Gen Path Labs 1-3

Question 1

How does autolysis differ from necrosis

Answer 1

autolysis will be diffuse, no inflammatory rxn

Question 2

How do the vacuolated areas accumulate in hepatocytes

Answer 2

damaged ER, decreased protein synth, lipids cannot leave hepatocyte

Question 3

How does CCL4 damage hepatocytes

Answer 3

metabolized to CCL3- Free radical = lipid peroxidation and membrane damage

Question 4

Antemortum ddx finding in CCL4 toxicity

Answer 4

bloodwork = elevated serum alanine aminotransferase (leaks from hepatocytes into serum)

Question 5

How do you tell if a lesion is older?

Answer 5

epithelial cell hypertrophy is an adaptive rxn to injury and necrosis

Question 6

Antemortum ddx finding in subacute renal infarct

Answer 6

UA = cellular casts

Question 7

How do you differentiate apoptotic bodies from necrotic pyknotic/karyorrhectic nuclei?

Answer 7

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.

Question 8

how do you tell the difference between necrotic and apoptotic cells?

Answer 8

electron microscopy can show that apoptotic cells have NO SWELLING (mitochondrial/ER)

Question 9

Spleen from foal with bacterial septicemia shows apoptotic bodies, what mechanisms can cause this?

Answer 9

1. endotoxin
2. stress - corticosteroids
3. TNF alpha from endotoxin response

Question 10

How does caseastion necrosis (Tb) develop

Answer 10

chronic inflammation - macs - coagulation necrosis w/o clean up = cell borders lost

Question 11

what agents cause caseation necrosis

Answer 11

mycobacteria, fusobacterium necrophorum, incite inflamm rxn that recruit lots of macs.

Question 12

What can cause hepatic lipidosis

Answer 12

1. increased lipid synth
2. mobilize peripheral = increased FFA to liver
3. decreased FA oxidation in liver
4. decreased apoprotein synth
5. decreased lipoprotein export

Question 13

What causes hepatic lipidosis in a peripartum cow?

Answer 13

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

Question 14

A lipidosis liver would appear grossly as

Answer 14

yellow/brown, greasy, floats

Question 15

Are hepatocellular lesions associated with hepatic lipidosis reversible?

Answer 15

Yes

Question 16

Infarcted lung from a dog with heartworms shows a brown pigment in macrophages, what is it?

Answer 16

hemosiderin (Fe bound to apoferritin from RBC breakdown)

Question 17

lipofuscin stains with

Answer 17

acid fast and autofluoresces

Question 18

biliruben stains with

Answer 18

bile stains

Question 19

hemosiderin stains with

Answer 19

prussian blue, perl’s iron stain

Question 20

What happens to the macs in the infarcted lung of the dog with heartworm?

Answer 20

mas are removed by lymphatics and mucociliary escalator and disposed/recycled

Question 21

A dog with chronic uremia shows gastric mineralizations - what is this? how would it look grossly?

Answer 21

metastatic calcification,

grey/off-white, granular, gritty

Question 22

special stain for calcification

Answer 22

von kossa stain (stains black)

Question 23

What type of amyloid is likely present in a dog with renal amyloidosis? how did it develop?

Answer 23

Secondary via SAA protein made by liver. Chronic inflammation - IL production by macs - hepatocytes make SAA - SAA undergoes PARTIAL proteolysis = amyloid deposits

Question 24

In glomerular amyloidosis, what mechanisms account for protein in renal tubules? What does this do for long term health of patient?

Answer 24

Glomerular permeability increased. Long term = hypoalbuminemia and generalized edema due to decreased oncotic pressure

Question 25

Amyloid stains grossly with

Answer 25

lugol’s iodine

Question 26

What 3 features would you expect to see histologically in the lung from a cow with fibrous pneumonia due to bacterial infection?

Answer 26

1. edema (interlobular septa, perivascular areas, distended lymphatics, eosionophilic/protein rich material
2. edema with protein in alveolar spaces
3. hyperemic BVs

Question 27

In the case of cow with fibrous penumonia what caused the edema?

Answer 27

increased vascular permeability (protein in edema!)

Question 28

What lab tests ddx confirm DIC

Answer 28

hemogram (thrombocytopenia, hypofibrinogenemia), elevated clotting times, elevated d-dimers

Question 29

__ is a component of glutathione peroxidase, a critical enzyme in enzymatic degradation of free radicals and lipid hydroperoxides

Answer 29

selenium