Week 2 Flashcards
Describe the path of the oesophagus
Continuation of laryngopharynx connecting pharynx to stomach
Dorsal to trachea, LHS
Travels through mediastinum (space between plural sacs)
Passes through oesophageal hiatus of diaphragm
Label the diagram
How do oesophageal muscles differ to other muscles in GI tract
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)
Describe the phases of swallowing
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)
Label the diagram
Label the stomach
What are the ridges for in the stomach
Ridges are known as rugae which increase surface area & lets stomach expand
Label the GI tract
Describe the glandular stomach
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
Label the stomach
What is the margo plicatus
folded margin between non-glandular and glandular portion of stomach
What are the 4 regions of the glandular stomach and their functions
Label the glandular stomach
describe the glandular stomach
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
Label
Describe the stomach innervation
Sympathetic fibres
Parasympathetic fibres
Intrinsic fibres of enteric nervous system (ENS)
describe the enteric nervous system
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
Describe the parasympathetic and sympathetic impulses of ENS
What do ENS plexuses contain
What are interstitial cells of Cajal (pacemaker cells)
Modified smooth muscle cells central to GI motility regulation
Function as a pacemaker for gut contraction
Different frequencies in different parts of GI tract
What is Ileus
GI stasis caused by stress/dehydration/other primary condition
Common in rabbits
Primary cause rarely diagnosed
Can occur after abdominal surgery
What is spasmodic colic
Change in gut activity causes muscular spasm of intestines
Underlying cause rarely identified
Common in horses
Opposite issue to ileus – too much activity
What is vagal indigestion
Motor disturbances that hinder passage of ingesta from reticulorumen, abomasum or both
Common in cows
Describe the layers of the GIT
Why would you want to image the oesophagus and what are some radiographic considerations
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
What is wrong with this x-ray
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
How do you view oesophagus via radiography
How do you view oesophagus via fluoroscopy
Label the anatomy
Label the anatomy
Label the x-ray
Label the x-ray
Fill in the table with gas/fluid in stomach depending on view
What view is this
dorsoventral
What view is this
ventrodorsal
What view is this
right lateral
What view is this
left lateral
what is gastric dilation and volvulus (GDV)
What condition is seen here
GDV
gastric dilation and volvulus
gas and gastric contents cant leave so stomach continues to stretch
What other structures are affected by GDV
Define sphincter
ring of muscle surrounding opening
Define peristalsis
involuntary constriction & relaxation of muscles creating wave-like movements that push contents forwards
define deglutition
process of swallowing
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
Where is the swallowing centre and how is it activated
in medulla oblongata & activated by pressure-sensitive sensors in pharynx
define dysphagia
swallowing difficulties
define regurgitation vs vomiting
regurgitation: action of bringing swallowed food up again into mouth
vomiting: eject matter from stomach through mouth
What should we find on gastroscopy
Label the horse gastroscopy
In what views were these radiographs taken
What abnormalities can you see in this radiograph
gas in stomach, contrast media in oesophagus, displaced abdominal organs
Define transit time
Define zymogen/proenzyme
Define autocatalyse
catalysis of a reaction by one of its products
Define paracrine
What is the stomach, where is it and what does it do?
What are the main functions of the stomach
What enzyme digests proteins
pepsin
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
Label the stomach gland
ECL = enterochromaffin like cells (release histamine)
endocrine cells include G cells & D cells
Describe the phases of gastric secretion
Describe the cephalic (first) phase of gastric secretion
Describe the gastric (second) phase of gastric secretion
Describe the intestinal (third) phase of gastric secretion
Describe how pepsinogen is activated in the stomach
Describe histamine & gastrin in control of HCl production
Describe the parasympathetic nervous system in control of HCL production
Fill in the table with roles of different cells in digestion
Describe factors that regulate appetite
Ghrelin stimulates appetite
Leptin supresses appetite
appetite affected by nutrient balance, sensory stimuli, feeding schedule, health/illness, exercise
Describe the major effects of sympathetic & parasympathetic stimulation of GI tract motility, including sphincter tone
Recall the mechanism of generation of an action potential
identify the positions of autonomic ganglia & plexuses within abdomen & pelvis
Describe the functions of the enteric nervous system
describe the distribution of the enteric nervous system
Describe the relationship between extrinsic autonomic innervations & intrinsic enteric innervations of tract
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
describe the anatomical & biophysical characteristics of GI tract smooth muscle
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
What are the features of segmentation
What are the features of peristalsis in SI
describe the importance of the ENS
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
What is the enterogastric reflex
What factors influence stomach emptying
Describe how gastric emptying can be affected by osmotic pressure or chemical composition of stomach contents
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
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
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
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
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
Describe origin, stimuli & effect of ghrelin
produced by D1 cells in stomach
stimulates hunger & promotes gastric emptying
stimulated by empty stomach
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
What are the methods of ion transport across membranes of cells
Describe mechanism of neuromediators release in synaptic cleft
describe the importance of kiss & run mechanism regarding leak of neuromediators in synaptic cleft
What are the stomachs of the ruminant
Rumen = fermentation vat
Reticulum = part of rumen
Omasum = water absorption
Abomasum = true stomach
describe lining of ruminant fore-stomachs
Lined by stratified keratinised epithelium (constantly renewed because wall is always being eroded)
describe lining of ruminant abomasum
Lined by simple columnar epithelium with occasional goblet cells
Label the ruminant LHS
surgery always done from LHS
label the ruminant RHS
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
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)
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.
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
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
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
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
What is this
Reticulum
keratinised
Ridges 1-2mm high & 1-2cm wide
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
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
Label the omasum
Describe rumen papillae
Leaf-shaped
Keratinised
Poorly developed in roof of dorsal sac
Increased surface area for flora and absorption
Label the rumen papillae
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
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
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
label the ruminant neonate stomach
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
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
What are the factors for a stable microbial population
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
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.
Fill in the chart showing fermentation steps
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
How are different bacteria involved in fermentation
What are common protozoa in rumen
Holotrichs and oliotrichs
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
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
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
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)
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.
How does helicobacter survive in monogastric stomach
- Drills into the mucus gel layer of the stomach
- Binds to membrane-associated lipids of epithelial cells
- Secretes large amounts of Urease
- Urease metabolizes urea to produce ammonia
- 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
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
Label the rumen papillae
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.
What do the abdominal silhouettes show
How can you assess rumen health
- rumen fill (has cow been eating?)
- palpate to feel consistency (should be doughy consistency & feel 3 contractions every 2 min)
- auscultation to listen to rumen contractions
- volume & consistency of faeces (score of 3 ideal)
Label the reticulum histology
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.
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.
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.
What is the function of the abomasum
digest protein from both feed (bypass protein) and ruminal microbes (ruminal protein).
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)
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.
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.
What buffers the acidifying effects of VFAs in ruminant fermentation
Acidifying affects of VFA buffered by bicarbonate & phosphate in large volumes of saliva
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)
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
Describe chain of carbohydrate digestion in ruminants
Describe fat digestion in ruminants
Limited
High fat diets depress microbial activity
Long chain fatty acids not absorbed
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
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…
What can cause acidosis in rumen
too much concentrate or not enough fibre can lead to increased levels of lactic acid
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
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
What typically causes acute acidosis in ruminants
grain engorgement
What are the by-products of carbohydrate fermentation in ruminants
Methane & CO2
What is bloat in ruminants
gases produced not removed by eructation
What are the 2 main forms of bloat
Gas bloat
Frothy bloat
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
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
How can bloat become fatal
Causes compression of other organs e.g., heart, lungs
What are some advantages & disadvantages of ruminant fermentation & digestion compared to non-ruminants
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)
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
Why is the optimisation of rumen function important? How can this be achieved? How does suboptimal function occur?
Why is forestomach motility important and how does it occur? How does suboptimal motility occur and what are the consequences?
What is the importance of the reticular groove reflex and what are the consequences and reasons for this not occuring
Compare roughage based diet to concentrate based diet
define ptyalism
hypersalivation
Which organs are in contact with the stomach
Spleen on greater curvature
Liver on lesser curvature
Pancreas
SI
Oesophagus
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
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
What occurs after birth that make translocation of the abomasum possible?
after birth there is lots of space for abomasum to move
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
