Health is generally said to be wealth. To acquire this wealth either for personal or national needs, one require to be healthy hence the need for adequate Medicare especially in the area of diagnosis. Since there is a good relationship between the job output and the health of the workers, a good Medicare is vital.

Unfortunately, in most developing notions including Nigeria, adequate Medicare is lacking due to low standard of technologies know how and manual handling of most medical problem. As observed by Iyiama H.C and Chukwu. D. C. very often, people in developing countries who are critically ill are rushed abroad for special treatment because it is felt that medical facilities at home is inadequate. This is simply because at home is inadequate. This is simply because computer aided Medicare has become a reality in many developed countries. It is also a known fact that the production of qualified medical doctors, medical lab. Scientists and other medical personnel is on the increase but this is not enough to meet the health needs of the increasing population. The return of patients to a doctors, samples to lab scientist is still high. This situation creates problem, because proper and adequate medical attention to patients is far fetched.


It has been observed that to receive medical treatment in most of our hospitals (or private laboratories) the patients queue up for several hours from one unit of the hospital to another. Starting from obtaining a new hospital folder or retrieving an old one before consulting a doctor to the laboratory unit far laboratory test than to the pharmacy to get the prescribed drugs and so on, with the manual processes involved in handling the patient most of them waste whole day in the hospital. This situation discouraging to most patients and sometimes force them to turn to non professionals or even resort to self medication for quick recovery. Due to the number of patients, who need the attention of the doctor, the doctors medical lab-scientist hurries over his work without adequate attention and expertise. Still at the end of the day he (is exhausted. In addition to this, the diagnosis and prescription depends on the doctor’s memory their brains are often loaded with different diseases, signs, systems and various drugs far third treatment. Some of which are very similar. To remember and process threes huge information in his clinical work is very asking for this reason accurate and urgent diagnosis and subsequent drug prescription may not always be obtained. The keeping and retrieval of accurate records an patients are poorly carried out in most of our hospitals. Files may be misplaced the record in them might be wrongly filled.

Finally the keeping of folder for each patient manually takes a lot of time and money. Some of the information are redundant. All these have not effect on loss of lines and inefficiency on the part of management.


Purposely, this work is designed at minimizing the time patients have to wait to get adequate medical attention. This delay usually pushes them into patronizing non-professionals. It will also help to reduce the workload which the doctor usually has to show especially where they are few in number. It will allow easy assessment of the previous clinical history of the patient in the shortest possible time.

It will also allow easy analysis of a medical laboratory result. Hence there is need far a system. That will achieve all these, designing a software far laboratory result analysis.


This study is centered on the following objectives: i. To examine the current procedure employed in our hematological laboratories with regards to diagnosis. ii. To examine the associated problem(s) in the current system.

iii. To improved or the already existing system by designing an efficient computer coded medical diagnosis aimed at an accurate, faster and reliable diagnosis therapy.


Due to the fact that it is difficult to develop a computer based system for diagnosing all disease at a time; financing and time constraints, this research is limited to medical diagnosis of sickle cell disease and erythropoiesis foetive.

This study will also improve method(s) of diagnosis especially the patient history, physical examinations and request for clinical laboratory test it the patient did not go directly to the medical lab scientists.


The aim of this study is not to replace medical doctors medical laboratory scientist but to assist them in accelerating in their diagnostic work; which will go a long way to eliminate the trial and error method of treatment (which the doctors usually do while waiting for the lab, result which could be detrimental to the patient. This work will also help both the lab scientist and doctors overcome mental stress and constancy of being overworked.

Furthermore, this research will educate our lab scientist/doctors on the need to accumulate salient aspects of the medical know-how of even the most experienced specialist, in the computer. So as to eliminate the vacuum that would be created when specialist dies or is incapacitated by old age.


It has been observed that the computerization of the procedures of hematological laboratory analysis is a difficult if not an impossible one. We then have to accept that complete computerization of any branch of the medical laboratory will still take scientists some more year.

Therefore, this work will be centered mainly on the computerization of the patient’s classical data and result documentation rather than the procedure involved in obtaining the results.


1. ANEMIA:- This is the most common of hematological disorder and is characterized by a multiplication of conditions which can be complicated and confusing. This is defined as a reduction in the peripheral in the pesidpherd blood which is below normal for the age and sex of the patient. Anemia must also relate to the level of hemoglobin the individual normally possessed for instance if an adult maintains hemoglobin of 160g/l and over a period of days is noted to have decreased to 140 gil. This must be considered significant even though both values are within the normal range of an adult male.

2. Hemoglobin – This is the most important agent on the red cell. This, like its quarter brother myoglobin of muscle, the ctyochrome, peroxides and catalyses enzymes, is a hemoprotein. The protein part, known as globins, is colorless and consists of far peptide chains arranged in hops. The hemoglobin molecule has the heme group surrounded by two pairs of polypeptide chains, normal adult hemoglobin has the pairs of chains alpha and data. The alpha chain has 141 amino acids in a strict sequence commencing at valine and ending with arginine. The beta chain has 146 amino acids also starting with value but ends at histidene. In the adult there as also a small amount of fetal hemoglobin. (HBF) in which the two beda chains are replaced by gumma chains.

HC – HC HC = = = HC 11 11 1 1

HC – – – HC HC = HC C – – – – CH

N Iron porphyrin nucleus. For of such heme group are present in each hemoglobin molecule, united to the protein globin.

3. sickle cell anemia (HBS Sickle cell disease). This is another hemoglobinopathy commonly seen in North America. It is inherited as a mendelian dominail. Although is inherited in a dominest pattern. It can be considered as a recessive characteristic in that it requires a homozygous to produce clinically evident symptoms; parental carriers are asymptomatic. The abnormality of the hemoglobin has been located at the beta chain, where in the 6th position, glutangl is replaced in a valley residue. The homozygote produces a characteristic sickle cells when the oxygen tension of the blood falls. The sickling is caused by the low reduced state, with the production of semi crystalline bodies (factoids) which distort and elongate the cells to produce the deformity. Sickle cell may also block small vessels and capillaries, promoting further reduction of oxygen tension and producing a vicious circle.


Fig 1-2 the outcome of the foetal genotype when both parents are sickle cell carriers.

The outcome of the foetal genotype when one parent is a carrier and the other a sickle.

Fig 1-4 the outcome of the foetal genotype when both parents have the sickle cell carriers disease.

Fig 1-5 the possible outcome of foetal genotype when s/c genes are combined.

Fig 1-6 shows that gene c is same in pothdogy as s.

4. Agglutination the furdatmental and most commonly used reaction in the immunohemotology laboratory to demonstrate the interactian of antigen and antibody is the phenomenon of agglutinatian. By board definition agtglitinatination is simply the clumping of cell into aggregates often as a result of the combination of an antibody’s binding site with antigen site of adjacent red cells. Certain red cell antibodies will agglutinate cell suspended in sdine (ie simply by bringing the two components antigen and antibody together in a test tube and allowing a period of time for the reaclian to take place at room temperature or by hastering the reaction by immediate centicitugatian). These antibodies are known as saline active (complete) antibodies. Other red cells antibodies do not agglutinate in a saline medium but require the presence of a potentially medium in order to allow clumping to occur subsequent to sensitization. These antibodies are sometimes called saline non-active (in complete antibodies. Complete antibodies are more often igra while they of incomplete are usually igci and igA with some execeptians. The demonstatian of red cell aglutintian for erythoropoiesis foetalis (hemolyte disease of the newborn HDN). HDN is a disease that starts in uterous and causes jaundice, anaemia aid hepatosphlenomegaly in the infant. The degree of sevesity of the disease ranges from mild anemia to mental retardation, brain damages, still birth.

The disease is caused by blood group incompatibility between the mother and the foetus. ABO and Rh antibodies especially anti-Rho (D) a most commonly implicated as the cause of the cause of hemolytic disease of the new born blood group antibodies seldom cause the disease although any iga antibody can be responsible far it because of the ability of the iga mediated antibodies to cross the placental barriers from mother to infant.


When hemolytic disease of the newborn results from anti Rho(D), the mother is RHO(D) negative and the infant is Rho D positive (the Rho (D) factor in the infant having been inherited from the father). The first Rh incompatible foctus is usually unaffected. Since the number of fetal red cell that cross the placenta into the maternal circulation during the pregnancy (after the 24th week of gestation) is usually small and insufficient to cause antibody production. In addition to this, elevated steroid levels and other factors associated with pregnancy may suppress the mothers primary immune response. At delivery, a transplacental hemorrhage is not uncommon, the amount of fetal blood entering the matern-1 circulation varying from less than imi or 10m1 or more. The total red cells simulate the production of anti-Rho(D) in about 7 percent of these Rho(D) negative in mothers, the antibody appears in the mother’s serum within months after delivery. When pregnancy with a second Rho(D) positive foetus occurs, fetal red cell crossing the placenta from about the 24th week of gestation stimulate the existing antibody to high liters. This is a secondary response, and therefore small amount of red cells are capable of causing drastic increase in the material antibody. The anti-Rho(D) formed is iga and it is therefore capable of crossing the placenta into circulation, where it combines fetal Rho(D) positive red cells, leading to their destruction. In ABO hemolytic disease of the newborn. The mechanisms of hemolytic disease of the newborn is caused by ABO incompatibility are similar to those of Rh incompatibility (i.e the passage of fetal red cells into the maternal circulation provokes an immune response in the newborn). However, the ABO form can and often does occur in the first pregnancy, since anti-A, B in group O subject is often partly iga the mother is invariably group O. (anti-A and Anti-B in group and A subjects, respectively, is usually I gm.

The ABO form of the disease is rarely severe, although mild forms are common than the Rh formed the ABO form of the disease is between five and six times more common in blacks than in whites.

Antigen – it is difficult to define an antigen rather than describing it as a substance that when injected in an animal recognized as foreign and of given access to immunologically competent cells, will provoke an immune reaction. Antibody, they are produced by immune competent cells in response to antigenic stimuli. Antibodies are serum proteins and together they are generally considered as immunoglobulins.