Thyroid gland pharmacology b.pharm 5th sem.pptx

1. Thyroid hormones- analogues and
their inhibitors
Pharmacology II
B.Pharm Vth Semester

2. Anatomy of Thyroid Gland
• The thyroid gland is the
largest, butterfly-shaped
endocrine glands & is
located at the base of
the neck immediately
below the Larynx, on
each side of & anterior
to the trachea.
• Over Trachea
• Two Lobes connected
together by an isthmus
• 15 to 20 g

3. • Thyroid gland is
composed over a million
cluster of follicles
• Follicles are spherical &
consists of epithelial cells
surrounding a central
mass (colloid)
• The thyroid gland consists
of 2 types of cells:
• Follicular cells: These are
more abundant, and the
major secretory cells.
They secrete Thyroid
hormone.
• Parafollicular cells or C-
cells: These are fewer in
number & interspersed.
They secrete Calcitonin

4. THYROID HORMONES
• The Thyroid gland secretes 3 major hormones:
1. Thyroxine or T4 : having 4 atoms of Iodine.
(secreted in largest amount)
2. Triiodothyronine or T3 : having 3 atoms of
Iodine (secreted in lesser amount)
3. Calcitonin: which is an important hormone of
calcium metabolism

5. DIFFERENCE BETWEEN T4 & T3
• The thyroid secretes about 80 micrograms of
T4, but only 5 micrograms of T3 per day.
• However, T3 has a much greater biological
activity (about 10X) than T4.
• An additional 25 micrograms/day of T3 is
produced by peripheral monodeiodination of
T4.

6. Thyroid hormone- 2 important
biological functions
1. Normal human growth & development, esp.CNS
2. In adults,maintain metabolic homeostasis,
affecting all organ systems
• Metabolism of thyroid hormone occurs in liver
and brain
• TSH regulates serum thyroid hormones by a
negative feedback system
• Bind to nuclear thyroid hormone receptors,
modulates gene transcription

7. BIOSYNTHESIS OF THYROID
HORMONES
• Thyroid gland is unique in storing large amount of preformed
hormone
• Thyroid follicular colloid stores thyroid hormone as amino residues
of thyroglobulin
• Iodide is required for synthesis of thyroid hormone
• Sea fish, eggs, milk and water - dietary sources of iodide, carried in
plasma as inorganic iodide
• Sources: Food, water or medication
• Daily Requirement for adult: 150 μg (200 μg in pregnancy and
lactation)
• Total body content of Iodine 30 – 50 mg (1/5th in thyroid gland)
• odine denotes all form of the element and Iodide denotes only the
ionic form (I-)
• 75 μg is utilized daily for hormone synthesis by thyroid gland

8. Synthesis , storage & secretion of thyroid hormone:
• Involve following steps;
1)Uptake of plasma iodide by follicle cells.
2)Oxidation of iodide & iodination of tyrosin residues of thyroglobuline.
3) Coupling.
4)Secretion of thyroid hormone.
5)Peripheral conversion of T4 to T3.
1)Uptake of plasma iodide by follicle cells:
• Regular I2 requirement of body is 30-50mg which fulfilled by food & water, about 1/5
is present in thyroid.
• Iodide is capture from blood & move to lumen by 2 transporter,
Na+/I- symporter (NIS)- Locate at basolateral surface of thyrocytes. Pendrin I-/Cl-
Porter( PDS)- At apical membrane.
• Iodine uptake is energy dependent process energy provided by Na+/K+ATPase

9. 2)Oxidation of iodide & iodination of tyrosin residues of thyroglobuline.
• Captured Iodide carried across the membrane by pendrine transport &
oxidised by thyroid peroxidase enzyme (Oxidising agent).
• Inside the cells, iodide is oxidized by membrane bound peroxidase system to
more reactive iodine (Iodinium(I+)/Hypoiodous acid (HOI)/Enzyme linked
hypoiodate (E-OI)
• Iodine immediately reacts with tyrosine residue on a thyroid glycoprotein
called “thyroglobulin” to form: MIT (Monoiodotyrosin ) (3rdposition)and DIT
(Diiodotyrosin ) (5th position)
• Both processes are catalyzed by thyroid peroxidase enzyme

10. • 3) Coupling:
• Coupling is oxidative reaction catalyzed by same thyroid peroxidase
enzyme .
• Thyroglobuline is efficient protein helps for reaction.
• Pair of iodinated tyrosil residue couple together to form T3 & T4.
• 2 molecule of diiodotyrosine-=Thyroxine (T4)
• 1 molecule of monoiodotyrosine + 1 molecule of diiodotyrosine =
Triidothyronine (T3).
• Normally high amount of T4 is formed

11. 4)Storage and Secretion of thyroid hormone:
• Normal human thyroid secretes- 60-90 μg of T4 & 10-30 μg of T3.
• The iodinated residue of thyrosin get transferred to the interior of the follicles
where it store as thyroid colloid. MIT, DIT, T3 and T4 - all attached to
thyroglobulin and stored in the colloid Thyroglobulin molecule
• After release it uptake by endocytosis after stimulation of TSH. This process is
stimulated by TSH
• Taken up by follicular cells by the process of endocytosis and broken down by
lisosomal proteases
• T3 and T4 released and also MIT and DIT. MIT and DIT are deiodinated and
reutilized
• T4 & T3 enter circulation directly from follicular cells
• Free (unbound) hormone is a small percentage, 0.03%T4 and 0.3%T3 of the
total plasma hormone
• Only unbound form has metabolic activity
5)Peripheral conversion of T4 to T3:
Peripheral tissue like liver, kidney convert T4 to T3.
Target tissue take T3 from plasma depended upon their metabolic need. While
brain and pituitary takes T4 and convert that to T3 with own cell.
Drugs like some propylthiouracil, propranolol etc. inhibit conversion of T4 to T3.

13. T3 Vs T4
• T3 is 5 times more potent > T4
• Half life of T4 is 6-7 days and T3 is 1-2 days – hyper and
hypothyroidism
• T4 is the major circulating hormone – bound more to
plasma proteins
• T4 is less active and a precursor of T3 - the major mediator
of physiological effects
• The term thyroid hormone is used to comprise both T4 plus
T3
• T4 deiodination to T3 or reverse T3
• T3 & reverse T3 deiodination to three diiodothyronines,
deiodinated to two monoiodothyronines - (inactive)

14. REGULATION OF THYROID HORMONE
LEVELS
Thyroid hormone synthesis and secretion is
regulated by two main mechanisms:
• - an “autoregulation” mechanism, which reflects
the available levels of iodine
• - regulation by the hypothalamus and anterior
pituitary

15. AUTOREGULATION OF THYROID
HORMONE PRODUCTION
The rate of iodine uptake and incorporation into
thyroglobulin is influenced by the amount of
iodide available:
• - low iodide levels increase iodine transport
into follicular cells
• - high iodide levels decrease iodine transport
into follicular cells
• Thus, there is negative feedback regulation of
iodide transport by iodide.

16. FEEDBACK REGULATION
THE HYPOTHALAMIC-PITUITARY-THYROID AXIS
• Hormones derived from the pituitary that
regulate the synthesis and/or secretion of
other
• hormones are known as trophic hormones.
• Key players for the thyroid include:
• TRH - Thyrotropin Releasing Hormone
• TSH - Thyroid Stimulating Hormone
• T4/T3 - Thyroid hormones

17. Mechanism Of Action of Thyroid
Hormone
• T3 & T4 penetrate cell by
active transport
• Combine nnuclear thyroid
hormone receptor (TR)
• T3 binds to high affinity
receptors
• Three thyroid hormone
receptor:- TR α1, TRβ1,
TRβ2
• TRα1, binds to DNA
sequence in specific genes
• Hormone receptor
complex bind to DNA via
zinc fingers undergo
• conformational changes
• T3 modulates gene
transcription and
Production of specific m-
RNA & protein synthesis
• T4 binds with lower affinity
than T3 but does not alter
gene transcription
• T3 causes all actions of
thyroid hormones at
transcriptional level
• Gives various metabolic &
anatomic effect

19. Actions:
• The T3 & T4 having almost
having same functions ;
1) Growth & Development.
2) Intermediary metabolism.
3)Calorigenesis.
4)Cardivascular system.
5) Nervous system.
6)Skeletal muscle.
7)GIT.
8)Kidney.
9)Haemopoiesis.
10) Reproduction.

20. 1) Growth & Development.
• Eessential for normal growth and development.
• The action cannot be categorised as catabolic or anabolic.
• T3 & T4 have role in protein synthesis i.e. translation of genetic
code therefore Congenital deficiency of T, and T, resulting in
cretinism & delayed development of organs or deficit dendrites
ramification, synapse formation & impaired myelination.
2) Intermediary metabolism.
Thyroid hormones have marked effect on Thyroid lipid,
carbohydrate and protein metabolism.
• Lipid: T3 & T4 potentiate action of catecholamine & lipolytic
action (Increases lipolysis)
• Suppress phosphodiestrase- Increases cAMP- Increases plasma
free fatty acid.
• Increases cholesterol metabolism- so causes
hypocholesterolemia.

21. • Carbohydrate: T3 & T4
• Increases carbohydrate metabolism.
• Increases sugar utilization by tissue but faster absorption
of glucose from blood. Increases absorption & less
metabolism causes hyperglycemia & diabetic like state.
• Therefore hyperthyroidism causes insulin resistance.
• Protein: T3 & T4
• Increases synthesis of certain protein which used as
protein source by body.
• But prolong action causes negative nitrogen balance &
weight loss.
• At low concentration of T3 & T4 inhibit mucoprotein
synthesis .
• T3 & T4 increses the oxygen consumption & heat
production.

22. 3)Calorigenesis:
• T3 & T4 increases basal metabolic rate by increasing cellular
metabolism.
• Which helps to maintain body temperature during calorigenesis causes
oxidative phosphorylation & that release heat but this reaction only
occurs in high dose.
4)Cardivascular system:
• T3 & T4 causes hyperdynamic state of circulation Increses blood
volume unknowingly). Also increases heart rate, contractility & output
of heart by acting on contractile element.
• During hyperthyroidism causes arterial fibrillation & other regularity
like CHF and angina.
5) Nervous system:
• T3 & T4 deficency causes mental retardation or cretinism. Also
hyperthyroid individuals are anxious, nervous, excitable or produces
tremors.

23. 6)Skeletal muscle:
• Hypothyroidism causes swelling of skin & underlying tissue.
• Hyperthyroidism causes increases muscle tone, tremor & weakness.
7)GIT:
• T3 & T4 causes increased gut activity which causes diarrhea.
8)Kidney:
• Hypothyroidism causes diuresis . While normal person not causes diuresis.
9)Haemopoiesis:
• T4 increases process of RBC formation (Erythropoiesis) Therefore T4 treatment
given to patient suffering from anemia.
10) Reproduction:
• Thyroid has an indirect effect on reproduction fertility is impaired in
hypothyroidism & Oligomenorrhoea(Infrequent menstrual periods).
• Normal thyroid function is required for maintenance of pregnancy and
lactation.

24. THYROID DISEASES
• If your thyroid is too active, it makes more thyroid hormones than
your body needs. That condition is hyperthyroidism. Too much
thyroid hormone can make you lose weight, speed up your heart
rate and make you very sensitive to heat.
• A thyroid gland that is not active enough, called hypothyroidism, is
far more common. It can make you gain weight, feel fatigued and
have difficulty dealing with cold temperatures
HYPERTHYROIDISM & HYPOTHYROIDISM
• Hyper-secretion or hypo-secretion will induce diseases:
• Too much secretion causes hyperthyroidism
• Too little secretion causes hypothyroidism

25. HYPOTHYROIDISM
• Hypothyroidism is a condition in which the thyroid gland fails to produce enough
thyroid hormone. Complications Untreated hypothyroidism can lead to a number of
health problems:
Complications-
• Heart problems.
• Mental health issues.
• Myxedema.
• Birth defects.
HYPERTHYROIDISM
• Hyperthyroidism is a condition caused by an overactive thyroid gland.
• The gland makes too much T4 and T3 hormones.
Complications-
• Hyperthyroidism can lead to a number of complications:
• Heart problems.
• Brittle bones.
• Eye problems. People with Graves' ophthalmopathy develop eye problems, including
bulging, sensitivity to light, and blurring or double vision.
• Thyrotoxic crisis —a sudden intensification of the symptoms, leading to a fever, a rapid
pulse and even delirium. If this occurs, seek immediate medical care.

26. Thyroid Preparations
These are synthetic compounds are identical to the natural hormones:
1) Levothyroxine (T4)
2) Liothyronine (T3)
Therapeutic Uses
The most important uses of thyroid hormone are as
replacement therapy deficiency states:
1)Cretinism
2)Adult hypothyroidism
3)Myxoedema coma
4)Nontoxic goiter
5) Thyroid nodule
6) Papillary carcinoma of thyroid.
7) Other uses.

27. Cretinism
• Endemic or sporadic
• Endemic - extreme iodine deficiency
• Sporadic – failure of thyroid to develop normally or
defective hormone synthesis
• Detectable at birth, may not be recognized until 3-5
mths of age
• Dwarfism ,mental retardation, short extremities,
inactive, puffy & expressionless face, enlarged
tongue, skin yellow, dry & cool, bradycardia, low
body temp., late teeth eruption, Poor appetite,
feeding slow, constipation, umbilical hernia
• Treatment with thyroxine (8-12 ug/kg) daily, prior to
pregnancy till end of 2nd trimester

28. Adult hypothyroidism(Myxoedema)
• commonest endocrine disorders - Caused due to autoimmune
thyroiditis, thyroidectomy.
• Antibodies generated against thyroid peroxidase or thyroglobuline.-
Causes adult hypothyroidism.
• Drugs that can cause hypothyroidism are 13 iodides, lithium and
amiodarone which treated with T4 50ug/day.
• Face: expressionless, puffy, pallid, Skin: cold, dry, scaly scalp
• Hair: coarse, brittle, sparse, Fingernails: thickened, brittle
• Voice: husky, low pitched, slow speech, Poor appetite, constipation
• Voluntary muscles weak and relaxation of deep tendon reflexes
delayed
• Dilated heart, pericardial effusion, ascites, Hyperlipidemia, anaemia,
Cold intolerance
• Subclinical hypothyroidism- In this disorder free serum thyroxine level
increases but TSH level decreases- This condition treated with T4.

29. Myxoedema coma
• It is an emergency condition were progressive mental
deterioration caused due to deficient production of
thyroid hormone(Hypothyroidism).
• Profound hypothermia, respiratory depression,
unconscious, bradycardia, delayed reflexes, dry skin etc.
• This condition treated with liothyroinine (T3) but high risk
of cardiac arrhythmia & angina.
• I V. dose T3(10μg/8hr).
Nontoxic goiter
• Endemic due to iodine deficiency.
• Sporadic due to defect in hormone synthesis.
• In above cases deficiency of thyroid hormone leads to
increases TSH causes enlargement of thyroid gland
treatment with T4.

30. Thyroid nodule:
• When T4 treatment is started TSH synthesis get
suppressed causes normal functioning of nodules
function while nonfunctional nodules not respond.
Papillary carcinoma of thyroid:
• This is type of cancer caused due to TSH over
production; treatment with T4 causes decreased
TSH production.
Other uses.
• T4 used for treatment of refractory anemia, mental
depression, menstrual disorder or infertility.

31. Anti-thyroid drugs/ Thyroid inhibitors
Definition: “ These are the pharmacological agents which are
used to lower the functional capacity of hyperactive thyroid
gland”
• These are the agents used in treatment of thyrotoxicosis ( It
is excess secretion of thyroid hormone due to disorders)
• The two main causes are- Graves disease( auto immune
disease) and Toxic nodular goiter.
• Graves’ disease is an autoimmune disorder: IgG class of
antibodies to the TSH receptor are detected in blood. They
bind to and stimulate thyroid cells, and produce other TSH
like effects.
• Toxic nodular goiter, which produces thyroid hormone
independent of TSH, mostly supervenes on old nontoxic
goiters. It is more common in the elderly

32. CLASSIFICATION
1. Inhibit hormone synthesis
(Antithyroid drugs)
Ex. Propylthiouracil, Methimazole,
Carbimazole.
2. Inhibit iodide trapping (Ionic inhibitors)
Ex. Thiocyanates (–SCN), Perchlorates (–
ClO4), Nitrates (–NO3).
3. Inhibit hormone release
Ex. Iodine, Iodides of Na and K, Organic
iodide.
4. Destroy thyroid tissue
Ex. Radioactive iodine (131I, 125I, 123I).
Compounds in groups 1 and 2 may be
collectively called goitrogens because,
if given in excess, they cause
enlargement of thyroid by feedback
release of TSH.

33. Antithyroid drugs: ( Thioamides)
• Hormone synthesis inhibitors called Antithyroid
• Mechanism of action:
• Thiocarbamide ( S-C-N) group essential for activity.
• Antithyroid drugs bind to thyroid peroxidase and prevent
oxidation of iodide/iodotyrosyl residues;
1)Inhibit iodination of tyrosine residues in thyroglobuline.
2) Inhibit coupling of iodotyrosine residues to form T3 and
T4 which occurs as low concentration.
• Simply this class drug decreases the output of thyroid
hormone from the gland so decreases the sign and
symptoms of thyrotoxicosis.
• Propyl Thiouracil- Inhibit conversion of T4-T3- Mostly in
type 1st diabetes mellitus- but methamizole & Carbamazole
not have this action. drugs.

34. • Adverse drug reaction:
1)Hypothyroidism and goiter – Due to over treatment- After
stopping of treatment reversible effect is observed.
• At normal dose goiter not develop because T4 concentration
which maintain TSH level normal.
• High does: Causes excess TSH production- Enlargement of
thyroid gland (Goiter).
2)Other side effects: GI intolerance, Skin rashes, joint pain.
3)Graying or loss of hair, loss of taste, fever & liver damage.
4) Agranulocytosis & Jaundice may occurs.
• Preparation:
Propylthiouracil(50mg-150mg TDS)
Methimazole (5-10mg)
Carbimaole (5-15mg) (Inhibition T4-T3 peripheral conversion)

35. Uses:
1)Control thyrotoxicosis in graves disease & toxic nodular goiter.
Some times patient take another treatment like cough preparation, contrast media, aminodarone- less
responsive to Antithyroid agent.
In those cases the dose should be modify depending on the patient.
As definitive therapy: In some patient after 1-2 year of treatment remission may occur.
After drug withdrawal if symptoms recur again start the treatment.
Above situation mostly occurs in patient having short history of graves disease & small goiter.
The case like nodular goitre remission are rare or toxic that time surgery or I 131 is preferred.
Some cases in elderly patient with multinodular goiter maintenance therapy causes less responsive to
I131 so surgery advised.
2) Preoperatively:
Surgery (thyroidectomy) is advised to thyrotoxicosis patients which is very risky so preoperative
treatment of carbimazole is given.
3) Treatment along with I131:
When there is prompt control of severe hyperthyroidism in older patient following sequence of therapy
employed;
Starting treatment with Antithyroid drug.
1-2 week gap.
Radioiodine dosing.
Again Antithyroid drug after 5-7 days.
Withdrawal of drug after 3 month.
Again start I131 treatment.

36. Advantages of Antithyroid drug over surgery / I131 treatment:
• No surgical risk, scar or chances of injury to parathyroid or
nearest laryngeal nerve.
• If treatment with Antithyroid shows side effect like
hypothyroidism then stoppage of treatment reverse the action.
• The Antithyroid drugs used for children as well as young adults.
Disadvantage:
• Prolonged (often life long) treatment is needed because
stoppage of treatment shows recurrence & relapse rate is high.
• Not practicable in uncooperative/unintelligent patient.
• High drug toxicity & side effects.
• During pregnancy thyroidectomy and I131 are contraindicated
because it develops risk of foetal hypothyroidism and goiter. in
this condition propylthiouracil is preferred.

37. IONIC INHIBITORS
• Certain monovalent anions inhibit iodide trapping
by NIS into the thyroid probably because of similar
hydrated ionic size—T4/T3 cannot be synthesized.
Perchlorate is 10 times more potent than
thiocyanate in blocking NIS, while nitrate is very
weak.
• They are toxic and not clinically used now.
• Thiocyanates: can cause liver, kidney, bone marrow
and brain toxicity.
• Perchlorates: produce rashes, fever, aplastic
anaemia, agranulocytosis.

38. Iodine/Iodide
• Even if the iodine is one of the constitute of thyroid hormone
but still it acts as faster acting thyroid inhibitor(Antithyroid).
• In the process of thyroid hormone release in one step iodine is
covered in to on vivo iodide (I-) and due to negative feedback
mechanism iodide inhibit release of thyroid hormone.
• Within 1-2 days of starting of treatment causes inhibition of
secretion of thyroid hormone while 10-14 days causes marked
reduction in vascularity of gland & which causes decreases the
size of gland.
• Iodine mostly orally in solution with potassium Iodide( Lugols
iodine)
• Effect seen in 15-15 days. But further treatment causes thyroid
escape & thyrotoxicosis or hyperthyroidism mostly occurs in
multinodular goiter.

39. Mechanism of action:
• Actual mechanism is unknown; It inhibits own transport in to thyroid cell (
Step 1 in thyroid synthesis) by acting on NIS (Sodium Iodide symporter)
• It attenuates TSH & cAMP & causes thyroid inhibition.
• Also excess iodide rapidly interferes with tyrosil ( Iodination step2)
• Inhibit thyroid ( Wolff chaikoff effect)
• Inhibition of hormone release causes thyroid constipation.
Uses:
1) Preoperative preparation:
• For thyroidectomy in graves disease; iodine for 10 days before surgery will
given which makes gland less vascular & easier to remove by operation.
2) Thyroid storm:
Lugol's iodine (6-10 drops) or iodine containing radiocontrast media (iopanoic
acid) are used orally to stop further release and conversion of T3/T4 from the
thyroid.
3) Prophylaxis of endemic goiter: It is used as "iodized salt“.
4) Antiseptic: The tincture of iodine, povidone iodine is used as antiseptic.

40. Adverse drug reaction:
1) Acute Acute reaction It occurs in sensitive people.
Shows symptoms like swelling of lips, eyelids, angio-
edema of larynx (may be dangerous), fever, joint pain,
petechial haemorrhages, thrombocytopenia,
lymphadenopathy.
2) Chronic overdose (iodism): Inflammation of mucous
membranes, salivation, rhinorrhoea, sneezing,
lacrimation, swelling of eyelids, burning sensation in
mouth, headache, rashes, g.i. symptoms.
3) Long-term use of high doses can cause
hypothyroidism & goiter.
4) If high dose given to pregnant women chance to
hypothyroidism & goiter in foetus.

41. Radioactive Iodine:
• Ex- I131, I123 I125.
• The stable form of isotope of iodine is I127 but
medically useful isotope is I 131 which having half
life 8 days available as sodium salt; given as oral
dose.
• But one of the advantage of radioactive iodine is it
produce necrosis of cell (affected thyroid follicular
cell) without damaging neighboring tissue.
• Radioactive iodine administration as sodium salt of
I 131 dissolve in water & take orally.
Diagnostic : 25-100μg given scanning is done at
interval ( No damage to thyroid cell occurs with this
dose).

42. Mechanism of action:
• 131I emits X-rays as well as β particles. The former
are useful in tracer studies, while the latter are
utilized for their destructive effect on thyroid cells.
• 131I is concentrated by thyroid, incorporated in
colloid—emits radiation from within the follicles.
• The β particles penetrate only 0.5–2 mm of tissue.
• The thyroid follicular cells are affected from within,
undergo pyknosis and necrosis followed by fibrosis
when a sufficiently large dose has been
administered, without damage to neighbouring
tissues
• Radioactive iodine is administered as sodium salt of
131I dissolved in water and taken orally.

43. Therapeutic:
• The hyperthyroidism is mainly occurs due to grave’s disease or toxic nodular
goiter at that time therapeutic dose is 3-6 mg curie.
• High dose is requirement for toxic multinodular goiter.
• The response to radio active iodine is start after 2 week & get increased after
3 month.
Advantages:
• Treatment with I 131 is inexpensive.
• No surgical risk, scar or thyroids/recurrent laryngeal nerves after treatment
with I 131
• Once hyperthyroidism is controlled, cure is permanently.
Disadvantages:
1) Hypothyroidism: About 5-10% patients of Graves' disease treated with 1311
become hypothyroid.
2) Very slow response was observed for treatment with I131.
3) during pregnancy drug is Contraindicated because it causes foetal thyroid
destruction.
4)I131 not suitable for young patients more likely to develop
hypothyroidism & genetic damage/cancer .

44. β- Adrenergic blocker:
• Nonselective B blockers- propranolol used for tretment of
thyrotoxicosis because in hyperthyroidism; over activity of
sympathetic nervous system was observed i.e. palpitation,
tremor, nervousness, myopath, swelling.
• Very little effect on thyroid function & hyper metabolic
state.
• B blockers used for tretment of hyperthyroidism in
following situation;
1) While response to carbimazole, propylthiouracil or I131
is low.
2) B blockers given along with iodide for preoperative
preparation before subtotal thyroidectomy.
3) Thyroid storm (thyrotoxic crisis-It is an emergency due
to decompensate hyperthyroidism.) In above condition
emergency treatment with B blockers are given.