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Physiology Y1 > Gastrointestinal Tract > Flashcards

Gastrointestinal Tract Flashcards

1
Q

What are the 6 major functions of the gastrointestinal tract?

A
  • Ingestion of food
  • Secretion of fluids and digestive enzymes
  • Mixing and movement of food and wastes through the body
  • Digestion of food into smaller pieces
  • Absorption of nutrients
  • Excretion of wastes
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2
Q

Describe the gross structure of the GI tract in carnivores.

A

Stomach > small intestine > large intestine

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3
Q

Describe the gross structure of the GI tract in ruminants.

A

Fore stomachs, where fermentation occurs > stomach/abomasum > small intestine > large intestine

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4
Q

Describe the gross structure of the GI tract in simple-stomached herbivores.

A

Stomach > small intestine > large intestine, where fermentation occurs

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5
Q

What 3 adaptations of the GI tract allow for increased surface area?

A
  • Folding of mucosa
  • Villi
  • Microvilli
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6
Q

Describe the bloods supply to the GI tract.

A

Coeliac artery supplies hepatic artery to the liver and the splenic artery to the stomach, spleen and pancreas.

Cranial mesenteric artery supplies small intestine.

Caudal mesenteric artery supplies the large intestine.

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7
Q

Describe the venous drainage of the GI tract.

A

Hepatic portal vein drains the stomach, spleen, pancreas, small intestine and large intestine to the liver.

Hepatic vein drains the liver to the caudal vena cava.

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8
Q

Describe the motor activity and regulation of the GI tract.

A
  • Contractile tissue is smooth muscle
  • Contraction has region specific patterns in motility, which relates to functions, such as mixing and propulsion.
  • Motility regulated and coordinated by the enteric nervous system, hormones and the autonomic nervous system.
  • Valves called sphincters are under control of enteric nervous system, with eth exception of the external anal sphincter, which is under somatic nervous control.
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9
Q

What is the function and motility at the ileocaecal sphincter?

A

Controls movement in one direction from the small to the large intestine.

  • Distending ileum relaxes sphincter to aid movement into the colon
  • Distending colon contracts sphincter to prevent retrograde movement from colon to ileum.
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10
Q

What is the cephalic phase of gastric secretion from the stomach?

A

Autonomic via the vagus nerve.

  1. Sight, smell, taste, chewing of food sends signals to the brain.
  2. Nerve impulses sent down vagal nerve.
  3. Impulses act on chief cells to release pepsinogen and parietal cells to release HCl.
  4. Impulses also act on endothelium of the stomach to release gastrin, which is released to the blood and acts on parietal cells to release HCl.
  5. The nerve pulses cause acetylcholine to stimulate chief cells to secrete pepsinogen.
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11
Q

What is the gastric phase of gastric secretion from the stomach?

A

Involves stretch receptors causing direct stimulation of gastrin release and stimulates reflexes.

  1. Food stimulates gastric phase.
  2. Sensory cells in stomach release short and long reflexes.
  3. Chief cells stimulated to release pepsinogen and parietal cells stimulated to release HCl.
  4. Sensory cells in stomach release short and long reflexes and products of digestion stimulate gastrin-producing cells to release gastrin.
  5. Gastrin in the blood stimulates parietal cells to release HCl.
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12
Q

How is parietal cell secretion controlled?

A

Stimulation (all 3 receptors necessary):

  • Acetylcholine – vagus nerve stimulation
  • Gastrin – G cells stimulated by vagus nerve and mechanical stimulation
  • Histamine – ECL cells stimulated by gastrin

Inhibition:

  • Somatostatin receptors inhibit adenylyl cyclase, opposite effect to histamine
  • Low pH inhibits release of gastrin
  • Histamine receptor type 2 blockade (Zantac)
  • Proton pump inhibitors
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13
Q

Which 2 things allow for epithelial protection?

A

Mucus layer from glycoproteins, which are resistant to enzymes and also secrete bicarbonate into the gel layer of cells formed.

Exchange of bicarbonate and chloride ions with epithelium close to pH7. Bicarbonate comes from plasma. Parietal cells secrete protons causing a surge of alkaline blood after a meal and secreted by gut mucosa and pancreas.

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14
Q

What stimuli are sent to the vomiting centre of the medulla oblongata?

A
  • Psychological factors via the cerebral cortex
  • Opiates, anaesthetics, ipecac, urea via the chemical trigger zone
  • Bacterial, viral toxins/distention via the vagus nerve
  • Motion or infection via the vestibular apparatus
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15
Q

Describe the process of vomiting.

A
  1. Distension or irritation of the duodenum, pain or tickling at the back of the throat causes small intestinal antiperistalsis.
  2. Mechanoreceptors in the throat, stomach and duodenum and chemoreceptors in the stomach and duodenum send signal to the vomiting centre. Labyrinthine receptors stimulated from pregnancy hormones, chemical trigger zones and general anaesthetics also send signals to the vomiting centre in the medulla oblongata.
  3. Postural adaptation
  4. Salivation stimulated
  5. Respiratory inhibitory muscles inhibited to decrease intrathoracic pressure
  6. Glottis closes and larynx raised
  7. Soft palate lifted
  8. Diaphragm and abdominal muscles contract to increase intra-abdominal pressure
  9. Intragastric pressure raised against constricted/closed lower oesophageal sphincter, causing retching
  10. LOS relaxes and the gastric contents are expelled in vomiting.
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16
Q

What are some normal physiological causes of vomiting?

A
  • Normal voiding of indigestible items from stomach

- Over-distention of the stomach (mainly dogs)

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17
Q

What are some chemical causes of vomiting?

A

Chemical – iatrogenic or intoxication is pathogen derived

  • Commonly used drugs, such as opioids
  • Enteric pathogens
  • Bacterial or viral toxins
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18
Q

What are some pathological causes of vomiting?

A
  • Inflammation or ulceration of stomach
  • Elevated blood urea or ammonia in liver or kidney origin
  • Infections of GI tract
  • Blockade of small or large bowel
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19
Q

What could be implicated if vomiting is chronic?

A
  • Significant loss of fluid = dehydration and CVS impairment
  • Loss of acid = metabolic alkalosis
  • Avoidance of foods consumed prior to vomiting = ‘train’ avoidance (emetics to food)
  • Pancreatitis - from reflux of gut contents into pancreatic ducts, diagnosed by pancreatic enzymes in blood
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20
Q

What are the species differences in vomiting?

A

Rodents, horses, rabbits (and possibly foxes) do not vomit.

Horses partly anatomical

Rodents partly neuroanatomical - mutations has broken the chain linking stimuli to the mechanics of emesis.

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21
Q

How is the GI tract coordinated and controlled?

A
  • Salivary glands are almost entirely controlled by parasympathetic nervous system
  • Stomach is evenly controlled by neural, hormonal and local (physical/stretch and chemical, such as histamine) control
  • The pancreas is largely hormonal control but also parasympathetic control
  • Small intestine and most of the large intestinal are largely due to local stimulation with some parasympathetic stimulation
  • The last part of the large intestine is largely parasympathetic stimulation with a small amount of local control
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22
Q

Describe neural coordination of the GI tract.

A
  1. Stimuli from GI tract lumen stimulate sensory cells.
  2. Signals to nerve plexuses to smooth muscle and glands or signals to the CNS.
  3. CNS also sends signals to nerve plexuses going tp smooth muscle and glands, and signals to salivary glands, pancreas and liver.
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23
Q

Which stimuli can trigger a response in GI tract epithelia?

A 
Presence of peptides 
Products of digestion 
Osmolarity 
pH
Presence of irritants
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24
Q

Describe enteric control of the GI tract.

A
  1. Sensory neurone is stimulated and a signal travels to motor fibres via an interneurone.
  2. Signals sent to gland cells and smooth muscle cells.
  3. Motor fibres send signals to preganglionic parasympathetic nerve fibres to the CNS.
  4. Signals from the CNS sent down pre and post-ganglionic sympathetic nerve fibres, acting on arterioles supplying the wall of the GI tract.
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25
Q

Describe the organisation of the enteric nervous system.

A

Myenteric plexus:

  • Between muscle layers
  • Regulates muscular activity
  • Major transmitters of acetylcholine, nitrogen oxide and VIP
  • 1/3 of neurones are sensory

Submucosal plexus:

  • At submucosa circular boundary
  • Regulates mucosal glands – secretion
  • Major transmitters of acetylcholine and VIP
  • Some sensory neurones
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26
Q

What are short and long reflexes in the enteric nervous system?

A

Short: signals from the stomach to the small bowel.

Long: signals from the stomach goes to the CNS and are sent to the large bowel via parasympathetic and sympathetic nerve fibres.

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27
Q

Name and describe 4 types of non-transmitter chemical messengers of GI tract control.

A
  • Endocrine – secreted and enters the bloodstream in order to reach its target
  • Paracrine – secreted into the extracellular fluid and diffuses a short distance to act on a different size of a cell
  • Autocrine – secreted into the extracellular fluid and diffuses a short distance to act on the same type of cell that released it
  • Neurocrine – released by a neurone to act on a different type of cell
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28
Q

Where is gastrin produced, its stimuli and effects?

A

Distal part of the stomach.

Peptides in the stomach and gastrin releasing peptide produced by the vagus nerve.

Stimulation (with ACh and histamine) of HCl production and supports growth of mucosa.

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29
Q

Where is secretin produced, its stimuli and effects?

A

Mainly duodenum

Low pH in the small bowel

Stimulates production of bicarbonate by the pancreas and Brunner’s glands.

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30
Q

Where is CCK produced, its stimuli and its effects?

A

Mainly duodenum

Fatty acids, monoglycerides and amino acids in the small bowel.

Stimulates enzyme production in the pancreas and gall bladder contraction.

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31
Q

Where is GIP produced, its stimuli and effects?

A

Proximal small bowel

Fat, glucose and amino acids in the small bowel.

Reduces HCl production and stomach emptying
(stimulates insulin release).

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32
Q

Where is somatostatin produced, its stimuli and effects?

A

Intestine and pancreas

Fats, amino acids and bile salts in the intestine.

Reduces acids secretion, gastric mobility and stomach emptying.

33
Q

Where is leptin produced, its stimuli and effects?

A

White adipose tissue

Fat reserve proportion

Stimulates satiety

34
Q

Where is ghrelin produced, its stimuli and effects?

A

Epithelium of small and large bowel.

Size of meal proportion.

Stimulates satiety to inhibit eating.

35
Q

What is the overall activity of gastric secretion?

A
  • Cephalic is 35% of total gastric secretion. Occurs at the thought, sight, smell and taste of food. Vagus nerve controls this and involved acetylcholine, gastrin-releasing peptide and histamine
  • Gastric is 55% of totally gastric secretion. Occurs at mechanical (distention) and amino acids. Involves gastric reflexes of short myenteric and long central reflexes using Ach, gastrin and histamine.
  • Intestinal accounts for 10% of total gastric secretion. Occurs when digestion products in the small intestine – protein, lipids, pH, osmolarity. Involves enterogastrones, increased gastrin secretion, secretin decrease, CCK decrease and GIP decrease.
36
Q

What does the small intestine secrete?

A

Mostly fluid, mucus, bicarbonate

This dilutes the products of digestion, protects mucosal epithelium and neutralises acid from the stomach. Brunner’s gland is a ducted mucus glands lying in the submucosa that secrete mucus and bicarbonate.

Stimuli is vagus Ach, secretin and mechanical stimulation.

37
Q

What do enterocytes secrete?

A
  • Crypt cells secrete almost pure extracellular fluid
  • Fluid is derived from plasma
  • Volume secreted per day is equivalent to plasma volume
  • Secretion is limited by cAMP which act on chloride channels called cystic fibrosus transmembrane conductance regulators, and allow fluid, chloride ion and sodium ion secretion.
38
Q

What are the 2 types of motility?

A
  • Segmentation – alternating contractions squeeze material back and forth so there is no net movement, only mixing to increase rate of digestion and absorption.
  • Peristalsis – initiated at a point and contraction of circular muscle on oral side. Relaxation of circular muscle on aboral side. Contraction propagated from several cm to propel gut contents along the GI tract.
39
Q

How is motility controlled?

A
  • Local distention causes oral propagating excitation and aboral propagating inhibition, producing peristaltic movement aborally.
  • Parasympathetic increases peristalsis
  • Sympathetic decreases peristalsis
40
Q

What factors affect the rate of stomach emptying and how?

A
  • Distention of the stomach > increases activity of stretch sensitive sensory cells > increasing contraction of smooth muscle cells > stomach empties faster.
  • Peptides in stomach > increases gastrin > increases contraction of smooth muscle cells > stomach empties faster
  • High concentration of peptides, high pressure, high osmolarity, low pH and high fat content in the duodenal lumen > increases activity of sensory cells in the duodenum > CNS > sympathetic activity of nerve fibres in the stomach increases > activity of parasympathetic nerve fibres to the stomach decrease > stomach empties faster. This is also aided by increased release of hormones form the duodenal epithelium.
41
Q

Describe pancreatic secretion of bicarbonate to control pH.

A
  1. Stomach has very low pH
  2. Detected by cells in the epithelial layer of the small bowel
  3. Hormone secretion of secretin increases
  4. Passes in blood stream and acts on ductile cells to increase their secretion of bicarbonate into the ducts.
  5. Bicarbonate passes down ductile system out into the lumen of the GI tract where bicarbonate acts with protons to forms carbonic anhydrase.
  6. This dissociates to from CO2 that is breathed out.
42
Q

Describe pancreatic secretion of enzymes.

A
  • In an inactive form that pass down the pancreatic duct.
  • Has a bit of peptide attached to enzyme that leaves it inactive.
  • Can be activated by enteropeptidase, the only enzyme made by the small bowel itself and are attached to the surface of the small bowel.
  • CCK is the stimulus for the production of these enzymes and is secreted into the bloodstream in response to the products of digestion in the lumen of the small bowel.
43
Q

What are the functions of the liver?

A 
Regulation of metabolism
Protein synthesis
Glycogen
Vitamin and iron storage 
Degrading steroid hormones
Detoxification
Fat digestion with bile salts 
pH control
44
Q

What is the function of bile salts?

A

Bile salts aid fat digestion by emulsifying fats and increasing their surface area for enzymes. They are stored in the gallbladder, which contracts and pushes them into the small intestine when they are needed. They act along the small intestine and then reabsorbed back to the liver at the end of the small intestine.

45
Q

What 2 routes can bile production occur by?

A

Recovery of bile acids from portal blood via sodium coupled transporters.

New synthesis from cholesterol.

46
Q

What happens to absorption and secretion in relevance to diarrhoea?

A

Pathogens that damage absorptive villus epithelium induce malabsorptive diarrhoea. Villi becomes blunted and have marked reduced height. Bacterial toxins and inflammatory stimuli cause massive chloride, bicarbonate and water secretion from the crypts. Absorption decreased and secretion increased.

47
Q

What mechanism do cells use because they cannot pump water?

A

Cells cannot pump water so have a mechanism in which salts are moved first and then water is moved by osmosis.
The osmotic gradient is established in the lateral space between the cells, and water is pulled in and generates a pressure. This pressure is small but large enough to push water across the basement membrane into the interstitium where it’s taken up by the bloodstream.

48
Q

How is water absorbed across a leaky epithelia with no cellular osmotic gradient?

A
  1. Sodium ion concentration is high in the lumen and low inside cells.
  2. Sodium and co-transported solutes are untaken and sodium is pumped into the lateral space.
  3. High bicarbonate from metabolic CO2 powers exchange for chlorides ions. Chloride ions enter lateral space, attracted by positive sodium ion charge.
  4. Osmotic movement of water into lateral space.
  5. Slight hydroststic pressure causes fluid to move across basement membrane into blood stream.
49
Q

What are some causes of diarrhoea?

A
  • Reduced transit time (increased motility)
  • Impaired active absorption (tissue damage?)
  • Stimulated secretion
  • Solute retention (osmotic effect)
  • Tissue damage (leaky epithelia)
50
Q

What are the effects of diarrhoea?

A

Dehydration and circulatory failure

Isotonic and hypotonic fluid loss

51
Q

How is diarrhoea treated?

A

Oral or intravenous rehydration therapy solutions contain sodium, glucose and a pH buffer, absorption of sodium and glucose leads to absorption of water. pH buffer helps raise and normalise blood pH.

52
Q

What are the 3 oral rehydration recipes?

A

Type I = 50 NaCl, 75 glucose, 20 KCl, 30 citrate

Type II = intermediate-higher potassium than type I

Type III (nutritive) = 150 Na, 30 K, 10 Ca & Mg, 300 glucose, 60 citrate, 50 glutamine/glycine

53
Q

What is the function of the colon?

A
  • Absorbs remaining water and sodium
  • Absorbs vitamins produced by commensal bacteria
  • Eliminates metabolic waste in bile
54
Q

What is the function of the microbiota?

A
  • Protection against pathogens
  • Synthesis of vitamins
  • Immune system development
  • Promotion of intestinal angiogenesis
  • Promotion of fat storage
  • SCFA production by fermentation of dietary fibre
  • Modulation of CNS
55
Q

What are some differences between ruminants and hindgut fermenters?

A

Ruminant has salivary secretion as a pH buffer and has fore-stomachs. Products of digestion are short chain fatty acids from rumen at 70%, microbial amino acids after the abomasum.

Hindgut fermenters have partly glandular stomachs and a larger hindgut. Products of digestion are limited glucose and amino acids from small bowel and shorter chain fatty acids. They lose microbial protein.

56
Q

What are some similarities between ruminants and hindgut fermenters?

A
  • Microbes metabolically similar
  • Anaerobic fermentation conditions
  • Small volatile fatty acids produced – 50% VFA absorbed in horses and 60-80% absorbed in ruminants
  • Bicarbonate used to buffer pH – from small intestine and colon in horse and from saliva and minorly small intestine in the ruminant
  • Gas production – eructated in ruminants and flatus in horses
57
Q

Describe the pathway that stimulates the gastric groove reflex.

A
  1. Milk in the oral cavity in the stimulus for this.
  2. Calcium and sodium in the milk stimulates chemoreceptors.
  3. Signals are sent to the medulla through the vagus nerve.
  4. A motor program in initiated: the groove closes, the reticular-omasum orifice dilates to allow the material into the omasum, dilation of the omasum canal to allow a direct route to the abomasum, and then there is pumping action from the distal oesophagus to force milk through.
  5. Even though chemoreceptors play a role, it has a strong Pavlovian effect and becomes the dominants input– as the animals anticipate being fed, this reflex is stimulates.
  6. Hunger through the hypothalamus also impacts on stimulating this reflex.
58
Q

Describe the fate of cellulose in fermentation.

A

Rumen: Cellulose > glucose > acetate + propionate > butyrate

Blood: acetate + propionate + butyrate + ketone bodies

Tissues: acetate + butyrate + ketone bodies > triacylglycerol and CO2 in muscle. Propionate > glycogen in the liver

59
Q

Describe the ‘rumen ecology’.

A
  • Multiple substrates and many microbes
  • End products of some species are substrates for others
  • Dynamically stable complex network of inter-dependency with ratios of particular bacteria and protozoa that are stable unless food types changes.
  • Relative abundance of bacteria species reflects rate of growth/division
  • Only about 7% of the energy produced by the microbes is used by the microbes, the majority is uptaken by the ruminant.
60
Q

Which sugar has a link to methane?

A

As acetate produced increases the methane produced increases, as there is a bacteria that will take acetate and from methane. This means that 15% of the carbon in the food material is lost as methane. In the US, there is a bacteria that can be used against methogenic bacteria to reduce losses.

61
Q

What 2 things does satiety and control of intake depend on?

A
  • High cereal diet – driven mostly by post-absorptive factors, such as volatile fatty acids in the blood that causes sensory output from the liver.
  • Normal high roughage content diet – driven mostly by pre-absorptive factors – such as rumen volume. This is important in young animals, as they have smaller rumens and less developed gut microbes so digestion of beta bonded carbohydrates is poor relative to adults. The young must try to choose to eat the young shoots of their food source, which are more easily digested.
62
Q

Describe the effect of cut and feeding levels on digestion rate.

A

Early cut is more digestible than immediate or late cut.

Increased feeding levels (feed it that 3 times) there is a reduced available energy extracted from food, as there is less time for nutrients to be absorbed, as food passes through the rumen quicker.

63
Q

What are the functions of salivary secretions in ruminants?

A 
Oral hygiene 
Food lubrication 
Primary source of pH buffer 
Replacement of fluid 
Anti-frothing proteins 
Wetting agents (proteins)

In the ruminants the digestive role is a minor one.

64
Q

What is the type, structure and innervation of ruminant salivary glands?

A

Parotid, mandibular and sublingual major salivary glands. Glands can be serous = parotid or mix of serous and mucosal = mandibular and sublingual.

Controlled by the ANS but the fore-stomachs are also controlled by the ANS.

  • Acinus are the duct like structures in salivary glands
  • Joined to intercalating ducts
  • Joined to a striated duct
65
Q

What are the principles of salivary secretion?

A
  1. Secretion derived from plasma
  2. Salt composition similar to plasma
  3. Blood vessels made reversibly leaky
  4. Fluids leak out
  5. Acinus cells transport salts
  6. Cell membranes highly permeable to water in osmotic water flow
66
Q

Describe salivation in ruminants.

A
  • 0.57-1.5 litres per kg body weight per day
  • For a dairy cow of 600 kg, this is between 70 to 180 litres a day
  • Body water is 60% body mass so 50% body water is circulated through the salivary glands
  • Parotid and sublingual nerve have zero secretion, as basal secretion is quite large
  • Main stimulus is anticipation of food and food in the mouth.
  • Additional stimuli: stretch of cardia. Reticular groove, reticular-ruminal fold
67
Q

How do monogastric and ruminants differ in vagal control?

A

Complex functions such as swallowing, mixing and segregation of ingesta by size, eructation and rumination.

Dependent on intact connection to ANS with vagus nerve. Monogastric species can have transplants between them but ruminants cannot survive if the vagus nerve is cut.

68
Q

Describe the nature and function of the primary contractions of the rumen.

A
  • 1-1.5 per minute in cattle, less in sheep
  • The primary purpose is mixing
  • Strength correlates with rumen fill
  • Absent only in deep sleep
  • Begins in reticulum and sweeps aborally is peristalsis
  • Sweeps fibrous mat from front to back, figure of 8 movement
69
Q

Describe the nature and function of the secondary contractions of the rumen.

A
  • About half of the primary contractions are followed by a secondary contraction, this can be a 1:1 ratio if there is a high fermentation rate
  • The primary purpose is eructation of gas
  • Relatively weak contractions
  • Begins in caudal sac and moves forwards in anti-peristalsis
  • Moves gas cap forwards to clear the cardiac and allow eructation of gas. Only when it covers the cardiac can it be eructated
70
Q

Describe mastication and rumination in ruminants.

A
  • Time consuming, as ruminants consume large mass of plant material er day
  • Plant material commonly quite hard/tough
  • Chewing occurs during both eating/mastication and rumination
  • Diet dictates the ratio of eating to rumination
  • High crude fibre content = slower fermentation
  • Longer retention = reduced drive to eat
71
Q

What is the consequence of increased feeding rate on digestibility?

A

Increased feeding rate reduces apparent digestibility. As feeding rate increases, time spent in the gut reduces. Less rumination, less fermentation and less of the energy in the food I released. The effect is more pronounced for food that is harder to digest = late cut course grass.

72
Q

Define and describe eructation in ruminants.

A
  • Fermentation liberates CO2 and methane, 1-2 litres per minute in cattle
  • Composition is 60% CO2 and 40% CH4
  • Eructation reflex involves stimulus from distention of the rumen, vago-vagal reflex arc (afferent and efferent), resulting in stimulation of a secondary ruminal wave.
  • Failure of the mechanism involves bloat/ruminal tympany
  • Causes of bloat are oesophageal block, foamy gas that fails to elicit reflex, liquid covering cardia for lung protection or inhibition of the secondary ruminal contraction.
  • Secondary ruminal wave in cranial propagation > oesophagus fills > rapid anti-peristalsis in somatic control > voided through nares (silent).
  • 50% of eructated gas is inhaled and can lead to milk taint.
73
Q

Describe ruminant hindgut fermentation.

A

High % digestion in the large intestine (20%) = low digestibility

Low % digestion in the large intestine (5%) = high deigestibility

74
Q

What are the limitations of hindgut fermenters?

A
  • Some microbes and microbial products are lost because fermentation goes on in the large bowel, so microbes and some vitamins are lost when the animal voids the material as faeces.
  • Means that the protein content of the faeces of a hind-gut fermenter is much higher.
  • While a ruminant has all the microbes in the foregut, so microbes are digested when material passes into the abomasum and extracts the protein from the microbes, while the hind-gut fermenter loses them.
75
Q

Name an adaptation of some hindgut fermenters (rabbits, rats, hares and beavers).

A

Coprophagic behaviour - produce 2 types of faecal pellets.

  • Discarded – hard, dark and familiar
  • Caecotrophes – produced in caecum, eaten directly from anus, high in protein and vitamins mainly B and K. They contain partially digested plant material and all the microbes encased in a thick mucus coat, which protects them when they are reintroduced into the stomach. They remain at a normal pH and fermentation continues, and microbes are also digested now, improving the availability of protein and vitamins.
76
Q

Name 4 disadvantages horses have compared to cows.

A
  • Dietary protein utilised more efficiently in horses and horses are more dependent on dietary protein, as microbial protein is largely lost.
  • Nitrogen content of faeces in high in horses.
  • Horses more prone to impaction than ruminant.
  • Overall efficiency of horses is quite similar to ruminants.
77
Q

What occurs in lactation ketosis?

A
  • In lactation ketosis, the rumen becomes fuller and the animal has a greater drive to eat.
  • More propionate is being converted to oxaloacetate, which goes off to lactate production.
  • Means there is less oxaloacetate that can be combined with acetyl-CoA to make citrate in the citrate cycle. This process is less efficient now.
  • So additional/left acetyl-CoA goes to milk fat production and excess is taken to the liver for production of additional fats and ketone bodies.
  • Lead to a reduction in available glucose in the body and is treated by an IV bolus injection of dextrose.
78
Q

What is the consequence of grain overload?

A
  1. Rumen full of grain
  2. Bacteria in the rumen will ferment that starch incredibly quickly.
  3. This will cause osmolarity to increase because the water is withdrawn into the rumen.
  4. This will cause dehydration and circulatory failure.
  5. Causes low arterial blood pressure, which impairs kidney function.
  6. Rapid fermentation also causes rumen pH to fall as the concentration of volatile fatty acids increases.
  7. Low pH is tolerated well by bacterial species producing lactate. This causes pH to reach 5 and species that metabolise lactate die.
  8. Lactophiles thrive and cause lactate concentration to increase.
  9. Lactate is absorbed and produces lactate acidosis and acidaemia.
  10. Causes all together compensation to acidosis: renal compensation of bicarbonate increase and respiratory compensation of hyperventilation.

Physiology Y1 (12 decks)

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