Comprehensive Cancer Center, provides definitions and terms used in cancer diagnosis and treatment. He explores the process of diagnosis from biopsies to imaging and how staging is established. He also discusses the multimodality approach to treatment which typically includes surgical oncology, medical oncology and radiation oncology. Series: "UCSF Osher Center for Integrative Medicine presents Mini Medical School for the Public

Buerger's disease (thromboangiitis obliterans) is a rare disease of the arteries and veins in the arms and legs. In Buerger's disease, your blood vessels become inflamed, swell and can become blocked with blood clots (thrombi). This eventually damages or destroys skin tissues and may lead to infection and gangrene. Buerger's disease usually first shows in your hands and feet and may eventually affect larger areas of your arms and legs. Virtually everyone diagnosed with Buerger's disease smokes cigarettes or uses other forms of tobacco, such as chewing tobacco. Quitting all forms of tobacco is the only way to stop Buerger's disease. For those who don't quit, amputation of all or part of a limb is sometimes necessary.

Eosinophilic granulomatosis with polyangiitis (EGPA)—or, as it was traditionally termed, Churg-Strauss syndrome—is a rare systemic necrotizing vasculitis that affects small-to-medium-sized vessels and is associated with severe asthma and blood and tissue eosinophilia. [1] Like granulomatosis with polyangiitis (Wegener granulomatosis), and the microscopic form of periarteritis (ie, microscopic polyangiitis), EGPA is an antineutrophil cytoplasmic antibody (ANCA)–associated vasculitide. [2, 3, 4, 5] In 1951, Churg and Strauss first described the syndrome in 13 patients who had asthma, eosinophilia, granulomatous inflammation, necrotizing systemic vasculitis, and necrotizing glomerulonephritis. [3] In 1990, the American College of Rheumatology (ACR) proposed the following six criteria for the diagnosis of Churg-Strauss syndrome [6] : Asthma (wheezing, expiratory rhonchi) Eosinophilia of more than 10% in peripheral blood Paranasal sinusitis Pulmonary infiltrates (may be transient) Histological proof of vasculitis with extravascular eosinophils Mononeuritis multiplex or polyneuropathy

Temporal arteritis is a condition in which the temporal arteries, which supply blood to the head and brain, become inflamed or damaged. It is also known as cranial arteritis or giant cell arteritis. Although this condition usually occurs in the temporal arteries, it can occur in almost any medium to large artery in the body. The journal Arthritis & Rheumatology states that approximately 228,000 people in the United States are affected by temporal arteritis. According to the American College of Rheumatology, people over the age of 50 are more likely than younger people to develop the condition. Women are also more likely than men to have temporal arteritis. It is most prevalent in people of northern European or Scandinavian descent. Although the exact cause of the condition is unknown, it may be linked to the body’s autoimmune response. Also, excessive doses of antibiotics and certain severe infections have been linked to temporal arteritis. There’s no known prevention. However, once diagnosed, temporal arteritis can be treated to minimize complications.

Ischemic colitis occurs when blood flow to part of the large intestine (colon) is reduced, usually due to narrowed or blocked blood vessels (arteries). The diminished blood flow doesn't provide enough oxygen for the cells in your digestive system. Ischemic colitis can cause pain and may damage your colon. Any part of the colon can be affected, but ischemic colitis usually causes pain on the left side of the belly area (abdomen). The condition can be misdiagnosed because it can easily be confused with other digestive problems. Ischemic colitis may heal on its own. But you may need medication to treat ischemic colitis or prevent infection, or you may need surgery if your colon has been damaged. Symptoms ShareTweet Oct. 13, 2015 References Products and Services Newsletter: Mayo Clinic Health Letter See also Abdominal pain Colonoscopy Color Blue Detects Colon Cancer CT scan CT scans: Are they safe? Diarrhea Ultrasound Advertisement Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. Advertising & Sponsorship PolicyOpportunitiesAd Choices Mayo Clinic Store Check out these best-sellers and special offers on books and newsletters from Mayo Clinic. NEW! – The Mayo Clinic Diet, Second Edition Treatment Strategies for Arthritis Mayo Clinic on Better Hearing and Balance Keeping your bones healthy and strong The Mayo Clinic Diet Online Ads by Swoop Psoriasis Treatment www.informationaboutpsoriasis.com Explore a Treatment Option for Moderate to Severe Plaque Psoriasis Immune Biomarker PD-L1 - Discover the Science iobiomarkers.bmsinformation.com Understanding Assay Results for PD-L1 is Crucial for Treatment Decisions. Biomarker PD-L1 Information - Easy to Download Resources iobiomarkers.bmsinformation.com Explore the Role of PD-L1 in Immuno-Oncology & the Evolving Biomarker Landscape.

Chronic mesenteric ischemia (CMI) usually results from long-standing atherosclerotic disease of 2 or more mesenteric vessels. [1] Other nonatheromatous causes of CMI include the vasculitides, such as Takayasu arteritis. Symptoms are caused by the gradual reduction in blood flow to the intestine. [2] (See Presentation.) In 1958, Shaw and Maynard described the first thromboendarterectomy of the superior mesenteric artery (SMA) for the treatment of both acute mesenteric ischemia (AMI) and CMI. Several other surgical procedures have since been attempted, ranging from reimplantation of the visceral branch into the adjacent aorta to using an autogenous vein graft. In 1972, Stoney and Wylie introduced transaortic visceral thromboendarterectomy and aortovisceral bypass, which have proved to be highly effective techniques.

Acute mesenteric ischemia (AMI) is a syndrome caused by inadequate blood flow through the mesenteric vessels, resulting in ischemia and eventual gangrene of the bowel wall. Although relatively rare, it is a potentially life-threatening condition. Broadly, AMI may be classified as either arterial or venous. AMI as arterial disease may be subdivided into nonocclusive mesenteric ischemia (NOMI) and occlusive mesenteric arterial ischemia (OMAI); OMAI may be further subdivided into acute mesenteric arterial embolism (AMAE) and acute mesenteric arterial thrombosis (AMAT). AMI as venous disease takes the form of mesenteric venous thrombosis (MVT).

What is a brain aneurysm? A brain (cerebral) aneurysm is a bulging, weak area in the wall of an artery that supplies blood to the brain. In most cases, a brain aneurysm causes no symptoms and goes unnoticed. In rare cases, the brain aneurysm ruptures, releasing blood into the skull and causing a stroke. When a brain aneurysm ruptures, the result is called a subarachnoid hemorrhage. Depending on the severity of the hemorrhage, brain damage or death may result.

Aortoiliac occlusive disease (AIOD) occurs commonly in patients with PAD. Significant lesions in the aortoiliac arterial segment are exposed easily by palpation of the femoral pulses. Any diminution of the palpable femoral pulse indicates that a more proximal obstruction exists. Obstructive lesions may be present in the infrarenal aorta, common iliac, internal iliac (hypogastric), external iliac, or combinations of any or all of these vessels. Occasionally, degenerated nonstenotic atheromatous disease exists in these vessels and may manifest by atheroembolism to the foot, the "blue toe" or "trash foot" syndrome. Generally, patients with aortoiliac PAD have a poorer general prognosis than those with more distal PAD.

According to the 2007 Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II), acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability [1]. The threatened limb may manifest as ischemic rest pain or the development of tissue loss (ulcers, gangrene). The clinical presentation depends upon the etiology and whether the patient has underlying peripheral artery disease. Patients who present later than two weeks after the onset of the acute event are considered to have chronic limb ischemia. The management of acute arterial occlusion remains a challenge for vascular specialists. Surgical thromboembolectomy and bypass grafting were the mainstays of therapy for many years [2]. Subsequently, thrombolytic therapy and percutaneous transluminal angioplasty (PTA) have become treatment options for selected patients [3,4]. Despite these advances, the morbidity, mortality, and limb loss rates from acute lower extremity ischemia remain high [5]. Thus, regardless of the treatment modality used, early diagnosis and rapid initiation of therapy are essential in order to salvage the ischemic extremity.

Claudication, which is defined as reproducible ischemic muscle pain, is one of the most common manifestations of peripheral arterial occlusive disease (PAOD) caused by atherosclerosis. Claudication occurs during physical activity and is relieved after a short rest. Pain develops because of inadequate blood flow. Examination of a patient with claudication should include a complete lower-extremity evaluation and pulse examination, including measuring segmental pressures. Attempt to palpate pulses from the abdominal aorta to the foot, with auscultation for bruits in the abdominal and pelvic regions. When palpable pulses are not present, a handheld Doppler device may be used to assess circulation.

Throughout the body, there are several points at which blood vessels unite. The junctions are termed anastomoses. In the simplest sense, an anastomosis is any connection (made surgically or occurring naturally) between tube-like structures. Naturally occurring arterial anastomoses provide an alternative blood supply to target areas in cases where the primary arterial pathway is obstructed. They are most abundant in regions of the body where the blood supply may can be easily damaged or blocked (such as the joints or intestines). This article focuses on the arterial anastomotic networks of the upper limb.

A circulatory anastomosis is a connection (an anastomosis) between two blood vessels, such as between arteries (arterio-arterial anastomosis), between veins (veno-venous anastomosis) or between an artery and a vein (arterio-venous anastomosis). An end artery (or terminal artery) is an artery that is the only supply of oxygenated blood to a portion of tissue. Examples of an end artery include the splenic artery that supplies the spleen and the renal artery that supplies the kidneys.

Both lower extremities must be evaluated to determine the presence or extent of any disease and to ascertain the pulse status of the patient. The feet are examined for signs of peripheral vascular disease and the anterior and posterior tibial pulses are palpated. Because an intact arch can supply retrograde flow to the major vessels of the foot, it can be helpful to put pressure on the anterior tibial artery when detecting the presence of a posterior tibial pulse and visa-versa. This "modified Allen's test" may detect proximal vessel obstruction masked by an intact foot arch. The need for preoperative angiography in young, healthy patients with a normal physical examination has been hotly debated. Our tendency has been to obtain preoperative angiograms as a guide. Although rare, we have seen lower extremities with a dominant peroneal artery nourishing the foot and distal anterior and posterior vessels, contraindicating sacrifice of the peroneal artery. MRI or CT angiography can also be used in many circumstances.

Simple microinstruments and a medical school laboratory microscope were used for anastomosis training. Chicken blood vessels were used as a material for this study. A long segment of blood vessel from the proximal brachial artery to the distal radial artery was used for training. End-to-side anastomosis was practiced first, and the training continued with end-to-end anastomosis of the appropriate segments.

The needle should pass through the tissue at a perpendiculaPlace the tips of the left-hand forceps on the underside of the tissue at the point where the needle will enter, and gently push the edge upward. With the right hand, bring the needle into contact with the tissue, and press downward. These movements create eversion. Pass the needle through. Do not grab the tissue with your left hand forceps since it will damage the intima. If needed, you can pick up adventitia or a nearby suture to help with exposure and eversion. r.The needle must pass through the other side at a perpendicular, too. Bring the tip of the needle to the place where you intend to bring it out on the other side. Put the tip of your left-hand forceps on the upper surface of the tissue at the intended exit point. Press down with the left-hand forceps and push up with the needle to give you the correct eversion. The width of the bite should be about three times the thickness of the needle. The bites on both sides must be equal, and the needle should cross exactly in a straight line (not diagonally). Pull the needle through the tissue following the curve of the needle

At first, grasping the needle is difficult because it will have a tendency to want to jump around. What can oftentimes help is to get hold of the thread with the left-hand forceps at a point 2 to 3 cm away from the needle. Dangle the needle until it just comes to rest on the surface. This will then allow you to use the angulated needle holder to grab the needle easily. Your needle is in a stable position if it is set up to 90 degrees to the axis of the tips of the forceps. You can make minor corrections by touching the needle with your left-hand forceps, or by partially relaxing your grip and nudging the needle tip against another firm object. You should hold the needle just behind its midpoint (If you hold it too near the tip, it will point downward. If you hold it too near the thread end, it will point upward.).

The epididymis is a long coiled tube that lies above and behind each testicle. The epididymis collects and transports sperm from the testis to the vas deferens (tubes that transport sperm to the urethra). An epididymal cyst is a cyst-like mass in the epididymis that contains clear fluid. Typically, epididymal cysts and spermatoceles do not cause symptoms. When discovered, the epididymal cyst is usually about the size of a pea and feels separate from the top of the testis. Spermatoceles typically arise from the head of the epididymis, and are felt on the top portion of the testicle. Epididymal cysts and spermatoceles are often incidental findings on testicular self-examination or routine physical examination. It is important that any mass noted in the scrotum be examined by a urologist in order to obtain an accurate diagnosis, especially a mass on the testicle itself. Our team in the Division of Urology will typically be able to confirm the diagnosis on physical exam. However, a scrotal ultrasound may also be used in order to rule out other conditions.

Surgery. A procedure to remove an epididymal cyst is carried out under general anaesthetic and involves removing the cysts through a small incision in your scrotum that is sealed with dissolvable stitches.

A spermatocele (SPUR-muh-toe-seel) is an abnormal sac (cyst) that develops in the epididymis — the small, coiled tube located on the upper testicle that collects and transports sperm. Noncancerous and generally painless, a spermatocele usually is filled with milky or clear fluid that might contain sperm. The exact cause of spermatoceles is unknown but might be due to a blockage in one of the tubes that transports sperm. Spermatoceles, sometimes called spermatic cysts, are common. They typically don't reduce fertility or require treatment. If a spermatocele grows large enough to cause discomfort, your doctor might suggest surgery.