There are lots of reasons your stomach could be hurting. Gas, UTI, and kidney stones are just a few. You should probably go see a doctor to be sure!
The stomach is a muscular, hollow, dilated part of the digestion system which functions as an important organ of the digestive tract in some animals, including vertebrates, echinoderms, insects (mid-gut), and molluscs. It is involved in the second phase of digestion, following mastication (chewing).
The stomach is located between the esophagus and the small intestine. It secretes protein-digesting enzymes called protease and strong acids to aid in food digestion, (sent to it via esophageal peristalsis) through smooth muscular contortions (called segmentation) before sending partially digested food (chyme) to the small intestines.
The word stomach is derived from the Latin stomachus which is derived from the Greek word stomachos (στόμαχος), ultimately from stoma (), "mouth". The words gastro- and gastric (meaning related to the stomach) are both derived from the Greek word gaster ().
Bolus (masticated food) enters the stomach through the esophagus via the esophageal sphincter. The stomach releases proteases (protein-digesting enzymes such as pepsin) and hydrochloric acid, which kills or inhibits bacteria and provides the acidic pH of two for the proteases to work. Food is churned by the stomach through muscular contractions of the wall called peristalsis – reducing the volume of the fundus, before looping around the fundus and the body of stomach as the boluses are converted into chyme (partially digested food). Chyme slowly passes through the pyloric sphincter and into the duodenum of the small intestine, where the extraction of nutrients begins. Depending on the quantity and contents of the meal, the stomach will digest the food into chyme anywhere between forty minutes and a few hours. The average human stomach can comfortably hold about a liter of food.
Gastric juice in the stomach also contains pepsinogen and prorennin. Hydrochloric acid activates these inactive forms of enzymes into active forms which are pepsin and rennin (proteases). Rennin digests the milk protein caesinogen (soluble) into caesin (insoluble) thus curdling the milk. Pepsin breaks down proteins into polypeptides.
The stomach lies between the esophagus and the duodenum (the first part of the small intestine). It is on the left upper part of the abdominal cavity. The top of the stomach lies against the diaphragm. Lying behind the stomach is the pancreas. The greater omentum hangs down from the greater curvature.
Two sphincters keep the contents of the stomach contained. They are the esophageal sphincter (found in the cardiac region, not an anatomical sphincter) dividing the tract above, and the pyloric sphincter dividing the stomach from the small intestine.
The stomach is surrounded by parasympathetic (stimulant) and orthosympathetic (inhibitor) plexuses (networks of blood vessels and nerves in the anterior gastric, posterior, superior and inferior, celiac and myenteric), which regulate both the secretions activity and the motor (motion) activity of its muscles.
In adult humans, the stomach has a relaxed, near empty volume of about 45 to 75 ml. Because it is a distensible organ, it normally expands to hold about one litre of food, but can hold as much as two to three litres. The stomach of a newborn human baby will only be able to retain about 30 ml.
The stomach is divided into four sections, each of which has different cells and functions. The sections are:
The lesser curvature of the stomach is supplied by the right gastric artery inferiorly, and the left gastric artery superiorly, which also supplies the cardiac region. The greater curvature is supplied by the right gastroepiploic artery inferiorly and the left gastroepiploic artery superiorly. The fundus of the stomach, and also the upper portion of the greater curvature, is supplied by the short gastric artery which arises from splenic artery.
Like the other parts of the gastrointestinal tract, the stomach walls are made of the following layers, from inside to outside:
Over the submucosa, the muscularis externa in the stomach differs from that of other GI organs in that it has three layers of smooth muscle instead of two.
Different types of cells are found at the different layers of these glands:
The movement and the flow of chemicals into the stomach are controlled by both the autonomic nervous system and by the various digestive system hormones:
Other than gastrin, these hormones all act to turn off the stomach action. This is in response to food products in the liver and gall bladder, which have not yet been absorbed. The stomach needs to push food into the small intestine only when the intestine is not busy. While the intestine is full and still digesting food, the stomach acts as storage for food.
Epidermal growth factor (EGF) results in cellular proliferation, differentiation, and survival. EGF is a low-molecular-weight polypeptide first purified from the mouse submandibular gland, but since then found in many human tissues including submandibular gland, parotid gland. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays also an important physiological role in the maintenance of oro-oesophageal and gastric tissue integrity. The biological effects of salivary EGF include healing of oral and gastroesophageal ulcers, inhibition of gastric acid secretion, stimulation of DNA synthesis as well as mucosal protection from intraluminal injurious factors such as gastric acid, bile acids, pepsin, and trypsin and to physical, chemical and bacterial agents.
The stomach can "taste" sodium glutamate using glutamate receptors and this information is passed to the lateral hypothalamus and limbic system in the brain as a palatability signal through the vagus nerve. The stomach can also sense independently to tongue and oral taste receptors glucose, carbohydrates proteins, and fats. This allows the brain to link nutritional value of foods to their tastes.
Although the absorption is mainly a function of the small intestine, some absorption of certain small molecules nevertheless does occur in the stomach through its lining. This includes:
A large number of studies have indicated that most cases of peptic ulcers, gastritis, and stomach cancer are caused by Helicobacter pylori infection. The stomach has to regenerate a new layer of mucus every two weeks, or else damage to the epithelium may result.
Although the precise shape and size of the stomach varies widely among different vertebrates, the relative positions of the esophageal and duodenal openings remain relatively constant. As a result, the organ always curves somewhat to the left before curving back to meet the pyloric sphincter. However, lampreys, hagfishes, chimaeras, lungfishes, and some teleost fish have no stomach at all, with the esophagus opening directly into the intestine. These animals all consume diets that either require little storage of food, or no pre-digestion with gastric juices, or both.
The gastric lining is usually divided into two regions, an anterior portion lined by fundic glands, and a posterior with pyloric glands. Cardiac glands are unique to mammals, and even then are absent in a number of species. The distributions of these glands vary between species, and do not always correspond with the same regions as in man. Furthermore, in many non-human mammals, a portion of the stomach anterior to the cardiac glands is lined with epithelium essentially identical to that of the esophagus. Ruminants, in particular, have a complex stomach, the first three chambers of which are all lined with esophageal mucosa.
In birds and crocodilians, the stomach is divided into two regions. Anteriorly is a narrow tubular region, the proventriculus, lined by fundic glands, and connecting the true stomach to the crop. Beyond lies the powerful muscular gizzard, lined by pyloric glands, and, in some species, containing stones that the animal swallows to help grind up food.
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The esophagus (oesophagus, commonly known as the gullet) is an organ in vertebrates which consists of a muscular tube through which food passes from the pharynx to the stomach. During swallowing, food passes from the mouth through the pharynx into the esophagus and travels via peristalsis to the stomach. The word esophagus is derived from the Latin œsophagus, which derives from the Greek word oisophagos, lit. "entrance for eating." In humans the esophagus is continuous with the laryngeal part of the pharynx at the level of the C6 vertebra. The esophagus passes through posterior mediastinum in thorax and enters abdomen through a hole in the diaphragm at the level of the tenth thoracic vertebrae (T10). It is usually about 25cm, but extreme variations have been recorded ranging 10–50 cm long depending on individual height. It is divided into cervical, thoracic and abdominal parts. Due to the inferior pharyngeal constrictor muscle, the entry to the esophagus opens only when swallowing or vomiting.
The layers of the oesophagus are as follows:
Similar to rectum, it lacks serosa layer.
Normally, the esophagus has three anatomic constrictions at the following levels:
The distances from the incisor teeth are important as is useful for diagnostic endoscopic procedures.
The junction between the esophagus and the stomach (the gastroesophageal junction or GE junction) is not actually considered a valve, although it is sometimes called the cardiac sphincter, cardia or cardias, it actually better resembles a structure.
In much of the gastrointestinal tract, smooth muscles contract in sequence to produce a peristaltic wave which forces a ball of food (called a bolus) while in the esophagus. In humans, peristalsis is found in the contraction of smooth muscles to propel contents through the digestive tract.
In most fish, the esophagus is extremely short, primarily due to the length of the pharynx (which is associated with the gills). However, some fish, including lampreys, chimaeras, and lungfish, have no true stomach, so that the esophagus effectively runs from the pharynx directly to the intestine, and is therefore somewhat longer.
In tetrapods, the pharynx is much shorter, and the esophagus correspondingly longer, than in fish. In amphibians, sharks and rays, the esophageal epithelium is ciliated, helping to wash food along, in addition to the action of muscular peristalsis. In the majority of vertebrates, the esophagus is simply a connecting tube, but in birds, it is extended towards the lower end to form a crop for storing food before it enters the true stomach.
A structure with the same name is often found in invertebrates, including molluscs and arthropods, connecting the oral cavity with the stomach.
H&E stain of biopsy of normal esophagus showing the stratified squamous cell epithelium
Layers of the esophagus.
Accessory digestive system.
Organs of the digestive tract.
Section of the neck at about the level of the sixth cervical vertebra.
Transverse section of thorax, showing relations of pulmonary artery.
Sagittal section of nose mouth, pharynx, and larynx.
The position and relation of the esophagus in the cervical region and in the posterior mediastinum. Seen from behind. |
Section of the human esophagus. Moderately magnified.
Microscopic shot of a cross section of human gastroesophageal junction wall.
Micrograph of herpes esophagitis. H&E stain.
Ultrasound image of the fetal esophagus at 19 weeks of pregnancy.
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Stomach cancer, or gastric cancer, refers to cancer arising from any part of the stomach. Stomach cancer causes about 800,000 deaths worldwide per year. Prognosis is poor (5-year survival <5 to 15%) because most patients present with advanced disease.
Stomach cancer is often either asymptomatic (producing no noticeable symptoms) or it may cause only nonspecific symptoms (symptoms which are not specific to just stomach cancer, but also to other related or unrelated disorders) in its early stages. By the time symptoms occur, the cancer has often reached an advanced stage (see below) and may have also metastasized (spread to other, perhaps distant, parts of the body), which is one of the main reasons for its relatively poor prognosis.][ Stomach cancer can cause the following signs and symptoms:
Note that these can be symptoms of other problems such as a stomach virus, gastric ulcer or tropical sprue.
Most stomach cancer is caused by Helicobacter pylori infection. Dietary factors are not proven causes, but some foods, such as smoked foods, salted fish and meat, and pickled vegetables are associated with a higher risk. Nitrates and nitrites in cured meats can be converted by certain bacteria, including H. pylori, into compounds that have been found to cause stomach cancer in animals. On the other hand, the American Cancer Society recommends eating fresh fruits and vegetables that contain antioxidant vitamins, such as A and C, and says that they lower the risk of stomach cancer, and a Mediterranean diet is associated with lower rates of stomach cancer.
Smoking increases the risk of developing gastric cancer significantly, from 40% increased risk for current smokers to 82% increase for heavy smokers. Gastric cancers due to smoking mostly occur in the upper part of the stomach near the esophagus Some studies show increased risk with alcohol consumption as well.
Other factors associated with increased risk are autoimmune atrophic gastritis, pernicious anemia, Menetrier's disease (hyperplastic, hypersecretory gastropathy), intestinal metaplasia, and genetic factors.
H. pylori is the main risk factor in 65–80% of gastric cancers, but in only 2% of such infections. The mechanism by which H. pylori induces stomach cancer potentially involves chronic inflammation, or the action of H. pylori virulence factors such as CagA. Approximately ten percent of cases show a genetic component. Some studies indicate that bracken consumption and spores are correlated with incidence of stomach cancer, though causality has yet to be established.
Gastric cancer shows a male predominance in its incidence as up to three males are affected for every female. Estrogen may protect women against the development of this cancer form. A very small percentage of diffuse-type gastric cancers (see Histopathology below) are thought to be genetic. Hereditary diffuse gastric cancer (HDGC) has recently been identified and research is ongoing. However, genetic testing and treatment options are already available for families at risk.
The International Cancer Genome Consortium is leading efforts to map stomach cancer's complete genome.][
To find the cause of symptoms, the doctor asks about the patient's medical history, does a physical exam, and may order laboratory studies. The patient may also have one or all of the following exams:
Abnormal tissue seen in a gastroscope examination will be biopsied by the surgeon or gastroenterologist. This tissue is then sent to a pathologist for histological examination under a microscope to check for the presence of cancerous cells. A biopsy, with subsequent histological analysis, is the only sure way to confirm the presence of cancer cells.
Various gastroscopic modalities have been developed to increase yield of detected mucosa with a dye that accentuates the cell structure and can identify areas of dysplasia. Endocytoscopy involves ultra-high magnification to visualize cellular structure to better determine areas of dysplasia. Other gastroscopic modalities such as optical coherence tomography are also being tested investigationally for similar applications.
A number of cutaneous conditions are associated with gastric cancer. A condition of darkened hyperplasia of the skin, frequently of the axilla and groin, known as acanthosis nigricans, is associated with intra-abdominal cancers such as gastric cancer. Other cutaneous manifestations of gastric cancer include tripe palms (a similar darkening hyperplasia of the skin of the palms) and the Leser-Trelat sign, which is the rapid development of skin lesions known as seborrheic keratoses.
Various blood tests may be done, including: Complete Blood Count (CBC) to check for anemia. Also, a stool test may be performed to check for blood in the stool.
If cancer cells are found in the tissue sample, the next step is to stage, or find out the extent of the disease. Various tests determine whether the cancer has spread and, if so, what parts of the body are affected. Because stomach cancer can spread to the liver, the pancreas, and other organs near the stomach as well as to the lungs, the doctor may order a CT scan, a PET scan, an endoscopic ultrasound exam, or other tests to check these areas. Blood tests for tumor markers, such as carcinoembryonic antigen (CEA) and carbohydrate antigen (CA) may be ordered, as their levels correlate to extent of metastasis, especially to the liver, and the cure rate.
Staging may not be complete until after surgery. The surgeon removes nearby lymph nodes and possibly samples of tissue from other areas in the abdomen for examination by a pathologist.
The clinical stages of stomach cancer are:
The TNM staging system is also used.
In a study of open-access endoscopy in Scotland, patients were diagnosed 7% in Stage I 17% in Stage II, and 28% in Stage III. A Minnesota population was diagnosed 10% in Stage I, 13% in Stage II, and 18% in Stage III. However in a high-risk population in the Valdivia Province of southern Chile, only 5% of patients were diagnosed in the first two stages and 10% in stage III.
Cancer of the stomach is difficult to cure unless it is found in an early stage (before it has begun to spread). Unfortunately, because early stomach cancer causes few symptoms, the disease is usually advanced when the diagnosis is made. Treatment for stomach cancer may include surgery, chemotherapy, and/or radiation therapy. New treatment approaches such as biological therapy and improved ways of using current methods are being studied in clinical trials.][
Surgery is the most common treatment. The surgeon removes part or all of the stomach, as well as the surrounding lymph nodes, with the basic goal of removing all cancer and a margin of normal tissue. Depending on the extent of invasion and the location of the tumor, surgery may also include removal of part of the intestine or pancreas. Tumors in the lower part of the stomach may call for a Billroth I or Billroth II procedure.
Endoscopic mucosal resection (EMR) is a treatment for early gastric cancer (tumor only involves the mucosa) that has been pioneered in Japan, but is also available in the United States at some centers. In this procedure, the tumor, together with the inner lining of stomach (mucosa), is removed from the wall of the stomach using an electrical wire loop through the endoscope. The advantage is that it is a much smaller operation than removing the stomach. Endoscopic submucosal dissection (ESD) is a similar technique pioneered in Japan, used to resect a large area of mucosa in one piece. If the pathologic examination of the resected specimen shows incomplete resection or deep invasion by tumor, the patient would need a formal stomach resection.
Surgical interventions are currently curative in less than 40% of cases, and, in cases of metastasis, may only be palliative.
The use of chemotherapy to treat stomach cancer has no firmly established standard of care. Unfortunately, stomach cancer has not been particularly sensitive to these drugs, and chemotherapy, if used, has usually served to palliatively reduce the size of the tumor, relieve symptoms of the disease and increase survival time. Some drugs used in stomach cancer treatment have included: 5-FU (fluorouracil) or its analog capecitabine, BCNU (carmustine), methyl-CCNU (Semustine), and doxorubicin (Adriamycin), as well as Mitomycin C, and more recently cisplatin and taxotere, often using drugs in various combinations. The relative benefits of these different drugs, alone and in combination, are unclear. Clinical researchers have explored the benefits of giving chemotherapy before surgery to shrink the tumor, or as adjuvant therapy after surgery to destroy remaining cancer cells. Combination treatment with chemotherapy and radiation therapy has some activity in selected post surgical settings. For patients who have HER2 overexpressing metastatic gastric or gastroesophageal (GE) junction adenocarcinoma, who have not received prior treatment for their metastatic disease, the US Food and Drug Administration granted approval (2010 October) for trastuzumab (Herceptin, Genentech, Inc.) in combination with cisplatin and a fluoropyrimidine (capecitabine or 5-fluorouracil). This was based on an improvement of the median overall survival (OS) of 2.5 months with trastuzumab plus chemotherapy treatment compared to chemotherapy alone (BO18255 ToGA trial). The combination of Herceptin with chemotherapy for treating metastatic gastric cancer was also sanctioned by the European regulatory authorities (2010 January).
Radiation therapy (also called radiotherapy) is the use of high-energy rays to damage cancer cells and stop them from growing. When used, it is generally in combination with surgery and chemotherapy, or used only with chemotherapy in cases where the individual is unable to undergo surgery. Radiation therapy may be used to relieve pain or blockage by shrinking the tumor for palliation of incurable disease.
While previous studies of multimodality therapy (combinations of surgery, chemotherapy and radiation therapy) gave mixed results, the Intergroup 0116 (SWOG 9008) study showed a survival benefit to the combination of chemotherapy and radiation therapy in patients with nonmetastatic, completely resected gastric cancer. Patients were randomized after surgery to the standard group of observation alone, or the study arm of combination chemotherapy and radiation therapy. Those in the study arm receiving chemotherapy and radiation therapy survived on average 36 months; compared to 27 months with observation.
Stomach cancer is the fourth most common cancer worldwide with 930,000 cases diagnosed in 2002. It is more common in men and in developing countries. As of 2010 deaths have decreased slightly from 774,000 in 1990 to about 755,000 in 2010 however it remains the second leading cause of cancer death after lung cancer.
It represents roughly 2% (25,500 cases) of all new cancer cases yearly in the United States, but it is more common in other countries. It is the leading cancer type in Korea, with 20.8% of malignant neoplasms.
Metastasis occurs in 80-90% of individuals with stomach cancer, with a six month survival rate of 65% in those diagnosed in early stages and less than 15% of those diagnosed in late stages.
Less than 1 in every 50 people going to the doctor with indigestion have cancer. Out of 10 million people in the Czech Republic, only 3 new cases of stomach cancer in people under 30 years of age in 1999 were diagnosed. Other studies show that less than 5% of stomach cancers occur in people under 40 years of age with 81.1% of that 5% in the age-group of 30 to 39 and 18.9% in the age-group of 20 to 29.
For Taiwan (statistic not shown on the above map), the mortality was 11.75 per 100,000 (1996).
The stomach is a muscular organ of the gastrointestinal tract that holds food and begins the digestive process by secreting gastric juice. The most common cancers of the stomach are adenocarcinomas but other histological types have been reported. Signs vary but may include vomiting (especially if blood is present), weight loss, anemia, and lack of appetite. Bowel movements may be dark and tarry in nature. In order to determine whether cancer is present in the stomach, special X-rays and/or abdominal ultrasound may be performed. Gastroscopy, a test using an instrument called endoscope to examine the stomach, is a useful diagnostic tool that can also take samples of the suspected mass for histopathological analysis to confirm or rule out cancer. The most definitive method of cancer diagnosis is through open surgical biopsy. Most stomach tumors are malignant with evidence of spread to lymph nodes or liver, making treatment difficult. Except for lymphoma, surgery is the most frequent treatment option for stomach cancers but it is associated with significant risks.
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7. Adrenal gland
Vessels: 8. Renal artery and vein, 9. Inferior vena cava, 10. Abdominal aorta, 11. Common iliac artery and vein
With transparency: 12. Liver, 13. Large intestine, 14. Pelvis
The urinary bladder is the organ that collects urine excreted by the kidneys before disposal by urination. A hollow muscular, and distensible (or elastic) organ, the bladder sits on the pelvic floor. Urine enters the bladder via the ureters and exits via the urethra.
Bladders occur throughout much of the animal kingdom, but are very diverse in form][ and in some cases are not homologous with the urinary bladder in humans.
The human urinary bladder is derived in embryo from the urogenital sinus and, it is initially continuous with the allantois. In males, the base of the bladder lies between the rectum and the pubic symphysis. It is superior to the prostate, and separated from the rectum by the rectovesical excavation. In females, the bladder sits inferior to the uterus and anterior to the vagina; thus, its maximum capacity is lower than in males. It is separated from the uterus by the vesicouterine excavation. In infants and young children, the urinary bladder is in the abdomen even when empty.
The detrusor muscle is a layer of the urinary bladder wall made of smooth muscle fibers arranged in spiral, longitudinal, and circular bundles. When the bladder is stretched, this signals the parasympathetic nervous system to contract the detrusor muscle. This encourages the bladder to expel urine through the urethra.
For the urine to exit the bladder, both the autonomically controlled internal sphincter and the voluntarily controlled external sphincter must be opened. Problems with these muscles can lead to incontinence.
The urinary bladder usually holds 300-350 ml of urine. As urine accumulates, the rugae flatten and the wall of the bladder thins as it stretches, allowing the bladder to store larger amounts of urine without a significant rise in internal pressure.
Since the urinary bladder has a transitional epithelium, it does not produce mucus.
The fundus of the bladder is the base of the bladder, formed by the posterior wall. It is lymphatically drained by the external iliac lymph nodes. The peritoneum lies superior to the fundus.
Frequent urination can be due to excessive urine production, small bladder capacity, irritability or incomplete empting. Males with an enlarged prostate urinate more frequently. One definition of overactive bladder is when a person urinates more than eight times per day, though there can be other causes of urination frequency.][ Though both urinary frequency and volumes have been shown to have a circadian rhythm, meaning day and night cycles, it is not entirely clear how these are disturbed in the overactive bladder.
The bladder receives motor innervation from both sympathetic fibers, most of which arise from the hypogastric plexuses and nerves, and parasympathetic fibers, which come from the pelvic splanchnic nerves and the inferior hypogastric plexus.
Sensation from the bladder is transmitted to the central nervous system (CNS) via general visceral afferent fibers (GVA). GVA fibers on the superior surface follow the course of the sympathetic efferent nerves back to the CNS, while GVA fibers on the inferior portion of the bladder follow the course of the parasympathetic efferents.
Disorders of or related to the bladder include:
Structure of the penis
Organs of the female reproductive system.
Coronal section of pelvis, showing arrangement of fasciæ. Viewed from behind.
Dissection of side wall of pelvis showing sacral and pudendal plexuses. (Bladder visible at lower left.) |
The peritoneum of the male pelvis.
Median sagitta section of male pelvis.
Male pelvic organs seen from right side.
Median sagittal section of female pelvis.
The interior of bladder.
Vertical section of bladder wall.
Fundus of the bladder with the vesiculæ seminales.
Vertical section of bladder, penis, and urethra.
Female pelvis and its contents, seen from above and in front.
Topography of thoracic and abdominal viscera.
The bladder can be seen highlighted in yellow in the illustration.
Layers of the urinary bladder wall and cross section of the detrusor muscle.
Urinary bladder (black butterfly-like shape) and hyperplastic prostate (BPH) visualized by Medical ultrasonography technique.
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The kidneys are organs that serve several essential regulatory roles in most animals, including vertebrates and some invertebrates. They are essential in the urinary system and also serve homeostatic functions such as the regulation of electrolytes, maintenance of acid–base balance, and regulation of blood pressure (via maintaining salt and water balance). They serve the body as a natural filter of the blood, and remove wastes which are diverted to the urinary bladder. In producing urine, the kidneys excrete wastes such as urea and ammonium, and they are also responsible for the reabsorption of water, glucose, and amino acids. The kidneys also produce hormones including calcitriol, erythropoietin, and the enzyme renin.
Located at the rear of the abdominal cavity in the retroperitoneum, the kidneys receive blood from the paired renal arteries, and drain into the paired renal veins. Each kidney excretes urine into a ureter, itself a paired structure that empties into the urinary bladder.
Renal physiology is the study of kidney function, while nephrology is the medical specialty concerned with kidney diseases. Diseases of the kidney are diverse, but individuals with kidney disease frequently display characteristic clinical features. Common clinical conditions involving the kidney include the nephritic and nephrotic syndromes, renal cysts, acute kidney injury, chronic kidney disease, urinary tract infection, nephrolithiasis, and urinary tract obstruction. Various cancers of the kidney exist; the most common adult renal cancer is renal cell carcinoma. Cancers, cysts, and some other renal conditions can be managed with removal of the kidney, or nephrectomy. When renal function, measured by glomerular filtration rate, is persistently poor, dialysis and kidney transplantation may be treatment options. Although they are not severely harmful, kidney stones can be painful and a nuisance. The removal of kidney stones involves ultrasound treatment to break up the stones into smaller pieces, which are then passed through the urinary tract. One common symptom of kidney stones is a sharp pain in the medial/lateral segments of the lower back.
In humans the kidneys are located in the abdominal cavity, more specifically in the paravertebral gutter and lie in a retroperitoneal position at a slightly oblique angle. There are two kidneys. One is on each side of the spine. The asymmetry within the abdominal cavity caused by the liver typically results in the right kidney being slightly lower than the left, and left kidney being located slightly more medial than the right. The left kidney is approximately at the vertebral level T12 to L3, and the right slightly lower. The right kidney sits just below the diaphragm and posterior to the liver, the left below the diaphragm and posterior to the spleen. Resting on top of each kidney is an adrenal gland. The upper (cranial) parts of the kidneys are partially protected by the eleventh and twelfth ribs, and each whole kidney and adrenal gland are surrounded by two layers of fat (the perirenal and pararenal fat) and the renal fascia. Each adult kidney weighs between 125 and 170 grams in males and between 115 and 155 grams in females. The left kidney is usually slightly larger than the right kidney.
The kidney has a bean-shaped structure; each kidney has a convex and concave surface. The concave surface, the renal hilum, is the point at which the renal artery enters the organ, and the renal vein and ureter leave. The kidney is surrounded by tough fibrous tissue, the renal capsule, which is itself surrounded by perinephric fat, renal fascia (of Gerota) and paranephric fat. The anterior (front) border of these tissues is the peritoneum, while the posterior (rear) border is the transversalis fascia.
The superior border of the right kidney is adjacent to the liver; and the spleen, for the left kidney. Therefore, both move down on inhalation.
The kidney is approximately 11–14 cm in length, 6 cm wide and 4 cm thick.
The substance, or parenchyma, of the kidney is divided into two major structures: superficial is the renal cortex and deep is the renal medulla. Grossly, these structures take the shape of 8 to 18 cone-shaped renal lobes, each containing renal cortex surrounding a portion of medulla called a renal pyramid (of Malpighi). Between the renal pyramids are projections of cortex called renal columns (of Bertin). Nephrons, the urine-producing functional structures of the kidney, span the cortex and medulla. The initial filtering portion of a nephron is the renal corpuscle, located in the cortex, which is followed by a renal tubule that passes from the cortex deep into the medullary pyramids. Part of the renal cortex, a medullary ray is a collection of renal tubules that drain into a single collecting duct.
The tip, or papilla, of each pyramid empties urine into a minor calyx; minor calyces empty into major calyces, and major calyces empty into the renal pelvis, which becomes the ureter. At the hilum, the ureter and renal vein exit the kidney while the renal artery enters. Surrounding these structures is hilar fat and lymphatic tissue with lymph nodes. The hilar fat is contiguous with a fat-filled cavity called the renal sinus. The renal sinus collectively contains the renal pelvis and calyces and separates these structures from the renal medullary tissue.
The kidneys receive blood from the renal arteries, left and right, which branch directly from the abdominal aorta. Despite their relatively small size, the kidneys receive approximately 20% of the cardiac output.
Each renal artery branches into segmental arteries, dividing further into interlobar arteries which penetrate the renal capsule and extend through the renal columns between the renal pyramids. The interlobar arteries then supply blood to the arcuate arteries that run through the boundary of the cortex and the medulla. Each arcuate artery supplies several interlobular arteries that feed into the afferent arterioles that supply the glomeruli.
The interstitium is the functional space in the kidney beneath the individual filters (glomeruli) which are rich in blood vessels. The interstitum absorbs fluid recovered from urine. Various conditions can lead to scarring and congestion of this area, which can cause kidney dysfunction and failure.
After filtration occurs the blood moves through a small network of venules that converge into interlobular veins. As with the arteriole distribution the veins follow the same pattern, the interlobular provide blood to the arcuate veins then back to the interlobar veins which come to form the renal vein exiting the kidney for transfusion for blood.
Renal histology studies the structure of the kidney as viewed under a microscope. Various distinct cell types occur in the kidney, including:
The renal artery enters into the kidney at the level of first lumbar vertebra just below the superior mesenteric artery. As it enters the kidney it divides into branches: first the segmental artery, which divides into 2 or 3 lobar arteries, then further divides into interlobar arteries, which further divide into the arcuate artery which leads into the interlobular artery, which form afferent arterioles. The afferent arterioles form the glomerulus (network of capillaries closed in Bowman's capsule). From here, efferent arterioles leaves the glomerulus and divide into peritubular capillaries, which drain into the interlobular veins and then into arcuate vein and then into interlobar vein, which runs into lobar vein, which opens into the segmental vein and which drains into the renal vein, and then from it blood moves into the inferior vena cava.
The kidney and nervous system communicate via the renal plexus, whose fibers course along the renal arteries to reach each kidney. Input from the sympathetic nervous system triggers vasoconstriction in the kidney, thereby reducing renal blood flow. The kidney also receives input from the parasympathetic nervous system, by way of the renal branches of the vagus nerve (cranial nerve X); the function of this is yet unclear. Sensory input from the kidney travels to the T10-11 levels of the spinal cord and is sensed in the corresponding dermatome. Thus, pain in the flank region may be referred from corresponding kidney.
The kidney participates in whole-body homeostasis, regulating acid-base balance, electrolyte concentrations, extracellular fluid volume, and regulation of blood pressure. The kidney accomplishes these homeostatic functions both independently and in concert with other organs, particularly those of the endocrine system. Various endocrine hormones coordinate these endocrine functions; these include renin, angiotensin II, aldosterone, antidiuretic hormone, and atrial natriuretic peptide, among others.
Many of the kidney's functions are accomplished by relatively simple mechanisms of filtration, reabsorption, and secretion, which take place in the nephron. Filtration, which takes place at the renal corpuscle, is the process by which cells and large proteins are filtered from the blood to make an ultrafiltrate that eventually becomes urine. The kidney generates 180 liters of filtrate a day, while reabsorbing a large percentage, allowing for the generation of only approximately 2 liters of urine. Reabsorption is the transport of molecules from this ultrafiltrate and into the blood. Secretion is the reverse process, in which molecules are transported in the opposite direction, from the blood into the urine.
The kidneys excrete a variety of waste products produced by metabolism. These include the nitrogenous wastes called "urea", from protein catabolism, as well as uric acid, from nucleic acid metabolism. Formation of urine is also the function of the kidney. The concentration of nitrogenous wastes, in the urine of mammals and some birds, is dependent on an elaborate countercurrent multiplication system. This requires several independent nephron characteristics to operate: a tight hair pin configuration of the tubules, water and ion permeability in the descending limb of the loop, water impermeability in the ascending loop and active ion transport out of most of the ascending loop. In addition, countercurrent exchange by the vessels carrying the blood supply to the nephron is essential for enabling this function.
Glucose at normal plasma levels is completely reabsorbed in the proximal tubule. The mechanism for this is the Na+/glucose cotransporter. A plasma level of 350 mg/dL will fully saturate the transporters and glucose will be lost in the urine. A plasma glucose level of approximately 160 is sufficient to allow glucosuria which is an important clinical clue to diabetes mellitus.
Amino acids are reabsorbed by sodium dependent transporters in the proximal tubule. Hartnup's disease is a deficiency of the tryptophan amino acid transporter which results in pellagra.
Pregnancy reduces the reabsorption of glucose and amino acids.
Two organ systems, the kidneys and lungs, maintain acid-base homeostasis, which is the maintenance of pH around a relatively stable value. The lungs contribute to acid-base homeostasis by regulating carbon dioxide (CO2) concentration. The kidneys have two very important roles in maintaining the acid-base balance: to reabsorb bicarbonate from urine, and to excrete hydrogen ions into urine
Any significant rise in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. An increase in osmolality causes the gland to secrete antidiuretic hormone (ADH), resulting in water reabsorption by the kidney and an increase in urine concentration. The two factors work together to return the plasma osmolality to its normal levels.
ADH binds to principal cells in the collecting duct that translocate aquaporins to the membrane, allowing water to leave the normally impermeable membrane and be reabsorbed into the body by the vasa recta, thus increasing the plasma volume of the body.
There are two systems that create a hyperosmotic medulla and thus increase the body plasma volume: Urea recycling and the 'single effect.'
Urea is usually excreted as a waste product from the kidneys. However, when plasma blood volume is low and ADH is released the aquaporins that are opened are also permeable to urea. This allows urea to leave the collecting duct into the medulla creating a hyperosmotic solution that 'attracts' water. Urea can then re-enter the nephron and be excreted or recycled again depending on whether ADH is still present or not.
The 'Single effect' describes the fact that the ascending thick limb of the loop of Henle is not permeable to water but is permeable to NaCl. This allows for a countercurrent exchange system whereby the medulla becomes increasingly concentrated, but at the same time setting up an osmotic gradient for water to follow should the aquaporins of the collecting duct be opened by ADH.
Although the kidney cannot directly sense blood, long-term regulation of blood pressure predominantly depends upon the kidney. This primarily occurs through maintenance of the extracellular fluid compartment, the size of which depends on the plasma sodium concentration. Renin is the first in a series of important chemical messengers that make up the renin-angiotensin system. Changes in renin ultimately alter the output of this system, principally the hormones angiotensin II and aldosterone. Each hormone acts via multiple mechanisms, but both increase the kidney's absorption of sodium chloride, thereby expanding the extracellular fluid compartment and raising blood pressure. When renin levels are elevated, the concentrations of angiotensin II and aldosterone increase, leading to increased sodium chloride reabsorption, expansion of the extracellular fluid compartment, and an increase in blood pressure. Conversely, when renin levels are low, angiotensin II and aldosterone levels decrease, contracting the extracellular fluid compartment, and decreasing blood pressure.
The kidneys secrete a variety of hormones, including erythropoietin, and the enzyme renin. Erythropoietin is released in response to hypoxia (low levels of oxygen at tissue level) in the renal circulation. It stimulates erythropoiesis (production of red blood cells) in the bone marrow. Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate. Part of the renin-angiotensin-aldosterone system, renin is an enzyme involved in the regulation of aldosterone levels.
The mammalian kidney develops from intermediate mesoderm. Kidney development, also called nephrogenesis, proceeds through a series of three successive phases, each marked by the development of a more advanced pair of kidneys: the pronephros, mesonephros, and metanephros.
Kidneys of various animals show evidence of evolutionary adaptation and have long been studied in ecophysiology and comparative physiology. Kidney morphology, often indexed as the relative medullary thickness, is associated with habitat aridity among species of mammals.
Medical terms related to the kidneys commonly use terms such as renal and the prefix nephro-. The adjective renal, meaning related to the kidney, is from the Latin rēnēs, meaning kidneys; the prefix nephro- is from the Ancient Greek word for kidney, nephros (νεφρός). For example, surgical removal of the kidney is a nephrectomy, while a reduction in kidney function is called renal dysfunction.
Generally, humans can live normally with just one kidney, as one has more functioning renal tissue than is needed to survive. Only when the amount of functioning kidney tissue is greatly diminished does one develop chronic kidney disease. Renal replacement therapy, in the form of dialysis or kidney transplantation, is indicated when the glomerular filtration rate has fallen very low or if the renal dysfunction leads to severe symptoms.
Many renal diseases are diagnosed on the basis of classical clinical findings. A physician (usually a nephrologist) begins by taking a detailed clinical history and performs a physical examination. In addition to medical history and presenting symptoms, a physician will ask about medication history, family history recent infections, toxic/chemical exposures and other historical factors which may indicate an etiology for the patient's renal disease. Often, some diseases are suggested by clinical history and time course alone. For example, in a formerly healthy child with a recent upper respiratory tract infection and facial/lower limb swelling, findings of proteinuria on urinalysis, a diagnosis of minimal change disease is highly suggested. Similarly, a patient with a history of diabetes who presents with decreased urine output is most likely to be suffering from diabetic nephropathy. Often, such cases do not require extensive workup (such as with renal biopsy). A presumptive diagnosis can be made on the basis of history, physical exam and supportive laboratory studies.
Laboratory studies are an important adjunct to clinical evaluation for assessment of renal function. An initial workup of a patient may include a complete blood count (CBC); serum electrolytes including sodium, potassium, chloride, bicarbonate, calcium, and phosphorus; blood urea, nitrogen and creatinine; blood glucose and glycocylated hemoglobin. Glomerular filtration rate (GFR) can be calculated.
Urine studies may include urine electrolytes, creatinine, protein, fractional excretion of sodium (FENA) and other studies to assist in evaluation of the etiology of a patient's renal disease.
Urinalysis is used to evaluate urine for its pH, protein, glucose, specific gravity and the presence of blood/hemoglobin. Microscopic analysis can be helpful in the identification of casts, red blood cells, white blood cells and crystals.
Imaging studies are important in the evaluation of structural renal disease caused by urinary tract obstruction, renal stones, renal cyst, mass lesions, renal vascular disease, and vesicoureteral reflux.
Imaging techniques used most frequently include renal ultrasound and helical CT scan. Patients with suspected vesicoureteral reflux may undergo voiding cystourethrogram (VCUG).
The role of the renal biopsy is to diagnose renal disease in which the etiology is not clear based upon noninvasive means (clinical history, past medical history, medication history, physical exam, laboratory studies, imaging studies).
A detailed description of renal biopsy interpretation is beyond the scope of this article. In general- a renal pathologist will perform a detailed morphological evaluation and integrate the morphologic findings with the clinical history and laboratory data, ultimately arriving at a pathological diagnosis. A renal pathologist is a physician who has undergone general training in anatomic pathology and additional specially training in the interpretation of renal biopsy specimens.
Ideally, multiple core sections are obtained and evaluated for adequacy (presence of glomeruli) intraoperatively. A pathologist/pathology assistant divides the specimen(s) for submission for light microscopy, immunofluorescence microscopy and electron microscopy.
The pathologist will examine the specimen using light microscopy with multiple staining techniques (hematoxylin and eosin/H&E, PAS, trichrome, silver stain) on multiple level sections. Multiple immunofluorescence stains are performed to evaluate for antibody, protein and complement deposition. Finally, ultra-structural examination is performed with electron microscopy and may reveal the presence of electron-dense deposits or other characteristic abnormalities which may suggest an etiology for the patient's renal disease.
Calculations of kidney performance are an important part of physiology and can be estimated using the calculations below.
The filtration fraction is the amount of plasma which is actually filtered through the kidney. This can be defined using the equation:
Normal human FF is 20%.
Renal clearance is the volume of plasma from which the substance is completely cleared from the blood per unit time.
More information regarding renal function can be found on the Renal function Wikipedia page.
In the majority of vertebrates, the mesonephros persists into the adult, albeit usually fused with the more advanced metanephros; only in amniotes is the mesonephros restricted to the embryo. The kidneys of fish and amphibians are typically narrow, elongated organs, occupying a significant portion of the trunk. The collecting ducts from each cluster of nephrons usually drain into an archinephric duct, which is homologous with the vas deferens of amniotes. However, the situation is not always so simple; in cartilaginous fish and some amphibians, there is also a shorter duct, similar to the amniote ureter, which drains the posterior (metanephric) parts of the kidney, and joins with the archinephric duct at the bladder or cloaca. Indeed, in many cartilaginous fish, the anterior portion of the kidney may degenerate or cease to function altogether in the adult.
In the most primitive vertebrates, the hagfish and lampreys, the kidney is unusually simple: it consists of a row of nephrons, each emptying directly into the archinephric duct. Invertebrates may possess excretory organs that are sometimes referred to as "kidneys", but, even in Amphioxus, these are never homologous with the kidneys of vertebrates, and are more accurately referred to by other names, such as nephridia.
The kidneys of reptiles consist of a number of lobules arranged in a broadly linear pattern. Each lobule contains a single branch of the ureter in its centre, into which the collecting ducts empty. Reptiles have relatively few nephrons compared with other amniotes of a similar size, possibly because of their lower metabolic rate.
Birds have relatively large, elongated kidneys, each of which is divided into three or more distinct lobes. The lobes consists of several small, irregularly arranged, lobules, each centred on a branch of the ureter. Birds have small glomeruli, but about twice as many nephrons as similarly sized mammals.
The human kidney is fairly typical of that of mammals. Distinctive features of the mammalian kidney, in comparison with that of other vertebrates, include the presence of the renal pelvis and renal pyramids, and of a clearly distinguishable cortex and medulla. The latter feature is due to the presence of elongated loops of Henle; these are much shorter in birds, and not truly present in other vertebrates (although the nephron often has a short intermediate segment between the convoluted tubules). It is only in mammals that the kidney takes on its classical "kidney" shape, although there are some exceptions, such as the multilobed reniculate kidneys of cetaceans.
The Latin term renes is related to the English word "reins", a synonym for the kidneys in Shakespearean English (e.g. Merry Wives of Windsor 3.5), which was also the time the King James Version was translated. Kidneys were once popularly regarded as the seat of the conscience and reflection, and a number of verses in the Bible (e.g. Ps. 7:9, Rev. 2:23) state that God searches out and inspects the kidneys, or "reins", of humans. Similarly, the Talmud (Berakhoth 61.a) states that one of the two kidneys counsels what is good, and the other evil.
The kidneys can be cooked and eaten (along with other offal).
Kidneys are usually grilled or sautéed, but in more complex dishes they are stewed with a sauce that will improve their flavor. In many preparations, kidneys are combined with pieces of meat or liver, as in mixed grill or meurav Yerushalmi. Dishes include the British steak and kidney pie, the Swedish hökarpanna (pork and kidney stew), the French rognons de veau sauce moutarde (veal kidneys in mustard sauce) and the Spanish riñones al Jerez (kidneys stewed in sherry sauce) .
Kidney Posterior View
Anterior relation of Left Kidney
Kidney Cross Section
noco/acba/cong/tumr, sysi/epon, urte
proc/itvp, drug (G4B), blte, urte
A kidney stone, also known as a renal calculus (from the Latin rēnēs, "kidneys" and calculus, "pebble") is a solid concretion or crystal aggregation formed in the kidneys from dietary minerals in the urine.
Urinary stones are typically classified by their location in the kidney (nephrolithiasis), ureter (ureterolithiasis), or bladder (cystolithiasis), or by their chemical composition (calcium-containing, struvite, uric acid, or other compounds). About 80% of those with kidney stones are men.
Kidney stones typically leave the body by passage in the urine stream, and many stones are formed and passed without causing symptoms. If stones grow to sufficient size (usually at least 3 millimeters (0.12 in)) they can cause obstruction of the ureter. Ureteral obstruction causes postrenal azotemia and hydronephrosis (distension and dilation of the renal pelvis and calyces), as well as spasm of the ureter. This leads to pain, most commonly felt in the flank (the area between the ribs and hip), lower abdomen, and groin (a condition called renal colic). Renal colic can be associated with nausea, vomiting, fever, blood in the urine, pus in the urine, and painful urination. Renal colic typically comes in waves lasting 20 to 60 minutes, beginning in the flank or lower back and often radiating to the groin or genitals. The diagnosis of kidney stones is made on the basis of information obtained from the history, physical examination, urinalysis, and radiographic studies. Ultrasound examination and blood tests may also aid in the diagnosis.
When a stone causes no symptoms, watchful waiting is a valid option. For symptomatic stones, pain control is usually the first measure, using medications such as nonsteroidal anti-inflammatory drugs or opioids. More severe cases may require surgical intervention. For example, some stones can be shattered into smaller fragments using extracorporeal shock wave lithotripsy. Some cases require more invasive forms of surgery. Examples of these are cystoscopic procedures such as laser lithotripsy or percutaneous techniques such as percutaneous nephrolithotomy. Sometimes, a tube (ureteral stent) may be placed in the ureter to bypass the obstruction and alleviate the symptoms, as well as to prevent ureteral stricture after ureteroscopic stone removal.
The hallmark of stones that obstruct the ureter or renal pelvis is excruciating, intermittent pain that radiates from the flank to the groin or to the genital area and inner thigh. This particular type of pain, known as renal colic, is often described as one of the strongest pain sensations known. Renal colic caused by kidney stones is commonly accompanied by urinary urgency, restlessness, hematuria, sweating, nausea, and vomiting. It typically comes in waves lasting 20 to 60 minutes caused by peristaltic contractions of the ureter as it attempts to expel the stone. The embryological link between the urinary tract, the genital system, and the gastrointestinal tract is the basis of the radiation of pain to the gonads, as well as the nausea and vomiting that are also common in urolithiasis. Postrenal azotemia and hydronephrosis can be observed following the obstruction of urine flow through one or both ureters.
Dietary factors that increase the risk of stone formation include low fluid intake and high dietary intake of animal protein, sodium, refined sugars, fructose and high fructose corn syrup, oxalate, grapefruit juice, apple juice, and cola drinks.][
Calcium is one component of the most common type of human kidney stones, calcium oxalate. Some studies suggest people who take supplemental calcium have a higher risk of developing kidney stones, and these findings have been used as the basis for setting the recommended daily intake for calcium in adults. In the Women's Health Initiative, postmenopausal women who consumed 1000 mg of supplemental calcium and 400 international units of vitamin D per day for seven years had a 17% higher risk of developing kidney stones than subjects taking a placebo. The Nurses' Health Study also showed an association between supplemental calcium intake and kidney stone formation.
Unlike supplemental calcium, high intakes of dietary calcium do not appear to cause kidney stones and may actually protect against their development. This is perhaps related to the role of calcium in binding ingested oxalate in the gastrointestinal tract. As the amount of calcium intake decreases, the amount of oxalate available for absorption into the bloodstream increases; this oxalate is then excreted in greater amounts into the urine by the kidneys. In the urine, oxalate is a very strong promoter of calcium oxalate precipitation, about 15 times stronger than calcium. In fact, current evidence suggests the consumption of diets low in calcium is associated with a higher overall risk for the development of kidney stones. For most individuals, other risk factors for kidney stones, such as high intakes of dietary oxalates and low fluid intake, would play a greater role than calcium intake.
Aside from calcium, other electrolytes appear to influence the formation of kidney stones. For example, by increasing urinary calcium excretion, high dietary sodium may increase the risk of stone formation. Fluoridation of drinking water may increase the risk of kidney stone formation by a similar mechanism, though further epidemiologic studies are warranted to determine whether fluoride in drinking water is associated with an increased incidence of kidney stones. On the other hand, high dietary intake of potassium appears to reduce the risk of stone formation because potassium promotes the urinary excretion of citrate, an inhibitor of urinary crystal formation. High dietary intake of magnesium also appears to reduce the risk of stone formation somewhat, because like citrate, magnesium is also an inhibitor of urinary crystal formation.
Diets in Western nations typically contain a large proportion of animal protein. Urinary excretion of excess sulfurous amino acids (e.g., cysteine and methionine), uric acid and other acidic metabolites from animal protein acidifies the urine, which promotes the formation of kidney stones.][ The body often balances this acidic urinary pH by leaching calcium from the bones, which further promotes the formation of kidney stones. Low urinary citrate excretion is also commonly found in those with a high dietary intake of animal protein, whereas vegetarians tend to have higher levels of citrate excretion.
Despite a widely held belief in the medical community that ingestion of vitamin C supplements is associated with an increased incidence of kidney stones, the evidence for a causal relationship between vitamin C supplements and kidney stones is inconclusive. While excess dietary intake of vitamin C might increase the risk of calcium oxalate stone formation, in practice this is rarely encountered. The link between vitamin D intake and kidney stones is also tenuous. Excessive vitamin D supplementation may increase the risk of stone formation by increasing the intestinal absorption of calcium, but there is no evidence that correction of vitamin D deficiency increases the risk of stone formation.
There are no conclusive data demonstrating a cause-and-effect relationship between alcohol consumption and kidney stones. However, some have theorized that certain behaviors associated with frequent and binge drinking can lead to systemic dehydration, which can in turn lead to the development of kidney stones. The American Urological Association has projected that increasing global temperatures will lead to an increased incidence of kidney stones in the United States by expanding the "kidney stone belt" of the southern United States.
When the urine becomes supersaturated (when the urine solvent contains more solutes than it can hold in solution) with one or more calculogenic (crystal-forming) substances, a seed crystal may form through the process of nucleation. Heterogeneous nucleation (where there is a solid surface present on which a crystal can grow) proceeds more rapidly than homogeneous nucleation (where a crystal must grow in liquid medium with no such surface), because it requires less energy. Adhering to cells on the surface of a renal papilla, a seed crystal can grow and aggregate into an organized mass. Depending on the chemical composition of the crystal, the stone-forming process may proceed more rapidly when the urine pH is unusually high or low.
Supersaturation of the urine with respect to a calculogenic compound is pH-dependent. For example, at a pH of 7.0, the solubility of uric acid in urine is 158 mg/100 ml. Reducing the pH to 5.0 decreases the solubility of uric acid to less than 8 mg/100 ml. The formation of uric acid stones requires a combination of hyperuricosuria (high urine uric acid levels) and low urine pH; hyperuricosuria alone is not associated with uric acid stone formation if the urine pH is alkaline. Supersaturation of the urine is a necessary, but not a sufficient, condition for the development of any urinary calculus. Supersaturation is likely the underlying cause of uric acid and cystine stones, but calcium-based stones (especially calcium oxalate stones) may have a more complex etiology.
Normal urine contains chelating agents, such as citrate, that inhibit the nucleation, growth, and aggregation of calcium-containing crystals. Other endogenous inhibitors include calgranulin (an S-100 calcium binding protein), Tamm-Horsfall protein, glycosaminoglycans, uropontin (a form of osteopontin), nephrocalcin (an acidic glycoprotein), prothrombin F1 peptide, and bikunin (uronic acid-rich protein). The biochemical mechanisms of action of these substances have not yet been thoroughly elucidated. However, when these substances fall below their normal proportions, stones can form from an aggregation of crystals.
Kidney stones often result from a combination of factors, rather than a single, well-defined cause. Stones are more common in people whose diet is very high in animal protein or who do not consume enough water or calcium. They can result from an underlying metabolic condition, such as distal renal tubular acidosis, Dent's disease, hyperparathyroidism, primary hyperoxaluria or medullary sponge kidney. In fact, studies show about 3% to 20% of people who form kidney stones have medullary sponge kidney. Kidney stones are also more common in people with Crohn's disease. People with recurrent kidney stones are often screened for these disorders. This is typically done with a 24-hour urine collection that is chemically analyzed for deficiencies and excesses that promote stone formation.
Diagnosis of kidney stones is made on the basis of information obtained from the history, physical examination, urinalysis, and radiographic studies. Clinical diagnosis is usually made on the basis of the location and severity of the pain, which is typically colicky in nature (comes and goes in spasmodic waves). Pain in the back occurs when calculi produce an obstruction in the kidney. Physical examination may reveal fever and tenderness at the costovertebral angle on the affected side.
Calcium-containing stones are relatively radiodense, and they can often be detected by a traditional radiograph of the abdomen that includes the kidneys, ureters, and bladder (KUB film). Some 60% of all renal stones are radiopaque. In general, calcium phosphate stones have the greatest density, followed by calcium oxalate and magnesium ammonium phosphate stones. Cystine calculi are only faintly radiodense, while uric acid stones are usually entirely radiolucent.
Where available, a noncontrast helical CT scan with 5 millimeters (0.20 in) sections is the diagnostic modality of choice in the radiographic evaluation of suspected nephrolithiasis. All stones are detectable on CT scans except very rare stones composed of certain drug residues in the urine, such as from indinavir.
Where a CT scan is unavailable, an intravenous pyelogram may be performed to help confirm the diagnosis of urolithiasis. This involves intravenous injection of a contrast agent followed by a KUB film. Uroliths present in the kidneys, ureters or bladder may be better defined by the use of this contrast agent. Stones can also be detected by a retrograde pyelogram, where a similar contrast agent is injected directly into the distal ostium of the ureter (where the ureter terminates as it enters the bladder).
Ultrasound imaging of the kidneys can sometimes be useful, as it gives details about the presence of hydronephrosis, suggesting the stone is blocking the outflow of urine. Radiolucent stones, which do not appear on KUB, may show up on ultrasound imaging studies. Other advantages of renal ultrasonography include its low cost and absence of radiation exposure. Ultrasound imaging is useful for detecting stones in situations where X-rays or CT scans are discouraged, such as in children or pregnant women. Despite these advantages, renal ultrasonography is not currently considered a substitute for noncontrast helical CT scan in the initial diagnostic evaluation of urolithiasis. The main reason for this is that compared with CT, renal ultrasonography more often fails to detect small stones (especially ureteral stones), as well as other serious disorders that could be causing the symptoms.
Laboratory investigations typically carried out include:
Kidney stones are typically classified by their location and chemical composition.
By far, the most common type of kidney stones worldwide contains calcium. For example, calcium-containing stones represent about 80% of all cases in the United States; these typically contain calcium oxalate either alone or in combination with calcium phosphate in the form of apatite or brushite. Factors that promote the precipitation of oxalate crystals in the urine, such as primary hyperoxaluria, are associated with the development of calcium oxalate stones. The formation of calcium phosphate stones is associated with conditions such as hyperparathyroidism and renal tubular acidosis.
Oxaluria is increased in patients with certain gastrointestinal disorders including inflammatory bowel disease such as Crohn disease or patients who have undergone resection of the small bowel or small bowel bypass procedures. Oxaluria is also increased in patients who consume increased amounts of oxalate (found in vegetables and nuts). Primary hyperoxaluria is a rare autosomal recessive condition which usually presents in childhood.
Calcium oxalate stones appear as 'envelopes' microscopically. They may also form 'dumbbells.'
About 10–15% of urinary calculi are composed of struvite (ammonium magnesium phosphate, NH4MgPO4·6H2O). Struvite stones (also known as "infection stones", urease or triple-phosphate stones), form most often in the presence of infection by urea-splitting bacteria. Using the enzyme urease, these organisms metabolize urea into ammonia and carbon dioxide. This alkalinizes the urine, resulting in favorable conditions for the formation of struvite stones. Proteus mirabilis, Proteus vulgaris, and Morganella morganii are the most common organisms isolated; less common organisms include Ureaplasma urealyticum, and some species of Providencia, Klebsiella, Serratia, and Enterobacter. These infection stones are commonly observed in people who have factors that predispose them to urinary tract infections, such as those with spinal cord injury and other forms of neurogenic bladder, ileal conduit urinary diversion, vesicoureteral reflux, and obstructive uropathies. They are also commonly seen in people with underlying metabolic disorders, such as idiopathic hypercalciuria, hyperparathyroidism, and gout. Infection stones can grow rapidly, forming large calyceal staghorn (antler-shaped) calculi requiring invasive surgery such as percutaneous nephrolithotomy for definitive treatment.
Struvite stones (triple phosphate/magnesium ammonium phosphate) have a 'coffin lid' morphology by microscopy.
About 5–10% of all stones are formed from uric acid. People with certain metabolic abnormalities, including obesity, may produce uric acid stones. They also may form in association with conditions that cause hyperuricosuria (an excessive amount of uric acid in the urine) with or without hyperuricemia (an excessive amount of uric acid in the serum). They may also form in association with disorders of acid/base metabolism where the urine is excessively acidic (low pH), resulting in precipitation of uric acid crystals. A diagnosis of uric acid urolithiasis is supported by the presence of a radiolucent stone in the face of persistent urine acidity, in conjunction with the finding of uric acid crystals in fresh urine samples.
As noted above (section on calcium oxalate stones), patients with inflammatory bowel disease (Crohn disease, ulcerative colitis) tend to have hyperoxaluria and form oxalate stones. These patients also have a tendency to form urate stones. Urate stones are especially common after colon resection.
Uric acid stones appear as pleomorphic crystals, usually diamond-shaped. They may also look like squares or rods which are polarizable.
Patients with hyperuricosuria can be treated with allopurinol which will reduce urate formation. Urine alkalinization may also be helpful in this setting.
People with certain rare inborn errors of metabolism have a propensity to accumulate crystal-forming substances in their urine. For example, those with cystinuria, cystinosis, and Fanconi syndrome may form stones composed of cystine. Cystine stone formation can be treated with urine alkalinization and dietary protein restriction. People afflicted with xanthinuria often produce stones composed of xanthine. People afflicted with adenine phosphoribosyltransferase deficiency may produce 2,8-dihydroxyadenine stones, alkaptonurics produce homogentisic acid stones, and iminoglycinurics produce stones of glycine, proline and hydroxyproline. Urolithiasis has also been noted to occur in the setting of therapeutic drug use, with crystals of drug forming within the renal tract in some people currently being treated with agents such as indinavir, sulfadiazine and triamterene.
Urolithiasis refers to stones originating anywhere in the urinary system, including the kidneys and bladder. Nephrolithiasis (from the Ancient Greek: , "kidney"; and , , "stone") refers to the presence of such calculi in the kidneys. Calyceal calculi refers to aggregations in either the minor or major calyx, parts of the kidney that pass urine into the ureter (the tube connecting the kidneys to the urinary bladder). The condition is called ureterolithiasis when a calculus is located in the ureter. Stones may also form or pass into the bladder, a condition referred to as cystolithiasis.
Preventative measures depend on the type of stones. In those with calciums stone drinking lots of fluids, thiazide diuretics and citrate are effective as is allopurinal in those with high uric acid levels in the blood or urine.
Specific therapy should be tailored to the type of stones involved. Diet can have a profound influence on the development of kidney stones. Preventive strategies include some combination of dietary modifications and medications with the goal of reducing the excretory load of calculogenic compounds on the kidneys. Current dietary recommendations to minimize the formation of kidney stones include:
Maintenance of dilute urine by means of vigorous fluid therapy is beneficial in all forms of nephrolithiasis, so increasing urine volume is a key principle for the prevention of kidney stones. Fluid intake should be sufficient to maintain a urine output of at least 2 litres (68 US fl oz) per day. A high fluid intake has been associated with a 40% reduction in recurrence risk.
Calcium binds with available oxalate in the gastrointestinal tract, thereby preventing its absorption into the bloodstream, and reducing oxalate absorption decreases kidney stone risk in susceptible people. Because of this, some nephrologists and urologists recommend chewing calcium tablets during meals containing oxalate foods. Calcium citrate supplements can be taken with meals if dietary calcium cannot be increased by other means. The preferred calcium supplement for people at risk of stone formation is calcium citrate because it helps to increase urinary citrate excretion.
Aside from vigorous oral hydration and consumption of more dietary calcium, other prevention strategies include avoidance of large doses of supplemental and restriction of oxalate-rich foods such as leaf vegetables, rhubarb, soy products and chocolate. However, no randomized, controlled trial of oxalate restriction has yet been performed to test the hypothesis that oxalate restriction reduces the incidence of stone formation. Some evidence indicates magnesium intake decreases the risk of symptomatic nephrolithiasis.
The mainstay for medical management of uric acid stones is alkalinization (increasing the pH) of the urine. Uric acid stones are among the few types amenable to dissolution therapy, referred to as chemolysis. Chemolysis is usually achieved through the use of oral medications, although in some cases, intravenous agents or even instillation of certain irrigating agents directly onto the stone can be performed, using antegrade nephrostomy or retrograde ureteral catheters. Acetazolamide (Diamox) is a medication that alkalinizes the urine. In addition to acetazolamide or as an alternative, certain dietary supplements are available that produce a similar alkalinization of the urine. These include sodium bicarbonate, potassium citrate, magnesium citrate, and Bicitra (a combination of citric acid monohydrate and sodium citrate dihydrate). Aside from alkalinization of the urine, these supplements have the added advantage of increasing the urinary citrate level, which helps to reduce the aggregation of calcium oxalate stones.
Increasing the urine pH to around 6.5 provides optimal conditions for dissolution of uric acid stones. Increasing the urine pH to a value higher than 7.0 increases the risk of calcium phosphate stone formation. Testing the urine periodically with nitrazine paper can help to ensure the urine pH remains in this optimal range. Using this approach, stone dissolution rate can be expected to be around 10 mm (0.39 in) of stone radius per month.
One of the recognized medical therapies for prevention of stones is the thiazide and thiazide-like diuretics, such as chlorthalidone or indapamide. These drugs inhibit the formation of calcium-containing stones by reducing urinary calcium excretion. Sodium restriction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Thiazides work best for renal leak hypercalciuria (high urine calcium levels), a condition in which high urinary calcium levels are caused by a primary kidney defect. Thiazides are useful for treating absorptive hypercalciuria, a condition in which high urinary calcium is a result of excess absorption from the gastrointestinal tract.
For people with hyperuricosuria and calcium stones, allopurinol is one of the few treatments that have been shown to reduce kidney stone recurrences. Allopurinol interferes with the production of uric acid in the liver. The drug is also used in people with gout or hyperuricemia (high serum uric acid levels). Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/100 ml) is often a therapeutic goal. Hyperuricemia is not necessary for the formation of uric acid stones; hyperuricosuria can occur in the presence of normal or even low serum uric acid. Some practitioners advocate adding allopurinol only in people in whom hyperuricosuria and hyperuricemia persist, despite the use of a urine-alkalinizing agent such as sodium bicarbonate or potassium citrate.
Stone size influences the rate of spontaneous stone passage. For example, up to 98% of small stones (less than 5 mm (0.20 in) in diameter) may pass spontaneously through urination within four weeks of the onset of symptoms, but for larger stones (5 to 10 mm (0.20 to 0.39 in) in diameter), the rate of spontaneous passage decreases to less than 53%. Initial stone location also influences the likelihood of spontaneous stone passage. Rates increase from 48% for stones located in the proximal ureter to 79% for stones located at the vesicoureteric junction, regardless of stone size. Assuming no high-grade obstruction or associated infection is found in the urinary tract, and symptoms are relatively mild, various nonsurgical measures can be used to encourage the passage of a stone. Repeat stone formers benefit from more intense management, including proper fluid intake and use of certain medications. In addition, careful surveillance clearly is required to maximize the clinical course for people who are stone formers.
Management of pain often requires intravenous administration of NSAIDs or opioids. Orally administered medications are often effective for less severe discomfort.
The use of medications to speed the spontaneous passage of ureteral calculi is referred to as medical expulsive therapy. Several agents, including alpha adrenergic blockers (such as tamsulosin) and calcium channel blockers (such as nifedipine), have been found to be effective. A combination of tamsulosin and a corticosteroid may be better than tamsulosin alone. These treatments also appear to be a useful adjunct to lithotripsy.
Extracorporeal shock wave lithotripsy (ESWL) is a noninvasive technique for the removal of kidney stones. Most ESWL is carried out when the stone is present near the renal pelvis. ESWL involves the use of a lithotriptor machine to deliver externally applied, focused, high-intensity pulses of ultrasonic energy to cause fragmentation of a stone over a period of around 30–60 minutes. Following its introduction in United States in February 1984, ESWL was rapidly and widely accepted as a treatment alternative for renal and ureteral stones. It is currently used in the treatment of uncomplicated stones located in the kidney and upper ureter, provided the aggregate stone burden (stone size and number) is less than 20 mm (0.79 in) and the anatomy of the involved kidney is normal. For a stone greater than 10 mm, ESWL may not help break the stone in one treatment; instead, two or three treatments may be needed. Some 80 to 85% of simple renal calculi can be effectively treated with ESWL. A number of factors can influence its efficacy, including chemical composition of the stone, presence of anomalous renal anatomy and the specific location of the stone within the kidney, presence of hydronephrosis, body mass index, and distance of the stone from the surface of the skin. Common adverse effects of ESWL include acute trauma, such as bruising at the site of shock administration, and damage to blood vessels of the kidney. In fact, the vast majority of people who are treated with a typical dose of shock waves using currently accepted treatment settings are likely to experience some degree of acute kidney injury. ESWL-induced acute kidney injury is dose-dependent (increases with the total number of shock waves administered and with the power setting of the lithotriptor) and can be severe, including internal bleeding and subcapsular hematomas. On rare occasions, such cases may require blood transfusion and even lead to acute renal failure. Hematoma rates may be related to the type of lithotriptor used; hematoma rates of less than 1% and up to 13% have been reported for different lithotriptor machines. Recent studies show reduced acute tissue injury when the treatment protocol includes a brief pause following the initiation of treatment, and both improved stone breakage and a reduction in injury when ESWL is carried out at slow shock wave rate.
In addition to the aforementioned potential for acute kidney injury, animal studies suggest these acute injuries may progress to scar formation, resulting in loss of functional renal volume. Recent prospective studies also indicate elderly people are at increased risk of developing new-onset hypertension following ESWL. In addition, a retrospective case-control study published by researchers from the Mayo Clinic in 2006 has found an increased risk of developing diabetes mellitus and hypertension in people who had undergone ESWL, compared with age and gender-matched people who had undergone nonsurgical treatment. Whether or not acute trauma progresses to long-term effects probably depends on multiple factors that include the shock wave dose (i.e., the number of shock waves delivered, rate of delivery, power setting, acoustic characteristics of the particular lithotriptor, and frequency of retreatment), as well as certain intrinsic predisposing pathophysiologic risk factors.
To address these concerns, the American Urological Association established the Shock Wave Lithotripsy Task Force to provide an expert opinion on the safety and risk-benefit ratio of ESWL. The task force published a white paper outlining their conclusions in 2009. They concluded the risk-benefit ratio remains favorable for many people. The advantages of ESWL include its noninvasive nature, the fact that it is technically easy to treat most upper urinary tract calculi, and that, at least acutely, it is a well-tolerated, low-morbidity treatment for the vast majority of people. However, they recommended slowing the shock wave firing rate from 120 pulses per minute to 60 pulses per minute to reduce the risk of renal injury and increase the degree of stone fragmentation.
Most stones under 5 mm (0.20 in) pass spontaneously. Prompt surgery may, nonetheless, be required with persons with only one working kidney, bilateral obstructing stones, a urinary tract infection and thus, it is presumed, an infected kidney, or intractable pain. Beginning in the mid-1980s, less invasive treatments such as extracorporeal shock wave lithotripsy, ureteroscopy, and percutaneous nephrolithotomy began to replace open surgery as the modalities of choice for the surgical management of urolithiasis. More recently, flexible ureteroscopy has been adapted to facilitate retrograde nephrostomy creation for percutaneous nephrolithotomy. This approach is still under investigation, though early results are favorable. Percutaneous nephrolithotomy or, rarely, anatrophic nephrolithotomy, is the treatment of choice for large or complicated stones (such as calyceal staghorn calculi) or stones that cannot be extracted using less invasive procedures.
Ureteroscopy has become increasingly popular as flexible and rigid fiberoptic ureteroscopes have become smaller. One ureteroscopic technique involves the placement of a ureteral stent (a small tube extending from the bladder, up the ureter and into the kidney) to provide immediate relief of an obstructed kidney. Stent placement can be useful for saving a kidney at risk for postrenal acute renal failure due to the increased hydrostatic pressure, swelling and infection (pyelonephritis and pyonephrosis) caused by an obstructing stone. Ureteral stents vary in length from 24 to 30 cm (9.4 to 12 in) and most have a shape commonly referred to as a "double-J" or "double pigtail", because of the curl at both ends. They are designed to allow urine to flow past an obstruction in the ureter. They may be retained in the ureter for days to weeks as infections resolve and as stones are dissolved or fragmented by ESWL or by some other treatment. The stents dilate the ureters, which can facilitate instrumentation, and they also provide a clear landmark to aid in the visualization of the ureters and any associated stones on radiographic examinations. The presence of indwelling ureteral stents may cause minimal to moderate discomfort, frequency or urgency incontinence, and infection, which in general resolves on removal. Most ureteral stents can be removed cystoscopically during an office visit under topical anesthesia after resolution of the urolithiasis.
More definitive ureteroscopic techniques for stone extraction (rather than simply bypassing the obstruction) include basket extraction and ultrasound ureterolithotripsy. Laser lithotripsy is another technique, which involves the use of a holmium:yttrium aluminium garnet (Ho:YAG) laser to fragment stones in the bladder, ureters, and kidneys.
Ureteroscopic techniques are generally more effective than ESWL for treating stones located in the lower ureter, with success rates of 93–100% using Ho:YAG laser lithotripsy. Although ESWL has been traditionally preferred by many practitioners for treating stones located in the upper ureter, more recent experience suggests ureteroscopic techniques offer distinct advantages in the treatment of upper ureteral stones. Specifically, the overall success rate is higher, fewer repeat interventions and postoperative visits are needed, and treatment costs are lower after ureteroscopic treatment when compared with ESWL. These advantages are especially apparent with stones greater than 10 mm (0.39 in) in diameter. However, because ureteroscopy of the upper ureter is much more challenging than ESWL, many urologists still prefer to use ESWL as a first-line treatment for stones of less than 10 mm, and ureteroscopy for those greater than 10 mm in diameter. Ureteroscopy is the preferred treatment in pregnant and morbidly obese people, as well as those with bleeding disorders.
Kidney stones affect all geographical, cultural, and racial groups. The lifetime risk is about 10 to 15% in the developed world, but can be as high as 20 to 25% in the Middle East. The increased risk of dehydration in hot climates, coupled with a diet 50% lower in calcium and 250% higher in oxalates compared to Western diets, accounts for the higher net risk in the Middle East. In the Middle East, uric acid stones are more common than calcium-containing stones. The number of deaths due to kidney stones is estimated at 19,000 per year being fairly consistent between 1990 and 2010.
In North America and Europe, the annual incidence (number of new cases per year) of kidney stones is roughly 0.5%. In the United States, the prevalence (frequency in the population) of urolithiasis has increased from 3.2% to 5.2% from the mid-1970s to the mid-1990s. The total cost for treating urolithiasis was US$2 billion in 2003. About 65-80% of those with kidney stones are men; most stones in women are due to either metabolic defects (such as cystinuria) or infection. (p. 1057) Men most commonly experience their first episode between 30 and 40 years of age, whereas for women, the age at first presentation is somewhat later. The age of onset shows a bimodal distribution in women, with episodes peaking at 35 and 55 years. Recurrence rates are estimated at 50% over a 10-year and 75% over 20-year period, with some people experiencing ten or more episodes over the course of a lifetime.
The existence of kidney stones was first recorded thousands of years ago, and lithotomy for the removal of stones is one of the earliest known surgical procedures. In 1901, a stone discovered in the pelvis of an ancient Egyptian mummy was dated to 4,800 BC. Medical texts from ancient Mesopotamia, India, China, Persia, Greece, and Rome all mentioned calculous disease. Part of the Hippocratic Oath suggests there were practicing surgeons in ancient Greece to whom physicians were to defer for lithotomies. The Roman medical treatise De Medicina by Aulus Cornelius Celsus contained a description of lithotomy, and this work served as the basis for this procedure until the 18th century.
Famous people who were kidney stone formers include Napoleon I, Napoleon III, Peter the Great, Louis XIV, George IV, Oliver Cromwell, Lyndon B. Johnson, Benjamin Franklin, Michel de Montaigne, Francis Bacon, Isaac Newton, Samuel Pepys, William Harvey, Herman Boerhaave, and Antonio Scarpa.
New techniques in lithotomy began to emerge starting in 1520, but the operation remained risky. After Henry Jacob Bigelow popularized the technique of litholapaxy in 1878, the mortality rate dropped from about 24% to 2.4%. However, other treatment techniques continued to produce a high level of mortality, especially among inexperienced urologists. In 1980, Dornier MedTech introduced extracorporeal shock wave lithotripsy for breaking up stones via acoustical pulses, and this technique has since come into widespread use.
Crystallization of calcium oxalate appears to be inhibited by certain substances in the urine that retard the formation, growth, aggregation, and adherence of crystals to renal cells. By purifying urine using salt precipitation, isoelectric focusing, and size-exclusion chromatography, some researchers have found that calgranulin, a protein formed in the kidney, is a potent inhibitor of the in vivo formation of calcium oxalate crystals. Considering its extremely high levels of inhibition of growth and aggregation of calcium oxalate crystals, calgranulin might be an important intrinsic factor in the prevention of nephrolithiasis.
noco/acba/cong/tumr, sysi/epon, urte
proc/itvp, drug (G4B), blte, urte
Gastritis is an inflammation of the lining of the stomach, and has many possible causes. The main acute causes are excessive alcohol consumption or prolonged use of nonsteroidal anti-inflammatory drugs (also known as NSAIDs) such as aspirin or ibuprofen. Sometimes gastritis develops after major surgery, traumatic injury, burns, or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract. Chronic causes are infection with bacteria, primarily Helicobacter pylori, chronic bile reflux, and stress; certain autoimmune disorders can cause gastritis as well. The most common symptom is abdominal upset or pain. Other symptoms are indigestion, abdominal bloating, nausea, and vomiting and pernicious anemia. Some may have a feeling of fullness or burning in the upper abdomen. A gastroscopy, blood test, complete blood count test, or a stool test may be used to diagnose gastritis. Treatment includes taking antacids or other medicines, such as proton pump inhibitors or antibiotics, and avoiding hot or spicy foods. For those with pernicious anemia, B12 injections are given, but more often oral B12 supplements are recommended.
Many people with gastritis experience no symptoms at all. However, upper central abdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp. Pain is usually located in the upper central portion of the abdomen, but it may occur anywhere from the upper left portion of the abdomen around to the back.
Other signs and symptoms may include:
Erosive gastritis is a gastric mucosal erosion caused by damage to mucosal defenses. Alcohol consumption does not cause chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid. NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the stomach, which increases the possibility of peptic ulcers forming. Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis.
Chronic gastritis refers to a wide range of problems of the gastric tissues. The immune system makes proteins and antibodies that fight infections in the body to maintain a homeostatic condition. In some disorders the body targets the stomach as if it were a foreign protein or pathogen; it makes antibodies against, severely damages, and may even destroy the stomach or its lining. In some cases bile, normally used to aid digestion in the small intestine, will enter through the pyloric valve of the stomach if it has been removed during surgery or does not work properly, also leading to gastritis. Gastritis may also be caused by other medical conditions, including HIV/AIDS, Crohn's disease, certain connective tissue disorders, and liver or kidney failure.
Mucous gland metaplasia, the reversible replacement of differentiated cells, occurs in the setting of severe damage of the gastric glands, which then waste away (atrophic gastritis) and are progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the causes or the consequences. Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum, and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia.
Coffee can damage the lining of the gastrointestinal organs, causing gastritis and ulcers. The consumption of coffee is therefore not recommended for people with gastritis, colitis, and ulcers.
Helicobacter pylori colonizes the stomach of more than half of the world's population, and the infection continues to play a key role in the pathogenesis of a number of gastroduodenal diseases. Colonization of the gastric mucosa with Helicobacter pylori results in the development of chronic gastritis in infected individuals, and in a subset of patients chronic gastritis progresses to complications (e.g., ulcer disease, gastric neoplasias, some distinct extragastric disorders). However, gastritis has no adverse consequences for most hosts, and emerging evidence suggests that H. pylori prevalence is inversely related to gastroesophageal reflux disease and allergic disorders. These observations indicate that eradication may not be appropriate for certain populations owing to the potentially beneficial effects conferred by persistent gastric inflammation.
Often, a diagnosis can be made based on the patient's description of his or her symptoms, but other methods which may be used to verify gastritis include:
Over-the-counter antacids in liquid or tablet form are a common treatment for mild gastritis. Antacids neutralize stomach acid and can provide fast pain relief. When antacids do not provide enough relief, medications such as cimetidine, ranitidine, nizatidine or famotidine that help reduce the amount of acid the stomach produces are often prescribed. An even more effective way to limit stomach acid production is to shut down the acid "pumps" within acid-secreting stomach cells. Proton pump inhibitors reduce acid by blocking the action of these small pumps. This class of medications includes omeprazole, lansoprazole, rabeprazole, and esomeprazole. Proton pump inhibitors also appear to inhibit H. pylori activity. Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate. Many people also drink milk to relieve symptoms, however the high calcium levels actually stimulate release of gastric acid from parietal cells, ultimately worsening symptoms. In addition to protecting the lining of stomach and intestines, bismuth preparations appear to inhibit H. pylori activity as well. Several regimens are used to treat H. pylori infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is also added to the regimen. The antibiotic aids in destroying the bacteria, and the acid blocker or proton pump inhibitor relieves pain and nausea, heals inflammation, and may increase the antibiotic's effectiveness.
anat (t, g, p)/phys/devp/enzy
proc, drug (A2A/2B/3/4/5/6/7/14/16), blte
Arthritis Dermatomyositis soft tissue (Myositis, Synovitis/Tenosynovitis, Bursitis, Enthesitis, Fasciitis, Capsulitis, Epicondylitis, Tendinitis, Panniculitis)
female: Oophoritis Salpingitis Endometritis Parametritis Cervicitis Vaginitis Vulvitis Mastitis
male: Orchitis Epididymitis Prostatitis Balanitis Balanoposthitis
Serotonergic: agonist35-HT responsible for GABAergic ( receptorAGABA PAM), glycinergic, and cholinergic (mAChR agonist) effects
A kidney stone, also known as a renal calculus (from the Latin rēnēs, "kidneys," and calculus, "pebble"), is a solid concretion or crystal aggregation formed in the kidneys from dietary minerals in the urine.
Urinary stones are typically classified by their location in the kidney (nephrolithiasis), ureter (ureterolithiasis), or bladder (cystolithiasis), or by their chemical composition (calcium-containing, struvite, uric acid, or other compounds). About 80% of those with kidney stones are men.
Gastrointestinal cancer refers to malignant conditions of the gastrointestinal tract (GI tract) and accessory organs of digestion, including the esophagus, stomach, biliary system, pancreas, small intestine, large intestine, rectum and anus. The symptoms relate to the organ affected and can include obstruction (leading to difficulty swallowing or defecating), abnormal bleeding or other associated problems. The diagnosis often requires endoscopy, followed by biopsy of suspicious tissue. The treatment depends on the location of the tumor, as well as the type of cancer cell and whether it has invaded other tissues or spread elsewhere. These factors also determine the prognosis.
Overall, the GI tract and the accessory organs of digestion (pancreas, liver, gall bladder) are responsible for more cancers and more deaths from cancer than any other system in the body. There is significant geographic variation in the rates of different gastrointestinal cancers.
Stomach cancer, or gastric cancer, refers to cancer arising from any part of the stomach. Stomach cancer causes about 800,000 deaths worldwide per year. Prognosis is poor (5-year survival <5 to 15%) because most patients present with advanced disease.
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