Degeneration and Necrosis Flashcards
(146 cards)
1
Q
Cell Injury
A
Any biochemical or structural alteration that impairs the ability of the cell to function normally.
2
Q
Four common causes of cell injury
A
- Hypoxia
- Free radicals and activated O2 species
- Some chemicals
- Viruses
3
Q
Total loss of oxygen
A
anoxia
4
Q
Deficiency of oxygen in the tissue
A
hypoxia
5
Q
Inadequate oxygen in the presence of adequate blood supply
A
Anoxic anoxia
6
Q
Decrease arterial blood flow and pressure with stagnation and decrease oxygen delivery
A
Ischemic anoxia
7
Q
Failure of the cell to use available oxygen
A
Cytotoxic anoxia
8
Q
Why are consequences of hypoxic anoxia greater in brain, heart, liver, and kidney?
A
-High metabolic rate
-With elaborated vascular system which shunts, anastomoses and double supply that protects them from hypoxia
-Duration and form of oxygen deficit are important determinants of cell injury
-Heart muscle extract 100% of the O2 from the whole volume of blood circulating in the myocardial capillaries.
9
Q
Cellular changes in anoxia
A
- Mitochindrial shutdown
- Ion shifts in the cytoplasm
- Metabolic shift
- Membrane lyse
10
Q
Define degeneration
A
means deterioration, Abnormal morphological changes or “sicked cells” . In general, considered as reversible if the function returns to normal
11
Q
Patterns of cell degeneration
A
- Water loading
- Metabolite loading
- Storage loading
12
Q
What pattern of cell degeneration is described as acute cell swelling and hydropic degeneration?
A
Water loading
13
Q
Glycogen degeneration, fatty degeneration, and hyaline degeneration are what pattern of cell degeneration?
A
Metabolite loading
14
Q
Lipidosis, mucopolysaccharidosis, mineralization and pigment loading are seen in what pattern of cell degeneration?
A
Storage loading
15
Q
Describe the degenerative changes in the cell membrane
A
Forms variety of configuration due to peroxidation of unsaturated lipids in the CM by free radicals that leads to degeneration of the phospholipids layer and protein components of the cell
Separation of intracellular junction
Formation of holes which is fatal to the cell
Injury that leads to the Na and CL into the cell together with water
16
Q
Describe the degenerative changes in the mitochondria
A
Loss of mitochondrial junction due to decrease ATP
Condensation with contraction of matrix
Swelling after ion and water movement inside with rupture of the outer membrane
Tubular formation from inner membrane
Calcium and phosphate deposition
Sometimes formation of the megamitochondrion
17
Q
Degenerative changes seen in the endoplasmic reticulum
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May lose ribosomes, break up or become greatly dilated into vesicular structures or may form a dense whorls when injured
18
Q
Degenerative changes seen in the lysosomes
A
Become quite prominent due to
Needs for digestion
Removal of particles brought into the cells by the process of heterophagy
Removal of degenerative components within the cell by the process of autophagy
19
Q
One of the earliest recognizable microscopic changes following injury, Universal manifestation of cell injury
A
Acute cellular swelling
20
Q
Severe acute cell swelling in which free water dilutes the cytoplasm. Common in epithelium and is called “ballooning degeneration”
Associated with blisters as seen in burns, bacterial toxins and epitheliotrophic viral diseases (FMD, VE,SVD. SVS)
A
Hydropic degeneration
21
Q
Membrane bound pumps rapidly moves ions and water out of the cytosol into the cisternae of the ER, which expands to create large filled cytoplasmic vacuoles. Very much like Hydropic degeneration except that water in large cytoplasmic vacuoles
A
Vacuolar degeneration
22
Q
What happens during glycogen degeneration?
A
Major deposits of glycogen in the liver, muscle, and kidney and this condition is essentially limited to these organs
23
Q
Abnormal accumulation of fat in the cytoplasm of the parenchymal cell. Liver is the best known location of this lesion lesser in the renal tubular epithelium and in the myocardium. Also known as lipidosis or fatty liver.
A
Fatty degeneration
24
Q
Excess lipids in the cells suggest that
A
-Long standing elevation of blood lipids
-Chronic hypoxia inhibiting lipid metabolizing enzymes
-Acute sub lethal injury that suppresses lipid pathways or,
-Chronic progressive metabolic disease arising from defective cell enzymes.
-Liver and kidney are apt to be involved in acute injury or metabolic disease.
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Fatty liver is well known in diabetes in?
dogs
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Fatty liver is well known as ketosis in?
Bovine
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Also known as fatty replacement. The presence of fat in adipose cell that accumulate in tissues in which they are not normally present usually replacing atrophied tissues.
Fatty infiltration
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A form of fatty infiltration in large areas of muscle having a pale or mottled color due to fatty infiltration
Steatosis
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Cell death can occur in two ways, these are?
Accidental cell (necrosis), Programmed cell death
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When the cell injury progressed to the point where irreversible cell injury occurs or passed the point of “no return". Death of cells and tissues in the living animal
Necrosis
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Involves the shrinkage or condensation of a cell with increased nuclear compactness or density. Nucleolus is no longer visible,
Loss of internal structure
Pyknosis
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Fragmentation of chromatin into tiny basophilic granules due to rupture of the nuclear membrane
Fragmented bits may remain in the original place of the nucleus or scattered throughout the cytoplasm
Karyorrhexis
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Refers to the earlier stage of cell death
Karyolysis
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Karyolysis
-Nucleus appear as hollow sphere surrounded by a faint outline, or ghost of nuclear membrane
-Dissolution or lysis of the nuclear chromatin by nucleases from leaking lysosomes of dead cells
-Solubilized chromatin diffuses out of the leaky nuclear membrane into the cytosol and interstitial fluid
-When complete, nuclear membrane disappears
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Nuclear changes during necrosis
loss of nucleus
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Changes in the cytoplasm during nercosis
Depletion of the cytoplasmic glycogen
Increased eosinophilia of the cytoplasm
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The cytoplasm tends to become less dense and ultimately disappears completely
Cyoplasmolysis
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Changes in the whole cell during necrosis
-Loss of cell outline
-Loss of differential staining
-Loss of cell
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Gross characteristic of a necrotic tissue
Dead tissue is paler than healthy one
Black if filled with blood
Dead tissue has less tensile strenght because of the enzymatic digestion of the cytoskeleton
Odors of putrefaction may emanate from or caused by saprophytic bacteria after gangrene or postmortem autolysis
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Forms of necrosis
1. Coagulative necrosis
2. Liquefactive necrosis
3. Caseous necrosis
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Sequence of events during necrosis
Necrosis begins with cell swelling, the chromatin gets digested, the plasma and organelle membranes are disrupted, the ER vacuolizes, the organelles break down completely and finally the cell lyses, spewing its intracellular content and eliciting an immune response (inflammation).
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Occurs when cells die due to a lack of blood supply
Coagulative necrosis
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How can you identify coagulative necrosis grossly?
Tissue is gray to white unless filled with blood, it is firm, dense and often depressed compared to the normal tissue
Focal necrotic areas are ussually surrounded by zones of inflammation.
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How can you identify coagulative necrosis microscopically?
The normal architecture of the tissue with its cellular components is recognizable, but the nuclie appear karyolitic, pyknotic, karyorrhectic or absent
The cytoplasm is strongly acidophilic
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Rapid enzymatic dissolution of the cells that result in complete destruction. It occurs in bacterial infection that lead to suppuration or pus formation when proteolytic enzymes released from WBC converts dead WBC and cellular debris into liquid amorphous materials.
Liquefactive necrosis
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How can you identify liquefactive necrosis grossly?
Lesion is a cavity with wall, small or large containing fluid that is usually yellow white and opaque
Wall cavity are frayed and irregular and more or less soft
Usually drained away by the lymphatic
Abscess is a localized collection of LN caused by suppuration deep in the tissue
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How can you identify liquefactive necrosis microscopically?
Necrotic tissue appear as empty space without definitive lining with frayed and irregular edge that may show some feature of necrosis
Pink staining proteinaceous precipitate may or may not remain in the fluid
Abscess contain large number of neutrophils whose enzyme liquefied areas of dead tissues and themselves, leaving liquefied mass of cellular debris
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It occurs when dead cells are converted into granular friable mass resembling cottage cheese. Occurs as part of typical lesions of tuberculosis, tularemia, syphilis, ovine caseous lymphadinitis, adenitis, and other granulomas.
Caseous necrosis
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How can you identify a caseous necrosis microscopically?
There is loss of cell outline and differential staining
Cell wall and other histologic structures disappears, and the tissue disintegrates to form finely granular mass that has purplish color with H&E. resulting from the mixture of blue chromatin material with red material derived from the cytoplasm.
The normal architectural pattern is totally obliterated.
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How can you identify caseous necrosis grossly?
White, grayish, or yellowish and is suggestive of milk curds or cottage cheese
Necrotic tissue is dry, slightly greasy and firm without any cohesive strength, rendering it easily separable into granular fragments with blunt instrument.
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Fat is often decomposed into fatty acid and glycerin
Fat combine with metallic ions Na, K, and calcium to form soap-like compounds
Fat necrosis
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a severe glassy or waxy hyaline degeneration or necrosis of striated muscle in acute infectious diseases.
Zenkers necrosis
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serous atrophy of fat in the coronary groove of the heart. This lesion is commonly seen in cachexia.
Myxomatous Degeneration
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Localized area of necrosis resulting from sudden obstruction of blood supply to the affected area.
Infarcts
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Types of infarcts
Red/Hemorrhagic
Pale/Anemic
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Infarcts in the kidney
Typically conical with the apex near the corticomedullary junction and the path of the arcuate arteries, anemic, multiple and often heal leaving only a narrow fibrous scar
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Infacts in the spleen
almost always hemorrhagic, many shallow subcapsular infarcts – seen in hog cholera
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Infacts of the myocardium
– rare in animals than in humans
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Brain infarcts
anemic and quickly reach the state of liquefaction necrosis. if animal survive, infarcted area may be represented by a hole in the brain parenchyma
Rare in animals
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Intestinal infarcts
usually involve considerable length of bowel
Always hemorrhagic
Ordinarily caused by strangulation of the bowel caught in hernial sac, intussusceptions or in the twisted loop of mesentery
If not promptly treated, develop gangrene that is fatal
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Infarcts of the lung
Occurs only when the circulation is also compromised by abnormally low blood pressure or perfusion.
emboli occluding the pulmonary artery are the usual cause
Not common in animals
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Why is infarcts in the liver non-existent?
Infarcts in the liver are non-existent because both the portal vein and the hepatic artery supply large amount of blood to this organ. If an infarct does occur, it is due to the obstruction of the a branch of the hepatic artery, obstruction of the portal vein does not cause infarction.
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Death is based on the irreversible cessation of activity of the heart, lungs or brain.
Somatic death
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Term used to describe the decay or death of an organ or tissue caused by a lack of blood supply.
Gangrene
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More frequent type of gangrene, occurs in tissue that are well filled with blood at the time of necrosis begins
Wet or moist Gangrene
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Microscopically, recognized as a mixture of coagulative and liquefactive necrosis in which large bacilli (rod shaped) are demonstrated.
Wet or Moist Gangrene
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Occurs in tissues that have limited content of blood and fluid or in tissues in which necrosis has develop slowly, with retardation of the natural circulation.
Dry tissue is not favorable so bacterial multiplication is slow.
Dry gangrene
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A group of diseases brought about by anaerobic spore- forming bacteria under Clostridium. They produce gas from constituent of dead tissue, which appears as bubbles in the affected tissue.
Gas gangrene
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Refer to alterations which accompanies or occurs after death of the entire body or somatic death
Postmortem changes
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Refer to those alterations that occur in cells, tissues, organs, etc. prior to somatic death or in the living individual.
Antemortem changes
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Why is it importantn to differentiate postmortem changes from antemortem changes?
It is important to differentiate postmortem changes from antemortem changes in order to interpret correctly those lesions encountered at necropsy.
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Rapidity of occurence of Postmortem changes depends on?
-Environmental temperature
-Humidity
-Condition of the animal
-Size of the individual
-External insulation
-Species of the animal
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Refers to self-digestion by enzymes that are present within or released into the cytoplasm of cells after death.
It is due to total diffuse anoxia.
Postmortem autolysis
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Refers to the stiffening of all muscles after death
Rigor Mortis
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Refers to the decomposition of tissues by bacterial enzymes.
Postmortem putrefaction
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The loss of body heat as the temperature of the body gradually equilibrates with its environment
Algor mortis
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Occurs after death when the heart beat stops and there is no longer a force which will maintain the circulation of blood and overcome gravity.
Livor mortis
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Occurs when the failing heart, prior to death, is no longer able to maintain blood pressure and blood accumulates in the veins in the ventral portions of the body.
Aginal hypostatic congestion
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Refers to the coagulation of blood in vessels and/or heart after death.
Postmortem clotting of blood
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Refers to the coagulation of blood in vessels and/or heart after death.
Postmortem coagulation
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Refers to the accumulation of gas in tissues as a result of bacterial fermentation.
Postmortem emphysema
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The leakage of bile through the autolyzed wall of the gall bladder. The adjacent liver tissue is stained a greenish hue.
Biliary imbibition
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Refers to the staining of tissues with hemoglobin.
Imbibition with hemoglobin
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Occurs when gases produced by bacterial fermentation cause progressive distention of body structures until they burst (stomach, intestine, diaphragm, etc.).
Postmortem rapture
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Occurs when the dead animal is rolled over or moved. The intestine is most commonly displaced after death.
Postmortem displacement of organs
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Glycogen deposition causes hyperglycemia in?
diabetes mellitus
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Glycogen deposition causes hyperadrenocorticism or what in dogs?
corticosteroid therapy
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These are autosomal recessive inherited disorders characterized by deficiencies of various enzymes involved in synthesis or degradation of glycogen
Glycogen storage disease or glycogenoses
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A collective term for dust retained in the lungs
Pneumoconiosis
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specialized form of pneumoconiosis (carbon)
Anthracosis
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Inhalation of silicon dioxide in rock quarries and mines or in any other conditions in which the rock is being cut or sandblasted.
Silicosis
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Inhalation of iron dust chiefly as hematite or iron oxide from mines
Siderosis
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From asbestos which is a widely used in manufacture of fire – retardant insulating material
Asbestosis
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Pigmentation of various silver containing compounds
Argyria
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Kind of clay derived from disintegration of an aluminous material such as feldspar or mica.
also known as China clay or Fuller’s earth. Causes pneumoconiosis which leads to dense pulmonary scarring in man and subhuman primates
Kaolin
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Greenish – yellow, fat soluble pigments from plant origin, normally occur in epithelial cells of adrenal gland, lutien cells of the corpus lutium, testis and seminal vesicles, kupffer cells, ganglion cells, egg yolk, butter fat, and adipose cells (horses, Jersey and Guersey cattle)
Carotenoid pigments
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Most important autogenous pigment, gives color to the skin, hair, and iris, and it provides the black, reflection proof choriod layer of the eye.
Melanin
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a deposition of melanin in various organs, especially lungs, and aorta
Melanosis
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Pathological absence of melanin resulting from inability of melanocytes to synthesize sufficient functionally active tyrosinase.
Albinism
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A type of hemoglobin loosely oxygenated, not oxidized, reason for the bright red color of arterial blood.
Oxyhemoglobin
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A type of hemoglobin that has given up its stored oxygen. venous blood
Reduced hemoglobin
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A type of hemoglobin, is a true oxide of hemoglobin and is reddish – brown (chocolate brown). Produced by poisonings with nitrites, chlorates, and some organic compounds.
Methemoglobin
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A type of hemoglobin, is a combination of reduced hemoglobin and inorganic sulfide and is dark brown in color.
Sulfhemoglobin
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A type of hemoglobin, formed after death and cause greenish discoloration to abdominal structure.
Sulfur Methemoglobin
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A type of hemoglobin, – bright cherry – red, and is the result of a combination of carbon monoxide with hemoglobin.
Carboxyhemoglobin
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Formed by the action of acids on hemoglobin, formed when acid aqueous solutions of formaldehyde acts on blood rich tissues.
Hematin or acid hematin
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Seen within and adjacent to gastric ulcers, is apparently formed from the action of gastric acid with hemoglobin
HCL Acid Hematin
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Shiny, golden yellow or golden brown pigment derived from hemoglobin, occurs locally when there has been hemorrhage into the tissue
Hemosiderin
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the cause of formation of hemosiderin is the excessive destruction or
hemolysis of erythrocytes
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Golden brown pigment formed in the lysosomes of cell undergoing progressive and prolonged autoxidation of unsaturated lipids
Lipofuscin pigment
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Tends to increased with advancing age thus the term “ aging pigment or wear and tear pigment”
Lipofuscin Pigment
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An early forms of lipofuscin, consisting of partially oxidized and polymerized unsaturated fatty acid.
Ceroid
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Common in salmonids nd catfish feed with rancid diet
Hepatic ceroidiosis
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Group of neurodegenerative dis. characterized by accumulation of fluorescent lipopigments in neurons and many other cells
Ceriod lipofuscinosis diseases
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An autosomal recessive dis. of English setter dogs characterized by intracellular accumulation of lipopigments in neurons and associated with loss of neuron and cerebral functions
Neuronal ceroid lipofuscinosis
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Yellow or yellow brown pigment in macrophages of the spleen, liver, bone marrow and sites of hemorrhage
Derived from degradation of heme
Bilirubin
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2 forms of bilirubin that can be detected thru van den Bergh test
Cojugated bilirubin or direct reacting bilirubin and Unconjugated bilirubin or indirect reacting bilirubin
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An important disorder in which the level of bilirubin reach such a high concentration in the blood the all tissues of the body have a yellow tinge.
Icterus, jaundice or hyperbilirubinemia
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Three types of Hyperbilirubinemia/ icterus / Jaundice
Pre-hepatic or Hemolytic
Hepatic or Toxic
Post-hepatic or Obstructive
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Jaundice that occurs in piroplasmosis, anaplasmosis, leptospirosis an equine infectious anemia
Pre-hepatic or Hemolytic
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Jaundice caused by toxic substance acting on the hepatocytes producing hydropic and fatty changes and necrosis
Hepatic or Toxic
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Type of jaundice that results from obstruction of the normal flow of bile
Post-hepatic or Obstructive
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Differentiate Pre-hepatic, Hepatic, and Post-Hepatic Jaundice
Pre-hepatic jaundice is caused by an increasing amt of hemolytic erythrocytes in the bloodstream. While hpatic or toxic jaundice is caused by toxic substances acting upon the the hepatocytes causing hydropic and fatty changes and necrosis. Lastly, post-hepatic or obstructive jaundice is caused by obstruction of the normal flow of the bile.
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How to diagnose jaundice/icterus/hyperbilirubinemia
Icteric index, Van den Bergh reaction
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Presence of bile in the urie
Choluria
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Icterus or jaundice is an important clue to what other diseases
It may indicate development of necrosis of renal epithelium in hepatorenal syndrome
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Photosensitizing pigments causing photosensitization or photosensitizational dermatitis
Porphyrins
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Three major types of photosensitization
Type I (Primary Photosensitization)
Type II (Congenital Erythropoietic Porphyria or Photophyria)
Type III (Secondary or Hepatotoxic Photosensitization)
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A pigment similar to hemosiderin is deposited in tremendous amounts in the cytoplasm in the epithelial cells in the liver and lesser amount in other organs.
Hemochromatosis
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A product formed during the metabolism of phenylalanine and tyrosine.
Homogentisic acid oxidase
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Unidentified pigment found in liver cells may be a lipofuscin but also shares many properties with melanin.
Mechanism in the production of this pigment is unknown
Dubin-Johnson Pigment
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First describes in Angora goats as dark brown, iron negative pigmentation that occurs in the basement membranes of the PCT of the kidney, which imparts the appearance in tissue section the reminiscent of enameled jewelry (cloisonne)
The nature and significance of the condition is unknown.
Cloisonne Kidney
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Deposition of calcium salts in tissues other than bone and teeth
Pathological Calcification
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2 types of pathological calcification
Dystrophic, Metastatic
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Deposition of calcium salts in dead or degenerating tissues
Type that occurs most often
Dystrophic calcification
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A variant of Dystrophic Calcinosis in which tissues are converted into masses of calcium salts surrounded by foreign body giant cells.
Tumorous calcinosis
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Precipitation of calcium salts as a result of persistent hypercalcemia of calcium in the blood
Tissue is not damaged previously
Metastatic Calcification
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Abnormal masses, usually calcium and other mineral salts that develop in organs as a result of secretion or inspissation or thickening of luminal content
Calcified bodies or calculi
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A condition in which crystals of uric acid or urates are deposited in the tissues due to disease in purine metabolism.
Chalky white masses of uric acid (tophi) develops in tissue and causes local inflammation
Gout
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Avian gout occur into two forms, both forms are initiated by renal failure in uric acid secretion and are promoted by dehydration and diets high in protein.
Visceral Gout, Articular Gout
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A form of avian gout common, the plasma uric acid is increased and the urates are deposited in the kidney, liver, joints and pericardium. Common sequela to dehydration
Visceral gout
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A form of avian gout limited to synovia and tendon sheaths of joints esp. on the foot and hock
Articular gout
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Genetically controlled homeostatic mechanisms that deletes cells that are no longer needed that in some way would be damaging to the animal
Apoptosis/Programmed Cell Death
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Cellular changes in Programmed Cell Death/Apoptosis
The cell shrinks and condenses. The cytoskeleton collapses, the nuclear envelope disassembles, and the nuclear DNA breaks up into fragments.
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The round, homogenous, anuclear remnants of the dead cell that remain are called
Apoptotic bodies
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Stages of Apoptosis
Initiation or priming
Commitment or decision
Execution and Clearance
