Nutrition GI Disease (11)

• absence of lactase activity at birth
• infants with this condition who're breastfed will get diarrhea from the milk

• a defect in absorption, NOT a defect of digestion
• lactose is usually absorbed in the intestine but in THIS case it's absorbed in the stomach & circulates in the blood stream as lactose which is abnormal & problematic
• not usually done & can cause multi-organ damage or dysfunction

• partial or complete loss of brush border lactase activity
• acquired or congenital - acquired is more common

• ACQUIRED Hypolactasia
• Primary: autosomal recessive genetically programmed loss of lactase gene expression & activity that occurs after weaning; often starts at 3-5 years
• Secondary: caused by disease, injury, drugs, radiation,
• surgery, or infection

• PRIMARY is permanent because it's caused by a genetic mutation
• secondary is reversible after whatever stimulus is causing the brush border impairment is removed

• Primary Acquired Lactase Nonpersistence is genetically based
• Caucasians/Europeans have the most lactase & therefore the greatest ability to digest lactose
• Asians & African Americans tend to have higher rates of primary LNP which can cause lactose intolerance

• LNP causes lactose maldigestion or lactose intolerance if SYMPTOMS occur
• symptoms result from:
• osmotic load, where unabsorbed lactose leads to water influx into SI
• cramping, distention
• lactose fermentation
• abdominal pain
• increased motility

• they can ferment it resulting in
• 1) short chain FAs: these are absorbed by colonocytes but if unabsorbed cause DIARRHEA
• 2) Gas: 50% H2 + methane & CO2 which causes cramps, flatus, & increased motility

• Degree of LNP: the more enzyme, the fewer symptoms
• Lactose load: amount ingested, rate of delivery to the SI, rate of gastric emptying; a mixed meal might slow release of lactose in intestines, help body keep up with lactase production
• Ability to ferment + absorb short chain FAs: flatus still produced in that situation

• 1. avoiding lactose-containing foods
• 2. limit RATE of lactose delivery to small intestine
• 3. eat β-galactosidase rich food (YOGURT)
• 4. add β-galactosidase to food

• that they might not get enough Calcium or Vitamin D because most people depend on dairy products for those micronutrients
• deficiencies of these puts people at risk for osteoporosis
• it is possible to get them outside of dairy, or one could eat dairy with less lactose like hard cheeses over soft ones (bacteria digest the lactose during the aging process)

• by having a mixed meal
• eg. fat slows digestion from the stomach

• a hydrolase enzyme that catalyzes the hydrolysis of β-galactosides (eg. lactose) into monosaccharides
• enzyme can be found in bacteria which itself is found in different foods (yogurt)
• bacteria are lysed in the upper GI tract upon food ingestion, liberating the β-galactosidase which can digest lactose
• can also take a capful of β-galactosidase or have β-galactosidase-enriched food (lactaid milk)

• an immune-mediated (IgA) response to dietary gluten
• it's more common in people of European descent
• it's UNDER diagnosed (1/133 people in the US)
• a person is at increased risk for Celiac's if a 1st degree relative has the disease (prevalence goes to 1/22)

• AUTOIMMUNE diseases
• type 1 Diabetes Mellitus 
• thyroid disease liver disease
• selective IgA deficiency
• inflammatory bowel disease (IBS)
• eosinophilic esophagitis
• down syndrome…

• a protein found in wheat, barley, rye, possibly oats, many medications, & hygiene products, where it's used as a filter/preservative
• ingestion of gluten if intolerant leads to destruction of the small intestine mucosa
• this manifests as diarrhea, bloating, nutrient malabsorption, & sometimes dermatitis herpetiformis, an itchy skin rash

• 1. indigestible fragments of gluten induce enterocytes to release zonulin → LOOSENS tight junctions between mucosal cells
• 2. gluten may move through now opened spaces between cells & accumulate underneath
• 3. enterocytes secrete IL-15 in response to deposited gluten → intraepithelial leukocytes squeeze through mucosa to target area
• 4. tissue transglutaminase (TTG) modifies the gluten, which is now picked up by APCs, presented to T cells, initiating an immune response
• 5. T cell activation occurs, B cells make Ig's to gluten, & damage mucosal enterocytes in the destruction process

• by measuring tissue transglutaminase (TTG), the enzyme that modifies gluten before it's presented in MHC class II molecules, activating an immune response
• a tissue biopsy is often collected for confirmation

• Consult w/ a skilled dietician
• Educate about the disease
• Lifelong adherence to a gluten-free diet*
• Identify + treat nutritional deficiencies
• Access should be provided to advocacy groups
• Continuous long-term follow up (by a multidisciplinary team)

• 1. could be blatant non-compliance to the diet
• 2. accidental ingestion of gluten
• 3. complete misdiagnosis
• 4. a concurrent disorder: another condition affecting GI tract (eg. cholitis)
• 5. refractory sprue: when someone never improves on a gluten-free diet
• 6. something completely unrelated (eg. ulcerative jejunitis, intestinal lymphoma)

• because if you don't that can result in intestinal damage which causes malabsorption
• manifests as diarrhea/steatorrhea, weight loss, vitamin deficiency, & mineral deficiency
• *in some cases unexplained IRON deficiency may be the first sign of Celiac Disease

• grain & many grain products
• grain vinegar - found in most condiments
• food starches added or dusted on many foods
• beer & grain alcohol
• medications
• hygiene products
• *because gluten-free diets can be difficult to follow, can focus on what a patient CAN have as opposed to what they can't (especially if they've had weight loss)

• 1. cannot contain wheat, rye, barley, or crossbreeds of these grains
• 2. any ingredient derived from these grains must have been processed to remove gluten
• 4. cannot contain 20 ppm or more gluten

• because damage to the GI tract will put them & risk for micronutrient deficiencies & the associated conditions that can result
• Osteoporosis ~ vitamin D + Calcium [also vitamin K]
• Lactose Intolerance ~ example of secondary persistence
• Small Bowel Lymphoma ~ related to intestine damage or immunosuppression treatment involved
• Pregnancy Complications ~ women w/ unmanaged Celiac's have poor pregnancy outcomes or trouble getting pregnant
• Stunting in children ~ if a child isn't absorbing nutrients they're not going to grow

• in some areas of the world children don't have a clean water supply
• as a result many get infectious diarrhea & die from dehydration
• eg. cholera toxin destroys GI tract & causes net pooling + secretion of water in GI tract lumen
• however transporters are still functional, so providing a sodium/glucose solution causes water to passively follow sodium into the circulatory system to maintain osmolality
• can pull fluid in across basolateral membrane & hydrate individual using such a solution

• inflammation of the pancreas
• may be acute or chronic (chronic presents with more long-term abdominal pain; smoking contributes to both types)

acute symptoms: sudden onset abdominal pain & elevated serum amylase and lipase

most common causes: Gallstones & Alcohol

• • Abdominal injury or surgery
• • Cystic fibrosis
• • Genetic predisposition
• • Hypercalcemia
• • Hyperparathyroidism
• • Hypertriglyceridemia
• • Infection
• • Medications
• • Pancreatic cancer
• • Smoking

• not a particularly common type of pancreatitis however it can be avoided by taking cautionary nutritional measures
• controlling a persons obesity, diabetes, alcohol intake, or certain hyperlipoproteinemias can help prevent this type of pancreatitis
• there's also a risk of high triglycerides during pregnancy

• most commonly caused by alcohol & gallstones
• for a mild/moderate case: nil per os (NPO) + IV fluids for up to a week
• for a severe case: enteral nutrition to stimulate the GI a little, as failure to do so may worsen the severity of disease
• VERY severe cases: parenteral nutrition in to prevent further malnutrition
• *fat in the diet produces the most pain b/c without pancreatic lipase fat digestion doesn't occur

• permanent impairment of the pancreas
• can lead to exocrine dysfunction - no production of pancreatic enzymes
• this leads to fat malabsorption which can lead to Steatorrhea, Weight loss (afraid to eat b/c painful), or Fat soluble vitamin deficiencies
• originally caused by alcohol, familial predisposition, a juvenile form limited to tropical areas of the developing world, or an unknown cause (idiopathic)

• pancreatic enzyme replacement therapy
• large pills that need to be consumed when something with fat is eaten

• less than or 3 stools per week
• is associated with inadequate fiber intake, dehydration, physical inactivity, medications, & intestinal disease

• high intracolonic pressure can cause colonic outpouchings, called DiverticulOSIS
• if in addition you have poor intestinal transit, things such as food, stool, or bacteria can get stuck in the outpouchings
• DiverticuLITIS: infection & inflammation due to impaction of stool or food particle in colonic outpouchings

*diverticular disease is managed with a HIGH FIBER diet; in societies with a HIGH fiber intake, there's a LOW prevalence of diverticular disease

• 1. decreases how long it takes for food to move from mouth to anus (Transit Time)
• 2. causes stool bulking, making it easier for peristaltic action to move it along
• 3. decreases intracolonic pressure → less diverticulosis

such a diet should consist of increased fruit, vegetables, & whole grain, adequate hydration, and possibly fiber supplements