Shailesh Patel, [08.07.18 11:23]

[Forwarded from Muskan] Sir, what would be the justifications for,

1. Leukotrienes are chemotactic agents.

2. Tryptophan rich diet causes drowsiness.

3. GABA deficiency may cause stiffman syndrome.

4. Use of antitubercular drug INH produces pyridoxine deficiency.

5. Most human cancers emerge from oncofetal gene.

6. Ingestion of PUFA decreases serum cholesterol.

7. Iron deficiency anaemia is seen in Cu deficiency.

Shailesh Patel, [08.07.18 11:23]

[Forwarded from Muskan] 8. Heparin is known as clearing factor.

Shailesh Patel, [08.07.18 11:23]

[Forwarded from Muskan] 9. About 40g carbohydrates will induce sleep, while protein rich food will cause alertness.

Shailesh Patel, [08.07.18 11:23] [Forwarded from Muskan] 10. Mechanism of action of Ciprofloxacin.

Shailesh Patel, [08.07.18 11:23]

[Forwarded from Shailesh Patel] 1. leukotriene, product from arachidonic acid, is released by leukocyte. it binds its receptors on other leukocyte. this causes movement of leukocyte from lower concentrations to higher concentration. as concentration of leukotriene is higher at site of inflammation, it causes movement of peripheral leukocyte move towards site of inflammation. this is called chemotaxis.

Shailesh Patel, [08.07.18 11:28] 2. Based on electrophysiological, neurochemical, genetic and neuropharmacological approaches, it is currently accepted that serotonin (5-HT) functions predominantly to promote wakefulness (W) and to inhibit REM (rapid eye movement) sleep (REMS). Yet, under certain circumstances the neurotransmitter contributes to the increase in sleep propensity.

it is oversimplification to say that high tryptophan diet cause drowsiness.

in some it cause sleep, in some it may have oppsite effect, based on preexisting CNS diseases.

tryptophan is coverted into serotonin and melatonin, both are involved in sleep and wakefulness physiology.

*correct question: high Tryptophan diet may alter sleep and weakfullness.*

Shailesh Patel, [08.07.18 11:46] 3. glutamate is coverted into gaba by removing co2. enzyme is glutamate decarboxylase.

in stiffman syndrome, there are autoantibodies against glutamate decarboxylase.

so, gaba deficiency.

gaba is involved in inhibition of many neurotransmitters.

its deficiency causes problems in sleep and muscle tone.

in this disease, there is stiffness in body in response to stress, sound, light etc. patients fear going out of house.

Shailesh Patel, [08.07.18 11:57] note that, gaba deficiency donot affect sleep, but, only affects muscle. probably, gaba antibodies are in peripheral blood. so, gaba in muscle is altered, bit cns gaba is unaffected.

it is better called stiff-person syndrome, rather than stiff-man syndromeπŸ˜„πŸ˜„πŸ˜„πŸ˜„πŸ˜„πŸ˜„

Shailesh Patel, [08.07.18 11:58] baba poorly cross blood brain barrier

Shailesh Patel, [08.07.18 11:58] gaba, i mean

Shailesh Patel, [08.07.18 12:00] you may be able to smile a bit, even when exam is due, if u read entire answer again, by replacing gaba with baba

Shailesh Patel, [08.07.18 13:30] 4.

INH (isoniazide) bind bacterial acyl-carrier protein (Fatty Acid synthatase). It prevent formation of mycolic acid(a fatty acid, in bacterial cell wall of tubercal bacilli). Thus, it work as anti tuberculosis drug.

a) INH bind pyridoxin. The complex is inactive. and lost in urine. b) INH inhibit enzyme which convert pyridoxal to pyrixoxal-phosphate (active form).

All patients of TB require multi drug tratment. One of which is INH. All TB patients receiving INH are supplimented with pyridoxin. RDA for pyridoxin is 2mg/day. In INH therapy 10-50 mg / day is given.

phyridoxin is required for decarboxylase ( Glu to GABA). This it interfere with amine neurotransmitter syntheis. So, its deficiency causes peripheral neuropathy.

Correlate INH mechanism of action, side effect etc.

Shailesh Patel, [08.07.18 13:39] 5. Oncofetal gene: produce oncofetal protein

They are physiologically important in foetal development. In adult life, where much of development stops, these genes are physiologically switched off. But, due to mutation in adult life, some of them are expressed again(produce protein). Their primary and tertiary structure is also altered. This leads to abnormal growth of cells. Such cells grow, penetrate surrounding tissue and reach distant site( That is cancer).

Shailesh Patel, [08.07.18 13:40] It is oversimplification to say that Most human cancers emerge from oncofetal gene correct question dysregulation and mutation of oncofetal genes can cause cancer

Shailesh Patel, [08.07.18 14:17] 6. PUFA = polyunsaturated fatty acid

they are of two types: omega-3 and omega-6. Omega-3 have double bond between 3rd and 4th catbon from -CH3 side. Omega-6 have double bond between 6th and 7th catbon from -CH3 side.

Omega-6 Omega-6 in food β†’ omega-6 in lipoprotein, cell membrane etc it alter metabolism of lipoprotein and β€œSOMEHOW” reduce serum cholesterol. But, evidence is inconcusive that is reduce cardiovascular mortality and morbidity.

Omega-3 Omega-3 in food β†’ omega-3 in lipoprotein, cell membrane etc There are good evidence that is reduce cardiovascular mortality and morbidity. a) It alter liporotein function, which reduce atherosclerosis. b) It alter membrane function, thus altering uptake of liporotein, relelase of cytokines (which cause atherosclerosis) c) it produces more of omega-3-prostaglandins which are less platelet-aggregating and more platelet-antiaggregating than omega-6-prostaglandins. This reduces coronary and cerebral thrombosis. (too much of omaga-3 increase bleeding and cerebral stroke.😑😑😑😑😑) d) It aliter membrane function, thereby altering action potential generation. This have benificial effect on cardiac arrythmia.

Shailesh Patel, [08.07.18 14:21] Arachidonic acid (animal) and linoleic acid (plant origin) is omega-6. ecosapentaeinoic acid (EPA) and docosahexaeinoic acid (DHA) are omega-3 (animal, fish) alpha-linolenic acid is omega-3 (plant, flaxseed, nuts)

Shailesh Patel, [08.07.18 14:22] Rest tomorrow. (But you read hard)

Shailesh Patel, [09.07.18 23:24] 7. cu2+ is present in ferroxidases (present in intestine and plasma). The enzyme convert fe2+ in to fe3+. the enzyme help iron bind with transferrin ( because Tf binds preferably with Fe3+)

In copper deficiency, this process is slowed, resulting in lesser iron absorption and anemia

Shailesh Patel, [09.07.18 23:29] 8. Lipoprotein lipase (+ charged) is bound to endothelium cell by heparan sulpate (-ve charge). When heparin(-ve charge) is given Intravenously, it remove LL from Heparan Sulphate and bind itself to LL. Thus, Heparin injections increase plasma free lipoprotein lipase.

Such plasma (with high LL) can repidly convert triacylglycerol emulsion in to FA and glycerol. This results in white/turbind emulsion become clear/transparent.

So, Heparin is called clearing factor.

Shailesh Patel, [09.07.18 23:49] 9. Orexin is a peptide neurotranmitter secreted by orexin cell in brain. it stimulate catabolism and weakfulness. glucose inhibit them and amino acid activate them. So high glucose diet stimulate drowsyness and high protein diet cause wakefullness.

But remember, high protein (with tryptophan) can have reverse effect.

Shailesh Patel, [11.07.18 20:42] 10.

Both human and bacteria need DNA topoisomerase. (differing in their structure) During DNA replication and protein synthesis both DNA strands needs to be unwind+separated. During unwinding of one region of DNA , another region get hyper-wind. This further inhibit unwinding (and replication, transcription). Topoisomerase funtion to decrease hyper-winding.

Ciprofloxacin (fluroquinolone group of drugs) inhibit Bacterial DNA topoisomerase. There by decrease bacterial growth. used as antibiotic to treat infection

Shailesh Patel, [11.07.18 20:42] [Forwarded from Sara Shah] Sir how to justify these questions 1 Carbohydrate are essential for the metabolism of fat. 2. Fibrinogen estimation cannot be done in serum. 3. 2-3 BPG concentration is higher in patient of COPD and cyanotic heart disease. 4. Excess use of barbiturate cause anemia. 5. In a patient with lipoprotein lipase deficiency, creamy layer is seen on the top of serum. 6. Niacin deficiency alone can not cause pellagra.

Shailesh Patel, [11.07.18 21:53] 1. Fatty acid oxidation produce Acetyl-Co-A. Acetyl-Co-A need small amount of oxaloacetate to enter TCA cycle. (Oxaloacetate is NOT consumed in TCA cycle - that is why it is small amount per cell) Oxaloacetate is produced from pyruvate. pyruvate is formed from glucose.

In experiment in vivo, when cell is kept in carbohydrate free medium, catolism of fatty acid is slow. Very small amount of glucose added in such experiment enhance fatty acid oxidation.

This is mostly not true about whole body, where small amount of glucose required for OA syntheis is always available.

In fact, if human take carbohyrate, lipids are spared from oxidation and stored.!!!!!

Wrong Question: Carbohydrate are essential for the metabolism of fat. Right question: In glucose deficient medium of cell growth, fatty acid oxidation is slowed down.

Shailesh Patel, [11.07.18 21:54] 2. Fibrinogen estimation cannot be done in serum because serum is removed from clotted blood.

Shailesh Patel, [11.07.18 23:11] 3. In COPD, O2 is not exchanged as effectly as CO2, resulting in low CO2 with Low O2

In cyanotic heart disease, there is low O2 in blood. This results in faster breathing, resulting in low O2 with Low CO2.

Both condition cause alkalosis. High pH stimulate bisphosphoglycerate mutase enzyme and inhibit DPG-phosphatase enzyme. It results in elevated 2-3 DPG.

This decrease O2 affinity of Hb. resulting in better release of O2.

2-3 BPG concentration is higher in patient of COPD and cyanotic heart disease.

Remember that, Alkalosis move O2 saturation curve to left, causing opposit effect. Thus, benifit of elevated 2-3 BPG donot appear to be as great.

Shailesh Patel, [11.07.18 23:13] 4.

many anticonvulsant cause megaloblastic anemia (Phenytoin for example. Barbiturates are less common in this effect) There are several possible mechanism.

1) Dietary folate-plyglutamate is converted to mono-glutamate by one enzyme, which is inhibited by the drug. 2) Drug elevate Duodenal pH, which decrease folate absorption. 3) Drug may block Folate receptor on instestinal mucosal cells

only folate monoglutamate can be absorbed

Shailesh Patel, [11.07.18 23:15] 5. In a patient with lipoprotein lipase deficiency, creamy layer is seen on the top of serum because Chylomicrone are not removed by blood. they are lighter than water and float in blood on standing. They are white in appearance

Shailesh Patel, [11.07.18 23:16] 6. Niacin deficiency alone can not cause pellagra. because niacin can be synthesised from tryptophan using pyridoxin as cofactor.