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Endocrinology
BYU PdBio 305 Dr. Rhees Endocrinology
Question | Answer |
---|---|
endocrine glands | anterior pituitary, posterior pituitary, thyroid, parathyroid pancreas, adrenal cortex, adrenal medulla, ovaries, testes |
receptor | integral membrane protein that receives hormones |
target cell has how many receptors for a particular hormone? | 2000-100,000 |
down-regulation | when a hormone is present in excess the number of target cell receptors may decrease |
steroids | lipids that are derived from cholesterol. These are lipid soluble and will thus cross the plasma membrane and enter cells rapidly. Estrogens, progesterone, testosterone, aldosterone, cortisol |
biogenic amines | synthesized by modifying amino acids; T3 and T4, epinephrine, histamine, serotonin |
peptides and proteins | these hormones consist of chains of 3 to 200 amino acids. Oxytocin, ADH, Insulin, parathyroid hormone, calcitonin, CCK and gastrin |
how are most hormones transported in the blood? | carrier proteins |
master gland | anterior pituitary, now known to be controlled by the hypothalamus. has structure of an endocrine gland |
seven hormones of anterior pituitary | growth hormone GH, Adrenocorticotripic hormone ACTH, Thyroid stimulating hormone TSH, prolactin PRL, follicle stimulating hormone FSH, luteinizing hormone LH, melanocyte stimulating hormone MSH |
two hormones of posterior pituitary | antidiuretic hormone ADH, oxytocin |
the hypothalamus makes hormones for which pituitary | posterior |
the hypothalamus transports hormones down the axons of the neurosecretory cells for which pituitary | posterior |
which pituitary is controlled by substances made in the hypothalamus | anterior |
releasing or inhibitory hormones | hypothalamic substances which regulate the anterior pituitary; CRH stimulates ACTH; TRH stimulates TSH and a little prolactin; GnRH or LHRH stimulates FSH and LH; GIH or somatostatin inhibits GH |
Growth Hormone | GH or somatotropin; stimulates the uptake of amino acids into cells; stims growth of long bones and soft tissues; closure of epiphyseal cartilage stops growth of long bones-puberty (sex hormones) |
pituitary adenoma causes | acromegaly and gigantism |
gigantism & acromegaly | gigantism-excess GH before puberty; acromegaly-excess GH in adults |
symptoms of acromegaly/gigantism | overgrowth of bone, particularly of the skull and mandible; nose thickened and puffy, large ears, large tongue, large hands, increased sweating, fatigue, and weight gain |
Pituitary Dwarfism | lack of GH or GRH before puberty; may also be caused by hypothalamic-pituitary tumor; symptoms-small body, normal proportions; mild obesity w/ lack of appetite |
How to diagnose pituitary dwarfism | inadequate rise in serum GH after provocative stimulus such as Arginine infusion, oral levodopa, or clonidine |
Prolactin | stimulates the production of milk; promotes breast development in pregnancy |
Thyroid stimulating hormone- TSH | promotes and maintains growth and development of the thyroid gland and stimulates it to secrete thyroxine (T4) and triidothyronine (T3) |
Follicle Stimulating Hormone FSH | stimulates growth and develpment of the follicle to maturity, stims the follicle to secrete estrogens, stimulates testicular growth, enhances production of androgen-binding protein in the Sertoli cells (this increases the conentratino of testosterone near |
Luteinizing hormone LH | acts with FSH in the development of the follicle, promotes ovulation, responsible for the formation of the corpus luteum, stims corpus luteum to produce estrogen and progesterone, stims production of testosterone by the interstitial cells in males |
Adrenocorticotropin ACTH or corticotropin | Promotes and maintains normal growth and development of the adrenal cortex and stims the secretion of the glucocorticoids (cortisol); also affects the secretion of the androgens and the mineralcorticoids (aldosterone). ACTH is a polypeptide that is 39 a |
osteoblast activity | stimulated by GH |
epiphyseal cartilage | stimulates by GH; makes space for bone formation |
somatomedins | GH exerts growth-promoting effects indirectly by stimulating somatomedins; somatomedin IGF is an insulin-like growth factor |
GH does not act directly on its target cells to bring about | cell division, enhanced protein sythesis, or bone growth |
where is IGF-I made | liver mostly |
production of IGF-I is controlled by | nutritional status, age, and tissue specific factors |
what closes the epiphyseal plate? | sex hormones among other things |
hormones of the posterior pituitary | oxytocin and ADH (vasopressin) |
where are posterior pituitary hormones synthesized | in the hypothalamus and then transported intracellularly to the posterior pituitary from which they are released |
oxytocin functions | stimulate milk secretion and strong uterine contractions |
milk secretion physiology | oxytocin causes contraction of myoepithelial cells surrounding mammary alveoli (women not secreting enough milk are given an oxytocin nasal spray) |
uterine contraction physiology | oxytocin alters transmembrane ionic currents in myometrial smooth muscle cells to produce sustained uterine contractions. Sensitivity to oxytocin of uterine muscle increases during pregnancy. |
diabetes insipidus | lack of ADH (often due to damage to the pituitary or the hypothalamus. loss of 75% of ADH secretory neurons is necessary before polyuria is evident) |
Alcohol's effect on ADH | decrease release of |
Narcotics effect on ADH | increase release of |
symptoms of lack of ADH | polyuria, polydipsia, dehydration, fever, dry tongue, delirium |
where are catecholamine hormones secreted | adrenal medulla; these are epinephrine and norepinephrine (these supplement the action of the sympathetic nervous system) |
what does the adrenal cortex secrete in general | corticosteroids |
chromaffin cells do what | secrete catecholamines in the adrenal medulla |
corticosteroid hormones of the adrenal cortex | mineralocorticoids, glucocorticoids, and gonadocorticoids |
three zones of adrenal cortex | zona glomerulosa, zona fasciculata, zona reticularis |
other name for mineralcorticoids | aldosterone |
other name for glucocorticoids | cortisol (hydrocortisone) |
other name for gonadocorticoids | sex hormones |
action of mineralcorticoids (aldosterone) | regulate the concentration of extracellular electrolytes, especially sodium and potassium, water balance |
regulation of mineralcorticoids (aldosterone) | renin-angiotensin system (angiotensin II) |
action of glucocorticoids (cortisol) | influence the metabolism of carbohydrates, proteins, and fats; promote vasoconstriction; anti-inflammatory; decrease antibody production |
regulation of glucocorticoids (cortisol) | ACTH from the adenohypophysis of the pituitary gland in response to stress |
action of gonadocorticoids (sex hormones) | supplement the sex hormones from the gonads |
addison's disease | inadequte secretion of glucocorticoids and mineralcorticoids which results in hypoglycemia, na+ and K+ impalance, dehydration, hypotension, weight loss, and general weakness |
cushing syndrome | hypersecretion of corticosteroids generally caused by a tumor of the adrenal cortex or by oversecretion of ACTH by the pituitary. Symptoms are puffy face, hyperglycemia, hypertension, decreased antibodies, and muscle weakness |
adrenogenital syndrome | alteration of enzymes required to produce mineralcorticoids and glucocorticoids, results in an increase in the production of sex hormones. symptoms: masculinization of females, facial and body hair, acne, paleness, increased muscularity, atrophy of breas |
what does the thyroid gland produce | thyroxine (T4) and triiodothyronine (T3), and calcitonin |
physical structure of thyroid | two laterla lobes interconnected by an isthmus (neck area) |
histological structure of thyroid | spherical sacs called thyroid follicles. Humans have about one million follicles. Each follicle is lined with principal cells which synthesize T3 and T4 and contain a protein-rich fluid called colloid. Between the follicles are perifollicular cells whi |
action of triiodothyronine and thyroxine | regulate metabolism; increase rate of protein synthesis; increase rate of energy release from carbs; regulate growth; stimulate maturity of nervous system; regulate body temp |
regulation of T3 and T4 | hypothalamus and release of TSH from adenohypophysis of the pituitary gland |
Action of Calcitonin (thyrocalcitonin) | lowers blood calcium by inhibiting the release of calcium from bone tissue |
regulation of calcitonin | calcium levels in the blood |
cretinism | insufficient secretion of T4 and T3 in infants and children. Stunted growth, thickened facial features, large protruding tongue, abnormal bone growth, mental retardation, decreased metabolic rate, general lethargy. Treat with T3 and T4 |
myxedema | insufficient secretion of T4 and T3 in adults. Weight gain, slow pulse, dry brittle hair, decreased basal metabolic rate, lack of energy, sensation of coldness, diminished perspiration, weakness. treat with T3 and T4 |
goiter | a pathological enlargment of the thyroid gland due to insufficient iodine intake. Take iodine. |
graves' disease (thyroxicosis) | excessive secretion of T4 and T3. Loss of weight, rapid pulse, warm, moist skin, increased appetite, increased basal metabolic rate, tremor, goiter, exophthalmos (bulging eyes); muscular weakness. Treatment: surgical removal of a portion of thyroid gland, |
what percent of calcium is in crystalline form | 99% |
lf the non crystalline calcium, what percent is in cells and what percent is in extracellular fluid | of 1%, .9% is inside the cells and .01% is in the extracellular fluid |
parafollicular or C cells | produce calcitonin in the thyroid gland; lower the blood calcium and phosphates by: 1. decreasing bone resorption by inhibiting the activity of osteoclasts 2. stimulating urinary excretion of calcium and phosphate by inhibiting their reabsorption in the k |
parathyroid glands | four small glands attached to the posterior surface of the thyroid glands. Principal or chief cells in the parathyroid glands secrete parathyroid hormone (PTH) or parathormone. |
what happens in the absence of PTH | death in a few days from hypocalcemia |
functions of PTH (parthormone) | stimulates the activity of osteoclasts to reabsorb bone (remove Ca++ from bones), stims the kidneys to reabsorb ca++ from the filtrate, promotes the formation of 1,25 dihydroxyvitamin D3 |
1, 25 dihydroxyvitamin D3 function | helps raise the plasma calcium and phosphate levels by stimulating 1. intestinal absorption of Ca++ and Phosphate 2. reabsorption of Ca++ from bones 3. renal absorption of ca++ and phosphate so that less is excreted in the urine |
hyperparathyroidism | usually caused by a tumor in one of the parathyroid glands. Is characterized by hypercalcemia- muscle weakness, neurological disorders, decreased alertness, poor memory |
hypoparathyroidism | used to be caused by removal of parathyroids during thyroid surgury. Could lead to death. Other symptoms- hypocalcemia, increased neuromuscular excitability |
endocrine gland in the pancreas | islets of langerhans (clusters of cells); alpha cells secrete glucogon, beta cells secrete insulin |
Glucogon | elevates blood glucose by stimulating glycogenolysis in the liver, this helps the body maintain sufficient blood glucose levels during fasting and starvation |
Insulin | promotes the cells to take up glucose; some tissue do not require insulin for glucose uptake (brain, kidney, intestinal, and red blood cells); stimulates glycolysis; lowers blood glucose levels |
diabetes mellitus | insulin deficiency |
genetic factors in diabetes mellitus | predisposition of diabetes is inherited, the genetic factors are complex (on chromosome 6), over 20% of the relatives of diabetic patients have abnormal glucose tolerance curves |
other possible causes (not hereditary) of diabetes mellitus | environmental chemicals and drugs, infectious agents (mumps virus, rubella, pancreatitis), autoimmune events (antibodies damage the beta cells, anti-insulin receptor antibodies |
two types of diabetes mellitus | type I-insulin-dependent (juvenile onset), type II-noninsulin-dependent (maturity onset) |
type I insulin-dependent (juvenile onset) diabetes mellitus | requires insulin injections (there is no insulin being secreted), often severe and complicated by ketoacidosis, onset usualy in youth but may occur at any age |
type II noninsulin-dependent (maturity onset) diabetes mellitus | 90-95% of diabetes, injections not required, patient usually obese, may use oral hypoglycemic drugs to stimulate insulin release from beta cells, insulin resistance is a factor for 60-80% of patients with type II diabetes |
how to diagnose diabetes mellitus | oral glucose tolerance test; oral administration of 1.75 g/Kg of glucose after at least 3 days on a 300 g carbohydrate diet |
symptoms of diabetes mellitus | glycosuria, polyuria (glucose acts as an osmotic diuretic), polydipsia, hyperglycemia, weakness, loss of weight, acetone breath (ketoacidosis), acetone in the urine |
increased risk of infection due to diabetes mellitus | factors that increase infection 1. pathogens proliferate rapidly b/c of excess glucose 2. hypoxia-glycosylated hemoglobin in RBC's impedes the release of O2 3. decreased blood flow to infected area b/c of vascular damage 4. white blood cells have impaired |
insulin excess results in | insulin shock (hyperinsulinism) |
gestational diabetes mellitus (GDM) | refers to diabetes that occurs during pregnancy (in 1 to 14% of pregnancies) and then disappears following delivery |
GLUT4 | transporter that moves glucose across the membrane |