Health Tips and Tricks

The ancient Greeks around 400 B.C. first recognized that ascites was associated with liver disease. Abdominal paracentesis is one of the oldest medical procedures; the first report of this procedure is dated about 20 B.C. Yet the bulk of the literature regarding the diagnosis and management of ascites and the details of paracentesis has been published only since 1980.
The causes of ascites in the United States have changed over the past 90 years. At the turn of the century, patients with ascites were usually found to have cardiac or renal failure. Now more than 80% of patients with ascites seen by general internists and gastroenterologists-hepatologists have liver disease (Table 9-1). As we head into the next century, chronic parenchymal liver disease, including cirrhosis and alcoholic hepatitis, is the predominate cause of ascites.
A history, physical examination, and careful analysis of ascitic fluid (Table 9-2, Table 9-3, Table 9-4, Table

Since the advent of routine automated serum testing, a common problem in gastroenterology has been the determination of the cause, and thus the importance, of abnormalities in liver chemistries. At first, such evaluations may be frustrating because of the lack of any well-defined diagnostic algorithms. However, armed with an understanding of the diverse panel of available measurements of liver function and serum markers of hepatobiliary disease and knowledge of the patterns by which specific hepatobiliary disorders typically present themselves, the clinician can usually approach these diagnostic challenges in an orderly and selective manner. The normal values of certain laboratory tests that either lead to or assist in diagnosis are listed in Table 8-1 with ranges or reference intervals in traditional and Système International d’Unités (SI).
Drug-induced abnormalities in liver chemistries are frequently encountered. Although familiarity with the hepatic side effects of all drugs used is not possible, knowledge of the potential for and clinical pattern of

The evaluation of jaundice begins with a thorough review of the history of presentation, medication usage, medical history, physical examination, and evaluation of liver function tests. In a diagnostic evaluation for a patient with jaundice, the key elements initially arise from the patient’s history and physical examination. The following key questions are to be asked:
1.    Is the elevated bilirubin conjugated or unconjugated? In general, most patients with jaundice do not have isolated unconjugated hyperbilirubinemia.
2.    If the hyperbilirubinemia is unconjugated, is it caused by increased production, decreased uptake, or impaired conjugation?
3.    If the hyperbilirubinemia is conjugated, is the problem intrahepatic or extrahepatic?
4.    Is the process acute or chronic?
Jaundice can appear among patients with both acute hepatitis and chronic liver disease. The general

Constipation is a symptom rather than a disease and therefore represents a patient’s subjective interpretation of a real or imaginary somatic disturbance. Although no single definition is applicable to all patients with constipation, for clinical purposes one may use a frequency of defecation less than three times a week, either alone or in conjunction with difficulty during defecation, especially if this represents a distinct change in regular bowel habits (Fig. 6-1).
Constipation may be regarded conceptually as disordered movement through the colon or anorectum. From a pathophysiologic standpoint, this can occur because of a primary motor disorder, in association with various diseases or as a side effect of many drugs.
The classic example of neurogenic constipation is Hirschsprung disease, which results from a developmental arrest of caudal migration of neural crest cells from the notochord during embryonic development. This is

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Diarrheal diseases have quite different prevalences and outcomes in developed and developing countries (Fig. 5-1, Fig. 5-2, Fig. 5-3). Infant and child mortality rates decreased in developing nations from 5 million a year in 1987 to 3.5 million a year in 1995. The infant mortality rate from diarrheal diseases in the United States is stable at 300-500 deaths per year over the same period. In the United States, the death rate from diarrhea among persons older than 74 years is nearly 10 times that of infants, children, and younger adults.
Diarrhea (stool volumes greater than 200 mL/24 h) results from alterations in water and electrolyte transport mediated through changes in intracellular messengers (Fig. 5-4 and Fig. 5-5) or from unabsorbed osmotic solutes that retain fluid within the intestinal lumen. Inflammatory diarrhea causes systemic symptoms through the release of cytokines (Fig. 5-6).
Acute diarrhea is defined as that less than 2 to 3 weeks in duration. The most common causes are infections

CLINICAL BACKGROUND

A wide spectrum of pathophysiologic mechanisms may come into play when ileus or obstruction involve the small and large intestines. The most life-threatening abnormality is ischemic necrosis that occurs as a result of complicated obstruction. When blood flow is compromised, the most vulnerable bowel layer, the mucosa, becomes nonviable. This disrupts the normal functions of absorption and secretion, but more important, it destroys the protective barrier against intralumenal microorganisms. Lethal bacteria and toxins traverse the intestinal wall, causing peritonitis, abscesses, toxemia, and sepsis. The process is accelerated if transmural necrosis and perforation occur. Because of the high mortality rate associated with this complication, prevention is the best clinical plan. Early recognition is not sufficient, because it is often too late to intervene when clinical signs become apparent. Anticipation of this lethal complication and early surgical intervention should be adopted as the therapeutic strategy in many, if not most cases of obstruction of the small and large intestine.
Because of intestinal stasis in progressive obstruction, the normal gram-positive aerobic flora of the small intestine are replaced by anaerobic and gram-negative flora. If ileus or obstruction is incomplete, the result