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scilearner

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Everything posted by scilearner

  1. In blood clotting disorders, clotting time is increased, but when there is plalete disorder clotting time is not affected. What is the reason for that. Aren't platelets required for blood clotting. Also when a fibrous mesh is formed, do red blood cells and platelets get stuck in it. Is it why blood clots. Thanks
  2. Hello everyone, The book says invivo extrinsic pathway is the one that gets activated, but intrinsic pathway is activated by surface collagen, so it must be activated as well. Both must be activated right, also if a person is deficient of intrinsic pathway clotting factors, would they have no problems with clotting because extrinsic pathway is the major one involved. Thanks
  3. Hello everyone, Ok so red blood cells break and release haemoglobin. Now I checked a book and it all it showed is that this haemoglobin binds to haptoglobin and goes to liver. Now billirubin is made by reticulocytes in spleen using haem. So does liver break this haemoglobin haptoglobin complex, and release haem into the circulation, so reticulocytes in spleen can act on it or does this haemoglobin travel to spleen? Thanks
  4. Hello everyone, So in renin angiotensin system, the NaCl concentration reaching the macula densa is monitored. Now my question if if there is loss of fluid from the body and both NaCl and water is lost from the body,plasma NaCl would be normal, now how would this affect macula densa. Okay so GFR decreases, but both NaCl and water filtration is decreased, so nacl reaching macula densa would be normal. I know I have really confused myself and I nedd some help. Thanks
  5. Hello everyone, Ok there are less nephrons, and they get more GFR. So the answer says more osmotically active particles are filtered leading to polyurea. My question is how can this happen, if there is more GFR shouldn't more water also be filtered with high amount of osmotically active particles, so as long as water is present it should reduce the effect of these substances. Thanks
  6. Hello everyone, MCV is packed cell volume divide by RBC count. Now I know reticulocytes increase in haemolytic anaemia. Why is that, is it to compensate for lost RBC? I want to know how this affects MCV. When you measure packed cell volume, do you measure the volume of blood occupied by RBC only or RBC+reticulocytes. Then when you measure RBC count do you count RBC only or RBC+reticulocytes. I just want to where the error occurs. Thanks
  7. Hello everyone, Bicarbonate concentration reduces in acidosis. My question is where actually does this buffering take place and why it reduces?Do Hydrogen ions move into cells (like red blood cells), where they are buffered by bicarbonate. I'm talking about this reaction that occurs inside cells CO2 + H20 <-> H2CO3<-> H+ + HCO3- If this is the case why does bicarbonate in extracellular fluid decrease. Is it because the reaction I mentioned above occurs, in reverse direction and there is less efflux of bicarbonate from cells. Also does bicarbonate from extracellular fluid move into cells, to carry out this reaction. or Are hydrogen ions buffered in extracellular fluid by bicarbonate. Does the same reaction occur in extracellular fluid as well. Thank you
  8. Hello everyone, Why does the velocity of flow decreases as the cross-sectional area of a tube increases. If a tube was constricted for sometime, its flow rate would be low due to resistance, now if you dilate the tube, the flow rate should increase. Am I confusing flow rate with velocity of flow. When they say velocity of flow do they mean, that when you dilate the tube more particles travel slower, but since there are more particles flow rate would be high. Thanks
  9. Hello everyone, What is dark adaptation of light? Is it the adaptation of rods and cones, when you are exposed to bright light for some time, and then move to a dark area. I know some chanes that occur. 1.the retinal and opsins in the rods and cones are converted back into the light-sensitive pigments 2. Pupils dilate- Why is that? I know light of more intensity enters, but if light sensitive pigments are not generated, how could this be beneficial. 3. The other mechanism is neural adaptation, involving the neurons in the successive stages of the visual chain in the retina itself and in the brain. What exactly is this neural adaptation. Also what is the textbook saying in this paragraph. Thanks
  10. Hello everyone, A 20 year old insulin dependent diabetic female was admitted to casuality in a semiconscious state. Her plasma values are as follows. a) on admission, b)eight hour after therapy with insulin,saline etc. Na+ a) 127, b)134, normal- 132-144 mmol/l K+ a) 7.0, b)3.1, normal- 3.2-4.8 mmol/l Urea a) 10.1, b)6.0, normal- 3.0-8.0 mmol/l Creatinine a) 0.18, b)0.07, normal- 0.06-0.12 mmol/l Phosphate a) 1.85, b)0.30, normal- 0.6-1.3 mmol/l This is what I think why these values have changed. Please add and correct me if I'm wrong. Na+ = Sodium has decreased initially. Due to osmotic diuresis. Large amount of sodium is lost in urine. I'm also thinking lack of insulin depresses the ativity of sodium potassium atpase pump, so more sodium enters cells not sure about this. K+ = Sodium potassium pump depression, creating efflux of Potassium. Also due to osmotic diuresis, water is lost so this increases plasma K+ concentration. Also after insulin treatment K+ moves into cells due to increased activity of sodium pottasium pump. Urea, creatinine, phosphte= Are they increased due to water loss or is diabetic nephropahy involved in this. If Diabetic nephropathy is involved how can they become normal after treatment. Your help is much appreciated. Thanks
  11. Ok I know that atria and ventricles contract independently and it makes sense heart would beat slower but what is the exact reason. The accesssory pacemaker that activates ventricles, is is lot slower than AV node is that the reason? Thanks
  12. Hello everyone, I don't understand the importance of this. Now I don't exactly understand what is the importance of filtration fraction. If normal GFR is 125 ml, in aortic stenosis filtration fraction increases, what does this mean? Does it mean that kidney has to now work harder to maintain 125 ml GFR? But in aortic stenosis both GFR and renal flow decreases. I don't understand the significance of filtration fraction? Also why does catecholamines constrict the efferent arteriole more than the efferent, I can understand how this would increase pressure up stream and increase GFR, is that the reason? Thanks
  13. Hello everyone, Wiki: The atrioventricular septum is a septum of the heart between the right atrium (RA) and the left ventricle (LV). I can't identify this in pics. I have not heard of a connection between right atrium ad left ventricle. Is this some embryological structure or can you see it in normal heart. Are tricupsid and mitral regions also called atrioventriclar regions? Can anyone provide me a clear pic. Thanks
  14. In aortic stenosis there is ventricular hypertrophy and this could lead to reduced cardiac ooutput. My question is why is the ventricular hypertrophy in aortic stenosis, inferior to ventricular hypertrophy you get in exercise. Why is their better ventricular hypertrophy that increases cardiac output occurs, in exercise. Thanks
  15. Hello everyone, Vasomotor centre for example, increases heart rate and increases blood vessel constriction and raises total peripheral resistance. The end result is increase in stroke volume. My question is if blood pressure is raised too much by constricting blood vessels, wouldn't that make it hard for the ventricles to pump blood and decrease stroke volume. Thanks
  16. Thanks SMF, that was a great answer , much better than the explantion I noted before. I understood everything, how relatively water moves in other direction, but I have simple question since my physics is not good. When you rotate the water bucket, why does water stay still. Is it because you are only rotating the bucket and not the water, so water remains still. If you move it hard though water would also move right. I understood all the rest of the explantion though.
  17. Hello everyone, First of all I don't understand the pic. Why is the endolymph moving in opposite direction to the movement of head, shouldn't it move the same way. How is inertia involved in this and what is the paragraph saying. Thanks
  18. Thanks for the reply swansont but I'm not a physics student. Could you please tell me if what I said above is right or wrong. I very much love to understand the physics concept though.
  19. Hello, I need to know what linear acceleration and angular acceleration of head is. This is not for physics, this is what I'm thinking, if I'm wrong please correct me and tell my why not Shaking head-angular acceleration Tilting head back- angular acceleration (Just in case this becomes linear, why? angle is changing right?) Nodding your head-angular accleration Moving your head back and forth, in a straight line- linear acceleration Thanks
  20. Thanks for the reply but I'm still confused. If I follow the cut nerves in B back to retina, pic doesn't support it. In case A, what do I see. If I close left eye, and look from right eye, is it the same thing I see in case A or do I only see half of an image. What I mean is, this is paris seen from normal eyes I don't understand this pic. Why do we see 2 things, don't we see only one thing with our eyes. For me this is like double vision. Paris with bitemporal hemianopia In real life what does a person with bitemporal hemianopia see, does he see these 2 images merged together.
  21. Hello everyone, I'm totally confused with this. If there is a lesion in A, why can't you see the left visual field. According to the arrows, if there is a lesion at A, you would not be able to see white areas in pic C. Are they talking about a particular eye or what you see, please either way I don't understand this. What I'm thinking is if there is a lesion at A, when you look at an object you see an object with some areas missing, I'm assuming this is wrong and you can see a whole image in lesion A, but I don't understand. Your help would greatly appreciated. Thanks
  22. Thanks Cypress However I have a little trouble understanding this. When you say human organism is one set of diploid chromomes, doesn't that mean 46 chromosomes. There are 46 chromosomes in a diploid cell right. Also isn't human a sexually reproducing organism? Also when there is a great deal of variation in G-C bonds, what does this mean, I can not picture it? Also if it is 23 chromosomes as you said, are there 2 different genoms for female and male?
  23. Ok I can see the 5 end is negative, is the 3 end positive due to OH. So in other strand this goes other way round. Is this what they mean when they say there is reverse polarity in a DNA molecule. Thanks!!
  24. Hello everyone, Ok I read the definitions but I'm confused. What I'm thinking is genome, is the amount of DNA in one diploid cell. So when they say we have 20 000 genes in our body, are they referring amount of DNA in one diploid cell. Also what do they mean when they say human genome is extremely heterogenous. Thank you
  25. Hello everyone, I have a very poor understanding in this area. 1. In gel electrophoresis, let's say I used many DNA fragments.Then I used a filter paper, and used a probe to detect a specific DNA fragment. Then the pictures you see of electrophoresis, is it this filter paper you see, I mean you can not see the position of fragments in the machine right. Also does this filter paper, exactly mimic the positions of fragments in electrophoresis. Please excuse the stupidity. 2. Gel electrophoresis can be used to measure the length of the DNA accurately. Ok if have standard pieces of known size you can do this, but I still don't get how this works. I mean how can the distance of a fragment exactly give the size of the molecule. In electrophoresis particles with different sizes can end up at the same place due to other factors like charge and resistance. So even if you have fragments with known size how does this work. Thanks
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