Red Blood Cells and Its Functions

Red blood cells are the more numerous type of cells present in the blood. They are also called as RBCs, red blood corpuscles, erythrocytes, etc. The red blood cells are red in color due to the presence of hemoglobin in their cytoplasm. An adult human male has about 5-6 million per cubic millimeter and has 20 to 30 trillion red blood cells at any given time in circulation. An adult human female has slightly less number such as 4-5 million erythrocytes per cubic millimeter. ​The erythrocytes or RBCs moves by the push of the blood flow in arteries and blood flow pull in the veins and squeezing through the capillaries. The flexibility of RBCs helps then to squeeze through smaller blood vessels and capillaries.

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Red Blood Cell Structure

The mature red blood cells are are flexible and biconcave shaped cells with no nucleus or organelles. The biconcave shape of the red blood cells provides them with good surface area compared to the volume that helps diffusion of gases. RBCs have a diameter of about 7.5 microns and the thickness at the periphery is 2 microns and at the center it is 1 micron. RBCs do not contain cellular structures such as nucleus, mitochondria, ribosomes, endoplasmic reticulum, or centrioles.

The cytoplasm of RBC is fully composed of hemoglobin and it is interwoven in the structure of the RBCs. About 95% of the dry weight of the RBC is due to the presence of hemoglobin. The hemoglobin is an iron containing compound that helps in the transport of oxygen and carbon dioxide through the blood. The presence of the hemoglobin gives the red blood cell its red color. The cell membrane of the erythrocytes contains lipids and proteins. The membrane of the red blood cells play important role in regulating their surface deformability, flexibility, adhesion, and immune recognition. These functions depend on the properties of the cell membrane. The red cell membrane is composed of 3 layers, the exterior glycocalyx that is rich in carbohydrates, a lipid bilayer, which contains transmembrane proteins, and the membrane skeleton which is a structural network of proteins located on the inner surface of the lipid bilayer. The lipid bilayer is composed of cholesterol and phospholipids.​

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​Red Blood Cell Formation

RBCs have a lifespan of 120 days in the blood stream. There is a huge loss of RBCs daily, and so to keep up with the number, there must be sufficient number of RBCs produced daily. Red blood cells are developed from 2 types of tissues:

1) Myloid tissue which is the red bone marrow, that produces RBCs. 

2) Lymphoid tissues include lymph nodes, the thymus, and the spleen.​

The formation of blood cells starts from the 3rd week of intrauterine life, which is called erythropoiesis. The most primitive form of RBC derives from pluripotent stem cells. The pluripotent stem cells divide and differentiate to produce progenitor cells. From the progenitor cells, pronormoblast develops, which is converted into early normoblast, intermediate normoblast, and the late normoblast to form reticulocyte. The reticulocyte later is turned into a matured erythrocyte or the RBC. The factors that influence the formation of red blood cells are hematopoietic growth factors such as erythropoietin, interoleukins, stem cell factor, colony stimulating factor, thrombopoietin, some vitamins, and minerals iron and copper.

A normal increase in RBC production occurs in severe hypoxemia and conditions of less oxygen in the air.

Functions of RBC

RBCs collect oxygen from the lungs and release it to the cells and tissues whereas they take up carbon dioxide from the cells and tissues and release it to the lungs. Hemoglobin present in the red blood cells helps in the transport of oxygen and carbon dioxide to and fro between the lungs and the cells.

​When there is a shear stress in the constricted blood capillaries, the RBCs release ATP which makes the vessel wall to relax and dilate to allow normal flow of the blood.

Due to the deoxygenation of the hemoglobin molecules the red blood cells release S-nitrosothiols that acts to dilate the blood vessels directing more blood to the areas of oxygen depletion.

Exposure of RBCs to physiological levels of shear stress activates them to synthesize nitric oxide enzymatically thus contributing to the regulation of the vascular tone.

Erythrocytes produce hydrogen sulfide that helps to relax the blood vessel walls.

RBCs helps in playing a role in the immune mechanism of the body. When lysed by the pathogenic bacteria, the hemoglobin in the RBCs releases free radicals that breaks down the cell wall of the pathogenic bacteria and thereby killing it.

Diseases Involving the Red Blood Cells

Anemia is a disease characterized by a low oxygen carrying capacity of the blood due to decrease in number of red blood cells or abnormality of the red blood cells. There are different types of anemia such as:

Iron deficiency anemia occurs due to the decreased intake or decreased absorption of iron from the diet.

Sickle cell anemia is a genetic disease due to the presence of abnormal hemoglobin molecules.

Hemolytic anemia is characterized by excessive breakdown of the red blood cells.

Thalassemia is a genetic disease that causes an abnormal ratio of hemoglobin.

Pernicious anemia is a disease where there is a decreased absorption of vitamin B12, which is necessary for the production of hemoglobin.

Spherocytosis is a disease that causes a defect in the red blood cell's cytoplasm where the RBCs become spherical in shape.

Aplastic anemia is disease caused by the inability of the bone marrow to produce blood cells.

Polycythemia is a disease characterized by an abnormal increase in number of red blood cells.

Hemolytic transfusion reaction is the destruction of the donated red blood cells after a blood transfusion. It is mediated by the antibodies present in the recipient's blood.

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GERD Causes Symptoms and Treatment

Gastroesophageal reflux disease or GERD is a condition where the contents of the stomach and acids return backward from the stomach to the esophagus and also the subsequent mucosal damage by that. It is also called as gastric acid disease, gastric reflux disease, acid reflux disease, etc. It can cause irritation of the esophagus, damage, heartburn, and other symptoms. When eating foods, it passes from the throat to the stomach through the esophagus, called the food pipe. When the food reaches the stomach it is prevented from returning back into the esophagus or regurgitate by the help of a ring of muscle fibers. These ring of muscle fibers are called the lower esophageal sphincter or LES. When the sphincter is not closed properly, food, liquids, and acids in the stomach can regurgitate back into the esophagus, and this reflux of food and acid is called as the acid reflux or gastroesophageal reflux disease.

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Causes

GERD is caused by the changes in barrier between the stomach and the esophagus due to abnormal relaxation of the lower esophageal sphincter, impaired expulsion of the gastric contents, impaired gastric reflux from the esophagus, or hiatal hernia. It can be a temporary phenomenon or a permanent one.

The trigger factors which initiate GERD are alcohol, obesity, hiatal hernia, pregnancy, scleroderma, smoking, etc. The drugs that induce the GERD symptoms are anticholenergics, beta-blockers, bronchodialators, calcium channel blockers, dopamine, progestin, sedatives, and tricyclic antidepressants.

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Other factors that contribute to GERD are Zollinger-Ellison syndrome, which is increased gastric acidity due to gastrin production, hypercalcemia, that increases the gastrin production and increased acidity, scleroderma and systemic sclerosis that can cause esophageal dysmotility, use of medicines such as prednisolone, visceroptosis in which the stomach has been reduced in the abdomen thereby upsetting the gastric motility and acid secretion etc.

​​Signs and Symptoms

The common symptoms of GERD are:

Heartburn or a burning sensation in the chest

Regurgitation or expulsion of material from the esophagus

Dysphagia or difficulty on swallowing

The less common symptoms of GERD are:

Odynophagia or pain with swallowing

Sialorrhea, or increased salivation

Nausea, or feeling of vomiting

Chest pain

Coughing and wheezing

Hiccups

Hoarceness

​Sore throat

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Some associated symptoms of GERD are:

Chronic cough

Laryngitis, inflammation of the larynx and hoarceness.

Asthma

Erosion of dental enamel due to acid leach of the enamel of the tooth

Dentine hypersensitivity due to decalcification of the dentine due to acids

Sinusitis

Pharyngitis

Globus pharyngeus or a choking sensation felt in the throat

Globus hystericus or sensation that a foreign body is present in the throat

Symptoms of GERD in children are:

Repeated vomiting

Effortless spitting up

Coughing

Wheezing.

Inconsolable crying, refusal of food, cry for food and then rejecting food or milk bottle and again crying for it, failure to gain weight, bad breath, belching and burping etc.

Complications ​

Asthma is caused due to difficulty in passage of air through the pharynx due to GERD.

Bronchospasm due to irritation and spasm of the airways due to gastric acid.​

Reflux esophagitis, which is the necrosis of the esophageal epithelium causing ulcers at the junction between the esophagus and the stomach.

Esophageal strictures, which is the persistent narrowing of the esophagus by the inflammation.

Dental erosion caused by the frequent exposure to reflux acid contents.

Barrett's esophagus or the change in lining of epithelium from squamous cells to intestinal columnar epithelial cells.

Esophageal adenocarcinoma, which is the cancer of the esophagus.

Diagnosis of GERD

​Detailed history is necessary for diagnosis. Other investigations for GERD include esophageal pH monitoring, barium swallow X-ray, esophageal manometry, and esophagogastroduodenoscopy.

Esophagogastroduodenoscopy is a type of endoscopy of the esophagus which involves insertion of a thin scope through the mouth and the throat into the esophagus and stomach to determine and assess the internal surface structures of the stomach and duodenum.

Biopsies of the esophageal, duodenum, and the walls of the stomach can be taken to identify, edema and basal hyperplasia, inflammation, Barretts esophagus, elongation of papillae, thinning of the lining squamous layer, dysplasia or precancer, or carcinoma.

​Treatment

The 3 modalities of treatment for GERD are lifestyle modification, medication, and surgery.

Certain foods seems to exacerbate the the symptoms of GERD and these needs to be curbed from the diet. Antacids such as calcium bicarbonate actually increase the acidity of the stomach and needs to be avoided. Drugs such as aspirin, ibuprofen, or naproxen are usually avoided because of reflex acid production and acetaminiphen is used instead. Habits such as smoking reduces the esophageal sphincter competence and thus allowing the acid to get into the esophagus and so smoking is stopped.

Lifestyle Modification

Certain positions of sleep seem to reduce night time reflux episodes in some people. Elevating the head seems to improve in reducing the GERD symptoms. The head of the bed can be elevated by bed risers that support bed post or legs, a therapeutic bed pillow, inflatable mattress lifter, or a bed elevator facility.

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Medications used to treat GERD

Proton pump inhibitors such as  omeprazole, esomeprazole, pantoprazole, lansoprazole, and rabeprazole etc. are used in effectively reducing the acid production. They stop acid production via proton pump inhibition.

Gastric H2 receptor blockers such as ranitidine, famotidine, cimetidine etc. reduces gastric acid secretion. Good relief is achieved by these drugs.

Antacids taken before meals or just after symptoms begin, can reduce gastric acidity.

Alginic acid may coat the mucosa of the GI tract and also increase pH thus decreasing GERD symptoms.

Surgery​

Surgical methods are used to treat GERD. The common surgical treatment for GERD is the  Nissen fundoplication. Here the upper part of the stomach around the lower esophageal sphincter LES is wrapped around. It is done to strengthen the sphincter and therefore preventing the acid reflux. Laparoscopic repair of a hernia is also done for reducing acid reflux. 

A treatment called transoral incisionless fundoplication (TIF) is used where the valve between the stomach and esophagus is rebuild by a device called Esophyx done intraorally.

Prevention

​GERD is prevented through lifestyle modification methods such as:

Sleeping on the left side or raising the upper side of the body significantly reduces GERD symptoms as mentioned in the treatment part. Raising the upper part of the body by raising the bed, using pillows, or elevating the head and body part of the bed. The entire upper part including the body and head should be raised to prevent acid reflux.

Sleeping on the left side also helps to reduce these reflux symptoms by the use of the gravity when the esophagus is at a higher level than the stomach.

Eating smaller meals causes lesser acid production and so reduced GERD symptoms. Avoiding eating just before sleeping also helps to prevent any reflux symptoms.

Losing weight helps to reduce the risk of acid reflux. More body fat will put more pressure on the stomach and its contents to reflux into the esophagus. Thus reducing the excessive body fat will help get relief from GERD symptoms.

Avoiding tight clothing around the body helps to prevent GERD symptoms as the tight clothing puts pressure on the stomach causing reflux symptoms.

Avoiding acidic foods and foods that trigger GERD symptoms help to prevent reflux. The acidic foods include fruit or juices, fatty foods, coffee, tea, onions, peppermint, chocolate, etc.

Avoiding taking foods shortly before going to bed, because it produces excess gastric acid that takes time to subside.

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Dengue Fever Causes Symptoms and Treatment

Dengue fever is a debilitating infectious disease caused by the dengue virus and transmitted by mosquitoes. It is characterized by the dengue triad, high fever, rashes, and intense headache, body ache, and joint aches. It is also called the "break-bone fever" because it causes severe body and joint aches and pains. The disease is found throughout the world and more prevalent in the tropics and the subtropics where the climate is especially hot and rainy. It is common in South and Southeast Asia, Northern Australia, SubSaharan Africa, Central and South America, parts of Caribbean etc. The disease occurs at the start of the rainy season and immediately after it. ​​The dengue virus has 4 different types, types 1, 2, 3, and 4. Infection with any one type gives lifelong immunity to that type of virus but only short term immunity to the other types. The mortality rate is 3 to 30 in every 100 cases.

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​Signs and symptoms

The characteristic symptoms of dengue include sudden-onset fever, headaches typically located behind the eyes, muscle and joint pains, swollen glands, and a characteristic rash that is similar to measles. The incubation period of dengue fever ranges from 3-14 days. Most people, 80%, who are infected with the dengue virus are asymptomatic. The other 5% have more severe symptoms, and for the rest it is life threatening.

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​Transmission and Clinical Course

The dengue virus is transmitted by the Aedes mosquitoes and more specifically by the genus Aedes eagypti. The other Aedes mosquito species that spread dengue include A. albopictus, A. polynesiensis, and A. scutellaris. These mosquitoes bite during the day and the infection can be acquired with a single bite. Female mosquitoes are those which causes the disease. Humans are the primary host of the disease. Dengue virus is present in the blood of an infected person suffering from the dengue fever. The female mosquito sucks the blood from the person suffering from dengue fever, and the mosquito themselves get infected with the virus in the cells lining the gut. The virus spreads to other tissues of the mosquito which involves the salivary glands and it is therefore is released into the saliva. In fact, the mosquito does not get any adverse effects of the disease while it is being infected and the virus stays in the mosquito for life. These mosquitoes prefer to lay their eggs in stagnant water near human dwelling and feed on the blood of human rather than on other vertebrates.

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When a mosquito that carries the dengue virus bites a person, the virus enters the skin along with the saliva of the mosquito. It enters the blood and binds with the white blood cells and reproduces inside it while they move throughout the body. The white blood cells responds by producing several proteins such as interferon and these proteins produces many symptoms such as fever, flu-like symptoms, severe pains and aches. In severe infection, the reproduction of the virus is greater and many organs and organ systems are affected such as the liver, bone marrow etc. The fluid and plasma from the blood leaks through the walls of the blood vessel into the body cavities. Due to this, there will be less blood that will circulate through the blood vessels and the blood pressure drops to low. Because there is less blood that is present in the blood vessels it cannot supply sufficient oxygen or nutrients to the the vital organs, thus producing serious effects. When the bone marrow is affected, it causes dysfunction that leads to reduced number of platelets resulting in decreased clotting of blood. Decreased clotting of blood leads to increased risk of bleeding mostly through soft mucous membranes, which is a serious complication.

Dengue can also be transmitted through blood transfusion, blood products and organ transplants. Vertical transmission from mother to the child does occur. Some rare person to person mode of transmission also occur.

​Predisposition

The severe effects of the dengue fever are seen mostly in children and babies. It is more common in children who are well nourished. It also affects women more than men. Dengue fever is a life threatening disease in people who have chronic diseases such as diabetes, asthma, clotting disorders etc.

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​Phases of Infection

There are 3 phases of infection, and they are febrile phase, critical phase, and recovery phase.

The febrile phase involves high fever often above 40 degree centigrade associated with generalized aches and pains and headache, which lasts for 2 to 7 days. A rash occurs in 50%-80% of those with symptoms. It occurs as a flushed-skin type to a measles-type rash. Some petechiae or red raised spots with bleeding are noted on the skin and there may be mild bleeding from the mucous membranes of the mouth and nose. The fever often fluctuates by breaking and then returning in 1 or 2 days.

The disease sometimes proceed to a critical phase in some people that follows the resolution of the fever and it lasts for 1 to 2 days. There is significant amount of fluid accumulation in the chest and abdominal cavity due to increased permeability and leakage. It leads to depletion of fluid from the blood vessels and decreased blood flow to the vital organs. Multiple organ dysfunction, abdominal pain and severe bleeding from the gastrointestinal tract may occur. Shock often known as dengue shock and the hemorrhage known as dengue hemorrhagic fever occur in less than 5% of the cases. Dengue hemorrhagic fever is a life threatening condition where there is low levels of blood platelets and bleeding and blood plasma leakage. It leads to the dengue shock syndrome characterized by extremely low blood pressure.Those previously infected with other types of dengue virus are at an increased risk.

The recovery phase is characterized by resorption of the leaked fluid into the blood stream and it can last about 2 to 3 days. There may be severe itching and slow heart rate. A severe fluid overload state may occur that affects various organs. When it affects the brain there will be reduced level of consciousness and seizures. Other dengue complications include neurological disorders like  transverse myelitis and Guillain-Barre syndrome and infections occur such as infection of the heart and acute liver failure.

Diagnosis

The diagnosis dengue is made clinically based on the reported symptoms and physical examination that includes fever, nausea and vomiting, rash, generalized pains, low white blood cell count, positive tourniquet test, or any warning signs such as abdominal pain, ongoing vomiting, liver enlargement, mucosal bleeding, high hematocrit count with low platelets, lethargy in someone who lives in an endemic area.

Laboratory Tests

Dengue fever can be diagnosed with laboratory testing methods done by virus isolation in cell cultures, nucleic acid detection by PCR, viral antigen detection, or specific antibodies.

Management

There are no specific treatments or vaccines for dengue fever. Treatment of dengue fever depends on the symptoms and their management, which includes oral rehydration therapy, close follow up, hospital admission with administration of intravenous fluids, blood transfusion etc. ​Invasive medical procedures such as nasogastric intubation or intramuscular injections are avoided to prevent any bleeding complications. Drugs such as paracetamol is used for fever and discomfort. NSAIDs such as ibuprofen and aspirin are avoided to prevent any risk of bleeding. Blood transfusion is given for patients presenting with unstable vital signs or decreasing hematocrit. Packed red blood cells or whole blood is given for severely hypovolemic patients. Platelets or fresh frozen plasma are usually not given.

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Prevention

There are no vaccines for dengue virus. Prevention of dengue virus is through the control of mosquitoes and avoiding mosquito bites.

The primary method of controlling Aedes eagypti is by eliminating its habitats. This is through various means such as:

Emptying water where it is collected such as containers or collectors either natural or artificial.

Adding insecticides or biological pest control agents in those water bodies.

Environmental modification or reduction of open collections of water.

Closing any air holes of septic tanks and other drainage pipes.

Draining of any stagnant water.

Wearing clothing to prevent mosquito bites such as clothing that fully covers the skin.

Using mosquito net closure on all doors, windows, ventilators, and other air channels at home.

Using mosquito net over the bed while sleeping.

Application of insect repellant on the skin.

Use of mosquito repellant smoking coil to deter mosquitoes.

Using mosquito electric bats and wire meshes to trap and kill mosquitoes.​

These are some of the methods that helps to control mosquitoes and mosquito bites and thus effectively preventing the spread of dengue fever.

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Platelets and Its Functions

Platelets are irregularly shaped cell fragments present in the blood. They are not actually true cells but merely the circulating fragments of cells. They are smaller and lighter than the other blood cells. They are colorless bodies with small nonnucleated protoplasm. These are cell fragments, which are derived from the fragmentation of precursor megakaryocytes. The size of the platelet is about 2 to 3 micrometer in diameter. The normal platelets count is 1.5 to 4 hundred thousand per microliter in peripheral blood. The average lifespan of a platelet is 5 to 9 days.

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Formation

Platelets are produced by thrombopoiesis in the bone marrow. Platelets are produced from very large bone marrow cells called megakaryocytes. When megakaryocytes develop itself into giant cells, they undergo a process of fragmentation which results in the release of platelets. Between 5,000 and 10,000 platelets per megakaryocyte are produced by fragmentation or budding. Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone produced by the liver and kidneys. When the platelets gets older, they are destroyed by a process called phagocytosis in the spleen and by Kupffer cells in the liver. The reserve platelets are stored in the spleen and are released when needed by splenic contraction.

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Functions

Hemostatic Function: Platelets are involved with hemostasis, leading to the formation of blood clots. When damage to the endothelium of blood vessels occurs, they form thrombi and prevent further bleeding. They contain many structures that are important for stopping the bleeding. Platelets contain proteins on their surface that allow them to stick to breaks in the blood vessel wall and also to stick with each other. They contain granules that secrete proteins required for creating a firm plug that seal the blood vessel breaks. Platelets also contain proteins similar to the muscle proteins that allow them to change shape when they become sticky. When the platelets are stimulated by a break in the blood vessel wall, they changes their shape. They become round and extends long filaments or pseudopods. They extend and reach out to make contact with the broken blood vessel wall and other platelets. With these filaments platelets form a plug and seals the broken blood vessel thus stopping the bleeding.

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Platelet Action: In normal blood flow, the platelets roll along the surface of the vessel wall, which is lined by endothelial cells. Endothelial cells produce a protein called the von Willebrand factor or vWF, a cell adhesion agent, which helps endothelial cells adhere to collagen of the basement membrane. When there is a cut or an injury, the collagen, vWF, and the tissue factor from the subendothelium is exposed to the bloodstream. When the platelets contact collagen, vWF or thrombin, they are activated and clump together. The tough fibers surrounding the vessel wall act like an envelop and attract platelets. These platelet changes in shape and then clump onto these fibers thus providing an initial seal preventing any further bleeding.

Wound Healing Function: Platelets release growth factors such as platelet-derived growth factor which is a chemotactic agent and TGF beta which stimulates deposition of extracellular matrix. These growth factors are involved with the repair and regeneration of connective tissues. Other growth factors produced by the platelets include basic fibroblast growth factor, insulin-like growth factor 1, platelet-derived epidermal growth factor, and vascular endothelial growth factor. These growth factors have been involved with the healing of wounds. Local application of these growth factors in high concentration in the form of platelet-rich plasma has been used for wound healing.

​Other functions of platelets include clot retraction, pro-coagulation, inflammation, cytokine signalling, and phagocytosis.

Platelet Disorders:

High Platelet Count: The condition is also called thrombocytosis. When the platelet count becomes too high than normal range, there is increased risk for formation of blood clots or thrombosis. Clot formation due to high number of leukocytes can cause obstruction of blood vessels and result in events such as stroke, myocardial infarction, pulmonary embolism, circulatory block etc.  The elevated platelet count is due to myeloproliferative disorder. Disorders due to an elevated count includes essential thrombocytosis. Elevated counts either reactive or as an expression of myeloproliferative disease may produce dysfunctional platelets.

Low Platelet Count: The condition is also called thrombocytopenia. When the platelet count becomes low than normal range, excessive bleeding occurs. This condition may be caused by the failure of bone marrow to produce normal amount of platelets. Thrombocytopenia is also produced by increased destruction of platelets after they have been formed and released into the blood. Disorders due to a reduced platelet count include thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytopenic purpura, drug-induced thrombocytopenic purpura, Gaucher's disease, and aplastic anemia​

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Vitamin D Deficiency Symptoms and Treatment

Vitamin D deficiency is a condition when the blood serum levels of vitamin D are lower than the normal range. It is is also called hypovitaminosis D. Vitamin D is essential for the body in developing strong bones. It helps the body to absorb calcium from the diet. Vitamin D is normally produced by the body on exposure to sunlight. It is also naturally available in foods containing vitamin D such as milk, fish, nuts, egg, meat etc.

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The compound 25-hydroxyvitamin D (calcidiol) is a precursor to the active form of 1,25-dihydroxy vitamin D (calcitriol) in the blood. The 25-hydroxyvitamin D is transformed into the active metabolite in the kidney. The active form of vitamin D controls the level of calcium and phosphorous present in the blood.

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Causes of Vitamin D Deficiency

Decreased dietary intake of vitamin D: Those who do not consume the adequate vitamin D in their diet are deficiency of vitamin D. People who are strictly vegetarian or people under malnutrition are more prone to have vitamin D deficiency.

Increased age: Older people are more prone to vitamin D deficiency because of decreased absorption from the gut.

Decreased exposure to sunlight. Vitamin D is produced by the skin during exposure to the sunlight. People who live their lives mostly at home, those who live in northern latitudes, people wearing long dresses covering most of their body, and those who do indoor jobs especially are prone to be vitamin D deficient.

Presence of dark skin color: The dark pigmentation on the skin by melanin reduces the skin's ability to make vitamin D when exposed to the sunlight.

Decreased absorption of vitamin D: Those medical conditions which inhibit the absorption of vitamin D from the intestine will cause deficiency of vitamin D.

Inability to convert vitamin D into its active form: Vitamin D is converted into its active form by the kidneys. The inability of the kidneys to convert vitamin D into the active from will cause deficiency of vitamin D in the body.

Obesity: Individuals who are obese have lower circulating vitamin D in their blood due to reduced bioavailability. The fat cells extract vitamin D from the blood and thus decrease the amount of it in the blood circulation. Excessive body fat will cause vitamin D deficiency.

Hereditary disorders: Disorders which cause decreased vitamin D metabolism in the body can cause vitamin D deficiency in certain people.

Signs and Symptoms

Vitamin D deficiency causes rickets, which is a childhood disease characterized by decreased mineralization of the bones, bone softening, skeletal deformities of the long bones, and stunted growth.

​Deficiency of vitamin D causes osteomalacia, which is a bone thinning disorder found in adults. It is characterized by proximal muscle weakness and fragility of the bones.

It causes osteoporosis in adults, which is a condition of reduced bone density and fragility.

It causes muscular aches and weakness.

​It causes twitching and fasciculations of the muscles.

It is a risk factor in developing depressive symptoms in older people.​

​Tests For vitamin D Deficiency

​Vitamin D deficiency is is diagnosed by measuring the concentration of the compound 25-hydroxyvitamin D (calcidiol) in the blood. A concentration of 75–80 nmol/L (30–32 ng/mL) is sufficient for a healthy adult​ and a level below this range indicates vitamin D deficiency.

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​Treatment For Vitamin D Deficiency

Vitamin D deficiency is treated through dietary supplementation and also by sun exposure. Foods such fish and fish liver oils, oysters, soy products, milk and diary products, eggs, and mushrooms are abundant in vitamin D.

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Adequate exposure to sunlight can provide the necessary daily vitamin D. Extreme sun light exposure should be avoided. Sunscreens inhibit the production of vitamin D on the skin. The most preferred time for sun exposure is before 8 in the morning and after 5 in the evening.

Vitamin D Supplements

Vitamin D is available as supplements in two forms D2 (ergocalciferol) and D3(cholecalciferol) that differ chemically  in their side-chain. Vitamin D2 is manufactured by the UV irradiation of ergosterol in yeast while vitamin D3 is manufactured by the irradiation of 7-dehydrocholesterol from lanolin and the chemical conversion of cholesterol. Both these forms are regarded as equivalent based on their ability to cure rickets. The steps involved in the metabolism and actions of vitamin D2 and vitamin D3 are identical as well as effectively raise serum 25-hydroxyvitamin D levels. These supplements usually available as granules can be taken alone or fortified with foods or calcium.