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Block 2 > Vitamins > Flashcards

Vitamins Flashcards

1
Q

methanol consumption vs. ethanol consumption

A
  • methanol leads to formation of formic acid (toxic)
  • ethanol leads to formation of acetaldehyde (toxic)
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2
Q

essential amino acids

A

histidine
isoleucine
leucine
lysine
methionine
phenylalanine
threonine
tryptophan
valine

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3
Q

conditionally essential amino acids

A

arginine
cysteine
glutamine
glycine
proline
tyrosine

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4
Q

nonessential amino acids

A

alanine
asparagine
aspartate
glutamate
serine

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5
Q

what can make some nonessential amino acids essential?

A
  • urea cycle defect (arginine)
  • inability to metabolize phenylalanine (tyrosine)
  • trauma/severe burns (proline)
  • growing (glycine)
  • being a pre-term baby (cysteine)
  • hypercatabolic state (glutamine)
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6
Q

ketogenic amino acids

A

leucine, lysine

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7
Q

branched chain amino acids

A

valine
leucine
isoleucine

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8
Q

Vitamin B names

A

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

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9
Q

Vitamin B1 cofactor

A

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).

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10
Q

Vitamin B1 deficiency

A

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

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11
Q

Vitamin B2 cofactor

A

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)

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12
Q

Vitamin B3 cofactor

A

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.

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13
Q

Vitamin B5

A

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)

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14
Q

Vitamin B6 coenzyme

A

Pyridoxal phosphate (PLP) is a coenzyme for:
- transamination reactions (AST & ALT)
- glycogenolysis
- amino acid metabolism
- decarboxylation
- heme synthesis

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15
Q

Vitamin B6 deficiency

A

Caused by:
- heavy drinking
- malnutrition

Clinical manifestations:
- sideroblastic anemia (heme synthesis dysfunction ==> impaired iron transfer to heme ==> accumulation of iron)
- irritability, seizures, peripheral neuropathy

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16
Q

Vitamin B7

A

Biotin is a coenzyme for carboxylase enzme complexes:
- fatty acid synthesis (acetyl-CoA carboxylase)
- gluconeogenesis (pyruvate carboxylase)
- fatty acid reduction (propionyl-CoA carboxylase)

17
Q

Vitamin B9

A

Active form: tetrahydrofolate (THF)

Folate is a coenzyme for:
- DNA synthesis
- amino acid metabolism
- neurotransmitter synthesis
- hormone synthesis
- protein synthesis

18
Q

Vitamin B9 deficiency

A

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

19
Q

Vitamin B12

A

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)

20
Q

Vitamin B12 deficiency

A

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

21
Q

water soluble vs. fat soluble vitamins

A

Water soluble:
- C (ascorbic acid)
- B (thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, biotin, folate, cobalamin)

Fat soluble:
- A (retinol)
- D (cholecalciferol)
- K
- E

22
Q

Vitamin C

A

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

23
Q

Vitamin A

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

24
Q

Vitamin D

A

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

25
Q

Vitamin E

A

Tocopherol:
- antioxidant

Deficiency is rare:
- fat malabsorption disorders (cystic fibrosis)
- neurologic dysfunction
- hemolytic anemia

Toxicity is rare:
- alteration of vitamin K metabolism ==> anticoagulation

25
Q

Vitamin K

A

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

Block 2 (10 decks)

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