NEET MDS Lessons
Biochemistry
Factors regulating blood calcium level
(i) Vitamin D
(a) Vitamin D and absorption of calcium: Active form of calcium is calcitriol. Calcitriol enters intestinal wall and binds to cytoplasmic receptor and then binds with DNA causes depression and consequent transcription of gene code for calbindin. Due to increased availability of calbindin, absorption of calcium increases leading to increased blood calcium level.
(b) Vitamin D and Bone: Vitamin D activates osteoblast, bone forming cells & also stimulates secretion of alkaline phosphatase. Due to this enzyme, calcium and phosphorus increase.
(c) Vitamin D and Kidney: Calcitriol increase reabsorption of calcium and phosphorus by renal tubules.
(ii) Parathyroid hormone (PTH)
Normal PTH level in serum is 10-60ng/l.
(a) PTH and bones: In bone, PTH causes demineralization. It also causes recreation of collagenase from osteoclast leads to loss of matrix and bone resorption. As a result, mucopolysacharides and hydroxyproline are excreted in urine.
(b) PTH and Kidney: In kidney, PTH causes increased reabsorption of calcium but decreases reabsorption of phosphorus from kidney tubules.
(iii) Calcitonin Calcitonin decreases serum calcium level. It inhibits resorption of bone. It decreases the activity of osteoclasts and increases osteoblasts.
Hyper Calcemia When plasma Ca2+ level is more than 11mg/dl is called Hypercalcemia. It is due to parathyroid adenoma or ectopic PTH secreting tumor. calcium excreted in urine decreases excretion of chloride causing hyperchloremic acidosis.
Hypocalcemia Plasma calcium level less than 8mg/dl is called hypocalcemia. Tetany due to accidental surgical removal of parathyroid glands or by autoimmune disease. In tetany, neuromuscular irritability is increased. Increased Q-7 internal in ECG is seen. Main manifestation is carpopedal spasm. Laryngismus and stridor are also observed.
FLUORIDE
The safe limit of fluorine is about 1PPM in water. But excess of fluoride causes Flourosis
Flourosis is more dangerous than caries. When Fluoride content is more than 2 PPM, it will cause chronic intestinal upset, gastroenteritis, loss of weight, osteosclerosis, stratification and discoloration of teeth
The input to fatty acid synthesis is acetyl-CoA, which is carboxylated to malonyl-CoA.
The ATP-dependent carboxylation provides energy input. The CO2 is lost later during condensation with the growing fatty acid. The spontaneous decarboxylation drives the condensation.
fatty acid synthesis
acetyl-CoA + 7 malonyl-CoA + 14 NADPH → palmitate + 7 CO2 + 14 NADP+ + 8 CoA
ATP-dependent synthesis of malonate:
8 acetyl-CoA + 14 NADPH + 7 ATP → palmitate + 14 NADP+ + 8 CoA + 7 ADP + 7 Pi
Fatty acid synthesis occurs in the cytosol. Acetyl-CoA generated in the mitochondria is transported to the cytosol via a shuttle mechanism involving citrate
The Hemoglobin Buffer Systems
These buffer systems are involved in buffering CO2 inside erythrocytes. The buffering capacity of hemoglobin depends on its oxygenation and deoxygenation. Inside the erythrocytes, CO2 combines with H2O to form carbonic acid (H2CO3) under the action of carbonic anhydrase.
At the blood pH 7.4, H2CO3 dissociates into H+ and HCO3 − and needs immediate buffering.
Functions of lipids
1. They are the concentrated fuel reserve of the body (triacylglycerols).
2. Lipids are the constituents of membrane structure and regulate the membrane permeability (phospholipids and cholesterol).
3. They serve as a source of fat soluble vitamins (A, D, E and K).
4. Lipids are important as cellular metabolic regulators (steroid hormones and prostaglandins).
5. Lipids protect the internal organs, serve as insulating materials and give shape and smooth appearance to the body.
Gluconeogenesis
It is the process by which Glucose or glycogen is formed from non carbohydrate substances.
Gluconeogenesis occurs mainly in liver.
Gluconeogenesis inputs:
The source of pyruvate and oxaloacetate for gluconeogenesis during fasting or carbohydrate starvation is mainly amino acid catabolism. Some amino acids are catabolized to pyruvate, oxaloacetate, Muscle proteins may break down to supply amino acids. These are transported to liver where they are deaminated and converted to gluconeogenesis inputs.
Glycerol, derived from hydrolysis of triacylglycerols in fat cells, is also a significant input to gluconeogenesis
Glycolysis & Gluconeogenesis pathways are both spontaneous If both pathways were simultaneously active within a cell it would constitute a "futile cycle" that would waste energy
Glycolysis yields 2~P bonds of ATP.
Gluconeogenesis expends 6~P bonds of ATP and GTP.
A futile cycle consisting of both pathways would waste 4 P.bonds per cycle.To prevent this waste, Glycolysis and Gluconeogenesis pathways are reciprocally regulated.
COPPER
The normal serum level of copper is 25 to 50 mg/dl.
Functions of copper
(a) Copper is necessary for iron absorption and incorporation of iron into hemoglobin.
(b) It is very essential for tyrosinase activity
(c) It is the co-factor for vitamin C requiring hydroxylation
(d) Copper increases the level of high density lipo protein and protects the heart.
Wilson’s disease
In case of Wilson’s disease ceruloplasmin level in blood is drastically reduced.
Wilson’s disease leads to
(i) Accumulation of copper in liver leads to hepatocellular degeneration and cirrhosis
(ii) Deposition of copper in brain basal ganglia leads to leticular degeneration
(iii) Copper deposits as green pigmented ring around cornea and the condition is called as Kayser-Kleischer ring
Over accumulation of copper can be treated by consumption of diet containg low copper and injection of D-penicillamine, which excretes copper through urine.
Menke’s kidney hair syndrome
It is X-linked defect. In this condition copper is absorbed by GI tract, but cannot be transported to blood. The defect in transport of copper to blood is due to absence of an intracellular copper binding ATPase.