Endocrinology 2 Flashcards

Question

what is hashimoto's?

Answer 1

This is the most common causes of hypothyroidism in the developed world. It is caused by autoimmune inflammation of the thyroid gland. It is associated with antithyroid peroxidase (anti-TPO) antibodies and antithyroglobulin antibodies. Initially it causes a goitre after which there is atrophy of the thyroid gland.

Answer 2

Replacement of thyroid hormone with oral levothyroxine is the treatment of hypothyroidism. Levothyroxine is synthetic T4, and metabolises to T3 in the body. The dose is titrated until TSH levels are normal.

Answer 3

it is defined as - normal serum free T3 and T4 levels - with TSH below the normal range

Answer 4

multinodular goitre, particularly in elderly females | excessive thyroxine may give a similar biochemical picture

Answer 5

The importance in recognising subclinical hyperthyroidism lies in the potential effect on the cardiovascular system (atrial fibrillation) and bone metabolism (osteoporosis). It may also impact on quality of life and increase the likelihood of dementia

Answer 6

TSH levels often revert to normal - therefore levels must be persistently low to warrant intervention a reasonable treatment option is a therapeutic trial of low-dose antithyroid agents for approximately 6 months in an effort to induce a remission

Answer 7

TSH raised but T3, T4 normal no obvious symptoms *risk of progressing to overt hypothyroidism is 2-5% per year (higher in men) risk increased by the presence of thyroid autoantibodies

Answer 8

Not all patients require treatment. TSH is between 4 - 10mU/L and the free thyroxine level is within the normal range if < 65 years with symptoms suggestive of hypothyroidism, give a trial of levothyroxine. If there is no improvement in symptoms, stop levothyroxine 'in older people (especially those aged over 80 years) follow a 'watch and wait' strategy, generally avoiding hormonal treatment' if asymptomatic people, observe and repeat thyroid function in 6 months ``` TSH is > 10mU/L and the free thyroxine level is within the normal range start treatment (even if asymptomatic) with levothyroxine if <= 70 years 'in older people (especially those aged over 80 years) follow a 'watch and wait' strategy, generally avoiding hormonal treatment' ```

Answer 9

TSH - low T4 - high * in T3 thyrotoxicosis the free T4 will be normal

Answer 10

TSH - high | T4 - low

Answer 11

TSH - low T4 - low *replacement steroid therapy is required prior to thyroxine

Answer 12

Antithyroid Peroxidase (anti-TPO) Antibodies are antibodies against the thyroid gland itself. They are the most relevant thyroid autoantibody in autoimmune thyroid disease. They are usually present in Grave’s Disease and Hashimoto’s Thyroiditis. Antithyroglobulin Antibodies are antibodies against thyroglobulin, a protein produced and extensively present in the thyroid gland. Measuring them is of limited use as they can be present in normal individuals. They are are usually present in Grave’s Disease, Hashimoto’s Thyroiditis and thyroid cancer. TSH Receptor Antibodies are autoantibodies that mimic TSH, bind to the TSH receptor and stimulate thyroid hormone release. They are the cause of Grave’s Disease and so will be present in this condition.

Answer 13

Ultrasound of the thyroid gland is useful in diagnosing thyroid nodules and distinguishing between cystic (fluid filled) and solid nodules. Ultrasound can also be used to guide biopsy of a thyroid lesion. Radioisotope scans are used to investigate hyperthyroidism and thyroid cancers. Radioactive iodine is given orally or intravenously and travels to the thyroid where it is taken up by the cells. Iodine is normally used by thyroid cells to produce thyroid hormones. The more active the thyroid cells, the faster the radioactive iodine is taken up. A gamma camera is used to detect gamma rays emitted from the radioactive iodine. The more gamma rays that are emitted from an area the more radioactive iodine has been taken up. This gives really useful functional information about the thyroid gland: Diffuse high uptake is found in Grave’s Disease Focal high uptake is found in toxic multinodular goitre and adenomas “Cold” areas (i.e. abnormally low uptake) can indicate thyroid cancer

Answer 14

Features of hyperthyroidism or hypothyroidism are not commonly seen in patients with thyroid malignancies as they rarely secrete thyroid hormones Most commonly presents as an asymptomatic thyroid nodule detected by palpation or ultrasound in a woman in her 30s or 40s.

Answer 15

Papillary carcinoma - (70%) often young females Follicular adenoma - (20%) Medullary - (5%) - cancer of parafollicular (C) cels, secrete calcitonin Anaplastic - (1%) - not responsive to treatment, can cause pressure symptoms, most common in elderly females, local invasion is common Lymphoma - rare - associated with hashimoto's thyroiditis

Answer 16

TSH - will usually be normal USS neck - nodules - suspicious features include micro-calcifications, a more-tall-than-wide shape, hypervascularity, marked hypoechogenicity, or irregular margins fine needle biopsy and cytology Laryngoscopy - paralysed vocal cord is highly suggestive of malignancy

Answer 17

hypovolaemic - Na+ lost and water follows - this loss can be from kidneys - due to diuretics, addison's disease ( increased potassium), kidney injury or osmotic diuresis) - this can be caused by loss from elsewhere - D+V, fistula, burns Euvolaemic - water gained - normal Na+ quantity - the water can be gained from the kidneys - SIADH, hypothyroidism, glucocorticoid insufficiency - the water gained from elsewhere - water intoxication ** Water excess (patient often hypervolaemic and oedematous) secondary hyperaldosteronism: heart failure, liver cirrhosis nephrotic syndrome IV dextrose psychogenic polydipsia

Answer 18

Plasma osmolality - to confirm if it is true hyponatremia (high = hypertonic hyponatremia, low = hypotonic hyponatremia (evolaemic), serum osmolality normal - indicates isotonic hyponatremia (pseudohyponatremia) serum sodium concentration urine sodium concentration urine osmolality urine electrolytes specific tests to confirm specific causes (e.g. 9am cortisol screening test for addison's, TFTs for hypothyroidism) serum lipids and serum protein electrophoresis - may exclude pseudohyponatremia

Answer 19

In hypovolaemic hyponatraemia, urine sodium concentration >20 mmol/L indicates renal sodium loss (e.g., diuretics), and ≤20 mmol/L indicates non-renal sodium loss (e.g., gastrointestinal losses). In hypervolaemic hyponatraemia, urine sodium concentration >20 mmol/L indicates acute kidney injury/chronic kidney disease or diuretic use, and ≤20 mmol/L indicates congestive heart failure, cirrhosis, or nephrotic syndrome. In euvolaemic hyponatraemia, urine sodium concentration is >20 mmol/L in most patients; however, patients with a concomitant low sodium intake may have a low urinary sodium.

Answer 20

High (≥300 mmol/kg): indicates syndrome of inappropriate antidiuretic hormone (SIADH) due to the inappropriate dilution of plasma as a result of pathological vasopressin release, or may also be due to medication-related effects. Intermediate (150-300 mmol/kg): indicates potomania or a partial effect of medications or mild SIADH in conjunction with high fluid intake. Low (<100-150 mmol/kg): indicates primary polydipsia. Variable: indicates prolonged physical exercise with high fluid intake. Urine osmolality may be variable as it reflects vasopressin release with high urine osmolality initially, followed by low urine osmolality as self-correction and aquaresis (loss of water) occur.

Answer 21

mild 130-134 mmol/l - Non-specific symptoms such headache, lethargy, nausea, vomiting, dizziness, confusion, and muscle cramps mild - 120-129mmol/l - same symptoms as mild severe less than 120mmol/l- seizures, coma and respiratory arrest

Answer 22

``` Treat underlying cause acute onset (<48hours) and/or symptomatic - 3% hypertonic saline infusion ``` chronic hypovolaemic - replace lost fluid with isotonic fluid infusion (0.9% saline) hypervolaemic - fluid restriction (max 1L/day) this should be adjusted according to urine output - and set as 500mL less than daily urine volume). Loop diuretic (furosemide) or spironolactone can be added) Euvolaemic - fluid restriction 2nd line for euvolaemic and hypervolaemic = vasopressin receptor antagonist and discontinue fluid restriction Vasopressin/ADH receptor antagonists (conivaptan): These act on V1 and V2 receptors. The V1 receptors cause vasoconstriction while the V2 receptors results in selective water diuresis, sparing the electrolytes. They should be avoided in patients who have hypovolemic hyponatremia. Vasopression/ADH receptor antagonists can stimulate the thirst receptors leading to the desire to drink free water. They can be hepatotoxic in patients with underlying liver disease.

Answer 23

Osmotic demyelination syndrome (central pontine myelinolysis) can occur due to over-correction of severe hyponatremia to avoid this, Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma patients are awake but are unable to move or verbally communicate, also called 'Locked-in syndrome’

Answer 24

stop active treatment | initiate free water intake and give desmopressin

Answer 25

free water loss: > osmotic diuresis/renal losses (ecovery from renal failure, poorly controlled diabetes mellitus, use of intravenous mannitol or loop diuretics, recovery from obstructive uropathy, diabetes insipidus) > GI losses - severe D&V > insensible sweat losses > during peritoneal dialysis when using dialysates that are high in dextrose Inadequate free water intake >inability to drink water or limited access >impaired thirst mechanism Sodium overload >Administration of large volumes of hypertonic sodium bicarbonate solutions (e.g., patients with metabolic acidosis) or hypertonic saline > mineralcorticoid excess (cushings or primary aldosteronism) > intake of large amounts of salt *diabetes insipidus is an uncommon cause of hypernatraemia as the patient's thirst mechanism is usually sufficiently intact to prevent electrolyte abnormalities

Answer 26

``` excessive thirst lethargy weakness irritability confusion muscle twitching or spasms tachycardia ```

Answer 27

serum electrolyte panel with glucose, urea and creatinine urine osmolality serum osmolality urine electrolytes fluid deprivation test -confirm diabetes insipidus

Answer 28

- oral or IV fluids - treat underlying cause Hypernatraemia should be corrected with great caution. Although brain tissue can lose sodium and potassium rapidly, lowering of other osmolytes (and importantly water) occurs at a slower rate, predisposing to cerebral oedema, resulting in seizures, coma and death should not be corrected at a rate greater than 0.5mmol/hour. also risk of osmotic demyelination if chronic hypernatremia is corrected too quickly.

Answer 29

``` Increased renal excretion: > diuretics - except potassium sparing > endocrinological - steoids, cushing's, Conn's > renal tubular acidosis > hpomagnesaemia ``` Increased cellular uptake > salbutamol > Insulin >acidosis Other K+ loss - intestinal fluid loss - D&V Decreased potassium intake ``` Hypokalaemia with alkalosis vomiting thiazide and loop diuretics Cushing's syndrome Conn's syndrome (primary hyperaldosteronism) ``` ``` Hypokalaemia with acidosis diarrhoea renal tubular acidosis acetazolamide partially treated diabetic ketoacidosis ``` Magnesium deficiency may also cause hypokalaemia. In such cases, normalizing the potassium level may be difficult until the magnesium deficiency has been corrected

Answer 30

Features muscle weakness, hypotonia hypokalaemia predisposes patients to digoxin toxicity - care should be taken if patients are also on diuretics ``` ECG features U waves small or absent T waves prolonged PR interval ST depression ```

Answer 31

Hypokalaemia with hypertension Cushing's syndrome Conn's syndrome (primary hyperaldosteronism) Liddle's syndrome 11-beta hydroxylase deficiency* Carbenoxolone, an anti-ulcer drug, and liquorice excess can potentially cause hypokalaemia associated with hypertension ``` Hypokalaemia without hypertension diuretics GI loss (e.g. Diarrhoea, vomiting) renal tubular acidosis (type 1 and 2**) Bartter's syndrome Gitelman syndrome ```

Answer 32

U&Es - concurrent low sodium suggests thiazide use or marked volume depletion. Serum bicarbonate. Serum glucose. Serum chloride. Serum magnesium - low serum magnesium often accompanies hypokalaemia and needs to be corrected to enable recovery of serum potassium. Spurious - potassium is taken up by cells outside the body - eg, white cells in leukaemia; especially likely to occur if there are delays in analysing the sample - as these cells take up the potassium it will lead to a false potassium reading ECG Urine tests ABG - to establish acidosis or alkalosis

Answer 33

inary potassium - where low, suggests poor intake, shift into the intracellular space, or GI loss. Where high, suggests renal loss. Urinary sodium - low urinary sodium combined with high urinary potassium suggests secondary hypoaldosteronism. Urinary osmolality - needed to interpret urinary potassium levels.

Answer 34

if K+ > 2.5mmol/L: sando-K 2 tablets TDS or add 20-400 mmol/L potassium chloride to IV fluids If K+ <2.5mmol/L give 40 mmol/L potassium chloride in 1L 0.9% saline over 6 hours ** never give >10mmol/hour K+ outside the ICU

Answer 35

a number of facots including - aldosterone - acid base balance - insulin levels

Answer 36

Renal causes (reduced renal excretion): AKI, CKS, hyperkalemia renal tubular acidosis, mineral corticoid deficiency, drugs (potassium sparing diuretics, ACE-i, NSAIDs, heparin can also cause hyperkalemia), addison's Increased cellular release: acidosis, tissue breakdown (rhabdomyolysis, haemolysis, tumour lysis syndrome) , medications (digoxin, suxamethonium, BB, theophylline) excess K+ load - iatrogenic, massive blood transfusion,potassium supplementation

Answer 37

Mild - 5.5-5.9 mmol/L. Moderate - 6.0-6.4 mmol/L. Severe - >6.5 mmol/L.

Answer 38

weakness fatigue occasionally patients will present with muscular paralysis or SOB chest pain palpitations occasionally there will be bradycardia due to heart block or tachypnoea from respiratory muscle weakness depressed or absent tendon reflexes

Answer 39

- any unexpected result - always repeat the test - urine output - urine electrolytes - FBC - looking for any anaemia which may suggest heamolysis, throbocytosis and/or leukocytosis - blood glucose levels - digoxin levels if they are taking it - ABG - ECG

Answer 40

``` Peaked or 'tall-tented' T waves (occurs first) Loss of P waves Broad QRS complexes Sinusoidal wave pattern Ventricular fibrillation ```

Answer 41

Untreated hyperkalaemia may cause life-threatening arrhythmias. Precipitating factors should be addressed (e.g. acute renal failure) and aggravating drugs stopped (e.g. ACE inhibitors) there should be ECG monitoring Calcium gluconate 10mls 10% IV over 5 mins - to protect and stabilize the cardiac membrane - check ECG - if not resolved repeat dose every 10 mins up to 50 mls. to shift potassium into the cells - Insulin dextrose IV infusion over 30 minutes and nebulised salbutamol can be used. You need to check blood glucose before, during and after. to remove potassium from body - calcium resonium - orally or enema (enemas are more effective), it works slowly. Give with regular lactulose as it can cause constipation.

Answer 42

In patients who are taking digoxin, give calcium gluconate in an infusion (add to 100 ml glucose 5%) and run over 20 minutes (otherwise, can precipitate myocardial digoxin toxicity).

Answer 43

> hypoparathyroidism (with low PTH levels) > secondary hyperparathyroidism (with high PTH levels - e.g. VD deficiency) > CKD > pseudohypoarathyroidism - where target cells are insensitive to PTH > rhabdomyolysis > acute pancreatitis > drugs - calcium chelators, bisphosphonates, calcitonin, drugs affecting VD > hypoalbuminaemia (correct for albumin)

Answer 44

As extracellular calcium concentrations are important for muscle and nerve function many of the features seen in hypocalcaemia seen a result of neuromuscular excitability ``` Features tetany: muscle twitching, cramping and spasm perioral paraesthesia if chronic: depression, cataracts ECG: prolonged QT interval ``` Trousseau's sign carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic wrist flexion and fingers are drawn together seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people Chvostek's sign tapping over parotid causes facial muscles to twitch seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people

Answer 45

renal function PTH phosphate and magnesium

Answer 46

if severe - calcium gluconate 10mls 10% over 30 mins if mild - oral calcium supplements treat cause e.g. if VD deficiency give VD If hypomagnesaemic then you need to correct that before the hypocalcaemia will resolve because magnesium helps to transport calcium and potassium in and out of cells

Answer 47

bones, stone, groans and psychic moans levels <2.8mmol/L: - Polyuria and polydipsia - Dyspepsia - due to calcium-regulated release of gastrin - Depression - Mild cognitive impairment ``` levels <3.5mmol/L : All of the previous plus: - Muscle weakness - Constipation - Anorexia and nausea - Fatigue ``` ``` levels >3.5mmol/L: All of the previous plus: - Abdominal pain - Vomiting - Dehydration - Lethargy - Cardiac arrhythmias, shortened QT interval - Coma - Pancreatitis ```

Answer 48

- primary hyperparathyroidism - excess PTH - usually only mild hypercalcaemia - malignancy (most common cause of non-PTH-mediated hypercalcaemia) - can be from bone mets, myeloma, Squamous cell lung cancer - granulomatous conditions - sarcoidosis and tuberculosis - endocrine disorders eg, thyrotoxicosis, phaeochromocytoma and primary adrenal insufficiency. - Drugs - eg, thiazide diuretics, vitamin D and vitamin A supplement - Familial - eg, familial hypocalciuric hypercalcaemia

Answer 49

``` renal function ALP PTH phosphate urine calcium and phosphate ``` myeloma screen/Bence Jones protein - if you suspect myeloma serum ACE - if you suspect sarcoidosis isotope bone scan

Answer 50

Raised PTH levels are suggestive of primary, secondary or tertiary hyperparathyroidism, or familial hypocalciuric hypercalcaemia. Low PTH levels are seen in granulomatous disease, iatrogenic causes (eg, renal dialysis), adrenal insufficiency, thyrotoxicosis,and vitamin D intoxication. The levels in malignancy may be low, normal or high.

Answer 51

The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days Other options include: calcitonin - quicker effect than bisphosphonates steroids in sarcoidosis Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.

Answer 52

drugs: diuretics, proton pump inhibitors total parenteral nutrition diarrhoea alcohol hypokalaemia, hypocalcaemia conditions causing diarrhoea: Crohn's, ulcerative colitis metabolic disorders: Gitleman's and Bartter's

Answer 53

``` Features may be similar to hypocalcaemia: paraesthesia tetany seizures arrhythmias decreased PTH secretion → hypocalcaemia ECG features similar to those of hypokalaemia exacerbates digoxin toxicity ```

Answer 54

<0.4 mmol/l intravenous replacement is commonly given. An example regime would be 40 mmol of magnesium sulphate over 24 hours >0.4 mmol/l oral magnesium salts (10-20 mmol orally per day) diarrhoea can occur with oral magnesium salts * correct hypomagnesemia before hypokalaemia, hypophosphatemia and hypocalcemia if possible * do not give IV magnesium and IV phosphate at the same time as it can precipitate as magnesium phosphate

Answer 55

``` alcohol excess acute liver failure diabetic ketoacidosis refeeding syndrome primary hyperparathyroidism osteomalacia ```

Answer 56

red blood cell haemolysis white blood cell and platelet dysfunction muscle weakness and rhabdomyolysis central nervous system dysfunction

Answer 57

Carcinoid syndrome occurs due to release of serotonin and other vasoactive peptides into systemic circulation from a carcinoid tumour. 20-30% of midgut neuroendocrine tumours (NETs), 5% of bronchial carcinoid tumours, and approximately 1% of pancreatic NETs secrete serotonin and other peptides. the liver is the most common site for mets

Answer 58

flushing (often earliest symptom) diarrhoea bronchospasm hypotension right heart valvular stenosis (left heart can be affected in bronchial carcinoid) other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing's syndrome pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour

Answer 59

``` urinary 5-hydroxyindoleacetic acid (elevated) serum chromogranin A/B - elevated LFTs FBC metabolic panel ```

Answer 60

surgical resection of disease somatostatin analogues e.g. octreotide diarrhoea: cyproheptadine may help

Answer 61

aka acute pituitary failure Acute pituitary failure is a rare medical emergency presenting with the sudden onset of headache (with or without neurological symptoms involving the second, third, fourth and sixth cranial nerves), vomiting, visual impairment and decreased consciousness. itary apoplexy is bleeding into or impaired blood supply of the pituitary gland.

Answer 62

It is caused by haemorrhage and/or infarction of the pituitary gland. it occurs in patients with a pituitary tumour, most commonly in a clinically non-functioning macroadenoma

Answer 63

Sheehan's syndrome is postpartum hypopituitarism caused by necrosis of the pituitary gland. It is usually the result of severe hypotension or shock caused by massive haemorrhage during or after delivery. Patients with Sheehan's syndrome have varying degrees of anterior pituitary hormone deficiency. Sheehan's syndrome usually presents progressively with a variety of developing symptoms (starting commonly with failure to lactate, breast involution and then amenorrhoea), rather than the more dramatic and acute presentation.

Answer 64

headaches vomiting diplopia visual feild defects

Answer 65

initially management should involve careful assessment of fluid and electrolyte balance, replacement of corticosteroids and supportive measures to ensure haemodynamic stability empirical steroid therapy (IV hydrocortisone) surgery is required urgently for patients with wrsening neuro symptoms

Answer 66

``` serum electrolytes serum and urine osmolarity 8 am cortisol 8 am testosterone, FSH, LH in men TFTs cranial nerve examination and visual fields ``` to confirm diagnosis urgent MRI scan must be done

Answer 67

it usually occurs in patients with underlying Graves disease or toxic multinodular goitre usually presents with: - hyperpyrexia (over 41), dehydration - Tachycardia, hypotension, atrial dysrthythmias, CCF - nausea, jaundice, vomiting, diarrhoea, abdominal pain - confusion, agitation, delerium, pyschosis, seizures or coma

Answer 68

Infection or other acute illness. Withdrawal of or non-compliance with antithyroid medication. Recent trauma, including surgical stress. Myocardial infarction or stroke. Diabetic ketoacidosis, hyperosmolar coma or hypoglycaemia. Following childbirth. Pulmonary embolism. Drugs: radio-iodine, amiodarone, radiographic contrast media. Overdose of thyroid hormone tablets. Vigorous palpation of the thyroid gland in hyperthyroid patients. Recent thyroid surgery.

Answer 69

- investigations for any underlying precipitant e.g. infection screen - TFTs - renal function tests, FBC, LFTs - to assess for decompensation of homeostasis - ECG - CXR - ABG

Answer 70

symptomatic treatment e.g. paracetamol treatment of underlying precipitating event beta-blockers: typically IV propranolol anti-thyroid drugs: e.g. methimazole or propylthiouracil Lugol's iodine dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

Answer 71

Myxoedema coma is the extreme manifestation of (usually untreated) hypothyroidism. It is a medical emergency the adaptations of the body to untreated hypothyroidism fail to maintain homoeostasis and become overwhelmed by hypothermia, infection or other precipitating factors. These adaptations include peripheral vasoconstriction to maintain core body temperature.

Answer 72

``` hypothermia - common infections - influenza, pneumonia, UTI medications - amiodarone, anaesthesia, BB, diuretics, lithium, phenytoin, rifampicin hypoglycaemia GI haemorrhage cerebrovascular disease surgery or trauma burns ```

Answer 73

their mental state will usually be affected they may not always present with a coma or non-pitting oedema they can present in a comatose state CNS symptoms - deterioration in mental state, confusion, apathy, psychosis, lethargy Metabolic - weight gain, growth reduction, low energy, hypothermia, resp acidosis, hypoxia generalised swelling and puffiness dry, cool skin, hair loss non pitting oedema of hands and feet CV - bradycardia, pericardial effusions, reduced heart sounds GI - consipation, mmyxoedema megacolon and paralytic ileus Renal impairment Respiratory distress, hypoventilation, hypoxia

Answer 74

hypothermia septic shock anything that could cause deterioration of mental state

Answer 75

TFTs routine biochemistry creatine kinase - often raised ECG (changes include: bradycardia, nonspecific ST and T wave changed, reduced voltages, varying degrees of heart block, prolonged QT syndrome) CXR - pleural effusion, pericardial effusion serum cortisol levels to rule out adrenal insufficiency

Answer 76

admission to intensive care ``` IV thyroid replacement IV fluid IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded) electrolyte imbalance correction sometimes rewarming ```

Answer 77

A phaeochromocytoma is a rare tumour that secretes catecholamines. usually derived from chromaffic cells in the adrenal medulla

Answer 78

``` hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety tremor ```

Answer 79

24 hr urinary collection of metanephrines (sensitivity 97%*) blood glucose often raised calcium may be elevated CT or MRI

Answer 80

Surgical resection of the tumour is the treatment of choice and usually results in cure of the hypertension. Pre-operative treatment with alpha-blockers ( phenoxybenzamine) and beta-blockers (propranolol) is required to control blood pressure and prevent intraoperative hypertensive crises.

Endocrinology 2 Flashcards

(104 cards)