- Decreased levels of T3 and T4 stimulate the release of thyrotropin-releasing hormone (TRH) from the hypothalamus and thyroid- stimulating hormone (TSH) from the anterior pituitary
- Hypothalamus(TRH) -> pituitary(TSH) -> Thyroid(T3 and T4).
- Elevated T3 and T4 levels, in turn, feed back to suppress the secretion of both TRH and TSH.
- 90% of circulating hormone is T4. T4 is less active.
- In the periphery, the majority of free T4 is deiodinated to T3.
- T3 binds to thyroid hormone nuclear receptors in target cells with tenfold greater affinity than does T4 and has proportionately greater activity.
Thyrotoxicosis is a hypermetabolic state caused by ele vated circulating levels of free T3 and T4
- High T3, T4, low TSH – primary hyperthyroidism
- High T3, T4, high TSH – secondary hyperthyroidism – rare tumours.
- Graves disease
- Antibody stimulates TSH receptor –> increased T3T4 production, growth of thyroid epithelium(goitre)
- Anti thyroid peroxidase and anti-thyroglobulin.
- Initially hyper–> later hypo
- Diffuse uptake on NM scan
- T cell mediated infiltrative ophthalmopathy.
- Usually qiuet but can have hot nodules
- Toxic adenoma or carcinoma.
- Subacute granulomatous thyroiditis(de quervain)
- Painful, post viral syndrome
- Thyroid follicular cell destruction by CD8 cells so no uptake on NM scan
- Transient hyperthyroidism for 2-8wks followed by hypothyroidism also transient for 2-8wks.
- Recovery is virtually always complete.
- Subacute lymphocytic thyroiditis
- Usually post partum. Thought to be autoimmune with Anti TG and TPO antibodies. Develops over 1-2wks and subsides over 2-8wks.
- Facticious and iodine OD
- White out on NM scan
- Carcinoma- papillary, follicular, medullary
- Adenoma- treat with radio iodine. Carcinoma- resect.
- Hypothyroidism is a condition caused by a structural or functional derangement that interferes with the production of thyroid hormone.
- Hypothyroidism is a fairly common disorder. Overt hypothyroidism is 0.3%, while subclinical hypothyroidism can be found in greater than 4%.
- The prevalence increases with age, and it is nearly tenfold more common in women than in men.
- Endemic iodine deficiency
- Hashimoto’s Thyroiditis
- Thyroid epithelial cell destruction – CD8 mediated and cytokine mediated, antibody mediated.
- Lymphocytic and plasma cell infiltrate. Usually euthyroid or hypothyroid. Diffusely lights up on nuclear scan. Commonly women 60-70yo. Anti body titres are high- anit thyroglobulin, anti-TPO, anti TSH receptor. Painless Goitre. High TSH
- Primary atrophic hypothyroidism(women, common, diffuse lymphocytic infiltrate, no goitre).
- Both are autoimmune and associated with- Addison’s, DM1, pernicious anaemia.
This can be caused by either surgical or radiation-induced ablation
- Due to excess cortisol – exogenous(commonest) or endogenous(70-80% ACTH high, 10-20% adrenal neoplasms 10% secretion of ectopic ACTH from other tumours)
- Insomnia, weakness
- Skin fagility, hirsuitism, striae
- Central adiposity, promimal myopathy, buffalo hump, moon facies,
- Adrenocortical insufficiency – low cortisol and aldosterone and sex hormones
- Causes – autoimmune 60-70%, TB, AIDS, metastases(breast, lung GI), lymphomas, amyloidosis, sarcoid, haemachromatosis
- Weakness and lethargy
- LOA, nausea, vomiting, LOW, diarrhoea
- Aldosterone lack – hyperkalaemia, hyponatraemia, hypotension(volume depletion)
- Testicular atrophy, amenorrhoea
Adisonian crisis (when unwell, post surgery etc) – intractable vomiting, abdo pain, hypotension, coma, vascular collapse. Possible death.
- Adrenal medullar chromaffin cells – neoplasm
- Synthesis and release catecholamines.
- Abrupt precipitous HTN with associated tachycardia, palpitations, headache, sweating, tremor, sense of aprehension. May have abdo or chest pain. May –> CCF, MI, VF, CVA.
- Precipitated by emotional stress, exercise, change in posture, palpation of the tumour.
- 10% arise in association with familial syndromes, 10% are extra-adrenal, 10% of non familial are bilateral, 10% are malignant, 10% come in childhood.
- Increased urinary excretion of free catecholamines, metanephrines, vanillamandelic acid.
- Sodium retention
- Potassium excretion
- HTN and hypokalaemia
- Causes – adrenocortical neoplasm (Conn’s syn), primary adrenocortical hyperplasia, glucocorticoid remediable hyperaldosteronism.
- Secondary hyperaldosteronism – from high renin
- Causes – reduced renal perfusion, arterial hypovolaemia, pregnancy.