د.نبيل
ابي اعرف وش اعراض قصور الغدة النخامية وايش العلاج وطريقته, كتبت موضوعين ومحد رد علي الله يخليك ساعدني .
ابي اعرف وش علاجة
لان امي قال لها الدكتور انه معاها قصور في الغدة
ومن الاعراض اللي معاها خمول
الام في المفاصل
انقطاع الدورة الشهرية

وبصرااحة انا ما اقتنعت بالعلاج اللي اعطاه امي ,اعطاها دواء منع حمل عشان تنتظم الدورة
وكورتيزون قال تستخدمة طول عمرها عبارة عن حبه ونص بعد الفطور ونص حبه بعد الغداء
واعطاها دواء ثاني وقال لها اذا حدث استفراغ كتب لها ابر تعطى في العضل ( هي تعطيها لنفسها )
وعلا اخر تاخذه عندهم بالمستشفى وقبل اعطائها اياه يقومون اخفاض مستوى السكر في جسمها لاقصى حد بصراااحة انا ما ارتحت لهذا العلااج احس انه مو لحالتها

لان انا درست ان الغده النخامية خصوصا الفص الامامي مسؤول عن المناسل (المبايض) وعن هرمون البرولاكتين
فافيدووني وساعدوني
واذا تعرفون دكاترة ممتازين في مدينه جدة خبروني عنهم

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Clinical manifestations of hypopituitarism

Peter J Snyder, MD


UpToDate performs a continuous review of over 350 journals and other resources. Updates are added as important new information is published. The literature review for version 14.2 is current through April 2006; this topic was last changed on March 2, 2005. The next version of UpToDate (14.3) will be released in October 2006.

INTRODUCTION — The presentation of hypopituitarism can be considered as the presentation of deficiency of each anterior pituitary hormone. The presentations of patients with deficiencies of those hormones that control target glands are often similar to the presentations of patients with primary deficiencies of the target gland hormones they control, with some notable exceptions.

An overview of the hormonal abnormalities that can occur in patients with hypopituitarism and of their clinical consequences will be provided here. The clinical manifestations and the specific diagnostic approaches to establishing the presence of hormone deficiency due to hypothalamic or pituitary disease are discussed separately as are the diagnosis and treatment of hypopituitarism. (See "Diagnosis of hypopituitarism" and see "Treatment of hypopituitarism").

Patients in whom the hypopituitarism is due to a pituitary or sellar mass may also have symptoms related to the mass, such as headache, visual loss, or diplopia. (See "Causes; presentation; and evaluation of sellar masses").

GENERAL PRINCIPLES — Damage to the anterior pituitary can occur suddenly or slowly, can be mild or severe, and can affect the secretion of one, several, or all of its hormones. As a result, the clinical presentation of anterior pituitary hormone deficiencies varies, depending upon the following factors:

The rapidity with which a disease affects anterior pituitary cells. Some diseases, such as pituitary apoplexy, develop rapidly, causing sudden impairment of ACTH (corticotropin) secretion and, consequently, sudden onset of symptoms of cortisol deficiency. Other insults, such as radiation therapy to the pituitary or hypothalamus, usually act slowly, causing symptoms many months or, more likely, years later. (See "Causes of hypopituitarism").
The severity of the hormonal deficiency. Complete ACTH and cortisol deficiency, for example, can cause symptoms under basal circumstances, while partial ACTH deficiency may cause symptoms only during times of physical stress.
How many kinds of anterior pituitary cells are affected, leading to impairment in the secretion of one, a few, or all the pituitary hormones (called panhypopituitarism). As a general rule, the secretion of gonadotropins and growth hormone is more likely to be affected than ACTH and thyroid-stimulating hormone (TSH). Many exceptions occur, however, so that one may see a patient who has only isolated ACTH deficiency. Thus, one cannot make an assumption about the status of one pituitary hormone from the status of another; if the physician jues that it is clinically important to know the status of a particular pituitary hormone, the status of that hormone must be tested directly.
ACTH deficiency — The presentation of ACTH deficiency is almost exclusively that of the resulting cortisol deficiency. In its most severe form, cortisol deficiency leads to death due to vascular collapse, because cortisol is necessary for maintenance of peripheral vascular tone. A less severe form of the same phenomenon is postural hypotension and tachycardia. Mild, chronic deficiency may result in lassitude, fatigue, anorexia, weight loss, decreased libido, hypoglycemia, and eosinophilia. (See "Clinical manifestations of adrenal insufficiency").

There are two important clinical distinctions between ACTH deficiency and primary adrenal insufficiency with a secondary increase in ACTH release:

ACTH deficiency does not cause salt wasting, volume contraction, and hyperkalemia, because it does not result in clinically important deficiency of aldosterone.
ACTH deficiency does not result in hyperpigmentation.
Both forms of adrenal insufficiency can cause hyponatremia. This abnormality is due to inappropriate secretion of antidiuretic hormone (vasopressin) that is caused by cortisol (not aldosterone) deficiency [1]. (See "Hyponatremia and hyperkalemia in adrenal insufficiency").

It is important to realize that moderately severe ACTH and cortisol deficiency may cause few or no symptoms and no physical findings. Consequently, the adequacy of ACTH secretion should be evaluated biochemically in all patients who have pituitary or hypothalamic disease. (See "Diagnosis of adrenal insufficiency").

TSH deficiency — The clinical presentation of TSH deficiency is exclusively that of thyroxine deficiency, which might include fatigue, lethargy, cold intolerance, decreased appetite, constipation, facial puffiness, dry skin, bradycardia, delayed relaxation phase of the deep tendon reflexes, and anemia. The degree of symptoms and abnormal physical findings usually parallels the degree of thyroxine deficiency, but, as the case with ACTH deficiency, some patients with marked TSH deficiency have few or no symptoms. (See "Clinical manifestations of hypothyroidism").

Gonadotropin deficiency — Deficient secretion of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) causes hypogonadism in both women and men.

In women, hypogonadism means ovarian hypofunction, which results in the inability to ovulate, infertility, and decreased estradiol secretion. The latter may be responsible for a variety of symptoms including oligo- or amenorrhea, vaginal dryness and atrophy, and fatigue. Estradiol deficiency due to hypopituitarism causes hot flashes, like estradiol deficiency due to ovarian disease. No physical findings of hypogonadism are detectable initially, but after several years, breast tissue decreases, fine facial wrinkles appear, and bone mineral density declines. (See "Evaluation of spontaneous premature ovarian failure").
Serum androgen concentrations in women with hypopituitarism (particularly those with both gonadotropin and ACTH deficiency) are lower than those in normal control women [2], and appear to be correlated with bone mineral density [3]. The clinical significance of this decrease has yet to be determined.

In men, hypogonadism means testicular hypofunction, which results in infertility and decreased testosterone secretion. The latter causes decreased energy and libido, and hot flashes if sufficiently severe, within weeks to months, but does not cause decreased muscle mass (and perhaps strength) for several years. Testosterone deficiency also causes decreased bone mineral density [4]. (See "Clinical features and diagnosis of male hypogonadism").
Growth hormone deficiency — Growth hormone deficiency in children typically presents as short stature. (See "Causes of short stature"). For many years, growth hormone deficiency beginning in adulthood was not thought to have any adverse consequences. However, evidence suggests that lack of growth hormone in adults might have a number of adverse effects [5]. The evidence is of two kinds (See "Growth hormone deficiency in adults").

The demonstration that patients who have growth hormone deficiency have a greater frequency of certain diseases than expected. Interpretation of this kind of evidence is confounded by the simultaneous deficiencies of other pituitary hormones and the variability of their replacement.
The improvement these patients experience when they are treated with growth hormone. Interpretation of this kind of evidence is made difficult by the lack of placebo controls in most studies of growth hormone treatment.
With the above qualifications, we should consider the possibility that growth hormone deficiency may result in the following:

Diminished muscle mass and increased fat mass [6-9]. This effect is the best documented.
Increased serum low-density-lipoprotein (LDL) cholesterol.
Decreased bone mineral density [10,11].
Diminished sense of well b**** [12-14].
Increased risk of cardiovascular disease [15] and increased inflammatory cardiovascular risk markers (IL-6 and C-reactive protein). (See "Screening for cardiovascular risk with C-reactive protein" and see "C-reactive protein in cardiovascular disease") [16].
Prolactin deficiency — The only known presentation of prolactin deficiency is the inability to lactate after delivery.


دي اعراض كسل الغده
د.نبيل

ده العلاج
Treatment of hypopituitarism

Peter J Snyder, MD


UpToDate performs a continuous review of over 350 journals and other resources. Updates are added as important new information is published. The literature review for version 14.2 is current through April 2006; this topic was last changed on May 8, 2006. The next version of UpToDate (14.3) will be released in October 2006.

INTRODUCTION — Treatment of patients with hypopituitarism is the sum of the treatments of each of the individual pituitary hormonal deficiencies detected when a patient with a pituitary or hypothalamic disease is tested. The treatments of corticotropin (ACTH), thyroid-stimulating hormone (TSH), and luteinizing hormone (LH) and follicle-stimulating hormone (FSH) deficiencies are in many ways the same as the treatments of primary deficiencies of the respective target glands, but in other ways they differ. Both the similarities and differences will be highlighted below. Treatment of growth hormone (GH) deficiency is unique to hypopituitarism.

One reason to optimize treatment is that in a retrospective study of 344 patients who had hypopituitarism after pituitary surgery, the long-term mortality was about double that of the general population [1]. Most of the excess mortality was due to cerebrovascular disease. The relationship between the hypopituitarism and the excess mortality remains unknown.

The specifics of therapy for hypopituitarism will be reviewed here. The causes, clinical manifestations, and diagnosis of hypopituitarism, are discussed elsewhere. Growth hormone deficiency in adults is also discussed in more detail elsewhere. (See "Causes of hypopituitarism" and see "Clinical manifestations of hypopituitarism" and see "Diagnosis of hypopituitarism" and see "Growth hormone deficiency in adults").

ACTH DEFICIENCY — Lack of ACTH primarily induces cortisol deficiency. As a result, treatment consists of the administration of hydrocortisone or other glucocorticoid in an amount and timing to mimic the normal pattern of cortisol secretion. Because there is no test to assess the adequacy of the replacement, the optimal replacement glucocorticoid and the optimal doses are not known. The author's practice is to use hydrocortisone, because that is the glucocorticoid the adrenals make, in a daily dose according to the patient's weight; suitable doses are approximately 20 mg/day for a patient who weighs 55 kg and 30 mg/day for a patient who weighs 80 kg. Although it would make sense physiologically to give two-thirds of the dose on arising and one-third in the early afternoon, many patients cannot remember the latter dose, so it more practical to give the entire dose on arising.

Some authorities, however, prefer dexamethasone or prednisone because of their longer durations of action. (See "Treatment of adrenal insufficiency"). Others use hydrocortisone but in lower doses, eg, 15 to 20 mg a day, because that is closer to the daily production rate of hydrocortisone [2]. Whatever the preparation and dose, the patient should be instructed in the need for larger doses in times of illness and other stresses.

An inadequate dose may result in persistence (or recurrence) of the symptoms of cortisol deficiency, while an excessive dose can lead to symptoms of cortisol excess and to bone loss. (See "Glucocorticoids and osteoporosis: Pathogenesis and clinical features"). Small deviations from the optimal dose are usually not detected, and there are no established biochemical tests for determining the adequacy of the dose. Plasma ACTH measurements cannot be used, because the values are low or normal before treatment. Serum cortisol values vary greatly depending upon when a dose of hydrocortisone was taken. Urinary cortisol values are also unreliable.

Unlike the situation in primary adrenal insufficiency, mineralocorticoid replacement is rarely necessary in hypopituitarism. Angiotensin II and potassium, not ACTH, are the major regulators of aldosterone secretion. (See "Chapter 6C: Aldosterone").

An unusual side effect of glucocorticoid replacement is the unmasking of underlying central diabetes insipidus, leading to marked polyuria [3]. Correction of cortisol deficiency can increase the blood pressure and renal blood flow, and, in patients with partial diabetes insipidus, reduce the secretion of vasopressin. All of these effects increase urine output. (See "Urine output in diabetes insipidus").

TSH DEFICIENCY — TSH deficiency results in thyroxine (T4) deficiency, and is treated with L-thyroxine. The goal of therapy should be a normal serum T4 value. The factors that influence dosing are similar to those of primary hypothyroidism (See "Treatment of hypothyroidism"), but treatment of secondary hypothyroidism differs in two ways:

T4 should not be administered until adrenal function, including ACTH reserve, has been evaluated and either found to be normal or treated. In a patient with coexisting hypothyroidism and hypoadrenalism, treatment of the hypothyroidism alone may increase the clearance of the little cortisol that is produced, thereby increasing the severity of the cortisol deficiency.
Measurement of serum TSH cannot be used as a guide to the adequacy of L-thyroxine replacement therapy. The treatment goal should be a serum T4 concentration in the middle of the normal range.
LH AND FSH DEFICIENCY — Treatment of LH and FSH deficiency depends upon gender and whether or not fertility is desired.

Men — Testosterone replacement is sufficient in men who have hypogonadism and who are not interested in fertility. The choice of treatment does not differ from that in men with primary hypogonadism, but serum LH measurements cannot be used to monitor the adequacy of therapy. This can be achieved by measurements of serum testosterone. (See "Testosterone treatment of male hypogonadism").

Men with secondary hypogonadism who wish to become fertile can be treated with gonadotropins, if they have pituitary disease or with either gonadotropins or gonadotropin-releasing hormone (GnRH) if they have hypothalamic disease. (See "Induction of fertility in men with secondary hypogonadism").

تكمله العلاج
Women — Women who have hypogonadism, ie, are deficient in estradiol and progesterone, and who are not interested in fertility, can be treated with estrogen-progestin replacement therapy. (See "Preparations for postmenopausal hormone therapy"). In women over age 50, the considerations for hormone therapy are the same as for women who undergo a natural menopause. (See "Postmenopausal hormone therapy: Benefits and risks"). The choice of treatment does not differ from that in women with primary hypogonadism.

Women with secondary hypogonadism who wish to become fertile may be treated with pulsatile GnRH or gonadotropins. (See "Congenital gonadotropin-releasing hormone deficiency (idiopathic hypogonadotropic hypogonadism) in adults", section on Treatment and see "Overview of ovulation induction", sections on Gonadotropin therapy and Pulsatile GnRH therapy).

Serum androgen concentrations in women with hypopituitarism, particularly those with both gonadotropin and ACTH deficiency, are significantly lower than those in normal control women [4]. In a study of women with testosterone deficiency due to hypopituitarism, who were taking exogenous estrogen orally, testosterone replacement transdermally at doses of 150 to 300 mcg/day for one year increased the serum free testosterone into the normal range, and increased mean bone mineral density of the hip and radius, but not the spine [5]. This treatment also increased fat-free mass and thigh muscle area but not fat mass. Treatment also improved some aspects of mood, sexual function, and quality of life, as assessed by questionnaires. Cognitive function was unchanged. One third of the women receiving testosterone developed acne but no patients developed hirsutism or other hyperandrogenic side effects.

GROWTH HORMONE DEFICIENCY — The availability of several recombinant human growth hormone preparations (Humatrope®, Nutropin®, Serostim®, and Genotropin®) for treating adults with growth hormone deficiency allows physicians in the United States to prescribe this treatment. Patients with GH deficiency acquired as an adult must meet at least two criteria for therapy: a poor GH response to at least two standard stimuli; and hypopituitarism due to pituitary or hypothalamic damage. The criteria are different in children in whom GH is required for normal growth. (See "Treatment of growth hormone deficiency in children").

Patients who develop GH deficiency in adulthood have unfavorable serum lipid profiles, increased body fat, decreased muscle mass, decreased bone mineral density, and a diminished sense of well-b****. There is substantial evidence that growth hormone treatment in these patients increases muscle mass and reduces body fat. The evidence for improvement in bone mineral density is less convincing, and the evidence concerning improvements in the sense of well-b****, muscle strength, and serum lipids is conflicting. Thus, we do not recommend recombinant human growth hormone as routine treatment for all patients with adult-onset growth hormone deficiency. (See "Growth hormone deficiency in adults").

PROLACTIN DEFICIENCY — The only known presentation of prolactin deficiency is the inability to lactate after delivery (for which there is currently no available treatment).

SUMMARY — Treatment of patients with hypopituitarism is the sum of the treatments of each of the individual pituitary hormonal deficiencies detected when a patient with a pituitary or hypothalamic disease is tested. The treatments of corticotropin (ACTH), thyroid-stimulating hormone (TSH), and luteinizing hormone (LH) and follicle-stimulating hormone (FSH) deficiencies are in many ways the same as the treatments of primary deficiencies of the respective target glands, but in other ways they differ.

Lack of ACTH primarily induces cortisol deficiency. Treatment consists of the administration of hydrocortisone or other glucocorticoid in an amount and timing to mimic the normal pattern of cortisol secretion (see "ACTH deficiency" above and see "Treatment of adrenal insufficiency").
TSH deficiency, which results in thyroxine (T4) deficiency, is treated with L-thyroxine. The goal of therapy should be a normal serum T4 value. T4 should not be administered until adrenal function, including ACTH reserve, has been evaluated and either found to be normal or treated. Measurement of serum TSH cannot be used as a guide to the adequacy of L-thyroxine replacement therapy. (See "TSH deficiency" above and see "Central hypothyroidism").
In men with gonadotropin deficiency, testosterone replacement is indicated when fertility is not desired. (See "Testosterone treatment of male hypogonadism"). Men with secondary hypogonadism who wish to become fertile may be treated with gonadotropins, if they have pituitary disease or with either gonadotropins or gonadotropin-releasing hormone (GnRH) if they have hypothalamic GnRH deficiency. (See "Induction of fertility in men with secondary hypogonadism").
In women with gonadotropin deficiency, treatment depends upon the patient's goals. Estrogen and progestin replacement is indicated in women who are not pursuing fertility, while gonadotropin or pulsatile GnRH therapy may be used when ovulation induction and fertility are the goal. (See "Postmenopausal hormone therapy: Benefits and risks" and see "Overview of ovulation induction").
We currently do not recommend recombinant human growth hormone as routine treatment for all patients with adult-onset growth hormone deficiency. This issue is reviewed in detail elsewhere. (See "Growth hormone deficiency in adults").

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