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Cardiogenic shock is a major, and frequently fatal, complication of a variety of acute and chronic disorders that impair the ability of the heart to maintain adequate tissue perfusion. Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state. Cardiogenic shock is the commonest cause of death after acute myocardial infarction. It occurs in 7% of patients with ST segment elevation myocardial infarction and 3% with non-ST segment elevation myocardial infarction. It most commonly occurs in association with, and as a direct result of, acute myocardial infarction. Decreased coronary perfusion pressure and increased myocardial oxygen demand play a role in the vicious cycle that leads to cardiogenic shock. Cardiogenic Shock is the most serious consequence of myocardial infarction, but can also result from other cardiac emergencies, such as cardiac tamponade. A sudden and severe drop in the blood pressure and blood flow through the body because the heart is not pumping normally. Cardiogenic shock is based upon an inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively. Patients who develop cardiogenic shock from acute MI consistently have evidence of progressive myocardial necrosis with infarct extension. Cardiogenic shock has a death rate of about 60% and is the major cause of death in patients hospitalized for a heart attack. Getting immediate medical treatment for a heart attack is important in preventing the development of cardiogenic shock.

Causes of Cardiogenic shock

The main causes of Cardiogenic shock:

• Myocardial Infarction (heart attack).
• Diastolic - Ventricular hypertrophy and restrictive cardiomyopathies.
• Losing about 1/5 or more of the normal amount of blood in your body causes hypovolemic shock.
• Severe valvular heart disease, particularly aortic stenosis.
• Acute, severe pulmonary embolism.
• Myocardial suppression due to bacteraemia/sepsis (although, strictly speaking, this would be defined as septic shock).

Signs and symptoms of Cardiogenic shock

Signs and symptoms often experienced with Cardiogenic shock are:

• Profuse sweating.
• Low blood pressure.
• Chest pain.
• Nausea and vomiting.
• Rapid breathing.
• Dyspnoea.
• Loss of ability to concentrate.
• Fatigue due to hyperventilation and hypoxia.

Treatment of Cardiogenic shock

Some most common treatmet of Cardiogenic Shock:

• Intra-aortic balloon counterpulsation (IABP) to improve heart and blood vessel ( cardiovascular ) function.
• Intravenous fluids, including blood and blood products, may be given if indicated.
• Medicines such as dopamine , dobutamine, epinephrine, and norepinephrine may be needed to increase blood pressure and the amount of blood pumped out of the heart.
• Careful monitoring in an intensive care unit is necessary. Further treatment depends on the cause. Fluids and medications given intravenously (through a vein directly into the bloodstream) are used to maintain blood flow.

May-Thurner syndrome is deep vein thrombosis of the iliofemoral vein. It is not a disease but a congenital anatomic variant. It is a genetic disorder that results from an abnormality of a chromosome. Chromosomes are thin strands of material found in the nucleus of each cell. They contain the genes that determine each person's characteristics. In may turner syndrome, one of the X chromosomes is missing or misshapen in most of the cells in the body. The reason for this total or partial loss of the chromosome usually cannot be found, but the loss occurs soon after the baby is conceived. There is nothing either parent can do to prevent this from happening; it is a biological accident for which no one is responsible. Girls with may turner syndrome are shorter than their peers and reach an average adult height of 4 feet 8 inches, although a few women may reach or exceed 5 feet in height. Their body proportions are normal. May turner syndrome is characterized by the presence of a single complete functioning sex-determining chromosome, the X chromosome, instead of two, either XX or XY. In may turner syndrome, female sexual characteristics are present but generally underdeveloped.

The most common features of may turner syndrome are short stature and reduced or absent development of the ovaries. As adults, women with this disorder are typically infertile. This condition occurs in about 1 in 2,500 female births worldwide, but is much more common among pregnancies that do not survive to term (miscarriages and stillbirths). Other complications of may turner syndrome include defects of the kidneys and heart, thyroid disease, arthritis and skeletal disorders, and development of type 2 diabetes. In early childhood, girls who have Turner syndrome may have frequent middle ear infections. Recurrent infections can lead to hearing loss in some cases. Girls with may turner Syndrome are usually of normal intelligence with good verbal skills and reading skills. Some girls, however, have problems with math, memory skills and fine-finger movements. People with may turner Syndrome are all different. Some may have many physical differences and symptoms, whereas others experience only a few medical problems. With early and appropriate medical care and ongoing support, most people with may turner Syndrome can lead normal, healthy, and productive lives.

Causes of May Thurner syndrome

Here are the list of the possible causes of May Thurner syndrome:

• The exect cause or factors that put a couple at risk of having a daughter with may turner syndrome are not known.
• An abnormality of a chromosome.

Symptoms of May Thurner syndrome

Some sign and Symptoms related to May Thurner syndrome:

• Short stature.
• Broad chest ( shield chest ) and widely-spaced nipples.
• Low-set ears.
• A webbed neck.
• Drooping eyelids.
• Hearing loss.
• Pigmented moles.

Treatment of May Thurner syndrome

Some most common treatmet of May Thurner Syndrome:

• Growth hormone may help a child with May turner syndrome grow taller.
• Estrogen replacement therapy is often started when the girl is 12 or 13 years old. This helps trigger the growth of breasts, pubic hair, and other sexual characteristics.
• Women with May turner syndrome who wish to become pregnant may consider using a donor egg.

Lown-Ganong-Levine syndrome is a syndrome of pre-excitation of the ventricles due to an accessory pathway providing an abnormal electrical communication from the atria to the ventricles. This condition causes people living with Lown-Ganong-Levine syndrome to experience rapid heartbeats, heart palpitations, and blackouts. It is not uncommon for people to live with Lown-Ganong-Levine syndrome well into adulthood before any they experience any symptoms. The heartbeat originates in a place called the sino-atrial node, situated in the right upper heart chamber. The Lown-Ganong-Levine syndrome is diagnosed by the presence of a short PR interval and normal QRS complex on the surface electrocardiogram. If you have Lown-Ganong-Levine syndrome, extra tissue in the way of your impulses may sometimes divert from their usual route down the bundle of His and conduct along other electrical tissues. This can sometimes lead to a rapid heartbeat, and possibly symptoms of palpitations and blackouts. Anti-arrhythmetic drugs help many people with Lown-Ganong-Levine or other heart rhythm problems.

Causes of Lown Ganong Levine syndrome

Here are the list of the possible causes of Lown Ganong Levine syndrome:

• The exact cause of lown ganong levine syndrome are not known.

Symptoms of Lown Ganong Levine syndrome

Some sign and Symptoms related to Lown Ganong Levine syndrome:

• Palpitations.
• Lightheadedness.
• Shortness of breath.
• Weakness.

Treatment of Lown Ganong Levine syndrome

Some most common treatmet of Lown Ganong Levine syndrome:

• Anti-arrhythmetic drugs help many people with Lown-Ganong-Levine or other heart rhythm problems.

Leriches syndrome usually occurs in men and commonly also causes impotence (erectile dysfunction). Impotence is common in men with lack of adequate blood flow. Leriches syndrome is characterized by the triad of symptoms consisting of absent or diminished femoral pulses, claudication or pain with walking in the buttocks and legs and penile impotence. A person with leriches syndrome must stop smoking immediately, or symptoms will relentlessly worsen. Amputation is then likely to become necessary. Exposure to cold, which causes blood vessels to narrow (constrict), and use of certain drugs should be avoided. Wearing shoes that fit well and have wide toe spaces can help prevent injury to the feet. For people who quit smoking but still have leriches syndrome, surgeons may perform bypass surgery in an attempt to avoid amputation. Surgery to remove blood clots (thromboendarterectomy) can be performed when thrombolytic drugs are ineffective or too dangerous.

Causes of Leriches syndrome

Here are the list of the possible causes of Leriches syndrome:

• Diseases that affect the nervous system, including strokes, spinal cord injuries, multiple sclerosis, long-standing diabetes, and Parkinson's disease.
• Anterior temporal-lobe lesions.
• Cigarette smoking.
• High blood pressure and high cholesterol.
• Diabetes Mellitus.
• Disease of dorsal-root ganglia.

Symptoms of Leriches syndrome

Some sign and Symptoms related to Leriches syndrome:

• The syndrome is characterized by the triad of symptoms consisting of absent or diminished femoral pulses, claudication or pain with walking in the buttocks and legs and penile
• A recurrent, sudden, or uncontrollable urge to urinate
• Pain relieved with dependent position.
• A frequent need to urinate, sometimes every 2 hours or less.

Treatment of Leriches syndrome

Some most common treatmet of Leriches syndrome:

• Although there is no cure, specific symptoms can usually be relieved by treatment. For example, a corticosteroid applied externally (rather than by mouth) can help heal inflamed eyes and skin sores.
• Thalidomide is being investigated for use. Needle punctures should be avoided because the skin may become inflamed.
• Angioplasty is often performed immediately after angiography. Angioplasty may be performed to relieve symptoms and thus postpone or avoid surgery.
• Surgery to remove blood clots can be performed when thrombolytic drugs are ineffective or too dangerous.

A lacunar stroke is a blockage of blood flow to a part of the brain supplied by one or more small arteries. A lacunar stroke occurs when one of the arteries that provide blood to the brain's deep structures is blocked. These arteries are small, and are uniquely vulnerable. Hypertension can lead to lacunar strokes because it causes a pounding pulse. High blood pressure can directly damage these arteries. It also can dislodge small clumps or clots that can block blood flow. Unlike strokes that damage the cortex, lacunar strokes are only rarely caused by a blood clot that forms elsewhere in the body, such as the neck or heart, and travels through the bloodstream to the brain. A clot traveling through the bloodstream is called an embolus. It is difficult for an embolus to make its way into the small arteries that can cause a lacunar stroke. Lacunar strokes, a subtype of ischemic stroke, have earned their name because the area rendered ischemic takes the form of a small lacune or cavity (usually less than 15mm in diameter). In lacunar stroke one of the tiny blood vessels deep inside the brain tissue becomes blocked, leading to the death of the small area of tissue that it supplies. Lacunar strokes are usually less severe.

Smoking is an established risk factor for lacunes. In a lacunar stroke, brain cells in a relatively small area are damaged or killed by lack of oxygen. These small areas of brain destruction are called lacunes. Lacunar strokes involve only small areas of the brain, but they cause significant disability. The symptoms of lacunar stroke vary depending on the part of the brain that is deprived of its blood supply. Different areas of the brain are responsible for different functions, such as sensation, movement, sight, speech, balance and coordination. In an intra-cerebral haemorrhage the bleeding occurs inside the brain itself. In a subarachnoid haemorrage the burst blood vessel bleeds into the subarachnoid space surrounding the brain. Unlike strokes that damage the cortex, lacunar strokes are only rarely caused by a blood clot that forms elsewhere in the body, such as the neck or heart, and travels through the bloodstream to the brain. A person with a severe stroke may need help with self-care or feeding. To prevent future strokes, it is very important to control high blood pressure. It helps to take a daily aspirin or other blood-thinning medication (ticlopidine or clopidogrel).

Causes of Lacunar stroke

Here are the list of the possible causes of Lacunar Stroke:

• Diabetes mellitus.
• A cerebral hemorrhage (bleeding in the brain) can cause a stroke by depriving blood and oxygen to parts of the brain.
• Alcohol consumption.
• Smoking is an established risk factor for lacunar stroke.
• History of prior of stroke.

Symptoms of Lacunar Stroke

Some sign and symptoms related to Lacunar Stroke:

• Sudden numbness.
• Difficulty with muscle movements, such as swallowing, moving arms and legs.
• Difficulty speaking.
• Weakness or paralysis of eye muscles.
• Clumsiness of a hand or arm.
• Dysarthria and dysphagia also may be present.

Treatment of Lacunar Stroke

Some most common treatmet of Lacunar Stroke:

• If doctors are able to provide treatment within three hours after symptoms start, they probably will use with a clot-dissolving medication.
• Patients with clot-related stroke who are ineligible for t-PA treatment may be treated with heparin or other blood thinners, or with aspirin or other anti-clotting agents in some cases.
• A speech-language therapist can assist with speech-language problems and swallowing disorders. Early assessment of a patient with swallowing problems may prevent dehydration and malnutrition from inadequate intake, as well as prevent aspiration and pneumonia.
• Surgery rarely is required, but patients with severe dysphagia may require long-term tube feeding.

Coarctation of the aorta is a narrowing of the aorta between the upper-body artery branches and the branches to the lower body. It's relatively common, accounting for 5 percent to 10 percent of all congenital heart conditions, and often occurs along with other heart defects. This blockage can increase blood pressure in your arms and head, reduce pressure in your legs and seriously strain your heart. Aortic valve abnormalities often accompany coarctation. Coarctation occurs most commonly in a short segment of the aorta just beyond where the arteries to the head and arms take off, as the aorta arches inferiorly toward the abdomen and legs. Coarctation of the aorta may range from mild to severe. The aorta carries blood from the heart to the vessels that supply the body with blood and nutrients. If part of the aorta is narrowed, it is hard for blood to pass through the artery. People with this condition often have high blood pressure in the upper body and arms (or one arm) and low blood pressure in the lower body and legs.

A coarctation can occur anywhere in the aorta, but it is most often found just beyond the point where the aorta sends a branch off to supply the left arm. In babies with coarctation, the aortic arch may be small (hypoplastic). Coarctation may also occur along with other cardiac defects, typically involving the left side of the heart. The defects most commonly seen with coarctation are bicuspid aortic valve and ventricular septal defect. Aortic coarctation occurs in approximately 1 out of 10,000 people. It is usually diagnosed in children or adults under age 40. Symptoms depend on how much blood can flow through the artery. In severe cases, symptoms are seen when the baby is very young. Coarctation of the aorta usually requires treatment, and there are a number of options to repair the constriction. While treatment for coarctation of the aorta is usually successful, it's a condition that requires careful follow-up through infancy and into adulthood.

Causes of Coarctation of the aorta

The main causes of Coarctation of the aorta:

• Improper development of the aorta in the first eight weeks of fetal growth.
• Genetic disorders, such as Turner's syndrome.
• Birth defects of the aortic valve, such as a bicuspid aortic valve.

Signs and symptoms of Coarctation of the aorta

Signs and symptoms often experienced with Coarctation of the aorta are:

• Muscle weakness.
• Dizziness or fainting.
• Chest pain.
• Leg cramps with exercise.
• Pounding headache.
• Nosebleeds.

Treatment of Coarctation of the aorta

Some most common treatmet of Coarctation of the aorta:

• Babies with severe coarctation of the aorta may receive a drug called prostaglandin E. This drug helps keeps the ductus arteriosis open, providing a bypass for blood flow around the constriction, until the coarctation is repaired.
• Surgery is usually recommended.
• If the problem area was small, the two free ends of the aorta may be re-connected. This is called anastomosis.
• If a large part of the aorta was removed, a Dacron graft (a synthetic material) is used to fill the gap.

Cerebellar hemorrhage occurs when bleeding takes place in the cerebellum, usually from a stroke. Cerebellar hemorrhage result from the same causes as other intracerebral hemorrhages. Long-standing hypertension with degenerative changes in the vessel walls and subsequent rupture is believed to be the most common cause of a typical cerebellar hemorrhage. Hemorrhage into tumor, blood dyscrasias, amyloid angiopathy, arteriovenous malformations, trauma, and sympathomimetic abuse are less common causes of cerebellar hemorrhage. Cerebellar hemorrhage may occur at any age, depending on the etiology. Generally, incidence increases with age; most hypertensive hemorrhages occur in patients older than 50 years. Rupture of a vascular malformation may be the most common cause in children. The cerebellum plays a major role in maintaining balance.

Causes of Cerebellar hemorrhage

The main causes of Cerebellar hemorrhage:

• Sympathomimetic drug use.
• Hemorrhage into tumor.
• Cocaine.
• Blood thinners such as Coumadin.
• Heavy alcohol consumption.
• High Blood Pressure.
• Brain Aneurysm.

Signs and symptoms of Cerebellar hemorrhage

Signs and symptoms often experienced with Cerebellar hemorrhage are:

• Nausea and vomiting.
• Headaches in lower back of skull.
• Swallowing difficulties.
• Balance problems with walking.
• Dizziness.
• Closed eyelid.
• Vertigo ("spinning sensation").

Treatment of Cerebellar hemorrhage

Some most common treatmet of Cerebellar hemorrhage:

• Mannitol or similar agent to lower the pressure in the brain.
• In symptomatic bradycardia reflecting Cushing response, atropine may be beneficial if hypotension is present.
• Mannitol 1 g/kg may be considered preoperatively in patients with tight posterior fossa.
• Surgical care has been the mainstay of therapy for cerebellar hemorrhage, although some patients with small hematomas may be treated successfully without surgery.

Cavernous sinus thrombosis is a blood clot in the cavernous sinus. Cavernous sinus thrombosis is usually a late complication of an infection of the central face or paranasal sinuses. Cavernous sinus thrombosis is generally a fulminant process with high rates of morbidity and mortality. The cavernous sinuses are situated within the skull, immediately behind each eye socket (orbit) and on either side of the pituitary gland. They are large veins and their purpose is to drain blood from the brain and face back to the heart. Other causes include bacteremia, trauma, and infections of the ear or maxillary teeth. It is an uncommon complication following infection of face,paranasal sinuses resulting in thrombosis of cavernous sinus and its surrounding anatomic structures including cranial nerves 3,4,5[maxillary and ophthalmic division],6 and the internal carotid artery. The most common signs of Cavernous sinus thrombosis are related to anatomical structures affected within the cavernous sinus, notably cranial nerves III-VI, as well as symptoms resulting from impaired venous drainage from the orbit and eye. Classic presentations are abrupt onset of unilateral periorbital edema, headache, photophobia, and proptosis.

Cavernous sinus thrombosis is often misdiagnosed because it is so uncommon. It may be confused with orbital cellulitis. Features that distinguish Cavernous sinus thrombosis from orbital cellulitis include cranial nerve dysfunction, bilateral eye involvement, and mental status changes. Without effective therapy, signs appear in the contralateral eye by spreading through the communicating veins to the contralateral cavernous sinus. Eye swelling begins as a unilateral process and spreads to the other eye within 24-48 hours via the intercavernous sinuses. This is pathognomonic for Cavernous sinus thrombosis. The condition can affect any one at any age but is not contagious or inherited. Bacterial infections caused by Streptococcus and Staphylococcus are the most common organisms found in patients with cavernous sinus thrombosis. Before antibiotics were discovered, the mortality from cavernous sinus thrombosis was 80% to 100%. Since the discovery of antibiotics, the mortality ranges between 20% and 30%. The condition can be easily treated with high doses of intravenous antibiotic drugs which are given immediately after diagnosis. If the condition does not improve, the sinus may be drained surgically.

Causes of Cavernous Sinus Thrombosis

The main causes of Cavernous Sinus Thrombosis:

• Due to the spread of bacteria from an infection in the sinus, eye, ears, and nose or on the face.
• Chronic sinusitis or diabetes mellitus.
• Streptococci, pneumococci, and fungi.

Signs and symptoms of Cavernous Sinus Thrombosis

Signs and symptoms often experienced with Cavernous Sinus Thrombosis are:

• High fever.
• Severe pain behind and around the eye.
• Rapid heart rate.
• Muscle weakness.
• Numbness in the face.
• Hearing loss or fluid from the ear.
• Swelling of the eye lids and of the membrane covering the white of the eye.
• Loss of vision.

Treatment of Cavernous Sinus Thrombosis

Some most common treatmet of Cavernous Sinus Thrombosis:

• The condition can be easily treated with high doses of intravenous antibiotic drugs which are given immediately after diagnosis.
• Oral antibiotics are given for mild cases; intravenous antibiotics are given for severe cases.
• Sometimes surgery is needed to drain a collection of pus or an infected sinus.
• You may also be placed on a blood thinner called heparin, but this remains controversial and the decision is made between you and your physician.

Angiodysplasia is a condition which can be defined as the abnormal or enlarged blood vessels in the gastrointestinal tract which can be a source of gastrointestinal bleeding and anemia. Angiodysplasia of the colon has been seen in about 3% of "nonbleeding persons" and in about 5% of patients evaluated for blood in the stool, anemia, or hemorrhage. Men and women are equally at risk for developing angiodysplasia of the colon. The condition is mostly related to the aging and degeneration of the blood vessels, and occurs in older adults. Angiodysplasia of the colon is not related to cancers or other disease of the blood vessels. It is different than diverticulosis, another very common cause of bleeding in older adults. The symptoms vary. Often, in elderly patients, the symptoms are anemia, weakness, fatigue, and shortness of breath. There may not be any signs of bleeding directly from the colon. Although angiodysplasia is probably quite common, the risk of bleeding is increased in disorders of coagulation. These are abnormal collections of blood vessels within the gastrointestinal tract. These are also called arteriovenous malformations.

Angiodysplasia is most readily diagnosed by endoscopy. The lesions are typically discrete, flat or slightly raised, and bright red and are often stellate in appearance. Celiac artery and superior mesenteric artery injections may fail to demonstrate the lesions. Some patients may have dark or black, tarry stools. There is no pain associated with angiodysplasia. When a patient is bleeding from the colon, it is important to determine the source of the bleeding and the rate of blood loss. The patient's condition must be evaluated continuously and may require admission to an intensive care unit. Administration of IV fluids, and blood products may be required. Actively bleeding vascular ectasia can also be treated by angiography by clotting the blood supply to the bleeding area of the colon. The use of chemicals that cause the blood vessels to constrict can also be administered, whether by angiography or colonoscope.

Causes of Angiodysplasia

Some causes of Angiodysplasia:

• Hereditary hemorrhagic telangiectasia (a rare genetic disease).
• Damaged veins as above.
• Autoimmune diseases such as Scleroderma.
• Congenital (born with these abnormal vessel connections).

Symptoms of Angiodysplasia

Some symptoms of Angiodysplasia:

• Bright red blood passed from rectum.
• Shortness of breath.
• Tarry black stool (melena).
• Fatigue and weakness.
• Vomiting blood or coffee-ground material.
• Usually painless.

Treatment of Angiodysplasia

Some most common treatmet of Angiodysplasia:

• Actively bleeding vascular ectasia can also be treated by angiography by clotting the blood supply to the bleeding area of the colon.
• The use of chemicals that cause the blood vessels to constrict can also be administered, whether by angiography or colonoscope.
• Administration of IV fluids, and blood products may be required.
• Injection of dyes, such as methylene blue, indigo carmine, and fluorescein, has been used to assist in localization of angiodysplasia before surgical resection.
• Selective infusion of vasopressin is less effective than embolization.

Adams stokes attacks are a type of syncope of cardiac origin resulting from a sudden reduction in blood flow from the heart to the brain. This can cause inadequate blood flow to the brain and fainting. This condition is also called Stokes-Adams or Morgangni, Adams-Stokes disease. The condition is characterized by sudden transient attacks of lightheadedness or unconsciousness, with or without convulsions, due to a temporary cessation of blood supply to the brain. In this condition, the normal heartbeat passing from the upper chambers of the heart to the lower chambers is interrupted. This results in a condition called a " heart block ." When a heart block occurs, the heart rate usually slows considerably. This condition goes by a baffling number of names including the Adams-Stokes, Morgagni, Morgagni-Adams-Stokes, Spens syndrome, and Stokes-Adams disease or syndrome.

Adams stokes attack is the common term for an attack of fainting. Deep and fast respiration changes to weak and slow pulse and respiration, convulsions and respiratory pauses that may last for 60 seconds. Other symptoms may be fixed pupils, incontinence, bilateral babinskis sign with resumption of heartbeats, and flushing of the face. It usually occurs after the age of 40. Loss of consciousness usually occurs suddenly without any cardiac symptoms. Approximately 100 per 1 million individuals develop Stokes-Adams syndrome. It is generally a syndrome connected with age. Treatment must be undertaken by a qualified cardiologist. Medication and a cardiac pacemaker may be required to prevent the sudden heart rate changes that prevent adequate flow of blood to the brain. Appropriate medications to regulate heart rate or surgical implantation of an electrical pacemaker.

Causes of Adams stokes attack

Some causes of Adams stokes attack:

• Inadequate blood flow to the brain.
• Arrhythmia.

Symptoms of Adams stokes attack

Some symptoms of Adams stokes attack:

• Recurrent attacks of fainting.
• Convulsive movements.
• Slow heart rate or multiple missed heart beats.
• Facial flushing occurs for a minute.
• Other symptoms may be fixed pupils, incontinence, bilateral Babinski's sign with resumption of heart beats, and flushing of the face.

Treatment of Adams stokes attack

Some most common treatmet of Adams stokes attack:

• Treatment must be undertaken by a qualified cardiologist. Medication and a cardiac pacemaker may be required to prevent the sudden heart rate changes that prevent adequate flow of blood to the brain.
• Modern surgery began in the mid-19th century with use of anesthetics and antiseptics.
• Included in the area of medicine are the clinical specialties of surgery, pediatrics, psychiatry, obstetrics, and others.

Aplastic anemia, or hypoplastic anemia, results from conditions in which blood cell production in the bone marrow or erythrocyte stem cells are underdeveloped, defective, or absent. Other cases of aplastic anemia are secondary and are caused by radiation, chemicals or viruses. The term aplastic anemia commonly implies a panhypoplasia of the marrow with associated leukopenia and thrombocytopenia. The theoretical basis for marrow failure includes primary defects in or damage to the stem cell or the marrow microenvironment. Aplastic anemia is a syndrome of bone-marrow failure characterized by peripheral pancytopenia and marrow hypoplasia.

Causes of Aplastic Hypoplastic Anemias

Common causes and risk factor's of Aplastic Hypoplastic Anemias include the following :

• Cancer Chemotherapy.
• Radiation therapy.
• Cartilage hair hypoplasia.
• Pregnancy.
• History of an autoimmune disease.
• Shwachman-Diamond syndrome.
• Exposure to certain toxins such as heavy metals.
• Some forms may be associated with thymomas (the types that only affect red blood cells .
• History of specific infectious diseases such as infectious hepatitis.

Symptoms of Aplastic Hypoplastic Anemias

Some of the common sign and symptoms of the disease Aplastic Hypoplastic Anemias are as follows:

• Fatigue.
• Shortness of breath.
• Gastrointestinal bleeding
• Headache.
• Infections.
• Bleeding in gums.
• Weakness.
• Nosebleeds.
• Bleeding under skin.

Treatment of Aplastic Hypoplastic Anemias

Find effective treatment methods of treating Aplastic Hypoplastic Anemias:

• Supportive therapy such as oxygen may be needed
• Antithymocyte Globulin (suppresses immune system to treat autoimmune cause, i.e., stops the body from mistakenly attacking the bone marrow).
• Bone marrow transplantation is the treatment of choice for severe aplasia and for those who need constant RBC replacement.
• Blood Transfusions
• Antibiotics are not given prophylactically because they tend to encourage resistant strains of organisms.
• Cyclosporin (used with Antithymocyte Globulin)
• G-CSF & GM-CSF (stimulate white blood cell production)
• Cyclophosphamide and predisone are also used in some cases.

Sickle cell anemia occurs when a person inherits two abnormal genes that cause their red blood cells to change shape. In sickle cell anemia, the body produces red blood cells that are shaped like a sickle. Under normal circumstances, your red blood cells are flexible and round, and they move easily through your blood vessels to carry oxygen to all parts of your body. Hemoglobin molecules in each red blood cell carry oxygen from the lungs to body organs and tissues and bring carbon dioxide back to the lungs. Although knowledge of the pathophysiological basis for sickle cell anemia has led to advances in its treatment, emergency physicians remain challenged by its varied clinical presentations, including vasoocclusive, hematologic, and infectious crises. Sometimes these red blood cells become sickle-shaped and have difficulty passing through small blood vessels. Characteristic features of this disorder include a low number of red blood cells, repeated infections, and periodic episodes of pain. This abnormality can result in painful episodes, serious infections, chronic anemia, and damage to body organs.

Sickle cell disease is a general term for a group of genetic disorders caused by sickle hemoglobin. With this disorder, sickle-shaped red blood cells are destroyed rapidly, causing anemia. Other symptoms of sickle cell anemia occur when the stiff, inflexible sickled red blood cells get stuck in small blood vessels, depriving organs and tissues of oxygen-rich blood. A serious complication of sickle cell anemia is high blood pressure in the blood vessels that supply the lungs (pulmonary hypertension). The disease primarily affects Africans and African Americans. It is estimated that in the United States, some 50,000 African Americans are afflicted with the most severe form of sickle cell anemia. Pulmonary hypertension occurs in about one-third of adults with sickle cell disease and can lead to heart failure. The National Institutes of Health recommends that all newborns be screened for sickle cell disease, and testing at birth is now required in almost every state. This helps infants with sickle cell anemia get the care and treatment they need right away.

Causes of Sickle Cell Anemia

Common Causes of Sickle Cell Anemia

• Dehydration .
• Pregnancy.
• Fever
• Infection .
• Drop in oxygen or change in air pressure (sometimes occurs during airplane travel) .

Symptoms of Sickle Cell Anemia

Some of the common sign and symptoms of the disease Sickle Cell Anemia follows:

• Paleness.
• Yellow eyes/skin.
• Fatigue.
• Breathlessness.
• Rapid heart rate.
• Delayed growth and puberty.
• Susceptibility to infections.
• Ulcers on the lower legs.
• Jaundice.
• Bone pain.
• Attacks of abdominal pain.
• Fever.

Treatment of Sickle Cell Anemia

Find effective treatment methods of treating Sickle Cell Anemia :

• Bed rest.
• Oral and intravenous fluids .
• Hydroxyurea is a medication that has recently been developed that may help reduce the frequency of pain crises and acute chest syndrome. It may also help decrease the need for frequent blood transfusions. The long-term effects of the medication, however, are unknown.
• Pain relief medications .
• Blood transfusions are generally used only in extreme situations, such as severe anemia or especially bad episodes of pain.
• Oxygen to reduce pain and prevent complications.

Secondary Polycythemia is a disorder of the blood-producing cells of the bone marrow that results in overproduction of red blood cells. Secondary polycythemia is an acquired form of a rare disorder characterized by an abnormal increase in the number of mature red cells in the blood. When RBC levels are low, the body's tissues cannot obtain enough oxygen. Secondary Polycythemia should be suspected in patients with elevated hemoglobin or hematocrit levels, splenomegaly, or portal venous thrombosis. Polycythemia vera also may result in production of too many of the other types of cells in your blood white blood cells and platelets. It is associated with several conditions in adulthood, but in children this condition is usually only diagnosed in the newborn. Polycythemia is also called plethora.

Causes of Secondary Polycythemia

Common causes and risk factor's of Secondary Polycythemia include the following :

• Exposure to high altitudes.
• Chronic heart or lung disease.
• Hormonal disorders.
• Carbon monoxide poisoning.
• Tumors of the brain, liver, or uterus.
• Kidney cysts.

Symptoms of Secondary Polycythemia

Some of the common sign and symptoms of the disease Secondary Polycythemia follows:

• Blood in the stool.
• Blood clots.
• Painful erythema.
• Warmth in parts of the limbs.
• Blackening of the fingers or toes.
• Fever.
• Heat tolerance.
• Weight loss.

Treatment of Secondary Polycythemia

Find effective treatment methods of treating Secondary Polycythemia :

• In relative polycythemia, the patient must avoid diuretics and drink fluids to replenish the liquid portion of the blood .
• For the treatment of polycythemia vera, see Myeloproliferative Disorders .
• Usually, blood is removed from the body in a procedure called phlebotomy, similar to the way blood is removed when donating blood.

Polycythemia is a condition in which there is a net increase in the total number of red blood cells in the body. Polycythemia vera is a disorder of the blood-producing cells of the bone marrow that results in over production of red blood cells. PV may cause shortness of breath, dizziness, itchy or flushed skin, fatigue and headaches. The thickened blood flows more slowly through your small blood vessels and can form clots. PV tends to evolve into acute leukemia or a condition with the marrow replaced by scar tissue. Polycythemia vera is a relatively rare, chronic disorder characterized by an increase in red blood cell mass and in the concentration of hemoglobin. The increase in blood cells makes the blood more viscous, leading to strokes or tissue and organ damage. It is possible that the main title of the report Polycythemia Vera is not the name you expected. This is accompanied by increased white blood cell and platelet production, which is due to an abnormal clone of the hematopoietic stem cells with increased sensitivity to the different growth factors for maturation.

Polycythemia vera is a rare blood disorder in which there is an increase in all blood cells, particularly red blood cells. To have PV, there must be polycythemia which formally exists when the hemoglobin, red blood cell count, and total RBC volume are all above normal. Polycythemia vera is an abnormal increase in blood cells resulting from excess production by the bone marrow. Polycythemia vera is a clonal disorder arising in a multipotent hematopoietic progenitor cell that causes the accumulation of morphologically normal red cells, white cells, platelets, and their progenitors in the absence of a definable stimulus and to the exclusion of nonclonal hematopoiesis. This disease rarely occurs early in life. In polycythemia vera, the excess of red blood cells increases the volume of blood and makes it thicker, so that it flows less easily through small blood vessels. The overproduction of red blood cells may be due to a primary process in the bone marrow , or it may be a reaction to chronically low oxygen levels or, rarely, a malignancy . Polycythemia vera (PV) is a stem cell disorder characterized as a panhyperplastic, malignant, and neoplastic marrow disorder.

Causes of Polycythemia Vera

Common causes and risk factor's of Folic Acid Deficiency Anemia include the following : -

• The exact cause of polycythemia vera is unknown.

• White blood cells.
• Red blood cells.
• Platelets .
• Bone marrow.

Symptoms of Polycythemia Vera

Some of the common sign and symptoms of the disease Polycythemia Vera follows:

• Fatigue.
• Headache.
• Dizziness.
• Shortness of breath.
• Inability to concentrate.
• Night sweats.
• Flushed complexion.
• Bleeding gums.
• Hemoptysis.
• Iitchy skin.
• Numbness.
• High blood pressure.

Treatment of Polycythemia Vera

Find effective treatment methods of treating Polycythemia Vera :

• Certain medications, including chemotherapy.
• Phlebotomy - a procedure that involves removing blood from the body.
• Bone marrow transplantation.
• The goals of treating PV are to control your symptoms and reduce the risk of complications, especially stroke or heart attack , caused by thickened blood and blood clots

Pernicious anemia is a rare disorder in which the body does not absorb enough vitamin B12 from the digestive tract, resulting in an inadequate amount of red blood cells (RBCs) produced. Anemia from an underlying autoimmune digestive disorder. Pernicious anemia is characterized by the presence in the blood of large, immature, nucleated cells that are forerunners of red blood cells. That's because anemia a condition in which there aren't enough healthy red blood cells to carry adequate oxygen to your tissues — can make you feel tired. The diagnosis of pernicious anemia is made by means of microscopic examination of the blood and measurement of vitamin B12 and the products of its breakdown in the blood. Vitamin B12 deficiency can have many causes including PA, malabsorption syndromes, and food cobalmin deficiency. Pernicious anemia is caused by a lack of intrinsic factor, a substance needed to absorb vitamin B12 from the gastrointestinal tract.Pernicious anemia is a condition in which the body does not make enough red blood cells due to a lack of vitamin B12 in the body.

Pernicious anemia is a type of anemia characterized by very large red blood cells. Pernicious anemia (PA) is an autoimmune condition of anemia caused by a deficiency of vitamin B12. Anemia from an underlying autoimmune digestive disorder. The disease was named pernicious anemia because it was fatal before treatment became available, first as liver therapy and, subsequently, as purified vitamin B-12. It usually occurs in people whose bodies have lost the ability to absorb vitamin B12 from food. Pernicious anemia is characterized by the presence in the blood of large, immature, nucleated cells that are forerunners of red blood cells. Anemia can be temporary or long term, and it can range from mild to severe. If you were diagnosed with PA at such a young age, chances are you need the B12 replacement now, at the age of 80, more than ever.

Causes of Pernicious Anemia

There are various factors which give rise to the disease Pernicious Anemia , but here we mentioned some of the common causes:

• Atrophic gastritis.
• Removal of all or part of the stomach.
• Genetics.
• Nutrition.
• Infection.
• Gastrointestinal disease.
• Drugs.
• Metabolic disorders.

Symptoms of Pernicious Anemia

Some of the common sign and symptoms of the disease Pernicious Anemia follows:

• Weak muscles.
• Numbness or tingling in hands and feet.
• Difficulty walking.
• Nausea.
• Decreased appetite.
• Weight loss.
• Irritability.
• Lack of energy or tiring easily.
• Diarrhea.
• Increased heart rate.

Treatment of Pernicious Anemia

Find effective treatment methods of treating Pernicious Anemia :

• Usually, injections of vitamin B12 are sufficient to overcome the deficiency.
• Prevent complications, such as heart or nerve damage.
• Provide ongoing followup to make sure that the treatment is working.
• There is also a preparation of Vitamin B12 that may be given intranasally.
• Therapy for pernicious anemia is administration of vitamin B12 as injections under the skin or into the muscle.

Iron deficiency anemia is the most common type of anemia , and the most common cause of microcytic anemia. Anemia is a condition where red blood cells are not providing adequate oxygen to body tissues. There are many types and causes of anemia. Iron deficiency anemia is a decrease in the number of red cells in the blood caused by too little iron. Your body needs the element iron to make hemoglobin, a substance in red blood cells that enables them to carry oxygen. Iron is needed to form hemoglobin. Iron is mostly stored in the body in the hemoglobin. The differential diagnosis includes thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning. IDA is usually due to a diet insufficient in iron or from blood loss. Blood loss can be acute as in hemorrhage or trauma or long term as in heavy menstruation. A decreased amount of hemoglobin and RBCs in the bloodstream is known as anemia. It is a decrease in the amount of red cells in the blood caused by having too little iron. In healthy people, the body concentration of iron is regulated carefully by absorptive cells in the proximal small intestine, which alter iron absorption to match body losses of iron. A lack of iron in the body can come from bleeding, not eating enough foods that contain iron, or not absorbing enough iron from food that is eaten.

Iron deficiency anemia is a decrease in the number of red cells in the blood caused by too little iron. Lack of iron in your diet is one cause of iron deficiency anemia, but there are other causes as well. For iron deficiency anemia in women, a diet with iron rich foods along with iron supplements is often recommended. When the reserves are depleted, the red blood cells are not only fewer in number but also abnormally small. Iron deficiency, whether it is severe enough to lead to anemia or not, can result from a number of health issues. When the body has sufficient iron to meet its needs (functional iron), the remainder is stored for later use in the bone marrow, liver , and spleen. Having iron deficiency anemia may cause you to feel tired and often look pale. Anemia is a condition where red blood cells are not providing adequate oxygen to body tissues.

Causes of Iron Deficiency Anemia

Common causes and risk factor's of Iron Deficiency Anemia include the following :

• Iron that is poorly absorbed in the digestive tract (may occur due to certain intestinal diseases or after surgery)
• A common cause in infants, children, and pregnant women
• Chronic bleeding, including heavy menstrual bleeding or GI tract bleeding
• Pregnancy
• Diets that contain insufficient iron (fairly rare in the United States)
• Babies who are given cow's milk to drink prior to age 12 months
• Heavy menstrual bleeding.
• Breastfed infants who have not started on solid food after six months of age

Symptoms of Iron Deficiency Anemia

Some of the common sign and symptoms of the disease Iron Deficiency Anemia follows:

• Pale skin color.
• Fatigue.
• Irritability.
• Weakness.
• Shortness of breath .
• Sore tongue.
• Brittle nail.
• Unusual food cravings.
• Decreased appetite.
• Headache - frontal.
• Blue tinge to sclerae.

Treatment of Iron Deficiency Anemia

Find effective treatment methods of treating Iron Deficiency Anemia :

• Iron supplements are typically continued for 6 months after the blood counts return to normal to fully replenish the body's reserves.
• The goals of treating iron-deficiency anemia are to restore normal levels of red blood cells, hemoglobin, and iron as well as to treat the condition causing the anemia.
• Treatment will depend on why the body is bleeding and where it is bleeding.
• Supplemental iron is needed during pregnancy and lactation because normal dietary intake rarely supplies the required amount.

Idiopathic thrombocytopenic purpura is a bleeding disorder characterized by too few platelets in the blood. People with idiopathic thrombocytopenic purpura, because of their low platelet count, tend to bruise easily and bleed longer when injured. Nosebleeds and bleeding gums also are common. Idiopathic thrombocytopenic purpura , also known as primary immune thrombocytopenic purpura and autoimmune thrombocytopenic purpura, is defined as isolated thrombocytopenia with normal bone marrow and the absence of other causes of thrombocytopenia. The bleeding is due to a low number of platelets , blood cells that help the blood clot and stop bleeding. Platelets are cells in the blood that help stop bleeding. In idiopathic thrombocytopenic purpura (ITP), the immune system treats a person's own platelets as if they were invaders in the body, attacking and destroying them. Thrombocytopenic means the blood doesn't have enough platelets.

Idiopathic thrombocytopenic purpura is often divided into two categories: acute and chronic. People with ITP often have purple bruises that appear on the skin. ITP is a decrease in the number of circulating platelets in the absence of toxic exposure or a disease associated with a low platelet count. Idiopathic means the exact cause of the disease is unknown. As most causes appear to be related to antibodies against platelets, it is also known as immune thrombocytopenic purpura. Idiopathic thrombocytopenic purpura (ITP), also called immune thrombocytopenic purpura, is a bleeding disorder in which your blood has difficulty clotting due to an unusually low number of platelets. The bruises are caused by bleeding has occurred in small blood vessels under the skin. quality of each study was graded by two reviewers using formal methodologic rules.

Causes of Idiopathic Thrombocytopenic Purpura

Common causes and risk factor's ofIdiopathic Thrombocytopenic Purpura include the following :

• Microangiopathic hemolytic anemias.
• Aggregation of platelets.
• Activation of coagulation.
• Blood vessels .
• Fibrin.
• Medications.
• Infection.
• Pregnancy.
• Immune disorders.

Symptoms of Idiopathic Thrombocytopenic Purpura

Some of the common sign and symptoms of the disease Idiopathic Thrombocytopenic Purpuraas follows:

• Fluctuating neurological.
• Kidney failure.
• Fever.
• Thrombocytopenia.
• Bruising.
• Bleeding that is hard to stop.
• Bleeding from gums.
• Nosebleeds.
• Heavy menstrual bleeding in women.
• Blood in the urine .
• Blood in the stool.

Treatment of Idiopathic Thrombocytopenic Purpura

Find effective treatment methods of treating Idiopathic Thrombocytopenic Purpura :

• Risk of bleeding relative to lifestyle, such as participation in sports or other vigorous physical activities that may predispose you to injury.
• Risk of bleeding based on other medical conditions or medications.
• Your tolerance for specific medications, procedures, or therapies.
• Expectations for the course of the disease.
• Prehospital airway control may be necessary for a large intracranial hemorrhage.
• EMS providers should be aware of the potential for serious bleeding complications in patients with idiopathic thrombocytopenic purpura.
• Passing the blood over a protein A column (Prosorba), which filters antibodies out of the blood stream.

Hyperbilirubinemia is one of the most common problems encountered in term newborns. A newborn may be bigger or smaller than usual or suffer from problems affecting blood, such as the levels of sugar in the blood being too high or too low. Kernicterus is chronic and irreversible bilirubin encephalopathy, and it is a preventable disorder. When neurological signs evident in the infant, permanent damage has already occurred, leading to death or long term disability. Babies are not easily able to get rid of the bilirubin and it can build up in the blood and other tissues and fluids of the baby's body.

Hyperbilirubinemia is a condition in which there is too much bilirubin in the blood. When red blood cells break down, a substance called bilirubin is formed. These babies often go untreated or are re-admitted to the hospital for salvage phototherapy to reduce bilirubin levels after they have already risen to harmful levels. The heme portion of the hemoglobin molecule is converted into a yellow pigment called bilirubin, which is carried in the blood to the liver where it is chemically modified and then excreted in the bile into the newborn's digestive tract.

Causes of Hyperbilirubinemia

Common Causes of Hyperbilirubinemia :

• A condition that results from the breakdown of red blood cells due to hemolytic disease of the newborn (Rh disease), polycythemia, or hemorrhage.
• Occurs in some baby's in the first week due to low intake or dehydration.
• About 2 percent of breastfed babies develop jaundice after the first week.
• Inadequate liver function due to infection or other factors.

Symptoms of Hyperbilirubinemia

Some of the common sign and symptoms of the disease Hyperbilirubinemia are as follows:

• Jaundice of the skin.
• Fatigue and weakness.
• Loss of appetite.
• Jaundice (yellowing) of the whites of the eyes.
• Abdominal pain .

Treatment of Hyperbilirubinemian

Find effective treatment methods of treating Hyperbilirubinemia :

• Another form of phototherapy is a fiberoptic blanket placed under the baby. This may be used alone or in combination with regular phototherapy.
• Treatment of breast milk jaundice often requires stopping the breastfeeding for one to two days and giving the baby formula often helps lower the bilirubin levels. Breastfeeding can then be resumed.
• When this is not the case or when multiple causes are possible, consultation with a gastroenterologist or hepatologist may be helpful.
• Babies who have bilirubin in their blood at a level that could be harmful need treatment.

Hereditary hemorrhagic telangiectasia is characterized by the presence of multiple arteriovenous malformations that lack intervening capillaries and result in direct connections between arteries and veins. Too much clotting can block blood vessels that are not bleeding consequently, the body has control mechanisms to limit clotting and dissolve clots that are no longer needed. Hereditary hemorrhagic telangiectasia is a condition characterized by abnormal blood vessels which are delicate and prone to bleeding. A child with HHT, also known as Osler-Weber-Rendu Syndrome, tends to form blood vessels that lack the capillaries between an artery and vein. It is usually referred to as the Osler-Weber-Rendu disorder, or simply the OWR. It is a rare inherited disorder that affects blood vessels throughout the body and is characterised by a tendency for bleeding in particular recurrent epistaxis, and skin telangiectasia.

Hereditary haemorrhagic telangiectasia is also known as Osler-Rendu-Weber syndrome. Telangiectasias are abnormally dilated blood vessels associated with a number of diseases. In this condition, without capillaries, arterial blood under high pressure flows directly into a vein. When clotting is uncontrolled, small blood vessels in critical places can become clogged with clots. Large AVMs often cause symptoms when they occur in the brain, lungs, or gastrointestinal tract complications from bleeding or shunting may be sudden and catastrophic.

Causes of Hereditary Hemorrhagic Telangiectasia

Common causes and risk factor's of Hereditary Hemorrhagic Telangiectasia include the following :

• Hereditary hemorrhagic telangiectasia.
• Ataxia - telangiectasia.
• Spider angioma.
• Cutis marmorata telangiectatica congenita.
• Bloom syndrome.
• Klippel-Trenaunay-Weber syndrome.
• Sturge-Weber disease.
• Xeroderma pigmentosa.
• Nevus flammeus such as port-wine stain.

Symptoms of Hereditary Hemorrhagic Telangiectasia

Some of the common sign and symptoms of the disease Hereditary Hemorrhagic Telangiectasia as follows:

• Anxiety.
• Lower back pain.
• Fatigue.
• Fever.

Treatment of Hereditary Hemorrhagic Telangiectasia

Find effective treatment methods of treating Hereditary Hemorrhagic Telangiectasia :

• Life-threatening GI bleeds can be effectively treated by segmental bowel resection.
• Embolization, ligation, or surgical excision is indicated for enlarging or symptomatic pulmonary AV fistulas or for intrahepatic fistulas that cause high-output cardiac failure.
• Pulsed dye laser treatment can be used to photocoagulate telangiectases in the nasal mucosa.
• Radiosurgery can be used to treat smaller cerebral AVMs.
• Humidification and the daily application of nasal lubricants by the individual may be helpful

Hemophilia is a disease that prevents a person's blood from clotting properly, which means that the person bleeds more than a person without hemophilia does. Babies born with hemophilia are missing or have a low level of a protein needed for normal blood clotting or blood coagulation. BeneFIX is indicated for the control and prevention of hemorrhagic episodes in patients with hemophilia B, including control and prevention of bleeding in surgical settings. People with hemophilia are deficient in one of those factors due to their disease genes, and as a result, their blood can't clot properly. Treating the bleeding episodes involves the prompt and proper use of clotting factor concentrates. The clotting process makes use of blood particles called platelets and clot-forming proteins called clotting factors. defective gene interferes with the ability of the body to produce the clotting factors that allow for normal clotting. People living with hemophilia do not have enough of, or are missing, one of the blood clotting proteins naturally found in blood. Hemophilia is a rare genetic blood clotting disorder that primarily affects males.

Hemophilia is a rare disorder in which a person's blood does not clot properly because they do not produce enough of, or are missing, blood clotting proteins called factors. Virtually all people who have hemophilia A or B are born with it. Sticky cells in the blood called platelets go to where the bleeding is and plug up the hole. If you have hemophilia and you have a cut, you'll bleed for a longer time than if your blood clotted normally. Human blood contains special proteins, known as clotting factors. Persons with hemophilia may bleed for a longer time than others after an injury or accident. In most cases, the disorder is passed down through families and most often affects males. Bleeding in the brain, a very serious complication of hemophilia, requires emergency treatment.

Causes of Hemophilia

Common causes and risk factor's of Folic Acid Deficiency Anemia include the following :

• Procoagulant proteins.
• Anticoagulant proteins.
• Fibrinolytic proteins.

Symptoms of Hemophilia

Some of the common sign and symptoms of the diseaseHemolytic Disease Of The Newbornare as follows:

• Anemial
• Jaundicel
• Neonatal jaundicel
• Edemal
• Hydrops fetalis.
• Tooth extraction.
• Surgery.
• Blood in the urine.

Treatment of Hemophilia

• If you have blood in your urine, drink plenty of fluids to ensure hydration.
• Avoid aspirin and anti-inflammatory agents such as ibuprofen because they may further interfere with blood clotting.
• Apply ice and put a splint on affected joints after bleeding to provide relief from symptoms.
• If you have the training on the disease process, you can give yourself factor replacement therapy.