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

Pg. 96-97 in First Aid 2014 Sections include: -Vitamin E (tocopherol/tocotrienol) -Vitamin K -Zinc -Ethanol metabolism -Malnutrition (28 cards)

1
Q

What are 2 other names for Vitamin E?

A

Vitamin E (tocopherol/tocotrienol)

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2
Q

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

A

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

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3
Q

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

A

Can enhance anticoagulant effects of warfarin

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4
Q

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

A

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

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5
Q

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

A

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

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6
Q

What is the function of Vitamin K?

A

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

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7
Q

What synthesizes Vitamin K?

A

Synthesized by intestinal flora

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8
Q

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

A

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

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9
Q

What drug functions as a Vitamin K antagonist?

A

Warfarin - Vitamin K antagonist

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10
Q

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

A

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

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11
Q

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

A

Can also occur after prolonged use of board-spectrum antibiotics

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12
Q

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

A

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

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13
Q

What are important functions of Zinc?

A

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

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14
Q

What are 6 signs/symptoms associated with Zinc deficiency?

A

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

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15
Q

To what condition may Zinc deficiency predispose patients?

A

May predispose to alcoholic cirrhosis

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16
Q

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

A

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

17
Q

What is the limiting reagent in ethanol metabolism?

A

NAD+ is the limiting reagent.

18
Q

By what kinetics does alcohol dehydrogenase operate?

A

Alcohol dehydrogenase operates via zero-order kinetics

19
Q

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?

A

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)

20
Q

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

A

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

21
Q

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

A

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

22
Q

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

A

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

23
Q

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

A

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

24
Q

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

A

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

25
What reaction does acetaldehyde dehydrogenase catalyze, and where? What effect does it have on NAD+/NADH?
Acetaldehyde conversion to Acetate in mitochondria; Makes NAD+ into NADH
26
What are 2 types of malnutrition?
(1) Kwashiorkor (2) Marasmus
27
What is Kwashiorkor, and what are 3 signs/symptoms that characterize it? What is its typical clinical picture?
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)."
28
What is Marasmus, and what are 4 signs/symptoms that characterize it?
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"