GIT and nutrition Flashcards
How is glucose transported into the cells epithelial cells of the GIT?
by the mechanism of active sodium-glucose cotransport, in which active transport of sodium provides energy for absorbing glucose against a concentration dif- ference.
How is glucose transported into cells other than the GIT epithelial cells ?
facilitated diffusion, made possible by the special binding prop- erties of membrane glucose carrier protein.
What hormone increases the facilitated diffusion of glucose into the cells?
insulin - when larger amounts are secreted the transport of glucose increases 10 fold
Can the cells absorb enough glucose to allow for all essential metabolic functions in the abscence of insulin?
with the exception of liver and brain cells, without insulin too little glucose can enter the cells to supply the required energy for metabolism.
What is the cells carbohydrate utilisation rate determined by
insulin
What is the first step of glucose metabolism once the sugar enters the cell?
Phsophorilation by glukokinase in the liver and hexokinase in other cells -> glucose combines with a phosphate radical
In what tissues is glocose phosphorilation by glukokinase or hexokinase reversible?
iver cells, renal tubular epithelial cells, and intestinal epithelial cells. In thse cells glucose phosphatase can dephosphorylate the glucose
Once in the cell, what two pathways can glucose take metabolically?
1) it can be utulised for release of energy
2) can be stored as glycogen
Which cells are best at storing glycogen?
All cells can store some glycogen, however, liver (5-8%) and muscle cells (1-3%) can sote lare amounts
What is the molecular weight of glycogen and why ?
The glycogen molecules can be polymerized to almost any molecular weight, with the average molecular weight being 5 million or greater. This conversion of monosaccharides into a high- molecular-weight precipitated compound (glycogen) makes it possible to store large quantities of carbohydrates without significantly altering the osmotic pressure of the intracellular fluids. High concentrations of low-molecular- weight soluble monosaccharides would play havoc with the osmotic relations between intracellular and extracel- lular fluids.
What is glycogenesis and glycogenolysis?
Glycogenesis - formation of glycogen from excess glucose
Glycogenolysis - breakdown of stored glycogen to reform glucose
What is the role of phosphorylase in glycogen metabolism?
How is the function of this enzyme controlled?
The breakdown of glycogen into glucose occurs through severeal phosphorulation steps caused by phosphorylase.
Phosphorylase is usually innactive and has to be activated by cyclic-AMP which is formed by hormones such as glucagon or epinepherine
What is the role of epinepherine in energy metabolism?
with increased sympathetic tone, epinepherine is released from the adrenal medulla, where it forms intracellular cyclic-AMP which activated phosphorylase which kicks off glycogenolysis. This is essentiial in the muscle and liver to promote glucose formation which is needed in the flight and fight response
What is the role of glucagon in the production of energy ?
When glucose levels drop too low glucagon is released by the alpha-islets of the pancreas. This stimulates cyclic-AMP production intracellularly which activated phosphorylase inducing glycogenolysis
How many moles ATP are produced by one mole of glucose
38
What is glycolysis ?
The most important mean of releasing energy from glucose. This consists of 10 steps which result in the production of 2 pyruvic acid molecules for each molecule of glucose. Each pyruvic acid molecule will then enter its own Krebs cycle.
What is the transition step between glycolysis and Krebs?
The two pyruvate molecuse bind to Coenzyme A to form acetyl-coa which can then enter the citirc acid (aka Krebs) cycle.
what is the tricarbxylic acid cycle?
the same things as citric acid or krebs cycle
What is the krebs cycle and where does this occur?
The citric acid cycle is a sequence of chemical reactions in which the acetyl portion of acetyl-CoA is degraded to carbon dioxide and hydrogen atoms. These reactions all occur in the matrix of mitochon- dria. The released hydrogen atoms add to the number of these atoms that will subsequently be oxidized through the electron transport chain
How much hydrogen is produced in the krebs and glycolysis pathways and what happens to this ?
4 hydrogen atoms during glycolysis, 4 during formation of acetyl-CoA from pyruvic acid, and 16 in the citric acid cycle; thus a total of 24 hydrogen atoms are released for each original molecule of glucose. they are released in packets of two, and in each instance, the release is catalyzed by a specific protein enzyme called a dehydrogenase. Twenty of the 24 hydrogen atoms immediately combine with nicotinamide adenine dinucleotide (NAD+),
Why is niacin an essential vitamin ?
because NAD+ is a derivative of this
What is the electron transport chain and where is it ?
IT is in the mitocondria and does it do;
(1) split each hydrogen atom into a hydrogen ion and an electron and (2) use the electrons eventually to combine dis- solved oxygen of the fluids with water molecules to form hydroxyl ions. Then the hydrogen and hydroxyl ions combine with each other to form water. During this sequence of oxidative reactions, tremendous quantities of energy are released to form ATP.
How is ADP converted to ATP in the ETC?
ATP synthase, which protrudes through the mitocondrial membrane oxidatively phosphorylates the the ADP to ATP
What are the main factors that control the quantity of ATP that is produced by the ETC?
1) [ATP and ADP]
- high [ATP] causes phosphofrutokinase inhibition - glycolysis rate reduction. Vice versa for ADP
2) citrate ion in the krebs cycle; an eccess inhibits phosphofrutokinae preventing glycolysis
3) Excess ATP concentration will prevent further formatio until the store is depleted (except with strenous exercise)
Why is anaerobic metabolism not preferentially used?
This process is extremely wasteful of glucose because only 24,000 calories of energy are used to form ATP for each molecule of glucose metabolized, which represents only a little over 3 percent of the total energy in the glucose molecule.
Which of the following 3 can function in an anaerobic environement?
1) glycolysis
2) Krebs
3) ETC
Glycolysisas the formation of 2 pyruvate does not need O2
How is the anaerobic metabolism pathway kicked in?
Krebs and ETC cannot work without O2. At the end of glycolysis you end up with 2x pyruvate + 2 H+. These build up in concentration and can rate limit glycolisis through phosphofructokinase. When their concentration accumlates excessively the end products react with each other forming lactic acid
What is the benefit of lactic acid?
Lactic acid diffuses readily out of the cells into the extracellular fluids and even into the intracellular fluids of other less active cells. Therefore, lactic acid represents a type of “sinkhole” into which the glycolytic end products can disappear, thus allowing glycolysis to proceed far longer than would oth- erwise be possible.
Heart muscle is especially capable of converting lactic acid to pyruvic acid and then using the pyruvic acid for energy. This is beneficial in heavy exercise as large volumes of lactic acid are produced which can be used by th e heart for energy and is a salvage mechanisms during infactation
When a person begins to breathe oxygen again after a period of anaerobic metabo- lism, the lactic acid is rapidly reconverted to pyruvic acid and NADH plus H+. Large portions of these substances are immediately oxidized to form large quantities of ATP. This excess ATP then causes as much as three fourths of the remaining excess pyruvic acid to be converted back into glucose.
Other than glycolysis which other important first step pathway exists for energy metabolism;
Pentose phosphate patheway (phosphocluconate pathwy) which is responsibe for 30% of the glucose breakdon in the live and even more in the fat cells
why does the pentose pathway exist?
This pathway is especially important because it can provide energy independently of all the enzymes of the citric acid cycle and therefore is an alternative pathway for energy metabolism when certain enzymatic abnormalities occur in cells. It has a special capacity for providing energy to multiple cellular synthetic processes.
What key differece exists in hydrogen untilisation in the pentose phosphate pathway compared to glycolysis?
The hydrogen released during the pentose phosphate cycle does not combine with NAD+ as in the glycolytic pathway but combines with nicotinamide adenine dinucleotide phosphate (NADP+), which is almost identical to NAD+ except for an extra phosphate radical, P. This difference is extremely significant because only hydrogen bound with NADP+ in the form of NADPH can be used for the synthe- sis of fats from carbohydrates - hence why this pathway is common in fat cells
What happens to the pentose pathway when glycolysis is downregulated due to cellular innactivity ?
he pentose phosphate pathway remains operative (mainly in the liver) to break down any excess glucose that continues to be transported into the cells, and NADPH becomes abundant to help convert acetyl-CoA, also derived from glucose, into long fatty acid chains. This is another way in which energy in the glucose molecule is used other than for the formation of ATP—in this instance, for the formation and storage of fat in the body.
What is excess glucose stored as?
Glucose is prefer- entially stored as glycogen until the cells have stored as much glycogen as they can—an amount sufficient to supply the energy needs of the body for only 12 to 24 hours.
When the glycogen-storing cells (primarily liver and muscle cells) approach saturation with glycogen, the addi- tional glucose is converted into fat in liver and fat cells and is stored as fat in the fat cells.
what is gluconeogensis ?
When the body’s stores of carbohydrates decrease below normal, moderate quantities of glucose can be formed from amino acids and the glycerol portion of fat. This process is called gluconeogenesis.
During prolonged fasting which processes mantain glucose levels?
Gluconeogenesis breaks down fats. kidneys also synthesize considerable amounts of glucose from amino acids and other precursors.
About 60 percent of the amino acids in the body proteins can be converted easily into carbohydrates; the remaining 40 percent have chemical configurations that make this conversion difficult or impossible.
What is the role of corticotropin and glucocorticoids on gluconeogenesis?
When normal quantities of carbohydrates are not available to the cells, the adenohypophysis, for reasons not completely understood, secretes increased quantities of the hormone corticotropin. This secretion stimulates the adrenal cortex to produce large quantities of glucocorticoid hormones, especially cortisol. In turn, cortisol mobilizes proteins from essentially all cells of the body, making these proteins available in the form of amino acids in the body fluids. A high proportion of these amino acids immediately become deaminated in the liver and provide ideal sub- strates for conversion into glucose. Thus, one of the most important means by which gluconeogenesis is promoted is through the release of glucocorticoids from the adrenal cortex.
What is the normal Bg of a person?
90mg/dl during fasting, 140mg/dl after a large meal.
what are the layers of the GIT ? what do these look like on US?
Same throughout;
- Mucosa (hypoechoic)
- Submucosa (hyperechoic)
- Muscularis (Hypoechoic)
- Serosa (hyperechoic)
what are the 4 major activities of the GIT?
1) motility = moving food from mouth to rectum
- mixes and reduces size of food
- rate is regulated to optimize digestion and absorbtion
2) secretions = juices from dalivary gland, pancreas and liver added to GI tract
- enzymes, electrolytes, fluid and mucus
3) Digestion -= food digested into absorbable molecues
4) absorbtion - nutrients, electrolytes, H20 are absobed from the lumen to the blood stream
What are the main regulators of function?
- innervation
- hormones
- autocrine secretions
- neurocrine secretions
What nerves innervate the GIT
1) Autnomic
- extrinsic
2) extrinsic component
- sympathetic
- parasympathetic
3) intrinsic
- enteric nervous system
what is the 2 key parasympathetic nerves of the git.
Are these efferent or afferent?
What stilmutea these nerves ?
What do they do?
What types of postganglionic neurons do they have ?
Two key nerves;
1) vagus
2) pelvic
VAGUS
Mainly afferent - take sensory info from mechano/chemo receptors to CNS
Some efferent = take motro info from CNS to muscle/secretory/endocrine cells
Two types of postganglionic neurons
1) peptodergic - release peptides like substance P or VIP
2) cholinerci = relese ACh
What does parasympathetic mean?
Long preganglionic nerve fibers which synapse on ganglia in the GI walls. Remeber parasympathetic is a longer word than sympathetic hence long ganglia
what are the 2 types of parasympathetic post ganglionic neurons
Two types of postganglionic neurons
1) peptodergic - release peptides like substance P or VIP
2) cholinerci = relese ACh
what is the sympathetic innervation of the GIT
What are the 4 sympathetic ganglia?
Is this afferent or efferent ?
short preganglionic neurons which synapse on ganglia outside of the GIT (sympathetic is shorter than parasympathetic, hence, shorter ganglia.
The 4 sympathetic ganglia are; Celiac, superior mesenteric, inferior mesenteric, hypogastric
The postganglionic fibers (release NE) then synapse on the plexus or directly on smooth muscle, endocrine or secretory cells
Sympathetic innervation is 50:50 efferent:afferent
what are the 4 sumpathetic ganglia?
Celiac, superior mesenteric, inferior mesenteric, hypogastric
what proportion of the Sympathetic innervtion of the GI tract is afferent or efferent
it is 50:50
draw a diagram of the GIT extrensic nervous system, what it secretes and where ?
What is the enteric nervous system?
this is the intrinsic NS.
Can direct all functions of the GI tract in abscence of the extrensic. It is modulated by para and sympathetic innervation
It is enterely in plexuses.
Tabulate all of the GIT neurocrines, the source of the these and what their actions are?
what are the 3 main categories of GI peptides
1) hormones -> endocrine cells of GIT - substances secred into the portal system, picked up by the liver and then go and work on cells elsewhere
2) pacrines -> endocrine cells of GIT but their target cell is close and they reach this by diffusion
3) neurocrines -> nerve cells that are transported by an action potential
what are the 4 main GI hormones ?
1) gastrin
2) cholicystokinin
3) secretin
4) glucose dependent insulinotropic peptid (also known as gastric inhibitory peptide or GIP)
what is a candidate hormone and what are examples (less important question)
Molecules that don’t met all of the criteria of what a hormone is;
- Motalin, pancreatic polypeptide, serotonin, somatostatin, ghrelin, leptin, GLP-1, GLP-2, enteroglucgon, peptide YY
tabulate the GI hormones, what family they belong to, site of secretion, stimulus of secretion and action
Describe the key features of gastrin;
Cells secreted from?
Stimuli for production?
Actions?
secreted by G cells in the stomach. when a meal is eaten.
- Stimuli for production are; are products of protein digestion (as), stomach distension, vagal stimulation, neuroen docrine-releasing peptide (bombesin)
- Stimuli for decreased production are; low pH, hastric contents, somatostatin
Actions
1) stimulates H+ secretion by gastric parietal cells (makes stomach more acidic)
2) stimulates growth of gastric mycosa
what is a gastrinoma?
What are the symptoms of this
gastrin secreting tumour usually in non-B cell pancrease -> results in increased H+ secretion by parietal cels, get ulcer, antral hypertrophy and statorrhea/diarrhoea (excessive gastrin inactivates lipase)
why is low pH an inhibitor of gastrin ?
hastrin secretes H+ so once the stomach is acidic enough it will inhibit the production of more acid as its not needed
if you suspect a gastrinoma what test could you run and what are the limitations ?
Texas A&M can measure gastin. 0.5 ml fasting (12-18 hours) non-hemolyzed serum
The reference interval for serum gastrin concentration in dogs using this assay was established as <28 ng/L, but most normal dogs will have undetectable serum gastrin concentrations. The test is recommended in chronic vomiting where there is suspicion of a gastrinoma. Until a more precise cut-off value for the diagnosis of a gastrinoma can be determined, recommend using the traditional cut-off value of 10 times the upper limit of the reference range, or >280 ng/L.
Can proton pump inhibitors affect gastrin secretion and testing ?
Giving PPI results in hypergastrinemia in chronic enteropathies, but the levels do not reach those where you may get a false positive result for a gastrinoma on the texas A&M test (ie recomended cut off is 10x the reference interval for gastrinoma)
what is the role and stimuli of secretion for cholcystokinin (CCK)?
What cells secrete this? And where?
What receptors does this bind to?
Stimuli of secretion?
Essential for fat digestion and absorbtion. It looks like gastrin and will have some gastrin activity.
2 receptors;
- CCKa–only recognises CCK
- CCKb- recognizes CCK and gastrin
Secreted by I cells of the duodenum and jejunal mucosa
Stimuli of secretion; monoglycerides and fatty acids, small peptides and AAs (aka fats and proteins)
End goal = make sure that the right pancreatic enzymes + bile salts are secreted to aid in digestion and absorbtion
what are 5 main actions of CCK ?
1) contract the gallbatter and relaxation of the sphincter of Odi -> ejection of bile - > essential for emulsification of fat
2) Secretion of pancreatic enxymes (lipase, protesase and amylase)
3) Secretio fo bicarb from pancreas
4) growth of exocrine pancreas and GB
5) inhibit gastric emptying (fat takes a LONG TIME to be digested)
what are amylases, proteases and lipases
Amylase -> break down varbs
Protease -> break down protein
Lipase -> break down fat
What is the secretin ?
Secreted by S cells of the duodenum (S for Secretin)
Funciton to promote secetion of pancreatic and billiary HCO3 -> which neutralises H+ in the SI (don’t want all the stomach acid produced by a gastrin to break down food in the SI).
Secretin is inhibited by the effects of Gastrin on parietal cells (turns off H= secretion and tissue growth)
why is secetin essential for fat digestion when fat requires a lot of digestion to be broken down?
Bicarb is needed for fat digestion as pancreatic lipase works best between pH of 6-8, and lipases do NOT work if pH<3. Without this the pH would be too low from gastrin
what are parietal cells;
Parietal cells, also known as oxyntic cells, are specialized epithelial cells found in the stomach lining. They play a crucial role in gastric acid secretion, which is essential for digestion
what is the role of glucose-dependent insulinotropic peptide (GIP)?
What are its functions?
Where is it secreted from?
One of the 4 fondamental GIT hormones
Secreded by K cells of the duodenum and jejunum. Secreted in response to glucose, AA, and FA.
Functions;
1) stimulation of insulin secretion by B-cells (referred to as an incretin because it stimulates insulin secretion)
2) inhibition of gastic H+ secretion
3) inhibition of gastric emptying
Why is PO glucose better utilised than IV ?
when you injest glucose, you have release of glucose-depndent insulinotropic peptide (GIP). This promotes insulin secretion from the ß cells allowing the glucose to be uptaken by the cells.
Iv glucose will only result in insulin seretion when this directly binds ß-cells in the pancreas
What is role of motilin?
this is a cadidate hormone secreted by the duodenum during fasting and increases GII motility and initiates interdigestive myoelectric complexes
What are the two main GI paracrins?
1) somatostatin
2) histamine
From secretion, how do paracrins reach the target tissue;
via capillaries and act locally. They travel short distances and do NOT enter the systemic circulation
What is the role of somatostatin?
SOMATOSTATIN SHUTS IT DOWN - key buzz phrase to remember
Inhibits hormone release, especially insulin, glucagon, growth hormone, tsh. It also reduces GIT motility and secretion
SECRETED by D (down) cells of the GI mucosa in response to decreased lumen pH. Also (less important) by the hypothalamus and by delta endoctine pancreatic cells
INHIBITED by; secretion of other GI hormones and inhibits gastric H+ secretion
what is the role of histamine?
What cells secrete this?
sereted by enterochromaffin like cells (H+ secreting region of the stomach)
Histamine (along with gastrin) stimulates H+ secretion by gastric parietal cells (bind H2 receptor)
where are enterochomaffin like cells found?
in the acid secreting region of the stomach
What are the main GI neurocrines?
Acetylcholine and norepinepherin
What is the major area of the body responsible for the regulation of satiety?
Hypothalamus
- satiety center -> inhibits appetite even in the presence of food
- Feeding center -> increases appetite
- Arcuate nucleous of the hypothalamus gives info to these centers via anorexigenic and oregigenic neurons
What are the main signalers of appetite ?
- POMC (proopiomelanocortin) -> decreases appetite -> released by anorexigenic neurons
- Neuropeptide Y -> increases appetite
->relesed by orexigenic neurons
What substances influence apetite:
KEY ONES YOU MUST KNOW FIRST
1) Leptin -> DECREASE appetite and INCREASES energy expenditure (Leptin-LEss of an aPeTIte Now, and LiPid cells secrete leptin in proportion to the amount of fat stored in adipose)
2) Insulin -> similar to leptin -> DECREASES eppetite
3) Ghrelin -> INCREASES apetite and food intake
LESS IMPORTANT AND SECONDARY
GLP-1; DECREASES appeite
Peptide YY (PYY): DECREASES appetite
Why would insulin decrease appetite?
insulin is secreted when there are plenty of available nutrients, and as a result more is not needed, hence its role in supressing appetite
Ghrelin secretin occurs when and how?
What is a key stimulator of Ghrelin?
secreted by gastic cells BEFORE ingestion of a meal. It stimulates orexigenic neurons and inhibits the anorexigenic neurons. It is stimulated by weight loss and starvation
what is a stimulus for leptin secretion and where does it act?
Sensed fat level -> leptin secreted by fat cells -> crosses BBB -> acts on arcuate nucleous of hypothalamus -> stimualtes anorexigenic neurons and inhibits orexigenic neurons
Of the 5 appetite influencing substances, which decrease appetite and which ones increases it?
Ghrelin is the ONLY INCREASOR
Leptin, insulin, GLP-1 and Peptide YY ALL DECREASE `
How can we stimulate hunger in patients and what pathway does this take?
Entice is a ghrellin receptor agonist which stimulates hunger and food intake in patients
What is the role of kidney disease in hunger control;
recent study has shown an increase in adoponectin and leptin in dogs with non proteinuric kidney disease which may exacerbate weight loss through reduced food intake
The GIT tract is made of what muscle type?
All is smooth muscle except the larync, cranial esophageal sphincter and parts of the oesephagous and external anal sphincter
Glucose and galactose are transported from the intestinal epithelial cells to the blood by facilitated diffusion through what transporter?
a) GLUT 2
b) GLUT5
c) SGLT1
d) SGLT2
a) glut 2
Trypsin is made into active trypsin by what important brush border enzyme?
Enterokinase
Lipase
Pepsinogen
Phospholipase A2
enterokinase
Pancreatic lipase is secreted as an active enzyme and hydrolyzes _________ to ___________ and ____________.
1 triglyceride molecule; 1 monoglyceride molecule; 2 fatty acid molecules
1 amino acid; 1 cholesterol; 1 fatty acid molecule
1 phospholipid molecule; lysolecithin; 2 fatty acid molecules
1 chylomicron molecule; 1 phospholipid molecule; 1 apoprotein molecule
1 triglyceride molecule; 1 monoglyceride molecule; 2 fatty acid molecules
what is the orientation of the muscle fibers in the GIT and why?
External layer is longitiudinal while internal is circular -> this allows for peristalsis to occur as the tissue milks the food aborally. The longitudinal layer crunches the intestine togeter while the circular propels the chyme forward.
what are the two types of muscle contraction ?
1) phasic (tension goes up and then relaxes in a wave like form) -> this occurs in the oesophagous, gastric antrum - aka places than need to mix and propel food forward
2) Tonic contraction (constant contra`ction without relaxation) -> occurs in orad stomach, LES, illeocolic sphincter, internal anal sphincter (ie sphincters should be closed until they are told to relax)
How do sphincters stay closed?
Specialised circular muscle - at rest they maintain a higher pressure than the adjacent regions thereby staying closed and preventing flow. For something to move past, the sphincter must relax
What are slow waves in the muscles of the GIT?
These are oscillating depolarization and representations of t›he smooth muscle cells. These are not true depolarization though. These are sub-threshold depolarization which allow the muscle to maintain its rigidity in a closed position, ie tonic contraction.
Waves that meet/exceed threshold result in phasic contraction
where do slow waves originate from ?
Interstitial celss of Cajal
what is the intrinsic rate of slow action potentials?
3-12 slow waves sets the frequency of AP’s thus contractions
other than the git where are slow waves found?
Nowhere else
what ion channels are involved in slow wave depolarisation and repolarisation ?
Depolarisation -> opening of Ca channels which causes Ca to enter and depolarise the membrane
Repolarisation -> opening of K channels and outward K current
if there is a slow wave, can depolarisation happen?
yes, depolarisation happens when the slow wave hits the membrane potential
What are the 3 phases of pharyngeal motility?
1) prehension -> with teeth and tongue
2) Mastication -> breaking food down and coating with saliva
3) Deglutition -> rostral to caudal pharyngeal contractions propel food bolus to the base of the tongue to cricopharyngeal/cranial esophageal sphincter opening
a) sphincter relaxes
b) bolus pases into cranial esophageal body
c) cranial esophageal sphincter contract and pharyngral muscles relax
what are the major nervous system structures involved in Oropharyngeal motility?
Medulla, vagus and glossopharyngeal
Is swallowing voluntary or involuntary
initially voluntary but once in the oropharyngeal area it is involuntary
abnormalities in the oropharyngeal phases results in what clinical findings ?
What are the two mechanisms of disease for oropharyngeal disease ?
Two main clinical signs are dysphagia and hypersalivation.
Two mechanisms can be;
1) functional -> mainly neuromuscular
2) Morphological -> strictures, FBs, neoplasia, trauma, inflammation of the oral cavity and pharynx
fill in the clinical signs and disease location table
what type of muscle makes up the oesophageal sphincters and oesophagous
UES (upper es sphinc) = crycopharyngeal is striated
esophageal body in dog is all striated. In cat 1/3 to 1/2 distal is smooth. Lower oesophageal sphincter = gastroesophageal is smooth
What is the name for the upper and lower esophageal sphincter?
UES= crocopharyngeus
LES= Gastroesophageal
(VI) what nerve innervates the oesophagous and the sphincters ?
vagus
Somatic branches -> glossopharungeal, pharyngeal and recurrent laryngeal (these innervate striated muscle)
Autonomic branches -> innervate smooth muscle
what is primary and secondary peristalsis ?
swallowing triggers primary which moves the food back and that kicks off sec
What is esophageal dismotility
This is when there is lack of synchronization between swallowing, primary and secondary peristalsis, and sphincter opening
Hallmark of esophageal dysmotility ?
Regurgitation!!
Also, painful swallowing, dysphagia, multiple swallowing attempts, excessive salivation, changes in appetite
What are the 5 distinct anatomical compartments of the stomach ?
1) cardia
2) fundis,
3) body
4) antrum
5) pylorus
How many layers of muscle are there in the stomach, what is their thickeneses, and what is the origtantion and name
1) Outer longitudial
2) Middle circular
3) Inner oblique
Thickness of the muscle increases from proximal to distal
what are the regions of the stomach on the image ?
How many and what are the physiological stomachs?
What are the roles of these section ?
What anatomical parts of the stomach make up these physiological sections and what are distinguishing features
there are 2
1) Proximal (orad) - cardia, fundus and first 1/3 of body
- has TONIC contractions (contracts until told to relax)
- thin wall
- Responsible for receptive relaxation which allows food to accumulate -> mediated by vagus and VIP
2) Distal (Caudad)- antrum, pylorus and second 2/3rd of the body
- has PHASIC contraction
- Thick wall
- Responsible for mixing and digestion of food
- Contractions push food into the SI
1)why does the distal physiologic stomach have phasic contraction?
2) why does proximal have tonic contractions
2) so that it can milk food into the SI.
2) it just needs to relax so that it can accomodate food
what are the 3 components of gastric motility?
1) relaxation of orad stomach - to receive food
2) contraction - help mix food
3) gastric emptying
(VI) the orad stomach relaxes in response to what nerve?
the vagus nerve and VIP
contraction phase of the stomach is determined by what? how often does it contract?
what hormones and neurons effect this?
Slow waves affect this. They are not affected by neurons or hormones. They contract at 3-5 waves/min=3/5 contractions per minute
during contraction of the stomach, why is all of the food not extruded into the intestine in one go? what allows for trickling of food out into the SI
The slow waves (3-5min) cause contractions, but each wave also causes the pyloric sphincter to contract. As a result, the waves of peristalsis and food bolus are interrupted by the sphincter being forced shut
(VI) How does neural input and hormonal input impact gastric contraction action potential frequency and force?
- Parasympathetic stimulation, gastrin, motalin = increase the frequency of action potentials and force of gastric contraction(i.e. when you are RESTING and DIGESTING)
- Sympatheric stimulation, secretin and GIP =DECREASE the frequency of action potentials and force of contraction (when fighting you are not digesting
why are secreting and GIP upregulated in sympathetic stimulation ?
Secretin and GIP are important for digestion that occurs in the SI, and thus they don’t want more gastric material until thats occurred
what are migrating myelotric comprexes (MMC)?
These are sfasting periodic contractions mediated by motalin. The role of these is to clear the stomach of any residual material.
They are only found in dogs
what are myoelectric spike complexes?
These are weaker versions of MMC’s, and consist of weaker migrating complexes found in cats and rabbits.
what steps have to occur during gastric emptying?
1) need to allow for neutralisation of gastric H+ in the duodenum
2) Neetd to allow time for adequate digestion and absorbtion
how is the rate of gastric emptying vary based on the type of nutrient, density of the nutrient, and acidity ?
List from fast to slow
Liquids»_space; solids»_space; indigestible solids
Carbohydrates»_space; proteins»_space; lipids
Neutral pH» acidic/alkaline (rare for it to be alkaline due to the acid in the stomach)
how does temperature affect gsastric emptying?
Hot and cold are slower than body temp
What are the 2 MAJOR factors that slow gastric emptying?
What physiological responses are there in response to this?
1) FAT - it takes time to digest fat. CCK is involved in digesting fat, and when there is a lot of fat, CCK is upregulated. CCK will then slow down gastric emptying
2) low pH (lot of H+); this has to be neutralised as low pH deactivates enzymes. Receptors in the duodenum sense low pH -> allows pancreatic HCO3 to neutralize which is essential for pancreatic enzyme function
what are the 3 main roles of the SI?
1) mix enzymes and bicarb with chyme
2) expose nutrients to the mucosa for absorbtion
3) move unabsorbed material to the LI
Where do slow waves occur?
stomack
SI - > these are a bit faster
What hormone regulates slow waves and MMC?
No hormones regulated slow waves
MMC are regulated by motalin
what drugs are used for increasing interstinal motility and how does these work ?
Erythromycin and azithromycin are motil analogues which increase migrating myelogenic complexes (MMC).
What is the nervous control of SI motility
Parasympathetic -> vagus
Sympathetic-> from ganglia
Enteric nervous system - > regulates the pattern of contraction
what is segmented vs peristaltic contraction?
Segmented- > acts to mix chyme and enxymes and does not move food forward (crashes and relaxes)
Peristaltic -> wave moves oral->aboral moving food forward
(VI) what causes the segmented and peristaltic contractions?
1) ECL (enterochromaphin like cells) in the intestinal mucosa sense bolus
2) 5-HT (serotonin) is released -> peristaltic reflex starts
3) behind the bolus; excitatory neurotransmitters ( ACh, Substance P, neuropeptide Y) cause contraction
4) in front of bolus: inhibitory signals (VIP, NO) cause relaxation
why does maropitant have visceral analgesic properties?
It is a substance P inhibitor. When there is a bolus of food, we have exitatory neurotransmittor release (substance P, neuropeptide Y, ACh) which cause contraction -> the stronger the contraction the more pain
where is the vomiting center?
medulla of the brain - collects info from a lot of places whcih can cause vomiting like medulla, stomach, SI, chemoreceptor trigger zone etc.
what physiological differences are there in vomiting and wretching?
Both coordinated by the medulla;
Vomiting = LES and UES are open
Wretching= LES open but UES CLOSED -> the contents as a result cannot pass past the UES hence nothing is vomited out
what is the role of the large intestine ?
What segments is this divided into ?
What are the distinguishing charachteristics of the waves of peristalsis in this region?
1) extract water and electrolytes
- proximal colon -> slow and weak contractions to allow for absorbtion
2) controls defecation
- descending colon -> fast and strong contractions to push faeces out
what are haustration contractions in the proximal colon?
Do they happen in the distal colon ?
These are segmental contractions. They break up the bolus so that it is exposed to the mucosa of the ascending colon so that water can be absorbed.
These can happen in the distal colon but this is mostly to break up the bolus so that it does not arrive all at once
what are the steps that occur in defecation ?
1) rectum fills with faecal material -> smooth muscle contracts and internal anal sphincter relaxes (rectosphincter reflex) -> this is a true sphincter
2) External anal sphincter still contracted (is striated muscle and under voluntary control) this no defecation until time permits -> this is under voluntary control!
What is the gastrocolic reflex?
distension of the stomach increases motility of the colon. Mediated by CCK and gastrin
what is the rectosphincter reflex?
it is a reflex where dilation of the smooth muscle of the recutm contracts and the internal anal sphincter relaxes.
This will not allow defecation as the external anal sphincter is under voluntary control
(VI) n the gastrointestinal tract, slow waves are a unique characteristic that provides tonic contraction of the smooth muscle. At the peak of the slow wave, if the membrane potential is maximally depolarized and meets threshold, an action potential occurs. Depolarization is caused by opening of what channels?
A) Calcium channels
B) Chloride channels
C) Potassium channels
D) Sodium channels
a
(VI) During peristaltic contractions in the small intestine, what substance contributes to relaxation of the intestinal smooth muscle in front of (aborad) the food bolus?
A) Acetylcholine
B) Neuropeptide Y
C) Substance P
D) VIP
VIP
(VI) Pick if the below substances increase or decrease appetite.
A) Leptin: DECREASES/INCREASES appetite
B) Insulin: DECREASES /INCREASES appetite
C) GLP-1: DECREASES/INCREASES appetite
D) Ghrelin: DECREASES/INCREASES appetite a
E) Peptide YY (PYY): DECREASES/INCREASES appetite
A) Decrease
B) Decrease
C) Decrease
D) Increase
E) Decrease
ONLY GHRELLIN INCREASES
(VI) Pick the correct neurotransmitter.
Postganglionic neurons of the parasympathetic NS within the GI tract release peptides or (ACETYLCHOLINE / NOREPINEPHRINE)
Postganglionic neurons of the sympathetic NS within the GI tract release (ACETYLCHOLINE / NOREPINEPHRINE)
1) ACETYLCHOLINE
2) NOREPINEPHRINE
Main secretion organs of the GIT?
Salivary glands
Gastric mucosa
Exocrine pancreas
Liver
Fill in the secretion table
2 major types of salivary secretion
Serous = alpha-amylase to start digestion of starches, water, ions, electrolytes
Mucous = lubrication
name the 3 salivary glands ?
What type of saliva do they secrete
Parotid = serous secretion only
Submandibular = mixed → serous and mucous
Sublingual = mixed → serous and mucous
What is the innervation of the salivary system and what determines secretions?
Salivary glands have BOTH parasympathetic and sympathetic control!
Parasympathetic dominates but saliva production is stimulated by BOTH
Parasympathetic innervation of the salivary glands is performed by which nerves and what effect does this have ?
When parasympathetic in control = increased flow rate
- Facial and glossopharyngeal CNs
- Postganglionic parasympathetic neurons release ACh which interacts on muscarinic receptors
Sympathetic innervation of the salivary glands occurs due to which nerves and what effect does this have?
When sympathetic in control = more viscous (thicker), high in protein
Innervation from T1-T3 segments
Postganglionic sympathetic neurons release NE which talks to B-adrenergic receptors
draw a schematic of the regulation of saliva secretion
Describe the cellular structure of the salivary gland and what each cell type does;
Acinar cells: make initial saliva which is water, ions, enzymes, mucus
Intercalated duct (just a tunnel)
Striated duct: lined with ductal cells which MODIFY the saliva (Na and Cl removed, K and HCO3 added)
Myoepithelial cells = eject the saliva
(VI) describe the formation of saliva;
1) Acinus makes initial isotonic fluid – has approximately the same lytes as plasma
2)Ductal cells modify initial saliva
a) 3 transporters in lumen: Na-H exchange, Cl-HCO3 exchange, and H-K exchange (HCO3, K, and H out, while Cl, Na, H in)
b) 2 channels in basolateral membrane
i) Na-K ATPase
ii) Cl channel
3) NET EFFECT = NaCl absorption and secretion of K+ and HCO3- (NaCl greater)
4) Final product = hypotonic b/c ductal cells are impermeable to water
(VI) How does flow rate affect the composition of saliva?
High flow rates - no time to alter saliva so it looks like it did when the acinar cells made it;
- higher concentration of NaCl (less time to reabsorb it!)
- lower concentration of K (less time to secrete it!)
Low flow rate - lots of time to modify the saliva
- lower concentration of NaCl (more time to reabsorb it!)
- higher concentration of K+ (more time to secrete i!)
**Bicarb doesn’t listen to this! Remember it’s secreted by ductal cells thus you’d think its concentration should be high at low flow rates…but it’s concentration is lowest at low flow rates and highest at high flow rates b/c secretion of bicarb is selectively stimulated when saliva production is stimulated. So more flow rate = more HCO3 - secretion
$
(VI) Describe the two gland times involved in gastric secretions and what cells make up each section?
Oxyntic glands = in body of stomach
- Parietal cells = Secrete HCl and intrinsic factor
- Chief cells = Secrete pepsinogen
Pyloric glands = in antrum of stomach
- G cells = Secrete gastrin into circulation
- Mucous neck cells =Make Mucus, HCO3-, and pepsinogen
Draw a table and diagram of the location of the cell gastric secretion cell types, location and secretion
(VI) what cells secrete HCL
Parietal cells
(VI) what is the role of HCL in the GIT?
make very acidic environment so pepsinogen (made by chief cells) can become pepsin (starts protein digestion)
(VI) what cells produce and what is the role of pepsinogen?
Pesinogen is made by chief cells and with exposure to acid it can become pepsin which starts protein digestion
(VI) what is the mechanism of HCL secretion by parietal cells?
1) H+ secreted into lumen via H+K+ ATPase
2) HCO3- is absorbed into the blood
NET EFFECT = secretion of HCl (into stomach lumen) and absorption of HCO3- into blood
(VI) How do proton pump inhibitors work?
PPIs block H+K+ATPase in the parietal cells. This proton pump is what secretes HCL into the stomach
What is an alkaline tide?
Post eating a meal, the blood pH becomes more alcaline as HCO3 is secreted into the blood stream.
(VI) Parietal cells secrete HCO3 into the circulation when acidifying the stomach. where is this HCO3 produced
HCO3 is a byproduct of H+ production by the parietal cells. The parietal cells have carbonic anyhydrase which produces H2HCO3 from CO2+H2O, after which one hydrogen ion is cleaved off, secreted into the lumen of the stomach, leaving HCO3 behind that is then secreted into the blood via the HCO3-Cl cotransporter
(VI) What Alters HCl secretion by PARIETAL cells? KNOW THIS.
1) Histamine - INCREASES HCl secretion
a) Released from Enterochromafin life (ECL) cells and mast cells
b) Binds to H2 receptors on parietal cells
i) Blocked by cimetidine / famotidine
2) ACh - INCREASES HCl secretion
a) Released by vagus nerve
b) Binds muscarinic (M3 receptors) on parietal cells
i) Blocked by atropine
c) Indirect stimulation– stimulates ECL cells to make histamine
3) Gastrin - INCREASES HCl secretion
a) Released into circulation by G cells
b) Binds CCK-b receptors on parietal cells
c) Indirect stimulation - stimulates ECL cells to make histamine
What are the sites of action of PPI, Famotidine, cimetidine and atropine
PPI; H+K+ ATPase in the parietal cells
Famotidine/cimetidine; H2 receptors on parietal cells reducing histmine release
Atropine; binds to muscarinic M3 receptors on parietal cells preventing ACh from binding thus reducing acid secretion
draw a diagram showing the main pathways of acid decretion and the inhibition of these
(VI) how is HCL secretion regulated
Vagus nerve stimulates parietal cells (via ACh) and G cells (via GRP)
Parietal cells make HCl, G cells make gastrin
Gastrin further stimulates HCl production by acting on parietal cells
(VI) what are the phases of HCL secretion ?
1) Basal phase -> occurs in abscence of all gastric/intestinal stimulation
2) Cephalic phase -> 30% of HCL in reponse to smell/tast/chew/swallowing/conditioned antivipation of food
Vagus- > ACh->parietal-> HCL
3) Gastric phase -> 60% of HCL
Stimuli= stomach distension, peptides, AA
Direct path; Distension -> vagus-> parietal/G-cells
Indirect path; AAs -> G cells ->Gastrin
4) Insteinal ->10% HCL
stimuli = proteins, distension
How do we have the inhibiton of HCL secretion ?
1) Major inhibitory control = decrease pH of gastric contents
2) somatostatin (secreted by D cells)
- Direct; binds to parietal cells
- indirect; inhibits histamine and gastrin release
3) Prostaglandins (prostaglandin E2)
- antagonizes histamine
(VI) How does the stomach protect its self from all of the acid?
1) Mucus - secreted by mucous neck glands
2) HCO3- - secreted by gastric epithelial cells
a) Helps neutralize H+ and any pepsin that accidentally gets activated
3) Prostaglandin E2
a) Maintains mucosal barrier and stimulates bicarb secretion
4) Mucosal cell renewal
5) Mucosal blood flow
(VI) decribe pepsinogen secretion and activation
1) Inactive precursor to pepsin
2) secreted by chief cells and mucous cells
3) Parietal cells secrete HCl→ lowers pH→ inactive pepsinogen made into pepsin→ starts protein digestion
4) Major stimulus = VAGUS
a) also stimulated by H+
what is intrinsic factor, where is it secreted?
This is needed for B12 absorbtion in the ileum
- humans secrete it from Parietal cells
- Dogs and cats, most is secreted by the pancreas
How much of the pancreas is exocrine?
90%
what anatomical differences are there between dog and cat pancreases?
dogs’ pancreatic duct does not empty into the common bile duct; cats’ pancreatic duct merges with the common bile duct
(VI) what are the two main cell families of the pancreas?
Acinar cells = secrete digestive enzymes
Ductal cells = secrete water and bicarbonate
(VI) what is the innervation of the pancreas? what does nerve stimulation result in?
Innervation
-sympathetic = inhibits secretion
-parasympathetic = VAGUS = stimulates secretion
(VI) 3 major functions of pancreatic juice
1) Neutralize the material in the duodenum
2) Provide enzymes for digestion of food
3) Secrete intrinsic factor (mediates B12 absorption in distal GI)
(VI) in what area of the pancreas is the endocrine component found and what are the 4 main cell types?
Islets of Langerhans = clumps of endocrine pancreas
4 major cell types in these islets
Alpha cells - glucagon
ß cells - insulin
Delta cell - somatostatin and gastrin
PP cell - pancreatic polypeptide
(VI) where are the exocrine Pancreatic Secretions ( Enzymatic Portion) formed?
What enzymes are produced?
Where are the enzymes stored?
1) Enzymatic component of pancreatic secretion made by acinar cells
a)Amylase - secreted active
i) Hydrolyzes starches
b) Lipases / Phospholipases - secreted active
i) Lipase = hydrolyzes triglycerides
ii) Phospholipase = hydrolyzes phospholipids
c) Proteases - secreted inactive and activated in duodenum
i) Hydrolyzes proteins
ii) Ex: trypsinogen → trypsin
2) Enzymes concentrated and stored in zymogen granules until stimulated to secrete (mainly parasympathetic and CCK)
a) ENTEROKINASE activates trypsinogen to trypsin which then activates all the other zymogens
describe the Formation of Pancreatic Secretions (Aqueous Component)?
Aqueous component is made by the ductal cells
1) Contains Na, Cl, K, HCO3
2) Na and K similar to plasma concentrations
3) Cl and HCO3 vary w/ flow rate
i) High flow rate = high concentration of HCO3 and low Cl- concentration
ii)Low flow rate = low concentration of HCO3 and high concentration of Cl-
4) Net result = secretion of HCO3 and absorption of H+
(VI) what part of the pancrea produces the aqueous component?
Ductal cells
What is the net result of production of the aqueous component of pancreatic solutions?
secretion of HCO3 and absorption of H+
(VI) what regulates the secretion fo the aqueous and enzymatic proportion of the pancreatic secretions?
Aqueous portion
- Stimulated by arrival of H+ in the duodenum, secretin, and VIP
Enzyme portion
- Stimulated by digestion products in the duodenum (peptides, AAs, FAs)
- ***3 major agonists of enzyme secretion = ACh, gastrin, CCK (need to reduce acid)`
what are the phases of pancreatic secretion ?
1) Cephalic = stimulated by smell, taste, conditioning via vagus; enzymes
a) ACh -> H+ secretion by parietal cells -> secretin release in duodenum -> pancreatic fluid and bicarb secretion
b) vagal stimulation -> gastrin from G cells -> pancreatic enzymes (gastrin like CCK in dogs )
2) gastric= stimulated by distension of stomach by vagus; enzymes
a) protein products in stomach -> gastrin -> pancreatic enzymes and gastric acid secretion
REMEBER THIS NEXT ONE - MOST IMPORTANT
3) Intestinal = MOST IMPORTANT, enzymes and aqueous portions secreted
a) 80% of secretion
b) H+ triggers release of SECRETIN → HCO3- secretion
i. Secretin also inhibits gastric secretions and emptying and gastrin release
c) CCK → ENZYME secretion
i. CCK released in response to AAs and FAs in SI
ii. Also potentiates effect of secretin on ductal cells
(VI) what are the most important enzymatic secretions from acinar cells?
-CCK is MOST IMPORTANT signaler for enzyme secretion
-AAs, peptides, FAs→ I cells→ CCK secretion→ CCKa receptors on acinar cells → enzymes!
(VI) which are the most important aqueous secretions from ductal cells?
-Secretin is the MOST IMPORTANT signaler for aqueous secretion
-H+ in duodenum → S cells → secretin → ductal cells → bicarb rich aqueous secretion
draw a diagram depicting the regulation of pancreatic secretion;
what happes in regards to bile secretion when chyme reaches the SI?
CCK secreted (by I cells) → CCK causes contraction of GB and relaxation of sphincter of Oddi → bile flows from GB into duodenum
once lipid absorbtion is complete what occurs to bile salts?
bile salts are recirculated to the liver via enterohepatic circulation
decribe the main steps in bile salts enterohepatic recirculation ?
- Absorption bile salts from the ileum into portal circulation
- Delivered back to liver
- Hepatocytes extract bile salts from portal blood
- Allows for conservation of bile salts–liver only has to replace the small amount that is lost in the feces
what is the composition of bile?
bile salts, bile pigments (bilirubin), cholesterol, phospholipids
How are bile salts formed?
Bile acids;
a) Primary Bile Acids = synthesized from cholesterol (cholic acid)
b) Secondary Bile Acids = made from primary BAs that are modified by intestinal bacteria (deoxycholic acid
are conjugated in the liver with glycine or taurine to form bile salts
why are bile acids converter to salts instead of being secreted to digest solutes
Bile salts are amphipathic which allows for lipids to be solubilized and they are more water soluble
what is billirubin and what is its life cycle ?
Byproduct of hemoglobin metabolism which is combined with bile acids, phospholipids and cholesterole to form bile.
Reticuloendothelial system degrades hemoglobin resulting in bilirubin -> transported into the liver by albumin -> live conjugates billirubin with glucoronic acid to form conjugated billirubin (this is yellow - also known as billirubin glucoronide) -> conjugated billirubin is unconjugated in the intestines and made into urobillinogen by bacteria -> urobillinogen is reticulated to the liver, some excreted in urine, some oxidised to urobillin and stercobilin (dark colour of faeces)
Note, while in the gallbladder the bile is concentrated by epithelial cells thar remove water and other ions.
what cell population is responsible for depositing bile in the gallbladder for future use
hepatocytes and ductal cells to make bile which is deposited in the gallbladder
what are the stimuli for bile ejection ?
Ejection of bile: occurs after a meal is ingested
- MAJOR STIMULUS = CCK → secreted by I cells in response to AAs, peptides, FAs
- CCK causes contraction of GB and relaxation of sphincter of Oddi
what ion channels are reponsible for bile salt re-absorbtion and where are these found?
Na-bile salt cotransporters in the Ileum re-absorb bile salts from the lumen of the intestine and eject them into the portal system
how does the liver determine how much bile acid to produce for the formation of bile salts?
The system is under negative feedback controle by bile salts which inhibite cholesterole-7-alpha hydroxylase (CYP7A1) which catalyses the first rate limiting step in bile acid synthesis where cholesterole is converted to 8a-hydroxycholesterole, a precurdor of by acid
CYP7A1 is what and what family of enzymes does it bellong to?
CYP7A1 is cholesterole 7 alpha-hydroxylase which is the enzyme that catalyzes cholesterole into 7alpha-hydroxycholesterole, a precursor of bile acids.
It belongs to the p450 enzyme family
In the following table, determine if the substance results in increased or decreased HCL secretion
where is somatostatin secreted by?
Somatostatin is secreted by delta cells at several locations in the digestive system, namely the pyloric antrum, the duodenum and the pancreatic islets
what is the effect of somatostatin on HCL secretion?
n the stomach, somatostatin acts directly on the acid-producing parietal cells via a G-protein coupled receptor (which inhibits adenylate cyclase, thus effectively antagonising the stimulatory effect of histamine) to reduce acid secretion.[14] Somatostatin can also indirectly decrease stomach acid production by preventing the release of other hormones, including gastrin and histamine which effectively slows down the digestive process.
fill in the table regarding bile salts
List the 4 fat soluble vitamins.
A,D,E,K
In the jejunum, ileum and colon, what electrolytes are absorbed and what electrolytes are secreted ?
All ingested carbohydrates must be broken down to _______ in order to be absorbed.
Disaccharides
Monosaccharides
Peptides
Polysaccharides
Monosacharides
Pancreatic secretions are made of 2 main components: the aqueous portion and the enzymatic portion. The aqueous portion is made by ______ and the enzymatic portion is made by ______.
Acinar cells, ductal cells
Ductal cells, acinar cells
Acinar cells, Zymogen cells
Ductal cells, Zymogen cells
Ductal cells, acinar cells
During peristaltic contractions in the small intestine, what substance contributes to relaxation of the intestinal smooth muscle in front of (aborad) the food bolus?
Acetylcholine
Neuropeptide Y
Substance P
VIP
VIP
Please label if the below substances increase or decrease the frequency of action potentials and force of gastric contractions.
In the gastrointestinal tract, slow waves are a unique characteristic that provides tonic contraction of the smooth muscle. At the peak of the slow wave, if the membrane potential is maximally depolarized and meets threshold, an action potential occurs. Depolarization is caused by opening of what channels?
Calcium channels
Chloride channels
Potassium channels
Sodium channels
Calcium channels
Pick the correct neurotransmitter.
Postganglionic neurons of the parasympathetic NS within the GI tract release peptides or (ACETYLCHOLINE / NOREPINEPHRINE)
Postganglionic neurons of the sympathetic NS within the GI tract release (ACETYLCHOLINE / NOREPINEPHRINE)
Postganglionic neurons of the parasympathetic NS within the GI tract release peptides or (ACETYLCHOLINE)
Postganglionic neurons of the sympathetic NS within the GI tract release (NOREPINEPHRINE)
Pick if the below substances increase or decrease appetite.
Leptin: DECREASES/INCREASES appetite
Insulin: DECREASES /INCREASES appetite
GLP-1: DECREASES/INCREASES appetite
Ghrelin: DECREASES/INCREASES appetite a
Peptide YY (PYY): DECREASES/INCREASES appetite
Leptin: DECREASESappetite
Insulin: DECREASES appetite
GLP-1: DECREASES appetite
Ghrelin: INCREASES appetite a
Peptide YY (PYY): DECREASES appetite
fill in the table
what occurs when there is disruption of water and electrolyte absorbtion?
diarrhoea -> what is not absorbed is secreted
what electrolytes does the jejunum absorb?
major Na absorption site in SI
Net absorption of NaHCO3
what electrolytes does the ileum absorb?
Net absorption of NaCl
what are the main molecules absorbed by the colon ?
- Na (this is how it is the principal absorber of water)
- Ammonia (product of ammino acid metabolism - produced by colonic bacteria)
- Volatile fatty acids (VFAs -> acetate, proprionate, butyrate [made by microbial fermentation in the colon])
what electrolyte is the colon responsible for secreting?
K
what effects does aldosterone have in the colon ?
it increases Na re-absobrtion which in turns re-absorbs water
