Biochem - Nutrition (Part 3: Vitamins E, K, Zinc, Ethanol metabolism, & Malnutrition)

Question 1

What are 2 other names for Vitamin E?

Answer 1

Vitamin E (tocopherol/tocotrienol)

Question 2

What is the function of Vitamin E (tocopherol/tocotrienol)?

Answer 2

Antioxidant (protects erythrocytes and membranes from free radical damage); Think: “E is for Erythrocytes”

Question 3

With what drug in particular can Vitamin E interact, and how so?

Answer 3

Can enhance anticoagulant effects of warfarin

Question 4

What are 4 signs/symptoms associated with Vitamin E (tocopherol/tocotrienol) deficiency?

Answer 4

(1) Hemolytic anemia (2) Acanthocytosis (3) Muscle weakness (4) Posterior column and Spinocerebellar tract demyelination

Question 5

Compare/Contrast Vitamin E (tocopherol/tocotrienol) deficiency to Vitamin B12 deficiency.

Answer 5

Neurological presentation may appear similar to vitamin B12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or increase serum methylmalonic acid levels

Question 6

What is the function of Vitamin K?

Answer 6

Cofactor for the gamma-carboxylation of glutamic acid residues on various proteins required for blood clotting; Think: “K is for Koagulation”

Question 7

What synthesizes Vitamin K?

Answer 7

Synthesized by intestinal flora

Question 8

What are the clotting factors and/or anticoagulatory proteins for which Vitamin K is necessary?

Answer 8

Necessary for the activation of clotting factors II, VII, IX, X, and proteins C and S.

Question 9

What drug functions as a Vitamin K antagonist?

Answer 9

Warfarin - Vitamin K antagonist

Question 10

In what patient population does Vitamin K deficiency typically present, and why? What are 3 lab findings of significance in this presentation?

Answer 10

Neonatal hemorrhage with increased PT and increased aPTT but normal bleeding time (neonates have sterile intestines and are unable to synthesize vitamin K).

Question 11

Besides in neonates, in what other context can Vitamin K deficiency occur?

Answer 11

Can also occur after prolonged use of board-spectrum antibiotics

Question 12

What are the considerations/approaches for Vitamin K deficiency prevention in neonates?

Answer 12

(Vitamin K) Not in breast milk; Neonates are given vitamin K injection at birth to prevent bleeding diathesis

Question 13

What are important functions of Zinc?

Answer 13

Essential for activity of 100+ enzymes. Important in the formation of zinc fingers (transcription factor motif).

Question 14

What are 6 signs/symptoms associated with Zinc deficiency?

Answer 14

(1) Delayed wound healing (2) Hypogonadism (3) Decreased adult hair (axillary, facial, pubic) (4) Dysgeusia (5) Anosmia (6) Acrodermatitis enteropathica

Question 15

To what condition may Zinc deficiency predispose patients?

Answer 15

May predispose to alcoholic cirrhosis

Question 16

Draw out the major reactions of ethanol metabolism, including its locations.

Answer 16

See p. 97 in First Aid 2014 for reactions at the top of the page

Question 17

What is the limiting reagent in ethanol metabolism?

Answer 17

NAD+ is the limiting reagent.

Question 18

By what kinetics does alcohol dehydrogenase operate?

Answer 18

Alcohol dehydrogenase operates via zero-order kinetics

Question 19

What molecular change does ethanol metabolism cause in the liver? What are 3 effects of this change related to chronic alcoholism? What is the end result of these effects? What additional effects does this molecular change have?

Answer 19

Ethanol metabolism increase NADH/NAD+ ratio in liver, causing: (1) Pyruvate => lactate (lactic acidosis) (2) Oxaloacetate => malate (prevents gluconeogenesis => fasting hypoglycemia) (3) Glyceraldehyde-3-phosphate => Glycerol-3-phosphate (combines with fatty acids to make triglycerides => hepatosteatosis); End result is clinical picture seen in chronic alcoholism; Additionally, increased NADH/NAD+ ratio disfavors TCA production of NADH => increased utilization of acetyl-CoA for ketogenesis (=> ketoacidosis) and lipogenesis (=> hepatosteatosis)

Question 20

What is the mechanism of Fomepizole? For what is it an antidote?

Answer 20

Fomepizole - inhibits alcohol dehydrogenase and is an antidote for methanol or ethylene glycol poisoning

Question 21

What is the mechanism of Disulfiram? What biochemical effect does it have, and how does this present?

Answer 21

Disulfiram - inhibits acetaldehyde dehydrogenase (acetaldehyde accumulates, contributing to hangover symptoms)

Question 22

Draw the reaction of pyruvate breaking down in anaerobic glycolysis, including factors involved and its product.

Answer 22

See p. 97 in First Aid 2014 for visual at right

Question 23

Draw the reaction of Oxaloacetate breaking down in the TCA cycle, including factors involved and its product.

Answer 23

See p. 97 in First Aid 2014 for visual at right

Question 24

What reaction does alcohol dehydrogenase catalyze, and where? What effect does it have on NAD+/NADH?

Answer 24

Ethanol conversion to Acetaldehye in cytosol; Makes NAD+ into NADH

Question 25

What reaction does acetaldehyde dehydrogenase catalyze, and where? What effect does it have on NAD+/NADH?

Answer 25

Acetaldehyde conversion to Acetate in mitochondria; Makes NAD+ into NADH

Question 26

What are 2 types of malnutrition?

Answer 26

(1) Kwashiorkor (2) Marasmus

Question 27

What is Kwashiorkor, and what are 3 signs/symptoms that characterize it? What is its typical clinical picture?

Answer 27

Protein malnutrition resulting in (1) skin lesions, (2) edema, (3) liver malfunction (fatty change due to decrease apolipoprotein synthesis). Clinical picture is small child with swollen belly. ; Think: “Kwashiorkor results from a protein-deficient MEAL - Malnutrition, Edema, Anemia, Liver (fatty).”

Question 28

What is Marasmus, and what are 4 signs/symptoms that characterize it?

Answer 28

Total calorie malnutrition resulting in (1) tissue and (2) muscle wasting, (3) loss of subcutaneous fat, and (4) variable edema; Think: “Marasmus results in Muscle wasting”