GI/Pancreatic funuction

List and describe the structure and function of the five major components of the gastrointestinal tract

Designed to ingest, digest, absorb nutrients, and eliminate waste. It utilizes both mechanical and chemical processes to break down food, moving it via peristalsis while absorbing essential nutrients and water into the bloodstream

Continuous 30-foot muscular tube

• Mouth

• Esophagus

• Stomach

• Small intestine

• Large intestine

Discuss the physiologic role of the pancreas in the digestive process.

Endocrine and exocrine tissue

Activity is under both nervous and endocrine control. Branches of the vagus nerve can cause a small amount of pancreatic fluid secretion when food is smelled or seen

List the hormones excreted by the pancreas, together with their physiologic roles.

Islet cells (with Greek alphabet names) secret 5 hormones into the blood:
▪ Alpha – glucagon
▪ Beta – insulin
▪ Delta – somatostatin
▪ Gamma – pancreatic polypeptide (PP) hormones
▪ Epsilon – ghrelin

Explain autonomic nervous system influence on gastrointestinal motility

regulates gastrointestinal (GI) motility through a complex interplay of parasympathetic (excitatory) and sympathetic (inhibitory) branches, modulating smooth muscle contraction, sphincter tone, and coordinating with the enteric nervous system

Explain the role of gastrin, cholecystokinin, and secretin in controlling gastrointestinal secretions

• Gastrin (from stomach G-cells) stimulates gastric acid secretion

• CCK (from duodenum) triggers pancreatic enzyme release and gallbladder contraction.

• Secretin (from duodenum) acts to neutralize chyme by stimulating pancreatic bicarbonate secretion and inhibiting stomach acid.

Describe the process by which complex carbohydrates, proteins, and lipids are digested and absorbed

Digestion breaks down complex carbohydrates, proteins, and lipids into absorbable units—monosaccharides, amino acids, and fatty acids/glycerol, respectively—primarily in the small intestine using enzymes from the pancreas and intestinal brush border

Relate the following digestive enzymes to the substance they help breakdown: pepsin, amylase, lipase

• pepsin breaks down proteins into peptides in the stomach

• amylase breaks down carbohydrates/starches into simple sugars in the mouth and small intestine

• lipase breaks down fats/lipids into fatty acids and glycerol.

Zollinger-Ellison’s syndrome

Etiology

• associated with multiple neoplasia type 1 (MEN1) syndrone.

Pathophysiology

• begins with a gastrin-producing tumor (gastrinoma) in the pancreas or duodenum, which causes excessive gastrin release

Clinical and laboratory findings

• Serum gastrin test will be elevated and used to diagnose

• gastric acid hypersecretion

• tumor of pancreas

• peptic and doudenal ulcers

Peptic Ulcer Disease

Etiology

• H. pylori

• Nonsterodial anti-inflammaroty drugs (NSIADs)

Pathophysiology

• Destructive processes exceed protective mechanisms

Clinical and laboratory findings

• Asymptomatic\Eoigastric -

• C-urea breath test

Celiac Disease

Etiology

• Intolerance to gluten due to exposure to gliadin

  • Anti-tissue tranglutaminase antibody or Enomysial antibody

Pathophysiology

• villus atrophy with decrease in digestive enzyme production. Causes malabsorption

Clinical and laboratory findings

• eliminate gluten, vitamen supplements

Inflammatory Bowel Disorders

Ulcerative Colitis and Chron's

Etiology - both

• Idopathic

Pathophysiology

• Ulcerative

  • Abscess formation

  • granulomatous tissue

• Chrons

  • fibrotic tissue can form

  • lymphatic structures become blocked

Clinical and laboratory findings

• Ulcerative

  • bleeding and diarrhea

  • toxic

• Chrons

  • Inabilty to absorb nutrients

  • perianal fissures, fistuals, and abscesses

No direct method of diagnoses

• Elevated WBC

• Positive stool occult blood

• increased c-reactive protien

Protein-losing enteropathy

Etiology

• A condition where large amounts of serum proteins pass into the bowel lumen and ultimately into the feces

  Caused by a wide range of underlying GI Tract disorders including inflammatory bowel syndromes, obstructions to lymphatic circulation, and food allergies

Pathophysiology

• Patient will typically have generalized GI Tract symptoms and will have a hypoalbuminemia upon chemistry work-up.

Clinical and laboratory findings

• Confirmation of diagnosis is done by finding an elevated fecal clearance of alpha-1-antitrypsin (AAT)

  Useful measure since AAT is not broken down by GI tract enzymes

  Must have a 24 hour stool sample and a serum sample collected during stool collection window to determine clearance rate

Lactase deficiency

Etiology

• Lactase is the enzyme needed to breakdown lactose into glucose and galactose for digestion to occur

Pathophysiology

• Without the enzyme lactose cannot be reabsorbed and stays in the intestinal lumen

Clinical and laboratory findings

• Can be detected via lactose tolerance test:

  Collect baseline blood glucose level

  Give patient 50g of lactose in 200mL of water

  Collect multiple blood glucose levels over two hour window

  Lactase deficiency is present if blood glucose does NOT increase by 30m

Colorectal cancer

Etiology

Pathophysiology

Clinical and laboratory findings

Describe the principal, clinical utility, preferred sample (if any) and expected results for the following tests of Gastrointestinal Function

Serum Gastrin Level

• Detect and evaluate stomach ulcers

• ZE syndrome

• Serum

Urea Breath Test

• detects h. pylori

• exhaled

h pylori antigen

• immunoaassay to detect h pylori proteins

• patients with gastris and peptic ulcers

Oral Lactose Tolerance Test

• if body can digest sugar, if it can break down lactose

• plasma

• normal is more than 30mg/

Transglutaminase antibody

• highly sensitive blood test used as the primary screening tool for celiac disease and, less commonly, dermatitis herpetiformis. It detects IgA antibodies that the immune system produces against the tissue transglutaminase enzyme when gluten is ingested.

• Celiac disease

• serum

• less than 4,0 u/ml, greater than 10

IgA-Endomysial antibody

Stool Occult Blood

CA19-9

Explain why an infection with mumps can increase amylase levels.

the virus causes inflammation of the glands that produce this enzyme, leading to its release into the bloodstream.

The mumps virus (a paramyxovirus) typically infects the salivary glands, particularly the parotid glands, causing them to swell and become painful (parotitis). The parotid glands produce saliva containing high levels of salivary amylase. When these glandular cells are inflamed and damaged by the virus, they leak this enzyme into the bloodstream, leading to elevated amylase levels

Correlate laboratory findings to a discussed Gastrointestinal Disorder

ibd

• Fecal Calprotectin (FC): Strongly elevated. It is a protein released by neutrophils in the stool, acting as a benchmark for intestinal inflammation. Fecal calprotectin correlates closely with endoscopic and histologic disease activity.

• C-Reactive Protein (CRP) & ESR: Elevated, indicating systemic inflammation.

• Hemoglobin/Hematocrit: Decreased (Anemia), often due to chronic blood loss or malabsorption.

• Albumin: Decreased, suggesting nutritional deficiency or protein-losing enteropathy.

• Platelets: Frequently elevated (thrombocytosis) as a reactive response to chronic inflammation. 

2. Celiac Disease

Laboratory findings for celiac disease are primarily immunological, reflecting an autoimmune response to gluten. 

• Tissue Transglutaminase (tTG) IgA: The preferred first-line blood test, showing high sensitivity and specificity.

• Total Serum IgA: Measured to ensure the patient is not IgA deficient, which could cause a false-negative tTG result.

• Hemoglobin/Ferritin: Low, indicating iron-deficiency anemia due to malabsorption in the small intestine. 

3. Gastrointestinal Infections (e.g., Bacterial Gastroenteritis) 

• Stool Culture: Identifies abnormal bacteria (e.g., Salmonella, Shigella) in the digestive tract, explaining acute diarrhea.

• White Blood Cells (WBCs) in Stool: Elevated (leukocytosis in stool), indicating acute inflammation or infection.

• Fecal Occult Blood Test: Positive, indicating damage to the intestinal mucosa. 

4. Irritable Bowel Syndrome (IBS) 

• Laboratory Profile: Generally, laboratory findings are normal.

• Role of Labs: Used to rule out IBD or celiac disease. Fecal calprotectin is typically low or within normal range, helping to distinguish IBS from IBD.

• Molecular Markers: Research indicates that while routine labs are normal, patients may show increased mast cell counts in the intestine and altered microbiome profiles (e.g., higher Firmicutes/Bacteroidetes ratio). 

5. Helicobacter pylori Infection (Peptic Ulcer Disease) 

• Urea Breath Test (UBT): Highly accurate, non-invasive test detecting active infection.

• Stool Antigen Test: Detects the presence of H. pylori proteins, also used for confirming eradication. 

6. Liver and Biliary Disorders

• Liver Function Tests (LFTs): Elevated AST, ALT, ALP, and Bilirubin indicate liver injury, hepatitis, or biliary obstruction. 

Summary of Key Biomarkers and Clinical Significance

• Inflammation: High Calprotectin, High CRP, High ESR, Elevated WBCs.

• Malabsorption/Nutritional Deficiencies: Low Hemoglobin, Low Ferritin, Low B12, Low Albumin.

• Tissue Damage: Positive Fecal Occult Blood.

• Infection: Positive Stool Culture. 

Determine the most likely cause of a gastrointestinal disorder when given appropriate laboratory data

Recall exocrine pancreatic function

essential for digestion, producing and secreting digestive enzymes (via acinar cells) and bicarbonate-rich fluid (via duct cells) into the duodenum to break down nutrients and neutralize gastric acid

Explain the etiology and pathogenesis of exocrine pancreatic insufficiency

The primary etiology is chronic pancreatitis, while cystic fibrosis (often in children), pancreatic cancer, and resection are major causes. Pathogenesis involves the destruction of pancreatic acinar cells, ductal obstruction, or reduced stimulation, generally leading to enzyme deficiency when >90% of function is lost. The primary etiology is chronic pancreatitis, while cystic fibrosis (often in children), pancreatic cancer, and resection are major causes. Pathogenesis involves the destruction of pancreatic acinar cells, ductal obstruction, or reduced stimulation, generally leading to enzyme deficiency when >90% of function is lost.

Describe the clinical utility of the fecal elastase test

to diagnose exocrine pancreatic insufficiency (EPI)

It measures pancreatic enzyme concentration to assess digestive function, aiding in the evaluation of conditions like chronic pancreatitis, cystic fibrosis, and pancreatic cancer.

Discuss the physiologic role of the pancreas in the digestive process.

Endocrine functions of the pancreas include production of insulin and glucagon

Exocrine function of the pancreas involves production of enzymes used in the digestive process

Activity is under both nervous and endocrine control. Branches of the vagus nerve can cause a small amount of pancreatic fluid secretion when food is smelled or seen.

List the hormones excreted by the pancreas, together with their physiologic roles.

Endocrine – hormone -releasing

Islet cells (with Greek alphabet names) secret 5 hormones into the blood:

Alpha – glucagon

Beta – insulin

Delta – somatostatin

Gamma – pancreatic polypeptide (PP) hormones

Epsilon – ghrelin - regualtes appetite

The primary hormones include insulin (lowers blood sugar), glucagon (raises blood sugar), somatostatin (inhibits other hormones), pancreatic polypeptide (manages digestion), and amylin (controls appetite). 

Describe the following pancreatic disorders and list the associated laboratory tests that would aid in diagnosis

1. Acute pancreatitis

• CMP

• elevated lipase and amylase levels

1. Chronic pancreatitis

2. alp high

3. bilirubin high

4. lactate high

5. alt high

6. Pancreatic carcinoma

• Pancreatic Tumor, malignant neoplasms

  • Tumour markers

  • Liver function tests

  • CMP

1. Cystic fibrosis

• An inherited autosomal recessive disorder characterized by dysfunction of mucous and exocrine glands throughout the body

  • Sweat Chloride Test

  • Fecal elastase-1

5. Pancreatic malabsorption.

• Fecal elastase-1,

• Fecal fatacut

List the tests used to assess intestinal function.

Clinical chemistry testing of intestinal function focuses almost entirely on the evaluation of absorption and its derangements in various disease states.

The lactose intolerance test, administered after ingestion of a dose of lactose and subsequent serum glucose testing, has been replaced largely by a breath test.

D-xylose is an exogenously administered simple (pentose) monosaccharide sugar. It is not ordinarily present in the blood in significant measurable quantities because it does not require pancreatic lytic enzymes for absorption and can therefore be used to differentiate malabsorption from an intestinal etiology or exocrine pancreatic insufficiency.

Carotenoids are phytochemicals, the chief precursors of vitamin A in humans found in over 600 species of plants and some fungi and alg

Evaluate a patient’s condition, given clinical data.

• e Blood Cells (WBCs):

  • High (Leukocytosis): Infection, inflammation, leukemia, stress, or tissue damage.

  • Low (Leukopenia): Bone marrow failure, autoimmune disease, or severe infection.

• Red Blood Cells (RBCs) / Hemoglobin / Hematocrit:

  • High: Dehydration (blood concentration), lung disease, or smoking.

  • Low (Anemia): Bleeding, iron deficiency, chronic disease, or bone marrow issues.

• Platelets:

  • High (Thrombocytosis): Infection, cancer, or inflammatory diseases.

  • Low (Thrombocytopenia): Clotting disorders, severe bleeding, or immune system destruction. 

2. Electrolytes and Minerals (Blood/Serum) 

• Sodium (Na+):

  • High (Hypernatremia): Dehydration, high salt intake.

  • Low (Hyponatremia): Kidney disease, heart failure, or excessive water intake.

• Potassium (K+):

  • High (Hyperkalemia): Kidney failure, tissue injury, or medication side effects.

  • Low (Hypokalemia): Vomiting, diarrhea, or diuretic use.

• Calcium (Ca2+):

  • High: Hyperparathyroidism, cancer.

  • Low (Hypocalcemia): Vitamin D deficiency, kidney disease.

• Magnesium (Mg2+):

  • High: Kidney failure, dehydration.

  • Low: Alcoholism, chronic diarrhea, malnutrition. 

3. Metabolic and Organ Function Panels 

• Glucose:

  • High: Diabetes mellitus, stress, or recent food intake.

  • Low: Insulin overdose, fasting, or metabolic issues.

• Creatinine & Blood Urea Nitrogen (BUN):

  • High: Kidney damage or dysfunction, dehydration.

  • Low: Liver disease, malnutrition (often less clinical significance).

• Liver Enzymes (ALT, AST, ALP, GGT):

  • High: Hepatocellular damage (hepatitis), fatty liver, alcohol abuse, or bile duct obstruction.

• Albumin:

  • High: Dehydration.

  • Low: Kidney disease (nephrotic syndrome), liver disease, malnutrition, or chronic inflammation. 

4. Inflammatory Markers 

• C-Reactive Protein (CRP):

  • High: Nonspecific inflammation, infection, or chronic autoimmune disease.

• Procalcitonin (PCT):

  • High: Specifically indicates bacterial infection or sepsis. 

Formulas to know

(Ucr mg/dl x U vol)/(Pcr mg/dl x collection time)

• Ucrcap U sub c r end-sub

  𝑈𝑐𝑟

  (Urine Creatinine Concentration): Creatinine concentration in the urine, measured in mg/dL.

• U vol (Total Urine Volume): Total volume of urine produced in the collection period, measured in mL.

• Pcrcap P sub c r end-sub

  𝑃𝑐𝑟

  (Plasma/Serum Creatinine Concentration): Creatinine concentration in the blood, measured in mg/dL.

• Collection time: Duration of the urine collection, usually 24 hours (1440 minutes). 

Standard 24-Hour Formula 

When using a 24-hour collection, the formula often appears as:

Creatinine Clearance (mL/min)=𝑈𝑐𝑟 (mg/dL)×Total Volume (mL)𝑃𝑐𝑟 (mg/dL)×1440 min

Key Information 

• Purpose: To measure the rate of glomerular filtration and assess kidney function.

• Normal Range: A normal 24-hour urine creatinine level is typically 500-2000 mg/day, though this varies by muscle mass, age, and sex.

• Importance of Accuracy: The 24-hour collection must be complete to avoid inaccuracies. An incorrect collection time or volume will lead to an incorrect result

Tot mg=Ucr(mg/dl) x (total volumeml/100)

Where: 

• Ucrcap U sub c r end-sub

  𝑈𝑐𝑟

  (Urine Creatinine): The concentration of creatinine measured in a small sample of the urine (in milligrams per deciliter).

• Total Volume: The total amount of urine collected over 24 hours (in milliliters).

• 100: This is the conversion factor used because concentration is measured per

  100 mL100 mL

  100 mL

  (

  1 dL=100 mL1 dL equals 100 mL

  1 dL=100 mL

  ). 

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Step-by-Step Calculation Example 

If a patient has a urine creatinine concentration of

120 mg/dL120 mg/dL

120 mg/dL

and a total 24-hour urine volume of

2,000 mL2 comma 000 mL

2,000 mL

: 

1. Divide Volume by 100:
   

   2,000 mL100=20 dLthe fraction with numerator 2 comma 000 mL and denominator 100 end-fraction equals 20 dL

   2,000 mL100=20 dL

2. Multiply by Concentration:
   

   120 mg/dL×20 dL=2,400 mg120 mg/dL cross 20 dL equals 2 comma 400 mg

   120 mg/dL×20 dL=2,400 mg

3. Result: The total creatinine excretion is

   2,400 mg2 comma 400 mg

   2,400 mg

   . 

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