REFLUX OESOPHAGITIS

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LABORATORY FINDINGS   Microcytic anaemia due to chronic blood loss Occult blood in stool due to oesophageal erosions

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LABORATORY FINDINGS Peptic ulcer - normal or increased gastric acid;  there is no correlation of the amount of gastric acid with the presence of peptic ulceration; lack of gastric acid excludes the diagnosis of peptic ulcer Zollinger-Ellison syndrome - increased volume of gastric secretions, increased basal acid secretion (greater than 60% of the maximal acid secretion following betazole {Histalog} or pentagastrin stimulation), and increased fasting serum gastrin level Pyloric obstruction with gastric retention and vomiting - dehydration and azotemia; decreased serum Na, CI, K; increased C02 content and increased pH (metabolic alkalosis) Perforation - leukocytosis with left shift, dehydration, increased amylase, increased lipase Haemorrhage - acute, normocytic anaemia, chronic, microcytic hypochromic anaemia;  occult blood in stool

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LABORATORY FINDINGS Occult blood in stool due to gastric mucosal erosions Hypochromic, microcytic anaemia due to chronic blood loss Macrocytic anaemia due to pernicious anaemia following atrophic gastritis of long duration Early decrease in gastric acid due to increased acid formation by injured and atrophic gastric parietal cells Late absence of gastric acid which is unresponsive to Histalog or pentagastrin stimulation Increased serum gastrin due to lack of gastric acid and loss of acid inhibition of gastrin secretion Parietal-cell antibodies frequently occur in atrophic gastritis. Intrinsic-factor antibodies occur in many cases of autoimmune chronic gastritis that result in pernicious anaemia. Decreased serum vitamin B12 due to decreased formation of intrinsic factor by atrophic gastric parietal cells

Penetrating gastric carcinoma: note nodularity of the base and the thickened nodular or rolled margins and that the rugae or folds do not radiate to the edge of the ulcer in most areas.Click on image for link to source.

LABORATORY FINDINGS   Gastroscopic biopsy and cytology - essential for diagnosis Hypochromic, microcytic anaemia due to chronic blood loss Occult blood in stool Blood in gastric contents Gastric analysis - 50% of patients have no gastric acid, even following stimulation;  50% have normal or decreased gastric acid Increased serum gastrin due to hypochlorhydria

REGIONAL ENTERITIS

LABORATORY FINDINGS

• Leukocytosis and increased sedimentation rate occur during the acute inflammatory phase.
• Hypochromic, microcytic anaemia due to chronic blood loss
• Occult blood in stool due to intestinal mucosal bleeding
• Decreased serum albumin and total protein due to loss of protein from the intestinal mucosa and to impaired dietary intake
• Increased alkaline phosphatase, serum glutamic-oxaloacetic transminase (SGOT) (AST {aspartate aminotransferase}) or bilirubin due to associated liver disease
• Increased urine oxalate and calcium oxalate renal calculi due to increased colonic absorption of dietary oxalate

• Peritonitis
• Gastrointestinal bleeding
• Impaired intestinal absorption
• Amyloidosis*
• Arthritis - synovial fluid similar to that of rheumatoid arthritis, but with negative rheumatoid factor
• Ankylosing spondylitis

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LABORATORY FINDINGS

• Increased urine 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin - occurs only when hepatic metastases are present
• Increased blood and urine serotonin, found only after hepatic metastases of intestinal carcinoid tumour and in gastric carcinoid tumours
• Laboratory findings of diarrhoea

LABORATORY FINDINGS
 

• Early increase in WBC (to 12,000/ul - 14,000/ul;  later up to 20,000/ul);  more than 75% neutrophils with a "shift to the left"
• Normal sedimentation rate

• Dehydration - decreased urine volume;  increased blood urea nitrogen (BUN), haematocrit, and urine specific gravity
• Abscess formation - increased sedimentation rate
• Peritonitis

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LABORATORY FINDINGS Definitive diagnosis requires a colonic mucosal biopsy. Normocytic anaemia (acute blood loss) or microcytic anaemia (iron deficiency due to chronic blood loss) Gross or occult blood in stool;  WBC in stool Leukocytosis during acute exarcerbation Increased sedimentation rate - indicates active inflammation Decreased serum K, Na CI - due to diarrhoeal loss Decreased serum albumin due to loss of protein from the diseased bowel wall;  the degree of hypoalbuminaemia parallels the severity of the disease Increased alkaline phosphatase, SGOT (AST) and bilirubin due to associated liver disease Laboratory Findings of Complications Carcinoma of the colon Gastrointestinal bleeding Arthritis

LABORATORY FINDINGS

Acute infarction

• Leukocytosis with a "shift to the left"
• Decreased  pH and C02 content (metabolic acidosis) reflect lactic acidosis from the necrotic bowel.
• Increased serum LDH, with all isoenzymes increased, reflects tissue necrosis.
• Increased haematocrit and BUN reflect haemoconcentration following intestinal fluid loss.
• Laboratory findings of intestinal bleeding, intestinal obstruction, and shock

• Laboratory findings of impaired intestinal absorption

Click on image for link to source document Approximately 6 - 8 litres of fluid enters the small bowel every 24hours. Most of this fluid is absorbed through the microvilli in the small intestine. The wall of the small bowel contains layers of smooth muscle and the nerve supply to this smooth muscle is from both the parasympathetic (vagus nerve - the 10th. cranial) and the sympathetic divisions of the autonomic nervous system. Parasympathetic stimulation increases movement through the lumen of the gut wall (motility). This is achieved through pendular contractions and waves of peristalsis. Sympathetic activity has the opposite effect, it brings about a reduction in intestinal motility and peristalsis. In small bowel obstruction these normal physiological functions are disrupted. Peristalsis is either severely reduced or absent. As a result, fluid, gas and intestinal contents accumulate and abdominal distention with nausea and vomiting occurs. This leads to fluid loss, dehydration and electrolyte imbalances involving sodium, potassium and chloride. These disturbances contribute further to the existing intestinal obstuction. Distention of the bowel wall brings about an increase in capillary permeability, and intestinal fluid and electrolytes leak (extravasation) into the peritoneal cavity causing peritonitis. Peritonitis is a major cause of paralytic ileus and together with fluid loss and electrolyte disturbances rapidly places the patient, unless treated correctly, in a state of hypovolaemic shock.

LABORATORY FINDINGS Leukocytosis - counts <15,000/ul suggest simple obstruction;  counts > 15,000/ul suggest impaired circulation;  counts > 25,000/ul suggest infarction.  Leukocytosis may not occur in older, debilitated patients or in those using corticosteroids or other immunosuppressive drugs. Leukopenia with left shift suggests infarction with sepsis. Increased serum amylase indicates bowel infarction, secondary pancreatitis, and leakage of pancreatic amylase into the peritoneum and bloodstream. Decreased pH and C02 content (metabolic acidosis) reflect lactic acidosis occurring with bowel infarction Increased pH and C02 content (metabolic alkalosis) secondary to vomiting with loss of fluid, H+, C1 and K Increased BUN suggests dehydration, blood in the intestine, or renal damage. Increased LDH (all isoenzymes) suggests infarction of the intestine. Decreased serum K and C1 seconary to vomiting Ascitic fluid - infarction is suggested by bloody fluid, fetid odour, bacteria, elevated amylase Gastric contents - presence of blood suggests infarction of the small intestine Rectal contents - presence of blood is common due to bleeding from infarcted bowel Laboratory Findings of Dehydration Decreased urine volume occurs early Increased haemoglobin and haematocrit Increased urine specific gravity Increased BUN

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LABORATORY FINDINGS Leukocytosis and increased sedimentation rate reflect acute inflammation. Occult blood in stool due to mucosal bleeding Laboratory Findings of Complications Intestinal haemorrhage Peritonitis due to perforation Obstruction of colon Pyelonephritis or cystitis due to inflammation from adherent diverticulitis

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LABORATORY FINDINGS Biopsy of colonic tumour is necessary for definitive diagnosis. Occult or gross blood in stool Leukocytosis and increased sedimentation rate indicate inflammation or necrosis of the tumour. Microcytic anaemia, iron-deficiency type, due to chronic blood loss Decreased serum potassium as a result of potassium loss from mucus-secreting villous tumour of the rectum Increased serum carcioembryonic antigen - this test is used to monitor the adequacy of treatment and evidence of recurrence Decreased serum protein reflects protein loss in stool or poor dietary intake. Laboratory findings of Complications Intestinal haemorrhage Peritonitis due to perforation Obstruction of the colon

INCREASED DELIVERY OF SMALL-INTESTINAL CONTENTS TO COLON
 

LABORATORY FINDINGS

• Culture of stool yielding Salmonella, Shigella, Yersinia, or Campylobacter
• Neutrophils in stool - ulcerative colitis, amebiasis, pseudomembranous colitis, enteritis due to Shigella, Campylobacter, Salmonella
• Presence in stool of Entamoeba histolytica or Giardia lamblia
• Increased haemoglobin, haematocrit, and BUN reflect haemoconcentration due to loss of fluid and electrolytes in stool.
• Decreased urine sodium and volume due to marked fluid and electrolyte loss in stool
• Decreased pH and C02 content (metabolic acidosis) due to intestinal loss of bicarbonate; less commonly, metabolic alkalosis occurs as a result of loss of fluid, acid, potassium, and chloride in the stool.  This occurs with congenital acid diarrhoea and with villous adenoma.
• Increased stool fat due to malabsorption or maldigestion
• Biopsy of small - or large - intestinal mucosa may show diagnostic pathologic changes.

CAMPYLOBACTER ENTERITIS

LABORATORY FINDINGS

• Presence of foecal leukocytes and gross or occult blood
• Stool culture yields Campylobacter.
• Phase-contrast microscopy of stool may reveal Campylobacter.

LABORATORY FINDINGS

• Presence of fecal leukocytes and gross or occult blood
• Presence of toxin of C. difficile

LABORATORY FINDINGS

• Culture of Shigella from stool, rectal swab, or sigmoidoscopic swab
• Smear of stool shows mucous, leukocytes, macrophages, and gross or occult blood

LABORATORY FINDINGS

Enterocolitis

• Stool culture, usually positive for S. typhimurium, for 1-4 weeks
• Stool may contain leukocytes.
• No systemic leukcytosis

• Stool and bloodstream cultures usually positive for S. paratyphi B or S. typhimurium

• Intermittently positive blood cultures, usually of S. choleraesuis
• Negative stool cultures
• Leukocytosis

• Meningitis, especially in infants
• Positive culture of organisms from local abscesses at various sites

LABORATORY FINDINGS

• Positive blood culture for S. typhi during the first 10 days (90%); fewer than 30% are positive at the end of the third week
• Positive bone marrow culture for S. typhi occurs even when blood cultures are negative.
• Positive stool culture for S. typhi after 10 days, especially during third to fifth week (85%); stool culture may remain positive for more than 1 year in 3% of patients, who are termed chronic enteric carriers.  The bacilli are harbored in the gallbladder.
• Positive urine culture for S. typhi during third to fourth week (25%)
• Leukopenia - 4000/ul - 6000/ul in first two weeks; 3000/ul - 5000/ul in second two weeks
• Normochromic, normocytic anaemia - chronic-disease type
• Proteinuria during febrile period
• No increase in sedimentation rate
• Serologic tests are nonspecific

• Liver involvement - increased serum LDH (especially LDH), alkaline phosphatase, SGOT (AST)
• Intestinal ulceration - blood in stool during second to third week
• Relapse - positive blood culture

LABORATORY FINDINGS

• Ascitic fluid - turbid, bloody, may contain fat globules; increased WBC; Gram's stain and aerobic and anaerobic cultures show multiple organisms;  increased amylase;  increased mononuclear cells and decreased glucose occur in tuberculous peritonitis
• Leukocytosis - up to 50,000/ul with 80% - 90% neutrophils;  may not occur in older patients
• Increased haemoglobin, haematocrit, and BUN - reflect haemoconcentration secondary to extracellular fluid loss into the peritoneal cavity
• Laboratory findings of any of the underlying conditions listed above

LABORATORY FINDINGS

• Gross or occult blood in stool, vomitus, or gastric contents
• Hypochromic, microcytic anaemia, iron-deficiency type, due to chronic blood loss
• Altered liver function tests suggest cirrhosis of the liver with oesophageal varices as the source of bleeding.
• Increased BUN due to breakdown of blood in the colon by bacteria resulting in increased nitrogen formation
• Laboratory findings or any of the underlying conditions listed above

LABORATORY FINDINGS

• Increased number and size of fat globules in stool;  increased neutral fat (unsplit fats) indicates impaired fat digestion;  increased free fatty acids (split fats) indicates normal fat digestion but impaired fat absorption
• Increased quantity of fat in 72-hr stool sample after the patient has been on a 100-g fat diet daily for three days
• Decreased serum carotene indicates fat malabsorption or decreased dietary intake of carotene.
• Impaired D-xylose tolerance test (decreased urinary excretion of a measured amount of ingested xylose) indicates impaired jejunal mucosal absorption of xylose.  Because this carbohydrate does not require digestion by pancreatic enzymes, the tolerance test is normal in pancreatic insufficiency and does not indicate maldigestion.
• Decreased serum levels of total protein, albumin, y-globulin, iron, folate, vitamin B12, calcium, phosphorous, magnesium, and cholesterol result from impaired intestinal absorption.
• Anaemia - macrocytic, due to impaired absorption of folate or vitamin B12; microcytic, due to iron deficiency
• Increased urine oxalate accompanying steatorrhea indicates an increase in colonic absorption of oxalates and their excretion in urine.
• Prolonged prothrombin time results from impaired vitamin-K absorption.
• Intestinal biopsy may show mucosal villous atrophy, tumour, or inflammation.

Malabsorption

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