GI Flashcards
lamina propria
layer of CT that contains glands, hormone-containing cells, LN and capillaries
submucosa
- layer of CT that contains glands, large bv, and lymphatics
- outermost region has nerve net called meissner’s plexus
- Meissner’s plexus = part of enteric nervous system; involved in secretory activity
an increase in sympathetic activity has what effects on the GI tract
- decrease motility, decrease secretion (through NE)
- increase constriction of sphincters (through NE)
an increase in parasympathetic activity has what effects on the GI tract
- promotes digestive and absorptive processes:
- incresaed motility and secretions (through ACh)
- increased gastrin (GRP stimulates G cells)
- decreased constriction of sphincters (through VIP = inhibitory parasympathetic transmitter)
nerve gas has what effect on GI tract
nerve gas increases GI and bronchial secretions
Electrical activity in GI Smooth muscle
- resting membrane potential = close to depolarization (-45 to -60)
- oscillation of membrane potential generated by interstitial cells of Cajal that act as pacemakers (creates the intrinsic motor activity)
- this is called slow waves or basic electrical rhythm (always some basal motor activity in the GI tract)
- slow waves create low-level contractions
- if threshold is reached, generates AP
- AP are generated by opening of slow channels that allow entry of BOTH Na and Ca
- AP strengthen the contractions
- duodenum contracts the most often
Response to stretch in the GI tract
- stretch produces a contractile response
- ex) stomach distention stimulates ACh and increased parasympathetic activity (increases stomach motility)
- overload of the duodenum decreases stomach motility
Secretin
- source
- stimulus
- effect
- source: S cells lining duodenum
- stimulus: acid entering duodenum
- inhibits stomach motility and secretion
- stimulates fluid secretion (HCO3-) from the pancreas
(neutralizes stomach acid entering duodenum) - stimulates insulin release (pancreas)
- no effect on gallbladder
anticholinergic medications have what effect on GI motility
slow GI motility
- ex) atropine or TCA
- however, atropine alone cannot slow the stomach, bc GRP bypasses ACh
Cholecystokinin (CCK)
- source
- stimulus
- effect
- source: cells lining duodenum
- stimulus: fat and AA entering duodenum
- inhibits stomach emptying (increase the degree of pyloric constriction)
- stimulates enzyme secretion from pancreas
- stimulates insulin release (from pancreas)
- stimulates Gallbladder contraction and relaxation of sphincter of Oddi for bile into the duodenum
Gastrin
- source
- stimulus
- effect
- source: G cells of stomach, stimulate stomach distention
- Source: Pyloric Antrum, stimulate parasym peptides (GRP)
- source: duodenum, stomach acid inhibits (negative feedback)
Gastric Inhibitory Peptide (GIP); Glucagon-like peptide (GLP)
- source
- stimulus
- effect
- source: duodenum
- stimulus: fat, carb, AA
- inhibits stomach motility and secretion
- effect on gallbladder:
1. GIP increases insulin
2. GLP decreases glucagon
In swallowing, how is relaxation of the LES triggered?
VIP acts as an inhibitory transmitter of the myogenic smooth muscle of the LES
Difficulty initiating swallowing
= oropharyngeal dysphagia, usually neural in origin
- bc swallowing is a reflex controlled from the brain stem
Stomach emptying in order from fastest (1) to slowest (4)
- liquids
- carb
- protein
- fat
ileocecal sphincter
- valve btw SI and LI
- distention of ileum creates a muscular wave that relaxes sphincter
- distension of colon creates a nervous reflex to constrict the sphincter
motilin
- SI hormone
- stimulates the migrating myoelectric complex (propulsive movement repeated every 90-120 mins during fasting that moves from stomach to colon)
- this movement prevents the back flow of bacteria from the colon into the ileum and its subsequent overgrowth in the distal ileum
composition of salivary secretions
- low in Na+ and Cl-, bc reabsorption
- high in K+, HCO3- , bc of secretion (pH = 8)
- salivary fluid is HYPOtonic bc of reabsorption of NaCl and impermeability of ducts to water
- alpha-amylase (ptyalin): secreted in the active form and begins the digestion of carbs
- mucus, glycoprotein
- immunoglobulins and lysozymes
- regulated via parasympathetic input
Parietal cells
- secrete HCL
- intrinsic factor combines w Vit B12 and is reabsorbed in the distal ileum
- this is the only substance secreted by the stomach that is required for survival
- it is released by the same stimuli that release HCL
Chief Cells
- pepsinogen is converted to pepsin by H+
- active pepsin continues the process
- only active in the acid pH medium of the stomach
- begins the digestion of protein but is NOT essential for life
- Pepsin is secreted by chief cells
Mucous Neck Cells
- secrete the protective mucous, HCO3 combination
- the epithelial cells that cover the gastric mucosa secrete a highly viscous alkaline fluid (mucin + HCO3) that protects the stomach lining from the acid
- NSAID decrease the secretion of mucin and HCO3
3 natural substances that stimulate parietal cells
- gastric acid secretion via a H/K-ATPase pump
1. ACh; release is stimulated by sight/smell of food and reflexly in response to stomach distention (vasovagal reflex)
2. locally released histamine; stimulated by ACh and gastrin
3. hormone gastrin; stimulated by release of GRP - as stomach pH falls, SOMATOSTATIN is released, and inhibits gastrin and reduces acid secretion (feedback regulation of acid secretion)
Diarrhea
- a loss of isotonic fluid that is high in HCO3 and K+
- EXCEPT in infants, where it can be HYPOtonic
pepsinogen is converted to pepsin by
- H+
- only active in the acid pH medium of the stomach
- begins the digestion of protein but is NOT essential for life
- Pepsin is secreted by chief cells
Carbonic anhydrase
- converts CO2 to H+ and HCO3
Compared to extracellular fluid, gastric secretions
- high in H+, K+, Cl-
- low in Na+
- the greater the secretion rate, the higher the H+ and lower the Na+
Trypsin inhibitor
- protein present in pancreatic secretions
- prevents activation of the proteases within the pancreas
how do you get active trypsin
- trypsinogen is secreted by the pancreas and activated to trypsin by enterokinase (aka enteropeptidase)
- enterokinase = enzyme secreted by the lining of the SI. NOT A BRUSH BORDER ENZYME.
- trypsin then goes on to activate the other proteases (i.e. chymotrypsinogen and procarboxypeptidase)
stercobilin
- produced from metabolism of bilirubin by intestinal bacteria
- gives stool its brown color
how does cholera produce diarrhea
- cholera toxin binds and activates Gs, increases cAMP
- cAMP opens luminal Cl- channels, causing massive secretory diarrhea
Where are bile salts reabsorbed
- distal ileum ONLY
- electrolytes and water (but not bile pigments or bile salts) can be absorbed from the gall bladder lumen
- distal ileum also absorbs intrinsic factor-Vit B12 complex
lipid digestion requires
- bile micelles and pancreatic lipase
- end products absorbed include 2-monoglycerides and FA
digestion of carbs requires
- pancreatic amylases and the small intestinal brush border enzymes
- end products absorbed: monosaccharides
- disaccharides can’t be absorbed from the SI
digestion of protein requires
pancreatic proteases (must be activated by enterokinase/enteropeptidase and the intestinal brush border enzymes)
Absorption in the colon
- net absorption of water and electrolytes
- influenced by aldosterone, but has a net secretion of HCO3 and K
- doesn’t have digestive enzymes or transporters to absorb products of digestion
