© 2013 Pearson Education, Inc. Surface epithelium Mucosa Lamina propria Muscularis mucosae Oblique layer Circular layer Longitudinal layer Submucosa (contains

© 2013 Pearson Education, Inc.

Surfaceepithelium

Mucosa Laminapropria

Muscularismucosae

ObliquelayerCircularlayerLongitudinallayer

Submucosa(containssubmucosalplexus)Muscularisexterna(containsmyentericplexus)Serosa

Layers of the stomach wallStomach wall

Figure 23.15a Microscopic anatomy of the stomach.


Enteroendocrine cell

Enlarged view of gastric pits andgastric glands

Chief cell

Parietal cell

Mucous neck cells

Surface epithelium (mucous cells)

Gastric pits

Gastricpit

Gastricgland

Figure 23.15b Microscopic anatomy of the stomach.


Figure 23.15c Microscopic anatomy of the stomach.

Mitochondria

Parietal cell

Chief cell

Enteroendocrine cell

Location of the HCl-producing parietal cellsand pepsin-secreting chief cells in a gastricgland

HCIPepsinPepsinogen


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


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


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


Figure 23.16 Photographs of a gastric ulcer and the H. pylori bacteria that most commonly cause it.

A gastric ulcer lesion H. pylori bacteria

Bacteria

Mucosalayer ofstomach


• 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.

http://en.wikipedia.org/wiki/Helicobacter_pylori

http://en.wikipedia.org/wiki/Helicobacter_pylori

http://consensus.nih.gov/1994/1994HelicobacterPyloriUlcer094html.htm


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.


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


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


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


HCIParietal cell

Interstitialfluid

HCO3−- Cl−

antiporter

Alkalinetide

H+-K+

ATPase

Stomach lumenChief cell

Gastric gland

H+

K+

CO2 CO2 H2O

H2CO3

+

HCO3−

H+

K+

Carbonicanhydrase

HCO3−

Bloodcapillary

Cl− Cl− Cl−

Figure 23.18 Mechanism of HCl secretion by parietal cells.


Figure 23.19 Deglutition (swallowing). Slide 4

Grinding: The most vigorous peristalsis and mixing action occur close to the pylorus.

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.

2 Propulsion: Peristaltic waves move from the fundus toward the pylorus.

1 3

Pyloricvalveclosed

Pyloricvalveclosed

Pyloricvalveslightlyopened


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


Presence of fatty, hypertonic,acidic chyme in duodenum

Duodenal entero-endocrine cells

Chemoreceptors andstretch receptors

Secrete Target

Enterogastrones(secretin, cholecystokinin,vasoactive intestinalpeptide)

Via shortreflexes

Via longreflexes

Duodenalstimulidecline

Entericneurons

CNS centers sympathetic activity; parasympathetic activity

Contractile force andrate of stomachemptying decline

Initial stimulus Stimulate

Inhibit

Figure 23.20 Neural and hormonal factors that inhibit gastric emptying.

Physiological response

Result



• 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)


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)


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


Figure 23.21 The duodenum of the small intestine, and related organs.

Right and left hepatic ducts of liver

Common hepatic duct

Bile duct and sphincterAccessory pancreatic duct

Tail of pancreasPancreas

Jejunum

Main pancreatic duct and sphincter

Head of pancreasHepatopancreaticampulla and sphincter Duodenum

Mucosawith folds

Gallbladder

Major duodenalpapilla

Cystic duct


Jejunum and Ileum

• Jejunum– Extends from duodenum to ileum– About 2.5 m long

• Ileum– Joins large intestine at ileocecal valve– About 3.6 m long


Structural Modifications

• Increase surface area for nutrient abs– Circular folds (plicae circulares)– Villi

• - Microvilli (brush border) – contain enzymes for carbs and protein dig


Figure 23.22a Structural modifications of the small intestine that increase its surface area for digestion and absorption.

Vein carryingblood tohepatic portalvessel

Musclelayers

Circularfolds

Villi

Lumen


Microvilli(brush border)

Absorptivecells

VillusLacteal

GobletcellBloodcapillaries

Mucosa-associatedlymphoidtissue

IntestinalcryptMuscularismucosae

Duodenalgland

Enteroendocrinecells

VenuleLymphatic vessel

Submucosa

Figure 23.22b Structural modifications of the small intestine that increase its surface area for digestion and absorption.



• Chemotherapy targets rapidly dividing cells– Kills cancer cells– Kills rapidly dividing GI tract epithelium

nausea, vomiting, diarrhea


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


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


The Liver and Gallbladder

• Accessory organs• Liver

– Many functions; only digestive function bile production• Bile – fat emulsifier

• Gallbladder– Chief function bile storage


• 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.


• 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.


Figure 23.25a–b Microscopic anatomy of the liver.

Lobule Centralvein

Connectivetissue septum


Liver: Microscopic Anatomy

• Liver sinusoids - leaky capillaries between hepatic plates

• Kupffer cells (hepatic or stellate macrophages) in liver sinusoids remove debris & old RBCs


Interlobular veins(to hepatic vein)

Central vein

Sinusoids

Plates ofhepatocytes

Portal vein

Stellate macrophagesin sinusoid walls

Bile canaliculi

Bile duct (receivesbile from bile canaliculi)

Fenestrated lining (endothelial cells) of sinusoids

Bile ductPortal venule

Portal arteriolePortal triad

Figure 23.25c Microscopic anatomy of the liver.


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


Liver

• Regenerative capacity– Restores full size in 6-12 m after 80% removal– Injury hepatocytes growth factors

endothelial cell proliferation


• Hepatitis– Usually viral infection, drug toxicity, wild

mushroom poisoning• Cirrhosis

– Progressive, chronic inflammation from chronic hepatitis or alcoholism

– Liver fatty, fibrous portal hypertension


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


Bile

• Enterohepatic circulation– Recycles bile salts– Bile salts duodenum reabsorbed from

ileum hepatic portal blood liver secreted into bile


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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© 2013 Pearson Education, Inc. Surface epithelium Mucosa Lamina propria Muscularis mucosae Oblique layer Circular layer Longitudinal layer Submucosa (contains