Page 237 - Concise Pathology for Exam Preparation ( PDFDrive )

222 SECTION I General Pathology

3. Delayed wound healing
4. Anaemia due to blood loss

Q. Write briefly about vitamin E deficiency.
Ans. Vitamin E belongs to a group of eight closely related fat-soluble compounds (four
tocopherols and four tocotrienols) of which a-tocopherol is the most active.
• Sources are vegetables, nuts, grains and their oils, dairy products, fish and meat
• Absorption requires normal biliary and pancreatic function
• Transported in the blood in chylomicrons
• Stored mainly in the fat depots; also in minor amounts in the liver and muscle.
• Functions as an antioxidant (terminates free radical generated lipid peroxidation
reactions and prevents damage to the cellular and subcellular membranes)
• Pathologic changes due to vitamin E deficiency are characteristically seen in the nervous
system (degeneration of axons in the posterior columns of the spinal cord and loss of
neurons in the dorsal root ganglia). Vitamin E–deficient RBCs are more susceptible to
oxidative damage and have a shorter half-life
• Manifestations include depressed tendon reflexes, ataxia, dysarthria, loss of position and
vibration sense, muscle weakness, impaired vision and disorders of eye movement

Q. Write briefly about vitamin K deficiency.
Ans. Vitamin K is a cofactor for a liver microsomal carboxylase, which carboxylates
the glutamyl residues in certain proteins to carboxyglutamates, eg, clotting factors like
prothrombin, factors VII, IX and X. Carboxylation provides a calcium-binding site to allow
calcium-dependent interactions of the clotting factors.
• Activation of proteins C and S also requires vitamin K-dependent carboxylation.
• Vitamin K–dependent carboxylation of osteocalcin (a protein secreted by osteo-
blasts) increases calcium and osteocalcin interaction and thereby favours bone calci-
fication.
• Endogenous intestinal bacteria synthesize the vitamin, therefore, it is required in very
small amounts in the diet.
• Active reduced form is converted to an epoxide after vitamin K reacts with its substrate;
the epoxide reduced back by a liver epoxide reductase.
• Deficiency is seen in
(a) Malabsorption syndromes (vitamin K is a fat-soluble vitamin)
(b) Ingestion of broad spectrum antibiotics (which destroy the gut flora)
(c) Neonatal period when the intestinal flora is not well developed, liver reserves are
small and breast milk is low on vitamin K
• Deficiency manifests as bleeding diathesis (haematomas, haematuria, melena, ecchymo-
ses and bleeding from the gums).

Q. Write briefly about thiamine deficiency.

Ans. Thiamine plays an important role in helping the body metabolize carbohydrates and
fats to produce energy.
• Absorption of thiamine in the gut is followed by its phosphorylation resulting in forma-
tion of thiamine pyrophosphate, which has three important functions:
• It regulates the oxidative decarboxylation of a-keto acids, responsible for synthesis of
adenosine triphosphate
• It is a cofactor for transketolase in pentose phosphate pathway
• It maintains the integrity of neural membrane and ensures normal nerve conduction
• Thiamine is essential for normal growth and development, and helps to maintain proper
functioning of the heart, nervous and digestive systems.
• It is water-soluble and cannot be stored in the body; however, once absorbed, the vita-
min concentrates in muscle tissue.

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