Please enable JavaScript.
Coggle requires JavaScript to display documents.
Vitamins - Coggle Diagram
Vitamins
Water Soluble
B1/ Thimine
Deficiencies Conditions
Beriberi (i cannot, i cannot in latin)
Weakness & lassitude
Cardiac symptoms: tachycardia, pathogenic heart remodeling, congestive heart failure,
Neuro symptoms
weakness, apathy, nerve tingling, poor coordination, paralysis (B1 catalyzes pyruvate --> acetyl-coA rxn; acetyl coA is needed for acetylcholine
Wernicke-Korsakoff syndrome
Linked to alcoholism
psychosis
Confusion
memory problems
coma
Diet
Found in grains, legumes, & meat (also used to fortify cereals breads, & other baked goods)
B2/ Ribo
f
lavin
coenzyme form =
FAD & FMN
(flavin adenine nucleotide; flavin mononucleotide)
Diet
Mainly found in
milk products
& meat. (also found in whole & enriched grains & some vegetables)
deficiency
Associated with alcoholism in the US, but globally where
milk
& meat consumption are low
Ariboflavinosis
Inflammation of the ...
lips
mouth
skin (seborrheic dermatitis besoming red, scaly, & greasy
tongue
eyes
influences iron absorption & mobilization (oxy-reduction of Fe2+/3+) thus can affect function of red blood cells
FAD & FMN are electron carriers
B3/
N
iacin
coenzyme form =
NAD
another important electron carrier
Diet
fish, meat, legumes, bran, peanuts
Deficiencies
Pellegra
endemic in places where unfortified corn is the staple diet
4 Ds
Diarhhea
Dermatitis
Death (if untreated)
Dementia
partially synthetic (we also make some not only dietary)
Tryptophan is taken up by same transporter
B7/ Biotin
Diet
liver, egg yolks, yogurt, nuts (not rly found in fruits & meats/ very minimal)
Only carboxylation rxns
Rxns: Pyruvate Carboxylase (Gluconeogenesis), Acetyl-CoA Carboxylase (FA synthesis), catabolism of some amino acids ( proponyl-coA, carboxylase, ect ...)
Deficiencies
Brittle fingernails, hair loss, skin rashes
, neurological deficits, & tingling extremities
B5/ Pantothenic acid
Diet
found in everything
rxns
acyl carrier, (eg. acetyl-CoA)
deficiencies
very rare but found in WWII Pacific prisoners of war
may also contribute to generalized vitamin B deficiencies in alcoholics
numbness & painful burning & tingling in extremities
B
6
/
P
yridoxine
forms PLP (pyridoxal phosphate)
Diet
both animal & plant products: meats, whole grains, brown rice, & some fruits & vegetables
Rxns
involved in many rxns
deficiencies
very rare except alcoholics
Some drugs can inactivate B6 derivatives
Take B6 along with these drugs
Cycloserine - tuberculosis
Isoniazid - tuberculosis
Hydralazine - high blood pressure
Theophylline - asthma
Penicillamine - rheumatoid arthritis
Monoamine oxidase inhibitors - depression
Carbidopa, a drug used in treating Parkinson's may also lead to a vitamin B6 deficiency.
Symptoms
Neurological features of B6 deficiency are thought to relate to its role in neurotransmitter synthesis and include:
Confusion
Depression
Headaches
Numbness or tingling in extremities, and seizures.
Anemia - microcytic anemia with ringed sideroblasts
B6 is a coenzyme in one of the 1st steps of heme synthesis
Seborrheic dermatitis
Glossitis
Cheilosis
Neurological features - Infants consuming the formula where B6 was inactivated by heat as a major food source began displaying abdominal problems, convulsions and other neurological symptoms.
B9/ Folate
Diet
Lentils & green vegetables
In the United States, since 1998, refined grain products are fortified with folic acid
Deficiencies
Megaloblastic anemia
Neural tube defects
Elevated homocysteine
elevated homocysteine is associated with cardiovascular disease
important cofactor for cell division so affects rapidly dividing cells like RBCs
B12/ Cobalamin
diet
almost exclusively in animal products, therefore vegans need to obtain cobalamin through fortified foods or supplements
Rxns
only used in 2 rxns
Methionine synthase
- methyl-cobalamin is used to methylate homocysteine to methionine by the enzyme methionine synthase.
Cobalamine formed in this reaction is converted back to methyl-cobalamin by the same enzyme using N5-methyl-tetrahydrofolate as a methyl group donor.
Since this is the only reaction where N5-methyl-tetrahydrofolate is converted to tetrahydrofolate and returned to the folate pool, this reaction forms the basis for the folate trap discussed above.
Methylmalony-CoA-Mutase
- adenosyl-cobalamin: reaction where methylmalonyl-CoA is rearranged to succinyl-CoA in a late step in the catabolism of certain amino acids and odd-chain fatty acids (VOMIT).
deficiencies
Causes
autoimmune/ immune mediated malabsorption problems
Pernicious anemia
Autoimmune process destroys parietal cells involved in the synthesis of intrinsic factor needed for B12 absorption in the ileum.
Atropic gastritis
affects acid secretion in the stomach, which can affect the release of B12 from proteins in the diet, reducing absorption.
Malabsorption syndromes such as celiac disease and tropical spruce
surgical resection
surgical resection of stomach or terminal ileum can result in the loss of cells secreting intrinsic factor or receptors for the intrinsic factor-B12
Drug Interactions
Proton pump inhibitors that reduce stomach acid can affect B12 absorption – prolonged use is generally necessary for B12 deficiency to develop.
Nitrous oxide – Nitrous oxide inactivates B12 and can lead to symptoms of B12 deficiency.
Metformin – metformin has an effect on B12 absorption by influencing levels of free calcium needed for uptake of the intrinsic factor-B12 complex.
Tetracycline – tetracycline can interfere with the absorption of B12, so if supplements are taken they should be taken at different times than tetracycline.
vegans
Clinical manifestatios
Macrocytic anemia
Homocystinuria
methylmalonic aciduria
Neurologic manifestations
Mechanisms
Folic acid crosses BBB as 5-methyl-THF
Upon entering neurons 5-methyl-THF is converted to THF via the methionine synthase reaction, with cobalamin as an essential co-enzyme.
The methyl group as part of methionine can then form S-adenosyl-methionine
1 more item...
symptoms
numbness and tingling of hands and feet
difficulty walking
memory loss
disorientation
dementia
Ascorbic acid/ Vitamin C
diet
citrus fruits, & other fruits/ vegetables
rxns (used directly no other coenzyme)
Hydroxylation
Hydroxylation of proline and lysine in collagen
Hydroxylation of dopamine to norepinephrine
Hydroxylation of hypoxia inducible factor used as an oxygen sensor in angiogenesis
Antioxidant!
protects the body from reactive oxygen species
Deficiencies
Hurts wound healing through disrupting collagen synthesis and supplying new blood flow
Scurvy
historically seen in sailors, now seen in the poor
clinical findings
Fragile blood vessels; pinpoint hemorrhages, bleeding gums, bruising
Poor wound healing
Bone fractures
Loose teeth
Joint pain and swelling
Anemia
caused by chronic bleeding due to weakened blood vessels. chronic bleeding leads to Fe+ deficiency
Vit. C aids Fe+ absorption
an effect of vitamin C on the conversion of folic acid to folate (could be a macrocytic anemia)
Fat Soluble
ADEK (A Don't Even Know!)
Retinoids/ Vitamin A
diet
Preformed retinoids (more efficiently absorbed)
liver, fish, egg yolks, dairy
Carotinoids
Vegetables & fruits w/ yellow & orange pigment
eg. carrots
rxns
visual cycle
signal transduction (gene expression @ transcriptional level)
Development
– retinoic acid derivatives play critical roles in human development affecting the formation of the cardiovascular system, nervous system, respiratory system and skeletal growth.
Immune system
– retinoic acid derivatives control cell fate decisions during erythropoiesis.
Epithelial tissue
– retinoic acid plays a role in the differentiation of epithelial layers.
Eyes
– mucus secreting cells of the eye require retinoic acid signaling for appropriate function
Skin
- retinoic acid plays in important role in controlling the differentiation of hair follicles and mucus secreting glands.
Bone
growth and remodeling
Deficiencies
Major problem for children in developing countries
causes (other than reduced Vit A consumption)
inadequate fat intake
decreases solubility
inadequate protein consumption
--> dec substrate available for retinol binding protein synthesis
inadequate zinc consump.
clinical features
Xerophthalmia
eye problems
including: night blindness, extreme dryness and softening of the cornea referred to as keratomalacia.
nutritionally acquired immunodeficiency
Follicular hyperkeratosis
hard dry skin surfaces with lesions that appear on extremities, shoulders, and buttocks.
Disruption of the skin barrier can lead to infections.
toxicities/ overdose clinical features
Adults
Adults Acute - nausea, headache, blurred vision, cerebral edema, and lack of muscle coordination
Chronic – weight loss, muscle and joint pain, liver damage, bone abnormalities, visual defects, anemia, and skin rashes
Infants
bulging frontanels
Pregnancy
teratogens (especially preformed!)
Pharmaceutical uses: used to treat ...
Acute promyelocytic leukemia
Psoriasis
Severe Acne/Acne Vugarus
Retinitis pigmentosa
Vitamin D/ Cholecalciferol
diet
naturally arises from animal derived products such as salmon, liver, & egg yolks
In the US, major sources of vitamin D in the diet come from fortified milk and cereals.
rxns
Ca2+ & phosphorus homeostasis
deficiencies
causes/ risk factors
exclusively breastfed infants (less fortified food eaten)
darker skin (less UV rays get through)
CKD, kidney cannot produce enzyme to activate Vitamin D
fat malabsorption syndromes
cystic fibrosis
obesity
vitamin D is stuck/ absorbed in body fat & not bioavailable for other functions
elderly
body enzymes less efficiency w/ age & nursing homes w/ reduced sunlight
clinical findings
Rickets (children
narrow rib cages and bowed legs
Osteomalacia
weaken bones leading to fractures in weight-bearing bones; promote osteoporosis
toxicity from too much vitamin supplementation
high blood calcium and calcium depositions in blood vessels, kidney and cardiovascular system.
drug interactions
Cholesterol sequesterants should not be taken at the same time as vitamin D supplements.
Drugs like phenytoin, carbamazepine and rifampin increase vitamin D catabolism.
Vitamin E/ Tocopherol
diet
nuts & vegetable oils
rxns
fat-soluble anti-oxidant
especially protecting cell membranes especially of RBCs, nerves & immune system
deficiency (is rare)
causes
Fat malabsorption syndromes
Genetics
Birth – little transfer of vitamin E occurs from mother to fetus until late in pregnancy
:Premature infants can have damaged red blood cell membranes and suffer from hemolytic anemia due to vitamin E deficiency
symptoms
Neurologic
- impaired balance and coordination, damage to sensory nerves, muscle weakness, and damage to the eye (peripheral neuropathy, ataxia, and retinitis pigmentosa – classic symptoms)
Hemolytic anemia
– see discussion above regarding premature infants
Vitamin K/ Phylloquinone
K for blood
Koagulation!
diet
leafy green plants and vegetable oils.
Some forms of vitamin K are also formed by bacteria within the digestive tract and absorbed
rxns
generating coagulation factors
serve as an essential co-enzyme for γ-glutamyl carboxylase
electron donor in this reaction
targeted by warfarin
Deficiencies
rare in adults, common in newborns!
causes
causes in newborns
Most infants receive a vitamin K injection within 6 hours of birth
little transfer of vitamin K from mother to fetus and the newborn GI tract is essentially free of bacteria
Fat-malabsorption syndromes can affect vitamin K absorption
Antibiotics that kill off GI bacteria coupled with a diet low in vitamin K can lead to vitamin K deficiency.