Nutrition III

Question 1

What are the symptoms of rickets?

Answer 1

Bone pain and deformity in children (p.94)

Question 2

What are the symptoms of osteomalacia?

Answer 2

Bone pain and muscle weakness in adults (p.94)

Question 3

What are the symptoms of Vitamin D overdose?

Answer 3

Hypercalcemia, hypercalciuria, loss of apatite, stupor (p.94)

Question 4

What condition predisposes a patient to Vitamin D excess?

Answer 4

Sarcoidosis (p.94)

Question 5

How does sarcoidosis cause Vitamin D excess?

Answer 5

By increased activation of vitamin D by epitheloid macrophages (p.94)

Question 6

What is the function of Vitamin E?

Answer 6

Antioxidant that protects erythrocytes and membranes from free radical damage (p.94)

Question 7

What are the symptoms associated with Vitamin E deficiency?

Answer 7

Increased fragility of erythrocytes causing hemolytic anemia, muscle weakness, posterior column and spinocerebellar tract demyelination (p.94)

Question 8

What is the function of Vitamin K?

Answer 8

Catalyzes y-carboxylation of glutamic acid residues on various proteins concerned with blood clotting (p.95)

Question 9

What is the mechanism of action of Warfarin?

Answer 9

Vitamin K antagonist (p.95)

Question 10

What are two causes of Vitamin K deficiency?

Answer 10

Neonates- have sterile intestines and are unable to synthesize Vitamin K. This causes hemorrhage with increased PT, aPTT, and normal bleeding time. Can also occur in pts with prolonged antibiotic use (p.95)

Question 11

Why are neonates given Vitamin K at birth?

Answer 11

Vitamin K is not in breastmilk; injection needed to prevent hemorrhage (p.95)

Question 12

What is the function of Zinc?

Answer 12

Essential for the activity of 100+ enzymes and important in the formation of zinc fingers (transcription factor motif) (p.95)

Question 13

What are the symptoms associated with a Zinc deficiency?

Answer 13

Delayed wound healing, hypogonadism, decreased adult hair (axillary, facial, pubic), dysguesia, anosmia; Predisposition to alcoholic cirrhosis (p.95)

Question 14

Describe the reactions involved in ethanol metabolism.

Answer 14

Ethanol is converted to acetylaldehyde in the cytosol by alcohol dehydrogenase and the conversion of NAD+ to NADH. Acetylaldehyde is shuttled into the mitochondria where it is converted to acetate by acetaldehyde dehydrogenase and the conversion of NAD+ to NADH (p.95)

Question 15

What is the limiting reagent in alcohol metabolism?

Answer 15

NAD+ (p.95)

Question 16

Describe the kinetics of alcohol dehydrogenase.

Answer 16

Zero order kinetics; alcohol is eliminated by zero order metabolism (p.95)

Question 17

What is the antidote for methanol or ethylene glycol poisioning?

Answer 17

Fomepizole (p.95)

Question 18

What is the mechanism of action of Fomepizole?

Answer 18

Inhibition of alcohol dehydrogenase (p.95)

Question 19

What is the mechanism of action of Disulfiram?

Answer 19

Inhibition of acetaldehyde dehydrogenase which causes the accumulation of acetaldehyde and the symptoms of a hangover (p.95)

Question 20

What is ethanol hypoglycemia?

Answer 20

Ethanol metabolism increases the ratio of NADH to NAD+ in the liver which causes diversion of pyruvate to lactate and OAA to malate. This inhibits gluconeogenesis and stimulates fatty acid synthesis which results in hypoglycemia, increased ketone production, and hepatic fatty change (hepatocellular steatosis) which is seen in chronic alcoholics. Excess lactic acid can cause an acidosis (p.95)

Question 21

What is the difference between Kwashiorkor and Marasmus?

Answer 21

Kwashiorkor is protein malnutrition; marasmus is energy malnutrition (p.96)

Question 22

What is the clinical picture of a patient with Kwashiorkor?

Answer 22

Skin lesions, edema, liver malfunction (fatty change), anemia, malnutrition. Typical picture is a child with a swolen belly (p.96)

Question 23

What is the clinical picture of a patient with Marasmus?

Answer 23

Tissue and muscle wasting, loss of subcutaneous fat, variable edema (p.96)