ABDOMINAL PAIN

Abdominal Pain

Types and Mechanism

Pain associated with the parietal peritoneum

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Steady and aching, worsened by changes in the tension of the peritoneum caused by pressure or positional change Accompanied by tension of the abdominal muscles to relieve such tension Another characteristic feature is tonic spasm of the abdominal musculature
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Dependent on the location of the inflammatory process

Abdominal Pain

Types and mechanism

Pain associated with obstruction of hollow viscus

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Intermittent or colicky, coinciding with peristaltic waves of the organ Experienced in early acute appendicitis and gastroenteritis and are somewhat relieved by writhing and massage

Abdominal Pain

Types and mechanism

pain associated with abdominal vascular disturbances (thrombosis or embolism)

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sudden or gradual in onset, and can be severe or mild

Pain that is felt in the abdomen may be "referred" from elsewhere

- e.g., a disease process in the chest may cause pain in the abdomen

GASTROENTERITIS

Gastroenteritis
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inflammation of the gastrointestinal tract, involving both the stomach and the small intestine and resulting in acute diarrhea

inflammation is caused most often by infection with certain viruses, less often by bacteria or their toxins, parasites, or adverse reaction to something in the diet or medication.

Acute Infectious Gastroenteritis

leading cause of mortality among children in developing countries several enteric viruses have been recognized as important etiologic agents of acute infectious gastroenteritis

Acute InfectiouGastroenteritis

Illness caused by these viruses is characterized by

acute onset of vomiting and/or diarrhea Fever Nausea Abdominal cramps Anorexia malaise

Etiologic Agents

Human Calcivirus

Norwalk Virus

prototype strain of a group of nonenveloped, small (24-70 nm), round, icosahedral, with relatively amorphous surface virus

2 genera: noroviruses and sapoviruses

Pathogenesis

Carbohydrates that are similar to humanblood group antigens present on gastroduodenal epithelium

Serve as ligands for the attachment of norwalk virus

After the infection of volunteers, reversible lesions are noted in the upper jejunum with:

Pathogenesis

broadening and blunting of the villi shortening of the microvilli vacuolization of the lining epithelium crypt hyperplasia infiltration of the lamina propria by polymorphonuclear neutrophils and lymphocytes

Pathogenesis

The lesions persist for at least 4 days after the resolution of symptoms and are associated with:

malabsorption of carbohydrates and fats decreased level of brush-border enzymes

There is also s delay in gastric motor function

- believed to contribute to the nausea and vomiting that are typical of this illness

Clinical Manifestations

Incubation Period: 12-72 hours (ave. 24 hrs) Illness lasts for 12-60 hrs Onset is sudden

Clinical Manifestations

S/Sx:

Nausea more prevalent in children Vomiting- affects a great portion of adults Abdominal cramps diarrhea headache, fever, chills, and myalgias

Constitutional Symptoms

Management

Treatment

Self-limited Oral rehydration IV fluid No specific antiviral therapy is available Control of contamination of food and water Exclusion of infected food handlers Reduction of person-person spread through good personal hygiene and disinfection of formites

Prevention

Etiologic Agent

Rotaviruses

members of the family Reoviridae viral genome consists of 11 segments of doublestrand RNA that are enclosed in a triple-layered, nonenveloped, icosahedral capsid 75 nm in diameter There are seven major groups (A-G)

Group A cause human illness Group B cause human illness to a lesser extent

Pathogenesis

Rotaviruses infect and ultimately destroy mature enterocytes in the villous epithelium of the proximal small intestine loss of absorptive villous epithelium, coupled with the proliferation of secretory crypt cells that results in secretory diarrhea

Pathogenesis

Brush-border enzymes characteristic of differentiated cells are reduced

leads to the accumulation of unmetabolized disaccharides and consequent osmotic diarrhea

may evoke fluid secretion through activation of the enteric nervous system in the intestinal wall

Clinical Manifestations

IP: 1-3 days Abrupt onset vomiting frequently preceding the onset of diarrhea stools are characteristically loose and watery and only infrequently contain red or white cells Gastrointestinal symptoms generally resolve in 37 days

Epidemiology

Nearly all children are infected by 3-5 years of age worldwide Reinfection is common but severity decreases More associated with dehydration

Management

Immunity

Protection is correlated with he presence of of virusspecific secretory IgA antibodies I the intestine and, to some extent, the serum Oral and IV fluids Antibiotics and antimotility drugs should be avoided Orally administered immunoglobulins and colostrum may resolve symptoms in immunocompromised patients

Treatment

Other Viral Agents

Adenoviruses Astroviruses Toroviruses Picobirnaviruses

Etiologic Agents

Bacteria that may cause Gastroenteritis

Escherichia coli Salmonella Vibrio Campylobacter jejuni Shigella Vibrio cholerae Clostridium difficile