Endocrine Conditions Flashcards
(43 cards)
What is the aetiology of Hyperthyroidism?
There are different types and causes of hyperthyroidism, including:
- Primary (abnormal thyroid) - Graves’ Disease (75% of cases), Toxic multinodular goitre (2nd biggest cause), toxic thyroid nodule (Plummer’s disease) (adenoma), and drugs.
- Secondary (excess TSH) - pituitary adenoma secreting TSH, high HcG can also stimulate thyroid, thyroid hormone resistance syndrome (very rare) where pituitary is resistant to t3/t4.
- Subclinical - This is where, although TSH is suppressed, FT3 + FT4 is in normal range.
- Thyrotoxicosis without hyperthyroidism - due to large doses of levothyroxine or thyroiditis.
What is the definition and epidemiology of Graves’ Disease?
Graves disease is an autoimmune condition resulting in hyperthyroidism. It is relatively common affecting 0.8/1000 women a year, with negligible incidence in men. It is the most common cause of hyperthyroidism in many countries.
Thyroid hormone overproduction is a result of stimulation of TSH receptors in thyroid by TSH receptor antibodies. This causes an increased basal metabolic rate, and increased protein, carbohydrate and fat metabolism.
What are the clinical features of Hyperthyroidism?
Patient’s present with heat intolerance, sweating, palpitations, anxiety, irritability and a tremor.
Weight loss (despite a good appetite), diarrhoea and pruritus are also common.
Females complain of menstrual abnormalities and reduced libido. Males complain of impotence.
- Grave’s orbitopathy* is present in 25% of cases, with tobacco use being a strong risk factor. Patient’s complain of blurred vision, diplopia, eye grittiness and eye protrusion.
- On examination*: The patient may be underweight, restless, sweaty, and have signs of other autoimmune diseases. Also notice pretibial myxoedema (raised pigmented orange-peel textured nodules or plaques on shins) and symmetricallyenlarged smooth goitre.
- Hands: Tremor, warm, moist, rapid or irregular pulse, onycholysis (nails dethatch from nailbed), clubbing and palmar erythema.
- Eyes: May notice lid lag and lid retraction
What are the potential complications of Hyperthyroidism?
Thyrotoxic crisis, heart failure, osteoporosis, infertility.
What are the investigations for Hyperthyroidism?
As with primary hyperthyroidism, blood tests will show suppressed TSH, and elevated T3 and T4.
To differentiate between the causes of primary hyperparathyroidism (Plummer’s disease [Toxic nodular goitre], Viral thyroiditis) perform radioactive iodine uptake test. In Grave’s disease, notice elevated diffuse uptake. In Plummer’s disease there is multiple areas of increased uptake, and in a solitary toxic adenoma there is a single ‘hot nodule’ of uptake. In de Quervain’s (viral) thyroiditis, there is absent uptake.
TSH receptor antibodies can also be detected, but is an expensive test.
Describe the management of Hyperthyroidism
All patients with primary hyperthyroidism should be told about the three options:
- Medical:* Prolonged antithyroid drug (ATD) therapy, involving carbimazole/thiamazole or propylthiouracil (all work by inhibiting thyroid peroxidase and hormone synthesis). Block and replace regimens are when ATDs are prescribed as well as levothyroxine.
- Patients told to look out for sore throat, fever etc. as agranulocytosis is an important side-effect.
Symptomatic therapy by beta-blockers such as propranolol or atenolol can be used to treat tremor, palpitations, tachycardia and anxiety.
- Radioactive iodine* :Must avoid pregnant women and young children for 4 months. Thyroid eye disease is a relative contraindication as can worsen. Most require thyroid replacement after 5 years.
- Surgery:* Reserved for patients with large goitres causing upper-airway obstruction, and those who cannot take ATD, and are either pregnant or cannot take radioiodine due to exophthalmos.
- Complicated by: left recurrent laryngeal nerve injury, which if cut can cause speech difficulty; hypothyroidismand hypoparathyroidism.
What is the definition and epidemiology of Hypothyroidism?
Hypothyroidism is the clinical syndrome resulting from the insufficient secretion of thyroid hormones. Affects up to 2% of adults and women more than men (6:1).
What is the aetiology of Hypothyroidism?
Primary causes (95%) include:
- Autoimmune (Hashimoto’s) thyroiditis (most common cause, affecting women up to 9x more).
- Iatrogenic (post-surgery, radioiodine, medication for hyperthyroidism)
- Severe iodine deficiency (most common cause worldwide) or iodine excess (Wolff-Chaikoff effect)
- Thyroiditis (De Quervain’s)
- Lymphocytic thyroiditis is developed by 6% of post-partum women.
- Congenital: thyroid dysgenesis
- Inherited defects in thyroid hormone biosynthesis
Secondary (5%) causes are pituitary or hypothalamic disease e.g. tumours.
What are the clinical features of Hypothyroidism?
A history of thyroid surgery or radioiodine surgery strongly points to hypothyroidism.
Onset is usually insidious. Patients complain of cold intolerance, lethargy, weight gain, constipation, dry skin, hair loss, hoarse voice. Can also complain of mental slowness, depression, dementia, cramps, ataxia and paraesthesia.
Females may experience menstrual disturbances (irregular cycles, menorrhagia).
Personal or family history of other autoimmune conditions can point to Hashimoto’s.
On examination: Note bradycardia and cold hands. Pale puffy face, goitre, oedema, dry skin, vitiligo. Also notice pericardial or pleural effusions. The patient may also have ascites, and have slow relaxation of reflexes, and signs of carpal tunnel syndrome.
What are the potential complications of Hypothyroidism?
Myxoedema coma, myxoedema madness (psychosis with delusions and hallucinations or dementia) in severe hypothyroidism (may be seen in the elderly after starting levothyroxine treatment).
What are the investigations for Hypothyroidism?
Blood: TFTs (Thyroid Function Test) - Primary: ↓ T4/T3 and ↑ TSH. Secondary: ↓ T4/T3 and ↓ or inappropriately normal TSH.
FBC may show normocytic anaemia
U&Es may show ↓ Na.
Cholesterol may be increased.
In suspected secondary cases: pituitary function tests, MRI and visual field testing.
Describe the management of Hypothyroidism
- Chronic:* Levothyroxine (synthetic T4) 50-200mcg a day. TSH levels should be checked 8-12 weeks after a change in dose. The ‘goal’ is to normalise TSH levels (i.e. to the normal range). Rule out adrenal insufficiency and treat before starting thyroid hormone replacement to avoid Addisonian crisis.
- Iron and calcium carbonate reduces the amount of iron absorbed, and so should be given at least 4 hours apart.
- Myxoedema coma:* Give oxygen, rewarming, rehydration, I.V liothyroxine or T4, IV hydrocortisone (in case hypothyroidism is secondary to hypopituitarism). After stable, treat the underlying disorder e.g. infection. Myxoedema coma has a mortality of up to 80%.
What are the different types of hyperparathyroidism and their causes?
Primary hyperparathyroidism is when there is increased PTH secretion unrelated to the plasma calcium concentration. Caused by adenomas or hyperplasia (98%), rarely parathyroid carcinomas (<1%).
Secondary hyperparathyroidism is when there is increased secretion of PTH secondary to hypocalcaemia. Often caused by chronic renal failure or vitamin D deficiency.
Tertiary is autonomous PTH secretion following chronic secondary hyperparathyroidism.
What are the clinical features and causes of Hyperparathyroidism?
Primary: Many patients have mild hypercalcaemia and are asymptomatic. A history of osteoporosis or osteopenia is common, as well as nephrolithiasis (as most kidney stones are of calcium phosphate).
Other symptoms of hypercalcaemia can be remembered with: Stones, Bones, Groans, Psychic Moans and Thrones. Stones = kidney stones. Bones = bone pain and osteoporosis. Groans = Abdominal pain, nausea, constipation. Psychic moans = depression, lethargy, fatigue, confusion, anxiety. Thrones = polyuria and polydipsia.
Secondary: May present with symptoms and signs of hypocalcaemia - see Osteomalacia and/or the underlying cause (chronic renal failure, or vitamin D deficiency).
Complications: Hypercalcaemia. Osteitis fibrosis cystica in secondary hyperparathyroidism due to renal failure.
What are the investigations for Hyperparathyroidism?
Bloods:
- Serum calcium is ↑ in primary and ↓ in secondary.
- A serum PTH can be measured with immunochemical assays, which will be elevated.
- Vitamin D may be low in someone with secondary hyperparathyroidism.
- ↑ Alkaline Phosphatase due to increase bone turnover.
Patient may also have hyperchloremic due to PTH inhibition of bicarbonate reabsorption.
A renal ultrasound can be used to look at renal calculi. A DXA of (lumbar spine, hip and forearm) should be completed to assess extent of disease.
Describe the management of Hyperparathyroidism
- Acute hypercalcaemia:* Rehydration with normal fluids.
- Primary hyperparathyroidism:*
- 1st line treatment is a parathyroidectomy (subtotal, or rarely total) which tends to be curative. Monitor serum calcium and creatinine. Bisphosphonate can be given if osteoporosis is present.
-
Select patients can be managed conservatively by regular follow ups:
- Calcium level is <0.25 mmol/L above upper limit AND
- The patient is >50
- No evidence of end-organ damage (such as kidney stones or osteoporosis)
Following surgery, calcium can be low requiring supplementation. The patient may experience signs of hypocalcaemia such as pins and needles.
Secondary hyperparathyroidism: Treat underlying renal failure or vitamin D supplements.
What is thyroid storm and its precipitants?
Thyroid storm is a rare but life-threatening complication of thyrotoxicosis. It is typically seen in patients with established thyrotoxicosis and is rarely seen as the presenting feature. Iatrogenic thyroxine excess does not usually result in thyroid storm.
Precipitating events:
- thyroid or non-thyroidal surgery
- trauma
- infection
- acute iodine load e.g. CT contrast media
What are the clinical features of thyroid storm?
Clinical features include:
- fever > 38.5ºC
- tachycardia
- confusion and agitation
- nausea and vomiting
- hypertension
- heart failure
- abnormal liver function test - jaundice may be seen clinically
What is the management of thyroid storm?
Emergency management usually involves:
- Beta-blockers: typically IV propranolol
- Anti-thyroid drugs: e.g. propylthiouracil or methimazole.
Generally patients should be managed in ICU and should receive treatment for hyperpyrexia (e.g. paracetamol) as well as treatment of underlying precipitating event.
Lugol’s iodine can be delivered orally or through NG tube, which inhibits further release of thyroxine.
Dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3.
What is the aetiology of adrenal insufficiency?
Adrenal insufficiency is the deficiency of adrenocortical hormones (mineralocorticoids, glucocorticoids and androgens).
Primary causes (problem with endocrine organ itself) - called Addison’s disease include:
- Autoimmune destruction of the adrenal cortex (>70% of cases)
- Infections such as tuberculosis, meningococcal septicaemia, CMV (HIV patients), histoplasmosis
- Can be caused by infarction, and congenital (adrenoleukodystrophy)
Secondary causes include due to pituitary or hypothalamic disease.
The most common cause is iatrogenic - where cortisol production is suppressed due to long-term steroid use, leading to negative feedback on hypothalamic-pituitary-axis. This results in decreased CRH (corticotrophin releasing hormone) and decreased ACTH production.
What are the clinical features of adrenal insufficiency?
Chronically presents with non-specific symptoms: dizziness, anorexia (causing weight loss), diarrhoea and vomiting (unknown reason), abdominal pain, lethargy, weakness and depression.
On examination:
- Postural hypotension
- Increased pigmentation (more noticeable in buccal mucosa, scars, skin creases, nails and pressure points) - this is absent in secondary causes (iatrogenic) as ACTH production is also dampened.
- Loss of body hair in women (due to androgen deficiency)
Can present with other autoimmune conditions such as vitiligo.
Acute presentation (Addisonian crisis): Acute adrenal insufficiency with major haemodynamic collapse often precipitated by stress (e.g. infection or surgery). On examination: tachycardia, pale, cold, clammy, oliguria.
What are the investigations for adrenal insufficiency?
In primary care, start with a 9am serum cortisol test. If <110 nanomol/L, likely adrenal failure. If >550, likely normal response. If between, or in secondary care, do a short synACTHen test:
- Short synACTHen is the best test to diagnose Addison’s disease - it is is administering a small amount of synACTHen and measuring response by cortisol production. Primary adrenal insufficiency (Addison’s) will not respond, while secondary (pituitary) will produced a delayed response, or no response.
- A long synACTHen test is administering more synACTHen, and measuring response over 24h. It will more consistently produce a response for secondary causes, and still no response for primary.
Identify the cause:
- Autoantibodies (against 21-hydroxylase).
- Abdominal CT or MRI
Addisonian crisis:
- FBC (neutropenia)
- U&Es (↑urea, ↓Na+, ↑K+)
- ↑ESR and CRP
CXR can be used to identify cause.
Describe the management of adrenal insufficiency
Chronic: Glucocorticoid replacement with hydrocortisone (three times a day) and mineralocorticoids with fludrocortisone.
- Hydrocortisone and not fludrocortisone needs to be increased during acute illness or stress (usually doubled).
Give them a steroid warning card (says patient is on steroids), Medic-alert bracelet, emergency hydrocortisone ampule and patient education (as missing doses of steroids is dangerous).
Prognosis: Adrenal function rarely recovers, but normal life expectancy can be expected if treated.
What is the definition and epidemiology of Acromegaly?
Acromegaly is the constellation signs and symptoms that are caused by hypersecretion of growth hormone (GH) in adults (if this happens before puberty it is known as gigantism).
- It is rare, incidence is 5 in 1,000,000.
