Physiology Lecture 50

Physiology Lecture 50

Tanveer Raza MD MS MBBS

[email protected]

Tanveer Raza MD MS [email protected]

ESOPHAGUS-STOMACH JUNCTIONLongitudinal section


Gastric Secretion

Tubular Glands Pyloric glands

Secretes Mucus Gastrin

Oxyntic Glands


Gastric Secretion Tubular Glands

Pyloric glands

Oxyntic Glands Type of cells

Mucous neck cells Mucus

Peptic or Chief Cells Pepsinogen

Parietal (or Oxyntic) cells Hydrochloric acid Intrinsic factorSTOMACH

Fundus


Gastric Secretion: Mechanism of HCL secretion

pH=0.8 (H+ concentration is 3 million times of

arterial blood) Concentration of 150-160 mEq/L


Gastric Secretion: Mechanism of HCL secretion


Gastric secretion: Postprandial Alkaline Tide

Postprandial alkaline tide Postprandial increased gastric acid

secretion results in more H+ being secreted

Raises pH of systemic blood

Urine becomes alkaline (Postprandial alkaline tide)


Gastric Secretion: HCl secretion

3 stimulators of acid secretion in Parietal cells Acetylcholine

via M3 muscarinic receptors, Increases intracellular free Ca++

Gastrin Increases intracellular free Ca++

Histamine via H2 receptors, Increases intracellular cAMP



Prostaglandin inhibits acid secretion by activating Gi


Enterochromaffin-like (ECL) cells

Neuroendocrine cells Found in gastric mucosa Synthesize and secrete

Histamine Other peptide hormones


Enterochromaffin-like (ECL) cells

ECL secrete histamine in response toGastrinVagal stimulation

Acetylcholine Other hormonal substance

Histamine secretion is inhibited by somatostatin


Enterochromaffin-like (ECL) cellsHCl secretion by parietal cells is directly related to the amount of histamine secreted by ECL cells


Enterochromaffin-like (ECL) cellsFood stimulates release of gastrin from antral G cells (G). Gastrin stimulates ECL cells to release histamine, which stimulates parietal cells (P) in the gastric corpus to secrete HCl. HCl stimulates release of somatostatin from somatostatin cells (S) in the antrum, inhibiting further gastrin release

BMJ. 2001 October 27; 323(7319): 980–982


Gastric Secretion: Pepsinogen

Pepsinogen

Pepsinogen PepsinProteolytic enzyme

HCl


Gastric Secretion: Intrinsic Factor

Intrinsic factor Essential for Vitamin B12 absorption in ileum Secreted by parietal cells If parietal cells are destroyed (Chronic

gastritis) achlorhydria and pernicious anemia will develop


Hormonal Control of GI motility

Gastrin

Cholecystokinin

Secretin

Gastric inhibitory peptide

Motilin


Hormonal Control of GI motility Gastrin

Secreted by "G" cells of antrum of stomach Cause of secretion

Presence of food in stomach Distention of the stomach Products of proteins digestion Gastrin releasing peptide

Function Stimulation of gastric acid and pepsin secretion Stimulation of growth of gastric mucosa


Hormonal Control of GI motility Cholecystokinin

Secreted by "I" cells in the mucosa of duodenum and jejunum

Cause of secretion Mainly in response to digestive products of fat,

fatty acids, and monoglycerides in intestinal contents

Function Strongly contracts gallbladder Inhibits stomach contraction moderately



Secretin Secreted by the "S" cells in the mucosa of

the duodenum Cause of secretion

Acidic gastric juice emptying into duodenum from stomach

Function Mild effect on GIT motility Promotes pancreatic secretion of HCO3



Gastric inhibitory peptide Secreted by the mucosa of the upper small

intestine Cause of secretion

Fatty acids and amino acids but to a lesser extent in response to carbohydrate

Function Mild effect in decreasing motor activity of the

stomach



Motilin Secreted by the upper duodenum during

fasting Function

Increase GI motility


GI Blood Flow: Splanchnic Circulation

Blood from GIT, spleen and pancreas flow into liver by portal vein. After passing liver sinusoids, through hepatic veins drains into inferior vena cava


GI Blood Flow: Splanchnic Circulation Reticuloendothelial (RE) cells lining liver

sinusoids remove potentially harmful agents Nonfat, water-soluble nutrients absorbed from

GIT (such as carbohydrates & proteins) are absorbed and stored temporarily by RE cells and hepatic cells

Fat is absorbed by intestinal lymphatics, then to systemic circulation by thoracic duct, bypassing liver


GI Blood Flow:"Countercurrent" Blood Flow in Villi

Similar to vasa recta in renal medulla

Arterial & venous flow in opposite directions

Vessels lie in close apposition


GI Blood Flow:"Countercurrent" Blood Flow in Villi

Much of O2 diffuses out of arterioles directly into venules without being carried to the tips of the villi Normal conditions: not harmful

Disease conditions when blood flow reduced: O2 deficiency can cause ischemia to the villus tip or the whole villus


GI Blood Flow: Nervous Control

Parasympathetic supply: Increases local blood flow to stomach and

lower colon

Sympathetic supply: Intense vasoconstriction of GIT arterioles

with greatly decreased blood flow


GI Blood Flow: Nervous Control Parasympathetic supply

Sympathetic supply: Importance

During heavy exercise, more flow to skeletal muscle & heart

In circulatory shock to body's vital tissues In hemorrhagic shock to general

circulation


GI Blood Flow: Autoregulatory Escape

After few minutes of vasoconstriction, flow often returns almost to normal by "autoregulatory escape"

Sympathetic vasoconstriction

Ischemia

Local metabolic vasodilator

Redilate the arterioles


Phases of Gastric Secretion 3 "phases"

Cephalic Gastric Intestinal


Phases of Gastric Secretion Cephalic Phase

Before food enters the stomach, especially while being eaten

20% of the secretion

Gastric Phase Intestinal Phase


Phases of Gastric Secretion Cephalic Phase

Gastric Phase Once food enters the stomach, Due to

long vagovagal reflexes local enteric reflexesGastrin

About 70% of total secretion

Intestinal Phase


Phases of Gastric Secretion Cephalic Phase Gastric Phase

Intestinal Phase Food in upper portion of small intestine

Thank You

Physiology Lecture 50

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