1. Layers of the stomach wall
Figure 23.15a Microscopic anatomy of the stomach.
Surface
epithelium
Mucosa
Lamina
propria
Muscularis
mucosae
Submucosa
(contains
submucosal
plexus)
Oblique
layer
Muscularis
externa
(contains
myenteric
plexus)
Circular
layer
Longitudinal
layer
Serosa
Stomach wall
Layers of the stomach wall
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2. Enlarged view of gastric pits and gastric glands
Figure 23.15b Microscopic anatomy of the stomach.
Gastric pits
Surface epithelium
(mucous cells)
Gastric
pit
Mucous neck cells
Parietal cell
Gastric
gland
Chief cell
Enteroendocrine cell
Enlarged view of gastric pits and
gastric glands
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3. Location of the HCl-producing parietal cells
Figure 23.15c Microscopic anatomy of the stomach.
Pepsinogen
Pepsin
HCI
Mitochondria
Parietal cell
Chief cell
Enteroendocrine
cell
Location of the HCl-producing parietal cells
and pepsin-secreting chief cells in a gastric
gland
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4. Gastric Gland Secretions
Parietal cell secretions
HCl
 pH 1.5–3.5 denatures protein, activates pepsin, breaks down plant cell walls, kills many bacteria
Intrinsic factor
Glycoprotein req for abs of vit B12 in SI
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5. Gastric Gland Secretions
Chief cell secretions
Pepsinogen - inactive enzyme
Activated to pepsin by HCl and by pepsin itself (a positive feedback mechanism)
and milk protein by rennin in infants
Lipases
Digest ~15% of lipids
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6. Homeostatic Imbalance
Gastritis
Inflammation caused by anything that breaches mucosal barrier
Peptic or gastric ulcers
Erosions of stomach wall
Can perforate  peritonitis; hemorrhage
Most caused by Helicobacter pylori bacteria
Some by NSAIDs
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7. Bacteria Mucosa layer of stomach A gastric ulcer lesion
Figure Photographs of a gastric ulcer and the H. pylori bacteria that most commonly cause it.
Bacteria
Mucosa
layer of
stomach
A gastric ulcer lesion
H. pylori bacteria
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8. Australia’s Barry Marshall, knew ulcers afflicted 10 % of all adults
Australia’s Barry Marshall, knew ulcers afflicted 10 % of all adults. In 1981 Marshall discovered the gut could be overrun by hardy, corkscrew-shaped bacteria Helicobacter pylori. Biopsying ulcers and culturing the organisms, Marshall traced not just ulcers but also stomach cancer to this gut infection. The cure, was readily available: antibiotics. But mainstream gastroenterologists were dismissive, holding on to the old idea that ulcers were caused by stress.
Unable to make his case in studies with lab mice (because H. pylori affects only primates) and prohibited from experimenting on people, he grew desperate. Finally he ran an experiment on the only human he could ethically recruit: himself. He took some H. pylori, stirred it into a broth, and drank it. As the days passed, he developed gastritis, the precursor to an ulcer: He started vomiting, his breath stunk and he felt sick. Back in the lab, he biopsied his own gut, culturing H. pylori and proving unequivocally that bacteria were the underlying cause of ulcers.
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9. Digestive Processes in the Stomach
Lipid-soluble alcohol and aspirin absorbed into blood
Only stomach function essential to life
Secretes intrinsic factor for vit B12 abs
Pernicious anemia, the body can't make enough RBCs because it doesn't have vit B12 to divide normally and are too large. They may have trouble getting out of bone marrow.
You may feel tired and weak. Severe, long-lasting pernicious anemia can damage the heart, brain, and can cause nerve damage, neurological problems (such as memory loss), and digestive problems.
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10. Regulation of Gastric Secretion
Neural and hormonal mechanisms
Gastric mucosa  up to 3 L gastric juice/day
Vagus nerve stimulation  secretion 
Sympathetic stimulation  secretion 
Hormonal control largely gastrin
 Enzyme and HCl secretion
Most SI secretions - gastrin antagonists
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11. Regulation of Gastric Secretion
Three phases of gastric secretion
Cephalic (reflex) phase – conditioned reflex triggered by aroma, taste, sight, thought
Gastric phase – lasts 3–4 hours; ⅔ gastric juice released
Stimulated by distension, peptides, low acidity, gastrin (major stimulus)
Enteroendocrine G cells stimulated by caffeine, peptides, rising pH  gastrin
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12. HCl Formation
Parietal cells pump H+ (from carbonic acid breakdown) into stomach lumen
K+ goes into cells to balance charge
HCO3– from carbonic acid breakdown
 blood (via Cl– and HCO3– antiporter)
 blood leaving stomach more alkaline  Alkaline tide
Cl– (from blood plasma via antiporter) follows H+ HCl
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13. Gastric gland Blood capillary Chief cell Stomach lumen CO2 CO2 + H2O
Figure Mechanism of HCl secretion by parietal cells.
Gastric gland
Blood
capillary
Chief cell
Stomach lumen
CO2
CO2 +
H2O
H+-K+
ATPase
Carbonic
anhydrase
H2CO3 H+ H+ K+ K+
HCO3−
HCI
Alkaline
tide
Parietal cell
HCO3−
Cl−
Cl−
Cl−
HCO3−- Cl−
antiporter
Interstitial
fluid
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14. Pyloric Pyloric Pyloric valve valve valve slightly closed closed
Figure Deglutition (swallowing).
Slide 4
Pyloric
valve
slightly
opened
Pyloric
valve
closed
Pyloric
valve
closed
Propulsion: Peristaltic waves move from the fundus toward the pylorus. 1
Grinding: The most vigorous peristalsis and mixing action occur close to the pylorus. 2
Retropulsion: The pyloric end of the stomach acts as a pump that delivers small amounts of chyme into the duodenum, simultaneously forcing most of its contained material backward into the stomach. 3
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15. Regulation of Gastric Emptying
As chyme enters duodenum
Receptors respond to stretch and chemical
Enterogastric reflex inhibit gastric secretion and duodenal filling
Carb-rich chyme moves quickly through
Fatty chyme remains duodenum 6 hrs or more
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16. Physiological response
Figure Neural and hormonal factors that inhibit gastric emptying.
Presence of fatty, hypertonic,
acidic chyme in duodenum
Duodenal entero-
endocrine cells
Chemoreceptors and
stretch receptors
Secrete
Target
Enterogastrones
(secretin,
cholecystokinin,
vasoactive intestinal
peptide)
Via short
reflexes
Via long
reflexes
Enteric
neurons
CNS centers
sympathetic
activity;
parasympathetic
activity
Duodenal
stimuli
decline
Contractile force and
rate of stomach
emptying decline
Initial stimulus
Stimulate
Physiological response
Inhibit
Result
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17. Homeostatic Imbalance
Vomiting (emesis) caused by
Extreme stretching
Intestinal irritants, e.g., bacterial toxins, excessive alcohol, spicy food, certain drugs
Chemicals/sensory impulses  emetic center of medulla
Excessive vomiting  dehydration, electrolyte and acid-base imbalances (alkalosis)
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18. Small Intestine: Gross Anatomy
Major organ of digestion and absorption
2-4 m long; from pyloric sphincter to ileocecal valve (TI)
Subdivisions
Duodenum (retroperitoneal)
Jejunum (attached posteriorly by mesentery)
Ileum (attached posteriorly by mesentery)
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19. Curves around head of pancreas; shortest part – 25 cm
Duodenum
Curves around head of pancreas; shortest part – 25 cm
Bile duct and main pancreatic
Join at hepatopancreatic ampulla
Enter duodenum at duodenal papilla
Entry controlled by hepatopancreatic sphincter
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20. Bile duct and sphincter Accessory pancreatic duct
Figure The duodenum of the small intestine, and related organs.
Right and left
hepatic ducts
of liver
Common hepatic duct
Bile duct and sphincter
Accessory pancreatic duct
Tail of pancreas
Pancreas
Jejunum
Main pancreatic duct and sphincter
Head of pancreas
Hepatopancreatic
ampulla and sphincter
Duodenum
Mucosa
with folds
Gallbladder
Major duodenal
papilla
Cystic duct
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21. Jejunum and Ileum Jejunum Ileum Extends from duodenum to ileum
About 2.5 m long
Ileum
Joins large intestine at ileocecal valve
About 3.6 m long
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22. Structural Modifications
Increase surface area for nutrient abs
Circular folds (plicae circulares)
Villi
- Microvilli (brush border) – contain enzymes for carbs and protein dig
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23. Vein carrying blood to hepatic portal vessel Muscle layers Lumen
Figure 23.22a Structural modifications of the small intestine that increase its surface area for digestion and absorption.
Vein carrying
blood to
hepatic portal
vessel
Muscle
layers
Lumen
Circular
folds
Villi
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24. Villus Venule Lymphatic vessel Submucosa
Figure 23.22b Structural modifications of the small intestine that increase its surface area for digestion and absorption.
Microvilli
(brush border)
Absorptive
cells
Lacteal
Villus
Goblet
cell
Blood
capillaries
Mucosa-
associated
lymphoid
tissue
Intestinal
crypt
Enteroendocrine
cells
Venule
Muscularis
mucosae
Lymphatic vessel
Duodenal
gland
Submucosa
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25. Homeostatic Imbalance
Chemotherapy targets rapidly dividing cells
Kills cancer cells
Kills rapidly dividing GI tract epithelium  nausea, vomiting, diarrhea
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26. Peyer's patches protect against bacteria
Mucosa
Peyer's patches protect against bacteria
B lymphocytes leave intestine, enter blood, protect intestinal with IgA
Duodenal glands of duodenum secrete alkaline mucus to neutralize acidic chyme
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27. 1-2 L secreted d in response to distension or irritation of mucosa
Intestinal Juice
1-2 L secreted d in response to distension or irritation of mucosa
Slightly alkaline
Largely water; enzyme-poor (enzymes of small intestine only in brush border); contains mucus
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28. The Liver and Gallbladder
Accessory organs
Liver
Many functions; only digestive function  bile production
Bile – fat emulsifier
Gallbladder
Chief function  bile storage
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29. Attorney General John Ashcroft was in intensive care after what he thought was a bout of stomach flu turned out to be a severe case of a pancreatic ailment. After complaining of stomach pain Ashcroft, 61, was taken to the ER
His condition was diagnosed as ''a severe case'' of gallstone pancreatitis, which is an inflammation of the pancreas. The department did not specify which type the attorney general had, but gallstone pancreatitis is usually considered the less serious variety.
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30. Physician Ron Shemenski 59, passed a gallstone and had pancreatitis
Physician Ron Shemenski 59, passed a gallstone and had pancreatitis. Subsequently the NYAir National Guard was mobilized for a medevac. Flights to the South Pole base are normally halted winter because of extreme cold with temp up to 75 degrees below zero..
But rescuers are worried that Dr Shemenski's condition could worsen in the coming months when an airlift would be virtually impossible.
In October 1999, Dr Jerri Nielsen, the lone physician at the Amundsen-Scott Station was evacuated after she discovered a breast tumor that was diagnosed as cancerous.
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31. Lobule Central vein Connective tissue septum
Figure 23.25a–b Microscopic anatomy of the liver.
Lobule
Central
vein
Connective
tissue septum
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32. Liver: Microscopic Anatomy
Liver sinusoids - leaky capillaries between hepatic plates
Kupffer cells (hepatic or stellate macrophages) in liver sinusoids remove debris & old RBCs
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33. Interlobular veins (to hepatic vein) Central vein Sinusoids
Figure 23.25c Microscopic anatomy of the liver.
Interlobular veins
(to hepatic vein)
Central vein
Sinusoids
Plates of
hepatocytes
Portal vein
Stellate macrophages
in sinusoid walls
Bile canaliculi
Bile duct (receives
bile from bile
canaliculi)
Fenestrated
lining (endothelial
cells) of sinusoids
Bile duct
Portal venule
Portal arteriole
Portal triad
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34. Liver: Microscopic Anatomy
Hepatocytes – increased rough & smooth ER, Golgi, peroxisomes, mitochondria
Hepatocyte functions
Process bloodborne nutrients
Store fat-soluble vitamins
Perform detoxification
Produce ~900 ml bile per day
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35. Regenerative capacity
Liver
Regenerative capacity
Restores full size in 6-12 m after 80% removal
Injury  hepatocytes  growth factors  endothelial cell proliferation
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36. Hepatitis
Usually viral infection, drug toxicity, wild mushroom poisoning
Cirrhosis
Progressive, chronic inflammation from chronic hepatitis or alcoholism
Liver  fatty, fibrous  portal hypertension
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37. Yellow-green, alkaline solution containing
Bile
Yellow-green, alkaline solution containing
Bile salts - cholesterol derivatives that function in fat emulsification and absorption
Bilirubin - pigment formed from heme
Bacteria break down in intestine to stercobilin  brown color of feces
Cholesterol, neutral fats, phospholipids, and electrolytes
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38. Enterohepatic circulation
Bile
Enterohepatic circulation
Recycles bile salts
Bile salts  duodenum  reabsorbed from ileum  hepatic portal blood  liver  secreted into bile
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39. Stores and conc bile by abs water
The Gallbladder
Stores and conc bile by abs water
Muscular contractions release bile via cystic duct, which flows into bile duct
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