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Rumen GI- F&F > Motility #2 > Flashcards

Motility #2 Flashcards

1
Q

Evaluating Motility

A

-Visual
-external palpation
-rectal exam
-asucultation

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2
Q

Visual evaluation

A

-chewing cud
-cud moves to esophagus
-left paralumbar fossa- looking for undulations and bloat

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3
Q

External palpation

A

-left paralumbar fossa
-should be soft and doughy; firm could mean bloat
-Ballottement

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4
Q

Rectal exam

A

-left side
-can feel caudodorsal rumen contractions

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5
Q

Auscultation

A

-stethoscope in left paralumbar fossa, caudal to ribs
>rumbling= primary contraction (~1/min)
>splashing or tinkling= can indicated reduced motility, and increased water in rumen from acidosis
>Percussion- ping= displaced abomasum

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6
Q

Decreased motility

A

-Can be a primary or secondary clinical sign; indicates an unhealthy animal
1.Hypomotility= less than normal
2. Atony or stasis= no motility

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7
Q

What directly decreases gastric centers?

A

-Medications eg. Xylazine (Rompun, Anased)
-Acute Phase Proteins (fever)
-Pain (Hardware disease)
**Results in decrease in stimulatory signals from peripheral receptors to the gastric centers AND increase in inhibitory signals
>chemoreceptors, stretch receptors, epithelial receptors

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8
Q

Decreased motility through poor neuromuscular transmission

A

-if failure of neuromuscular transmission occurs, the impulse down the vagus nerve will not send signals to rumen/reticulum smooth muscle contraction
>eg. Hardware disease causing adhesions to body wall, affecting signals and contraction

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9
Q

Decreased motility through sympathetic stimulation

A

-increased sympathetic stimulation through the splanchnic nerve can result in decreased motility

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10
Q

Displaced Abomasum occurrence

A

-occurs in high producing dairy cows, early lactation
-Left displaced is more common than right

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11
Q

Displaced abomasum

A

-abomasum distended with air or fluid
-stimulates abomasal tension receptors sending inhibitory signals to gastric center
-Pain will also result in more inhibition

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12
Q

Cows not eating

A

-Lumpy jaw (Actinomycosis), wooden tongue
-starvation
-decreased stimulatory signals to gastric centers
-pain=direct depression of gastric centers

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13
Q

How does not eating decrease stimulatory signals to gastric centers?

A

-results in
1.decreased buccal mechanoreceptors
2.Decreased rumen tension receptor stimulation
3.decreased Rumen epithelial (mechano) receptor stimulation =decreased rumination

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14
Q

Traumatic reticuloperitonitis

A

-hardware disease
>foreign object punctures reticulum=infection and inflammation
»direct depression of gastric centers (pain, acute phase proteins-inflammation and fever)
»inappetence

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15
Q

Bloat (Ruminal Tympany)

A

1.Free gas bloat
2.Frothy Bloat

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16
Q

Free gas bloat

A

-failure to eructate through secondary contractions (Not the same as gas overproduction)
>often linked to other problems
>results in high rumen pressure and high tension (inhibitory signals to gastric centers)

17
Q

Frothy Bloat

A

-most common form of bloat
-formation of foam/froth in the rumen
>can be from legumes/alfalfa, proliferation of Streptococcus bovis at lower pH which produces slime

18
Q

Frothy Bloat results

A

-high surface tension= gas bubbles do not coalesce into free gas cap
-froth covers the cardia which results in no free gas and no eructation reflex
-high tension results in increased inhibitory signals to gastric centers

19
Q

How to treat frothy bloat?

A

-treat with surfactant
Eg. Poloxalene, mineral oil

20
Q

Rumen impaction

A

-Large quantities of poor quality or indigestible feed (eg. Straw, oat hulls) or foreign bodies (eg.bale netting, plastic, rope)
>results in the microbes being unable to ferment (not broken down and too large to pass)

21
Q

Rumen distention from impaction

A

-results in high tension, the tension receptors will increase inhibitory signals to gastric centers

22
Q

Ruminal Acidosis

A

1.Grain overload- ingestion of large quantities of grain/concentrate which is highly fermentable and results in the rapid production of VFAs
2.Rumen pH falls which promotes the lactic acid-producing bacteria
3.pH drops even more
4.Rumen epithelial (chemo) receptors will increase inhibitory signals to the gastric center
5.May also cause bloat= decrease in motility and frothy bloat

23
Q

Hypocalcemia (milk fever) occurrence

A

-seen in periparturient dairy cattle

24
Q

Hypocalcemia

A

-low ECF and plasma Ca concentrations
-results in the failure of neuromuscular transmission due to lack of Ca which is needed for NT release at synapse, and therefore impulse down vagus nerve is inhibited. Also smooth muscle requires Ca for contraction.

25
Q

Downer cow

A

-inappetant (decrease gastric center stimulation)
-fluid covering cardia decrease in eructation)

26
Q

Vagal indigestion

A

-Has a distinct “papple” shape
>apple on left (dorsal sac distended), pear on right (ventral sac distended)
-originally thought to be due to vagus nerve dysfunction but this is rarely involved
-Due to adhesions around reticulum which inhibits motility
>less separation of particles within the reticulum, and less outflow to omasum

27
Q

Stress/Fear effects on motility

A

-eg. Moving a flighty cow into chute
-results in increased sympathetic activation through splanchnic nerve
>will slow activity but not eliminate it

28
Q

Atropine effect on motility

A

-competitive Acetylcholine antagonist
-blocks parasympathetic transmission at post-synaptic receptors through vagus nerve

29
Q

Sedatives, tranquilizers, anesthetics effect on motility

A

-Xylazine, opioids, gas anesthetics
-results in central depression of gastric centers

30
Q

Drugs to increase motility

A

1.Metoclopramide
2.Neostigmine
**however they cannot stimulate the coordinated sequence of contractions required for rumen motility. The only treatment is to fix underlying cause

31
Q

Metoclopramide

A

-increases gastric motility in other species

32
Q

Neostigmine

A

-competitive inhibitor of cholinesterase results in increases Ach in synapse
-increases parasympathetic effects

Rumen GI- F&F (10 decks)

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