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GI 1-3

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imissyou419's version from 2017-04-06 19:28

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Question Answer
Salivacomplex solution made up of water, ions, enzymes
Parotid gland makes what kind of salivawatery saliva with lots of enzymes (important for chemical digestion)
Submandibular gland and sublingual gland makes what kind of salivamucous saliva with less enzymes
Acinar cellssecrete macromolecules (proteins, ions, mucus, bicarb), primary secretion is isotonic
Ductal cellsmodifies the primary secretion by transport of ions and water based on the speed of salivary flow (i.e. faster flow -> less modified, more isotonic; slower flow -> reabsorb Na+, Cl-, hypoosmotic)
Saliva composition1. water,
2. chloride,
3. bicarb (neutralize acidic food and phosphate ions (help buffer acidity),
4. mucus (lubrication),
5. amylase (digest carbs particularly starch, Cl- helpful for activity of amylase),
6. lipase (babies have lot of lingual lipase, cystic fibrosis have more lingual lipase as compensatory mechanism, lingual lipase inactive in mouth),
7. immunoglobulin A (target pathogens for destruction), lysosomes (destroy bacteria cell walls)
What is the benefit of having a mostly unmodified salivary secretion (closer to primary secretion)? Saliva flow fast so end up mostly unmodified, the increased Cl- activate amylase, better it is to digest starches
Salivary gland ductSaliva glands are on either side (3 on each side), each gland has 1 major duct that go into mouth
Neural regulation of salivary secretion (PNS and SNS)1. PNS - major pathway to stimulate saliva secretion, initiates and sustains high levels of saliva (by causing vasodilation of blood vessels around salivary glands -> more blood to pull from to produce saliva),
2. SNS - can't initiate saliva secretion but potentiates the effect of PNS
How does ADH and aldosterone control saliva compositionIT DOES NOT AFFECT FLOW RATE; ADH - reduce amount of water in saliva (more viscous), Aldosterone - hypoosmotic saliva
How does higher brain order, like emotions affect saliva productionProduce more saliva when you smell something you like
Mechanical digestionconverting food into a bolus
Chemical digestionsalivary amylase & lingual lipase (IT DOES NOT FUNCTION UNTIL STOMACH)
Voluntary StageBolus pushed voluntarily to pharynx and against the palette
Pharyngeal StageInvoluntary, palette pulled upward (to close off nasal sinus), then larynx opening closed off by epiglottis
Esophageal StageInvoluntary, opening of upper esophageal sphincter
XerostomiaInsufficient production of saliva, aka "dry mouth",
unpleasant for affected individuals, can lead to poor nutrition (can't lubricate food so hurt to eat and swallow), and depression (food is social thing),
increased tooth decay, opportunistic infections
What causes xerostomiamedication, long term dehydration, pathogens, inflammation of salivary glands, autoimmune disease - attack of tissue, neck radiation -> damage salivary glands
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Question Answer
Peristalsisdo not need gravity,
unidirectional movement of bolus from top of esophagus towards stomach,
co-ordinated contraction & relaxation of muscles under control of medulla oblongata,
secondary peristalsis (more vigorous) initiated in esophagus if bolus becomes lodged
Stomach functionreservoir
Which part of the stomach are exocrine?fundus and body make HCl, intrinsic factor (parietal cells) mucous (mucus neck cells), pepsinogen, gastric lipase (chief cells)
Which part of the stomach are endocrine?antrum release gastrin
Rugaefolds in stomach that cause expansion of stomach
Mucus neck cellsin fundus and body, secrete mucus
Chief cellsin fundus and body, secrete pepsinogen and gastric lipase
Parietal cellsin fundus and body, secrete intrinsic factor (helps with vitamin B12 absorption), HCl
G cellsin antrum, In response to food in stomach/peptide, secrete gastrin (acts within stomach to increase HCl secretion from parietal cells, increase stomach motility, relaxation of pyloric sphincter)
Mucosa of stomachEnterocytes secrete acid, gastric lipase (digest fat), pepsinogen (pepsin digest proteins), intrinsic factor;
folds called rugae, invaginations called pits (chief, parietal, stem cells in pits)
Submucosa of stomachsimilar characteristics to rest of the tract - thicker lay of stretchy connective tissue with lacteals and blood vessels, adhere mucosa to mucularis externa
Muscularis externa of stomachcircular, longitudinal, AND OBLIQUE muscle layer, provides strength to mix and churn contents
Serosa of stomachcontinuous with lesser and greater omentum
Stomach motility purposeconvert bolus into chyme (liquid food)
Emptying of gastric contents regulated by opening ofpyloric sphincter
Mechanical digestion in stomachmuscular contractions to grind stomach contents and mix with the secretions of the stomach
Stomach motilityPropulsion (push food toward antrum),
Grinding (pyloric sphincter closed so pushed backwards),
Retropulsion (pyloric sphincter opens, some chyme exit and majority goes back to body region to be mixed)
Pyloric stenosisHypertrophy of pyloric muscles - failure of pylorus to relax - prevent gastric emptying,
Infantile Hypertrophic Pyloric Stenosis - most common, 1 in 500 infants, most frequently first born male, hereditary linkage, causes projectile vomiting & babies not getting enough nutrients;
Treatment: cut pyloric muscle to release pressure so muscle can resolve itself
Stomach chemical digestion1. Carbohydrates digestion halts - salivary amylase doesn't function in the acidic environment of stomach (protein folds differently in acidic environment)
2. Protein digestion begins - pepsinogen is cleaved in presence of acid to form enzyme pepsin in stomach
3. Lipid digestion begins - gastric lipase secreted by chief cells is active in an acidic environment, lingual lipase activated in acidic environment
Function of acid in the stomach1. Activate lingual lipase (folds in certain formation in acidic environment which cause the active site of enzyme to be folded properly so it begins cleaving lipids)
2. Activate pepsin (cleavage event cutting pepsin from pepsinogen, digest protein)
3. Inactivate salivary amylase (different folding of amylase in acidic compared to neutral)
4. Kill microbes
5. Denature proteins
6. Stimulates secretion of hormones (presence of acid from stomach into small intestines -> secretin released)
How is acid secreted into stomachInside cell, have H2O + CO2 -> H2CO3 by CA
HCO3- goes to blood stream through HCO3-/Cl- exchanger
H+ is pumped to lumen of stomach through K+/H+ ATPase (K+ moves into enterocyte while H+ moves out into lumen)
K+ leak channel allow K+ to leak back to lumen drives ^
Cl- moves to lumen through Cl- leak channel (build up of + charge outside the cell due to H+ moving out and K+ moving in so Cl- move because of electrical gradient)
HCl combine outside of mucosa layer
Regulation of HCl secretionProteins/AA detected by G cells secrete gastrin
Gastrin-CCK2 receptor stimulate HCl secretion
Gastrin stimulates ECL cell (through part of lamina priopia) to secrete Histamine
Histamine-H2 receptor stimulate HCl secretion
Thought of food is enough for PNS activation, release of Ach
Ach-Muscularic 3 receptor stimulate HCl secretion

Stretching of stomach causes submucosa plexus neurons release GRP (gastrin releasing peptide) -> stimulate G-cells to release Gastrin
PNS activation release Ach onto ECL cell to cause histamine release

These signals are SYNERGISTIC to get a lot of HCl secretion
UlcersLoss of protective barrier (mucous) in stomach so acid and pepsin erode stomach lining -> Bleeding of mucosal vessels
Causes: H.pyloric and NSAIDs
Gastric or duodenal
Treatment:
- For chronic NSAID: reduce acid and pepsin production (antiacid) but 2 options most common: block H2 receptor to reduce HCl secretion (so gastrin, PNS, histamine cannot affect HCl secretion), H+/K+ ATPase inhibitor(H+ pump) to completely block HCl secretion
- For H.pylori: antibiotics
Protein digestionPepsinogen once it comes in contact with acidic environment, fold differently and become autocatalytic into pepsin (digest proteins)
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Question Answer
DuodenumLocation of enzymes mixing with chyme, most digestion occurs here
Can increase or decrease motility to optimize chemical digestion
JejunumMany villi to increase SA for optimal absorption
Most absorption here
IleumLess villi but can still absorb nutrients if necessary
Vitamin B12, intrinsic factor are only absorbed in the ileum, bile acids are reabsorbed and go back to liver
Mucosa in small intestineAbsorptive epithelia - transporters for macronutrients (stomach does not have this)
No acid secreting cells (unlike stomach)
Finger-like projections called villi
Plicae which increase SA (in stomach have rugae which allow for expansion)
Submucosa in small intestineSame with stomach - thicker lay of stretchy connective tissue with lacteals and blood vessels, adhere mucosa to mucularis externa
Muscularis externa in small intestineLongitudinal, circular (does not have oblique layer that stomach has to help with crushing of food)
Serosa in small intestineSame with stomach - continuous with lesser and greater omentum
Absorptive cellsEpithelial cells with microvilli (increase SA for absorption)
Goblet cellsSecrete mucus
Intestinal gland cellsSecrete alkaline water mucus (neutralize acid in chyme)
Paneth cellsSecrete lysozyme (destroy pathogens in chyme)
S cellsSecrete secretin (In response to acid in small intestines, secretin travel in blood, stimulate ductal cells in pancreas to secrete bicarb and water, acts on ductal cells of bile canaculi to stimulate secretion of bicarb and water to make higher volume bile solution)
CCK cellsSecrete cholecystokinin (CCK) (In response to food in small intestine esp PROTEIN > lipid > carbs, CCK travel in blood and act on acinar cells of pancreas to secrete digestive enzymes, act on liver and gallbladder to stimulate bile production and secretion)
Open Oddi
Close pyloric sphincter
K cellsSecrete glucose dependent insulinotrophic peptide (GIP) (released in response to carbs, stimulate beta cells of pancreas to release insulin)
Stomach vs. Small intestinesStomach - mechanical digestion, food reservoir
Has rugae (stretch out)
Pits (glands)
Small intestine - chemical digestion, absorption of nutrients
Has plicae (folds to increase SA)
Crypts (glands)

Both contain stem cell - epithelial layer are replaced frequently
Microvillibrush border, increases SA for nutrient absorption, cells on the microvilli have brush border enzymes, final digestion for some nutrients to allow for absorption (we can only absorb monosaccharides)
Lactasebreak down lactose
Sucrasebreak down disaccharide sucrose
Maltasebreakdown disaccharide maltose
Alpha-dextrinasebreakdown of alpha-dextrin (complex carb) - digest amylopectin to alpha dextrin
Aminopeptidasebreakdown protein (digest from last a.a. on amino terminus -> leaves you with 1 a.a. and a longer peptide)
Dipeptidasebreakdown dipeptides (take 2 a.a. stuck together and break them into individual a.a.)
Nucleosidasesbreakdown nucleosides (DNA)
Enterokinaseprocessing of proteases from pancreas so they become active
Phosphotasesremove phosphate groups
Small intestine motilitysegmentation and peristalsis
Segmentationunique to small intestine, specialized localized contractions for mixing chyme with digestive juices, increased interactions of particles of food in chyme with absorptive cells of the mucosa layer, motility that enhances chemical digestion and therefore absorption
Peristalsispropels chyme from pyloric sphincter towards the large intestine, propulsive type of motility (doesn't improve chemical digestion)
Migrating motility complextype of peristalsis initiated in the fastened state (from stomach through the intestines), remaining lumen content moved unidirectionally, interrupted when new foods introduced into GI tract; intestines moving gases make sound
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