GI Physiology 3 Flashcards
Mucosal surface of the stomach - antrum
Just before the pyloric sphincter
Important endocrine organ
Important in regulating GI function
Mucosal surface of the stomach - describe
It has pits and is highly invaginated
Gastric cells and secretions - Cells include
Surface mucous and neck cells
Parietal cells
Chief cells
Gastric cells and secretions - Surface mucous cells and neck cells - secrete what
What is their function
Secrete mucus bicarbonate
Function in gastroprotection
Gastric cells and secretions - Parietal cells - secrete what
What are their functions?
HCl - protein digestion sterilization, nutrient absorption
Intrinsic factor - Vit B12 absorption
Gastric cells and secretions - Chief cells - secrete what
What is their function
Secrete pepsinogen
Function in protein synthesis
Important regulatory cells include
ECL cells
Neurons
G cells
D cells
Important regulatory cells - ECL cells secrete what?
What is their function
Secrete histamine
Function in promoting HCl secretion
Histamine is an important paracrine regulator
Important regulatory cells - Neurons - secrete what? Function how?
Secrete ACh
Function to promote mucus secretion, promote HCO3 secretion, and promote HCl secretion
Important regulatory cells - G cells - secrete what? Function?
Secrete gastrin
Functions to promote HCl secretion
Important regulatory cells - D cells - secrete what? Function?
Secrete somatostatin
Functions in suppressing HCl secretion
It is a negative regulator - works in both paracrine and endocrine function
Direct regulation of the parietal cell - acid secretion is regulated directly through
Paracrine pathways (histamine) Endocrine pathways (gastrin) Neurocrine pathways (Ach)
Direct regulation of the parietal cell - how is acid secretion regulated directly through paracrine pathway?
Histamine!
Binds to H2 receptors
H2 promotes acid secretion
If taking drug that blocks H2 receptor - acid suppression
Direct regulation of the parietal cell - how is acid secretion regulated directly through endocrine pathways?
Gastrin!
Gastrin is a hormone that binds to CCK2
Gastrin is released from the antrum
Gastrin stimulates the parietal cell to secrete acid
Direct regulation of the parietal cell - how is acid secretion regulated directly through neurocrine pathways?
Ach!
Muscarinic receptors respond to Ach
Intrinsic factor is released by what cells
Parietal!
Parietal cell secretions - IF
Vit B12 is released during gastric disruption
Once released, vit B12 binds to haptocorrin
IF will bind to Vit B12 to form a complex
Complex will remain bound throughout intestine and will be absorbed in the ileum
Our body cannot see vit B12 unless it is in complex with IF
Diseases that impact parietal cells will cause changes in
IF secretion which will then change vit B12 absorption which can then lead to anemia
Stomach atrophy can also lead to vit B12 deficiency
Deficiency in IF and/or vit B12 can lead to
Inc risk of infection
Changes in nutrient absorption
Key gastric secretions
Acid (HCl)
Pepsinogen
Mucus
Intrinsic Factor
Components of gastric secretions - Pepsinogen
Pepsinogen is released and as moves through mucosal gel layer is inactive (pH is not right)
Lower pH will activate pepsinogen - we don’t want this to happen until it is in the lumen
Once activated, pepsin can help convert pepsinogen to pepsin
Components of gastric secretions - Pepsinogen - what is required for the activation of pepsinogen to pepsin
HCl!
Optimal activity for pepsin activation is pH of 1.8 to 3.5
Components of gastric secretions - Mucus - Protective factors - the mucus layer is made up of
Mucin Phospholipids Electrolytes Water Bicarbonate
Components of gastric secretions - Mucus - Within the gel layer we have mucin which is
a glycosylated protein
Important for coding and protecting throughout the GI tract
Components of gastric secretions - Mucus - Protective factors - The mucus layer protects by
Creating a physical barrier
Inc pH at mucosal surface
Preventing activation of pepsinogen
Components of gastric secretions - Mucus - Mucus secretion is stimulated by
Neurocrine = Ach Paracrine = Prostaglandins
Components of gastric secretions - Mucus - Mucus secretion stimulated by Ach and Prostaglandins - Prostaglandins key roles include
Mucus and HCO3 secretion
Suppression of HCl secretion (negative regulator)
Inc gastric blood flow
Components of gastric secretions - Mucus - If disruption of mucosal layer
Pepsinogen can become activated at the stomach surface (rather than waiting until lumen) and it will attack the tissue and eventually lead to ulcer development
Things that increase acid secretion?
Things that decrease acid secretion?
Increase = Ach, Histamine, Gastrin Decrease = Prostaglandins
Components of gastric secretions - Mucus - Acid secretion is regulated directly through
Protaglandins (specifically PGE2) which decreases or inhibits signaling through the histamine pathway
Targets the same pathway that histamine does - so prostaglandins turn off the histamine response
Acid-Peptic Disease includes
Gastritis
Ulcers
Acid-Peptic Disease - Gastritis
Infiltration of inflammatory cells without a break in the mucosal barrier
Acid-Peptic Disease - Ulcer
Breakthrough in mucosal lining
Acid-Peptic Disease - Primary causes of acid peptic disease
H pylori infection
NSAIDs and Aspirin
Acid-Peptic Disease - Other causes
Inc number of parietal cells High serum gastrin levels Loss of acid mediated neg feedback on gastrin secretion (loss of somatostatin) Rapid gastric emptying Cigarette smoking Alcohol use Dec mucosal HCO2 secretion GERD
Acid-Peptic Disease - H pylori are key inducers of gastritis and gastric ulcers - H pylori description
It expresses urease which will help to buffer HCl by generating NH3 and CO2
NH3 is also toxic to gastric epithelium
So H pylori can set up its own domain that is more neutral than that of the stomach (pH of 1 or 2)
Acid-Peptic Disease - H pylori are key inducers of gastritis and gastric ulcers - H pylori expresses virulence factors that will what
Allow for adhesion to the epithelium
Will induce immune response
Breakdown mucus layer that protects the epithelium
Acid-Peptic Disease - Caused by NSAIDs - NSAIDs do what
Inhibit the enzyme COX1 and COX 2 and dec prostaglandin synthesis (COX normally produces PGE2)
So in presence of chronic NSAID use, you get gastric irritation and inhibit healing
Acid-Peptic Disease - Caused by NSAIDs - Decrease in prostaglandins leads to (opp of func of prostaglandins)
Dec in gastric blood flow
Dec in mucus/HCO3 secretion
Inc in acid secretion
Therefore NSAIDs will cause damage to the mucosa when prostaglandin synthesis is inhibited
Gastric motor activity
Storing
Churning
Emptying
Gastric motor activity - Storing
Reservoir function in which the stomach fills and stores contents
2 steps = Receptive relaxation and Gastric accommodation
Gastric motor activity - Churning
Mixing and initiation of digestion
After food enters the stomach a propulsive movement (peristalsis) will begin
Pyloric sphincter stays closed though so moving contents of stomach towards a wall
Contents move back and forth (Retropulsive movement)
The rhythmic phase of these contractile forces is called antral systole
Gastric motor activity - Churning - end result
Products smaller than 2 mm will eventually pass through the pylorus
Particles larger than that will pass into the duodenum during interdigestive period (approx 2 hours later)
Gastric motor activity - Storing - steps
Receptive Relaxation
- Mediated by vagus
- Initiated by swallowing
- Relaxation in anticipation of food
Gastric accommodation
- Relaxation in response to gastric and duodenal filling or stretch
- Mediated by ENS
Gastric motor activity - Emptying
Delivery of food to duodenum
Gastric motor activity - Rate of emptying
Depends on the content of the ingested material Liquid will move through first Glucose moves through quickly Protein slower Fat is even slower
Gastric motor activity - Emptying - Control of emptying rate
Controlled through neuronal and hormonal regulation
Hormones = secretin, CCK, gastrin
Neurons = ACh, NO, 5HT, VIP
Gastric motor activity - Emptying - Stimulus/Mediator/Result
Stimulus = HCl in duodenum
Mediator = secretin
Result = humeral regulators from the duodenum and stomach decrease emptying (they dec relaxation of pyloric sphincter so it stays closed)
DELAYS GASTRIC EMPTYING
Gastric motor activity - Emptying - Stimulus/Mediator/Result
Stimulus = Fat n duodenum
Mediator = CCK
Result = humeral regulators from the duodenum and stomach decrease emptying (they dec relaxation of pyloric sphincter so it stays closed)
DELAYS GASTRIC EMPTYING
Gastric motor activity - Emptying - Stimulus/Mediator/Result
Stimulus = protein in the stomach
Mediator = gastrin
Result = humeral regulators from the duodenum and stomach decrease emptying (they dec relaxation of pyloric sphincter so it stays closed)
DELAYS GASTRIC EMPTYING! This is a big one!
Gastric motor activity - Emptying - Stimulus/Mediator/Result
Stimulus = duodenal distention and osmolarity
Mediator = Ach and 5HT Result = Feedback reflexes from the duodenum cause pyloric contraction
Gastric motor activity - Emptying - Stimulus/Mediator/Result
Stimulus = Vagal efferents (the one he said to know)
Mediator = NO
Relaxation of the pyloric region and therefore promotes gastric emptying
PROMOTES GASTRIC EMPTYING
Multiple roles of CCK - what stimulates its release (relating to its function in the stomach)
Fat stimulates CCK release
Functions to reduce emptying
Emesis - definition
Expulsion of gastric and duodenal contents from the GI tract via the mouth
Emesis - preceded by
Nausea, Tachycardia, Dizziness, Sweating, Mydriasis, Retching, Inc saliva production
Emesis - key motility events
Wave of reverse peristalsis
Contraction of abdominal mm and resp mm
Emesis - sign of
Pathophysiological condition that may or may not be GI related
Emesis - purpose of inc saliva
Protection of the oral cavity from the acid that is about to come up (inc mucin and bicarb with inc in saliva)
Emesis - reverse peristalsis of what
The duodenum and the stomach (NOT THE esophagus)
Emesis - Key NTs
5HT
Ach
Dopamine
Histamine
Key NT for the gut is 5HT (relays signal from gut to CNS)
Emesis - causes can be (general)
Medications GI disorders CNS causes Endocrine Infections
Emesis - causes - Medications
Chemo
Analgesics
Antibiotics
Narcotics *
Emesis - causes - GI disorders
5HT will be involved!
Mechanical obstruction Gastroparesis Radiation injury Functional bowel disorders Intraperitoneal inflammation
Emesis - causes - CNS
Inc ICP
Emotional responses
Psychiatric conditions
Tumors
Emesis - causes - Endocrine
Pregnancy
Uremia
Diabetic ketoacidosis
Emesis - causes - Infections
VIral/Bacterial gastroenteritis
