Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

15 Cards in this Set

  • Front
  • Back
What does MMC stand for and what does it do?
Migrating Myoelectric Complex (MMC)
It's the waves that start at mid-stomach and ends at the terminal ileum, right up to the ileocecal sphincter. MMC occurs 2-3 hours after u eat a meal. There are 4 phases of the MMC, and the whole cycle takes about 90-120 min of which phase 3 only takes 6-10 min total. But while phase 3 is short is the only important one for us. So Phase 3... motilin is a hormone found in the blood that stimulates phase 3 contractions.
As soon as u put food in your mouth the MMC stops.
What does your body / GI system due in response to food?
So prolonged time w/o food triggers the MMC.
When u r stimulated with the prospect of food u start salivating and there is a cephalic phase of HCL secretion. The salivation is not from the Vagus n. but from the PNS (Hypoglossal and Facial n.'s)
You take your first bite and so it begins:
More saliva is secreted which begins the digestion of starches, lipids, and caps B12 for protection from stomach acid.
-Alpha-amylase from the salivary acinar cells starts to digest the starches.
-Lingual Lipase from the von Ebner's glands of the tongue - which breaks down lipids.
-R-protein combines with any B12 to protect it from the stomach.
With all this chewing one more thing happens... vagus n. stimulation causing parietal cells to secrete more HCL and the vagus also starts motility in the lower GI tract.
What does your body do when u swallow?
There are 4 different phases to swallowing:
1. Oral Preparatory Phase - Mastication
2. Oral Phase - the tongue propels food posteriorly until the pharyngeal swallow is triggered.
3. Pharyngeal Phase - food bolus goes through pharynx down the esophagus.
4. Esophogeal Phase - the vocal cords adduct (closes) and the UES relaxes. esophogeal peristalsis carries the bolus from the cricopharyngeal juncture or UES through the esophagus to the LES.
Primary Esophogeal Peristalsis then occurs to push the bolus down.
The three places in the GI tract that have skeletal muscle are the: 1. mouth, 2. UES, 3.EAS. So we can control what goes in and what comes out, but everything in between is smooth muscle (involuntary).
If the bolus gets stuck then 'painful' Secondary Esophogeal Peristalsis takes over with mucous secreted, both stimulated by Vagus and Enteric n.'s sensing the 'stretch' in the throat. This is a local reaction.
Achalsia - a disease of the enteric n.'s, which prevents the LES from relaxing. Hard/painful to eat, pts stop eating. Tx is to clip the sphincter open, but this can cause indigestion.
What goes on in your stomach?
When the bolus enters the stomach, the stomach undergoes "receptive relaxation" (which is stimulated by the Vagus n. and can also occur in the duodenum). Because of 'receptive relaxation' it takes about a Liter of food in your stomach to get full. If you have a vagotomy then what happens? You don't get the receptive relaxation and you feel full a lot sooner.
The antral area of the stomach is found right before the pyloric sphincter and it's where grinding occurs.
The stomach breaks down stomach contents into three groups: 1. Saline, 2. Acid, 3. Fatty.
When more food comes in Mechanoreceptors sense the stretch and send the hormone gastrin (from G cells) into the blood. Gastrin acts on the parietal cells and causes them to release a tremendous amount of HCL. Gastrin also increases the motility of the lower GI tract. HCL is also modulated by the hormones:
Hist - increases HCL
SS - decreases HCL
intrinsic factor (IF) also comes from the parietal cells, binding to the R-Protein/B12 complex, protecting it until it gets into the SI. In the SI trypsin cleaves the R-protein from the complex and the IF/B12 dimer travels down to the terminal ileum.
-Coming out of the Chief Cells is pepsinogen (inactive form of pepsin, a protease) that becomes active and thrives in the acidic environment of the stomach.
Pepsin - digests proteins
Gastric Lipase - digests lipase
All of the secreting cells of the stomach can be found in the 'Gastric Pits'. Except for the mucous which has glands that secrete a ton of mucous laced w/ bicarb to protect the stomach lining.
Describe the different types of waves that occur in digestion?
There are 1. Slow Waves, and 2. Action Potentials (spike potentials)
Slow Waves (also called Basal Electrical Rhythm or BER) are not AP but are undulations in the resting membrane potential that occur from the mid-stomach to the anus.
Stomach 3/min, duodenum (12/min), distal SI (10/min), and colon (3/min). These differences allow for different rates of contractions in the different sections of the tract when there is an AP. Slow waves favor mixing, while fast waves favor propulsion. These slow waves originate in the interstial cells of Cajal, and are probably due to the activity of the Na/K ATPase pump.
So once again, slow waves are NOT APs and they do NOT cause Cxs! They merely make it possible for these AP and Cxs to occur. Spike potentials only occur at the crests of slow waves.
Stimuli that Hyperpolarize slow waves are Norepi, SNS, Vasoactive Intestinal Peptide (VIS)
Stimuli that Depolrize slow waves are stretch, PNS, ACh, and tachykinin (substance P)
The AP in these cells are caused by Ca influx into the cells, where it binds to calmodulin. This then activates myosin, making it more attractive to actin, creating a cx. It is the active influx of Ca and the Ca/calmodulin interaction that causes depolarization. Thus the AP is generated if it goes above -40 mV!
Also the more depolarized it gets not only are the AP more frequent but there also stonger!
What happens when Chyme is released into the SI? (important)
Chyme comes out into the duodenum with a pH of 2. The endocrine cells in the Crypts of Leiberkuhn put secretin into the blood which tells the pancreas to secrete bile which b/c of solvent drag carries electrolytes (think bicarb) so it buffers the acidic pH.
Secretin also stimulates the Paneth Cells in the Crypts to release buffer.
And lastly, the secretin acts on the G-cells to decrease the amount of Gastrin being released, thus decreasing the amount HCL. So due to all this only a couple of centimeters down and the pH is up to 7!
In addition, Gastric Inhibitory Peptide (GIP) is secreted into the duodenum, GIP reduces gastric emptying by keeping the pyloris constricted. GIP also decreases Gastrin levels in the blood. GIP also acts on the pancreas to make it release insulin.
Now insulin increases HCL
While, GIP decreases HCL
What is the function of the gall bladder?
Contraction of the gall bladder is stimulated by both the Vagus n. and CCK. The Vagus n. will also relax the Sphincter of Oddi which happened early on in the cephalic phase. CCK is released by cells in the duodenum. CCK circulates through the blood and it facilitates 1. gall bladder cx, 2. activates the liver to make more bile, 3. facilitate mass movements in the colon, and it will finally act on the 4. pancreas to stimulate enzyme secretion.
Pancreatic enzymes released are: 1. pancreatic alpha-amylase (starch digestion), 2. pancreatic co-lipase, 3. pancreatic lipase, and 4. pancreatic proteases. These are in zymogen form in the pancreas, and are prevented from transforming by having trypsin inhibitor throughout the pancreas and the pancreatic ducts. Once in the duodenum trypsinogen is activated by enterokinase.
What's involved in propulsion in the small intestine?
Peristalsis and Segmentation
Peristalsis follow The Law of the Intestine which states, if there is a bolus of chyme, there will be cx on the oral side and relaxation on the aboral side. Behind the bolus of chyme you'll get an AP causing cx while in front of the bolus you'll get hyperpolarization and therefore relaxation to allow it too pass. The only exception to this directional flow is retrograde peristalsis, which occurs when you vomit or hold in your BM.
The second type of motility is a rebel and does not follow The Law of the Intestine.
Segmentation cause cx behind and in front of the bolus and relaxation in the middle. This type of movement accounts for mixing and propulsion of chyme through the intestine. Occurs over a wider amount of the intestine and therefore accounts for the majority of propulsion in the SI.
How does starch from the gut get absorbed and digested for usuable energy?
The starches have been processed to oligosaccharides by salivary alpha-amylase and a little by HCL. Lactose and sucrrose (disaccharides) are also present. Must be monos to slip into the enterocytes. This final digestion occurs at the BB by the enzymes maltase, isomaltase, sucrase, and lactase. Sucrose makes glucose and fructose. Fructose enters the enterocyte by facilitated transport.
Maltase and iso-maltase make a lot of glucose molecules from the long chains of starches. Lactase makes glucose and galactose, which are carried in by secondary active transport with sodium. There's a big drive for to get glucose in, and since Na comes with glucose, water follows and what the hell u gotta keep electroneutrality so Cl comes along too for the ride.
The glucose, galactose, and fructose that get through the enterocyte, into the portal blood to the liver. The liver then metabolizes the sugars and monitors how much gets into the blood and how much get stored as glycogen and fat. In order to keep blood flowing out of the hepatic vein, the pressure is 0 mmHg.
About 25-30% of digestion has occured preduodenally.
How does fat go from free flowing in the gut to being processed for multiple uses by the liver?
So now we've got a load of bile and pancreatic lipase heading our way. The bile latches onto the fat w/ the polar face sticking out, (bile is polar b/c it's conjugated w/ taurine and lysine) but now our pancreatic lipase can't get to it. So pancreatic co-lipase comes in and binds to the bile, which makes it so pancreatic lipase can get through the bile to the fat and do it's job of breaking up the fat, eventually creating a micelle. The water-taxi (micelle) gets the fat through the unstirred water layer covering up the BB w/ a mucuos layer on top of it. The fats are deposited and the bile stays in the intestine and goes to the terminal ileum to be reabsorbed to go back into the system. When you've finished your meal the bile will head over to the gall bladder where it's stored for future use. By The Way, bile also gets rid of bilirubin and excess CHL. So bile is the only way both of these can get into the intestine to get out of the body!
Wait! That's not it! What happened to the lipids! Well, the lipids get re-esterified w/ FFAs and get incorporated into chylomicrons in the smooth ER of the cell. The chylomicron has a beta-lipoprotein coat for exocystosis. Now remember it can't get into the blood directly... the chylomicrons go through the lymph lacteals to get deposited in the venous blood in the thorax. Remember, lipids do not have first pass effect! So now once the chylomicrons make it to the liver they are metabolized and processed into phospholipids,CHL, lipoproteins, steroid hormones, bile, membranes, ect. That's it for Lipids!
How does protein get digested?
Protein digestion starts in the stomach with pepsin. In the SI protein is broken down by pancreatic proteases (trypsin, and what else?) Once the protein is reduced to oligopeptides they go to the BB. Only aa's and di- and tripeptides are allowed in. After entering the enterocytes they can only leave the cells as aa's so cytoplasmic proteases finish the job. The aa's are shuttled off to the liver where they are deaminated and ammonia is produced. Since ammonia is toxic it is immediately combined with CO2 to make urea.
Review all of the positive and negative feedback signals in the GI tract. (a work in progress please add on to this)
Peptide YY - released by fat in the duodenum it inhibits HCL and motility.
What does the colon do with feces?
There are three bands of muscle running longitudinally along the colon called the teneia coli. When they contract they form haustrae. They can stay contracted for long periods of time. This is called "segmental propulsion", which is not like the segmentation motility of the SI. "segmental propulsion" is a system to make stack of feces and keep them there. NO mixing is needed in the LI. The formation of these haustrae allows for Na and water to be absorbed. The term for this absorption of Na and H2O is called "colonic salvage".
What are mass movements and what stimulates them?
The process of feces formation is started in the region of the transverse colon. Feces travels very slow here at a rate of 5 cm/hr. Remember slow waves in the colon undulate at about 3 times/min. But occassionally there are quicker movements in the colon. There are called "Mass Movements". These are stimulated by Gastrin, CCK, and Vagus n. stimulation. Mass movements work by taking down the Haustae and making the colon a straight tube.
What are some of the reflexes of the GI tract?
Rectosphincteric Reflex - The IAS relaxes b/c your colon is full which then causes your EAS to tense up so u don't pooh your pants.
Gastrocolic Reflex - Food in the stomach stimulates mass movements, by CCK, Gastrin, and the Vagus n.
ileogastric reflex: Food in the ileum limits gastric emptying of the stomach.