NEET MDS Lessons
Biochemistry
1. Kwashiorkor
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Cause: Severe protein deficiency with adequate or near-adequate calorie intake.
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Typical Age: 1–3 years (post-weaning)
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Clinical Features:
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Edema (due to hypoalbuminemia)
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Moon face and swollen abdomen
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Dermatosis and skin depigmentation
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Fatty liver
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Apathy and irritability
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Key Insight: Protein is lacking, but energy (carbohydrates) may be sufficient.
2. Marasmus
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Cause: Deficiency of both protein and calories
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Typical Age: Infants under 1 year
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Clinical Features:
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Severe wasting and muscle loss
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Prominent ribs and sunken eyes
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No edema
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Alert but irritable
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Key Insight: Total energy deficit leads to extreme emaciation.
IRON
The normal limit for iron consumption is 20 mg/day for adults, 20-30 mg/day for children and 40 mg/day for pregnant women.
Milk is considered as a poor source of iron.
Factors influencing absorption of iron Iron is absorbed by upper part of duodenum and is affected by various factors
(a) Only reduced form of iron (ferrous) is absorbed and ferric form are not absorbed
(b) Ascorbic acid (Vitamin C) increases the absorption of iron (c) The interfering substances such as phytic acid and oxalic acid decreases absorption of iron
Regulation of absorption of Iron
Absorption of iron is regulated by three main mechanisms, which includes
(a) Mucosal Regulation
(b) Storer regulation
(c) Erythropoietic regulation
In mucosal regulation absorption of iron requires DM-1 and ferroportin. Both the proteins are down regulated by hepcidin secreted by liver. The above regulation occurs when the body irons reserves are adequate. When the body iron content gets felled, storer regulation takes place. In storer regulation the mucosal is signaled for increase in iron absorption. The erythropoietic regulation occurs in response to anemia. Here the erythroid cells will signal the mucosa to increase the iron absorption.
Iron transport in blood
The transport form of iron in blood is transferin. Transferin are glycoprotein secreted by liver. In blood, the ceruloplasmin is the ferroxidase which oxidizes ferrous to ferric state.
Storage form of iron is ferritin. Almost no iron is excreted through urine.
Anemia
Anemia is the most common nutritional deficiency disease. The microscopic appearance of anemia is characterized by microcytic hypochromic anemia
The abnormal gene responsible for hemosiderosis is located on the short arm of chromosome No.6.
The main causes of iron deficiency or anemia are
(a) Nutritional deficiency of iron (b) Lack of iron absorption (c) Hook worm infection (d) Repeated pregnancy (e) Chronic blood loss (f) Nephrosis (g) Lead poisoning
The Bicarbonate Buffer System
This is the main extracellular buffer system which (also) provides a means for the necessary removal of the CO2 produced by tissue metabolism. The bicarbonate buffer system is the main buffer in blood plasma and consists of carbonic acid as proton donor and bicarbonate as proton acceptor :
H2CO3 = H+ + HCO3–
If there is a change in the ratio in favour of H2CO3, acidosis results.
This change can result from a decrease in [HCO3 − ] or from an increase in [H2CO3 ]
Most common forms of acidosis are metabolic or respiratory
Metabolic acidosis is caused by a decrease in [HCO3 − ] and occurs, for example, in uncontrolled diabetes with ketosis or as a result of starvation.
Respiratory acidosis is brought about when there is an obstruction to respiration (emphysema, asthma or pneumonia) or depression of respiration (toxic doses of morphine or other respiratory depressants)
Alkalosis results when [HCO3 − ] becomes favoured in the bicarbonate/carbonic acid ratio
Metabolic alkalosis occurs when the HCO3 − fraction increases with little or no concomitant change in H2CO3
Severe vomiting (loss of H+ as HCl) or ingestion of excessive amounts of sodium bicarbonate (bicarbonate of soda) can produce this condition
Respiratory alkalosis is induced by hyperventilation because an excessive removal of CO2 from the blood results in a decrease in [H2CO3 ]
Alkalosis can produce convulsive seizures in children and tetany, hysteria, prolonged hot baths or lack of O2 as high altitudes.
The pH of blood is maintained at 7.4 when the buffer ratio [HCO3 − ] / [ H2CO3] becomes 20
| Enzyme | Clinical Use | Indicates |
|---|---|---|
| ALT (SGPT) | Specific to liver injury | Hepatitis, liver necrosis |
| AST (SGOT) | Found in liver, heart, muscle | Liver disease, myocardial infarction |
| ALP | Bile duct obstruction, bone disease | Cholestasis, bone metastases |
| GGT | Alcoholic liver disease, biliary obstruction | Alcohol abuse, hepatobiliary disease |
| LDH | Non-specific, elevated in many conditions | Liver, cardiac, or hemolytic disorders |
ESSENTIAL FATTY ACIDS (EFAs) Polyunsaturated FAs,such as Linoleic acid and g(gamma)- Linolenic acid, are ESSENTIAL FATTY ACIDS — we cannot make them, and we need them, so we must get them in our diets mostly from plant sources.
Vitamin B12: Cobalamin
Vitamin B12, also known as cobalamin, aids in the building of genetic material, production of normal red blood cells, and maintenance of the nervous system.
RDA The Recommended Dietary Allowance (RDA) for vitamin B12 is 2.4 mcg/day for adult males and females
Vitamin B12 Deficiency
Vitamin B12 deficiency most commonly affects strict vegetarians (those who eat no animal products), infants of vegan mothers, and the elderly. Symptoms of deficiency include anemia, fatigue, neurological disorders, and degeneration of nerves resulting in numbness and tingling.
These are normally non-essential but become essential during stress, illness, or in infants.
| Conditionally Essential | When Needed |
|---|---|
| Arginine | Growth, trauma, immune stress |
| Cysteine | Liver disease, oxidative stress |
| Glutamine | Critical illness, burns |
| Tyrosine | PKU (phenylketonuria) patients |
| Proline, Glycine | Wound healing, collagen synthesis |