VITAMINS

Fat Soluble Absorption depends on gut Water Soluble vitamins all wash out easily
(ileum) and pancreas. Toxicity is more from the body EXCEPT B12 and folate
common than for water-soluble, because (stored in the liver). B-complex deficiencies
these accumulate in fat. Malabsorption often result in dermatitis, glossitis, and
syndromes (steatorrhea), such as cystic diarrhea.
fibrosis and sprue, or mineral oil intake can  B1 (thiamine: TPP);
cause fat-soluble vitamin deficiencies.  B2 (riboflavin: FAD, FMN);
 B3 (niacin: NAD+);
 A;  B5 (pantothenic acid: CoA);
 D;  B6 (pyridoxine: PLP);
 E;  B7 (biotin);
 K;  B9 (folate);
 B12 (cobalamin);
 C (ascorbic acid);

VITAMIN FUNCTION DEFICIENCY EXCESS

Vitamin A 1. Antioxidant;
(retinol) 2. Visual pigments (Rhodopsin);
3. Normal differentiation of
Found in liver epithelial cells into specialized
and leafy tissues (e.g. pancreatic cells,
vegetables; mucus secreting cells);
4. Prevents squamous metaplasia;
5. Used to treat measles and AML
(M3);
Vitamin B1
(thiamine) Thiamine pyrophosphate (TPP) is a
cofactor for several enzymes in
decarboxylase reactions:
1. Pyruvate dehydrogenase (links
glycolysis to TCA cycle);
2. Alpha-ketoglutarate
dehydrogenase (TCA);
3. Transketolase (HMP shunt);
4. Branched-chain amino acid
dehydrogenase;
 Night blindness;  Cerebral edema,
 Dry skin; headaches (bear liver
 Keratomalacia consumption);
(softening of cornea);  Arthralgias, fatigue;
 Follicular hyperplasia;  Skin changes;
 Failure to thrive;  Sore throat;
 Alopecia;
 Teratogenic;
Deficiency results in impaired glucose breakdown  ATP
depletion that is WORSENED by glucose infusion. Highly aerobic
tissues (brain and heart) are affected first.
Wernicke-Korsakoff – confusion, ophthalmoplegia, ataxia +
confabulation, personality change, memory loss (permanent) due to
damage to medial dorsal nucleus of thalamus and mammillary
bodies;
Dry BeriBeri – polyneuritis, symmetrical muscle wasting (need
ATP for myelin synthesis);

Wet Beriberi – high output cardiac failure (dilated

cardiomyopathy, edema;
Vitamin B2 Cofactor in oxidation and reduction
(riboflavin) reactions (e.g. FADH2).

Necessary for the regeneration of

oxidized glutathione.

Deficiency
 Cheliosis (inflammation of the
lips, scaling, and fissures at the
corners of the mouth);
 Corneal vascularization;
Vitamin B3 Constituent of NAD+ and NADP+ (used DEFICIENCY: EXCESS:
(niacin) in redox reactions).  Glossitis;  Facial Flushing (due
 Pellagra = diarrhea, to pharmacologic doses
It is derived from tryptophan and its dermatitis, dementia; for treatment of
synthesis requires vitamin B6. hyperlipidemia);

Deficiency can be caused by:

1. Hartnup’s Disease (decreased
tryptophan absorption);
2. Malignant carcinoid
syndrome (tryptophan
consume to make 5-HT);
3. INH (reduces vitamin B6);
4. Corn-based diets;

Vitamin B5 DEFICIENCY:
(pantothenate) Essential component of CoA (a cofactor  Dermatitis;
for acyl transfers) and fatty acid  Enteritis;
synthase.  Alopecia;
 Adrenal insufficiency;

Vitamin B6 Converted to pyridoxal phosphate, a DEFICIENCY

(pyridoxine) cofactor used in:  Convulsions due to decreased neurotransmitters;
1. Transamination;  Hyperirritability;
2. Decarboxylation reactions;  Peripheral neuropathy (def. induced by INH and oral
3. Glycogen phosphorylase; contraceptives);
 Sideroblastic anemias due to impaired hemoglobin
Synthesis of: synthesis and iron excess;
 Cystathione;
 Heme;
 Niacin;
 Histamine;
 Neurotransmitters (5-HT, E,
NE, and GABA);
Vitamin B7 Cofactor for carboxylation enzymes DEFICIENCY is relatively rare but can be caused by antibiotic use or
(Biotin) (add 1 carbon groups): excessive ingestion of raw eggs;
1. Pyruvate carboxylase (pyruvate  Dermatitis;
 oxaloacetate);  Alopecia;
2. Acetyl Co-A Carboxylase (acetyl  Enteritis;
Co-A  malonyl CoA);  Lactic acidosis (excess conversion of pyruvate to lactate)
3. Propionyl-CoA carboxylase  Fasting hypoglycemia (cannot initiate gluconeogenesis);
(propionyl-CoA 
methylmalonyl-CoA);
Vitamin B9 Converted to Tetrahydrofolate (THF), a DEFICIENCY is the most common vitamin deficiency seen in the US
(Folic Acid) coenzyme for 1-carbon especially in pregnancy and alcoholism.
transfer/methylation reactions;  Macrocytic, megaloblastic anemia with NO neurologic
Found in leafy symptoms (as opposed to B12 deficiency0;
green Important for the synthesis of
vegetatbles; nitrogenous bases in DNA and RNA. Small Drugs can precipitate deficiency:
reserve pool in the liver;  Phenytoin;
 Sulfonamides;
 Methotrexate;
 5-FU;
 TMP;

HIGH FOLATE MAY ANTAGONIZE PHENYTOIN AND INDUCE

SEIZURE.

TREATMENT OF B12 DEF. WITH FOLATE CAN WORSEN

NEUROLOGIC DYSFUNCTION;
VITAMIN B12 Cofactor for homocysteine
(Cobalamin) methyltransferase (transfers CH3
groups as methylcobalamin) and
Found in methylmalonyl CoA mutase;
animal
products. Very large reserve pool in the liver.
Use Schilling Test to detect etiology of
deficiency:
The normal test will result in a
higher amount of the radiolabeled
cobalamin in the urine because it
will have been absorbed by the
intestinal epithelium, but passed
into the urine because all hepatic
B12 receptors were occupied. An
abnormal result will cause less of
the labeled cobalamin to appear in
the urine because it will remain in
the intestine and be passed into the
feces.
VITAMIN C
(Abscorbic FUNCTIONS:
Acid) 1. Antioxidant (regenerates
Vitamin E and reduces
oxidation of LDL);
2. Facilitates iron absorption by
keeping iron in Fe2+ reduced
state;
3. Hydroxylation of proline and
lysine in collagen synthesis;
4. Necessary for Dopamine B-
Hydroxylase which converts
dopamine to NE;
VITAMIN D D2 = ergocalciferol – ingested from
plants;
D3 = cholecalciferol – consumed in milk,
formed in sun-exposed skin;
25-OH D3 = storage form;
1,25-OH2-D3 (calcitriol) = active form
Functions:
1. Increase intestinal absorption
of calcium and phosphate;
2. Increase bone mineralization
via stimulation of osteoblasts to
release ALP;
3. Stimulates macrophage stem
cells to become osteoclasts;
VITAMIN E Functions as an antioxidant that
Symptoms of Deficiency:
 Macrocytic, megaloblastic anemia;
 Hypersegmented PMNs;
 Neurologic symptoms (paresthesias, subacute combined
degeneration) due to abnormal myelin;
 Prolonged deficiency leads to irreversible nervous system
damage.
DEFICIENCY is usually caused by:
1. Malabsorption (sprue, enteritis, Diphyllobothrium latum);
2. Lack of intrinsic factor (pernicious anemia or gastric
bypass surgery);
3. Absence of terminal ileum (Crohn’s Disease)
DEFICIENCY is seen in those on a EXCESS
“tea and toast diet”, homeless,  Nausea;
severely malnourished, IVDAs,  Vomiting;
alcholics;  Diarrhea;
 Fatigue;
Scurvy – swollen gums, bruising,  Sleep problems;
hemarthrosis, anemia, poor wound
healingl Can increase risk of IRON
TOXICITY in predisposed
Weakened immune response individuals (e.g. those with
transfusions or hereditary
hemochromatosis);
DEFICIENCY can be caused by EXCESS
renal failure, inadequate sun  Hypercalcemia;
exposure, fat malabsorption, liver  Hypercalciuria
disease and drugs that induce p450 (stones);
(metabolize 25-H enzyme);  Loss of appetite;
 Stupor;
Rickets in children (bone pain,
derformity), osteomalacia in Seen in sarcoidosis
adults (bone pain and muscle (increased activation of
weakness); vitamin D by epithelioid
macrophages);
Hypocalcemia tetany;
Breast milk has reduced Vitamin D
(must supplement in dark skinned
patients).
DEFICIENCY: TOXICITY
 protects erythrocyte membranes from
free-radical damage;
Vitamin K Catalyzes the gamma carboxylation of
glutamic acid residues on various
proteins concerned with blood clotting.
Synthesized by intestinal flora.
Activated by epoxide reductase which
is inhibited by warfarin.
Coagulation factors require Ca2+ to work
– gamma carboxylation brings Ca2+ to
bind to factors via carboxylation enabling
clot formation.
 Increased fragility of
erythrocytes  hemolytic Prevents synthesis of vitamin
anemia; K coagulative factors –
 Muscle weakness; results in over anti-
 Posterior column and coagulation with warfarin;
spinocerebellar tract
demyelination (protects
cell membrane with high
fatty acid content from
oxidative injury);
DEFICIENCY occurs in neonates and also after prolonged use of
broad-spectrum antibiotics;
 Neonatal hemorrhage with increased PT and PTT but
normal bleeding time;
 Rat Poison consumption (treat with IM vitamin K)
It is not present in breast milk – so neonates are given vitamin K
injection at birth to prevent hemorrhage. After 5D, the bacteria
have colonized the gut and begin to produce vitamin K.