V. Vijayanthi: Pharmacology & Management of Hypothyroidism

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PHARMACOLOGY

&
MANAGEMENT OF HYPOTHYROIDISM

BY

V. VIJAYANTHI
HYPOTHYROIDISM

 Hypothyroidism is a common endocrine


disorder resulting from abnormally low
levels of thyroid hormones.
HYPOTHYROIDISM

CLASSIFICATION

SECONDARY TERTIARY
PRIMARY
HYPOTHYROIDISM HYPOTHYROIDISM
HYPOTHYROIDISM
Primary hypothyroidism
 It results from the inability of the
thyroid gland to produce its hormones.

 The most common forms include


hashimoto’s thyroiditis and radio-iodine
therapy for hyperthyroidism.
Secondary hypothyroidism
 Occurs if the pituitary gland does not
create enough TSH to induce the
thyroid gland to produce enough
hormones.
 It is usually caused by damage to the
pituitary gland as by a tumour, radiation
or surgery.
Tertiary hypothyroidism
 Tertiary hypothyroidism occurs when
the hypothalamus fails to produce
sufficient thyrotropin releasing
hormone(TRH).

 Also termed hypothalamic-pituitary axis


hypothyroidism.
Causes of hypothyroidism
 Hashimoto’s thyroiditis.
 Thyroid destruction from radioactive
iodine or surgery.
 Severe iodine deficiency.
 Pituitary or hypothalamic disease.
 Medications .
 Lymphocytic thyroiditis.
Symptoms of hypothyroidism
 Fatigue, lethargy and sleepiness.
 Weight gain
 Decreased appetite
 Dry skin
Cold intolerance
Hair loss
Constipation
 Menstrual disturbances, impaired
fertility.
 Hoarseness of voice
Muscle pain, joint pain and weakness in
the extremity.
 Depression.
 Forgetfulness, impaired memory,
inability to concentrate.

Signs of hypothyroidism
 Hypothermia
 Goitre
 Weight gain
 Dry skin
 Pallor
 Slowed speech and movements
 Coarse facial features
 Myxedema
 Hoareseness
 Loss of scalp, axillary and pubic hairs
 Bradycardia
 Decreased systolic B.P and increased
diastolic B.P
 Hyporeflexia.
DRUGS USED IN
HYPOTHYROIDISM
 LEVOTHYROXINE
 LIOTHYRONINE
 DESSICATED THYROID
 However levothyroxine is the preparation of choice for
thyroid replacement and supression therapy because of
its
i) stability, content uniformity
ii) lack of allergenic foreign protein
iii) easy laboratory measurement of serum levels
iv) long half-life
 Although Liothyronine is 3 to 4 times more potent than
Levothyroxine, it is not used because of consequent greater
risk of cardiotoxicity and arrhythmias.

 PHARMACO KINETICS

i) Oral bio availability of l-thyroxine is 75%

ii) Its oral absorption may be impaired by sucralfate, iron and


calcium and by certain foods. Hence, it should be
administered in empty stomach.

iii) Its long half-life of 7 days permits once – daily dosing.


DOSAGE

1. The average dosage for an infant of 1 to 6 months age is


10 to 15 microgram / Kg./day.
 2. For an adult : 1.7 microgram / Kg. / day.

 3. In long standing hypothyroidism, in older patients and in

patients with underlying cardiac disease, it is imperative to


start treatment with reduced dosages.
 4. In such patients l-thyroxine is given in a dosage of 12.5

– 25 microgram / day for 2 weeks, increasing the dose by


25 microgram every 2 weeks until euthyroidism or drug
toxicity is developed.
TOXICITY

 Toxicity of thyroxine is directly related to the


hormone level.
 Signs of thyroxine toxicity in children: Restlesness,
Insomnia, Accelerated bone maturation and
growth.
 In adults: increased nervousness, heat
intolerance, episodes of palpitation and
tachycardia, unexplained weight loss.
 Chronic overtreatment with T4 in elderly patients
increases the risk of atrial fibrillations and
accelerated osteoporosis.
MANAGEMENT OF
HYPOTHYROIDISM
 Cretinism
 Cretinism is a condition of severely stunted physical
and mental growth due to untreated congenital
deficiency of thyroid hormones resulting from
maternal nutritional deficiency of iodine.
 It is of two types:
 Sporadic cretinism: due to failure of thyroid
development or a defect in hormone synthesis.
 Endemic cretinism: due to extreme iodine deficiency.
 Thyroxine 8-12 mcg/kg/day should be started
as early as possible because the mental
retardation that has already ensued is only
partially reversible.
 Response is dramatic: physical growth and
development are restored and further mental
retardation is prevented.
 Rarely l-thyroxine replacement is associated
with pseudo tumour cerebri in children.
ADULT HYPOTHYROIDISM

 If there is no residual thyroid function,


levothyroxine- 1.5 mcg/kg/day (typically
100-150 mcg ) is given.
 If the residual thyroid tissue is not
destroyed, it is wise to start with a low
dose – 50 mcg of l-thyroxine daily and
increase every 2-3 weeks with an
optimum of 100-200 mcg/day.
 The dose is adjusted on the basis of TSH
levels.
 Adjustment of l-thyroxine dosage is made in
12.5 -25 mcg increments if the TSH is high.
 Once full replacement is achieved and TSH
levels are stable, follow up measurement of
TSH is recommended at annual intervals and
may be extended to every 2-3 years.
HYPOTHYROIDISM AND
PREGNANCY
 In a pregnant hypothyroid patient, it is
extremely important that the daily dose
of thyroxine be adequate because early
development of fetal brain depends on
maternal thyroxine.
 During pregnancy, an increase in
thyroxine dose by 30-50% is required
to normalize the serum TSH levels.
MYXEDEMA COMA

 Myxedema coma is a severe form of


hypothyroidism that results in an altered mental
status, hypothermia, bradycardia, hypothermia,
hyponatremia and hypercapnia.

 Clinical manifestations include reduced level of


consciousness associated with seizures and
other symptoms of hypothyroidism may be
present
 Myxedema coma most commonly occurs in
patients with untreated or undiagnosed
hypothyroidism who are subjected to an
external stress such as low temperature,
infection or medical intervention ( surgery or
hypnotic drugs.
 Levothyroxine should be initially administered
as a single intravenous bolus of 500 mcg,
which serves as a loading dose.
 Levothyroxine can initially be administered as
a single intravenous bolus of 500 mcg, which
serves as a loading dose.
 An alternative is to give liothyronine
intravenously or via nasogastric tube, in
doses ranging from 10-25 mcg every 8 to 12
hours.
 Another commonly used option is to combine
l-thyroxine( 200 mcg ) and liothyronine( 25
mcg) as a single intravenous bolus followed
 By daily treatment with levothyroxine( 50-100
mcg/day ) and liothyronine( 10 mcg every 8
hrs ).
 Supportive therapy should be provided to
correct any associated metabolic disorders.
 External warming is induced only if the
temperature is <30◦c , as it can result in
cardiovascular collapse.
 Space blankets should be used to prevent
further heat loss.
 Parenteral hydrocotisone ( 50 mg every 6 hrly )
should be administered as there is impaired
adrenal reserve in profound hypothyroidism.
 Any precipitating factors should be treated.
 Ventilatory support with regular blood gas
analysis is usually needed during the first 48
hrs
 Hypertonic saline or intravenous glucose may
be needed if there is hyponatremia or
hypoglycemia.
 The metabolism of most medications is
impaired, and sedatives should be avoided if
possible or used in reduced doses.
 Blood levels should be monitored when
available , to guide medication dosage.
SUBCLINICAL HYPOTHYROIDISM

 It refers to the biochemical evidence of thyroid


hormone deficiency in patients who.
 Thyroid hormone therapy should be have few or
no apparent features of hypothyroidism
considered for patients with TSH levels>10mIU/L
while close monitoring is appropriate for those
with lower TSH elevations.
Thank you

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