Deuk Laser Disc Repair vs Traditional Spinal Fusion Comparison, Laser versus Fusion

Watch that video of The 10 Most Invasive Parasites in the World

1. What is hemodialysis?
2. Why do you do hemodialysis?
3. How does hemodialysis remove body waste?
4. What are the symptoms and side effects of hemodialysis?
5. How should I eat food when I do hemodialysis?
6. What are some precautions for patients during hemodialysis?


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Here's a quick simple way to determine if a pH disturbance is respiratory or metabolic.

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Bleeding usually occurs from only one nostril. If the bleeding is heavy enough, the blood can fill up the nostril on the affected side and overflow within the nasopharynx (the area inside the nose where the two nostrils merge), spilling into the other nostril to cause bleeding from both sides. Blood can also drip back into the throat or down into the stomach, causing a person to spit or even vomit blood. Signs of excessive blood loss include dizziness, light-headedness, confusion, and fainting. Excessive blood loss from nosebleeds is rare. Additional bleeding from other parts of the body, such as bleeding gums when brushing teeth, blood in urine or bowel movements, or easy bruising may indicate an inability of the blood to clot. Additional bleeding or easy bruising can be a sign of a more significant medical problem.

Renal agenesis is a condition in which a newborn is missing one or both kidneys. Unilateral renal agenesis (URA) is the absence of one kidney. Bilateral renal agenesis (BRA) is the absence of both kidneys. Both types of renal agenesis occur in fewer than 1 percent of births annually, according to the March of Dimes. Fewer than 1 in every 1,000 newborns has URA. BRA is much rarer, occurring in about 1 in every 3,000 births.

Learn a simple way to tell if you might be suffering from an undiagnosed autoimmune condition. Examples of autoimmune conditions include: • alopecia areata

Stay active and push your body to its limit – tips on how you can mend strained muscles and prevent injury.

The examination consists of three portions: Inspection, Palpation, and Synthesis of data from these techniques In addition to palpating for size, also note the gland texture, mobility, tenderness and the presence of nodules. Inspection Inspection: Anterior Approach The patient should be seated or standing in a comfortable position with the neck in a neutral or slightly extended position. Cross-lighting increases shadows, improving the detection of masses. To enhance visualization of the thyroid, you can: Extending the neck, which stretches overlying tissues Have the patient swallow a sip of water, watching for the upward movement of the thyroid gland. quicktime video 251KB video demo from Return to the Bedside Inspection: Lateral Approach After completing anterior inspection of the thyroid, observe the neck from the side. Estimate the smooth, straight contour from the cricoid cartilage to the suprasternal notch. Measure any prominence beyond this imagined contour, using a ruler placed in the area of prominence. Palpation Note: There is no data comparing palpation using the anterior approach to the posterior approach so examiners should use the approach that they find most comfortable. Palpation: Anterior Approach placement of hands for palpatation of thyroid in anterior approach The patient is examined in the seated or standing position. Attempt to locate the thyroid isthmus by palpating between the cricoid cartilage and the suprasternal notch. Use one hand to slightly retract the sternocleidomastoid muscle while using the other to palpate the thyroid. Have the patient swallow a sip of water as you palpate, feeling for the upward movement of the thyroid gland. quicktime video 454KB video demo from Return to the Bedside. Palpation: Posterior Approach placement of hands for palpatation of thyroid in posterior approach The patient is examined in the seated or standing position. Standing behind the patient, attempt to locate the thyroid isthmus by palpating between the cricoid cartilage and the suprasternal notch. Move your hands laterally to try to feel under the sternocleidomstoids for the fullness of the thyroid. Have the patient swallow a sip of water as you palpate, feeling for the upward movement of the thyroid gland.

It involves placing a small, expandable tube called a stent in the narrowed artery. This procedure is also called carotid angioplasty and stenting. There are two carotid arteries-one on each side of the neck-that supply blood to the brain. These arteries can be narrowed and damaged by fatty deposits called plaque.

Motivation for Medical Students!

Skin Cysts Cysts are noncancerous, closed pockets of tissue that can be filled with fluid, pus, or other material. Cysts are common on the skin and can appear anywhere. They feel like large peas under the surface of the skin. Cysts can develop as a result of infection, clogging of sebaceous glands (oil glands), or around foreign bodies, such as earrings.

Harvesting and prepare fat for grafting

Although drug treatment of hypertension is associated with improved survival and decreased vascular complications, drug compliance is a major problem in the control of hypertension. All antihypertensive medications are associated with side effects; thus, it is a physician's responsibility to explain to each patient the side effects of the drugs he prescribes to treat hypertension, and to instill in the patient a sense of necessity for the treatment of hypertension. The choice of antihypertensive drug should be made based on each patient's lifestyle, overall health and ability to tolerate the drug. Ideally, the antihypertensive regimen should be simple, effective, convenient to take and have very few side effects.

intracranial hematoma occurs when a blood vessel ruptures within your brain or between your skull and your brain. The collection of blood (hematoma) compresses your brain tissue. An intracranial hematoma may occur because the fluid that surrounds your brain can't absorb the force of a sudden blow or a quick stop. Then your brain may slide forcefully against the inner wall of your skull and become bruised. Although some head injuries — such as one that causes only a brief lapse of consciousness (concussion) — can be minor, an intracranial hematoma is potentially life-threatening and often requires immediate treatment. An intracranial hematoma often, but not always, requires surgery to remove the blood.

This implantation method is very common and used in both FUE hair transplant surgery and strip surgery (FUSS). During this implantation method, site creation and graft implantation are performed simultaneously as part of a one or two step process.

Common causes of the knee pain
Knee pain is very common and in this video we will present the most common problems that can cause pain in the knee. (Patella) itself, which is in front of the knee, or from the tendons that are attached to the kneecap (patellar tendon and quadricep tendon). One of the most common problems is patellar chondromalacia which is chronic pain due to the softening of the cartilage beneath the kneecap. The cartilage of the kneecap will have some erosions, defects, or holes from mild to complete inside the joint (exactly in the back of the kneecap).
• Pain in the front of the knee
• Occurs more in young people
• Becomes worse from climbing up stairs and going downstairs
Treatment is usually nonsteroidal anti-inflammatory medication, physical therapy, and surgery is very rare. Also in front of the kneecap, the patient may get pain due to prepatellar bursitis.
When there is prepatellar bursitis, the patient will see that the swelling, the inflammation, and the pain is located over the front of the kneecap. The bursa becomes inflamed and fills with fluid at the top of the knee, causing pain, swelling, tenderness and a lump in that area on top of the kneecap. If the pain is in front of the knee but below or above the patella, this may indicate that the patient has tendonitis. Patellar tendonitis is an overuse condition that often occurs in athletes who perform repetitive jumping activities. Patellar tendonitis is a knee pain that is associated with focal patellar tendon tenderness and it is usually activity related. It is located below the kneecap and is called "jumper's knee". Patellar tendonitis affects approximately 20% of jumping athletes. There will be tenderness to palpation at the distal pole of the patella in extension and not in flexion. Quadriceps inflexibility, atrophy and hamstring tightness are predisposing factors for this condition. Treatment is rest, anti-inflammatory medication, stretching and strengthening of the hamstrings and quadriceps. Use an eccentric exercise program. The early stages of patellar tendonitis will respond well to nonoperative treatment. Another important cause of knee pain is a meniscal tear. The meniscus is the cushion that protects the cartilage in the knee. Injury will cause pain on the medial or the lateral side of the knee exactly at the level of the joint. The patient will complain of a history of locking, instability and swelling of the knee. McMurray test will be positive. A painful pop or click is obtained as the knee is brought from flexion to extension with either internal or external rotation of the knee. Arthritis of the knee Knee arthritis is very common. The cartilage cells die with age and its repair response decreases in the joint collapses with increased breakdown of the framework of the cartilage. The patient will have progressive blurring away of the cartilage of the joint with decreased joint space as seen on x-rays. Another source of pain is the Baker's cyst. The cyst is in the back of the knee between the semimembranosus yes and the medial gastrocnemius muscles. Another important source of knee pain is a ligament injury. Here is a normal knee without a ligament injury. Here you can see from the front, you can see the lateral and medial collateral ligament. You can see the ACL and PCL from the side view. These ligaments are usually injured as a result of a sports activity. Here is an example of a sports knee injury. Here is an example of the medial collateral ligament injury. This is the most commonly injury knee ligament injury to this ligament is on the inner part of the knee. Here is an example of an injury of the anterior cruciate ligament. It involves a valgus stress to the knee. Lachman test is usually positive, and MRI is diagnostic. Another important cause of knee pain is iliotibial band syndrome of the knee. Inflammation of the thickening of the iliotibial band results from excessive friction as the iliotibial band slides over the lateral femoral condyle. The iliotibial band is a thick band of fascia that extends along the lateral thigh from the iliac crest to the knee. And as the knee moves, the IT band was repeatedly shifted forwards and backwards across the lateral femoral condyle. The patient will complain of swelling, tenderness, and crepitus over the lateral femoral condyle. The condition occurs in the ITB S occurs in runners, cyclist and athletes that require repeated knee flexion and extension. The pain may be reproduced by doing a single-leg squat. The Ober's test is used to at assess tightness of the iliotibial band. MRI may show edema in the area of the ITB. Treatment is usually nonoperative with rest and ice, physical therapy, with stretching, proprioception, and improvement in neuromuscular coordination. Training modification and injections may be helpful. Surgery is a last resort. Surgical excision of the scarred inflamed part of the iliotibial band.

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

A ventricular septal defect (VSD), a hole in the heart, is a common heart defect that's present at birth (congenital). The hole occurs in the wall that separates the heart's lower chambers (septum) and allows blood to pass from the left to the right side of the heart. The oxygen-rich blood then gets pumped back to the lungs instead of out to the body, causing the heart to work harder. A small ventricular septal defect may cause no problems, and many small VSDs close on their own. Larger VSDs need surgical repair early in life to prevent complications.