Stomach Flashcards
Chief Cells
- Secrete pepsinogen, rennin, lipase
- Lots of RER for enzyme production and storage in apical granules
- Inc secretion if Ach and dec if somatostatin
- Location: mainly fundus and body
Parietal Cells
- Secrete HCl and Intrinsic Factor for Binding Vit B12
- Round w/ central nucleus and homogeneous bright pink cyto b/c so much mito (need oxygen to pump H+ out via H-K-ATPase)
- Many folds w/ intracellular canaliculi (microvilli) and tubulovesicular system to aid in acid secretion/inc SA (many H-K pumps on surface)
- Stim by … histamine, gastrin, Ach (has receptors for these on basal side)
- Inhib by… somatostatin, VIP, prostaglandins
- Location: cardia, fundus, body
G Cells
- Produce gastrin which stim parietal cells to inc HCl release by binding CCK receptors on parietal cells
- Gastrin also inc histamine secretion; proliferation of mucosa; promotes peristalsis (gastro-colic reflex)
- Inc secretion if proteins/AA in lumen –> Galpha Q -> IP3/DAG –> Ca++ and secondary messengers
- look like pale fried eggs on histo
- Location: esp in antrum and pylorus
ECL Cells
- histamine release –> bind H2 receptors on parietal cells –> G alpha s –> inc cAMP –> up-reg kinases –> activate more H/K ATPases
D Cells
- somatostatin release (FEEDBACK) –> inhibit G cells, ECL cells, parietal cells and chief cells
- inhibit stomach contractions and initiate housekeeping MMC waves in duodenum
- Somatostatin directly binds parietal cell membrane –> G alpha i –> dec cAMP –> down-reg kinases –> dec activation of H/K ATPase
- Somatostatin indirectly binds G cells to inhibit gastrin release
- Location: mainly antrum
Blood Supply + Venous Drainage (esophageal v. gastric varices)
- Branches off celiac artery (rich and redundant so very rarely ischemic)
- Lesser curve - L and R gastric
- Greater curve - L and R gastoepiploic arteries
- Fundus - short gastric arteries off splenic
- Venous Drainage
- Drains into portal system
- Collaterals b/n gastric vein and esophageal vein –> esophageal varices in portal HTN
- If short gastric veins that drain fundus and superior greater curve back up –> gastric varices (if splenic vein thrombosis)
- Drains into portal system
3 Phases of Secretion Regulation
- Cephalic Phase - sight, smell, thought of food stimulates acid secretion
(vagus Ach release –> M3 receptors on parietal cell basolateral membrane –> G alpha q –> PIP2 –> Ca++ –> up-reg kinases –> activate more H/K ATPases) - Gastric Phase - distention in stomach, nutrients and chemicals stimulate acid secretion
(gastrin and histamine effects on parietal cells) - Intestinal Phase - FEEDBACK INHIB of acid secretion based on fats, low pH, distention in SI
3 Ways to Inhibit Parietal Cells
- Somatostatin - directly binds parietal cell membrane –> G alpha i –> dec cAMP –> down-reg kinases –> dec activation of H/K ATPase AND indirectly binds G cells to inhibit gastrin release
Prostaglandins - directly binds parietal cell membrane –> G alpha i –> dec cAMP –> down-reg kinases –> dec activation of H/K ATPase
VIP (from D1 cells)
3 Functions of Stomach Beyond Secretion
1- Filling - requires relaxation - vagal receptive relaxation in response to swallowing + local reflexes and paracrine factors
2- Mixing - powerful contractions (esp in antrum) to disintegrate food
3- Emptying
- Liquids empty quickly - Solids - LAG phase then gradual emptying phase
Hypertrophic Pyloric Stenosis
- congenital outlet obstruction due to loss of inhibitory NO neurons in pylorous
- Infants projectile vomit; dx by barium swallow or ultrasound then repair surgically
Gastric Volvulus
- RARE; abnormal rotation >180 degrees
- Acute - due to compromise/block of blood supply
- Chronic - causing vague discomfort
- Tx - surgery
Zollinger Ellison Syndrome
- Rare disease of excess gastrin secretion by endocrine tumor (usually in upper ab- in or near pancreas)
- Gastrin secretion not down-reg by acid like normal G cells
- Leads to hypertrophy of gastric folds, proliferation of parietal cells, excess acid secretion –> injury/ulcers/reflux
- Can also cause high volume loos bowel movements
- Dx and Tx - use somatostatin analogue (octreotide)
What is the most common gastric infection? (details and how to treat)
H Pylori
- Gram neg, microaerophillic (hard to cx), spiral bacillus
- Urease enzyme (dec acidity of stomach) so only colonizes stomach; urease breath test
- Flagella, adhesins, catalase
- Fecal-oral transmission
- Histo - see band-like infiltrate (just affects superficial band of stomach along lumen)
- Goal is to eradicate in all pts w/ or w/o ulcers due to role in peptic ulcer disease (triple treatment - 2 abx to avoid resistance and PPI esp if pH dep abx)
H Pylori Tx
Std -PPI + Clarithomycin + Amox
If PCN allergy - PPI + Clarithomycin + Metro
If PCN allergy or tx fails - PPI + Tetracycline + Metro + Bismuth
**All regimens for 10-14 days
Other Gastric Infections
- Rarely mycobacterium tuberculosis or MAC or treponema pallidum (syphilitic gastritis)
- Viral can be CMV and HSV in immune-comp
- Fungi rare but can include Candida, aspergillus, histo and mucor
- Parasites = cryptosporidium, Giardia, anisakis marina (in ingested fish) and Strongyloides stercoralis