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Leah GIL > Week 2 > Flashcards

Week 2 Flashcards

1
Q

Describe the path of the oesophagus

A

Continuation of laryngopharynx connecting pharynx to stomach

Dorsal to trachea, LHS

Travels through mediastinum (space between plural sacs)

Passes through oesophageal hiatus of diaphragm

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2
Q

Label the diagram

A
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3
Q

How do oesophageal muscles differ to other muscles in GI tract

A

Oesophageal muscles differ from elsewhere in GI tract in that they are striated (facilitates swallowing & vomiting)

Circular muscle layer particularly well developed in upper region & at junction of stomach (sphincters)

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4
Q

Describe the phases of swallowing

A

Oral phase
1. Food mixed with saliva to form bolus
2. Tongue moves bolus to back of the mouth

Pharyngeal stage
3. Vocal folds close
4. Epiglottis covers entrance to trachea

Oesophageal phase
5. Upper sphincter of the oesophagus opens
6. Food passes into oesophagus, entrance to trachea is reopened & upper oesophageal sphincter closes. Breathing resumes
7. Swallowing centre in medulla initiates wave of contractions in circular muscle layer (swallowing no longer voluntary)
8. Peristaltic wave travels along oesophagus carrying bolus ahead of it to the lower oesophageal sphincter (0.5-1m/s)
9. In many species function of lower (aka cardiac) sphincter is aided by sharp angle at which oesophagus enters stomach (acts as 1-way valve)

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5
Q

Label the diagram

A
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6
Q

Label the stomach

A
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7
Q

What are the ridges for in the stomach

A

Ridges are known as rugae which increase surface area & lets stomach expand

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8
Q

Label the GI tract

A
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9
Q

Describe the glandular stomach

A

Part of stomach closest to oesophageal opening = oesophageal portion

Small in most species (except horses & rats)

Lined with stratified squamous epithelium (like oes. & oral cavity)

Proportion of non-glandular region varies between species

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10
Q

Label the stomach

A
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11
Q

What is the margo plicatus

A

folded margin between non-glandular and glandular portion of stomach

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12
Q

What are the 4 regions of the glandular stomach and their functions

A
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13
Q

Label the glandular stomach

A
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14
Q

describe the glandular stomach

A

Stomach wall contains millions of glands (gastric pits) with secretory cells

1-3 mm deep

Ducts of glands open into stomach lumen through glandular neck

Most gastric juice formed in corpus and pylorus

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15
Q

Label

A
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16
Q

Describe the stomach innervation

A

Sympathetic fibres

Parasympathetic fibres

Intrinsic fibres of enteric nervous system (ENS)

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17
Q

describe the enteric nervous system

A

Motility and secretion largely regulated by reflexes:
- Long reflex arcs – involve the CNS
- Short reflex arcs - contained within wall of the GIT = ENS

Can function independently from the CNS

Controls:
- Motility (peristalsis)
- Exocrine and endocrine secretions
- Microcirculation of the gastrointestinal tract
- Regulating immune and inflammatory processes

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18
Q

Describe the parasympathetic and sympathetic impulses of ENS

A
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19
Q

What do ENS plexuses contain

A
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20
Q

What are interstitial cells of Cajal (pacemaker cells)

A

Modified smooth muscle cells central to GI motility regulation

Function as a pacemaker for gut contraction

Different frequencies in different parts of GI tract

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21
Q

What is Ileus

A

GI stasis caused by stress/dehydration/other primary condition

Common in rabbits

Primary cause rarely diagnosed

Can occur after abdominal surgery

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22
Q

What is spasmodic colic

A

Change in gut activity causes muscular spasm of intestines

Underlying cause rarely identified

Common in horses

Opposite issue to ileus – too much activity

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23
Q

What is vagal indigestion

A

Motor disturbances that hinder passage of ingesta from reticulorumen, abomasum or both

Common in cows

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24
Q

Describe the layers of the GIT

A
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25
Q

Why would you want to image the oesophagus and what are some radiographic considerations

A
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26
Q

Label the radiograph

A

Can be hard to see if problem is in trachea of oesophagus when looking at cranial aspect

black (gas) high up in abdomen is probably stomach (not lungs

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27
Q

What is wrong with this x-ray

A
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28
Q

What is wrong with this x-ray

A

Can be congenital (puppy wont gain weight & is always regurgitating clumps of food with no liquid)

Also in older dogs because NS is damaged/changed & oesophagus doesn’t contract anymore (spinal tumour, nervous system disorder etc.)

Dogs cant rely on gravity because their chest is so flat so food sits in oesophagus

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29
Q

How do you view oesophagus via radiography

A
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30
Q

How do you view oesophagus via fluoroscopy

A
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31
Q

Label the anatomy

A
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32
Q

Label the anatomy

A
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33
Q

Label the x-ray

A
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34
Q

Label the x-ray

A
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35
Q

Fill in the table with gas/fluid in stomach depending on view

A
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36
Q

What view is this

A

dorsoventral

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37
Q

What view is this

A

ventrodorsal

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38
Q

What view is this

A

right lateral

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39
Q

What view is this

A

left lateral

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40
Q

what is gastric dilation and volvulus (GDV)

A
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41
Q

What condition is seen here

A

GDV
gastric dilation and volvulus

gas and gastric contents cant leave so stomach continues to stretch

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42
Q

What other structures are affected by GDV

A
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43
Q

Define sphincter

A

ring of muscle surrounding opening

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44
Q

Define peristalsis

A

involuntary constriction & relaxation of muscles creating wave-like movements that push contents forwards

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45
Q

define deglutition

A

process of swallowing

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46
Q

define primary vs secondary peristalsis

A

primary: classic coordinated motor pattern of oesophagus initiated by swallowing

secondary: if food gets stuck, oesophagus will distend. local reflexes at these distention sites trigger forceful secondary waves

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47
Q

Where is the swallowing centre and how is it activated

A

in medulla oblongata & activated by pressure-sensitive sensors in pharynx

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48
Q

define dysphagia

A

swallowing difficulties

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49
Q

define regurgitation vs vomiting

A

regurgitation: action of bringing swallowed food up again into mouth

vomiting: eject matter from stomach through mouth

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50
Q

What should we find on gastroscopy

A
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51
Q

Label the horse gastroscopy

A
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52
Q

In what views were these radiographs taken

A
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53
Q

What abnormalities can you see in this radiograph

A

gas in stomach, contrast media in oesophagus, displaced abdominal organs

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54
Q

Define transit time

A
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55
Q

Define zymogen/proenzyme

A
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56
Q

Define autocatalyse

A

catalysis of a reaction by one of its products

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57
Q

Define paracrine

A
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58
Q

What is the stomach, where is it and what does it do?

A
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59
Q

What are the main functions of the stomach

A
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60
Q

What enzyme digests proteins

A

pepsin

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61
Q

How does the stomach prevent digestion of chief cells & parietal cells

A

Pepsin (breaks fown proteins) would digest chief cells so chief cells produce/store pepsin as inactive proenzyme (pepsinogen)

HCl would dissolve parietal cells so they produce H+ & Cl- ions instead which they release into lumen where HCl forms

Mucosal mucous cells secrete mucus containing HCO3- to create protective layer protecting against pepsin & HCl in stomach

Negative feedback loops prevent constant release of gastric juiuces

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62
Q

Label the stomach gland

A

ECL = enterochromaffin like cells (release histamine)

endocrine cells include G cells & D cells

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63
Q

Describe the phases of gastric secretion

A
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64
Q

Describe the cephalic (first) phase of gastric secretion

A
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65
Q

Describe the gastric (second) phase of gastric secretion

A
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66
Q

Describe the intestinal (third) phase of gastric secretion

A
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67
Q

Describe how pepsinogen is activated in the stomach

A
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68
Q

Describe histamine & gastrin in control of HCl production

A
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69
Q

Describe the parasympathetic nervous system in control of HCL production

A
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70
Q

Fill in the table with roles of different cells in digestion

A
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71
Q

Describe factors that regulate appetite

A

Ghrelin stimulates appetite
Leptin supresses appetite

appetite affected by nutrient balance, sensory stimuli, feeding schedule, health/illness, exercise

72
Q

Describe the major effects of sympathetic & parasympathetic stimulation of GI tract motility, including sphincter tone

A
73
Q

Recall the mechanism of generation of an action potential

A
74
Q

identify the positions of autonomic ganglia & plexuses within abdomen & pelvis

A
75
Q

Describe the functions of the enteric nervous system

A
76
Q

describe the distribution of the enteric nervous system

A
77
Q

Describe the relationship between extrinsic autonomic innervations & intrinsic enteric innervations of tract

A
78
Q

explain what is meant by electrical coupling between smooth muscle cells & its importance for generating waves of activity along gastrointestinal tract

A
  • electrical coupling refers to smooth muscle cells being in communication with each other & responding together (being a synctium) to electrical stimulus (action potential)
  • achieved by gap junctions between smooth muscle cells which allow ions to pass between smooth muscle cells, thus allowing adjacent cells to contract as one
  • spread of action potential down muscle also allows for relaxation of muscle that just contracted to get ready for another wave of contraction
79
Q

describe the anatomical & biophysical characteristics of GI tract smooth muscle

A
80
Q

what is the origin and physiological significance of slow wave development in GI tract smooth muscle

A
  • interstitial cells of Cajal (ICC) are coupled with another type of interstitial cell & smooth muscle to form syncytium
  • ICC have intrinsic pacemaker activity that is responsible for waves of contraction/relaxation that run down GI tract
  • waves of depolarisation are propagated along ICC network to create segmented contractions
81
Q

What are the features of segmentation

A
82
Q

What are the features of peristalsis in SI

A
83
Q

describe the importance of the ENS

A
84
Q

Describe contractions in the stomach

A

Contractions are peristaltic and start in the fundus

They appear at intervals of 15 seconds lasting 2-3 seconds

Contractions lead to circular narrowing of lumen of stomach, moving from fundus towards duodenum

Muscles in upper part of stomach are poorly developed so contractions are weak & content is not well mixed

Contractions become stronger moving towards pylorus

Large part of pylorus wall contracts simultaneously –> increases luminal presses –> forces chyme through pyloric sphincter into intestine

Most pyloric content remains in stomach for further mixing & dividing

85
Q

What is the enterogastric reflex

A
86
Q

What factors influence stomach emptying

A
87
Q

Describe how gastric emptying can be affected by osmotic pressure or chemical composition of stomach contents

A
88
Q

Describe integrated reflexes that initiate vomiting

A

Nausea
Chemoreceptors in GI tract
CNS (medulla oblongata)
Pharynx contracts to close respiratory passages
Deep inspiration
Closure of glottis
Contraction of abdominal muscles to increase intra-abdominal pressure
Lower sphincter relaxes

89
Q

Describe origin and release of gastrin

A

produced by G cells in lower part of stomach

stimulate gastric acid secretion & enhance motility

stimulated by vagal nerve fibres & activation of stretch receptors

90
Q

Describe origin and release of secretin

A

produced by S cells in duodenum & upper jejunum

stimulates pancreas to secrete bicarbonate-rich pancreatic juice to neutralise acidic chyme in SI & inhibits gasric acid secretion

stimulated by chyme entering duodenum

91
Q

Describe origin and release of cholecystokinin (CCK)

A

produced by I cells in duodenum & jejunum

stimulates release of digestive enzymes from pancreas

Induces contraction of gallbladder to release bile into duodenum & inhibits gastric emptying

stimulated by presence of peptides, amino acids, fatty acids & monoglycerides in SI

92
Q

Describe origin and release of motilin

A

produced by M cells in duodenum & jejunum

stimulates migrating motor complex (MMC) in stomach & SI during fasting

Enhances gastric & SI motility

stimulated by absence of food in digestive tract & acid in duodenum

93
Q

Describe origin, stimuli & effect of ghrelin

A

produced by D1 cells in stomach

stimulates hunger & promotes gastric emptying

stimulated by empty stomach

94
Q

Describe origin and release of somatostatin

A

produced by D cells in stomach & duodenum

inhibits release of gastrin, insulin, glucagon & growth hormone

suppresses gastric acid secretion

stimulated by acidic chyme in stomach

95
Q

What are the methods of ion transport across membranes of cells

A
96
Q

Describe mechanism of neuromediators release in synaptic cleft

A
97
Q

describe the importance of kiss & run mechanism regarding leak of neuromediators in synaptic cleft

A
98
Q

What are the stomachs of the ruminant

A

Rumen = fermentation vat

Reticulum = part of rumen

Omasum = water absorption

Abomasum = true stomach

99
Q

describe lining of ruminant fore-stomachs

A

Lined by stratified keratinised epithelium (constantly renewed because wall is always being eroded)

100
Q

describe lining of ruminant abomasum

A

Lined by simple columnar epithelium with occasional goblet cells

101
Q

Label the ruminant LHS

A

surgery always done from LHS

102
Q

label the ruminant RHS

A
103
Q

Describe ruminant stomach capacity

A

Total capacity of stomach is approx. 100-250L in adult cow
- Rumen ~ 80%
- Reticulum ~ 5%
- Omasum ~ 7%
- Abomasum ~ 8%

In sheep & goats reticulum is relatively larger whilst omasum is relatively smaller than in cattle

104
Q

Describe ruminant oesophagus

A

Large (diameter up to 6 cm) and distensible

Striated muscle along its whole length

Mucosa is insensitive

Heavily keratinised
- Helps protect it from abrasive plant material

“Chock” (obstruction of oesophagus) most commonly occurs close to pharynx & at thoracic inlet (potatoes, sugar beet)

105
Q

Describe the reticulorumen

A

Large volume - ~ 200 L in the adult cow

Warm (close to body temperature)

Moist (~ 90% of contents is water)

Anaerobic –> “Fermentation”

pH ~ 6.5
- Important
- Too much grain can cause acidosis which kills flora

Environment suitable for range of microorganism that digest & degrade plant material
- Particularly cellulose & hemicellulose

Fermentation results in production of volatile fatty acids, carbon dioxide & methane

Fibrous feedstuffs remain long enough for complex carbohydrate digestion

Surface area increased by initial mastication & ruminating (long fibre particles are regurgitated & re-chewed)

Rumen-reticulo contractions (~3 every 2 mins)
- Stirs, redistributes and mechanically grinds
- Partitions fibre for re-chewing.

106
Q

Describe the abomasum

A

Structure and function similar to monogastrics

Divided into fundus, body and pylorus

Approximately a dozen large longitudinal rugae (persist when distended)

Glands producing mucus, pepsinogen & hydrochloric acid

pH ~3-4 (diluted by large volumes of fluid from forestomach)

Weak, rhythmical contractions

No proper pyloric sphincter – wall thickening (torus) acts as valve

107
Q

Compare chamber sizes in young vs mature ruminants

A

Abomasum proportionately larger in young ruminants

Growth of Re/Ru/Om commences as calf/lamb eats more roughage

Rumen not developed in lambs

108
Q

Describe ruminant stomach development at weaning

A

After birth the forestomach starts to develop and grow

Development is promoted by presence of forage in rumen as young animal starts to pick at solid food

A rumen flora develops within a couple of weeks of birth

Functional by 6-8 weeks

By the time animals are weaned forestomach is capable of digesting adult diet

109
Q

Why do calves have milk clots in abomasum

A

During process of digestion in preruminant calf, casein protein in cows’ milk clots in abomasum due to action of enzymes pepsin & rennin (chymosin) & hydrochloric acid

110
Q

What is this

A

Reticulum

keratinised

Ridges 1-2mm high & 1-2cm wide

111
Q

describe rumination time vs feed quality

A

Poor quality feed e.g., rough hay spends more time in the rumen - this is good for the rumen as ruminants are designed to be slow digesters
Grains - spend less time in rumen but leads to acidity problems

112
Q

Describe the omasum structure

A

Function still remains unclear:
- Probably water absorption
- Pumping of ingesta from reticulum into abomasum

Contains approx. 100 laminae (like leaves in book) covered with conical papillae which hugely increase its surface area

Laminae are in 3 distinct size groups i.e. not random sizes

Regular biphasic contractions squeeze material into recesses & then general contraction progresses fluid forward

Relatively smaller in sheep and goats

Not present in tylopods (camelids)

Bolus gets squashed in omasal leaves so water squeezed out & then drier bolus flows along bottom

113
Q

Label the omasum

A
114
Q

Describe rumen papillae

A

Leaf-shaped

Keratinised

Poorly developed in roof of dorsal sac

Increased surface area for flora and absorption

115
Q

Label the rumen papillae

A
116
Q

Describe rumen papillae size & growth

A

Vary in size & shape depending on age, diet & location in rumen

Growth stimulated by:
- High concentration of VFAs (esp. butyrate)
- Long fibre

Thus longest at top of fluid layer, where long fibre floats

Shortest at top of rumen, where the gas cap sits

Medium length in middle to bottom of rumen

They take time to adapt to dietary changes

117
Q

Describe digestion in neonatal ruminant

A

Milk is digested in the abomasum

Fundic glands produce rennin which coagulates casein (milk protein) in acidic environments

Clot retains milk to allow complete digestion by pepsin

118
Q

How does milk bypass the reticulum & rumen in neonates

A

In neonates, milk needs to go directly to abomasum, otherwise it ferments in rumen & causes scour

Special structure, reticular groove, acts as diversion for milk

Relaxed: oesophagus empties into reticulum/rumen

Contracted: edges of groove curl up & create tunnel between oesophagus & reticulo-omasal orifice

Groove persists but only works in calves

119
Q

label the ruminant neonate stomach

A
120
Q

Describe the reticular groove reflex

A

When stimulated by vagus, groove contracts to form closed tube

The reflex is stimulated by:
- Suckling milk / pharyngeal stimulation
- Noises associated with the “feeding routine”

The reflex is poorly reactive to:
- Drinking – hence bucket-fed calves are prone to scour since milk enters rumen
* Also drink too fast which floods groove
- Stomach tubing

Reflex still works in adults:
- Dehydration via ADH
- Drenches containing copper (sheep) or sodium salts (cattle)
- Apart from this, reflex can be considered inactive in adult feeding & drinking

121
Q

Describe the rumen microbiota

A

The rumen ‘microbial population’ is very dense
- ca. 10^10 bacteria/ml
- 10^6 protozoa/ml
- 10^3 fungi/ml

Rumen microbes specialized to survive & thrive within rumen

Conditions are strictly anaerobic

Oxygen is toxic to many rumen microbes

If microbiota is disrupted, then nutrition of ruminant is disrupted

122
Q

What are the factors for a stable microbial population

A
123
Q

Why do herbivores need bacteria for digestion

A

Food of ruminants consists mainly of β-linked polysaccharides e.g. cellulose

These can’t be broken down by mammalian digestive enzymes

Ruminants have evolved to use microbial fermentation of food prior to normal digestion

Bacteria produce products that can be directly used by animal

Bacteria also multiply on poor food to provide accessible form of proteins, nucleic acids, sugars & lipids that can be digested by ruminant

124
Q

What does microbial fermentation provide

A

High-Quality Protein from Poor quality feed

Nitrogen Incorporation: Rumen microbes use nitrogen from non-protein sources like urea for protein synthesis

Hard-to-Digest Carbon: Microbes convert difficult-to-digest carbon into microbial proteins and nucleic acids.

Essential Amino Acids: Rumen microbes synthesize all essential amino acids that vertebrates cannot produce.

B Vitamins Production: Rumen microbes produce all B vitamins, preventing deficiencies common in other mammals.

125
Q

Fill in the chart showing fermentation steps

A
126
Q

What is fermentation

A

Catabolic reactions producing ATP in which organic compounds serve as both primary electron donor & ultimate electron acceptor
- Don’t use oxygen as terminal electron acceptor in respiration

Fermentation requires anaerobic conditions

127
Q

How are different bacteria involved in fermentation

A
128
Q

What are common protozoa in rumen

A

Holotrichs and oliotrichs

129
Q

Describe the role of anaerobic fungi in rumen fermentation

A

Actively ferment cellulose & soluble sugars (but not all) resulting in generation of mixture of products

Products include acetate, lactate, ethanol, formate, succinate, CO2 & H2

130
Q

How does a diet change affect rumen microbiota

A

When a diet changes the microbiota will adjust

This takes time

Can take up to two weeks to re-establish a balance

The balance of organisms may be different

Sudden changes in diet composition can have undesired effects on rumen function

131
Q

Describe the effect of antibiotics on rumen microbiota

A

Bacteria of rumen (& hind gut) flora will vary in susceptibility to antibiotics
- Oral antibiotics can affect bacteria in rumen & lower intestine
* This can impact on both rumen and gut health

Oral antibiotics are NOT given for adult ruminants as they can disrupt rumen function

Some species are susceptible to oral antibiotics as they disturb balance of gut microbes & cause disease

132
Q

Describe the monogastric stomach microbiology

A

A barrier to infection of the lower intestinal tract

Minimal Microbiology (but there is a base microflora)

One bacterial pathogen to consider (Helicobacter)

Bacteria killed by acid pH

Disruption of acid can lead to infection or breakdown of protection

Age may impact on pH barrier function

Neonatal stomachs may be infected by overgrowth

Food type may effect the barrier function

Pharmacology can effect the barrier function (i.e. antacids)

133
Q

Describe the helicobacter species in monogastric stomachs

A

Helical / ‘s’ shaped Gram –ve

Related to Campylobacter

Range of species effected:
- Ferrets, dogs, cats, lab rodents but found in many other species

Chronic gastritis in ferrets

Found in gastric mucosa of dogs and cats

Considered limited pathogenic significance to animals but possibly zoonotic.

134
Q

How does helicobacter survive in monogastric stomach

A
  1. Drills into the mucus gel layer of the stomach
  2. Binds to membrane-associated lipids of epithelial cells
  3. Secretes large amounts of Urease
  4. Urease metabolizes urea to produce ammonia
  5. Ammonia will neutralize gastric acid

Survival in the acidic stomach is dependant on urease

The ammonia that is produced is toxic to the epithelial cells

Also produces other products protease, catalase & phospholipases which can cause damage to those cells

135
Q

How can you test for helicobacter in monogastric stomach

A

Diagnosis of infection with Helicobacter is rare in practice as there is lot of asymptomatic carriage in range of species

The following approaches can be used
- Non invasive tests
- blood antibody test
- Stool antigen test
- carbon urea breath test, uses radio labelled urea which urease metabolises to produce radiolabelled CO2 which can be monitored
- Most reliable method is combination of biopsy check during endoscopy with rapid urease test, histological examination & microbial culture

136
Q

Label the rumen papillae

A
137
Q

Role of the rumen

A

The rumen is designed to digest cellulose, which is from the plant cell walls. This digestion results in the production of volatile fatty acids (VFAs), which are the primary energy source of the ruminant.

138
Q

What do the abdominal silhouettes show

A
139
Q

How can you assess rumen health

A
  1. rumen fill (has cow been eating?)
  2. palpate to feel consistency (should be doughy consistency & feel 3 contractions every 2 min)
  3. auscultation to listen to rumen contractions
  4. volume & consistency of faeces (score of 3 ideal)
140
Q

Label the reticulum histology

A
141
Q

What is the location of the reticulum

A

The reticulum is adjacent to the diaphragm, lungs, abomasum, rumen and liver. It is in the cranial abdomen, situated on ventral abdominal wall, just to the left of the midline.

142
Q

What is the location of the omasum

A

The omasum is located in the cranial abdomen, on the ventral abdominal wall, just to the right of the midline. It is covered by lesser omentum and is bilaterally flattened.

143
Q

What is the location of the abomasum

A

The abomasum sits on the ventral wall of the cranial abdomen, to the right hand side of the midline. It is divided into the fundus, body and pylorus.

144
Q

What is the function of the abomasum

A

digest protein from both feed (bypass protein) and ruminal microbes (ruminal protein).

145
Q

describe the abomasum absorptive surface

A

There are approximately 12 large folds

Surface is columnar epithelial cells

There are also glands which produce mucus, pepsinogen and hydrochloric acid (resulting pH 3-4)

146
Q

Describe the omasum absorptive surface

A

Contains approximately 100 laminae (leaf-like structures) which are grouped into different sizes; these leaf-like fronds drastically increase the surface area for absorption

The interior surface is lined by stratified squamous epithelial cells.

147
Q

Describe the reticulum function

A

Main Role: Collects smaller digesta particles, moving them to the omasum; larger particles stay in the rumen for further digestion.

Fluid Role: Helps in particle separation.

Biphasic Contractions:
First Contraction: Sends large particles back to the rumen.
Reticulo-omasal Orifice: Allows finer particles to pass to the omasum.

148
Q

What buffers the acidifying effects of VFAs in ruminant fermentation

A

Acidifying affects of VFA buffered by bicarbonate & phosphate in large volumes of saliva

149
Q

Explain protein digestion in rumen

A

protein is digested into rumen undegradable protein (moved into abomasum and SI) and rumen degradable protein
Rumen degradable protein is broken down into amino acids which is either converted to microbial protein (this uses energy) or ammonia (if no energy available)

150
Q

Explain process of urea cycling in protein digestion in the rumen

A

Protein degraded into ammonia when no energy present to convert it to microbial proteins

Ammonia transported to liver where it is converted to urea

Some is excreted in urine

Some is recycled back into saliva where it returns to the rumen to be converted back to ammonia

this ammonia can be converted into microbial protein (uses energy) or be recycled again

151
Q

Describe chain of carbohydrate digestion in ruminants

A
152
Q

Describe fat digestion in ruminants

A

Limited
High fat diets depress microbial activity
Long chain fatty acids not absorbed

153
Q

What happens if more protein is present than energy in rumen

A

If more protein is present than energy, amount of MCP produced is limited by energy

Increase ammonia - elevated blood urea

Can recycle but high urea causes issues with reproduction

154
Q

What happens if more energy is present than protein in rumen

A

If more energy is present than protein, amount of MCP produced is limited by protein

Wasted energy to methane…

155
Q

What can cause acidosis in rumen

A

too much concentrate or not enough fibre can lead to increased levels of lactic acid

156
Q

What are the consequences of decreased rumen pH?

A

Balance of rumen microflora changes
Decreased rate of digestion due to decreased number of viable microorganisms
Changes proportion of different VFAs produced

157
Q

What are the clinical signs of chronic acidosis and where is it most common

A

High producing animals fed diets high in concentrate
- sub-optimal rumen function
- reduced food intake
- pain
- indigestion
- loose faeces
- low milk fat levels

158
Q

What typically causes acute acidosis in ruminants

A

grain engorgement

159
Q

What are the by-products of carbohydrate fermentation in ruminants

A

Methane & CO2

160
Q

What is bloat in ruminants

A

gases produced not removed by eructation

161
Q

What are the 2 main forms of bloat

A

Gas bloat
Frothy bloat

162
Q

Describe gas bloat

A

Something blocks or hinders normal eructation

Physical obstruction
- e.g. foreign bodies blocking the oesophagus
* e.g. potatoes or neoplastic growths

Cessation of normal rumination
- e.g. ruminal acidosis, vagal indigestion

Gas being unable to reach the oesophagus
- e.g lateral recumbency

163
Q

Describe frothy bloat

A

Pastures rich in clover
- Soluble leaf proteins form a gassy foam with rumen gases
- Gassy foam can’t be removed by eructation & builds up in rumen
- Lots of air trapped in liquid

164
Q

How can bloat become fatal

A

Causes compression of other organs e.g., heart, lungs

165
Q

What are some advantages & disadvantages of ruminant fermentation & digestion compared to non-ruminants

A
166
Q

List the differences in forestomach & forestomach digestion between camelids & other ruminants

A

Camelids only have 3 compartments (lack omasum) instead of 4

Rumen & reticulum are combined (c1 - most nutrient absorption here)

167
Q

What are the features that permit continuous fermentation in ruminants

A

multicompartmental stomach
Rumen microbial population
Cud chewing
Large surface area
Reticulorumen contractions
Large amount of saliva

168
Q

Why is the optimisation of rumen function important? How can this be achieved? How does suboptimal function occur?

A
169
Q

Why is forestomach motility important and how does it occur? How does suboptimal motility occur and what are the consequences?

A
170
Q

What is the importance of the reticular groove reflex and what are the consequences and reasons for this not occuring

A
171
Q

Compare roughage based diet to concentrate based diet

A
172
Q

define ptyalism

A

hypersalivation

173
Q

Which organs are in contact with the stomach

A

Spleen on greater curvature
Liver on lesser curvature
Pancreas
SI
Oesophagus

174
Q

Identify common reasons for milk production drop in post partum cow

A

Fe/Se/Cu/Co deficiency
hypocalcaemia (milk fever)
bacterial imbalance
LDA
Rumen acidosis
dehydration

175
Q

What does a high pitch tinkling sound suggest in cow left abdomen auscultation

A

LDA due to gas in abomasum

ping between 9th and 13th rib

176
Q

What occurs after birth that make translocation of the abomasum possible?

A

after birth there is lots of space for abomasum to move

177
Q

What factors can influence gaseous distension of the abomasum in ruminants?

A

Ingestion of high concentrate, low roughage diets reduced emptying of abomasum
Sudden change in diet can stress the abomasum
More volatile acids -> hypomotility of abomasum -> more gas -> blocks entrance and exit

Leah GIL (12 decks)

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