Metabolic disturbances

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  1. Define bloat
    over distension of the rumen and reticulum with gases of fermentation
  2. another name for bloat?
    ruminal tympany
  3. Define Primary ruminal tympany.
    frothy bloat- of dietary origin (occurs in cattle on pasture and feedlot cattle on high grain diets)
  4. Define secondary bloat.
    free gas bloat- physical or physiological interference with eructation
  5. What is the most common cause of sudden death in cattle?
  6. How fast can bloat occur?
    Within 15 min of feeding
  7. How fast can gas be produced in unfed vs. fed cattle?
    • unfed 0.2L/min
    • fed 2.0L/min
  8. Function of the rumen?
    soaking, fermentation, and mixing
  9. Function of the reticulum?
    • Pump that causes food to move in and out of rumen
    • directs ingesta to rumen or from rumen to omasum
    • Floods cardia prior to regurgitation
  10. Functions of the omasum?
    Grinds and triturates (squeezes out fluid) rumen contents located within folds.
  11. Functions of the abomasum?
    • True stomach- functions like non-ruminants 
    • starts digestion of degraded concentrates and roughages 
    • starts digestion of microbes of fermentation
  12. Define eructation.
    process by which gas from the forestomach is removed via the esophagus to the pharynx
  13. How long does eructation take?
  14. How is eructation initiated?
    mechanoreceptors in dorsal sac of rumen and cardia sense gas pressure- goes to CNS: reflex center in medulla
  15. Describe the mechanisms by which eructation occurs.
    • rumen contracts-moves gas bubble forward
    • reticulum relaxes
    • cardia opens 
    • gas released (most inspired by lungs)
  16. Explain how interference with eructation could occur.
    Gas bubbles produced are very tiny and thus they are not sensed by mechanoreceptors in the rumen or cardia, which prevents eructation and = BLOAT!!
  17. Define primary rumen contraction.
    Reticulum to rumen (coordinated waves of contractions and relaxations)
  18. Define secondary rumen contractions.
    Rumen only- associated with eructation.
  19. List five groups of possible causes for secondary ruminal tympany.
    • Intraesophageal foreign body (may cause scarring(stenosis))
    • Paraesophageal obstruction- swollen lymph nodes
    • Diaphragmatic hernia, muscle trauma, toxins
    • Interference of nerve pathways
    • Metabolic derangements
  20. What are some disease that could cause paraesophageal obstruction?
    tuberculosis, bovine leukosis virus and chronic pneumonia
  21. What could cause interference with nerve pathways, leading to secondary ruminal tympany?
    • injury to vagal nerve
    • injury to central processing centers for digestion (medulla)
  22. Which metabolic derangements could cause secondary ruminal tympany?
    hypocalcemia, acidosis
  23. How can consumption of certain plants cause primary ruminal tympany?
    Rapid digestion of plants rich in cytoplasmic protein causes a release of plant proteins that act as frothing agents and form many tiny gas bubbles.
  24. When is bloat more common in pasture cattle?
    In the spring and fall when pastures are lush.
  25. Which plants have high bloat potential?
    • legumes (alfalfa, landino clover)> red and white clover>crimson and subterranean clovers
    • Also cereal crops (young plants), cabbage, canola, peas and beans
  26. Which plants have the ability to reduce the potential for bloat?
    legumes with high concentrations of tannin (Sainfoin and Lotus)- precipitate protein
  27. Why do animals bloat in feedlots?
    Production is rushed, high grain diets are fed 90% grain 10% forage
  28. Why are such high grain diets used in feedlots?
    • greater energy density
    • easy to transport
    • ability to manipulate blend/diet easily
    • demand for fatty, marbled meat
  29. Problem with high grain diets?
    • high energy source that cattle are not accustomed to
    • rumen can accommodate large quantities of forage as it is broken down over a 12-24 hour time period
    • microbial fermentation changes from slow ( cellulose and hemicellulose) to rapid (starch)
    • Bacteria grow rapidly in starch and produce a sick ass slime (excessive mucopolysaccarides)- which form froth and viscous ruminal fluid
    • Alters feed stratification (layers of gas, liquid, solid in rumen)
    • Streptococcus bovis like high starch and sugar concentrations and produce lactic acid that can lead to bloat
    • A drop in the number of protozoa can also lead to bloat as they are responsible for engulfing bacteria and starch
  30. How can bloat lead to death?
    • - respiratory and/or cardiovascular failure
    • - absorption of toxic gases, toxic amine (histamine) and hydrogen sulfide
  31. What is an indicator of bloat when performing a post mortem?
    BLOAT LINE- demarcation between bloodless distal esophagus and the congested proximal esophagus at thoracic inlet
  32. Treatment for secondary bloat?
    remove foreign body
  33. treatment for primary bloat?
    • -trochar in caudal dorsal rumen (left paralumbar fossa)
    • - De-gas by placing a stomach tube (for free gas bloat)
    • -Anti-foaming agent (aka detergent)- works best for pasture bloat
  34. Ways to prevent bloat?
    • -watch diet: lower grain content, don't use lush pasture
    • - processing: don't make feed fine or processed
    • -use more forage in diet- reduces fermentation rate, increases pH and increases salivation( antifoaming properties)
    • -add ionophores (inhibits growth of gram positive bacteria (steptococcus and lactobacillus)
  35. Define acidosis?
    A decrease in the alkali in body fluids relative to acid content.
  36. Acidosis is not a disease but rather a _____ of _______.
    continuum of change
  37. two types of ruminal acidosis
    acute or chronic
  38. What defines acute acidosis ?
    • rumen pH of 4-5
    • rapid increase of lactic acid (D lactate 50-300 uM (normal=5uM))
    • increase in Gram positive bacteria (lactate producers)
    • decrease in Gram negative bacteria & protozoa
    • Physiological change
  39. What are some physiological changes from acute acidosis?
    • rumen stasis
    • dehydration
    • acidosis leading to coma and death
  40. What is the most prevalent form of acidosis?
    chronic acidosis
  41. What is often the only sign of chronic acidosis?
    decrease in food intake
  42. What defines chronic acidosis?
    • Decrease in protozoa
    • pH: 5.0-5.5
  43. Describe reaction 1 for acidosis in ruminants.
    Increased starch- increases glucose concentration in the rumen
  44. Describe reaction 2 for acidosis in ruminants.
    Decreased forage- shorter eating time, less salivation (buffer) and faster fermentation and digestion
  45. Describe reaction 3 for acidosis in ruminants.
    Increase pyruvate which increases the substrate for increased lactate = decreased pH
  46. Describe reaction 4 for acidosis in ruminants.
    • Increased D-lactate50-300uM- metabolizes 1/5 rate of L-lactate and is a potent neurotoxin 
    • can cause ataxia, lethargy, depression/ confusion, nystagmus
  47. Describe reaction 5 for acidosis in ruminants.
    Increase VFAs = decreased pH, also other microbes involved in acidosis will release ethanol, methanol, histamine, tyramine and endotoxin
  48. Describe reaction 6 for acidosis in ruminants.
    Drop in pH due to rumen, reticulum or omasum injury
  49. Define chemical rumenitis?
    swelling of the rumen due to lactic acid
  50. Define mycotic rumenitis.
    Swelling of the rumen due to the presence of a fungal infection
  51. What percentage of feedlot cattle have liver abscesses?
  52. Are there any production issues related to liver abscesses?
    • decrease in animal performance
    • lowers carcass yield- not growing as well
  53. What is polioencephalomalacia?
    Wasting of grey matter of the brain.
  54. Is there a correlation between polioencephalomalacia and acidosis?
    Yes, polioencephalomalacia increases with rumen acidosis.
  55. What type of bacteria does acidosis favor?
    bacteria that produces thiaminase I: forms thiamin analogs that compete for thiamine= get polioencephalomalacia
  56. What are clinical signs of polioencephalomalacia?
    blind, down, convulsions, hypermetria, staggering
  57. Name two types of fungus that cause liver abscessation.
    • Aspergillus
    • Zygomycetes
  58. Name a type of bacteria that can lead to liver abscessation.
    Fusobacterium necrophorum
  59. Describe reaction 7 for acidiosis in ruminants.
    Increased osmolarity- causes fermentation products in the rumen such as lactate, VFAs, metabolites and pyruvate to withdraw large amounts of water from blood= severe dehydration
  60. Describe reaction 8 for acidosis in ruminants.
    Absorption of fermentation products such as VFAs, metabolites, lactate and pyruvate in the intestine. Also causes withdraw of large amounts of water from blood = severe dehydration and diarrhea.
  61. Describe reaction 9 for acidosis in ruminants.
    decreased blood pH= severe acidosis
  62. Describe reaction 10 for acidosis in ruminants.
    Increased blood osmolarity (hemoconcentration)- associated with laminitis
  63. Which type of bacteria is laminitis associated with?
    endotoxin release of gram negative bacteria-following a drop in rumen pH
  64. Describe reactions 11 and 12 for acidosis in ruminants
  65. List four ways to prevent acidosis.
    • Decrease rate of introducing grain
    • Increase roughage
    • Ionophores (monensin good choice)
    • Add Buffers (bicarbonates) to feed
Card Set:
Metabolic disturbances
2013-03-06 04:08:16

Midterm 2
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