Thyroid Flashcards
What is hyperthyroidism?
over-production of thyroid hormone by the thyroid gland
What is thyrotoxicosis?
Thyrotoxicosis = abnormal and excessive quantity of thyroid hormone in the body
Primary hypyperthyroidism?
Thyroid pathology causing thyroid to secrete excessive hormone
Secondary hyperthyroidism?
excessive thyroid hormones as a result of TSH overstimulation. due to pituitary or hypothalamic pathology
What is Graves disease
What are the markers of Graves?
Most common cause of hyperthyroidism
Autoimmune condition
TSH receptor stimulating antibodies *
anti-thyroid peroxidase antibodies
What is toxic multinodular goitre (Plummer’s disease)
what are the unique features of multi nodular goitre?
where nodules develop in the thyroid which act independently of the normal feedback system and continuously produce excess thyroid hormone
second most common cause of thyrotoxicosis after graves
unique features:
- Goitre with firm nodules
- most patients over 50
What are the causes of hyperthyroidism? which is the most common?
Grave’s disease (most common)
Toxic multinodular goitre
Toxic adenoma (solitory toxic thyroid nodule)
Amiodarone, Thyroxine
Thyrotoxic phase of thyroiditis (De Quervain’s, Hashimotos, post partum)
How does hyperthyroidism present?
Which are specific to Graves disease?
- General: weight loss, restlessness, heat intolerance
- Cardiac: palpitations, can provoke arrhythmias e.g AF
- Skin + hair: hair thinning, increased sweating, pretibial myxoedema (thyroid dermopathy) - erythematous oedematous lesions above the lateral malloeli
- GI: diarrhoea
- Gynae: oligomenorrhoea
- Neuro: anxiety, tremor, manic
Specific to Graves:
- Ophthalmopathy: exophthalmos, ophthalmoplegia, eye discomfort and grittiness
- Dermopathy: pretibial myxoedema
- Thyroid acropachy
- diffuse goitre - without nodules, increased iodine uptake
what is de quervains thyroiditis?
How is it managed?
Diffuse painful goitre
occurring following viral URTI
fever, neck pain, tenderness and dysphagia
Hyperthyroid phase followed by hypothyroid then resolves spontaneously
- self limiting condition, supportive management, NSAIDs for pain & inflammation and beta blockers for symptomatic relief
What investigations and findings would you see in hyperthyroidism?
- low TSH, raised T3,T4
- Abs: TSH receptor antibody
- Raised calcium, raised LFTs
- isotope scan: raised in graves, low in thyroiditis
What conditions is graves disease associated with?
autoimmune conditions:
T1DM
Vitiligo
Addisson’s
What is a thyroid storm/thyrotoxic crisis?
- Fever
- Tachycardia
- confusion and agitation
- nausea and vomiting
- heart failure
- abnormal LFTs - jaundice may be seen
- hypertension
What causes a thyroid storm?
recent thyroid surgery or radio-iodine
infection
MI
trauma
How is hyperthyroidism managed?
1st line: Carbimazole - succesful at tx graves in 4-6 weeks
Once normal levels the dose is either:
titrated to maintain at normal levels - titration block
or
dose is sufficient to block all function and the patient takes levothyroxine titrated to effect - block and replace
complete remission can be achieved in 18 months and carbimazole can be stopped
50% relapse - surgery or radiodine
S.E of carbimazole = agranulocytosis
2nd line: propylthiouracil (risk of hepatic reactions)
Non-medical
Radio-iodine - most become hypothyroid, need to take levothyroxine. CI: pregnancy, lactation, must avoid contact with children and pregnant for 3 weeks
surgical:
thyroidectomy - levothyroxine for life
s.e recurrent laryngeal n palsy
symptom management
B-Blockers - propanol is non selective adrenergic blocker
How is a thyroid storm managed?
- symptomatic tx e.g paracetamol
- tx precipitating factors
- beta blockers - IV propanolol
- antithyroid drug e.g carbimazole then Lugol’s iodine 4hrs later
- dexamethasone - blocks conversion of T4 to T3
