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Flashcards in TA Review of Vitamins and GI Disease Deck (99):

Vitamin C
-active form
-made by
-destroyed by
-preserved by
-excreted by

-L ascorbic acid
-plants and some non-primates
-oxidation, heat, eposure to air or alkaline medium, contact with copper or iron
-organic acids and antioxidants


actions of vitamin C (4)

-collagen synthesis: proline and lysine hydroxylation, bone formation and wound healing, for skin, teeth, and bone
-carnitine synthesis
-iron absorption: non heme iron absorbed better with VC because keeps in reduced form
-antioxidant: plays role in lipid peroxidation, mega doses are not helpful to ward off heart disease, smokers need a lot more because it will be used up as an antioxidant


vitamin C excess
-what is UL based on?
-other potential effects

-based on diarrhea and bloating
-enhanced iron absorption, hyperoxaluria (kidney stones)


risk factors for vitamin c def

-poor diet


manifestaions and cause of scruvy

-caused by a vitamin c def
-weakness and lassitude
-lack of skin and soft tissue integrity (petichiae and ecchymoses, bleeding), impaired healing
-oral: gingival swelling and bleeding, tooth loss
-bone: impaired growth and healing, bowing of long bones, subperiosteal hemorrhage
-infection and internal bleeding


Thiamin (B1)
-major biochemical roles
-body pool

-whole grains, animal foods, etc.
-NADPH biosynthesis: transketolase needed (PPP)
-energy metabolism: dehydrogenases
-synthesis of neurotransmitters: Ach, glutamate, GABA


sources of thiaminases and antithiaminases

-thiaminases: fish, shelfish, ferns, microorganisms
-antithiamine compounds: coffeee, tea, betel nuts


diagnostic risk factors of thiamine def

-Persistent vomiting
-alcohol inhibition of transport and phosphorylation
-refeeding syndrome


thiamine deficiency causes what serious diseases

-wernicke encephalopathy
-koraskoff psychosis


dry beriberi

-peripheral neuropathy
-calf wasting, tenderness, tingling


wet beriberi

-heart failure


infant beriberi

-when mother is defiient during gestation or vomits a lot


-wernicke encephalopathy

-opthalmoplegia (eye manifestations)
-ataxia/balance problems
-confusion (lateral gaze and stuttering of the eye)


korsakoff's psychosis

-amnesia, confabulation, loss of spontaneity and initiative
-not alwyass preceded by wernicke
-usually an irreversible form of thiamine def


Niacin (B3)
-active forms
-biochemical roles

-nicotinic acid and nicotinamide
-whole grains, tryptophan, meat and fish
-energy utilization and synthesis; synthesis of fatty acids, cholesterol, steroid homrones, glutamate and ribonucleotides; DNA repair* ; cell replication and differentiation*


toxicity of niacin (VB3)
-symptoms (two important)

-usually due to supplements
-vasodilation and flushing *
-heartburn, nausea, vomiting
-hyperuricemia and gout *
-decreased insulin sensitivity/ glucose intolerance


diagnostic risk factors for niacin deficiency

-hartnups: decreased absorption
-carcinoid tumors: use up tryptophan



-niacin deficiency



-folate is found in food, folic acid is synthetic and found in fortified foods/supps
-functions in 1 carbon transfers, nucleotide synthesis, and methylation


folate deficiency

-manifests in rapidly proliferating tissues
-megaloblastic anemia
-diarrhea and malabsorption


-protein bound VB12

-meat, poultry, fish, dairy egges
-crystalline B12 is more readily absorbed (can be fortified in cereals)
-functions as a cofactor in conversion of homocystein to methionine, methylmalonyl CoA to succinyl CoA
-protein bound B12 requires gastric acid to liberate B12 and make it bioavailable


absorption of B12

-in the stomach gastric acid liberates B12
-R protein binders bind to B12
-in intestin, IF replaces R binder protein and B12 is absorbed in the ileum then stored in liver


vitamin B12 def
-risk factors
-assessed by

-dietary for vegetariens and older adults
-reduced gastric acid or IF, pernicious anmeia (loss of IF)
-manifestations of megaloblastic anemia and neurological/psychiatric
-assessed by serum B12, methylmalonic acid, and homocystein


what are the fat soluble vitamins

-ADEK and carotenoids


characteristics of vat soluble vitamins
-mechanism of absorption

-increased bioavailability
-solubilized by bile, digestion by lipases
-absorbed with fat and is transporter dependent
-transported in lymphatics as chylomicrons


dietary sources of vitaminA and provitamin A

-vitamin A: preformed in food, family of compound related to retinol, function determines specific compound
-provitamin A: carotenoids, converted to vitamin A in intestine and elsewhere


Provitamin A
-different forms

-plant and algae pigments
-3 are provitamin A (alpha and beta carotenes and beta cryptoxanthin)
-cleavage: central cleavage gives you vitamin A; eccentric cleavage gives other compounds; cleavage is regulated by vitamin A stores (central cleavage is down regulated if you have good vitamin A stores)


food sources of preformed vitamin A

-meat, poultry, fish, liver, animal oils


food sources of carotenoids (the provitamin version of vitmain A)

-green leafy veggies
-brightly colored fruit and vegetables
-vegetable oils


biological roles of vitamin A (not carotenoids)

-vision (pigments of rods and cones)
-cell division and differentiation
-immune function
-bone growth


biological roles of carotenois



absorption, transport and storage of vitmain A

-stored in liver
-trasnported in circulation on retinol binding protein and lipoproteins


storage and transport of carotenoids

-transported in and out of liver on lipoproteins
-stored in adipose tissue


risk for primary and secondary vitamin A deficiency

-primary: observed to accompany protein energy malnutrition and zinc deficiency
-secondary: very low fat diets, disorders of fat digestion or absorption (pancreatic insufficiency, disorders of bile production or flow, small intestine)


vitamin A deficiency causes

-decreased night vision
-increased keratinization of the epithelium (xeropthalmia)
-decreased immune function (increased infection risk)
-decreased bone growth leading to stunting


risk for vitamin A tox

-primary: dietary excess, preformed vitamin A only, dietary supplements, rarely get enough from food to be toxic
-secondary: chronic kidney disease


symptoms of acute vitamin A toxicity

-abdominal pain
-increased intracranial pressure leading to altered mental state, blurred vision,m and headache
-nausea and vomiting
-muscle pain and weakness


symptoms of chronic vitamin A toxicity

-liver dysfucntion
-anorexia and weight loss
-hair loss
-dryness of mucus membranes, lips, skin


utility of carotenoid supplements

-no consistent effect on chronic disease prevention
-increased mortaility due to lung cancer in smokers
-not recommended for routine consumption. Could be pro carcinogenic because eccentrically cleaved products can possibly incerase oxidative stress
-may improve outcomes in age and macular degeneration


-vitamin D2
-scientific name

-plants, fungi, invertebrates, supplements


vitamin D 3
-scientific name

-skin synthesis (main), animal foods, fortified foods, supplements


formation of active vitamin D
-what organ does it go to first? second?
-what happens there?
-what is the result of the production of the active form?
-how is this regulated?
-what is the inactive metabilte?

-D2/D3 goes to liver for first hydroxylation to become 25-(OH)D; this is the most stable circulating form, basis of status assessment
-goes to kidneys where parathyroid hormone stimulates the second hydroxylation to form the active molecule 1, 25 (OH)2D; PTH also acts on bone to stimulate turnover, the active Vit D acts on intestine to increase Ca absorption (increased Ca will then inhibit PTH)
-inactive metabolite: 24, 25(OH)2D


traditional roles of vitaminD

-calcium homeostasis and bone health
-muscle function


emerging roles of vitamin D

-cancer (colon, prostate, breast)
-diabetes type 2
-cardiovascular disease
-immune function


risk for loss of vitamin D def due to skin synthesis

-limited sun exposure
-darker skin


dietary risks for viatmin D deficiency

-Obesity ** (FSV's trapped in fat)
-infants who are exclusively breast fed
-lactose intolerance
-fat malabsorption
-end stage liver or kidney disease
-medications (corticosteroids, anticonvulsants)


obesity's effect on vitamin D

-as body fat increases, vitamin D goes down
-if you do not have curculating vitamin D, you will not absorb enough calcium
-low calciu causes an increase in PTH (which should be stimulating the conversion of 25 (OH)D into 1, 25(OH)2D)
-this increase in PTH causes secondary hyperthyroidism


vitmain D deficiency in children

-growth retardation
-bowing of lower extremities from weight bearing in setting of abnormal mineralization


vitamin D def in adults

-bones have stopped growing so you do not see bowing
-diffuse bone and muscle pain
-muscle weakness
-acceleration of osteoperosis and an increased risk


vitamin D excess

-not from UV exposure
-usually from supps
-hypercalcemia is the big one, calciuria and kidney stones, arrhythmias


assessment of vitamin d status
-what can we measure

-25-OH D has a half life of 15 days
-1,25-OH2 D has a half life of 4 to 6 hours
-calcium concentrations
-bone mineral density by DEXA


vitamin E
-natural form
-synthesized alpha tocopherol contains

-family of tocopherols and tocotrienols
-R or S
-alpha, beta, gamma, delta
-natural form: RRR alpha-tocopherol
-synthesized alpha tocopherol contains R and S


vitamin E sources

-vegetable oil
-wheat germ
-green leafy vegetables
-fortified foods
-dietary supps


biological roles of vitamin E
-creation of active form

-antioxidant ** : prevents RBC hemolysis and lipid peroxidation; reduced by vitamin C (you need VC to reduce VE into its active form)
-immune function
-DNA repair


risk for vitamin E deficiency

-dietary insufficiency
-premature very low birth weight infants
-fat malabsorption
-alpha tocopherol transfer protein (TTP) defects **


vitamin E deficiency results in

-peripheral neuropathy
-ataxia with vitamin E def fue to TTP mutations
-immune dysfunction
-RBC hemolysis


assessment of vitamin E status

-serum VE


vitamin E excess
-caused by

supplement use
-causes bleeding
-supplements may worsen risk or outcomes for some cancers
-may increase mortality risk above 400 IU/day


vitamin K
-two dietary forms

-phylloquinone(K1): most common in US
-menaquinones (K2): most common in japan, fermented foods, animal feeds


sources of phylloquinone

-green leafy veggies
-vegetable oil
-fortified foods


sources of menaquinones

-some fermented foods
-animal foods
-intestinal bacteria


absorption, tranport, and storage of vitamin K

-absorbed with dietary fats as chylomicrons
-transported in lipoproteins
-stored in liver and adipose


vitamin K mechanism of action

-enters as dietary sources and is hydroxylated
-in the liver, glutmic acid ues vitamin K as a coenzyme and casues it to be carboxylated to GLA (gamma carboxyglutamate)
-this allows for the binding of calcium and the initiation of the clotting cascade


what regenerates vitamin K?




interferes with regeneration of vitamin K in order to inhibit the clotting cascade
-it is a blood thinner


prothrombin time

-how long it takes someone to clot


epoxide reductase variations

-we can assess someones variation in this enzyme in order to preduct how they will react to warfarin


risk factors for vitamin K deficiency

-fat malabsorption
-liver disease
-poor intake
-alcoholoism (can cause cirrhosis meaning that someone may not have enough tissue to effectively produce and carboxylate clotting proteins)


vitamin K deficiency in adults and babies

-adults: bleeding
-babies: bleeding
-embryopathy (from warfarin use or severe deficiency in mothers)
-possible disorders of soft tissue and bone calcification


warfarin embryopathy
leads to (fancy name)

-warfarin use and severe vitamin K def
-chondrodysplasia punctata: bony deformities with excess calcification
-nasal hypoplasia
-mental retardation: warfarin can effect calficcation of tissue and brain development


name the disorders of lactose

-congenital lactase deficiency
-congenital lastose intolerance



-partial or complete loss of brush border lastase activity
-congenital (rare) or acquired


congenital lactase deficiency

-absence of lactase activity at birth
-associated with diarrhea in breast fed infants


congenital lactose intolerance

-not a defect of digestion but a defect in absorption
-lactose absorbed by stomach into circulation instead of in the intestine
-causes multi organ dysfunction


primary and secondary acruired hypolactasia (lactase nonpersistence)

-primary: genetically programmed loss of lactase activity, occurs after weaning and often starts at 3-5 years, permanent
-secondary: associated with disease, injury, drugs, radiation, surgery, infection; reversible after stimulus is removed


primary acquired lactase nonpersistence continued
-genetic basis
-who is it most common in

-genetic basis: autosomal recessive, loss of lactase gene expression, possible post translational modification of lactase
-very common in middle eastern , indian, african american, and asian


lactose intolerance

-osmotic load: unabsorbed lactose causes water influx in small intestine which leads to cramping, abdominal pain, and increased motility


lactose can be fermented by colonic bacteria to

-short chain fatty acids which are absorbed by colonocytes, if not absorbed then they contribute to diarrhea
-gas: hydrogen, methane, and CO2 - causes cramps and flatus and incresed motility


what determines the severity of lactose intolerance symptoms

-degree of LNP: if you have some enzymes, symptoms will be lessened
-lactose load is a big one: amount digested andrate of delivery to SI (rate of gastric emptying)
-ability to ferment and absorb chort chain FA's


what are the 4 approaches to lactose intolerance?

-avoidance: no dairy (may be a problem for calcium and vitamin D intake
-limit the rate of lactose delivery: : small doses, consume as part of a mixed meal
-eat foods that contain bacteria with beta galactosidase activity so they will be lysed and the enzyme released
-take beta galactosidase suppleents


2 big diseases associated with malabsorption

-celiac disease
-chronic panreatitis


celiacs disease

-celiac sprue, non-tropical sprue, gluten sensitive enteropathy
-immune mediated response to dietary gluten


celiacs disease is associated with

-type 1 diabetes mellitus
-down syndrome
-thyroid disease
-liver disease
-selective IgA deficiency
-eosiniphilic esophagitic
-inflammatory bowel disease



-a protein found in wheat, rye, barley, and oats
-also found in certain medications and hydiene products


characterisitics of celiacs

-may occur with even trivial aounts of gluten
-T lymphocyte mediated inflammatory response affecting proximal small intestinal mucosa in response to gluten ingestion: different from an allergic reaction
-destruction of the small bowel mucosa leading to diarrhea and bloating, malabsroption of nutrients


management of celiacs disease

-consultation with a skilled dietician
-education about the disease
-lifelong adherence to a gluten-free diet
-identification and treatment of nutritional deficiencies
-access to an advocacy group
-continuous long-term follow-up by a multidisciplinary team


celiacs patients that do not follow a gluten free diet man

-develop ulcerative jejunitis and intestinal lymphoma


celiacs and malabsorption

-if you do not follow a lguten free diet, the damage to SI epithelium can cause serious absorption problmes
-weight loss
-vitamin deficiency
-mineral deficiency (iron def may be one of the first signs of celiacs)


gluten free labeling

-can not contain an ingredient that is any type of wheat, rye, barley, or crossbreeds of these grains
-or must have been processed to remove gluten (to be lower than 20 or more parts per million)


what can a persistent poor diet casue which is asymptomatic

-micronutrient deficiencies even without symptoms


oral rehydration solutions

-oral sodium and glucose are absorbed by the cotransporter into the intestinal cell
-water passively follows sodium
-this is very important in areas with a poor water supply because even in illness this cotransporter remains intact, this allows them to pull water back in after diarrhea
-6 teaspoons sugar, 1/2 teaspoon salt, 1 liter of water


-what is it

-inflammation of the pancreas; enzymes are being acitvated within the pancreas instead of being released into the duodenum
-sudden onset abdominal pain
-elevated serum amylase and lipase **


causes of pancreatitis

-gallstones and hypertriglyceridemia


risk factors for triglyceride induced pancretitis



acute pancreatitis
-most common casue
-nutrtitional management

-alcohol consumption and gall stones
-standard care if mild to moderate
-severe cases may require enteral nutrition, failure to use GI tract may worsen the disease (parenteral nutrition may be required to prevent malnutrition)


chronic pancreatitis

-permanent impairment of the pancreas
-decreased secretion of pancreatic enzymes leads to fat malabsorption (steatorrhea, weight loss, fat soluble vitamin deficiency)
-ethanol, idiopathic, familial, tropical
-pancreatic enzyme replacement


-defined as
-associated with

-less than or equal to 3 stools per week
-inadequate fiber intake, dehydration


diverticular disease

-diverticulosis: colonic outpouchings from high intercolonic pressure
-diverticulitis: infection/inflammation due to impaction of stool or food particle


fiber and diverticula disease
-diet of a patient

-fiber may decrease disease via faster transit time, stool bulking, and decreased intrcolonic pressure
-increased fruit, veggies, and whole grains, fiber supps, adequate hydration