clinical pathophysiology of the digestive system

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Clinical pathophysiology of the digestive system

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Page 1: Clinical pathophysiology of the digestive system

Clinical pathophysiology of the digestive system

Page 2: Clinical pathophysiology of the digestive system

Disorder of stomach secretory function

According to mechanism:•Organic disturbances of stomach glands•Change I functional activity of secretory cells According to kind of disturbance•Hypersecretion•Hyposecretion

Page 3: Clinical pathophysiology of the digestive system

Key-points for hypersecretion

Page 4: Clinical pathophysiology of the digestive system

The four inputs to parietal cells that regulate acid secretionby controlling the transfer of the H,K-ATPase pumps incytoplasmic vesicle membranes to the plasma membrane.

Page 5: Clinical pathophysiology of the digestive system

Gastritis

Page 6: Clinical pathophysiology of the digestive system

Gastritis

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Disorder of stomach motor function

• Hypercinesis – increased motility• Hypertonus – increased degree of contraction• Hypocinesis - decreased motility• Hypotonus - decreased degree of contraction Pathological reflexes• Nausea• Vomiting• Belching

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Gastric Juice Secretion, Mucosal Protection and Risk of Ulcer

Page 13: Clinical pathophysiology of the digestive system

Gastric Juice Secretion, Mucosal Protection and Risk of Ulcer

Page 14: Clinical pathophysiology of the digestive system

Gastric Juice Secretion, Mucosal Protection and Risk of Ulcer

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Disorders After Stomach Surgery

Page 18: Clinical pathophysiology of the digestive system

Disorders After Stomach Surgery

Page 19: Clinical pathophysiology of the digestive system

Disorder of digestion in intestine• Disorders of the pick out of bile and pancreatic juice

are accompanied by disorders of all types of digestion, development of putrefaction and fermentation in the intestine (at closing, or squeezing the excretory ducts of glands in cystic fibrosis mucoviscidosis, because of pancreatic cancer, acute and chronic pancreatitis and duodenitis, violating the neurohumoral mechanisms of regulation of secretion, particular functions of the vagus nerve, the allocation of secretin, cholecystokinin, pancreatic polypeptide).

• Disorders of digestion of nutrients combined in maldigestion syndrome.

• Malabsorption of substances in the gut combined into a syndrome, which is characterized by diarrhea, weight loss, protein deficiency, signs of hypovitaminosis.

Page 20: Clinical pathophysiology of the digestive system
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Causes of Acute Pancreatitis

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Consequences of Acute Pancreatitis

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Causes of Chronic Pancreatitis

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Consequences of Chronic Pancreatitis

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Causes of Constipation

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Consequences of Constipation and (Pseudo-)Obstruction

Page 29: Clinical pathophysiology of the digestive system

Etiology and pathogenesis of liver insufficiency

• Infectious agents (hepatitis B virus, tuberculosis bacillus, helmints)• Hepatotropic poison (drugs - tetracycline, sulfonamides, industrial poisons - carbon tetrachloride, arsenic, chloroform, vegetable poisons - aflatoxin, muscarine)• Physical impacts (ionizing radiation)• Biological drugs (vaccines, serums)• Violation of blood circulation (thrombosis, embolism, venous congestion)• Endocrine pathology (diabetes mellitus, hyperthyroidism)• Tumors• Hereditary ensymopathy

Page 30: Clinical pathophysiology of the digestive system

Causes of Liver Failure

Page 31: Clinical pathophysiology of the digestive system

Consequences of Liver Failure

Page 32: Clinical pathophysiology of the digestive system

Fibrosis and Cirrhosis of the Liver

Page 33: Clinical pathophysiology of the digestive system

Fibrosis and Cirrhosis of the Liver

Page 34: Clinical pathophysiology of the digestive system

Clinical syndromes in liver injury

Lack of liver disorders manifested its functions lesion:• metabolic (involved in carbohydrate, fat, protein metabolism, metabolism of vitamins, hormones, biologically active substances)• protection (phagocytic and antitoxic)• digestive and excretory (the formation and release of bile)• hemodynamic (involved in maintaining systemic circulation).

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Cholelithiasis: Abnormal Cholesterol to Bile Salt Ratio

Page 36: Clinical pathophysiology of the digestive system

Clinical syndromes of jaundice• Acholia associated with non-receipt of bile in the

intestine due to violations of the formation and outflow of bile. Acholia manifested disorders of digestion and absorption of fats, hypovitaminosis A, E, K, decreased intake of unsaturated fatty acids of phospholipids to build cell membranes, intestinal motility violation, increasing decay and fermentation.

• Dyscholia - violation of the physical-chemical properties of bile, causing it acquires the ability to form stones (due to genetic predisposition, poor nutrition, metabolic disorders, infectious-inflammatory processes, cholestasis).

Page 37: Clinical pathophysiology of the digestive system

Cholelithiasis: Abnormal Cholesterol to Bile Salt Ratio

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Etiology and pathogenesis of jaundice

• Jaundice - a syndrome caused by an increase in blood bilirubin (hemolytic, parenchymal, mechanical).

• In hemolytic jaundice due to destruction of a large number of red blood cells accumulate indirect, protein bound bilirubin.

• When parenchymal jaundice disturbed capture, and excretion of bilirubin in hepatocytes due to their injuries.

• In mechanical jaundice occurs outflow obstruction of bile, compression of biliary tract tumor or scar, closing within a stone, worms, thick bile.

Page 43: Clinical pathophysiology of the digestive system

Mechanisms and Consequences of Cholestasis

Page 44: Clinical pathophysiology of the digestive system

Methods of experimental study of liver pathology

• hepatic-cell failure simulating full or partial removal of the liver, the introduction of poisons (carbon tetrachloride, chloroform, trinitrotoluene);• cholestatic model obtained by squising bile ducts by ligature;• hepatic vascular insufficiency simulating by overlapping portocaval anastomosis, ligation portal vein, hepatic vein, hepatic artery.