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Lab Med II > Upper GI > Flashcards

Upper GI Flashcards

1
Q

Zollinger-Ellison Syndrome

A

Caused by a pancreatic islet cell gastrin-secreting tumor (gastrinoma) that stimulates the acid-secreting cells of the stomach (parietal cells) to maximal activity, with consequent gastrointestinal mucosal ulceration

May occur sporadically or as part of an autosomal dominant familial syndrome called multiple endocrine neoplasia type 1 (MEN 1)

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2
Q

Zollinger-Ellison Syndrome Clinical presentation

A

Abdominal and esophageal pain
Chronic diarrhea (steatorrhea)
Nausea
Malnourishment/ Weight loss

ZES is suspected in patients who have severe ulceration of the stomach and small bowel, especially if they fail to respond to treatment

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3
Q

What is the best single screening test for ZES?

A

Fasting serum gastrin

Serum gastrin will be normal in patients with routine peptic ulcers and greatly elevated in ZES.

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4
Q

Gastrin provocative test

A

Differentiation between the causes of hypergastrinemia can be made with the aid these tests.

Includes:
1. Secretin stimulation test (preferred; the most sensitive and specific for the diagnosis of gastrinoma)
In ZES, there is a paradoxical promotion of gastrin secretion with secretin administration

2.Calcium infusion study

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5
Q

Secretin Stimulation test for ZES

A

Secretin is administered after an overnight fast with serum levels of gastrin drawn at 0,2,5,10,15.

If gastrin levels rise 120pg within 15 mins of secretin injection, >90% sensitive and specific for ZES

Increase of gastrin levels >200pg/mL at 15 minutes is diagnostic of ZES

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6
Q

Secretin stimulation and PPI

A

A false-positive secretin test result may occur if the patient has PPI–induced hypochlorhydria or achlorhydria (low or absent stomach acidity), which means that this agent must be stopped for 1 week prior to testing

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7
Q

Calcium infusion testing for ZES

A

Not used as frequently. 15mg Ca/kg in 500mL nml saline is administered over 4 hours with baseline fasting serum gastrin drawn prior to infusion and at 1, 2, 3, 4 hrs.

Normal: if little or no increase occurs over the baseline gastrin level

Positive: if there is a marked increase in gastrin with the calcium infusion

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8
Q

G-cell hyperplasia

A

Rare condition associated with increase in the number of G cells and marked hypergastrinemia.

Unlike ZES, antral G-cell hyperplasia is characterized by a poor response to secretin stimulation test, and absence of gastrinoma on imaging.

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9
Q

Pernicious anemia

A

Pernicious anemia is a vitamin B12 deficiency related to atrophic gastritis, parietal cell loss, or loss of intrinsic factor

An autoimmune destruction of gastric parietal cells leading to a lack of intrinsic factor, which is essential for vitamin B12 absorption in the ileum

Serum gastrin is increased in pernicious anemia to compensate for the hypochlorhydria

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10
Q

Gastrin testing: Pre-test prep

A

Patients should fast 12 hours prior to the test. Water is permitted.

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11
Q

Gastrin testing: Specimen care

A

Collect 5mL of venous blood in a red topped tube (Freeze if not tested immediately)

Indicate any medications on the lab slip that may affect results

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12
Q

Gastrin can be falsely increased/decreased in:

A
  1. Non-fasting patients or a protein rich meal
  2. Elderly patients
  3. Diabetic patients taking insulin
  4. Drugs (antacids, H₂-blocking agents, PPIs, steroids, calcium, amphetamines (Adderall), caffeine, pseudoephedrine)
  5. Peptic ulcer surgery (partial gastrectomy, pyloroplasty) - creates a persistant alkaline environment, stimulating gastrin production

Falsely decreased in those treated with:
1. Anticholinergics (benadryl, atrovent, bupropion, dextromethorphan) and TCAs (Elavil, Pamelor)

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13
Q

Gastrin level increased interpretation

A

ZES
G-cell hyperplasia
Pernicious anemia/atrophic gastritis
Gastric carcinoma: stomach CA usually exists in an alkaline environment
Chronic renal failure: gastrin is metabolized by the kidney, so if inadequate renal function, gastrin levels will increase
Pyloric or gastric outlet obstruction: causes stomach distention, which is a stimulant of gastrin secretion
Retained antrum after gastrectomy: Antral tissue contains G cells, which if left on the duodenal stump is constantly bathed in duodenal alkaline juices, is a strong stimulant for gastrin production

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14
Q

Gastrin level decreased interpretation

A

Antrectomy
Vagotomy
Hypothyroidism

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15
Q

Gastric acid composition

A

HCl (hydrochloric acid, KCl (potassium chloride), and NaCl (sodium chloride)

Normal pH of gastric acid in the stomach lumen is 1.5-3.5

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16
Q

Gastric analysis uses

A

Examines stomach contents for abnormal substances and measures gastric acidity.

Used to:
diagnose ulcers, obstructions, pernicious anemia, or gastric carcinoma

evaluate the effectiveness of medical or surgical therapies

identify mycobacterial infection (e.g., TB studies) when previous sputum tests have been negative

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17
Q

Gastric acid analysis: pre-test

A

Should be fasting 10-12 hours prior to the procedure from food, fluids, smoking, and gum chewing.

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18
Q

Gastric analysis procedure: Aspirate the stomach contents

A

using a 50cc syringe until no more gastric juice may be aspirated.

Record volume, color, and pH of gastric juice

If residual volume (the volume aspirated) is >100mL or if food particles are present, a gastric outlet obstruction should be considered (possibly caused by PUD around pylorus, scarring, or gastric CA).

19
Q

Gastric acid procedure: Basal gastric acid output (BAO)

A

Calculation of stomach acid production after the stomach contents are aspirated.

20
Q

Gastric acid procedure: Stimulated gastric analysis

A

SC injection of pentagastrin (gastrin stimulant) is collected every 15 minutes.

21
Q

Gastric analysis: Increased levels interpretation

A

Peptic or duodenal ulcer
Zollinger-Ellison Syndrome
G-cell hyperplasia
Post small intestine resection

22
Q

Gastric analysis: Decreased levels interpretation

A

Pernicious anemia
Atrophic gastritis
Gastric malignancy
Post vagotomy

23
Q

Gastric acid analysis and ZES

A

Basal acid output (BAO) of >15mEq/hr supports diagnosis of ZES.

BAO >5mEq/hr if a previous acid reducing surgery (vagotomy/partial gastrectomy) has been performed is suggestive of ZES

Basal gastric secretory volume >140mL has a high sensitivity and specificity for ZES

Basal gastric pH <2.0 in the presence of a large gastric volume (>140mL) is highly suggestive of ZES

24
Q

H. pylori neutralization of stomach acid

A

H. pylori neutralizes the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia.

Ammonia, which is basic, neutralizes stomach acid

25
Q

Methods of detecting the presence of H. pylori

A 
Gastric mucosal biopsy (from antrum and greater curvature of the corpus) through EGD (esophagogastroduodenoscopy)
Rapid urease test
Stool antigen test
Carbon 13 urea breath test
Serology
26
Q

Who should be tested for H. pylori?

A

Patients with active gastric or duodenal ulcers

Patients with a documented history of peptic ulcers

Patients with early gastric cancer (following resection)

Patients with low-grade MALT (mucosa associated lymphoid tissue) lymphoma

Current guidelines recommend treatment for H. pylori whenever it is detected – so only test if you plan to treat if positive

27
Q

H. pylori gastric mucosal biopsy

A

Upper EGD + biopsy is considered gold standard and reference method of diagnosis, but it is invasive.

28
Q

EGD gastric mucosal biopsy morphology on Giemsa stain:

A

Variable number of H. pylori organisms adhering to the gastric epithelium, both coating the gastric wall and lining the gastric glands

29
Q

Rapid urease test

A

A small piece of gastric mucosa (obtained from gastroscopy) is inserted into testing gel containing urea and an indicator such as phenol red

The urease produced by H. pylori hydrolyzes urea to ammonia, which raises the pH of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE)
Sensitivity of 96% and specificity of 90%

30
Q

H. pylori stool antigen test

A

H. pylori does not survive in the stool, but H. pylori antigens are present.

ELISA using a polyclonal anti-H. pylori capture antibody detects the presence of H. pylori antigen in a fresh stool specimen

Positive: presence of detectable antigen in the stool
Negative: no detectable antigen in the stool

Used in initial stages of infection but can also detect eradication after treatment.

31
Q

H. pylori Carbon 13 urea breath test

A

Carbon 13 urea breath test (UBT) is based on the capability of H. pylori to metabolize urea to CO₂ because of the organism’s capability to produce urease

It is expensive!

False-negative results:
1. infection with coccoid forms of H pylori that do not produce as much urease

  1. related to the intake of antibiotics, bismuth, H₂ blockers, or proton pump inhibitors
32
Q

H. pylori serology testing

A

Easy to perform, non-invasive, and requires no preparation or abstinence from antacids

Lab-based ELISA testing to detect immunoglobulin G (IgG) antibodies against H. pylori

Lab-based ELISA testing to detect immunoglobulin G (IgG) antibodies against H. pylori

Helpful for detecting a newly infected patient, but not used for follow-up because difficult to differentiate active and past infection

33
Q

Celiac disease

A

Autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy onward

Symptoms: Abdominal discomfort, chronic constipation and diarrhea, failure to thrive (in children), anemia and fatigue

34
Q

Celiac disease pathophysiology

A

Celiac disease is caused by a reaction to gliadin, a gluten breakdown product found in wheat, barley, rye
Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the gliadin and the immune system cross-reacts with the small-bowel tissue, causing an inflammatory reaction
This inflammatory reaction leads to a shortening of villi lining the small intestine (villous atrophy) which interferes with absorption
Autoimmune response involves plasma cells that produce IgA and IgG

35
Q

Who should be tested for celiac disease?

A
  1. Those with GI symptoms including chronic or recurrent diarrhea, malabsorption, weight loss, and abdominal distension or bloating (including pts with symptoms suggestive for IBS or lactose intolerance)
2. Individuals without other explanations for signs and symptoms of disorders of the following types:
Nutritional deficiencies
Elevated liver enzymes
Reproductive abnormalities
Nervous system abnormalities
Persistent aphthous stomatitis
  1. Pts with type I diabetes and first-degree relatives of individuals with celiac disease if they have signs, symptoms, or lab evidence of possible celiac disease
  2. Testing for celiac disease may be considered in asymptomatic first-degree relatives of patients with confirmed diagnosis of celiac disease, particularly children, and in those with Down syndrome
36
Q

American college of gastroenterology (ACG) clinical guidelines for celiac disease

A
  1. Patients should be tested prior to being placed on a gluten-free diet
  2. Antibody testing, especially immunoglobulin A anti-tissue transglutaminase antibody (IgA tTG), is the best first test, although biopsies are needed for confirmation.

In children younger than 2 years, the IgA tTG test should be combined with testing for IgG-deamidated gliadin peptides (DGP)

  1. Patients diagnosed with celiac disease should be examined for deficiencies, including low bone density
  2. Patients already on a gluten-free diet without prior testing need to be evaluated to assess the likelihood that celiac disease is present
    Genetic testing and a gluten challenge are most helpful
37
Q

Celiac disease: IgA anti-tissue transglutaminase (tTG)

A

single preferred test for detection of celiac disease in individuals over the age of two years.

Want to check in combination with total IgA to make sure that they do not just have IgA deficiency.

38
Q

Who is considered high probability for celiac disease?

A
  1. Those with certain conditions frequently associated with celiac disease:
    dermatitis herpetiformis, Down syndrome, selective IgA deficiency, and other conditions with autoimmune features (type 1 diabetes mellitus, thyroid disease, autoimmune liver disease)
  2. Those with family history of celiac disease
  3. Patients with suggestive clinical features, including:
    severe diarrhea, weight loss, or persistent anemia
39
Q

Who should have duodenal biopsy via upper endoscopy to confirm celiac disease?

A
  1. patients with a positive serology

2. patients with a high probability of celiac disease, regardless of the serology

40
Q

Gross appearance of celiac disease on endoscopy:

A

duodenal mucosa may appear atrophic with loss of folds, contain visible fissures, have a nodular appearance or the folds may be scalloped

41
Q

Histology of celiac disease: Mild alteration

A

characterized only by increased intraepithelial lymphocytes (IEL)

42
Q

Histology of celiac disease: Severe

A

flat mucosa with total mucosal atrophy, complete loss of villi, enhanced epithelial apoptosis, and crypt hyperplasia

43
Q

Monitoring response to gluten-free diet

A

Timing: evaluate 4-6 weeks following the initiation of a gluten-free diet

Tests performed:

  1. complete blood count
  2. folate, B12, iron studies
  3. liver chemistries (ALT, AST, ALP, bilirubin)
  4. serologic testing

Serologic testing for monitoring treatment response:
IgA tTG or IgA (or IgG) DGP

For any assay that is used, a pretreatment antibody level should be determined at time of diagnosis

44
Q

Expected test results of successful treatment

A

Exclusion of gluten from the diet results in a gradual decline in serum IgA tTG and IgA DGP levels (half-life of 6-8 weeks).

Normal baseline value is typically reached within 3-12 months depending upon pre-treatment concentrations.
Normal IgA tTG levels do not reliably indicate recovery from villous atrophy

Conversely, if the levels do not fall as anticipated, the patient is usually continuing to ingest gluten either intentionally or inadvertently

Lab Med II (2 decks)

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