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Endocrine > Thyroid Gland > Flashcards

Thyroid Gland Flashcards

1
Q

what does the thyroid gland produce?

A

a. Produces tetraiodothyronine (T4) and the active H triiodotyronine (T3)

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2
Q

thyroid follicle

A

a. functional unit of the gland
i. Surrounded by a single layer of epithelial cells
ii. Follicular lumen itself is filled with colloid—place for storage and production of thyroid H
1. Colloid is composed of newly synthesized TH attached to thyroglobulin
2. Epithelium sits on basal lamina—outermost part of follicle
iii. Size of epithelial cells and amount of colloid change with activity

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3
Q

thyroid gland general: which cells?, secretory products?

A

a. Also contains C cells—parafollicular cells
i. Secretes calcitonin
b. Receives rich blood supply
c. Secretory products of the gland are iodothyronines
i. Tyrosine gives rise to monoiodotyrosine (MIT) and diiodotyrosine (DIT)
1. 2 DIT–>T4
2. 1 MIT + 1 DIT–>T3
ii. TH contain a large amount of iodine
iii. Synthesis of Hs occurs part intracellularly and part in the extracellular compartment
iv. T 4 is the major secretory product

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4
Q

peripheral conversion of T4 to T3

A

i. Peripheral conversion occurs thru the action of deiodonase
1. 10-20% of circulating T3 comes from direct secretion of the thyroid gland
2. 80-90% is produced by peripheral conversion—by deiodonase
ii. provides circulating T3 for uptake by other tissues in which T3 supply is too low
iii. there are some clinical states associated with a reduction in the conversion of T4 into T3:
1. fasting
2. medical and surgical stress
3. catabolic diseases

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5
Q

2 types of deiodonases

A
  1. type 1—predominant around peripheral tissue
  2. type 2—form of this enzyme in the brain which is important when the body goes into starvation, it will prevent starvation effects on the brain
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6
Q

increasing conversion of T4 to 3

A
  1. obesity
  2. cold exposure
  3. hyperthyroid
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7
Q

dec conversion of T4 to 3

A
  1. pregnancy
  2. fasting
  3. beta-blockers
  4. hepatic renal failure
  5. aging
  6. hypothyroid
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8
Q

synthesis of thyroid Hs

A

i. start with tyrosine which is involved in synthesis of TGB which is protein with tyrosine molecules that is extruded thru the follicular lumen thru exocytosis
ii. Na-iodide symporter pulls iodide into the cell from the blood, so will work thru secondary active transport b/c the conc of iodide is very high in the cell, so have to use the energy of Na moving down its gradient to get iodide to move up its gradient
1. Excess of iodide in the cell—“I trap”
iii. Pendrin is a transport mechanism using Cl—iodide is taken to the follicular lumen and then immediately converted to iodine by peroxidase to enzyme
iv. Peroxidase then combines TGB and I2 to make TGB bound to MIT and DIT
v. Peroxidase then forms T4 from 2 molecules of DIT and T3 from 1 MIT and 1 DIT
1. Can have 4 types of products here
2. All of this is stored as colloid in the follicular epithelial cell
vi. In order to get H into the cell, we need a stimulus which is TSH for pinocytosis
vii. Proteases in the lysosomes of the cell pushes T3 and T4 out to blood
viii. Intrathyroidal deiodonases will convert MIT and DIT back to get further production of TGB

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9
Q

PTU

A
  1. PTU is an effective treatment for hyperthyroidism
    a. PTU knocks out peroxidase
  2. High levels of I- inhibit organification (step 4) and dec synthesis of thyroid Hs—Wolff Chaikoff effect
  3. Perchlorate and thiocynate knocks out the Na/I symporter, so then we also get a decrease in the TH produced
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10
Q

radioactive iodine uptake

A
  1. radioactive iodide uptake occurs during first 6 hours
    a. when significant uptake occurs, then we have hyperthyroidism
    b. when uptake of the iodide occurs, then we have hypothyroidism
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11
Q

Graves Disease*

A

a. associated thyrotoxicosis
i. Overproduction of TH
ii. Extreme stimulation of thyroid gland—high turnover

  1. TSH R can be activated but not necessarily by TSH
    a. This is done by certain antibodies that perfectly fit in the TSH R and these are thyroid stimulating immunoglobulin and can have same effect as TSH which will cause and overstimulation of the thyroid gland and an increased overproduction of TH
    i. TSH levels will dec b/c TH levels are so high so feedback and inhibit TSH secretion
    1. TSH levels are lower than normal b/c the high circulating levels of TH inhibits TSH secretion
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12
Q

perchlorate in the synthesis of THs

A
  1. Perchlorate inhibits the Na/I symporter which will inhibit production of TH but will lead to an organification defect
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13
Q

transport of thyroid Hs

A

i. Circulate in the bloodstream either bound to plasma proteins (99%) or free (1%)
1. There is an equilibrium b/w bound and free circulating T3/4 in the bloodstream
ii. Main binding proteins
1. TBG—thyroxine binding protein is synthesized in the liver
a. Binds 1 mc of T3 or T4
b. Has higher affinity for T4 than T3
2. Transtheyretin (TTR)
3. Albumin
iii. Most circulating thyroid hormone is T4
1. T4 has a half life of 6 days
2. T3 has a half life of 1 day

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14
Q

T3 resin uptake test

A

a. Circulating levels of TBG can be indirectly assessed with T3 resin uptake test
1. TBG with bound T4 from serum is put in an incubator with unbound and labeled T3
2. Unbound TBG sites bind labeled T3
3. Anti T3 antibody or non specific resin which absorbs T3 is added
a. Absorbed T3 on the antibody precipitates and we can measure T3 uptake
In solution, we have TBG with bound T4 and labeled T3 is removed

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15
Q

changes in the blood levels of TGB and free THs in the following:

  • hyperthyroidism
  • hypothyroidism
  • high TBG
  • low TBG
  • hepatic failure
  • pregnancy
A
  1. Hyperthyroidism
    a. inc T4
    b. inc T3 resin uptake
  2. hypothyroidism
    a. dec T4
    b. dec T3 resin uptake
  3. high TBG
    a. inc T4
    b. dec T3 resin uptake
  4. low TBG
    a. dec T4
    b. inc T3 resin uptake
  5. hepatic failure
    a. dec TBG
    b. inc T3 resin uptake
  6. pregnancy
    a. inc TBG
    b. dec T3 resin uptake
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16
Q

hepatic failure*

A
  1. Dec blood levels of TBG
  2. Transient inc in the level of free T3, T4
  3. Followed by inhibition of synthesis of T3, T4—negative feedback
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17
Q

pregnancy*

A
  1. Inc blood levels of TBG
  2. Inc bound T3, T4; dec free T3, T4
  3. Transient dec in free T3, T4 causes an increase in synthesis and secretion of T3, T4
  4. Inc total levels of T3, T4, but levels of free, physiologically active, THs are normal
    a. Person is said to be clinically euthyroid
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18
Q

HPT axis and the control of synthesis and secretion of TH

A

i. Role of TSH is to regulate:
1. The growth of thyroid gland—trophic effect
2. Secretion of THs
ii. TSH is regulated by:
1. Thyrotropin releasing H—TRH
a. Anterior pituitary has enzyme to convert T4 to T3 and this regulates how much TSH will be secreted
2. Free T3
iii. TSH secretion, in contrast, to the secretion of GH, occurs at a steady state

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19
Q

actions of TSH on thyroid gland

A

i. cAMP is the second messenger for TSH
ii. TSH has 2 types of actions on the thyroid gland:
1. Increases the synthesis and secretion of THs
2. Trophic effect on thyroid gland

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20
Q

stimulatory effects on TH secretion

A
  1. TSH
  2. Thyroid stimulating immunoglobulins
  3. Increased TBG levels—pregnancy
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21
Q

inhibitory effects on TH secretion

A
  1. Iodide deficiency
  2. Deiodinase deficiency
  3. Excessive iodide uptake—Wolff Chaikoff effect
  4. Perchlorate, thiocyanate
  5. Propylthiouracil (PTU)
  6. Decreased TBG levels—liver disease
22
Q

proteins synthesized under the direction of TH

A
  1. Na/K ATPase
  2. Transport proteins
  3. B1 adrenergic Rs
  4. Lysosomal enzymes
  5. Proteolytic proteins
  6. Structural proteins
23
Q

what stimulates Na/K ATPase?

A

THs

24
Q

proteins synthesized in cardiac muscle under TH

A
  1. Myosin
  2. B1 adrenergic Rs
  3. Ca ATPase
25
Q

actions of THs on growth

A
  • growth formation

- bone maturation

26
Q

actions of THs on CNS

A

-maturation of CNS

27
Q

actions of THs on BMR

A
  1. Inc Na/K ATPase
  2. Inc O2 consumption
  3. Inc heat production
  4. Inc BMR
28
Q

actions of THs on metabolism

A
  1. Inc glucose absorption
  2. Inc glycogenolysis
  3. Inc gluconeogenesis
  4. Inc lipolysis
  5. Inc protein synthesis and degradation (net catabolic)
29
Q

actions of THs on CV

A

inc CO

30
Q

how does TH inc BMR?

A

i. Increased activity of Na/K ATPase accounts for most of the increase in metabolic rate
1. Leads to inc O2 consumption and heat production
ii. The inc in BMR produced by a single dose of thyroxine (T4) occurs after several hours but it is long lasting (>6 hours)
i. Hyperthyroidism leads to a high BMR
ii. Hypothyroidism leads to a low BMR

31
Q

actions of TH on lipid metabolism

A
  1. Stimulate fat mobilizationincreased concentration of FA in plasma
  2. Enhance oxidation of FA
  3. Plasma concentration of cholesterol and triglycerids are inversely correlated with THs
    a. Inc blood cholesterol concentration in hypothyroidism
  4. Required for conversion of carotene to vitamin A
    a. Hypothyroid patients can suffer from blindness and yellowing of the skin
32
Q

actions of TH on carbohydrate metabolism

A
  1. Increased gluconeogenesis and glycogenolysis to generate free glucose
  2. Enhancement of insulin dependent entry of glucose into cells
33
Q

indirect CV effects of THs

A

i. contribution thru indirect means is higher than direct
1. Inc heat production and CO2 in tissues–>
2. Dec peripheral vascular resistance–>
3. Dec diastolic BP–>
4. reflex inc adrenergic stimulation–>

34
Q

direct CV effects of THs

A
  1. inc cardiac muscle myosin heavy chain alpha/beta ratio, Na/K ATPase, sarcoplasma Ca-ATPase, beta adrenergic signaling, G protein stimulatory/inhibitory ratio
  2. inc ventricular contractility and function
  3. dec peripheral vascular resistance
35
Q

what do both direct and indirect CV effects of TH cause?

A

i. both indirect and direct CV effects of TH lead to inc blood volumeinc cardiac rate and output

36
Q

TH and beta 1 adrenergic Rs

A

i. TH stimulates the synthesis of cardiac B1 adrenergic Rs
1. When thyroid H levels are high, the myocardium has an increased number of beta1 Rs and is more sensitive to stimulation by SNS which causes inc CO and heart rate

37
Q

cretinism*

A

a. Neural changes induced by TH deficiency during the perinatal period are irreversible and lead to cretinism unless replacement therapy is started soon after birth
i. causes of cretinism
1. impaired development of thyroid gland
2. maternal intake of antithyroid medication or excess iodine
3. inherent deficit in the synthesis of THs
ii. symptoms
1. feeding problems
2. respiratory difficulty
3. protruding tongue
4. curse facial features
5. growth retardation
6. mental retardation
7. jaundice, dry skin
8. hypotonia

38
Q

deficiency of TH during perinatal period leads to:

A

i. Abnormal development of synapses

ii. Decreased dendritic branching and myelination

39
Q

causes of primary hypothyroidism

A
  1. Agenesis—failure of an organ to develop
  2. Gland development—surgical removal, irradiation, autoimmune dz, idiopathic atrophy
  3. Inhibition of THs synthesis and release—iodine deficiency, inherited enzyme defects, drugs that interfere with thyroid homeostasis
  4. Transient—after surgery or therapeutic radioiodine, postpartum, thyroiditis
40
Q

Hashimoto’s thyroiditis*

A

a. Hashimoto’s thyroiditis
i. TH synthesis is impaired by thyroglobulin or TPO antibodies, which leads to dec T3/4 secretion
ii. TSH levels are high
1. Have trophic effect—goiter
2. Occurs due to negative feedback which will not work b/c not enough T3/4 so more TSH will be released to inc the levels of T3/4

41
Q

causes of secondary hypothyroidism

A
  1. Hypothalamic dz
  2. Pituitary dz
    a. Sheehan’s Syndrome
  3. Resistance to TH
42
Q

symptoms of hypothyroidism

A

i. Dec BMR
ii. Dec heat production
iii. Cold sensitivity
iv. Weight gain
v. Positive N2 balance
vi. Dec CO
vii. Hypoventilation
viii. Lethargy
ix. Drooping eyelids
x. Myxedema
xi. Growth retardation
xii. Mental retardation
xiii. Goiter
xiv. Menstrual dysfunction

43
Q

treatment of hypothyroidism

A

i. Replacement doses of T4
1. b/c metabolism of T4 dec and the plasma half life decreases with age, higher doses are required in younger pts
2. in women beyond menopause, overprescribing T4 can contribute to the development of osteoporosis (Osteoclastogenesis)

44
Q

hypothyroidism due to iodine deficiency

A

i. leads to transient dec in the synthesis of THs
ii. TSh levels are elevated due to low T3/4
iii. Goiter due to TSH elevation
1. If gland maintains normal blood levels of Ths, pt is euthyroid and asymptomatic
2. If gland cannot maintain normal blood levels of THs, patient enhibits hypothyroid

45
Q

causes of primary hyperthyroidism

A
  • Graves Disease
    i. Other causes:
    1. TSH secreting pituitary adenoma—secondary hyperthyroidism
      ii. TSH levels
    2. Dec due to negative feedback of T3 on the anterior lobe of the pituitary gland
    3. If defect is in the anterior pituitary, TSH levels are increasing
46
Q

Graves Disease*

A

i. most common cause of hyperthyroidism, primary endocrine disorder
1. Major clinical signs: exophthalmos (bulging of eyes) and periorbital edema (due to recognition by the anti TSH receptor antibodies of a similar epitope within the orbital cells
2. Diagnosed by: elevated serum free and total T4/3 level and clinical signs of goiter and ophthalmophaty
3. TSH levels are low—due to negative feedback by high levels of TH
4. Presence of circulating TSI—thyroid stimulating immunoglobulins
a. Helps distinguish Graves from adenoma of pituitary thyrotrophs—secondary endocrine dz

47
Q

hyperthyroidism

A

a. too much TH in bloodstream
i. Inc speed of bodily fcns
1. leads to weight loss
2. Sweating
3. Rapid HR
4. High BP

48
Q

hypothyroidism

A

a. not enough TH for the body’s needs
i. Without enough TH, many of the body’s functions slow down
1. Ppl may have fatigue
2. Weight gain
3. Cold intolerance

49
Q

goiter

A

a. Goiter can develop in response to multiple imbalances and disease within the HPT axis, coexisting with hypothyroidism, euthyroidism (normal), hyperthyroidism
b. These imbalances include:
i. Hyperthyroidism
1. Excessive stimulation of the TSH R by an autoantibody (Graves Dz)
2. Excessive secretion of TSH from a TSH producing tumor (secondary hyperthyroidism)
3. Thyroid H producing (toxic) adenoma (nodular) or toxic multinodular goiter
ii. Primary hypothyroidism
1. Lack of adequate iodine in the diet (nontoxic goiter, endemic goiter)
2. Sporadic hypothyroidism of unknown etiology (nontoxic goiter)
3. Chronic thyroiditis (Hashimoto dz, autoimmune induced deficiency in thyroid fcn)

50
Q

TSH test

A
  1. TSH test is used for diagnosing both hyper/hypothyroidism

Endocrine (15 decks)

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