11: GI Secretions And Exocrine Pancreas Flashcards
Parotid gland secretion contents
Water, ions, enzymes (amylase rich)
Submaxillary and sublingual gland secretion
Aqueous fluid + mucin glycoproteins
How does saliva compare to plasma?
Hypotonic; higher in K and bicarb but lower in Na and Cl
Salivary ductal cell mechanism for absorbing NaCl and secreting K and bicarb
- Na/K ATPase utilization to form gradient
- Cotransport of bicarb + Na into ductal cell
- Bicarb enters lumen as chlorine enters ductal cell
Salivary gland innervation
Both symp and parasymp stimulate it, but parasymp dominates
What does Omeprazole block? What’s the point?
Blocks H/K ATPase in parietal cells -> H cant enter lumen from cell
What does atropine block?
Direct pathway where vagus nerve stimulates parietal cells
What two things can cause lack of intrinsic factor?
Absence of parietal cells, achlorydia
Pernicious anemia
Stomach doesn’t produce enough IF, so decreases B12 absorption
Four common causes of pernicious anemia
- Atrophic gastritis
- Autoimmune metaplastic atrophic gastritis
- Gastrectomy
- Gastric bypass
Atrophic gastritis
Chronic inflammation of stomach mucosa -> loss of parietal cells
Why can gastric bypass cause pernicious anemia?
Loss of stomach, duodenum, and jejunum from B12 absorption
Two main parts of the stomach’s mucosal barrier
Mucus, bicarb
Four things that protect the mucosal barrier
- Prostaglandins
- Blood flow
- Gastrin
- GFs
8 things that damage the mucosal barrier
- Stress
- Acid
- Pepsin
- NSAIDs
- H pylori
- Alcohol
- Smoking
- Bile
Two component model for gastric secretion
- Parietal secretions: H and K and Cl - slightly hyperosmotic
- Non-parietal secretions: basal alkaline secretion at constant low volume made of Na, Cl, and bicarb
Potentiation
combined response of 2 stimulants exceeds sum of individual responses
Gastrinoma
duodenal or pancreatic NE tumors that secrete gastrin
What causes Zollinger-Ellison Syndrome
Gastrinomas
How do gastrinomas work?
Cause increased H secretion by parietal cells -> enzymes in SI are overwhelmed
Four effects of excess H in duodenum in Zollinger-Ellison Syndrome
- Inactivates pancreatic digestive enzymes -> les digestion
- Inhibits absorption of Na and water -> diarrhea
- Interferes with fat emulsification -> steatorrhea
- Damages intestinal villi -> ulcers
How to test for Zollinger-Ellison Syndrome
Secretin stimulation test: inject secretin -> paradoxical increase in gastrin
Two mechanisms of peptic ulcer disease
- Loss of mucosal barrier
2. Excess H and pepsin
Main causes of gastric vs duodenal ulcers
Gastric: defective mucosal barrier
Duodenal: high H secretion rates
Which type of peptic ulcer is more common?
Duodenal
H pylori mechanism
Release cytotoxins like urease that breakdown mucosal barrier and underlying cells
How does urease from H pylori work?
Converts urea to ammonia -> alkalizes the environment -> damage
Diagnostic test for peptic ulcer disease
Based on urease activity
Three things that stimulate I cells to produce CCK
- Phenylalanine
- Peptides and AAs
- FAs
Sympathetic innervation to exocrine pancreas
Post-ganglionic s from celiac and superior mesenteric plexuses
Parasymp innervation to exocrine pancreas
Vagus nerve, with a ganglionic synapse in the ENS
What causes cystic fibrosis
Mutation in CFTR, a Cl channel
One of the first organs to fail in cystic fibrosis
Pancreas
What can CFTR cause in the pancreas
Loss of bicarb secretions + inability to flush active enzymes out of pancreatic ducts -> can cause acute or chronic pancreatitis
