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Transcript
Pathology Lecture 43 Intestinal Infections and Inflammation 1) To be familiar with abnormal patterns of fluid/stool handling in the GI tract. Diarrhea is stool production in excess of 250 g containing 70-95% water. Dysentery is low-volume, painful, bloody diarrhea. Secretory diarrhea: net intestinal fluid secretion, >500 mL isotonic fluid. Osmotic diarrhea: high luminal osmolarity, >500 mL, abates upon fasting. Exudative diseases: mucosal destruction leads to output of purulent bloody stools. Deranged motility: improper gut neuromuscular function, highly variable patterns. Malabsorption: produces voluminous, bulky stools with increased osmolarity and combined with excess stool fat (steatorrhea). 2) To know the basic elements of GI tract protection against infection, and the broad categories of pathogenesis in GI infection. Protective mechanisms: Intrinsic to GI tract: gastric acidity, native intestinal flora (competition, toxic metabolites), bowel motility, local immune response (GALT, IgA), digestive enzymes, and other (intestinal mucus, bile). Behavioral/social: personal hygiene and community sanitation. Broad categories of pathogenesis: - Organisms specifically pathogenic for GI tract. - Native mixed flora of GI tract become pathogenic due to decreased bowel integrity, risk of peritonitis, septicemia. 3) For the various viral, bacterial, protozoal, and metazoal diseases of GI tract, be able to recognize the following (in each group): common infectious agents, clinical manifestations, at-risk population groups, pathologic features, and special features. Disease Infectious agents Viral Rotavirus Enteric adenovirus Norwalk virus Bacterial Ingested toxin (Staph, Vibrio cholerae) Toxigenic organisms (toxigenic E. coli) Enteroinvasive (Salmonella, Shigella, Yersinia) Clinical manifestation Nausea, vomiting, watery diarrhea Explosive diarrhea and abdominal pain; neurotoxin of C. botulinum may produce respiratory failure. Incubation hoursdays, Secretary and the toxins produced area and dehydration. Cytotoxic enterotoxins and enteroinvasive processes produce dysentery. At-risk pop. Pathologic features Special features Infants <2 years Older children, adults Locations of poor hygiene, developing nations, consuming uncooked foods especially chicken and pork. Micro: nonspecific; small bowel villus blunting or flattening: ↑mononuclear cells Variable, typically surface epithelial damage (ulceration); increased mitotic rate (regeneration); edema, congestion; variable leukocyte population. May resemble Crohn's disease (Yersinia, mycobacterial). All enteroinvasive organisms may simulate acute ulcerative colitis Incubation 1-2 days Symptomatic period 1-3 days Salmonella: linear ulcers localized over Peyer’s patches Shigella: distal colon purulent exudate. Yersinia: Peyer’s patches necrotizing granulomas Clostridium Perfringens: necrotizing lesions Mycobacterium tuberculosis: granulomatous infection with tendency for transmural scarring and constriction. Protozoal Metazoal Amebiasis (Entamoeba histolytica) Dysentery, intestinal pain, fever Developing countries Giardiasis (Giardia lamblia) Acute or chronic diarrhea; crampy abdominal pain; possible steatorrhea Institutionalize and day care populations commonly affected Hookworm, strongyloides, tapeworm Usually minor GI tract symptoms: more likely to produce nutritional deficiencies and/or anemia of blood loss Unsanitary conditions , consuming raw or undercooked meat Flasks shaped ulcer "undermining" produces larger areas of ulceration Pear-shaped binucleate, flagellate trophozoite resembles "ghost" sickle-shaped forms adherent to villus services of epithelial cells Parasites attach and small bowel, reproduce eggs are excreted in feces, some may invade locally. May spread to liver producing amoebic liver abscess. Agammaglobulinemic patients at risk for severe disease 4) To understand the microbiologic basis for different types of pathogenesis within the area of bacterial enterocolitis. Differences among bacterial pathogens with regards to adhesion/replication, enterotoxins, and invasion produce different types of pathogenesis. 5) For “Other Inflammatory Processes,” to be familiar with at-risk patient groups, the pathophysiology of the process, range of clinical disease, preferred anatomic sites of involvement, and pathologic features. See number 6. 6) To know, in detail, the information under #5 (above) for common causes of GI tract inflammation such as diverticulitis and appendicitis. Disease At-risk groups Pathophysiology Clinical disease Anatomic sites Pathologic features Necrotizing enterocolitis of newborn 1st 3 months, premature, low-birth-weight, formula fed Ischemia, pathogenic organisms, high protein concentration, GI tract immaturity. Anabiotic-associated (pseudomembranous) colitis Patients finishing a full course of broadspectrum antibiotics Proliferation of toxinforming organisms (Clostridium difficile) Diverticulitis Appendicitis 50% of Patients >60 yr in developed nations Adolescents and young adults Outpouching (<1 cm diameter) along taeniae coli due to weak wall and increased pressure Abdominal distention, tenderness, paralytic ileus, bloody diarrhea. Severe cases perforation, septicemia, and shock. Terminal ileum and ascending colon Mucosal ulceration to full-thickness necrosis of bowel wall Acute, chronic diarrhea; usually no history of prior GI disease. Usually asymptomatic (80%); may have cramping, vague abdominal discomfort, constipation, and distention Sigmoid colon Obstruction of appendix lumen (fecalith), ↑ pressure, compressed veins, ischemic injury, bacteria proliferate = acute inflammation Periumbilical pain localizing to RLQ, nausea and vomiting, guarding, rebound tenderness, low-grade fever, elevated WBC's Appendix Obstruction and/or perforation of diverticulum produces inflammation, with granulation tissue and fibrosis Gross: edema, injected serosal vessels, exudates micro: mucosal ulceration, neutrophils through wall, fibrinopurulent exudate Colon Denuding of surface epithelium; mucopurulent exudate merging to form "pseudomembrane" 7) To recognize patients in special risk categories for GI tract infection/inflammation, as covered in “Special circumstances for GI inflammation/infection.” HIV-infected patients: wide array of opportunistic infections; possible entity of primary AIDS associated enteropathy. Bone marrow transplantation: direct GI injury due to pre-transplant therapy (radiation, chemotherapy); opportunistic infections; graft-versus-host disease. Granulocytopenia: peripheral WBC count <1000/cubic mm carries high risk of infection, normal gut flora are a potential source of gram-negative sepsis. Acute typhilitis (cecitis): necrotizing colitis, preferentially localized to cecum; cancer patients were neutropenia; 70% incidence gram-negative or Clostridial species. 8) To understand the concept of peritonitis, its causes, pathologic findings and outcomes. Peritonitis is localized or generalized inflammation of the peritoneal cavity. Causes: may be infectious due to bacteria escaping through the GI wall or spontaneous growth of natural flora (due to proteinaceous effusion - ascites). May be non-infectious due to bile, pancreatic enzymes, or foreign body. Pathologic findings: edema, vascular congestion (injected appearance) of small blood vessels; fibrinopurulent exudate on peritoneal surface (pus appearance). Outcomes: resolution; walled off abscesses; organization of exudate as fibrous adhesions. 9) To be responsible for all material covered in Lecture Notes for “Intestinal Infections and Inflammation.” Review notes.