Download Methodological Instruction to Practical Lesson № 13

MINISTRY OF PUBLIC HEALTH OF UKRAINE
BUKOVINIAN STATE MEDICAL UNIVERSITY
Approval on methodological meeting
of the department of pathophisiology
Protocol №
Chief of department of the pathophysiology,
professor
Yu.Ye.Rohovyy
“___” ___________ 2008 year.
Methodological Instruction
to Practical Lesson
Мodule 2 : PATHOPHYSIOLOGY OF THE ORGANS AND SYSTEMS.
Contenting module 6. Pathophysiology of digestion, liver and kidney.
Theme 13: PATHOPHYSIOLOGY OF DIGESTION
Chernivtsi – 2008
1.Actuality of the theme. The diseases of digestive organs take
considerable place in general morbiditi of the population. Chronic gastritis and
peptic ulcer meet in all agegroups and don’t the tendencies to decrease. The
most of them course chronically and is characterized by bend to relapses and
acute. It lead to loss of working ability and disability. It should account, that not
only organic, but also the functional disorders of alimentary system seriosly
influence on state of the whole organism, on it metabolism. The leading
etiological factors of disturbance of digestion are the errors in digestion,
infectious agents, toxic substances and medicines drugs abusing by alcohol and
nicotine, psychic, traumas, negative emotions. Pathogenetical the grounded
methods of prevention and treatments of illnesses of gastrointestinal tract is
based on knowledge of the nature of these pathogenic factors and mechanisms
of those disorders, which arise under their action.
2.Length of the employment – 2 hours.
3.Aim:
To khow: Characterize the common signs and symptoms of gastrointestinal
dysfunction.
Etiological factors and to be able explain mechanisms of disturbance of
digestion with the purpose of diseases discern of gastrointestinal сhannel organs.
The causes of digestion disorder in the stomach and the intestine.
Displays and mechanisms of disorder secretory and motor evacuation of
stomach functions.
he kinds of digestion disorder in the intestine, their causes and mechanisms
To be able: To analyse the mechanisms of the ulcer diseases.
To give an account etiology and pathogenesis of gastritis
To give an account etiology and pathogeny of pancreatitis.
To evaluate role of the hereditary, local and endocrine factors in the etiology
of peptic ulcer.
To characterize digestive disturbances of deficit bile and pancreatic juice.
To give an account nature of membranous digestion disorder.
To explain mechanisms of disorder of vital activity for intestinal obstruction.
To give an account nature of intestinal endointoxication.
To perform practical work: to analyse the mechanisms of the acute and
chronic gastritis.
4. Basic level.
The name of the previous
disciplines
1.
histology
2.
biochemistry
3.
physiology
The receiving of the skills
Structure of gastrointestinal сhannel.
Digestion in stomach.
Digestion in an intestine.
5. The advices for students.
1. List sequentially the parts of the alimentary canal from mouth to anus.
2. Describe the structure and function of the mouth, esophagus, stomach,
small and large intestine.
The gastrointestinal system includes the oral structures (mouth, salivary glands,
pharynx), the alimentary tract (esophagus, stomach, small and large intestine,
appendix, anus) and the accessory organs of digestion (liver, gallbladder, bile
ducts, pancreas). The function of the alimentary tract is to digest masticated food,
to absorb the digestive products, and to excrete the digestive residue and certain
waste products excreted by the liver through the bile duct.
The digestive process begins in the mouth, where carbohydrate-splitting
enzymes or amylases from the salivary glands mix with the food during
mastication. In the stomach the proteolytic pepsin and hydrochloric acid are added
to the digesting mixture in duodenum. These include amylases, proteolytic trypsin
and fat splitting enzymes or lipases. In addition, bile salts secreted by the liver and
stored in the gallbladder are added to emulsify lipids into small water-soluble
micelles. The final phase of digestive process occurs at the surface of small
intestinal epithelial cells. Complex endocrine and nervous mechanism coordinate
the timing of secretion of digestive enzymes, hydrochloric acid, and bile salts. The
sight of food may cause salivation and gastric secretion because of nervous
stimulation. Distension of the stomach causes release of gastrin, which stimulates
acid production and gastric emptying.
3. Characterize the common signs and symptoms of gastrointestinal
dysfunction.
ANOREXIA is the absence of a desire to eat despite to physiologic stimuli that
would normally produce hunger. Anorexia is a nonspecific symptom often
associated with nausea, abdominal pain, and diarrhea.
VOMITING is the forceful emptying of stomach and intestinal contents or
chyme through the mouth. The metabolic consequences of vomiting are fluid,
electrolyte, and acidbase disturbances.
NAUSEA is a subjective experience, associated with duodenum and antrum of
the stomach going in spasm.
DIARRHEA is an increased frequency of defecation, accompanied by changes
in fecal fluidity and volume. There are large-volume, small-volume, and motility
diarrhea. Motility diarrhea can be caused by reaction of small intestine or fistula
formation between loops of the intestine.
Numerous disorders cause ABDOMINAL PAIN, BLEEDING which are
characterized by HEMATOMESIS (the presence of blood in the vomitus) and
HEMATORRHEA or MELENA (bleeding from the rectum as result is dark tarry
stools)
4. Compare the various disorders of digestive motility
Disorder
Dysphagia (swallowing difficulty)
Gastroesophageal reflux (chyme reflux into esophagus)
Hiatal hernia (protrusion of upper stomach through the diaphragm into thorax)
Pyloric obstruction (narrow pylorus)
Intestinal obstruction (impaired chyme flow through intestinal lumen)
Causes
Esophageal obstructions, tumors, strictures, or diverticula.
Impaired esophageal motility, neural dysfunction, muscular disease, CVA.
Achalasia (decreased ganglion cells in myenteric plexus, muscle atrophy)
Increased abdominal pressure, ulcers, pyloric edema and strictures, hiatal hernia
Congenitally short esophagus, trauma, weak diaphragmatic muscle at
gastroesophageal junction, increased abdominal pressure.
Peptic ulcer or carcinoma near pylorus.
Hernia, telescoping of one part of intestine into another, twisting, inflamed
diverticula, tumor growth, loss of peristaltic activity
Manifestation
Distension and spasm of esophagus after swallowing, regurgitation of
undigested food
Regurgitation of chyme within 1 hour of eating.
Gastroesofageal reflux, dysphagia, epigastric pain.
Epigastric fullness, nausea and pain, vomitus without bile.
Colicky pain to severe and constant pain, vomiting, diarrhea, constipation,
dehydration, hypokalemia and acidosis with complications.
5. Describe the pathogenesis of acute and chronic gastritis.
Gastritis is an inflammatory disorder of the gastric mucous that may be acute or
chronic and that affects the fundus or antrum or both. Aspirin and other antiinflammatory drugs are known to cause acute gastritis with erodes the epithelium,
probably because they inhibit prostaglandins that normally stimulate the secretion
of protective mucus. Alcohol, histamine, digitalis, and metabolic disorders such as
uremia are contributing factors for gastritis. The clinical manifestation of acute
gastritis can include vague abdominal discomfort, epigastric tenderness, and
bleeding. Healing usually occurs spontaneously within a few days. Discontinuing
injurious drugs, using antacids, or decreasing acid secretion with drugs facilitate
healing.
Chronic gastritis is a progressive disease that tends to occur in elderly
individuals. This gastritis causes thinning and degeneration of the stomach wall.
Chronic fundal gastritis is the most severe type, as the gastric mucosa degenerates
extensively. The loss of chief and parietal cells diminishes secretion of pepsinogen,
hydrochloric acid, and intrinsic factor. Pernicious anemia develops because
intrinsic factor is unavailable to facilitate vitamin B12 absorbtion. Chronic fundal
gastritis becomes a risk factor for gastric carcinoma, particularly in individuals
who develop pernicious anemia. A significant number of individuals with chronic
fundal gastritis have antibodies to parietal cells in their sera thus suggesting an
autoimmune mechanism as the pathogenesis of the disease.
Chronic antral gastritis is more frequent than fundal gastritis. It is not associated
with decreased hydrochloric acid secretion, pernicious anemia, or the presence of
parietal cells antibodies. Helicobacteria pylori is a major etiologic factor
associated with the inflammation seen in this chronic gastritis. The long-standing
inflammatory process and gastric atrophy may develop without a history of
abdominal distress. Individuals may report vague symptoms including anorexia,
fullness, nausea, vomiting, and epigastric pain. Gastric bleeding may be the only
clinical manifestation of gastritis.
6. Characterize ulcer disease .
The cause and risk-factors
Pathogenesis
Nonsteroidal antiinflammatory drug (NSAID), smoking, alcohol
Corrosive agents (HCl and pepsin)
Helicobacteria pylori
Stress-syndrome
1. All these factors diminish the mucosal barrier, regeneration of epithelium,
supply of blood, neutralization of the secrets XII thus excluding them from the
system
2. Mucosal ischemia develops
3. Genetic and environmental predisposition
4. Mechanical traumatisation
5. Chronic gastritis and duodenitis
6. Hyperacidosis. Increased gastrin secretion
7. Exhaustion hypothalamo-pituitary-adrenal system due to stress
8. Motility defect may lead to return of bile acids, which act as irritants to
mucosal barrier
According to the data, therapy should be directed at intensification of the
protective factors and weakening of the agressive factors, inhibiting acidopepsin
secretion.
7. Ileus
Classification
Mechanical: a) compression b) occlusion c) strangulation
Dynamical: a) spastic b) paralytic
The main cause: Poor quality food. Helminthiasis. Tumor. Postoperative
complication
Pathogenesis: Intestinal autointoxication Acid/base disbalance Neuro-humoral
disbalance
Clinical manifestations : vomiting dehydration Abdominal pain Gaseous
bowel distension Hypotension Loss of Na, K, H, Cl ions
8. APUD-system and APUD-pathy of GIT.
(APUD – amino precusor uptake and decarboxylase)
It is well-known that food due to mechanical and chemical stimuli irritates the
Kulchitsky's cells of stomach and duodenum via central neurous system and then
they true hormones are released: gastrin, secretin, gastrointestinal peptide (GIP).
Gastrin stimulates acid secretion and the growth of gastric oxyntic gland mucosa.
Secretin stimulates: 1) pancreatic bicarbonate secretion; 2) biliary secretion; 3)
growth of exocrine pancreas and inhibits gastric acid secretion and trophic effects
of gastrin.
GIP stimulates insulin release and inhibits gastric acid secretion. APUD-pathy is
associated with tumor of pancreas and Zollinger — Elison syndrome (peptic ulcer
disease)
5.1. Content of the theme. List sequentially the parts of the alimentary
canal from mouth to anus. Describe the structure and function of the mouth,
esophagus, stomach, small and large intestine. Characterize the common signs
and symptoms of gastrointestinal dysfunction. Compare the various disorders of
digestive motility. Describe the pathogenesis of acute and chronic gastritis.
Characterize ulcer disease. Discribe ileus, the acute intestinal obstruction.
APUD-system and APUD-pathy of GIT.
1.
2.
3.
4.
5.2. Control questions of the theme:
List sequentially the parts of the alimentary canal from mouth to anus.
Describe the structure and function of the mouth, esophagus, stomach, small
and large intestine.
Characterize the common signs and symptoms of gastrointestinal
dysfunction.
Compare the various disorders of digestive motility.
5.
6.
7.
8.
Describe the pathogenesis of acute and chronic gastritis.
Characterize ulcer disease.
Discribe ileus, the acute intestinal obstruction
APUD-system and APUD-pathy of GIT.
5.3. Practice Examination.
1. The digestive function performed by the saliva and salivary amylase
respectively are: A. Moistening and protein digestion B. Deglutition and fat
digestion C. Peristalsis and polysaccharide digestion D. Lubrication and
carbohydrate digestion
2. The nervous pathway involved in salivary secretion requires stimulation
of: A. Receptors in the taste buds, impulsed to the motor cortex, and somatic motor
impulses to salivary glands B. Receptors in the mouth, sensory impulses to a center
in the brain stem, and parasympathetic impulses to salivary glands C. Taste
receptors, sensory impulses to centers in the brain stem, and somatic motor
impulses to salivary glands D. Pressoreceptors in blood vessels, motor impulses,
and autonomic impulses to salivary glands
3. Food would pass rapidly from the stomach into the duodenum if it were
not for the: A. Fundus B. Epiglottis C. Rugae D. Cardiac sphincter E. Pyloric
sphincter
4. The secretion of gastric juice: A. Occurs only when the stomach comes in
contact with swallowed food B. Is entirely under the control of the hormone gastrin
C. Is entirely under the control of the hormone epigastrone D. Is stimulated by the
presense of saliva in the stomach E. Occurs in 3 phases: cephalic, gastric and
intestinal
5. During nevous control of gastric secretion, the gastric glands secrete
before food enters the stomach. This stimulus to the glands comes from
A. Gastrin B. Impulses over somatic nerves from the hypothalamus C. Motor
impulses from the cerebral cortex and cerebellum D. Parasympathetic impulses
over the vagus nerve
6. Pepsinogen: A. must be activated by HCl B. is secreted by chief cells C. is
important in breakdown of proteins D. all of the above are correct
7. Beginning at the lumen of the tube, the sequence of layers of the of the
gastrontestinal tract is: A. Mucosa, submucosa, muscularis, serosa B.
Submucosa, mucosa, serous membrane, muscularis C. Submucosa, mucosa,
muscularis, skeletal muscle
D. Serous membranes, muscularis, mucosa,
submucosa
8. Normally, when chyme leaves the stomach: A. The nutrients are ready for
absorbtion into the blood B. The amount of inorganic salts has been increased by
the action of hydrohloric acid C. Its pH is neutral D. The proteins have been partly
digested E. All above is correct
9. Which layer of small intestine includes microvilli: A. Submucosa
B. Mucosa C. Muscularis D. Serosa
10. Which is not an example of mechanic digestion: A. Chewing B. Churning
and mixing of food in the stomach C. Peristalsis and mastication D. Conversion of
protein molecules into amino acids
11. Pancreatic juice is to trypsin as gastric juice is to A. Salivary amylase B.
Pepsin C. Mucin D. Intrinsic factor
12. Which part of small intestine is most distal from pylorus: A. Jejunum B.
Pyloric sphincter C. Duodenum D. Cardiac sphincter E. Common bile duct
13. The chief role played by the pancreas in digestion is to: A. Secrete insulin
and glucagons B. Churn the food and bring it into contact with the digestive
enzymes C. Secrete enzymes that digest food in the small intestine D. Assist in the
absorbtion of digested food
14. Among the structural features of the small intestine are villi, microvilli,
circular folds. Their function is to: A. Liberate hormones B. Promote peristalsis
C. Liberate digestive enzymes D. Increase the surface area of absorbtion
15. The fate of carbohydrates in the small intestine is: A. Digestion by
amylase, sucrase, maltase, and lactase to monosaccharides B. Convertion to simple
sugars by the activity of trypsin and lipase C. Hydrolysis to aminoacids by the
activity of amylase, sucrase, maltase, and lactase D. Conversion to glycerol and
fatty acids by the activity of lipase and amylase
16. The absorbtive fate of the end products of digestion may be summarized
as: A. Most fatty acids are absorbed into the blood; glucose and amino acids are
absorbed into the lymphatic system B. Amino acids and monosaccharides are
absorbed into the blood capillaries; most fatty acids are absorbed into the lymph
C. Amino acids and fatty acids are absorbed into the lymph capillaries; glycerol
and glucose are absorbed into the blood capillaries D. Fatty acids are absorbed into
the blood capillaries; glycerol, amino acids and glucose are absorbed into lymph
17. Intestinal obstruction causes: A. Decreased intralumenal tension
B. Hyperkalemia C. Deccreased nutrient absorbtion D. Both A and B are correct E.
A, B, and C are correct
18. Peptic ulcers may be caused by: A. NSAIDs B. H. Pylori C. Habitual
alcohol cosumption D. Mucus secretion E. A, B, and C are correct
19. Gastric ulcers: A. may lead to malignancy B. Occur at a younger age than
duodenal ulcer C. Always have increased acid production D. Exibit nocturnal pain
E. Both A and C are correct
20. Duodenal ulcers: A. Occur four times more frequently in females than in
males. B. May be comlicated by hemorrhage C. Are associated with sepsis
D. May cause inflammatory and scar tissue formation around the sphincter Oddi
Literature:
1.Gozhenko A.I., Makulkin R.F., Gurcalova I.P. at al. General and clinical
pathophysiology/ Workbook for medical students and practitioners.-Odessa, 2001.P.203-210.
2. Gozhenko A.I., Gurcalova I.P. General and clinical pathophysiology/ Study
guide for medical students and practitioners.-Odessa, 2003.- P.266-277.
3.Robbins Pathologic basis of disease.-6th ed./Ramzi S.Cotnar, Vinay Kumar,
Tucker Collins.-Philadelphia, London, Toronto, Montreal, Sydney, Tokyo.-1999.