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scilearner

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Everything posted by scilearner

  1. How can a villous adenoma arise in colon, if colon naturally doesn't have villi. Thanks
  2. Hello everyone, Stomach normal epithelium is simple columnar, intestine it is the same. Now in intestinal type of adenocarcinoma of stomach, intestinal metaplasia of stomach occurs. I don't get it , columnar has changed to columnar, how is this metaplasia. Thanks
  3. Hello guys, I'm bit confused here, hope you guys can help me out. 1. Crystalloid- Ok they contain water soluble molecules. So eg is Saline (NaCl). Now book says if I infuse crystalloids then only 1/3 of of my infusion would remain in the intravascular compartment. Now my question is why is this? If I add lot of salt to intravascular compartment eg by giving saline, shouldn't I suck more water from extracellular compartment, why am I losing 2/3 instead. What I think: Is it because Saline contains like 0.9% Saline. So this is actually more like you are adding more water to the intravascular compartment rather than salts, so some water may leak out. Does this mean if I give 5% Saline solution more water would stay in the intravascular compartment than 0/9%. 2. Colloid- Ok why are they called plasma expanders What I think: Ok they are big molecules, increasing colloid osmotic pressure and sucking water from extracellular environment into blood vessels. But crystalloids should also then be considered plasma expanders because add the end, they also increase the fluid even if it is not as great as colloids. Thanks a lot in advance.
  4. Hello everyone, Haemosiderin definition says that it is a pigment that occurs when there is a local or systemic excess of iron. Does that mean excess iron deposition can cause haemosiderin pigment, I mean you don't alway need macrophages to eat Hb and make it, just iron is enough. Thanks
  5. What does myxoid change mean and how does it look like in microscope. I searched but I can't understand it. They say it is a mucoid change but I don't get it. Thanks
  6. Hello everyone, In metabolic acidosis, normal anion gap means cholride has increased causing hypercholaemic acidosis. My question is how can Chloride increase in metabolic acidosis, because in such a case chloride shift strongly favours chloride going inside the RBC, decreasing plasma chloride concentration. Thanks
  7. In leukaemia since immature white blood cells increase, do they overcrowd and decrease mature white blood cells. So does neutropenia and thrombocytopenia, leucocytopenia occur in leukaemia. Or does this deped on subtypes eg in some leukaemia B lymphocytes increase. Thanks
  8. Hello everyone, Ok my textbook says inhibition of transmitter release, vasoconstriction and more things. Now my question is what does inhibition of transmitter release mean. Since alpha 1 receptor is present on post synaptic membrane, and alpha 2 is present in pre synaptic membrane, does this mean alpha 2 actually controls the action of alpha 1 receptors by inhibiting neurotransmitter release. If that is the case why are there actions similar, shouldn't alpha 2 have oppposite actions of alpha 1 and actually decrease sympathetic activity. Also if you give a non selective alpha agonist which acts on both alpha 1 and alpha 2 receptors does vasodilation occur, how? Thank you
  9. Hello everyone, Ok Acetylchlone is released from postganglionic parasympathetic fibres and preganglionic nerve fibres of both sympathetic and parasympathetic nerves. It also cause muscle contraction in neuromuscular junction. So anticholinesterase would increase acetylcholine level---> Now what would be the effects of increased acetylcholine. Ok I understand parasympathetic activity would be increased, but if lots of acetylcholine is there in preganglionic nerve fibres of sympathetic fibres now, shouldn't sympathetic activity also increase. So what is the final effect.Also in anticholinesterase poisoning what are the clinical effects. I can't work it out because of my previous confusion. Is is like pupillary constriction and bronchoconstriction if parasympathetic predominates. Also increased muscle contraction. Also if I use anticholinesterase in combination with a competitive agonist and neuromuscular blocking agent such as tubocurarine would this decrease the action of tubercurine, because now it has compete with acetylcholine. Thanks for help in advance
  10. Hello everyone, Ok if a vessel was damaged, there is a platelet plug formation at the damaged site, then fibrin mesh forms, and red cells get stuck in that forming a blood clot in that area. Now in a test tube how does blood clot, does the same mechanism occur? how? Thanks
  11. Thank you both for your replies lol yes I needed it for drinking, I'm so stupid sometimes, this explains the mild stomach ache I had the other day.
  12. Hello everyone, Let's say I want cool sterilised water. If I get water from my tap and put it in the fridge does that sterilize the water, or do I have to boil it first and then put it in fridge. I'm just asking this from a pratical point of view, from sterilisation I don't mean complete removal of microorganisms, I'm just asking if I boil and put it in fridge am I wasting my time. Thanks
  13. Hello everyone, I'm very new to microbiology and does not have any background knowledge, so I have some simple questions on identifying different bacteria on agar plates. I have some questions and I have answered them the way I think. Please correct me where nessecary. 1. First of all what do all the lines in that plate mean, and how do you make a culture plate? Ok so you get the agar medium, and dip a bacterial loop into your sample eg CSF and then streak them on agar plate. So I'm thinking those lines are bacterial streaks. 2. Now how do I know there is growth in the culture plate and what is the difference between streaks and circles in the above pic? Do the circles mean bacterial colonies , then what do the streaks mean?I would like to see an agar plate where there is no bacterial growth, how does that agar plate look like, does it still have original streaks, or would it just be the agar without any streaks. 3. Ok this is a picture of proper streaking and growth of H. influenzae on a CAP. Now how do I differentiate this bacteria from other bacteria capable of growing on choclate agar. Also my orginal pic is proper streaking and growth of N. meningitidis on a BAP, same question prevails for this. 4. Are bacterias able to grow on all agar types or do they have specific ones. If anyone can answer thanks a lot in advance I'll post more pics depending on the replies.
  14. Tell me if I'm right. Endophillic - rest indoors Exophillic- rest outdoors Endophagic- bite indoors Exophagic -bite ourtdoors. Now my questions is in terms of fogging and indoor residual spraying do we do it by considering the resting habits of mosquitoes or biting habits. Also Culex quinquefasciatus rests indoor but indoor residual spraying is not useful. Why? Thanks
  15. For example candida fungus is a commensal in our skin and mucus membrane, but it can cause infection. So I'm asking why is it not causing infection in everyone, are the commensal form of candida harmless, so to get the infection we must inhale patogenic candida. Thanks
  16. Thanks for the reply CharonY But I'm still not sure. I mean if you belong to lance field group you must show beta haemolysis right, I mean all beta haemolysis bacteria are divided further by lance field groups. . So do you mean enterococcus show both. Thanks
  17. Previously it belonged to lance field group D, that means it must show beta haemolysis. But now it is classified in gamma group. I'm confused does enterococcus show beta or gama haemolysis or both. Thanks
  18. Hello, I'm reading tuberculosis pathology and I'm finding it hard to understand because my general poor knowledge in pathology. This is what I gathered from the reading. 1. Tubercle bacilli reach alveoli of lung and ingested by macrophages. 2. Then macrophages call other macrophages and T cells to wall off the bacilli in lung(forming a tubercle). Now my question is phagosome-lysosome fusion is inhibited by these bacilli, how can macrophages kill these bacilli. Now what is the difference between this tubercle and a granuloma. In a granuloma is it only macrophages that wall off the foreign substance or T cells as well. 3. After few weeks macrophages die releasing bacilli and forming caseous necrotic centre. Why does this cause caseous necrosis, is any necrosis in lung causes cheesy like appearance which is called caseous, is caseous necrosis always covered by granuloma. 4. Now when the tubercle/granuloma ruptures how do cavities form in lungs, and how does this allow for the infection to spread in lung? 6.Why is this a type IV hypesensitivity reaction? 5. What on earth is Ghon's complex? Thanks
  19. If u get infected with X serotype of dengue. And then you get infected again with Y serotype you get a severe infection. What is the exact pathology behind this. Also what happens if you get infected by X serotype again, do you get severe infection then as well. Thanks
  20. I'm not asking about the mechanism exactly, I know it is about evolution and survival of the fittest. But for example, when u take antibiotics for a viral infection. Why do they say bacteria will develp resistance? What bacteria are they referring to, the bacteria living inside your body (commensals), but they are not harmful so even if they are resistant why does it matter? Thanks for replies so far
  21. Hello everyone, Ok I have an infection due to to X bacteria. I take too much antibiotics. How does the X bacteria develop resistance then? For the commensals I can understand. I take antibiotics commensals die and the minority that are resistance will survive and multiply and now the new commensals would be resistant. But I'm asking about outside bacteria. Thanks
  22. Hello everyone, 1. My first question is when there is a wound, blood leaks and collects in the space as shown in the A diagram. Is it this blood that clots and fills the wound? 2. Now if the wound contracts a lot in C diagram, how can there be a scar left. Also epithelium always heals, so can not it hide the scar tissue. I mean why do we see darker scars in wounds. Isn't the epithelium over it unable to hide it? Thanks
  23. Hello everyone, This is the life cyle of H.diminuta. My question is the 4th point. It says ingestion of these arthropods/fleas by rats or humans. Do rats actually eat these fleas, or do the fleas live on rats's skin and suck their blood and via that infects rats, same for humans. Is it ingestion or do these fleas live on the skin of these individuals? This is H.nana. My question is about 1st point. Can humans get infected by eating infected eggs of rats, which are passed in their faeces? Thanks
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