Clinical Pathology Exam 3

Front 1

Leakage enzymes are released as a result of membrane damage. List some reasons for this damage.

Back 1

-hypoxia
-lipid accumulation
-glycogen accumulation
-toxin exposure
-trauma

Front 2

What are 3 common hepatocellular leakage enzymes?

Back 2

AST, ALT (small animals), SDH (lg animals)

Front 3

What is AST specific for?

Back 3

muscle, liver, RBC

Front 4

What are the 2 induced hepatic enzymes?

Back 4

ALP and GGT

Front 5

What is ALP specific for?

Back 5

liver, steroids (dogs only), bone

Front 6

What are differentials for elevation is ALT?

Back 6

D - degenerative
A - anomalous
M - metabolic
N - neoplastic/non-infectious/nutritional
I - inflammation
T - toxix/trauma

Front 7

What does it mean when AST is elevated, but CK is not?

Back 7

greater decree of liver damage

Front 8

Which type of hepatocytes have first contact with blood and therefore oxygen, nutrients and toxins?

Back 8

periportal

Front 9

Where are the centrilobular hepatocytes?

Back 9

in the center around the central vein - most affected by anemia, dehydration and shock

Front 10

What 4 structures are at the portal area?

Back 10

-portal vein
-hepatic artery
-lymphatic vessel
-bile duct

Front 11

What is the flow of blood flow in the liver?

Which way does lymph and bile flow?

Back 11

-from portal vein into sinusoids, thru sinusoids, to central vein
-hepatosites line these sinusoids and remove toxins from the blood

-lymph flows in the opposite direction

Front 12

What is bilirubin conjugated to?

Back 12

glucuronic acid

Front 13

Is unconjugated bilirubin water soluble?

Back 13

No

Front 14

What is the rate limiting step for bile?

What does this mean?

Back 14

secretion into the SI

-overwhelmed hepatocytes can regurgitate bilirubin back into the circulation where it is eliminated byt the kidneys

Front 15

Why is pee yellow?

Why is poop brown?

Back 15

urobilinogen + O2

stercobilinogen stays in feces because it is water insoluble

Front 16

What does poop look like if the common bile duct is completely blocked?

urine?

Back 16

grey feces (bc no urobilinogen or stercobiligion can be produced in the SI)

-urine is brown bc of massive regurgitation of conjugated bilirubin and its passage into the urine (bilirubinuria)

Front 17

What is a cause of pre-hepatic hyperbilirubinemia?

hepatic?

Post-hepatic?

Back 17

(1) accelerated RBC destruction - lysis

(2) diffuse blockage of bile ducts or canaliculi (liver injury, necrosis, fibrosis, swelling)

(3) common bile duct obstruction --> grey poop

Front 18

What supports intra and post hepatic causes of hyperbilirubinemia (cholestasis)?

Back 18

-elevation of ALP and GGT
-elevation in leakage enzymes with liver damage

Front 19

What comes first hyperbillirubin - uria or nemia?

Back 19

hyperbilirubinuria comes first

Front 20

What will be elevated in horses with anorexia?

Back 20

unconjugated bilirubin - no elevation in liver enzymes

Front 21

Is bilirubin a specific indicator of hepatic disease in the ruminant?

Back 21

no

Front 22

What are bile acids made from in the hepatocytes?

Back 22

cholesterol

Front 23

What do bile acids do?

Back 23

released with bile after a meal to aid pancreatic enzymes with lipolysis
-then 90% are reabsorbed in terminal ileum
-5% absorbed in colon
5% lost in poop (replaced by hepatic synthesis)

Front 24

What is more difficult - to replace lost bile acids or recycle them?

Back 24

recycle

Front 25

Why is it not necessary to evaluate the bile acids of a hyperbilirubinemic patient?

Back 25

bile acids will regurgitate into systemic circulation with intra or post hepatic biliary obstruction

Front 26

What happens to bile acid levels when > 80% of hepatocellular mass is lost?

Back 26

increase in bile acids because hepatocytes can't take up the bile acids from circulation

-this is also true in a PSS

Front 27

What happens to ammonia after it is made from proteins in the gut?

Back 27

absorbed into portal circulation from GI
-removed by hepatocytes and converted to urea
-urea released into circulation and cleared b kidneys and helps maintain the concentration gradient

Front 28

What are some common causes of hyperammonemia?

Back 28

-decreased functional hepatic mass
-decreased presentation of ammonia to the liver (PSS)
-urea toxicosis
-severe GI disease in horses

Front 29

Why might isothenuria occur with liver disease?

Back 29

decreased conversion of ammonia to BUN therefore reduced concentrating ability

Front 30

What might happen to cholesterol with cholestsis?

Back 30

increase

Front 31

Are vitamin K def. possible with cholestasis? Why?

Back 31

yes - fat digestion and absorption is negatively affected (K is fat slouble)

Front 32

Why might FDPS be increased with liver failure?

Back 32

the liver clears FDPs

Front 33

What are 2 causes of hypcholesterolemia?

Back 33

1 - PSS
2 - PLE

Front 34

How is glucose derived?

Back 34

-intestinal absorption
-hepatic production --> gluconeogenesis (non CHO sources) and glycogenolysis (from stored gylcogen)

Front 35

In what 3 ways are blood glucose concentrations regulated?

Back 35

(1) time since last meal
(2) hormonal influences
(3) peripheral utilization of glucose

Front 36

What do the following hormones do for blood glucose levels?
-insulin
-glucocorticoids
-glucagon
-catecholamine
-growth hormone

Back 36

-insulin --> decrease
-glucocorticoids --> increase (promote gluconeogenesis)
-glucagon --> increase
-catecholamine --> increase (promote glycogenolysis)
-growth hormone --> increase

Front 37

What are the 5 top reasons for hyperglycemia?

Back 37

(1) post-prandial
(2) corticosteroids-mediated stress
(3) catecholamine release
(4) DM
(5) hyperadrenocortism (Cushings)

Front 38

What are causes of hypoglucemia?

Back 38

-starvation/malabsorption
-increased insulin production
-decreased glucocorticoid production (addisons)
-liver failure
-sepsis
-neoplasia
-ketosis in cattle
pregnancy toxemia in sheep

Front 39

What does an amended insulin: glucose ratio greater than 30 suggest?

Back 39

hyperinsulinism

Front 40

What does PTH target and what does it do?

Back 40

bone, intestine, kidney

-increases Ca (intestinal and renal absorption)
-decrease P (renal excretion)

-mobilization of both from the bone
-increase formation of active vitamin D

Front 41

Where does vitamin D3 come from?

-which animal lacks the kidney enzyme so that they are less dependent on the renal function for activation of vitamin D3

Back 41

diet
-conversion of cholesterol by UV light to cholecalciferol (vitamin D3)

-D2 (ergocalciferol from plants)


--horses

Front 42

What does vitamin D3 do?

Back 42

-increases Ca and P

-action on GI, bone and kidney

-when Ca is low, PTH in increased and enhances formation of active vitamin D

Front 43

Where is calcitonin made and what does it do?

Back 43

parafollicular cells of thyroid (C-cells)

-decreases Ca and P

Front 44

What are the major fractions of Ca?

Back 44

- free or ionized (50%) --> regulated by hormones and contributes to pathologic states

-anion-bound Ca (40-50%) --> bound to albumin

-bound to non-protein ions

Front 45

What are the 6 determinants of serum Ca?

Back 45

1 - Age (higher in older, not kittens or foals)
2 - albumin concentration
3 - GI absorption
4 - resorption from or deposition of calcium in the bone
5 - kidneys
6 - Calcium and P interaction (if product is greater than 70, mineralization can occur)

Front 46

What are causes of hypercalcemia?

Back 46

Granulomatous (increase Ca and P)
Osteolytic
Spurious
Hyperparathyroidism
D- Vitamin D (indirectly with granulomatous)
Addison's disease (lack aldosterone, Na decreases)
R - ARF in horses and rabbits
Neoplasm (secretion of PTHrp)

Front 47

What are causes of hypocalcemia?

Back 47

-hypoalbuminemia
-decreased PTH (hypomagnesemia - grass tetany)
-decreased vitamin D
-EPI
-lactational causes
-furosemide treatment

Front 48

What 5 factors determine serum phosphorous concentrations?

Back 48

1 - renal function and hydration status
2 - IC and EC shifts
3 - GI absorption
4 - bone resorption
5 - age (young will have increased levels)

Front 49

What are causes of hyperphosphatemia?

Back 49

- decreased GFR
-increased GI absorption
- ICF - ECF

(acute renal failure, exertional rhabdomyolysis, cholechalciferol intoxication)

Front 50

What are causes of hypophosphatemia?

Back 50

-increased GFR
-decreased intestinal absorption
- ECF - ICF shift
- defective mobilization of P from bone

(hyperparathyroid, administration of insulin --> ECF - ICF)

Front 51

Cortiocosteroid administration can result in a 5 fold increase in what?

Back 51

lipase

Front 52

What type of increase in amylase and lipase is seen in animals with pancretis?

Back 52

3 fold increase

Front 53

What is TLI and is it specific?

Back 53

trypsin-like immunoreactivity
-yes

Front 54

What does an elevate TLI mean?

decreased?

Back 54

- pancreatis or decreased GFR

- EPI

Front 55

What animal is cPLI used in?

Back 55

dogs - improved sensitivity to TLI in cases of pancreatis

Front 56

What is the test of choice for diagnosis pancreatis?

-EPI?

Back 56

PLI

-TLI

Front 57

What are the 3 main diseases of the exocrine pancreas that can be detected by lab eval?

Back 57

-pancreatisi
-pancreatic neoplasia
-EPI

Front 58

What is seen with pancreatis?

Back 58

-inflammation
-azotemia
-increased liver enzymes
-increase in amylase, lipase, TLI and PLI
-hyperglycemia
-hypocalcemia

Front 59

Increased serum folate could mean what?

decreased?

Back 59

-EPI or bacterial overgrowth

-severe intestinal disease

Front 60

Will cobalamin be increased or decreased with EPI?

Back 60

decreased

Front 61

Hyperadrenocorticism includes 3 types, what are they?

Back 61

1 - pituitary dependent
2 - adrenal dependent
3 - iatrogenic

Front 62

In hyperadrenocortisim, what does primary disease at the adrenal gland produce?

what does secondary disease at the pituitary gland produce?

Back 62

-adrenal --> excess glucocorticoids

-pituitary --> excess ACTH

Front 63

What is more common - primary or secondary Cushings?

Back 63

secondary - 85% at pituitary

Front 64

What type of hypoadrenocortism is more common?

Back 64

-adrenal gland failure - most common -- immune mediated destruction

Front 65

What test would you use to take advantage of the normal negative feedback mechanism in the HPA axis?

Back 65

Low-dose dexamethasone suppression test

-used to SCREEN animals for PDH or ADH

Front 66

What is the high-dose dexamethasone test used for?

-which lesion should suppress?

Back 66

to distinguish between PDH and ADH

-PDH should suppress
adrenal tumor will not suppress

-this test is not really used

Front 67

What test helps determine:

hypoaderenocortism
iatrogenic hyperadrenocorticism
SCREENING test for hyperadrenocorticism

Back 67

ACTH stim test

Front 68

What is the best test to differentiate PDH from adrenal tumors?

Back 68

Endogenous ACTH