Vitamins Flashcards
methanol consumption vs. ethanol consumption
- methanol leads to formation of formic acid (toxic)
- ethanol leads to formation of acetaldehyde (toxic)
essential amino acids
histidine
isoleucine
leucine
lysine
methionine
phenylalanine
threonine
tryptophan
valine
conditionally essential amino acids
arginine
cysteine
glutamine
glycine
proline
tyrosine
nonessential amino acids
alanine
asparagine
aspartate
glutamate
serine
what can make some nonessential amino acids essential?
- urea cycle defect (arginine)
- inability to metabolize phenylalanine (tyrosine)
- trauma/severe burns (proline)
- growing (glycine)
- being a pre-term baby (cysteine)
- hypercatabolic state (glutamine)
ketogenic amino acids
leucine, lysine
branched chain amino acids
valine
leucine
isoleucine
Vitamin B names
B1: thiamine
B2: riboflavin
B3: niacin
B5: pantothenic acid
B6: pyridoxine
B7: biotin
B9: folate
B12: cobalamin
the red ninja paid prue and berry for cake
Vitamin B1 cofactor
Thiamine is a cofactor for:
- pyruvate dehydrogenase (pyruvate ==> acetyl CoA)
- a-ketoglutarate dehydrogenase (a-ketoglutarate ==> succinyl CoA)
- transketolase (PPP: ribulose-5-phosphate ==> fructose-6-phosphate ==> glycolysis)
- branched-chain ketoacid dehydrogenase (valine/isoleucine ==> propionic acid; leucine ==> acetyl CoA)
Enzymes thiamine is a cofactor for:
Thiamine PATs your Back! (Pyruvate dehydrogenase, Alpha-ketoglutaric acid dehydrogenase, Transketolase, Branched-chain ketoacid dehydrogenase).
Vitamin B1 deficiency
Caused by:
- heavy drinking
- malnutrition
Pathophysiology:
- impaired glucose breakdown ==> decreased ATP ==> tissue damage in heart, brain
Clinical manifestations:
- Dry Beriberi: symmetrical peripheral neuropathy
- Wet Beriberi: high-output cardiac failure
- Wenicke encephalopathy: confusion, ophthomoplegia, ataxia
Vitamin B1 deficiency causes Ber1ber1
Vitamin B2 cofactor
Active form: flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD)
Riboflavin is a cofactor for:
- succinate dehydrogenase (TCA cycle)
- glutathione reductase (in RBCs: breaks disulfide bond in GSSG ==> GSR)
Vitamin B3 cofactor
Active forms:
- Nicotinamide adenine dinucleotide (NAD+/NADH)
- Nicotinamide adenine dinucleotide phosphate (NADP+/ NADPH)
Niacin is a cofactor for:
- redox reactions (alcohol dehydrogenase, G6PD)
3 typical features of severe vitamin B3 Deficiency: Dermatitis, Diarrhea, and Dementia.
Vitamin B5
Pantothenic acid: essential component of coenzme A
- Cofactor for fatty acid, cholesterol, and acetylcholine synthesis
- Activation of carboxylic acids (e.g., pyruvate dehydrogenase, α-ketoglutarate dehydrogenase)
Vitamin B6 coenzyme
Pyridoxal phosphate (PLP) is a coenzyme for:
- transamination reactions (AST & ALT)
- glycogenolysis
- amino acid metabolism
- decarboxylation
- heme synthesis
Vitamin B6 deficiency
Caused by:
- heavy drinking
- malnutrition
Clinical manifestations:
- sideroblastic anemia (heme synthesis dysfunction ==> impaired iron transfer to heme ==> accumulation of iron)
- irritability, seizures, peripheral neuropathy
Vitamin B7
Biotin is a coenzyme for carboxylase enzme complexes:
- fatty acid synthesis (acetyl-CoA carboxylase)
- gluconeogenesis (pyruvate carboxylase)
- fatty acid reduction (propionyl-CoA carboxylase)
Vitamin B9
Active form: tetrahydrofolate (THF)
Folate is a coenzyme for:
- DNA synthesis
- amino acid metabolism
- neurotransmitter synthesis
- hormone synthesis
- protein synthesis
Vitamin B9 deficiency
Most common vitamin deficiency in the U.S.
Caused by:
- malnutrition/chronic alcohol use
- malabsorption
- increased requirement
Pathophysiology:
- decreased DNA synthesis ==> megaloblastic erythropoiesis ==> megaloblastic anemia
- increased homocysteine, decreased methionine ==> endothelial damage ==> increased risk of cardiac disease
- neural tube defects in fetal development
Clinical manifestations:
- anemia
- NO neurological symptoms
Vitamin B12
Cobalamin:
- produced by microorganisms in colonic flora, but needs to be ingested
- large reserve pool in body; deficiency in B12 takes a long time
Cofactor for:
- methionine synthase (DNA synthesis): homocysteine ==> methionine; N5-methyl-THF ==> THF
- methylmalonyl-CoA mutase (odd-chain fatty acid metabolism)
Vitamin B12 deficiency
Caused by:
- decreased intrinsic factor (IF): malabsorption, chronic alcohol use, Crohn’s disease, celiac disease, pernicious anemia (autoimmune disease against IF)
- malnutrition
- increased demand
Pathophysiology:
- decreased methionine ==> folate trapped as methyl THF, decreased active THF ==> decreased DNA synthesis ==> large nucleated hematopoietic cells ==> pancytopenia
- decreased methionine ==> neuropathy
- increased homocysteine ==> increased risk of cardiac disease
- can cause secondary folate deficiency
- acetyl CoA replaced by propionyl CoA in neurons ==> demyelination ==> neurological symptoms
Clinical manifestations:
- anemia
- symmetrical peripheral neuropathy
- subacute combined degeneration of spinal cord
- neuropsychiatric disease
water soluble vs. fat soluble vitamins
Water soluble:
- C (ascorbic acid)
- B (thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, biotin, folate, cobalamin)
Fat soluble:
- A (retinol)
- D (cholecalciferol)
- K
- E
Vitamin C
Ascorbic acid:
- antioxidant
- promotes iron resorption
- coenzyme for collagen synthesis, noradrenaline synthesis
Deficiency due to:
- malnutrition
Clinical manifestations:
- Scurvy: impaired collagen synthesis, easily damaged connective tissue
Toxicity:
- increased risk of iron toxicity in transfusion patients
“absorbic acid” since it promotes the intestinal absorption of iron
Vitamin A
Retinol:
- Retinal: component of rhodopsin (vision)
- Retinoic acid, retinol: gene transcription and tissue maintenance
Deficiency caused by:
- disorders associated with fat metabolism
- malnutrition
Clinical manifestations:
- night blindness
- Bitot spots on conjunctiva
- retinopathy
Toxicity:
- teratogenic
Vitamin D
Calciferol:
- only vitamin that the human body can produce entirely on its own
- stored as 25-hydroxycholecalciferol, mainly in adipose tissue (25-OH D3)
- ↑ Absorption of calcium and phosphate in the intestine
Deficiency caused by:
- lack of sun exposure
Clinical manifestations:
- adults: osteomalacia
- children: rickets
Toxicity:
- hypercalciuria
Vitamin E
Tocopherol:
- antioxidant
Deficiency is rare:
- fat malabsorption disorders (cystic fibrosis)
- neurologic dysfunction
- hemolytic anemia
Toxicity is rare:
- alteration of vitamin K metabolism ==> anticoagulation
Vitamin K
Phytomenadione:
- active form: vitamin K hydroquinone
- important for coagulation (factors II, VII, IX, X)
- bone formation
Deficiency caused by:
- liver failure
- fat malabsorption
- vitamin K antagonists (warfarin)
- neonatal deficiency
Clinical manifestations:
- hemorrhage
- newborns: vitamin K deficiency bleeding (VKDB) ==> increased PT and PTT
Toxicity is rare
