Presentation on the thyroid gland and drugs which modify action of the gland

1. THYROID HORMONES AND ANTI- THYROID
DRUGS.
Hormones secreted from the thyroid gland
include:L-thyroxine (l- tetra iodo –l thyronine or T4
and triiodo-l thyronine or T3.
Term thyroxine or thyroid hormone is commonly
used to include both T3 and T4
 T3 is 3- 5 times more potent than T4 and is the
major physiologically active thyroid hormone
Thyro- calcitonin is also secreted by the thyroid
gland and is involved in calcium metabolism .

2. SYNTHESIS ,RELEASE AND
METABOLISM OF THYROID HORMONES
• The functional unit of the thyroid gland is
the thyroid follicle-consists of a cavity
lined with a single epithelial cell layer.
• The lumen of the follicle is filled with
thyroglobulin-large glycoprotein of MW
600,000
• Throglobulin is synthesized in the thyoid
and has 115 tyrosine residues.

3. steps in the synthesis of
thyroid hormones

4. SYNTHESIS ,RELEASE AND
METABOLISM OF THYROID HORMONES
Cont…
• Synthesis of thyroid hormone occurs in steps:
• Step 1- Iodide trapping or uptake of
circulating iodides by follicle cells.
• Energy dependent active process ,stimulated by
TSH and is also dependent on thyoid iodine
concentration
• Uptake is stimulated in case of iodine deficiency
and decreased when the thyroid iodine content
is high.

5. SYNTHESIS ,RELEASE AND METABOLISM OF
THYROID HORMONES Cont…
• Step 2-Oxidation of iodide to iodine atom or
free radical .
• Reaction occurs inside the follicle lumen and is
catalyzed by the enzyme thyroperoxidase.
• Thyroperoxidase requires hydrogen peroxide as
the oxidizing agent.
• Step3-Iodination of tyrosine residues of
thyroglobulin.
• Process also under the influence of
thyroperoxidase.
• Mono iodo tyrosine (MIT) and di iodo tyrosine
(DIT) are formed.

6. SYNTHESIS ,RELEASE AND METABOLISM OF
THYROID HORMONES Cont…
• Step 4- Coupling of iodotyrosine molecules to
form T3 andT4.
• MIT +DIT =T3 and DIT + DIT=T4—these
reactions are all under peroxidase.
• The iodinated thyroglobin is secreted and
stored in the follicular lumen.
• Step 5-Uptake of iodinated thyroglobulin TG.
• Under the influence of thyrotropin (TSH), the
iodinated thyroglobulin is taken back by the follicle
cells by aprocess of endocytosis where the cells
engulf some amount of the thyroglobulin colloid.

7. SYNTHESIS ,RELEASE AND METABOLISM OF
THYROID HORMONES Cont…
• Step6 Release of thyroid hormone into
circulation.
• Thyroglobulin is acted upon by proteolytic
enzymes to release thyroid hormones into
the circulation.
• Most of the hormone released is T4 , and
80% of T4 is de iodinated in peripheral
tissues into active T3.

8. • Step 1 Trapping of iodide—inhibited by
Thiocyanates ,perchlorates and nitrates.
These anions in high concentration
competitively inhibit the iodide transport
into the cell.
• Iodide trapping is stimulated by TSH.
DRUG ACTION ON THE THYROID GLAND

9. DRUG ACTION ON THE
THYROID GLAND
• Ionic inhibitors are no longer used in
hyperthyroidism:
1.Perchlorates-produce hypersensitivity
reactions-rashes, fever, aplastic anaemia
and agranulocytosis.
2.Thiocyanates- can cause liver, kidney,
bone marrow and brain toxicity.
3.Nitrates-induce methaemoglobinemia and
vascular effects

10. • Step 2 –oxidation of iodide—stimulated
by TSH but inhibited by antithyroid agents
and iodides.

11. DRUG ACTION ON THE
THYROID GLAND
• Step3 iodination of tyrosine into
MITand DIT –stimulated by TSH and
inhibited by antithyroid agents.
• Step 4 Coupling of MIT and DIT into
T3andT4 –stimulated by TSH and
inhibited by antithyroid agents.
• Step 5 endocytosis of thyroglobulin,TG
into follicular cells –stimulated by TSH

12. DRUG ACTION ON THE
THYROID GLAND
• Step6 proteolytic release of T4 and T3
–stimulated by TSH and inhibited by
iodides.
• Step 7 –de iodination of T4 into T3 –
inhibited by propyl thio uracil, propranolol
and ipodate.

13. TRANSPORT OF T3 AND T4
• They are transported in plasma bound to
plasma proteins.
• The main binding plasma protein is the
thyroxine binding globulin(TBG ) and
thyroxin binding albumin (TBA)
• Binding of thyroid hormones is important
because:
1.Only the free or unbound hormone is
pharmacologically active

14. TRANSPORT OF T3 AND T4.
2. Only the free or unbound hormone is
metabolized or excreted. Binding therefore
prolongs the duration of action of the
hormones by increasing their half lifes.
3.Certain factors affect the levels of TBA
and TBA and hence the pharmacological
actions of T3 and T4.

15. • TBG and TBA levels in plasma are raised
by: estrogens ,oral contraceptives
,clofibrate ,neuroleptics and pregnancy
TRANSPORT OF T3 AND T4

16. TRANSPORT OF T3 AND T4 Cont…
• In the presence of the above factors, more
thyroxine is bound and plasma
concentration is low. WHAT IS THE
THERAPEUTIC IMPLICATION?
• Concentrations of TBG andTBA are
lowered by corticosteroids, androgens
,anabolic steroids, furosemide.
• In the presence of the above factors less
thyroxine is bound and concentration of
thyroxine in plasma is high. WHAT IS THE
THERAPEUTIC IMPLICATION?

17. TRANSPORT OF T3 AND T4 Cont…
• Phenytoin and salicylates displace thyroid
hormones from plasma protein binding sites
and increases levels of the free hormone.
• Systemic factors e.g. liver disease. porphyria
and HIV infection decrease the binding
proteins.
• Plasma protein binding of thyroid hormones
increases their half lifes by protecting them
from metabolism and excretion,(free unbound
T4 in plasma is 0.03% and T3 0.3% )

18. METABOLISM OF THYROID HORMONES.
• Part of T4 is de iodinated to active T3
• The thyroid hormones are enventually de-
iodinated in the liver ,deaminated and
partly conjugated.
• Free and conjugated metabolites are
excreted in bile and urine.

19. REGULATION OF THYROID FUNCTION
• Secretion is mainly under thyrotropin
(TSH) secreted by the anterior pituitary.
• Secretion of thyrotropin is increased by the
hypothalamic TRH and decreased by
somatostatin.
• TSH stimulates all aspects of thyroid
hormone synthesis I.e steps 1-6.

20. REGULATION OF THYROID FUNCTION
Cont…
• TSH exerts a trophic effect on thyroid follicular cells
and influences thyroid circulation .Increase TSH
activity will thus lead to hypertrophy of follicular cells
,increase in blood flow and stimulation of thyroxin
synthesis and release.
• Plasma iodide levels also influence the thyroid
function i.e iodine defiency results in reduced
plasma iodide levels, reduced thyroxine synthesis
and increased levels of TSH and vice-versa.
• Iodide administration will lead to decrease in size
and vascularity of the thyroid gland due to reduced
TSH activity.

21. EFFECTS OF DRUGS ON THYROID FUNCTION/
drug interactions involving thyroid hormones
• Dopamine, l-dopa corticosteroids—
Inhibition of TRH and TSH secretion.
• Iodides, lithium--- Inhibition of thyroxine
synthesis and hypothyroidism.
• Cholestyramine
,colestipol,sucralfate,aluminium salts---
Inhibit thyroxine absorption from the gut.
• Phenytoin ,carbamazepine ,rifampicin,
phenobarbitone--- Enzyme inducers and
may increase T3 and T4 metabolism.

22. EFFECTS OF DRUGS ON THYROID
FUNCTION Cont…
• Propyl thiouracil, amiadarone,
corticosteroids ,beta blockers--- Inhibition of
conversion of T4 to T3.
• Androgens, glucocorticoids---- Decrease
thyroxin- binding globulin.
• Estrogens, tamoxifen ,mitotane--- Increase
thyroxin –binding globulin.
• Salicylates ,mefenamic acid furosemide----
DisplacesT3 andT4 from thyroxin binding
globulin.

23. PHARMACOLOGICAL EFFECTS OF
THYROID HORMONE.
• The physiological effects are mainly due to T3
because it is 3-5 times more potent than T4.
• REGULATION OF GROWTH AND
DEVELOPMENT.
– Regulation of growth and development of the skeletal
system and CNS.
– Above effect is partly direct and partly by
• GH ,parathormone and calcitonin potentiation.---
may involve protein synthesis by inducing
synthesis of specific MRNA and proteins in
target cell
• Thyroid hormone deficiency during fetal and
post natal growth and development –cretinism(
physical and mental retardation.)

24. METABOLIC EFFECTS.
• Stimulate metabolism of carbohydrates, proteins
and lipids.
• Above effects may be exerted directly or by
modulating effects of other hormones e.g.
insulin,glucagon catecholamine ,corticosteroids
and parathormone. WHAT WOULD BE THE
EFFECT OF THYROXINE ON INSULIN LEVELS?
• Basal metabolic rate is increased by calorigenic
effect i.e increased oxygen consumption by the
tissues.
• Uptake and utilization of glucose is increased and
lipolysis in tissues results in increased levels of
triglycerides, cholesterol and free fatty acids.

25. CARDIAC EFFECTS.
• Increased HR and cardiac output due to
sensitization of cardiac beta receptors to
catecholamines
AUTO REGULATION OF THYROID FUNCTION
• By negative feedback inhibition of
thyrotopin (TSH) from the pituitary by T3
and T4.

26. C N S. AND G.I.T
C N S.
• Increased thyroid hormone leads to
nervousness and many psycho neurotic
tendencies e,g anxiety , paranoia and
extreme worries.
• G .I.T
– Increase appetite and food intake.
– Increased rate of secretion of digestive juices.
– Increased gut motility I.e hyperthyroidism can
cause diarrhea and hypothyroidism can lead
to constipation.

27. EFFECT ON MUSCLE FUNCTION
• Increased thyroid hormone---increase in
skeletal muscle contractility.
• Hyperthyroidism manifests with fine
muscle tremors. This is caused by
increased reactivity of the neuronal
synapses in the areas of the spinal cord
that controls muscle tone
• Very high levels_----muscle weakness
due to excessive protein catabolism.

28. EFFECT ON SLEEP
• Hyperthyroidism leads to exicitability and
lack of sleep due to CNS excitation.
• Hypothyroidism causes extreme
somnolence ,with sleep lasting 12-14 hrs
a day.

29. EFFECT ON SEXUAL FUNCTION
• Hypothyroidism causes loss of libido in males
while very high levels may lead to impotence.
• In women ,hypothyroidism may cause:
• a) Menorrhagia ( excessive menstrual bleeding )
• b) Poly menorrhea (frequent menstrual bleeding)
• c) Irregular periods and amenorrhea.
• d) Decreased libido.
• Above effects may be due to excitatory and
inhibitory effects of thyroid hormones on anterior
pituitary hormones that control sexual function
(FSH and LH).
• Normal thyroid hormone levels is required for
maintenance of pregnancy and lactation.

30. VITAMIN REQUIREMENT
• Increases vitamin requirement because of
increase metabolic rate.
• Metabolic reactions require enzymes
which need vitamins as co- factors.
• Hyperthyroidism may cause vitamin
deficiency unless dietary intake is
increased.

31. Mechanism of action of thyroid
hormones
• Thyroid hormones, T3 and T4 penetrate
cells by active transport and produce most
of their actions by combining with a
nuclear thyroid hormone receptor (TR)
which belong to the steroid and retinoid
super family of intracellular receptors.
• There is increased synthesis of RNA
which leads to accelerated protein
synthesis and enhanced enzymatic and
cellular activities.

32. Mechanism of action of thyroid
hormones.
• Thyroid hormones also stimulate sodium –
potassium ATP- ase directly thus
facilitating membrane transport of sodium
and potassium and increasing cellular
utilization of oxygen.

33. Summary of Pharmacological
actions of thyroid hormones
• Increase rate of metabolism, total heat
production and oxygen consumption in
most body tissues.
• Promote normal physical and mental
development and growth.
• Potentiate the cardiovascular and
metabolic actions of catecholamines.

34. Summary of Pharmacological
actions of thyroid hormones
• At cellular level, they accelerate protein
synthesis, mainly by T3 .
• Approximately 1/3 of T4 is converted to T3
in the periphery, liver, kidneys and the
primary effect of the thyroid hormones is
apparently due to T3 activity.

35. DISORDERS IN THYROID GLAND FUCTION
HYPERTHYROIDISM. (THYROTOXICOSIS).
In most patients manifests with:
• Increase in size of thyroid gland 2-3
times its normal size.( hyperplasia)
• Each follicular cell increases the rate
of secretion of thyroid hormone 5-15
times the normal.
• Two types: Graves disease and toxic
nodular goiter.

36. Graves Disease./Exophthalmic goiter
/Diffuse toxic goiter.
• Auto immune disease in which antibodies
called thyroid stimulating immunoglobulin
(TSIs) form against the TSH receptor in
the thyroid (TD ).
• The antibodies bind with the same
membrane receptors that bind TSH and
induce continual activation of the cAMP
system of the the cells with resultant
development of hyperthyroidism.

37. Graves Disease./Exophthalmic goiter
/Diffuse toxic goiter. Cont…
• The TSI have a stimulating effect on the
thyroid gland (12 hr effect in contrast to
1hr for TSH).
• The high level of thyroid hormone
secretion caused by TSI in turn
suppresses the anterior pituitary formation
of TSH.
• TSH concentration is therefore less than
normal.

38. Toxic Nodular Goitre.
• Localised benign adenoma or tumour in
the TD tissue may cause hyperthyroidism
by secreting large quantities of TD
hormone.
• There is no evidence of an auto immune
disease.
• Increased secretion of TD hormones by the
adenoma depresses the TSH levels by the
pituitary gland .This in turn suppresses all
the secretory functions in the remainder of
the TD gland.

39. Other causes
• Anti arrhythmic drug amiadarone is rich in
iodine and can cause either hyper or hypo
thyodism .

40. GENERAL SYMPTOMS OF HYPERTHYROIDISM.
• A state of excitability.
• Intolerance to heat.
• Increased sweating
• Mild to extreme weight loss (50 kg or less).
• Varrying degrees of diarrhea.
• Muscle weakness.
• Nervousness or other psychic disorders.
• Extreme fatigue but inability to sleep.
• Tremors of the hands.
• Exopthalmos or protrusion of the eye ball.

41. Exopthalmos
• Affects about a third of hyperthyroidism patients
especially of diffuse toxic goiter. Toxic nodular
goiter does not present with exophalmos.
• Protrusion of the eyeball stretches the optic
nerve which in turn leads to poor vision.
• The eyes are eventually damaged because the
eyelids do not close completely when the person
blinks or falls asleep.
• There is increased irritation, ulceration and
infection of the cornea,
• Patients have high levels of circulating TSIs ,
suggesting an auto immune component.

42. DIAGNOSIS OF HYPERTHYROIDISM.
• Direct measurement of free T4 OR T3 in the
plasma by radio immuno assay.
• Measurement of basal metabolic rate .-usually
increased to +30 to +60 in severe
hyperthyroidism
• Concentration of TSH in the plasma is measured
by radioimmuno assay. In thyrotoxicosis TSH
levels are low.
• The concentration of TSI is measured by radio
immuno assay. it is usually high in Graves
disease but low in toxic nodular goiter.

43. TREATMENT OF HYPER THYROIDISM.
– 1) Surgical removal of most of the thyroid.
Propyl thio uracil is administered before
surgery to reduce the basal metabolic rate.
– 2) Iodides : given for 1-2 weeks before
surgery .Iodides cause the gland to recede in
size and its blood supply to diminish.
– Procedures 1 and 2 before surgery reduces
operative mortalities .( 1 in 1000 ,before it was
1:25)

44. TREATMENT OF HYPER THYROIDISM.
Cont…
• Radio active iodine - -Destroys most of
the secretory cells of the TD because
when hyperplastic the TD can absorb
about 90% of iodine. 5millicuries of
radioactive iodine is given for several
weeks.Additional doses may be
administered until normal thyroid states
is achieved.
• Others: Perchlorates ,lithium, and
propranolol.

45. HYPOTHYROIDISM.
Effects are opposite to hyperthyroidism.
• Autoimmune component that destroys the
gland and not stimulate it ( Hashimoto
disease).
• There is decreased secretion of TD
hormones due to fibrosis of the gland.
• Due to low production of TD hormones
there is an associated enlargement of the
TD gland.

46. TYPES OF HYPOTHYROIDISM.
• Endemic Colloidal Goitre
–Due to dietary iodide deficiency.
–Lack of iodine leads to no production of
T3 andT4 by the TD gland.
–T4 and T3 always exert a negative
feedback on TSH levels.TSH production
rises and this causes the TD to to
increase the conc. Of thyroglobulin
colloid into the follicles causing the TD
gland to enlarge.

47. Idiopathic non toxic colloid goiter
• These people do not suffer from iodine
deficiency but goitrous glands may secrete
low quantities of thyroid hormones.
• Colloid goiter may be caused by the
abnormality in the enzyme system required
for the formation of the thyroid hormones e.g.
• Deficient iodide trapping mechanism – iodine
is not pumped adequately into the thyroid
cells.
• Deficient peroxidase system – in which
iodides are not oxidized to iodine state.
• Deficient coupling of iodinated tyrosines in
the thyroglobulin molecule, so the final thyroid
hormone cannot be formed.

48. Myxedema (Adult hypothyroidism)
• This develops in patents with almost total lack of
thyroid hormone function. Manifests with:
• Baggines under the eyes .
• Swelling of the face.
• Pitting oedema due to increase in intestinal fluid.
• Development of atherosclerosis (lack of thyroid
hormones causes increase blood cholesterol
because of altered fat and cholesterol metabolism
and dimished liver excretion of cholesterol in bile.
• Atherosclerosis can occur in other types of
hypothyroidism but is more enhanced in myxedema
• Atherosclerosis will lead to peripheral vascular
diseases, coronary artery disease and early death.

49. Cretinism
• This is called congenital or neonatal
hypothyroidism: It is due to:
• Dysgenesis or poorly formed thyroid.
• Iodine deficiency .
• In born errors of iodine metabolism.

50. Other causes of Hypothyroidism
• Goitrogenic substances – excessive intake
of these substances e.g cabbages and
turnips. These foods contains compounds
with anti thyroid activity (similar to propyl
thiouracil) and cause TSH stimulated
enlargement of the thyroid gland.

51. Clinical manifestation of hypothyroidism
• Hypothroidism may be due to:
• Thyroiditis or thyroid inflammation.
• Endemic colloid goiter.
• Destruction of the thyroid gland by
irradiation .
• Surgical removal of the thyroid .
• Myxedema and cretinism .

52. Effects Of hypothyroidism
• Fatigue and extreme somnolence with prolonged
sleep of upto 14hrs a day .
• Extreme muscular sluggishness.
• Slowed heart rate.
• Decrease CO, decrease BV.
• Increase BW .
• Constipation, mental sluggishness .
• Depressed growth of hair and scaliness of the
skin .
• Development of frog like husky voice.
• In severe cases development of odematous
appearance throughout the body called
myxedema.

53. EFFECTS OF HYPOTHYROIDISM.
• Mental retardation and dwarfism due to
delayed skeletal maturation
• Thick dry skin, protruding tongue,
hypothermia and lethargy.

54. Diagnosis of hypothyroidism
• Free thyroxin in the blood- decreases
• Basal metabolic rate in myxedema
range from -30 and -50.
• Secretion of TSH by anterior pituitary
when a test dose of TRH is
administered is usually increased.

55. Treatment of Hypothyroidism
• Use thyroid hormone replacements
• Preparations
• Thyroxine – Sodium salt of L-thyroxine
• Liothyronine Sodium (T3) – NOT for long
term use because of high potency and
incidence of cardiac side effects. 25 ug of T3
has similar clinical response as 100ug of
thyroxine.
• Liotrix (25 ug T4 with 6.5 ugT3. It does not
offer any special advantage over l-thyroxine.

56. Therapeutic uses Of Thyroid Hormones
• Replacement or substitution therapy of
primary hypothyroidism e.g cretinism,
myxedema, non toxic goiter, hypothyroid
states of childhood.
• Also hypothyroidism resulting from other
causes e.g. surgery, radiation, drugs,
pregnancy or ageing.
• Adjuncts to thyroid – inhibiting agents.
• Adjunctive therapy of follicular and
papillary carcinoma of the thyroid in
conjuction with radioactive iodine.

57. Side effects /adverse of thyroid
hormones
• Palpitations, sweating, nervousness
• Heat intolerance
• Insomnia
• Allergic skin reaction
• CCF and shock

58. Contra indications and precautions
thyroid hormones
• CI – patients with thyrotoxicosis, nephrosis and
myocardial infarction, obesity.
• Caution – CVS diseases (angina)
• concomitant diabètes mellitus or adrenal isufficiency.
Interactions involving thyroid hormones
• Potentiates cardiovascular effects of catecholamines.
• Potentiate effects of oral anticoagulants
• Thyroid hormones increase effectiveness and toxicity of
cardiac glycosides
• May increase blood glucose levels thus increasing
requirement for insulin and oral hypoglycemics.

59. ANTITHYROID DRUGS
These drugs are used in hyper
thyroidism.
a) Thioamides
• These reduce the synthesis of thyroid
hormones and include carbimazole,
methimazole and propylthiouracil. They
are called antithyroid drugs.
• b) Iodide – In high doses
• c) Radioactive iodine – 131

60. ANTITHYROID DRUGS
Cont…
d) Ionic inhibitors – These inhibit iodide
uptake e.g. thiocyanates, perchlorates,
nitrates. Their use is obsolete due to toxicity.
e) Propranolol – use as an adjunct therapy
in thyrotoxicosis.

61. Thioamides
Mechanism of action
These drugs inhibit all the steps catalyzed
by thyroperoxidase- steps 2 3 and 4 in the
biosynthetic pathway viz:
• Preventing conversion of iodide to iodine
atom or free radical, inhibiting iodination of
tyrosine and coupling of iodotyrosine to
form T3 and T4
• In addition propylthiouracil inhibits the
peripheral conversion of T4 toT3.

62. Mechanism of action of
thioamides
• There is also evidence to suggest that the
drugs may suppress the synthesis of auto
antibodies implicated in the aetiology of
Graves disease.

63. PHARMACOKINETICS OF
THIOAMIDES
• Drugs are absorbed orally
• Carbimazole is a pro-drug and is converted to methimazole
.
• T ½ (methiomazole 4 hrs, propylthioracil 2 hrs)
.
• These short t ½ are not clinically important because there is
cumulation of these drugs in the thyroid where they act for
25-35hrs.

64. PHARMACOKINETICS OF
THIOAMIDES
• A single dose of carbimazole or
propylthiouracil can reduce iodination of
tyrosine by 70-90% within 7-12 hrs.
• These drugs are excreted in urine and
mothers milk and cross the placental
barrier.
• Methimazole crosses the placental barrier
to a greater extent than propyl thiouracil.

65. THERAPEUTIC USES
THIOAMIDES
1. Graves disease
• Carbimazole orally 30-60mg/day until
remission of symptoms with maintenance
dose of 5 -15 mg/d.
• Propyl thiouracil – orally 300 – 450mg/d
maintenance dose 50-150 mg/day

66. THERAPEUTIC USES
THIOAMIDES
ii) Toxic nodular goiter
iii) Prior to surgery for hyperthyroidism
iv) Combined with radioactive iodine to
decrease symptoms of hyperthyroidism
before radiation effects are manifested.

67. ADVERSE EFFECTS OF
THIOAMIDES
• Pruritic rash and hypothyroidism- most
common
• Rare effects include: Vasculitis, arthralgia,
Cholestatic jaundice, lymphadenopathy,
Hair pigmentation and SLE like syndrome.

68. ADVERSE EFFECTS OF
THIOAMIDES
• Adverse effects are reversible on
discontinuation of the drug.
• Adverse cross sensitivity between propyl
thiouracil and methimazole is 50% i.e. one
cannot be substituted for the other.

69. Iodides
• Iodides after food intake are selectively
trapped by the thyroid gland, uptake being
increased in hyperthyroidism and reduced
in hypothyroidism.
• Large doses of iodides:e.g. lugols iodine
(5%iodine in 10% potassium iodide
solution):

70. MECHANISMS OF ACTION OF
IODIDES
1. Inhibit secretion of thyroid hormones
2. Inhibit hormone release by inhibiting
thyroglobulin proteolysis
3. Decrease vascularity of the gland.

71. THERAPEUTIC USES OF
IODIDES
1. Pre-operative use in thyroid surgery.
Potassium iodide 60mg orally tds. Antithyroid drugs
are first used to control symptoms of
hyperthyroidism and iodides are began 10 days
before surgery to reduce gland size and vascularity
.
2. Thyroid crisis – defined as sudden aggravation of
hyperthyroidism (thyrotoxicity)

72. THERAPEUTIC USES OF
IODIDES
3. Accidental over-dosage of radioactive
iodine. It appears to protect the thyroid
follicles.
4. Prophylactic use in endemic goitre. It is
added to salt (1:100,000 parts ) as iodized
salts.
5. As an expectorant
6. As antiseptic for topical use

73. ADVERSE DRUG REACTIONS
OF IODIDES
• Acute hypersensitivity Rx e.g.
angioedema, skin haemorrhage and drug
fever
• Iodism on chronic administration
(salivation, lacrimation, soreness of throat)
conductivities, coryza like symptom, skin
rashes.

74. ADVERSE DRUG REACTIONS
OF IODIDES
• Foetal or neonatal goiter can occur after
administration to pregnant or lactating
mothers.

75. RADIOACTIVE IODINE
Mechanism
• Emits both beta and gamma rays. It is
absorbed after oral administration and is
trapped by the thyroid follicles and
incorporated into thyroblogulin.
• The emitted beta rays have a short range
and act on thyroid tissues without injuring
surrounding areas including the
parathyroid gland.

76. THERAPEUTIC USES OF RADIOACTIVE
IODINE
• It is used as radio active sodium iodide
• Radioactive sodium iodide is administered
orally in the dose of 5-8 millicurie in the
following conditions:

77. THERAPEUTIC USES OF
RADIOACTIVE IODINE
1. Graves disease – including relapse after
sub total thyroidectomy.
2. Toxic nodular goiter
3. Thyroid carcinoma
Clinical response with radioactive iodine is
slow and may take 6-12 weeks for
suppression of hyperthyroid symptoms.
Repeated doses may be necessary in
some cases.

78. ADVERSE DRUG REACTIONS
OF RADIOACTIVE IODINE.
• Hypothyroidism is fairly common.
• Should be avoided in children (mutagenic
effect) and pregnancy (teratogenicity and
cretinism.
• Lactating mothers (hypothyroidism,
cretinism).

79. PROPRANOLOL
• It is not strictly an anti-thyroid drug but is a
beta adrenergic antagonist which inhibits
many symptoms of hyperthyroidism e.g.
palpitation or tachycardia, tremors, anxiety
and thyrotoxic periodic paralysis due to
increased muscle activity.

80. THERAPEUTIC USES OF
PROPRANOLOL
1. In thyroid crisis
2. As an adjunct in thyrotoxicosis or
hyperthyroidism
3. Prior to thyroid surgery to reduce
symptoms like tachycardia
4. Thyroiditis (or inflammation of the thyroid)
– prevents palpitations.

81. THYROID CRISIS OR
THYROID STORM
• Hyperthyroidism / thyrotoxicosis
with sudden elevation of thyroid
hormones.
• It is a medical emergency.

82. DRUGS FOR THYROID
STORM
• Propranolol I.V
• Diltiazem
• Sodium iodide
• Propylthiouracil
• Hydrocortisone

83. THYROID CRISIS/STORM
PROPRANOLOL
• Given I.V 5-10mg followed by oral
administration 20-40 mg 6hourly.
• Propranolol decreases palpitations,
agitations, and anxiety and muscle
tremors.
• It also prevents peripheral conversion of
T4 TO T3.

84. THYROID CRISIS OR
THYROID STORM
DILTIAZEM
• 5-10mg IV is used if adequate control is
not attained by propranolol or in cases
where propranolol is contraindicated
(CHF, bronchial asthma.)

85. THYROID CRISIS OR
THYROID STORM
SODIUM IODIDE.
• I.V 1-2 g/day followed by saturated
solution of potassium iodide 10 drops
orally daily.
• Increased concentration of iodides
prevents hormone synthesis and
peripheral conversion of T4 to T3.

86. THYROID CRISIS OR
THYROID STORM
PROPYL THIOURACIL
• The antithyroid drug is given orally or
through orogastric tube 150-200mg 4-6
hourly.
• It prevents incorporation of iodine into
tyrosine residues and peripheral
conversion of T4 to T3.

87. THYROID CRISIS OR
THYROID STORM
GLUCOCORTICOIDS E.G.
HYDROCORTISONE.
• Is given I.V 100-200 mg 8 hourly.
• It prevents peripheral conversion of T4 to
T3.
• Increased thyroid hormones may lead to
increased glucocorticoid secretion and
possible adrenal suppression. This is one
reason for glucocorticoid administration (IV
hydrocortisone is used).

88. THYROID CRISIS OR
THYROID STORM
SUPPORTIVE MEASURES.
• Sedation,
• Oxygen,
• I.V glucose,
• Vitamins,
• Treatment of infections

89. SUPPORTIVE MEASURES
• Digitalis to maintain the cardiac status,
rehydration,
• Treatment of hyperpyrexia with
analgesics.

90. SUPPORTIVE MEASURES
Elimination of precipitating causes of
storm.
• E.g. infections, trauma, inadequate
preparation prior to thyroidectomies,
surgical operation, Stress, diabetic
acidosis, pregnancy, emboli, abrupt
discontinuation of antithyroid medication,
RAI therapy

91. #END#