Endocrine Patho Ogena

8/14/2019 Endocrine Patho Ogena

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Hypothyroidism results from decreased levels of

circulating thyroid hormone. may result from malfunction of the

thyroid gland, the pituitary, or thehypothalamus.


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Myxedema the non-pitting, boggy edema

eyesFeet

hands

and infiltrates other tissues aswell.


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thyroid gland malfunction

low TH levels high TSH

high TRH


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pituitary malfunction

low levels of TH low TSH.

High TRH


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Medically-induced hypothyroidism

previous thyroid therapy

surgery radioiodine therapy

drugs such as cytokines,

amiodarone, and lithium.


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Hashimoto's disease also called autoimmunethyroiditis autoantibody destruction of

thyroid gland tissue.


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Hashimoto's diseaseThis results in decreased TH, with

increased TSH and TRH levels

caused by minimal negativefeedback. cause of autoimmune thyroiditis is

unknown but there appears to be a genetic

tendency to develop the disease


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Endemic goiter hypothyroidism caused by a

dietary deficiency of iodide.A goiter is an enlargement

of the thyroid gland.


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Endemic goiter Goiter occurs with a deficiency of iodide

because the thyroid cells becomeoveractive and hypertrophic (larger) in anattempt to sequester all possible iodidefrom the bloodstream.

Low TH levels are accompanied by highTSH and TRH because negative feedback isminimal.


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Thyroid carcinoma

may causehypothyroidism orhyperthyroidism.


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Thyroid carcinoma Treatment of this rare cancer may include

thyroidectomyTSH suppression drugs

radioactive iodine therapy to destroy thyroidtissue.

All of these treatments may result inhypothyroidism.


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Thyroid carcinoma Exposure to radiation, especially during

childhood, is a cause of thyroid cancer. Iodine deficiency may also increase the

risk of developing thyroid cancer

because it stimulates thyroid cellproliferation and hyperplasia


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Sluggishness, slow thinking, andclumsy, slow movements.

Decreased heart rate, enlarged heart(myxedemic heart), and decreasedcardiac output.

Bogginess and edema of the skin,

especially under the eyes and in theankles.


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Intolerance to cold temperatures.Decreased metabolic rate, decreased

caloric requirements, decreasedappetite and nutrient absorption acrossthe gut.

Constipation.

Change in reproductive function.Dry, flaky skin and brittle, thin bodyand head hair


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Diagnostic Tools A good history and physical examination

Blood tests measuring levels of TH (bothT3 and T4), TSH, and TRH will allowdiagnosis of the condition andlocalization of the problem at the level of

the central nervous system or thethyroid gland.


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Complications Myxedema coma

a life-threatening situationcharacterized by exacerbation(worsening) of all symptoms ofhypothyroidism, including

hypothermia without shivering,hypotension, hypoglycemia,hypoventilation, and a decrease inconsciousness resulting in coma.


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Death can occur without TH replacementand stabilization of symptoms.

There are also risks associated with the

treatment of thyroid deficiency. Theserisks include hormone over-replacement,anxiety, muscle wasting, osteoporosis andatrial fibrillation.


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TreatmentTreatment always includes replacement of

thyroid hormone with synthetic thyroxine. For endemic goiter, iodide replacement

may relieve symptoms. If the cause of hypothyroidism is related to

a central nervous system tumor, it may betreated with chemotherapy, radiation, orsurgery.


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Hyperthyroidism is excessive levels of circulating TH.

can result from dysfunction of thethyroid gland, pituitary, orhypothalamus.

Thyroid gland malfunction

Increase Th

decreased TSH and TRF


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Pituitary Gland Malfunction high TH and high TSH.

low TRH Hypothalamus Malfunction

TH accompanied excess TSH and TRH.


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Graves' disease the most common cause of

hyperthyroidism

an autoimmune disorder characterized by production of

autoantibodies that mimic the action ofTSH on the thyroid gland.

These IgG autoantibodies, termedthyroid-stimulating immunoglobulins,turn on the production of TH, but are notinhibited by rising levels.


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TSH and TRH levels are low because theyare inhibited by high TH.

cause is unknown genetic predisposition to autoimmune

disease. Women in their 20s and 30s are most

often diagnosed, although the disease

may start during the teen years.


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an increase in the size of the thyroid glandcaused by increased demand for thyroidhormone.

Increased demand for thyroid hormoneoccurs during periods of growth or excessmetabolic demand such as puberty orpregnancy.

In these cases, increased TH is caused by

metabolically driven activation of thehypothalamus, and therefore isaccompanied by increased TRH and TSH.


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When the demand for thyroid hormone is lessened, thethyroid gland usually returns to its previous size.

Occasionally, irreversible changes may have occurredand the gland does not regress.

The enlarged thyroid may continue to produce excessTH. If the individual remains hyperthyroid, thecondition is referred to as a toxic nodular goiter.

Pituitary adenomas of TSH-producing cells orhypothalamic diseases rarely occur.


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Increased heart rate. Increased muscle tone, tremors, irritability, increased

sensitivity to catecholamines. Increased basal metabolic rate and heat production,

intolerance to heat, excess sweating.

Weight loss, increased hunger. A staring appearance. Exophthalmos (bulging of the eyes) may develop. Increased number of bowel movements. Goiter (usually), which is an increase in the size of the

thyroid gland. Changes in skin and hair condition may occur. Reproductive irregularities.


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A good history and physical examination.Blood tests measuring levels of TH (both T3

and T4), TSH, and TRHlocalization of the problem at the level of the

CNS or the thyroid gland.Decreased serum lipids may accompany

hyperthyroidism.Decreased sensitivity to insulin, which may

result in hyperglycemia


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Arrhythmiasare common in patients with

hyperthyroidismmay be the presentingsymptom of the disorder


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A life-threatening complication ofhyperthyroidism is thyrotoxic crisis (thyroidstorm) which may develop spontaneously in

patients with hyperthyroidism undergoingtherapy or during surgery on the thyroidgland, or may occur in undiagnosedpatients with hyperthyroidism.

The result is a large burst of TH releasethat causes tachycardia, agitation, tremors,hyperthermia (up to 106F), and, ifuntreated, death.


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depends on the site and causeof hyperthyroidism.

Thyroid gland:anti-thyroid drugs that blockTH productionbeta-blocking drugs todecrease sympathetic hyper-responsiveness.


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Drugs that destroy thyroid tissue also maybe used. radioactive iodine (I131) administered inoral form is actively taken up byhyperactive thyroid cells.

I131 destroys the cells. a permanent treatment forhyperthyroidism and frequently results in

the individual becoming hypothyroid andrequiring lifelong TH replacement.


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Partial or total thyroidectomy may be atreatment choice

Total thyroidectomy

Percutaneous ethanol injection of thethyroid benign thyroid nodule and those withincreased surgical risk due to cardiac

or pulmonary diseases, advanced age,multimorbidity, or dialysis.


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Adrenal insufficiency a decrease in the circulating level of the

glucocorticoids.

The mineralocorticoid aldosterone may alsobe reduced. may be caused by dysfunction of the adrenal

gland, called primary adrenal insufficiency

by dysfunction of the pituitary orhypothalamus. Both of these latter conditionscause secondary adrenal insufficiency


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Primary adrenal insufficiency is characterized by low levels

of glucocorticoids, especiallycortisol

accompanied by high ACTH andhigh CRH


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If the entire adrenal gland is destroyed ormalfunctioning adrenal androgens and aldosterone will be low.

If only the glucocorticoid-secreting cells aremalfunctioning the high ACTH levels that accompany primary

adrenal insufficiency will cause high levels ofcirculating adrenal androgens.

Aldosterone secretion is primarily determined bythe renin-angiotensin system, but may be slightlyincreased by elevated ACTH


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If the cause of adrenal insufficiency issecondary to a pituitary dysfunction low glucocorticoids will be accompanied by

low ACTH and high CRH. In this case, adrenalandrogens will also be low. If there is zeroACTH, aldosterone levels will be reduced. Ifadrenal insufficiency is caused by a

hypothalamus malfunction, theglucocorticoids, ACTH, and CRH will be low.


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Primary adrenal insufficiencycalled Addison's diseaseoccurs from destruction ofthe adrenal cortex.usually autoimmuneresults from IgG antibodiesdirected against all or partof the adrenal gland.


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also may result from infections such astuberculosis.

Tuberculosis of the adrenal gland is a

common cause of adrenal insufficiencyin developing countries and does nottypically resolve with treatment of theinfection.

Destructive adrenal gland tumors alsomay lead to adrenal insufficiency.


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Addison's diseasecharacterized by low

glucocorticoid levelsaccompanied by high ACTHand high CRH.

Total loss of the adrenalgland results in the loss ofadrenal androgens andaldosterone as well.


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Aldosterone deficiency leads to increasedloss of sodium in the urine, resulting inhyponatremia (decreased sodium in theblood), dehydration, and hypotension

(because water loss in the urine frequentlyaccompanies the loss of sodium). Decreased potassium excretion in the

urine will lead to hyperkalemia (increased

potassium concentration in the blood).


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Secondary adrenal insufficiency can occur as a result of hypopituitarism

or hypothalamic dysfunction. With secondary adrenal insufficiency,

ACTH is not released, so the adrenals donot secrete glucocorticoids or

androgens. Aldosterone synthesis may also be

affected.


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Secondary adrenal insufficiency if cortisol is used therapeutically for anti-

inflammatory purposes.

When one takes pharmacologic levels ofcorticosteroids, the pituitary secretion of ACTHis inhibited in a negative feedback manner.

Judicious treatment of inflammatory illnesses

with glucocorticoids for fewer thanapproximately 10 days will not result inpituitary suppression.


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Depression, because cortisol levelsinfluence mood and emotions.

Fatigue, related to hypoglycemia, and

decreased gluconeogenesis. Anorexia, vomiting, diarrhea, and

nausea. Hyperpigmentation of the skin if ACTH

levels are high (primary adrenalinsufficiency) as a result of ACTH havingmelanin-stimulating hormone likeeffects on the skin.


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Sparse body hair in women, ifthe adrenal cells producing

androgens are destroyed or ifACTH levels are very low. Inability to respond to stressful

situations, perhaps leading tosevere hypotension and shock.


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A good history and physical examination willhelp diagnose glucocorticoid deficiency.

Blood tests measuring levels of CRH, ACTH,and different glucocorticoids will allow

diagnosis of the condition and localization ofthe problem at the level of the CNS oradrenal gland.

Hyponatremia, hyperkalemia, andhypotension may be present if the adrenal

cells that produce aldosterone are destroyedor if ACTH levels are undetectable.


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Adrenal crisis may occur afterphysical or mental stress in anaffected individual. This can be life-threatening and is characterized byvolume depletion, hypotension, andvascular collapse.


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Glucocorticoid replacement such asthe use of hydrocortisone orcortisone acetate is required.

Health providers should monitor thehistory of glucocorticoid doseadjustments; potential adverseevents including any crisis since lastvisit; the individual's ability to cope

with daily stressors; the individual'sbody weight; and signs that suggestover-replacement or under-replacement.


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Monitoring blood pressure, peripheral edema, serumsodium, serum potassium, and plasma renin activityprovides clues to treatment efficacy.

Aldosterone replacement (only in primary adrenalinsufficiency) may be necessary.

Glucocorticoid administration may need to beincreased during periods of stress, includinginfection, trauma, and surgery. Morbidity andmortality are high without treatment.

If the cause of adrenal insufficiency is related to apituitary tumor, it may be treated withchemotherapy, radiation, or surgery.


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Glucocorticoid excess refers to any condition in which there are very

high levels of circulating glucocorticoids.

The cause of glucocorticoid excess may resideat the level of the adrenal gland or at thepituitary/hypothalamic level.

If the cause of glucocorticoid excess is primaryadrenal gland hypersecretion, usually an adrenal tumor present. low ACTH and low CRH levels will be present as a

result of negative feedback from high glucocorticoids. Adrenal androgen levels will be low because ACTH is

low.


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If glucocorticoid excess results from anadenoma of the pituitary cells producingACTH, elevated ACTH also will cause excess adrenal

androgen production. Bronzing of the skin will occur because of

crossover effects between ACTH and melanin-

stimulating hormone. CRH levels will be low as a result of negative

feedback from ACTH and the glucocorticoids.


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Excess ACTH also may occur as a result of theproduction of ACTH by a tumor outside of thepituitary or hypothalamus.

This is referred to as an ectopic (abnormal)source of ACTH. Many tumors demonstrate ectopic production

of ACTH, especially lung tumors.

Excess adrenal androgens and skin bronzingwill accompany ACTH-secreting tumors.


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Cushing's syndrome refers to any condition of high

glucocorticoids

includes glucocorticoid excess caused bytherapeutic administration of corticosteroids.

Cushing's disease refers to high glucocorticoids caused

specifically by malfunction of the anteriorpituitary resulting in excess ACTH


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Altered fat metabolism leading to fat padson the back (subclavian buffalo hump),moon face, protruding abdomen with thinextremities,and stretch marks on breasts, thighs, andabdominal surface. Muscle weakness fromprotein breakdown.

Hypertension as a result of increasedcatecholamine responsiveness.

Weight gain resulting from strong appetitestimulation. Because of effects on hepaticgluconeogenesis, a reversible form ofdiabetes mellitus may result.


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Inhibition of immune and inflammatoryreactions, leading to poor wound healing.

Extreme emotional swings (lability), sometimes

causing psychosis and occasionally resulting insuicide. Masculinization of women and children as a

result of adrenal androgen stimulation if ACTHlevels are high.

Bronzing of the skin if ACTH levels are high.


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A good history and physicalexamination will help diagnoseglucocorticoid excess.

Blood tests measuring levels of CRH,ACTH, and different glucocorticoids willallow diagnosis of the condition andlocalization of the problem at the level

of the CNS or adrenal gland.Loss of normal diurnal (morning)pattern of cortisol release.


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Hyperglycemia, hypernatremia and hypokalemiamay be present because of aldosterone-likeproperties of the glucocorticoids. This can contributeto hypertension and cardiac and neural

irregularities. A dexamethasone challenge test commonly used in clinical practice to evaluate states of

glucocorticoid excess. In healthy individuals, a low dose of dexamethasone will

suppress ACTH secretion; in those with Cushing'ssyndrome, suppression does not occur.


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Morbidity and mortality are highwithout treatment andapproximately 50% of individuals diewithin 5 years.

Causes of death include suicide,overwhelming infections, and

coronary artery disease from severehypertension.


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Correction of high glucocorticoid levelsdepends on the cause of the problem.

Surgery for tumors of the adrenal,

pituitary, or other tissue (e.g., the lung) isfrequently performed. Radiation therapy isdone if a tumor is present.

Drugs that block steroid synthesis may beused if the tumor is inoperable.

Discontinue corticosteroid therapy, byweaning down, if syndrome is caused bymedication.


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the total or relative unresponsiveness of theadrenal glucocorticoid-producing cells toACTH during gestation, resulting in very lowlevels of glucocorticoids and masculinization

of the genitalia in a female fetus.Female masculinization occurs because the androgen-producing

cells of the adrenal gland respond to thecontinuously high levels of ACTH resulting

from little or no negative feedback on ACTHrelease.


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autosomal-recessive genetic alterationwhereby there is a deficiency in one ormore of the five enzymes needed toproduce cortisol.

Mineralocorticoid production (aldosterone)may be affected.The most common enzyme deficiencies

are of 21-hydroxylase or 11-hydroxylase. Enzyme deficiencies may be partial or

total. Carriers of the disorder do not appear tobe affected.


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Masculinization of the female infant is apparent atbirth and may include ambiguous genitalia with an enlarged clitoris, fused labia,

and malformation of the urogenital area.

The degree of abnormality is variable. Male fetuses are usually normal at birth or have slightlyenlarged genitalia.

If aldosterone production is blocked, salt wasting,dehydration, vomiting, hyperkalemia, andhypotension develop.

In the rare case of enzyme 11-deoxycorticosteronedeficiency, mineralocorticoid levels increase,resulting in salt retention, hypokalemia, andhypertension.


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Physical examination at or soon afterbirth will help diagnose the conditionin females.

Blood tests will demonstrate enzymedeficiency in either sex.


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Because cortisol is essential tosurviving even relatively minorstresses, illnesses or surgeries in the

newborn period may be fatal if thediagnosis of congenital adrenalhyperplasia has not been made.

Psychological distress to the child andfamily may result from delayeddiagnosis.


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Cortisol, and possibly aldosterone,replacement therapy will be requiredthroughout life.

Therapy must be monitored andadjusted appropriately for growthand in times of excess physical

stress


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a decrease in circulating levels of GH. Most cells of the body will be affected. is usually clinically recognized only in children. Usually caused by a pituitary adenoma of

another anterior pituitary hormone producing celltype.

can also be a result of hypoxic necrosis (deathcaused by lack of oxygen) and inflammation ofthe pituitary.

ay also be at the hypothalamic level, resultingfrom malnutrition, sleep deprivation, orstimulation of somatostatin released duringperiods of prolonged physical or emotional stress.


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Dwarfism.A reduction of growth potential may

occur in children.Alteration in metabolic functioning,

including insulin resistance andabnormal lipid profile, may occur in

children and adults.


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In children, GH deficiency results inproportional short stature (below thethird percentile for their age).

Affected children have decreasedmuscle mass and increasedsubcutaneous fat stores.

They are typically bright mentally.Short stature different frompredicted based on familial patterns

may be observed if a reduction ingrowth potential occurs.


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Delayed onset of puberty mayaccompany GH deficiency

Adult-onset GH deficiency may result innonspecific changes in functioning,including alterations in physical andmental well-being, cardiac function andmetabolic parameters.

Adults with GH deficiency may

experience lower levels of energy andlibido.


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Diagnostic Tools A good history and physical examination will

help diagnose growth hormone deficiency.

Blood tests measuring decreased levels of GHwill support diagnosis of the condition.

Neuroimaging tests to identify pituitary tumorscan improve diagnosis.

Lack of responsiveness to GH provocation willassist in confirming GH deficiency


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TreatmentTreatment of GH deficiency in children

involves subcutaneous injections ofrecombinant GH several times per weekduring the pubertal years or earlier.Success is greater in children treatedearly.

GH deficiency in adults may also betreated with GH injections.


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Growth hormone excess is the increase in circulating levels of GH. Increased levels of GH result in increased

somatomedin levels and increased growth ofbone, cartilage, and other tissues.

Direct effects of GH on the breakdown ofcarbohydrates and on protein synthesis alsooccur.

Growth hormone excess is usually caused by aGH-secreting tumor of the anterior pituitary.


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Gigantism a disease of excess longitudinal growth of the

bones of the skeleton, is seen as a result of GHexcess before puberty.

Acromegaly a disease of connective tissue proliferation Because long bone growth has stopped in adults,

GH excess cannot cause growth of the skeleton.

It is associated with growth of the cartilage of thehands, feet, nose, jaw, chin, and facial bones. Connective tissue proliferation of internal organs,

including the heart, also occurs.


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Tall stature with gigantism. Thickening of the fingers, jaw, forehead, hands, and feet

with acromegaly. Because GH excess is usually caused by an aggressively

growing adenoma, other hormone-secreting cells of theanterior pituitary are frequently destroyed. symptoms of GH excess often include those associated with

deficiencies of other hormones. For example, if the growing tumor displaces the gonadotropin-

secreting cells of the anterior pituitary, decreased reproductivefunction may occur.

If the tumor affects any other hormone-producing cells,

manifestations particular to that hormone will prevail.Increased intracranial pressure can also occur with a growingtumor. Symptoms include headache, vomiting, andpapilledema (swelling where the optic nerve enters the eyechamber).


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A good history and physical examinationwill help diagnose growth hormoneexcess.

Blood tests measuring increased levels ofGH will support diagnosis of gigantism oracromegaly.

Increased blood glucose levels may bepresent with either condition.

The secretory pattern of GH release is nolonger predictable and is unrelated tosleep with either condition.


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TreatmentTreatment of GH excess is usually by

surgical excision of the GH-secretingtumor. Radiation therapy may also beapplied.

Bromocriptine, a dopamine antagonist,

may be effective in decreasing GHlevels.


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characterized by increased release of ADH fromthe posterior pituitary in the absence of normalstimuli for ADH release.

Increased ADH release usually occurs in response

to increased plasma osmolality (a decrease inplasma water concentration) or, to a lesserextent, decreased blood pressure.

With SIADH, ADH is high in the face of lowplasma osmolality. Plasma osmolality continues

to decrease because of ADH stimulating waterreabsorption by the kidneys. Release of ADHcontinues without feedback control, in spite oflow osmolality and increased blood volume


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most commonly induced by drugs.Other causes of SIADH include

disease, injury, or tumors of the CNS,

pain, stress, and temperatureextremes.Surgery may result in a transient

occurrence of SIADH.Tumors outside the CNS, especially

bronchogenic carcinomas, frequentlyproduce ADH ectopically.


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Clinical Manifestations Water retention and weight gain.

Decreased urinary output. Nausea and vomiting worsening with thedegree of water intoxication.


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Blood tests measuring increasedlevels of ADH with decreased plasmaosmolality and hyponatremia

(decreased sodium concentration,mild: serum sodium decreased to130 mEq/L; severe: serum sodium

below 126 mEq/L) will allowdiagnosis of the condition.


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For mild cases, fluid restriction is adequate tocontrol symptoms until the syndromespontaneously regresses.

If the condition is more severe, diuretics and

drugs that block ADH action on the collectingtubules will be administered. A hypertonicsolution of sodium chloride may occasionallybe used to increase plasma sodiumconcentration.

If ADH is arising from ectopic tumorproduction, treatment will be aimed ateliminating the tumor.


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is a disease of decreased ADHproduction, secretion, orfunction.

The term diabetes insipidusrefers to the quantity and qualityof the urine: the disease isassociated with copious amountsof dull, or tasteless, urine.


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Without ADH, the renal-collectingtubules cannot reabsorb water andcannot concentrate the urine.

may result from a partial or totallack of ADH production by thehypothalamus, or decreased releaseof ADH from the posterior pituitary.


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Clinical ManifestationsLarge volumes of diluteurine.Polydipsia (excessive

thirst).


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Diagnostic Tools Blood tests measuring decreased levels

of ADH with increased plasma osmolalityand hypernatremia will allow diagnosisof the condition.


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Complications Severe dehydration may occur if large

volumes of drinking water areunavailable


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Treatment Drugs are available that mimic the

action of ADH. desmopressin, was previouslyoffered only as a nasal spray forhome use but is now available inpill form.


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is a metabolic disorder characterized byhyperglycemia (elevated serum glucoselevel) resulting from lack of insulin, lack ofinsulin effect, or both.


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Three general classifications arerecognized:

type 1, absolute insulin insufficiency

type 2, insulin resistance with varyingdegrees of insulin secretory defects

gestational diabetes, which emerges

during pregnancy.


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Onset of type 1 usually occurs before theage of 30 years (although it may occur atany age); the patient is usually thin and

requires exogenous insulin and dietarymanagement to achieve control.


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Type 2 usually occurs in obese adults after the age of 40 years treated with diet and exercise antidiabetic drugs insulin therapy.


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Causes

Evidence indicates that diabetesmellitus has diverse causes, including:

heredity

environment (infection, diet, toxins,stress)

life-style changes in geneticallysusceptible persons.


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In persons geneticallysusceptible to type 1 diabetes, atriggering event, possibly a viral

infection, causes production ofautoantibodies against the betacells of the pancreas.

The resultant destruction of thebeta cells leads to a decline inand ultimate lack of insulinsecretion.


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Insulin deficiency leads tohyperglycemia, enhancedlipolysis (decomposition of fat),

and protein catabolism.These characteristics occurwhen more than 90% of the betacells have been destroyed.


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Type 2 diabetes mellitus is a chronicdisease caused by one or more of thefollowing factors: impaired insulin production inappropriate hepatic glucose production peripheral insulin receptor insensitivity Genetic factors are significant, onset is

accelerated by obesity and a sedentary lifestyle. Again, added stress can be a pivotal factor.


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polyuria and polydipsia due to highserum osmolality caused by highserum glucose levels

anorexia (common)

Polyphagiaweight loss (usually 10% to 30%;persons with type 1 diabetes oftenhave almost no body fat at time ofdiagnosis) due to prevention of normal

metabolism of carbohydrates, fats,and proteins caused by impaired orabsent insulin function


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headaches, fatigue, lethargy, reducedenergy levels, and impaired school andwork performance due to low

intracellular glucose levelsmuscle cramps, irritability, and

emotional lability due to electrolyteimbalance

vision changes, such as blurring, due

to glucose-induced swelling


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numbness and tingling due to neuraltissue damage

abdominal discomfort and pain due

to autonomic neuropathy, causinggastroparesis and constipationnausea, diarrhea, or constipation

due to dehydration and electrolyteimbalances or autonomicneuropathy.

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