ต่อมไร้ท่อ

โปรแกรมที่ให้แพทย์สูติฯ เรียนต่อไปทางต่อมไร้ท่อโดยตรงเนี่ยส่วนมากจะมีชื่อเป็นภาษาอังกฤษว่าอะไรคะ


ความคิดเห็นที่ 139 

jan_km2p@hotmail.com (แจน) (Guest)
18 ธ.ค. 2553 09:19
  1. อยากทราบว่าต่อมไร้ท่อที่เป้นอิสระต่อมใต้สมองมีอะไรบ้าง
    ต่อมไร้ท่อที่ถูกควบคุมด้วยระบบประสาทมีอะไรบ้าง
    ต่อมไร้ท่อที่ควบคุมจากต่อมใต้สมองส่วนหน้า



ความคิดเห็นที่ 128

spider
14 ส.ค. 2549 05:09



ความคิดเห็นที่ 120

เด็กดี (Guest)
7 ส.ค. 2549 15:35
  1. ขอบคุงคราบ



ความคิดเห็นที่ 91

U (Guest)
2 มิ.ย. 2549 10:29
  1. ต่อมไร้ท่อๆๆๆๆๆๆๆๆๆๆๆ สร้างฮอร์โมนหลายชนิดครับๆๆๆๆๆๆๆๆๆๆ



ความคิดเห็นที่ 88

นู๋แนนค่า (Guest)
29 พ.ค. 2549 19:04
  1. อยากรู้ว่าต่อมไพนีลมีลักษณะอย่างไร



ความคิดเห็นที่ 98

พเเด (Guest)
7 มิ.ย. 2549 11:47
  1. เดเพ



ความคิดเห็นที่ 99

konan_doy_5@hotmail.com (Guest)
13 มิ.ย. 2549 19:57
  1. อวัยวะที่เกี่ยวกับต่อมไร้ท่อมีไรบ้างคะ



ความคิดเห็นที่ 112

ยานี (Guest)
10 ก.ค. 2549 22:22
  1. เป็นต่อมบาโทลีนอักเสบ ปวดมากต้องให้คุณหมอเจาะเอาหนองออกมา น่ากลัว ขนาด 3 เซนติเมตร ไม่อยากเป็นอีก

    ถามว่า 1. เกิดจากอะไรค่ะ ดิฉันเป็นคนรักษาความสะอาดอยู่เสมอ นี่เป็นมา 2 หนแล้ว อายมากด้วย

    2. จะกลับมาเป็นอีกหรือเปล่า

    ขอบคุณค่ะ



ความคิดเห็นที่ 101

แจม (Guest)
14 มิ.ย. 2549 20:13
  1. อยากทราบความรู้เรื่องต่อมใต้สมองมากกว่านี้



ความคิดเห็นที่ 129

Naruto_13_9@hotmail.com (Guest)
24 ส.ค. 2549 19:32
  1. อยากรู้เกวียวกับต่อมไร้ท่อ ใครรู้บ้าง



ความคิดเห็นที่ 71

Sora (Guest)
18 ม.ค. 2549 00:18
  1. อยากทราบโครงสร้างคร่าวๆของ ต่อมไร้ท่อ หน่อยครับ



ความคิดเห็นที่ 102

ปกรฐนิส ผลพิมาย (Guest)
15 มิ.ย. 2549 13:40
  1. เอาเป็นว่า ผมสรุปง่ายๆ จะได้เข้าใจหลักๆของต่อมต่างๆน่ะครับ



    ร่างกายคนเราสามารถสร้าง ฮอร์โมนได้จาก

    1.ต่อมมีท่อ

    2.ต่อมไร้ท่อ

    3.เนื้อเยื่อ

    4.เซลประสาท



    งิงิงิ เอาล่ะมาแยกดูกันเลย



    1.ต่อมมีท่อ ชื่อมันก็บอกอยู่แล้วว่ามีท่อ เอาไว้คอยส่งสารที่มันสร้างออกมา กระจายไปทั่วร่างกาย เช่นพวกเซลตับ เซลสร้างน้ำย่อยต่างๆ



    2.ต่อมไร้ท่อ ผมจะถนัดอธิบายตัวนี้มากก่า ต่อมไร้ท่อ คือ มันไม่มีท่อในการขนสารออกมาโดยตรง แต่จะมีเส้นเลือด ไปรับสารที่มันสร้างออกมา เพื่อกระจายไปทั่วร่างกาย เช่น



    ต่อมไอส์เลต ออฟแลงเกอฮาน มันจะมี 2 ชนิด

    คือ แอลฟาเซล จะสร้าง glucagon

    และ บีตาเซล จะสร้าง Insulin



    ต่อไปเป็นต่อมไทรอยด์

    ต่อมนี้จะสร้าง ไทรอกซิน ควบคุมอุณหภูมิร่างกาย และอื่นๆ

    กะ แคลซิโตนิน ควบคุมปริมาณ แคลเซี่ยมไอออน



    ต่อมไพเนียล ต่มนี้ในจิงๆแล้ว สามารถรับแสงได้น่ะ โดยเฉพาะในตัว.. อาไรหว่า ลืมล่ะ คล้ายๆกิ่งก่าอ่ะ ซาลามานเดอร์ป่ะ อิอิอ ลองไปค้นดูน่ะงับ

    สร้าง เมลาโตนิน ควบคุม สีผิวหนังให้เข้มขึ้นโดยมีแสงเป็นตัวกระตุ้นงับ



    ต่อม พาราไทรอยด์(4 ต่อม)

    ต่อมนี้สร้าง พาราทอร์โมน เอาไว้ควบคุม เกี่ยวกะ ประมาณแคลเซี่ยม ทำงานร่วมกะวิตามินดีน่ะงับ



    ต่อมใต้สมอง (อันนี้ตัวหลักงับ)

    แบ่ง เป็น 3 ส่วน

    1.ส่วนหน้า สร้างฮอร์โมนเองได้

    มี GH

    เอนดรอฟิน

    TSH

    LH

    ง่าลืมง่ะ เดี๋ยวไปค้นมาให้ใหม่ง่ะงับ งิงิงิ



ความคิดเห็นที่ 109

pookpick_physiology (Guest)
8 ก.ค. 2549 14:58
  1. ต่อมที่ผลิตฮอร์โมนควบคุมการทำงานของต่อมไร้ท่ออื่นๆคือ

    ต่อมใต้สมองหรือ pituitary gland เป็นต่อมที่อยู่ในแอ่งที่เรียกว่า sella turcica อยู่ภายใต้การควบคุมของ hypothalamus

    แบ่งออกเป็น สองส่วน คือ ต่อมใต้สมองส่วนหน้าหรือ Anterior Lobe และต่อมใต้สมองส่วนหลังหรือ Posterior Lobe

    โดยต่อมใต้สมองส่วนหน้านั้นสร้างและหลั่งฮอร์โมน

    1.Growth Hormone (GH)เพื่อไปกระตุ้นการเจริญเติบโต เพิ่มขนาดของกล้ามเนื้อและกระดูก

    2.Luteinizing hormone(LH) ทำหน้าที่กระตุ้นรังไข่ให้สร้างฮอร์โมนestrogenและกระตุ้นการตกไข่ในผู้หญิงและกระตุ้นให้มีการสร้างฮอร์โมนtestosterone ในเพศชาย

    3.Adrenocorticotrophic hormone(ACTH)กระตุ้น adrenal cortex ที่ต่อมหมวกไตให้สร้างฮอร์โมน

    4.Prolactin(PRL) กระตุ้นการสร้างน้ำนม

    5.Thyroid-stimulating hormone(TSH)กระตุ้นต่อมthyriod ให้มีการหลั่งฮอร์โมน

    6.Follicle-stimulating hormone(FSH)ในผู้หญิงกระตุ้นการสร้างestrogen และการเจริญเติบโตของไข่ ในชายกระตุ้นการสร้างเสปิร์ม



    ที่ต่อมใต้สมองส่วนหนังมีหน้าที่หลั่งฮอร์โมนที่สร้างจากต่อมใต้สมองส่วนหน้าแล้วนำมาเก็บไว้ที่ต่อมใต้สมองส่วนหลัง ได้แก่

    1.Antidiuretic Hormone (ADH) กระตุ้นการดูดกลับน้ำที่ไต

    2.Oxytocin กระตุ้นการบีบตัวของ uterus ขณะคลอดและกระตุ้นการหลั่งของน้ำนม



ความคิดเห็นที่ 110

pookpick_physiology (Guest)
8 ก.ค. 2549 15:01
  1. Endocrine System and Disorders



    Mark E.Peterson & John F. Randolf







    THE ENDOCRINE GLANDS



    The endocrine system is composed of glands that secrete hormones directly into the bloodstream. These hormones regulate many body processes. The endocrine system of the cat includes the following glands: thyroid, parathyroids, adrenals, pancreas, gonads (testicles and ovaries), and pituitary.







    The thyroid in the cat is a single gland with right and left lobes, situated in the neck alongside the upper part of the trachea (windpipe). The thyroid lobes produce two major hormones, thyroxine (T-4) and trfiodothyronine (T-3). These hormones help control the overall metabolism of the body. Adherent to the thyroid gland are the parathyroid glands. These four small glands (two per thyroid lobe) produce parathyroid hormone (PTH), which regulates calcium and phosphorus concentrations in the body.



    Adjacent to the front of each kidney in the cat is an adrenal gland. These glands consist of an outer region, or cortex, that surrounds a centrally located inner part, or medulla. The adrenal cortex elaborates glucocorticoid (e.g., cortisol) and mineralocorticoid (e.g., alclosterone) hormones, whereas the adrenal medulla produces catecholarnine hormones (e.g., adrenaline). The glucocorticoids affect the metabolism of carbohydrates, fat, and protein; the mineralocorticoids, help regulate salt and water balance-, and the catecholamines alter blood pressure and heart function.



    The pancreas of the cat lies along the upper part of the small intestine near the stomach. The endocrine activity of the pancreas resides in clusters of cells called the islets of Langerhans that are dispersed among the more predominant pancreatic cells that produce digestive enzymes. The pancreatic islets secrete several hormones including glucagon, somatostatin, gastrin, and insulin. Insulin is especially important in regulating the metabolism of glucose (blood sugar) and other fuels for the body.



    The gonads serve as a source of the sex hormones that govern reproduction and fertility. in the mate cat, the testicles produce testosterone; in the female cat, the ovaries produce progesterone and estrogen.



    The pituitary gland is located at the base of the brain. just as the brain is the "nerve center" for the nervous system, so the pituitary gland is the control center for many of the endocrine glands. The pituitary gland exerts this control by secreting hormones that affect particular endocrine glands. For example, pituitary-derived adrenocorticotropic hormone (ACTH) stimulates the adrenal cortex to produce cortisol, whereas pituitary production of thyroid-stimulating hormone (TSH) stimulates the thyroid to make T-4 and T-3 The pituitary gland also secretes growth hormone (GH) which stimulates growth, and vasopressin (also called antidiuretic hormone [ADH]) which acts to conserve body water by reducing urine output. Should the pituitary gland malfunction, then other endocrine glands under its control may also malfunction.



    Disorders of the endocrine system develop when there is an overproduction (hyper-) or underproduction (hypo-) of hormones. Certain endocrine disorders such as hyperthyroidism are common diseases in cats, whereas other diseases such as hypoadrenocortism are less well recognized.







    DISEASES OF THE ENDOCRINE SYSTEM



    Hyperthyroidism



    Hyperthyroidism results from excessive production of the thyroid hormones T-4 and T-3 In the cat, hyperthyroidism is most commonly caused by a functional benign tumor involving one or both thyroid lobes. Hyperthyroidism occurs in middle- to old-aged cats (average age, approximately thirteen years). There is no breed or sex predisposition.



    The most common clinical signs of hyperthyroidism in cats are weight loss, ravenous appetite, vomiting, excessive drinking and urinating, hyperactivity, and diarrhea. Often the haircoat looks unkempt and lull. Heart abnormalities including murmurs, rapid heart rate, arrhythmias (variations in the normal heartbeat), and even secondary cardiomyopathy (disorder of the heart muscle) may develop, occasionally in cats with hyperthyroidism, hyperexcitability and increased appetite are replaced by weakness and inappetance.



    Because the clinical signs of hyperthyroidism in cats mimic other diseases such as diabetes mellitus, kidney failure, heart disease, and gastrointestinal disorders, a thorough evaluation of the cat should include a complete physical exam and screening laboratory tests (complete blood count, serum biochemical profile, and urinalysis). Results of these tests may show alterations that will aid in the diagnosis of hyperthyroidism. Even more important, however, results of such routine screening tests may reveal the presence of a concurrent disorder not directly related to the hyperthyroidism, a situation that should not be surprising considering the old age of most cats with hyperthyroidism. During the physical examination, the veterinarian will carefully feel the neck region of the cat to determine if the lobes of the thyroid are enlarged and listen to the heart for any abnormalities. Findings on physical examination may prompt the need for further testing, such as electrocardiogram, radiographs, or echocardiogram.



    A definitive diagnosis of hyperthyroidism in cats is made when the blood concentrations of T-4 and/or T-3. are increased. Rarely, cats with hyperthyroidism may have normal concentrations of thyroid hormones. In these instances, repeating the thyroid hormone measurement or performing other thyroid function tests may be necessary.



    Thyroid imaging (scanning after administration of a small tracer dose of a radionuclide) is helpful in determining the extent of thyroid gland involvement in hyperthyroid cats, especially when no enlargement of the thyroid gland can be felt, when the enlarged thyroid gland has descended into the chest, or in the rare instance when the thyroid tumor is malignant.



    Hyperthyroidism in cats can be treated in three ways: surgical removal of the affected thyroid lobe(s), radioactive iodine therapy, or antithyroid drugs. Each form of treatment has its advantages and disadvantages. The treatment of choice for an individual cat depends on several factors, including the presence of heart disease or other medical problems (e.g., kidney failure) and the availability of a nuclear medicine facility.



    Surgical removal of the enlarged thyroid lobe(s) thyroidectomy-is an effective treatment for hyperthyroidism in cats. However, hyperthyroid cats may have increased anesthetic and surgical risks because of the effect the disease has had on the cat's heart and metabolism. The most serious complication of thyroidectomy is hypocalcemia (low blood calcium). This occurs when the parathyroid glands are inadvertently injured or removed during surgery. Exacting and special attention must be given to try and save at least one of the four parathyroid glands which are closely associated with the thyroid glands. This can be tricky, especially to maintain the microscopic blood supply to these tiny organs. Careful skill and keen surgical vision is essential to maintain parathyroid gland function for these cats to avoid the cat having a hypoparathyroid crisis. If both glands were removed, there is always a question as to how well the parathyroid glands will function; if they fail the cat could have a fatal seizure due to a severe drop in blood calcium. Some cats never have complications, others will require supplements and vitamin D therapy to help them otherwise maintain their blood calcium levels. Regular post-surgical thyroid checks are also needed to guard against recurrence and/or see if there is a need for thyroid supplementation.



    If both lobes of the thyroid are removed, thyroid hormone supplementation should be given daily with periodic measurement of blood T-4 concentration. If only one thyroid lobe is removed, the remaining lobe usually can maintain the proper hormone balance without additional treatment. However, if only one parathyroid gland remains, it can maintain normal calcium levels. If hypocalcemia does develop, it usually occurs within the first three days of surgery. Signs of hypocalcemia associate with hypoparathyroidism include: Lethargy, anorexia, and depression (100%); seizures (50%); muscle trembling, twitching, and fasciculations (83%); panting (33%); posterior lenticular cataracts (33%); bradycardia (17%); fever (17%); hypothermia (17%). There is an approximately 10% fatality rate associated with this surgery.



    Preparing hyperthyroid cats for surgery by pretreating them with an antithyroid drug may minimize the anesthetic and surgical complications. After antithyroid drugs have maintained normal thyroid hormone blood concentrations for 1 to 3 weeks, most systemic complications associated with hyperthyroidism will have improved. In hyperthyroid cats that cannot tolerate antithyroid drug treatment, alternate preoperative preparation with B-adrenoreceptor-blocking drugs (e.g., propranolol) may be tried. The beta-blockers do not lower thyroid hormone concentrations but instead block many of the effects of excess thyroid hormones on the heart.



    Radioactive iodine I-131 is the safest, most effective cure for cats with hyperthyroidism because it selectively destroys functioning thyroid tissue while sparing the parathyroid glands. The procedure involves first a nuclear medicine scan in which the cat receives an injection of the radioactive compound pertechnetate . The resulting scan shows the location of the cat’s thyroid glands, confirms the disease, and, most importantly, determines the cat’s dose of the radioactive agent iodine 131. Iodine is joined to the amino acid tyrosine in the thyroid gland to create T4. Iodine 131 is carried directly to the thyroid gland as though it were regular iodine. Iodine 131, being radioactive, emits high speed electrons which kill the surrounding abnormal thyroid tissue. Because these electrons penetrate only fractions of an inch, only the thyroid gland experiences the radiation and the rest of the body is spared. Radioactive iodine treatment does not require surgery or anesthesia. In most cats with hyperyroidism, a single treatment with radioactive iodine sufficient to return thyroid hormone concentrations normal. Cats that remain hyperthyroid can be successfully retreated with radioiodine. Cats whose T4 levels drop too low can be supplemented with T-4 At present the major disadvantage of radioactive iodine treatment is the unavailability of nuclear medicine facilities and the period of quarantine for treated cats. Cats receiving radioactive iodine need to be confined a nuclear medicine facility. This amounts to about nine days of hospitalization.(depending on the dose of radioiodine used and radiation safety regulations). This method of therapy is the safest and most effective cure for feline hyperthyroidism.



    If kidney function is not thoroughly investigated prior to this therapy, latent kidney failure may be unmasked irreversibly by this therapy. This

    can be avoided simply by screening potential candidates for kidney failure prior to recommending radiotherapy. Those who have possible

    kidney insufficiency should be treated with medication to bring the thyroid levels under control. If kidney function begins to show

    deterioration on this therapy, medication is discontinued and one must reevaluate the need for treating thyroid disease. If kidney function

    remains stable on treatment with anti-thyroid medications, then radiotherapy can proceed. A glomerular filtration rate test may well be an

    excellent predictor of possible kidney problems after I-131treatment and should be considered before I-131 radiotherapy.



    Antithyroid drugs inhibit the production of thyroid hormones, but they do not destroy the thyroid tumor. If doses of antithyroid drugs are missed, the signs of hyperthyroidism will recur. The most commonly used antithyroid drug is methimazole. In cats in which long-term methimazole treatment is planned, the goal of treatment is to maintain the blood T4 concentrations within the low-normal range with the lowest possible daily dose. Adverse reactions associated with methimazole include loss of appetite, vomiting, and lethargy. In most cats, these mild reactions disappear in a few days. However, if these gastrointestinal signs persist, the drug may need to be discontinued. Other, less common side effects of methimazole requiring cessation of the drug include severe scratching of the head and neck, liver damage, severe thrombocytopenia (low clotting-cell count predisposing to bleeding episodes), severe leukopenia (low white blood cell count predisposing to infection), immune-mediated hernolytic anemia, and lupus-like syndrome.



    Some cats simply cannot take methimazole or other drugs of its class. In most cases, there was a good reason why oral therapy was selected over radiotherapy and surgery. These factors are still present even if side effects preclude the use of methimazole. Fortunately there is an alternative: IPODATE (ORAGRAFFIN®)



    Ipodate blocks the activation of T4 into T3. It may also block the activity of existing T3. Because Ipodate does not block T4 production, T4 levels will remain high. In other words, T4 levels cannot be used to monitor success of Ipodate treatment. Further, because Ipodate is an iodine containing substance just as T3 & T4 are, Ipodate may interfere with the uptake of iodine 131 should radiotherapy be selected after Ipodate treatment has been underway. (The most current recommendation is to withdraw Ipodate for 3-4 weeks prior to radiotherapy). Ipodate may, however, be used up until the day of thyroid surgery with no ill effects.



    So far, no negative side effects have been reported with Ipodate in the treatment of feline hyperthyroidism even at the highest doses tested. One might ask, why this medication has not replaced Methimazole as “drug of choice?” Indeed, in the future, we may see that Ipodate does eclipse Methimazole; however, one recent study performed at the Animal Medical Center in New York City, found that a full 30% of hyperthyroid cats did not respond to ipodate (these cats were felt to be the most severely affected). Further, the Veterinary profession must still be concerned about “off-label” use of medications. Neither Methimazole nor Ipodate is licensed for use in animals; it is simply too expensive for pharmaceutical companies to pursue this kind of registration. The FDA recognizes that most animal diseases could not be treated if veterinarians were restricted to prescribing only those medications licensed for animal use; however, the FDA expects off-label drugs to be used only if there is extensive literature published supporting their use. Ipodate’s use in hyperthyroid cats is still newly recognized and not widely published whereas Methimazole’s use has been well reported for over ten years. Most veterinarians choose to reserve Ipodate for cats unable to tolerate Methimazole. If a cat has not had a clear response to ipodate after 6 weeks of treatment, one of the other treatment methods should be selected.



    In hyperthyroid cats with compromised kidney function, a trial course of antithyroid drug therapy may be advisable prior to more permanent treatment modalities (thyroidectomy or radioiodine). Deterioration of kidney function may occur in some cats after correction of the hyperthyroid state. If no decompensation of kidney function develops when normal thyroid levels are achieved by methimazole treatment, then more permanent intervention may be attempted.



    Hypothyroidism



    Naturally occurring hypothyroidism (decreased T-4 and T-3 production resulting from a loss of functioning thyroid tissue) is an extremely rare clinical disorder in the adult cat. However, hypothyroidism can be created in adult cats by complete surgical removal or radioiodine destruction of the thyroid gland in the treatment of hyperthyroidism. Kittens may develop a congenital hypothyroidism resulting from defects in thyroid hormone synthesis.



    The clinical signs associated with hypothyroidism in the adult cat include lethargy, weight gain, dullness, low body temperature, dry scaly skin, matting of hair, and possibly hair loss. Kittens afflicted with hypothyroidism may also show retarded growth (with an enlarged head and short neck and limbs) and constipation.



    A tentative diagnosis of hypothyroidism can be made on the basis of clinical signs, physical examination, exclusion of nonthyroidal disease, and the finding of a low blood T4 concentration. However, because many factors can falsely lower blood T4 levels, a definitive diagnosis of hypothyroidism usually requires thyroid function testing (i.e., TSH response test or thyrotropin-releasing hormone stimulation test).



    Treatment of hypothyroid cats consists of administering a thyroid hormone supplement. Dosage of the supplement is adjusted based on clinical response and serial blood T-4 concentrations. In hypothyroid kittens, dullness, constipation, and growth abnormalities may persist despite thyroid hormone supplementation,







    . Hyperparathyroidism



    The parathyroid glands are sensitive to the balance of calcium and phosphorus in the blood. If there is a chronic excess of phosphorus or a deficit of calcium, the parathyroid glands will overproduce the parathyroid hormone (PTH) resulting in secondary hyperparathyroidism. This overproduction causes calcium to be removed from the bones to reestablish the proper calcium-to-phosphorus ratio in the blood. Secondary hyperparathyroidism may develop as a result of kidney disease or feeding all-meat diets.



    In contrast, primary hyperparathyroidism is caused by a tumor of one or more parathyroid glands that results in an overproduction of PTH that is totally unrelated to the calcium-to-phosphorus ratio in the blood. in fact, the increased PTH in this instance causes hypercalcemia (high blood-calcium concentration). Primary tumors of the parathyroid glands are rare in the cat. When they occur, they seem to develop more commonly in older female Siamese cats. The most common clinical signs of primary hyperparathyroidism in cats are lethargy and inappetance.



    Primary hyperparathyroidism may be suspected when a cat with appropriate clinical signs is found to be consistently hypercalcemic on screening laboratory tests. However, other causes of hypercalcernia (e.g., nonparathyroid tumors, vitamin D toxicity, kidney disease, hypoadrenocorticism, and spurious factors) must be ruled out. Determination of blood concentrations of PTH and ionized calcium may help differentiate among these causes of hypercalcemia.



    Treatment of primary hyperparathyroidism involves surgical removal of the parathyroid tumor. Postoperatively, the blood-calcium concentration might fall too low, until the remaining parathyroid glands resume their function. Temporary vitamin D and calcium supplementation may be required during this transition.







    Hypoparathyroidism



    In the cat, the most common cause of hypoparathyroidism is inadvertent injury or removal of the parathyroid glands during thyroidectomy for hyperthyroidism. In contrast, naturally occurring hypoparathyroidism is a rare disorder in the cat, affecting mainly young to middle-aged cats. The most common clinical signs of hypoparathyroidism, regardless of cause, are lethargy, inappetance, and muscle tremors.



    The diagnosis of hypoparathyroidism is based on history, clinical signs, laboratory evidence of hypocalcemia and hyperphosphatemia (high blood-phosphorus concentration), and exclusion of other causes of hypocalcemia (e,g., phosphate enema toxicity, kidney failure, pancreatitis, intestinal malabsorption). if naturally occurring hypoparathyroidism is suspected, the disorder may be confirmed by determination of blood PTH concentrations or biopsy of parathyroid tissue.



    Treatment of hypoparathyroidism, regardless of cause, includes the use of calcium supplements and vitamin D. With naturally occurring hypoparathyroidism, long-term management is necessary; however, with hypoparathyroidism following thyroidectomy, calcium and vitamin D therapy usually may be tapered off and eventually discontinued based on results of serial blood-calcium concentrations.





    Hyperadrenocorticism



    Hyperadrenocorticism (Cushing's syndrome) results from excessive production of glucocorticoids by the adrenal glands. The syndrome appears to be quite rare. Most cases of hyperadrenocorticism in the cat are caused by overstimulation of the adrenal glands by a pituitary tumor, or by an overly active pituitary gland producing excess amounts of ACTH; the remaining cases result from functional adrenal tumors. Hyperadrenocorticism occurs mainly in middle-aged to older cats, with a slightly greater incidence in females.



    The most common clinical signs associated with hyperadrenocorticism, in cats include excessive drinking and urinating, increased appetite, enlarged abdomen, hair loss, thin skin, and lethargy. A cat afflicted with Cushing's syndrome may also exhibit extreme fragility of the skin that results in skin tears during routine handling.



    Cats with hyperadrenocorticism are predisposed to developing diabetes mellitus because of the effects of chronic glucocorticoid excess on blood sugar metabolism. In fact, more than 90 percent of the cats with hyperadrenocorticism have concurrent diabetes mellitus. Interestingly, many of these cats with hyperadrenocorticism and secondary diabetes mellitus require exceptionally high doses of insulin (more than 1 to 2 units per pound of body weight per day), because the excess glucocorticoids antagonize the actions of the insulin.



    The ideal diagnostic testing protocol for hyperadrenocorticism in cats is still unknown, but helpful procedures include adrenal function testing (e.g., dexamethasone suppression test), measurement of ACTH concentrations, and radiographic studies (e.g., ultrasound, computed tomography).



    In general, surgical removal of the adrenal gland(s) -adrenalectomy-appears to be the most successful means of treating cats with hyperadrenocorticism. Only the affected adrenal gland is removed in cats. with a functional adrenal tumor, whereas both adrenal glands are removed in cats with an overstimulating pituitary tumor/gland. Permanent replacement therapy with glucocorticoids and mineralocorticoids is necessary in cats that have had both adrenal glands removed. Temporary glucocorticoid supplementation may be required in cats following removal of the adrenal gland tumor.



    Unfortunately, drugs used in dogs with Cushing's syndrome to destroy the adrenal cortex or block glucocorticoid synthesis do not seem to be consistently effective in the cat. Similarly, radiation therapy directed at the causative pituitary tumor has had variable results in cats.





    Hypoadrenocorticism



    Naturally occurring hypoadrenocorticism (also known as primary hypoadrenocorticism or Addison's disease) is caused by destruction of the adrenal cortices. The resultant deficiency of both glucocorticoids and mineralocorticoids causes the clinical signs observed. Primary hypoadrenocorticism is a rare disease in the cat.



    The most common clinical signs of primary hypoadrenocorticism in the cat are lethargy, inappetance, and weight loss. Vomiting and diarrhea are less frequently encountered. in some cats, the symptoms may wax and wane. Physical examination may reveal depression, weakness, dehydration, and low body temperature.



    Primary hypoadrenocorticism should be suspected in a cat with appropriate clinical features and laboratory abnormalities. Classic laboratory findings in a cat with Addison's disease include low blood sodium and high blood potassium concentrations (resulting from the lack of mineralocorticoids), as well as hyperphosphatemia, azotemia, (excess urea in the blood), and mild anemia. However, these laboratory findings also can be seen with other diseases. The most accurate screening test for hypoadrenocorticism is the ACTH stimulation test, in which the response of the adrenal glands to a test dose of commercial ACTH is evaluated.



    Therapy for the cat with primary hypoadrenocorticism consists of lifelong glucocorticoid and mineralocorticoid supplementation, either oral or injectable. Initial treatment also may require fluid administration. The dosage of mineralocorticoid replacement is adjusted based on the results of serial blood sodium and potassium concentrations.



    Secondary hypoadrenocorticism develops when pituitary ACTH secretion is deficient, resulting in inadequate stimulation of adrenal glucocorticoid production. Certain drugs containing glucocorticoids or progesterone can inhibit pituitary ACTH secretion. The resultant deficiency in glucocorticoid production may result in clinical signs similar to those observed in primary hypoadrenocorticism, except the electrolyte (sodium and potassium) disturbances associated with mineralocorticoid deficiency arc absent.





    Diabetes mellitus



    Diabetes mellitus, a common endocrine disorder in the cat, is caused by decreased insulin production by the pancreatic islet cells, or decreased responsiveness of the cat's body cells to the action of insulin. When insulin quantity or activity is decreased, most body tissues cannot use glucose. Hyperglycemia (high blood sugar concentration) and subsequent glucosuria (sugar in the urine) rapidly develop. The glucosuria leads to excessive urination and thirst. Because the body's cells cannot use the available glucose, lethargy and weight loss develop, despite a good appetite. As the disease progresses, derangements in fat and protein metabolism accelerate, causing inappetance, vomiting, weakness, and dehydration.



    Diabetes mellitus occurs in cats of any age, breed, or sex, but typically it is seen in aged (older than ten years), obese (over fifteen pounds), castrated male cats. A veterinarian's diagnosis of diabetes mellitus is based on clinical signs, physical examination, laboratory tests, and the persistent presence of hyperglycemia and glucosuria. Diagnosis usually is not based on a single elevated blood sugar test, especially in the cat with equivocal clinical signs, because stressed cats can have temporary sugar levels that are abnormally high. The presence of ketones, a by-product of the body's digestion of its own tissues to produce energy when sugar cannot be metabolized, in urine or blood indicates the disease has progressed.



    Proper treatment of diabetes mellitus is based on the severity of the disorder. Diabetic cats that are ill (i.e., inappetance, vomiting, dehydration) with ketones in their blood and urine require intensive care. Their hospitalized treatment program will probably include fluid therapy to correct dehydration and electrolyte abnormalities, and short-acting insulin (e.g., regular insulin given frequently during the day) to lower blood glucose and stop ketone production. Once the ill diabetic cat starts to feel better (i.e., eating with no vomiting, normal hydration), then the fluid therapy is tapered off and discontinued, and a longer acting insulin given once or twice a day is substituted for the short-acting insulin.



    In diabetic cats that are not ill, the longer acting insulins (NPH insulin, lente insulin, or ultralente insulin) given once or twice a day by injection under the skin may be started initially. Alternatively, in diabetic cats that are not ill and do not have ketones, an attempt may be made for management without insulin treatment by use of dietary modification and oral hypoglycemic drugs, These cats should be monitored carefully; if they become ill, develop ketones, or remain persistently hyperglycemic, then insulin therapy should be initiated.



    INSULIN. In general, home therapy for diabetic -cats involves the injection of ultralente insulin once or twice daily, or NPH or lente insulin twice daily, or NPH or lente insulin twice daily. Selection of the type and dose frequency of insulin of an individual diabetic cat should be based on eighteen- to twenty-four-hour blood glucose profiles following insulin administration. These in-hospital profiles involve frequent determinations of blood glucose values throughout the day to assess how long the insulin action lasts and how effectively the insulin lowers the blood glucose. The dose of insulin is also variable for each cat and may need to be adjusted based on blood glucose profiles, intermittent blood glucose determinations, clinical response, and at home urine glucose monitoring. Obtaining a urine sample from a diabetic cat to check urine glucose may be facilitated by using nonabsorbent Kitty Litter substitutes, such as plastic beads or aquarium gravel.



    One of the most potentially dangerous complications of insulin therapy is hypoglycemia (low blood sugar). Signs of hypoglycernia include weakness, lethargy, wobbly gait mimicking a drunken state, convulsions, and coma. Should these signs develop, you should offer the cat its normal food if it will eat, or rub a tablespoon of Karo syrup on its gums. Food or fluids should never be forced down the mouth, nor should fingers be placed inside the mouth of a convulsing cat. If no response to food or Karo syrup is observed within a few minutes, the cat should be taken to a veterinarian. Whenever signs of hypoglycemia occur, your cat's veterinarian should be contacted and subsequent doses of insulin should be reduced until appropriate insulin dosage adjustments can be made based on the results of serial blood glucose determinations.



    Some diabetic cats lose their need for insulin injections. These temporary diabetics may develop hypoglycemia as their insulin requirements gradually decrease. Once the diabetic state has resolved, these cats may go for weeks to years without requiring insulin, although diabetes mellitus may recur.



    In contrast, other diabetic cats seem to require excessive doses of insulin (greater than 1 to 2 units of insulin per pound of body weight per day). These cats may have concurrent diseases (e.g., hyperadrenocorticism, infections, acrornegaly) that are blocking insulin's action, technical problems with insulin administration (e.g., inadequate mixing of the insulin, outdated or denatured insulin), poor absorption of insulin, too rapid metabolism of insulin, or even overdosage of insulin. Your cat's veterinarian can help you sort out most of these conditions by careful history, thorough physical examination, screening laboratory tests, and a blood glucose profile.



    DIET. Obese diabetic cats should lose weight to better control their diabetes. The weight loss should be gradual, with no greater a loss than 3 percent of body weight weekly. High-fiber diets have been recommended in the management of diabetic cats, because they help promote weight loss and may help control the increase in blood glucose after eating. Thin diabetic cats should be fed a high-calorie diet initially and then be switched to a lower calorie, high-fiber diet once their ideal body weight is reached.



    Diabetic cats receiving insulin should have their meals spaced according to their insulin administration. With once-daily injection of insulin, the cat is fed one-half of its food at the time of insulin injection and the remainder at the time of peak insulin activity (about eight to twelve hours later). When a cat is receiving insulin twice daily, feedings should coincide with insulin injections. Diabetic cats that are being given oral hypoglycemic drugs rather than insulin should be encouraged to eat several small meals throughout the day to minimize the increase in blood sugar after eating.



    ORAL HYPOGLYCEMIC DRUGS. Oral hypoglycemic drugs are not "oral insulins," but rather drugs that stimulate insulin secretion from the cat's own pancreatic islet cells. The oral hypoglycemic drug that is most commonly used in diabetic cats is glipizide. Diabetic cats receiving glipizicle should have their blood glucose levels monitored weekly by a veterinarian. The ideal goal of treatment is a normal blood glucose, at which time the dose of glipizicle may be discontinued or tapered. Side effects of glipizide in cats include vomiting, inappetance, and liver damage. If the diabetic cat receiving glipizide becomes ill, develops ketones, or remains persistently hyperglycemic after one to two months of treatment, then the glipizide should be discontinued and insulin therapy should be started.





    Pancreatic Islet Cell Tumors



    Pancreatic islet cell tumors (e..g., insulinoma, gastrinorna) are extremely rare in the cat. Insulin-secreting islet cell tumor (insulinoma) seems to occur most commonly in older, castrated, male Siamese cats. Clinical signs are related to hypoglycemia and include weakness and convulsions. Laboratory findings of hypoglycemia and increased blood insulin concentration are consistent with the diagnosis of insulinoma. Treatment has included surgical removal of the insulinoma. and medical management with frequent feedings and oral glucocorticoids. Unfortunately, most insulinomas in cats seem to be malignant.



    Gastrin-secreting pancreatic tumor (gastrinoma) results in vomiting and weight loss. The increased gastrin secreted by these tumors causes excessive production of stomach acid that leads to intestinal ulcers. Possible treatment includes surgical removal of the tumor and management of the ulcers with antacids.





    Acromegaly



    Acromegaly occurs when there is an excess of growth hormone (GH) in an adult cat. Although uncommon, acromegaly in the cat is most often caused by a GH-secreting pituitary tumor. Most of the cats diagnosed with acromegaly have been middle-aged or old, and male.



    The clinical features of acromegaly are caused by the excess GH. They include large head and paws, forward-jutting lower jaw, weight gain, enlarged abdomen, thick skin, and enlargement of many of the organs in the body (e.g., heart, liver, kidneys). The overgrown heart and kidneys may fail as the disease progresses.



    Cats with acromegaly are prone to the development of diabetes mellitus because of the effect of chronic GH excess on blood sugar metabolism. So far, all the cats diagnosed with acromegaly have had concurrent diabetes mellitus. In fact, cats with acromegaly and secondary diabetes mellitus require very large doses of insulin (greater than I to 2 units per pound of body weight daily), because the excess GH antagonizes the action of insulin.



    Acromegaly should be suspected in any diabetic cat that is persistently hyperglycemic throughout the day despite daily insulin doses exceeding 20 units, especially if accompanied by clinical signs characteristic of acrornegaly (e.g., weight gain, changes in facial features and body dimensions). The definitive diagnosis of acromegaly generally requires finding increased blood GH concentrations. However, because GH determinations in the cat are not performed by most laboratories, a tentative diagnosis is based on characteristic clinical and laboratory features, normal results on thyroid and adrenal testing, and demonstration of a pituitary tumor by brain scan. Measurement of somatomedin C (a substance produced in response to GH) also may be helpful diagnostically.



    Acromegaly can be treated in three ways: surgical removal of the pituitary tumor, radiation of the pituitary tumor, or drugs that inhibit GH secretion. Unfortunately, at this time, there does not appear to be a consistently effective treatment for acromegaly in cats. Surgical removal of GH-secreting pituitary tumors has not been evaluated in cats. Radiation of the pituitary tumor is temporarily effective in lowering GH levels in some cats, yet ineffective in other cats. Long-acting somatostatin, a drug that inhibits GH secretion in people with acromegaly, does not have the same effect in acromegalic cats.





    Diabetes insipidus



    Diabetes insipidus is caused by deficient pituitary secretion of vasopressin (also called antidiuretic hormone or ADH), or by the kidneys' inability to respond to the vasopressin hormone. The kidneys' inability to respond to vasopressin can be caused by various drugs and diseases. The reasons for the pituitary's decreased secretion of vasopressin include pituitary tumor, pituitary cyst, head trauma, and unknown factors. The following discussion pertains to deficient secretion of vasopressin by the pituitary gland.



    All the cats diagnosed with diabetes insipidus have been kittens or young adults, and most have been males. The major clinical signs of this rare condition are extreme thirst and the elimination of vast quantities of urine.



    .The diagnosis of diabetes insipidus requires that it be differentiated from other, more common causes of increased drinking and urinating in the cat, such as kidney failure, diabetes mellitus, and hyperthyroidism. A veterinarian can help distinguish many of these disorders by evaluating the cat's history, performing a complete physical examination, and completing some laboratory tests (e.g., routine hemogram, serum biochemical profile, analysis of the urine, T4 concentration). However, definitive diagnosis of diabetes insipidus requires more extensive testing; these additional in-hospital procedures monitor the cat's ability to make more concentrated urine as water is withheld and following an injection of vasopressin.



    The treatment of choice for diabetes insipidus is desmopressin (DDAVP), a synthetic form of vasopressin. Desmopressin is available as a nose spray for people that can be converted to an eye drop for cats. The number of drops is adjusted to control the excessive drinking and urinating. Adverse side effects of DDAVP are uncommon but could include excess water retention.



ความคิดเห็นที่ 30

F_kornvika@hotmail.com (Guest)
14 ก.ค. 2548 12:54
  1. ตำแหน่งต่างๆของต่อมไร้ท่อมีอยู่ที่ไหนบ้างคะ

    แล้วสามารถบอกตำแหน่งได้อย่างไร



ความคิดเห็นที่ 118

soda_yajok_dream@hotmail.com (Guest)
31 ก.ค. 2549 13:25
  1. จะอธิบายได้หรือไม่ว่า ความสามารถในการตอบสนองต่อ สิ่งเร้าของร่างกายที่ควบคุมโดยระบบต่อมไร้ท่อ แตกต่างจากที่ควบคุม โดยระบบประสาทอย่างไร



ความคิดเห็นที่ 11

kid (Guest)
17 ม.ค. 2548 21:31
  1. Islet of Langerhans คืออะไรหรอคับ



ความคิดเห็นที่ 114

ลี่katoon9636@hotmail.com (Guest)
14 ก.ค. 2549 19:11
  1. อยากทราบว่าต่อมไร้ท่อนี้ชื่อว่าอะไรAdrenal glandมีหน้าที่และความสำคัญอย่างไร



ความคิดเห็นที่ 17

อยากรู้อยากเห็น (Guest)
14 มี.ค. 2548 14:24
  1. Islet of Langerhans คือ ชื่อ cell ที่ตับอ่อน แบ่งเป็น 2 ชนิด คือ แอลฟา กับ เบต้า ที่ต่างกันเห็นๆคือ อัลฟาผลิตฮอร์โมนกลูคากอน(เพิ่มปริมาณน้ำตาลกลูโคสในกระแสเลือด) เบต้าก็ผลิตฮอร์โมนอินซูลิน(ช่วยลดปริมาณน้ำตาลในกระแสเลือด ก็คือเอาไปใช้นั่นแหละ)



ความคิดเห็นที่ 56

sky_upk7@hotmail.com (Guest)
13 ก.ย. 2548 12:10
  1. อยากทราบว่าใน exocrine pancreas มีเซลล์ที่สร้าง pancreatic juice ประกอบด้วยเซลล์ชนิดใดบ้าง สร้างอะไรบ้าง ตอบให้ด้วยนะคะ จะเป็นพระคุณอย่างสูง

แสดงความคิดเห็น

กรุณา Login ก่อนแสดงความคิดเห็น