Hyperthyroidism is caused by excess thyroid hormones due to conditions like Graves' disease. It causes symptoms like weight loss, rapid heart rate, nervousness, and eye changes. Treatment options include antithyroid drugs which suppress hormone production, radioactive iodine which destroys the gland, and surgery. Hypothyroidism is caused by insufficient hormone levels and results in fatigue, weight gain, constipation, and intolerance to cold. Levothyroxine replacement is the standard treatment.

1. HYPERTHYROIDISM

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.

22. HYPOTHYROIDISM

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