Contains both clinical features and treatment in special cases

1. Okoli E. V.

2. Outline
 Introduction
 Classification and Aetiology
 Clinical features
 Investigations
 Treatment
 Conclusion

3. Introduction
 Hypothyroidism is a common endocrine disorder in
which the thyroid gland does not produce enough
thyroid hormones.
 Worldwide, iodine deficiency remains the foremost
cause. In areas of adequate iodine intake, autoimmune
thyroid disease (Hashimoto disease) is the most common
cause.
 There are three types of hypothyroidism: primary,
secondary, and tertiary

4. The Thyroid gland
oid  Gland that regulates metabolism
 Located in the front of the neck
just below the voice box (larynx)
 The thyroid gland releases two
hormones: thyroxine (T4) and
triiodothyronine (T3)
 The thyroid gland, as well as the
pituitary gland and hypothalamus,
control how much of these
hormones are produced

6. Synthesis and Secretion
 Follicular cells arranged in clumps.
 Clumps of cells contain colloid.
 Colloid contains an iodine containing protein called
thryoglobulin. This is the precursor and storage form
of thyroid hormone.

7. Thyroid hormone action
 T4 and T3 circulate in the blood bound to plasma
proteins.
 TBG(70%), TBPA(20%) and albumin(10%).
 T3 is the active form, 5 times more active than T4.
 T4 is converted to T3 outside the thyroid, mostly in
liver and kidney.
 T3 binds to a nuclear receptor

8. Regulation of the H-P-T axis
 TRH secreted from hypothalmus controls TSH
production.
 TSH from anterior pituitary stimulates secretion of T4
and T3 from thyroid.
 Regulated by a negative feedback loop.

10. Effects of thyroid hormones
• Increases cardiac output
 Increases heart rate
 Increases ventilation rate
 Increases basal metabolic rate
 Potentiates the effects of catecholamines (i.e. increases sympathetic
activity)
 Potentiates brain development
 Thickens endometrium in females
 Increases metabolism of proteins and carbohydrates

12. Primary hypothyroidism
 Due to a defect in the gland, the thyroid cannot make
enough T3 and T4. The most common cause is iodine
deficiency.
 The most common cause of primary hypothyroidism in the
United States is the destruction of the thyroid gland by the
immune system (Hashimoto’s thyroiditis)
 Other causes of primary hypothyroidism include:
 certain drugs such as lithium
 radiation exposure to the neck
 radioactive iodine used for treatment of hyperthyroidism
 special x-ray dyes
 surgical removal of part or all of the thyroid gland
 some women develop after pregnancy (postpartum thyroiditis)

13. Secondary & Tertiary Hypothyroidism
 In secondary hypothyroidism the thyroid gland produces too little
hormone due to disorders of the pituitary gland (i.e. pituitary
hypothyroidism)
 Tertiary hypothyroidism is caused by disorders of the hypothalamus

15. 15
Goiter: an enlargement of the thyroid gland, often
resulting from the deficiency of iodine in the diet
(simple goiter)

17. Potential difficulties
 Children with hypothyroidism may not show classic
features but often have a slow growth velocity, poor school
performance and sometimes arrest of pubertal
development.
 Young women with hypothyroidism may not show
obvious signs. Hypothyroidism should be excluded in all
people with oligomenorrhoea/amenorrhoea,
menorrhagia, infertility or hyperprolactinaemia.
 The elderly show many clinical features that are difficult
to differentiate from normal ageing.

18. 18
HYPOTHYROIDISM

19. Clinical Features
 Hypothyroidism commonly manifests as a slowing in
physical and mental activity but may be asymptomatic
 Symptoms and signs of this disease are often subtle and
neither sensitive nor specific.
 Classic signs and symptoms (eg, cold intolerance, puffiness,
decreased sweating, and coarse skin) may not be present as
commonly as was once believed.

20.  General: Lethargy, Easy fatiguability, Weight gain,
Cold intolerance, Pallor or yellow skin
Goitre, Hyperlipidaemia, Puffy face and hands
 Gastrointestinal: Constipation, Ascites, Ileus

21. 21
THYROID HORMONE DEFICIENCY
 Cardiovascular
 Angina
 Bradycardia
 Cardiac failure
 Pleural effusion
 Pericardial effusion
 Low voltage complexes (ECG)
 Dermatological
 Dry skin, Vitiligo
 Alopecia, Erythema ab igne

 Genitourinary
 Water retention
 Menorrhagia
 Infertility
 Hyperprolactinaemia
 Haematological
 Anaemia-iron or folate
deficiency
 Pernicious anaemia

22. 22
THYROID HORMONE DEFICIENCY
 Mental state
 Mental slowing
 Inability to concentrate
 Poor memory
 Hypersomnolence
 Depression
 Psychosis (myxoedema
madness)
 Neuromuscular
 Weakness
 Muscle cramps
 Paraesthesiae
 Hoarseness
 Deafness
 Cerebellar ataxia
 Delayed reflexes
 Entrapment
neuropathies

23.  Features of other autoimmune diseases
 Family history of autoimmune diseases

24. Myxoedema Coma
 Myxoedema coma is an uncommon complication of long-
standing hypothyroidism
 Typically seen in the elderly,
 often precipitated by severe infection, therapy with
sedative agents, or by inadequate heating during cold
weather.
 It is has a high mortality.
 It is characteristically associated with depression of the
level of consciousness, and hypothermia.
 Alveolar hypoventilation leading to carbon dioxide
retention and a dilutional hyponatremia are often seen.

25. • Body temperature may be as low as 25°C, convulsions are
not uncommon and cerebrospinal fluid (CSF) pressure
and protein content are raised
 Mortality rate is 50% and survival depends on early
recognition and treatment of hypothyroidism and other
factors contributing to the altered consciousness level,
such as medication, cardiac failure, pneumonia,
dilutional hyponatraemia and respiratory failure.

26. Investigation
 Purpose of investigations is: a) to establish diagnosis of
hypothyroidism
b) to distinguish between transient
& long-lasting hypothyroidism
c) to determine whether it is
primary, secondary/tertiary
d) to establish the specific cause of
hypothyroidism &
e) ultimately, to treat appropriately

27. Findings
 TFT
>T4/FT4 reduced
>T3/FT3 reduced
>TSH elevated
 Thyroid Antibodies may indicate aetiology.
 If TSH is reduced or normal in the presence of a low
T4, pituitary function necessary.

29.  T3 does not add extra information
 Free hormones are more useful than total hormones
because of affectatation of the latter by TBG levels
 TBG levels are proportional to total hormone levels.

30.  TRH stimulation test is used to distinguish between
secondary and tertiary hypothyroidism
 TSH levels are measured.
 Increased TSH(may be normal) =tertiary hypothyroidism
 Reduced TSH(may be normal)= secondary hypothyroidism

31. Additional abnormal tests.
 Fasting cholesterol and triglycerides may be raised
 Hyponatremia(dilutional)
 Ck, AST and LDH may be raised
 FBC- Anemia
 ECG -Slow rate,low voltage complexes complexes.
 Imaging studies & FNAb to rule out carcinoma

32. `1

33. Treatment
 Treatment is with levothyroxine replacement. It is customary to start
with a low dose of 50 µg per day for 3 weeks, increasing thereafter to
100 µg per day for a further 3 weeks and finally to a maintenance dose
of 100–150 µg per day.
 In younger patients, it is safe to initiate levothyroxine at a higher dose
(for example, 100 µg per day), to allow a more rapid normalisation of
thyroid hormone levels.
 Levothyroxine has a half-life of 7 days so it should always be taken as a
single daily dose and at least 6 weeks should pass before repeating
thyroid function tests and adjusting the dose, usually by 25 µg per day.
 Patients feel better within 2–3 weeks. Reduction in weight and
periorbital puffiness occurs quickly, but the restoration of skin and
hair texture may take 3-6 months

34.  The dose of levothyroxine should be adjusted to maintain
serum TSH within the reference range(0.40-4.2 mIU/L)
 Some physicians advocate combined replacement with T4
and T3 or preparations of animal thyroid extract, but this
approach remains controversial and is not supported by
robust evidence.
 It is important to measure thyroid function every 1–2 years
once the dose of levothyroxine is stabilised.

35.  In some poorly compliant patients, levothyroxine is taken
diligently or even in excess for a few days prior to a clinic
visit, resulting in the seemingly anomalous combination
of a high serum T4 and high TSH
 Levothyroxine absorption is maximal when the
medication is taken before bed and may be further
optimised by taking a vitamin C supplement.
 Treat complications eg HF ,anaemia , carpal tunnel
syndrome

36. Special circumstances
 IHD: exacerbation of myocardial ischaemia, infarction and
sudden death are recognised complications of levothyroxine
replacement, even using doses as low as 25 µg per day.
 In patients with known ischaemic heart disease, thyroid
hormone replacement should be introduced at low dose and
increased very slowly under specialist supervision.
 It has been suggested that T3 has an advantage over T4, since T3
has a shorter half-life and any adverse effect will reverse more
quickly, but the more distinct peak in hormone levels after each
dose of T3 is a disadvantage.
 Coronary angioplasty or bypass surgery may be required if
angina is exacerbated by levothyroxine replacement therapy

37.  Pregnancy:Most pregnant women with primary
hypothyroidism require an increase in the dose of
levothyroxine of approximately 25–50 µg daily to maintain
normal TSH levels.
 Inadequate maternal T4 therapy may be associated with
impaired cognitive development in an unborn child and so
women are usually advised to increase their daily
levothyroxine dose by 25 µg when pregnancy is confirmed. S
 . Serum TSH and free T4 should be measured during each
trimester and the dose of levothyroxine adjusted to
maintain a normal TSH.

38. Treatment of Myxoedema Coma
 It is a medical emergency and treatment must begin before
biochemical confirmation of the diagnosis.
 Suspected cases should be treated with an intravenous
injection of 20 µg triiodothyronine, followed by further
injections of 20 µg 3 times daily until there is sustained
clinical improvement.
 Hydrocortisone 100 mg IM 3 times daily can be given.
 Other measures include slow rewarming , glucose for
hypoglycaemia, cautious use of intravenous fluids, broad
spectrum antibiotics and high-flow oxygen. Occasionally,
assisted ventilation may be necessary.

39. Conclusion
 Hypothyroidism is an endocrine disorder where the
thyroid gland is unable to secrete sufficient quantities ot
the thyroid hormones,T3 & T4
 It could be primary, secondary or tertiary
 It is essential that the hypothyroid patient be evaluated
properly(which includes identification of clinical features
and laboratory studies).This is to ensure that appropriate
management measures are instituted
 Treatment is individualised and treatment response
should be evaluated periodically

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