Diarrhoea Flashcards

1
Q

What time frame distinguishes acute and chronic diarrhea?

A

Diarrhea is the frequent (> 3 times per day) evacuation of liquid feces. Acute diarrhea is often self-limiting and lasts for a few days. Diarrhea is considered chronic when lasting > 3 weeks.

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2
Q

What is the most common cause worldwide of epidemic diarrhea?

A

Norovirus. These single-stranded RNA viruses are believed to be responsible for at least 50% of all gastroenteritis outbreaks worldwide and a major cause of foodborne illness. With the widespread use of rotavirus vaccination, norovirus has become the most common cause of medically attended acute gastroenteritis in children

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3
Q

What are other common causes of acute diarrhea?

A
  • Viral (others include rotavirus, enterovirus)
  • Bacterial (e.g ., Escherichia coli, Shigella, Salmonella, Yersinia, Campylobacter, Clostridium difficile )
  • Protozoal
  • Allergic
  • Medication side effect (e.g., antibiotic usage)
  • Extra-intestinal infections (e.g., respiratory, urinary, sepsis)
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4
Q

Which historical questions are key when seeking the cause of diarrhea?

A
  • Recent medications, especially antibiotics
  • History of immunosuppression (e.g., recurrent major infections, history of malnutrition, acquired immunodeficiency syndrome, immunosuppressive medications)
  • Illnesses in other family members or close contacts
  • Travel outside of the United States
  • Travel to rural or seacoast areas (i.e., involving the consumption of untreated water, raw milk, or raw shellfish)
  • Attendance in day care
  • Recent foods particularly focus on juice and fructose consumption
  • Presence of family pets
  • Food preparation and water source
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5
Q

In what settings can diarrhea be a severe, life-threatening illness?

A
  • Intussusception
  • Salmonella gastroenteritis (neonatal or compromised host)
  • Hemolytic-uremic syndrome
  • Hirschsprung disease (with toxic megacolon)
  • Pseudomembranous colitis (classically due to C. difficile )
  • Inflammatory bowel disease (with toxic megacolon)
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6
Q

Why is true diarrhea during the first few days of life especially concerning?

A

In addition to the greater potential for dehydration in a newborn, diarrhea in this age group is more commonly associated with major congenital intestinal defects involving electrolyte transport (e.g., congenital sodium- or chloride-losing diarrhea), carbohydrate absorption (e.g., congenital lactase deficiency), immune-mediated defects (e.g., autoimmune enteropathy), or those characterized by villous blunting (e.g., microvillus inclusion disease). Although viral enteritis can occur in the nursery, any newborn with true diarrhea warrants thorough evaluation and possible referral to a tertiary center.

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7
Q

What are the most useful stool tests for diagnosing fat malabsorption?

A

Measurement of 72-hour fecal fat is the gold standard test for fat malabsorption. The patient must ingest a high-fat diet for 3 to 5 days (100 g daily for adults), and all stool is collected for the final 72 hours. A complete and accurate dietary history should be obtained concomitantly so the coefficient of fat absorption can be calculated. Steatorrhea is present if more than 7% of dietary fat is malabsorbed. In normal infants, up to 15% of fat can be malabsorbed. Other tests include Sudan staining of stool for fat globules (a qualitative test that, if positive, indicates gross steatorrhea), the steatocrit, and monitoring absorbed lipids after a standardized meal.

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8
Q

What stool test is most useful for helping diagnose GI protein loss?

A

Fecal α 1 -antitrypsin measurement is the most useful stool marker of protein malabsorption. It is important to concomitantly measure serum α 1 -antitrypsin to ensure that the patient does not have α 1 -antitrypsin deficiency, which could result in a false-negative stool study.

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9
Q

How do patterns of secretory or enterotoxigenic and inflammatory diarrhea vary?

A

Secretory or enterotoxigenic disease is characterized by watery diarrhea and the absence of fecal leukocytes. Inflammatory disease is characterized by dysentery (i.e., symptoms and bloody stools), as well as fecal leukocytes and red blood cells.

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10
Q

What is the primary pathophysiologic difference between secretory and osmotic diarrhea?

A

In osmotic diarrhea , undigested nutrients increase the osmotic load in the distal small intestine and the colon leading to decreased water absorption. In secretory diarrhea , a noxious agent causes the intestinal epithelium to secrete excessive water and electrolytes into the lumen.

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11
Q

How can osmotic diarrhea be distinguished from secretory diarrhea?

A

In true osmotic diarrhea, symptoms should cease when the patient is made NPO. In addition, a fecal osmotic gap can be calculated. In osmotic diarrhea, the fecal electrolyte content becomes lower than the serum. Stool electrolytes should be collected and compared with a normal serum osmolality, 290 mOsm/kg. The fecal osmotic gap is [290 − 2(Na + K)].

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12
Q

How should children with secretory diarrhea be managed?

A

After the child is taken off feeds, a vigorous attempt must be initiated to maintain fluid and electrolyte balance. If this is successful, the child should be evaluated for proximal small bowel damage, enteric pathogens, and a baseline malabsorption workup. If abnormalities of the mucosal integrity are suspected, a small bowel biopsy is performed; if the findings are significantly abnormal, the patient may be given parenteral alimentation and gradual refeeding. Electron microscopy may reveal congenital abnormalities of the microvillus membrane and the brush border. Hormonal causes of secretory diarrhea (e.g., a VIPoma, hypergastrinoma, or carcinoid syndrome) must be considered if initial studies are negative

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13
Q

What rare tumors can cause true secretory diarrhea?

A
  • Gastrinoma : Children present with typical ulcer pain, hematemesis, vomiting, and melena. High acid output into the proximal small bowel leads to precipitation of bile salts and steatorrhea.
  • VIPoma: Children present with profuse watery diarrhea with marked fecal losses (20 to 50 mL/kg/day) due to high levels of vasoactive intestinal peptide (VIP).
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14
Q

What features characterize “toddler diarrhea”?

A

Toddler diarrhea , which is also known as chronic nonspecific diarrhea , is a clinical entity of unclear etiology that occurs in infants between 6 and 40 months of age, often following a distinct identifiable enteritis and treatment with an antibiotic. Loose, nonbloody stools (at least two per day but usually more) occur without associated symptoms of fever, pain, or growth failure. Malabsorption is not a key feature.

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15
Q

What is primary lactose intolerance?

A

In more than 50% of the population, beginning at the age of 5 years, lactase levels decline progressively after having been normal in infancy. These levels decline at different rates for different people depending on their genetics. Most adults with primary lactose intolerance have lactase levels of about 10% of those seen during infancy. Symptoms of lactose intolerance (e.g., bloating, nausea, cramps, diarrhea after dairy foods) may develop if excessive lactose loads are ingested.

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16
Q

What conditions produce secondary lactose intolerance?

A
Any disorder that alters the mucosa of the proximal small intestine may result in secondary lactose intolerance
Microvillus and brush border:
• Post-enteritis
• Bacterial overgrowth
• Inflammatory lesions (Crohn disease)
Level of the villus:
• Celiac disease
• Allergic enteropathy
• Eosinophilic gastroenteropathy
Bulk intestinal surface area:
• Short bowel syndrome
Altered transit with early lactose entry into colon:
• Hyperthyroidism
• Dumping syndromes
• Enteroenteral fistulas
17
Q

How is lactose intolerance diagnosed?

A

The most common noninvasive method of diagnosing lactose intolerance is a breath hydrogen test . The fasted patient is fed 2 g/kg (up to 25 g) of lactose, and end-expired air is collected every 15 minutes for the next 2 to 3 hours for the purpose of measuring hydrogen concentration. Fermentation of carbohydrate by bacteria in the colon results in hydrogen expiration after lactose ingestion. A peak hydrogen level of 20 parts per million above the baseline after about 60 minutes in concert with a symptomatic response is considered a positive test. Because of the need for colonic bacteria to ferment carbohydrate and produce hydrogen gas, it is important that the patient not receive antibiotics immediately before the test.

18
Q

What is the role of stool elastase measurement?

A

Measurement of fecal pancreatic elastase is a screen for pancreatic insufficiency , which can be a cause of fat malabsorption (e.g., cystic fibrosis). A decreased measurement of pancreatic elastase is associated with pancreatic insufficiency, although values can be falsely decreased when the sample is obtained from diarrheal specimen.

19
Q

What three individual clinical features are the most accurate for predicting 5% dehydration?

A
  • Abnormal capillary refill
  • Abnormal skin turgor
  • Abnormal respiratory pattern
20
Q

What is the role of antiemetic agents in children with gastroenteritis?

A

Published guidelines have not yet formally recommended the use of antiemetic medications, particularly domperidone, metoclopramide, prochlorperazine, and promethazine, because of concerns of increased emergency department (ED) revisits rates of misdiagnosis, and health care costs. Oral ondansetron, a centrally acting 5-hydroxytryptamine antagonist, has been found to be useful in decreasing the risk for persistent vomiting, lessening the need for intravenous therapy in ED settings and reducing the likelihood of hospitalization.

Freedman SB, Hall M, Shah SS, et al: Impact of increasing ondansetron use on clinical outcomes in children with gastroenteritis, JAMA Pediatr 168:321–329, 2014.

21
Q

Why is Salmonella enteritis so concerning in a child who is younger than 12 months?

A

In older children with Salmonella gastroenteritis, secondary bacteremia and dissemination of disease rarely occur. In infants, however, 5% to 40% may have positive blood cultures for Salmonella , and in 10% of these cases, Salmonella can cause meningitis, osteomyelitis, pericarditis, and pyelonephritis. Thus, in infants who are younger than 1 year, outpatient management of diarrhea assumes even greater significance, particularly if Salmonella is suspected.

22
Q

What are the clinical manifestations of typhoid fever?

A

Typhoid fever is caused by Salmonella species typhi and paratyphi . It is characterized by fever, abdominal pain, nausea, decreased appetite, and constipation over the first week. The fever is sometimes paradoxically associated with bradycardia (Faget sign or sphygmothermic dissociation). Leukopenia is common. Diarrhea begins after approximately a week. If untreated it can last for 2 to 3 weeks and cause significant weight loss and melena. Treatment of typhoid fever is necessary only in patients with sepsis or bacteremia with signs of systemic toxicity or a metastatic focus, which can include otitis, endocarditis, cholecystitis, or encephalitis.

23
Q

What strains of E. coli are associated with diarrhea?

A
  • Enterotoxigenic (ETEC): responsible for travelers’ diarrhea
  • Enteropathogenic (EPEC): similar mechanism as ETEC; adheres to epithelial cells and releases toxins that induce intestinal secretions and limit absorption; responsible for epidemics in daycare settings and nurseries
  • Enteroinvasive (EIEC): invades mucosa and causes bloody diarrhea
  • Enterohemorrhagic (EHEC): produces a Shiga-like toxin that is responsible for hemorrhagic colitis; usually associated with contaminated food and undercooked beef; usually a self-limited gastroenteritis
24
Q

What clinical entity has been attributed to EHEC, specifically strain O157:H7?

A

Hemolytic uremic syndrome (HUS), which is the triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure

25
Q

What is the most common cause of antibiotic-associated colitis?

A

Clostridium difficile (C. difficile) . Fever, abdominal pain, and bloody diarrhea begin as early as a few days after starting antibiotics (especially clindamycin, ampicillin, and cephalosporins). Definitive diagnosis is made by sigmoidoscopy, which reveals pseudomembranous plaques or nodules

26
Q

How is the diagnosis of C. difficile made?

A

C. difficile causes diarrhea by producing two diarrheagenic toxins (A and B). Essay immunoassay for the toxins was previously the diagnostic test of choice. However, in 2013, the American College of Gastroenterology recommended that nucleic acid amplification tests , such as PCR assays , which detect toxin-encoding genes should be the standard diagnostic test because of superior sensitivity and specificity.

27
Q

How common is asymptomatic C. difficile carriage?

A

Colonization rates in infants can be up to 70%, with percentages decreasing with age. By the second year of life, the rate declines to about 6%, and above age 2 years to 3%, which is the approximate rate in adults. These high colonization rates make the interpretation of positive tests in younger infants problematic. Toxin assays are more indicative of C. difficile –associated disease than culture. However, the toxin may be present without any symptoms, especially in infants, who typically do not have the toxin receptors necessary for disease. Unless there is evidence of histologic colitis, asymptomatic carriers do not require treatment.

28
Q

What are the three most common presenting symptoms of giardiasis?

A
  • Asymptomatic carrier state
  • Chronic malabsorption with steatorrhea and FTT
  • Acute gastroenteritis with diarrhea, weight loss, abdominal cramps, abdominal distention, nausea, and vomiting
29
Q

How reliable are the various diagnostic methods for detecting Giardia ?

A
  • Three stool examinations (ideally 48 hours apart) for same: 95%
  • Single stool examination and stool enzyme-linked immunosorbent assay test for Giardia antigen: > 95%
  • Duodenal aspirate or string test: > 95%
  • Duodenal biopsy (gold standard): Closest to 100%
30
Q

What are the potential complications of amebiasis?

A

The parasite Entamoeba histolytica disseminates from the intestine to the liver in up to 10% of patients and to other organs less commonly.

  • Liver abscess
  • Pericarditis
  • Cerebral abscess
  • Empyema