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
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
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)
4
Q
risk factors for vitamin c def
A
- poor diet
- malabsorption
- alcoholism
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
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
7
Q
sources of thiaminases and antithiaminases
A
- thiaminases: fish, shelfish, ferns, microorganisms
- antithiamine compounds: coffeee, tea, betel nuts
8
Q
diagnostic risk factors of thiamine def
A
- Persistent vomiting
- HIV/AIDS
- alcohol inhibition of transport and phosphorylation
- refeeding syndrome
9
Q
thiamine deficiency causes what serious diseases
A
- beriberi
- wernicke encephalopathy
- koraskoff psychosis
10
Q
dry beriberi
A
- peripheral neuropathy
- calf wasting, tenderness, tingling
11
Q
wet beriberi
A
- heart failure
- edema
12
Q
infant beriberi
A
-when mother is defiient during gestation or vomits a lot
13
Q
-wernicke encephalopathy
A
- opthalmoplegia (eye manifestations)
- ataxia/balance problems
- confusion (lateral gaze and stuttering of the eye)
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
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*
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
17
Q
diagnostic risk factors for niacin deficiency
A
- hartnups: decreased absorption
- carcinoid tumors: use up tryptophan
18
Q
pellagra
- cause
- symptoms
A
- niacin deficiency
- dermatitis
- diarrhea
- dementia
- death
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
20
Q
folate deficiency
A
- manifests in rapidly proliferating tissues
- megaloblastic anemia
- diarrhea and malabsorption
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
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
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
24
Q
what are the fat soluble vitamins
A
-ADEK and carotenoids
25
characteristics of vat soluble vitamins
- digestion
- absorption
- mechanism of absorption
- transport
- increased bioavailability
- solubilized by bile, digestion by lipases
- absorbed with fat and is transporter dependent
- transported in lymphatics as chylomicrons
26
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
27
Provitamin A
- different forms
- cleavage
- 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)
28
food sources of preformed vitamin A
- meat, poultry, fish, liver, animal oils
- dairy
- eggs
29
food sources of carotenoids (the provitamin version of vitmain A)
- green leafy veggies
- brightly colored fruit and vegetables
- vegetable oils
- eggs
30
biological roles of vitamin A (not carotenoids)
- vision (pigments of rods and cones)
- cell division and differentiation
- reproduction
- immune function
- bone growth
31
biological roles of carotenois
-antioxidants
32
absorption, transport and storage of vitmain A
- stored in liver
| - trasnported in circulation on retinol binding protein and lipoproteins
33
storage and transport of carotenoids
- transported in and out of liver on lipoproteins
| - stored in adipose tissue
34
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)
35
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
36
risk for vitamin A tox
- primary
- secondary
- primary: dietary excess, preformed vitamin A only, dietary supplements, rarely get enough from food to be toxic
- secondary: chronic kidney disease
37
symptoms of acute vitamin A toxicity
- abdominal pain
- increased intracranial pressure leading to altered mental state, blurred vision,m and headache
- nausea and vomiting
- anorexia
- muscle pain and weakness
38
symptoms of chronic vitamin A toxicity
- liver dysfucntion
- osteoporosis/fracture
- teratogenicity
- anorexia and weight loss
- hair loss
- dryness of mucus membranes, lips, skin
- headache
- bleeding
39
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
40
- vitamin D2
- scientific name
- sources
- ergocalciferol
| - plants, fungi, invertebrates, supplements
41
vitamin D 3
- scientific name
- sources
- cholecalciferol
| - skin synthesis (main), animal foods, fortified foods, supplements
42
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
43
traditional roles of vitaminD
- calcium homeostasis and bone health
| - muscle function
44
emerging roles of vitamin D
- cancer (colon, prostate, breast)
- diabetes type 2
- cardiovascular disease
- immune function
- depression
45
risk for loss of vitamin D def due to skin synthesis
- aging
- limited sun exposure
- darker skin
46
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)
47
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
48
vitmain D deficiency in children
- rickets
- growth retardation
- bowing of lower extremities from weight bearing in setting of abnormal mineralization
49
vitamin D def in adults
- 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
vitamin D excess
- cause
- manifestations
- not from UV exposure
- usually from supps
- hypercalcemia is the big one, calciuria and kidney stones, arrhythmias
51
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
- PTH
- bone mineral density by DEXA
52
vitamin E
- family
- stereochem
- forms
- 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
53
vitamin E sources
- nuts
- seeds
- vegetable oil
- wheat germ
- green leafy vegetables
- olives
- fortified foods
- dietary supps
54
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
55
risk for vitamin E deficiency
- dietary insufficiency
- premature very low birth weight infants
- fat malabsorption
- alpha tocopherol transfer protein (TTP) defects **
- abetalipoproteinemia
56
vitamin E deficiency results in
- peripheral neuropathy
- ataxia with vitamin E def fue to TTP mutations
- myopathy
- retinopathy
- immune dysfunction
- RBC hemolysis
57
assessment of vitamin E status
-serum VE
58
vitamin E excess
- caused by
- manifestations
supplement use
- causes bleeding
- supplements may worsen risk or outcomes for some cancers
- may increase mortality risk above 400 IU/day
59
vitamin K
| -two dietary forms
- phylloquinone(K1): most common in US
| - menaquinones (K2): most common in japan, fermented foods, animal feeds
60
sources of phylloquinone
- green leafy veggies
- vegetable oil
- soybean
- fortified foods
61
sources of menaquinones
- some fermented foods
- animal foods
- dairy
- intestinal bacteria
62
absorption, tranport, and storage of vitamin K
- absorbed with dietary fats as chylomicrons
- transported in lipoproteins
- stored in liver and adipose
63
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
64
what regenerates vitamin K?
-epoxide
65
warfarin
- purpose
- action
interferes with regeneration of vitamin K in order to inhibit the clotting cascade
-it is a blood thinner
66
prothrombin time
-how long it takes someone to clot
67
epoxide reductase variations
-we can assess someones variation in this enzyme in order to preduct how they will react to warfarin
68
risk factors for vitamin K deficiency
- 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
vitamin K deficiency in adults and babies
| -pregnancy
- adults: bleeding
- babies: bleeding
- embryopathy (from warfarin use or severe deficiency in mothers)
- possible disorders of soft tissue and bone calcification
70
```
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
71
name the disorders of lactose
- hypolactasia
- congenital lactase deficiency
- congenital lastose intolerance
72
-hypolactasia-
- partial or complete loss of brush border lastase activity
| - congenital (rare) or acquired
73
congenital lactase deficiency
- absence of lactase activity at birth
| - associated with diarrhea in breast fed infants
74
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
75
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
76
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
77
lactose intolerance
| -symptoms
- osmotic load: unabsorbed lactose causes water influx in small intestine which leads to cramping, abdominal pain, and increased motility
- fermentation
78
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
79
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
80
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
81
2 big diseases associated with malabsorption
- celiac disease
| - chronic panreatitis
82
celiacs disease
| -cause
- celiac sprue, non-tropical sprue, gluten sensitive enteropathy
- immune mediated response to dietary gluten
83
celiacs disease is associated with
- type 1 diabetes mellitus
- down syndrome
- thyroid disease
- liver disease
- selective IgA deficiency
- eosiniphilic esophagitic
- inflammatory bowel disease
84
gluten
- a protein found in wheat, rye, barley, and oats
| - also found in certain medications and hydiene products
85
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
86
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
87
celiacs patients that do not follow a gluten free diet man
-develop ulcerative jejunitis and intestinal lymphoma
88
celiacs and malabsorption
- 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
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)
90
what can a persistent poor diet casue which is asymptomatic
-micronutrient deficiencies even without symptoms
91
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
92
pancreatitis
- what is it
- signs/symptoms
- 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
causes of pancreatitis
-gallstones and hypertriglyceridemia
94
risk factors for triglyceride induced pancretitis
- obesity
| - diabetes
95
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)
96
chronic pancreatitis
- manifestation
- casues
- treatment
- 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
constipation
- defined as
- associated with
- less than or equal to 3 stools per week
| - inadequate fiber intake, dehydration
98
diverticular disease
- diverticulosis
- diverticulitis
- diverticulosis: colonic outpouchings from high intercolonic pressure
- diverticulitis: infection/inflammation due to impaction of stool or food particle
99
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
