what are the characteristics of a red cell and platelet?

Answer 1

Both are cells without a nucleus. They both are involved in formation of a clot.


Red Blood Cell (Erythrocyte)
This is a cell found in the human blood stream which is a biconcave disc approx 7microns in diameter. It has the properties of carrying oxygen in the blood, transporting it bound to the haemoglobin protein.

Platelet (Thrombocyte)
This is a cell found in the human blood stream which is a small disc about 2-3 microns in diameter. It arises from the Megakaryocytes. It is able to change the nature of its outer coat to become "sticky" and bind to other platelets and form a plug or clot when a blood vessel is damaged.

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Answer 2

Red blood cells are spherical shape and are red because O2 attaches to iron molecules producing the red color that gives it its name. Sorry I'm not sure what patelets look like, but I believe they are black small balls that swim in the blood along w/ the other cells in the blood. Platelets cover cuts that occur by breakage of the skin to keep germs out(most recognized as a scab) to allow the white blood cells to destroy germs that have already invaded the body through the cut.

Answer 3

RED CELL

Vertebrate erythrocytes

From left to right: erythrocyte, thrombocyte, leukocyte.Erythrocytes consist mainly of haemoglobin, a complex molecule containing heme groups whose iron atoms temporarily link to oxygen molecules in the lungs or gills and release them throughout the body. Oxygen can easily diffuse through the red blood cell's cell membrane. Haemoglobin also carries some of the waste product carbon dioxide back from the tissues. (In humans, less than 2% of the total oxygen, and most of the carbon dioxide, is held in solution in the blood plasma). A related compound, myoglobin, acts to store oxygen in muscle cells.

The color of erythrocytes is due to the heme group of haemoglobin. The blood plasma is straw-colored alone, but the red blood cells change colors due to the state of the hemoglobin: when combined with oxygen the resulting oxyhaemoglobin is scarlet and when oxygen has been released, the resulting deoxyhaemoglobin is darker, appearing bluish through the blood vessel walls.

The keeping of oxygen-binding proteins in cells (rather than having them dissolved in body fluid) was an important step in the evolution of vertebrates; it allows for less viscous blood and longer transport ways of oxygen.


[edit] Mammalian erythrocytes
Erythrocytes in mammals are anucleate when mature, meaning that they lack a cell nucleus and thus have no DNA. In comparison, the erythrocytes of nearly all other vertebrates have nuclei; the only known exception is salamanders of the Batrachoseps genus. Mammalian erythrocytes also lose their other organelles including their mitochondria and produce energy by fermentation, via glycolysis of glucose followed by lactic acid production. Furthermore, red cells do not have an insulin receptor and thus glucose uptake is not regulated by insulin. As a result of the lack of nucleus and organelles, the cells cannot produce new structural or repair proteins or enzymes and their lifespan is limited.

Mammalian erythrocytes are biconcave disks: flattened and depressed in the center, with a dumb-bell shaped cross section. This shape (as well as the loss of organelles and nucleus) optimizes the cell for the exchange of oxygen with its surroundings. The cells are flexible so as to fit through tiny capillaries, where they release their oxygen load. Erythrocytes are circular, except in the camel family Camelidae, where they are oval.

In large blood vessels, red blood cells sometimes occur as a stack, flat side next to flat side. This is known as rouleaux formation, and it occurs more often if the levels of certain serum proteins are elevated, as for instance during inflammation.

The spleen acts as a reservoir of red blood cells, but this effect is somewhat limited in humans. In some other mammals such as dogs and horses, the spleen sequesters large numbers of red blood cells which are dumped into the blood during times of exertion stress, yielding a higher oxygen transport capacity.


Erythrocytes: (a) seen from surface; (b) in profile, forming rouleaux; (c) rendered spherical by water; (d) rendered crenate by salt. (c) and (d) do not normally occur in the body.
[edit] Human erythrocytes
The diameter of a typical human erythrocyte disk is much smaller than most other human cells. A typical erythrocyte contains about 270 million hemoglobin molecules, with each carrying four heme groups.

Adult humans have roughly 2–3 × 1013 red blood cells at any given time (women have about 4 million to 5 million erythrocytes per cubic millimeter (microliter) of blood and men about 5 million to 6 million; people living at high altitudes with low oxygen tension will have more). Red blood cells are thus much more common than the other blood particles: There are about 4,000–11,000 white blood cells and about 150,000–400,000 platelets in a cubic millimeter of human blood. The red blood cells store collectively about 3.5 grams of iron, more than five times the iron stored by all the other tissues combined.


[edit] Life cycle
The process by which red blood cells are produced is called erythropoiesis. Erythrocytes are continuously being produced in the red bone marrow of large bones, at a rate of about 2 million per second. (In the embryo, the liver is the main site of red blood cell production.) The production can be stimulated by the hormone erythropoietin (EPO), synthesised by the kidney; which is used for doping in sports. Just before and after leaving the bone marrow, they are known as reticulocytes which comprise about 1% of circulating red blood cells. Erythrocytes develop from stem cells through reticuloctyes to mature erythrocytes in about 7 days and live a total of about 120 days. The aging cells swell up to a sphere-like shape and are engulfed by phagocytes, destroyed and their materials are released into the blood. The main sites of destruction are the liver and the spleen. The heme constituent of hemoglobin is eventually excreted as bilirubin.


[edit] Proteins
There are two main types of proteins on the surface:

Band 3
Glycophorins such as glycophorin C
The blood types of humans are due to variations in surface glycoproteins of erythrocytes.


[edit] Separation
Red blood cells can be separated from blood plasma by centrifugation. During plasma donation, the red blood cells are pumped back into the body right away, and the plasma is collected. Some athletes have tried to improve their performance by doping their blood: First about 1 litre of their blood is extracted, then the red blood cells are isolated, frozen and stored, to be reinjected shortly before the competition. (Red blood cells can be conserved for 5 weeks at −79 °C.) This practice is hard to detect but may endanger the human cardiovascular system which is not equipped to deal with blood of the resulting higher viscosity.


[edit] Diseases and diagnostic tools

Affected by Sickle-cell disease, red blood cells alter shape and threaten to damage internal organs.Blood diseases involving the red blood cells include:

Anemias (or anaemias) are diseases characterized by low oxygen transport capacity of the blood, because of low red cell count or some abnormality of the red blood cells or the hemoglobin.
Iron deficiency anemia is the most common anemia; it occurs when the dietary intake or absorption of iron is insufficient, and hemoglobin, which contains iron, cannot be formed
Sickle-cell disease is a genetic disease that results in abnormal hemoglobin molecules. When these release their oxygen load in the tissues, they become insoluble, leading to mis-shaped red blood cells. These sickle shaped red cells are rigid and cause blood vessel blockage, pain, strokes, and other tissue damage.
Thalassemia is a genetic disease that results in the production of an abnormal ratio of hemoglobin subunits.
Spherocytosis is a genetic disease that causes a defect in the red blood cell's cytoskeleton, causing the red blood cells to be small, sphere-shaped, and fragile instead of donut-shaped and flexible.
Pernicious anemia is an autoimmune disease wherein the body lacks intrinsic factor, required to absorb vitamin B12 from food. Vitamin B12 is needed for the production of hemoglobin.
Aplastic anemia is caused by the inability of the bone marrow to produce blood cells.
Pure red cell aplasia is caused by the inabilty of the bone marrow to produce only red blood cells.
Hemolysis is the general term for excessive breakdown of red blood cells. It can have several causes.
The malaria parasite spends part of its life-cycle in red blood cells, feeds on their hemoglobin and then breaks them apart, causing fever. Both sickle-cell disease and thalassemia are more common in malaria areas, because these mutations convey some protection against the parasite.
Polycythemias (or erythrocytoses) are diseases characterized by a surplus of red blood cells. The increased viscosity of the blood can cause a number of symptoms.
In polycythemia vera the increased number of red blood cells results from an abnormality in the bone marrow and releases through the women's vagina which causes a menstrual period.
Several microangiopathic diseases, including disseminated intravascular coagulation and thrombotic microangiopathies, present with pathognomonic (diagnostic) RBC fragments called schistocytes. These pathologies generate fibrin strands that sever RBCs as they try to move past a thrombus.
Several blood tests involve red blood cells, including the RBC count (the number of red blood cells per volume of blood) and the hematocrit (percentage of blood volume occupied by red blood cells). The blood type needs to be determined to prepare for a blood transfusion or an organ transplantation.


[edit] History
In 1658, the Dutch biologist Jan Swammerdam was the first to describe red blood cells. He had used an early microscope


PLATELETS

Production
Platelets are produced in the bone marrow; the progenitor cell for platelets is the megakaryocyte. It is about twelve times larger than an erythrocyte, possesses a lobed nucleus and sheds platelets into the circulation. Thrombopoietin (c-mpl ligand) is a hormone, mainly produced by the liver, that stimulates platelet production. It is bound to circulating platelets; if platelet levels are adequate, serum levels remain low. If the platelet count is decreased, more thrombopoeitin circulates freely and increases marrow production.


[edit] Circulation
The circulating life of a platelet is 8–10 days. After this it is sequestered in the spleen. Decreased function (or absence) of the spleen may increase platelet counts, while hypersplenism (overactivity of the spleen, e.g. in Gaucher's disease, leukemia, and cirrhosis) may lead to increased elimination and hence low platelet counts.


[edit] Function
Platelets are activated when brought into contact with collagen (which is exposed when the endothelial blood vessel lining is damaged), thrombin (primarily through PAR-1), ADP, receptors expressed on white blood cells or the endothelial cells of the blood vessels, a negatively charged surface (e.g., glass), or several other activating factors. Once activated, they release a number of different coagulation factors and platelet activating factors. Platelet activation further results in the scramblase-mediated transport of negatively charged phospholipids to the platelet surface. These phospholipids provide a catalytic surface (with the charge provided by phosphatidylserine and phosphatidylethanolamine) for the tenase and prothrombinase complexes. The platelets adhere to each other via adhesion receptors or integrins, and to the endothelial cells in the wall of the blood vessel forming a haemostatic plug in conjunction with fibrin. The high concentration of myosin and actin filaments in platelets are stimulated to contract during aggregation, further reinforcing the plug. The most common platelet adhesion receptor is glycoprotein (GP) IIb/IIIa; this is a calcium-dependent receptor for fibrinogen, fibronectin, vitronectin, thrombospondin and von Willebrand factor (vWF). Other receptors include GPIb-V-IX complex (vWF) and GPVI (collagen)


[edit] Activators

From left to right: erythrocyte, thrombocyte, leukocyte.There are many known platelet activators. They include

Collagen, which is exposed when endothelial blood vessel lining is damaged and binds to its receptors GPVI and alpha2b-beta1 on the platelet surface;
von Willebrand factor which circulates in the blood and binds to its receptor GPIb-IX-V on the platelet surface.
Thrombin, primarily through cleavage of the extracellular domain of PAR1 and PAR4;
Thromboxane A2 (TxA2), which binds to its receptor, TP;
ADP through an action on its two cell surface receptors, P2Y1 and P2Y12.
Adrenaline that activates its receptor (alpha 2) on the platelet surface. Note that adrenaline will also activate an inhibitory beta2 receptor on platelets, but this effect is normally masked by its predominant effect on alpha 2.
Serotonin that activates its receptor (5HT-2c) on the platelet surface.
Human neutrophil elastase (HNE) cleaves the αIIbβ3 integrin on the platelet surface;
P-selectin, which binds to PSGL-1 on endothelial cells and white blood cells and which is normally exposed on the surface of platelets following initial activation by other activators.

[edit] Inhibitors
Prostacyclin opposes the actions of most if not all platelet agonists by increasing intracellular cAMP levels
Adenosine through an action on its cell surface receptor (A2 receptor) by increasing intracellular cAMP levels
Nitric oxide released by the endothelium (and platelets themselves in some instances)
Clotting factors II, IX, X, XI, XII
Nucleotidases such as CD39 ecto-ADP'ase break down ADP

[edit] Drugs that inhibit platelet function
Aspirin inhibits cyclooxygenase-1, preventing positive feedback
Clopidogrel inhibits ADP receptors
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis
Abciximab blocks fibrinogen receptors
β-lactam antibiotics alteration of agonist receptors
Quinidine calcium channel blocker

[edit] Role in disease

[edit] High and low counts
A normal platelet count in a healthy person is between 150,000 and 400,000 per mm³ of blood (150–400 x 109/L). 95% of healthy people will have platelet counts in this range. Some will have statistically abnormal platelet counts while having no abnormality, although the likelihood increases if the platelet count is either very low or very high.

Both thrombocytopenia (or thrombopenia) and thrombocytosis may present with coagulation problems. Generally, low platelet counts increase bleeding risks (although there are exceptions, e.g. immune heparin-induced thrombocytopenia) and thrombocytosis (high counts) may lead to thrombosis (although this is mainly when the elevated count is due to myeloproliferative disorder).

Low platelet counts are generally not corrected by transfusion unless the patient is bleeding or the count has fallen below 5 x 109/L; it is contraindicated in thrombotic thrombocopenic purpura (TTP) as it fuels the coagulopathy. In patients having surgery, a level below 50 x 109/L) is associated with abnormal surgical bleeding, and regional anaesthetic procedures such as epidurals are avoided for levels below 80-100.

Normal platelet counts are not a guarantee of adequate function. In some states the platelets, while being adequate in number, are dysfunctional. For instance, aspirin irreversibly disrupts platelet function by inhibiting cyclooxygenase-1 (COX1), and hence normal hemostasis; normal platelet function may not return until the aspirin has ceased and all the affected platelets have been replaced by new ones, which can take over a week. Similarly, uremia (a consequence of renal failure) leads to platelet dysfunction that may be ameliorated by the administration of desmopressin.


[edit] Diseases
Disorders leading to a reduced platelet count:

Thrombocytopenia
Idiopathic thrombocytopenic purpura - also known as immune thrombocytopenic purpura (ITP)
Thrombotic thrombocytopenic purpura
Drug-induced thrombocytopenia, e.g. heparin-induced thrombocytopenia (HIT)
Gaucher's disease
Aplastic anemia
Alloimmune disorders

Fetomaternal alloimmune thrombocytopenia
Some transfusion reactions
Disorders leading to platelet dysfunction or reduced count:

HELLP syndrome
Hemolytic-uremic syndrome
Chemotherapy
Dengue
Disorders featuring an elevated count:

Thrombocytosis, including benign essential thrombocytosis (elevated counts, either reactive or as an expression of myeloproliferative disease); may feature dysfunctional platelets
Disorders of platelet adhesion or aggregation:

Bernard-Soulier syndrome
Glanzmann's thrombasthenia
Scott's syndrome
von Willebrand disease
Hermansky-Pudlak Syndrome
Disorders of platelet metabolism

Decreased cyclooxygenase activity, induced or congenital
Storage pool defects, acquired or congenital
Disorders that compromise platelet function:

Haemophilia

[edit] Discovery
Brewer[1] traced the history of the discovery of the platelet. Although red blood cells had been known since van Leeuwenhoek, it was the German anatomist Max Schultze (1825-1874) who first offered a description of the platelet in his newly founded journal Archiv für mikroscopische Anatomie[2]. He describes "spherules" much smaller than red blood cells that are occasionally clumped and may participate in collections of fibrous material. He recommends further study of the findings.

Giulio Bizzozero (1846-1901), building on Schultze's findings, used "living circulation" to study blood cells of amphibians microscopically in vivo. One of his findings was the fact that platelets clump at the site of blood vessel injury, which precedes the formation of a blood clot. This observation confirmed the role of platelets in coagulation[3].