HYPERTHYROIDISM
background
• Clinical syndrome resulting from exposure
of tissues to excess circulating levels of
free thyroid hormones
• It is five times more commoner in females
• Highly vascular gland located anteriorly in
the lower neck
• Synthesises and stores two important but
different types of hormones:
➢Iodothyronine hormone –Thyroxine (T4)
➢Triiodothyronine(T3) –released from T4 in
the peripheral tissues ; most active hormone
➢essential for normal growth and
development
• The function of the thyroid gland is
regulated by a feedback mechanism
involving hypothalamic-pituitary axis in the
brain.
• TSH from the anterior pituitary gland which
is regulated by the TRH from the
hypothalamus.
TSH stimulate T4 and T3 production from
the glands
THYROID HORMONES
• THYROXINE
• T4: (Thyroxine) is made exclusively in
thyroid gland
• Secretion of T4 to T3 : 10:1
• Potency of T4 to T3; 1:10
• T4 is the most important source of T3 by
peripheral tissue deiodination“ T4 to T3 “
Etiology
• Gravis disease-76%
• Multinodular goitre
• Autonomously functioning solitary thyroid
nodule
• Thyroiditis
Subacute
Pospartum
• Drugs - amiodarone
Grave’s disease
• Autoimmune process in which serum IgG
antibodies bind to TSH receptors and
stimulate thyroid hormone production,
behaving like TSH
• These antibodies are called thyroid
stimulating antibodies
• Most pts are aged between 30-50
Clinical features
• Goitre- diffuse + bruit, nodular
• GIT
Wt loss despite normal or increased
appetite
Hyperdefaction (frequent bowel motions)
Diarrhea
Anorexia, vomiting
Clinical features
• Cardiorespiratory
Palpitations, sinus tachycardia
Increased pulse pressure
Ankle oedema in absence of cardiac
failure
Angina, cardiomyopathy, ccf
Dyspnoea, exacerbation of asthma
Clinical features
• Neuromuscular
 Nervousness, irritability, psychosis
• Dermatology
 Increased sweating, pruritus, palmar erythema,
 Alopecia, vitiligo, myxoedema
Clinical features
• Reproductive
Amenorrhea/ oligomenorrhea
Infertility, spontaneous abortion
Loss of libido, impotence
• Ocular
 Excessive lacrimation, exophalmos,
diplopia, papilloedema, loss of visual
acuity
Clinical features
• Other
Heat intolerance
Fatigue, apathy
Lyphadenopathy
Thirst
osteoporosis
Management
• Three methods
Antithyroid drugs
Subtotal thyroidectomy
Radioactive iodine
Treatment
• ANTITHYRIOD DRUGS :
• CARBIMAZOLE
• METHIMAZOLE
• PROPYLTHIOURACIL
CARBIMAZOLE
These drugs inhibit thyroid hormone
production.
Full dose of carbimazole (40mg/day) are
give to suppress the thyroid gland
completely while replacing thyroid activity
with100 mcg of thyroxin daily once
euthyroid state is achieved.
This continues for 18 months
METHIMAZOLE
• Same mechanism of action as
carbimazole
Dose; 30mg/day until someone is
euthyroid ( 4- 6 weeks)
Maintenance dose; 5-10mg
PROPYLTHIOURACIL
• Inhibits production of thyroxine hormone
and stops the conversion of T4 to T3 in the
peripherals.
• 300 -450mg /day
• Maintenance dose of 50-100mg/day
Adverse effects
• Rash
• Fever
• Anorexia & nausea
• Agranulocytosis
• Aplastic Anaemia
• Liver damage
Radioiodine
• Emits beta radiation that destroys the
gland.
• Cant be used in pregnant women.
Surgery
• Surgical remove of the gland in individuals
that cant use radioiodine.
Beta blockers
• Propranolol : used for symptomatic relief
• Blocks beta receptors that are activated by
increased amount of the hormone
• Blocks the conversion of T4 to T3.
HYPOTHYROIDISM
introduction
• It may be primary from the disease of the
thyroid gland or secondary to
hypothalamic –pituitary disease
CLINICAL FEATURES
• General;
Tiredness, wt gain, cold intolerance
Hoarseness
Goitre
Bradycardia
Constipation
Impotence
Skin problems
Thyroid Preparations
These preparations may be synthetic (levothyroxine,
liothyronine, liotrix) or of animal origin (desiccated thyroid).
 Synthetic levothyroxine is the preparation of choice for
thyroid replacement and suppression therapy because of its
 1- stability
 2- content uniformity
 3- low cost
 4- lack of allergenic foreign protein
 5- easy laboratory measurement of serum levels
 6- long half-life (7 days), which permits once-daily
administration.
• In addition, T4 is converted to T3 intracellularly; thus,
administration of T4 produces both hormones.
 Although liothyronine (T3) is three to four times more potent
than levothyroxine, it is not recommended for routine
replacement therapy because of its
 1- shorter half-life (24 hours), which requires multiple daily
doses
 2- its higher cost
 3- the greater difficulty of monitoring
 4- its greater hormone activity and consequent greater risk of
cardiotoxicity,
 T3 should be avoided in patients with cardiac disease. It is best
used for short-term suppression of TSH.
Treatment
• Levothyroxine(T4)
• Dose: 50 -100microgram/day
• Liothyronine (T3)
• 5-20microgram/day
Adverse effects
• Increase in the metabolic rate
• Myocardial ischaemia
• Atrial fib

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HYPERTHYROIDISM-lecture.ppt

  • 2. background • Clinical syndrome resulting from exposure of tissues to excess circulating levels of free thyroid hormones • It is five times more commoner in females
  • 3. • Highly vascular gland located anteriorly in the lower neck • Synthesises and stores two important but different types of hormones: ➢Iodothyronine hormone –Thyroxine (T4) ➢Triiodothyronine(T3) –released from T4 in the peripheral tissues ; most active hormone ➢essential for normal growth and development
  • 4. • The function of the thyroid gland is regulated by a feedback mechanism involving hypothalamic-pituitary axis in the brain. • TSH from the anterior pituitary gland which is regulated by the TRH from the hypothalamus. TSH stimulate T4 and T3 production from the glands
  • 5. THYROID HORMONES • THYROXINE • T4: (Thyroxine) is made exclusively in thyroid gland • Secretion of T4 to T3 : 10:1 • Potency of T4 to T3; 1:10 • T4 is the most important source of T3 by peripheral tissue deiodination“ T4 to T3 “
  • 6. Etiology • Gravis disease-76% • Multinodular goitre • Autonomously functioning solitary thyroid nodule • Thyroiditis Subacute Pospartum • Drugs - amiodarone
  • 7. Grave’s disease • Autoimmune process in which serum IgG antibodies bind to TSH receptors and stimulate thyroid hormone production, behaving like TSH • These antibodies are called thyroid stimulating antibodies • Most pts are aged between 30-50
  • 8. Clinical features • Goitre- diffuse + bruit, nodular • GIT Wt loss despite normal or increased appetite Hyperdefaction (frequent bowel motions) Diarrhea Anorexia, vomiting
  • 9. Clinical features • Cardiorespiratory Palpitations, sinus tachycardia Increased pulse pressure Ankle oedema in absence of cardiac failure Angina, cardiomyopathy, ccf Dyspnoea, exacerbation of asthma
  • 10. Clinical features • Neuromuscular  Nervousness, irritability, psychosis • Dermatology  Increased sweating, pruritus, palmar erythema,  Alopecia, vitiligo, myxoedema
  • 11. Clinical features • Reproductive Amenorrhea/ oligomenorrhea Infertility, spontaneous abortion Loss of libido, impotence • Ocular  Excessive lacrimation, exophalmos, diplopia, papilloedema, loss of visual acuity
  • 12. Clinical features • Other Heat intolerance Fatigue, apathy Lyphadenopathy Thirst osteoporosis
  • 13. Management • Three methods Antithyroid drugs Subtotal thyroidectomy Radioactive iodine
  • 14. Treatment • ANTITHYRIOD DRUGS : • CARBIMAZOLE • METHIMAZOLE • PROPYLTHIOURACIL
  • 15. CARBIMAZOLE These drugs inhibit thyroid hormone production. Full dose of carbimazole (40mg/day) are give to suppress the thyroid gland completely while replacing thyroid activity with100 mcg of thyroxin daily once euthyroid state is achieved. This continues for 18 months
  • 16. METHIMAZOLE • Same mechanism of action as carbimazole Dose; 30mg/day until someone is euthyroid ( 4- 6 weeks) Maintenance dose; 5-10mg
  • 17. PROPYLTHIOURACIL • Inhibits production of thyroxine hormone and stops the conversion of T4 to T3 in the peripherals. • 300 -450mg /day • Maintenance dose of 50-100mg/day
  • 18. Adverse effects • Rash • Fever • Anorexia & nausea • Agranulocytosis • Aplastic Anaemia • Liver damage
  • 19. Radioiodine • Emits beta radiation that destroys the gland. • Cant be used in pregnant women.
  • 20. Surgery • Surgical remove of the gland in individuals that cant use radioiodine.
  • 21. Beta blockers • Propranolol : used for symptomatic relief • Blocks beta receptors that are activated by increased amount of the hormone • Blocks the conversion of T4 to T3.
  • 23. introduction • It may be primary from the disease of the thyroid gland or secondary to hypothalamic –pituitary disease
  • 24. CLINICAL FEATURES • General; Tiredness, wt gain, cold intolerance Hoarseness Goitre Bradycardia Constipation Impotence Skin problems
  • 25. Thyroid Preparations These preparations may be synthetic (levothyroxine, liothyronine, liotrix) or of animal origin (desiccated thyroid).  Synthetic levothyroxine is the preparation of choice for thyroid replacement and suppression therapy because of its  1- stability  2- content uniformity  3- low cost  4- lack of allergenic foreign protein  5- easy laboratory measurement of serum levels  6- long half-life (7 days), which permits once-daily administration. • In addition, T4 is converted to T3 intracellularly; thus, administration of T4 produces both hormones.
  • 26.  Although liothyronine (T3) is three to four times more potent than levothyroxine, it is not recommended for routine replacement therapy because of its  1- shorter half-life (24 hours), which requires multiple daily doses  2- its higher cost  3- the greater difficulty of monitoring  4- its greater hormone activity and consequent greater risk of cardiotoxicity,  T3 should be avoided in patients with cardiac disease. It is best used for short-term suppression of TSH.
  • 27. Treatment • Levothyroxine(T4) • Dose: 50 -100microgram/day • Liothyronine (T3) • 5-20microgram/day
  • 28. Adverse effects • Increase in the metabolic rate • Myocardial ischaemia • Atrial fib