Fa Med - Metabolic Diseases Of Small Ruminants

Front 1

Maximum copper uptake
-sheep
-cattle
-horses

Back 1

-sheep: 25 ppm

-cattle: 100 ppm

-horses: 800 ppm

*sheep very low --> very susceptible

Front 2

Copper toxicosis
-when do problems occur in sheep

Back 2

-when fed cattle or horse rations

*goats not as susceptible

Front 3

Copper toxicosis
-ratio

Back 3

Cu:Mo & Su
>10:1

Front 4

Effect of Mo & Su on Copper

Back 4

-bind dietary copper and decrease liver accumulation

Front 5

Where is Copper toxicity a problem?

Back 5

-pastures fertilized with poultry/swine manure from animals fed CuSo

-lambs fed calf milk replacers

-grazing pasture with a high Cu:Mo ratio (young plants low in Mo; clover high in copper)

-hepatogenous form

Front 6

Where does copper accumulate in the body?

Back 6

-hepatocytes

Front 7

Hepatogenous copper toxicity
-describe

Back 7

-plant toxins damage liver parenchyma

*senecio, helotropium

Front 8

Copper toxicity
-pathogenesis

Back 8

Cu binds with proteins ---> Cu accumulates in liver lysozymes ---> necrosis of parenchymal cells ---> release of Cu into blood due to stress or spontaneously ---> acute IV hemolysis due to fragile RBCs, dec. blood glutathione, methemaglobinemia

Front 9

Cu toxicity
-signs

Back 9

-watery, dark feces
-anemia
-hemaglobinuria
-methemaglobinemia
-icterus
-muddy mucus membranes

Front 10

Cu toxicity
-necropsy signs

Back 10

-liver: yellow, friable

-kidney: gunmetal grey (dark red-black)

Front 11

Cu toxicity
-necropsy diagnosis

Back 11

Liver and Kidney
*after Copper release, the liver may not be useful to test due to normal Copper levels
*test other organs instead of liver

Front 12

Cu toxicity
-prognosis

Back 12

-poor

Front 13

Cu toxicity
-treatment

Back 13

-ammonium molybdate & Na sulfate
-ammonium tetrathiomolybdate
-methylene blue

Front 14

Cu deficiency
-causes

Back 14

-overcautious owners

Nutritional deficit
-Ca, Fe, Se, Zn, alakaline soil, Vit C
-Molybdenum + Cu (blocks availability)
-Improved pastures (decreased Cu in forage, fertilizer with Mo)
-grass/fresh gras > hay/legumes

Front 15

Cu deficiency
-clinical signs

Back 15

-anemia
-dec. milk production
-heart failure
-dec. fertility
-dec. growth
-lameness
-diarrhea

Front 16

Enzootic neonatal ataxia
-cause

Back 16

-lamb born to a Cu deficient dam (usually from high Mo or sulfate levels)

Front 17

Enzootic Neonatal Ataxia
-signs

Back 17

-progressive incoordination and paresis starting at the hind limbs
-loss of wool crimp
-diarrhea
-unthrifty
-low weight gain
-lost hair color
-fractures

Front 18

Enzootic Neonatal Ataxia
-prognosis

Back 18

-death in 3-4 days of clinical signs

Front 19

Enzootic Neonatal Ataxia
-diagnosis

Back 19

-usually neonates
-2-3 months old
-recover with supplementation
-same clinical signs

-liver copper biopsy antemortem
-histopath --> demyelination of spinal cord and cerebral white matter cavitation

Front 20

copper deficiency
-antemortem diagnosis

Back 20

-liver biopsy (levels may be normal before Cu release from liver)
-take biopsy in 9th IC space, off cranial aspect of 10th rib

Front 21

Copper deficiency
-prevention

Back 21

-adequate Cu intake
-trace mineral supplements
-evaluate feed
-Cu:Mo (5:1-10:1 for adequate absorption)

Front 22

Vitamin E/Selenium Deficiency
-aka

Back 22

-stiff lamb disease
-white muscle disease

Front 23

Vit E/Selenium Deficiency
-animals affected

Back 23

-young/rapidly growing

Front 24

Vit E/Selenium Deficiency
-causes

Back 24

-PUFAs
-Milk replacer with fish oil, linseed oil, corn oil, soybean oil (contain PUFAs)
-High moisture grains have lower levels of Vit E
-young growing plants (high in PUFAs)

Front 25

Vitamin E/Selenium Deficiency
-effect of PUFAs

Back 25

-polyunsaturated fatty acids result in the release of free radicals

Front 26

Vitamin E/Selenium Deficiency
-MOA

Back 26

-antioxidant deficiencies causing the breakdown of cell membranes

Front 27

Vitamin E/Selenium deficiency
-forms

Back 27

-cardiac
-skeletal

Front 28

Vitamin E/Selenium Deficiency
-cardiac form

Back 28

-peracute
-myocardial decompensation
-pulmonary edema (nasal froth)
-increased heart rate/irregular rhythm
-lesion in heart, diaphragm, intercostals
-death in 24 hrs

Front 29

Vitamin E/Selenium Deficiency
-skeletal form

Back 29

-weak/stiff
-swollen/painful supporting muscles (differentiate from Cu deficiency) [gastroc, semi-membrinosis, neck, gluteals]
-increased heart rate from pain

*may improve with treatment

Front 30

Vitamin E/Selenium Deficiency
-diagnosis

Back 30

Selenium
-serum
-liver
-Se dependent glutathione peroxidase
-found in RBCs
-spin down immediately or keep refrigerated prior to testing because RBCs will consume

Vit E difficult to evaluate

Front 31

Vitamin E/Selenium deficiency
-rule outs

Back 31

-Clostridial myositis ***** (will get gas crackles on palpation)
-sepsis
-toxemia
-meningitis
-spinal cord trauma
-neurotoxins
-etc.

Front 32

Vitamin E/Selenium Deficiency
-Treatment

Back 32

Vitamin E/Selenium combo injectable (Vit E only for preservative, not medicinal effect)
-Bo-Se
-L-Se

*Don't use Me-Se in Sheep (cause abortion in pregnant females)

Front 33

Vitamin E/Selenium
-prevention

Back 33

-test forage
-selenium dietary supplements
-mixture of fresh legumes and grasses
-avoid diets high in grains

Front 34

Hypocalcemia
-often seen when in small ruminants

Back 34

-with pregnancy toxicosis in last 2 weeks of gestation
(seen post parturition in cattle)

Front 35

Hypocalcemia
-cause

Back 35

-high demand for calcium by pregnant ewes

Front 36

When are ewe's serum calcium levels considered critical?

Back 36

< 7 mg/dl

Front 37

hypocalcemia
-clinical signs

Back 37

-inital hyperactive muscles
-ataxia/flaccid paralysis
-bloat**** (S-shaped spine)

Front 38

Hypocalcemia
-hyperactive muscles due to

Back 38

-poor membrane stabilization from lack of calcium

Front 39

Hypocalcemia
-ataxia/flaccid paralysis due to

Back 39

-no Calcium at synapses to cause Ach release

Front 40

Hypocalcemia
-bloat due to

Back 40

-no ruminal contractions

Front 41

Hypocalcemia
-treatment

Back 41

-Oral calcium drench (can kill with overdose IV)

Front 42

Hypocalcemia
-prevention

Back 42

-alfalfa

Front 43

Pregnancy toxicosis
-aka

Back 43

-ketosis

Front 44

Pregnancy toxemia
-occurs when in Small ruminants

Back 44

-last trimester of pregnancy with multiple feti

*post parturition in dairy cattle due to high energy demand for milk production

Front 45

Pregnancy toxemia
-predisposed animals

Back 45

-thin
-excessively obese
-stressed (storm, movement, etc.)

Front 46

Pregnancy toxemia
-due to

Back 46

Negative energy balance
-decreased intake
-increased demand

Front 47

Pregnancy Toxemia and the Krebs Cycle

Back 47

Oxaloacetate can't be converted to glucose due to a lack of proprionate for kreb cycle function
-Oxaloacetate backs up to Acetyl CoA --> Acetoacetate --> Ketones (acetone, beta-hydroxybutyrate)

Front 48

Ketones
-can be used for energy by

Back 48

-muscle (won't lose muscle tone)

Front 49

Ketones
-can't be used for energy by

Back 49

-RBCs
-Brain
-Fetus

*only glucose

Front 50

Pregnancy toxemia
-clinical signs

Back 50

-recumbency (but with muscle tone)
-stargazing*
-incoordination*
-bruxism*

Front 51

Pregnancy toxemia
-diagnosis

Back 51

-ketonuria
-history/clinical signs
-acidemia
-hypoglycemia

Front 52

Pregnancy toxemia
-why could there be hyperglycemia

Back 52

-stress (cortisol)

Front 53

Animal that will pee when suffocated

Back 53

-sheep

Front 54

Pregnancy toxemia
-treatment

Back 54

Slightly affected;
-IV dextrose
-propylene glycol (metabolized to proprionate)
-transfaunation

Severely affected
-C-section
-support ewe to allow fetal development to 10 days pre-term (will often lose both ewe and feti)

Front 55

Pregnancy toxemia
-prevention

Back 55

Ultrasound @ 50 days to determine if multiple pregnancy
-separate multiple feti ewes and give higher energy feed ration
-shear early to decrease heat

Front 56

Goiter
-causes

Back 56

-Breed susceptibility (Boer, Angora, polled dorset)
-Ingestion of Brassica family plants during gestation (goitrogenic compounds - peanuts, soybeans, cherries, kale)
-Iodine deficient diet in Dam
-iodine deficient diet during gestation
-congenital

Front 57

Goiter
-induction in pre-disposed breeds

Back 57

-iodine induces

Front 58

Iodine deficient diet during gestation due to

Back 58

-high nitrates blocking absorption
-iodine deficient soil
-sandy soil

Front 59

Animals with congenital goiter

Back 59

-merino sheep
-dutch
-pygmy
-nubian goats

*outgrow by 1 yr old

Front 60

Goiter
-clinical signs of iodine deficient form

Back 60

-enlarged thyroid
-dyspnea
-weak, hairless neonate
-poor fiber quality
-dry skin
-tendon laxity
-low libido, fertility, semen quality
-poor growth rate
-low milk production

Front 61

Goiter
-diagnosis

Back 61

-clinical signs of enlarged thyroid
-history of poor growth, wt loss, fleece quality
-low Iodine in serum, plasma, milk
-low thyroxine level (unreliable)

Front 62

Goiter
-treatment

Back 62

-trace mineral supplement during pregnancy
-avoid brassica plants
-potassium iodine PO late gestation
-Lugols iodine in milk to newborn

*poor response to treatment in congenitals