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LA DX & TX I > Exam 3 - Forestomach Disorders > Flashcards

Exam 3 - Forestomach Disorders Flashcards

1
Q

how is rumen health assessed by rumen fluid analysis?

A

protozoal numbers & activity

new methylene blue reduction

sedimentation examination

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2
Q

what is the new methylene blue reduction test? what is an abnormal result?

A

qualitative measure of the redox potential of rumen fluid generated by microbial fermentation to check for the function of anaerobic bacteria

abnormal - > 8-10 minutes, indicates microbial inactivity/death

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3
Q

what is a sedimentation rate used for rumen fluid analysis? what is an abnormal result?

A

qualitative estimate of microbial activity & dietary particle size

floatation is minimal or not observed with inactive/decreased particle-associated bacteria - can indicate frothy bloat

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4
Q

what is simple indigestion/rumen dysbiosis?

A

transient inappetence due to changes in rumenal microenvironment

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5
Q

what are some general causes of simple indigestion/rumen dysbiosis?

A

moldy/spoiled feed, indigestible roughage, too much feed, & new type/batch of feed

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6
Q

how is simple indigestion/rumen dysbiosis diagnosed?

A

rule out - usually multiple animals are affected

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7
Q

what are the clinical signs associated with rumen dysbiosis/simple indigestion?

A

decreased appetite, decreased milk production, rumen hypomotility, mild bloat, & abnormal feces

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8
Q

how is simple indigestion/rumen dysbiosis treated?

A

usually resolves spontaneously once the feeding error has been corrected

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9
Q

what causes rumen acidosis?

A

overindulgence on carbs

readily digestible carbohydrates (such as starch. sugar, or pectin) are rapidly fermented an unadapted rumen resulting in increased VFA & lactate concentrations & a reduction in rumen pH

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10
Q

what are some common offenders that cause rumen acidosis?

A

cereal grains - corn, wheat, barley

high sugar/starch fruit or root crops

corn or milo stubble fields

byproduct feeds - bakery waste & brewer’s grain

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11
Q

what is the pathogenesis of rumen acidosis?

A
  1. within 2-6 hours after ingestion, rumenal bacterial population begins to shift towards increased numbers of gram positive bacteria
  2. fermentation is altered with a shift in VFA production from acetic > propionic > butyric to propionic > acetic > butyric and increased concentrations of undissociated VFAs lactate & glucose
  3. rumen protozoa decline & lactate begins to accumulate at pH of 5.5 - dying protozoa release amylase & contribute to increased glucose generation from starch
  4. these conditions favor proliferation of strep bovis & other gram positives that produce lactate & once pH falls to 5.0, gram negative organisms decline rapidly & there is a local release of endotoxin
  5. pH 4.5, lactobacillus spp. predominate with rapid production of lactate & histamine
  6. ability of the rumen to buffer acid is overwhelmed at pH <5, and D- & L- lactate accumulate causing a systemic lactic acidosis & metabolic acidosis
  7. rumen epithelium is damaged as a result of acids & other mediators released during acute acidosis
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12
Q

what bacteria predominate during rumen acidosis?

A

step. bovis & lactobacillus

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13
Q

what is going on with d-lactate & l-lactate during rumen acidosis?

A

l-lactate is metabolized but d-lactate isn’t & it builds up causing a metabolic acidosis

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14
Q

what damage occurs to the rumen epithelium in rumen acidosis?

A

chemical rumenitis, epithelial necrosis, absorption of bacteria into portal blood, & bacterial & fungal rumenitis

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15
Q

T/F: acute rumen acidosis is an individual animal disease while subacute rumen acidosis is a herd disease

A

true

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16
Q

what are some clinical signs associated with acute rumen acidosis?

A

individual animal disease!!!! sick!!!!

anorexia, depression, splashy/distended/static rumen, dehydration, tachycardia, cold extremities, weak or recumbent, diarrhea with or without grain, & death

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17
Q

what factors can influence the development of acute rumen acidosis?

A

rate of dietary adaption, type of carb & processing method, forage availability, feed sorting, feeding frequency, feed intake, & feed mixing/delivery

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18
Q

why are clinical signs of subacute rumen acidosis not as severe as acute?

A

the changes in fermentation rate, pattern, & rumen pH are temporary & not as severe

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19
Q

what is supportive of acute rumen acidosis on rumen fluid analysis?

A

foul smell, pH <5.5, & dead protozoa & gram positive bacteria

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20
Q

what may be seen on lab tests in an animal with acute rumen acidosis?

A

metabolic acidosis, increased anion gap, hemoconcentration, pre-renal azotemia, & mild-to-moderate hypocalcemia

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21
Q

what are some clinical signs associated with subacute rumen acidosis?

A

herd disease!!!

decreased/variable feed intake, decreased performance/increased culling, increased incidence of lameness, milk component changes (decreased milk fat % & inversion of fat:protein ratio), & loose feces

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22
Q

T/F: history & physical exam findings will not be pathognomic for subacute rumen acidosis

A

true

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23
Q

how can subacute rumen acidosis be diagnosed?

A

ration analysis, rumenocentesis (pH >5.8, normal), manure scoring, lameness scoring, & milk fat inversion

24
Q

why does sudden introduction of fermentable carbs or a sudden change in amount of fermentable carbs carry a higher risk of developing acute rumen acidosis?

A

dietary adaption is necessary to build up populations of lactate-using bacteria, and you need to maintain the equilibrium between acid production & acid utilization

25
Q

what is the classic example of acute rumen acidosis?

A

animals accidentally gain access to a grain storage area & engorge themselves

26
Q

why does processing method carry risk for an animal developing rumen acidosis?

A

small particle size (fine grinding), heat or pressure processing, & high moisture storage of grain increase starch availability

27
Q

list the types of carbs that carry the highest risk of rumen acidosis

A

wheat = barley > corn > sorghum = oats

28
Q

how can feeding smaller meals frequently help prevent rumen acidosis?

A

not as much grain in the food when compared to 1 large meal

29
Q

what are some examples of causes for fluctuations in feed intake?

A

inclement weather, disease, management changes

30
Q

what animals may show predisposition to developing acute rumen acidosis?

A

feedlot animals/dairy cattle in transition from the dry to lactating period

dairy cattle in early lactation

animals being fitted for show or sale

31
Q

T/F: acute rumen acidosis is one of the rare conditions that results in metabolic acidosis in adult ruminants

A

true

32
Q

what are the principles for treating rumen acidosis?

A

remove further access to carbs - evacuate rumen contents (surgical or rumen lavage), correct dehydration & systemic acidosis, neutralize rumen pH

stop acidification, correct metabolic abnormalities, reestablish flora, prevent sequelae, surgical/medical intervention

33
Q

what are some possible sequelae of rumen acidosis?

A

bacterial rumenitis, bacteremia/septicemia, fungal rumenitis, liver abscesses, metastatic pneumonia, polioencephalomalacia, & laminitis

34
Q

how is rumen acidosis prevented?

A

prevent accidents, transition cattle slowly to high concentrate diets, use ionophores, & buffers

35
Q

how is subacute rumen acidosis treated?

A

managed by dietary changes rather than treatment of individual animals

36
Q

what is bloat?

A

occurs when eructation is impaired & the rumen becomes overdistended with froth or gas

37
Q

what is primary ruminal tympany?

A

dietary factors lead to frothy or foamy rumen contents - gas bubbles are trapped by the froth/foam & eructation of gas is prevented

38
Q

what is secondary ruminal tympany?

A

following physical obstruction of the cardia or impairment of the rumenoreticular function with accumulation of free gas in the rumen

39
Q

what is the similar appearance & clinical signs shared between animals with primary & secondary ruminal tympany?

A

distended rumen & left paralumbar fossa

dyspnea, abdominal pain, staggering, & death

40
Q

how does a stomach tube help differentiate between primary & secondary ruminal tympany?

A

primary - stomach tube passes easily but does not relieve bloat, frothy contents may be seen at the end of the tube

secondary - stomach tube passes & relieves bloat or the stomach tube will not pass

41
Q

primary ruminal tympany affects what animals?

A

ruminants on pasture - pasture bloat

ruminants fed high concentrate diets - feed lot bloat

42
Q

when can frothy bloat affect feedlot cattle?

A

those fed high protein pelleted rations early in the feeding period

43
Q

what is the pathogenesis of pasture bloat?

A

foaming agents (soluble proteins) are contained in the plant - lush, rapidly growing legumes (alfalfa, clover, winter wheat) that contain large amounts of proteins that are rapidly degradable & produce gas at a rapid rate - gas is trapped in the froth/foam

44
Q

what is the pathogenesis of feedlot bloat?

A

high grain diets slow rumen motility & decrease saliva production

ingestion of high grain, low roughage (> 50% grain) diets results in mucopolysaccharide (slime) production by bacteria within the rumen which increases the viscosity of rumen fluid resulting in trapped gas & formation of stable foam

45
Q

why do finely ground diets increase the risk of feedlot bloat?

A

they increase the fermentation rate & decrease salivation

46
Q

when is feedlot bloat most likely to occur?

A

transition to a high grain diet is rapid or when very high concentrate diets are fed for a long time late in the finishing period

47
Q

what are some clinical signs of primary ruminal tympany?

A

severe abdominal distension, gasping for breath, prolapsed rectum, raised tailhead, & dead

48
Q

what is the preferred treatment for pasture bloat?

A

poloxalene - ionic surfactant that lowers the surface tension of foam

49
Q

what is the preferred treatment for feedlot bloat?

A

intraruminal administration of mineral oil to destabilize froth

50
Q

with both pasture bloat & feedlot bloat, why tie a rag in the animals mouth?

A

helps increase saliva production & stimulates chewing which increase rumenoreticular motility

51
Q

how is primary rumen tympany prevented?

A

antifoaming agents, grazing control - rotational or strip grazing, limit overgrazing, graze mature pasture, mixed pastures, feed prior to turnout

feed ionophores

52
Q

what is secondary rumen tympany?

A

occurs when gas production continues but eructation of gas is limited - failure of eructation

53
Q

what are some examples of causes of secondary rumen tympany?

A

esophageal blockage & during step up to a high concentration diet

54
Q

how is secondary rumen tympany diagnosed?

A

pass a tube - try to release gas & treat the underlying cause

55
Q

how is secondary rumen tympany treated?

A

cause dependent - if you can’t pass a tube, can do an indwelling rumen trochar or temporary rumenostomy

56
Q

when is rumen fluid analysis indicated?

A

off-feed animal

rumen atony

abdominal or rumen distension of undetermined origin

history consistent with indigestion, acidosis, or urea toxicosis

assist in diagnosis of feed quality or feed mixing/delivery problems

LA DX & TX I (45 decks)

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