Week 2 Flashcards

(177 cards)

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
Why would you want to image the oesophagus and what are some radiographic considerations
26
Label the radiograph
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
27
What is wrong with this x-ray
28
What is wrong with this x-ray
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
29
How do you view oesophagus via radiography
30
How do you view oesophagus via fluoroscopy
31
Label the anatomy
32
Label the anatomy
33
Label the x-ray
34
Label the x-ray
35
Fill in the table with gas/fluid in stomach depending on view
36
What view is this
dorsoventral
37
What view is this
ventrodorsal
38
What view is this
right lateral
39
What view is this
left lateral
40
what is gastric dilation and volvulus (GDV)
41
What condition is seen here
GDV gastric dilation and volvulus gas and gastric contents cant leave so stomach continues to stretch
42
What other structures are affected by GDV
43
Define sphincter
ring of muscle surrounding opening
44
Define peristalsis
involuntary constriction & relaxation of muscles creating wave-like movements that push contents forwards
45
define deglutition
process of swallowing
46
define primary vs secondary peristalsis
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
47
Where is the swallowing centre and how is it activated
in medulla oblongata & activated by pressure-sensitive sensors in pharynx
48
define dysphagia
swallowing difficulties
49
define regurgitation vs vomiting
regurgitation: action of bringing swallowed food up again into mouth vomiting: eject matter from stomach through mouth
50
What should we find on gastroscopy
51
Label the horse gastroscopy
52
In what views were these radiographs taken
53
What abnormalities can you see in this radiograph
gas in stomach, contrast media in oesophagus, displaced abdominal organs
54
Define transit time
55
Define zymogen/proenzyme
56
Define autocatalyse
catalysis of a reaction by one of its products
57
Define paracrine
58
What is the stomach, where is it and what does it do?
59
What are the main functions of the stomach
60
What enzyme digests proteins
pepsin
61
How does the stomach prevent digestion of chief cells & parietal cells
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
62
Label the stomach gland
ECL = enterochromaffin like cells (release histamine) endocrine cells include G cells & D cells
63
Describe the phases of gastric secretion
64
Describe the cephalic (first) phase of gastric secretion
65
Describe the gastric (second) phase of gastric secretion
66
Describe the intestinal (third) phase of gastric secretion
67
Describe how pepsinogen is activated in the stomach
68
Describe histamine & gastrin in control of HCl production
69
Describe the parasympathetic nervous system in control of HCL production
70
Fill in the table with roles of different cells in digestion
71
Describe factors that regulate appetite
Ghrelin stimulates appetite Leptin supresses appetite appetite affected by nutrient balance, sensory stimuli, feeding schedule, health/illness, exercise
72
Describe the major effects of sympathetic & parasympathetic stimulation of GI tract motility, including sphincter tone
73
Recall the mechanism of generation of an action potential
74
identify the positions of autonomic ganglia & plexuses within abdomen & pelvis
75
Describe the functions of the enteric nervous system
76
describe the distribution of the enteric nervous system
77
Describe the relationship between extrinsic autonomic innervations & intrinsic enteric innervations of tract
78
explain what is meant by electrical coupling between smooth muscle cells & its importance for generating waves of activity along gastrointestinal tract
- 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
describe the anatomical & biophysical characteristics of GI tract smooth muscle
80
what is the origin and physiological significance of slow wave development in GI tract smooth muscle
- 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
What are the features of segmentation
82
What are the features of peristalsis in SI
83
describe the importance of the ENS
84
Describe contractions in the stomach
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
What is the enterogastric reflex
86
What factors influence stomach emptying
87
Describe how gastric emptying can be affected by osmotic pressure or chemical composition of stomach contents
88
Describe integrated reflexes that initiate vomiting
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
Describe origin and release of gastrin
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
Describe origin and release of secretin
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
Describe origin and release of cholecystokinin (CCK)
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
Describe origin and release of motilin
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
Describe origin, stimuli & effect of ghrelin
produced by D1 cells in stomach stimulates hunger & promotes gastric emptying stimulated by empty stomach
94
Describe origin and release of somatostatin
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
What are the methods of ion transport across membranes of cells
96
Describe mechanism of neuromediators release in synaptic cleft
97
describe the importance of kiss & run mechanism regarding leak of neuromediators in synaptic cleft
98
What are the stomachs of the ruminant
Rumen = fermentation vat Reticulum = part of rumen Omasum = water absorption Abomasum = true stomach
99
describe lining of ruminant fore-stomachs
Lined by stratified keratinised epithelium (constantly renewed because wall is always being eroded)
100
describe lining of ruminant abomasum
Lined by simple columnar epithelium with occasional goblet cells
101
Label the ruminant LHS
surgery always done from LHS
102
label the ruminant RHS
103
Describe ruminant stomach capacity
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
Describe ruminant oesophagus
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
Describe the reticulorumen
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
Describe the abomasum
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
Compare chamber sizes in young vs mature ruminants
Abomasum proportionately larger in young ruminants Growth of Re/Ru/Om commences as calf/lamb eats more roughage Rumen not developed in lambs
108
Describe ruminant stomach development at weaning
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
Why do calves have milk clots in abomasum
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
What is this
Reticulum keratinised Ridges 1-2mm high & 1-2cm wide
111
describe rumination time vs feed quality
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
Describe the omasum structure
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
Label the omasum
114
Describe rumen papillae
Leaf-shaped Keratinised Poorly developed in roof of dorsal sac Increased surface area for flora and absorption
115
Label the rumen papillae
116
Describe rumen papillae size & growth
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
Describe digestion in neonatal ruminant
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
How does milk bypass the reticulum & rumen in neonates
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
label the ruminant neonate stomach
120
Describe the reticular groove reflex
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
Describe the rumen microbiota
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
What are the factors for a stable microbial population
123
Why do herbivores need bacteria for digestion
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
What does microbial fermentation provide
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
Fill in the chart showing fermentation steps
126
What is fermentation
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
How are different bacteria involved in fermentation
128
What are common protozoa in rumen
Holotrichs and oliotrichs
129
Describe the role of anaerobic fungi in rumen fermentation
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
How does a diet change affect rumen microbiota
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
Describe the effect of antibiotics on rumen microbiota
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
Describe the monogastric stomach microbiology
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
Describe the helicobacter species in monogastric stomachs
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
How does helicobacter survive in monogastric stomach
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
How can you test for helicobacter in monogastric stomach
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
Label the rumen papillae
137
Role of the rumen
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
What do the abdominal silhouettes show
139
How can you assess rumen health
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
Label the reticulum histology
141
What is the location of the reticulum
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
What is the location of the omasum
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
What is the location of the abomasum
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
What is the function of the abomasum
digest protein from both feed (bypass protein) and ruminal microbes (ruminal protein). 
145
describe the abomasum absorptive surface
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
Describe the omasum absorptive surface
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
Describe the reticulum function
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
What buffers the acidifying effects of VFAs in ruminant fermentation
Acidifying affects of VFA buffered by bicarbonate & phosphate in large volumes of saliva
149
Explain protein digestion in rumen
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
Explain process of urea cycling in protein digestion in the rumen
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
Describe chain of carbohydrate digestion in ruminants
152
Describe fat digestion in ruminants
Limited High fat diets depress microbial activity Long chain fatty acids not absorbed
153
What happens if more protein is present than energy in rumen
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
What happens if more energy is present than protein in rumen
If more energy is present than protein, amount of MCP produced is limited by protein Wasted energy to methane…
155
What can cause acidosis in rumen
too much concentrate or not enough fibre can lead to increased levels of lactic acid
156
What are the consequences of decreased rumen pH?
Balance of rumen microflora changes Decreased rate of digestion due to decreased number of viable microorganisms Changes proportion of different VFAs produced
157
What are the clinical signs of chronic acidosis and where is it most common
High producing animals fed diets high in concentrate - sub-optimal rumen function - reduced food intake - pain - indigestion - loose faeces - low milk fat levels
158
What typically causes acute acidosis in ruminants
grain engorgement
159
What are the by-products of carbohydrate fermentation in ruminants
Methane & CO2
160
What is bloat in ruminants
gases produced not removed by eructation
161
What are the 2 main forms of bloat
Gas bloat Frothy bloat
162
Describe gas bloat
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
Describe frothy bloat
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
How can bloat become fatal
Causes compression of other organs e.g., heart, lungs
165
What are some advantages & disadvantages of ruminant fermentation & digestion compared to non-ruminants
166
List the differences in forestomach & forestomach digestion between camelids & other ruminants
Camelids only have 3 compartments (lack omasum) instead of 4 Rumen & reticulum are combined (c1 - most nutrient absorption here)
167
What are the features that permit continuous fermentation in ruminants
multicompartmental stomach Rumen microbial population Cud chewing Large surface area Reticulorumen contractions Large amount of saliva
168
Why is the optimisation of rumen function important? How can this be achieved? How does suboptimal function occur?
169
Why is forestomach motility important and how does it occur? How does suboptimal motility occur and what are the consequences?
170
What is the importance of the reticular groove reflex and what are the consequences and reasons for this not occuring
171
Compare roughage based diet to concentrate based diet
172
define ptyalism
hypersalivation
173
Which organs are in contact with the stomach
Spleen on greater curvature Liver on lesser curvature Pancreas SI Oesophagus
174
Identify common reasons for milk production drop in post partum cow
Fe/Se/Cu/Co deficiency hypocalcaemia (milk fever) bacterial imbalance LDA Rumen acidosis dehydration
175
What does a high pitch tinkling sound suggest in cow left abdomen auscultation
LDA due to gas in abomasum ping between 9th and 13th rib
176
What occurs after birth that make translocation of the abomasum possible?
after birth there is lots of space for abomasum to move
177
What factors can influence gaseous distension of the abomasum in ruminants?
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