Page 238 - Concise Pathology for Exam Preparation ( PDFDrive )

9 Environmental and Nutritional Pathology 223

• Sources include green peas, spinach, liver, beef, pork, beans, nuts, bananas, whole
grains, unpolished rice and legumes.
• Deficiency manifests as Wernicke–Korsakoff syndromes or dry and wet beriberi,
and usually results from malnutrition, alcoholism, diets high in thiaminase-rich foods
(raw freshwater fish, raw shellfish and ferns) and antithiamine factors (tea and coffee),
debilitating illness, consumption of polished rice and protracted diarrhoea.
• Dry beriberi causes wasting and partial paralysis resulting from damaged peripheral nerves.
It is also associated with tingling or loss of feeling (sensation) in hands and feet, mental
confusion, speech difficulties and involuntary eye movements (nystagmus). It is thought to
result from degeneration of myelin.
• Wet beriberi mainly affects the heart; it causes vasodilation, peripheral oedema,
paroxysmal nocturnal dyspnoea, increased heart rate and eventually heart failure.
The chronic form of wet beriberi consists of three stages. In the first stage, periph-
eral vasodilatation occurs, leading to a high-cardiac-output state. This leads to salt
and water retention mediated through renin–angiotensin–aldosterone system in the
kidneys. As the vasodilation progresses, the kidneys detect a relative loss of volume
and respond by conserving salt. With salt retention, fluid is also absorbed into the
circulatory system. The resulting fluid overload leads to oedema of dependent ex-
tremities. By the time significant oedema occurs, the heart has been exposed to a
severely high workload in order to pump required cardiac output needed to satisfy
end-organ requirements. This causes parts of the heart muscle to undergo overuse
injury.
• A more rapid form of wet beriberi is termed acute fulminant cardiovascular beriberi
or Shoshin beriberi. In this form, oedema may not be present. Instead, cyanosis of
hands and feet, tachycardia, distended neck veins, restlessness and anxiety occur. It
is because of damage to the heart muscle and its inability to cope with the demands of
the body. Treatment with thiamine causes low-output cardiac failure because systemic
vasoconstriction is reinstated before the heart muscle recovers.

Q. Write briefly about riboflavin deficiency.

Ans. Riboflavin is a yellow or yellow-orange coloured vitamin which can be used as a
food colouring.
• Large quantities of riboflavin are often included in multivitamins. The excess is excreted
in the urine, causing the urine to be coloured bright yellow.
• Deficiency of riboflavin can be primary, which is diet related, or secondary, which
may be a result of conditions that affect absorption in the intestine, the body not being
able to use the vitamin, or an increase in the excretion of the vitamin from the body.
• Riboflavin deficiency manifests as cracked and red lips, inflammation of the lining of
mouth and tongue, mouth ulcers, cracks at the corners of the mouth (angular cheilitis)
and a sore throat.
• Deficiency may also cause dry and scaly skin, scrotal dermatitis, fluid in the mucous
membranes and iron-deficiency anaemia. The eyes may become bloodshot, itchy, watery
and sensitive to bright light (photophobia).

Q. Write briefly about niacin deficiency.
Ans. Niacin (Vitamin B 4 ) refers to both nicotinic acid and its amide derivative nicotin-
amide (niacinamide). Both of the above are required for formation of coenzymes
nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide
phosphate (NADP).
• The coenzymes NAD and NADP are required for many biological oxidation–reduction
(redox) reactions responsible for energy generation in tissues by the biochemical degra-
dation of carbohydrates, fats and proteins.
• The exogenous sources of niacin are meat, fish, eggs, legumes and groundnut. Trypto-
phan can be converted to niacin in the human body.

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