Upper GIT Physiology and disorders Flashcards
Exocrine cells
Mucous cells – secrete mucus
- Important because it sits at the top of internal muscuso and acts as a cell layer to prevent burning of ACID
- seen as the protective cells
• Chief cells – secrete pepsinogen & gastric lipase
- is in active form
• Parietal cells – secrete HCl & intrinsic factor (glycoprotein for B12 absorption)
- B12 is absorbed at the end of small intenstine
Endocrine/ Paracrine cells
- Enterochromaffin-like (ECL) cells
- G cells
- D cells
other cells
Stem cells filled in Stomach and small intestine
Roles of HCl
• Activates pepsinogen (zymogen) -
converts it in active pepsin
• Contributes to nonspecific disease resistance by destroying most ingested pathogens
Mucus is a protective barrier
- Impermeable mucosal cells: luminal membranes are impermeable to H+
- Tight junctions: prevent HCl from penetrating
- Mucous coat: physical barrier to HCl
- Chemical barrier: HCO3- neutralizes HCl
Regulation of gastric secretion
- neural control
Acetylcholine (ACh) – released by intrinsic nerve plexuses within the stomach, under the control of short local reflexes and vagal stimulation
Regulation of gastric secretion
- hormonal control
• Enterochromaffin-like (ECL) cells – secrete histamine among the parietal and chief cells (oxyntic mucosa)
• G cells – secrete gastrin into the bloodstream
- Food reaches mouth > g cells release gastin > stimulates
ECL and D cells > Histamine
• D cells – secrete somatostatin in response to acid
Shut down system
d cells sense change in pH and produce somatostatin
And has opposite affect and shuts down system
Control of gastric secretion involves three phases:
- cephalic phase -factors arising before food reaches the stomach (thinking of food - long reflex)
- gastric phase -factors resulting from food in the stomach (food is present)
- intestinal phase -factors in the duodenum after food has left the stomach
- Cephalic phase
– sight and thought of food increase gastric juices.
- Gastric phase
– begins when food is in the stomach (especially proteins).
- Intestinal phase
factor that originates in the small intestine (duodenum). Inhibitory phase, which helps with stomach emptying.
Gastritis
Breakdown of the mucus barrier can result in inflammation. >
Chemical breakdown of mucosal barrier: alcohol, aspirin and non steroidal
anti-inflammatory drugs (NSAIDs such as ibuprofen) > GASTRITIS
Redness (erythema) is caused by excessive production of HCl and gastric juices when no need it
Gastritis treatment
• antacids tablets: neutralize HCl
• lifestyle changes: avoid aggravating food (spicy food, coffee, chocolate, mint and
tomato).
Peptic ulcers
Extreme gastritis or bacterial infection increase the chance of developing peptic ulcers.
Discovery of the acid-resistant bacteria Helicobacter pylori • Flagella • Prefer to settle in the antrum (no parietal cells) • Production of urease to buffer HCl
Peptic ulcers trmt and diagnosis
Diagnosis: urea breath test (UBT), if positive endoscopy to check for ulcers
Treatment:
• antibiotics (2 weeks)
• proton pump inhibitors (action on H+-K+ ATPase pump)
• blocker for histamine receptor 2 (H2) (cimetidine): inhibits production of HCl, no effect on H1 receptors (involved in allergic respiration disorders)
• lifestyle changes