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chinkins tentres

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Dear Dr Sufyan,

What is the significance of basophillic stippling and target cells?

Thank you.

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1) Will patient with lymphoma present with leukopenia?

2) Does Alkaline phosphatase value increase or decrease in polycythemia vera ?

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Q: What is meant by clotting factors are 'consumed' when clotting occurs? (e.g. factor V and VIII) and how does over consumption of factors lead to DIC?

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Q: What is meant by clotting factors are 'consumed' when clotting occurs? (e.g. factor V and VIII) and how does over consumption of factors lead to DIC?

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Does "trauma to the blood" that activates the intrinsic pathway mean activation due to diseases like bacteremia? 

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Does "trauma to the blood" that activates the intrinsic pathway mean activation due to diseases like bacteremia? 

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It has long been known that blood often coagulates during sepsis or bacterial infections, but this has generally been regarded as a host's immune and inflammatory response. It also has been known that bacteria can activate factors that precede coagulation, probably through the intrinsic pathway.

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 Is prothrombin activator the same as prothrombinase?

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 Is prothrombin activator the same as prothrombinase?

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Yes.

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If nociception and thermoception of the spinothalamic tract are important in avoiding dangerous situations, why does the tract still relay information at a slower velocity than the discriminative touch relay of the dorsal column medial lemniscus tract?

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If nociception and thermoception of the spinothalamic tract are important in avoiding dangerous situations, why does the tract still relay information at a slower velocity than the discriminative touch relay of the dorsal column medial lemniscus tract?

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It is not that slow, it's just 'slower' in comparison to dorsal column. Reflex activity occurs instantly, its only the conscious perception which is slightly delayed.
In addition, sensory signals carried through dorsal column have high convergence and better localization.

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B9/B12 deficiency leads to macrocytosis due to nascent erythroblasts being constantly stuck in the G1 cell cycle phase. However, how does iron deficiency alone lead to microcytosis?

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B9/B12 deficiency leads to macrocytosis due to nascent erythroblasts being constantly stuck in the G1 cell cycle phase. However, how does iron deficiency alone lead to microcytosis?

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As haemoglobin is the main content of RBCs, inability to form haemoglobin leads to smaller RBCs (microcytic anaemia (low MCV)). The RBCs are usually hypochromic as well, meaning that they appear paler than usual (low MCHC). Thus, iron deficiency typically presents as 'microcytic hypochromic anaemia'

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Dr, does low platelet count caused one of the symptoms of Dengue Fever which is BLEEDING UNDER THE SKIN? Can you explain more on how the bite of a mosquito can cause this?

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Dr, does low platelet count caused one of the symptoms of Dengue Fever which is BLEEDING UNDER THE SKIN? Can you explain more on how the bite of a mosquito can cause this?

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Yes, Dengue fever can lead to low platelet count.
It's not just a mosquito bite, it's an injection of 'Dengue Virus'.
Check the WHO website for more info on Dengue:
http://www.who.int/mediacentre/factsheets/fs117/en/

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Sir, What is the difference between the intrinsic and the extrinsic pathway? and What are the cases in which a fibrous growth occurs? are plasma proteins and clotting factors the same? Thank you

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Sir, What is the difference between the intrinsic and the extrinsic pathway? and What are the cases in which a fibrous growth occurs? are plasma proteins and clotting factors the same? Thank you

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Both are coagulation pathways, but having different starting points, involving different clotting proteins and culminating at the final common pathway (i.e; activation of Prothrombin activator). Usually both are activated when there's an injury to blood vessel. Extrinsic is more robust than intrinsic.

Fibrous growth occurs, if the blood vessel wall can't be regenerated.

Plasma proteins is a very wide term (includes many types of proteins). Clotting factors are a group of proteins present in plasma.

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Blood coagulation. Sir, how are phospholipids utilized in blood coagulation?Is the dendritic state and the contracted state if platelets the same?

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Blood coagulation. Sir, how are phospholipids utilized in blood coagulation?Is the dendritic state and the contracted state if platelets the same?

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Significance of phospholipids in the haemostatic process is an area of active research. What is known is that plasma membranes of activated platelets provide a catalytic phospholipid surface on which certain clotting factors can be assembled. Plays an important role in intrinsic pathway.
Moreover, tissue-factor, which plays a key role in blood coagulation by initiating the extrinsic coagulation pathway, requires the presence of phospholipids for optimal biological activity.

Dendritic shape is the early stage of platelet activation (contraction).

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Hello Dr, I just wanted to ask: during your presentation on clot formation you said that in case of an injury, there is vasoconstriction to prevent excessive blood flow out of the vessel, however in our consequent lecture on acute inflammation we were told that in case of an injury, there is vasodilation because the blood has to deliver substances required for healing - which is which?

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Hello Dr, I just wanted to ask: during your presentation on clot formation you said that in case of an injury, there is vasoconstriction to prevent excessive blood flow out of the vessel, however in our consequent lecture on acute inflammation we were told that in case of an injury, there is vasodilation because the blood has to deliver substances required for healing - which is which?

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These are two different things. Local vasoconstriction occurs at and around the site of vessel injury (to reduce blood loss). In inflammatory response (which could be triggered by many factors, one of these could be vessel injury) the blood vessels supplying the affected area dilate to allow for delivery of cells and chemicals. But remember, these two responses could be happening next to each other.

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Q: What is the difference between hypochromic and microcytic anaemia ? thank you Dr.

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Q: What is the difference between hypochromic and microcytic anaemia ? thank you Dr.

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It's simple. Microcytic means RBCs are smaller in size (low MCV). Hypochromic means their haemoglobin content is low (low MCH). These two may co-exist. Iron deficiency anaemia usually presents as Microcytic Hypochromic.

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Q: What is the function of microtubules and tubular system in platelets? Thank you Dr. 

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Q: What is the function of microtubules and tubular system in platelets? Thank you Dr. 

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The process of megakaryocyte maturation and the formation of pro-platelets are essential steps in the production of mature platelets and both depend heavily on the actin and microtubule cytoskeletons.
Understanding the key molecules and signalling pathways that regulate actin and microtubule crosstalk is important for the development of in vitro platelet production which will help to treat thrombocytopenia as well as produce model systems for studying platelet-associated disorders.
You can read the attached article if interested...

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Q: In the lecture of blood coagulation, you mentioned the positive feedback effect of thrombin on Factor V prevent the clot from spreading in the blood vessel. But isn't the positive feedback mechanism promotes the formation of clot while the negative feedback prevents the formation of clot? Thank you

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Q: In the lecture of blood coagulation, you mentioned the positive feedback effect of thrombin on Factor V prevent the clot from spreading in the blood vessel. But isn't the positive feedback mechanism promotes the formation of clot while the negative feedback prevents the formation of clot? Thank you

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Positive feedback of thrombin on it's own activation leads to an explosive reaction in the area where clot is forming. The anti-thrombins are also activated simultaneously which prevent the clot from becoming too big and extending beyond the vessel injury site. So, it is the balance which matters... positive feedback at the site of clot formation and anti-thrombins around the clot forming area

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Q: In end arteries, how does the blood flow? The blood have to be drained back to the vein right?

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Q: In end arteries, how does the blood flow? The blood have to be drained back to the vein right?

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Also known as terminal artery. It is an artery that is the only supply of oxygenated blood to a particular area or tissue.
The end artery will break down into arterioles and capillaries, which will then join to form venules and veins (the usual pattern).
Usually arteries form anastomoses to provide alternative supplies of fresh blood. This is not the case with end arteries.
Examples of an end artery include the splenic artery that supplies the spleen and the renal artery that supplies the kidneys.

Thus, in summary, an end artery has insufficient anastomoses to maintain viability of the tissue supplied if occlusion of the artery occurs.

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Q: In the prevention of blood clotting, why is the inhibitor of tissue plasminogen activator be inactivated by protein c. 

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Q: In the prevention of blood clotting, why is the inhibitor of tissue plasminogen activator be inactivated by protein c. 

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It's teamwork among anti-coagulant pathways. Protein C is member of the anti-coagulant pathway. Plasmin activation is also an anti-coagulant pathway (will lead to clot dissolution).

Statement that “Protein C inactivates inhibitors of plasminogen activators” means that Protein C will allow Plasmin pathway to go ahead. In simple terms it shows the cooperation among anti-coagulant pathways.

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Q: What are the differences between mast cells and basophils?

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Q: What are the differences between mast cells and basophils?

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Essentially, not much. The Mast cells are very similar to Basophils in both appearance and functions. In blood, only basophils are found. In tissues, both basophils and mast cells are found. Thus, it is postulated that basophils transform into mast cells after leaving the blood circulation.

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Q: How do red blood cells act as acid-base buffer?

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Q: How do red blood cells act as acid-base buffer?

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Haemoglobin is an excellent intracellular acid-base buffer.Histidine residues in haemoglobin can accept protons, thus acting as buffer by removing excess H+

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Q: How does tissue necrosis cause the increase of neutrophils?

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Q: How does tissue necrosis cause the increase of neutrophils?

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Tissue necrosis leads to accumulation of debris. Neutrophils get attracted to inflammatory tissue and also to necrotic tissue. In both cases their job is to clear the area by phagocytozing the debris and thus, limiting the spread of inflammation to surrounding tissues.

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Generally speaking, the immune system comprises of many biological structures and processes that protects against disease. Immune system should be able to detect and attack a wide variety of disease-causing agents, and distinguish them from the “self.”
Immune system can be classified into two sub-categories: the innate immune system and the adaptive immune system.:
INNATE immune system is built-in, doesn’t require learning and activation. Includes skin (the barrier), inflammation, complement proteins in the blood, phagocytes like macrophages and neutrophils, etc…
ADAPTIVE immune system is activated only upon exposure to a specific pathogen (containing “antigens”, which are recognized as “non-self”). Major members of this system are T and B lymphocytes. After first exposure to an antigen, B and T lymphocytes are formed that are specific against the antigen and upon subsequent exposures to this antigen, lymphocytes come into action very quickly and launch an attack against that specific antigen.

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Whether absorbed from intestine (after digestion of food) or released by macrophages (after processing of Haemoglobin), Iron is transported in blood bound to a protein called “Transferrin”.
Our body can store excess iron in the liver, bone marrow, and skeletal muscles bound to a protein called “Ferritin”.