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Endo/Repro Block1 > Thyroid Hormone Phys/Pharm [TRH] > Flashcards

Thyroid Hormone Phys/Pharm [TRH] Flashcards

1
Q

What form is TRH translsated in?

WI its mature form?

A

translated as: preprohormone

mature= tripeptide

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2
Q

Besides the thyroid/hypothalmus/pit, where can you find TRH in the body?

What are the major roles of TRH?

A
  • TRH is also in the cerebral cortex, GI, & pancreas
  • Roles/regulation:
    • regulates energy homeostasis [thru stimulation of TSH & regulating circulating thyroid H levels]
    • feeding behavior
    • thermogenesis
    • autonomic regulation
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3
Q

What is the structure of TSH?

A
  • alpha chain: same as other pit. H’s [listed below]
  • beta chain: specific to TSH [and each gonadotropin; LH, FSH, hCG]
    • confers specificity of H action
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4
Q

What is the structure of T4?

What is the structure of T3?

A
  • T4: 2 tyrosines + 4 Iodine
  • T3: 2 tyrosines + 3 iodine
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5
Q

7 steps of thyroid H synthesis?

A
  1. dietary iodide required & active transport of I- into thyroid follicular cell
  2. Oxidation of I- [iodide] to I2 [iodine]…aka organification
  3. Iodination of tyrosines bound to thyroglobulin backbone–>
    • MIT & DIT
  4. conjugation of MIT & DIT –> TriiodoT [T3] & TetraiiodT [T4]
    • dependendent on thyroid peroxidase
  5. endocytosis of conjugates
  6. proteolysis of conjugates into mature T3 & T4
  7. move T3 & T4 out of cell
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6
Q

Compare T3 & T4?

  • activity
  • circulation []
A

T3:

  • more active
  • shorter circulating half life [1 day]
  • binds thyroid H R’s

T4:

  • less active
  • longer circulation half life [6 days]
  • binds thyroid H R’s
  • converted intracellularly to T3!!!!
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7
Q

What are the 3 main thyroid H carrier proteins?

-what do they bind respectively?

A

Thyroxine binding globulin [TBG]

  • binds 75% of T3 & T4
  • 1 binding site for 1 thyroid H molecule

Transthyretin

  • binds 20% of T4, 5% of T3
  • 2 binding sites

Albumin

  • binds 5% T4 & 20% T3 [has several binding sites]
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8
Q

When are serum [thyroid H] carrier proteins highest?

lowest?

A

increased: in pregnancy OR estrogen/androgen Tx

Decreased: hyperthyroidism, malnutrition & nephritic syndrome [diseases that cause protein loss]

note: 99.98% of T4 & 99.95% of T3 are bound to carriers

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9
Q

What does total H mean?

A

bound + free = total

***total can fluctuate

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10
Q

What molecules deactivate & activate T4 & T3?

A

Deactivate:

  • DI & III
    • converts T4 –> rT3 = not active

Activate:

  • DI & II
    • convert T4 –> T3 =active
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11
Q

Which Deiodinase is responsible for both activation & deactivation of thyroid H’s?

  • where is it most abundant?
  • one more unique thing about it?
A

Deiodinase I:

  • highly prevalent in liver and kidney
  • converts T4 to T3 [more active] & increases T3 in cell/circul8
  • converts T4 to rT3 [inactive] for disposal
  • drug target for **prophylthiouracil **
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12
Q

What are DII & III responsible for repectively?

-where are they most abundant?

A

DII:

  • in brain, pit, sk. & cardiac muscles
  • converts T4 to T3 [activates intracellularly]

DIII:

  • in brain, skin, placenta
  • deactivates hormones
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13
Q

What process does TSH stimulate?

A
  • secretion/release of mature H’s [T3 & T4]
  • thyroid peroxidase synthesis
  • Na+/I- symporter activity [^^ I- availability to follicular cell]
  • Thyroglobulin transcription
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14
Q

Biochemically, how is T4 converted to T3?

A

DI removes a 5’ iodine!

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15
Q

Which has a higher thyroid H [], intracellular or plasma/serum?

Why is this?

A

intracellular [] > serum/plasma []

**this is due to 10+ different energy-dependent thyroid H transporters –> help maintain the above gradient

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16
Q

What effects are seen in congenital hypothyroid [caused often by maternal hypothyroidism] in infants

A
  • profound mental retardation
  • short stature
  • delay in motor development
  • coarse hair
  • protuberant abdomens
17
Q

What are the causes of maternal hypothyroidism?

A
  • lack of Iodine in maternal diet [rare now]
  • mother has Hashimoto’s thyroiditis –> makes anti-TSH R antibodies
  • exposure to radioactive Iodine or antithyroid drugs during pregnancy
18
Q

What is the RDA of iodine?

-where can we get it in our diets?

A

RDA: 150 mcg/day for men & women

TUL: 1,100 mcg/day

dietary sources: sea food, esp. kelp, & plants grown in iodine-rich soil

**iodized salt too

19
Q

HYpothyroid effects/**cretinism **in infants

A

respiratory difficulty

cyanosis

jaundice

poor feeding

hoarse cry

umbilical hernia

slowed bone maturation: prox. tibial & distal femoral epiphysis lengths shorter than expected indicate hypoThyroidism

20
Q

How do we Tx hypoThy in infants?

A

if hormone replacement occurs w/in few days of birth, development will proceed normally

***if delayed Tx; physical development will be fine but mental development will be retarded

thus we should screen newborns [although not all states have made this mandatory yet]

21
Q

HypoThy effects in adults

A

lethargy

somnolence

slowed intellect fxn’s; speech!

stiff & aching muscles

cold intolerance

delayed deep tendon reflexes

anovulation & amenorrhea common, menorrhagia less common

22
Q

HyperThy effects in adults

A
  • promote rapid contraxn & relax of muscles –>^^HR
  • ^^# if Beta adrenerguc R’s in heart, Sk.M, fat & lymphocytes –>^^catecholamine sensitivity
  • amplified post-R axn of catecholamines
  • ^^contrxn–>^^O2 demand –>^^EPO prdxn –> ^^erythropoesis
  • ^^GI motility–> D
  • promote bone turnover w/ net bone loss & hyperCa+
  • ^^protein turnover –> net loss of Sk.M & myopathy
    • heat intolerance
  • ^^hepatic GluNeo & GlyLys & intestinal absorption of Glu
  • ^^ LDL-R #’s –> ^^LDL clearance –> decreased LDL levels
  • alters prdxn, responsiveness, & met. clearance of many H’s
  • precocious puberty
  • ^^aromatization of androgens to estrogens & ^^sex H binding globulins –> gynecomastia in men
  • impairs GnRH & regulation of ovulation –> infertility
23
Q

WI thyrotoxicosis?

WI thyroid storm?

How do we Tx/prevent?

A

Thyrotoxicosis: any cause of excessive thyroid H [] & its effects

Thyroid storm: extreme manifestation of thyrotoxicosis & one of most critical endocrine illnesses [less than 10% of pts with tox get storm]

Thus we Tx thyrotoxicosis as if they will progress to a STORM:

  • B-adrenergic blockers, thioamides [antithyroid], corticosteroids [covers fxnl hypoadrenalism induced by thyrotox]
24
Q

What are the causes of 1’ Hypothyr?

2’/tertiary?

A

1’: problem in thyroid gland itself

  • congenital
  • gland destrxn [surg, radiation, external rad]
  • Iodine deficiency
  • Autoimmune [hashimoto]

2’/tertiary: problem in pit gland or hypothalamus

note: you can also have thyroid H resistance syndromes [norm thyroid H prodxn]

25
Q

WI Graves disease?

A

produxn of thyroid stimulating immunoglobulins [TSI’s]

  • T cells become sensitive to thyroid Ag–> stimul8 B cells –> produce antibodies that mimic TSH
  • –> hyperstimulates thyroid H prodxn!!
  • IgG can cross placental membranes & affect the fetus
26
Q

What causes a goiter in HypoThyr?

A
27
Q

What does TSH test test for?

A

thyroid activity

ex: low TSH= hyperthyroidism [^^levels T3/4]

28
Q

What test is used to look for Graves disease?

WI a radioactive Iodine uptake test?

A

TSI test: thyroid stimulating antibody test

radioactive Iodine: measures amt of iodine thyroid takes up from blood (low levels might b hypo, high Graves/hyper)

29
Q

What does a thyroid scan measure?

A

shows how and where Iodine is distributed in the thyroid

30
Q

What are 2 replacement medications for thyroid H?

What are radioactive Iodines & what are they used for?

A

levothyroxine [T4]

liothyronine [T3]

radioactive I:

  • 131-I used for ablation
  • 123-I for thyroid imaging
31
Q

What are thioamides [aka thionamides]?

A

used for Tx’s of hyperT & to prep for thyroid surgery

  • Methimazole & carbimazole: metabolites of methimazole
  • propylthiouracil [PTU]
  • Potassium Iodide (KI)
    • used in Fukushima nuclear disaster to counter radioactive potential exposures to I-131
32
Q

Levothyroxine

[ADME]

A
  • once daily
  • narrow toxic to therapeutic index
  • long t1/2 [7 days, 6-8 weeks before steadyst8 reached]
  • absorption is variable & incomplete [decreased by Fe, Ca, AIOH & soy]
  • pregos need 30-50% increased in dose
  • SE [iatrogenic hyperT]: palpitations, tremors, anxiety, w8 loss, tachC, ^^bowel movements, bone loss w/chronic med
    • CVD pts: arr’s, angina, & MI risk ^^
    • elderly: Afib
33
Q

When is Liothyronine used?

A

T3

  • short onset [4-6hrs
  • t1/2 is 2 days
  • greater potency
  • used when want quick onset
34
Q

What are Thioamides (propylthiouracil [PTU] & methimazole/carbimazole] used to Tx

[MOA/ADME]

A
  • Tx’s hyperT & prep for thyroid surg
  • methimazole & PTU inhibit thyroid peroxidase
  • PTU also inhibits DI [inhibits peripheral conversion T4 to T3]
  • rapid & complete oral absorption
  • accumulates in thyroid [PTU= 12 hrs, met=24hrs duration]
  • 2 weeks for effect
  • 1st line of defense for Graves

note: recent FDA warning on PTU= serious liver injury/hepatotox

35
Q

How is Iodine used as a Tx for thyroid disease?

A
  • prep for thyroidectomy, Tx thyroid storm, & protect from radioactive Iodine
  • ^^[]’s inhibit all aspects of Iodine met (transport, synth & release of thyr H)
  • “escape” from Iodine Tx can happen
  • SE’s: HSR, sore teeth & gums, excess salivation
36
Q

What are the advantages & disadvantages of radioactive iodine Tx

A
  • 131-I: destroys thyroid
    • advantage: painless, easy to admin, cheap & effective
    • disadvantage: too much destrxn!
    • need to supplement Thyroid H’s after Tx
37
Q

How do we Tx Graves disease?

A
  • antithyroid H’s [ATD]!!!
    • course of 12-18 months
    • recurrence of Graves after discontinuing ATD is high
      • 30-50% in adults
      • 30% in kids
38
Q

Which is preferred in hyperT/Graves methimazole or PTU?

A

Methimazole!!

unless pregnant: then use PTU

Endo/Repro Block1 (11 decks)

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