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Forensic Pathology for Police - Brainshare Public Online Library

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Gastrointestinal and Hepatobiliary System 239<br />

something protrudes into or through something that it should not. Examples of<br />

herniation sites involving segments of bowel (usually small intestine) include the<br />

inguinal regions (groin), the anterior abdominal wall, a defect within the mesentery,<br />

and intra-abdominal adhesions (which develop following surgery). A segment of<br />

herniated bowel can become entrapped (“incarcerated”) (Fig. 10.25). It can subsequently<br />

twist on itself, or otherwise swell to such an extent that its blood supply is<br />

cut off. When this occurs, the hernia is said to have “strangulated.” A strangulated<br />

hernia will eventually die (infarct), and per<strong>for</strong>ation, inflammation, hemorrhage, or<br />

sepsis, with possible death, can occur. Segments of bowel can undergo ischemic<br />

infarction, with similar results. In some persons, the bowel actually telescopes on<br />

itself, which can lead to compression of blood vessels with infarction, per<strong>for</strong>ation,<br />

etc. This process is referred to as “intussusception.” When a segment of bowel twists<br />

on itself, or its mesentery, with eventual infarction, the condition is referred to as a<br />

“volvulus.” Intussusception and volvulus may occur in association with a tumor,<br />

which acts as a mass that predisposes to the conditions. Alternatively, each of these<br />

conditions can occur in the absence of a tumor in children.<br />

Fig. 10.25 A strangulated hernia case. Note that a portion of small intestine has herniated through<br />

a small defect in the abdominal wall and that it cannot be removed. The arrow indicates where the<br />

intestine enters the defect in the abdominal wall<br />

Hemochromatosis<br />

Hemachromatosis refers to excess levels of iron in the body . It can result from<br />

a genetic abnormality (primary or hereditary hemochromatosis) or from various<br />

iron-overload conditions, including multiple blood transfusions, various blood/bone<br />

marrow disorders, increased oral intake of iron, and chronic liver diseases. Humans<br />

are at risk <strong>for</strong> the disorder because they have no normal way in which to get<br />

rid of excess iron. The genetic condition is an autosomal recessive disorder (see<br />

below), caused by a mutation of the HFE gene, which normally regulates intestinal<br />

absorption of iron. In primary hemochromatosis, too much iron is absorbed. The

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