Endocrinology Flashcards
What does a HBa1c have to be equal or greater than to be diagnostic of diabetes mellitus?
What can cause a false HbA1c?
HbA1c > 6.5%. If it is less than 6.5% then it does not exclude diabetes, as it is less sensitive.
HbA1c readings can be influenced by increased red cell turnover, such as in aneamia and heamoglobinopathies, and pregnancy.
What constitutes an impaired fasting glucose?
An impaired fasting glucose is when fasting glucose is between 6 and 7. People with an impaired fasting glucose should be offered a glucose tolerance test.
Describe the physiology of thyroid hormone secretion.
Thyroid Releasing hormone (TRH) is secreted from the hypothalamus. It acts on the pituitary that then secretes Thyroid Stimulating Hormone (TSH). TSH stimulates the thyroid to secrete thyroxine (T4), and triiodothyronine (T3) (which exert a negative feedback on TSH production). The thyroid mainly produces T4, which is 5 times less active than T3. 85% of T3 is formed by the peripheral conversion of T4. Unbound T3andT4 increased cell metabolism and catecholamine effects.
What tests are you interested in ordering to investigate thyroid function?
TSH, FreeT3 and T4 for hyperthyroidism, and only TSH and T4 for hypothyroidism or monitoring. May also consider Anti-thyroid Peroxidase (TPO) antibodies or anti-thyroglobulin antibodies which are increased in autoimmune diseases (Hashimoto’s or Grave’s disease). TSH receptor antibody (May be positive in Grave’s), thyroglobulin, ultrasound, isotope scan.
What would be your diagnosis for:
a) High TSH, Low T4
b) High TSH, normal T4
c) High TSH, highT4
d) High TSH, High T4, Low T3
a) High TSH, Low T4 - Hypothyroidism
b) High TSH, normal T4 - Treated/subclinical hypothyroidism
c) High TSH, High T4 - TSH secreting tumour or resistance
d) High TSH, High T4, Low T3 - Slow conversion of T4 toT3 (deiodinase deficiency, euthyroid hyperthyroxineamia), or thyroid hormone antibody artefact.
What are the causes of the following test results:
a) Low TSH, high T4, or T3
b) Low TSH, normal T3 and T4
c) Low TSH, Low T4
a) Low TSH, high T4 or T3 - Hyperthyroidism
b) Low TSH, normal T3 and T4- Subclinical hyperthyroidism
c) Low TSH, Low T4 - Central hypothyroidism (hypothalamic or pituitary disease)
What causes the following results?
a) Low TSH,Low T4, Low T3
b) Normal TSH, abnormal T4
a) Low TSH, Low T4, Low T3 - Sick euthyroidism (systemic disease) or pituitary disease
b) Normal TSH, abnormal T4 - consider changes in thyroid binding globulin, assay interference, amiodarone, or pituitary TSH tumour.
Free T3 andT4 are more useful than total T3 and T4 and total T# andT4 are affected by Thyroxine Blinding Globulin (TBG) (only the unbound portion is the active part). Total T3 andT4 are high when TBG is high. TBG is high in pregnancy, oestrogen therapy, and hepatitis.
Which patients should be screened for thyroid function?
Patients with atrial fibrillation, hyper lipidaemia, diabetes mellitus (on annual review), patients on amiodarone or lithium, Patients with Down’s or Turner’s syndrome, or Addison’s disease.
What are the symptoms of Thyrotoxicosis?
Diarrhoea, decreased weight, increased appetite (may result in a paradoxical weight gain), overactive, sweats, heat intolerance, palpitations, tremor, irritability, labile emotions, oligomenorrhoea, infertility, rarely psychosis, chorea, panic, itch, alopecia and urticaria.
What are the signs of thyrotoxicosis?
Pulse is fast/irregular (AF, or SVT), warm moist skin, fine tremor, palmar erythema, thin hair, lid lag (eyelids lags behind eye’s descent as patient watches your finger descend slowly). lid retraction, goitre, thyroid nodules, thyroid bruit. Signs of Grave’s disease: Exopthalmos, opthalmoplegia. Pretibial myoedema (oedematous swellings above the lateral malleoli), Thyroid acropatchy (an extreme manifestation producing clubbing, painful finger and tow swelling, periosteal reaction on the limb bones).
What tests would you conduct for thyrotoxicosis?
Low TSH, High T4 and T3. There may be normocytic anaemia and mild neutropenia (in Grave’s disease) , raised ESR, raised Ca2+, raised LFT. Also check thyroid autoantibodies. Isotope scan if the cause is unclear, test visual fields, acuity, and eye movements.
What is Grave’s disease?
Grave’s disease is responsible for 2/3 s of hyperthyroidism. It has a female preponderance and tends to present in the 4th or 5th decade. Grave’s disease is caused the autoantibodies binding to and activating the G protein coupled thyrotropin receptor. This causes smooth thyroid enlargement and increased hormone production (especially T3). Grave’s disease is triggered by stress, pregnancy, or infection. Patients are generally hyperthyroid but may become hypo or euthyroid. Associated with autoimmune diseases eg. vitiligo, Addison’s, type 1 diabetes mellitus.
What is toxic multinodular goitre?
Toxic multinodular goitre is seen in the elderly and iodine deficient area. There are nodules that secrete thyroid hormones. Treat by controlling the thyrotoxicosis first with medications, then with radioidodine. Surgery is indicated for compressive symptoms from the goitre such as dysphagia or dyspnoea.
What is a toxic adenoma?
A toxic adenoma is when there is a solitary nodule in the thyroid producing T3 and T4. On an isotope scan, the nodule is ‘hot’ and the rest of the thyroid is supressed. Treat with radioiodine.
What is Subacute (De Quervain’s) Thyroiditis?
Sub acute (De Quervain’s) thyroiditis is thought to be a post viral syndrome that causes hyperthyroidism, tender goitre, raised ESR and globally reduced uptake on iodine 131/technecium scan. The condition is usually self resolving and does not require treatment. Steroids can be used if it becomes problematic
What are the causes of hyperthyroidism?
Grave’s Disease, toxic multinodulat goitre, Toxic adenoma, Subacute De quervain’s thyroiditis, Ectopic thyroid tissue (choriocarcinoma or ovarian teratoma), Iodine excess (food, supplements, contrast media causing thyroid storm), Amiodarone, or lithium (more commonly causes hypothyroidism).
How do you treat hyperthyroidism?
Drugs: treat using Beta-blockers (propranolol) for rapid control of symptoms and give carbimazole. Depending on the dose you may need to give thyroxine as well to avoid iatrogenic hypothyroidism. Carbimazole causes agrunulocytosis and can lead to sepsis.
Radioiodine treatment, but leads to hypothyroidism post treatment. Thyroidectomy may also be considered.
What are the complications of hyperthyroidism?
Heart failure caused by thyrotoxic cardiomyopathy, angina, AF, osteoporosis, opthalmopathy, gyneacomastia, thyroid storm.
What are the causes of goitre?
Diffuse goitre: -Physiological -Grave's Disease -Hashimoto's -Subacute De Quervain's thyroiditis Nodular: -Multinodular goitre -Adenoma -Carcinoma
What are the features of hypercalceamia?
‘Stones, bones, abdominal groans, thrones, and psychiatric moans’
- Renal calculi
- Bone pain, fractures
- Peptic ulceration, constipation, pancreatitis
- Polydipsia, polyuria, hypertension
- Depression
What are the causes of hypercalceamia?
- Hyperparathyroidism
- False Test Reading
- Immobilisation
- Excess Vitamin D (seen in sarcoidosis, tuberculosis, lymphoma)
- Thiazides, lithium
- Malignancy (multiple myeloma, bone metastases, secretion of Parathyroid related hormone produced by some squamous cell lung cancers, breast, and renal cell carcinomas).
Describe the physiology of Parathyroid hormone.
Parathyroid hormone is secreted from the four parathyroid glands situated posterior to the thyroid. It is normally secreted in response to low ionised calcium levels. The glands are controlled by negative feedback from the calcium levels. PTH acts by:
- Increasing osteoclast activity releasing calcium and phosphate from bones.
- Increased calcium and decreasing phosphate reabsorption in the kidney causing calcium retention and phosphate dumping.
- Active Vitamin D production is increased.
Overall there is an increase in calcium and decrease in phosphate.
What is primary hyperparathyroidism?
80% of primary hyperparathyroidism is caused by a solitary adenoma, 20% is cause by hyperplasia of all glands, and (but not in retrospect) with increased calcium on routine tests. Symptoms include typical bones, stones, groans, thrones and moans of hypocalcaemia. Associated with hypertension and MENS 1 and 2.
What investigations would you order and what results would you see in Primary hyperparathyroidism?
Increased Calcium
Increased PTH (or inappropriately normal)
Decreased PO4 (unless in renal failure)
Increased Alkaline Phosphatase from bone activity
Increased 24 hourly urinary calcium,
Imaging: Technecium sestamibi scan to determine cause. Osteitis fibrosa cystica (rare, due to severe resorption, may show up as Brown tumours of the phalanges), Pepper pot skull, DEXA for osteoporosis.
What is secondary hyperparathyroidism?
Secondary hyperparathyroidism presents with a decreased calcium and an appropriately raised PTH. It caused by a decrease in calcium (eg. vitamin D intake, chronic renal failure. Treat by correcting the causes, phosphate binders. If tricky give Cinacalcet (increases sensitivity of Parathyroid cells to calcium), and consider parathyroidectomy,
What is tertiary hyperparathyroidism?
In tertiary hyperparathyroidism there is increased calcium and inappropriately very high levels of PTH. This occurs after prolonged secondary hyperparathyroidism, causing the glands to act autonomously after having undergone hyperplastic or adenomatous change. This causes increased calcium from the hugely increased secretion of PTH unlimited by feedback control. This is seen in chronic renal failure.
What is primary hypoparathyroidism?
Primary hypoparathyroidism is decreased PTH due to gland failure. Tests show decreased calcium, increased phosphate (or normal), normal alk phos. Caused by autoimmune phenomenon, di George syndrome, calcium supplements plus calcitriol.
What are the signs of hypocalcaemia?
(apparent hypocalcaemia may be an artefact of hypoalbumineamia).
‘SPASMODIC”
Spasms (Trousseau’s Sign: Carpopedal spasms on inflating BP cuff)
Perioral parathesiae
Anxious, irritable, irrational
Seizures
Muscle tone increased in smooth muscle (colic, wheeze, and dysphagia)
Orientation impaired (time, place and person)
Dermatitis (atopic/exfoliative)
Impetigo herpatiformis (rare and serious)
Chvostek’s Sign:(corner of mouth twitches when the facial nerve is tapped over the paratid).
Also Cateracts, and cardiomyopathy (long QT interval on ECG).
What are the causes of secondary hyperparathyroidism?
Secondary hyperparathyroidism is caused by radiation or surgery (thyroidectomy, parthyroidectomy), hypomegnesia (magnesium is required for PTH secretion).
What are the causes of pseudohypoparathyroidism?
Pseudohypoparathyroidism is the failure of the target cell to respond to PTH. Signs of Pseudohypoparathyroidism includes short metacarpals (especially the 4th and 5th), a round face, short stature, calcified basal ganglia, and decreased IQ. Tests show decreased calcium, high PTH, alk pho is normal or increased.
What is pseudopseudohypoparathyroidism?
In pseudohypoparathyroidism, the morphological features of pseudohypoparathyroidism are present, but there is normal biochemistry. The cause for both in genetic. Morphological features include short metacarpals, a round face, short stature, and decreased IQ.
What are the different types of medications available to treat type two diabetes?
- Biguanides/Metformin (Diabex, diaformin, Formet, glucomet)
- Sulphonylureas/Gliclazides (diamicron)
- Thiozolidinediones/Glitazones (Avandia,Actos)
- Metglitinides
- Alpha glucosidase inhibitor (Acarbose)
