What is hyperpituitarism?The pituitary gland produces hormones that regulate many functions in the body. A person with hyperpituitarism has an overactive pituitary gland that leads to high levels of one of the pituitary hormones in the bloodstream. The most common cause of hyperpituitarism is a non-cancerous tumor of the pituitary gland. Hyperpituitarism is very rare. What are the symptoms of hyperpituitarism?The symptoms of hyperpituitarism depend on the hormone that is over-produced by the pituitary gland. Symptoms of hyperpituitarism may include hyperprolactinemia symptoms, Cushing's disease symptoms, acromegaly symptoms, and hyperthyroidism symptoms.How does the doctor treat hyperpituitarism?The treatment for hyperpituitarism depends upon which hormone is over-produced by the pituitary gland. Treatment for hyperpituitarism may include medications, surgery, and hormone replacement therapy.The following are statistics from various sources about hospitalizations and Hyperpituitarism: 0.2% (2,482) of hospital consultant episodes were for hyperfunction of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 92% of hospital consultant episodes for hyperfunction of pituitary gland required hospital admission in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 41% of hospital consultant episodes for hyperfunction of pituitary gland were for men in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 59% of hospital consultant episodes for hyperfunction of pituitary gland were for women in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 16% of hospital consultant episodes for hyperfunction of pituitary gland required emergency hospital admission in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 9.6 days was the mean length of stay in hospitals for hyperfunction of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 4 days was the median length of stay in hospitals for hyperfunction of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 49 was the mean age of patients hospitalised for hyperfunction of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 48% of hospital consultant episodes for hyperfunction of pituitary gland occurred in 15-59 year olds in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 15% of hospital consultant episodes for hyperfunction of pituitary gland occurred in people over 75 in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 63% of hospital consultant episodes for hyperfunction of pituitary gland were single day episodes in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 0.13% 6,877 of hospital bed days were for hyperfunction of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03)
Hypopituitarism is a clinical syndrome of deficiency in pituitary hormone production. This may result from disorders involving the pituitary gland, hypothalamus, or surrounding structures. Panhypopituitarism refers to involvement of all pituitary hormones; however, only 1 or more pituitary hormones are often involved, resulting in isolated or partial hypopituitarism. (See Pathophysiology and Etiology.) Hormone replacementPatients with hypopituitarism are maintained on hormone replacement therapies for life, unless the causative disorder is reversed by treatment or by natural history. These medically replaced patients are generally asymptomatic but require increased doses of glucocorticoids following any form of stress, emotional or physical. The most common stressor is infection. Not matching glucocorticoid dose to stress causes acute decompensation. These patients present with nausea and vomiting and may be hypotensive and ill-appearing. A patient's initial presentation of undiagnosed hypopituitarism may be with this life-threatening decompensated state under stress. Patient educationEducation emphasizes the need for lifelong hormone replacement, increased glucocorticoid replacement during stress, and prompt medical attention as appropriate. Regular monitoring to avoid excessive hormone replacement is important. All patients with hypopituitarism should carry some identification. This is often in the form of an identification bracelet worn on the wrist or neck. Some vendors include more than 20 lines of information in a tiny pendant. Some may need to have a vial of hydrocortisone (Solu-Cortef) 100 mg and a syringe for emergency purposes at home and while travelling. Society statistics for HypopituitarismHospitalization statistics for Hypopituitarism: The following are statistics from various sources about hospitalizations and Hypopituitarism: 0.016% (2,061) of hospital consultant episodes were for hypofunction and other disorders of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 94% of hospital consultant episodes for hypofunction and other disorders of pituitary gland required hospital admission in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 54% of hospital consultant episodes for hypofunction and other disorders of pituitary gland were for men in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 46% of hospital consultant episodes for hypofunction and other disorders of pituitary gland were for women in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 14% of hospital consultant episodes for hypofunction and other disorders of pituitary gland required emergency hospital admission in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 6.3 days was the mean length of stay in hospitals for hypofunction and other disorders of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 2 days was the median length of stay in hospitals for hypofunction and other disorders of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 38 was the mean age of patients hospitalised for hypofunction and other disorders of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 58% of hospital consultant episodes for hypofunction and other disorders of pituitary gland occurred in 15-59 year olds in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 6% of hospital consultant episodes for hypofunction and other disorders of pituitary gland occurred in people over 75 in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 60% of hospital consultant episodes for hypofunction and other disorders of pituitary gland were single day episodes in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03) 0.008% (4,109) of hospital bed days were for hypofunction and other disorders of pituitary gland in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03)
Pituitary adenomas are relatively common, occurring in 1 out every 1000 adults. Most pituitary tumors are benign and are called adenomas. Pituitary adenomas are typically slow growing Some pituitary adenomas, although still benign, can invade adjacent structures (such the cavernous sinus, an area where the carotid arteries run) Pituitary carcinomas, a malignant tumor, are rare. Pituitary adenomas have separate names based on their size A microadenoma is less than 1 cm in diameter A macroadenoma is larger than 1 cm in size Most pituitary adenomas occur spontaneously, meaning they are not inherited. Cases of familial pituitary tumors, or inherited tendencies to develop pituitary adenomas, are rare.Multiple Endocrine Neoplasia type 1 (MEN 1) is a rare condition characterized by simultaneous tumors of the pituitary, pancreas and parathyroid glands. Pituitary adenomas develop in 25 percent of patients with MEN 1.Symptoms Caused by Pituitary AdenomasPituitary adenomas are generally thought of as either hormone-producing or hormone-inactive tumorsHormone-producing pituitary adenomas produce an active hormone in excessive amounts. Patients usually present with symptoms related to the hormonal imbalanceHormone-inactive (non-functional) pituitary adenomas typically cause problems related to the size of the tumor pushing on surrounding brain structures Large pituitary tumors can compress the normal pituitary gland and cause pituitary failure. This is why is it important to obtain a comprehensive evaluation of pituitary function if a pituitary tumor is diagnosed.Large hormone-producing pituitary tumors can also cause problems related to compression of brain structures. Hormone-producing pituitary adenomasThe three most common hormone-producing (called endocrine-active) adenomas are:Prolactin-secreting pituitary adenoma (prolactinoma): over-production of prolactin by the pituitary tumor causes loss of menstrual periods and breast milk production in women.Growth hormone-secreting pituitary adenoma: excessive growth hormone (GH) production causes acromegaly in adults or gigantism in children.ACTH-secreting pituitary adenoma: excessive ACTH hormone produced by the pituitary gland causes Cushing's disease. Other hormone producing pituitary tumors are very rareThyroid stimulating hormone (TSH) producing pituitary adenomas cause hyperthyroidismSymptoms related to the mass effect from large pituitary adenomasVisual Loss When large pituitary adenomas ("macroadenomas") grow upward, the tumor can elevate and compress the optic chiasm.A progressive loss of the outer peripheral vision occurs (called a "bitemporalhemianopsia")When severe, a patient can only see what is directly in front of themOther visual problems can include: Loss of visual acuity (blurry vision), especially if the macroadenoma grows forward and compresses an optic nerve. Changes in color perceptionPituitary Failure Compression of the normal pituitary gland can lead to various degrees of pituitary failure (hypopituitarism): Symptoms can include: Sexual dysfunction and/or loss of sex driveInadequate body cortisol levels, causing low blood pressure, fatigue, and inability to handle stressful situationsLow thyroid functioning (hypothyroidism)The "Stalk Effect" Compression of the pituitary stalk, the structure that connects the brain to the pituitary gland, can cause a mild elevation in the hormone prolactin. This can cause irregular menstrual periods. It is important to distinguish "stalk effect" from a prolactinoma.HeadachePituitary ApoplexyPituitary adenomas can suddenly bleed internally, leading to an abrupt increase in size. In other cases, the tumor can outgrow its blood supply, leading to swelling of the dead tissue. These scenarios are termed "pituitary apoplexy." Pituitary apoplexy generally presents with sudden onset headache and visual loss, and is a surgical emergency.Learn more about:ProlactinomaAcromegalyCushing's DiseaseNonfunctioning Pituitary AdenomaDiagnosisThe diagnosis of a pituitary adenoma is made based on a combination of pituitary function testing (blood hormone levels) and pituitary imagingPituitary Function TestingThe diagnosis of a hormone-producing pituitary adenoma may require the assistance of a pituitary endocrinologistThe medical diagnosis of Cushing's disease can be very difficult to make and may require highly specialized tests not available in most hospitals.Imaging Adenomas larger than 4 mm can be reliably detected by MRI scans (using a special pituitary protocol)In some cases, a powerful 3-Tesla MRI scanner may detect smaller tumors not visible using lower magnet strength scannersAlthough larger adenomas can be seen on computed tomography (CT), an MRI scan is preferred.TreatmentThe optimal treatment of a pituitary adenoma depends on multiple factors, including: Hormone production by the tumor (if present)Size of the tumorHow invasive the tumor is into surrounding structuresThe age and health of the patientTypically, more than one specialist is involved in the management of pituitary adenomas. The UCLA Pituitary Tumor Program has experts in each of the specialties who work closely together to provide patients the most comprehensive, state-of-the-art medical and surgical treatmentsMedical ManagementHormone-producing pituitary adenomas should be treated in conjunction with an endocrinologist. Prolactinomas often require only medical (nonsurgical) therapy.Medical therapy can play an important role in the management of Cushing's disease and acromegaly.It may be equally important to address pituitary failure (hypopituitarism), especially prior to surgery Inadequate cortisol or thyroid levels can be life-threatening if not recognized prior to surgeryUCLA has world-class endocrinologists who are available for consultationSurgical ManagementThe vast majority of pituitary adenomas that require surgery are best removed through the nose. This minimally-invasive technique leaves no facial scarUCLA neurosurgeons are experts in advanced endoscopic techniques, that are generally more effective in removing all the tumor while at the same time minimizing complications, hospitalization time, and discomfort. Our surgeons also have extensive experience with traditional techniques using the operating microscopeRadiation therapyStereotactic radiotherapy is a technique in which a high dose of radiation can be delivered to the tumor target. Remarkably, the surrounding brain structures receive only a fraction of the radiation dose and are typically unharmed (with the exception of the normal pituitary gland).UCLA uses the advanced Novalis Beam-Shaped radiation delivery system, which allows treatment of irregularly shaped tumors that are close to critical brain structures.One of the main drawbacks of radiation treatment is that it leads to delayed pituitary failure. This typically occurs several years after treatment, necessitating complete hormone replacement.Radiation therapy is typically reserved for pituitary tumors that cannot be cured surgically and are not controlled with medical drug therapyTo learn more about the Pituitary Tumor Program at UCLA, click here.The Neuro-ICU cares for patients with all types of neurosurgical and neurological injuries, including stroke, brain hemorrhage, trauma and tumors. We work in close cooperation with your surgeon or medical doctor with whom you have had initial contact. Together with the surgeon or medical doctor, the Neuro-ICU attending physician and team members direct your family member's care while in the ICU. The Neuro-ICU team consists of the bedside nurses, nurse practitioners, physicians in specialty training (Fellows) and attending physicians. UCLA Neuro ICU Family Guide
What is a prolactinoma?A prolactinoma is a benign-noncancerous-tumor of the pituitary gland that produces a hormone called prolactin. Prolactinomas are the most common type of pituitary tumor. Symptoms of prolactinoma are caused by hyperprolactinemia-too much prolactin in the blood-or by pressure of the tumor on surrounding tissues.Prolactin stimulates the breast to produce milk during pregnancy. After giving birth, a mother’s prolactin levels fall unless she breastfeeds her infant. Each time the baby nurses, prolactin levels rise to maintain milk production.[Top]ProlactinomaGeneral InformationThe UCLA Pituitary Tumor Program offers comprehensive management of prolactinomasThis type of pituitary tumor (adenoma) produces an excessive amount of the hormone prolactin. Prolactinomas are the most common type of hormonally-active pituitary tumor. What is Prolactin?Prolactin is a hormone produced by the pituitary gland that is makes breastfeeding of newborns possible.At the end of pregnancy, the pituitary gland begins producing more prolactin. This important hormone causes several body changes: Breast milk is produced (doctors call this "galactorrhea")Menstrual periods are stopped ("amenorrhea")Sexual interest (libido) is decreasedOnce breastfeeding is stopped (or never begun), prolactin levels drop back to normal and normal menstrual periods begin againThe brain controls the amount of prolactin production using a natural chemical ("neuropeptide") called dopamine. The more dopamine is sent down to the pituitary gland, the less prolactin that is made.Prolactin is a hormone essential for milk production by the breast. The release of prolactin is controlled by the amount of dopamine produced by the brainSymptomsIn women:Relatively small increases in prolactin cause irregular menstrual periods or complete loss of menses. For this reason, most prolactinomas are discovered when they are small in size.In many cases (more common with higher prolactin levels), there is milk production by the breastsSome women complain of a reduced sex driveLarge prolactinomas are uncommonly found in women. If the tumor is large enough, it may cause hypopituitarism, visual loss, and headache (see Symptoms In Men below)In men:Symptoms are usually caused as a result of the size of the tumor rather than the hormonal effects of prolactinIn some cases, men experience enlargement of the breast tissue ("gynecomastia")Large pituitary tumors ("macroadenomas") may cause: Some degree of pituitary failure (hypopituitarism) due to compression of the normal pituitary gland. The most common symptom is loss of sex drive (low libido).Visual loss from compression of the optic nerves. This is typically loss of peripheral vision first.HeadacheA minority of patients with large tumors may have acute bleeding into the tumor (pituitary apoplexy), causing the sudden onset of headache, visual loss, double vision, and/or pituitary failure. Immediate medical attention is usually requiredDiagnosisHormonalA blood test, measuring the level of prolactin, usually establishes the diagnosis.Not all cases of elevated prolactin are due to prolactinomas. Other possible causes include: PregnancyStressLow thyroid functionKidney failureLiver failureA large pituitary tumor (or other tumor occuring in the same area) that causes compression of the pituitary stalk (the connection between the brain and the pituitary gland). Compression of the pituitary stalk interferes with dopamine from the brain reaching the pituitary gland. Because dopamine normally inhibits prolactin release, the normal pituitary gland produces more prolactin (prolactin levels are usually less than 200)The blood prolactin level is usually proportional to the size of the tumor. Large tumors may have prolactin levels in the thousandsIn some cases, very high prolactin levels can overwhelm the blood test, resulting is a falsely measured prolactin level (typically reported as only slightly above normal). If a prolactinoma is suspected based on clinical symptoms, it is important to have the test repeated using a diluted sample of blood (the so-called "Hook Effect")MRI ImagingMost prolactinomas can be detected using magnetic resonance imaging (MRI) of the pituitary gland It is best to obtain a special MRI "Pituitary Protocol" in order to best visualize the tumorSmaller tumors may not be visible using computed tomography (CT) scans MRI image of the side-view of the head (midway through the brain) showing a prolactinoma. On the right is the same image that has been colorized, showing that the top part of the tumor (shown in red) elevates the optic nerve (actually, the optic chiasm)TreatmentMedical therapyIn general, the first line of treatment for patients with a prolactinoma is medical rather than surgical. Most patients (80 percent) will have their prolactin levels restored to normal with medication alone.The medications mimick the activity of dopamine, thereby sending the message to the prolactin-producing cells to stop making prolactin. Cabergoline (Dostinex) is usually the preferred medication because it is very effective, has the fewest side effects, and the easiest dosing schedule (twice a week). It is more expensive, howeverBromocriptine (Parlodel) is sometimes used, but its effectiveness is commonly limited by side effects (most common are nausea, headache, and dizziness)With treatment, most women experience a return of menses and many become fertile again. The size of the prolactinoma will be reduced in the majority of patients, which can improve vision and end headaches.The management of medical therapy for fertility and during pregnancy requires special consideration. As of now, Cabergoline is not FDA-approved for use during pregnancy, and therefore bromocriptine may be necessarySurgeryFor patients that do not respond to medical treatment with cabergoline or bromocriptine, surgery is considered Ideally, surgery should be performed within six months of starting medical treatment because the tumor may become more difficult to remove thereafter. Transsphenoidal surgery is effective for women with relatively small adenomas. The long-term cure rate is 80 percent to 90 percent. The cure rate is lower for larger tumors, particularly in men. Urgent transphenoidal surgery is advised for patients with pituitary apoplexy.RadiotherapyBecause most patients with prolactinomas respond well to medical therapy, radiation is used in few patients. Stereotactic radiation is generally preferred over external beam radiation therapy because a higher dose of radiation can be delivered to the tumor and less to normal brain structures. The Neuro-ICU cares for patients with all types of neurosurgical and neurological injuries, including stroke, brain hemorrhage, trauma and tumors. We work in close cooperation with your surgeon or medical doctor with whom you have had initial contact. Together with the surgeon or medical doctor, the Neuro-ICU attending physician and team members direct your family member's care while in the ICU. The Neuro-ICU team consists of the bedside nurses, nurse practitioners, physicians in specialty training (Fellows) and attending physicians. UCLA Neuro ICU Family Guide
The posterior (back) lobe of the pituitary gland releases ADH (antidiuretic hormone) and oxytocin (a hormone to contract the uterus during childbirth and stimulate milk production). Antidiuretic hormone (ADH), which is also called vasopressin, helps the kidneys (and body) conserve the right amount of water. For example, when a person becomes dehydrated, more ADH is produced to help the body conserve the water it contains. Lack of ADH leads to too much excretion of water (diabetes insipidus), and too much ADH leads to excessive retention of water by the body (syndrome of inappropriate antidiuretic hormone secretion).Listed in the directory below you will find additional information regarding these posterior pituitary disorders, for which we have provided a brief overview.The posterior lobe of the pituitary gland, the parathyroid glands, and the adrenal medulla are not governed by the anterior pituitary gland. The posterior pituitary produces a secretion called antidiuretic hormone which acts on the kidneys to control the amount of urine produced. A deficiency of this hormone causes diabetes insipidus, which results in the production of an excessive amount of urine, sometimes as much as 25 quarts a day. (A normal amount is about one quart.) The natural consequence of this disorder is an unquenchable thirst. It is an extremely rare disease, the cause of which is often unknown, although it may result from a brain injury or tumor. Treatment involves curing the cause if it is known. If not, the patient is given an antidiuretic hormone.Posterior Pituitary Disorders See also ...Handouts/Teaching sheetsThe posterior (back) lobe of the pituitary gland releases ADH (antidiuretic hormone) and oxytocin (a hormone to contract the uterus during childbirth and stimulate milk production). Antidiuretic hormone (ADH), which is also called vasopressin, helps the kidneys (and body) conserve the right amount of water. For example, when a person becomes dehydrated, more ADH is produced to help the body conserve the water it contains. Lack of ADH leads to too much excretion of water (diabetes insipidus), and too much ADH leads to excessive retention of water by the body (syndrome of inappropriate antidiuretic hormone secretion).
An enlarged pituitary fossa may also be caused by primary hypothalamic tumors extending into the pituitary fossa.(table 1). Hypothalamic tumors may extend into the pituitary fossa thereby leading to endocrine, visual, and neurological symptoms similar to those observed in patients with primary pituitary tumors. Furthermore, in contrast to primary pituitary tumors, hypothalamic tumors may cause posterior pituitary failure. Thus, diabetes insipidus is not seen in patients with pituitary tumors before surgery, though it is frequently observed in patients with primary suprasellar tumors in the pituitary stalk- or hypothalamic region (Fig. 1). Furthermore, hypothalamic tumors can cause disturbances of thirst control and dysregulation of osmolality, may lead to massive obesity by abnormal control of satiety, or to dysregulation of body temperature control. Extension of the hypothalamic tumor into upper parts of the brain may lead to blockage of the foramen of Monroe , internal hydrocephalus, and at the end, coma. Many hypothalamic tumors are developmental tumors, the most common is the craniopharyngioma followed by the rare germinomas, chordomas and hamartomas (Table 1). Furthermore, whereas metastases of solid cancers usually develop within the pituitary, systemic malignant diseases such as Hodgkin's disease, leukemia, histiocytosis X (Langherhan's cell histiocytosis), and Wegner's granulomatosis manifest as space occupying lesions of the basal hypothalamus. In addition, benign granulomatous or infectious diseases such as neurosarcoidosis, tuberculosis, syphilis, and cysticercosis are rare causes of a suprasellar mass.The diagnostic work-up of pituitary or hypothalamic tumor patients should therefore answer the following questions: 1. What is the nature of the pituitary or hypothalamic space-occupying lesion?2. Is there hormone hypersecretion? 3. Is there impairment of pituitary function? 4. Is there involvement of the optic pathways with visual field defects or other cranial nerve abnormalities?Since patients with pituitary or hypothalamic tumors are rarely cured completely or at least harbor one or several hormonal deficits needing substitution therapy, lifelong follow-up of these patients is warranted, though this may be at extended intervals (2-3 yearly) if patient’s tumour is stable..
A multinodular goiter is a specific thyroid condition that can cause symptoms that can effect a person's quality of daily life. Cardiovascular ChangesA multinodular goiter can cause changes in the cardiovascular system. A multinodular goiter is often accompanied by an overabundance of thyroid hormone in the body, which can cause heart palpitations, heart arrhythmia, high blood pressure, or shortness of breath. It is common for people to mistake cardiovascular changes that are caused by a multinodular goiter for a heart attack or stroke.Nervous System ChangesThe nervous system is directly connected to the thyroid gland, and therefore affected by the presence of a multinodular goiter. People have experienced symptoms such as anxiety, depression the sudden onset of phobias or panic attacks as a result of having a multinodular goiter and too much thyroid hormone in the body.Sponsored LinksLaptop Job - $34/Hr.Earn $34 per hour. Flexible. 2-3 hours per day. Work at Home.www.LionBridge.comPalpable ChangesPalpable changes can either be felt by your doctor or by yourself, depending on how large or advanced the goiter is. If the multinodular goiter is smaller, it may go unnoticed until your doctor inspects your thyroid gland during a routine visit. If the multinodular goiter is larger, you can easily feel a swelling in the neck, which may or may not be accompanied by a few round and hard thyroid nodules. Typically 95% of these nodules are benign, and do not indicate that cancer is present.Weight ChangesWeight can be affected by having either too much or too little thyroid hormone in the body. When a multinodular goiter is present, there is typically an overabundance of thyroid hormone, which can cause the metabolism to speed up and an unexpected or sudden loss of weight.Sleep ChangesExcess thyroid hormone in the body from a multinodular goiter can cause the system to speed up and can interfere with the body's ability to sleep. Over time, lack of sleep can negatively effect a person's overall health and wellness. In order to reclaim a more sound sleep, have your thyroid gland and hormone levels checked by your doctor. If your thyroid gland has a multinodular goiter, you may need to take a thyroid hormone suppressant medication to reduce thyroid hormone in the body.
Cretinism - Symptom, Causes, Treatment of CretinismCretinism is a situation induced by a insufficiency of thyroid hormone at birth and during minority, as a ensue of abnormal evolution of the thyroid gland about 1 in 4000 babies is impacted. Actual cretinism is a constitute of hypothyroidism, where need of thyroid gland activity, often expected to an iodine imperfection, stunts growth. Cretinism reasons very life-threatening retardation of physical and mental progress; if the situation is left untreated, progress is stunted and the physical stature progress is that of a dwarf. In addition, the skin is thick, flabby, and waxy in color, the nose is planated, the abdomen protrudes, and there is a common deliberate of movement and speech.Cretinism (also known as congenital hypothyroidism) may not evident at birth because thyroid hormone frornt mother's blood can profit the baby before and various months after birth. The three diagnostic features of neurological endemic cretinism in its fully germinate form are highly intense mental insufficiency unitedly with squint, deaf mutism and motor spasticity with disorders of the arms and legs of a characteristic nature. Most newborn babies are consistently screened for thyroid insufficiency, which can be observed by a blood test even if there are symptoms. If the situation is not noticed at birth, symptoms will have noticed within 6 months. Symptoms of CretinismSymptoms include execute growth, twined facial features, increased tongue and mental detainment. The typical: floppy infant thick, protruding tongue poor feeding choking episodes constipation prolonged jaundice short stature Frequent Signs and tests: sutures - separated widely and a big posterior fontanelleextensive fontanelle and posterior fontanelle (soft spots) dull-appearing facial features dry, brittle hair and low hairline short, thick neck growth failure short extremities broad hands with short fingers myxedemahypotoniahoarse-sounding cry or voice Types of CretinismMyxedematous Cretinism has a less ascetic degree of mental detainment than the neurological cretin. It has all the countenance of dreadfully stern hypothyroidism exhibit since premature life, as in non realised sporadic congenital hypothyroidism, life-threatening growth retardation, unfinished maturation of the features including the naso-orbital configuration, atrophy of the mandibles, intumescent features, myxedematous, thickened and dry skin, dry and infrequent hair, eyelashes and eyebrows and much delayed sexual maturation. Other signs may include inspissate skin and a protruding abdomen. Endemic cretinism develops from a diet inadequate in iodine and has involved for more people worldwide and proceed to be a major public health difficulty in a lots of countries. Iodine is an necessary trace element, necessary mainly for the synthesis of thyroid hormones. Although it is establish in many foods it is not worldwide present in all soils in adequate amounts. The soils of many another inland areas on all continents are iodine inferior, and plants and animals grown there are correspondingly deficient. Populations realistic in those areas without outside food sources are most at chance for iodine inadequacy diseases.Diagnosis and Treatment of CretinismAdvance diagnosis, and life long cure with thyroid hormone by mouth, afford the child a better adventure of evolving usually. Newborns analysed and treated in the first month to month and a half typically produce general intelligence. Nonattendance of thyroid hormone during beginning life afford a poor outlook in terms of mental progress. Replacement therapy with thyroxine is the common approach to treatment of hypothyroidism. Once medication begins, the blood levels of T3 and T4 are monitored to observed the values within a usual range.
What are the symptoms of myxedema?Symptoms of myxedema include thickening of the skin and other symptoms associated with hypothyroidism, including fatigue, weight gain, depression, dry skin, and brittle hair, among others. Skin thickening or swelling associated with myxedema is often described as nonpitting edema. In other words, if you press on the skin of the affected area and then remove your finger, you will not see an imprint.More serious associated symptoms include puffiness in the hands and face and slowing of speech. Rarely, serious or life-threatening symptoms, such as slowed breathing, low body temperature, or unresponsiveness, may be a sign of myxedema coma.Common symptoms of myxedemaMyxedema is usually part of a larger group of symptoms associated with hypothyroidism. At times any of these symptoms can be severe and include:Brittle hair or fingernailsConstipationDecreased sweatingDepressionDry or pale skinFatigueMalaise or lethargyMusculoskeletal painSensitivity to coldThickening of the skinWeakness (loss of strength)Weight gainRare or serious symptoms of myxedemaOther symptoms occur more rarely with myxedema, but may indicate a specific cause, type, or more serious condition. These symptoms include:Decreased senses of taste and smellFullness in the neck (a mass in the neck, called a goiter, is a very rare symptom)Thinning of hair, including eyebrowsSlowed speechSerious symptoms that might indicate a life-threatening conditionIn some cases, myxedema can be life threatening. Seek immediate medical care (call 911) if you, or someone you are with, have any of these life-threatening symptoms including:Change in level of consciousness or alertness, such as passing out or unresponsivenessChest painDifficulty breathing or decreased rate of breathingLow blood sugar (hypoglycemia)Low body temperature (hypothermia)INTRODUCTION What is myxedema?Myxedema is a condition marked by thickening and swelling of the skin caused by insufficient production of thyroid hormones by the thyroid gland. The function of thyroid hormones is to regulate your metabolism. Myxedema is associated with other symptoms of underactive thyroid, also called hypothyroidism, including lethargy, weight gain, fatigue, Read more about myxedema introduction CAUSES What causes myxedema?Myxedema is caused by an accumulation of tissue products, such as glycosaminoglycans, in the skin. Myxedema is almost always a result of hypothyroidism. Specific causes of hypothyroidism that can lead to myxedema include Hashimoto’s thyroiditis, thyroidectomy (surgical removal of the thyroid), and Graves’ disease.... Read more about myxedema causes TREATMENTS How is myxedema treated?Myxedema is most often addressed by treating the underlying cause of hypothyroidism that led to the thickening and coarseness of the skin. Medication to replace the reduced thyroid hormones is the most common treatment, and when dosed appropriately, may halt the progression of myxedema.... Read more about myxedema treatments
What is thyroiditis?Thyroiditis (thy-roi-DY-tiss) is inflammation, or swelling, of the thyroid. There are several types of thyroiditis, one of which is Hashimoto's thyroiditis. What are other types and symptoms of thyroiditis?Postpartum thyroiditisLike Hashimoto's thyroiditis, postpartum thyroiditis seems to be caused by a problem with the immune system. In the United States, postpartum thyroiditis occurs in about 5 to 10 percent of women. The first phase starts 1 to 4 months after giving birth. In this phase, you may get symptoms of hyperthyroidism because the damaged thyroid is leaking thyroid hormones out into the bloodstream. The second phase starts about 4 to 8 months after delivery. In this phase, you may get symptoms of hypothyroidism because, by this time, the thyroid has lost most of its hormones. Not everyone with postpartum thyroiditis goes through both phases. In most women who have postpartum thyroiditis, thyroid function returns to normal within 12 to 18 months after symptoms start.Risk factors for postpartum thyroiditis include having:An autoimmune disease, like type 1 diabetesA personal history or family history of thyroid disordersHaving had postpartum thyroiditis after a previous pregnancySilent or painless thyroiditisSymptoms are the same as in postpartum thyroiditis, but they are not related to having given birth.SubacutethyroiditisSymptoms are the same as in postpartum and silent thyroiditis, but the inflammation in the thyroid leads to pain in the neck, jaw, or ear. Unlike the other types of thyroiditis, subacutethyroiditis may be caused by an infection.ThyroiditisIntroduction:Thyroiditis is an inflammation of the thyroid gland. It may be painful and tender when caused by an infection or trauma, or painless when caused by an autoimmune condition or medications. There are several types of thyroiditis. The most common forms are Hashimoto's disease, subacutegranulomatousthyroiditis, postpartum thyroiditis, subacute lymphocytic thyroiditis and drug induced thyroiditis. Most forms of thyroiditis result in three phases: overactive thyroid (hyperthyroidism), underactive thyroid (hypothyroidism), and return to normal. When the thyroid is inflamed, it often releases an excess of thyroid hormone, resulting in hyperthyroidism. Alternatively, when the supply of thyroid hormone is depleted, the body has too little, and hypothyroidism results. Young to middle aged women are at greatest risk, however, some forms of thyroiditis occur in both men and women of all ages. With some forms, hypothyroidism may develop years later, even if the thyroiditis has resolved.Signs and Symptoms:Depending on the type of thyroiditis, the thyroid gland can have one of the following characteristics:Firm and enlarged, but not tenderEnlarged and painful, with pain extending to the jaw or earsEnlarged, but not painfulEnlarged on only one side, hard like a stone, and sticking to other neck structuresYou may also have one or more of the following symptoms:Cool, dry skin, slow pulse rate (fewer than 60 beats per minute), swelling around the eyes, hoarseness, or slow reflexesNo desire to eat, feeling tired and unenergetic, and a slight feverConstipationA rapid heartbeat, slight nervousness, anxiety, weight loss of 5 - 10 pounds, and increased sweatingWhat Causes It?:Immune disorders, viruses, and fever disorders can cause thyroiditis. Sometimes thyroiditis develops if you have Graves' disease (an autoimmune disorder that causes hyperthyroidism). Certain drugs, such as amiodarone, interferon-alpha, inter leukin-2, or lithium can also cause thyroiditis. Pregnant women who test positive for the thyroid antibody during their first trimester have a 30 - 50% chance of developing thyroiditis during the postpartum period. Excessive iodine intake may also contribute to thyroid disorders. In some cases or thyroiditis, there is no identifiable cause.What to Expect at Your Provider's Office:Your health care provider will feel your neck to see if the thyroid gland is enlarged or inflamed and may request an ultrasound of your thyroid gland. Your provider may also order blood tests to check the levels of thyroid hormones and antibodies. You may receive medication to help alleviate your symptoms.Natural medicine practitioners often take a different view of laboratory analysis of thyroid function. Many naturally oriented doctors pay particular attention to levels of T3 hormone, the active form of thyroid hormone that is converted in the body from T4, an inactive thyroid hormone. Conventional lab tests usually monitor T4 and thyroid stimulating hormone (TSH) without examining levels of T3. People with hypothyroidism may be treated with T4 to bring their levels of T4 to normal limits. Meanwhile, if you are unable to convert T4 to T3, your tests may be normal but you may still experience the symptoms of hypothyroidism. Talk to your doctor about including T3 lab tests in the treatment of hypothyroidism.Treatment Options:Thyroiditis generally involves three phases: overactive phase, underactive phase, and return to normal. Treatment is individualized to type and phase.Drug TherapiesDepending on the particular type of thyroiditis, a physician may prescribe one or more of the following treatments:Levothyroxine, if hypothyroidism or large goiter presentAspirin, to relieve pain and inflammationCorticosteroid medications (such as prednisone or dexamethasone), to reduce inflammation in severe casesPropanolol, for hyperthyroidismThyroxine, to replace thyroid hormone (in cases of hypothyroidism)Short term beta blockers, for hyperthyroid symptomsAntibioticsSurgical and Other ProceduresIn rare cases, partial thyroid removal may relieve pressure.Complementary and Alternative TherapiesAlternative therapies can help when used along with the medications your health care provider prescribes, but do not replace conventional medications. Make sure your doctor knows about any alternative therapies you are using or considering using. Some supplements can interfere with conventional medications.Nutrition and SupplementsFoods that depress thyroid activity are broccoli, cabbage, Brussels sprouts, cauliflower, kale, spinach, turnips, soy, beans, and mustard greens. You should include these foods in a diet for hyperthyroid conditions -- and avoid them if you have a hypothyroid condition. Use caution because people with thyroiditis can switch from hyperthyroidism to hypothyroidism very quickly.Avoid refined foods, sugar, dairy products, wheat, caffeine, alcohol.Essential fatty acids (1,000 - 1,500 mg three times per day), found in flaxseed oil, fish oil, and borage oil, are anti-inflammatory and necessary for hormone production. Essential fatty acids can increase the blood thinning effects of certain medications, including Coumadin, Plavix, or aspirin. Check with your health care provider.Bromelain (250 - 500 mg 3 times per day between meals), an enzyme from the pineapple plant, may reduce inflammation. Bromelain can increase blood thinning effects of certain medications. Check with your physician.Vitamin C (1,000 mg per day), vitamin A (10,000 - 25,000 IU per day), B complex [(50 -100 mg per day), augmented with vitamins B2 (riboflavin, 10 mg), B3 (niacin, 10 - 25 mg), and B6 (pyridoxine, 5 - 15 mg)], selenium (200 mcg per day), vitamin E (400 IU per day), and zinc (30 mg per day) are necessary for normal thyroid hormone production.Calcium (1,000 mg per day) and magnesium (200 - 600 mg per day) may help metabolic processes function correctly.If you take thyroid hormone medication, talk to your doctor before consuming soy products. Some evidence suggests that soy may interfere with absorption of thyroid hormone.Iron may also interfere with the absorption of thyroid hormone medication.Your health care provider may also recommend specific nutritional supplements for a hyperthyroid or hypothyroid condition.HerbsHerbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, you should work with your health care provider to diagnose your problem before starting treatment. You may use herbs as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, make teas with 1 tsp. herb per cup of hot water. Steep covered 5 - 10 minutes for leaf or flowers, and 10 - 20 minutes for roots. Drink 2 - 4 cups per day. You may use tinctures alone or in combination as noted.Talk to your health care provider before taking herbs for thyroiditis, particularly if you are also taking prescription medication.For hyperthyroid conditions:Bugleweed (Lycopusvirginica) and lemon balm (Melissa officinalis) help normalize the overactive thyroid. Steep the following amount in one cup of boiling water. Strain and cool. For bugleweed, 1 - 2 g; for lemon balm, 2 tablespoons. These herbs may be combined. Bugleweed may interact with some diabetes medications.Motherwort (Leonuruscardiaca) can help regulate rapid heartbeat. Steep 2 g in one cup of boiling water. Strain and cool. Drink 3 times per day. Do not take motherwort along with sedating medications.Turmeric (Curcuma longa) makes the effect of bromelain stronger and should be taken between meals, 500 mg 3 times per day. Turmeric can increase the blood thinning effects of certain medications, such as Coumadin. Speak with your physician.Avoid ashwagandha (Withaniasomnifera) and bladderwrack (Fucusvesiculosus), as they can stimulate hyperthyroidism.For hypothyroid conditions:Coleus forskohlii (50 - 100 mg 2 - 3 times per day) may stimulate thyroid function to increase thyroid hormone. Do not take coleus if you are taking blood thinning medications or Nitrates. Coleus may increase the blood thinning effects of cetain medications, such as Coumadin.Herbs such as guggul (Commiphoramikul) (25 mg of guggulsterones 3 times per day) and hawthorne (Crataegusmonogyna) (500 mg twice a day) are taken to counteract high cholesterol, which often accompanies hypothyroidism. Guggul can interact with many medications, particularly hormone medications, such as oral contraceptives, and other medications, such as Diltiazem (Cardizem, Dilacor, Tiazac). Guggul may also increase bleeding. Speak with your physician. Hawthorne can interact with various blood pressure medications and can increase the blood pressure lowering effects of drugs used to treat male sexual dysfunction, such as Viagra. Hawthorne may also interfere with Nitrate medications. You should carefully monitor any treatment for lowering or raising thyroid function because thyroiditis may switch from hyperthyroidism to hypothyroidism very quickly.HomeopathyHomeopathy may be useful as a supportive therapy for both hypothyroidism and hyperthyroidism.Physical MedicineExercise helps improve thyroid function for both hypothyroidism and hyperthyroidism.AcupunctureAcupuncture may help correct hormonal imbalances and address underlying deficiencies and excesses involved in thyroiditis.MassageTherapeutic massage may relieve stress and increase the sense of well being.Following Up:Your health care provider may perform frequent blood tests to make sure your thyroid hormone levels fall within the normal range.Special Considerations:Thyroid disorders are one of the most common endocrine disorders in pregnant women. Even mild maternal thyroid hormone deficiency can lead to neurodevelopment complications in the fetus. Careful monitoring is necessary.Alternative Names:Thyroid inflammationReviewed last on: 6/13/2010Steven D. Ehrlich, NMD, Solutions Acupuncture, a private practice specializing in complementary and alternative medicine, Phoenix, AZ. Review provided by VeriMed Healthcare Network.http://www.umm.edu/altmed/articles/thyroiditis-000164.htm#ixzz2AwMKwK49
INTRODUCTIONPainless thyroiditis is characterized by transient hyperthyroidism, followed sometimes by hypothyroidism, and then recovery (figure 1). Synonyms for this disorder include silent thyroiditis, subacute lymphocytic thyroiditis, and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. Painless thyroiditis accounts for 1 to 5 percent of cases of hyperthyroidism . It has many similarities with postpartum thyroiditis, but by definition excludes women who have a painless thyroiditis syndrome within one year after a delivery or an abortion. (See "Postpartum thyroiditis".) The diagnosis and management of painless thyroiditis will be reviewed here. An overview of thyroiditis is discussed separately. (See "Overview of thyroiditis".)PATHOGENESISPainless thyroiditis is considered a variant form of chronic autoimmune thyroiditis (Hashimoto's thyroiditis), suggesting that it is part of the spectrum of thyroid autoimmune disease . The two disorders have some pathologic similarities (see below), and many patients with painless thyroiditis have high serum concentrations of antithyroidperoxidase (TPO) and anti-thyroglobulin (Tg) antibodies, many have a family history of thyroid autoimmune disease, and some develop overt chronic autoimmune thyroiditis several years later . It affects women more often than men.Painless thyroiditis is associated with specific HLA haplotypes, most often HLA-DR3, findings that suggest an inherited susceptibility . However, the association is considerably weaker than that between HLA-B35 and subacutethyroiditis. (See "Subacutethyroiditis".)Factors postulated to initiate painless thyroiditis include excess iodine intake and various cytokines. A syndrome very similar to this disorder can occur in patients treated with interferon-alpha, interleukin-2, lithium, and tyrosine kinase inhibitors. These observations raise the possibility that cytokines released in response to some (subclinical) injury or infection might initiate the disorder. (See "Overview of thyroiditis", section on 'Drug-induced thyroiditis'.)Painless Thyroiditis/Silent ThyroiditisPainless thyroiditis is also frequently referred to as silent thyroiditis or subacute lymphocytic thyroiditis. It's thought that painless thyroiditis may be responsible for as much as 10 percent of hyperthyroidism, because the typical course of painless thyroiditis is a temporary period of hyperthyroidism, which is then sometimes followed by a period of hypothyroidism, and then a return to normal thyroid function. In painless thyroiditis, your thyroid usually does not become enlarged. Find out more about the signs, symptoms, diagnosis and treatment of this form of thyroiditis.Painless (silent) thyroiditisDefinitionPainless (silent) thyroiditis is an inflammation of the thyroid gland characterized by passing hyperthyroidism, followed by hypothyroidism and recovery.Alternative NamesLymphocytic thyroiditis; Subacute lymphocytic thyroiditisCauses, incidence, and risk factorsThe cause of this type of thyroiditis is unknown. The disease affects women more often than men and usually develops in people between age 13 and 80. The symptoms are those of hyperthyroidism (overactivity of the thyroid gland), and may last for 3 months or less.SymptomsSymptoms in painless thyroiditis are usually mild. Most symptoms are due to hyperthyroidism and may include:weight lossincreased appetitenervousness, restlessnessheat intoleranceincreased sweatingfatiguemuscle crampsfrequent bowel movementsmenstrual irregularitiesweaknessirritabilitypalpitationsSigns and testsA physical examination reveals an enlarged thyroid gland. The pulse (heart rate) may be rapid and the hands may shake.Radioactive iodine uptake is decreased.Serum T3 and T4 are elevated.A thyroid biopsy shows invasion of lymphocytes (a type of white blood cells) into the gland. TreatmentTreatment is based on symptoms. Beta-blockers (Propranolol and others) relieve rapid heart rate and excessive sweating. Generally, painless thyroiditis will resolve on its own in time.Expectations (prognosis)The disease is usually resolved within 1 year, with the acute phase ending in 3 months. Some people may develop hypothyroidism over time, so regular follow-up is recommended.ComplicationshypothyroidismCalling your health care providerCall your health care provider if symptoms of this disorder develop.If you have had this disease, regular follow-up is recommended to watch for the development of hypothyroidism
A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result from an inflammatory or neoplastic process and is not associated with abnormal thyroid function. Endemic goiter is defined as thyroid enlargement that occurs in more than 10% of a population, and sporadic goiter is a result of environmental or genetic factors that do not affect the general population.About thyroid diseasePresence of nodes in the thyroid gland or its volume increase it is accepted to call as nodular or diffuse goiter. These nodes in 2-4 times more often are revealed among women, with prevalence of about 20-65 per cents. From the morphological point of view, this disease is revealed in local or diffuse (general) structural TG nodes volume increase – follicles, peculiar “bricks”, which form this building of this endocrine organ. Follicles are globular elements, consisted on the periphery of cells and internal colloid “lake”. It is comparatively often condition modification of these structural thyroid elements is connected with its function effort in response to organism need in hormones, generated by the thyroid gland.Thyroid treatmentTreatment at the Th-d nodular and diffuse goiter should be directed on functional load’s reduction on this organ. This will allow the gland, functioning in the usual mode, not to use its additional opportunities at the expense of functioning elements’ increase and to exclude critical situations, revealing locally. The second way of treatment should be related to the renewable, as elimination of the reasons, conditions and factors, provocative the functional thyroid intension (revealing in nodular formation and volume increase), leads to the stable renewable transformation of the Th-d tissue. Developed and practically approved treatment method of the thyroid nodular and diffuse goiter (A.V. Ushakov, 2002)includes correction of energetic (calorie-gene) condition, renewal of hormonal balance in interrelations between internal organs, elimination and reduction of the harmful factors’ influence, and functional “maintenance” of the TGitself. These measures are realized by means of acupunctural influence, assessment of mode of living and recommendations on the not difficult (but necessary) food correction, some habits, and the other factors, having an influence on pathology. Definition of Goiter, diffuse toxicGoiter, diffuse toxic: Graves disease, the most common cause of hyperthyroidism (overactivity of the thyroid gland), with generalized diffuse overactivity ("toxicity") of the entire thyroid gland which becomes enlarged into a goiter. There are three clinical components to Graves disease: Hyperthyroidism (the presence of too much thyroid hormone), Ophthalmopathy specifically involving exophthalmos (protrusion of the eyeballs),Dermopathy with skin lesions. The ophthalmopathy can cause sensitivity to light and a feeling of "sand in the eyes." With further protrusion of the eyes, double vision and vision loss may occur. The ophthalmopathy tends to worsen with smoking. The dermopathy of Graves disease is a rare, painless, reddish lumpy skin rash that of Graves disease is an autoimmune process. It is caused by thyroid-stimulating antibodies which bind to and activate the thyrotropinreceptor on thyroid cells. Graves disease can run in families. The rate of concordance for Graves' disease is about 20% among monozygotic (identical) twins, and the rate is much lower among dizygotic (nonidentical) twins, indicating that genes make only a moderate contribution to the susceptibility to Graves disease. No single gene is known to cause the disease or to be necessary for its development. There are well-established associations with certain HLA types. Linkage analysis has identified gene loci on chromosomes 14q31, 20q11.2, and Xq21 that are associated with susceptibility to Graves disease.Factors that can trigger the onset of Graves disease include stress, smoking, radiation to the neck, medications (such as interleukin-2 and interferon-alpha), and infectious organisms such as viruses. The diagnosis of Graves disease is made by a characteristic thyroid scan (showing diffusely increase uptake), the characteristic triad of ophthalmopathy, dermopathy, and hyperthyroidism, or blood testing for TSI (thyroid stimulating immunoglobulin) the level of which is abnormally high.Current treatments for the hyperthyroidism of Graves disease consist of antithyroid drugs, radioactiveiodine, and surgery. There is regional variation in which of these measures tends to be used -- for example, radioactive iodine is favored in North America and antithyroid drugs nearly everywhere else. The surgery, subtotal thyroidectomy, is designed to remove the majority of the overactive thyroid gland.The disease is named for Robert Graves who in 1835 first identified the association of goiter, palpitations, and exophthalmos.
Definition: Colloid nodular goiter is the enlargement of an otherwise normal thyroid gland.Alternative Names: Endemic goiterCauses, incidence, and risk factors:When the thyroid gland is unable to make enough thyroid hormone, it may attempt to compensate by enlarging. Thyroid enlargement may also be caused by certain environmental factors.A colloid nodular goiter occurs when the thyroid gland is unable to meet the metabolic demands of the body with sufficient hormone production. The thyroid gland compensates by enlarging, which usually overcomes mild deficiencies of thyroid hormone.If the thyroid gland is then re-exposed to iodine, the nodules may produce thyroid hormone independently. Occasionally, the nodules may produce too much thyroid hormone, causing thyrotoxicosis. This is called a toxic nodular goiter.Colloid nodular goiters are also known as endemic goiters and are usually caused by inadequate iodine in diet. They tend to occur in certain geographical areas with iodine-depleted soil, usually areas away from the sea coast. An area is defined as endemic for goiter if more than 10 % of children aged 6 to 12 years have goiters.Small to moderate-sized goiters are relatively common in the United States. The Great Lakes, Midwest, and Intermountain regions were once known as the "goiter belt." The routine use of iodized table salt now helps prevent this deficiency.Risk factors are being female, being older than 40, having an inadequate dietary intake of iodine, living in an endemic area, and having a family history of goiters.Symptoms: Thyroid enlargement -- may vary from a single small nodule to massive enlargement Breathing difficulties from compression of the trachea (rare) Swallowing difficulties from compression of the esophagus (rare) Neck vein distention and dizziness when the arms are raised above the head (large goiter)Signs and tests: Thyroid scanThyroid ultrasoundBlood tests to monitor thyroid function including thyroid stimulating hormone (high if underactive, low if overactive) Radioactive iodine uptake (normal or increased) Urinary excretion of iodine (low)Treatment: Thyroid hormone replacement therapy is prescribed for iodine deficiency. Hormone replacement inhibits thyroid stimulating hormone (TSH) and allows the thyroid to recover.A large goiter that is unresponsive to medical management or restricts swallowing and breathing may require partial or complete removal of the thyroid gland.If the goiter is producing too much thyroid hormone, treatment with radioactive iodine, antithyroid medication, or surgery may be necessary.Support Groups: Expectations (prognosis): The prognosis is good with treatment. A persistent goiter may become toxic, causing symptoms of excess thyroid hormones to develop. Sudden enlargement of a thyroid gland may indicate internal bleeding or immune disorder, and requires immediate medical attention.Complications: Progressive thyroid enlargement or the development of hardened nodules may indicate thyroid malignancy (cancer). If there is a single, dominant nodule or if a nodule is enlarging, a fine needle biopsy should be performed to exclude malignancy. A simple goiter may progress to a toxic nodular goiter. Thyrotoxicosis may occur spontaneously with iodine re-exposure. Medications such as amiodarone and lithium can affect thyroid function.Calling your health care provider: Call your health care provider if signs of thyrotoxicosis develop:Fever Increased pulse ratePalpitationsDiarrhea or constipation NauseaFatigue Dry Skin SweatingTremorsAnxietyShortness of breathPrevention:Use iodized salt, or foods supplemented with iodine.DefinitionColloid nodular goiter is the enlargement of an otherwise normal thyroid gland.See also: GoiterAlternative NamesEndemic goiter Causes, incidence, and risk factorsColloid nodular goiters are also known as endemic goiters. They are usually caused by inadequate iodine in diet.Colloid nodular goiters tend to occur in certain geographical areas with iodine-depleted soil, usually areas away from the sea coast. An area is defined as endemic for goiter if more than 10 % of children aged 6 to 12 have goiters.Certain things in the environment may also cause thyroid enlargement.Small- to moderate-sized goiters are relatively common in the United States. The Great Lakes, Midwest, and Intermountain regions were once known as the "goiter belt." The routine use of iodized table salt now helps prevent this deficiency.Risk factors for colloid nodular goiters include being female, being older than 40, not getting enough iodine in your diet, living in an endemic area, and having a family history of goiters.
Parathyroid glands are small glands of the endocrine system which are located in the neck behind the thyroid. Parathyroid glands control the calcium in our bodies--how much calcium is in our bones, and how much calcium is in our blood. Calcium is the most important element in our bodies (we use it to control many systems), so calcium is regulated very carefully. Parathyroid glands control the calcium.Parathyroid glands (we all have 4 of them) are normally the size of a grain of rice. Occasionally they can be as large as a pea and still be normal. The four parathyroids are shown in this picture as the mustard yellow glands behind the pink thyroid gland. Normal parathyroid glands are the color of spicy yellow mustard. The light blue tube running up the center of the picture is the trachea (wind pipe). The voice box is the pink structure at the top of the picture sitting on top of the trachea. The carotid arteries are shown on both sides of the thyroid running from the heart up to the brain. NOTE: we are looking at the back side of the thyroid so we can see the parathyroids. Remember, the parathyroids are behind the thyroid. Also note that this drawing shows three small (normal) parathyroid glands and one big diseased one--this is the typical situation of a patient with parathyroid disease--one of the parathyroid glands grows into a tumor and makes too much hormone. If you have parathyroid disease, you very likely have 3 normal parathyroid glands the size of a grain of rice and one parathyroid tumor that is as big as an olive, grape, or even a walnut. If you have parathyroid disease (hyperparathyroidism) you will need an operation to remove the one parathyroid gland which has become a tumor. More about parathyroid disease on other pages...this page is about NORMAL parathyroid function. One more introductory note... We must make sure you understand that the thyroid and parathyroid are NOT related. Although they are neighbors and both are part of the endocrine system, the thyroid and parathyroid glands are otherwise unrelated--they do not have the same function--just similar and confusing names! Parathyroid FunctionNormal and AbnormalThe sole purpose of the parathyroid glands is to control calcium within the blood in a very tight range between 8.5 and 10.5. In doing so, parathyroid glands also control how much calcium is in the bones, and therefore, how strong and dense the bones are. Although the parathyroid glands are intimately related to the thyroid gland anatomically, they have no related function. The thyroid gland regulates the body’s metabolism and has no effect on calcium levels while parathyroid glands regulate calcium levels and have no effect on metabolism. Calcium is the primary element which causes muscles to contract. Calcium levels are also very important to the normal conduction of electrical currents along nerves. Knowing these two major functions of calcium helps explain why people can get a tingling sensation in their fingers or cramps in the muscles of their hands when calcium levels drop below 8.5 (like immediately after a successful parathyroid operation). Likewise, too high a calcium level can cause a person to feel run down, cause them to sleep poorly, make them more irritable than usual, and even cause a decrease in memory.Even though half of patients with this hyperparathyroidism (Parathyroid Disease) will state that they feel just fine, after a successful parathyroid operation more than 85 percent of these patients will claim to "feel much better"! Some say its like "someone turned the lights on".Normal Parathyroid ActivityAlthough the four parathyroid glands are quite small, they are very vascular. This suits them well since they are required to monitor the calcium level in the blood 24 hours a day. As the blood filters through the parathyroid glands, they detect the amount of calcium present in the blood and react by making more or less parathyroid hormone (PTH). When the calcium level in the blood is too low, the cells of the parathyroids sense it and make more parathyroid hormone. Once the parathyroid hormone is released into the blood, it circulates to act in a number of places to increase the amount of calcium in the blood (like removing calcium from bones). When the calcium level in the blood is too high, the cells of the parathyroids make less parathyroid hormone (or stop making it altogether), thereby, allowing calcium levels to decrease. This feed-back mechanism runs constantly, thereby maintaining calcium (and parathyroid hormone) in a very narrow "normal" range.You may be interested in these related articles:Osteoporosis and Parathyroid DiseaseHyperparathyroidism Diagnosis and TreatmentYour Parathyroid GlandsHyperparathyroidismHow Does Parathyroid Hormone Increase Blood Calcium?Like all endocrine glands, parathyroids make a hormone (a small protein capable of causing distant cells in the body to react in a specific manner). Parathyroid hormone (PTH) has a very powerful influence on the cells of the bones which causes them to release their calcium into the bloodstream. Calcium is the main structural component of bones which give them their rigidity. Under the presence of parathyroid hormone, bones will give up their calcium in an attempt to increase the blood level of calcium. Under normal conditions, this process is very highly tuned and the amount of calcium in our bones remains at a normal high level. Under the presence of too much parathyroid hormone, however, the bones will continue to release their calcium into the blood at a rate which is too high resulting in bones which have too little calcium. This condition is called osteopenia and osteoporosis and is illustrated in the bone segment on the top which has larger "pores" and less bone mass. When bones are exposed to high levels of parathyroid hormone for several years they become brittle and much more prone to fractures. Another way in the parathyroid hormone acts to increase blood levels of calcium is through its influence on the intestines. Under the presence of parathyroid hormone the lining of the intestine becomes more efficient at absorbing calcium normally found in our diet.
Home > Diseases and Conditions > HyperparathyroidismPrintPubMed Health. A service of the National Library of Medicine, National Institutes of Health.A.D.A.M. Medical Encyclopedia. Atlanta (GA): A.D.A.M.; 2011. A.D.A.M. Medical Encyclopedia.HyperparathyroidismParathyroid-related hypercalcemiaLast reviewed: July 19, 2012.Hyperparathyroidism is a disorder in which the parathyroid glands in your neck produce too much parathyroid hormone (PTH).Causes, incidence, and risk factorsThe parathyroid glands are located in the neck, near or attached to the back side of the thyroid gland. They produce parathyroid hormone. This hormone controls calcium, phosphorus, and vitamin D levels in the blood and bone.When calcium levels are too low, the body responds by making more parathyroid hormone. This hormone causes calcium levels in the blood to rise, as more calcium is taken from the bone and reabsorbed by the intestines and kidney. One or more of the parathyroid glands may grow larger. This leads to too much parathyroid hormone (a condition called primary hyperparathyroidism). Most often, the cause is not known. The disease is most common in people over age 60, but it can also occur in younger adults. Hyperparathyroidism in childhood is very unusual.Women are more likely to be affected than men.Radiation to the head and neck increases the risk.Rarely, the disease is caused by parathyroid cancer.Medical conditions that cause low blood calcium levels or increased phosphate levels can lead to secondary hypoparathyroidism. Common causes include:Conditions that make it hard for the body to break down phosphateKidney failureNot enough calcium in the dietToo much calcium lost in the urineVitamin D disorders (which are often seen in children who do not get enough nutrition, and in older adults who do not get enough sunlightProblems absorbing nutrients from food (called malabsorption)SymptomsOften hyperparathyroidism is diagnosed before symptoms occur.Symptoms are mostly caused by damage to organs from high calcium levels in the blood, or by the loss of calcium from the bones. Symptoms can include:Bone pain or tendernessDepression and forgetfulnessFeeling tired, ill, and weakFragile bones of the limbs and spine that can break easilyIncreased amount of urine producedKidney stonesNausea and loss of appetiteSigns and testsBlood tests will be done to check for increased levels of parathyroid hormone (PTH), calcium, and alkaline phosphatase, and lower levels of phosphorous. A 24-hour urine collection test can help determine how much calcium is being removed from the body.Bone x-rays and bone mineral density (DXA) tests can help detect bone loss, fractures, or bone softening.X-rays, ultrasound, or CT scans of the kidneys or urinary tract may show calcium deposits or a blockage.TreatmentIf you have mildly increased calcium levels from primary hyperparathyroidism and you do not have symptoms, you may choose to have regular checkups or get treated.If you decide to have treatment, it may include:Drinking more fluids to prevent kidney stones from formingExercisingAvoiding thiazide-type diuretics ("water pills")Having surgery to remove the overactive glands (recommended for people under age 50)If you have symptoms or your calcium level is very high, you may need surgery to remove the parathyroid gland that is overproducing the hormone.Treatment for secondary hyperparathyroidism depends on the cause. Your doctor may suggest:A special form of prescribed vitamin D, if you have low vitamin D levelsSurgery for cancerPatients whose hyperparathyroidism is caused by kidney failure may be treated with:Extra calcium and vitamin DAvoiding phosphate in the dietThe medicine cinacalcet (Sensipar)Dialysis or a kidney transplantParathyroid surgery, if the parathyroid levels become uncontrollably highExpectations (prognosis)The outlook depends on the type of hyperparathyroidism.Long-term problems that can occur when hyperparathyroidism is not well controlled include:Increased risk of bone fracturesHigh blood pressure and heart diseaseKidney stonesHyperparathyroidism is a disease of the parathyroid glands...Too much parathyroid hormone is produced by an overactive parathyroid gland. This is called hyperparathyroidism.hyper-parathyroid-ism = condition of too much parathyroid gland activityhyper = too muchparathyroid = parathyroid glandism = a disease or condition= HYPERPARATHYROIDISM"There is no other disease that is so easily cured which has such a tremendous impact on a patient's health and their quality of life"Hyperparathyroidism occurs when one (or more) of the four parathyroid glands grows into a tumor and behaves inappropriately by constantly making excess parathyroid hormone. This video explains it all in 5 minutes... We put a lot of effort into making this video--so watch it! You will see one of the parathyroid glands grow into a tumor and make too much parathyroid hormone which goes to the bones and removes calcium from the bones. This tumor has lost its control mechanism and makes large amounts of parathyroid hormone. Thus, even when the blood calcium level is high--when the parathyroids should not be making any hormone at all--one of the glands keeps making hormone. Remember as you read about hyperparathyroidism on these pages, it is a hormone problem secreted by a benign parathyroid tumor. It is not a cancer problem, however it can increase the occurrence of other cancers.Sometimes hyperparathyroidism it makes people miserable within the first year or two of having high blood calcium (see our page on symptoms). Other times it can go 10 years without causing too much problems other than fatigue, bad memory, kidney stones, and osteoporosis. But make no mistake about it, hyperparathyroidism kills people--it just takes 20 or so years to do so. What Causes Excess Parathyroid Hormone Production?The most common cause of excess hormone production (hyperparathyroidism) is the development of a benign tumor in one of the parathyroid glands. This enlargement of one parathyroid gland is called a parathyroid adenoma which accounts for about 94 percent of all patients with primary hyperparathyroidism (see chart below). This situation is illustrated in the picture on the right: one of the parathyroid glands has developed a tumor which is secreting all the hormone...the other three glands are small and responding appropriately to the high calcium by becoming dormant (the parathyroids are yellow and are situated behind the larger thyroid lobes shown in light pink). This out of control parathyroid gland is essentially never cancerous (less than one in 5000 is cancer---essentially all of them are benign tumors), however, it slowly causes damage to the body because it induces an abnormally high level of calcium in the blood which can slowly destroy a number of tissues. Parathyroid adenomas typically are much bigger than the normal "grain-of-rice" parathyroid and will frequently be about the size of an olive or grape. Thus, the typical patient with hyperparathyroidism will be cured of the disease when this "olive" size tumor is removed. They will live just fine forever with their three remaining normal parathyroid glands that will be about the size of a grain of rice. The picture to the left is a picture of a typical parathyroid adenoma (parathyroid tumor) that causes hyperparathyroidism. This is a very average tumor size, shape, and color. Most people with hyperparathyroidism will have a tumor in their neck about this size. Remember, the normal parathyroid gland is about the size of a grain of rice... but one cell inside this normal parathyroid gland went out of control and started reproducing itself until a large tumor developed. This tumor will almost always continue to grow until it is removed. As it grows, it makes more hormone and will make you feel worse. This tumor is constantly making parathyroid hormone which is what takes the calcium out of your bones and makes the calcium in your blood too high. (We have an entire page of photographs of parathyroid tumors so you can see what these little boogers look like!). Where did this parathyroid tumor come from? This is a great question, and the answer is quite simple... In most cases we don't know WHY parathyroid tumors form. But this is HOW a parathyroid tumor forms... The normal parathyroid gland is made up of about 80,000 very small parathyroid cells. Each one is exposed to lots of blood flow and they all measure the calcium in the blood. When the calcium is low, they make parathyroid hormone (called PTH). When the calcium is high, they stop making hormone. They normally turn on and off hundreds of times per day. All of these cells act independent of the other. Occasionally, one of these cells will go nuts and start reproducing itself... a million or more times. The crazy "mother" cell divides into two, then does it again, and again, and again; many times a day. Over a period of several years a tumor develops. This tumor mass (seen in the photos on this site) is made up of millions of cells all of which are sisters from one crazy "mother" cell. Each of these "daughter" cells inherited the craziness of the mom, and they don't pay attention to the calcium level in the blood. They are out of control, making PTH whenever they want, in as much concentration as they want. When you look at all the pictures of the parathyroid tumors on this web site, you will see a small (rice-size) yellow NORMAL gland with a dark-red tumor growing out of it. The tumor mass is composed of millions of crazy daughter cells from one mother cell that went nuts. If you have surgery at the Norman Parathyroid Center, you will get a photo of your tumor, and you can almost always see the normal gland from which the tumor arose. This graph shows the blood parathyroid hormone levels in 18,000 patients operated on at the Norman Parathyroid Center for primary hyperparathyroidism. Normal blood levels of parathyroid hormone vary according to the lab that measures the hormone, but most labs have a normal level between 15 and 65 pg/ml. Each of the patients represented here had a parathyroid tumor removed from their neck. As you can see, most (but not all!) of them have parathyroid hormone levels that are above normal (above 65). Note that most patients with primary hyperparathyroidism (due to a benign tumor in their neck) have PTH levels ranging from 60 to 150. When patients have PTH levels above 200 it is because their tumor is very old (usually this means over 10-12 years old) and the tumor is composed of MANY cells. If your PTH level is over 200, then some doctor somewhere was asleep at the wheel for at least 8 years. This should not be allowed to happen, and the amount of destruction to your body is generally worse. Also note that about 15% of patients that have a parathyroid tumor in their neck will have PTH levels that are in the "normal range". Let us say that again... about 15% of patients with hyperparathyroidism will have high calcium levels and NORMAL PTH levels. Realize that this is still hyperparathyroidism and they still have a parathyroid tumor in their neck... We say their PTH level is "inappropriately normal". In other words, it still shows that there is a tumor full of crazy, out of control cells because if they were normal parathyroid cells they would sense the high calcium and they would shut down. If your calcium is high, and your PTH is not near zero (consistently 20 or below), then you almost certainly have a parathyroid tumor. GET IT OUT! One final note... this graph shows Parathyroid Hormone (PTH) levels in patients with primary hyperparathyroidism. This graph is DIFFERENT from the graph at the bottom of our diagnosis page which shows CALCIUM levels in patients with primary hyperparathyroidism. These graphs have the same shape and thus you could confuse them... but one looks at the hormone levels in the blood, and the other looks at the calcium level in the blood. These two graphs are central to the diagnosis of hyperparathyroidism. Approximately 18% of patients with primary hyperparathyroidism who have two parathyroid adenomas while having two normal glands. This is one of the reasons why parathyroid surgery is tricky--because some people will have one tumor while others will have more than one. This is why surgeons who do LOTS of parathyroid surgery will not just take one parathyroid tumor out and quit the operation, instead they will spend the necessary time to make sure there isn't a second tumor (watch our surgery video to see Dr Norman find a second tumor). The most common reason that people have an unsuccessful parathyroid operation is because the surgeon couldn't find the tumor. The second most common cause for people to have a failed parathyroid operation is because they had two tumors and the surgeon removed only one. We operate on an average of one person per day for this reason (8% of all our patients). (For clarification, the number one reason people need a second parathyroid operation is because they had only one parathyroid tumor and their inexperienced surgeon couldn't find it--we do one or two of these every day too!). An even rarer situation occurs in about 1.5 percent of all patients with primary hyperparathyroidism will have an enlargement of all four parathyroid glands, a term called parathyroid hyperplasia. In this instance, all of the parathyroid glands become enlarged and produce too much parathyroid hormone. This is a much less common scenario but the end results for the patient are identical. On a different page of this web site we discuss the importance of an experienced parathyroid surgeon. Now you can see why experience is so important--sometimes the disease is caused by one gland, sometimes two glands, and sometimes four glands. Experience matters when operating on parathyroid glands! One last word on parathyroid hyperplasia... it is not very common. Unless you are on kidney dialysis or have taken lithium for over 20 years, we can tell you the the chance of you having parathyroid hyperplasia as the cause of your hyperparathyroidism is less than 1%. Please do not dwell on this. It makes no difference to you, nor does it make any difference to an experienced surgeon. Please, we beg you, forget you ever heard the term "4-gland hyperplasia"... you do NOT have this... so don't ask us about it--it makes our eyes glaze over!.Does Too Much Parathyroid Hormone and Calcium Cause Symptoms?Hyperparathyroidism causes symptoms in almost everybody, but sometimes they are quite subtle. We have put all of this information on a different page: Click here to learn about Symptoms and dangers of Parathyroid Disease. It is important for you to understand these few facts about blood calcium:It is almost never normal to have a high calcium level in your blood. Said differently, it is almost never for adults over 40 to have persistent calcium levels of 10.1 or higher. Almost all patients with high calcium in the blood have a single bad parathyroid gland that is causing it. Your doctor may look for other causes... but the overwhelming odds are that you will end up with parathyroid disease. We have an entire page discussing the other even more rare causes of high blood calcium on this web site, but don't spend too much time there reading about things you don't have. Persistent calcium levels over 10.1 (in an adult) is almost always a parathyroid tumor. The one bad parathyroid gland is a tumor. It is a benign tumor (not cancer), but it is a tumor. Most parathyroid tumors are between the size of peanut and a grape. Occasionally they can be as big as a golf ball... or bigger. However, the size of the tumor doesn't matter too much... just how much hormone it produces and how much calcium it is taking out of your bones. We have photos of these tumors on another page. If you have a big tumor, you are the loser not the winner. These are slow growing tumors and if you have a large one, it usually means your doctors have missed it for years. An expert in parathyroid surgery can fix this problem in 20 minutes or less. So if your surgeon says that it will take 2 or 3 hours in the operating room... You may want to find an expert surgeon. If he says it may take about 1.5 hours, then you may want to ask if it might take longer--you can be assured that he will say "yes, it could take as long as 4 hours or more". As you will read on this site and every other web site (or book) ever printed on the topic, picking your surgeon is the most important step, since the outcomes (cure rates and complications) are directly related to surgeon experience. There is no other area of the body that has such variable anatomy. Removing the bad parathyroid tumor will cure the hyperparathyroidism and will make the calcium level go back to normal WITHIN HOURS. It is almost unheard of for people to get parathyroid disease (hyperparathyroidism) twice. Said differently, surgery CURES this disease, it is not a TREATMENT for the disease. You should never get this again if you have a surgeon who cures you the first time. If your surgeon can't tell you that his/her cure rate for you will be 97% or higher, then go somewhere else. Removing the parathyroid tumor will change the patient's life. It often will make you feel 10 years younger, and literally, change your life. Read about symptoms.Read testimonials from about 1000 patients. Removing the parathyroid tumor will make you live longer (statistically). From a statistical standpoint, patients with hyperparathyroidism die an average of 5-6 years sooner than expected. This is because the incidence of several cancers is increased by 1.8 to 3-fold (breast, colon, kidney, and prostate), the incidence of high blood pressure is 2.5 times higher, stroke is 2 times higher, heart disease is 2.5 times higher. This is all explained in more detail on our Symptoms page, including footnotes to medical journals. Thus, parathyroid tumors are benign (not cancerous), but they slowly destroy your body, eventually making you feel miserable, and increasing your chance of several cancers dramatically. Do NOT "watch" your high calcium levels! How Many People Get Parathyroid Disease?(Hyperparathyroidism) ?The incidence of parathyroid disease (hyperparathyroidism) is 1 in 800 people. This rate is much higher in women over 50 where the rate is 1 in 250 or so. All of you will know somebody with hyperparathyroidism. Unfortunately, it is our opinion that about 70% of patients with hyperparathyroidism do not know they have it... they have high calcium levels but their doctors don't know what this means and so the high calcium is ignored. Often, when something bad happens (kidney stones, bad osteoporosis, severe depression), then the doctors pay attention to the high calcium. Hyperparathyroidism occurs in women more often than men (almost exactly 75% women, 25% men), and the average age is about 59 years old--but people of any age can get it. Young people do get parathyroid disease, but this is rare. We have an entire page dedicated to this topic--Read about Who Gets It?How Many Parathyroid Glands are Bad?Since everybody has 4 parathyroid glands, we could potentially get tumors in all four glands. This is almost impossible, however. It is usually just one, and occasionally two. In January, 2011 we published our data on 10,000 patients that we operated on and cured for hyperparathyroidism. In 2012 we published another article on 15,500 patients in the Journal of the American College of Surgeons. 83.5 % = one enlarged, overactive gland (termed a single adenoma) 15 % = two or three large glands (termed multiple adenomas)...(this group is over-reported) 1.5 % = four enlarged, overactive glands (termed four-gland hyperplasia) (this group is over-reported) <<<1 % = cancer of the parathyroid (very, very, very, very, very, very, very RARE.) Importantly... most patients with hyperparathyroidism have 1 parathyroid tumor and three normal parathyroid glands. Many of those patients with 4 bad parathyroid glands (remember, only about 1.5% will have 4 bad parathyroids) have 4 bad glands because they are 1) on the drug Lithium for many years, or 2) have a parent and/or brothers/sisters with this disease (called "familial hyperparathyroidism"). Thus, if you don't have a parent with this disease and you have not been on the drug Lithium for 20 or more years, then you have less than a 1% chance that you have 4 bad parathyroid glands. Bottom line, if your doctor thinks treating hyperparathyroidism complex or complicated and dangerous, and tells you that you could have 4 bad glands then you may want to take this page to them (or find a different doctor because they are talking about something that they simply don't know about). Hyperparathyroidism can be cured quite easily if you chose a surgeon that does this operation on a weekly basis (discussed on other pages of our web site). ALMOST EVERYBODY can be cured in 20 minutes or less (we examine all four glands in almost every one of our patients in less than 20 minutes). If your doctor or surgeon tells you that surgery is dangerous and complicated... then you may want to find a surgeon that thinks it's safe and simple. DO NOT let the concept of having one bad gland versus 4 bad glands confuse you or influence your treatment! This is one of our biggest pet peeves--the misunderstanding of 4-bad glands. You do not have four bad glands!Nearly all patients with hyperparathyroidism will benefit from having surgery... the only choice you really need to make is to choose your surgeon. Then let the surgeon worry about 1 bad gland, 2 bad glands, or 4 bad glands. As an example, the only difference in an operation for one bad gland and 4 bad glands when we are performing the operation is that those who have one bad gland have an operation that takes about 16 minutes on average, and operations for 4 bad glands takes about 19 minutes on average. Everything else is exactly the same... same anesthesia, same incision, same 1.5 hours in the recovery room... everything is the same. Why are we spending so much time talking about this? Because this is a very frequent worry that people have. They worry that they are one of the 1 percent of patients that have more than one bad gland... If you pick your surgeon wisely, you will not have to worry about this! We don't care--everybody at our center gets the same simple operation. If we don't care, then you shouldn't care!Click here to read more about parathyroid anatomy and where the four parathyroid glands are located. Understand why it can be very hard to find the four parathyroid glands, and why surgeons who do hundreds of these operations per year have a much higher cure rate.How the One Bad Parathyroid (the Adenoma)Affects the Other Three.To teach how the parathyroid glands respond normally to calcium levels and how the parathyroid glands are supposed to work, we will use your home's heating system in the winter as an example.We all have a heater in our homes that is controlled by a thermostat. When we set the thermostat on 70 degrees, it is this temperature that the thermostat will constantly monitor and turn on the heater when the temperature drops. If the temperature drops to about 68 degrees, the thermostat detects it and turns on the heater. The heater warms the room until the thermostat recognizes the increase in temperature, and when it reaches 72 degrees the thermostat turns OFF the heater. In reality, the heater in your home will turn on and off about 50 times per day. The temperature in the room will vary some, from a little above 70 degrees to a little below, but we don't notice it when the thermostat is working normally.All of our parathyroid glands have a built in "thermostat" (all endocrine glands do!). The thermostat in the parathyroid glands is very sensitive to calcium levels in the blood. The normal 'setting' for the thermostat in the parathyroid glands is for a calcium level between 8.5 and 10.2. Calcium is not just responsible for our bone strength, but it is the source of electrical energy in our nervous system and muscles, thus humans want this element controlled very, very well. Calcium is the ONLY element in the body that has its own control system!Normal parathyroid glands constantly monitor the calcium in the blood. When the calcium levels drop, the parathyroid glands turn on... and make parathyroid hormone (PTH). The PTH acts directly on the bones within minutes and takes some calcium out of the bones (we use the bones as a storage system for calcium). Now the level of calcium in the blood will increase a little--and the parathyroid glands recognize this and turn themselves off. Just like the thermostat that turned on when the temperature got low, the normal parathyroid glands turned on when the calcium got low. And, just like the thermostat that turned off when the temperature in the room got warm, the normal parathyroid glands turn off and stop making PTH when the calcium rose a little bit. This is why your calcium will vary every time your doctor measures it... it's always a little different, but it is ALWAYS supposed to be in the normal range.What happens in patients with Hyperparathyroidism? Well that is now a simple answer. One of the parathyroid glands developed a tumor. That tumor (an overgrowth of cells) will be about the size of an olive (typically) and it will do what it likes to do...MAKE HORMONE! So, you have this one big, bad parathyroid gland that is making hormone 24 hours per day... its thermostat is broken! It does NOT respond to the high calcium levels and turn off...instead it is stuck in the "on position", and constantly makes parathyroid hormone (PTH). Well, this PTH keeps working on your bones, taking calcium out of the bones and putting it in your blood. The bones become thin (osteoporosis), and the calcium in the blood is elevated out of the normal range. We get nervous system symptoms due to the brain not liking the high calcium levels (depression, tiredness, mean-ness, lack of energy, problems sleeping, etc). We can also get kidney stones and other problems due to all the extra calcium floating around.What happens to the NORMAL parathyroids when you have one bad parathyroid gland? Well that answer is now clear also. In the overwhelming majority of people with hyperparathyroidism, they will have one bad gland and 3 normal glands. The one bad gland is big and producing PTH all day long...making the calcium go high. Well, the three normal glands will still have a normal thermostat. They will recognize the high calcium and shut down their hormone making apparatus. Thus they become dormant and go to sleep. Since most people with parathyroid disease don't get diagnosed until they have had it for years--the normal parathyroid glands will have been dormant for years by the time the surgeon operates to take out the bad one. This is why experienced surgeons will provide their patients with calcium pills to take for the first few weeks after parathyroid surgery. It will take a week or two for the normal parathyroid glands to wake up and begin to regulate the calcium normally (to get their thermostats working properly). Without taking lots of calcium during that time, your calcium can drop too low and you will get sick (have problems with your nervous system and brain, like feel bad, feel 'foggy' and confused, fell anxious and 'doomed', feel out of control; get tingling in your hands and fingers and around your mouth, get cramps in your hands and feet). These are all symptoms of LOW calcium, and they can happen to patients after a successful parathyroid operation. The symptoms are temporary, and will go away after the nervous system gets used to the new 'normal' calcium levels. It may take 2 - 5 days, but these symptoms will always go away, and they are always treated the same way--take more calcium! If you get these symptoms after a parathyroid surgery--it means the surgery was successful, but your body doesn't like the new calcium levels yet and wants more calcium. You MUST give it more calcium if you have these symptoms. (Please understand, 94% of people will NOT have these symptoms as long as they take their calcium pills after the surgery)... and the ones that do have symptoms of low calcium simply have to take more calcium. (Note, these statistics come from our recent publication where we studied this in 6000 consecutive patients who went home within 1.5 hours of their operation. Of course, this is why all our patients get our home phone and cell phone numbers).
Pseudohypoparathyroidism (PHP) is a heterogeneous group of disorders characterized by hypocalcemia, hyperphosphatemia, increased serum concentration of parathyroid hormone (PTH), and insensitivity to the biologic activity of PTH. (See Pathophysiology, Presentation, and Workup.) Several variants of PHP have been identified. The molecular defects in the gene (GNAS1) encoding the alpha subunit of the stimulatory G protein (Gsa) contribute to at least 3 different forms of the disease: PHP type 1a, PHP type 1b, and pseudopseudohypoparathyroidism (pseudo-PHP). PHP type 1a is the best understood form of the disease. (See Etiology.) In 1942, Fuller Albright first introduced the term pseudohypoparathyroidism to describe patients who presented with PTH-resistant hypocalcemia and hyperphosphatemia along with an unusual constellation of developmental and skeletal defects, collectively termed Albright hereditary osteodystrophy (AHO). These features included short stature, rounded face, shortened fourth metacarpals and other bones of the hands and feet (see the image below), obesity, dental hypoplasia, and soft-tissue calcifications/ossifications. In addition, administration of PTH failed to produce the expected phosphaturia or to stimulate renal production of cyclic adenosine monophosphate (cAMP). (See Presentation and Workup.)Patient with pseudohypoparathyroidism showing shortened fourth metacarpals. EpidemiologyIn 1998, a nationwide epidemiologic survey of PHP was conducted in Japan based on hospital visits in 1997; the period prevalence was 3.4 cases per 1 million people. No information is available regarding the prevalence of PHP in the rest of the world. PHP occurs approximately twice as frequently in females as in males. Patients' ages range from infancy to senescence.Patient educationFor patient education information, see the Osteoporosis Center.TestotoxicosisTestotoxicosis with PHP type 1a can occur. Gonadotropin-independent sexual precocity has been reported in 2 boys who presented in infancy with classic PHP type 1a. Usually, patients with PHP type 1a show resistance to luteinizing hormone, which could lead to primary testicular insufficiency. The paradoxical presentation of testotoxicosis in these boys resulted from an identical point mutation in the GNAS1 gene, which caused both a loss and gain of Gsa function. PHP type 1a, characterized by a loss of Gsa function, is caused by thermal inactivation of the mutant protein at body temperature. Testotoxicosis indicates an organ-specific gain of Gsa function, resulting from the expression of the mutant protein. The lower temperature of the testes protects the mutant protein from thermal inactivation. Growth plate defectsA study by Sanchez et al found that an imprinting defect in GNAS may lead to growth plate defects in patients with PHP type 1b, including brachydactyly and Madelung deformity. This suggests that GNAS signaling has a more extensive role in chondrocyte maturation than was previously believed. Etiology As previously discussed, several variants of PHP have been identified, with PHP type 1a being the best understood form of the disease. The molecular defects in the gene (GNAS1) encoding the alpha subunit of the stimulatory G protein (Gsa) contribute to at least 3 different forms of the disease: PHP type 1a, PHP type 1b, and pseudopseudohypoparathyroidism (pseudo-PHP). All patients are heterozygous, with 1 normal Gsa allele; the mutant allele leads to production of inactive Gsa or to small amounts of active Gsa. HistoryPatients with pseudohypoparathyroidism (PHP) can present in infancy, especially if significant hypocalcemia occurs.Patients with PHP type 1a present with a characteristic phenotype, collectively called Albright hereditary osteodystrophy (AHO). The constellation of findings includes the following: Short statureStocky habitusObesity Developmental delayRound faceDental hypoplasiaBrachymetacarpalsBrachymetatarsalsSoft tissue calcification/ossificationPatients may develop paresthesias, muscular cramping, tetany, carpopedal spasm, or seizure. Hypocalcemia in children or adolescents is often asymptomatic. Patients with PHP type 1a may have disturbances in taste, smell, vision, and hearing, and they may be hyporesponsive to the biologic effects of other peptide hormones that use the alpha subunit of the Gsa protein to enhance cAMP production. The hormones under this class include thyrotropin, antidiuretic hormone, the gonadotropins, glucagon, adrenocorticotropin, and growth hormone–releasing hormone. Evaluate patients for signs and symptoms suggestive of deficiencies of any of these hormones. Primary hypothyroidism occurs in most patients with PHP type 1a.[10, 11] Reproductive dysfunction commonly occurs in persons with PHP type 1a. Women may have delayed puberty, oligomenorrhea, and infertility. Features of hypogonadism may be less obvious in men. Testes may show evidence of maturation arrest or may fail to descend normally. Fertility appears to be decreased in men with PHP type 1a. Within the spectrum of PHP type 1a, variability exists in osteoclast responsiveness to PTH. Some patients may have osteopenia and rickets. Mentation is impaired in approximately half of patients with PHP type 1a and appears to be related to the Gsa deficiency rather than to chronic hypocalcemia, because patients with other forms of PHP and hypocalcemia have normal mentation. Unusual presenting manifestations include neonatal hypothyroidism, Parkinson disease, and spinal cord compression. An interesting association between PHP type 1a and hypercalcitoninemia without any evidence of medullary thyroid carcinoma has been described.
Add “Also called the seat of the soul” (Pineal gland)Pineal tumors are a heterogeneous group of mass lesions originating in or located adjacent to the pineal gland. Neoplasms in this region cause symptoms when they compress or invade local structures or are disseminated beyond the confines of the tumor. When these tumors occlude the cerebral aqueduct, obstructive hydrocephalus with intracranial hypertension occurs; if the superior colliculus and pretectal area are involved, characteristic eye signs develop, which may include impairment of upward gaze and abnormalities of the pupil, paralysis or spasm of convergence and nystagmusretractorius. This sylvian aqueduct syndrome is indicative of a periaqueductal lesion. Parinaud's syndrome, the paralysis of upward gaze alone, is often and incorrectly used as synonymous with the sylvian aqueduct syndrome. The anatomic substrate underlying these functions is located just anterior to the aqueduct and below the posterior part of the third ventricle. Downward gaze. which also may be impaired in these patients, has its localization caudal to that of upward gaze in the brain stem. Compression or invasion of the cerebellum results in dysmetria, hypotonia and intention tremor. There may be altered consciousness due to intracranial hypertension or direct invasion of the brain stem by tumor. Malignant pineal tumors may metastasize to the spinal cord or caudaequina or to structures outside the nervous system. These metastases may also pass through the shunts inserted to treat intracranial hypertension. Less common symptoms, occurring in less than 10 percent of male patients with pineal tumors are precocious puberty or delayed onset of sexual maturation. Even less common is the occurrence of pineal apoplexy, in which a patient undergoes sudden neurological deterioration secondary to intratumoral hemorrhage and sudden expansion in the size of the posterior third ventricular tumor.PathologyThe lesions in the posterior third ventricle represent a diverse group of tumors; however, the crucial differentiation prognostically is between those lesions which are benign and those which are malignant. Approximately 10 percent of lesions in this area are truly benign, including pineal cysts, lipomas. arteriovenous malformations and aneurysms, pineocytomas. and meningiomas. Another 10 percent of tumors are relatively benign lesions. including low-grade gliomas and dermoids. The remaining 80 percent of pineal region neoplasms are highly malignant lesions. These include the germ cell tumors typified by the atypical teratoma (pineal germinoma) and also represented by the choriocarcinoma, endodermal sinus tumor. embryonal carcinoma. and malignant teratoma: and the non-germ cell malignancies such as pineoblastoma, glioblastoma, metastatic tumor and sarcoma.Associated lesionsThesuprasellargerminomas are included in this family of neoplasms. These are a subgroup of tumors, histologically identical to the pineal germinoma, which arise in or beneath the anterior part of the third ventricle. Germinomas represent a distinct pathologic entity arising from germ cells that originate from yolk-sac endoderm, migrate widely and settle in the gonadal ridges of the embryo. Normally, the nongonadal cells disappear from these sites; a failure of these cells to involute in the retroperitoneum, sacrococcygeal region, mediastinum, cerebral hemisphere or pineal or suprasellar region forms the cellular basis for an identical group of tumors which occasionally arise at these diverse locations. Many suprasellargerminomas represent an anterior extension of a pineal germinoma: however, suprasellargerminomas have been shown to exist free of pineal involvement.Kageyama and Belsky categorized these suprasellar tumors. The type 1 suprasellargerminoma is a metastatic tumor from the pineal region which invades the floor of the third ventricle, hypophysis and optic pathways. The symptoms are usually caused initially by hypothalamic and chiasmatic involvement. In one study, germ cell tumors with synchronous lesions in the pineal and suprasellar regions constituted 12.8 percent of germ cell tumors in a brain tumor registry. Type 2 germinomas are those which arise within the third ventricle and produce an obstructive hydrocephalus early in the disease: later findings are indicative of invasion of the hypothalamus, pituitary and optic pathways. Type 3 germinomas are those which originate in the region of the optic chiasmal region, grow outside the ventricular system, and only late in the disease invade the third ventricle and hypothalamus.When there is suprasellar involvement, the patient may present with a triad of findings including diabetes insipidus, visual defects and endocrine dysfunction. Diabetes insipidus is the most common manifestation of these tumors and may precede the development of other findings by years. The abnormalities of the visual system encountered include reduction in visual acuity, often in conjunction with optic atrophy. There are isolated reports of extraocular paralysis or severe exophthalmos due to infiltration of the tumor into the optic chiasm, nerves and orbit. Papilledema may not be evident, even in the presence of severe intracranial hypertension, because of the associated optic atrophy. Visual field studies may demonstrate bitemporal inferior scotomas, indicating a lesion on the dorsum of the chiasm. Macular fiber involvement by tumor growing into the posterior and superior part of the chiasm, associated with a bitemporal inferior scotomatous defect, is particularly characteristic of this tumor. Hypopituitarism is the third most common finding, after diabetes insipidus and visual abnormalities, and is often associated with growth arrest when the tumor occurs before puberty or with hypogonadism and amenorrhea when it occurs in older patients. Pathologic obesity, neurogenichypernatremia, hyperphagia with amnesia, abnormalities in temperature regulation, and excessive somnolence are uncommon manifestations reported in conjunction with these lesions. Elevated intracranial pressure is seen in tumors arising by extension from pineal region neoplasms. Suprasellargerminomas may also metastasize throughout the neuraxis and outside the nervous system.The occurrence of multiple tumors involving the nervous system occurs not only with synchronous germ cell tumors presenting in the pineal and suprasellar regions, but may be seen with the trilateral retinoblastoma in which a patient with an intraocular retinoblastoma or bilateral intraocular retinoblastomas presents with either a pineal, suprasellar, or parasellar retinoblastoma. In a report from the Wills Eye Hospital, this phenomenon was seen in seven (3 percent) of 245 consecutive cases of retinoblastoma, and five of these seven patients died of the intracranial disease.Molecular genetic studies have shown that transgenic mice expressing the large T-antigen of the simian virus 40 (SV 40) under the control of the Moloneymurine sarcoma virus (MSV) enhancer and the SV 40 promoter, develop heritable midline brain and ocular neoplasms with the features of a trilateral retinoblastoma. In these systems there is controversy about whether the pineal tumors arise from the subependymal cells of the cerebral aqueduct or are the result of the neoplastic transformation of pineal parenchymal cells.DiagnosisComputed tomography (CT) of the head with enhancement indicates the size and position of the lesion; whether there is a calcific, cystic, or hemorrhagic component; the degree of hydrocephalus; and whether there is evidence of subependymal extension or extension into the lateral ventricles or the suprasellar region. The suprasellar extension from a posterior third ventricular mass may be quite subtle and may require serial thin CT sections for detection, especially of subependymal enhancement. The suprasellargerminomas may show obliteration of the suprasellar cistern, irregular margins, moderate enhancement by contrast material and tumor infiltration of the walls of the third ventricle and both lateral ventricles. There may also be extension into the orbit and expansion of the optic nerves or chiasm caused by tumor infiltration.Germinomas appear on CT as high-density homogeneous lesions with intense contrast enhancement. Teratomas are often multilocular, heterogeneous appearing masses containing lipid areas. However, there are no pathognomonic CT features which allow differentiation among the various tumor types found in this region.Magnetic resonance imaging (MRI) with enhancement provides exquisite anatomic detail, outlining the lesion, the cerebrospinal fluid (CSF) pathways, and the venous anatomy around the vein of Galen. Also, MRI can aid in the detection of tumor seeding to other parts of the nervous system. However, as with CT, the MRI characteristics of pineal region tumors are usually nonspecific.Cytologic examination of the cerebrospinal fluid is important, because the presence of malignant cells may establish the nature and extent of the lesion. Seeding of the cerebrospinal fluid is a particularly characteristic feature of the germinomas, although this property is also exhibited by an occasional pineoblastoma and glioblastoma. Among brain tumors, the medulloblastomas have the highest incidence of malignant cells in the cerebrospinal fluid, 61.9 percent; however, the incidence of this phenomenon in patients with malignant pineal tumors is not known. There are reports of this occurrence in up to 60 percent of cases examined serially, especially when the sensitivity of the cerebrospinal fluid examination is improved by the use of millipore-filtered CSF tissue culture techniques.The MR or catheter angiographic examination of the intracranial arterial and venous vasculature allows identification of aneurysms of the posterior cerebral artery. arteriovenous malformations, abnormalities of the vein of Galen, and meningiomas. Although germinomas are vascular, it is unusual for them to contain neovascularity demonstrable by angiography, whereas embryonal carcinoma and teratocarcinoma show tumor vessels, and the presence of such tumor vascularity is suggestive of these malignant tumors. In addition, angiography provides important preoperative information about the relation of the internal cerebral veins, vein of Galen, basal veins of Rosenthal and precentralcerebellar vein to the mass lesion, information which can be important in planning the surgical approach.In the presence of either a pineal region tumor or synchronous lesions in the anterior and posterior third ventricle, MRI examination of the entire spine is also carried out to identify asymptomatic spinal metastases or assess the response of such lesions to therapy. In the absence of an obstructive hydrocephalus, one also samples CSF for malignant cells. The presence of malignant cells in the CSF is of major diagnostic and therapeutic importance, particularly since one cannot determine with a high degree of accuracy the nature of an isolated posterior third ventricular mass on the basis of current radiographic studies alone.The patient with a posterior third ventricular tumor requires as part of the investigation a careful assessment of endocrine function. Diabetes insipidus is the most common endocrine abnormality associated with pineal tumors; when present, it is probably due to anterior third ventricular extension of the neoplasm. Such cases are often overlooked. The physician should be suspicious and should undertake appropriate provocative tests. Tests of anterior pituitary function are also part of the investigation, to exclude adrenocorticotropic hormone deficiency and secondary, possibly life-threatening, adrenocortical insufficiency. Abnormalities of sexual maturation require that the levels of luteinizing hormone, follicle-stimulating hormone, testosterone. prolactin, growth hormone and melatonin of the cerebrospinal fluid and serum be surveyed.Neuro-ophthalmologic examination is mandatory in search of the defects seen in conjunction with these lesions and to provide evidence of the extent of the tumor involvement - which may not be apparent from the other studies - as well as a baseline for comparison after treatment. Immunoassay of serum, CSF and tumor cyst fluid for alpha fetoprotein (AFP) and the beta chain of human chorionic gonadotropin (hCG) may allow the diagnosis of an intracranial germ cell tumor (e.g. germinoma, teratocarcinoma, choriocarcinoma, or embryonal carcinoma). The AFP level may be elevated in endodermal sinus tumors. and the hCG-beta level is characteristically elevated in choriocarcinoma. Elevations of both of these tumor markers are seen with malignant teratomas and with undifferentiated germ cell tumors. In addition, the plasma level of these tumor markers correlates with tumor growth and regression and may be used to assess the response to therapy.The S-antigen, a 48 kilodalton protein also called "arrestin," is found in the retina and pineal. S-antigen reactivity has been detected in the preoperative CSF of one patient with a pineocytoma, and subsequently the tumor specimens were shown to have S-antigen immunoreactive cells. The same patient also had high levels of CSF melatonin. In experimental studies utilizing transgenic mice expressing the large T-antigen of SV 40, the large T-antigen was found exclusively in nuclei of cells containing S-antigen immunoreactivity in their cytoplasm, and these cells composed the neoplasm of one pineal region.TreatmentSince pineal region tumors are among the most dangerous intracranial masses to excise, there has been an ongoing debate for at least the last half-century concerning their surgical management. The debate centers on whether it is in the patient's best interest to explore these lesions at the time of their diagnosis, or whether the obstructive hydrocephalus should be treated with a shunt and the posterior third ventricular tumor irradiated without a tissue diagnosis-maneuvers which can be carried out with a low morbidity and mortality rate.Even though it has been demonstrated repeatedly that it is feasible for highly experienced surgeons to operate on lesions in the posterior third ventricle with a combined morbidity and mortality rate of under 10 percent, whether all patients with a pineal region tumor require surgical intervention remains a matter of judgment. For example, patients in whom cytologic examination of the cerebrospinal fluid shows malignant cells, patients with evidence of either spinal or extraneural metastases, and patients harboring synchronous anterior and posterior third ventricular tumors and in whom a tumor marker is elevated, most likely have a germinoma or other malignant germ cell tumor and may not require direct intervention.In contrast to these cases, there is a group of patients in whom surgical exploration is mandatory. These are patients previously treated with a shunt and radiation therapy without a tissue diagnosis who present with progressive neurological problems in the presence of a functioning shunt. Such patients have often survived for a period of years, and benign or relatively benign tumors are particularly frequent among this select group. The controversy centers on the posterior third ventricular lesion whose nature cannot be established preoperatively in spite of the best available diagnostic modalities. In centers in Japan and in England these patients are managed on a protocol of local field irradiation followed by assessment by MRI as to whether tumor regression occurs. If this does occur, the patients are subjected to whole-brain or whole-CNS irradiation. Among two groups of patients treated in Tokyo between 1975 and 1988 there was a 73 percent 5-year survival of those with histologically diagnosed germinomas and an 83 percent 5-year survival of those with suspected germinomas, outcomes which the investigators reported to be statistically the same. Patients not responsive to the 20 Gy local field irradiation are approached surgically. Among patients with this group of nongerminomatous tumors, the 5-year survival rate was 28 percent. Hoffman et al. have reported a 45 percent survival among patients with non-germ cell tumors treated with surgery and radiation.In the reported experience from the Royal Marsden Hospital. 50 patients with pineal tumors were managed with an initial 20 Gy local field irradiation. Responders were then given another 30 Gy to the brain and to the spine. These authors reported an 81 percent 5-year survival rate among patients with histologically diagnosed germinomas who respond to 20 Gy irradiation, 64 percent 5-year survival among those with non-germ cell tumors, and 18 percent 5-year survival among those with malignant teratomas.The malignant teratomas have a particularly bad prognosis and are those tumors which often present with elevations in the tumor markers and which recur rapidly following irradiation or surgical excision. It is particularly in these tumors and in patients with tumor recurrence that chemotherapeutic approaches seem to have a particular value. Currently cisplatin-based therapy of VP-16 and cisplatin alternating with vincristine, methotrexate, and bleomycin have been used to treat these cases with encouraging results.Even then, a pineal tumor referred to as a pineoloma is a rare occurrence in comparison to diseases affecting surrounding tissues and glands.The diagnostic radiographic approach to pineal tumors has changed over the past 30 years. Skull radiography, once an important study for detecting possible pineal neoplasm, has fallen into disuse because of its low sensitivity in detecting tumors. Unless the neoplasm is calcified, or unless the calcification in the pineal gland is displaced by a contiguous tumor or hydrocephalus, or unless changes of increased intracranial pressure are reflected in the sella, sutures, or calvarium, the plain x-ray film of the skull is not informative. Carotid and vertebral arteriography have been used in the past to identify the arterial blood supply to the pineal gland, venous drainage, and vascular displacement due to mass effect and obstructive hydrocephalus. However, at present, plain and contrast-enhanced computed tomography (CT) scans, with or without reconstruction (sagittal and coronal), are sufficient to make the diagnosis of a mass in the region of the pineal gland. In the last 20 years, magnetic resonance imaging (MRI) has proved to be the most informative imaging procedure for determining the anatomical localization of the mass, its relationship to adjacent vascular structures, and its spread by either direct invasion or subarachnoid dissemination. Both CT and MRI, while diagnostically highly accurate in determining the presence of a pineal region mass, lack specificity as to the histological nature of the tumor. Some relative specificity can be gained by paying attention to the density of the tumor on CT, the enhancement of the tumor on CT and MRI, and the intensity of the tumor on MRI. New in the diagnostic armamentarium is magnetic resonance spectroscopy. The role of magnetic resonance spectroscopy in the evaluation of pineal region tumors is, at present, relatively unknown but promising. Cerebral angiography retains a role in the evaluation of pineal region masses only in defining the arterial anatomy and venous relationships, information that may be useful when surgical resection is contemplated. Occasionally, characteristics of blood supply, such as duraltentorial blood supply (tentorialmeningioma) may indicate the likely histological nature of the lesion.Plain RoentgenographyA normal pineal gland measures 5 to 9 mm in length, 3 to 5 mm in height and up to 6 mm in width. The calcified pineal gland that is larger than 1 cm in any dimension should be looked upon with suspicion. Not only the size of the pineal calcification and its location are important but also the age at which the calcification appears. In the literature on the evaluation of skull roentgenograms it had generally been held that calcification of the pineal gland under the age of 10 was abnormal. However, Schey found that physiologic calcification could be seen in persons as young as 6 years. The overall incidence of calcification in childhood has been given by Willich et al. as 0.83 percent and by Peterson and Kieffer as 5.1 percent.It is clear from the literature on pineal calcification detected on skull roentgenograms that the incidence varies according to the age of the population examined, the quality of the examination, and the genetic makeup of the population. The overall incidence of pineal calcification is around 13 percent.Another factor in the incidence of skull radiographic evidence of pineal calcification is genetics. There is a body of literature that gives different rates for pineal calcification, according to the country of origin. Thus the incidence for Nigerians has been reported as 5 percent, for Japanese as 9.9 percent, for Fijians as 15 percent and for Indians as 19 to 24 percent. In contrast to these reports are the similar incidences found for calcification per decade of life by Adeloye and Felson in the American population and by Bhatti and Khan in the Pakistani population. For the first decade of life the incidence was zero in both series, for the second decade it was between 1.5 and 2.3 percent and for the third decade it was 10.5 percent. The incidence of pineal calcifications in both Americans and Pakistanis rises to 30 percent as the population ages into the middle and later years.Roentgenograms of the skull may be of diagnostic value in the patient with a pineal tumor if (1) the tumor produces calcification that is visible on the skull films; (2) the pineal tumor produces obstructive hydrocephalus with increased intracranial pressure that demineralises the floor of the sella or separates the sutures or the dilated third ventricle amputates the dorsum sellae; or (3) the obstructive hydrocephalus causes inferior and posterior displacement of the pineal calcification(s).The frequency of positive plain skull films in a series of pineal tumors varies. Abay et al., in a series of 24 patients with pineal tumors, found that in 25 percent the skull roentgenograms were abnormal on the basis of pineal tumor calcification, pineal calcification position, or evidence of increased intracranial pressure. Lin et al. reported a series of 32 pineal neoplasms, with calcifications seen in the region of the pineal in 75 percent. Of those with pineal calcification, the pineal gland was abnormal in size in 21 percent and in an abnormal position in 67 percent. The presence of the pineal calcification was abnormal in four of five patients who were 5 years of age or under (80 percent). The histologic classification of the tumors in the patients with abnormally large pineal calcification was teratoma in two, atypical teratoma in one, and pineoblastoma in two.Computed TomographyFactors that affect the detection of pineal calcification by CT are the thickness of the CT section, the size of the gland, the portion that is calcified, and the density of the calcification. Denser calcifications, thinner sections, and greater calcific portions make identification easier. It has been demonstrated that 8-mm-thick CT sections are eight times more sensitive than skull roentgenograms in the detection of 3-mm calcifications and 22 times more sensitive for 10-mm calcifications.The youngest patient with a normally calcified pineal gland on CT was age 6.5 years in the series of Zimmerman and Bilaniuk. In this series, from ages 8 to 14 years the incidence of pineal calcification ranged between 8 and 11 percent. At age 15 the incidence rose to 30 percent, and at age 17, to 40 percent. Thus, the incidence of pineal calcification as detected by CT shows an increase that coincides with the onset of puberty. The presence of a small pineal calcification on CT, in and of itself, from age 6.5, upward is not evidence of a pineal neoplasm. Calcification under age 6 should be looked upon with suspicion.CT has become an important diagnostic test for demonstrating the presence or absence of a pineal tumor. In the series of Abay et al. eight of nine CT studies were positive for pineal tumors. In one instance the CT was thought to be normal. In this false-negative study done on a first-generation CT scanner, the image quality was not ideal. In the first 44 pineal neoplasms diagnosed in the author's department since the advent of CT, there were two instances (4.5 percent) in which the pineal tumor was not appreciated initially. In one case. a 12-year-old girl presented with abnormal contrast enhancement of the subarachnoid space and a normal pineal region. Several subsequent CT examinations showed the same findings. Eight months after the onset of her headaches, a high-resolution. thin-section CT examination revealed a small pineal tumor. Biopsy revealed a pineoblastoma (primitive neuroectodermal tumor) and examination of the subarachnoid space revealed evidence of tumor seeding. The other patient had previously been treated for bilateral retinoblastomas. He was found to have an "incidental" CT finding of a pineal calcification at age 2 months. The patient was followed for a year, during which time a soft tissue mass grew around the calcification, producing obstructive hydrocephalus. Biopsy of this mass revealed a pineoblastoma. The first case represents a false-negative CT examination due to the small size of the lesion, while the second case represents a failure to appreciate the significance of a too-early-appearing pineal calcification.Thirty-one patients with pineal, parapineal or histologically related tumors were reported by Zimmerman et al. The CT characteristics in that series allowed differentiation between benign (germinal) tumors, such as teratomas and epidermoids from malignant germinal tumors, such as the germinoma and embryonal cell carcinoma. Primary pineal tumors (pineoblastoma, pineocytoma) could not be differentiated from malignant germinal tumors on the basis of CT criteria alone. Germinomas appeared as soft tissue masses of slightly greater density than normal brain tissue. Calcification was not a feature of the tumor matrix in germinomas. Frequently the germinoma surrounded a centrally placed normal-appearing pineal calcification. In the smaller tumors, the germinoma was well defined and did not appear to invade the surrounding brain or subarachnoid spaces. Uniform contrast enhancement was the rule. With larger germinomas the margins became poorly defined and infiltration into the adjacent brain parenchyma and subarachnoid spaces became more common. Cystic changes within a non-operated tumor were unusual. Embryonal cell carcinomas had soft tissue densities similar to those of the germinomas and they commonly contained tumor calcification; but in contrast to the germinomas, the embryonal cell carcinomas more often showed cystic areas. The benign teratomatous tumors also showed cystic areas. In addition, the benign teratomatous tumors showed evidence of tissue derived from all three germinal layers, such as calcification, ossification, teeth, fat and soft tissue densities.Epidermoid tumors of the pineal region have a density in the range of cerebrospinal fluid (CSF) and do not enhance with contrast administration. Thus, they may be confused with an arachnoid cyst or encysted ventricular structures.Both the pineocytomas and pineoblastomas show an isodense to hyperdense tumor matrix, contrast enhancement and a tendency toward parenchymal calcifications within the tumor matrix. Two patients with pineoblastomas, when followed by sequential CT examinations prior to treatment, showed rapid tumor growth. All but one of the pineoblastomas presented within the first 12 years of life. The case in which the pineoblastoma presented later at age 40, occurred in the mother of the child who had presented at age 12 with a pineoblastoma. The increased incidence of pineoblastomas in patients with congenital bilateral retinoblastomas and the occurrence of pineoblastoma in mother and daughter raise the interesting question of a genetic predisposition in at least some patients.Astrocytomas that arise within the pineal gland or adjacent to it will expand the gland, invade it or displace it. Since a glialstroma supports the pineocytes and is an integral part of the gland, some astrocytomas, presumably a small proportion of those involving the gland, arise directly from the pineal gland. Most often these tumors are of decreased density relative to brain parenchyma. The contrast enhancement that occurs is usually inhomogeneous.Calcification occurs infrequently in these tumors, but when it does, its nature and position may make the differential diagnosis between astrocytoma of adjacent structures and non-astrocytic pineal tumor difficult. Because of their location, posterior hypothalamic astrocytomas and astrocytomas of the tectum of the mesencephalon may also be difficult to differentiate from primary pineal tumors on transverse section CT. They frequently abut on the cerebral aqueduct or on the posterior third ventricle, producing obstructive hydrocephalus similar to that produced by a primary pineal neoplasm. To differentiate these tumors by location, careful attention needs to be paid to the size and shape of the tectal region: the radiologist needs to look for forward displacement of the calcified pineal gland by an upper brain stem mass. Sagittally reconstructed sections may be of particular advantage in this situation, as may be the use of a subarachnoid non-ionic water soluble contrast agent at the time of CT sectioning.In interpreting the CT findings, attention should be paid to the patient's age and sex. Teratomatous tumors of the pineal region occur almost exclusively in males. Germinomas occur in both males and females, most frequently in the second and third decades. Embryonal cell carcinoma occurs most often in the male in the second decade. Both germinomas and embryonal cell carcinomas are radiosensitive, but only the germinoma is radiocurable. After a period of regression, embryonal cell carcinoma tends to recur promptly. Sex distribution in the pineocytoma-pineoblastoma group seems equal. In a female patient with a calcified tumor in the pineal region, the most likely diagnosis is a tumor of primary pineal origin.Cerebral AngiographyThe major blood supply to the pineal gland arises from the posterior medial choroidal artery, a branch of the posterior cerebral artery. This vessel arises from the interpeduncular segment of the posterior cerebral artery. extends superiorly through the cistern of the lamina tecti and comes to lie on the lateral surface of the pineal gland. The artery continues on past the pineal to supply blood to the choroid plexus in the roof of the third ventricle. The pineal gland is drained by veins that originate from its superior and inferior surfaces. These veins drain into either the internal cerebral vein or the great vein of Galen. Superimposed upon the pineal vein anatomy on the lateral vertebral angiogram are the thalamic veins. It is difficult to differentiate pineal from thalamic veins. The internal cerebral vein lies in the roof of the third ventricle and then extends posteriorly through the velum interpositum into the cistern of the lamina tecti, where it joins the opposite internal cerebral vein and, with both basilar veins of Rosenthal, forming the vein of Galen. The vein of Galen lies just beneath the splenium of the corpus callosum and extends posteriorly to join the inferior sagittal sinus to form the straight sinus, which lies at the point of insertion of the falxcerebri onto the tentorium.In the pathologic situation, a number of adjacent arterial and venous structures may be displaced or deformed or may provide an abnormal source of blood supply or venous drainage. How often these findings are appreciated angiographically is uncertain. It is probable that the degree to which these findings are appreciated depends upon the quality of the examination. A high-quality examination requires magnification angiography with subtraction, following the delivery of an adequate volume of contrast agent to the tumor bed in a patient who is able to cooperate. Abay et al. in a series of 12 pineal tumors studied by angiography, reported the presence of tumor vascularity or stain in four (33 percent).More important than the presence of tumor stain is the recognition of the displacement of adjacent arteries and veins. Vascular displacements are dependent upon the direction of growth of the neoplasm and upon enlargement of the ventricular system resulting from obstruction of the posterior third ventricle or aqueduct. When the pineal gland is enlarged, the posterior medial choroidal artery is displaced posteriorly and laterally, and the superior and inferior pineal veins become more separated. The internal cerebral vein, which lies just above the pineal gland, is impinged on, elevated, and stretched. If the mass effect is sufficient, an angular deformity occurs at the point of juncture between the internal cerebral vein and the vein of Galen. If the tumor is large and extends posterolaterally, the vein of Rosenthal can also be deformed. As the tumor extends back into the cistern of the lamina tecti, down onto the tectum of the mesencephalon, and against the anterior-superior vermis, other changes occur. The superior cerebellar arteries are spread apart within the lamina tecti cistern (shown best with a Towne projection of the vertebral arteriogram); the precentralcerebellar veins are flattened and displaced from front to back (seen on the lateral projection of the vertebral angiogram); and the superior cerebellar artery branches, as they go over the anterior superior vermis, are flattened and deformed from front to back (seen on the lateral projection of the vertebral arteriogram). If the tumor extends forward (inferiorly), into the floor of the third ventricle, or as the third ventricle dilates from obstructive hydrocephalus, the thalamic perforating branches that arise from the proximal posterior cerebral arteries and posterior communicating arteries are displaced and stretched (seen on the lateral projection of the vertebral arteriogram). With obstructive hydrocephalus, the posterior lateral choroidal arteries (branches of the posterior cerebral artery that supply the choroid plexus of the lateral ventricles) are stretched. In the rare instance of a parapinealtentorialmeningioma, selective injection of the internal carotid artery may show its dural blood supply, which is derived from the intracavernous portion of the internal carotid artery through the tentorial branch of the meningohypophyseal trunk. Both internal carotid arteriography and vertebral arteriography are of use in the differential diagnosis of pineal neoplasms when the lesion proves to be a vascular anomaly (such as a vein of Galen aneurysm) that stimulates a pineal tumor on CT examination.Magnetic Resonance ImagingSince 1983. MRI has come to play a major role in the pre- and postoperative evaluation of patients with pineal region masses. Superior anatomic localization is the first and foremost reason. MRI can show direct sagittal images of the pineal region, demonstrating the gland's relationship to the tectum of the midbrain, corpus callosum and posterior third ventricle. Coronal and axial images complement the sagittal views.The combination of T1-weighted, proton density, and T2weighted images allows detection of abnormal alterations in signal intensity within the pineal gland and adjacent structures, such as the thalamus or brain stem. Tumors or disease processes characterized by an abnormal increase in interstitial water content within the lesion appear as regions of increased signal intensity on proton density images. CSF and fluidfilled cystic spaces appear high in signal intensity on T2-weighted images. Thus, the frequently occurring pineal cysts (a normal anatomic finding) are shown by a combination of T1 - and T2weighted images. On T1-weighted images, the cyst is hypointense and on proton density and T2-weighted images, bright.The normal pineal gland tissue enhances with gadolinium on MRI. This is because the pineal gland lacks a blood-brain barrier. Thus, contrast enhancement within the pineal gland, in and of itself, does not denote abnormality. Mamourian and Towfighi used MRI to obtain images from six patients with pineal cysts measuring between 7 and 15 mm in size and found that with immediate imaging, enhancement initially showed a rim-like margin, but with delayed imaging (60 to 90 minutes) the cysts also enhanced because of diffusion of the contrast material into the cyst. Tamaki et al. evaluated 32 cases of pineal cysts and found that they did not enlarge on follow-up studies over the next 3 months to 4 years. None of the patients in either series was symptomatic secondary to the pineal cyst. It is thought that pineal cysts may arise from incomplete fusion of the third ventricular diverticulum that gives rise to the pineal gland. However, pineal cysts with both glial and ependymal linings have been found.Calcification is best seen by CT and poorly seen by MRI. Calcification may be seen as a focal hypointensity, when the calcification occupies a sufficient portion of the volume of the slice. It is possible to have a pineal neoplasm that is not larger than the normal-size pineal gland but is identifiable on CT because of the presence of calcification too early in life. Such is the case in trilateral retinoblastoma. Under these circumstances it is possible to have the tumor not seen on MRI because the calcification cannot be visualized and the pineal gland is not increased in size and the enhancement of the pineal gland is considered a normal phenomenon.MRI shows flowing blood as a hypointense flow void within the lumen of the vessel. This is true for both arteries and veins. Thus, on the routine T1-weighted, proton density and T2weighted images, the internal cerebral veins, vein of Galen and straight sinus can be identified clearly, along with their relationship to any pineal mass. Should the mass be a vascular malformation, then the hypointense flow voids that make up the mass can be identified as such and characterized as a vein of Galen malformation.Despite the superior anatomic demonstration of a pineal mass by MRI it is not always possible to determine the site of origin. Thus, sometimes it is not possible to determine whether a mass in this region has arisen from the tectal plate, pineal gland or adjacent thalamus.In the demonstration of dissemination of tumor into the subarachnoid pathways, gadolinium-enhanced MRI of the brain and spinal canal has proved superior to contrastenhanced CT and/or myelography with a water-soluble agent. Thus, the method of choice for determining the presence or absence of disseminated tumor is gadolinium-enhanced MRI of the brain and spine. This should be done before surgery in order to avoid confusion with postoperative blood products in the form of methemoglobin, which can be bright on T1-weighted images. MRI is also superior to CT in demonstration of blood products, whether acute, subacute or chronic. This is important in the case of occult vascular malformations, such as those arising in the midbrain, thalamus, splenium or corpus callosum, masses that may mimic pineal region tumors. In these instances. the pattern of signal intensity changes on T1-weighted, proton density and T1-weighted images may help characterize the presence of blood products, giving a pattern that suggests the presence of a vascular anomaly.With teratoid tumors, the presence of fat produces increased signal intensity on T1-weighted images. That this is fat and not methemoglobin can be verified by the use of a fatsuppression pulse sequence, which will turn the high signal of fat to a low one but will leave the high signal of methemoglobin unaffected.Germinomas on MRI appear as masses hypo- to isointense to gray matter on T1-weighted images. On proton density images they are often of slightly increased signal intensity, whereas on T1-weighted images they are most often iso- to hypointense. The reason for this decrease in signal intensity on long time to repetition (TR) images seems to be related to their dense cellularity. This signal intensity change is not unique to germinomas but occurs in lymphomas and primitive neuroectodermal tumors as well. The pineoblastoma is a primitive neuroectodermal tumor and has a similar signal intensity change on T1-weighted images. Germinomas enhance intensely. They are radiation-responsive and often disappear on imaging following the initial 3000 rad. Gadolinium-enhanced T1weighted images of the brain and spinal canal are used pre- and postoperatively to evaluate for disseminated disease. Choriocarcinomas and embryonal cell carcinomas arising in the pineal region have a more variable signal intensity on MRI. This is due to the frequent presence of haemorrhage in the tumor. Haemorrhage can have a variety of signal intensity appearances, including areas of hypo-, iso- or hyperintensity on T1-weighted, proton density, and T2-weighted images, depending upon the chemical state of the blood (oxy- or de oxyhemoglobin, intra- or extracellular methemoglobin, or hemosiderin). Teratomas of the pineal region often contain fat, which can be seen as a zone of increased signal intensity on T1-weighted images. Fat decreases in signal intensity on long TR images as the time to echo (TE) increases, and it disappears on fatsuppressed sequences. Pineoblastomas are a form of primitive neuroectodermal tumor. Calcification, if present in these tumors, is seen poorly or not at all on MRI. On T1weighted images they are hypo- to isointense masses; on proton density images the masses are of slightly increased signal intensity; and on T2-weighted images they are hypointense. They enhance strongly with contrast medium. The pineocytoma has a signal intensity pattern somewhat different from that of the pineoblastoma. On T2-weighted images pineocytomas are more often somewhat increased in signal intensity. Again, contrast enhancement is usually present. Astrocytomas arise from adjacent structures, such as the tectum of the midbrain, thalamus, and splenium of the corpus callosum, and intrinsically from within the pineal gland. These tumors are usually of low signal intensity on T1-weighted images and of increased signal intensity on proton density and T2-weighted images. Enhancement is variable and may or may not be present.Arteriovenous malformations (AVMs) and fistulae within the thalamus and midbrain drain into the adjacent venous structures, such as the vein of Galen and straight sinus (the vein of Galen malformation), giving rise to their enlargement. These high-flow vascular structures, both arterial and venous, become enlarged hypointense flow voids on T1-weighted, proton density, and T2weighted images. Gadolinium can produce some enhancement within portions of the nidus of the AVM. Magnetic resonance angiography serves a role in anatomically delineating the feeding arteries, the nidus, and the draining veins.Magnetic Resonance Angiography and Magnetic Resonance SpectroscopyWithin the last 14 years, magnetic resonance angiography has come into its own as a diagnostic technique. Two methods, time-of-flight and phase-contrast, have been used to produce images of flowing blood within vessels. Resolution remains a problem but is adequate to show major feeding arteries, the nidus of an AVM and draining veins. This is useful in the region of the pineal gland when there is a vein of Galen malformation. It can also be useful in giving a clear anatomical picture of the configuration of the internal cerebral veins, vein of Galen and straight sinus when a surgical approach is being contemplated for a solid tumor that is displacing or encasing these structures.Proton magnetic resonance spectroscopy in the last 13 years has begun to come into its own as a diagnostic technique. Singlevoxel spectroscopy, using a 2 x 2 x 2 cm voxel size, can show the levels of choline, phosphocreatine, creatine, N-acetylaspartate (NAA), and lactate within the region studied. Preliminary work in paediatric brain tumors has shown that elevation of choline, a cell membrane metabolite, is increased to a larger extent in malignant tumors than in benign tumors. By calculating ratios of choline to NAA, an index of the tumour's relative malignancy can be determined.
Vestigiality describes those similar characters of organisms that have seemingly lost all or most of their original function in a species through evolution. A structure or organ or even a function is vestigial if it has diminished in size or usefulness in the course of evolution. Vestigial structures are markers of evolutionary descent. These may take various forms such as anatomical structures, behaviors and biochemical pathways. Some of these disappear early in embryonic development, but others are retained in adulthood. The idea that we are carrying around useless relics of our evolutionary past has long fascinated scientists and laypeople alike. Although some researches show nothing is rudimentary at all but having them is not a necessity.10. Vermiform Appendix<img class="size-large wp-image-5982 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/Appendix-600x450.jpg" alt="Appendix" width="600" height="450" />Image SourceThe vermiform appendix is a vestige of the cecum, an organ that would have been used to digest cellulose by humans’ herbivorous ancestors. One potential ancestral purpose put forth by Charles Darwin was that the appendix was used for digesting leaves as primates. It may be a vestigial organ, evolutionary baggage, of ancient humans that has degraded down to nearly nothing over the course of evolution. Evidence can be seen in herbivorous animals such as the koala. The cecum of the koala is very long, enabling it to host bacteria specific for cellulose breakdown. Human ancestors may have also relied upon this system and lived on a diet rich in foliage. As people began to eat more easily digested foods, they became less reliant on cellulose-rich plants for energy. The cecum became less necessary for digestion and mutations that previously had been deleterious were no longer selected against. These alleles became more frequent and the cecum continued to shrink. After thousands of years, the once-necessary cecum has degraded to what we see today, with the appendix. Analogous organs in other animals similar to humans continue to perform that function, whereas other meat-eating animals may have similarly diminished appendices. In line with the possibility of vestigial organs developing new functions, some research suggests that the appendix may guard against the loss of symbiotic bacteria that aid in digestion. An alternative explanation would be the possibility that natural selection selects for larger appendices because smaller and thinner appendices would be more susceptible to inflammation and disease.9. Goose Bumps<img class="size-large wp-image-5983 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/Goose-Bumps-600x488.jpg" alt="Goose Bumps" width="600" height="488" />Image Source Goose bumps, also called chicken skin or the medical term cutis anserina, are the bumps on a person’s skin at the base of body hairs which may involuntarily develop when a person is cold or experiences strong emotions such as fear, awe, admiration or sexual arousal. The reflex of producing goose bumps is known as piloerection and the vestigial structures involved are the piloerector muscles. It occurs not only in humans but also in many other mammals; a prominent example are porcupines which raise their quills when threatened, or sea otters when they encounter sharks or other predators. Goose bumps do not appear on the face. As a response to cold: in animals covered with fur or hair, the erect hairs trap air to create a layer of insulation. Goose bumps can also be a response to anger or fear: the erect hairs make the animal appear larger, in order to intimidate enemies. This can be observed in the intimidation displays of chimpanzees, in stressed mice and rats, and in frightened cats. In humans, it can even extend to piloerection as a reaction to hearing nails scratch on a chalkboard, listening to awe-inspiring music, or feeling or remembering strong and positive emotions (e.g., after winning a sports event). Some people have learned to will goose bumps at any time they please. Piloerection as a response to cold or emotion is vestigial in humans. As we retain only very little body hair, the reflex now provides no known benefit. Humans also bear some vestigial behaviors and reflexes. The formation of goose bumps in humans under stress is a vestigial reflex; its function in human ancestors was to raise the body’s hair, making the ancestor appear larger and scaring off predators. Raising the hair is also used to trap an extra layer of air, keeping an animal warm. Due to the diminished amount of hair in humans, the reflex formation of goosebumps when cold is now vestigial.8. Musculature<img class="size-large wp-image-5991 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/palmaris-longus-600x450.jpg" alt="palmarislongus" width="600" height="450" />Image SourceA number of muscles in the human body are thought to be vestigial, either by virtue of being greatly reduced in size compared to homologous muscles in other species, by having become principally tendonous or by being highly variable in their frequency within or between populations. The Occipitalis Minor is a muscle in the back of the head which normally joins to the muscles of the ear. This muscle is very sporadic in frequency—always present in Malays, in 56% of blacks, 50% of Japanese, 36% of Europeans, and is nonexistent in the Khoikhoi people of southwestern Africa and in Melanesians. In many non-human mammals the upper lip and sinus area is associated with whiskers or vibrissae which serve a sensory function. In humans these whiskers do not exist but there are still sporadic cases where elements of the associated vibrissal capsular muscles or Sinus hair muscles can be found. Similarly the palmarislongus muscle of forearm, the pyramidalis muscle of abdomen and plantaris of the leg are considered useless or vestigial.7. Vomeronasal Organ<img class="size-large wp-image-5984 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/Vomeronasal-Organ-600x525.jpg" alt="Vomeronasal Organ" width="600" height="525" />Image SourceRodents and other mammals secrete chemical signals called pheromones that carry information about their gender or reproductive state, and influence the behaviour of others. Pheromones are detected by a specialised sensory system, the vomeronasal organ (VNO), which consists of a pair of structures that nestle in the nasal lining or the roof of the mouth. Although most adult humans have something resembling a VNO in their nose, neuroscientists have no hesitation in dismissing it as a remnant. If you look at the anatomy of the structure, you don’t see any cells that look like the sensory cells in other mammalian VNOs. You don’t see any nerve fibres connecting the organ to the brain. Genetic evidence suggest that the human VNO is non-functional. Virtually all the genes that encode its cell-surface receptors – the molecules that bind incoming chemical signals, triggering an electrical response in the cell – are pseudogenes, and inactive. So what about the puzzling evidence that humans respond to some pheromones? Larry Katz and a team at Duke University, North Carolina, have found that as well as the VNO, the main olfactory system in mice also responds to pheromones. If that is the case in humans too then it is possible that we may still secrete pheromones to influence the behaviour of others without using a VNO to detect them.6. Nictitating Membrane The Third Eyelid<img class="size-large wp-image-5986 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/Nictitating-membrane-600x450.jpg" alt="Nictitating membrane" width="600" height="450" />Image SourceThe nictitating membrane is a transparent or translucent third eyelid present in some animals that can be drawn across the eye for protection and to moisten the eye while also maintaining visibility. Various reptiles, birds, and sharks have a full nictitating membrane, whereas in many mammals including humans, there is a small vestigial remnant of the membrane present in the inner corner of the eye having no known function. Some mammals, such as camels, polar bears, seals, and aardvarks, also have a full nictitating membrane. It is often called a third eyelid or haw and may be referred to as the plicasemilunaris in scientific terminology.5. Coccyx the Tailbone<img class="size-large wp-image-5987 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/coccyx-600x533.jpg" alt="" width="600" height="533" />Image SourceThe coccyx, commonly referred to as the tailbone, is the final segment of the ape vertebral column. Comprises three to five separate or fused vertebrae (the coccygeal vertebrae) below the sacrum. In humans and other tailless primates (e.g. great apes) the coccyx is the remnant of a vestigial tail, but still not entirely useless; it is an important attachment for various muscles, tendons and ligaments — which makes it necessary for physicians and patients to pay special attention to these attachments when considering surgical removal of the coccyx. Additionally, it is also part of the weight-bearing tripod structure which act as a support for a sitting person. Nevertheless coccyx, or tailbone, is the remnant of a lost tail. All mammals have a tail at one point in their development; in humans, it is present for a period of 4 weeks, during stages 14 to 22 of human embryogenesis. This tail is most prominent in human embryos 31–35 days old. The tailbone, located at the end of the spine, has lost its original function in assisting balance and mobility, though it still serves some secondary functions, such as being an attachment point for muscles, which explains why it has not degraded further.4. Wisdom Teeth<img class="size-large wp-image-5988 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/Wisdom-Teeth-600x435.jpg" alt="" width="600" height="435" />Image SourceWisdom teeth are the four third molars, present in the upper and lower jaws. Wisdom teeth usually appear between the ages of 17 and 25. Most adults have four wisdom teeth, but it is possible to have more, in which case they are called supernumerary teeth. Wisdom teeth commonly affect other teeth as they develop, becoming impacted or “coming in sideways”. They are often extracted when this occurs. About 35% of the population does not develop wisdom teeth at all. Wisdom teeth are vestigial third molars that human ancestors used to help in grinding down plant tissue. The common postulation is that the skulls of human ancestors had larger jaws with more teeth, which were possibly used to help chew down foliage to compensate for a lack of ability to efficiently digest the cellulose that makes up a plant cell wall. As human diets changed, smaller jaws were selected by evolution, yet the third molars, or “wisdom teeth,” still commonly develop in human mouths.Currently, wisdom teeth have become useless and even harmful to the extent where surgical procedures are often done to remove them.3. Outer Ear<img class="size-full wp-image-5989 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/ear.jpg" alt="" width="600" height="671" />Image SourceThe ears of a Macaque monkey, and most other monkeys, have far more developed muscles than those of humans and therefore have the capability to move their ears to better hear potential threats. Humans and other primates such as the chimpanzee however have ear muscles that are minimally developed and non-functional, yet still large enough to be identifiable. A muscle attached to the ear that cannot move the ear, for whatever reason, can no longer be said to have any biological function. In humans there is variability in these muscles, such that some people are able to move their ears in various directions, and it has been said that it may be possible for others to gain such movement by repeated trials. In such primates the inability to move the ear is compensated mainly by the ability to turn the head on a horizontal plane, an ability which is not common to most monkeys—a function once provided by one structure is now replaced by another. The outer structure of the ear also shows some vestigial features, such as the node or point on the helix of the ear known as Darwin’s tubercle which is found in around 10% of the population. Darwin’s point, or tubercle, is a minor malformation found in a substantial minority of people and takes the form of a cartilaginous node or bump on the rim of their outer ear, which is thought to be the vestige of a joint that allowed the top part of the ancestral ear to swivel or flop down over the opening to the ear.2. Male Nipples<img class="size-large wp-image-5990 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/Male-Nipple-600x337.jpg" alt="" width="600" height="337" />Image SourceMen’s nipples, cited as vestigial structures, are in a sense vestigial and are analogous to vestigial structures such as the remnants of useless pelvic bones in whales but are not truly vestigial because they are not remnants of functional male nipples in ancestral species. They occur because nipple precursors are grown early in the development of the human embryo, before sexual differentiation. Later in life these structures become more fully developed in women. The presence of nipples in male mammals is a genetic architectural by-product of nipples in females. So, why do men have nipples? Because females do.1. Palmar Grasp Reflex<img class="size-large wp-image-5992 aligncenter" src="http://www.smashinglists.com/wp-content/uploads/2011/02/palmar-grasp-reflex-600x425.jpg" alt="palmar grasp reflex" width="600" height="425" />Image SourceNot a structure but a vestigial behavior, the palmar grasp reflex appears at birth and persists until five or six months of age. When an object is placed in the infant’s hand and strokes their palm, the fingers will close and they will grasp it. The grip is strong but unpredictable; though it may be able to support the child’s weight, they may also release their grip suddenly and without warning. The reverse motion can be induced by stroking the back or side of the hand. The palmar grasp reflex is supported to be a vestigial behavior in human infants. When placing a finger or object to the palm of an infant, it will securely grasp it. This grasp is found to be rather strong. Some infants—37% according to a 1932 study—are able to support their own weight from a rod, although there is no way they can cling to their mother. The grasp is also evident in the feet too. When a baby is sitting down, its prehensile feet assume a curled-in posture, much like what is observed in an adult chimp.An ancestral primate would have had sufficient body hair to which an infant could cling unlike modern humans, thus allowing its mother to escape from danger, such as climbing up a tree in the presence of a predator without having to occupy her hands holding her baby.
The Human Suprachiasmatic NucleusIn mammals, the controlling clock component that generates a 24-hour rhythm is the suprachiasmatic nucleus (SCN), located in a part of the brain called the hypothalamus. The SCN produces a signal that can keep the rest of the body on an approximately 24-hour schedule. This animation illustrates the location of the SCN in the human brain.1 minute 40 secondsPlay Large: MOV / WMV (3 MB)Play Small: MOV / WMV (2 MB)To download the videos, in Internet Explorer right-click the link and select "Save Target As..." In Firefox right-click and select "Save Link As..." In Safari right-click and select "Download Linked File As..."More About Human SCN AnatomyEven in the absence of external time cues, humans maintain a sleep-wake rhythm very close to 24 hours. Typically an organism's circadian system is made up of components that receive environmental input, that generate the 24-hour rhythm, and that mediate rhythmic output to all the tissues of the body. In mammals, the controlling clock component that generates a 24-hour rhythm is the suprachiasmatic nucleus (SCN), located in a part of the brain called the hypothalamus. The SCN produces a signal that can keep the rest of the body on an approximately 24-hour schedule. However, because the internal clock's period is not exactly 24 hours, environmental cues—most importantly, light—are required to reset the clock each morning and keep the organism in sync with the external world. Watch this animation to see how sunlight is turned into a signal that can reset neurons in the SCN.Light enters the eye and activates neurons in the retina that convert photons (light particles) to electrical signals. The retinal neurons transmit the electrical signals from the retina via long axons in the optic nerve. Along the way is the optic chiasm, where the optic nerves from the left and right eye meet and cross. At the optic chiasm, visual information continues toward the back of the brain, where it is processed into images that we can consciously perceive. The neurons carrying information to the SCN, however, take a different path. They exit the optic chiasm and turn upward, toward the SCN (suprachiasmatic means "above the chiasm").The SCN is a small, paired, wing-shaped structure in the hypothalamus, located at the base of the brain. The animation shows the isolated left SCN, optic nerve, and eye, while the right SCN is shown embedded within the hypothalamus in the brain. Within each side of the SCN is a network of up to several thousand neurons. Experiments with individual isolated SCN neurons suggest that each SCN cell is a functional clock, normally synchronized with the activity of its neighbors. Inside a single SCN neuron, the protein product of a biological clock gene turns off production of more protein, forming a negative feedback loop. Go to the animation entitled "The Mammalian Molecular Model" to see how these molecular oscillations result in circadian rhythms. Even in the absence of external time cues, humans maintain a sleep-wake rhythm very close to 24 hours. Typically an organism's circadian system is made up of components that receive environmental input, that generate the 24-hour rhythm, and that mediate rhythmic output to all the tissues of the body. In mammals, the controlling clock component that generates a 24-hour rhythm is the suprachiasmatic nucleus (SCN), located in a part of the brain called the hypothalamus. The SCN produces a signal that can keep the rest of the body on an approximately 24-hour schedule. However, because the internal clock's period is not exactly 24 hours, environmental cues—most importantly, light—are required to reset the clock each morning and keep the organism in sync with the external world. Watch this animation to see how sunlight is turned into a signal that can reset neurons in the SCN.Light enters the eye and activates neurons in the retina that convert photons (light particles) to electrical signals. The retinal neurons transmit the electrical signals from the retina via long axons in the optic nerve. Along the way is the optic chiasm, where the optic nerves from the left and right eye meet and cross. At the optic chiasm, visual information continues toward the back of the brain, where it is processed into images that we can consciously perceive. The neurons carrying information to the SCN, however, take a different path. They exit the optic chiasm and turn upward, toward the SCN (suprachiasmatic means "above the chiasm").The SCN is a small, paired, wing-shaped structure in the hypothalamus, located at the base of the brain. The animation shows the isolated left SCN, optic nerve, and eye, while the right SCN is shown embedded within the hypothalamus in the brain. Within each side of the SCN is a network of up to several thousand neurons. Experiments with individual isolated SCN neurons suggest that each SCN cell is a functional clock, normally synchronized with the activity of its neighbors. Inside a single SCN neuron, the protein product of a biological clock gene turns off production of more protein, forming a negative feedback loop. Go to the animation entitled "The Mammalian Molecular Model" to see how these molecular oscillations result in circadian rhythms. Human SCN Anatomy BackgroundLiving organisms have evolved internal timekeeping mechanisms to synchronize behavior and physiology with the cycles of day and night. These biological clocks have been found in organisms as diverse as fungi, fruit flies, hamsters, and humans. The biological clock of humans is found deep within the brain. This animation takes the viewer on a three-dimensional tour following the path of light input to the suprachiasmatic nucleus (SCN), a collection of neurons that regulates our circadian rhythms. This animation was designed in conjunction with HHMI's 2000 Holiday Lectures on Science series Clockwork Genes: Discoveries in Biological Time. Human SCN Anatomy Teaching TipsThe animations in this section have a wide variety of classroom applications. Use the tips below to get started but look for more specific teaching tips in the near future. Please tell us how you are using the animations in your classroom by sending e-mail to firstname.lastname@example.org.Use the animations to make abstract scientific ideas visible and concrete.Explain important scientific principles through the animations. For example, the biological clocks animations can be used to demonstrate the fundamentals of transcription and translation.Make sure that students learn the material by repeating sections of the animations as often as you think necessary to reinforce underlying scientific principles. You can start, restart, and play back sections of the animations.Urge students to use the animations in accordance with their own learning styles. Students who are more visually oriented can watch the animations first and read the text later, while others might prefer to read the explanations first and then view the graphics.Incorporate the animations into Web-based learning modules that you create to supplement your classroom curricula.Encourage students to incorporate the animations into their own Web-based projects.
Hyperpituitarism An overactive pituitary gland that leads to high levels of one of the pituitary hormones in the bloodstream. The most common cause of hyperpituitarism is a non-cancerous tumor of the41% of hospital consultant episodes for hyperfunction ofpituitary gland were for men in England 2002-03 pituitary gland.59% of hospital consultant episodes for hyperfunction ofpituitary gland were for women in England 2002-03
Hypopituitarism 54% of hospital consultant episodesfor hypofunction and other disorders of pituitary gland were for men in England 2002-03 46% of hospital consultant episodesfor hypofunction and is a clinical syndrome of deficiency in other disorders of pituitary hormone production. This may pituitary gland were result from disorders involving the pituitary for women in gland, hypothalamus, or surrounding England 2002-03 structures.
Pituitary Adenomas Pituitary adenomas are relatively common Typically slow growing Some pituitary adenomas can invade adjacent structures even if thy are benign Can be 1cm in diameter to 1 cm in size Most adenomas occur spontaneously, and are not inherited. Inherited pituitary adenomas are very rare1 out every 1000 adults
Prolactinoma •Benign noncancerous tumor of the pituitary gland that produces a hormone called prolactin. •Most common type of pituitary tumor.•Some symptoms include; irregular menstrual periods, milk production in the breasts, loss of sex drive, in men enlargement of the breasts, vision loss, headaches, and double vision.
Posterior Pituitary Syndromes Diabetes insipidus High ADH ADH deficiency Levels Excessive Cerebral urination edema sometimes upHyponatremia to 12 gallons a Neurologic day dysfunction Excessive thirst Polydipsia
HypothalamicSuprasellar Tumor Hypothalamic tumors may extend into the pituitary fossa leading to endocrine, visual, and neurological symptoms that are similar to pituitary tumor symptoms. Symptoms; disturbance in thirst control, massive obesity by abnormal control of satiety, and dysegulartion of body temperature. May lead to blockage of the foramen of Monroe, internal hydrocephalus, and at the end, coma.
Multinodular Goiter •Cardiovascular changes •Nervous system changes •Palpable changes •Weight changesEffects a persons •Sleep Changes quality of life
Cretinism AKA Congenital Hypthyroidism Signs and Symptoms Thick, Protruding tongue Chocking episodes Prolonged Jaundice Short stature Dry, brittle hair Short, thick neck Broad hands with short fingers Horse sounding voice Hypotonia1 in 4000 babies Myxedema impacted
MyxedemaMyxedema- a condition markedby thickening and swelling ofthe skin caused by insufficientproduction of thyroid hormonesby the thyroid gland. Can becaused by an accumulation oftissue products in the skin. Symptoms Thickening of Skin Hypothyroidism Fatigue Weight gain Depression Dry Skin Brittle Hair
Thyroiditis An inflammation of the thyroid gland. It may be painful and tender when caused by an infection or trauma, or painless when caused by an autoimmune condition or medications. Types Hashimoto’s diseaseSubacute granlumatous thyroiditis Postpartum thyroiditis Subacute lymphocytic thyroiditis Drug induced thyroiditis Three phases: Overactive thyroid Underactive thyroid Return to normal
Granulomatous ThyroiditisSubacute granulomatous thyroiditis is a self-limited thyroid disorder that presents with localized neck pain and/or low-grade fever. The basic clinical and laboratory data are needed for making thediagnosis, and a biopsy is rarely required. The number of diagnoses made by using biopsies is not high. However, with the broadapplication of thyroid ultrasonography, the frequency of performing cytopathological diagnosis is increasing.
Painless ThyroiditisPainless (silent) thyroiditis is an inflammation of the thyroidgland characterized by passing hyperthyroidism, followed by hypothyroidism and recovery. Signs and Symptoms Weight loss Increased appetite Nervousness, Restlessness Heat intolerance Increased sweating Fatigue Muscle cramps Frequent bowel movements Menstrual irregularities Weakness
Diffused Goiter •A nontoxic goiter that does not result from an inflammatory or neoplastic process and it is not associated with abnormal thyroid function. •Nodes appear 2-4 times more likely in women than men.
Colloid Goiter •Enlargement of an otherwise normal thyroid gland. •Compensation for not making enough thyroid hormone •Environmental Factors •Happens in areas with iodine-depleted soils •Risk factors: female, older than 40, inadequate intake of iodine, living in endemic area, and genetics
Parathyroid Glands We have 4 parathyroid glands. They regulate calcium within the body by creating parathyroid hormone (PTH). When too high less PTH is made, when too low more PTH is made.
Hyperparathyroidism Information InformationWomen are more Increased urine likely productionOver the age of 60 Kidney stones Kidney Failure Nausea Bone pain or Loss of appetite tenderness Treatment includes: Depression Exercise Tired, ill, weak Drink plenty ofFragile bones and fluids limbs
Pseudohyperparathyroidism Characterized Information Hypocalcemia 1942 Albright, F.Hyperphosphatemia Short stature Increased serum Rounded Faceconcentration of PTH Shortened 4th Insensitivity to metatarsal biological activity of Obesity PTH Dental Hypoplasia In 1998, a nationwide epidemiologic survey of PHP was conducted in Japan based on hospital visits in 1997; the period prevalence was 3.4 cases per 1 million people. No information is available regarding the prevalence of PHP in the rest of the world.
Pinealomas The pineal gland is known as the seat of the soul Uncommon type of tumor associated with pineocytes, astrocytes, and germ cells. Can be characterized as a pineoblastoma or a pineocytoma. Worldwide 1%, Japan Korea and China 3-8%, and of all brain tumors about 10% of all pediatric.Symptoms: Insomnia, Headache, Nausea, Vomiting,Obstructive hydrocephalus.Account for 15%-32% of all tumors in the pineal region.Occurs more frequently in late childhood or early adulthood.
Vestigial Remnant Vestigal Remnant – Describesan organ that we as humans still have in our bodies that isn’t used anymore. Examples Coccyx (No tail) Appendix Wisdom Teeth Outer Ear Male Nipples
Suprachiasmatic Nucleus In mammals, the controlling clock component that generates a24-hour rhythm is the suprachiasmatic nucleus (SCN), located in a part of the brain called the hypothalamus. The SCN produces asignal that can keep the rest of the body on an approximately 24- hour schedule. This animation illustrates the location of the SCN in the human brain.
REFRENCES"Colloid nodular goiter: UCLA Endocrine Surgery Encyclopedia." Parathyroid Surgery: Endocrine Surgery, Thyroid Adrenal Surgery | UCLA Los Angeles, CA. N.p., n.d. Web. 1 Nov. 2012.<http://endocrinesurgery.ucla.edu/patient_education_adm_colloid_nodular_goiter.html>."Conditions: Pituitary Adenoma (Tumor) | UCLA Neurosurgery." Neurosurgery: Brain Tumor Surgery, Stroke, Minimally Invasive Surgery, Brain Aneurysms, Spinal Disorders, Trigeminal Neuralgia- UCLA. N.p., n.d. Web. 31 Oct. 2012. <http://neurosurgery.ucla.edu/body.cfm?id=1123&ref=80&action=detail>."Conditions: Prolactinoma | UCLA Neurosurgery." Neurosurgery: Brain Tumor Surgery, Stroke, Minimally Invasive Surgery, Brain Aneurysms, Spinal Disorders, Trigeminal Neuralgia - UCLA. N.p.,n.d. Web. 31 Oct. 2012. <http://neurosurgery.ucla.edu/body.cfm?id=1123&ref=86&action=detail>."Cretinism - Symptom, Causes, Treatment of Cretinism." Health Issues. N.p., n.d. Web. 31 Oct. 2012. <http://www.health-issues.org/diseases/cretinism.htm>."HHMIs BioInteractive - The Human Suprachiasmatic Nucleus." Howard Hughes Medical Institute (HHMI) | Biomedical Research & Science Education . N.p., n.d. Web. 1 Nov. 2012.<http://www.hhmi.org/biointeractive/clocks/SCN.html>."Hyperparathyroidism - PubMed Health." National Center for Biotechnology Information. N.p., n.d. Web. 1 Nov. 2012. <http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002195/>."Hyperparathyroidism: the Development of Parathyroid Tumors. Hyperparathyroidism Causes High Calcium, Parathyroidism.." Parathyroid.com Discusses Parathyroid Disease,Hyperparathyroidism, Parathyroid Diagnosis and Surgery. Parathyroid Operations, Parathyroid Treatment and Parathyroid Tumors.. N.p., n.d. Web. 1 Nov. 2012.<http://www.parathyroid.com/parathyroid-disease.htm>."Hypopituitarism - MayoClinic.com." Mayo Clinic. N.p., n.d. Web. 31 Oct. 2012. <http://www.mayoclinic.com/health/hypopituitarism/DS00479>."IMAGING OF PINEALOMAS." NEUROSURGERY NEURORADIOLOGY. N.p., n.d. Web. 1 Nov. 2012. <http://www.neuroradiology.ws/pinealimaging.htm>."Medscape: Medscape Access." Medscape: Medscape Access. N.p., n.d. Web. 1 Nov. 2012. <http://emedicine.medscape.com/article/120392-overview>."Myxedema - Symptoms - Better Medicine." Local Health â€“ Health and Medical Information You Can Trust â€“ LocalHealth.com - Better Medicine. N.p., n.d. Web. 31 Oct. 2012.<http://www.localhealth.com/article/myxedema/symptoms>."Pinealomas Pinealoma." Pinealomas Pinealoma. N.p., n.d. Web. 1 Nov. 2012. <http://www.pinealomas.com/>."Posterior Pituitary Disorders." Childrens Hospital of Wisconsin in Milwaukee, WI, is a member of Childrens Hospital and Health System - Home Page. N.p., n.d. Web. 31 Oct. 2012.<http://www.chw.org/display/PPF/DocID/22673/router.asp>."Posterior Pituitary Disorders." CHP: Posterior Pituitary Disorders. N.p., n.d. Web. 31 Oct. 2012. <http://www.chp.edu/CHP/P01972>."Prolactinoma Page - National Endocrine and Metabolic Diseases Information Service." Home Page - National Endocrine and Metabolic Diseases Information Service. N.p., n.d. Web. 31 Oct.2012. <http://www.endocrine.niddk.nih.gov/pubs/prolact/prolact.aspx#whatis>."Remnants & Organs of Human Body We No Longer Require." Best Top 10 Lists - Smashing Lists - Top Ten. N.p., n.d. Web. 1 Nov. 2012. <http://www.smashinglists.com/10-remnants-of-human-body-we-no-longer-require/>."Search: Images." Earn Reward Points and Redeem Them For Free Stuff at Swagbucks.com. N.p., n.d. Web. 31 Oct. 2012. <http://www.swagbucks.com>."Statistics about Hyperpituitarism - RightDiagnosis.com." Right Diagnosis. N.p., n.d. Web. 31 Oct. 2012. <http://www.rightdiagnosis.com/h/hyperpituitarism/stats.htm>."Statistics about Hypopituitarism - CureResearch.com." Symptoms, Diseases and Diagnosis - CureResearch.com. N.p., n.d. Web. 31 Oct. 2012.<http://www.cureresearch.com/h/hypopituitarism/stats_printer.htm>.Sundstrom, Kelly. "Multinodular Thyroid Symptoms | eHow.com." eHow | How to Videos, Articles & More - Discover the expert in you. | eHow.com. N.p., n.d. Web. 31 Oct. 2012.<http://www.ehow.com/about_5208992_multinodular-thyroid-symptoms.html>."Thyroiditis." University of Maryland Medical Center | Home. N.p., n.d. Web. 31 Oct. 2012. <http://www.umm.edu/altmed/articles/thyroiditis-000164.htm>."Thyroiditis." Medicine Net. N.p., n.d. Web. 31 Oct. 2012. <www.medicinenet.com/thyroiditis/article.htm>."Ultrasonographic Characteristics of Subacute Granulomatous Thyroiditis." National Center for Biotechnology Information. N.p., n.d. Web. 1 Nov. 2012.<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2667608/>.