Page 268 - Textbook of Pathology, 6th Edition

252 poor preservation and maturation of fibroblasts; and dry beriberi (peripheral neuritis);
localisation of infections in the wounds. wet beriberi (cardiac manifestations), and
4. Anaemia. Anaemia is common in scurvy. It may be the cerebral beriberi (Wernicke-Korsakoff’s syndrome).
result of haemorrhage, interference with formation of folic It is worth-noting that lesions in beriberi are mainly
acid or deranged iron metabolism. Accordingly, anaemia is located in the nervous system and heart. This is because the
most often normocytic normochromic type; occasionally it energy requirement of the brain and nerves is solely derived
may be megaloblastic or even iron deficiency type. from oxidation of carbohydrates which is deranged in
beriberi, while lesions in the heart appear to arise due to
5. Lesions in teeth and gums. Scurvy may interfere with reduced ATP synthesis in beriberi which is required for
development of dentin. The gums are soft and swollen, may cardiac functions.
SECTION I
bleed readily and get infected commonly.
The features of 3 forms of beriberi are as under:
6. Skin rash. Hyperkeratotic and follicular rash may occur
in scurvy. 1. Dry beriberi (peripheral neuritis). This is marked by
neuromuscular symptoms such as weakness, paraesthesia
and sensory loss. The nerves show polyneuritis, myelin
VITAMIN B COMPLEX
degeneration and fragmentation of axons.
The term vitamin B was originally coined for a substance 2. Wet beriberi (cardiac manifestations). This is charac-
capable of curing beriberi (B from beriberi). Now, vitamin B terised by cardiovascular involvement, generalised oedema,
complex is commonly used for a group of essential compounds serous effusions and chronic passive congestion of viscera.
which are biochemically unrelated but occur together in certain The heart in beriberi is flabby (due to thin and weak
foods such as green leafy vegetables, cereals, yeast, liver and myocardium), enlarged and globular in appearance due to
milk. Most of the vitamins in this group are involved in 4-chamber dilatation (Fig. 9.12).
metabolism of proteins, carbohydrates and fats.
The principal members of vitamin B complex are thiamine Microscopic examination of the heart shows hydropic
(vitamin B ), riboflavin (vitamin B ), niacin/nicotinic acid degeneration of myocardial fibres, loss of striations,
1
2
(vitamin B ), pantothenic acid (vitamin B ), pyridoxine interstitial oedema and lymphocytic infiltration.
5
3
(vitamin B ), folate (folic acid), cyanocobalamin (vitamin B )
12
6
and biotin. There is no definite evidence that any clinical 3. Cerebral beriberi (Wernicke-Korsakoff’s syndrome).
disorder results from deficiency of pantothenic acid (vitamin It consists of the following features:
B ). i) Wernicke’s encephalopathy occurs more often due to
5
conditioned deficiencies such as in chronic alcoholism. It is
General Pathology and Basic Techniques
Thiamine (Vitamin B ) characterised by degeneration of ganglia cells, focal
1
demyelination and haemorrhage in the nuclei surrounding
PHYSIOLOGY. Thiamine was the first in the family of the region of ventricles and aqueduct.
vitamin B complex group and hence named B . Thiamine
1
hydrochloride is available in a variety of items of diet such Microscopic examination shows degeneration and
as peas, beans, pulses, yeast, green vegetable roots, fruits, necrosis of neurons, hypertrophy-hyperplasia of small
meat, pork, rice and wheat bran. The vitamin is lost in refined blood vessels and haemorrhages.
foods such as polished rice, white flour and white sugar. A
few substances in the diet (strong tea, coffee) act as anti- ii) Korsakoff’s psychosis results from persistence of psychotic
thiamines. Since the vitamin is soluble in water, considerable features following brain haemorrhage in Wernicke’s
amount of the vitamin is lost during cooking of vegetables. encephalopathy.
The vitamin is absorbed from the intestine either by passive
diffusion or by energy-dependent transport. Reserves of
vitamin B are stored in the skeletal muscles, heart, liver,
1
kidneys and bones.
The main physiologic function of thiamine is in
carbohydrate metabolism. Thiamine after absorption is
phosphorylated to form thiamine pyrophosphate which is
the functionally active compound. This compound acts as
coenzyme for carboxylase so as to decarboxylate pyruvic
acid, synthesises ATP and also participates in the synthesis
of fat from carbohydrate. In addition, thiamin plays a role in
peripheral nerve conduction by an unknown mechanism.
LESIONS IN THIAMINE DEFICIENCY. Thiamine
deficiency can occur from primary or conditioned causes,
chronic alcoholism being an important cause. The deficiency
state leads to failure of complete combustion of carbohydrate
and accumulation of pyruvic acid. This results in beriberi
which produces lesions at 3 target tissues (peripheral nerves, Figure 9.12 Wet (Cardiac) beriberi. Flabby, thin-walled, enlarged
heart and brain). Accordingly, beriberi is of 3 types: and globular appearance of the heart due to four-chamber dilatation.