Ruminant Nutrition Flashcards

1
Q

What are the three different layers in the ruminant stomach? What is in each layer?

A

• 3 different layers. Gas is most dorsal. Then todays hay since it is not as broken down yet. Followed by grain and yesterdays hay (which has had some time to ferment and settle. Bottom Layer is higher in liquids and smaller particles.

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2
Q

What is the path of objects after being swallowed?

A

Feed/water, and saliva are delivered to the reticulorumen through the esophageal orafice.

Foreign objects like rocks and nails go to the reticulum.

Food is broken down into smaller pieces, that then is pushed into the retiuculum through the reticulo- omasal orifice into the omasum.

It will eventually make it into the rumen or the fermentation vat.

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3
Q

What is the purpose of saliva? What is the gas that makes up the majority of the ruminal gasses?

A

Saliva is used as a buffer

Much of gas that fills rumen is methane

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4
Q

What occurs during the first month of life for ruminants? What are they considered? What is milk curdled by?

A
  • Breaks down particles to smaller size. Smaller more dense material is pushed to the reticulum through the reticulo-omasal orifice into the omasum.
  • For first month of life, ruminant is functionally a mono-gastric animal. If milk goes to rumen it rots. Closure of gastric groove directs milk from esophagus to the omasum. Stomach milk is curdled by rennin and eventually digested.
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5
Q

What is rumination? When does it occur?

A
  • Rumination- regurgitation of ingesta from the reticulum followed by remastication and reswallowing.
  • Effective mechanical breakdown and increases substrate surface area to fermentive microbes.
  • Usually occurs when cow is at rest.
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6
Q

What are carbohydrates metabolized to in the rumen? What VFA is converted to glucose? How?

A
  • Fermentation of carbohydrates to VFA’s (alot)
  • Propionate (VFA) is metabolized to glucose via hepatic gluconeogenesis.
    • Butyrate and acetate cannot be converted to glucose.
    • Provides > 70 % energy supply
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7
Q

What occurs in VFA metabolism? What is acetic acid oxidixed for? What is propionic acid used for? What is Butyric acid used for?

A

VFA’s absorbed across ruminal epitheleum to ruminal veins, portal vein and liver. Removal of VFA important to prevent rumen acidosis

Acetic acid oxidized to generate ATP and used as source of acetyl COA for lipid synthesis

Propionic acid -> gluconeogenesis

-Almost no glucose makes it to the small intestines for absorption.

Butyric acid metabolized by rumen epithelium to ketone beta hydroxybutyric acid. Used for energy production.

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8
Q

What is the relationship of lactation and glucose demand? Lactose and milk production?

A
  • Higher lactation (or lactation in general), more milk produced. More lactose more volume of milk.

Glucose + galactose = lactose

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9
Q

How much glucose is needed to produce milk? What does that mean for cows? What is the most common milk cow in the US? How many lbs of milk can a cow make in a day? When is another time the reqiures more glucose?

A
  • 2 lbs glucose needed to make 6 gallons of milk.
  • Liver is in state of constant gluconeogenesis during lactation and requires constant supply of propionate.
  • Can make 150 lbs of milk (18 gallons) per day.
  • Requires more glucose during third trimester of gestation.
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10
Q

What is the process of gluconeogenesis in ruminants?

A

• Non esterfied Fatty acids sent to liver to become Triglycerides ( which then becomes VLDL), Ketone bodies ( exportable energy source used by extra hepatic tissues) or for fuel for hepatic metabolism to make energy.

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11
Q

What happens when energy requirements are not met? What happens when intake is low? When glucose is low?

A
  • more impactful when this occurs during lactation
  • Energy requirements > energy intake = negative energy balance

• When intake is low, insulin is decreased and glucagon is increased ( increases gluconeogenesis), When glucose is in short supply, fats/ triglycerides are used as substitutes since lipids are “energy dense”

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12
Q

What is lipolysis? What is the enzyme that facilitates lipolysis? What is lypolyis promoted by?

A
  • Lipolysis - process of breaking down lipids to glycerol and 3 free fatty acids (FFA)
  • HSL (hormone sensitive lipase) is enzyme that facilitates it
  • It is promoted by:

Negative energy balance

High glucagon and low insulin

Stress -> cortisol release

Stress -> epinephrine release

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13
Q

What is the long term complications of negative energy balance?

A
  • Limited reserve muscle so it is not primary source of alternative energy.
  • Acetyl CoA is chemically unstable, so the body does not want excess of it since it can cause oxidative damage.
  • Glycogen reserves depleted quickly
  • Fat reserves are main source of energy.

Oxaloacetate is limited and is depleted before all acetyl coa units are used up

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14
Q

What occurs with the formation of ketone bodies?

A
  • Ketones can be normal in moderate amounts when energy requirements are high (i.e lactation, ewes or does with large brood in last trimester)
  • Ketones remove unstable Acetyl CoA.
  • Ketones can be found and be normal, but excessive ketones can cause ketosis/ ketoacidosis.
  • Presentations of neurological signs, decreased appetite, pica, ect.
  • Can occur in severe chronic negative energy balance.
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15
Q

What are the 3 ketones?

A
  • acetoacetate, betahydroxybutyrate, acetone
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16
Q

What is ketosis? What are the clinical signs? What are your diagnostics? Prognosis?

A

Causes:

  • Can be primary - low carb diet
  • Secondary- unable to feed due to another issue.

• Common underlying reasons: orthopedic, LDA/RDA, mastitis

  • High concentrations of FFA, Hypoglycemia, increased blood ketones.
    • Usually in lactation which drives requirements.

Clinical signs:

  • vitals normal unless influenced by another primary disease. Decreased rumen motility, dry feces, dehydration, behavioral changes, dullness, nervousness ( can be dangerous to the vet)

Diagnostic Results:

  • Ketones can be detected in the breath. Acetone smell.
  • Reagents and tablets, can detect kin milk
  • Ketonuria can be diagnosed with urine dip stick
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17
Q

What is the treatments for ketosis?

A

Treatment

  • Treat underlying disease, or feeding high quality carbohydrate meals.
  • Add molasses in the water, orogastric tube feeding.
  • Transfaunation: If you have a fistulated cows, you can transfer rumen fluid from healthy cow to sick cow, can be administered via orogastric tube.
  • Adminsiter propylene glycol: metabolized by the liver to propionate. If animal has liver failure no point to give since it wont be metabolized. Overdose can cause diarrhea, ataxia, coma ect.
    • Glucose IV (decreases ketone formation)
    • Corticosteroids: enhances gluconeogenesis, reduce milk production. improve how animal feels.
    ◦ Negatives: Can induce abortion if pregnant. Stimulates hormone sensitive lipase, which increases FFA production which is not ideal in these patients.
  • Glucose IV + insulin SC: can be given together to reduce lipolysis -> you will see decrease of phosphorus, magnesusm, and potassium.
  • Give B vitamins : likely low, synthesized by rumen microbiota, niacin and choline (can help form lipoprotiens and transport fat from the liver in fattyliver disease)
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18
Q

How can you prevent ketosis in ruminants?

A
  • Prevention is key.
  • Monitor high risk patients and make sure high risk are getting supportive measures for prevention.
  • Cows feel fuller during pregnancy so they eat less and will also have increased nutritional needs due to lactation status, so making sure they are on a diet that is calorically and nutritionally dense for their needs are essential.
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19
Q

What are NEFA levels?

A

• Measure NEFA is blood at various intervals pre and post partum at random to make sure they are receiving essential nutrition.
- If more than 40% of cows in group are above normal values this indicates a problem.

How to improve: increase energy density, review BCS in mid lactation and dry cows, ensure sufficient space per cow, make sure feed is always available.

20
Q

What is fatty liver disease? What are the clinical signs?What is the treatments?

A

Can occur with cows with normal BCS, and is a result of prolonged negative energy balance in the immediate period before and after calving.

  • Result of decreased appetite and high energy needs during lactation.
  • Happens quicker in obease animals. High access of FFA, the ketone synthesis pathways become saturated.

Clinical signs:

  • Usually after calving
  • Depression
  • Anorexia
  • Weight loss
  • Decreased GI/ rumen motility
  • Weakness

Treatment:

  • Same as ketosis, but more severe so requires more intensive care
  • No propylene glycol -> cannot metabolize it
  • Cows with high BCS should be encouraged to lose weight.

Treatment is costly and long.

  • Put pedometers on cow, and move feed/ water on opposite sides of pen to make them increase exercise.
21
Q

What is pregnancy toxemia? What is the gestation period of small ruminants? What is the correlation between number of embryos and metabolic strain?

A
  • Another disease associated with chronic negative energy balance. Occurs in does and ewes in pregnancies with multiple offspring. Gestation in small ruminants last 142-150 days. Most embryonic development and growth takes place in the last trimester.

More embryos -> Higher metabolic strain

22
Q

What are the clinical signs of pregnancy toxemia in cattle? Pathophysiology? Treatment?

A

Clinical signs:

  • Illness ( poor doer) in last trimester
  • Poor appetite
  • Seperated from flock
  • Stargazing
  • Weakness

Pathophysiology: Unrelenting glucose requirement from fetus, this can be fatal. Ketosis also usually occurs and ewes get ketoacidosis.

Treatment:

  • Termination of pregnancy
  • Alternatively can try supportive care but likely wont work

Supportive care : IV glucose, propylene glycol, transfaunation, highly digestible high carbohydrate food (even sugary cerals can be supplemental)

23
Q

What is calcium important for?

A
  • Found in every cell
  • Bone is major storage pool for calcium of hydroxyapatite
  • Component in milk (high requirement during lactation)
  • Important muscle activity ( actin- myosin coupling)
  • Influx in cells may trigger cell death (both in normal and pathologic processes)
  • Calcium is required in hormone/ neurotransmitter release.
  • Dampen neuronal excitation potential that requires sodium channel activity.
24
Q

How does Calcium dampen the neuronal excitation potential that requires sodium channel activity?

A
  • Terminus of neuron, calcium enters the cell in response to action potential.
  • Calcium ion promotes fusion of vesicles containing acetylcholine with the membrane.
25
Q

What facilitates calcium absorption? What dietary factors can affect calcium absorption?

A

Activated Vitamin D, and Parathyroid Hormone.

  • Phosphorus and magnesium content
  • High dietary zinc (many times due to formulation error)
  • Oxalates (can be posionous)
26
Q

What is oxalate poisoning? What does it cause?

A

High oxalate plants have potential to be posionous. Rumen can detoxify oxalates but is dependent on bacterial content and can be overwhelmed when large ammounts are ingested.

  • Forms insoluable salts that precipitate in the kidney causing kidney failure.
27
Q

Who is more suceptible to oxalate poisoning?

A
  • Sheep are most susceptible
  • Livestock should be adapted to oxalate plants over 4 days incrementally increasing time allowed to graze these plants.
  • Becomes more resistant to these plants over time.
28
Q

What percentage of extracellular calcium in the blood is ionized? When is more calcium bound to albumin? What will this cause? Can these cause any clinical signs? In ruminants, what do you normally see concurrently and why?

A
  • More calcium bound to albumin during alkalosis, resulting in slightly lower Ca++ in the blood and ECF
  • Alkalosis can cause signs of hypocalcemia.
  • In ruminants normally occurs with diseases that impair abomasal emptying since hcl is trapped in abomasum and forestomachs, metabolic alkalosis.
29
Q

What occurs with calcium in acidosis?

A
  • Less calcium is bound, causing the release of calcium from the bones. Calcium from bone can also be used as a buffer.
30
Q

What is PTH released from? What do they do? What occurs in young animals? Older animals?

A

PTH released by chief cells of parathyroid in response to low ionized calcium. This acts to increase Ca2+ in ECF.
- PTH promotes bone resorption to provide Ca2+.
• Bones of younger animals (12-24 hours) responds more rapidly than older animals(24-48+ hours).

• Reabsorption of calcium ion from the glomerular filtrate in the kidney.

  • Loss of phosphate ion in saliva and urine.
  • Transformation of inactive vitamin D to active vitamin D
31
Q

What is calcitonin? What does it do?

A
  • Released from thyroid C cells in response of excessively high Ca2+
  • Promotes deposition of calcium, into bone
  • Promotes calcium loss in kidneys
  • Effect: decreases CA2+ in the ECF
32
Q

What is milk fever? Who is most affected by it?

A

Older cows : bone and gut less responsive to pth and calcitriol than heifers.

Peripartuant hypocalcemia occurs in 3 progressive stages, and can occur in both dairy and beef cattle.

33
Q

What are the 3 stages of milk fever clinical signs?

A

◦ Stage 1: standing, apprehensive, hypersensitive, tremors. This is loss of dampening on sodium channels.
◦ Stage 2: Loss of Ca2+ influx at motor end plate of the axon causes less acetyl choline to be released per action potential. Decreased calcium ECF. Cows recumbent and too weak to stand, head may be turned to back if too heavy to lift.
◦ Stage 3: Comatose. Death can occur from cardiac/ respiratory failure/ can also cause rumen regurgitation and cause aspiration pneumonia.

34
Q

What is the treatment of hypocalcemia? How can it be prevented?

A
  • Calcium salts: usually in form of calcium borogluconate, iv slowly ( Rapid iv administration can result in cardiac arrest (stone heart syndrome). Therefore ascult while administering, if heartrate decreases below 60 bpm or you hear severe arrhythmia then stop administration for 20-30 seconds
  • pad areas, likely to fall and can become injured

Prevention:

Method 1: 1 month prior to calving, decrease Ca2+ so they could gear up PTH and Vitamin D3 homeostasis early on (this will prevent them from being “blindsided” by drop in calcium). Increasing calcium in feed will have opposite effect and induce milk fever.

Method 2: Feed anionic salts for 2 weeks postpartum- inducing mild metabolic acidosis. This will aid calcium absorption in the gut, makes mineral more labile and improves renal activity of 1-alpha hydroxylase ( which activates vitamin D3)

Risks: Can cause bone mineral liability, expensive, and may not work.

35
Q

What is important abut magnesium in milk fever?

A

• Magnesium is important to have in diet at adequate amounts since it is an important cofactor for PTH.

36
Q

What is magnesium an important cofactor for? What does it compete with?

A
  • Cofactor for acetylcholinesterase, the ECF enzyme that cleaves Ach and terminates the stimulatory signal.
  • Cofactor for release of PTH from parathyroid gland.
  • Hypomagnesimia ( low mg2+ in ECF) may result in impaired PTH release.
  • Competes with calcium ( both are 2+ cations) and inhibits its stimulatory activity.
37
Q

What is important about magnesium in relation to its regulation? What are sources of magnesium in diets?

A
  • Doesnt have specific hormones to regulate it
  • Doesnt mobilize bone mineral release.

Mg absorption from gi tract is only regulatory mechanism for ECF. Animal must ingest from diet.

Magnesium Sources:

  • Variety of plants, (legumes better than grasses) and nuts.
  • Animal tissues and liver are sources of mg ( for carnivores)
38
Q

What are other things that can decrease magnesium absorption from diet?

A
  • GI tract absorption of Magnesium is generally inefficient.
  • High nitrogen (protein) as well as high dietary K+ will reduce magnesium absorption from the rumen since their will be a change in the electrical gradient.
  • Rapidly growing grasses have a lot of nitrogen and potassium.
39
Q

What is grass tetany? What is the clinical signs?

A
  • Graze lush pastures can lead to hypomagnesemia.
  • Clinical signs: repetitive muscle contractions that are uncontrolled, hyperirritability and convulsions.
  • Start with muscle tremors and progress to tetany.

Clinical signs by stage:

Early: Muscle fasiculations, hyperesthesia, stiff goose stepping gait. Animal may be irritable or maybe aggressive. Can be bellowing with an overly alert , nervous expression

Later: Recombency and convulsion, paddling motions with limb, extensor rigidity, opisthotonus, death can occur from respiratory/ cardiac arrest.

40
Q

What occurs with magnesium and calcium in grass tetany?

A

Low Mg2++ -> less competition for Ca2++ at axon terminus so more acetylcholine is released, which allows for more vigorous, sustained muscle contracctions.

Acetylcholine will not be broken down effectively since magnesium is needed as a cofactor for acetylcholinersterase. Sustained muscle contraction. Same occurs in cholinergic CNS so thats why you can see both tetany and seizures.

41
Q

What is the treatment of hypomagnesemic tetany? What is the prevention?

A

• Magnesium SO4 via rectum as well as Calcium/ magnesium salt solution. Wear boots and get ready to run ( Salts can cause diarrhea and the cows can wake up aggressive)

IV magnesium slowly

Prevention:

  • one gram elemental magnesium absorbed per head per day.
42
Q

What is phosphorus? Where can you find it? What is it used for? What can it compete with?

A

It is a component of bone mineral and tooth enamel.

85% of total body P in hydroxyapatite

Phospholipids in cell and cellular organelle membranes.

Energy metabolism: ATP

Sources:

  • Grains
  • Wheat bran
  • Supplements
  • Grasses are low in Phosphorus

Phosphorus competes with calcium and can reduce its absorption.

43
Q

What can occur when you have high phosphorus and low calcium? What about too high of phosphorus? Where does phosphorus excretion occur?

A

• Can compete with calcium and reduce bone absorption. Low Ca++ and High Phosphorus in blood triggers chronically elevated PTH.

Can cause bone resorption and condition called rubber jaw.
• Ruminants on high grain diets may develop phosphate based urinary calculi if urine becomes highly concentrated ( i.e struvite ( magnesium ammonium phosphate). Disease termed urolithiasis.

In ruminants: Phosphorus is usually excreted in the saliva and gi tract.

  • Saliva : supplies rumen bacteria with P source for ATP
  • Allows phosphorus recycling from blood into gut, minimizing urinary losses.
44
Q

What is hypophosphatemia? What can occur/clinical signs? What triggers it? What is the treatment?

A

• Low phosphorus in ECF.

  • relatively uncommon, can occur with milk fever.

Clinical presentation: usually alert but show weakness/ and inability to stand. Cows can attempt to rise on multiple occasions pushing part way up on legs and moving around pen on abdomen. “termed creeper cows”

Trigger: Lactation triggers heavy ca2+ loss in milk, triggers pth secretion, pth moves alot of phosphate into urine, and persistent weakness is likely due to ATP depletion from muscle cells.

Treatment:

Blood Samples: Note hemolysis increases blood phosphorus because it leaks from ruptured RBC

  • IV Monosodium phosphate. Cannot mix Ca++ containing soluion. CaPO4 aggregrates and will precipitate.
  • Phos supplements
  • Offer phosphorus rich grains
  • Consider checking vitamin D status of diet
45
Q

What is hypophosphotemic rickets? Who is more susceptible?

A
  • More common in young animals. Camelids
  • More likely occurs in dark finer llamas due to UV not penetrating their darker skin as well. This is problem in pacific northwest and occurs primarily in the winter.

Without Vitamin D, inadequate Ca and Phos absorption from gut to mineralize bones. Results in microfractures, wich cause lameness and angular deformities of the long bones.

Clinical signs:

  • Reluctant to play, lethargic,

Diagnostic indications:

  • Widened growth plates and flared metaphyses are hallmark signs
  • Typically normal serum calcium, low serum phosphorus