Pulsenotes | Hypothyroidism notes

7/21/2019 Pulsenotes | Hypothyroidism notes

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ENDOCRINOLOGY (/ENDOCRINOLOGY/NOTES)

Hypothyroidism

OTES

Definition & classification

Hypothyroidism is a common endocrine condition caused by a deficiency in thyroid

hormone.

has a prevalence of 1-2 per 100 and more frequently a!

ects women, ! 9:1 ". It is almostways caused by disease intrinsic to the thyroid gland.

Onset is often insidious and clinical features non-specific, a high index of clinical suspicion may

e needed.

Thyroid physiology

Thyroid hormone release is controlled by the hypothalamic-pituitary-thyroid axis.

Thyrotropin releasing hormone

RH is secreted from the paraventricular nucleus of the hypothalamus. As the name suggests

is a tropic hormone i.e one that acts upon another endocrine gland.

reaches the anterior pituitary via the hypophyseal portal system. Here it causes the release of

hyroid stimulating hormone.

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. Thyroid stimulating hormone

SH, produced by the thyrotrophs of the anterior pituitary, is released following stimulation

y TRH.

ransported in the blood, TSH acts upon the thyroid gland promoting the synthesis and

elease of thyroid hormone.

. Triiodothyronine and thyroxine

he thyroid is stimulated to synthesise and release thyroid hormone by TSH. The thyroid

roduces two hormones, thyroxine (T4) and triiodothyronine (T3).

hese thyroid hormones complete a negative feedback loop through the suppression of TRH

nd TSH release.

hough T3 is more biologically active than its counterpart T4, secreted thyroid hormone is

0% T4. Peripherally much of T4 is converted to T3.

oth are highly lipophilic, act on intracellular receptors and bind to thyroxine-binding globulin

TBG) in the blood. Only the ‘free pool’ is active: <0.1% T4 and <1% of T3.

he e! ects to T3/T4 are numerous:

BMR: increases the basal metabolic rate.

Metabolism: it has anabolic e! ects at low serum levels and catabolic e! ects at higher levels.

Growth: increases release and e! ect of GH and IGF-1.

Cardiovascular: increases the heart rate and contractility through increasing sensitivity to

catecholamines.

Aetiology



Hypothyroidism may be caused by disease a! ecting any part of the hypothalmic-

pituitary-thyroid axis.

Primary hypothyroidism

he majority of cases of hypothyroidism are caused by disease intrinsic to the gland itself. This

termed primary hypothyroidism.

n primary hypothyroidism, we expect to find reduced levels of thyroid hormone accompanied

y a raised TSH (due to lack of negative feedback).

. Secondary hypothyroidism

arely disease or damage to the pituitary may reduce the production or release of TSH. This is

ermed secondary hypothyroidism. It is most frequently caused by pituitary adenomas.

n these conditions, we expect to find reduced levels of thyroid hormone accompanied by

educed TSH (due to lack of production).

n even rarer cases the TSH level is normal (or high) but the structural abnormalities cause theormone to have less biological activity.

. Tertiary hypothyroidism

arely disease or damage to the hypothalamus or the hypophyseal portal system may reduce

he production, release or transport of TRH. This is termed tertiary hypothyroidism.

n this condition, we expect to find reduced levels of thyroid hormone accompaniedy reduced TSH and TRH.

esistance to thyroid hormone



n rare circumstances, individuals may su! er from resistance to thyroid hormone. This

enetically inherited disorder is caused by an unresponsive form of one of the T3 receptors.

is characterised by raised levels of thyroid hormone and TSH (as negative feedback is

omewhat inhibited by hormone resistance).

his compensatory increase means most individuals are clinically euthyroid.

rimary hypothyroidism

Autoimmune disease is the most common cause of primary hypothyroidism in the

western world.

hronic autoimmune (Hashimoto’s) thyroiditis

n chronic autoimmune thyroiditis cell and antibody mediated processes cause destruction of

he thyroid gland. It exists in two forms:

Goitrous: characterised by a firm and rubbery goitre

Atrophic: characterised by an atrophic gland

is estimated to a! ect between 0.5% and 2% of the population. It is most frequently seen in

women and becomes increasingly common with age.

he condition is associated with a number of other autoimmune conditions such as type 1

iabetes mellitus. Other associations include the genetic conditions Turner's and Down's

yndrome.

odine deficiency



Worldwide, iodine deficiency is the leading cause of hypothyroidism. Iodine is a key component

f thyroxine and its deficiency results in ‘endemic’ goitres.

his has led to a number of countries opting to fortify food products with iodine e.g Salt.

ostpartum thyroiditis

his is typically a transient change that occurs in the six months following birth, it may be

receded by a period of hyperthyroidism.

he condition is thought to a! ect between 6-10% of women with an increased incidence in

iabetic patients.

Most women will show complete resolution of the condition.

Amiodarone-induced hypothyroidism

miodarone is a lipophilic class III anti-arrhythmic drug with a high iodine content. Its e! ects

n the thyroid can be alarming and it may cause both hypothyroidism and hyperthyroidism.

he e! ects of amiodarone are dependent on whether there is pre-existing thyroid disease:

Pre-existing autoimmune disease: hypothyroidism may occur secondary to the Wol! –

Chaiko! e! ect - a phenomenon in which raised iodine intake results in reduced levels of thyroid hormone.

Normal thyroid gland: those with a normal gland may also develop hypothyroidism,

frequently a! ecting T3.

ongenital hypothyroidism

ongenital hypothyroidism is screened for with the Guthrie screen to prevent cretinism (the

yndrome caused by congenital hypothyroidism). It may be due to:

Dyshormonogenesis

Abnormal gland development

linical features

Hypothyroidism presents with non-specific symptoms, though patients may complain of

a goitre.

ymptoms

Tiredness



Lethargy

Weight gain

Cold intolerance

Amenorrhoea

Reduced libido

Goitre

igns

Hair loss - characteristically the outer third of the eyebrows

Dry skin

Goitre

Bradycardia

Myxoedema - deposition of mucopolysaccharides in the skin leading to swelling

Delayed relaxation phase of deep tendon reflexes

nvestigations & diagnosis

Measurement of TSH and fT4 is usually su! icient to diagnose hypothyroidism.

Hypothalamic-pituitary-thyroid axisrimary hypothyroidism: raised TSH (> 10mU/L) and reduced fT4 (< 9 pmol/L).

ubclinical hypothyroidism: moderately raised TSH (4.5-10 mU/L) and normal fT4.



econdary or tertiary hypothyroidism: normal (inappropriately normal) or lowered TSH

r TRH and a reduced fT4.

Autoantibodies

number of antibodies may be detectable in autoimmune thyroiditis. None of these are

outinely measured:

Anti-thyroid peroxidase (anti-TPO) antibodies: may be measured in subclinical

hypothyroidism, if positive the patient may require additional monitoring.

Anti-thyroglobulin (Anti-Tg) antibodies

Thyroid stimulating hormone receptor (TSHR) antibodies: may be measured if the patient

su! ers with thyroid eye disease.

Other

FBC

U&E

Serum CK

Cholesterol

uspicion of malignancy

Ultrasonography

Specialist referral

Management

Replacement of thyroxine is the mainstay of management.



Younger than 50

he initial dose of levothyroxine is typically 50-100 mcg with a TSH target of 0.4–4.5 mU/L.

he dose is titrated up and down by 25 mcg as needed. TSH levels are checked every 2-3

months then yearly once stable.

. Over 50 or with cardiovascular risk factors

he initial dose of levothyroxine is typically 25 mcg with a TSH target of 0.4–4.5 mU/L.

he dose is titrated up and down by 25 mcg as needed. TSH levels are checked every 2-3

months then yearly once stable.

. Pregnancy

reatment should be started, typically a lower (and trimester dependent) TSH target is usede.g. 0.4–2 mU/L). It requires specialist referral.

. Subclinical hypothyroidism

ypically prompts further confirmatory test at 3-6 months. Treatment is not routine and

monitoring for overt hypothyroidism is required.

may be treated if the patient is symptomatic, has a goitre, rising TSH or is pregnant (requires

pecialist referral).

Myxoedema coma

Myxoedema coma is a rare but potentially fatal outcome of untreated/undertreated

hypothyroidism.

he term is a misnomer as myxoedema may not be present and the patient may not be

omatose.

is a medical emergency requiring admission to hospital and often results from acute

ecompensation during an intercurrent illness.

atients are hypotensive, hypothermic, bradycardic and demonstrate cognitive decline.

V levothyroxine is the mainstay of management. Electrolyte imbalances and hypothermia

hould be addressed. IV hydrocortisone may be needed unless hypopituitarism is ruled out as a

ause.



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