Gen Path Labs 1-3 Flashcards
How does autolysis differ from necrosis
autolysis will be diffuse, no inflammatory rxn
How do the vacuolated areas accumulate in hepatocytes
damaged ER, decreased protein synth, lipids cannot leave hepatocyte
How does CCL4 damage hepatocytes
metabolized to CCL3- Free radical = lipid peroxidation and membrane damage
Antemortum ddx finding in CCL4 toxicity
bloodwork = elevated serum alanine aminotransferase (leaks from hepatocytes into serum)
How do you tell if a lesion is older?
epithelial cell hypertrophy is an adaptive rxn to injury and necrosis
Antemortum ddx finding in subacute renal infarct
UA = cellular casts
How do you differentiate apoptotic bodies from necrotic pyknotic/karyorrhectic nuclei?
Both are small nuclear fragments. Karyorrhectic nuclei fragment full sized with swollen, hyper eosinophilic cytoplasm where apoptotic bodies bud off with thin cytoplasm and are smaller.
how do you tell the difference between necrotic and apoptotic cells?
electron microscopy can show that apoptotic cells have NO SWELLING (mitochondrial/ER)
Spleen from foal with bacterial septicemia shows apoptotic bodies, what mechanisms can cause this?
- endotoxin
- stress - corticosteroids
- TNF alpha from endotoxin response
How does caseastion necrosis (Tb) develop
chronic inflammation - macs - coagulation necrosis w/o clean up = cell borders lost
what agents cause caseation necrosis
mycobacteria, fusobacterium necrophorum, incite inflamm rxn that recruit lots of macs.
What can cause hepatic lipidosis
- increased lipid synth
- mobilize peripheral = increased FFA to liver
- decreased FA oxidation in liver
- decreased apoprotein synth
- decreased lipoprotein export
What causes hepatic lipidosis in a peripartum cow?
reduced feed intake = mobilize fat stores to meet E needs for parturition and lactation. FA are converted to TG at high rates, liver exports them slowly = build up
A lipidosis liver would appear grossly as
yellow/brown, greasy, floats
Are hepatocellular lesions associated with hepatic lipidosis reversible?
Yes
Infarcted lung from a dog with heartworms shows a brown pigment in macrophages, what is it?
hemosiderin (Fe bound to apoferritin from RBC breakdown)
lipofuscin stains with
acid fast and autofluoresces
biliruben stains with
bile stains
hemosiderin stains with
prussian blue, perl’s iron stain
What happens to the macs in the infarcted lung of the dog with heartworm?
mas are removed by lymphatics and mucociliary escalator and disposed/recycled
A dog with chronic uremia shows gastric mineralizations - what is this? how would it look grossly?
metastatic calcification,
grey/off-white, granular, gritty
special stain for calcification
von kossa stain (stains black)
What type of amyloid is likely present in a dog with renal amyloidosis? how did it develop?
Secondary via SAA protein made by liver. Chronic inflammation - IL production by macs - hepatocytes make SAA - SAA undergoes PARTIAL proteolysis = amyloid deposits
In glomerular amyloidosis, what mechanisms account for protein in renal tubules? What does this do for long term health of patient?
Glomerular permeability increased. Long term = hypoalbuminemia and generalized edema due to decreased oncotic pressure
Amyloid stains grossly with
lugol’s iodine
What 3 features would you expect to see histologically in the lung from a cow with fibrous pneumonia due to bacterial infection?
- edema (interlobular septa, perivascular areas, distended lymphatics, eosionophilic/protein rich material
- edema with protein in alveolar spaces
- hyperemic BVs
In the case of cow with fibrous penumonia what caused the edema?
increased vascular permeability (protein in edema!)
What lab tests ddx confirm DIC
hemogram (thrombocytopenia, hypofibrinogenemia), elevated clotting times, elevated d-dimers
__ is a component of glutathione peroxidase, a critical enzyme in enzymatic degradation of free radicals and lipid hydroperoxides
selenium
