HUMAN MEDICAL BIOLOGY, ANATOMY, PHYSIOLOGY AND PATHOLOGY - Y.I. Fedoniuk 2010

ANATOMY, PHYSIOLOGY, PATHOLOGY

CHAPTER 7. NUTRITION PROCESS AND ITS PATHOLOGY

PATHOLOGY OF THE DIGESTIVE SYSTEM

DISORDERS OF INTESTINAL DIGESTION

PERITONITIS

Peritonitis is an acute or chronic inflammation of the Peritoneum accompanied by both general and local symptoms of the disease, as well as severe functional Disorders of the body's Organs and systems.

Depending on The pathway of microflora penetration into the Abdominal cavity, Primary and secondary peritonitis are distinguished. In primary peritonitis, microflora enters the abdominal cavity via hematogenous, lymphogenous pathways, or through the Fallopian tubes. Primary peritonitis is rare, accounting for approximately 1% of all cases. Secondary peritonitis is caused by the spread of microflora from inflamed abdominal organs (Appendix, Gallbladder, etc.), perforation of hollow organs, or penetrating abdominal wounds.

Based on the etiological factor, microbial and aseptic peritonitis are distinguished. Microbial peritonitis can be caused by the gastrointestinal microflora (Escherichia coli, Proteus, enterococci, etc.) and pathogens unrelated to the digestive tract (gonococci, Mycobacterium tuberculosis, pneumococci, etc.). Bacterial peritonitis develops when various non-infectious agents capable of exerting an aggressive effect on the peritoneum (Blood, urine, Bile, pancreatic Enzymes) enter the abdominal cavity.

Depending on the character of the exudate, serous, fibrinous, fibrino-purulent, purulent, hemorrhagic, and putrid peritonitis are distinguished.

Depending on the spread of the inflammatory process across the peritoneal surface, generalized and localized peritonitis are distinguished.

Localized peritonitis (abscess) has no tendency to spread further to other Regions of the abdominal cavity, from which it is clearly demarcated by adhesions, fibrinous deposits, the greater omentum, or intestinal loops.

Diffuse peritonitis lacks clear boundaries and a tendency to delimitation. Diffuse peritonitis localized in the immediate vicinity of the infection source and occupying only one anatomical region of the abdomen is called local. Diffuse peritonitis occupying several anatomical regions of the abdomen is called widespread. Involvement of the entire peritoneum is referred to as generalized peritonitis.

Three conventional stages are distinguished in the Pathogenesis of peritonitis.

Stage I (reactive) is the body's response to the appearance of an infection focus in the abdominal cavity. It is characteristic of the first 24 hours from the onset of peritonitis. This stage is clearly pronounced in sudden infection of the abdominal cavity (perforation of a hollow organ). The contact of microorganisms with the peritoneum triggers an inflammatory reaction with typical signs: hyperemia, increased capillary permeability, edema, and exudation. Initially, the exudate is serous in nature, but as Bacteria and leukocytes accumulate in it, it becomes purulent.

Stage II (toxic) is the body's response to The entry of exotoxins and endotoxins into the general bloodstream, as well as protein-breakdown products formed during Cell disintegration. It develops 24–72 hours after the onset of the disease.

Stage III (terminal) develops 72 hours after the onset of the disease. Septic Shock is frequently observed in this stage. The local and general defense mechanisms of the body prove ineffective. While localization of the infection and even recovery from peritonitis are possible in The First stage of the disease, such an outcome is impossible in the terminal stage without surgical intervention and intensive care.

Having started as a local condition, peritonitis rather rapidly causes life-threatening functional disorders across all organs and systems of the body.

Hemodynamic changes characteristic of the body's response to stressors (accelerated pulse rate, elevated blood pressure, increased Cardiac Output, etc.) occur at the early stage of the disease development. In the terminal stage, Hypertension is replaced by hypotension, tachycardia increases, and profound changes occur in The Cardiovascular system.

Renal Dysfunction develops As a result of vascular spasm occurring in the reactive stage, and subsequently due to hypotension, microcirculatory disorders, and a decrease in circulating blood volume. As a result, diuresis decreases, azotemia increases, and acute renal or hepatorenal failure develops.