The Celiac Patient
Week 8: Gastrointestinal System | Difficulty: Intermediate | Time: 35 minutes
Learning Objectives
- Understand the structure and function of the small intestinal villi
- Explain the pathophysiology of celiac disease
- Connect immune mechanisms to GI tissue damage
- Describe nutrient absorption and consequences of malabsorption
- Apply knowledge of the gut-associated lymphoid tissue (GALT)
Case Presentation
Patient: Lisa Anderson, 24-year-old female
History: Hashimoto's thyroiditis
Chief Complaint: Chronic diarrhea, bloating, fatigue for 6 months
History: Hashimoto's thyroiditis
Chief Complaint: Chronic diarrhea, bloating, fatigue for 6 months
Lisa presents with 6 months of loose stools (3-5 times daily), abdominal bloating after meals, and progressive fatigue. She reports unintentional weight loss of 6kg. Symptoms worsen after eating bread, pasta, or pizza. She has developed iron deficiency anemia despite oral supplementation. Her mother has celiac disease.
Physical Examination
- General: Thin, pale, anxious-appearing female
- Abdomen: Soft, mildly distended, hyperactive bowel sounds, mild diffuse tenderness
- Skin: Pale conjunctiva, dry skin, aphthous ulcers in mouth
- Hair: Dry, brittle hair with increased shedding
Investigations
Serology:
• Tissue Transglutaminase IgA (tTG-IgA): 85 U/mL (normal < 20)
• Endomysial Antibody IgA: Positive
• Total IgA: Normal (rules out IgA deficiency)
Endoscopy with Biopsy:
• Duodenal mucosa: Villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes
• Marsh 3b classification (partial villous atrophy)
Labs:
• Tissue Transglutaminase IgA (tTG-IgA): 85 U/mL (normal < 20)
• Endomysial Antibody IgA: Positive
• Total IgA: Normal (rules out IgA deficiency)
Endoscopy with Biopsy:
• Duodenal mucosa: Villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes
• Marsh 3b classification (partial villous atrophy)
Labs:
| Test | Result | Normal |
|---|---|---|
| Hemoglobin | 98 g/L | 120-160 g/L |
| Ferritin | 8 μg/L | 15-200 μg/L |
| Vitamin D | 32 nmol/L | > 50 nmol/L |
| Albumin | 28 g/L | 35-50 g/L |
Clinical Reasoning Questions
1. What is the pathophysiological mechanism of tissue damage in celiac disease?
Correct! Autoimmune T-cell mediated reaction
Celiac disease is an autoimmune disorder, not an allergy or direct toxicity:
• Gluten peptides (gliadin) cross the intestinal barrier
• Tissue transglutaminase (tTG) modifies gliadin
• HLA-DQ2/DQ8 positive T-cells recognize modified gliadin
• T-cell mediated inflammatory response damages villi
• Also produces autoantibodies against tTG
• Strong genetic component (HLA-DQ2/DQ8, family history)
Celiac disease is an autoimmune disorder, not an allergy or direct toxicity:
• Gluten peptides (gliadin) cross the intestinal barrier
• Tissue transglutaminase (tTG) modifies gliadin
• HLA-DQ2/DQ8 positive T-cells recognize modified gliadin
• T-cell mediated inflammatory response damages villi
• Also produces autoantibodies against tTG
• Strong genetic component (HLA-DQ2/DQ8, family history)
2. Why does Lisa have iron deficiency anemia despite taking oral iron supplements?
Correct! Villous atrophy reduces absorption surface
Iron is primarily absorbed in the duodenum. In celiac disease:
• Villous atrophy flattens the mucosa, reducing surface area by 70-90%
• Enterocytes (absorptive cells) are damaged and reduced in number
• Inflammation impairs transport proteins
• Iron absorption requires intact villi and functional enterocytes
• Even high-dose oral iron cannot be absorbed without treating the underlying celiac disease first
Iron is primarily absorbed in the duodenum. In celiac disease:
• Villous atrophy flattens the mucosa, reducing surface area by 70-90%
• Enterocytes (absorptive cells) are damaged and reduced in number
• Inflammation impairs transport proteins
• Iron absorption requires intact villi and functional enterocytes
• Even high-dose oral iron cannot be absorbed without treating the underlying celiac disease first
3. Which nutrients are most likely to be malabsorbed in celiac disease?
Correct! Iron, folate, calcium, fat-soluble vitamins
The proximal small intestine (duodenum and jejunum) absorbs:
• Iron: Duodenum - explaining Lisa's anemia
• Folate: Jejunum - causes macrocytic anemia
• Calcium: Duodenum - leads to osteopenia/osteoporosis
• Fat-soluble vitamins (A, D, E, K): Require intact villi and bile acids
• Vitamin D deficiency causes hypocalcemia and bone disease
Vitamin B12 is absorbed in the ileum, typically spared in celiac disease unless extensive disease.
The proximal small intestine (duodenum and jejunum) absorbs:
• Iron: Duodenum - explaining Lisa's anemia
• Folate: Jejunum - causes macrocytic anemia
• Calcium: Duodenum - leads to osteopenia/osteoporosis
• Fat-soluble vitamins (A, D, E, K): Require intact villi and bile acids
• Vitamin D deficiency causes hypocalcemia and bone disease
Vitamin B12 is absorbed in the ileum, typically spared in celiac disease unless extensive disease.
Bioscience Integration
Small Intestinal Anatomy and Function
- Villi: Finger-like projections that increase surface area 10-fold
- Microvilli: Brush border on enterocytes, further increase surface area 20-fold
- Total surface area: ~250 square meters (size of tennis court)
- Enterocytes: Absorptive cells with 3-5 day lifespan
- Goblet cells: Secrete protective mucus
In celiac disease, the villi are flattened (villous atrophy), dramatically reducing absorptive capacity.
Nursing Implications
- Dietary education: Strict gluten-free diet for life
- Nutritional support: Supplementation with iron, calcium, vitamin D, B-vitamins
- Monitoring: Weight, hemoglobin, bone density, tTG antibody levels
- Complications: Monitor for lymphoma, osteoporosis, infertility