Endocrine System for copying

Endocrine vs nervous system act together to coordinate body’s activities both: – use chemical messengers to communicate cell to cell – major function: homeostasis endocrine: slower response time – hormones transported thru circulatory system – target cells (any cell with hormone receptor) anywhere in body nervous: quicker conduction of signals – neurotransmitters – act on cells close by

Glands EndocrineExocrine no ducts secretions released and diffuse into blood capillaries have ducts secretions released onto surface example: sweat glands, salivary glands

2 types of hormones PeptideSteroid bind to protein receptors in cell membranes (do not enter cell) receptor-hormone activate enzyme in cytoplasm  series of reactions result in cell response enter cell & bind to receptor in cytoplasm or nucleus Activates transcription of gene  protein produced generally action slower than peptide hormone

Endocrine system

hypothalamus part of brain secretes “releasing” hormones that act on pituitary gland axons that store the 2 posterior pituitary hormones end there

Pituitary gland 2 lobes: posterior & anterior

Negative Feedback Inhibition

Thyroid Gland stimulated by TSH secretes thyroxin (T4) and triiodothyronine (T3) – (-) feedback inhibition both have similar effects on target cells

hypothyroidism Thyroid produces too little hormone several causes: Hashimoto’s autoimmune/ lack of Iodine in diet  goiter (enlargement of thyroid due to increased TSH stimulation Symptoms: – Adults: lethargy, weight gain, anovulatory cycles – Infants:cretinism: dwarfism, low IQ, failure to reach sexual maturity

hyperthyroidism excessive secretion of thyroid hormones

Parathyroid Glands 4 small glands embedded in posterior surface of thyroid gland secrete: parathyroid hormone (PTH) – regulated by serum Ca++ levels actions: 1.stimulates removal of Ca++ from bone 2.increases kidney tubules reabsorption of Ca++ 3.activates vit D which enhances Ca++ absorption from food

thymus upper thorax, posterior to sternum largest in infants, decreases as we age produces: thymosin – programs T cells

Adrenal Cortex outer layer produces 2 kinds of steroid hormones 1.Glucocorticoids – major 1 – cortisol: – reduces swelling by inhibiting immune system/ raises serum glucose (stimulates liver to make glucose from proteins or lipids 2.Mineralocorticoids – major 1- aldosterone – acts on kidney to promote absorption of Na+ & excretion of K+

pancreas 1.Insulin – protein – reduces blood glucose by increasing entry of glucose into cells/making glycogen in hepatocytes – regulated by blood glucose levels 2.Glucagon – protein – raises blood glucose by acting on glycogen stores in liver – regulated by blood glucose levels

testes paired oval organs suspended in scrotum site of: – spermatogenesis – production of androgens: 1.Testosterone major one – made by interstitial cells/stimulated by FSH & LH – produces male 2 ◦ sex characteristics in puberty – promotes growth & maturation of reproductive system organs – increases libido

ovaries paired, almond-shaped organs in pelvic cavity produce ova release: estrogens & progesterone begin functioning in puberty in response to anterior pituitary gonadotrophins

estrogens Estrone &Estradiol made by follicle where ova is maturing stimulate: – development of 2◦ sex characteristics work with progesterone to prepare uterine lining for implantation help maintain pregnancy & prepare breasts to lactate(those estrogens made in placenta)

progesterone made &secreted by corpus luteum acts with estrogen to prepare uterine lining for implantation quiets uterine muscle during early pregnancy helps prepare breasts for lactation

placenta produces hCG (human Chorionic Gonadotropin) – stimulates corpus luteum of ovary to continue producing estrogens and progesterone so lining of uterus does not slough off (like in menstruation) – turns pregnancy tests + – by 3 rd mo pregnancy placenta produces estrogen & progesterone (ovaries become inactive rest of pregnancy) – also produces hPL (human placental lactogen) works w/E & P in preparing breasts for lactation

Pituitary disorders Anterior Pituitary Posterior Pituitary Giantism : hypersecretion hCG during chidhood abnl increse in length of long bones hypersecretion hCG in adulthood  acromegaly (epiphyseal plates sealed) see thickening of bones of hands, face & thickening of skin on brow Diabetes Insipidus: defects in ADH excrete large volumes of urine  dehydration & thirst (bed-wetting in children) can die w/in 2 days from the dehydration

Thyroid gland disorders Hypothyroidism: Cretinism: congenital hypothyroidism – severe mental retardation if not tx’d – most states require testing new borns Myxedema:adults – hallmark:edema of facial tissues, slow HR, low body temp, sensitivity to cold, dry skin & hair, muscle weakness

Thyroid gland disorders Graves Disease most common form of hypothyroidism 7 – 10 x more common in females autoimmune disorder: autoantibodies that mimic TSH  causes thyroid to grow & make thyroid hormones signs: enlarged thyroid, exophthalmos tx: surgical excision of all or part of thyroid or use of antithyroid drugs to block synthesis of hormones

goiter enlarged thyroid could be associated with hypo- or hyperthyroidism, or euthyroidism (normal level of hormones) seen when intake of iodine too low

Adrenal Gland disorders Cushing’s Syndrome: hypersecretion of cortisol caused by tumors that secrete – cortisol (in adrenal cortex) – ACTH  stimulates more cortisol production in adrenal cortex muscle wasting  spindly arms & legs, “moon” face, “buffalo hump” red face ~80% have hypertension

Adrenal gland disorders Addison’s Disease: hyposecretion of glucocorticoids & aldosterone most are autoimmune: antibodies cause adrenal cortex destruction or block binding of ACTH to its receptors TB can destroy adrenal cortex symptoms: (after 90% of cortex destroyed) mental lethargy, anorexia, N/V, wt loss, hypotension, hypoglycemia, muscular weakness

Pancreatic islet disorders Diabetes mellitus: (honey-sweetened) inabillity to use or produce insulin 4 th leading cause death in USA blood glucose levels high  glucosuria 3 polys: polyuria, polydipsia, polyphagia

Diabetes Mellitus Type 1: autoimmune abys destroy beta cells – mostly develops <20 yrs old – most common in northern European heritage – cells starved for glucose so switch to breaking down fatty acids  ketone production  ketoacidosis  untx’d  death – transport of lipids from adipocytes  plaque formation in walls of arteries = atherosclerosis – excess glucose attaches to proteins in lens  catarracts – small vessel disease: blindness, kidney failure, amputation of toes  legs, impotence

Diabetes Mellitus Treatment self-monitoring of blood glucose levels  injections of insulin Diet: – 45 – 50% carbohydrates – <30% fats Exercise

Type 2 Diabetes non-insulin-dependent diabetes (NIDDM) more common (90% of all cases) typically occurs in obese people > 35 yrs old – #s children diagnosed increasing many control it with diet, exercise, wt loss oral hypoglycemic drugs – stimulates secretion of insulin from beta cells