Diet not a cause of PUD
Restrict foods now to increase acid secretions or cause irritation to mucosa (caffeine and coffee, decaf or regular, alcohol, black and red pepper)
Acidic foods are allowed
Frequent small meals (6-8 meals/day)
Billroth I = top half of stomach is reconnected to duodenum (less invasive)
Billroth II = top half of stomach is reconnected to the Jejunum (remove the are with hem orange/ulcers in PUD), like Roux-en Y but no pouch made
Bariatric surgery
Not as common in treating GI issues; usually to treat obesity
Dumping syndrome- food enters the small intestine to quickly, causing fluid to move in quickly to dilute the high osmotic load
Early symptoms: 10-20 min. After eating; decrease in blood volume = dizzy, weakness, and rapid heart rate
Intermediate symptoms: 20-30min after eating; abdominal distention, bloating, flatulence, pain, and diarrhea
Late symptoms: 1-3 hrs after eating; Reactive hypoglycemia after eating simple CHO die to rapid absorption of glucose and release of insulin (not really digesting, but still sensing the amount of CHO)
Small meals throughout the day
Lying down and avoiding activity an hour after eating
High-protein, moderate fat foods, complex carbs (acid simple carbs)
No liquid with meals (will increase GI transit)- small amounts of fluid during day, 1 hr after meal
Defect in digestion (gastric resection, pancreatic enzymes and bile acids, brush border enzymes)
Defect in absorption or transport (biochemical or genetic abnormality, mucosal structure damage, shorten length of intestines, shortened transit time)
Defect in lymphatics and vascular system
Bacterial over growth (main cause = slowed transit makes food into breeding ground)
NOTE: main symptom is diarrhea
Autoimmune disease in genetically suceptible individuals caused by immunological reaction to gluten
Characterized by chronic inflammation, mucosal atrophy, and malabsorption triggered by gluten (not an allergy)
Mucosal structure damaged (flattened) with immune response
Loss of surface area
Diarrhea = decrease in growth, wt. loss
Inappropriate T-cell mediated immune response caused by gliadin in genetically predisposed people (chronic inflammation of small intestinal mucosa
Production of IGA anti tissue transglutaminase (anti-tTG) (seen in biopsy), antiendomysial (EMA) and anti gliadin (AGA) antibodies (Used as diagnostic indicators)
Biopsy (anti-tTG)
Antibodies (EMA and AGA)
Gold Standard: small bowel biopsy
Positive Screen → Biopsy → Damage → GF diet → Biopsy → no more symptoms
Also can look for positive genetic markers (but this is not equal to a definite diagnosis)
Note: being gluten free before screening can show a false negative
Diarrhea (decreased growth, weight loss)
Abdominal pain, bloating, cramping, and gas
Dermatitis
Anemia
Joint pain, arthritis
Muscle cramps
Dental enamel hypoplasia
Osteopenia or osteoporosis
Delayed puberty
Infertility and miscarriages
Depression
Fatigue
Mouth sores
Head ache
Protein in wheat, rye, malt, and barley
Gliadin is resistant to digestion, so it stays in lumen and can cause inflammation
Lifelong gluten free diet (gluten foods and cross contaminates like oats); may als restrict lactose (secondary malabsorption)
Symptoms improve by 2-8 week in 70% cases
Restore nutritional status, vitamin-mineral supplement is often needed
Gluten sensitivity is not an autoimmune response (no antibodies); possibly a subset of IBS
No genetic link
Celiacs is 2:1 females:males; sensitivity is 3:1
Celiacs can occur at any age; gluten sensitivity rare in children
Diagnosed using the Rome IV criteria in the prior 6 months
Abdominal pain or discomfort that is present at least one day a week for 3 moths and associated with at least two of the following: pain relief with defecation, pain associated with change in frequency of stool, pain associated with change in form of stool
Largely unknown
Functional diagnosis: diagnosis is made after ruling out all other causes of patient's symptoms
Symptoms are aggravated by stress and emotional trauma (gut-brain axis)
Greater sensitivity to serotonin (abnormal motility)
Elevated response to infection (dysbiosis)
Enteric and central nervous systems have cross talk
IBS increases risk of neurologic disorders
Establish regular eating pattern and avoid large meals
Identify food intolerances (triggers)- elimination diet: FODMAPS, high fat, caffein, lactose, caffeine, alcohol, sorbitol, gas producing foods (beans, peas, cabbage, and bran) and fructose
Peppermint oil- reduces abdominal pain
Prebiotic, probiotic, and symbiotic
Imbalance of the gut; loss of diversity
IBS causes the loss of beneficial microorganisms and the expansion of harmful ones
Effects: increased permeability (less protection form pathogens), malabsorption, altered motility, sensitivity to pain with gas and water in gut, immune changes, changes in gut-brain axis
Fermentable Oligosaccharides Disaccharides Monosaccharides and Polyols
Apples, milk, legumes, gluten grains, honey, fructose, onions, etc.
Wheat and Rye and Barley are all high in FODMAPS and contain gluten
Gluten intolerance can contribute to IBS
Elimination
Determine sensitivities and start reintroduction
Personalization as needed for symptom management
Low FODMAP diets reduces bifidobacteria and other beneficial bacteria that produce short chain fatty acids
Stool pH increases with the diet- pathogens may grow
FODMAPs have effects on microbiota diversity- many FODMAPS are prebiotics
Reintroduce foods one at a time for 3 days and observe symptoms
Endurance athletes with GI distress
IBD with quiescent disease and IBS symptoms
Celiac disease with IBS symptom overlap
CNS cross talk
FODMAPS become SCFAs by microbiota draw water into LI and create gas causing discomfort
Defect in digestion
Defect in absorption or transport
Small intestine bacterial overgrowth
Lack of bile (liver disease, biliary tract obstruction,
Ileal dysfunction (Lower reabsorption of bile acids), small intestine bacterial overgrowth
Pancreatic disease, cystic fibrosis → lowers lipase
Mucosal damage →impairs fat absorption (celiac, surgery, infection)
Genetic disorders of metabolism (less chylomicrons)
72 hr fecal fat test = 100 g/d dietary fat and collect all stool for 3 days; >6g/d of fat in stool = steatorrhea
Fecal N excretion reflects protein malabsorption (>6 g/day of N in stool = protein malabsorption
Breath H2 test (lactose hydrogen breath test) = consume 25 g of lactose and measure breath H concentration (>20th suggest carbohydrate malabsorption)
Fat in stool > 6g/d fat in stool
Diagnosed with 72 hr fecal fat test, D-xylophone and Shillings test, or small bowel X-ray with barium swallow
Consequences: energy loss of up to 40g/day (360kcal), diarrhea, lowered absorption of fat soluble vitamins, kidney stones, abdominal pain, and cramping
Limit oxalate to < 50 mg/d and avoid foods high oxalate (spinach, black tea, nuts, etc.)
Ca at each meal (150 mg) to bind to oxalate
Low fat diet (<30% of energy from fat)
Avoid large vitamin C supplements (converted to oxalate)
Cross contamination of bacteria from the colon due to weak illogical valve, fistula, IBS, or bariatric surgery
Bacteria deconjugate bile acids = toxic to nucosa and Michelle formation (steatorrhea)
CHO malabsorption (when bacteria ferment lactose)
Bacteria use thiamin and B12 for their own growth
MNT: MCT, lactose-free diet and vitamin/mineral supplements
Medical Rx: treat cause (surgery may be needed) and control bacterial growth with antibiotic and pre/probiotics
An abnormal opening in the stomach or intestines that allows the contents to leak; can be enteroenteric or enterocutaneous
Severe complications; need surgical resection
Acute: loss of water, HCO3, Na, K, Mg, and Cl; metabolic acidosis and dehydration
Chronic: weight loss, micronutrient deficiencies
Osmotic = high number of osmotically active particles that draw water into the gut; disappears with fasting
Infectious = food poisoning, often bloody; persists with fasting
Secretory = active secretion of water and electrolytes; large volume of non bloody diarrhea; persists with fasting
Osmotic = high number of osmotically active particles that draw water into the gut (dumping syndrome, lactose intolerance, hyper osmotic enteral tube feeding
Infectious diarrhea = food poisoning (campylobacter, E.coli, Salmonella, etc.)
Secretory diarrhea = cholera toxin, C. Diff, etc.
MNT: Manage fluid and electrolyte losses (oral rehydration solutions to help Na glucose/galactose transporter, restrict lactose and raw fruits and vegetables to decrease fecal bult) and pre and probiotics
Infectious and secretory: treat with antibiotics
Osmotic: disappears with fasting
Replenish gut microbiota depleted by diarrhea (especially if antibiotics were used
Increase SCFAs (decrease luminal pH = less favorable to pathogens, energy source for colonocytes, promotes water and electrolyte absorption
Still emerging
Fermented foods are time-tested sources
Strong evidence for certain probiotics but no recommendations yet
Good bacteria increase immunity, vitamins, and metabolism
Bad bacteria (dysbiosis) increase obesity, inflammation, and autism
Sensitivity = say that someone has the disease if they have it
Specific = say that they do not have it if they do not
Precursors of colon cancer
Looks like beads
Family history
Red or processed meats increase risk
Whole grains and vitamins C and D decrease risk
More common in men than women
Causes liquid stool output
Colon, anus, and rectum are removed; stoma formed from the ileum to the outside
Stool output depend on location; solid stool in distal colon
Anus and rectum removed; stoma is formed from the remaining colon to the outside
Low fiber diet initially
Avoid problem foods: Odor: beans, cabbage, spicy food, fish; Plug up: Seeds/kernels and fibrous veggies
Minimize odor via yogurt, cranberry juice, butter milk, and pre- and probiotic foods
Flatulence: chew foods well, avoid drinking with straw, increase CHO foods likely to be malabsorbed and fermenred
Adequate fluid (water is absorbed in colon the most)
B12 supplement with distal ileum resection
Chrohn's disease
Ulcerative Colitis
Autoimmune disease, chronic inflammation
Etiology unknown; may be a genetic link as well as environmental triggers to cause immune response and inflammation (bacteria related, smoking, alcohol)
Mechanisms: epithelial cell barrier dysfunction, defects in innate immune system that affect commensal (good) bacteria, dysbiosis (decrease in bifidobacteria; increase in Proteobacteria), Environmental factors (diet and sanitation)
Food intolerance
Diarrhea and weight loss
Fever (infection)
Anemias (blood loss or malabsorption)
Extra intestinal manifestations (arthritic, osteopenia, dermatologic)
Crohn's - Patches spread throughout large intestine and ileum; mucosal thickening; surgery and fistulas common; incidence increasing
U.C. - Continuous strand from rectum, sigmoid colon, and some descending colon; mucosal thinning; incidence stable; rectal bleeding; less malnutrition