Toxicology Lecture 15 Renal Toxins

Front 1

What is the reserve capacity of the kidney?

Back 1

60-70% reserve
-minimal signs until reserve gone

Front 2

Azotemia develops when ____% of tubules gone.

Back 2

75%

Front 3

What are 4 ways that the kidneys can be damaged by toxins?

Back 3

1) Diminished blood supply
2) *Tubular obstruction
3) *Tubular cell damage
-incapable of re-absorption
4) Glomerular leakage

Front 4

How much of cardiac output goes to the kidneys?

Back 4

1/4 of CO

Front 5

There is a large ________ surface exposed in the kidneys.

Back 5

Endothelial surface

Front 6

What has to be intact for tubular cells to regenerate?

Back 6

Basement membrane

Front 7

What happens when there is tubule cell damage?

Back 7

Leaky tight junctions-->
more permeable to water-->
inability to concentrate urine (tubules don't reabsorb water)
-Active transport systems impaired (electrolytes, glucose etc. not reabsorbed)
-urea not diffused into collecting ducts

Front 8

What are 5 signs of renal failure?

Back 8

1) Anorexia, depression, wt. loss
2) Polyurea, polydypsia
-tubular function impaired
3) Edema
4) Anemia if chronic (EPO)
5) Ulcers, tartar, halitosis

Front 9

What are 5 abnormal lab values that are detected in renal failure?

Back 9

1) Azotemia, uremia
2) Isosthinuric
3) GFR
4) GGT in urine
5) Blood:urine creatinine ratio > 50: 1

Front 10

What is the source of oxalates? (2)

Back 10

1) Plants
2) Some produced in body naturally

Front 11

What do oxalates form when absorbed?

Back 11

Calcium oxalate crystals
-tie up calcium
-plug up kidney tubules

Front 12

What are 2 plants that we eat that contain oxalate?

Back 12

Rhubarb, beets

Front 13

What are 6 plants that contain oxalate?

Back 13

1) Rhubarb
2) Beets
3) Lamb's quarters
4) Halogeton glomeratus
5) Red root pigweed*
6) Dock or sorrel*

Front 14

What animal is most frequently affected by oxalate poisoning?

Back 14

Sheep

Front 15

What is the circumstance of oxalate poisoning?

Back 15

Livestock graze oxalate containing plants when they are not accustomed to eating the plants
-rumen MOs will metabolize some, tolerate more w/ time & gradual change of diet

Front 16

What is the toxic dose of oxalate poisoning?

Back 16

One dose could be fatal

Front 17

Oxalates are less toxic in ________.

Back 17

Ruminants
-if accustomed to consumption
-oxalates precipitated before absorbed

Front 18

What are the clinical signs of oxalate toxicity due to hypocalcemia?

Back 18

1) Muscle twitching, tetany
2) Weakness, prostration
3) Death
4) Hyperkalemia

Front 19

What are the clinical signs of oxalate toxicity as a consequence of acute renal failure?

Back 19

Depression, anorexia, azotemia

Front 20

How do you diagnose oxalate poisoning?

Back 20

-History of consuming plant
-Hypocalcemia
-Oxalate crystals in urine or kidney
-signs of renal failure

Front 21

What 3 lesions are found postmortem due to oxalate toxicity?

Back 21

1) Kidney swollen, pale
2) Crystals in tubules
3) Perirenal edema

Front 22

What are the 4 components of treating oxalate toxicity?

Back 22

1) Precipitate in GI w/ charcoal or limewater
2) IV fluids to dilute urine
-more water going through= less likely to plug things up
3) Calcium to replace bound
-Ca gluconate, glucose, Mg
-could form more crystals
4) Treat acute renal failure

Front 23

How do you prevent oxalate poisoning?

Back 23

-don't graze on oxalate containing plants (introduce gradually)
-Supplement w/ dicalcium phosphate

Front 24

What is the source of oak poisoning?

Back 24

Consuming oak leaves or acorns
-more when wind blows leaves and acorns to ground

Front 25

What animal do we usually see oak poisoning in?

Back 25

Cattle
-rumen converts tannins to gallic acid

Front 26

**What is acorn calf syndrome?

Back 26

=malformed
-protein malnutrition and acorns to dam

Front 27

What is the oak toxin?

Back 27

Tannins, gallotannin
-gallic acid + tannic acid
-still present if frozen or dried

Front 28

Tannins can be both ______toxic and ______toxic.

Back 28

Nephrotoxic and hepatotoxic

Front 29

Tannins are irritating to ______ tract.

Back 29

GI

Front 30

What is the mechanism of action of tannins?

Back 30

Denature cell protein--> cell death
-especially renal tubule cells

Front 31

Gallic acid is toxic to _______.

Back 31

Renal tubules

Front 32

What is the main clinical sign of oak toxicity?

Back 32

**Constipation followed by hemorrhagic diarrhea

Front 33

What are the 4 lab abnormalities found in an animal with oak toxicosis?

Back 33

1) Azotemia
2) Hypocalcemia
3) High anion gap
4) Isosthenuria
-urine specific gravity remains 1.008-1.014

Front 34

What are the 2 gross postmortem findings of oak toxicity?

Back 34

1) Mucoid, hemorrhagic, gastroenteritis
2) Kidneys pale & swollen
-Perirenal edema & hemorrhage

Front 35

What do you see on histology of the kidney in an animal w/ oak toxicity? (2)

Back 35

1) Renal tubular necrosis
-could be hepatocyte damage too
2) Eosinophilic material in lumen of proximal convoluted tubules

Front 36

How do you diagnose oak toxicosis?

Back 36

-History of oak availability (acorns or oak leaves in GI tract)
-Microscopic lesions of kidneys

Front 37

What are 4 components to treating oak toxicity?

Back 37

1) Remove from oak
2) Ca(OH)2 may precipitate in gut
3) IV fluids to rehydrate and promote renal function
4) Treat as for renal failure

Front 38

What are 3 ways to prevent oak toxicity?

Back 38

1) Introduce gradually
2) Provide other feed
3) Supplement w/ CaOH