Post Mortem Changes And Pigments PDF
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University of Prince Edward Island
Paul Hanna
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This document provides an overview of post-mortem changes. It covers topics such as somatic death, autolysis, various pigments (exogenous and endogenous), and their impact on different animal tissues, such as liver, kidney, lungs, and gut. The document also discusses factors influencing post-mortem autolysis, such as body temperature, and how these factors are relevant for medicolegal cases.
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Post-mortem changes and Pathological Pigments Somatic Death death of the body as a whole When respiration and cardiac action have stopped, the animal is said to have undergone somatic death After death, the cells undergo certain changes (post mortem change...
Post-mortem changes and Pathological Pigments Somatic Death death of the body as a whole When respiration and cardiac action have stopped, the animal is said to have undergone somatic death After death, the cells undergo certain changes (post mortem changes), which a pathologist must have knowledge of to distinguish them from lesions found in disease Post mortem changes can interfere with accurate interpretation of gross and microscopic lesions; minimize by cooling the carcass at 5c (1-3 days) for small animals not with ruminants and horses By a careful study of a postmortem changes one can determine the probable time of death and this is of great importance in medicolegal cases Post-mortem autolysis Autolysis/putrefaction -self digestion by the tissue enzymes after somatic death due to accelerated decomposition of the bacteria from the gut and blood -liver, pancreas, and kidney change relatively quickly -Loss and increase of weight in organs -Fixed ASAP: retina is the most sensitive, seminiferous tubules, intestine Postmortem Changes Edema fluid – found beneath skin commonly observed in sheep. Differential diagnosis with blackleg and malignant edema Softening –caused by autolysis commonly observed in livers, kidneys, and pancreas Distention – fermentation with gas production in digestive tract; rupture of stomach or diaphragm Postmortem Changes Pressure – due to distention of abdomen or intestines to other organs - liver may be pale because blood has been pushed out or imprints of intestine - mottled semi-cooked myocardium confusing with degeneration - gas bubbles in liver and kidney which appear pale Postmortem Changes Displacement – twist in the intestine, intussusceptions, or herniation. - Tear/rupture before death: hemorrhage at the edge of lesion whereas no hemorrhage in a postmortem tear. - mucus on the surface of intestine during autolysis - Bile will seep into nearby tissues stain yellowish brown Pigments( extracellular and Intracellular) Exogenous pigments Exogenous pigments Pneumoconiosis( dust disease) - due to inhalations of compounds in mineral/organic dust visible in respiratory tract and draining lymph nodes - An occupational pathological pigmentation eg. Silicon, asbestos, carbon, coal, lead, cotton fibers, iron dust - Chronic in nature; more of human concern Exogenous pigments Anthracosis - due to inhalations of carbon compounds found in animals exposed to too much dust - Grossly: gray/mottled lungs, black bronchial nodes - Microscopic: centered around small bronchioles as collection of black granules Exogenous pigments Canine, lung, mild anthracosis (likely due to secondhand smoke) note slight black discoloration of pulmonary parenchyma. Carbon is inert; not metabolized; remains in the tissue for life Exogenous pigments Endogenous pigments( colored substance which originate within the body) Lipofuscin – derived from lipids Melanin- derived from melanin Copper – derived from hemoglobin Hemosiderin- derived from hemoglobin Hematin-derived from hemoglobin Bilirubin-derived from hemoglobin Porphyrin- derived from hemoglobin Endogenous pigments( colored substance which originate within the body) Endogenous pigments - aka "wear-and-tear" or aging pigment - lysosomal breakdown products of lipids - sites: aged or chronically injured cells. - significance: doesn’t injure cell, but a sign of aging or excess free radical damage Endogenous pigments Lipofuscin Well known in neurons of dogs, myocardial cells in cattle, exhausted adrenal and thyroid glands “brown atrophy of the heart” associated with vitamin E deficiency; “brown dog gut”; carotenoids ( yellow fat) in Jersey and Guernsey cattle Endogenous pigments Endogenous pigments Endogenous pigments Endogenous pigments Hemoglobin - microscopic: reddish-orange in renal tubules if it crosses the glomerulus - grossly: black kidney as an indication of acute hemolytic crisis - Classic example is chronic copper poisoning in sheep and cattle Endogenous pigments Hemosiderin - An indication of iron stores or of blood breakdown - Seems to collect in clumps of macrophages which occur in renal epithelial cells ( xanthomatosis), hepatocytes, chronic left heart failure Endogenous pigments Endogenous pigments Results from action of acid or alkali on hemoglobin which occur after death Common as “formalin pigment” when unbuffered formalin is used for fixation mainly in blood vessels Used to identify blood in forensic lab and identify the specie Endogenous pigments Endogenous pigments Endogenous pigments Endogenous pigments Endogenous pigments Porphyrins - Cause pigmentation of tissues along with jaundice and photosensitization known as porphyria - Collect in teeth and bone of cattle known as “pink tooth” Acknowledgement: Paul Hanna of Atlantic Veterinary College University of Prince Edward Island