Gastrointestinal Function Flashcards
Digestive Enzymes
Amylase, Lipase, Pepsin, Collapse, Phospholipase, Trypsin, Chymotrypsin, Enterokinase, Disaccharides, Dipeptidases
Salivary Glands
Enzymes: amylase, lipase
Targets: starch, TGLs
Stomach
Enzymes: pepsin, lipase
Targets: proteins, TGLs
Pancreas
Enzymes: amylase, lipase/colipase, phospholipase, trypsin, chymotrypsin
Targets: starch, TGLs, phospholipids, peptides,
Intestine
Enzymes: enterokinase, disaccharides, dipeptides
Targets: activates trypsin, complex sugars, peptides
“entero”
= gut
enterocyte: absorbs nutrients - lipids in the SI
GI tract anatomy
Mesentery - OUTER layer containing blood vessels
Mucosa - Epithelial, lamina propria, muscularis mucosa
Submucosa - Meisseners plexus
Muscular Propria - circular muscle (auerbachs myenteric plexus), longitudinal muscle
Serosa - cell lining around the mesentery
Trypsin
attracts:
lys (+) - aromatic won’t fit
arg (+) - activates chymotrypsin & collapse
Epithelial vs. Endothelial
Epithelial - in contact with outside world
Endothelial - inside only (i.e.: blood vessels)
How to make food usable?
1) Mechanical disruption (mastication in mouth and churning in stomach)
2) Chemical digestion (lipids, aa, carbs)
Pepsin
ONLY zygomen that is is not activated by cleavage - activated by LOW pH
Enterokinase
enteropeptidase that activates trypsinogen by converting it to trypsin
GI peptides/modulators
1) Endocrine - SLOW
- ALL GI endocrine hormones are peptides
2) Paracrine
- peptides: somatostatin
- non-peptides: histamine
3) Neurocrine - FAST
- peptides: VIP
- non-peptides: ACh, NE
- nerve release diffuse to target cells
GI Hormones
Secretin Gastrin Cholecystokinin (CCK) Glucose-Dependent Insulinotropic Peptide Motilin
Hormonal Control of Digestion
1) Physiological even in one part that alters activity in another
2) Effect persists after denervation
3) Eliminating source tissue prevents response
4) Isolated substance produces response when injected into blood at proper dose
Gastrin
ANTRUM! (duodenum & jejunum too)
- related to CCK (Trp-Met-Asp-Phe-NH3)
- G cells
- gastric acid secretion is 1,500x MORE potent than histamine
- trophic activity: stimulates growth of oxyntic mucosa of stomach, duodenal mucosa, and colon mucosa
- surgical removal of antrum causes atrophy
- patients with gastrin-secreting tumors have mucosal hyperplasia and hypertrophy
Tyrosine
MUST be sulfated in Gastrin & CCK
CCK
- related to Gastrin (Trp-Met-Asp-Phe-NH3)
- digests fat and slows down chyme to slow gastric emptying
- emptying of gallbladder
- pancreatic exocrine enzymatic secretion
- inhibits gastric emptying
- delivery of pancreatic enzymes and bile into small intestine
- trophic effects: exocrine pancreas and gallbladder mucosa
Secretin
- natures antacid
- requires ALL 27 AA for activity
- released from S cells of duodenal mucosa
- stimulates bicarb and pepsin to inhibit gastric secretion
- acid (less than 4.5pH) and fatty acids cause release
- trophic effect on exocrine pancreas
GIP (gastric inhibitory polypeptide)
- released from K cells of the duodenum and proximal jejunum
- oral glucose
- all food (protein, carb, fat)
- fat MUST be hydrolyzed
- stimulates insulin release
- inhibits gastric acid secretion
Motilin
- released from M cells of duodenum and proximal jejunum during FASTING (100+ min)
- peptide family
- Neural controls release
- stimulates upper GI motility
- “housekeeping contractions”
Hypertrophy vs. Hyperplasia
trophy - cell size
plasia - replication
Zollinger-Ellison Syndrome
Gastrinoma!!!
- ChiRhoStim (synthetic secretin) used to inhibit gastric secretions! if gastrin production doesn’t stop, indicative of a gastrinoma (NOT a peptic ulcer)
- Loss of K+ in stool
- increase in parietal cell mass: increase acid production
- intestinal hyperacidity leads to peptic ulcer
- decrease in bile salts and lipase activity
= diarrhea, steatorrhea, hypokalemia
Low pH
- inactivates pancreatic lipase
- bile salts precipitate
= steatorrhea
Hypokalemia
- results from loss of K+ GI secretions in stool
IMPORTANT for movement - nerve/muscle
Histamine
- acid secretion
- Gastrin and ACh cause histamine release from cells in stomach
- histamine H2 receptor blockers decrease acid secretion! (ex: cimetidine (tagamet) and ranitidine (zantac))
Cimetidine
ie: Tagamet
histamine H2 blocker that decreases acid secretion
Ranitidine
ie: Zantac
histamine H2 blocker that decreases acid secretion
Paracrines
Somatostatin (peptide) and Histamine
Somatostatin
- release stimulated by acid
- inhibited by ACh
- directly inhibits parietal cell acid secretion
- mediates acid induced inhibition of gastric release
Parietal Cell
- secretes acid
Neurocrines
VIP, GRP (Bombesin), Enkephalins
VIP
- decrease in Ca++ relaxes gut smooth muscle
- located in gut mucosa and smooth muscle
GRP (Bombesin)
- gastrin releasing peptide from G cells
- located in gastric mucosa
- with CCK, stops hunger signals
Enkephalins
- increases smooth muscle tone
- located in gut mucosa and smooth muscle
Enteric Nervous System
- intrinsic nervous system
- network of neurons that control GI system
- second brain: MORE neurons than spinal cord and can operate independently of the brain
- myenteric auerbach’s plexus
- submucosal meissner’s plexus
Autonomic Nervous System
- extrinsic nervous system
- parasympathetic stimulates ACh (preganglionic) & VAGUS NERVE
- sympathetic inhibits NE (postganglionic)
Mast Cell
- immune control of GI function
- resting mast cell and activated mast cell
1) GI tract - increased fluid secretion and increased peristalsis lead to expulsion of GI tract content (diarrhea/vomitting)
2) Airway - decreased diameter and increased mucous secretion leads to expulsion of airway contents (phlegm/coughing)
3) Blood Vessels - increased blood flow and increased permeability lead to edema, inflammation, increased lymph flow and carriage of antigen to lymph nodes
Cytokine
TNF-a promotes inflammation, stimulates cytokine production bu many cell types and activates endothelium
Tryptase, Chemise, Cathespin G & Carboxypeptidase
enzymes that remodel connective tissue matrix
Toxic Mediators
Histamine and herapin are toxic to parasites to increase vascular permeability and cause smooth muscle contraction
Heparin
toxic mediator that is toxic to parasites to increase vascular permeability and cause smooth muscle contraction
