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47 Cards in this Set

  • Front
  • Back

What are the 3 function of GI motility?

1. Propulsive motility - propel food from one location to the next

2. Retentive motility - retain ingest for digestion, absorption or storage

3. Mixing - break up food and mix with digestive secretions

Esophageal motility - what is primary peristalsis and secondary peristalsis in ruminants?

Primary = contraction caused by swallowing movements

Secondary = contraction caused by local stimulation of a blolus

Ratio of striated:smooth muscle? (highest striated to lowest?)

Which muscle increases rate?

(striated) ruminants, dogs, pigs, rats, mice > cats > equine > primates > birds (smooth)

Greater rate in striated muscle

What is reverse peristalsis?

Eructation of gases and regurgitation of luminal contents

What are the functions of rumination?

1. Increases saliva flow

2. Re chewing to reduce particle size

-preparation for swallowing

-release soluble constituents

-damage plant tissues for microbes

What is the time budget for a grazing animal?

-8hrs eating

-8hrs ruminating

-8hrs resting

What are the main factors affecting rumination time?

Physical form of the diet

Fiber content of the diet

Rumination steps...

1. Triphasic contraction of reticulum

2. Production of negative pressure in thorax that is transmitted to esophagus ('vacuum')

3.Cardia opens and esophagus dilates (negative pressure sucks digesta into esophagus)

4. Rapid reverse peristalsis

5. Bolus is rechewed (slower)

6. Digesta is rein salivated and increases reticule-rumen motility

7. Reswollowing

What does the triphasic contraction of the reticulum do?

-Forces digesta to cardia

-epithelial receptor is activated by larger particles (>10mm)

-stimulation of rumination centre (hypothalamus)

How is the negative pressure in thorax created?

Inspiratory effort with tongue and soft palate raised to close oral cavity and nasopharyngeal opening (animal inhales with epiglottis close)

How does the saliva composition differ with rumination?

Parotid glads secrete increased saliva rich in bicarb (HCO3-)

After reswallowing, what does the rumen under go?

The rumen undergoes a primary contraction

Rumeno-reticular contractions are located where?

Contractions of the entire sac but primarily muscular contractions on the pillars

Rumeno-reticular contraction funtions?

1. Mix contents

-minimize stratification

-moved fermentation product to rumen wall

2. Particle sorting and passage

3. Rumination and eructation

What is the primary contraction sequence through the rumen?

What is the function?

Sequence = reticulum -> dorsal sac -> ventral sac

Function: mixing and inoculation of digesta and particle sorting across the reticuloruminal and anterior folds

Rumeno-reticular contractions - primary contraction (A-wave or back ward moving or mixing cycle) steps...

Rumeno-reticular contractions - primary contraction (A-wave or back ward moving or mixing cycle) steps...

1.Swollwed colus enters cadia (Air bubbles make bolus float near cardia)

2. 2nd contraction of reticulum forces fluid and bolus into Rumen - caudal contraction pushes bolus into dorsal sac

3. microbes release air bubbles

4. Dissolution of bolus causes particles to sink

5. Ventral sac contraction push material into dorsal sac and dense particles over cranial pillar into cranial ventral sac

6. Reticular contraction of next cycle opens reticulo-omasal orfice and dense particles are forced into omasum

Explain the Reticulum biphasic contractions

What is open during this contraction?

-1st contraction is weak and incomplete (half size)


-2nd contraction is complete and strong

**Reticulo-omasal orifice is open during contraction, but closes when reticulum dilates

(digestive passage to omasum is dependent on duration of contraction)

Explain the reticulum biphasic contraction...

-extra complete contraction that precedes a biphasic contraction

-associated with movement of digesta up to the cardiac sphincter before rumination (regurgitation)

When does the secondary contraction (bwave, forward moving, or eructative contraction) occur?

What is its sequence?

Occurs in association with every 2nd or 3rd primary contraction for eructation

Sequence: caudo-ventral blind sac -> caudo-dorsal blind sac -> dorsal sac -> cranial pillar elevation and cranial sac relaxation -> liquid moves away from cardia -> gas eructed

What are the factors that affect the rumens-reticular contractions?

1. Feeding - increases frequency and amplitude of contractions (2/minute)

2.Diet composition - high grain or fine forage decreases rate and amplitude

3. Volatile FA - decrease primary contractions (acetic, propionic, and butyric acids)

4. Metabolic disorders - decrease primary contractions (i.e. hardware disease)

Epithelial, mucosal and tension receptors regulate RR motility - what is the location and stimuli of each receptor?

Epithelial = basement membrane (RR), stimulated by chemical and mechanical (light tactile)

Mucosal = mucosa (abomasum, intestines), stimulated by chemical and mechanical (acidity/hyperosmolarlity)

Tension = muscle, stimulated by mechanical (distention, contractions)

What Stimulates RR motility?

(Increased salivation, rumination and RR motility) - salivation and gastric centres of the medulla oblongata

1. Moderate RR distension activates gastric and salivation centers (medulla oblongata)

2. Abomasal mucosal receptor activation (acid) = increased RR motility and rumination

3. Mediated by neural (vagus, splanchnic) and hormonal (CCK) signals

Inhibition of RR motility (negative feedback)

Inhibits medullary gastric and salivation enters = decreasing salivation, rumination and RR motility

1. Severe RR distention

2. Abomasal tension/mucosal receptor activation leads to decreased R motility to limit RR emptying

3. Duodenal tension/mucosal receptor activation leads to decrease abomasa motility to limit abomasal emptying

4. Mediated by Neural (vagus, spanchnic) and hormonal (CCK) signals

Gas production occurs 30 min to 2 hrs post feeding and is composed of what?

**CO2 65% and CH4 27% of rumen gas (also N2, O2, H2, H2S)

-25%-35% of CO2 is produced in the rumen, absorbed in the blood and removed though the lungs, remainder through the mouth

-20% of CH4 is removed though the lungs, remainder through the mouth

Mechanism of eructation...

1. Stimulus = gas distension of RR

2. Increase secondary cycle contractions: gas layer from dorsal rumen to cardia or reticulum.

-Rumino-reticular fold and cranial rumen pillar hold rumen contents (cardia free of fluid)

3. Opening of lower esophageal sphincter

4. Esophagus filled with gas and rapid reverse peristalsis of gas

**most expelled through mouth but some into lungs -> blood -> milk taint

Inhibition of eructation

(can cause animals to bloat - pressure 45-100mmHg)

1. Presence of digesta (fluid and froth) near cardia

2. lowering of esophageal sphincter (inhibition)

**hormones = epinephrine, histmine

What is bloat?

**usually frothy bloat (90%) some free gas bloat (10%)

Impaired eructation mechanisms

-frothy/foamy contents inhibit neural control of esophageal opening

-gas/froth accumulates

-rumen expands (increasing pressure)

-pressure on diaphragm


What is free gas bloat and what does it cause?

Usually due to physical obstruction of esophagus or cardia (incomplete chewing of foods) irregular feed intake

-Vagus nerve damage due to chronic pneumonia or hardware disease

How does hardware disease cause damage and free gas bloat?

Metal object punctures the reticulum


-esophagus is compressed

-decreased RR motility

What is frothy bloat and how is it caused?

Dispersion of gas-liquid-feed particles (legume pasture)

-often with high grain or fresh alfalfa

-Increased production of bacterial mucopolysaccharides (slime) and cell lysis (release of protein)

-Increases rumen fluid viscosity

-Bubble are tapped in fluid increasing stability of froth

Name the type of motility disorder...

Name the type of motility disorder...

Top left: Normal

Top right: free gas bloat

Bottom left: Frothy Bloat

Bottom right: frothy bloat (vagus indigestion)

What are 5 ways to measure GI motility?

1. Gastric emptying scintigraphy

2. Stable Isotope Breath Tests (13C isotope)


4. Functional ultrasonography (volume, contraction and emptying)

5. Other - absorbable markers (drugs), non absorbable markers (phenol red, wireless pH)

How do you evaluate gastric capacity and accommodation?

1. Balloon Measurements (barostat) - tone, compliance and postprandial accommodation.

-maintains contrant pressure

2. SPECT (single photon emission computed tomography)

-CT images of stomach after IV [99mTc] is taken up by parietal and mucin-secreting cells of gastric mucosa

Stomach (abomasum) functional regions?

Gastric pump - phasic contractions 
Gastric reservoir - tonic contractions

Gastric pump - phasic contractions

Gastric reservoir - tonic contractions

What are the 3 phases of the gastric pump?

Phase of propulsion 
Phase of emptying 
Phase of retropulsion

Phase of propulsion

Phase of emptying

Phase of retropulsion

What is the phase of propulsion?

Peristaltic wave begins at junction of proximal and distal stomach

= rapid flow of liquids with small particles

= delay of large particles towards the pylorus

What is the phase of emptying?

Peristaltic wave middle of antrum opening the pylorus...

Emptying of liquids with small particles

Retention of large particles in the bulge of the terminal antrum

What is the phase of retropulsion?

Distal antral contraction closing the pyloris

Retropulsion of large particle sad clearing of the terminal antrum (shear force)

What controls Relaxation of the gastric reservoir?

1. Receptive relaxation

2. Adaptive relaxation

3.Feed back relaxation

4. Regulation by NANC (nonadrenergeric, noncholinergic) inhibition

What is Receptive Relaxation?

1. Receptive relaxation: brief relaxation and swallowing (vago-vagal reflex)

-acts directly on the vagus centre (usually mechanical stimuli)

-glossopharyngeal,facial, trigemial nerves

What is Adaptive Relaxation?

2. Adaptive relaxation: prolonged relaxation caused by digesta in the stomach (gestro-gastric reflex between gastric reservoir - astral pump, and ago-vagal reflex)

-usually due to tension receptors

What is feedback relaxation?

3.Feed back relaxation: prolonged relaxation by nutrients in small intestine (duodenal brake, jejunal break, or ill brake)

-nutrients or release of CCK

What is regulation of NANC inhibition?

4. Regulation by NANC (nonadrenergeric, noncholinergic) inhibition: inhibitory vagal efferents (Ach) activate the ENS to release NO, PACAP, VIP, ATP which relax muscle

What are the 3 entero-gastric reflexes?

1. Activation of sensory vagal afferents (integration in vagal center) 
2.Effects of stimulation of vagal efferents 
3. Feed-back control by gastro-intestinal hormones

1. Activation of sensory vagal afferents (integration in vagal center)

2.Effects of stimulation of vagal efferents

3. Feed-back control by gastro-intestinal hormones

What effects the activation of sensory vagal afferents?

Intestinal nutrients, osmolality, acid, hormones

Effects of stimulation of vagal efferents on proximal and distal stomach?

Proximal = adaptive relaxation of gastric reservoir (decrease muscle activity) caused by inhibitory vagal efferents (NO, VIP)

Distal = increased contraction of pyloric sphincter (Ach)

Feed back control of gastric motility by what gastro-intestinal hormones?

Inhibition by...

-Duodenal brake = CCK, secretin, GIP

-Ileal brake = GLP, PYY

Stimulation by...

-Ghrelin, neurotensis, gastrin