Ulcerative Colitis is a painful disease that affects over 100,000 Canadians.

A new treatment option for men suffering from a fatal form of prostate cancer.

Rhinoplasty enhances facial harmony and the proportions of your nose. It can also correct impaired breathing caused by structural defects in the nose. Rhinoplasty surgery can change: Nose size in relation to facial balance. Nose width at the bridge or in the size and position of the nostrils.

Have you watched a surgery on a horse before?

A subdural hematoma (SDH) is a collection of blood below the inner layer of the dura but external to the brain and arachnoid membrane (see the images below). Subdural hematoma is the most common type of traumatic intracranial mass lesion. Subdural hematoma occurs not only in patients with severe head injury but also in patients with less severe head injuries, particularly those who are elderly or who are receiving anticoagulants. Subdural hematoma may also be spontaneous or caused by a procedure, such as a lumbar puncture (see Etiology). Rates of mortality and morbidity can be high, even with the best medical and neurosurgical care (see Prognosis). Subdural hematomas are usually characterized on the basis of their size and location and the amount of time elapsed since the inciting event age (ie, whether they are acute, subacute, or chronic). When the inciting event is unknown, the appearance of the hematoma on neuroimaging studies can help determine when the hematoma occurred. These factors, as well as the neurologic and medical condition of the patient, determine the course of treatment and may also influence the outcome. Generally, acute subdural hematomas are less than 72 hours old and are hyperdense compared with the brain on computed tomography scans. The subacute phase begins 3-7 days after acute injury. Chronic subdural hematomas develop over the course of weeks and are hypodense compared with the brain. However, subdural hematomas may be mixed in nature, such as when acute bleeding has occurred into a chronic subdural hematoma. Presentation varies widely in acute subdural hematoma (see Clinical). Many of these patients are comatose on admission. However, approximately 50% of patients with head injuries who require emergency neurosurgery present with head injuries that are classified as moderate or mild (Glasgow Coma Scale scores 9-13 and 14-15, respectively). Many of these patients harbor intracranial mass lesions. In a large series of patients who developed intracranial hematomas requiring emergent decompression, more than half had lucid intervals and were able to make conversation between the time of their injury and subsequent deterioration. In a more comprehensive review of the literature on the surgical treatment of acute subdural hematomas, lucid intervals were noted in up to 38% of cases. These patients may be more likely to benefit from medical and surgical intervention when instituted in a timely fashion (ie, before further neurological deterioration).

HIV is spread only in certain body fluids from a person infected with HIV. These fluids are blood, semen, pre-seminal fluids, rectal fluids, vaginal fluids, and breast milk. In the United States, HIV is spread mainly by having sex or sharing injection drug equipment, such as needles, with someone who has HIV. To reduce your risk of HIV infection, use condoms correctly every time you have vaginal, oral, or anal sex. Don’t inject drugs. If you do, use only sterile injection equipment and water and never share your equipment with others. Pre-exposure prophylaxis (PrEP) is an HIV prevention option for people who don’t have HIV but who are at high risk of becoming infected with HIV. PrEP involves taking a specific HIV medicine every day. PrEP should always be combined with other prevention options, such as condoms.

Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal, temporal and parietal lobes, the corona radiata, globus pallidus, caudate and putamen. The MCA is the most common site for the occurrence of ischemic stroke.[1] Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal.[1] In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the oedematus cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion. Contralateral hemiparesis and hemisensory loss of the face, upper and lower extremities is the most common presentation of MCA syndrome.[1] Lower extremity function is more spared than that of the faciobrachial region.[2] The majority of the primary motor and somatosensory cortices are supplied by the MCA and the cortical homunculus can, therefore, be used to localize the defects more precisely.it is important to note that middle cerebral artery lesions mostly affect the dominant hemisphere i.e. the left cerebral hemisphere.

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An aortic dissection is a serious condition in which the inner layer of the aorta, the large blood vessel branching off the heart, tears. Blood surges through the tear, causing the inner and middle layers of the aorta to separate (dissect). If the blood-filled channel ruptures through the outside aortic wall, aortic dissection is often fatal. Aortic dissection is relatively uncommon. The condition most frequently occurs in men in their 60s and 70s. Symptoms of aortic dissection may mimic those of other diseases, often leading to delays in diagnosis. However, when an aortic dissection is detected early and treated promptly, the chance of survival greatly improves.

Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection injury of the spinal cord, often in the cervical cord region. (See Presentation.) Patients with Brown-Séquard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrome. (See Etiology, Presentation, and Workup.) As an incomplete spinal cord syndrome, the clinical presentation of Brown-Séquard syndrome may range from mild to severe neurologic deficit. (See Presentation.) Brown-Séquard–plus syndrome The pure Brown-Séquard syndrome reflecting hemisection of the cord is not often observed. A clinical picture composed of fragments of the syndrome or of the hemisection syndrome plus additional symptoms and signs is more common. These less-pure forms of the disorder are often referred to as Brown-Séquard–plus syndrome.[1] Interruption of the lateral corticospinal tracts, the lateral spinal thalamic tract, and at times the posterior columns produces a picture of a spastic, weak leg with brisk reflexes and a strong leg with loss of pain and temperature sensation. Note that spasticity and hyperactive reflexes may not be present with an acute lesion.

What Causes Chest Pain ?

The dog bite victim needs to be taken to a safe place away from the assailant dog to prevent further attack and injury. Since dog bites can cause significant damage beneath the skin, a type of injury that cannot always easily be appreciated, medical care should be accessed by a health care practitioner. Wounds should be kept elevated and, if possible, washing the wound with tap water may be attempted. Information should be obtained from the dog's owner about the dog's rabies immunization status, but if this is not possible, hospital, animal control centers, or law enforcement personnel will help gather any required information.

The key difference between monophasic and biphasic defibrillator is that the monophasic defibrillator is a type of defibrillation waveform where a shock is delivered to the heart from one vector as shown below. Whereas, in biphasic defibrillation, shock is delivered to the heart via two vectors.

Cystinuria is a condition characterized by the buildup of the amino acid cystine, a building block of most proteins, in the kidneys and bladder. As the kidneys filter blood to create urine, cystine is normally absorbed back into the bloodstream. People with cystinuria cannot properly reabsorb cystine into their bloodstream, so the amino acid accumulates in their urine. As urine becomes more concentrated in the kidneys, the excess cystine forms crystals. Larger crystals become stones that may lodge in the kidneys or in the bladder. Sometimes cystine crystals combine with calcium molecules in the kidneys to form large stones. These crystals and stones can create blockages in the urinary tract and reduce the ability of the kidneys to eliminate waste through urine. The stones also provide sites where bacteria may cause infections.

The virus was first discovered in 1964 when Sir Michael Anthony Epstein and Ms. Yvonne Barr found it in a Burkitt lymphoma cell line. In 1968, the virus was linked to the disease infectious mononucleosis. Infection with Epstein-Barr virus (EBV) is common and usually occurs in childhood or early adulthood. EBV is the cause of infectious mononucleosis (also termed "mono"), an illness associated with fever, sore throat, swollen lymph nodes in the neck, and sometimes an enlarged spleen. It is also known as human herpes virus 4. Although EBV can cause mononucleosis, not everyone infected with the virus will get mononucleosis. Less commonly, EBV can cause more serious disease. Symptoms caused by EBV are usually mild and self-limited, but the virus persists in the body for life. It can be reactivated quietly without causing symptoms and may contaminate saliva. Thus, otherwise healthy people can spread the virus to uninfected people through kissing or sharing

A cornea transplant, also called keratoplasty, is a surgical procedure to replace part of your cornea with corneal tissue from a donor. Your cornea is the transparent, dome-shaped surface of your eye that accounts for a large part of your eye's focusing power. A cornea transplant can restore vision, reduce pain and improve the appearance of a damaged or diseased cornea. Most cornea transplant procedures are successful. But cornea transplant carries a small risk of complications, such as rejection of the donor cornea.

The most common symptoms noticed by people with haemochromatosis (inherited iron overload disorder) are • Fatigue, weakness and lethargy • Joint pains leading to osteoarthritis * Other symptoms include: • Abdominal pain • Diabetes • Liver disorders; enlarged liver, cirrhosis • Sexual disorders; loss of sex drive in both male and female, impotence in men, absent or scanty menstrual periods and early menopause in women • Decrease in body hair • Discolouration or bronzing of the skin • Cardiomyopathy; disease of the heart muscle • Neurological/psychiatric disorders; impaired memory, mood swings, severe irritability, depression. These symptoms, if present, take time to develop. No two people are alike and symptoms will vary from person to person. Some people never develop any symptoms at all. All of the symptoms of haemochromatosis can also be caused by other medical conditions or even just the stresses of modern life. They develop slowly and people often do not notice what is happening for a long time. This can make haemochromatosis difficult to diagnose. Symptoms are caused by high levels of iron stored in the body. One indicator of the level of iron stored is serum ferritin. If iron stores are high the serum ferritin level will be high, but serum ferritin levels can also be raised by other factors. The normal range is 20 – 300 micrograms per litre (µg/L) for men and 10 – 200 µg/L for women. There is strong medical evidence of a potential for significant organ damage when iron stores cause serum ferritin levels above 1,000 µg/L. However some people seem to experience symptoms with levels between 300 and 1,000 µg/L. Higher levels are more likely to be associated with more severe symptoms. If haemochromatosis is diagnosed and treated before serious iron overload and significant damage occurs, most symptoms will decrease or disappear. However there is evidence that treatment may not alleviate arthritis symptoms.

The bones, ligaments and tendons that make up your shoulder joint are encased in a capsule of connective tissue. Frozen shoulder occurs when this capsule thickens and tightens around the shoulder joint, restricting its movement. Doctors aren't sure why this happens to some people, although it's more likely to occur in people who have diabetes or those who recently had to immobilize their shoulder for a long period, such as after surgery or an arm fracture.

Specific treatment for menorrhagia is based on a number of factors, including: Your overall health and medical history The cause and severity of the condition Your tolerance for specific medications, procedures or therapies The likelihood that your periods will become less heavy soon Your future childbearing plans Effects of the condition on your lifestyle Your opinion or personal preference Drug therapy for menorrhagia may include: Iron supplements. If you also have anemia, your doctor may recommend that you take iron supplements regularly. If your iron levels are low but you're not yet anemic, you may be started on iron supplements rather than waiting until you become anemic. Nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs, such as ibuprofen (Advil, Motrin IB, others) or naproxen (Aleve), help reduce menstrual blood loss. NSAIDs have the added benefit of relieving painful menstrual cramps (dysmenorrhea). Tranexamic acid. Tranexamic acid (Lysteda) helps reduce menstrual blood loss and only needs to be taken at the time of the bleeding. Oral contraceptives. Aside from providing birth control, oral contraceptives can help regulate menstrual cycles and reduce episodes of excessive or prolonged menstrual bleeding. Oral progesterone. When taken for 10 or more days of each menstrual cycle, the hormone progesterone can help correct hormone imbalance and reduce menorrhagia. The hormonal IUD (Mirena). This intrauterine device releases a type of progestin called levonorgestrel, which makes the uterine lining thin and decreases menstrual blood flow and cramping. If you have menorrhagia from taking hormone medication, you and your doctor may be able to treat the condition by changing or stopping your medication.