THE ENDOCRINE

SYSTEMHonors Anatomy & Physiology

ENDOCRINE VS NERVOUSSYSTEM

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

Endocrine Exocrine

no ducts secretions released

and diffuse into blood capillaries

have ducts secretions released

onto surface example: sweat

glands, salivary glands

2 TYPES OF HORMONES

Peptide Steroid

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

GOITER

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 bone2. 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 GLAND

ADRENAL CORTEX outer layer produces 2 kinds of steroid hormones1. 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+

PANCREAS1. 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 3rd 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

AnteriorPituitary

PosteriorPituitary

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:adultshallmark:edema of facial tissues, slow HR, low body temp, sensitivity to cold, dry skin & hair, muscle weakness

CRETINISM & MYXEDEMA

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

GRAVES DISEASE

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

CUSHING’S SYNDROME

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 4th leading cause death in USA blood glucose levels high glucosuria 3 polys: polyuria, polydipsia,

polyphagi

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 drugsstimulates secretion of insulin from beta

cells