Why some HbF is always found in patients with Sickle cell anemia ?
539915
Hbf, is the type oh Hemoglobin that's supposed to be found \n(In high percentages) in fetuses, hence the "F", and almost 0% in adults. Sickle cell anemia is inherited as an autosomal (meaning that the gene is not linked to a sex chromosome) recessive condition whereas sickle cell trait is inherited as an autosomal dominant trait. This means that the gene can be passed on from a parent carrying it to male and female children. In order for sickle cell anemia to occur, a sickle cell gene must be inherited from both the mother and the father, so that the child has two sickle cell genes. \n\nThe inheritance of just one sickle gene is called sickle cell trait or the "carrier" state. Sickle cell trait does not cause sickle cell anemia. Persons with sickle cell trait usually do not have many symptoms of disease and have normal hospitalization rates and life expectancies.It's supposed to carry both recessive genes to have the disease.\nSickling of the red blood cells in patients with sickle cell anemia results in cells of abnormal shape and flexibility. The sickling is promoted by conditions which are associated with low oxygen levels, increased acidity, or low volume (dehydration) of the blood. These conditions can occur as a result of injury to the body's tissues, dehydrating states, or anesthesia. \n\n This disease occurs exclusively in Black people for an unknown reason.
928157
You can write on Sickle Cell Anemia...
470656
My boyfriend has sickle cell anemia and I'm learning how to deal with it and learn about especially considering we don't have medicare for him to get prescriptions.  From what I've read, the anemia does not affect your diet but your diet can affect the anemia or at least its symptoms.  For example, those with sickle cell anemia have a reduction in oxygen at times and therefore, it is very important to always drink plenty like 10 or more glasses of water a day.  Also, fruits and vegetable are often aids in oxidation and help to keep the body healthy.  Exercise, not smoking or drinking alcohol, and staying away from agitates like dust are also important.
878022
If your anemic it means you don't have enough red blood cells. Anemia can be common, especially for women that are menstrating once a month, or serious. I was anemic when I was a kid, but I out gew it with proper nutrition and vitamins.\n\nYou need to eat foods rich in iron or take an iron supplement. Maybe your doctor gave you a prescription. \n\nHere are some other resources for you.\n\nhttp://www.kidshealth.org/parent/medical/heart/anemia.
426999
This depends on the type of surgery and the comfort level of the surgeon.  In some surgeries, you are expected to lose more blood than others, so your hemoglobin should likely be higher.  Other surgeries might result in no blood loss at all, so it might be okay to do it with a slightly low hemoglobin.  It is hard to give you a solid number, because some surgeons I work with might do an knee replacement in a person with a hemoglobin of 10, while others would never do that procedure unless their hemoglobin was above 11.5 or so.  Also, the normal hemoglobin level is different for men and women, so these numbers are just hypothetical examples.
152924
Sickle cell trait/disease is an example of heterozygote advantage, in that homozygous recessive individuals (people with two sickle cell genes) have sickle cell anemia, which is bad, but people who are heterozygous for the gene (one normal and one mutant) have sickle cell trait, which provides resistance against malaria, which is good.\n\nAnother example of heterozygote advantage is cystic fibrosis.  As you probably know, cystic fibrosis is a fairly nasty recessive genetic disorder.  People with the recessive condition typically have a life expectancy of only a few years.  However, the heterozygous condition provides some defense against diseases that invovle loss of body fluid (typically diarrhea).  Cystic fibrosis is relatively common among people of European descent because carriers of the allele were more likely to survive cholera, which was a problem throughout European history.\n\nThere is also some evidence to suggest that the heterozygous carriers of the Tay-Sachs allele may have increased resistance to tuberculosis, although this has yet to be confirmed.
1025351
oh definitely. People with sickle cell traits are just as good as people with AA if not better.The trait was acquired to better protect from malaria................. Besides people with sickle cell do get fat. I know a lot of people with the traits who are fat.
571244
I work at a blood bank and I have never seen anything get past our lab it is possible but rare. Most hospitals make sure that the centers that they receive blood from has excellent track records.
419261
When a Full Blood Count (FBC) is requested the haematology analysers count the numbers of all the different blood cells - white cells, red cells and platelets. It also measures the size and shape of the cells. In healthy control patients the red cells will all be similar in size and shape, but in patients who are recovering from an anaemia, blood loss, or have received a recent blood transfusion or in patients with abnormalities of the red blood cells (thalassemia, sickle cell) the red cells can vary in size. This is measured by the Red Cell Distribution Width (RDW). So it is a variation in size of the red cells. If a patient has been anaemic, a raised RDW would be considered a good response to treatment as new healthy sized cells are being produced.
13809
Blood types are not evenly distributed throughout the human population. O+ is the most common, AB- is the rarest. There are also variations in blood-type distribution within human subpopulations. The figures given here are for people of European descent.\n\nType Frequency \nO+ 38% \nA+ 34% \nB+ 9% \nO- 7% \nA- 6% \nAB+ 3% \nB- 2% \nAB- 1%
394437
Alpha (α) thalassemias\nThe alpha thalassemias involve the genes HBA1 (OMIM 141800) and HBA2 (OMIM 141850), inherited in an autosomal co-dominant fashion. α thalassemias result in excess β chain production in adults and excess γ chains in newborns. The excess β chains form unstable tetramers that have abnormal oxygen dissociation curves.\n\nThere are four genetic loci for α globin. The more of these loci that are deleted or affected by mutation, the more severe will be the manifestations of the disease:\n\nIf all four loci are affected, the fetus cannot live once outside the uterus: most such infants are dead at birth with hydrops fetalis, and those who are born alive die shortly after birth. They are edematous and have little circulating hemoglobin, and the hemoglobin that is present is all tetrameric γ chains (hemoglobin Barts). Usually, this involves homozygous inheritance of an alpha thalassemia trait, type 1. \nIf three loci are affected, Hemoglobin H disease results. Two unstable hemoglobins are present in the blood, both hemoglobin Barts (tetrameric γ chains) and hemoglobin H (tetrameric β chains). There is a microcytic hypochromic anemia with target cells and Heinz bodies (precipitated Hb H) on the peripheral blood smear. The disease may first be noticed in childhood or in early adult life, when the anemia and splenomegaly are noted. This is usually due to compound heterozygous inheritance of alpha thalassemia type 1 and type 2 traits. \nIf two of the four α loci are affected, alpha thalassemia trait, type 1 results. Two α loci permit nearly normal erythropoiesis, though there is a mild microcytic hypochromic anemia. There is a high prevalence (about 30%) of deletion of one of the two α loci on chromosomes of people of recent African origin, and so the inheritance of two such chromosomes is not uncommon. The disease in this form can be mistaken for iron deficiency anemia and treated inappropriately with iron. Two modes of alpha thalassemia trait, type 1 has been noted. One involves cis deletion of two alpha loci on the same chromosome; another involves trans deletion of allelelic genes on homologous chromosomes (no. 16). \nIf one of the four α loci is affected, alpha minor or alpha+ thalassemia trait or alpha thalassemia trait, type 2 results and there is minimal effect. Three α-globin loci are enough to permit normal hemoglobin production, and there is no anemia or hypochromia in these people. They have been called α thalassemia carriers. \n[edit]\nBeta (β) thalassemias\nBeta thalassemia is due to mutations in the HBB gene on chromosome 11 (OMIM 141900), also inherited in an autosomal co-dominant fashion. In β thalassemia, excess α chains are produced, but these do not form tetramers: rather, they bind to the red blood cell membranes producing membrane damage, and at high concentrations have the tendency to form toxic aggregates. The severity of the damage depends on the nature of the mutation. Some mutations (βo) prevent any formation of β chains; others (β+) allow some β chain formation to occur. Recently, increasing reports suggest that upto 5% of patients with beta-thalassemias produce fetal hemoglobin (HbF), and use of hydroxyurea also has a tendency to increase the production of HbF, by as yet unexplained mechanisms.\n\nAny given individual has two β globin alleles:\n\nIf both have thalassemia mutations, a severe microcytic, hypochromic anemia called β thalassemia major or Cooley's anemia results. Untreated, this results in death before age twenty: treatment consists of periodic blood transfusion; splenectomy if splenomegaly is present, and treatment of transfusion-caused iron overload. Cure is possible by bone marrow transplantation. \nIf only one β globin allele bears a mutation, β thalassemia minor results (sometimes referred to as β thalassemia trait). This is a mild anemia with microcytosis. Symptoms include weakness and fatigue - in most cases β thalassemia minor may be asym
585730
What causes sickle cell disease? \n\nSickle cell disease, a group of blood disorders, is inherited, passed from parent to child. Children with sickle cell disease have two defective genes, one from each parent. \n\nA child born with sickle cell trait inherited one defective gene from one parent, and a normal gene from the other parent. These children don't have sickle cell disease but are carriers of the defective gene and may pass it on to their children.\n\nHow is it treated? \n\nThe best possible treatment for a person with sickle cell disease is a partnership between the affected family and a team of health professionals. Successful treatment requires: \n\nEarly diagnosis using infant screening (shortly after birth). \nPreventive antibiotic treatment and immunizations starting at 3 to 4 months of age. \nAn aggressive pain treatment plan. \nConsultation with doctors skilled in the care of patients with sickle cell disease. In severe cases, doctors may recommend regular blood transfusions, drug treatment with hydroxyurea, or (rarely) bone marrow transplant.
497817
they do have a nucleus when they are still being formed in the red bone marrow, but once they are mature enough the nucleus is excluded so that there is maximum room to store-hole hemoglobin in the rbc.  less than 1% of rbcs are found in the cirulation-blood.  If more than that,it is indicative of disease and needs to be treated since rbcs with nucleii can't carry oxygen, are too big,and get squished-damaged in the capillaries.  Without a nucleus they can fit single file and go thru without getting too beat up-bruised and live their usual life of 120 days.
643756
Sickle cell anemia? I dont know what the question is...or what disease you are talking about.
724539
Sickle-cell disease is a general term for a group of genetic disorders caused by sickle hemoglobin (HbS). In many forms of the disease, the red blood cells change shape upon deoxygenation because of polymerization of the abnormal sickle hemoglobin.\n\nHbN and HbS are alleles which are alternative forms of gene. All humans have 2 alleles for every gene (one from each parent).\nNormal healthy people have HbN HbN (HbN=normal hemoglobin).\nCarriers have HbN HbS (HbS=sickle hemogloblin).\nPeople suffering from sickle cell anaemia have HbS HbS. \n\nIn people heterozygous for HbS (carriers), the polymerization problems are minor, hence they don't suffer the effects of sickle cell anaemia. In people homozygous for HbS, the presence of long chain polymers of HbS distort the shape of the red blood cell, from a smooth donut-like shape to ragged and full of spikes, making it fragile and susceptible to breaking within capillaries. Carriers only have symptoms if they are deprived of oxygen (for example, while climbing a mountain) or while severely dehydrated.\n\nThe sufferers of the illness have a reduced life span. It is believed that carriers (sickle cell trait) are relatively resistant to malaria. Since the gene is incompletely recessive, carriers have a few sickle red blood cells at all times, not enough to cause symptoms, but enough to give resistance to malaria. Because of this, heterozygotes (HbS HbN) have a higher fitness than either of the homozygotes (HbN HbN & HbS HbS). This is known as heterozygote advantage. Those with HbN HbN are susceptible to malaria while those with HbS HbS will suffer from sickle cell anaemia.  \n\nThe malaria parasite has a complex life cycle and spends part of it in red blood cells. In a carrier, the presence of the malaria parasite causes the red blood cell to rupture, making the plasmodium unable to reproduce. Further, the polymerization of Hb affects the ability of the parasite to digest Hb in the first place. Therefore, in areas where malaria is a problem, people's chances of survival actually increase if they carry sickle cell anaemia.\n\nDue to the above phenomenon, the illness is still prevalent, especially among people with recent ancestry in malaria-stricken areas, such as Africa, the Mediterranean, India and the Middle East. In fact, sickle-cell anemia is the most common genetic disorder among African Americans; about 1 in every 12 is a carrier.
730231
The blood treats the problem..eg anaemia is lack of quality red bloods cells-> -> blood given, now patient has good quality blood cells, for a short while anyway...;
254574
Common signs include:\n\npaleness \nyellow eyes/skin \ngrowth retardation \nTests commonly performed to diagnose and monitor patients with sickle cell anemia include:\n\nComplete blood count (CBC) \nHemoglobin electrophoresis \nSickle cell test \nPatients with sickle cell may have abnormal results on certain tests, as follows:\n\nperipheral smear displaying sickle cells \nurinary casts or blood in the urine \nHemoglobin; serum decreased \nelevated bilirubin \nhigh white blood cell count \nelevated serum potassium \nelevated serum creatinine \nblood oxygen saturation may be decreased \nCT scan or MRI can display strokes in certain circumstances