Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
357 Cards in this Set
- Front
- Back
|
4 major functions of the GI tract
|
- Motility
- Secretion - Digestion - Absorption |
|
|
Four layers of the GI tract (inner to outermost)
|
- Mucosa
- Submucosa - Muscularis externa - Serosa |
|
|
Function of the mucosa (2)
|
- Absorption
- Mucous secretion |
|
|
What's located in the submucosa? (2)
|
- Lymph ducts and blood vessels
- Submucosal plexus |
|
|
What's located in the muscularis externa?
|
- Myenteric plexus
|
|
|
What's the function of the muscularis externa?
|
Provides segmented and peristaltic contractions for mixing and moving food
|
|
|
What's the function of the serosa?
|
Reduces friction with the movements the GIT make
|
|
|
Two epithelial modifications
|
- Villi
- Crypts Both function in secretion, absorption, and immunity |
|
|
What nervous system is involved with intrinsic control of the GIT?
|
ENT
|
|
|
What nervous system is involved with extrinsic control of the GIT?
|
ANS
|
|
|
Three things used in sensory communication of the GIT
|
- Chemoreceptors
- Mechanoreceptors - Osmoreceptors |
|
|
What provides excitatory effects to the GIT?
|
PSNS
|
|
|
Two primary nerves that supply innervation to the GIT
|
- Vagus n. to level of transverse colon
- Pelvic nn. from Descending colon to exit |
|
|
What provides inhibitory effects to the GIT?
|
SNS
|
|
|
What mediates SNS innervation to the GIT?
|
Adrenergic receptors
|
|
|
Where is the myenteric plexus located?
|
Between longitudinal and circular muscle layers
|
|
|
Where is the submucosal plexus located?
|
In the submucosa
|
|
|
What do the myenteric plexi regulate?
|
Motor neurons
|
|
|
What do the submucosal plexi regulate?
|
Glandular, endocrine, and epithelial secretions
|
|
|
What do the cephalic and oral phase cause?
|
Increase of PSNS outflow
- Salivary secretion - Gastric acid secretion - Pancreatic enzyme secretion - Gall bladder secretion |
|
|
6 functions of saliva
|
- Lubricates mouth and teeth
- Aids swallowing - Provides antibacterial and digestive enzymes - Maintains chemical balance of tooth enamel - Buffer - Cooling |
|
|
What do serous acinar cells have?
|
Zymogen granules
|
|
|
What do mucous acinar cells secrete?
|
Glycoprotein mucins
|
|
|
When is saliva hypotonic to plasma?
|
At all flow rates
|
|
|
What in saliva increases directly with flow rate?
|
Tonicity
|
|
|
What ion in saliva is more than the concentration in plasma? (2)
|
HCO3
- Except at lower flow rates K+ - All flow rates |
|
|
Why are saliva ionic concentrations clinically significant?
|
Electrolyte loss due to hyper-salivation
|
|
|
Two stages of salivary secretion
|
- Amylase containing primary secretion in the gland itself
- Modification of ionic content as it goes out the duct |
|
|
How does saliva become hypotonic in the salivary ducts? (2)
|
- Addition of K+ and HCO3
- Removal of Na+ and Cl- |
|
|
Four things that increase secretion of salivary amylase and saliva flow rate
|
- ACH **
- NE - Substance P - Vasoactive Intestinal Protein (VIP) |
|
|
What is salivary amylase released from?
|
Serous acinar cells
|
|
|
Three hormones that increase amylase production by acting on receptors to elevate cytosolic Ca++
|
- NE
- ACH - Substance P |
|
|
Two hormones that increase amylase production by elevating cAMP
|
- NE
- VIP |
|
|
Three functions of the upper esophageal sphincter
|
- Allows entry of food into esophagus
- Protects airway from swallowed material - Protects airway from gastric reflux |
|
|
What allows entry of food into the esophagus?
|
Upper esophageal sphincter
|
|
|
What allows entry of food into the stomach?
|
Lower esophageal sphincter
|
|
|
2 functions of the lower esophageal sphincter
|
- Protects esophagus from gastric reflux
- Allows entry of food into stomach |
|
|
Two fiber types found in the LES
|
- Vagal inhibitory fibers (VIF)
- Vagal excitatory fibers (VEF) |
|
|
What's required for the LES to relax?
|
Increase in VIF and decrease VEF
|
|
|
What's required for the LES to regain tone?
|
Increase VEF, decrease VIF
|
|
|
Another name for the body of the stomach
|
Oxyntic glandular mucosa
|
|
|
Four glands located in the stomach
|
- Cardiac glands
- Oxyntic glands - Pyloric glands - Chief cells |
|
|
What do cardiac glands secrete?
|
Mucous only
|
|
|
What do the oxyntic glands secrete?
|
- HCl
- HIstamine - Somatostatin |
|
|
What in the oxyntic glands secretes histamine?
|
Enterochromaffin like cells (ECL)
|
|
|
What in the oxyntic glands secretes somatostatin?
|
D cells
|
|
|
What do the chief cells produce?
|
Pepsinogens
|
|
|
What do the pyloric glands have in them?
|
G cells
|
|
|
What do G cells produce?
|
Gastrin
|
|
|
Where are G cells located?
|
Pyloric glands
|
|
|
What is the concentration of H+ in gastric juices at higher flow rates?
|
High
- Almost isotonic |
|
|
What two ions in gastric juice are inversely related?
|
- Na+
- H+ |
|
|
What ion concentration in the gastric juice is hypertonic?
|
K+
|
|
|
What is the major anion in the gastric juices?
|
Cl-
|
|
|
How does the parietal cell conform from non-secreting to secreting?
|
IC Caniculus fuses with apical side of the cell to dump secretions into lumen
|
|
|
Study diagram of parietal cell in diagrams packet
|
Basically:
- Cl-HCO3 antiporter (Cl- in; basolateral) - K+ leak (out, basolateral) - Na-K pump (basolateral, Na out) - Cl leak (out, lumen) - H+/K+ antiporter (H+ out, lumen) |
|
|
What in the parietal cell is used to drive more Cl- out of the cell?
|
K+ efflux from basolateral leak channel
|
|
|
What stimulates the K+ leak channel in the parietal cell? (2)
|
- Increase cAMP
- Increase Ca++ Used to drive more Cl- into lumen |
|
|
What does distension of the stomach lead to?
|
Vasovagal reflex
|
|
|
Three things that increase due to vasovagal reflex
|
- H+
- Pepsinogen - Gastrin |
|
|
What does the presence of CNH in the stomach cause?
|
- Production of peptides which move gastrin into endocrine system to produce H+ and pepsinogen
|
|
|
5 things that control gastric secretion of HCl
|
- Histamine
- ACH - Gastrin - Vagal stimulation - Somatostatin |
|
|
In regards to HCl production, what does Histamine do?
|
Stimulates parietal cells
|
|
|
What produces histamine?
|
ECL
|
|
|
Two things ACH stimulates in the stomach
|
- Parietal cells
- ECL cells |
|
|
Two things that gastrin stimulates
|
- Parietal cells
- ECL cells |
|
|
What does vagal stimulation do in regards to HCl production?
|
Increases secretion of Histamine, Gastrin, and HCl
|
|
|
What does somatostatin due in regards to HCl production? (2)
|
- Suppresses HCl secretion
- Inhibits G cells (which produce gastrin which stimulates parietal glands) |
|
|
What is somatostatin produced by?
|
D cells
|
|
|
What is somatostatin stimulated by?
|
H+
|
|
|
What do chief cells produce?
|
Pepsinogen
|
|
|
What do parietal cells produce?
|
HCl
|
|
|
What do ECL cells produce?
|
Histamine
|
|
|
What do G cells produce?
|
Gastrin
|
|
|
Two general things that inhibit gastric acid production during oral and gastric phase
|
- Vasovagal reflex (promotes gastrin --> somatostatin)
- Low pH in stomach (inhibits G and Parietal cells) |
|
|
Two general things that inhibit gastric acid production during intestinal phase
|
- Low pH in duodenum
- Digestion products of fats and protein |
|
|
What's the primary control of gastric emptying?
|
Pyloric sphincter
|
|
|
What secretes pepsin?
|
Chief cells
|
|
|
What is pepsinogen?
|
Inactive proenzyme of pepsin
|
|
|
What activates pepsinogen into pepsin? (2)
|
- Low pH
- Pepsin itself |
|
|
What inactivates pepsinogen?
|
Neutral or alkaline pH
|
|
|
5 secretagogues to chief cells
|
o ACH
o Gastrin o Histamine o CCK o Secretin |
|
|
Three secretagogues for acid secretion
|
- ACH
- Histamine - Gastrin |
|
|
Two antagonists for acid secretion
|
- Prostaglandin I and E
- Somatostatin |
|
|
What helps keep the mucous layer in tact?
|
Viscosity of the layer
|
|
|
What primarily makes up the mucous layer?
|
HCO3
|
|
|
What inhibits the secretion of mucous? (2)
|
- NSAIDs
- HCO3 |
|
|
Parasite that destroys the mucous layer
|
- H. pylori
|
|
|
What are slow waves in GI smooth muscle created by?
|
Interstitial cells
|
|
|
Which nervous system increases the amplitude of GI smooth muscle?
|
PSNS
|
|
|
Which nervous system decreases the amplitude of GI smooth muscle?
|
SNS
|
|
|
Where are slow waves absent?
|
Fundus
|
|
|
Where do AP spikes occur in plateaus of the slow waves? (2)
|
- Terminal antrum
- Pylorus |
|
|
Two hormones that stimulate gastric motility
|
- ACH
- Gastrin |
|
|
Hormone that inhibits gastric motility
|
NE
|
|
|
What does localized stimulation of the mucosa elicit? (2)
|
- Contraction above (oral) point of stimulation
- Relaxation below (aboral) point of stimulation |
|
|
What is receptive relaxation?
|
Stomach can accommodate a large increase in volume (stretch) without a significant increase in smooth muscle tension (intragastric pressure)
|
|
|
What is the largest rumen compartment for newborns?
|
Abomasum
|
|
|
Newborn calf
------------------ Rumen: 34% Abomasum: 56% |
Mature Cow
------------------ Rumen: 64% Abomasum: 11% |
|
|
What closes the esophageal groove?
|
Suckling reflex
|
|
|
What does the esophageal groove do?
|
Funnels liquid into abomasum
|
|
|
What bacteria type dominates the rumen?
|
G-
|
|
|
What kind of environment is the rumen?
|
Anaerobic
|
|
|
Three things the bacteria in the rumen do
|
- Help digest COHs
- Breaks up protein and lipids - Produces B vitamins |
|
|
What happens due to an increase in grain in diet? (3)
|
- G+ bacteria increases
- pH decreases - VFA increases |
|
|
Which protozoa have cilia all around? (2)
|
- Isotrichs
- Holotrichs |
|
|
Which protozoa have cilia on one end? (2)
|
- Oligotrichs
- Entodeiniomorphs |
|
|
Three general functions of protozoa in the rumen
|
- Buffers
- Detoxifies - Digests |
|
|
What contribution does saliva have to the rumen?
|
Increases pH
|
|
|
Where does most energy come from in the rumen?
|
VFAs
|
|
|
What is regurgitation?
|
Bringing cud into mouth
|
|
|
What is eructation?
|
Burping
|
|
|
Functions of the primary contractions
|
Mixes and stratifies
|
|
|
3 stimulants of contractions in the rumen
|
- Eating and chewing
- Cold - Low tension stretch receptors |
|
|
2 inhibitors of contractions
|
- Systemic disease
- Lack of stimulants |
|
|
Function of secondary contractions
|
Clears the cardia of fluid
|
|
|
What stimulates secondary contractions?
|
Distension of rumen
|
|
|
What part of the brain stimulates primary contractions of the rumen?
|
Medulla
|
|
|
What is normal rumen pH?
|
5.5 - 7.0
|
|
|
Function of rugae
|
Allows for stomach to distend
|
|
|
4 basic functions of stomach
|
- Short term storage
- Liquefication of food - Preduodenal digestion - Controlled release of chyme into duodenum |
|
|
What is the primary function of the proximal stomach?
|
Creates pressure in the stomach that helps move food
- Leads to gastric emptying |
|
|
3 functions of the distal stomach
|
- Creates strong peristaltic waves
- Acts as a grinder to liquefy food - Keeps pylorus tightly shut |
|
|
What's considered the 'housekeeper' of the GIT?
|
Migrating motor complex
|
|
|
When does the Migrating motor complex occur?
|
Interdigestive period
|
|
|
Where does the Migrating motor complex start?
|
Stomach
|
|
|
Two components of neural control of motility
|
- ENS
- ANS |
|
|
What digests proteins in preduodenal digestion? (2)
|
- Pepsin
- HCl |
|
|
Three species that digest lipids with gastric lipase
|
- Pigs
- Dogs - Cats |
|
|
Species that digests lipids with lingual lipase
|
Rats/mice
|
|
|
Two species that digest lipids with pharyngeal lipase
|
- Cattle
- Sheep |
|
|
What digests starch?
|
Oral amylase
|
|
|
What protects the stomach from digesting itself?
|
High HCO3- concentration in gastric mucous
|
|
|
What enzyme is important for H+ and HCO3- secretion?
|
Carbonic anhydrase
|
|
|
What drug class directly inhibits H/K ATPase pump?
|
Proton pump inhibitors
- Decreases amount of H+ excreted into lumen of stomach |
|
|
4 steps of pepsinogen synthesis
|
- Translation of mRNA at rER
- Internalization into rER and cleavage of a signal peptide - Transport into Golgi Apparatus for post-translational modifications - Excretion |
|
|
What activates pepsinogen?
|
Pepsin hydrolyzing the activation peptide at the active site
- Low pH allows access to the active site |
|
|
4 potential consequences of vomiting
|
o Hypovolemia
o Electrolyte imbalances o Aspiration pneumonia o Malnutrition |
|
|
What is antral contraction rate set by?
|
Interstitial cells
|
|
|
What is magnitude of antral contraction rate controlled by?
|
Chemically
|
|
|
What is the relationship of the antrum to the duodenum?
|
When antrum contracts, duodenum relaxes (and vice versa)
|
|
|
What mediates tone of the pyloric sphincter?
|
ACH
|
|
|
How fast do COHs empty?
|
85% within first hour
|
|
|
How quickly do fats empty?
|
Late, due to forming oily layer on top
|
|
|
How fast does protein empty?
|
Takes up to 4 hours on a linear curve
|
|
|
What is the endocrine portion of the pancreas?
|
Islets of Langerhans
|
|
|
What do beta cells release?
|
Insulin
|
|
|
What do alpha cells release?
|
Glucagon
|
|
|
What do delta cells release?
|
Somatostatin
|
|
|
Two portions of the exocrine pancreas
|
- Aqueous
- Enzymatic |
|
|
What does the aqueous exocrine pancreas portion do?
|
Rich in HCO3 to neutralize duodenal contents
|
|
|
What does the enzymatic exocrine pancreas portion digest? (3)
|
- COH
- CNH - Fat |
|
|
What two non-hormonal things increase enzymatic and aqueous activity of the pancreas?
|
- Vagal stimulation
- Pancreatic neuronal stimulation |
|
|
2 hormones that increase the enzymatic portion of the pancreas
|
- CCK
- ACH |
|
|
2 enzymes that increase the aqeuous portion of the pancreas
|
- Secretin
- ACH |
|
|
Which three enzymes are synergistic in regards to the pancreas?
|
- CCK
- ACH - Secretin |
|
|
During what phases does stimulation of the pancreas occur? (3)
|
- Cephalic
- Gastric - Intestinal |
|
|
Two ions in pancreas that are flow rate independent
|
- Na+
- K+ |
|
|
Two ions in the pancreas that are inversely related
|
- HCO3
- Cl- |
|
|
4 ions in the pancreas that are closely isotonic to plasma at all flow rates
|
- Na+
- K+ - Cl- - HCO3- |
|
|
What is pancreatic secretion stimulated by? (2)
|
- ACH
- Gastrin |
|
|
What's the major stimulus to pancreatic acinus?
|
CCK
|
|
|
What does secretin stimulate in the pancreas?
|
Extra-lobar ducts
|
|
|
What do the extra-lobar ducts in the pancreas produce?
|
Fluid that's high in HCO3-
|
|
|
What inhibits pancreas secretions?
|
Somatostatin
|
|
|
Two things that compete in proteolytic degradation
|
- CCK-RP
- Monitor peptide |
|
|
Three hormones that elevate IP3 and DAG to mobilize IC Ca++ in pancreatic acinar cells
|
- ACH
- CCK - GRP |
|
|
Two hormones that enhance adenyl cyclase activity to increase cAMP levels in pancreatic acinar cells.
|
- Secretin
- VIP |
|
|
How does somatostatin act on pancreatic acinar cells?
|
Inhibits secretion by decreasing cytosolic cAMP
|
|
|
What form must COH be in to be absorbed?
|
Monosaccharide
|
|
|
Three monosaccharides
|
- Glc
- Galactose - Frc |
|
|
Two disaccharides
|
- Lactose (Glc + Galactose)
- Sucrose (Glc + Frc) |
|
|
Cellulose
|
B - 1,4 linked Glc
|
|
|
Amylose
|
a-1,4 linked Glc
|
|
|
Which linked glucose form can monogastrics digest?
|
Amylose
|
|
|
Glycogen
|
Polysaccharide of Glc
|
|
|
What's the major short term energy storage?
|
Glycogen
|
|
|
Two biggest stores of glycogen in the body
|
- Liver
- Muscle |
|
|
Digestion of COH (5 steps)
|
- Starts in mouth
- Stops in stomach - Begins again in duodenum with secretion of pancreatic amylase - Oligosaccharidases break COH into monosaccharides - Monosaccharides are absorbed into intestinal epithelial cells |
|
|
Two components that are broken down by oligosaccharidases to monosaccharides
|
- a-limit dextrins
- Oligoasaccharides |
|
|
What is Glc and Gal transported into the brush border by?
|
SGLT1
|
|
|
How does Frc enter the brush border?
|
GLUT5 carrier via facilitated diffusion
|
|
|
How do all three monosaccharides leave the cell into the vasculature?
|
GLUT2
|
|
|
What does LPL do in regards to fats?
|
Directs chylomicrons into adipose tissue
|
|
|
What is the mother of all conversion enzymes?
|
Trypsinogen
|
|
|
Protein digestion (4 steps)
|
- Begins in stomach
- Continues in duodenum - Proteins are broken down into oligopeptides by pancreatic enzymes - Brush border enzymes convert oligopeptides into AAs, dipeptides, and tripeptides |
|
|
Two major sites of protein digestion
|
- Duodenum
- Jejunum |
|
|
What converts trypsinogen to trypsin?
|
Enterokinase
|
|
|
Two parts of the GIT that secrete enterokinase
|
- Duodenum
- Jejunum |
|
|
Three things the brush border enzymes convert oligopeptides into
|
- AAs (70%)
- Dipeptides and tripeptides (30%) |
|
|
How are di- and tri- peptides converted into AAs?
|
Cytosolic peptidases
|
|
|
3 reasons neonates can absorb antibody proteins
|
- Acid secretion is delayed
- Pancreatic function is delayed - Specialized intestinal epithelial cells capable of engulfing proteins are present |
|
|
Important enzyme in neonates for milk digestion
|
Gastric lipase
|
|
|
Where does emulsfication occur?
|
Duodenum
|
|
|
What causes emulsifcation? (2)
|
- Detergent action of bile salts
- Mechanical mixing |
|
|
What's the major source of fat digesting enzymes?
|
Pancreas
|
|
|
What forms micelles?
|
Bile acids
|
|
|
3 primary products of lipid degredation
|
- Free fatty acids
- Cholesterol - 2-monoacylglycerol |
|
|
4 things that form mixed micelles
|
- Free fatty acids
- Cholesterol - 2-monoacylglycerol - Bile salts |
|
|
What's the primary reason for micelles?
|
Allows lipid to be in solution in an aqeous environment
|
|
|
How are mixed micelles absorbed?
|
Mixed micelles migrate through unstirred layer
|
|
|
How are fatty acids and cholesterol absorbed?
|
Transport proteins
|
|
|
What binds the fatty acids within the cell?
|
Cytosolic fatty acid binding proteins
|
|
|
What binds cholesterol within the cell?
|
Sterol carrier proteins
|
|
|
How do chylomicrons leave the intestines?
|
Exocytosed into lacteals and then leave via lymph into thoracic duct
|
|
|
When is dietary lipid absorption complete?
|
Midjejunum
|
|
|
When are bile acids reabsorbed?
|
Ileum
|
|
|
Chylomicrons are directed into adipose tissue by what?
|
Lipoprotein Lipase
|
|
|
What do emetics work on centrally?
|
Chemoreceptor trigger zone (CTZ)
|
|
|
Two things emetics work on peripherally
|
- Duodenal receptors
- Pharynx |
|
|
How do anticholinergics work for anti-emetic action? (2)
|
- Block vagal afferents
- Block transmission from vestibular system |
|
|
How do anti-histamines work for anti-emetic action?
|
- Block transmission from vestibular system
|
|
|
How do centrally acting anti-emetics work? (2)
|
- Inhibits CTZ
- Inhibits vomiting center |
|
|
How do prokinetic anti-emetics work?
|
Enhance peristalsis in stomach without increasing secretions
|
|
|
4 forms of small intestine motility
|
- Segmentation
- Peristalsis - Contractile activity of muscularis mucosae - Electrical and contractile activity in SI |
|
|
How does segmentation SI motility work?
|
Closely spaced contractions of circular smooth muscle divides SI into small neighboring segments
|
|
|
What's the most frequent SI motility?
|
Segmentation
|
|
|
What does segmentation SI motility do from an oral to aboral direction?
|
Slows down
- Allows forward chyme movement to slow down to allow time for absorption |
|
|
How does contractile activity of the muscularis mucosae aid in motility?
|
Irregular contractions of muscularis mucosa causes a change in the topography of the internal surface of the GIT
|
|
|
How does contractile activity of the muscularis mucosae aid in absorption?
|
Irregular contractions of muscularis mucosa enhances contact between mucosal surface and contents of GIT
|
|
|
Two things that occur due to the contractile activity of the muscularis mucosae
|
- Emptying of central lacteals
- Increase of lymph flow |
|
|
Three things caused by APs eliciting strong contractions in the SI
|
- Major mixing of chyme
- Propulsion of chyme - Local segmentation and peristalsis |
|
|
What is the slow wave of contractile activity in the SI generated by?
|
Intrinsic factors
|
|
|
3 things that APs in SI motility can be modulated by
|
- ANS
- Intrinsic Nervous System - Hormones |
|
|
What does Relaxation of the SI do?
|
Moves electrical potential waves further from threshold
- Basal tone still won't be 0 though |
|
|
Three things that cause the Migrating Myoelectric Complex (MMC)
|
- Fasting in non-ruminants
- Fed and fasted ruminants - Ad libitum feeding of horses and pigs |
|
|
What is the Migrating Myoelectric Complex?
|
Bursts of intense electrical and contractile activity separated by longer periods of quiescence
|
|
|
Origin and end of Migrating Myoelectric Complex
|
O: Stomach
E: Terminal Ileum |
|
|
What is the 'housekeeper of the small intestines'?
|
Migrating Myoelectric Complex
|
|
|
What is the primary function of the Migrating Myoelectric Complex?
|
Sweeps bowel clean and empty its contents into the colon
|
|
|
What two things relax the ileocecal sphincter?
|
- Short range peristalsis
- Distension of terminal ileum |
|
|
What controls the rate of entry of chyme into cecum?
|
Ileocecal sphincter
|
|
|
What is the purpose of the ileocecal sphincter?
|
Controls the rate of entry of chyme into cecum
- Allows colon enough time to absorb water and salts |
|
|
What causes the ileocecal sphincter to contract?
|
Distention of cecum
|
|
|
What enhances ileal emptying after eating?
|
Gastroileal reflex
|
|
|
Three intestinal reflexes
|
- 'Law of the Intestines'
- Gastroileal reflex - Gastrocolic reflex |
|
|
What is the 'law of the intestines'?
|
When a bolus is placed in the small intestines, it typically contracts behind the bolus and relaxes ahead of it which propels the bolus in an aboral direction
|
|
|
What is the gastroileal reflex?
|
Elevated secretory and motor functions in the stomach increase the motility of the terminal ileum and accelerate movement into the cecum
|
|
|
What is the gastrocolic reflex?
|
After a meal, the motility in the proximal and distal colon is increased and the frequency of mass movements increase
|
|
|
Two functions of colonic contractions
|
- Mix chyme
- Circulate chyme across mucosal surface |
|
|
What type of contractions occur in the colon?
|
High amplitude propagating contractions
- Sustained contractions that push contents over a longer distance |
|
|
What kind of movement predominates in the proximal colon?
|
Antipropulsive patterns
- Reverse peristalsis and segmental propulsion toward the cecum |
|
|
Function of antipropulsive patterns in the proximal colon
|
Helps chyme be retained longer to facilitate reabsorption of water and salts
|
|
|
Effect of contractile agonists in the colon
|
Increases duration of the slow waves for sustained contraction
|
|
|
What is the internal anal sphincter innervated by?
|
Pelvic nn.
- Smooth m. |
|
|
What is the external anal sphincter innervated by?
|
Caudal rectal n.
- Striated m. |
|
|
Normal state of rectum
|
Empty
- Fills just before defecation |
|
|
What does filling of the rectum cause?
|
- Reflexive relaxation of internal anal sphincter
- Reflexive contraction of external anal sphincter |
|
|
What is impaired motility called?
|
Ileus
|
|
|
Two basic categories of ileus
|
- Mechanical (obstructive or dynamic)
- Functional (paralytic or adynamic) |
|
|
What type of ileus can be a post-operative complication?
|
Functional ileus
|
|
|
What is secreted in the duodenum?
|
HCO3-
|
|
|
What is absorbed in the jejunum? (5)
|
- Na+ (active)
- K+ (passive) - Cl- - HCO3- - H2O |
|
|
What is absorbed in the ileum? (5)
|
- Na+ (active)
- K+ (passive) - Cl- - Bile acids - B12 (cobalamin) |
|
|
What is secreted in the ileum?
|
HCO3-
|
|
|
What is absorbed in the colon? (2)
|
- Na+ (active)
- Cl- |
|
|
What is secreted in the colon? (2)
|
- K+ (if [K] > 25 mM)
- HCO3- |
|
|
Where is the highest rate of Na+ absorption?
|
Jejunum
|
|
|
Two things that enhance Na+ absorption
|
- Glc
- AA |
|
|
Where is the most water absorbed?
|
Jejunum
|
|
|
What does diarrhea do in regards to K+?
|
Decreases reabsorption due to increase in [K+]
|
|
|
In the colon, how does NaCl enter the cell?
|
Epithelial Na+ Channel (ENaC)
- Leaks into cell from lumen |
|
|
3 channels in colon enterocytes
|
- ENaC (Na in, lumenal)
- Na-K ATPase (Na out, basolateral) - K+ leak (out, basolateral) |
|
|
What is paracellular absorption of Cl- driven by in the colon?
|
Electronegativity created by Na+ absorption
|
|
|
What keeps Cl- leak channels in the SI and LI open?
|
cAMP
|
|
|
What is the consequence of increased cAMP in the SI and LI?
|
Large efflux of Cl- into lumen (accompanied by H2O and Na+)
- Causes secretory diarrhea |
|
|
Two types of diarrhea
|
- Secretory
- Malabsorptive |
|
|
When does secretory diarrhea occur?
|
When secretion increases and overwhelms absorptive capacity
|
|
|
What are most cases of secretory diarrhea caused by?
What's another way? |
Abnormal stimulation of SI crypts causing inappropriate secretion
Enterotoxins stimulating cAMP production |
|
|
When does a malabsorptive diarrhea occur?
|
When absorption is inadequate to recover the sufficient portion of water
|
|
|
What is the primary cause of a malabsorptive diarrhea?
|
Loss of GI epithelia
|
|
|
What is required for water absorption?
|
Nutrient absorption
|
|
|
How does Ca++ enter the cell in SI?
|
Leak channel
|
|
|
What happens to Ca++ in the cell? (2)
|
- Transported with Calbindin
- Transported in vesicles |
|
|
3 ways Ca++ leaves the cell
|
- Ca-ATPase
- Ca-Na Exchanger - Exocytosis of vesicles containing Ca++ |
|
|
What does vitamin D do in regards to Ca++? (2)
|
- Increases synthesis of calbindin
- Increases basolateral Ca-ATPase pumps |
|
|
What form must iron be in to enter the cell?
|
Fe++ (ferrous)
|
|
|
What reduces iron so it can enter the cell?
|
Iron reductase
|
|
|
What transporter allows iron into the cell?
|
Fe - H cotransporter
|
|
|
What happens to iron in the cytosol?
|
Oxidized to Fe+++ and bound to iron binding proteins
|
|
|
Why is Fe+++ bound to iron binding proteins in the cell?
|
Prevents it from forming insoluble complexes with anions
|
|
|
What transports Fe+++ across the basolateral membrane
|
IREG1/Hephaestin
|
|
|
What binds iron in the blood?
|
Transferrin
|
|
|
When is Iron Reabsorption protein bound?
|
When [Fe] is high
|
|
|
What determines how much iron can be trapped into a cell?
|
Apoferrin
|
|
|
What is Apoferrin used for?
|
Traps iron in cells so that the body can excrete iron by sloughing the cell
|
|
|
What does Iron Reabsorption Protein do? (2)
|
- Binds iron
- Regulates level of translation of proteins involved in iron reabsorption |
|
|
3 things inhibition of IRP causes
|
- Decrease in IREG1
- Decrease in Fe-H cotransporter protein - Increase in apoferrin |
|
|
Young animals more at risk of iron deficiency because they have fewer iron stores and high erythropoiesis rate since growing
|
Young animals more at risk of iron deficiency because they have fewer iron stores and high erythropoiesis rate since growing
|
|
|
3 conditions caused by iron deficiency
|
- Chronic hemorrhage
- Malabsorption problem - Dietary deficiency |
|
|
Where is Vitamin B12 absorbed?
|
Ileum
|
|
|
What's required for absorption of Vitamin B12?
|
Intrinsic factor (a dimer)
|
|
|
What produces intrinsic factor in dogs and cats?
|
Exocrine pancreas
|
|
|
What is required for absorption of Vitamin B12?
|
A dimer
|
|
|
What part of the horse's intestines have the largest diameter?
|
Right dorsal colon
|
|
|
Three things IRP causes
|
- Increase in IREG1
- Increase in Fe-H cotransporter protein - Decrease in apoferritin |
|
|
What inhibits IRP?
|
HIgh amounts of iron
|
|
|
What binds Fe+++ to prevent it from leaving the cell?
|
Ferritin
|
|
|
How much of the CO is delivered to the liver?
|
25%
|
|
|
How much blood supply does liver receive from portal vein?
|
70%
|
|
|
What does bile collect in?
|
Bile canaliculi --> bile ducts
|
|
|
Three ways that the liver regulates Glc
|
- Glycogen synthesis
- Glycogenolysis - Gluconeogenesis |
|
|
Review hormones and mechanisms associated with blood Glc homeostasis
|
Review hormones and mechanisms associated with blood Glc homeostasis
|
|
|
Two things that the liver does to fat
|
- Degredation of fatty acids
- Synthesis of fatty acids Can't do both at once |
|
|
Three things the liver can do with fatty acids
|
- Form triglycerides
- Form ketones - Utilize for energy via oxidation |
|
|
What enzyme processes Chylomicrons?
|
Lipoprotein Lipase
|
|
|
What is released from chylomicrons? (2)
|
- Glycerol
- FA |
|
|
4 things liver does to CNH
|
- Deamination of AAs
- Conversion of NH3 to urea - Synthesis of all non-essential AAs - Synthesis of all major plasma proteins |
|
|
What are Chylomicrons made up of?
|
Triglycerides
|
|
|
What are Micelles made up of?
|
Bile acids / salts
|
|
|
4 classes of lipoproteins
|
- Chylomicrons
- VLDL - LDL - HDL |
|
|
Two functions of Lipoproteins
|
- Keep component lipids soluble as they transport in the plasma
- Provides mechanism for transporting lipid to and from tissues |
|
|
When can triglycerides enter circulation?
|
After being incorporated into lipoproteins
|
|
|
When does fat accumulate in liver?
|
When rate of fatty acids being brought into liver is > rate of fatty acids leaving the liver
- Can be due to LPL impairment |
|
|
What's unique about nitrogen and the liver?
|
Only organ to process urea
|
|
|
What does the liver do in regards to urea?
|
Converts ammonia to urea
|
|
|
What can an increase in [urea] due to liver dysfunction do?
|
Cause hepatic encephalopathy
|
|
|
3 ways to manage hepatic encephalopathy
|
- Protein restricted diet
- ABs to reduce enteric urease producing flora - Lactulose |
|
|
What is the scientific name for Fatty Liver?
|
Hepatic Lipidosis
|
|
|
What causes hepatic lipidosis?
|
Expenditure of calories, causing fat production
|
|
|
What is contraindicated for treating hepatic lipidosis?
|
Corticosteroids
|
|
|
What causes pregnancy toxemia?
|
Inadequate nutrition during late gestation resulting from insufficient energy density of the ration and/or decreased rumen capacity as a result of fetal growth
|
|
|
What may result from pregnancy toxemia?
|
Ketoacidosis
- May smell like acetone |
|
|
Two treatments for Pregnancy Toxemia
|
- Remove source of Glc drain on ewe (suckling lamb)
- Correct energy and electrolyte imbalances |
|
|
Function of bile acids
|
Act as emulsifying agents to prepare lipids for degradation by pancreatic digestive enzymes
|
|
|
What synthesizes bile acids?
|
Liver
|
|
|
How do bile acids become bile salts?
|
Conjugated to glycine or taurine
|
|
|
What do dogs conjugate to form bile salts?
|
To taurine
|
|
|
What converts a bile salt to a bile acid so it can be reabsorbed?
|
Bacteria in the gut
|
|
|
Bile salts are better emulsifiers than bile acids
|
Bile salts are found only in the bile
|
|
|
What provides the only significant mechanism of cholesterol secretion?
|
Bile salts
|
|
|
What do bile and pancreatic secretions enter the duodenum via?
|
Sphincter of Oddi
|
|
|
Excretion of bile salts is very low in comparison to production
|
So majority is used, recycled, reabsorbed
|
|
|
What decreases de novo synthesis of bile acids?
|
Feeding more bile acids
- Increases portal blood levels |
|
|
What increases de novo bile acid synthesis?
|
Ileal resection
- Decreases portal blood levels |
|
|
What does the choleretic effect do?
|
Enhances secretion of bile acids
|
|
|
Reciprocal relationship exists between rate of de novo synthesis and rate of secretion of bile acids
|
Reciprocal relationship exists between rate of de novo synthesis and rate of secretion of bile acids
|
|
|
4 substances actively secreted into bile canaliculi
|
- Bile acids
- Phosphatidylcholine - Conjugated bilirubin - Xenobiotics |
|
|
6 substances passively secreted into bile
|
o Water
o Glc o Ca++ o Glutathione o AAs o Urea |
|
|
What is Na+ transported into the lateral IC spaces of the gall bladder via?
|
Na-K ATPase
|
|
|
What follows Na+ in the gall bladder to preserve electroneutrality? (2)
|
- Cl-
- HCO3- |
|
|
What causes osmotic flow of water from gall bladder lumen into IC space?
|
Hypertonic concentration of NaCl
|
|
|
Effect of water moving into IC space of gallbladder
|
Distension of IC space, increasing hydrostatic pressure causing ions and water to move across basement membrane of the epithelia to be carried away by capillaries
|
|
|
Net effect of bile duct epithelial transporters
|
Secretion of HCO3- rich fluid
|
|
|
Flow of Bile Acids (5 steps)
|
- Fatty meal is fed
- CCK stimulates contraction of gall bladder and release of bile - Bile salts mix with chyme to emulsify fats - Bile acids are reabsorbed in ileum - Port circulation delivers to the liver bile acids that were removed from circulation |
|
|
Two things that stimulate gall bladder contraction
|
- ACH
- CCK |
|
|
Two things that relax the sphincter of Oddi
|
- NO
- VIP |
|
|
Two processes that are involved with drug interactions that involve the cytochrome P450 isoforms
|
- Enzyme inhibition
- Enzyme induction |
|
|
Enzyme inhibition
|
Usually involves competition with another drug fro the enzyme binding site
|
|
|
Enzyme induction
|
Enzyme induction occurs when a drug stimulates the synthesis of more enzyme protein, enhancing the enzymes metabolizing capacity
|
|
|
What is bilirubin formed from?
|
Heme
|
|
|
What is used as a measure of liver function?
|
Bilirubin value
|
|
|
What is bilirubin excreted in?
|
Bile
|
|
|
3 major causes of icterus
|
- Hemolytic
- Obstructive - Hepatocellular |
|
|
What is hemolytic icterus?
|
Liver is overwhelmed by large amount of bilirubin and can't conjugate it fast enough
|
|
|
What is obstructive icterus?
|
Bile stasis
- Conjugated bilirubin will leak into circulation |
|
|
What is hepatocellular icterus?
|
Decreased conjugation due to damage/disease of liver
|
