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Flashcards in Endocrinology Deck (78):

What is the most common cause of hyperthyroidism?

Graves' disease - serum IgG antibodies bind to TSH receptors in the thyroid and stimulate thyroid hormone production


What is viral thyroiditis also known as?

de Quervains aka subacute granulomatous


What occurs in de Quervain's thyroiditis?

Hyperthyroidism from acute inflammatory process --> damage to thyroid follicular cells and breakdown of stored thyroglobulin --> unregulated release of T4 and T3 until stores are deplete


How is hyperthyroidism managed?(3)

1. Medical therapy: Carbimazole - blocks thyroid hormone synthesis; PTU - blocks thyroid hormone synthesis, also inhibits peripheral conversion of T4 to T3; Beta-blocker - propranolol; for symptomatic control

2. Radioactive iodine - if antithyroid drugs contraindicated or failed medical therapy

3. Thyroidectomy - if antithyroid drugs contraindicated, malignancy present or suspected, compressive symptoms


What side effects will you need to consider in the management of hyperthyroidism with carbimazole/PTU?



What is the most common cause of hypothyroidism in iodine-sufficient areas?

vs worldwide?

Hashimoto's or chronic autoimmune thyroiditis

Worldwide - iodine deficiency


What is the pathophysiology behind Hashimoto's thyroiditis? (2)

1. Cell-mediated destruction of thyroid follicles due to defect in clone of T-suppressors

2. B lymphocytes produce antibodies against thyroid components including thyroglobulin, thyroid peroxidase, TSH receptor, Na+/I symporter


Name 6 causes of diffuse goitres.

1. Simple - physiological (puberty, pregnancy)
2. Autoimmune - Hashimoto's, Graves'
3. Thyroiditis - de Quervain's
4. Iodine deficiency
5. Dyshormonogenesis
6. Goitrogens (e.g. SUs)


Name 4 causes of nodular goitres.

1. MNG
2. Solitaryndule
3. Fibrotic
4. Cysts


How is hypothyroidism managed?

Replacement therapy (levothyroxine)


How is thyrotoxicosis investigated? (3)

1. Biochemistry: TFTs, beta-HCG (apparently first trimester of pregnancy can cause subclinical hyperthyroidism), baseline FBE

2. Anti-thyroid antibodies - anti-TPO, anti-TG, anti-TSH receptor (if positive suspect Graves')

3. Thyroid nuclear scan/radioactive iodine - if the aetiology of the thyrotoxicosis is not evident from the clinical presentation and laboratory tests


What thyroid conditions reveal an increased uptake on a thyroid nuclear scan? (3)

1. Graves'
2. Toxic MNG (patchy)
3. Toxic adenoma - benign


What are the potential complications/disadvantages of radioactive iodine therapy? (5)

1. Permanent hypothyroidism
2. Development or exacerbation of ophthalmopathy in around 15%
3. Need to delay pregnancy and avoid breastfeeding - NOT SAFE TO TAKE DURING PREGNANCY
4. Radiation thyroiditis in 10%
5. Radiation safety precautions - avoid close contact with children


What are the potential complications/disadvantages of thyroidectomy? (3)

1. Permanent hypothyroidism
2. Surgical complications - recurrent laryngeal nerve damage, hypoparathyroidism
3. Post-operative pain or discomfort, scarring


What three differential diagnosis of hyperthyroidism would you consider in a pregnant lady (first trimester)?

1. Graves' disease

2. hCG-induced hyperthyroidism (assoc. with hyperemesis)

3. Toxic adenoma/MNG


How is hyperthyroidism treated in pregnancy?

Antithyroid drugs - at lowest possible dose



Define subclinical hyperthyroidism

TSH suppressed with normal T4 and T3


List 4 causes of painful thyroiditis

1. Infectious thyroiditis
2. Radiation thyroiditis - occasionally seen post-radioactive iodine therapy for Graves'
3. Palpation or trauma-induced
4. Subacute granulomatous (de Quervain's - most common!)


List 4 causes of painless thyroiditis

1. Subacute lymphocytic
2. Post-partum
3. Drug-induced (amiodarone, interferon-alpha)
4. Hashimoto's


What is the difference between Type 1 and Type 2 amiodarone-induced thyroiditis?

Type 1- due to excess iodine, often underlying thyroid pathology present

2. Type 2 - destructive thyroiditis due to direct toxic effect of amiodarone


How is AIT managed?

Type 1 - antithyroid therapy

Type 2 - corticosteroids


How is postpartum thyroiditis managed? (2)

1. Beta-blocker for symptoms
2. Thyroxine if hypothyroid is prolonged, symptomatic


What is the typical appearance of someone with hypothyroidism?

1. Puffy and pale facies
2. Dry, brittle hair
3. Sparse eyebrows
4. Dry skin
5. Thickened and brittle nails
6. Myxoedema - fluid infiltration of tissues


How is suspected hypothyroidism investigated? (3)

1. TFTs - TSH should be elevated, free T4 level levels should be decreased

2. Thyroid autoantibodies - anti-TPO and anti-TG are positive in 95% of patients with autoimmune thyroiditis

3. Thyroid US only if suspicious structural thyroid abnormalities suspected


What TFT findings would make one suspicious of a central hypothyroidism?

Low serum T4 without expected increase in serum TSH raises possibility of central hypothyroidism due to pituitary or hypothalamic pathology


can be seen transiently during recovery from severe illness (euthyroid sick syndrome)


Which result definitively confirms autoimmune/Hashimoto's thyroiditis as a cause of hypothyroidism?

Positive TPO antibody assay


Describe the HPA Axis

Hypothalamus produces CRH which acts on the pituitary - ACTH is produced. This acts on adrenal cortex - mineralocorticoids, glucocorticoids and sex hormones produced.

Cortisol acts on hypothalamus and pituitary in negative feedback loop to reduce CRH and ACTH production


What is the difference between primary and secondary adrenal dysfunction?

Primary = disorder in the gland

Secondary = disorder in the regulatory system


What is Cushing's syndrome?

Clinical state in which there is glucocorticoid excess resulting in loss of normal feedback mechanisms of the HPA axis - can have both ACTH-dependent and ACTH-independent causes


What is the most common cause of Cushing's syndrome?

Oral steroid therapy - ACTH-independent


What investigations are conducted in suspected Cushing's syndrome? (3)

1. Overnight dexamethasone suppression test - dexamethasone should suppress cortisol in normal people, in Cushing's cortisol is not suppressed

2. Midnight salivary cortisol - salivary sample collected at home and sent to lab - elevated in Cushing's

3. Urinary free cortisol (not as useful)


What is Cushing's disease?

ACTH-dependent cause: Bilateral adrenal hyperplasia from ACTH-secreting pituitary adenoma


Name three ACTH-dependent causes of Cushing's syndrome

1. Cushing's disease

2. Ectopic ACTH production - small cell lung and carcinoid, pancreatic

3. Ectopic CRH production - some thyroid (medullary) and prostate cancers


Name three ACTH-independent causes of Cushing's syndrome

1. Adrenal adenoma/cancer
2. Adrenal nodular hyperplasia
3. Iatrogenic - oral steroid therapy


How is Cushing's syndrome treated? (2)

Depends on cause

1. If iatrogenic, stop medications if possible

2. Remove tumours!


What is Nelson's syndrome?

Can occur if bilateral adrenalectomy is conducted in people with Cushing's disease -

Overproduction of ACTH from ACTH-secreting tumour in pituitary - leading to hyperpigmentation


What is Addison's disease? List three causes

Primary adrenal insufficiency - destruction of adrenal cortex leading to glucocorticoid and mineralocorticoid deficiency. (loss of negative feedback - increased CRH and ACTH)

can be due to autoimmunity, TB infection, metastatic tumour (lung and breast cancer)


What are the symptoms of Addison's disease? (4)

Chronic symptoms result from cortisol deficiency, aldosterone deficiency and excess ACTH

Abdo: N& V, abdo pain, diarrhoea/constipation

Skin: pigmented palmar creases and buccal mucosa

Mood: depression, psychosis, low self-esteem

Well-being: tired, dizzy, flu-like myalgias/arthralgias


How would you investigate Addison's disease?

1. Blood work: decreased Na+ and increased K+, decreased glucose, plasma

2. Short ACTH stimulation test: give ACTH, normally cortisol should rise, in Addison's it doesn't.


How would you differentiate between primary and secondary adrenal insufficiency?

Short ACTH

Primary: give ACTH, normally cortisol should rise, in Addison's it doesn't

Secondary: give ACTH, cortisol should increase dramatically


How do you treat Addison's disease? (2)

Replace hormones that glands are not making

1. Cortisol replaced with hydrocortisone tabets

2. Deficient aldosterone: fludrocortisone acetate and increased salt intake


List 4 causes of secondary adrenocortical insufficiency

1 Exogenous glucocorticoid therapy
2. Idiopathic hypopituitarism
3. Post-surgical cure of Cushing's disease
4. Pituitary tumour


What is Conn's syndrome?

Primary hyperaldosteronism - characterised by refractory hypertension, Na+ and H2O retention, potassium excretion


What are the two main causes of primary hyperaldosteronism?

1. Aldosterone-producing adenoma
2. Bilateral idiopathic hyperplasia


How is primary hyperaldosteronism treated?

Depends on cause!

Bilateral idiopathic hyperplasia - treat with mineralocorticoid antagonist e.g. spironolactone

Adenoma - adrenalectomy


What is a phaeochromcytoma?

Rare catecholamine-producing tumours - arise from sympathetic paraganglia cells (collections of chromaffin cells) found within adrenal medulla


What are the causes of phaeochromocytoma?

Rule of 10s

10% malignant
10% extra-adrenal
10% bilateral
10% familial


What is acromegaly caused by?

Increased secretion of growth hormone from a pituitary tumour usually - GH stimulates bone and soft tissue growth through increased secretion of insulin-like growth factor-1


What diagnostic tests can be done for acromegaly? (3)

1. Serum IGF-1 - if serum IGF-1 is high,(2) serum GH should be measured after oral glucose administration. Inadequate suppression of GH after a glucose load confirms the diagnosis of acromegaly.

3. Radiologic testing to determine the cause of excess GH secretion - pituitary MRI


What is a diabetes insipidus and what are the different types?

Passage of large volumes of dilute urine due to impaired water resorption by the kidney because of:

1. Reduced ADh secretion from posterior pituitary (Cranial DI)

2. Nephrogenic DI - mimpaired response of kidney to ADH


What can cause cranial DI? (4)

1. Idiopathic
2. Trauma
3. Infiltration - sarcoidosis
4. Vascular - haemorrhage


How would you differentiate between cranial DI and nephrogenic DI?

Give desmopressin (synthetic vasopressin) and measure urine output and omsolarity

Desmopressin will fix in cranial DI (should reduce urine output and increase osmolarity)
Doesn't fix nephrogenic DI


List two risk factors for thyroid malignancy. Which is the most important?

1. History of head and neck irradiation in childhood or teenage years - most important risk factor

2. Family history of medullary carcinoma


What type of thyroid nodules carry a low risk of malignancy, and how can this be evaluated? (2)

Hyperfunctioning nodules

1. Measurement of TSH - suppression suggests a nodule is hyperfunctioning

2. Radiouptake scan showing a 'hot' nodule


When should an FNA of a thyroid nodule be considered? (2)

In the absence of TSH suppression (i.e. TSH is normal or elevated) or after a radiouptake scan shows a cold nodule


What BMD (from DEXA scan) values would suggest normal vs osteopaenia vs osteoporosis?

Normal - T score greater than -1

Osteopaenia - T score greater than -2.5 but less than -1

Osteoporosis - T score less than -2.5

i.e. the smaller the number, the worse it is!


What are the diagnostic criteria for Type 2 diabetes? (3)

FBG equal to or greater than 7.0 mmol/L (on two separate occasions)

2 hour postprandial equal to or greater than 11.0 mmol/L on OGTT (on two separate occasions)

HbA1c equal to or greater than 6.5% (48 mmol/mol) (on two separate occasions)


When is an OGTT indicated?

1. FBG between 5.5-6.9 mmol/L


2. RBG between 5.5-11.0 mmol/L


Define impaired fasting glucose

FBG is between 6.1-6.9 mmol/L

(i.e. not high enough to be classified as diabetes (more than 7))


Define impaired glucose tolerance

2 hour postprandial on OGTT is between 7.8 and 11.0 mmol/L

(i.e. not high enough to diagnose diabetes (more than 11))


What is involved in an OGTT?

In the three days leading up to the test you should eat and drink adequate carbohydrates, greater than 150gms per day

You will need to fast for 8 hours before the test

A FBG is taken. You are then given a sweet drink that contains 75g of glucose

Your blood glucose is checked at one hour and again at two hours after the glucose drink

If FBG is between 6.1-6.9 - impaired fasting glucose
If 2 hour postprandial is between 7.8 and 11.0 - IGT


What is the biochemical criteria for the diagnosis of DKA? (3)

Hyperglycaemia (BG level of greater than 11)

Venous pH less than 7.3 or bicarb less than 15

Ketnoaemia and ketonuria


How is DKA managed in emergency? (5)

1. Bloods: FBE, UEC, glucose, CMP, bicarb, ketones

2. Urinalysis: ketones

3. Culture (blood, urine or throat) and consider CXR to exclude infection unless there is a clear alternative explanation

4. Fluid replacement - 0.9% saline

5. Insulin therapy: o.1 unit/kg/hour. Add 5% glucose once plasma glucose falls to 15. Can add potassium if hypokalaemic.


What lab studies help distinguish primary aldosteronism from other cases of hypertension?

Elevated aldosterone levels in the setting of suppressed plasma renin activity


How does parathyroid hormone regulate serum calcium? (3)

PTH ultimately tries to increase calcium concentrations in the body.

1. Bone: Stimulates formation of osteoclasts, increased bone resorption.

2. Kidneys: Enhances active reabsorption of calcium and magnesium

3. Intestine (via kidney): enhances the absorption of calcium in the intestine by increasing the production of activated Vitamin D (Vit D activation occurs in the kidney)


What are the symptoms/signs of hypercalcaemia?

BONES, STONES, (Psychiatric) MOANS AND (abdominal) GROANS


What are the symptoms/signs of hypocalcaemia?


C - convulsions
A - arrhythmias
T - tetany (trousseau's + chvostek's sign)
S - spasms, seizures, and stridor

Numb - numbness in fingers, feet, mouth and lips


What is Paget's disease of the bone?

Disease characterised by accelerated bone turnover and abnormal bone remodeling, resulting in overgrowth of bone at selected sites and impaired integrity of affected bone. ?Overactivity of osteoclast (bone resorption)


How does Paget's disease of the bone usually manifest?

Majority are asymptomatic, however two main manifestations are pain and deformities in affected areas


How is Paget disease of the bone primarily diagnosed?

Radiologic, but in most patients serum alkaline phsophatase is also elevated. Normal phosphate and calcium usually.


Name one fatal complication of Paget's

Osteosarcoma - rare, typically presents in those with longstanding skeletal disease


How should one counsel a patient on the use of bisphosphonates?

Must be taken with plain water first thing in the morning and at least 30 minutes before food. Patient should not lie down during this period to prevent GORD


What is osteomalacia?

Softening of the bones caused by defective bone mineralisation secondary to inadequate levels of available phosphate and calcium or because of overactive resorption of calcium from bone

Only occurs after growth plates have fused


What lab findings are found in osteomalacia? (5)

1. Elevated ALP
2. Reduced serum calcium and phosphate
3. Reduced urinary calcium
4. Reduced Vitamin D
5. elevated PTH


What radiologic findings are seen in Paget's? (2)

1. Osteoporosis circumscripta - osteolytic lesions in skill
2. Thickening of cortical bone


What radiologic findings are seen in osteomalacia?

Reduced bone density with thinning of cortex


What are the aims of treating osteomalacia? (3)

1. Relieve symptoms
2. Reverse underlying causes, if possible
3. Correct hypophosphataemia, hypocalcaemia, Vit D deficiency and secondary hyperparathyroidism


What is rickets?

Essentially, the kid's form of osteomalacia. Deficient mineralisation and architectural disruption of growth plate (will only occur if growth plates are open)