Hyper

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