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Thyroid & Antithyroid Drugs




  Fig 1                         Fig 2

* Thyroid follicles are the structural & functional units of the thyroid gland.
* Each follicle is surround mainly by simple cuboidal epithelium and is
filled with a colloid which mainly composed by thyroglobulin.
* Thyroid hormones are mainly synthesized in colloid while the simple
cuboidal epithelium undertaking thyroglobulin production, iodide intake &
thyroid hormones release.                               1
●Synthesis of thyroid hormones
Thyroid hormones                     MIT: monoiodotyrosine
   triiodothyronine (T3)             DIT: diiodotyrosine
   tetraiodothyronine (T4, thyroxine)
Materials
   iodine & tyrosine         Thioamid
                                     e drugs
Steps
1. Iodide is trapped by sodium-iodide symporter
2. Iodide is oxidized by thyroidal peroxidase to iodine
3. Tyrosine in thyroglobulin is iodinated and forms MIT & DIT
4. Iodotyrosines condensation
     MIT+DIT→T3;       DIT+DIT→T4              2
Intra-thyroidal synthesis and processing of thyroidal hormones
1.    Iodide is taken up at the basolateral cell             thyroidal peroxidase
      membrane and transported to the apical
      membrane
2.    Polypeptide chains of Tg (thyroglobulin) are
      synthesized in the rough endoplasmic reticulum,
      and posttranslational modifications take place in
      the Golgi
3.    Newly formed Tg is transported to the cell surface
      in small apical vesicles (AV)
4.    Within the follicular lumen, iodide is activated and
      iodinates tyrosyl residues on Tg, producing fully
      iodinated Tg containing MIT, DIT, T4 and a small
      amount of T3 (organification and coupling), which
      is stored as colloid in the follicular lumen
5.    Upon TSH stimulation, villi at the apical
      membrane engulf the colloid and endocytose the
      iodinated Tg as either colloid droplets (CD) or
      small vesicles (MPV)
6.    Lysosomal proteolysis of the droplets or vesicles
      hydrolyzes Tg to release its iodinated amino acids
      and carbohydrates
7.    T4 and T3 are released into the circulation
8.    DIT and MIT are deiodinated, and the iodide and
      tyrosine are recycled                                  3
●Regulation   of thyroid function




                             TRH: thyrotropin-releasing hormone
                             TSH: thyroid-stimulating hormone




                                             4
●Physiological actions of thyroid hormones

 To normalize growth and development, body temperature,
  and energy levels
   ▲Insufficiency→ cretinism (infant & child), and
  myxedema (adult);
  ▲Excess→hyperthyroid

 To enhance CNS excitability & sensitivity of CVS to NA



# T3 is 3 to 4 times more potent than T4 in heat production;
# T4 in colloid is about 4 times more numerous than T3 ;



                                                           5
hyperthyroid




cretinism
myxedema
            6
Myxedema
Stems from both the hyperthyroid and hypothyroid conditions,
results from the accumulation of increased amounts of
hyaluronic acid and chondroitin sulfate in the dermis in both
lesional and normal skin.
The mechanism that causes myxedema is still not yet
understood. Sympotoms include:
●Skin thickening ●Coarse skin ●Change in facial appearance

●Thickening nose ●Swollen lips ●Puffiness around the eyes

●Jelly-like infiltrations in subcutaneous tissues ●Slow speech

●Mental dullness              ●Lethargy         ●Mental problems

●Dry skin        ●Yellow skin       ●Swollen subcutaneous tissue

●Weight gain               ●Constipation           ●Thinning hair

● Brittle hair             ●Bald patches           ●Muscle pains
                                                 7
●Mechanism   of actions
     of thyroid hormones
                                      T3, via its nuclear
• Some of T4 are converted to T3 in
                                      receptor, induces
  kidney and liver
                                      new proteins
•    The actions of T3 on several
    organ systems are shown           generation which
                                      produce effects
• BMR: basal metabolic rate; CNS:
  central nervous system




                                          8
Thyroid drugs

    ● Representative    drugs
      levothyroxine (L-T4, levoxyl, synthroid)
      liothyronine (T3, cytomel, triostat)
      liotrix (T4 plus T3) (euthyroid, thyrolar)

●   Pharmacokinetics
    po easily absorbed; the bioavailablity of T4 is 80%, and T3 is
95%.
    Drugs that induce hepatic microsomal enzymes (e.g., rifampin,
phenbarbital, phenytoin, and etc) improve their metabolism.
                                                  9
●Pharmacological   effect
    see physiological effect

● Clinical   use
1. Hypothyroidism: cretinism & myxedema;
2. simple goiter: for pathogeny remaining unclear
   (endemic goiter directly supply iodine)
3. Others:
● Adverse   reactions
   Overmuch leads to thyrotoxicosis;
   Angina or myocardial infarction usually appears in
ageds
                                           10
Antithyroid drugs
● Drugs

  Class                       Representative
                            propylthiouracil
                            methylthiouracil
  Thioamides
                            methimazole
                            carbimazole
  Iodides                    KI, NaI
  Radioactive iodine        131
                                I
  β-adrenoceptor blockers   propranolol

                                       11
І. Thioamides

 ◆Structure




The thiocarbamide
group is essential for
antithyroid activity



                         12
Pharmacological action
   Inhibition of the synthesis of T3 & T4
Mechanism
All thioamides inhibit peroxidase-catalyzing reactions
  Iodine organification               First choice for
  Iodotyrosines condensation           thyroid crisis
Propylthiouracil also inhibit T4 converting to T3
Characteristics
① Result appears slowly: in 3-4 w hyperthyroid
ameliorated, and in 2-3 months BMR normalized;
② Long-term use leads to thyroid hyperplasia
③ Methimazole is 10 times as potent as propylthiouracil
                                          13
Clinical use
  treatment of hyperthyroid
    1. Mild hyperthyroid and those surgery & 131I
not permitted;
    2. Operation preparation;
    3. Thyroid crisis (comprehensive therapy).

Adverse reactions
   1. Long-term use leads to thyroid hyperplasia;
   2. Pruritic maculopapular rash is the most common
adverse raaction
   3. The severe adverse reaction is agranulocytosis
                                             14
Iodides (NaI, KI)
Pharmacological action
   Inhibition of T3 & T4 release and synthesis
   Decrease of size & vascularity of the hyperplastic gland

Clinical use
  Ministrant treatment of hyperthyroid
   1. Operation preparation;
   2. Thyroid crisis.

Adverse reactions
  1. Acneiform rash (similar to that of bromism);
   2. Swollen salivary glands, mucous membrane ulcerations, and etc.
                                                    15
Radioactive iodine (131I)

131
   I is the only isotope for treatment of thyrotoxicosis.
Its therapeutic effect depends on emission of β rays with an
effective half-life of 5 days & a penetration range of 0.4-2 mm.
Woman in pregnancy or lactation is forbidden!

                 β-adrenoceptor blockers

βblockers are effective in treatment of thyrotoxicosis.
Propranolol is the most widely studied and used.

                                               16

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thyroid & antithyroid drugs..

  • 1. Thyroid & Antithyroid Drugs Fig 1 Fig 2 * Thyroid follicles are the structural & functional units of the thyroid gland. * Each follicle is surround mainly by simple cuboidal epithelium and is filled with a colloid which mainly composed by thyroglobulin. * Thyroid hormones are mainly synthesized in colloid while the simple cuboidal epithelium undertaking thyroglobulin production, iodide intake & thyroid hormones release. 1
  • 2. ●Synthesis of thyroid hormones Thyroid hormones MIT: monoiodotyrosine triiodothyronine (T3) DIT: diiodotyrosine tetraiodothyronine (T4, thyroxine) Materials iodine & tyrosine Thioamid e drugs Steps 1. Iodide is trapped by sodium-iodide symporter 2. Iodide is oxidized by thyroidal peroxidase to iodine 3. Tyrosine in thyroglobulin is iodinated and forms MIT & DIT 4. Iodotyrosines condensation MIT+DIT→T3; DIT+DIT→T4 2
  • 3. Intra-thyroidal synthesis and processing of thyroidal hormones 1. Iodide is taken up at the basolateral cell thyroidal peroxidase membrane and transported to the apical membrane 2. Polypeptide chains of Tg (thyroglobulin) are synthesized in the rough endoplasmic reticulum, and posttranslational modifications take place in the Golgi 3. Newly formed Tg is transported to the cell surface in small apical vesicles (AV) 4. Within the follicular lumen, iodide is activated and iodinates tyrosyl residues on Tg, producing fully iodinated Tg containing MIT, DIT, T4 and a small amount of T3 (organification and coupling), which is stored as colloid in the follicular lumen 5. Upon TSH stimulation, villi at the apical membrane engulf the colloid and endocytose the iodinated Tg as either colloid droplets (CD) or small vesicles (MPV) 6. Lysosomal proteolysis of the droplets or vesicles hydrolyzes Tg to release its iodinated amino acids and carbohydrates 7. T4 and T3 are released into the circulation 8. DIT and MIT are deiodinated, and the iodide and tyrosine are recycled 3
  • 4. ●Regulation of thyroid function TRH: thyrotropin-releasing hormone TSH: thyroid-stimulating hormone 4
  • 5. ●Physiological actions of thyroid hormones  To normalize growth and development, body temperature, and energy levels ▲Insufficiency→ cretinism (infant & child), and myxedema (adult); ▲Excess→hyperthyroid  To enhance CNS excitability & sensitivity of CVS to NA # T3 is 3 to 4 times more potent than T4 in heat production; # T4 in colloid is about 4 times more numerous than T3 ; 5
  • 7. Myxedema Stems from both the hyperthyroid and hypothyroid conditions, results from the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin. The mechanism that causes myxedema is still not yet understood. Sympotoms include: ●Skin thickening ●Coarse skin ●Change in facial appearance ●Thickening nose ●Swollen lips ●Puffiness around the eyes ●Jelly-like infiltrations in subcutaneous tissues ●Slow speech ●Mental dullness ●Lethargy ●Mental problems ●Dry skin ●Yellow skin ●Swollen subcutaneous tissue ●Weight gain ●Constipation ●Thinning hair ● Brittle hair ●Bald patches ●Muscle pains 7
  • 8. ●Mechanism of actions of thyroid hormones T3, via its nuclear • Some of T4 are converted to T3 in receptor, induces kidney and liver new proteins • The actions of T3 on several organ systems are shown generation which produce effects • BMR: basal metabolic rate; CNS: central nervous system 8
  • 9. Thyroid drugs ● Representative drugs levothyroxine (L-T4, levoxyl, synthroid) liothyronine (T3, cytomel, triostat) liotrix (T4 plus T3) (euthyroid, thyrolar) ● Pharmacokinetics po easily absorbed; the bioavailablity of T4 is 80%, and T3 is 95%. Drugs that induce hepatic microsomal enzymes (e.g., rifampin, phenbarbital, phenytoin, and etc) improve their metabolism. 9
  • 10. ●Pharmacological effect see physiological effect ● Clinical use 1. Hypothyroidism: cretinism & myxedema; 2. simple goiter: for pathogeny remaining unclear (endemic goiter directly supply iodine) 3. Others: ● Adverse reactions Overmuch leads to thyrotoxicosis; Angina or myocardial infarction usually appears in ageds 10
  • 11. Antithyroid drugs ● Drugs Class Representative propylthiouracil methylthiouracil Thioamides methimazole carbimazole Iodides KI, NaI Radioactive iodine 131 I β-adrenoceptor blockers propranolol 11
  • 12. І. Thioamides ◆Structure The thiocarbamide group is essential for antithyroid activity 12
  • 13. Pharmacological action Inhibition of the synthesis of T3 & T4 Mechanism All thioamides inhibit peroxidase-catalyzing reactions Iodine organification First choice for Iodotyrosines condensation thyroid crisis Propylthiouracil also inhibit T4 converting to T3 Characteristics ① Result appears slowly: in 3-4 w hyperthyroid ameliorated, and in 2-3 months BMR normalized; ② Long-term use leads to thyroid hyperplasia ③ Methimazole is 10 times as potent as propylthiouracil 13
  • 14. Clinical use treatment of hyperthyroid 1. Mild hyperthyroid and those surgery & 131I not permitted; 2. Operation preparation; 3. Thyroid crisis (comprehensive therapy). Adverse reactions 1. Long-term use leads to thyroid hyperplasia; 2. Pruritic maculopapular rash is the most common adverse raaction 3. The severe adverse reaction is agranulocytosis 14
  • 15. Iodides (NaI, KI) Pharmacological action Inhibition of T3 & T4 release and synthesis Decrease of size & vascularity of the hyperplastic gland Clinical use Ministrant treatment of hyperthyroid 1. Operation preparation; 2. Thyroid crisis. Adverse reactions 1. Acneiform rash (similar to that of bromism); 2. Swollen salivary glands, mucous membrane ulcerations, and etc. 15
  • 16. Radioactive iodine (131I) 131 I is the only isotope for treatment of thyrotoxicosis. Its therapeutic effect depends on emission of β rays with an effective half-life of 5 days & a penetration range of 0.4-2 mm. Woman in pregnancy or lactation is forbidden! β-adrenoceptor blockers βblockers are effective in treatment of thyrotoxicosis. Propranolol is the most widely studied and used. 16