Malaria fever is a disease caused by the cytoxoic protozoon, Plasmodium spp. This parasite is transmitted by an infected female Anopheles mosquito during a blood meal. There are four types of Plasmodium spp viz; Plasmodium falciparum (causes malignant tertian malaria), Plasmodium vivax (causes benign tertian malaria), Plasmodium malariae (causes quartan tertian malaria) and Plasmodium ovale (causes ovala tertian malaria). The main factors which influence the epidermology of malaria are; the intensity of transmission and the immune response of the infected person. Blood smear or film stained with Leishmans stain ,Giemsa’s stain or Field’s stain helps to indentify the parasite.
Life cycle of Plasmodium spp is very distinct in both the infected female Anopheles mosquito and man. The tissue phase comprises the pre-erythrocytic stage which occurs in the liver. The pre-erythrocytic schizonts leave ruptured liver cells and transforms to merozoites which enters the erythrocytes immediately inorder to remain alive.
The large number of merozoites overpowers the lymphocytes (soldiers of the immune system) and attack the erythrocytes. The merozoites develop into trophozoites. The trophozoites are characterized by a ringed type of cytoplasm with a chromatin dot. These trophozoites multiply rapidly and migrate to the bone marrow, spleen, liver and brain. Schizogamy occurs and the rupturing of the affected cells results in the fever.
The gametophyte stage results from some of the merozoites that did not develop into schizonts. They begin the sexual cycle in the mosquito. They become a zygote and transforms into ookinete. Ookinete develops into oocyst and thereafter sporocyst. These sporocysts move to the proboscis as developed sporozoites. Man becomes infected when the mosquito takes a blood meal.
Symptoms include general body weakness especially the joints, increased body temperature, anaemia, splenomegaly and so on. Malaria is a serious disease in subtropical Africa that results in loss of life and decreased productivity. Pregnant women can suffer miscarriage as a result of malaria fever.
Measures taken to prevent and control malaria include; avoiding mosquito bites via the use of mosquito repellant cream, use of mosquito treated nets, preventing the breeding of mosquito larvae.
Treatment of malaria include the use of antimalarials such as chloroquine, Fansidar, Halofantrine, Metakelfin and so on. These drugs contain sulphadozine (500mg) and pyrimethimine (25mg). However, with the development of chloroquine resistance, new and more effective antimalarials are now in use. Examples include Artesunate, Coarten, Lonart and so on.
The development of a malaria vaccine would go a long way in eradicating malaria. Nevertheless, the vaccine that would be developed should be able to attack the trophozoite ,gametophyte and schizont stages of Plasmodium spp. If this medical breakthrough is achieved, the burden of this debilitating global disease would be solved.
Sunday, December 20, 2009
DNA FINGERPRINTING AND ITS MEDICAL IMPORTANCE
A DNA fingerprint is the pattern of fragmented DNA molecules obtained from electrophoresis. Restriction enzymes are used to cleave DNA molecules into specific fragments that can easily be analyzed. Examples of restriction enzymes include EcoR1 , mst II ,Alu I ,Taq I and so on. DNA fingerprinting is also called DNA typing or DNA profiling and is based on sequence polymorphisms.
Variations that occur in the pattern of restriction fragments produced by the same restriction enzyme from DNA of different individuals of same species is termed restriction fragment length polymorphisms (RFLPs). RFLP analysis is therefore invaluable in Forensic Medicine and in screening for mutations and genetic diseases such as sickle cell anaemia.
In Forensic Medicine, restriction fragment length polymorphism analysis can distinguish one individual from millions of people. DNA obtained from congealed blood ,hair follicles and seminal fluid can be used to catch culprits in criminal investigations such as murder, rape, and theft respectively.
The use of techniques such as complementary DNA radiolabeled probes , southern transfer technique, and restriction enzymes are very essential in detecting and screening for mutations and genetic diseases.
The detection of RFLPs utilizes a specialized hybridization technique termed Southern Blotting or Southern Transfer. DNA fragments from digestion of genomic DNA by restriction endonucleases or enzymes by size (in kilobases) electrophoretically. These fragments are denatured by soaking the agarose gel in alkali, and then blotted onto a nylon membrane to reproduce the distribution of fragments in the gel. The membrane is then placed in a solution containing a radioactively labeled DNA probe. Autoradiography is then used to reveal the fragments to which the radiolabeled DNA probe hybridizes.
It is pertinent to note that the number of repeated units in these DNA regions differs in humans (except between identical twins.). Combining the use of several radiolabeled probes makes DNA fingerprinting so selective that it gives accurate results.
However ,the southern transfer technique requires relatively fresh DNA samples and larger amounts of DNA are generally present at a crime scene. RFLP analysis sensitivity is complemented by the use of polymerase chain reaction (PCR) which helps to amplify small amounts of DNA. Forensic investigators can easily obtain DNA from hair follicle, congealed blood ,seminal fluid ,vaginal secretions from victims and suspects to carry out their investigations. Accurate results can be obtained from samples that have stayed for months or even years.
Results obtained from DNA profiling have been useful in convicting criminals and acquitting suspects. Murder mysteries have been solved and paternity disputes have been amicably resolved. An interesting discovery that was achieved with DNA fingerprinting was the discovery and indentification of the bones of the last Russian Czar and his family who were assassinated in 1918 by Forensic investigators in 1996.
Variations that occur in the pattern of restriction fragments produced by the same restriction enzyme from DNA of different individuals of same species is termed restriction fragment length polymorphisms (RFLPs). RFLP analysis is therefore invaluable in Forensic Medicine and in screening for mutations and genetic diseases such as sickle cell anaemia.
In Forensic Medicine, restriction fragment length polymorphism analysis can distinguish one individual from millions of people. DNA obtained from congealed blood ,hair follicles and seminal fluid can be used to catch culprits in criminal investigations such as murder, rape, and theft respectively.
The use of techniques such as complementary DNA radiolabeled probes , southern transfer technique, and restriction enzymes are very essential in detecting and screening for mutations and genetic diseases.
The detection of RFLPs utilizes a specialized hybridization technique termed Southern Blotting or Southern Transfer. DNA fragments from digestion of genomic DNA by restriction endonucleases or enzymes by size (in kilobases) electrophoretically. These fragments are denatured by soaking the agarose gel in alkali, and then blotted onto a nylon membrane to reproduce the distribution of fragments in the gel. The membrane is then placed in a solution containing a radioactively labeled DNA probe. Autoradiography is then used to reveal the fragments to which the radiolabeled DNA probe hybridizes.
It is pertinent to note that the number of repeated units in these DNA regions differs in humans (except between identical twins.). Combining the use of several radiolabeled probes makes DNA fingerprinting so selective that it gives accurate results.
However ,the southern transfer technique requires relatively fresh DNA samples and larger amounts of DNA are generally present at a crime scene. RFLP analysis sensitivity is complemented by the use of polymerase chain reaction (PCR) which helps to amplify small amounts of DNA. Forensic investigators can easily obtain DNA from hair follicle, congealed blood ,seminal fluid ,vaginal secretions from victims and suspects to carry out their investigations. Accurate results can be obtained from samples that have stayed for months or even years.
Results obtained from DNA profiling have been useful in convicting criminals and acquitting suspects. Murder mysteries have been solved and paternity disputes have been amicably resolved. An interesting discovery that was achieved with DNA fingerprinting was the discovery and indentification of the bones of the last Russian Czar and his family who were assassinated in 1918 by Forensic investigators in 1996.
HAEMOGLOBINOPATHIES-PATHOGENESIS AND MANAGEMENT
Haemoglobins are globular proteins found in red blood cells. They are able to bind molecular oxygen and transport oxygen through the lungs and other blood vessels in the body. Haemoglobin variants include;haemoglobin A, haemoglobin S, haemoglobin C, haemoglobin D, haemoglobin E and haemoglobin F (fetal haemoglobin).
Haemoglobinopathies are genetic disorders or abnormalities which result in abnormal structure of one of the globin chains of the haemoglobin molecule. Also ,low levels of synthesis of the normal polypeptide chains (i.e alpha and beta) and production of abnormal chains(i.e delta and epsilon ) result in haemoglobinopathy. These disorders result in thalassemias (alpha and beta), haemoglobin S (Hb S) disease ,haemoglobin C (Hb C) disease, haemoglobin D (Hb D ) disease, and haemoglobin E (Hb E) disease.
Alpha thalassemia results from genetic deletion and this occurs because the α-globin genes are duplicated. This results in unequal crossing over between adjacent α-alleles. Beta thalassemia results from mutations that produces frameshift in the β-globin coding sequence. Studies reveal that majority of β-thalassemias result from mutations affecting the biosynthesis of β-globin mRNA. Thalassemias are classified as major, minor, and intermediate respectively.
Haemoglobin A is the normal haemoglobin found in humans. Two subgroups exists viz; HbA1 and HbA2. The polypeptide chain composition of both HbA1 and HbA2 are α2β2 and α2δ2 respectively. This type of haemoglobin is found in normal shaped erythrocytes and do not possess pathological problem.
In haemoglobin S , there is a replacement of the amino acid glutamic acid with valine at the sixth position in the β-chain. In haemoglobin C, the replacement of the amino acid glutamine with lysine occurs at the sixth position of the β-globin chain. It is pertinent to note that HbC exhibits less haemolysis than HbS. Both HbS and HbC mutant haemoglobins are commonly found among certain black African population. Individuals with HbSC disorder will have an intermediate anaemia from that observed for HbSS. HbSS individuals suffer from sickle cell disease. It is characterized by sickle-shaped erythrocytes, formation of tactoid structure. Victims experience trauma and crises, and require blood transfusions.
HbAS individuals possess the sickling trait but do not suffer from sickle cell disease. However ,when two HbAS individuals marry, they are likely to produce an offspring with the HbSS genetic combination ( i.e a sickler )
Studies reveal that disease conditions associated with these disorders include splenomegaly, haemolytic anaemia, urobilinuria, jaundice and so on.
Management of these disorders include the use of blood transfusion coupled with desferoxamine, folic acid supplement, use of hypoxurea and bone marrow transplantation. HbAS individuals should be discouraged from marrying other HbAS individuals.
Haemoglobinopathies are genetic disorders or abnormalities which result in abnormal structure of one of the globin chains of the haemoglobin molecule. Also ,low levels of synthesis of the normal polypeptide chains (i.e alpha and beta) and production of abnormal chains(i.e delta and epsilon ) result in haemoglobinopathy. These disorders result in thalassemias (alpha and beta), haemoglobin S (Hb S) disease ,haemoglobin C (Hb C) disease, haemoglobin D (Hb D ) disease, and haemoglobin E (Hb E) disease.
Alpha thalassemia results from genetic deletion and this occurs because the α-globin genes are duplicated. This results in unequal crossing over between adjacent α-alleles. Beta thalassemia results from mutations that produces frameshift in the β-globin coding sequence. Studies reveal that majority of β-thalassemias result from mutations affecting the biosynthesis of β-globin mRNA. Thalassemias are classified as major, minor, and intermediate respectively.
Haemoglobin A is the normal haemoglobin found in humans. Two subgroups exists viz; HbA1 and HbA2. The polypeptide chain composition of both HbA1 and HbA2 are α2β2 and α2δ2 respectively. This type of haemoglobin is found in normal shaped erythrocytes and do not possess pathological problem.
In haemoglobin S , there is a replacement of the amino acid glutamic acid with valine at the sixth position in the β-chain. In haemoglobin C, the replacement of the amino acid glutamine with lysine occurs at the sixth position of the β-globin chain. It is pertinent to note that HbC exhibits less haemolysis than HbS. Both HbS and HbC mutant haemoglobins are commonly found among certain black African population. Individuals with HbSC disorder will have an intermediate anaemia from that observed for HbSS. HbSS individuals suffer from sickle cell disease. It is characterized by sickle-shaped erythrocytes, formation of tactoid structure. Victims experience trauma and crises, and require blood transfusions.
HbAS individuals possess the sickling trait but do not suffer from sickle cell disease. However ,when two HbAS individuals marry, they are likely to produce an offspring with the HbSS genetic combination ( i.e a sickler )
Studies reveal that disease conditions associated with these disorders include splenomegaly, haemolytic anaemia, urobilinuria, jaundice and so on.
Management of these disorders include the use of blood transfusion coupled with desferoxamine, folic acid supplement, use of hypoxurea and bone marrow transplantation. HbAS individuals should be discouraged from marrying other HbAS individuals.
GLUT TRANSPORTERS AND DISEASES
Glut protein family mediate glucose transport or uptake in a wide variety of cells. The term “GLUT” is derived from glucose transporter. They are facilitative hexose transporters. GLUT transporters are uniport systems (i.e they transport only one solute such as glucose and other hexoses such as fructose.)
Glut proteins encourage cellular glucose uptake in cells and tissues where they are found. These facilitative glucose transporters form special selective pathways between three major pools of glucose viz; the blood ,the extracellular fluids and the cellular cytoplasm. Most GLUT isoforms have been cloned using techniques such as polymerase chain reaction, reverse transcriptase ,and complementary DNA.
Detailed research reveals that GLUT transporters possess the following characteristics; they possess a putative 12 transmembrane domains with both the amino (NH3+) and carboxyl (COO-) ends inside the membrane, several isoforms have been identified with the designation GLUT1, GLUT2, GLUT3, GLUT4, GLUT5, and up to GLUT 12, possess identical genome SLC2A, are expressed in a tissue and cell specific manner, and they exhibit distinct kinetic and regulatory properties that reflect their roles in cells where they are expressed.
GLUT1 (SLC2A1) is a highly expressed isoform present in almost all cells, contain 492 amino acids and a reduction in blood glucose makes GLUT1 proteins readily available, and this encourages increased flux of glucose across the blood-brain barrier, GLUT2 (SLC2A2) is expressed in hepatocytes, pancreatic β-cells, and so on. GLUT 2 has 524 amino acids. GLUT3 (SLC2A3) is found in neurons and contains 496 amino acids.
GLUT4 (SLC2A4) is expressed in adipocytes and myocytes. GLUT4 has 509 amino acids and is responsible for glucose transport in insulin-sensitive tissues. GLUT 5 (SLC2A5) is a fructose transporter found in the plasma membrane of mature spermatozoa with 501 amino acids. Sperm cells utilize fructose in seminal fluid.
GLUT6 (SLC2A6) has been found in spleen, leukocytes and brain respectively with 507 amino acids.
GLUT7 (SLC2A7) is expressed in liver microsomes and contain 528 amino acids. It encourages diffusion of free glucose in gluconeogenic tissues. GLUT8 (SLC2A8) is expressed in testis, spleen, skeletal muscle and adipose tissues. GLUT8 has 477 amino acids. GLUT9 (SLC2A9) is found expressed in the liver and kidney, has between 511 and 540 amino acids.
GLUT10 (SLC2A10) is expressed in the liver and pancreas and contains 541 amino acids. GLUT11 (SLC2A11) is found in heart and skeletal muscles. It can transport fructose and contain 496 amino acids. GLUT12 (SLC2A12) is expressed in skeletal myocytes, adipocytes and small intestine. GLUT12 encodes 617 amino acids.
Studies show that there is a correlation between GLUT transporters malfunction and diseases. GLUT2 isoform has been implicated in insulin dependent diabetes mellitus. The reason is that this isoform is present in the β-cells of the pancreas where it regulates influx of glucose through insulin secretion. Derangements in glucose homeostasis as regards GLUT4 malfunction is also linked to insulin dependent diabetes mellitus. GLUT 4 is expressed in insulin-sensitive tissues such as myocytes and adipocytes. GLUT10 has been associated with non-insulin dependent diabetes mellitus.
The link between GLUT expression and cancer has been established. Studies involving the use of tec hniques such as reverse transcriptase, polymerase chain reaction, Northern blot analysis and immunochemistry and so on have been able to detect GLUT messenger RNA (mRNA) in sarcomas and carcinomas. Hence ,in cancerous tissues ,there is an abnormal or over-expression of GLUT isoforms especially GLUT1. However ,some tumour cells express specific GLUT mRNA.
Glut proteins encourage cellular glucose uptake in cells and tissues where they are found. These facilitative glucose transporters form special selective pathways between three major pools of glucose viz; the blood ,the extracellular fluids and the cellular cytoplasm. Most GLUT isoforms have been cloned using techniques such as polymerase chain reaction, reverse transcriptase ,and complementary DNA.
Detailed research reveals that GLUT transporters possess the following characteristics; they possess a putative 12 transmembrane domains with both the amino (NH3+) and carboxyl (COO-) ends inside the membrane, several isoforms have been identified with the designation GLUT1, GLUT2, GLUT3, GLUT4, GLUT5, and up to GLUT 12, possess identical genome SLC2A, are expressed in a tissue and cell specific manner, and they exhibit distinct kinetic and regulatory properties that reflect their roles in cells where they are expressed.
GLUT1 (SLC2A1) is a highly expressed isoform present in almost all cells, contain 492 amino acids and a reduction in blood glucose makes GLUT1 proteins readily available, and this encourages increased flux of glucose across the blood-brain barrier, GLUT2 (SLC2A2) is expressed in hepatocytes, pancreatic β-cells, and so on. GLUT 2 has 524 amino acids. GLUT3 (SLC2A3) is found in neurons and contains 496 amino acids.
GLUT4 (SLC2A4) is expressed in adipocytes and myocytes. GLUT4 has 509 amino acids and is responsible for glucose transport in insulin-sensitive tissues. GLUT 5 (SLC2A5) is a fructose transporter found in the plasma membrane of mature spermatozoa with 501 amino acids. Sperm cells utilize fructose in seminal fluid.
GLUT6 (SLC2A6) has been found in spleen, leukocytes and brain respectively with 507 amino acids.
GLUT7 (SLC2A7) is expressed in liver microsomes and contain 528 amino acids. It encourages diffusion of free glucose in gluconeogenic tissues. GLUT8 (SLC2A8) is expressed in testis, spleen, skeletal muscle and adipose tissues. GLUT8 has 477 amino acids. GLUT9 (SLC2A9) is found expressed in the liver and kidney, has between 511 and 540 amino acids.
GLUT10 (SLC2A10) is expressed in the liver and pancreas and contains 541 amino acids. GLUT11 (SLC2A11) is found in heart and skeletal muscles. It can transport fructose and contain 496 amino acids. GLUT12 (SLC2A12) is expressed in skeletal myocytes, adipocytes and small intestine. GLUT12 encodes 617 amino acids.
Studies show that there is a correlation between GLUT transporters malfunction and diseases. GLUT2 isoform has been implicated in insulin dependent diabetes mellitus. The reason is that this isoform is present in the β-cells of the pancreas where it regulates influx of glucose through insulin secretion. Derangements in glucose homeostasis as regards GLUT4 malfunction is also linked to insulin dependent diabetes mellitus. GLUT 4 is expressed in insulin-sensitive tissues such as myocytes and adipocytes. GLUT10 has been associated with non-insulin dependent diabetes mellitus.
The link between GLUT expression and cancer has been established. Studies involving the use of tec hniques such as reverse transcriptase, polymerase chain reaction, Northern blot analysis and immunochemistry and so on have been able to detect GLUT messenger RNA (mRNA) in sarcomas and carcinomas. Hence ,in cancerous tissues ,there is an abnormal or over-expression of GLUT isoforms especially GLUT1. However ,some tumour cells express specific GLUT mRNA.
IODINE REQUIREMENT AND GOITRE
Iodine is one of the halogens. It is one of the essential micronutrients needed by humans. The body contains 20-50mg of iodine and is an essential component of the secretions of the thyroid gland. The thyroid gland synthesizes, stores and secretes the thyroid hormones thyroxine,T4 and tri-iodothyronine,T3. The rate of synthesis and secretion of thyroid hormones are controlled by the pituitary gland. Thyroxine (T4) and tri-iodothyronine (T3) regulate oxygen consumption and heat production including a wide range of metabolic processes. They are also essential for normal growth and development. Iodine after peroxidation, becomes attached to tyrosine residues of thyroglobulin.
Food sources rich in iodine include sea foods such as crayfish, oyster, prawn, lobster and crabs, seeds, eggs, dairy products, cereals. Consumption of iodine is highly variable in different parts of the World.
The minimum requirement for adults has been estimated at 50-75µg/day. Children and mothers require more. Studies have shown that people who live in mountainous regions suffer from iodine deficiency because the soil contain little quantity of iodine. Hence, local produce have little iodine content .Such people suffer from endemic goiter. Endemic goitre results from low levels of thyroid hormones. Endemic goitre is characterized by enlarged thyroid gland.
The development of iodine deficiency can be averted through these methods viz; the addition of potassium iodate to salt used in cooking or in bread (i.e food fortification).In long standing goitre, the use of tyrosine treatment (9.3µg/day) yields appreciable results. Foods rich in gutrogens should be avoided. Examples of such foods are turnips and cabbages.
Iodine toxicity results when doses exceeding the normal daily requirement are administered. The addition of potassium iodate to food for the prophylaxis to endemic goitre is not devoid of hazards if overdose are added. In studies involving animal models, excessive amounts have been shown to inhibit thyroid hormone synthesis. Thyroid necrosis has also been reported.
Food sources rich in iodine include sea foods such as crayfish, oyster, prawn, lobster and crabs, seeds, eggs, dairy products, cereals. Consumption of iodine is highly variable in different parts of the World.
The minimum requirement for adults has been estimated at 50-75µg/day. Children and mothers require more. Studies have shown that people who live in mountainous regions suffer from iodine deficiency because the soil contain little quantity of iodine. Hence, local produce have little iodine content .Such people suffer from endemic goiter. Endemic goitre results from low levels of thyroid hormones. Endemic goitre is characterized by enlarged thyroid gland.
The development of iodine deficiency can be averted through these methods viz; the addition of potassium iodate to salt used in cooking or in bread (i.e food fortification).In long standing goitre, the use of tyrosine treatment (9.3µg/day) yields appreciable results. Foods rich in gutrogens should be avoided. Examples of such foods are turnips and cabbages.
Iodine toxicity results when doses exceeding the normal daily requirement are administered. The addition of potassium iodate to food for the prophylaxis to endemic goitre is not devoid of hazards if overdose are added. In studies involving animal models, excessive amounts have been shown to inhibit thyroid hormone synthesis. Thyroid necrosis has also been reported.
URIC ACID AND ITS CLINICAL CORRELATIONS
Uric acid is the end product of purines and nucleic acid metabolism in man. Uric acid emanates from two routes; from oxidation of purine moieties of degraded nucleic acids (i.e Ribonucleic and deoxyribonucleic acids),from glycine via a direct pathway not involving nucleic acid. Uric acid is filtered by glomerulli and both reabsorped and secreted by the renal tubules. Reasons for requesting uric acid assay include; suspected gout and uric acid nephropathy, renal failure.
Total daily output of uric acid depends partly on the purine content of the diet. Uric acid excretion is diminished when the diet has low purine content, low protein content. Normal levels of serum uric acid is 1-5mg/100ml and it rises to between 8-15mg/100ml in Gout. Diseases such as leukaemia, myeproliferative disorders, plasma cell myeloma and severe haemolytic anaemia, there is considerable breakdown of nuclei of leukocytes. This ultimately results in elevated serum uric acid level.
Gout is a chronic disorder of purine degradation. Types include ; acute gout and chronic gout. Features of gout is as follows viz; hyperuricemia, deposits of sodium monourates in the articular structures, and recurring attacks of acute arthritis with deposits of crystals of monosodium urate in and around the structures the affected joint.
Treatment of gout include the following; restrict the consumption of organ meats since these are rich in purines. Acute gout is treated with drugs such as colchine, phenylbutazone and indomethacin.Chronic gout is characterized by increased excretion of uric acid can be treated with drugs that discourage reabsorption of urates. Drugs such as probenecid (Benemid) and salicylates. Allopurinol inhibits the enzyme xanthine oxidase and this ultimately reduces uric acid synthesis.
Increased secretion of uric acid lowers serum uric acid levels in as much as reabsorption by the renal tubules is not encouraged.
Total daily output of uric acid depends partly on the purine content of the diet. Uric acid excretion is diminished when the diet has low purine content, low protein content. Normal levels of serum uric acid is 1-5mg/100ml and it rises to between 8-15mg/100ml in Gout. Diseases such as leukaemia, myeproliferative disorders, plasma cell myeloma and severe haemolytic anaemia, there is considerable breakdown of nuclei of leukocytes. This ultimately results in elevated serum uric acid level.
Gout is a chronic disorder of purine degradation. Types include ; acute gout and chronic gout. Features of gout is as follows viz; hyperuricemia, deposits of sodium monourates in the articular structures, and recurring attacks of acute arthritis with deposits of crystals of monosodium urate in and around the structures the affected joint.
Treatment of gout include the following; restrict the consumption of organ meats since these are rich in purines. Acute gout is treated with drugs such as colchine, phenylbutazone and indomethacin.Chronic gout is characterized by increased excretion of uric acid can be treated with drugs that discourage reabsorption of urates. Drugs such as probenecid (Benemid) and salicylates. Allopurinol inhibits the enzyme xanthine oxidase and this ultimately reduces uric acid synthesis.
Increased secretion of uric acid lowers serum uric acid levels in as much as reabsorption by the renal tubules is not encouraged.
VITAMINS AND THEIR MEDICAL RELEVANCE
Vitamins are nutritional requirements needed in small amounts by animals for healthy living. Vitamins are classified into 2 groups; water-soluble vitamins and fat-soluble vitamins. Examples of water-soluble vitamins are vitamin C (ascorbic acid) and the B vitamins(i.e vitamin B1,vitamin B2,vitamin B6 and vitamin B12). Fat-soluble vitamins include vitamin A, vitamin D, vitamin E and vitamin K.
Water-soluble vitamins have diverse chemical structures and are polar molecules. They can be synthesized by plants and are therefore provided by food sources such as legumes, whole grains, green leafy vegetables , yeast ,meat and milk. Water-soluble vitamins serves as co-factors (co-enzymes) in enzymatic reactions.
With the exception of vitamin B12 (cyanocobalamin),water-soluble vitamins are not stored in the body. Continuous intake in the diet is required. The human liver can store vitamin B12. They are absorbed in the water along the gastrointestinal tract and are excreted easily along with urine.
Water-soluble vitamins occur in interrelated biochemical pathways and deficiency diseases caused by lack of a single vitamin is rare. Generally ,lack of water-soluble vitamins affect tissues that are growing or metabolizing rapidly such as skin, blood, the digestive tract and the nervous system.
Symptoms of their deficiency include dermatitis, beri-beri, anaemia ,pellagra ,digestive and neurologic disorders. Ascorbic acid (vitamin C) is liable to heat including other water-soluble vitamins. Other important B vitamins include pantothenic acid (vitamin B5), biotin, folic acid (pteroylglutamic acid).
Fat-soluble vitamins are absorbed along with fats in the body. Hence, any substance or factor that favours the absorption of fats and lipids would aid their absorption. Fat-soluble vitamins include vitamin A, vitamin D, vitamin E and vitamin K respectively.
Vitamins A is derived from the precursor beta carotene. Cleavage at the centre of the structure produces retinol. It functions as a hormone. Food sources include fish liver oils, whole milk, carrots and sweet potatoes. Deficiency of retinol results in a variety of symptoms such as dryness of skin, eyes, mucous membranes and night blindness.
Vitamin D is one of the isoprenoid compounds. It exists in diverse forms such as cholecalciferol(vitamin D3),ergocalciferol (vitamin D2). Vitamin D3 is the precursor of 1,25-dihydroxycholecalciferol,a hormone that regulates calcium metabolism. Deficiency of vitamin D results in rickets and bone diseases such as osteomalacia,osteoporosis.
Vitamin E is also referred to as tocopherol. Vitamin E associates with cell membranes, lipid deposits and blood lipoproteins. They serve as biological anti-oxidants. Dietary sources include eggs and vegetable oil. Deficiency of vitamin E results in scaly skin, muscular weakness, and fragile erythrocytes.
Vitamin K has subgroups such as vitamin K1 (phylloquinone) and vitamin K2 (menaquinone). Vitamin K possess an aromatic ring. Detailed research discovered vitamin K as a required factor for blood clotting. Deficiency of vitamin K results in avitaminosis. Steatorrhea and biliary system disorders can result in malabsorption of the fat-soluble vitamins.
Vitamins are essential nutritional requirements required in the life processes of humans. Hence ,fat-soluble vitamins should be consumed with care since they can accumulate in the body to cause metabolic problems. Water-soluble vitamins should be continuously supplied in the diet.
Water-soluble vitamins have diverse chemical structures and are polar molecules. They can be synthesized by plants and are therefore provided by food sources such as legumes, whole grains, green leafy vegetables , yeast ,meat and milk. Water-soluble vitamins serves as co-factors (co-enzymes) in enzymatic reactions.
With the exception of vitamin B12 (cyanocobalamin),water-soluble vitamins are not stored in the body. Continuous intake in the diet is required. The human liver can store vitamin B12. They are absorbed in the water along the gastrointestinal tract and are excreted easily along with urine.
Water-soluble vitamins occur in interrelated biochemical pathways and deficiency diseases caused by lack of a single vitamin is rare. Generally ,lack of water-soluble vitamins affect tissues that are growing or metabolizing rapidly such as skin, blood, the digestive tract and the nervous system.
Symptoms of their deficiency include dermatitis, beri-beri, anaemia ,pellagra ,digestive and neurologic disorders. Ascorbic acid (vitamin C) is liable to heat including other water-soluble vitamins. Other important B vitamins include pantothenic acid (vitamin B5), biotin, folic acid (pteroylglutamic acid).
Fat-soluble vitamins are absorbed along with fats in the body. Hence, any substance or factor that favours the absorption of fats and lipids would aid their absorption. Fat-soluble vitamins include vitamin A, vitamin D, vitamin E and vitamin K respectively.
Vitamins A is derived from the precursor beta carotene. Cleavage at the centre of the structure produces retinol. It functions as a hormone. Food sources include fish liver oils, whole milk, carrots and sweet potatoes. Deficiency of retinol results in a variety of symptoms such as dryness of skin, eyes, mucous membranes and night blindness.
Vitamin D is one of the isoprenoid compounds. It exists in diverse forms such as cholecalciferol(vitamin D3),ergocalciferol (vitamin D2). Vitamin D3 is the precursor of 1,25-dihydroxycholecalciferol,a hormone that regulates calcium metabolism. Deficiency of vitamin D results in rickets and bone diseases such as osteomalacia,osteoporosis.
Vitamin E is also referred to as tocopherol. Vitamin E associates with cell membranes, lipid deposits and blood lipoproteins. They serve as biological anti-oxidants. Dietary sources include eggs and vegetable oil. Deficiency of vitamin E results in scaly skin, muscular weakness, and fragile erythrocytes.
Vitamin K has subgroups such as vitamin K1 (phylloquinone) and vitamin K2 (menaquinone). Vitamin K possess an aromatic ring. Detailed research discovered vitamin K as a required factor for blood clotting. Deficiency of vitamin K results in avitaminosis. Steatorrhea and biliary system disorders can result in malabsorption of the fat-soluble vitamins.
Vitamins are essential nutritional requirements required in the life processes of humans. Hence ,fat-soluble vitamins should be consumed with care since they can accumulate in the body to cause metabolic problems. Water-soluble vitamins should be continuously supplied in the diet.
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