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Nutrition > TA Review of Vitamins and GI Disease > Flashcards

TA Review of Vitamins and GI Disease Flashcards

1
Q

Vitamin C

  • active form
  • made by
  • destroyed by
  • preserved by
  • excreted by
A
  • 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
  • kidney
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2
Q

actions of vitamin C (4)

A
  • 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
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3
Q

vitamin C excess

  • what is UL based on?
  • other potential effects
A
  • based on diarrhea and bloating

- enhanced iron absorption, hyperoxaluria (kidney stones)

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4
Q

risk factors for vitamin c def

A
  • poor diet
  • malabsorption
  • alcoholism
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5
Q

manifestaions and cause of scruvy

A
  • 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
  • CNS
  • infection and internal bleeding
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6
Q

Thiamin (B1)

  • sources
  • major biochemical roles
  • body pool
  • UL
A
  • whole grains, animal foods, etc.
  • NADPH biosynthesis: transketolase needed (PPP)
  • energy metabolism: dehydrogenases
  • synthesis of neurotransmitters: Ach, glutamate, GABA
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7
Q

sources of thiaminases and antithiaminases

A
  • thiaminases: fish, shelfish, ferns, microorganisms

- antithiamine compounds: coffeee, tea, betel nuts

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8
Q

diagnostic risk factors of thiamine def

A
  • Persistent vomiting
  • HIV/AIDS
  • alcohol inhibition of transport and phosphorylation
  • refeeding syndrome
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9
Q

thiamine deficiency causes what serious diseases

A
  • beriberi
  • wernicke encephalopathy
  • koraskoff psychosis
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10
Q

dry beriberi

A
  • peripheral neuropathy

- calf wasting, tenderness, tingling

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11
Q

wet beriberi

A
  • heart failure

- edema

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12
Q

infant beriberi

A

-when mother is defiient during gestation or vomits a lot

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13
Q

-wernicke encephalopathy

A
  • opthalmoplegia (eye manifestations)
  • ataxia/balance problems
  • confusion (lateral gaze and stuttering of the eye)
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14
Q

korsakoff’s psychosis

A
  • amnesia, confabulation, loss of spontaneity and initiative
  • not alwyass preceded by wernicke
  • usually an irreversible form of thiamine def
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15
Q

Niacin (B3)

  • active forms
  • sources
  • biochemical roles
A
  • 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*
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16
Q

toxicity of niacin (VB3)

  • cause
  • symptoms (two important)
A
  • usually due to supplements
  • vasodilation and flushing *
  • heartburn, nausea, vomiting
  • hepatotoxicity
  • hyperuricemia and gout *
  • decreased insulin sensitivity/ glucose intolerance
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17
Q

diagnostic risk factors for niacin deficiency

A
  • hartnups: decreased absorption

- carcinoid tumors: use up tryptophan

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18
Q

pellagra

  • cause
  • symptoms
A
  • niacin deficiency
  • dermatitis
  • diarrhea
  • dementia
  • death
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19
Q

folate

  • source
  • function
A
  • folate is found in food, folic acid is synthetic and found in fortified foods/supps
  • functions in 1 carbon transfers, nucleotide synthesis, and methylation
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20
Q

folate deficiency

A
  • manifests in rapidly proliferating tissues
  • megaloblastic anemia
  • diarrhea and malabsorption
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21
Q

B12

  • family
  • sources
  • function
  • protein bound VB12
A
  • cobalamins
  • 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
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22
Q

absorption of B12

A
  • 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
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23
Q

vitamin B12 def

  • risk factors
  • manifestation
  • assessed by
A
  • 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
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24
Q

what are the fat soluble vitamins

A

-ADEK and carotenoids

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25
Q

characteristics of vat soluble vitamins

  • digestion
  • absorption
  • mechanism of absorption
  • transport
A
  • increased bioavailability
  • solubilized by bile, digestion by lipases
  • absorbed with fat and is transporter dependent
  • transported in lymphatics as chylomicrons
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26
Q

dietary sources of vitaminA and provitamin A

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
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27
Q

Provitamin A

  • different forms
  • cleavage
A
  • 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)
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28
Q

food sources of preformed vitamin A

A
  • meat, poultry, fish, liver, animal oils
  • dairy
  • eggs
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29
Q

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

A
  • green leafy veggies
  • brightly colored fruit and vegetables
  • vegetable oils
  • eggs
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30
Q

biological roles of vitamin A (not carotenoids)

A
  • vision (pigments of rods and cones)
  • cell division and differentiation
  • reproduction
  • immune function
  • bone growth
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31
Q

biological roles of carotenois

A

-antioxidants

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32
Q

absorption, transport and storage of vitmain A

A
  • stored in liver

- trasnported in circulation on retinol binding protein and lipoproteins

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33
Q

storage and transport of carotenoids

A
  • transported in and out of liver on lipoproteins

- stored in adipose tissue

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34
Q

risk for primary and secondary vitamin A deficiency

A
  • 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)
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35
Q

vitamin A deficiency causes

A
  • decreased night vision
  • increased keratinization of the epithelium (xeropthalmia)
  • decreased immune function (increased infection risk)
  • decreased bone growth leading to stunting
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36
Q

risk for vitamin A tox

  • primary
  • secondary
A
  • primary: dietary excess, preformed vitamin A only, dietary supplements, rarely get enough from food to be toxic
  • secondary: chronic kidney disease
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37
Q

symptoms of acute vitamin A toxicity

A
  • abdominal pain
  • increased intracranial pressure leading to altered mental state, blurred vision,m and headache
  • nausea and vomiting
  • anorexia
  • muscle pain and weakness
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38
Q

symptoms of chronic vitamin A toxicity

A
  • liver dysfucntion
  • osteoporosis/fracture
  • teratogenicity
  • anorexia and weight loss
  • hair loss
  • dryness of mucus membranes, lips, skin
  • headache
  • bleeding
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39
Q

utility of carotenoid supplements

A
  • 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
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40
Q
  • vitamin D2
  • scientific name
  • sources
A
  • ergocalciferol

- plants, fungi, invertebrates, supplements

41
Q

vitamin D 3

  • scientific name
  • sources
A
  • cholecalciferol

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

42
Q

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?
A
  • 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
43
Q

traditional roles of vitaminD

A
  • calcium homeostasis and bone health

- muscle function

44
Q

emerging roles of vitamin D

A
  • cancer (colon, prostate, breast)
  • diabetes type 2
  • cardiovascular disease
  • immune function
  • depression
45
Q

risk for loss of vitamin D def due to skin synthesis

A
  • aging
  • limited sun exposure
  • darker skin
46
Q

dietary risks for viatmin D deficiency

A
  • 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)
47
Q

obesity’s effect on vitamin D

A
  • 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
48
Q

vitmain D deficiency in children

A
  • rickets
  • growth retardation
  • bowing of lower extremities from weight bearing in setting of abnormal mineralization
49
Q

vitamin D def in adults

A
  • osteomalacia
  • bones have stopped growing so you do not see bowing
  • diffuse bone and muscle pain
  • muscle weakness
  • frailty
  • acceleration of osteoperosis and an increased risk
50
Q

vitamin D excess

  • cause
  • manifestations
A
  • not from UV exposure
  • usually from supps
  • hypercalcemia is the big one, calciuria and kidney stones, arrhythmias
51
Q

assessment of vitamin d status

-what can we measure

A
  • 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
  • PTH
  • bone mineral density by DEXA
52
Q

vitamin E

  • family
  • stereochem
  • forms
  • natural form
  • synthesized alpha tocopherol contains
A
  • family of tocopherols and tocotrienols
  • R or S
  • alpha, beta, gamma, delta
  • natural form: RRR alpha-tocopherol
  • synthesized alpha tocopherol contains R and S
53
Q

vitamin E sources

A
  • nuts
  • seeds
  • vegetable oil
  • wheat germ
  • green leafy vegetables
  • olives
  • fortified foods
  • dietary supps
54
Q

biological roles of vitamin E

-creation of active form

A
  • 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
55
Q

risk for vitamin E deficiency

A
  • dietary insufficiency
  • premature very low birth weight infants
  • fat malabsorption
  • alpha tocopherol transfer protein (TTP) defects **
  • abetalipoproteinemia
56
Q

vitamin E deficiency results in

A
  • peripheral neuropathy
  • ataxia with vitamin E def fue to TTP mutations
  • myopathy
  • retinopathy
  • immune dysfunction
  • RBC hemolysis
57
Q

assessment of vitamin E status

A

-serum VE

58
Q

vitamin E excess

  • caused by
  • manifestations
A

supplement use

  • causes bleeding
  • supplements may worsen risk or outcomes for some cancers
  • may increase mortality risk above 400 IU/day
59
Q

vitamin K

-two dietary forms

A
  • phylloquinone(K1): most common in US

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

60
Q

sources of phylloquinone

A
  • green leafy veggies
  • vegetable oil
  • soybean
  • fortified foods
61
Q

sources of menaquinones

A
  • some fermented foods
  • animal foods
  • dairy
  • intestinal bacteria
62
Q

absorption, tranport, and storage of vitamin K

A
  • absorbed with dietary fats as chylomicrons
  • transported in lipoproteins
  • stored in liver and adipose
63
Q

vitamin K mechanism of action

A
  • 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
64
Q

what regenerates vitamin K?

A

-epoxide

65
Q

warfarin

  • purpose
  • action
A

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

66
Q

prothrombin time

A

-how long it takes someone to clot

67
Q

epoxide reductase variations

A

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

68
Q

risk factors for vitamin K deficiency

A
  • infancy
  • 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)
69
Q

vitamin K deficiency in adults and babies

-pregnancy

A
  • adults: bleeding
  • babies: bleeding
  • embryopathy (from warfarin use or severe deficiency in mothers)
  • possible disorders of soft tissue and bone calcification
70
Q 
warfarin embryopathy
leads to (fancy name)
A
  • 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
71
Q

name the disorders of lactose

A
  • hypolactasia
  • congenital lactase deficiency
  • congenital lastose intolerance
72
Q

-hypolactasia-

A
  • partial or complete loss of brush border lastase activity

- congenital (rare) or acquired

73
Q

congenital lactase deficiency

A
  • absence of lactase activity at birth

- associated with diarrhea in breast fed infants

74
Q

congenital lactose intolerance

A
  • 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
75
Q

primary and secondary acruired hypolactasia (lactase nonpersistence)

A
  • 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
76
Q

primary acquired lactase nonpersistence continued

  • genetic basis
  • who is it most common in
A
  • 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
77
Q

lactose intolerance

-symptoms

A
  • osmotic load: unabsorbed lactose causes water influx in small intestine which leads to cramping, abdominal pain, and increased motility
  • fermentation
78
Q

lactose can be fermented by colonic bacteria to

A
  • 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
79
Q

what determines the severity of lactose intolerance symptoms

A
  • 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
80
Q

what are the 4 approaches to lactose intolerance?

A
  • 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
81
Q

2 big diseases associated with malabsorption

A
  • celiac disease

- chronic panreatitis

82
Q

celiacs disease

-cause

A
  • celiac sprue, non-tropical sprue, gluten sensitive enteropathy
  • immune mediated response to dietary gluten
83
Q

celiacs disease is associated with

A
  • type 1 diabetes mellitus
  • down syndrome
  • thyroid disease
  • liver disease
  • selective IgA deficiency
  • eosiniphilic esophagitic
  • inflammatory bowel disease
84
Q

gluten

A
  • a protein found in wheat, rye, barley, and oats

- also found in certain medications and hydiene products

85
Q

characterisitics of celiacs

A
  • 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
86
Q

management of celiacs disease

A
  • 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
87
Q

celiacs patients that do not follow a gluten free diet man

A

-develop ulcerative jejunitis and intestinal lymphoma

88
Q

celiacs and malabsorption

A
  • if you do not follow a lguten free diet, the damage to SI epithelium can cause serious absorption problmes
  • diarrhea/steatorrha
  • weight loss
  • vitamin deficiency
  • mineral deficiency (iron def may be one of the first signs of celiacs)
89
Q

gluten free labeling

A
  • 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)
90
Q

what can a persistent poor diet casue which is asymptomatic

A

-micronutrient deficiencies even without symptoms

91
Q

oral rehydration solutions

A
  • 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
92
Q

pancreatitis

  • what is it
  • signs/symptoms
A
  • 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 **
93
Q

causes of pancreatitis

A

-gallstones and hypertriglyceridemia

94
Q

risk factors for triglyceride induced pancretitis

A
  • obesity

- diabetes

95
Q

acute pancreatitis

  • most common casue
  • nutrtitional management
A
  • 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)
96
Q

chronic pancreatitis

  • manifestation
  • casues
  • treatment
A
  • 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
97
Q

constipation

  • defined as
  • associated with
A
  • less than or equal to 3 stools per week

- inadequate fiber intake, dehydration

98
Q

diverticular disease

  • diverticulosis
  • diverticulitis
A
  • diverticulosis: colonic outpouchings from high intercolonic pressure
  • diverticulitis: infection/inflammation due to impaction of stool or food particle
99
Q

fiber and diverticula disease

-diet of a patient

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

Nutrition (18 decks)

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