Lecture 10 Flashcards
small intestine
lenghth: 400cm
duodenum: 25-30cm
jejunum: 160-200
ileum: the rest
Celiac Disease
Gluten-Sensitive Enteropathy, Celiac Sprue, Nontropical Sprue
Autoimmune disease caused by immunological reaction to gluten
– Estimated prevalence in Canada: 1/133 (~0.75% of population)
– Similar in USA
• Exposure to gliadin à inappropriate T-cell mediated inflammatory
response
– ↑ production of antibodies:
• IgA-human tissue transglutaminase (tTG)
• Antiendomysial (EMA)
• Antiglidin (AGA)
Celiac Disease: Etiology
Exact triggers unknown
• Strong genetic predisposition
• Several other disorders associated with it
Type 1 DM Autoimmune thyroid disease Hyper/hypothyroidism Dermatitis herpetiformis Addison disease Autoimmune hepatitis Systemic lupus erythematosus Connective tissue disease Sjögren syndrome Atrophic gastritis Alopecia Rheumatoid arthritis Primary biliary cirrhosis Down syndrome Turner syndrome William syndrome Congenital heart defects Immunoglobulin A deficiency Psoriasis
Pathophysiology of celiac
• Absorptive surface of the small intestine damaged by inflammatory
response/reaction to gluten proteins
– Small intestinal inflammation à damage to enterocytes
• Reduced absorptive surface area
• Loss of digestive enzymes
– Villi
• Height reduced
• Flattened
• Small amounts of gluten can lead to gut mucosal changes (biopsy)
Symptomology of celiac
Gastrointestinal • Diarrhea • Abdominal pain • Cramping • Bloating • Gas production
Extraintestinal (non–GI) • Bone and joint pain • Muscle cramping • Fatigue • Peripheral neuropathy • Seizures • Skin rash • Mouth ulcerations • Depression • Infertility/adverse reproductive outcomes
Other Clinical Features Encountered in Celiac Disease
Vitamin and mineral deficiencies
– Iron deficiency anemia
• Can be sole manifestation of Celiac disease in absence of diarrhea
• Most common clinical presentation of Celiac disease
– B12 deficiency
– Fat-soluble vitamins, Zn, Mg, Folate deficiencies
• Secondary lactase deficiency
– Due to damaged villi / enzyme secretion
• Metabolic bone disease
– Osteoporosis (can impact up to 75% untreated patients)
• Decreased calcium absorption à secondary hyperparathyroidism, increased bone resorption turnover and loss
• Malabsorption of Vitamin D and Ca
• Inadequate Ca and Vitamin D intake d/t lactose intolerance
Treatment
Lifelong elimination of gluten
after initiation of GFD, symptomatic improvement seen within 2-weeks in 30-95% of patients
histological improvements may not be seen for years
Dietetic Management of patients with celiac disease
c: consultation with dietitan skilled in celiac disease
Education about the disease
Lifelong adherance to GFD
Identification and treatment of nutrient deficiency
Access to an advocacy group
Continuous long-term followup by multidisiplinary team
Non-celiac gluten sensitivity
Clinical state in which individuals develop symptoms related to celiac disease when they consume gluten and feel better on a GFD but do not have celiac
no biomarkers
antibodies are absent
no villouis atrophy
difficult to study epidemiologically
Gluten Free Diets
Massive expansion in GF foods available in last decade
• Cost?- expensive 242% most expensive
• Nutritional quality? low protein , fe, folate, high fat and cho, prepackages
Large Intestine Digestion & Absorption
no enzymatid digestion
primary function- resoption of water, electrolyte, some vitamins
considerable adaptive capacity- increased absorption 3-5x when disease affects small intestine
Common Disorders of the Large Intestine
Irritable Bowel Syndrome (IBS) • Abdominal pain or discomfort that occurs in association with altered bowel habits for at least 3 months. • “Functional disorder” – Diagnosed when all other organic causes ruled out • Cause unknown
Inflammatory Bowel Disease (IBD)
• Autoimmune, chronic inflammatory
condition of the GIT -> Crhons and colitis
Low FODMAP Diet
(Fermentable Oligosaccharides Disaccharides Monosaccharides and Polyols)
foods high in FODMAP:
EXCESS FRUCTOSE FRUCTANS LACTOSE GOS POLYOLS
Pathophysiology of IBD
Abnormal activation of the mucosal and systemic inflammatory
response, resulting in:
– Damage to intestinal cells w/ malabsorption
– Ulceration
– Strictures
• Triggers of this response?
– Environment, microbes, diet…
• UC and Crohn’s characterized by exacerbationsinterspersed
with periodes of remission .
Pathophysiology (cont.)
Crohn’s
• Can involve any part of the GIT • 50-60% cases: distal ileum and colon • 15-25% of cases: small intestine or colon only • Disease often ”skips” areas of intestine
Ulcerative Colitis
• Involves only the colon • Disease always extends from the rectum • Generally continuous disease• Involves only the colon • Disease always extends from the rectum • Generally continuous disease
Laboratory Markers (Exacerbations)
• Serology
– Inflammatory markers
• Cytokines (IL-1, IL-6, TNF-α); CRP, ESR
– Antiglycan antibodies • Antisaccharomyces cerevisiae (ASCA), anitneutrophil cytoplasmic autoantibodies (ANCA)
– WBC
– Albumin (decreased)
• Stool
– Calprotectin (Cal), lactoferrin (Lf), polymorphonuclear neutrophil elastase
(PMN-e)
Extraintestinal Manifestations of IBD
Osteopenia, osteoporosis • Dermatitis • Rheumatological conditions – i.e. ankylosing spondylitis • Ocular symptoms • Hepatobililary complications
Osteopenia, osteoporosis • Dermatitis • Rheumatological conditions – i.e. ankylosing spondylitis • Ocular symptoms • Hepatobililary complications
Pharmocotherapies 1. Aminosalicylates 1a. Antibiotics 2. Corticosteroids 3. Immunomodulators 4. Biologics - i.e. anticytokine therapies • Surgery • Nutrition (supportive)
Corticosteroids (i.e. Prednisone)
Significant nutritional implications:
sodium and fluid retension : increase BP, Edema, chipmunk cheeks
high protein breakdown losses
decrease calcium absoprtion
increased chol/lipid
high bloop glucose
decrease Na, high protein, high calcium, manipulation of other diatary compnents - decrease lipids, decreased chols
Nutritional Implications of IBD
• Nutrition Assessment – Comprehensive assessment vital • Nutrition Diagnosis – Malnutrition – Inadequate oral / energy intake – Inadequate vitamin/mineral intake – Increased nutrient needs – Impaired nutrient utilization – Food-medication interaction – Altered nutrition-related lab values
Common Nutrient Deficiencies Seen in Adult IBD
Energy Insufficient intake; anorexia; increased requirements; poor intake d/t fear of
pain / diarrhea after eating
Protein Increased protein needs (losses from GIT, inflammation), catabolism (steroidinduced,
infection/abscesses), surgical healing
Fluid & Electrolytes Short bowel syndrome, high-volume diarrhea
Iron Blood loss, malabsorption
Magnesium, Zinc Intestinal losses (especially in short bowel syndrome, high-volume diarrhea)
Calcium & Vitamin D Long-term steroid use; decreased dairy intake d/t lactose-restricted diets
B12 Surgical resections of stomach (loss of IF) and/or terminal ileum (absorption)
Folate Medications used to treat IBD
Water-soluble vitamins Surgical resections – loss of terminal ileum
Fat-soluble vitaminsSteatorrhea
Nutritional
Goals of Care
in IBD
normatize bowel function
prevent/minimize GI Symptoms
Prevent malnutrition restore nutritionsal status
Nutrition Therapies
Exacerbation of Disease Assess energy needs depending on case (predictive equations are suitable) • ↑ protein needs (1.2 -1.5 g/kg/d) • Maintain fluid & electrolyte balance • Low residue (i.e. low fibre) • Lactose-free • Small, frequent meals • Assess for micronutrient deficiencies – Vitamin/mineral supplementation usually required • ↓ fat if steatorrhea (MCT) • Advanced nutrition therapy as needed – EN preferred (polymeric seems to be more effective vs elemental, but ax/monitor)
Rehabilitative / Remission
• Primary goal: maximizing protein and
energy intake to promote rehab
– Energy needs similar to healthy adults
– Protein ~1.0 g/kg/d
– Increased needs if repleting
– Physical activity (restore muscle mass)
• No “IBD” diet (limited evidence/trials)
– Considerations: ↑ omega-3, antioxidants
• Lactose-free as required
