Ruminant Nutrition Flashcards
What are the three different layers in the ruminant stomach? What is in each layer?
• 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.

What is the path of objects after being swallowed?
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.
What is the purpose of saliva? What is the gas that makes up the majority of the ruminal gasses?
Saliva is used as a buffer
Much of gas that fills rumen is methane
What occurs during the first month of life for ruminants? What are they considered? What is milk curdled by?
- 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.
What is rumination? When does it occur?
- 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.
What are carbohydrates metabolized to in the rumen? What VFA is converted to glucose? How?
- 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
What occurs in VFA metabolism? What is acetic acid oxidixed for? What is propionic acid used for? What is Butyric acid used for?
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.
What is the relationship of lactation and glucose demand? Lactose and milk production?
- Higher lactation (or lactation in general), more milk produced. More lactose more volume of milk.
Glucose + galactose = lactose
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?
- 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.
What is the process of gluconeogenesis in ruminants?
• 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.
What happens when energy requirements are not met? What happens when intake is low? When glucose is low?
- 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”
What is lipolysis? What is the enzyme that facilitates lipolysis? What is lypolyis promoted by?
- 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
What is the long term complications of negative energy balance?
- 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
What occurs with the formation of ketone bodies?
- 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.
What are the 3 ketones?
- acetoacetate, betahydroxybutyrate, acetone
What is ketosis? What are the clinical signs? What are your diagnostics? Prognosis?
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
What is the treatments for ketosis?
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)
How can you prevent ketosis in ruminants?
- 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.
What are NEFA levels?
• 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.
What is fatty liver disease? What are the clinical signs?What is the treatments?
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.
What is pregnancy toxemia? What is the gestation period of small ruminants? What is the correlation between number of embryos and metabolic strain?
- 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
What are the clinical signs of pregnancy toxemia in cattle? Pathophysiology? Treatment?
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)
What is calcium important for?
- 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.
How does Calcium dampen the neuronal excitation potential that requires sodium channel activity?
- Terminus of neuron, calcium enters the cell in response to action potential.
- Calcium ion promotes fusion of vesicles containing acetylcholine with the membrane.