GI2- Ruminant Phys

  1. What is an abnormal result of the NMB reduction test?
    takes longer than 5 min for color to return to that of normal rumen fluid (microbes not functioning/not there)
  2. What are tests to assess rumen function? (6)
    auscultation (2-3 ruminations per 2 min), visualize protozoa, NMB reduction test, smell, pH (should be alkaline), chloride (inc. Cl- in rumen and low systemic Cl- indicates decreased pyloric outflow)
  3. The omasum lives in the __________ abdomen and functions to...
    right cranial; absorb water, electrolytes, VFAs.
  4. The __________ of a neonatal ruminant is the biggest compartment of the GI, but when they are weaned and begin to eat forages and grains, the ___________ becomes the biggest compartment.
    abomasum; rumen
  5. In the neonate, the ___________ is essential to prevent milk from entering the rumen.
    rumenoreticular groove (aka- esophageal groove, gastric groove)
  6. The glandular mucosa of the abomasum secretes... (3)
    HCl (fundus), pepsinogen (pylorus), and mucus (pylorus)
  7. The ruminant upper GI is suppled blood by the ___________; it is drained by the ___________.
    celiac artery; portal system
  8. What are the innervations of the ruminant upper GI?
    • vagus nerve dorsal trunk- rumen
    • vagus nerve ventral trunk- omasum, abomasum, reticulum
  9. Within the rumen, the host provides __(3)__ and the microbes provide __(3)__.
    nutrients, warmth, and a buffered environment; B vitamins, VFAs, and microbial proteins
  10. What types of rumen bacteria are there? (6)
    cellulose/pectin degraders (degrade plant cell walls), starch degraders (amylolytics), protein degraders (proteolytics), lipid degraders (lipolytics), lactate users, methanogens
  11. What is the function of methanogens in the rumen?
    regulate overall fermentation by removal of hydrogen
  12. What is the function of rumen protozoa?
    ingest bacteria for intraluminal nitrogen recycling
  13. What are the functions of ruminal fungi? (3)
    degrade cellulose and xylans, contribute to fiber degradation, facilitate bacterial colonization
  14. What is the gradation of rumen contents in ruminants?
    [on top] gas cap, fiber mat (today's hay), heavy particles (grain and yesterday's hay) [on bottom]
  15. What kind of bacteria live in the rumen and why?
    only anaerobes because oxygen is only 0.5% of the gas in the rumen gas cap
  16. What are advantages of pre-gastric fermentation? (3)
    energy from fibrous materials (VFAs), microbes are an amino acid source, production of B vitamins
  17. What are the disadvantages of pre-gastric fermentation? (3)
    inefficient use of nutrients (starches, sugars, proteins) compared to intestinal digestion, value of high-quality proteins decreased, fermentation can get out of control
  18. Primary rumen contractions are responsible for ___________; secondary contractions are responsible for ______________.
    mixes contents; eructation of fermentation gases
  19. _______ provide 80% of the animal's energy needs; they are produced in the __________ and absorbed through the ___________.
    VFAs; rumen; rumen wall
  20. What are the major VFAs produced in the rumen? (3)
    acetate, proprionate, butyrate
  21. __(2)__ move to the abomasum and are broken down as ___________ for host.
    Microbes and undigested material; protein source
  22. Ruminal tympany results from ___________, not __________.
    failure of eructation; overproduction of gas
  23. Potential causes of rumen tympany. (3)
    esophageal obstruction, rumen motility disorders, fluid/foam at cardia (frothy bloat, recumbancy)
  24. What causes free gas bloat? (2) How can you identify it?
    physical obstruction prevents gas from eructation, rumen hypomotility; passage of tube relieves bloat
  25. What causes frothy bloat? How can you identify it?
    thick foam from grain overload/lush legumes; tube does not relieve bloat (foam doesn't pass through tube)
  26. Hw can bloat result in death?
    rumen fills and pushes on diaphragm--> inhibition of respiration--> dyspnea--> death
  27. What are signs of choke? (3) What is a sequelae of choke?
    dysphagia, drooling, (late change) acidosis; free gas bloat (cannot eructate)
  28. ____________ is the hallmark of ruminal motility disorders, leading to... (5)
    Vagal indigestion; interference with vagal innervation of rumen, hypomotile rumen, frothy/free gas bloat, disruption of normal rumen flora, failure to clear cardia before eructation
  29. Describe the pathogenesis of frothy bloat.
    lush legumes/high conc diets--> rapid digestibility--> microbial proliferation--> multiplying bacteria release mucopolysaccharide--> slime/biofilm and stable foam
  30. How do you treat free gas bloat? (4)
    esophageal intubation/lavage, FB retrieval (if needed), rumenotomy, [emergency] rumen trocar for decompression
  31. How do you treat frothy bloat? (2)
    Poloxalene (TheraBloat), +/- rumenotomy
  32. Why is rumen trocar for emergency decompression of bloat ONLY for emergency use (respiratory distress)?
    peritonitis will result
  33. When is a rumenostomy indicated?
    relief of chronic bloat
  34. What are the classifications of vagal indigestion? (4)
    failure of eructation (free gas bloat), omasal transport failure (anterior functional stenosis- most common type), pyloric outflow obstruction (posterior functional stenosis), indigestion of late pregnancy
  35. What parts of the GI are distended with omasal transport failure?
    rumen distention WITHOUT absomasal distention [PAPPLE]
  36. What parts of the GI are distended with pyloric outflow failure?
    abomasal distension, omasal distention, rumen distention
  37. Causes of vagal indigestion. (6)
    traumatic reticuloperitonitis [hardware], reticular abscess [hardware], liver abscess, pneumonia, abomasal volvulus, abomasal ulcers [all things that interfere with the vagus nerve]
  38. What are clinical signs of vagal indigestion? (5)
    Papple abdominal distension, how HR, hypermotile/weak rumen, scant feces, undigested feedstuff in manure
  39. Grain overload causes ____________.
    rumen acidosis/lactic acidosis
  40. What are highly fermentable feeds? (3)
    cereal grains, root crops (beets/potatoes), fruit
  41. Describe the pathophysiology of grain overload/rumen acidosis.
    excessive carb ingestion--> increased bacterial growth and VFA production--> lower pH--> Strep bovis flourishes (lactate producer)--> increased lactic acid--> lactic acid users start dying off due to low pH--> pH further decreases--> Strep bovis dies (due to low pH) and lactobacillus flourishes (lactic acid producer)--> more lactic acid production--> further drop in rumen pH--> increased osmolality--> increased thirst, rumen distention, hypovolemia, rumenitis
  42. What are direct consequences of the pathophysiology of excessive carb ingestion? (9)
    increased rumen osmolality leading to increased thirst, rumen distention (filling with fluid), hypovolemia, rumenitis; increased VFAs leads to lactate and ketones released into systemic circulation, decreased rumen motility, systemic acidosis
  43. What form of lactic acid accumulates in the rumen wall?
    D-lactate (produced by microbes) (b/c animals produce L-lactate, therefore they are better at clearing it)
  44. Where is lactate metabolized in the body? What is a by-product of its metabolism?
    liver; bicarbonate
  45. What are systemic effects of rumen acidosis and damage to rumen epithelium? (3)
    endotoxemia, laminitis, liver abscesses/caval syndrome
  46. How does caval syndrome secondary to grain overload present? (3)
    bleeding from nose, [on necropsy] liver abscesses, caudal vena cava thrombi
  47. What are clinical signs of grain overload? (6)
    depression, abdominal distention, tachycardia, diarrhea, death, laminitis
  48. How do you treat grain overload? (5)
    rumen evacuation (kingman tube or rumenotomy), transfaunation (put healthy rumen fluid in), systemic antibiotics (rumenitits/liver abscesses), antifungals (mycotic rumenitis), IV fluids (hypovolemia)
  49. What are the 3 types of hardware disease?
    traumatic reticulitis (usually asymptomatic), traumatic reticuloperitonitis (most common presentation), traumatic reticulopericarditis (most serious)
  50. How do you treat hardware disease? (4)
    antibiotics (peritonitis), magnet, +/- rumenotomy to remove FB/drain abscess, +/- pericardiocentesis/ 5th rib resection/ pericardectomy
  51. What are predisposing factors to DAs? (7)
    GI (abomasal) atony due to a change in diet, high conc diet, concurrent diseases (esp. ketosis); recent calving leads to increased metabolic demands and a void in the abdomen
  52. Clinical signs of simple DA? (5)
    decreased milk, decreased appetite, depression, ketosis, ping
  53. What are clinical signs of a abomasal volvulus? (9)
    down on milk, decreased appetite, depression, ketosis, ping, colic, tachycardia, shock, death
  54. What metabolic derangements are usually associated with DAs? (4)
    hypochloremic, hypokalemic, metabolic alkalosis, [late dz-volvulus] lactic acidosis
Card Set
GI2- Ruminant Phys
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