Guyton Phys 76: Thyroid Metabolic Hormones

Front 1

what does complete lack of thyroid secretion cause

Back 1

basal metabolic rate to fall 40 to 50 percent below normal

Front 2

how much iodide is required to prevent deficiency

Back 2

50 mg ingested each year or 1 mg/week

Front 3

how are iodides absorbed in GI tract

Back 3

similar to Cl-

Front 4

kidney removal of iodides

Back 4

rapidly excreted, but only after 1/5 selectively removed by cells of thyroid gland

Front 5

first stage in formation of thyroid hormones

Back 5

transport of iodides from blood into thyroid glandular cells and follicles; iodide trapping

Front 6

what are major substarates within thyroglobulin that combine with iodine to form thyroid hormones

Back 6

tyrosine aas (~70 of them)

Front 7

what is oxidation of iodide to iodine promoted by

Back 7

peroxidase and its accompaning hydrogen peroxide

Front 8

organification of thyroglobulin

Back 8

binding of iodine with thyroglobulin

Front 9

when are effects of thyroid hormone synthesis ceasing seen

Back 9

several months after onset due to storage of Thyroid hormones

Front 10

how much of the iodinated tyrosine in thyroglobulin never becomes thyroid hormones

Back 10

about 3/4 remains monoiodotyrosine and diiodotyrosine - iodide cleaved and recycled

Front 11

what so T3 and T4 bind once entering blood

Back 11

99% bind either thyroxine-binding globulin or thyoxine-binding prealbumin and albumin

Front 12

how quickly are T3 and T4 releaseed into tissues from blood

Back 12

thyroxine - haf released every 6 days; triiodothyrorine - half released every 1 day

Front 13

what happens to T3 and T4 one inside tissue cells

Back 13

bind storage proteins T4 stronger than T3 - used over a period of days or weeks

Front 14

how long does it take for effects of T3 and T4 to be seen

Back 14

2 to 3 days and reaches max in 10 to 12 days; half-life ~15 days

Front 15

how long does some of the activity of TH last

Back 15

6 weeks to 2 months

Front 16

what accounts for the long latent period of THs

Back 16

storage on proteins and how they perform their fxns in cells

Front 17

general affect of TH

Back 17

activate nuclear transcription of large numbers of genes

Front 18

thyroid hormone nuclear receptors

Back 18

either attached to DNA or in proximity to DNA

Front 19

what does THR form a heterodimer with

Back 19

retinoid X receptor (RXR) at specific TH response elements on DNA

Front 20

how much are protein synthesis increased by TH

Back 20

some only slightly and some up to 6 fold; protein catabolism also increased

Front 21

mitochondria and TH

Back 21

increase in number and in SA; may be due to increased activity of cell and not directly from TH

Front 22

Thyroid hormone and Na+/K+ ATPase

Back 22

increases leakiness to Na+ and increases ATPase pump action

Front 23

TH in children

Back 23

sets growth rate; too little retards and too much increases (but also causes growth plates to close earlier and may yield short stature)

Front 24

Carb metabolism and TH excess

Back 24

stimulates - glucose uptake, enhanced glycolysis, enhanced gluconeogenesis, increased GI absorption rate, increased insulin secretion; due to increase in cellular metabolic enzymes

Front 25

Fat metabolism and TH excess

Back 25

lipids mobilized from fat tissue, increased free fatty acid concentration in plasma which accelerates oxidation of free fatty acids by cells

Front 26

Plasma and TH excess

Back 26

decreases concentrations of cholesterol, phospholipids, and triglycerides in plasma and increases free fatty acids

Front 27

TH excess and Liver fats

Back 27

increase rate of cholesterol secretion in bile; may induceincreased numbers of LDL receptors on liver cells

Front 28

CO and TH excess

Back 28

vasodilation in tissues to increase blood flow, CO increases

Front 29

Heart rate and TH excess

Back 29

increases more than expected from looking at CO

Front 30

heart strength and TH excess

Back 30

increases, but long term heart muscle strength becomes depressed due to excessive protein catabolism

Front 31

Arterial P and TH excess

Back 31

mean about normal; due to increased blood flow to tissues pulse P is often increased - systolic elevated 10-15 mmHg and diastolic decreased the same amount

Front 32

Respiration and TH excess

Back 32

increase rate and depth

Front 33

GI and TH excess

Back 33

increased appetite and food intake, increased secretion of digestive juices and motility; often diarrhea present

Front 34

CNS and TH excess

Back 34

nervousness and many psychoneurotic tendencies

Front 35

muscles and TH excess

Back 35

react with more vigor, when excessive muscles weaken due to protein catabolism

Front 36

muscle tremor and TH excess

Back 36

fine muscle tremor 10-15 times per second

Front 37

Sleep and TH excess

Back 37

feeling of constant tiredness, but difficult to sleep

Front 38

sleep and TH lack

Back 38

somnolence with sleep up to 12-14 hours per day

Front 39

sex drive and TH in men

Back 39

lack of thyroid likely to cause loss of libido, excesses can sometimes cause impotence

Front 40

sex drive and TH in women

Back 40

lack have depressed libido

Front 41

menstruation and TH

Back 41

lack of often causes menorrhagia and polymenorrhea (excessive and frequent), sometimes amenorrhea; hyperthyroid causes oligomenorrhea (reduced) and occasionally amenorrhea

Front 42

TSH alternative name

Back 42

thyrotropin

Front 43

what secretes thyrotropin releasing hormone

Back 43

nerve endings in the median eminence of the hypothalamus

Front 44

what is TRH

Back 44

a tripeptide amide - pyroglutamyl histidyl proline amide; TSH not reduced to 0 if TRH not released

Front 45

what seconds messenger does TRH use to cause secretion of TSH

Back 45

phospholipase to produce phospholipase C

Front 46

what affect do anxiety and excitement have on TSH secretion

Back 46

decrease; they increase sympathetic system and cause increased metabolism and body heat without TH

Front 47

how do we know the cold affect and anxiety/excitement affect are caused by the hypothalamus

Back 47

not seen whrn hypophysial stalk is cut

Front 48

antithyroid substances

Back 48

thiocyanate, propylthiouracil, and high concentration of organic iodides

Front 49

thiocyanate action

Back 49

competative inhibition of iodide transport into cell; can cause goiter

Front 50

propylthiouracil action

Back 50

prevents formation of TH from iodides and tyrosine; block peroxidase enzyme and coupling of teo iodinated tyrosines to form T3 and T4; goiter formation

Front 51

high iodide concentration action

Back 51

reduce rate of iodide trapping and normal endocytosis of colloid from follicles; decrease thyroid size and blood supply

Front 52

What TSH analog is present in the blood of patients with Graves' disease

Back 52

thyroid-stimulating immunoglobulin (TSI)

Front 53

thyroid adenoma

Back 53

no evidence of autoimmune disease; normal thyroid tissue atrophy

Front 54

exophthalmos

Back 54

protrusion of the eyeballs; mild degree in ~1/3 hyperthyroidism patients

Front 55

cause of exophthalmos

Back 55

edematous swelling of retro-orbital tissues and degenerative changes in extraocular muscles; believed to be autoimmune

Front 56

most accurate diagnostic test for hyperthyroidism

Back 56

free thyroxine in plasma

Front 57

treatment of hyperthyroidism presurgery

Back 57

propylthiouracil for several weeks to get BMR normal, then iodides for 1-2 weeks to reduce size/blood supply of gland

Front 58

myxedema cause

Back 58

increased quantities of hyaluronic acis and chondroitin sulfate bound with protein form excessive tissue gel in interstitial spaces; nonpitting

Front 59

cretinism

Back 59

extreme hypothyroidism during fetal life, infancy, or childhood; failure of body growth and mental retardation