesis:
- conversion of tyrosine to DOPA (catalyzed by tyrosinase - Cu containing enzyme)
- lack of tyrosinase results in albinism
- sheep/cattle w/ copper defficiency = fading coat color
Melanin + Diseases
Non-hematogenous Endogenous Pigments
partial albinism in Chediak-Higashi Syndrome
- recognized in mink, persians + mice
- caused by mutation of LYST (lysosomal trafficking regulator protein)
- melanocytes have enlarged melanosomes but melanin not transferred effectively to keratinocyes
- coat color is pastel shade of what should’ve been
normally pigmented skin + hair can also become depigmented bc of immune-mediated attack of menalocytes (vitiligo) or basilar keratinocytes (lupus erythematosus)
dead keratinocytes spill melanin into dermis (pigmentary incontinence) + phagocytized by macrophages (melanophages)
hyperpigmentation = excessive melanin
- can be common epidermal response to chronic injury
- often assoc. w/ endocrine skin dz
- melanin granules numerous but in all layers of epidermis
neoplasms of melanocytes can be darkly pigmented or amelanotic
Lipofuscin
Non-hematogenous Endogenous Pigments
yellow-brown lipoprotein
- accumulates as residual bodiesin secondary lysosomes
- esp. in long-lived post-mitotic cells
- esp. in aged animals
known as wear-&-tear pigment of aging
- accumulation in myocardium has linear correlation with age of dog
- little or no bad effect on cells
autoflourescent
reacts w/ fat stains
carb moieties = PAS +
Ceroid
Non-hematogenous Endogenous Pigments
lipofuscin-like pigment
- accumulates in dz states such as neuronal ceroid-lipofuscinosis, cachexia, vit. E deficiency, or other oxidative stress.
can be grossly evident in tunica muscularis of SI in dogs w/ vit. E deficiency or in dogs w/ ceroid-lipofuscinosis
Lipofuscin + Ceroid
Non-hematogenous Endogenous Pigments
both are autoflourescent lipoproteins w/ similar but not identical spectra
ultrastructurally, lipofuscin has granular appearance while ceroid forms membranous stacks or whorls
protein content of lipofuscin heterogenous
- subunit c of mitochondrial ATP sythase is predominant component of ceroid in neuronal ceroid-lipofuscinis
lectin histochemistry = distinguish neurona ceroid from lipofuscin by its sugar moieties
Hemoglobin
Hematogenous Pigments
consists of 4 globular protein subunits each folded around a central, non-protein, iron-containing heme group
oxyhemoglobin = gives oxygenated blood ins red color + pink tinge to well-oxygenated tissues
deoxygenated hgb explains blue cast to venous blood + accounts for cyanosis of hypoxic tissues
Hgb + Cyanide
CN- bocks oxidative phosphorylation in mito by binding cytochrome oxidase
- result = cells can’t use oxygen in hgb
in cases of cyanide poisoning = venous blood as read as arterial
herbivores = caused by consumption of plants w/ cyanogenic glycosides
Hgb + CO
Hgb has much higher affinity for CO than for oxygen
carboxyhemoglobin colors blood bright cherry head + imparts bright pink color to tissues in cases of CO poisoning
Hemoglobin + Nitrite
Nitrite poisoning = consumption of nitrate-accumulating plants in ruminants or from water source contaminated w/ nitrate runoff from fertilized fields
nitrate converted into rumen to nitrite ->- oxidize iron in heme group of Hgb to Fe3+ state -> converts hemoglobin to methemoglobin -> turns color of blood to a chocolate brown
Hemoglobin + IV Hemolysis
released Hgb imparts transparent pink tinge to plasma/serum
kidneys = IV Hgb passes throughglom. capillaries into urinary filtrate (hemoglobinuria) w/ formation of Hgb casts in renal tubules + reddisch discoloration of ruine
- turns color of renal parecnhyma from dark red to gunmetal blue
similar or browner discoloration of kidney + urine occurs with myogobinuria
- derived from injured skeletal m. fibers
Hematin
Hematogenous Pigments
brown-black, Fe3+ containing pigment formed by oxidation of Hgb
can be removed by soaking dewaxed tissue section before H&E staining in saturated alcoholic solution of picric acid
Acid hematin
Hematogenous Pigments
forms in tissues fixed in un-buffered, acidic formalin
appears as dark brown to nearly black granular or crystalline material in vessels or other areas where erythrocytes are numerous
postmortem change = not a lesion
Parasitic Hematin
Hematogenous Pigments
prasites infecting or consuming RBCs liberate heme during proteolysis of Hgb
free heme is toxic but parasites have evolved to aggregate it into heme dimers
accounts for blacking of migration tracts by juvenile liver flukes in ruminants + for black speckling of lungs in macaques infested w/ lung mite
Hemosiderin
Hematogenous Pigments
free iron is toxic to cells by catalyzing formation of ROS via Fenton reaction
Ferritin present in all tissues, binds free iron + stores it in nontoxic form for use by cell
serum ferritin conc. correlate with iron stores
accumulations of ferritin bound with iron are converted to golden bronw granules of hemosiderin, mainly in macrophages + less so in hepatocytes or renal tubular epithelial cells
prussian blue reaction detects iron of hemosiderin in tissue sections
iron stores most conspicuous in speen + hemosiderosis occurs when there’s increase in erythrocyte destruction
rarely excess iron can be derived from diet or other external sources
presence of hemosiderin-laden macrophages can also indicate chronic passive congestion
if abundant, imparts brownish discoloration to tissues
one of the pigments that typifies a bruise
Hematoidin
Hematogenous Pigments
bright-yellow crystalline pigment derived from hemosiderin but is free of iron
biochemically similar t bilirubin
deposited in tissues at sites of hemorrhage
Bilirubin
Hematogenous Pigments
normally present in low amounts in plasma as breakdown product of RBCs
RBCs phagocytized + lysed by macrophages -> globular protein components of Hgb broken down into AAs -> after removal of iron, heme converted by heme oxygenase to billiverdin -> converted to bilirubin by biliverdin reductase -> unconjugated bilirubin released into blood + carried as albumin-bilirubin complex to liver -> conjugation wiht glucoronic acid + secretion into bile canaliculus
mutant corrieale + southdown sheep = dev. conjugated hyperbilirubinemia
- atrributed to defective ATP-dependent transport system
- can conjugate bilirubin but can’t secrete into bile efficienctly
Porphyria
hematogenous pigments
heme synthesis disorders resulting in deposition of porphyrrin pigments in tissues
porphyrrin ring in Hgb mol. composed of 4 pyrrole moieties linked together around central iron
congetinal erythropoietic porphyrias (pink tooth) of calves, cats + pigs
- result of genetic defects caused by deficiency of uroporphyrinogen III synthase
- teeth, bone + urine red-brown + fluoresce red under UV light
feline disease mapped to 2 missense gene mutations in the synthase
