Pathology 1 General 2

sihirlifil's version from 2016-09-05 14:28

post mortem changes

Question Answer
what is post mortem autolysis, and how does it happen?autolysis of cells after somatic death. Results from total hypoxia and changes follows as in hypoxic cell injury.
post mortem changes can vary in onset and rate depending on (3)(1) cause of death (2) environmental and body temp (3) microbial flora
what is rigor mortis?contraction of muscles occurring after death, because of depletion of ATP in muscle.
what is algor mortis?gradual cooling of carcass (al-gor is now worried about global cooling)
what is livor mortis? aka?aka hypostatic congestion. it is gravitational pooling of blood to the down side of the animal (a POOL of livers--- because pooling blood. yeah it's a stretch.)
what would you say happens with blood clotting, post mortem?there is post mortem clotting, which will eventually liquefy again after a while.
what is hemoglobin imbibition?red staining of tissues by hemoglobin released from lysed erythrocytes.
what is bile imbibition?yellow staining of tissues adjacent to gall bladder. Seen in 1-6 hours after death.
what is pseudomelanosis?blue green discoloration of tissues by iron sulfide, seen between 18 to 24 hours after death. (a pseudo [suit-o] iron)
what causes softening of tissues post mortem?autolysis and bacteria
what causes bloating post mortem?result of post mortem bacterial gas formation in the digestive tract. More pronounced in herbivores.
how would you be able to tell if a ruminant died from ruminal tympany, or if it was just bloated from being dead?there will be a "BLOAT LINE" present if the ruminant died from tympany. the bloat line is where theres a line in the esophagus where part of it was pale and white, and the other part is flushed red
what is the bloat line?if a bloat line is present on the ruminant's esophagus, it died from ruminal tympany, NOT that it became bloated after death
what do you see on the liver after death? what causes this? (2)PALE FOCI ON THE LIVER. (this happens within an hour after death). it is caused by (1) inc intra-abdominal pressure which squeezes blood from the liver (2) bacteria disseminated from gut to portal vein
mucosal sloughing occurs after death at about what time?1-6 hrs after death

intracellular and extracellular depositions

Question Answer
hepatic lipidosis/steatosis happens when fat gets to the liver 2 ways(1) from fat deposits in form of free fatty acids (2) from intestine- in form of short chain fatty acids
once fat reaches the liver, what happens? (one thing or the other)(1) oxidized and used directly for energy (2) esterified to triglycerides/converted into cholesterol or phospholipid, or oxidized to ketone bodies
conditions (situations) related to fatty changes (3)(1) excess fat reaching liver (2) liver and other tissues not able to handle fat (defects in formation of lipoproteins-- poisons/toxins interfering with synthesis such as carbon tetrachloride) (dietary deficiency of protein) (3) dec oxidation of fatty acids to ketones (in hypoxia and toxins)
idiopathic hepatic lipidosis affects which animal most commonly?in fat cats (ohhh yes, hope you were paying attention to zeiger)
hyperlipidemia affects which animals most commonly?dogs and horses (there is a H and a D in the word)
is glycogen deposition intracellular or extracellular?intracellular
what are the causes of glycogen deposition? (3)(1) hyperglycemia in diabetes (2) drug induced metabolic dz with use of corticosteroids (3) glycogen storage disease
glycogen storage disease- glycogenosis. what is the broad definition?These are autosomal recessive inherited disorders characterized by deficiencies of various enzymes involved in the synthesis or degradation of glycogen.
what is Type-1 glycogen storage disease(glycogenosis)? (who, what, etc)occurs in toy breeds; due to deficiency of glucose-6- phosphatase. Glycogen storage is more in the liver; hypoglycemia develops. (1 can't break it down, because he feels so small, so it just builds up inside him, in his liver)
what is type-2 glycogenosis? (aka? who, what, where etc)POMPE'S DZ. Deficiency of lysosomal acid maltase (glucosidase). Reported in Brahman and shorthorn cattle calves,Corriedale sheep, Lapland dogs, cats, turkeys and Japanese quail. Glycogen accumulates in lysosomes of cells of brain, muscle and liver. (Two went to Pompeii, which is full of death [like a lysosome] where through sympathy and tasting acid she got sweeter)
what is type-3 glycogenosis? (aka, who, what, develops what etc)Cori's dz. Affects GSDs! Deficiency of amylo 1,6- glucosidase, (involved in break down of glycogen to glucose) GSD develops hepatomegaly and and hypoglycemia (Three once owned a German Shepard named Cori, but his girlfriend Amy punched it in the liver....sad)
what is type-4 glycogenosis? (not horse one) (who, what, where, prognosis)norwegian forest cats, deficiency of glycogen branching enzyme, glycogen deposits in many places esp. skele and cardiac mm. die soon after birth or develop progressive mm degeneration till ~5-7mo (Four once saw a norwegian cat up on some branches, but his muscles weren't strong enough to climb and get it, it broke his heart. it was a poor prognosis for the cat)
type-4 glycogenosis in horses-- which breeds? what's lacking? what happens because of this? prognosis?quarter horses and paint horses. congential lack of glycogen branching enzyme, so long unbranched chains accumulate in skele mm and CARDIAC mm so you get abnormal glycogen formation and deposition. affected foals are still born, aborted, or weak. (Four has some long, branching chains on him, and through his heart)
type-7 glycogenosis affects who? what is lacking? what happens because of that? clinical signs?english springer spaniel and cocker spaniels. lack of type M phosphofructokinase (PFK), and glycogen accumulates in the mm to cause hemolytic anemia, intravascular hemolysis, and hemoglobinuria. clinical signs incld exercise intolerance, mm wasting/cramping (Seven especially hated spaniels, because of how bouncy they were, they scratched him up and made him bleed. Also Type M-phospho-whatever has M as in Muscles)
what is PSSM? who does it affect? what is the prob and what does it cause?Polysaccharide storage myopathy in horses. SIMILAR TO PFK (phosphofructokinase) enzyme deficiency. excessive storage of **glycogen** in skele mm. familial component in certain horse breeds. **DEFICIENCY OF GLYCOGEN SYNTHASE ENZYME
lysosomal storage dz's are classified by what?by the major stored material, such as "mucolipidosis"
describe the lesions of a lysosomal storage dzINC in size and number of lysosomes, and abnormal intra and extracellular products
define amyloidosis (is it intra or extracellular?)EXTRACELLULAR deposition of of abnormal PROTEINACEOUS substances in the tissues. (amy likes to be on the outside)
the amyloid in amyloidosis looks uniform, but it is actually composed of what two things? where do those things come from?(1) amyloid light chain protein (AL) which comes from plasma cells (plasma brings us light, like the sun) (2) serum amyloid associated protein (SAA) which is made by liver cells (the liver makes serum stuff)
amyloidosis is classified based on what, and what are the 5 types? (he just lists the types, doesn't go into them specifically)based on clinical settings, anatomic location, and biochem. composition. There is primary, secondary, heredo-familial, amyloid of aging, and localized
what are the common sites of amyloidosis?liver, kidney, spleen. ( L and S are in the name, K?)
describe amyloid lesions in the liverexternal and cut surfaces waxy. also hard, pale, firm and enlarged (Amy has liver wax, which is pale and hard to work with)
describe amyloid lesions in the kidney. sp diff?large/grey/firm. dogs= deposit in glom. cats=extend to peritubular tissue also
describe amyloid lesions in spleen?"sago spleen" or "bacon spleen" either way it's firm, pale, gray and waxy. Yum! (amy would LOVE to eat this bacon-y spleen)
how do you STAIN amyloid to diag?congo red for pink/red. toluidine blue for blue (red and blue candies from the congo will take a tol on your stomach)
amyloidosis of renal involvement causes what probs?proteinuria, loss of antithrombin III---> thrombosis in many arteries. advanced cases lead to renal failure and uremia
amyloidosis with liver involvement causes what probs?metabolic derangement.
amyloidosis with pancreatic involvement causes what problems? in who specifically?non insulin dependent DM (type 2)- esp in cats
prognosis of amyloid pts?poor
amyloid changes are depositions of?proteins
hyaline changes are depositions of?proteins
what does a hyaline change look like?pink and glassy (think cartilage)
is hyaline intra or extra cellular?both, but intracellular is only ppl really (only people would have invented hydlide, but then animals suffer too, but differently)
intracellular hyaline affects who, and where?ppl, prox tubule of kidney
extracellular hyaline occurs in what situations?collagen fibrous tissue in old scars, glom. in chronic renal dz, equine intimal bodies (small calcified hyaline body found under endothelium of arteries), hyaline membrane dz, subendothelial hyaline in arterioles of pig brain in edema dz.

Mineral deposits

Question Answer
what are the two types of pathologic calcification?dystrophic and metastatic
what is dystrophic calcification?deposition of Ca in DEAD AND DEGENERATING tissue. NOT RELATED TO INC IN BLOOD Ca++ LEVELS. (think D= dead)
what is metastatic calcification?deposition of Ca in tissues b/c INC LEVELS OF CA IN BLOOD!!
what are the 5 causes of metastatic calcification?(1) hyperparathyroid activity (2) renal failure where phosphates are retained in the blood. (3) hypercalcemia of malignancy (4) granulomatous dz (5) excessive vit D
appearance of gross calcification lesionswhite or grey irregularly round particles which sound gritty when cut with a knife
appearance of micro. calcification lesionsseen as small irregular granules
what stain would you use to see calcification?van Kossa stains Ca++ BLACK
which is the "good" calcification and which is the bad?dystrophic is good for the body, metastatic is bad
which calcification is related to blood Ca++ levels?metastatic
which calcification manifests in dead or degenerating tissues?dystrophic
which calcification affects mainly BVs?metastatic
hypercalcemia USUALLY doesn't cause metastatic calcification in dogs and cats, but what DOES it do? (body systems affected-3)Ca++ deposits in epithelial cells of kidney (and other places) so polyuria and polydipsia since the kidney then cant concentrate urine, decreased excitability of GI leads to anorexia, vomiting, constipation. Dec neuromuscular activity leads to weakness, depression, twitching and seizures
what is CALCINOSIS?calcification in or under the skin
what are the two forms of CALCINOSIS?(Calcification in or under the skin) (1) calcinosis cutis (2) calcinosis circumscripta
what is happening in calcinosis cutis? (who does it affect?)happens in DOGS w/ hyperadrenocorticism, it is the mineralization of dermal collagen, epidermal and follicular basement membranes (curtis the dog has cushings)
what is happening in calcinosis circumscripta? (who does it affect?)mostly Lg breeds of dogs. calcification in connective tissue of dermis (esp at pressure points and trauma, so can be considered a form of dystrophic calcification) (circle of calcium around the elbow)
what does a calcinosis circumscripta lesion look like?raised nodule, cut surface shows white-grey masses of gritty material. Ca deposit is filled with LYMPHOCYTES, HISTIOCYTES, and GIANT CELLS.
what is gout? what are the two forms of it?deposit of uric acid/urates in tissues. (1) articular form (in joints) (2) visceral form (serous membranes, liver, kidney)
gross appearance of gout?greyish chalky material on serous membranes, joints, and kidney
microscopic appearance of gout?granulomatous reaction around the deposit