NURS 245 Ch. 41 part one: Disorders of Endocrine Control of Growth and Metabolism

hypofunction

underproduction of a hormone

what causes hypofunction

congenital defects; disruption in blood flow, infection, inflammation, autoimmune, neoplastic growth; decline in function; atrophy from drug therapy; receptor defects

hyperfunction

excessive hormone production

what causes hyperfunction?

excessive stimulation and hyperplasia of the endocrine gland, hormone-producing tumor on a gland

primary endocrine disorders

originate in the target gland that is responsible for producing the hormone

secondary endocrine disorders

target gland is normal, but its function is altered by defective levels of stimulating hormones or releasing factors from the pituitary system

tertiary endocrine disorders

result from hypothalamic dysfunction and both the pituitary and target organ are understimulated

releasing hormones

tell the pituitary what to release into the blood

trophic hormones

from pituitary; tell specific peripheral glands to grow and produce their hormones

adenomas are the most common cause of

pituitary disorders

adenomas effect of mass and on hormone secretion

the mass can cause pressure in the skull that causes headaches, seizures drowsiness, visual deficits. the effect on hormone secretion depends on the cells and location involved that can alter the release of hormones

direct and indirect control of hormones

the hypothalamus' control of growth hormone release

GHRH stimulates the anterior pituitary to release growth hormone, somatostatin inhibits the release

GH secretion is stimulated by

hypoglycemia, fasting, starvation, stress

GH secretion is inhibited by

increased glucose levels, free fatty acid release, obesity, cortisol

functions of the growth hormone

promotes growth through increased bone and cartilage, size and function of organs, and lean muscle mass via IGF-1 release in the liver.

promotes anti-insulin effects in adipose tissue with increased lipolysis and decreased adiposity and through carbohydrate metabolism decreases glucose use and increases blood glucose

dwarfism

deficit in growth hormone production and release. idiopathic GH deficiency (lack in hypothalamus), pituitary tumors and agenesis of pituitary (cannot product GH)

Laron-type dwarfism

hereditary defect in IGF production

gigantism

excess in GH prior to puberty and fusion of epiphysis

acromegaly

excess GH secretion in adults that is often associated with an adenoma. bones will become broader and heavier, soft tissue will grow causing enlarged hands and feet, along with changes in facial features.

what happens when there is an excess in GH in adults?

overgrowth of cartilaginous parts of the skeleton, enlargement of organs including the heart, metabolic disturbances that alter fat metabolism and impairs glucose tolerance

causes of acromegaly

most of the time, somatotrope adenoma. other causes include excess secretion of GHRH by hypothalamic tumors, ectopic GHRH secretion by nonendocrine tumors like carcinoid tumors, ectopic secretion of GH by nonendocrine tumors.

treatment for acromegaly

normalize GH response to oral glucose load, normalize IGF-1 levels to age and sex match, remove tumor or mass, relieve central pressure effects, improve adverse clinical features

thyroid hormones

T3 and T4 - released in response to TSH. disorders can result from pituitary or thyroid gland dysfunction causing goiter, hyperthyroidism, hypothyroidism

negative feedback loop in hypothalamus-pituitary-thyroid gland

a stimulus such as cold or stress will cause the hypothalamus to increase secretion of TRH in to the blood. pituitary glandular cells will increase secretion of TSH into circulation, causing the thyroid gland to increase T3 and T4 into the blood. target cells will see this and increase metabolism. the negative feedback loops occurs in response to high levels of T3 and T4, inhibiting secretion of TSH and TRH.

how do thyroid hormones effect peripheral tissues?

elevates rates of oxygen consumption and energy, increases heart rate and contraction (BP), increases sympathetic sensitivity, maintains sensitivity of respiratory centers, stimulates erythrocytosis, stimulates endocrine activity in tissues, accelerates turnover of minerals in bone

hypothyroidism

decreased metabolic rate, accumulation of hydrophilic mucopolysaccharide substance (myxedema) in connective tissues, elevates serum cholesterol

hyperthyroidism

increased metabolic rate and oxygen consumption, increased use of metabolic fuels, increased sympathetic nervous system responsiveness

manifestations of hyperthyroidism

thyroid storm, restlessness and irritability, wakefulness, increased CO, tachy and palpitations, diarrhea and increased appetite, dyspnea, heat intolerance, diaphoresis, thin and silky skin and hair, weight loss

thyroid storm

very high fever, extreme cardio (tachy, congestive failure, angina), CNS effects (agitation, restlessness, delirium) high mortality rate.

manifestations of hypothyroidism

mental and physical sluggishness, somnolence, decreased CO and brady, constipation, decreased appetite, hypovent, cold intolerance, coarse dry skin and hair, weight gain, myxedema in severe cases (nonpitting in face)

somnolence

sleepiness

myxedema coma

severe hypothyroidism; acute hypotension, hypoglycemia, hypothermia that can cause loss of consciousness

endemic goiter

hypothyroid condition in regions with low iodine levels in soil and food

goitrogens

food that contains elements to block synthesis of triiodothyroinine (T3) and thyroxine (T4)

toxic goiter

results from hyperactivity of thyroid gland

hyperthyroidism

grave's disease (autoimmune), thyroid tumors that cause hypermetabolism, toxic goiter, exophthalamos

grave's disease

autoimmune disorder in which the body makes abnormal antibodies directed against thyroid follicular cells. they mimic TSH which stimulates TH release. metabolic rate is increased, sweating, rapid and irregular heartbeats, nervousness, weight loss x

hypothyroidism

iodine deficit (endemic goiter), hashimoto thyroiditis, tumor, cretinism

congenital hypothyroidism

thyroid hormone is essential for normal growth and development. untreated cases cause mental retardation and impairment of physical growth - manifestations here are referred to as cretinism.

cretinism

results in short stature and cognitive defects that can be related to iodine deficit during pregnancy or untreated congenital hypothyroidism.

hashimoto thyroiditis

autoimmune disorder in women that destroys the thyroid, causing hypothyroidism

how are thyroid disorders measured?

measures of T3, T4, TSH; resin uptake, thyroid autoantibodies, radioiodine uptake test, thyroid scans, ultrasonography, CT and MRI scans, fine-needle aspiration biopsy of nodule

mineralocorticoids (aldosterone)

function in sodium, potassium, and water balance

glucocorticoids (cortisol)

aid in regulating metabolic functions of body and controlling inflammation. essential for survival in stressful situations

adrenal sex hormones (androgens)

serve mainly as a source of androgens for women

what are the actions of cortisol?

plasma proteins increase and immune systems are suppressed. catabolism increases, which causes muscle breakdown, free fatty acid increase, blood sugar increase, and SNS response increase

adrenal cortical insufficiency

inability to make all 3 hormones: primary adrenal being Addison disease, secondary adrenal cortical insufficiency, acute adrenal crisis

excessive adrenal secretion

glucocorticoid hormone excess (Cushing syndrome), hyperaldosteronism

congenital adrenal hyperplasia

decreased cortisol synthesis - other hormones may be increased or decreased

primary adrenal cortical insufficiency (Addison Disease)

aldosterone and cortisol levels are decreased, ACTH levels are elevated because of a lack of feedback inhibition

ACTH

adrenocorticotropic hormone

secondary adrenal cortical insufficiency

occurs as a result of hypopituitarism or because the gland has been removed. lack of ACTH.

acute adrenal crisis

bilateral adrenal hemorrhage, life-threatening situations of dehydration, acute hypotension, vascular collapse, muscle weakness

Addison disease

deficiency of adrenocorticoid secretions caused by an autoimmune reaction. the adrenal gland may be destroyed by hemorrhage or infection.

what causes addison disease?

destruction of the adrenal gland and glucocorticoid insufficiency.

clinical findings of Addison disease

anorexia and weight loss, fatigue and weakness, GI symptoms, myalgia and arthralgia, orthostatic hypotension, hyponatremia, hyperkalemia, hyper pigmentation, decreased blood volume

hypercortisolism (cushing syndrome)

pituitary form: excessive production of ACTH by a tumor of the pituitary gland

adrenal form: benign or malignant adrenal tumor

ectopic form: nonpituitary ACTH-secreting tumor

latrogenic: long-term glucocorticoid treatment

manifestations of hypercortisolism

altered fat metabolism, muscle weakness and wasting, purple striae, osteoporosis, derangements in glucose metabolism, hypokalemia, gastric acid secretion, hirsutism, acne, menstrual irregularities

Cushing syndrome appearance changes

round and ruddy face, truncal obesity with fat pad between scapulae, thin limbs and hair, fragile skin and striae

cushing syndrome

retention of sodium and water, suppression of immune response and stimulation of erythrocyte production. emotional lability and euphoria, increased catabolism of bone and proteins, delayed healing, increased insulin resistance and glucose intolerance

compare and contrast of addison disease and cushing syndrome

both have high risk of infection and poor stress response.