The Digestive System

1. The Digestive System Gastrointestinal tract Physiology Dr. Suaad M. Ghazi MBChB, MSc, PhD

2. Objectives of lecture 5 1. Explain the mechanism of vomiting. 2. Explain the function of the small intestine and ileocecal valve. 3. Describe how entry of pancreatic juice into the small intestine is regulated and state the role of pancreatic juice in digestion.

3. Peptic ulcer disease Gastric ulcer Duodenal ulcer Gastric mucosa cannot protect itself by existing level of gastric juice due to reduced defence capacity. Result of increased exposure of duodenal mucosa to gastric juice. Factors that maintaining mucosal resistance : 1. adequate blood flow to the gastric mucosa. 2. production of mucus. 3. cellular renewal. 4. chemical factors ( gastrin, PG, EGF), increase the resistance of cells to toxic conditions. ♦ Chronic use of NSAID inhibiting PG synthesis.

4. ♦ Recent studies have shown that major acquired factor responsible for both gastric and duodenal ulcers is the bacterium Helicobacter pylori. ♦ H. pylori infections are present in 95% of patients with duodenal ulcers and 100% of patients with gastric ulcers, suggesting that this is one of multiple contributing factors. ♦ H. Pylori cytotoxicity because NH4 + directly damages epithelial cells and weakens the mucosal barrier. It may also increase gastric acid production by unknown mechanism. Treatment of ulcers H2-receptor blockers or omeprazole in combination + Flagyl + Antibiotics.

5. The dumping syndrome: Develop after surgery to remove all or part of stomach or after bypass stomach.  It occurs because food moves from stomach into small bowel too quickly.  Rapid emptying of the stomach can lead to low pH, elevated tonicity in the duodenum,  Incomplete digestion and absorption, particularly of fat and protein.

6.  The unabsorbed food retains osmotically water, which in conjunction with the increased rate of intestinal transport  diarrhea and steatorrhea (fat in the feces).  The by-products of the bacterial metabolism of undigested food in the terminal ileum and colon can cause intestinal cramping, gas, and bloating. Weakness, dizziness, sweating, and hypoglycemia.  Rapid entry of a hypertonic meal into the intestine promotes the movement water into the gut hypovolemia and hypotension.

7. Gastric digestion and absorption:  Carbohydrate digestion in the stomach  salivary amylase.  Protein digestion occurs in the stomach by about 10% and mediated by HCl and later by gastric pepsin.  Fat digestion is minimal in the stomach due to restriction of gastric lipase activity.  Very little absorption of nutrients takes place in the stomach (highly lipid-soluble substances e.g., the non-ionized triglycerides of acetic, propionic, and butyric acids).

8.  Aspirin at gastric pH is non-ionized and fat soluble, after absorption, it ionizes intracellularly, damaging mucosal cells and ultimately producing bleeding.  Ethanol is rapidly absorbed in proportion to its concentration.  Water moves in both directions across the mucosa. Water-soluble substances including Na+, K+, glucose, and amino acids, are very poorly absorbed.  Speed of delivery of nutrients from stomach to small intestine is as follow: CHO > protein > fat

9. Vomiting (emesis)  It is a forceful expulsion of contents of the stomach and upper intestinal tract through the mouth.  Vomiting is a reflex coordinated by the region in the brain stem medulla known as the vomiting center  parasympathetic vagal and sympathetic nerves  motor spinal nerves  diaphragm and abdominal muscles.

10. Stimuli elicit vomiting • Tactile (touch) stimulation of the back of the throat. • Irritation or distension of the stomach and duodenum. • Stimulation of higher cortical centers by memory, feel, anticipation, sensory input (pain, smell, sight). • Elevated ICP (vomiting after a head injury bad sign  swelling or bleeding. • Rotation or acceleration of the head producing dizziness, such as in motion sickness. • Body chemistry disturbances and chemical agents (drugs or noxious substances, chemotherapeutic agents).

12. The vomiting reflex Vomiting centre medulla oblongata Vomit Efferent fibres: phrenic & vagus nerve LES, UES & pharynx relaxed Afferent fibres: pain, bloating, inflammation, irritants, toxins.... Diaphragm fixed for inspiration Contraction of duodenum, pylorus and antrum Intercostal muscles contracted… High abdominal muscular pressure

14.  The importance of vomiting is to remove the ingested toxic substances before they can be absorbed. • Vomiting begins with: • Increased salivation, sweating, increased heart rate, pallor, and feeling of nausea. •  Retching is the reverse movement (peristalsis) of the stomach and esophagus without vomiting. • Deep inspiration, closure of the glottis, and elevation of the soft palate. • The abdominal and thoracic muscles contract. • The lower esophageal sphincter relaxes. •  Excessive vomiting  large losses of fluid and salts  severe dehydration.

15. Small intestine

16. Small intestine Gross Anatomy

17. Small intestine  The small intestine has three parts: the duodenum, the jejunum, and the ileum.  It is approximately 5 m long.  The major site of digestion and absorption of carbohydrates, proteins, and fats.  An absorptive area of over 250 m2  numerous folds of the intestinal mucosa (valvulae conniventes or plica circulares)  finger-like projections called villi and microvilli (enterocytes) .

18.  The microvilli give the intestinal mucosa its characteristics brush border appearance.  The exposure of the lamina propria to digestive enzymes can cause internal bleeding and other serious problems.  Peristalsis in the small intestine is very weak, intense irritation of the intestinal mucosa (infectious diarrhea), can cause both very powerful and rapid peristalsis called the peristaltic rush  initiated by vagovagal nervous reflexes to the brain stem  sweep the contents into the colon and thereby relieving the small intestine of either irritative chyme or excessive distension.

19. Function of the ileocecal valve  Ileocecal valve is prevent backflow of fecal content from the colon into the small intestine by ileocecal sphincter .  Following meal, both gastroileal reflex (intensifies peristalsis) and gastrin (relaxant effect on the ileocecal sphincter)  increase emptying.  Distended cecum intensified ileocecal sphincter contraction and ileal peristalsis is inhibited  delays emptying chyme. Also, any irritant in the cecum delays emptying. Which all are mediated by enteric nervous system and vagovagal reflexes.

20. Gastroileal Reflex • Promotes movement of GI contents (chyme) from small intestine to large intestine (colon). • Activated by gastrin and autonomic nervous system (ANS). ANS Colon Gastrin

21. The Intestinal Wall

22. Figure 24.17d, e

25. Pancreas & gall bladder

26. Duodenal ampulla & papilla d.

27. Pancreatic secretions • 1200 to 1500 ml daily about pH 8. • Pancreatic juice is secreted mainly in response to the presence of chyme. • It contains enzymes for digesting proteins, carbohydrates, and fats. • It contains large quantities of bicarbonate ions  neutralizing the acid chyme. • Pancreatic juice is isotonic and with the same Na+ and K+ concentrations and much lower Cl- concentration than plasma.

28. The digestive enzymes of the pancreas are: • The digestive enzymes for proteins (proteolytic enzymes)  trypsin, chymotrypsin, carboxypolypeptidase, ribonuclease, and deoxyribonuclease. • The digestive enzyme for carbohydrates is pancreatic amylase which hydrolyzes starches, glycogen and most other carbohydrates except cellulose to form disaccharides and a few trisaccharides. • The digestive enzyme for fat lipase that is capable of hydrolyzing neutral fat into fatty acids and monoglycerides, cholesterol esterase which cause hydrolysis of cholesterol esters, and phospholipase which splits fatty acids from phospholipids.

29. Prevention of pancreatic self-digestion 1. When synthesized in the pancreatic cells, the proteolytic enzymes are in the inactive forms (zymogens) 2. These become activated only by trypsin 3. Trypsin is activated only after it is secreted into the intestinal tract by enterokinase 4. Pancreas secretes simultaneously trypsin inhibitor

30. Pancreatic enzymes

31. When the pancreas becomes severely damaged or when a duct becomes blocked  large quantities of pancreatic secretion become pooled in the damaged areas of the pancreas  trypsin inhibitor become activated and digest the pancreas  Acute Pancreatitis.

32.  Pancreatic enzymes are secreted entirely by the acini of the pancreatic glands.  Bicarbonate ions and water are secreted as an active process in large amounts mainly by the epithelial cells of the ductules.  The alkaline ions neutralize acid emptied into the duodenum from the stomach.  Bicarbonate secreted by the pancreas = Acid secreted by the stomach.  Bicarbonate released into the blood by the stomach = Acid released into the blood by the pancreas.

33. Intestinal secretion of water and electrolytes

35.  Alkaline blood leaving the stomach mixes with the acidified blood from the pancreas no change in the acidity of the blood.  Prolonged diarrhea  a loss of large quantities of bicarbonate ions  accumulation of acid in the blood.  Vomiting loss of acid from the stomach alkalinization of the blood.

36. Phases of pancreatic secretion • Cephalic phase: • Thought, sight, smell, or taste of food • Activated through the vagus nerve • Results in low volume (low bicarbonate), high enzymes secretion • 2. Gastric phase: • Pancreatic secretion is slightly enhanced by: • Distention of the antrum and the body of the stomach, which initiates a vagovagal reflex  low volume of pancreatic secretion containing both bicarbonate ions and enzymes. • Food breakdown digestion products (primarily amino acids and peptides)  stimulate pancreatic secretions  release gastrin from the G cells of the antrum low-volume, high-enzyme pancreatic secretion.

37. 3. Intestinal phase: • Is the majority of secretion • Activated through CCK and secretin released from endocrine cells in the duodenum and jejunum • Results in high volume (high bicarbonate), high enzymes secretion CCK(effect on gallbladder + potent stimulant of pancreatic enzyme secretion) Protein and fat are the major stimuli  Pancreatic acinar cell  enzyme-rich pancreatic juice Secretin gastric acid (HCl) is a potent stimulus  Pancreatic ductule cell  HCO3- (Low pH < 4.5) rich pancreatic juice The importance of secretin mechanism [A] Neutrilization of the acidic chyme [B] Provides a proper alkaline medium for the action of pancreatic enzymes