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LAB FINDINGS IN GASTROINTESTINAL DISEASES


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Reflux Oesophagitis Peptic Ulcer Gastritis Carcinoma of the Stomach
Regional Enteritis Carcinoid Tumour Acute Appendicitis Ulcerative Colitis
Mesenteric Infarction Intestinal Obstruction Intestinal Infections Antibiotic-Ass. Pseudomembranous Colitis
Carcinoma of the Colon Nontyphoidal Salmonellosis Diverticular Disease Shigellosis
Diahorrea Typhoid Fever Peritonitis Gastrointestinal Bleeding
Impaired Intestinal Absorption . .
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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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PEPTIC ULCER

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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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GASTRITIS

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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




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CARCINOMA OF THE STOMACH

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




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REGIONAL ENTERITIS

LABORATORY FINDINGS

Laboratory Findings of Complications



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CARCINOID TUMOUR

Carcinoid tumours are rare neuroendocrine lesions. Approximately 1000 cases are seen each year in the United Kingdom. Most arise from the gastrointestinal tract. The commonest sites of the primary tumour are the appendix (30%), small bowel (20%), colon (20%) and stomach less than 10%. Tumours can also arise from the bronchial tree. In most series a firm diagnosis has not been established before an operative procedure has been performed. They often present with vague right-sided abdominal pain. This has often been present for a number of years. Many patients have had numerous normal investigations. Urgent surgery, has often been precipitated by the onset of intestinal obstruction. When tumours have metastasised, symptoms related to excess hormonal production are often seen; the carcinoid syndrome. Symptoms include diarrhoea and flushing. The flushing is usually intermittent and lasting for only several minutes. Episodes become more frequent as the disease progresses. Flushing may be precipitated by the ingestion of either chocolate or alcohol and is often associated with palpitations and episodes of hypotension. Clinical examination is often normal. A right-sided abdominal mass or hepatomegaly may be present. In those with carcinoid syndrome features of pellagra, tricuspid regurgitation or pulmonary stenosis may be present.


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LABORATORY FINDINGS





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ACUTE APPENDICITIS

LABORATORY FINDINGS
 

Laboratory Findings of Complications
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ULCERATIVE COLITIS

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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




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MESENTERIC INFARCTION

LABORATORY FINDINGS

Acute infarction

Chronic Ischaemia



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INTESTINAL OBSTRUCTION

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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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DIVERTICULAR DISEASE

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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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CARCINOMA OF THE COLON

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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




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DIARRHOEA

INCREASED DELIVERY OF SMALL-INTESTINAL CONTENTS TO COLON
 

LABORATORY FINDINGS





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INTESTINAL INFECTIONS

CAMPYLOBACTER ENTERITIS

LABORATORY FINDINGS

ANTIBIOTIC-ASSOCIATED PSEUDOMEMBRANOUS COLITIS

LABORATORY FINDINGS

SHIGELLOSIS

LABORATORY FINDINGS

NONTYPHOIDAL SALMONELLOSIS

LABORATORY FINDINGS

Enterocolitis

Paratyphoid Fever Bacteremia Local infections TYPHOID FEVER

LABORATORY FINDINGS

Laboratory Findings of Complications



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PERITONITIS

LABORATORY FINDINGS





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GASTROINTESTINAL BLEEDING

LABORATORY FINDINGS





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IMPAIRED INTESTINAL ABSORPTION

LABORATORY FINDINGS


Malabsorption

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