MRSC Flashcards
parathyroid glands function
control the level of calcium and phosphates in the blood.
role of calcium
Calcium is involved with:
Contraction of skeletal, cardiac and smooth muscle
Blood clotting
Control of nerve impulses
Increases in the level of calcium cause depression of the nervous system
Decreases in the level of calcium causes excitation of the nervous system
PTH – hormone
PTH will cause a rise in serum concentrations of calcium and a fall in serum concentrations of phosphate
increasing calcium and phosphate absorption from the gut.
Calcitonin
hormone released by the thyroid gland in response to high levels of calcium in the blood
Decreased absorption of bone by osteoclasts
Decreased formation of new osteoclasts –
Primary Hyperparathyroidism
Normal PTH
High calcium
causes = tumour of parathyroid
2ndary
high PTH
low calcium
Low levels of Ca2+ are commonly due to chronic renal failure. Can also be caused by insufficient vit D, insufficient Ca2+ in the diet, excessive Mg2+ in the diet
Medullary thyroid carcinoma
This is associated with parathyroidism (often tertiary) as a result of hyperadrenalism. Together, these are all classed as multiple endocrine neoplasia syndrome (MEN) type I
Multiple endocrine neoplasia (MEN) type 2
a genetic condition characterised by neoplasia of the thyroid (medullary cell carcinoma), parathyroid (parathyroid adenoma) and adrenal glands (phaeochromocytoma
primary hypothyroidism
autoimmune disorder affecting thyroid tissue
Hashimoto’s thyroiditis
most common cause in the developed world
autoimmune disease, associated with type 1 diabetes mellitus, Addison’s or pernicious anaemia
may cause transient thyrotoxicosis in the acute phase
5-10 times more common in women
High TSH, Low T3/4
secondary hypothyroidism
disorder with the pituitary gland (e.g.pituitary apoplexy) or a lesion compressing the pituitary gland
low TSH low t3/4
Subacute thyroiditis (de Quervain’s)
associated with a painful goitre and raised ESR
Sick euthyroid syndrome
low TSH low t3/4
Poor compliance with thyroxine
high TSG and Low T3/4
Patients who are poorly compliant may only take their thyroxine in the days before a routine blood test. The thyroxine levels are hence normal but the TSH ‘lags’ and reflects longer term low thyroxine levels
Graves’ disease
TSH down, T4 and T3 up
thyroid autoantibodies
other investigations are not routinely done but includes isotope scanning
thyroid malignancies - papillary cancer
Papillary -> most common - Often young females - excellent prognosis
Usually contain a mixture of papillary and colloidal filled follicles
Histologically tumour has papillary projections and pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominate
Haematogenous metastasis rare
Follicular thyroid cancer (adenoma)
Usually present as a solitary thyroid nodule
Malignancy can only be excluded on formal histological assessment
Management of papillary and follicular cancer
total thyroidectomy
followed by radioiodine (I-131) to kill residual cells
yearly thyroglobulin levels to detect early recurrent disease
thyroid Follicular carcinoma
May appear macroscopically encapsulated, microscopically capsular invasion is seen. Without this finding the lesion is a follicular adenoma.
Vascular invasion predominates
Multifocal disease raree
Medullary carcinoma
C cells derived from neural crest and not thyroid tissue
Serum calcitonin levels often raised
Familial genetic disease accounts for up to 20% cases
Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.
thyroglossal cysts
More common in patients < 20 years old.
Features
usually midline, between the isthmus of the thyroid and the hyoid bone
moves upwards with protrusion of the tongue
may be painful if infected
Thyroid surgery: complications
Complications following surgery
Anatomical such as recurrent laryngeal nerve damage.
Bleeding. Owing to the confined space haematoma’s may rapidly lead to respiratory compromise owing to laryngeal oedema.
Damage to the parathyroid glands resulting in hypocalcaemia.
prevention of thyroid eye disease
smoking is the most important modifiable risk factor for the development of thyroid eye disease
radioiodine treatment may increase the inflammatory symptoms seen in thyroid eye disease.
In a recent study of patients with Graves’ disease around 15% developed, or had worsening of, eye disease. Prednisolone may help reduce the risk
thyroid eye disease
exophthalmos conjunctival oedema optic disc swelling ophthalmoplegia inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
Management topical lubricants may be needed to help prevent corneal inflammation caused by exposure steroids radiotherapy surgery
Primary hyperparathyroidism
Indications for surgery
Elevated serum Calcium > 1mg/dL above normal
Hypercalciuria > 400mg/day
Creatinine clearance < 30% compared with normal
Episode of life threatening hypercalcaemia
Nephrolithiasis
Age < 50 years
Neuromuscular symptoms
Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of more than 2.5 standard deviations below peak bone mass (T score lower than -2.5)
Secondary hyperparathyroidism treatment
Usually managed with medical therapy.
Indications for surgery in secondary (renal) hyperparathyroidism:
Bone pain
Persistent pruritus
Soft tissue calcifications
Side-effects of thyroxine therapy
hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation
Pseudohypoparathyroidism
target cells being insensitive to PTH
due to abnormality in a G protein
associated with low IQ, short stature, shortened 4th and 5th metacarpals
low calcium, high phosphate, high PTH
diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH. In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels. In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.
Riedel’s thyroiditis
characterised by dense fibrous tissue replacing the normal thyroid parenchyma. On examination a hard, fixed, painless goitre is noted. It is usually seen in middle-aged women. It is associated with retroperitoneal fibrosis.
Congenital adrenal hyperplasia causes
Cause
21-hydroxylase deficiency (90%)
11-beta hydroxylase deficiency (5%)
17-hydroxylase deficiency (very rare)
21-hydroxylase deficiency features
virilisation of female genitalia
precocious puberty in males
60-70% of patients have a salt-losing crisis at 1-3 wks of age
11-beta hydroxylase deficiency features
virilisation of female genitalia
precocious puberty in males
hypertension
hypokalaemia
17-hydroxylase deficiency features
non-virilising in females
inter-sex in boys
hypertension
Addison’s disease
Autoimmune destruction of the adrenal glands is the commonest cause of primary hypoadrenalism in the UK,
eatures
lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia
Cushings causes
ACTH dependent causes
Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes
ACTH independent causes
iatrogenic: steroids
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
Carney complex: syndrome including cardiac myxoma
micronodular adrenal dysplasia (very rare)
Pseudo-Cushing’s
mimics Cushing’s
often due to alcohol excess or severe depression
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
insulin stress test may be used to differentiate
Primary hyperaldosteronism
bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases
adrenal adenoma, termed Conn’s syndrome also a cause
Features hypertension hypokalaemia e.g. muscle weakness this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients alkalosis
Primary hyperaldosteronism investigations
vestigations
the 2016 Endocrine Society recommend that a plasma aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism
should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone)
following this a high-resolution CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
Adrenal Venous Sampling (AVS) can be done to identify the gland secreting excess hormone in primary hyperaldosteronism
Conditions where HbA1c may not be used for diagnosis:
haemoglobinopathies haemolytic anaemia untreated iron deficiency anaemia suspected gestational diabetes children HIV chronic kidney disease people taking medication that may cause hyperglycaemia (for example corticosteroids)
The following are key messages that should be given to all patients with diabetes if they become unwell:
Increase frequency of blood glucose monitoring to four hourly or more frequently
Encourage fluid intake aiming for at least 3 litres in 24hrs
If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake
It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis
