• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/47

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

47 Cards in this Set

  • Front
  • Back

Innervation of the GI tract

The autonomic nervous system of the GI tract comprises both extrinsic and intrinsic nervous systems

Extrinsic innervation

Parasympathetic; vagus and pelvic nerves, excitatory on the functions of the GI tract




Sympathetic; inhibitory on the functions of the GI tract,

Intrinsic innervation

Local reflexes to relay information within the GI tract




Control most functions of the GI tract,


- Myenteric plexus (motility)


- Submucosal plexus (secretion and blood flow)

What are the official GI hormones?

- Gastrin


- Cholecystokinin (CCK)


- Secretin


- Glucose-dependent insulinotropic peptide (GIP)

Gastrin

- G cells of stomach


- Stimulated by; small peptides and amino acids, distention of stomach, vagus (GIP),


- Inhibited by; H+ in stomach, somatostatin


- Actions; increase gastric H+ secretion (parietal cells), stimulates growth of gastric mucosa

CCK

- I cells of duodenum and jejunum


- Stimulated by; small peptides and amino acids, fatty acids


- Actions; contraction of gallbladder and relaxation of sphincter of Oddi, increased; pancreatic enzyme and bicarbonate secretion and growth of exocrine pancreas/gallbladder, inhibit gastric emptying

Secretin

- S cells of duodenum


- Stimulated by; H+ in duodenum, fatty acids in duodenum


- Actions; increase pancreatic bicarbonate secretion and biliary bicarbonate secretion, decreased gastric H+ secretion

GIP

- Duodenum and jejunum


- Stimulated by; fatty acids, amino acids and oral glucose


- Actions; increased insulin secretion, decreased gastric H+ secretion

Motilin

Increases GI motility and is involved in interdigestive myoelectric complexes

Pancreatic polypeptide

Inhibits pancreatic secretion

Glucagon-like peptide-1 (GLP-1)

Binds to pancreatic beta cells and stimulates insulin secretion. Analogue of GLP-1 may be helpful in the treatment of type II diabetes mellitus

Paracrines

- Diffuse short distances to act on target cells located in the GI tract


- The GI paracrine are somatostatin and histamine

Somatostatin

- Secreted in response to H+ in the lumen


- Inhibited by vagal stimulation


- Inhibits the release of all GI hormones and gastric H+ secretion

Histamine

- Secreted by mast cells of the gastric mucosa


- Increases gastric H+ secretion directly and by potentiating the effects of gastrin and vagal stimulation

Neurocrines

- Synthesized in neurons of the GI tract, moved by axonal transport down the axons and released by action potentials in the nerves


- GI neurons are; VIP, GRP and enkephalins



VIP

- Released from neurons in the mucosa and smooth muscle of the GI tract


- Produces relocation of GI smooth muscle, inkl. lower esophageal sphincter


- Stimulates pancreatic HCO3- secretion


- Inhibits gastric H+ secretion

GRP

- Released from vagus nerves that innervate the G cells


- Stimulates gastrin release from G cells

Enkephalins

- Secreted from nerves in the mucosa and smooth muscle of GI tract


- Stimulate contraction of GI smooth muscle


- Inhibit intestinal secretion of fluid and electrolytes

Leptin

- Secreted by fat cells


- Decreases appetite

Ghrelin

- Secreted by gastric cells


- Increases appetite

Slow waves

Are oscillating membrane potentials inherent to the smooth muscle cells of some parts of the GI tract (Cajal cells)

Gastric motility

Gastric contractions are increased by vagal stimulation and decreased by sympathetic stimulation

Gastric emptying

- Fastest when the stomach contents are isotonic


- Fat inhibits gastric emptying (CCK)


- H+ in the duodenum inhibits gastric emptying

Small intestinal motility

Parasympathetic stimulation increases intestinal smooth muscle contraction and sympathetic stimulation decreases it

Segmentation contractions


(small intestine)

Mix the intestinal contents

Peristaltic contractions


(small intestine)

Propel the chyme through the small intestine toward the large intestine




Coordinated by the enteric nervous system

Gastroileal reflex


(small intestine)

Mediated by the extrinsic ANS and possibly by gastrin.




The presence of food in the stomach triggers increased peristalsis in the ileum and relaxation of the ileocecal sphincter.

Segmentation contractions


(large intestine)

In the proximal colon mic the contents and are responsible for the appearance of haustra

Gastrocolic reflex


(large intestine)

The presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements.The reflex has a rapid parasympathetic component that is initiated when the stomach is stretched by food. A slower, hormonal component is mediated by CCK and gastrin.

Formation of saliva

By the parotid, submandibular and sublingual glands.

Regulation of saliva production

- Controlled by parasympathetic and sympathetic nervous systems (increased by both)

Parasympathetic regulation of saliva production

- Cranial nerves VII and IX


- By increasing transport processes in the acinar and ductal cells and by causing vasodilation

Sympathetic regulation of saliva production

Increases the production of saliva and the growth of salivary glands, although the effects are smaller than those of parasympathetic stimulation

Which factors affect saliva production?

Increased by;


food, smells, conditioned reflexes and nausea




Decreased by; sleep, dehydration, fear, anticholinergic drugs

What stimulates gastric H+ secretion?

- Vagal stimulation


- Gastrin


- Histamine

What inhibits gastric H+ secretion?

- Negative feedback of gastrin


- Somatostatin; inhibit release of histamine and gastrin


- Prostaglanding

Which drugs block gastric H+ secretion?

- Antropine


- Cimetidine


- Omeprazole

Antropine

A cholinergic muscarinic antagonist, inhibits H+ secretion by blocking the direct pathway, which uses ACh as a neurotransmitter. However, atropine does not block H+ secretion to completely because it does not inhibit the indirect pathway, which uses GRP as a neurotransmitter.

Pancreatic secretion

Much higher bicarbonate concentration than plasma - to neutralize the acidic chyme. Contains enzymes essential for the digestion of protein, carbohydrate and fat.




Isotonic

Stimulation of pancreatic secretion

- Secretin


- CCK


- ACh

Composition of bile

Bile contains;


bile salts, phospholipids, cholesterol and bile pigments (bilirubin)

Production of bile

- Produced continuously by hepatocytes


- Stored in the gallbladder


- The bile acids are conjugated with glycine or taurine to form bile salts

Carbohydrates

Absorbed in the small intestine by Na+-dependent cotransport (glucose, galactose) and facilitated diffusion (fructose).

Proteins

Absorbed in the small intestine by Na+-dependent cotransport (amino acids) and H+-dependent cotransport (di- and tripeptides)

Digestion of proteins

- Endopeptidases; degrade proteins by hydrolyzing interior peptide bonds


- Exopeptidases; hydrolyze one amino acid at a time from the C terminus of proteins and peptides


- Pepsin; pepsinogen activated to pepsin when low pH


- Pancreatic proteases; trypsinogen activated to trypsin by enterokinase

Lipids

- Absorbed in the small intestine


- Micelles form with bile salts in intestinal lumen


- Diffusion of fatty acids, monoglycerides and cholesterol into cell


- re-esterification in cell to triglycerides and phospholipids


- Chylomicrons form in cell to and are transferred to lymph

Bilirubin production and excretion

Hemoglobin is degraded to bilirubin by the reticuloendothelial system. Bilirubin binds to albumin in the circulation system. In the liver bilirubin is conjugated with glucuronic acid. A portion of conjugated bilirubin is excreted in the urine, and a portion into bile. In the intestine, it is converted to urobilinogen, which is returned to the liver and excreted as stercobilin and urobilin in feces.