Vitamine deficiencies and hypervitaminoses

Question 1

General information about vitamines

Answer 1

13 vitamines are essential for health. ADEK are Fat soluble, while all the other are water-soluble. Some of them can be synthesized endogenously such as vitamin D from precursor steroids, vitamin K and biotin from intestinal flora, Niacin from tryptophan

Question 2

General information about Vit. A

Answer 2

Obtained from animal-derived food and vegetables such as carrots, squash and spinach. Required bile and pancreatic enzymes in order to be properly absorbed.

• Retinol is absorbed through the intestinal wall. The chylomicron apolipoprotein E receptor takes it up into the liver where it is stored in Ito cells.
• When it is needed retinol binds to retinol-binding protein (RBP) and this complex is released into the circulation and later taken up by tissues.

Question 3

Functions of Vitamin A

Answer 3

Maintains normal vision in reduced light.
Potentiates the differentiation of specialized epithelial cell, mainly mucus secreting cells.
Enhances immunity to infections - particularly in children with measles.

Question 4

Deficiency of Vitamin A

Answer 4

Occurs due to poor nutrition or far malabsorption. Malabsorption may be because of:
Celiac disease
Crohn disease
Colitis
Surgery
Continuous use of laxatives

Question 5

Effects of Vitamin A deficiency

Answer 5

Impaired vision, particularly night vision
Metaplasia and keratinization due to the role of vitamin A in maintaining the specialized function of some epithelial cells:
- In the cornea: Lacrimal and mucus secreting epithelium is replaced by keratinized epithelium which leads to xerosis conjuctivae. Keratin can build up and form Bitot spots on the eyes and eventual erosion leading to keratomalacia.
- In the upper respiratory tract: loss of mucocilliary epithelium which predisposes to pulmonary infections
- In the urinary tract: keratinizing epithelium here will give keratin debris in the tract predisposing to renal and bladder stones

Also leads to immune deficiencies.

Question 6

Vitamine A toxicity

Answer 6

Signs and symptoms of acute toxicity:
Headache, dizziness, vomiting, stupor, blurred vision, hepatocellular damage, bone changes.

Signs and symptoms of chronic toxicity:
weight loss, anorexia, nausea, vomiting, bone and joint pain.

May be confused with brain tumors due to the symptoms

Question 7

General information about Vit. D

Answer 7

Synthesized in the skin by UV light from the precursor 7-dehydrocholesterol. Promotes intestinal calcium and phosphorus absorption enhanced bone calcification.

Question 8

Vitamine D deficiency

Answer 8

Symptoms: Rickets (children) and osteomalacia (in adults), hypocalcemia (if PTH managed to normalize the hypocalcemia, hypophosphatemia can rather be seen).

Question 9

Vitamine D toxicity

Answer 9

Symptoms: calcification of soft tissue and growth retardation, bone pain, hypercalciuria, hypercalcemia, nephrocalciosis, renal caliculi

Question 10

Vitamine C deficiency

Answer 10

Symptoms: scurvy

Question 11

Vitamine C toxicity

Answer 11

Symptoms: May cause uricosuria and increased absorption of iron, not really a big danger

Question 12

Vitamine B1 deficiency

Answer 12

Associated with severe malnutrition such as that seen in alcoholics and dieters.

Thiamine is important for carbohydrate and amino acid intermediate metabolism, thus deficiencies lead to:

• Dry beriberi, peripheral neuropathy, atrophy of muscles in the extremities
• Wet beriberi, marked by high output cardiac failure, dilated cardiomyopathy, and general edema
• Wernicke-Korsakoff syndrome

Question 13

Treatment of B1 deficiency

Answer 13

Thiamine is available as IV, intramuscular or oral preparations

Question 14

Vitamin B2 deficiency

Answer 14

Rare, as riboflavin is almost always added to commercially prepared bread and cereals. Occurs in alcoholics, fad dieters, elderly, people with chronic illness.
B2 is a component of FAD and FMN essential for redox processes.

Question 15

Vitamine B3 deficiency

Answer 15

Develops when the diet lacks both Niacin and tryptophan. May occur in Carcinoid syndrome and with usage of anti-TB drugs (isoniazid). Niacin is a component of NAD/NADP, so it is essential to glycolysis, TCA etc..

Deficiency manifests as pellagra (dementia, dermatitis, diarrhea - three Ds).

Question 16

Vitamine B3 treatment

Answer 16

Education, electrolyte replacement, nicotinamide

Question 17

Vitamin B12 deficiency

Answer 17

Daily requirement is 1g/day, liver stores are 1mg. It is usually caused by malabsorption, may occur in strict vegetarians.

Malabsorption causing B12 deficiency:

• Atrophic gastritis
• Pernicious anemia (due to lack of IF)
• Crohn’s disease
• Blind loop syndrome
• Fish tape worm infestation
• Can also occur secondarily to gastrectomy or ill resection

Question 18

Symptoms of B12 deficiency

Answer 18

Leads to a marked reduction of DNA replication and cell division – cobalamin is needed for folate synthesis and activation of THF. Megaloblastic anemia with neurologic dysfunction may occur.

Symptoms of anemia, combination of pallor and mild jaundice, glossitis, angular cheilosis, irritability, depression, psychosis, paresthesia, peripheral neuropathy

Question 19

Schilling test

Answer 19

Determines whether low B12 is due to malabsorption from terminal ileum or due to lack of intrinsic factor by comparing the amount of an oral dose (1g) of radioactive B12 which is absorbed and concurrently excreted in the urine with and without the concurrent administration of intrinsic factor.

If addition of intrinsic factor increases the absorption and thus the urinary excretion, then Pernicious anemia is most likely the cause

Question 20

Treatment for B12 deficiency

Answer 20

Hydroxycobalamine is available as IM and oral preparations

Question 21

Folic acid deficiency

Answer 21

Daily requirement is 50g. Deficiency is usually of dietary origin, often occurs in alcoholics and dieters. Can also be secondary to malabsorption diseases such as celiac, tropical sprue, jejunal resection.
Can also occur due to increased demand for folic acid such as in pregnancy, lactation, hemolytic anemia.
Can occur in cancer chemotherapy - megaloblastic anemia occurs without peripheral neuropathy

Question 22

Vitamine C deficiency

Answer 22

due to lack of the vitamin in the diet - ascorbic acid is needed for pro and lys hydroxylation and DA hydroxylation in NE synthesis. It leads to:

• Defective formation of mesenchymal tissue, and osteoid matrix due to decreased synthesis of hydroxyproline and hydroxylysine
• Defective collagen fribrillogenesis, impaired wound healing, fragile capillaries
• Scurvy: muscle, joint and bone pain. Bleeding gums, subperiosteal hemorrhage, perifolicular petechial hemorrhages. Bone changes are secondary to the defective osteoid synthesis

Question 23

Treatment of Vitamin C deficiency

Answer 23

Ascorbic acid - around 250mg/24h per os

Question 24

Vitamine K deficiency

Answer 24

Vitamine K is essential for the synthesis of clotting factors II, VII, IX, and X and of protein C. Deficiency results from fat malabsorption or alterations in the intestinal flora caused by antibiotics.

Question 25

Diagnosis of vitamin K deficiency

Answer 25

Characterized by hemorrhagic diatheses - bleeding tendency
Prolonged PT and aPTT
Low plasma vitamin K

Question 26

Treatment of vitamin K deficiency

Answer 26

10mg vitamin K IV