Midterm 2 - metabolic disorders, contagious & non-contagious disease, abdominal surgery

Question 1

What three volatile fatty acids are produced in the rumen?

Answer 1

1. Proprionate
2. Butyrate
3. Acetate

Question 2

Why can’t oral glucose be used to supplement ruminants with glucose? What precursor do we feed instead?

Answer 2

Would be consumed by bacteria before cow could absorb

Starch/Carbohydrate source

Question 3

List the three pathways by which ruminants produce energy

Answer 3

1. Citric acid/Krebs cycle
2. Fatty-acid oxidation
3. Gluconeogenic/glycolytic

Question 4

List precursors of glucose that are produced and stored in the body

Answer 4

1. Propionate, mainly produced by liver using starch, protein, and fibre, makes up 30-60% glucose source
2. Lactate, fermented from propionate in rumen, produced in skeletal mm., makes up 10% G source
3. Glycerol - adipose tissue, 5% G course
4. Fatty acid oxidation, diet, adipose tissue
5. Amino acids, diet, smooth muscle; 10%

Question 5

What is the physiologic purpose of ketone bodies, BHB & 3-acetone?
What determines the amount of ketone bodies produced?

Answer 5

1. BHB is important for milk fat synthesis
2. 3-acetone: some can be converted to glucose. Important substrate for heart, kidney muscle, and mammary gland
3. Proportion of propionate present –> gluconeogenesis: ketogenesis link –> FA are metabolized into KB. More proprionate decreases incidence of subclinical ketosis

Question 6

In times of negative energy balance, adipose tissue releases what substance to help supplement energy? What about skeletal muscle?

Answer 6

1. non-esterified fatty acids - triglycerides are stored in adipose tissue in the form of fatty acids
2. amino acids from protein breakdown

Question 7

Can a displaced abomasum lead to secondary ketosis?

Answer 7

YES!

Question 8

What is nervous ketosis?

What treatment is helpful in these cases?

Answer 8

BHB is converted to isopropyl alcohol, and affects the brain
Neurological signs will be seen, that might appear like rabies or BSE. Occurs in 10% of ketotic cows
2. Choral hydrate –> increases breakdown of starch in the rumen

Question 9

What is subclinical ketosis, what are its impacts?

How do you test for it?

Answer 9

1. Elevation in ketone bodies without clinical signs
2. loss in milk production, increased risk of periparturient disease (metritis, mastitis, DA, time to return to cycling increased, elevated risk of cystic ovaries)
3. BHB levels in the blood, milk, or urine (4x higher in urine than milk)

Question 10

Treatment of ketosis

Answer 10

Glucocorticoids (dexamethasone) –> stimulates release of energy sources –> AA from skeletal muscle, gluconeogenesis in liver

+/- Insulin (slightly better effects)
+/-glucose (this prevents decreased in milk production otherwise seen by glucocorticoids alone)

Others

1. Propylene glycol, added to silage –> used by liver to make G precursor, too much = CNS depression
2. Nicotinic acid –> decreases lipolysis, dramatic improvement on day 1, then relapse
3. Methionine/cholin: Increases fat mobilization from liver
4. Choral hydrate: increases starch metabolism in rumen
5. Slow release ionophore bolus –> rumen produces more propionate, impt VFA used for energy!

Question 11

What are the effects of treating ketosis with glucocorticoids?

Answer 11

1. Increased gluconegenesis (exacerbates ketosis), more glycogen in the liver
2. Increased citric acid cycle intermediates
3. Decreased uptake of Glucose by peripheral tissues, including mammary tissues
4. Decreased milk production
5. Increased appetite
6. Decreases immune system

Question 12

Calcium intake
1. Dry period
2. Lactating cow
So, should we give high amounts of Ca leading up to parturition?

Answer 12

1. 50g/day
2. > 100g/day (35g/day used for milk production)
3. No, need body to be ready to adjust to sudden change in expenditure of Ca. If high in diet, will decrease active absorption and release from bone. Diet [<20g/day] during the last 2 weeks before parturition will eliminate MF

Question 13

Describe the changes in plasma levels of Ca, P, and Mg at time of calving

Answer 13

Ca & P decrease

Mg increases

Question 14

Milk Fever can lead to parturient paresis. Describe these effects on the cow

Answer 14

1. Neuromusular dysfunction –> flaccid paralysis
   - Skeletal mm. –> paresis
   - Smooth muscle –> GI atony, bloat, constipation, loss of anal reflex, dilatation of pupils, reduced uterine contractions
2. Circulatory collapse
   - low BP, CO decreases (heart has to work harder, often tachycardic)
   - Hypoxia to tissues: cool extremities, mm. damage, paresis
3. Depression of consciousness

Question 15

Why is the time immediately before & after parturition a common time for milk fever to occur?

Answer 15

1. Sudden change in calcium requirements a time of milking
2. Production of colostrum in preparation for calving –> Ca requirements spike for this
3. Fetus utilizes some of Ca, grows the most in final trimester

Question 16

How might a milk fever cow close to calving present?

Answer 16

1. Dilated but no progression of parturition –> reduced uterine contractions, can’t expel fetus
2. Recumbent
3. Depressed
4. Paretic/weak
5. Blood test –> low calcium, and likely low P too

Question 17

Severity of parturient paresis is related to degree of hypophosphatemia. How might hypocalcemia contribute to low phosphorus? What other negative effects does low phosphorus have?
Could hypophosphatemia be a reason why treatment of hypocalcemia/milk fever be unresponsive?

Answer 17

1. Hypocalcemia –> increased PTH in response to increase re-absorption of Ca cause net loss of P
2. RBC fragility –> a lot of P in RBCs
3. YES! Consider: phosphate buffered saline added to water given IV, Cal-Dex also contains 1% P (as well as Ca, dextrose, and Mg)

Question 18

List diagnostic Rule-outs of milk fever?

Answer 18

1. Trauma
2. Infection: peritonitis, metritis, mastitis
3. Acute impaction of the rumen/grain overload
4. Bloat, ruminal tympany
5. Dystocia/torsion of the uterus
6. Other causes of hypocalcemia
7. Metabolic: grass staggers, hepatic lipidosis, PP hemoglobinuria
8. Severe toxemia/peracute infectious processes

Question 19

What helps prevent relapse of milk fever after administration of IV Calcium gluconate?

Answer 19

Administration of similar amount Subcutaneously

Question 20

What is the most reliable parameter to measure when concerned with hepatic lipidosis?

Answer 20

[non-esterified fatty acids] in the serum

Question 21

What is pregnancy toxemia in sheep?

Answer 21

Late gestation high energy demands resulting in energy imbalance. Fetus & placenta require 30-40% total glucose intake in late gestation. Just like ketosis in cattle.

• Hypoglycemia
• elevated ketone bodies
• Acidosis from ketone bodies
• electrolyte imbalance (Ca, K may be decreased)

Question 22

How do you treat pregnancy toxemia?

Answer 22

1. Provide energy source: propylene glycol, IV fluids to correct dehydration + glucose +/- insulin
2. Induce parturition if severe –> alleviate cause of extreme energy requirement
3. Dexamethasone if sign of infection, given prior to PGF2alpha injection if aborting

Question 23

What does vitamin E/selenium deficiency cause?

Answer 23

Nutritional myodegeneration. These are natural anti-oxidants to protect muscle against oxidizing agents. In young rapidly growing animals, muscle becomes damaged

1. Cardiac mm: arrhythmias, difficulty breathing, sudden death
2. Skeletal muscle (white mm. disease): stiff sore muscles, can only stand for short periods of time, weakness
3. Respiratory muscles: struggling to breathe, recumbent, gasping

Question 24

What are some causes of elevated rumen pH?

Answer 24

1. Simple indigestion
2. Urea indigestion
3. rumen content putrefaction
4. GI stasis, pyloric outflow problems

Question 25

What causes a decreased rumen pH?

Answer 25

1. Grain overload
2. Chronic ruminal acidosis
3. Concentrate feeding vs roughage

Question 26

When assessing the ruminal flora, list the tests associated with each function

1. Anaerobic fermentation
2. Carbohydrate digestion
3. Protein digestion
4. Fiber digestion

Answer 26

1. Methylene blue reduction test
2. Glucose fermentation test
3. Nitrate reduction test
4. Cellulose digestion test

Question 27

For a sedimentation activity test of rumen contents, what does the following indicate

1. rapid sedimentation
2. No sedimentation or flotation
3. 4-8 minutes –> sedimented layer, liquid layer, coarse hay/top layer

Answer 27

1. No active microflora, ruminal acidosis
2. vagal indigestion, frothy bloat
3. normal rumen flora

Question 28

List historical factors associated w. simple indigestion/”off-feed”

Is treatment necessary?

Answer 28

1. Sudden feed changes
2. Indigestible or damaged feed stuffs –> moldy, over-heated, spoiled
3. Too much carbohydrate
4. Not enough water
5. Prolonged Ab therapy

B. most cases resolved spontaneously within 24 hours

Question 29

List the three types of bloat (ruminal tympany)

Answer 29

1. Pasture or “legume” bloat
2. Grain or feedlot bloat
3. Free gas bloat

Question 30

For legume bloat

1. What causes it
2. How quickly do signs develop
3. What does it progress to that is life threatening?
4. How can we treat it?
5. Prevention?

Answer 30

1. Access to pasture with >50% legumes. Alfalfa poses the highest risk. Leads to formation of stable proteinaceous foam that traps natural air & fills cardia, preventing natural eructation of gas
2. Signs can develop within 2 hours (or sooner)
3. Expanded rumen puts pressure on major veins (posterior vena cava –> decreased venous return –> hypoxia)
4. Feed coarse stemmy hay, DRENCH with anti-bloat solutions s.a. non-ionic detergens (alfasure), alcohol ethoxylate detergent (blocare), peanut, olive oil
   -anti-bloat breaks up surface tension & allows formation of air bubbles, drenching clears cardia of froth = eructation
   IN SEVERE emergent cases: trochar & cannula
5. Anti-bloat supplements - polaxalene, ionophores, avoid heavy legume pastures

Question 31

For feedlot/grain bloat

1. what causes it
2. How quickly do signs develop
3. What produces the stable foam that traps air bubbles?
4. How can we treat it?

Answer 31

1. Sudden change to high grain diet, finely ground feed. Multiple animals usually affected at once –> feedlot calves recently arrived
2. Bloat develops slowly
3. Bacterial slime - strep bovis
4. No effective medication. Use anti-bloat supplement polaxalene, ionophores, mineral oil, reduce grain intake

Question 32

For free gas bloat

1. List functional causes
2. List mechanical causes
3. Positional causes
4. Treatment

Answer 32

1. Esophageal spasm (tetany, damage to vagal nn.), GI atony, severe toxemia, hypocalcemia
2. Esophageal obstruction (through or at entry to rumen), foreign body, stenosis, abscess, tumor
3. Lateral or dorsal recumbency incl. for surgery, facing downhill –> all cause obstruction of the cardia
4. not mentioned, but could likely pass stomach tube to alleviate gas

Question 33

For vagal indigestion where abomasal emptying has been impaired, how will this impact acid-base balance? How does this compare with vagal indigestion where reticulum emptying is impaired?

Answer 33

metabolic alkalosis

normal acid-base

Question 34

For vagal indigestion, where is the problem most commonly located?
Where do abomasal ulcers usually form?

Answer 34

Reticulum

fundus, pyloric region

Question 35

What are the presenting signs of a cow with vagal indigestion?

Answer 35

all GRADUAL onset - anorexia, decreased milk production, weight loss, intermittent bloat, ruminal distension

Question 36

Why do an atropine sulfate test?

Answer 36

Atropine blocks the inhibitory effects of vagus nerve. WIth a bradycardic cow suspected to have vagal indigestion, a reflex increase in heart rate with this test = increased vagal tone. May help support suspicion, though does not on its own = vagal indigestion

Question 37

What is the prognosis for cows with vagal indigestion?

Answer 37

Not good! Depends on cause though, reticular abscess carries the best prognosis after treatment - 66%

Question 38

Do most cases of abomasal ulceration show clinical signs?

Which group of cows are most commonly affected?

Answer 38

No
Veal calves
High producing, fresh cow with concurrent disease are the most common group to be affected AND have clinical signs

Question 39

What are some causes of abomasal ulcers?

Answer 39

1. Stress, confinement, hypocalcemia, histamine absorption, eating high amount of concentrates, high milk production, fresh cow, trauma (foreign bodies, hair balls, straw), hypoxia of the mucosa (volume overload for ex.), neoplasia, copper deficiency, C.perfringens
   - Some cause a decrease in mucous production, and others cause increased acid secretion

Question 40

List the four categories of abomasal ulcers

Answer 40

1. Non-perforating, minimal blood loss - most common
2. Non-perforating, massive blood loss (erosion of major vessel located in the submucosa), high mortality rate
3. Perforate wall, acute local peritonitis (perforation is VERY RARE, 50% occur in first month after calving in adult cows)
4. Perforating, acute diffuse peritonitis

Question 41

When is melena noted, for non-perforating, or perforating abomasal ulcers?

Answer 41

non-perforating
perforating ulcers penetrate all the way through the abomasal wall without involving any major vessels. Disease is the result of peritonitis, not vessel damage & blood loss.