Hypothyroidism Flashcards
(13 cards)
Background
what are the thyroid hormones
The pituitary gland releases thyrotrophin (also known as thyroid-stimulating hormone [TSH]) when it is stimulated by thyrotrophin-releasing hormone (TRH) from the hypothalamus.
TSH lead to the release of the thyroid hormones from the thyroid gland (lies in the front of your neck just below your Adam’s apple).
A decreased activity of the thyroid.
Decreased production of thyroid hormones or rarely from tissue resistance.
Thyroid hormones - thyroxine [T4]and tri-iodothyronine [T3].
T4 is converted to the more biologically active T3 in peripheral tissues.
Circulating thyroid hormone levels are controlled through the process of negative feedback on the hypothalamus and pituitary.
Essential for normal growth, development, and metabolism.
Types - primary and secondary explain them
Types
Primary hypothyroidism(95% of cases -MORE COMMON) occurs when there is thyroid hormone deficiency due to the thyroid gland beingunable to produce thyroid hormones because of iodine deficiency or an abnormality within the gland itself.
Secondary (or central) hypothyroidism is the result of insufficient thyroid stimulation due toa pituitary or hypothalamic disorder
Some people may show raised TSH levels in the presence of normal thyroid hormone levels (free T 4 and T 3 ). This biochemical abnormality may or may not be associated with hypothyroidism-related symptoms and is termed as subclinical hypothyroidism.It may gradually develop into clinical hypothyroidism over many years; an additional test for thyroid antibodies will help to determine the risk.
Severe case of hypothyroidism- can lead to myxoedema.
Hypothyroidism is more common in which gender?
what does prevalence increase with
women
age
HYPOTHYROIDISM HAS AN INSIDIOUS ONSET!! - SYMPTOMS GRADUALLY. HAPPEN
Causes
Iodine deficiency
Iodine, a trace element is essential raw material for thyroid synthesis. Iodine deficiency is the commonest cause of hypothyroidism globally
Autoimmune disease
Leads to failure of the thyroid gland is the common cause of more than 95% of adult cases.
Drugs
Hyperthyroidism drugs (carbimazole and propylthiouracil), Amiodarone, lithium, sodium valproate, thalidomide
Congenital hypothyroidism
Absence or underdevelopment of the thyroid gland, or the absence of enzymes required for thyroid hormone synthesis and iodide transfer.
Post-ablative therapy or surgery
Thyroid damage can occur after thyroid or other neck surgery, radioiodine therapy (for example for Graves’ disease or toxic nodular disease), or post-radiotherapy to the head or neck.
Others causes : Tumours, Pituitary infarction, Hypopituitarism, Hypothalamic disorders
Symptoms
Hypothyroidism can affect multiple body systems, but symptoms are mainly non-specific and gradual in onset:
Fatigue/lethargy
Sensitivity to cold
Weight gain
Constipation
Muscle pain and weakness
Menstrual irregularities; infertility or subfertility.
Depression, impaired concentrationand memory.
Dry skin andhair loss (such as loss of lateral eyebrows)
Puffy face and eyes
Hoarseness or deepening of the voice
Goitre
Bradycardia
Differential diagnosis
Conditions which may present similarly to hypothyroidism include:
Endocrine/autoimmune conditions such as type 1 diabetes mellitus, Addison’s disease, coeliac disease, atrophic gastritis with pernicious anaemia, hypopituitarism, or rheumatoid arthritis.
Haematological conditions such as anaemia and multiple myeloma
End-organ damage such as chronic kidney disease, chronic liver disease, and heart failure
Vitamin and mineral deficiencies such as D/B 12 /folate/iron deficiency
Adrenal insufficiency
Depression and anxiety
Dementia
Obesity and obstructive sleep apnoea
Menopause
When a diagnosis of hypothyroidism issuspected - what do we ask about
Typicalsymptomsof hypothyroidism.
Anydrug treatmentthat can cause it.
Family history of thyroid or autoimmune disease; personal or family history of hypothalamic-pituitary disease.
Personal history or signs of any conditions that may be confused with hypothyroidism such as autoimmune disorders or pernicious anaemia, coeliac disease, type 1 diabetes mellitus,
Previous radiotherapy to the head and neck, radioiodine treatment, or thyroid or neck surgery.
History of iodine deficiency
Examine for thyroid enlargement (a goitre) and/or thyroid nodules or thyroid pain
Test results
Universal screening for hypothyroidism in asymptomatic adults is not recommended, however case findingusingthyroid function tests(TFTs) is appropriate inspecific clinical situations- for example:
Has goitre — screen at initial presentation
Has type 1 diabetes — screen at initial presentation, then annually.
Has dyslipidaemia — screen at initial presentation.
Has suspected dementia — consider screen at initial presentation.
Has had previous neck radiotherapy or surgery involving the thyroid gland for head and neck cancer, including lymphoma — screen annually.
Has other autoimmune disorders — screen at baseline and annually in Addison’s disease. Have a low threshold for testing in other autoimmune disorders
Has a history of subfertility, abnormal menstrual cycle, or miscarriage — screen at initial presentation.
Is takingdrug treatmentsuch as amiodarone orlithium— screen at baseline and every 6 months. If amiodarone is stopped, monitoring should continue for a further 12 months.
Has postnataldepression — screen at presentation.
Management
Arrange emergency admission if a serious complication such as myxoedema coma is suspected.
Arrange urgent referral to an endocrinologist for specialist assessment of the underlying cause, if secondary hypothyroidism is suspected.
The only effective treatment for hypothyroidism, unless it is caused by iodine deficiency (which is treated with iodide), is to administer the thyroid hormones themselves as replacement therapy
Thyroxine (levothyroxine)- T4 : preferred due to being better tolerated and having longer t1/2
Triiodothyronine- T3
The dose of levothyroxine should be individualized on the basis of clinical response and thyroid function test (TFT) results. Treatment must be monitored regularly to determine an adequate dose and to avoid both under- and over-treatment.
Patients with risk factors
age over 65 years
cardiac disease
severe hypothyroidism
thyroid cancer
adrenal insufficiency
who are pregnant
For these patients adjust doses cautiously, for example, every 4 weeks in increments of 25 micrograms according to response
During pregnancy, an increase in the dose of levothyroxine by 25– 50% is needed to maintain TSH levels in a trimester-specific reference range.
Counselling
make sure they are well educated on that they need to take this for life
written advice should ve provided and monitoring of dosage should be continued anyally
can give leaflets
Counselling for Levothyroxine
Dose to be taken preferably 30–60 minutes before breakfast, caffeine-containing liquids (e.g. coffee, tea), or other medication.
Commonly used medications such as antacids, iron, calcium tablets and proton pump inhibitors (PPIs) may also interfere with absorption of levothyroxine therapy, and it is useful to advise the patients to take levothyroxine tablets separately from these medications
Adverse effects usually occur with excessive dosage and usually stop on reduction of dosage or withdrawal of treatment for a few days. They include:
Report side effects- See BNF
Unwanted effects
adverse effects may result from prolonged over-treatment
They include signs and symptoms of hyperthyroidism – nervousness, intolerance to heat and unexplained weight loss.
There is a risk of precipitating angina pectoris, cardiac dysrhythmias or even cardiac failure.
A proportion of patients may remain persistently symptomatic in spite of receiving an optimum dose of thyroxine replacement therapy despite the TSH levels being in the normal range. In these patients referral and alternate aetiologies should be investigated
