Gastrointestinal Flashcards
(355 cards)
1
Q
Secretion
A
- delivery of digestive enzymes, mucus, ions, and fluid to create an aqueous phase
- chemical digestion
2
Q
Digestion
A
- mechanical function of the teeth (grinding, birds: beak) and smooth muscle contraction (birds: gizzard)
- chemical action of enzymes and secretions
3
Q
Absorption
A
- transport of nutrients, water and ions across the epithelium to the blood
4
Q
Motility
A
- smooth muscle contractions to mix, crush and propel contents
- mechanical digestion
5
Q
Regulation
A
- hormonal and neuronal regulation to adjust the function according to the incoming food
6
Q
Mouth
A
- mechanical breakdown of food
- addition of saliva as a lubricant
7
Q
Esophagus
A
- conduit of the mouth/stomach
8
Q
Stomach
A
- chemical digestion of proteins, liquefaction of food
- > the process of making or becoming liquid
9
Q
Liver
A
- provision of bile salts for digestion and absorption of fats
10
Q
Pancreas
A
- Provision of major digestive enzymes, and gut pH control
11
Q
Small Intestines
A
- provision of enzymes, chemical digestion and absorption of nutrients and water
12
Q
Large Intestines
A
- absorption of water, feces formation, bacterial fermentation
- > major species difference are hindgut fermenters
13
Q
Forestomachs
A
- ruminants
- bacterial fermentation and absorption
14
Q
Beak and Tongue
A
- drinking, prehension, mechanical digestion, moisturizing (limited) and swallowing
15
Q
Oropharynx and Esophagus
A
- taste and swallowing
16
Q
Crop
A
- storage of food, particularly in discontinuous feeding pattern
17
Q
Proventriculus and Gizzard
A
- true stomach compartments
- where hydrochloric acid and pepsinogen are secreted by the proventriculus and mixed with contents due to muscular movements in the gizzard
18
Q
Small Intestine in Birds
A
- is the site for most digestion and practically all absorption of nutrients occurs
19
Q
Ceca
A
- electrolyte and water absorption
- fermentative function depends on the diet
20
Q
Cloaca
A
- the digestive, urinary and reproductive tracts common excretion component
21
Q
Pancreas and Liver
A
- chemical and enzymatic digestion
22
Q
Mucosa
A
- contributes to mechanical digestion, secretion, absorption and endocrine functions
- three layers
- > epithelium, lamina propria and muscularly mucosae
23
Q
Submucosa
A
- contains glands, vascular supply and nervous plexus
24
Q
Muscular
A
- circular, longitudinal layers of smooth muscle and myenteric plexus
25
Serosa
- the outer connective tissue layer in the abdominal cavity
| - > outside the abdominal cavity is called the adventitia
26
Slow waves
- spontaneous rhythmical undulations of the resting membrane potential around a baseline of -50 to -60 mV
- > caused by undulating electrical activities
27
Spike Potential
- When a slow wave peak reaches a critical threshold potential
- > voltage gated calcium channels open! (influx of Ca2+)
- true action potentials that elicit a contraction
28
Peristalsis/Propulsion
- Circular contraction cranial to a bolus with relaxation caudal to the bolus
- responsible for forward movement of bolus towards anus
- adaptive relaxation
29
Segmentation/Mixing
- Localized contraction of mostly circular muscles
- has a chopping, or mixing effect on gut content
- little or no net forward movement because alternate segments contract
30
Migrating Motility Complex (MMC)
- Occasional strong peristaltic waves occurring between the stomach and ileum while the pylorus is relaxed during fasting phases
- clears the stomach and small intestine of undigested food particle
- > intestinal housekeeper of GI tract
- prevention of small intestinal bacterial overgrowth (SIBO)
31
Enteric Endocrine System
- controls digestive functions by secreting endocrine and paracrine hormones
32
Enteric Nervous System
- intrinsic NS works independently
- Myenteric and Submucosal Plexus
- > Brain of the gut
- a local reflex system enabling communication among adjacent GI sections
33
Myenteric Plexus
- GI tract motility
| - mechanoreceptors to monitor degree of muscle stretch
34
Submucosal Plexus
- GI tract secretions
| - chemoreceptors to monitor chemicals such as nutrients and pH
35
Peristaltic Rush
- powerful and rapid peristaltic movements of the small intestine caused by intense mucosal inflammation
- protective response to quickly push potentially harmful contents into the Large Intestines
36
Sialocele
- a salivary mucocele
- is an accumulation of saliva in the submucosal or subcutaneous tissues after damage to the salivary duct or gland capsule
37
Ranula
- sublingual mucocele
38
Mumps
- a viral infection that primarily affects saliva-producing (salivary) glands that are located near your ears
- can cause swelling in one or both of these glands
39
Prehension
- requires highly coordinated movements of voluntary muscles, using lips, tongue, teeth, forelimbs, nose
- grasping of food
40
Mastication
- chewing
- the first step of mechanical digestion
- which breaks down food and lubricates it for swallowing
41
Swallowing
- deglutition
| - has a voluntary phase and a reflex phase which guarantees the correct closure of nasal and tracheal passageways
42
Voluntary Phase
- tongue moves bolus into pharynx
43
Reflex Phase
- Touch receptors stimulate swallowing centre via CN IX
- initiates lifting of soft palate and closure of larynx
- > a peristaltic wave moves over the pharynx
- > upper esophageal sphincter relaxes
- > bolus enters esophagus
44
Esophageal Phase
- bolus is propelled by peristalsis towards stomach -> lower esophageal sphincter relaxes ahead of peristalsis to allow entry of bolus into stomach
45
Achlasia
- can cause megaesophagus
- lower sphincter fails to relax due to genetic malfunction of myenteric plexus, or persistent right aortic arch (mechanical obstruction)
46
Myasthenia Gravis
- can cause megaesophagus
- acetylcholine receptor deficit or damage
- > nicotinic receptors
- cause is idiopathic
47
The cephalic, or pregastric phase
- involves grasping (prehension), chewing and mixing of food with saliva in preparation for swallowing
48
Pressure Pump
- includes the anatomic fundus and proximal corpus
49
Peristaltic Pump
- includes the distal corpus and pyloric antrum
50
Grinder
- includes the anatomic pyloric canal and pyloric sphincter
51
Stem Cells
- enable continual replenishment of all GI cells
52
Mucus Layer
- essential to protect the gastric mucosa against mechanical stress, acids and digestive enzymes
53
Mast Cell Tumor
- degranulate and produce histamine
| - > causes an overproduction of HCl and therefore gastric issues (gastric ulcer) can occur
54
Zollinger-Ellison Tumor
- caused by a gastrinoma that secretes gastrin
| - > causes an overproduction of HCl and therefore gastric issues (gastric ulcer) can occur
55
Intrinsic Factor
- binds to vitamin B12 (cobalamin) and protects it from being digested
- > Vitamin B12 is a necessary cofactor for erythropoiesis
56
Gastric Phase
- arrival of food in the stomach
57
Intestinal Phase
- when chyme arrives in the duodenum
- inhibition of gastric glands and motility due to the activation of receptors in the small intestines
- > prevents overloading of small intestines (negative feedback)
- > enterogastric reflex
58
CCK (Cholecystokinin)
- stimulated by fats and proteins
| - reduces gastric motility
59
Functions of Stomach
1. Temporary storage of food
- fundus
2. Mixing of food with gastric secretions and grinding / liquefaction of ingesta into chyme
- corpus and antrum
3. Chemical and enzymatic digestion, particularly of proteins
- Secretion.
4. Controlled release of liquefied chyme into the small intestine
5. Absorption of drugs and alcohol ONLY
60
Gastric Accommodation Reflex
- storage that occurs in the proximal stomach
| - expansion of stomach without pressure increase
61
Propulsive Unit
- pressure pump and peristaltic pump
62
Mucus
- produced by goblet cells
63
Koilin Membrane (cuticula gastris)
- developed internal lining of a carbohydrate/protein complex in avian gizzards
64
Koilin Membrane (cuticula gastris)
- secreted by the ventricular and pyloric glands
65
Synthesis of Prostaglandin
- increases mucus and bicarbonate release
66
Hydrochloric Acid
- secreted by parietal cells
| - involves an active proton pump (H+ and K+ exchanger)
67
Functions of Hydrochloric Acid
1. to macerate ingesta into fluid
2. to denature proteins
3. to begin emulsification of fats
4. to activate the proteolytic enzymes pepsinogen or prochymosin
5. to be bactericidal
68
Gastrin
- released from G cells into blood in response to peptides
| - stimulates Enterochromaffin cells to release histamine
69
Histamine
- acts as a paracrine and is the strongest stimulator of HCl release
70
Intrinsic Factor
- produced by parietal cells in humans
| - produced by pancreatic acinar cells in dogs and cats
71
Pepsinogens
- produced by chief cells
72
Pepsinogen
- precursor for pepsin (proteolytic enzyme)
| - > protein digestion
73
Prochymosin/Rennin in calves
- nursing animals secrete this instead of pepsinogens
| - specific for coagulation of casein
74
Secretin
- duodenal endocrine cells react to low pH values (high acid in small intestine)
- releases this into circulation
- stimulates pancreas and liver to release buffers into the gut
- reduces gastric secretions and emptying when involved in enterogastric reflex
75
Stimuli that trigger the Enterogastric Reflex
1. distention of small intestines
2. high acidity
3. high nutrient content
4. irritation of mucosa
76
Enterogastric reflex
- largely mediated by endocrines
| - > secretin and CCK
77
Vomiting
- emesis
| - the forceful expulsion of stomach / small intestinal contents through the mouth.
78
Signals that Elicit vomiting
1. GI mechanoreceptors and chemoreceptors,
- mucosal distension and irritation
2. Viscera other than GI tract
3. Extramedullary centers
- psychogenic
4. Chemoreceptor trigger zone
- stimulated by drugs, toxins, inflammation products
79
Consequences of severe vomiting
1. loss of fluid
- hypovolemia
- dec blood pressure
- circulatory shock
2. loss of K+
- hypokalemia
- hyperpolarization of membranes
- reduced excitability of nerve/muscle cells
- weakness and hyporeflexia
3. loss of H+
- metabolic alkalosis
- hypoventilation
80
Gastro-intestinal barrier
- GI mucosa forms a barrier between the gut lumen and the body
- allows the transfer of nutrients while protecting the body against harmful chemicals and bacteria
81
Components of the Gastro-intestinal barrier
1. Mucus and Bicarbonate
- coat cells, neutralize acids, binds to bacteria
2. Prostaglandin E2
- increases mucus, blood flow, and bicarbonate secretions
3. Epithelial cells with tight junctions and stem cells
- high regenerative capacity
4. Bactericidal peptides/immunoglobulins A
82
Causes of disruptions of the Gastro-intestinal barrier
1. Stress
- sympathetic stimulation and cortisol release
- > reduce blood flow, mucus, HCO3, impact healing
2. NSAIDs (non-steroidal anti-inflammatory drugs) via inhibition of prostaglandins
3. Ischemia
- cell damage
4. Infections
- tissue damage
- > helicobacter pylori
83
Consequences of the GI barrier breaking
- cell injury
- gastritis
- auto digestion
- erosion
- ulceration
84
Therapy to fix the GI barrier
- stress relief
- histamine blockers
- proton pump blockers
- antibiotics
85
Smooth Muscle Contractility
- regulated by the presence of food in the lumen and the ANS release of neurotransmitters
- > ACh and NE
86
Cells of Cajal
- self-excitatory cells
| - exhibit slow waves and spike potentials
87
Priming Factors
- depolarize smooth muscle membrane
- GI motility increases
- > gut wall stretching, parasympathetic stimulation and some GI hormones
88
Depriming Factors
- hyperpolarizing factors
- GI motility decreases
- > sympathetic stimulation and some GI hormones
89
Amplitude of slow waves can be modified by:
- priming and depriming factors
90
endocrine vs paracrine
- via blood stream
| - via diffusion
91
Enteroendocrine cells of the enteric endrocrine system
- sense luminal contents and secrete regulatory peptides into submucosa to act via blood stream or diffusion
92
Immune System
- defense system concerned with potential pathogens
| - if challenged releases inflammatory mediators
93
Inflammatory mediators
- act as paracrines
| - stimulate secretory and motility functions of the GI leading to peristaltic rush
94
Splanchnic Circulation
- GI blood flow is largely autoregulated and adjusts to the level of local activity
- it can increase by a factor of 8 between inactivity and active digestion
95
Splanchnic Circulation is stimulated by:
1. the pumping action of GI motility
2. several endocrines (mediators)
- by bradykinin and kallidin
3. decreased oxygen / increased CO2 partial pressures during activity phases
96
GI mucosa
- very sensitive to any longer than one hour of a disruption of its blood supply
- > sympathetic stimulation leads to constriction of GI blood vessels, but can be overruled by autoregulatory mechanisms to protect mucosa
97
Salivary Glands
- parotid
- mandibular
- sublingual
- buccal in ruminants and birds
98
Functions of Saliva
1. to moisten, lubricate and bind food into a bolus
2. to control bacterial growth.
3. to start carbohydrate digestion via salivary amylase mainly in omnivores (pig)
4. to cool body through evaporation (carnivores, birds)
5. to regulate rumen pH
99
Acini
- secrete mucus and plasma like fluid which is altered during duct passage
- Na+ and Cl- exchanged against K+ and HCO3-
- > net result hypotonic saliva
100
Saliva
- hypotonic
- alkaline
- K+ rich
101
Parasympathetic Reflex
- chemoreceptors and mechanoreceptors in the mouth -> salivary center/brain stem -> parasympathetic efferent pathway via the Cranial Nerve -> salivation
102
Conditioned Reflex
- anticipation and smell -> higher CNS -> salivary center -> salivation
103
Warming Up Phase
- anticipation and smell activate CN X(vagus nerve) and initiate vagal reflexes that cause mild stimulation of the stomach, small intestines, pancreas and bile
104
Ruminants
- produce large volumes of alkaline saliva rich in bicarbonate and phosphate buffers essential to neutralize fermentation products in the rumen
105
Carnivores
- equally wide jaws
- vertical jaw movements
- cutting action
106
Herbivores
- lower jaw is more narrow than upper jaw
- horizontal and vertical jaw movements
- > grinding
- requires constant growth of teeth
- > hypsodont
107
Chewing Reflex
- mastication is controlled by this
- involves CN V
- Presence of bolus -> pressure against palate -> inhibition of cheek muscles -> lower jaw drops -> stimulates stretch receptors in cheek muscles -> contraction -> pressure against palate
108
When not in Swallowing process
- upper (cricopharyngeal muscle) and lower esophageal sphincter (cardia) are tightly closed
- avoids entry of air and esophageal reflux of gastric contents
109
Disturbances of pregrastric digestion
- may lead to reduced nutrient intake and/or insufficient mechanical preparation of food
110
Pregastric Digestion disturbances due to oral cavity
- horses are prone to getting sharp enamel points
- > need to float enamel ridges
- gingivitis with periodontitis in dog and cat (plaque/inflammations)
- broken teeth
111
Pregastric Digestion disturbances due to nervous system
- encephalitis
- tetanus
- rabies
- trigeminal paralysis (CN V / drop-jaw)
- facial trauma
112
Pregastric Digestion disturbances due to anesthesia
- swallowing reflex is blocked
| - very important in ruminants
113
Chyme
- when leaving the stomach
- it is a fluid mixture of:
1. Polypeptides and Oligopeptides
2. Large emulsified fat globules
3. Unchanged dietary carbohydrates
- None can be absorbed
114
Two events in the that must occur via cooperation of the pancreas, bile and small intestinal mucosa
1. Neutralization of gastric acid to avoid mucosal damage
| 2. Hydrolysis of macromolecules into micromolecules for absorption
115
Pancreas
- provides buffers and digestive enzymes
116
Bile (liver)
- provides buffers and a fat emulsifier
117
Small Intestine Mucosa
- provides buffers, digestive enzymes and absorptive mechanisms
118
Functions of the Exocrine Pancreas
1. Bicarbonate production
| 2. Produce Digestive Enzymes
119
Bicarbonate
- secreted by the pancreatic duct system
- neutralizes gastric acid
- enables pancreatic enzymes to function that require a neutral pH
120
Digestive Enzymes
- produced in the pancreatic acini
| - 3 major groups are amylolytic, proteolytic and lipolytic
121
3 major groups of Digestive Enzymes
1. Amylolytic
2. Proteolytic
3. Lipolytic
122
Alpha Amylase
- digests most soluble (starch and glycogen), but not structural carbohydrates
- splits 1-4 alpha glycosidic linkages
- splits polysaccharides into oligosaccharides and disaccharides
123
Proteolytic Enzymes
- produce mostly oligopeptides
124
Proteolytic Enzymes
- are stored in vesicles (zymogens)
| - are secreted into ducts as inactive pro-enzymes to avoid autodigestion of the pancreas
125
Trypsinogen
- is activated by GI-mucosal enteropeptidase (enterokinase) to trypsin
- trypsin activates all others and its own precursor
126
Essential to avoid autodigestion in the pancreas
- containing a trypsin inhibitor
| - strict separation from lysosomes
127
Lipases
- depend on bile salts for further emulsification to be effective
128
Lipases
- attaches to the surfaces of fat globules and hydrolyze Triglycerides into fatty acids and monoglycerides for absorption
129
Pancreatic enzymes
- are essential for chemical digestion, but do not provide many absorbable micromolecules
130
Colipase
- is not an enzyme, but contributes to fat digestion
131
The Cephalic Phase
- vagal stimulation is involved
132
Gastric Phase
- will mildly stimulate the exocrine pancreas to secrete enzymes and bicarbonate
- > “warming up”
- caused by gastrin release
133
Intestinal Phase
- main phase of pancreatic stimulation through two hormones
1. Secretin
2. Cholecystokinin (CCK)
134
Secretin
- released from duodenal endocrine cells into blood when pH of chyme is low
- stimulates bicarbonate secretion
135
Cholecystokinin (CCK)
- proteins and fats stimulate release of this from duodenal endocrine cells into the blood
- stimulates release of pancreas enzymes
136
Pancreatic Disorders
1. Acute Pancreatitis
| 2. Exocrine Pancreas Insufficiency (EPI)
137
Acute Pancreatitis
- caused by infections, trauma, neoplasms, toxoplasma (cats) and fat-rich or spicy, unusual food (?)
1. Tissue, membrane, or vesicle damage
2. lysosomes and digestive zymogens mix
3. trypsinogen is activated and becomes trypsin
4. trypsin-inhibitor becomes overwhelmed
5. activation of all enzymes within the pancreatic tissue
6. pancreatic auto-digestion and leakage of enzymes into circulation
- apical block hypothesis
138
Exocrine Pancreas Insufficiency (EPI)
1. heritable atrophy (German Shepard dogs), idiopathic, or consequence of chronic inflammations (leads to scarring and reduced function)
2. reduced or lack of enzyme secretion
3. maldigestion
4. starvation
- weight loss or steatorrhea(fat rich feces)
5. Can also affect endocrine secretion
- Diabetes mellitus
139
Direct digestive functions of the Liver are
1. To facilitate digestion and absorption of fats and lipophilic vitamins through secretion of bile acids
2. To neutralize acidic chyme via bicarbonate secretion
140
Hepatocytes of the Liver
- secrete bile acids
| - secrete lipophilic waste products
141
Duct Cells of the Liver
- secrete bicarbonates
| - secrete electrolytes and water
142
Bile Acids
- derived from cholesterol
143
Cholesterol
- a detergent
| - has a hydrophilic and lipophilic end
144
Synthesis of Bile Acids
Cholesterol -> cholic acid -> is conjugated to an amino acids (glycine or taurine)
145
Bile Acid Functions
1. Emulsification of lipid aggregates
| 2. Transport of lipids in an aqueous environment
146
Emulsification Function of Bile Acids
1. Bile salts attach to surfaces of fat globules
2. vigorous mixing in aqueous chyme
3. globules break up into smaller pieces
4. increases the surface area for action of pancreatic lipases
147
Transport Function of Bile Acids
1. After hydrolysis by lipases, fatty acids and monoglycerides aggregate with bile acids to form micelles
- micelles have hydrophilic ends pointing outwards and lipophilic ends inside
3. This avoids re-condensation into triglycerides
4. Keeps lipids in solution and enables their transport within the aqueous chyme to the mucosa for absorption
148
Micelles
- fatty acids and monoglycerides that aggregated with bile acids
- have hydrophilic ends pointing outwards and lipophilic ends inside
- avoids recondensation of monoglycerides and fatty acids into triglycerides
149
Cholecystokinin (CCK)
- stimulates gall bladder contraction
| - which releases stored bile
150
Bile Juice
- some is released during the cephalic and gastric phases
| - the main stimulation occurs during the intestinal phase via hormones (CCK and secretin)
151
In animals without a Gall Bladder
- the Sphincter of Oddi is not an efficient Barrier
| - bile is continuously released into the duodenum
152
Recycling of bile acids
- 95% of bile acids are re-absorbed in the ileum, then re-enter liver and are secreted again and again
- > up to 20 times
153
Choleretic effect of bile acids
- The re-uptake of bile acids into the liver stimulates hepatocytes to secrete more bile juice
- > positive feedback
154
Effect of damaged hepatocytes
- cannot extract bile acids from portal blood
- bile acid concentration may increase in the plasma
- > sensitive diagnostic indicator of deficits in hepatic function
155
Small intestines
- the center of the food processing plant
| - where macronutrients are digested and absorbed as simple molecules
156
Main Functions of the Small Intestine
1. To receive, mix and propel chyme, pancreatic enzymes, bile juice, and buffers
- luminal digestion
2. To add large volumes of buffered fluid to create a suitable aqueous dilution enabling digestion and absorption
3. To provide additional means to finalize the digestive process started by gastric and pancreatic enzymes
- > via its mucosal enzymes (membrane digestion)
4. To absorb virtually all micromolecules, and the majority of water and electrolytes
157
Mixing and peristaltic contractions of the small intestine
- stimulated by incoming chyme
| - > via mechanoreceptors and chemoreceptors
158
Mixing and peristaltic contractions of the small intestine assist in:
1. Mixing incoming chyme with intestinal fluid, pancreatic juice and bile
2. Distributing chyme along the small intestines
3. Enabling contact between digestive products and absorptive cells
159
The Ileocecal Sphincter
- impedes flow of ingesta into the large intestines during the digestive phase
- > closed
- avoids backflow of bacteria from the large intestine into the small intestine
160
The Small Intestine tube and its mucosa
- characterized by a vast increase in surface area by having folds, villi and microvilli
161
Intestinal Mucosa
- contains numerous stem cells found within the crypts of Lieberkuehn
162
Stem cells
- differentiate into all the small intestinal epithelial cells
- replenishes the mucosa every 5 days
163
Consequences of Small intestinal Mucosa
1. Great regenerative capacity after injury
| 2. Highly active tissue and is therefore vulnerable
164
Stem Cells in the small intestine differentiate into:
1. Young Enterocytes
2. Mature enterocytes
3. Enteroendocrine cells
4. Mucus cells and Goblet cells
5. Paneth cells
165
Young Enterocytes
- secretory cells
| - line the crypts of lieberkuehn
166
Mature enterocytes
- absorptive cells
| - line the villus
167
Enteroendocrine cells
- produce endocrines
| - > CCK and secretin
168
Paneth Cells
- provide host defense against microbes in the small intestine
- > alpha-defensins, or cryptdins
169
Young Enterocytes
- secrete large volumes of intestinal fluid to facilitate digestion and absorption through:
1. active Cl- secretion into the guy lumen
2. creates an electrical gradient
3. pulls Na+ into the lumen
4. Creates an osmotic gradient
5. Pulls water
6. Dilution of chyme
170
Mature enterocytes
- develop numerous microvilli called Brush Border Membrane (BBM)
- contains digestive enzymes and absorptive mechanisms
171
End products of the luminal digestion
- largely not absorbable
- have to be hydrolyzed further by BBM-bound enzymes
- > membraneous, or BBM digestion before being absorbed
172
Luminal Phase of digestion for starch and glycogen
- salivary pancreatic enzyme
- > amylase hydrolyses a-1,4 linkages
- products are oligosaccharides and disaccharides (maltose) which can not be absorbed
173
Brush Border phase of digestion for starch and glycogen
- oligosaccharides and disaccharides (maltose) within the BBM are hydrolyzed
- end products are monosaccharides that are absorbable
174
Digestion of dietary disaccharides
- can not be hydrolyzed by alpha-amylase, but require Disaccharidases in BBM
175
Sucrose
- table sugar
176
Sucrose
- digested by BBM sucrase
| - produced into glucose and fructose
177
Lactose
- milk sugar
178
Lactose
- hydrolyzed by BBM lactase
179
Lactose
- hydrolyzed into glucose and galactose
180
Sucrose
- hydrolyzed into glucose and fructose
181
Galactose
- the only carbohydrate digesting enzyme in newborns
182
Lactose Intolerance
- genetic lactase deficiency (man, kittens) or acquired lack
1. Lactose
2. Fermented to Lactic Acid
3. Mucosal Irritant
4. Diarrhea
183
Absorption of Glucose and Galactose
- occurs through a secondary active Na cotransport mechanism
184
Secondary active Na cotransport mechanism
- depends on the electrochemical sodium gradient
185
Electrochemical sodium gradient
- created by the Na/K pump at the basolateral side of the mature enterocyte
186
Fructose
- absorbed via facilitated diffusion through the glucose transporter (GLUT5)
- exception for absorption of monosaccharides
187
Basolateral membrane
- Monosaccharides leave enterocytes by facilitated diffusion into interstitium, then blood, then tissue
188
Structural carbohydrates
- have a B glycosidic bond
- can not be hydrolyzed by any mammalian enzyme
- > fermented by microbial action
189
Proteins
- converted into tripeptides, dipeptides, or mainly amino acids for absorption
190
Luminal Phase for digestion of proteins
- HCl denature proteins and activates pepsin
191
Pepsin
- hydrolyses proteins into polypeptides
192
Pancreatic endopeptidases and exopeptidases
- hydrolyse polypeptides into oligopeptides
193
BBM Phase for digestion of proteins
- oligopeptides are hydrolyzed into tripeptides, dipeptides and amino acids
194
Brush Border enzymes
- hydrolyse oligopeptides into tripeptides, dipeptides and amino acids
195
Newborns
- can absorb colostral immunoglobulins via endocytosis
196
Digestion of Colostral immunoglobulins avoided by
1. limited HCl secretion
2. limited pro-chymosin secretion
3. a trypsin inhibitor in the colostrum
197
Absorption of end products from carbohydrate and protein digestion
1. depends on intact enterocytes
- BBMs (brush border membrane enzymes)
2. need specific transporters
3. depends on Na absorption
4. requires energy
198
Sodium
- crucial to guarantee the absorption of glucose and amino acids
199
Specific transporters for absorption of protein and carbohydrate end product absorption
- inhibited by enterotoxins
1. EPEC
- enteropathogenic E. Coli
2. CT
- cholera toxin
3. NSP4
- Rotavirus non-structural protein 4
200
Digestion and Absorption of Fats
- depends on pancreatic enzymes and bile salts
| - does not require any brushborder enzymes, or transporters
201
Fat Globules
- are emulsified by HCl
| - are conjugated by bile acids
202
Pancreatic Lipase and Colipase
- attach to fat globule surface
| - hydrolyze triglycerides into monoglycerides and free fatty acids
203
Micelles
- Monoglycerides and free fatty acids form aggregates with conjugated bile acids
204
Micelle Formation
- avoids recondensation
| - facilitates transport of monoglycerides and free fatty acids to the brushborder membrane
205
Monoglycerides and free fatty acids
- diffuse into the epithelial cell at the brushborder membrane
206
Free conjugated bile acids
- emulsify more fat globules or form new micelles
207
After diffusion into the enterocyte
- after this free fatty acids and monoglycerides are mostly recombine to triglycerides
208
Chylomicrons
- triglycerides, cholesterol, phospholipids, fat soluble vitamins and newly formed lipoproteins aggregate and become this
209
Chylomicrons
- transport formation for lipids in the plasma
210
Chylomicrons
- leave the enterocyte cell by exocytosis and enter the lymphatic system into the circulation
- > plasma can turn milky
211
Number of Micromolecules
- this increases dramatically once hydrolysis of nutrients begins
- osmotic pressure of chyme increases before absorption
- water is sucked into the gut lumen via osmotic pull
212
Osmotic Pull
- water is pulled into the gut lumen due to this
213
Water content of chyme
- 80-90% of this is reabsorbed before chyme leaves the small intestine
214
Water
- always follows the osmotic gradient!
215
Water
- its absorption entirely depends on absorption of electrolytes and nutrients
- > specifically sodium
216
K+ absorption
- is passively absorbed along its chemical gradient
| - mostly by the paracellular pathway
217
Reversing the Osmotic Gradient Effect
- causes water to follow passively from the GI lumen back into the GI mucosa and is reabsorbed
218
Reverses the Osmotic Gradient
- the accumulation of electrolytes and nutrients intracellularly and then in the lateral spaces between enterocytes
219
Bicarbonate
- has to be recovered to maintain pH neutrality
220
Recovery of Bicarbonate
- depends on Sodium gradients
| - is achieved as absorption of Carbon Dioxide (CO2)
221
Na+ gradient
- facilitates Na+ / H+ exchanger at the brushborder membrane (BBM)
- > H+ is excreted into gut lumen
222
CO2
- absorbed easily
| - combines with water to form H+ and bicarbonate
223
Bicarbonate Recycling
- H+ is excreted into the gut lumen and bicarbonate is returned to circulation
224
Diarrhea
- increased fecal fluidity, usually accompanied by increased defecation frequency and volume of feces
225
Diarrhea
- caused by an imbalance between water absorption and secretion
- > leads to loss of body water, electrolytes and bicarbonate via feces
226
Osmotic Diarrhea (malabsorptive)
- increased osmotic pull
227
Osmotic Diarrhea (malabsorptive) Steps
1. If gut lumen contains a large number of molecules which are poorly or not absorbed 2. high osmolality of chyme
3. water is “sucked” into the lumen
4. ingesta and fluid accumulation
5. distention
6. motility increases
7. diarrhea
228
Causes of Osmotic Diarrhea (malabsorptive)
1. Intake of nonabsorbable or low absorbable compounds
2. Accumulation of partially digested ingesta
3. Loss of absorptive cells due to mucosal damage
- digestion can not be completed and micromolecules cannot be absorbed
4. Toxins inhibit many Na-cotranporter mechanisms
- micromolecules accumulate
229
Secretory diarrhea
- direct stimulation of secretory cells and mucus cells to secrete more fluid into the gut lumen
- increased volume causes distention, increases motility, the diarrhea
230
Secretory Diarrhea is caused by
1. Some Toxins
2. Inflammatory mediators released during gastritis/enteritis
3. Mucosal Irritants
4. Parasympathetic stimulation
231
Exudative Diarrhea
- severe mucosal damage
- leads to massive fluid
- electrolyte and protein loss
232
Consequences of Diarrhea
1. Fluid loss
- hypovolemia
- hypoxia/metabolic acidosis/tissue damage and shock and circulatory collapse
2. bicarbonate loss
- metabolic acidosis
- tissue damage
3. K+ loss
- hypokalemia
- hyperpolarization of nerve/muscle membranes
- weakness, hyporeflexia
4. Epithelial defects/intestines
- denuding of villi
- loss of barrier effect
- septicemia
233
Small intestine
- Enzymatic digestion should have been completed
| - nutrients have been absorbed
234
Large Intestine
- receives largely indigestible material
235
Large Intestine Functions
1. Propulsion of chyme towards rectum
2. Absorption of remaining water and electrolytes
3. Microbial fermentation of undigested organic matter
- nonruminant herbivores
4. Storage and expulsion of feces
236
Ileocecal sphincter of the Large Intestine
- controls flow of ingesta between small and large intestines
- is closed during active digestion of the Small Intestine
237
Gastro-ileal reflex (vagal) of the Large Intestine
- at the end of small intestine digestion, an animal takes in the next meal
- gastric distention occurs
- then this occurs
- causes the ileocecal sphincter to open and ingesta is propelled into the caecum
238
Large Intestine Motility Pattern
- arrival of chyme in LI
- > induces increased motility to propel chyme towards the rectum which induces increased motility to propel chyme towards the rectum
239
Large Intestine Motility
1. Mixing and Segmentation Movements
2. Peristaltic and Anti-peristaltic movements
3. Mass Movements
240
Mass Movements of large intestine
- between the distal colon and rectum to forward fecal matter
241
Mass Movements of large intestine are Induced By:
1. Gastro-colic reflex (vagal)
2. Irritation of the Colon
3. Stimulation of PNS
242
Fermentation of LI
- Indigestible matter and “escaped” nutrients are fermented by bacterial enzymes into Volatile Fatty Acids, CO2 and CH4.
243
Secretion of LI
- Bicarbonate-rich fluid and mucus buffer the fermentation products to protect mucosa
244
Absorption of Li
- Sodium via the active Na-K pump is followed by chloride and water
- Na K pump is regulated by aldosterone!
245
Absorption of Li
- Fermentation products are absorbed by simple diffusion, followed osmotically by water and some vitamins produced by bacteria are also absorbed
246
Intense Irritation or psychogenic tension of large intestine
- leads to copious secretion of mucous and fluid
| - > diarrhea
247
Myenteric Reflex of Large Intestine
1. Mass movements move feces from colon into rectum
2. stimulates pressure receptors in rectum
3. stimulates this
4. peristalsis and internal sphincter relaxation
5. defecation
248
Myenteric Reflex of Large Intestine
- is a weak reflex of the large intestine
| - needs to be supported by the parasympathetic reflex
249
Parasympathetic Reflex of the Large Intestine
- The pelvic nerves stimulate intensified peristalsis
250
Parasympathetic Reflex of the Large Intestine
1. Rectum Distention
2. Afferent parasympathetic fibers
3. Spinal cord
4. Efferent parasympathetic fibers
5. Pelvic nerves
6. Intensified peristalsis
251
Defecation reflexes
- can be blocked by voluntary constriction of external spinchter and puborectal muscles
- through the pudendal nerve
252
Pelvic Nerve Damage
- causes paralyses defecation reflex (PNS not working)
| - constipation occurs
253
Pudendal Nerve Damage
- abolishes control of the parasympathetic reflex
| - fecal incontinence occurs
254
Ruminants
- the most successful group of land mammals
255
Problem: Structural carbohydrates
- the most abundant component of natural food resources
| - cannot be digested by any mammalian enzymes system
256
Solution: Ruminants
- developed a symbiotic relationship with microbes
| - which are able to ferment these structural carbohydrates and leave energy-rich products for their hosts
257
Ruminants four compartment stomach (fermentation chambers)
1. The rumen
- paunch
2. The Reticulum
- honeycomb
3. The Omasum
- manyplies
4. The abomasum
- true stomach
258
Complex Motility Pattern in Ruminants
1. Mix and retain ingesta to enable microbiotic activity
2. Enable the release of gas
3. Co-ordinate regurgitation
4. Pass on fermented matter into the omasum
259
Material in the Rumen
- less dense, or lighter large particles are at the top
- more dense, or heavier and smaller particles are at the bottom
- > stays at the top until broken down and fermented by microbes
260
Solid Zone, or Plant Material
- site of active fermentation
- dorsal rumen receives undigested plant matter
- forming a mat of entangled fibers with air and gas trapped in between (floating mat)
261
Gas Cap
- microorganisms produce gas during fermentation
| - gas floats to the top
262
Liquid Zone
- mixing and fermentation break fibers up and small particles sediment into the liquid zone (saliva and water) according to the gravity gradient
263
Omasal Orifice, or Potential escape zone
- only sufficiently fermented, or small particles and fluid move from here into the omasum
264
Primary Contraction of Ruminants
- mixing cycle
| - A cycle
265
A Cycle of primary contraction in ruminants
- occur with a frequency of 3 contractions per 2 min depending on the coarseness of the diet
- are only absent in deep sleep
266
Primary Contraction of Ruminants: Movements
1. Reticulorumen Movements
| 2. Ingesta Movements
267
Reticulorumen Movement Step 1
- Biphasic contraction of
reticulum
-> During the second contraction, the omasal orifice dilates and the omasum relaxes (suction)
268
Ingesta Movement Step 1
- coarse, light particles go to the dorsal sac
| - small heavy particles and fluid move to the cranial sac and omasum
269
Reticulorumen Movement Step 2
- reticulum relaxes
- cranial sac contracts
- cranio-caudal contraction of dorsal sac and dorsal blindsac
270
Ingesta Movement Step 2
- fluid flows back into the reticulum
- Coarse, light particles are mixed in dorsal rumen
- Small, heavy particles and fluid are pressed ventrally
271
Reticulorumen Movement Step 3
- Cranio-caudal contraction of
ventral sac and ventral blind sac
- Followed by caudo-cranial moving contraction
272
Ingesta Movement Step 3
- Small particles and fluid are pressed dorsally and flow back into the cranial sac and reticulum
- Coarse fibers remain in dorsal sac
273
Stratification of ruminal ingesta
- mostly achieved by differences in gravity
274
The overall effects of the
| stratification and the A Cycle are
1. Freshly swallowed food is moved into the rumen and added to the floating material
2. The floating mat is compressed and mixed
3. Small fermented particles are pressed out and sink into the fluid
4. Small particles and fluid move via the cranial sac back into reticulum and pass through the omasal orifice with next reticular contraction
275
Secondary Contraction of the Rumen
- B cycle
276
B Cycle of secondary contraction in ruminants
- eructation contraction of the reticulorumen and ructus
| - gasses formed during fermentation must be released
277
B cycle movements
- follows after 2-3 A cycles depending on the rate of gas formation
278
B cycle movements
1. A caudo-cranial contraction of rumen push gas cap forward to the cardia region
2. activates cardia receptors
3. sphincter relaxation
4. gas enters esophagus
5. antiperistaltic wave moves gas orally
6. part of gas inhaled and exhaled
279
Inhibition of Ructus
1. Gas accumulates
2. Bloat occurs
3. Pressure on the thoracic organs occurs
4. Circulatory failure occurs
280
Vagal reflex
- controls the reticulorumen motility
281
Vagal reflex involved in the reticulorumen motility
- receptors in the mouth, forestomach, and stomach.
- vagal afferent, or sensory fibers
- motility center in the medulla oblongata
- vagal efferent, or motor fibers
282
Main receptors of the reticulorumen
- stretch receptors and chemoreceptors
283
Stretch Receptors in the reticulorumen
- stimulated by mild to moderate distention of reticulorumen wall
- increase motility and rumination
- inhibited by severe distention!!
284
Chemoreceptors in the reticulorumen
- monitor pH
| - depresses motility when pH falls below 5.0 to slow down fermentation
285
Moderate distention of the reticulorumen wall
- increases motility and rumination
| - but if too severe inhibits it
286
When pH of reticulorumen falls below 5.0
- slows down fermentation by depressing the motility
287
Pain and fever
- inhibit reticulorumen activity
288
Motility Center (medulla oblongata) of the reticulorumen
- shows no spontaneous activity
| - needs to be driven by excitatory signals from receptors
289
- Receptor Damage or Inhibition in the reticulorumen
- ruminal stasis occurs
- vagal indigestion
Ex: traumatic reticuloperitonitis (TRP)
-> Magnets are used to prevent it…
290
Traumatic reticuloperitonitis (TRP)
- receptor damage or inhibition in the reticulorumen
| - magnets can be used to prevent this
291
Ejection, or Rumination (remastication)
- is a crucial part of a ruminant’s digestion to break up coarse fibers, increasing the surface area for microbes
- stimulate saliva secretion to stabilize rumen environment
- > buffers!
292
Circadian rhythm
- periods of feeding alternate with periods of rumination
293
Rumination: Complex vagal reflex
- react to fiber coarseness and degree of filling
- involves the rumination center, or medulla oblongata
- stimulated by mechanoreceptors
294
Rumination
- occurs immediately before an A-cycle
- > an extra contraction of the reticulum, cardia relaxes, glottis closes, inspiration movement sucks bolus into esophagus, anti-peristaltic wave propels bolus into mouth, water is pressed out and swallowed, rechewing occurs
295
Rumination
- is a good indicator of an animal’s well-being, as rumination is disturbed during stress, sickness or pain
296
Reticular Groove
- The groove is formed by muscular lips between the cardia and the omasal orifice
- they contract and twist to form a closed tube
297
Reticular Groove Reflex
- a vagal reflex that is stimulated by suckling (oral receptors) and by anticipation
298
Purpose of the Reticular Groove Reflex in suckling ruminants
- In suckling ruminants milk reaches the abomasum directly without passing, or being fermented in the forestomach
- purpose is to avoid loss of proteins to microbes and fermentation of lactose to lactic acid (mucosal irritant)
299
Purpose of Reticular Groove Reflex in adults
- this reflex can be activated by Antidiuretic (thirst), or oral application of copper salts or sodium salts
300
Omasum Motility: Second Contraction of the reticulum (pushing action)
- during this contraction, ingesta passes through the reticulo-omasal orifice while the omasum relaxes (sucking action)
- > causing fluid and particles to enter the omasum
301
Pumping Action of the Reticulo-omasal orifice
- Orifice closes briefly, the canal contracts pressing ingesta between leaves
- then the body contracts and presses ingesta forward into abomasum
302
Omasum Function of passing on particles from the reticulum to abomasum
- depends on correct stratification of food in the reticulum
| - can be impaired due to TRP
303
Omasum Motility
- controlled by the intrinsic nervous system
| - > enteric nervous system
304
Omasum Function
1. To pass on fermented particles from the reticulum to abomasum
2. Absorption of residual VFA, Water and bicarbonate
3. Grinding effect
305
Symbiotic Relationship
- relationship between the host/ruminant and microorganisms
| - > both partners benefit and would not survive without the other
306
What the Host Provides to the microorganism
1. shelter
2. food and water
3. removes waste products
4. *Maintains constant environmental conditions
- > temperature, pH, osmolality, low oxygen
307
What the Microorganism Provides to the host
- leaves energy-rich waste products for the host after fermentation of otherwise indigestible food
- nutrients through synthesis
308
Fermentation
- anaerobic metabolism (hydrolysis) of nutrients by microbes
309
Bacteria
- colonize the rumen after birth
| - mostly anaerobic
310
Protozoa
- colonize rumen after birth
| - contact to other ruminants is necessary
311
Protozoa
- constitute half of the microbial biomass
- provide essential proteins to the host
- fermentation pattern are similar to bacteria, but NOT essential for host's survival
312
Fungi
- anaerobic
- metabolize a wide range of carbohydrates
- fermentation pattern are similar to bacteria, but NOT essential for host's survival
313
Bacteria
- are essential for the host's survival
314
Volatile Fatty Acids
- are the major source of energy for the ruminant host
| - > cover 60-80% of the host's energy requirements
315
Absorption of Volatile Fatty Acids Occurs
1. As free acids
- they are lipophilic
- > requires low rumen pH
2. An ionized form
- involving probably a bicarbonate, or VFA exchanger
316
Starch (soluble carb)
- broken down to fructose by amylolytic microbes
317
Cellulose, Hemicellulose, and Pectin (structural carbs containing B-linkages_
- broken down to fructose by cellulolytic, hemicelulolytic and microbes
318
Fructose
- synthesized pyruvate while also producing energy (ATP)
319
Pyruvate
- synthesizes the volatile fatty acids (VFA)
1. Acetate (60-70%)
2. Proprionate (20-30%)
3. Butyrate (10%)
4. Lactate
- proprionate and acetate
320
Acetate
- produces energy (ATP)
- fermentation produces CO2 which produces methane (CH4)
- > bad for the environment
321
Ruminants
- can digest soluble carbohydrates, but not structural carbohydrates
- microbes extract energy from the food and produce waste products from fermentation
- absorb the waste product for energy yield
- eventually digests microbes for a protein source
322
Increase in VFAs during fermentation
- this decreases the rumen pH
| - > can be harmful
323
Rumen Content is buffered by
- buffered by the flow of saliva and bicarbonate
324
Soluble Carbohydrates (concentrates)
- are fermented faster than structural carbohydrates
- more VFAs are released
- provides more energy for the host
325
Problem with soluble carbohydrate fermentation
- rapid acid increase challenges the buffering capacity
- can suppress useful bacterial populations
- > potentially harmful
326
Protein Fermentation
- most are fermented by microbes to NH3 (ammonia) and VFAs
327
Microbes
- for their own growth, they synthesize proteins
328
Protein synthesis by microbes
- requires a carbon skeleton (VFA), a nitrogen source and ATP
- > nitrogen being the bottleneck
329
Natural sources of nitrogen for microbial protein synthesis
1. Ammonia from proteinolysis
| 2. Urea (non-protein nitrogen) recycling
330
Urea
- waste product of protein catabolism
| - formed in the liver to detoxify NH3
331
Urea is detoxifies NH3 from
1. catabolism of endogenous amino acids
| 2. ammonia absorption from the rumen and large intestines
332
If ruminal NH3 concentration is high
- urea is excreted via the kidneys
333
If ruminal NH3 concentration is low
- urea is secreted directly, or through saliva into the rumen for bacterial growth
- > rumino-hepatic nitrogen recycling
334
Rumino-hepatic nitrogen recycling
- when ruminal NH3 concentration is low
| - urea is secreted directly, or through saliva into the rumen for bacterial growth
335
Cause of Rumen Acidosis
- imbalance between VFA production and buffering capacity
| - > sudden ingestion of large quantities of highly digestible carbohydrates
336
Rumen Acidosis Effects
- VFA increase
- Salivation and rumination decreases
- pH decreases
337
Rumen Acidosis Consequences
- Damage to epithelium
- barrier function and absorption impaired
- systemic infections
- metabolic acidosis
- ruminal stasis
- dehydration
- renal failure
- shock
- death
338
Low pH
- favors lactate producers and inhibits fermentation to VFA
| - lactic acid is not absorbed easily, pH drops further, osmolarity rises and water enters the rumen
339
Functions of the hindgut
1. Absorption of water and electrolytes
2. Fermentation
3. Formation and storage of feces
340
Cecum Fermentors
- rabbit, chinchilla, guinea pig and koala
341
Colon Fermentors
- horse, elephant, rhinoceros, pigs and some primates
342
Equine Cecum
- receives slurry-like ingesta from the SI
- mixing movements between the haustra
- occasional mass movements
- > ingesta moves through cecocolic orifice into the ventral right colon
343
Equine Ventral Colon
- haustric segmentation
- > mixing, peristalsis and anti-peristalsis originating from the pelvic flexure
- > long retention of ingesta from here
344
Equine Pelvic Flexure
- marked reduction of diameter
- function similar to pylorus
- helps to retain large particles and to pass on liquid and small (fermented) particles
345
Equine Dorsal Colon
- junction to the small colon
| - movements similar to ventral colon with retention of ingesta at junction
346
Hindgut fermentation
- very similar to ruminal fermentation
347
Hindgut
- receives pre-digested mixture of feeds
| - endogenous fluids and cells
348
Digestion in the small intestine of horses
- not very efficient
- fast passage of ingesta
- many soluble carbohydrates reach the large intestines
349
Hindgut fermentation
- large water movements occur
- absorption of water also occurs
- daily fluid entering and leaving equals the total ECF volume of the horse
350
Buffering of VFAs
- achieved through mucosal secretion of HCO3-
351
Acetate
- produced instead of methane
| - > less energy loss
352
Nitrogen Recycling
- exists with urea secretion into cecum and colon
353
Microbial proteins and vitamins
- are hardly available to the host
354
Coprophagia and Lagomorphs
- microbe rich cecum content is excreted once daily through rapid peristalsis
- proteins and vitamins are recovered through small intestine digestion and absorption
355
Purpose of Coprophagia and Lagomorphs
- microbial proteins and vitamins K and B complex
