1. Honors Anatomy & Physiology

2.  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

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

4. 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

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

9.  2 lobes: posterior & anterior

11.  stimulated by TSH  secretes thyroxin (T4) and triiodothyronine (T3)  (-) feedback inhibition  both have similar effects on target cells

12.  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

14.  excessive secretion of thyroid hormones

15.  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

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

19.  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+

20. 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

22.  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

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

25.  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)

26.  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

27.  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

29. 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

31.  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

33.  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

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

36.  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

38.  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

40.  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, polyphagi

41.  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

42.  self-monitoring of blood glucose levels  injections of insulin  Diet:  45 – 50% carbohydrates  <30% fats Exercise

43.  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