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Does anyone have any easy to read (understand)


trs

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I am trying to compile a few short to the point Cushings articles for a disability appeal. I have decided to use an attorney and would like to take some information on Cushings with me to the appt. I have Vs. article and some others for what Cushings is I really need some that tell the damage it causes in more detail than the basic heart problems, diabetes and infection. I have some that are really long and detailed with various aspects of symptoms but, I think these would be a little to long for the intial appeal. The attorney won't have much time to file the appeal.

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Well I kept telling the man filling out the intial form that I thought Cushings was my trouble but, there is not a category or whatever it is they call that. So he listed obesity and heart problems. I didn't have the Cushings diagnosis then I do now. Since obesity is a major symptom of Cushings along with cognitive problems (short term memory loss per their psychologist) and heart problems I would think a good lawyer could put that together. I hope anyway.

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Trish,

Here is a web site http://www.socialsecurity.gov/disability/p...crine-Adult.htm

check it out. It tells you how you can qualify for disability. This is form social securtity web site.

 

 

Medical/Professional Relations

 

--------------------------------------------------------------------------------

 

 

 

 

 

 

Evidentiary Requirements

 

 

 

 

Listing of Impairments

(overview)

 

 

 

Disability Evaluation Under Social Security

(Blue Book- June 2006)

 

9.00 Endocrine System - Adult

 

Section 9.00 Endocrine System

 

9.01

Category of

Impairments,

Endocrine

System

 

9.02

Thyroid

disorders

 

9.03

Hyper-

parathyroidism

 

9.04

Hypo-

parathyroidism

 

9.05

Neurohypophyseal

insufficiency

(diabetes

insipidus)

 

9.06

Hyperfunction

of the adrenal

cortex

 

9.08

Diabetes

Mellitus

 

 

 

 

 

Cause of impairment. Impairment is caused by overproduction or underproduction of hormones, resulting in structural or functional changes in the body. Where involvement of other organ systems has occurred as a result of a primary endocrine disorder, these impairments should be evaluated according to the criteria under the appropriate sections. Medically acceptable imaging includes, but is not limited to, x-ray imaging, computerized axial tomography (CAT scan) or magnetic resonance imaging (MRI), with or without contrast material, myelography, and radionuclear bone scans. "Appropriate" means that the technique used is the proper one to support the evaluation and diagnosis of the impairment

 

9.01 Category of Impairments, Endocrine System

 

9.02 Thyroid disorders. Evaluate the resulting impairment under the criteria for the affected body system.

 

9.03 Hyperparathyroidism. With:

 

A. Generalized decalcification of bone on appropriate medically acceptable imaging study and elevation of plasma calcium to 11 mg. per deciliter (100 ml) or greater; or

 

B. A resulting impairment. Evaluate according to the criteria in the affected body system.

 

9.04 Hypoparathyroidism. With:

 

A. Severe recurrent tetany; or

 

B. Recurrent generalized convulsions; or

 

C. Lenticular cataracts. Evaluate under the criteria in 2.00ff.

 

9.05 Neurohypophyseal insufficiency (diabetes insipidus). With urine specific gravity of 1.005 or below, persistent for at least 3 months and recurrent dehydration.

 

9.06 Hyperfunction of the adrenal cortex. Evaluate the resulting impairment under the criteria for the affected body system.

 

9.08 Diabetes mellitus. With:

 

A. Neuropathy demonstrated by significant and persistent disorganization of motor function in two extremities resulting in sustained disturbance of gross and dexterous movements, or gait and station (see 11.00C); or

 

B. Acidosis occurring at least on the average of once every 2 months documented by appropriate blood chemical tests (pH or pC02 or bicarbonate levels); or

 

C. Retinitis proliferans; evaluate the visual impairment under the criteria in 2.02, 2.03, or 2.04.

 

11.05 Benign brain tumors

Evaluate under 11.02, 11.03, 11.04 or the criteria of the affected body system.

 

Here is a site also http://www.socialsecurity.gov/disability/p...ultListings.htm

which lists all the disorders. Gather as much info and records to take to the lawyers also show him these sites and what they are requiring.

 

If nothing else go to the psych and get on disability to start with with a mental disorder. This also goes along with cushings. THis is how I got on disabilty intially is from depression and bipolor. I have staid on becakuse of my depression and also my deteriating medical.

 

I was under review not to long ago and I had to send to them all the dr apt's and things I had had in the past 3 years including hospital visits. They gave me like three line. I sent a note enoough paper for 1 subject note book. I got my reponse back in like 2 weeks. They said we do not need to review your case at this time. SHould we need more info we will contact you, and your benefites witll contiue. LOL I do not even think they got thru the info before approving me.

 

I am not sure if this info will help you, but cushings is a part of the disability if it is worded right.

 

Amanda

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I just applied myself, I used the term Hypercortisolism and not cushings since I don't have an official cushing diagnosis, but they can't deny that I have hypercortisolism, and all of the symptoms and complications that go along with it!

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Ok this is what I have so far. What do you guys think. I just cut and pasted it so try to ignore the highlights etc. I fix those before I print. I am trying to make it easy on the attorney so they can get a quick overview of Cushings. I didn't know to use hypercortisolism to late now.

 

Cushing?s disease

Definition

Cushing?s disease is a pituitary tumor that releases excessive amounts of cortisol (a steriod). Cortisol is a hormone that controls the sleep/wake cycle, metabolism, immunity, and the relative composition of body between fat/bone and muscle.

Cortisol is the hormone that the body produces in response to stress.

Cortisol, a very potent glucocorticoid?a group of adrenocortical hormones that protects the body from stress and affect protein and carbohydrate metabolism? is involved in regulating the functioning of nearly every type of organ and tissue in the body, and is considered to be one of the few hormones absolutely necessary for life. Cortisol is normally released during stressful situations. It controls the body's use of carbohydrates, fats, and proteins and also helps reduce the immune system's response to swelling (inflammation).

Cortisol is involved in:

 complex processing and utilization of many nutrients, including sugars (carbohydrates), fats, and proteins

 normal functioning of the circulatory system and the heart

 functioning of muscles

 normal kidney function

 production of blood cells

 normal processes involved in maintaining the skeletal system

 proper functioning of the brain and nerves

 normal responses of the immune system

 

Causes

Cushing's disease is caused by a tumor or excess growth ( hyperplasia) of the pituitary gland. This gland is located at the base of the brain.

People with Cushing's disease have too much ACTH. ACTH stimulates the production and release of cortisol, a stress hormone. Too much ACTH means too much cortisol.

The adrenal glands are located on top of each kidney, and are responsible for releasing cortisol. The site of cortisol production is in the outer layer of the adrenal gland called the adrenal cortex. Release of cortisol is stimulated by ACTH, which is produced by the pituitary gland. The pituitary is juxtaposed to the base of the brain and serves as a type of control center for many other glands in the body. ACTH production occurs only when there is a low concentration of cortisol in the blood. Therefore, cortisol production can be abnormal due to abnormalities in the function of the adrenal gland or the pituitary gland. It can also be overproduced by abnormal regulation of ACTH

 

Symptoms

 Abdomen that sticks out and thin arms and legs (central obesity)

 Acne or skin infections

 Collection of fat on the back of the neck (buffalo hump)

 Depression

 Diabetes

 Easy bruising

 Excessive facial hair growth in females

 Headache

 Impotence

 Increased urination

 Moon face (round, red, and full)

 Osteoporosis

 Purple stretch marks on the abdomen, thighs, and breasts

 Stopping of menstruation

 Weakness

 Weight gain

 

Other clinical manifestations resulting from excessive cortisol production can be quite serious. Myopathy, or wasting away of the muscles often occurs. Due to the abnormal blood cell development that results from cortisol overproduction, the skin bruises more frequently and wounds do not heal as quickly. Skin tends to be fragile and thin. People with Cushing syndrome are susceptible to developing fractures, especially in the pelvic and spinal regions. Women are at a higher risk for developing osteoporosis or brittle bones. For all affected individuals, difficulty with activities such as lifting objects or getting up from a sitting position can lead to back pain and fractures. Because cortisol is also important for regulating insulin, patients with Cushing syndrome are at risk for developing diabetes. The function of cortisol is to regulate blood pressure, act as an anti-inflammatory mediator, and to regulate insulin metabolism. Cortisol plays a role during the metabolic activities associated with fat, protein, and carbohydrate metabolism. High levels of cortisol can cause sodium and water retention. Therefore, overproduction of cortisol can have medically important health-related implications that affect muscle contractions, heartbeat, and blood cell function.

 

Possible Complications

 Compression fractures

 Diabetes

 High blood pressure

 Infections

 Kidney stones

 Anxiety, cognitive dysfunction, psychosis

 

Most people have severe fatigue, weak muscles, high blood pressure and high blood sugar. Irritability, anxiety and depression are common.

An individual with HPA-axis suppression cannot increase steroid production appropriately during a medical illness or other stress and would need to receive stress doses of steroids to avoid adrenal crisis. Thus, in an emergency, the potential for relative adrenal insufficiency should be considered in any patient with Cushing syndrome.

 

Morbidity and Mortality

Morbidity and mortality associated with Cushing syndrome are related primarily to the effects of excess glucocorticoids. However, a large primary pituitary tumor may cause panhypopituitarism and visual loss.

 Two catastrophic medical crises that occur in glucocorticoid excess states are perforated viscera and opportunistic fungal infections.

 Exposure to excess glucocorticoids results in multiple medical problems, including hypertension, obesity, osteoporosis, fractures, impaired immune function, impaired wound healing, glucose intolerance, and depression, emotional lability psychosis.

 

The higher mortality rate observed in CS seems to be mainly caused by cardiovascular complications. Chronic hypercortisolism is associated with an increased incidence of cardiovascular risk factors such as systemic arterial hypertension, impaired glucose tolerance or diabetes, central obesity, hyperlipidemia, and hypercoagulability.

 

Hypercortisolism promotes the development of hyperglycemia and decreased carbohydrate tolerance by increasing hepatic glycogen and glucose production and decreasing glucose uptake and utilization by peripheral tissues

 

Increased body weight is one of the earliest signs of CS, with a characteristic redistribution of fat from peripheral to central parts of the body, mainly in the abdominal region. Glucocorticoids play a central role in the abdominal accumulation of body fat. An increased local generation of cortisol may take place in visceral adipose tissue because of high activity of 11?-hydroxysteroid dehydrogenase type I, resulting in high local concentrations of cortisol, by converting inactive cortisone into active cortisol. Visceral obesity is an independent risk factor for reduced life expectancy and also correlates with increased risk for disorders such as insulin resistance and diabetes, hyperlipidemia, hypertension, and atherosclerosis of coronary, cerebral, and peripheral vessels

 

In hypercortisolism, there is an increase in circulating very low-density lipoprotein and low-density lipoprotein, but not high-density lipoprotein, with consequent elevation of total triglycerides and cholesterol levels. The insulin resistance state induced by glucocorticoid excess is likely to play a key role in the determination of lipid abnormalities.

A complex derangement of the hemostatic system, characterized by both hypercoagulability and impaired fibrinolysis, is responsible for the thrombophilic state observed in patients with CS. Increased cortisol levels stimulate the synthesis of several clotting factors, such as fibrinogen by the liver, and von Willebrand factor by endothelial cells. Glucocorticoids also up-regulate the synthesis of plasminogen activator inhibitor type 1, the main inhibitor of the fibrinolytic system. This hypercoagulability state is a crucial factor predisposing CS patients to thromboembolic events, mostly after surgery and during IPS sampling. Therefore, patients with active CS should be treated as having a prothrombotic disorder, and antithrombotic prophylaxis should be considered.

 

Glucocorticoids affect behavior, mood, neural activity, and a number of specific biochemical processes in the central nervous system. A number of psychiatric and psychological disturbances may be associated with CS, regardless of its etiology. Depending on the series, 50?80% of patients with CS meet Diagnostic and Statistical Manual of Mental Disorders IV criteria for major depression. A minority of patients have other psychopathological manifestations including mania, anxiety, and cognitive dysfunction. If psychotic symptoms occur, they are likely to be a complication of mania or severe depression. Suicidal tendency also has been reported in patients with CS.

 

The somatotropic axis is negatively affected by exogenous or endogenous hypercortisolism, which reduces spontaneous GH secretion as well as the GH response to various stimuli, although with apparently minor changes in circulating IGF-I.

 

Patients with CS develop the manifestations of the metabolic syndrome or syndrome X, including insulin resistance, visceral adiposity, dyslipidemia, carbohydrate intolerance, and/or diabetes mellitus type 2, coagulopathy, and hypertension as a direct or indirect consequence of concurrent and chronic cortisol excess. The abnormalities enhance the global cardiovascular risk that is responsible for the increased mortality of these patients.

 

Prognosis

The prognosis for individuals who receive treatment for Cushing syndrome is good with a high likelihood of being cured. However, in affected individuals that are not treated, the prognosis can be poor, with death eventually resulting from complications from hypertension, diabetes, or heart disease

Despite cure of hypercortisolism, many patients exhibit residual symptoms in the first postoperative year or even longer, including problems with social and interpersonal relationships, anxiety, irritability, and demoralization.

Adults with hypercortisolism have also impaired cognitive function associated with reversible apparent loss of brain volume. Cognitive deficits are often specific to the medial temporal lobe declarative memory system. Adult patients studied 1 yr after surgical cure show improvement in mood but no change in cognitive function, with a concomitant increased, but not normalization, of brain volume.

 

Treatment

Treatment depends on the specific reason for cortisol excess and may include surgery, radiation, chemotherapy or the use of cortisol-inhibiting drugs. If the cause is long-term use of glucocorticoid hormones to treat another disorder, the doctor will gradually reduce the dosage to the lowest dose adequate for control of that disorder. Once control is established, the daily dose of glucocorticoid hormones may be doubled and given on alternate days to lessen side effects.

Pituitary Adenomas

Several therapies are available to treat the ACTH-secreting pituitary adenomas of Cushing's disease. The most widely used treatment is surgical removal of the tumor, known as transsphenoidal adenomectomy. Using a special microscope and very fine instruments, the surgeon approaches the pituitary gland through a nostril or an opening made below the upper lip. Because this is an extremely delicate procedure, patients are often referred to centers specializing in this type of surgery. The success, or cure, rate of this procedure is over 80 percent when performed by a surgeon with extensive experience. If surgery fails, or only produces a temporary cure, surgery can be repeated, often with good results. After curative pituitary surgery, the production of ACTH drops two levels below normal. This is a natural, but temporary, drop in ACTH production, and patients are given a synthetic form of cortisol (such as hydrocortisone or prednisone). Most patients can stop this replacement therapy in less than a year.

For patients in whom transsphenoidal surgery has failed or who are not suitable candidates for surgery, radiotherapy is another possible treatment. Radiation to the pituitary gland is given over a 6-week period, with improvement occurring in 40 to 50 percent of adults and up to 80 percent of children. It may take several months or years before patients feel better from radiation treatment alone. However, the combination of radiation and the drug mitotane (Lysodren?) can help speed recovery. Mitotane suppresses cortisol production and lowers plasma and urine hormone levels. Treatment with mitotane alone can be successful in 30 to 40 percent of patients. Other drugs used alone or in combination to control the production of excess cortisol are aminoglutethimide, metyrapone, trilostane and ketoconazole. Each has its own side effects that doctors consider when prescribing therapy for individual patients.

 

Surgical Care

 Cushing disease

 Treatment of choice for classic Cushing disease is transsphenoidal surgery by an experienced neurosurgeon. The goal of surgery is to remove the adenoma, preserving as much pituitary function as possible.

 The more extensive the mass and the resulting resection, the greater the risk for loss of pituitary function. Successful amelioration of hypercortisolism occurs in 60-80% of cases. Both open and laparoscopic techniques are possible. If unsuccessful, MRI-guided pituitary surgery, a new procedure, may be indicated. Lateralization of ACTH secretion via IPS catheterization and sampling is sometimes helpful in difficult cases.

 Pituitary irradiation is employed when transsphenoidal surgery is not successful or not possible. The procedure is less successful than surgery in adults, with a 45% cure rate in adults and 85% cure rate in children. Late-onset adverse effects include hypopituitarism.

 Bilateral adrenalectomy is an option if transsphenoidal surgery, pituitary irradiation, and medical therapy fail or if rapid normalization of cortisol levels is required. The patient then requires lifelong glucocorticoid and mineralocorticoid therapy.

 In individuals who undergo bilateral adrenalectomy, Nelson syndrome, that is symptomatic enlargement of the pituitary gland and adenoma, may occur in one quarter to one half of adults not treated with pituitary irradiation and in as many as one quarter of patients pretreated with radiation therapy.

 

Outlook (Prognosis)

If the tumor can be surgically removed, the outlook is fair to good, depending upon whether the entire tumor is removed.

 

Possible Complications

The most serious complication is blindness, which can occur if the optic nerve is seriously damaged.

Permanent hormonal imbalances may be caused by the tumor or its removal. This may require replacement of the affected hormones.

 

(I have diagrams for this part but they would not paste)

 

The pituitary gland is one of the body?s endocrine glands. It is sometimes called the ?master gland,? because it controls the functions of other endocrine glands.

Endocrine glands release chemical messengers (hormones) into the bloodstream to be carried to organs and tissues throughout the body.

The pituitary is located at the base of the brain. It is small and is divided into three parts: anterior lobe, intermediate lobe and posterior lobe. The anterior lobe is largest, making up about 80 percent of the gland.

The anterior lobe produces the following hormones:

 Growth hormone, which affects many other glands

 Prolactin, which stimulates milk production in women after giving birth

 Adrenocorticotropic hormone, which stimulates the adrenal glands

 Thyroid-stimulating hormone, which stimulates the thyroid gland

 Luteinizing hormone , which stimulates the ovaries or testes

 Follicle-stimulating hormone, which stimulates ovaries or testes

The intermediate lobe produces melanocyte, a hormone that controls skin pigmentation.

The posterior lobe of the pituitary stores and releases an antidiuretic hormone that increases the absorption of water by the kidneys. This lobe also stores and releases oxytocin, a hormone that causes the uterus to contract , helps to slow blood flow during the birthing process and causes milk to flow when a woman breast-feeds.

The pituitary is intimately involved in growth, development, maintenance and reproduction. The pituitary supplies growth hormone, which is responsible for growth from before birth to the end of growth at the end of puberty. The pituitary determines the timing for the onset of puberty and the cycling of the female menstrual cycle. It regulates the production of thyroid hormones that govern the overall metabolism of the body. It also controls the production of corticosteroids, which help govern such functions as electrolyte maintenance, blood pressure, inflammatory response and response to stress.

 

Sources

NIH

Medline Plus

The Hormone Foundation

The Pituitary Society

Mayo Clinic

The Journal of Clinical Endocrinology and Metabolism

 

Thanks everyone for your help.

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