Endo/ Electrolyte Abnormalities On Ward Flashcards

Question

What are some SES of amiodarone?

Answer 1

Pneumonitis and fibrosis Liver failure Arrythmias Sley grate Effect on thyroid… Type 1 when you give it to normal thyroid= hypothyroid Type 2 when you give it to hyperthyroid pts= hyperthyroidism and need to give steroids

Answer 2

Unlike normal adrenal medulla, there is no stimulus for adrenaline release Phaeochromocytomas occur in certain familial syndromes, including: Multiple endocrine neoplasia syndrome Neurofibromatosis Von Hippel LIndau disease

Answer 3

MEN2B syndrome | They will have phaeochromocytomas

Answer 4

Normal or low

Answer 5

Caused by uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands. This leads to hypercalcaemia It is treated surgically by removing the tumour

Answer 6

This is where insufficient vit D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bone. This causes hypocalcaemia (low level of calcium in thr blood) The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone Over time, the total number of cells in the parathyroid glands increase as they respond to the increased need to produce parathyroid hormone, this is called hyperplasia and leads to tertiary hyperparathyroidism.

Answer 7

This is when secondary hyperparathyroidism continues for a long period of time It leads to hyperplasia of the glands The baseline level of PTH increases dramatically Treated surgically

Answer 8

Classical signs of hypercalcaemia Stones, bones, groans (pancreatitis, peptic ulcers), thrones (constipation) proximal muscle weakness If pts have acute high calcium >3cm then patients should be admitted with IV bisphosphonates and IV fluids Will take about 7 days for bisphosphonate to kick in Normally give Iv fluids for 24 hours then give bisphosphonates Calcium can cause long QT so do an ECG

Answer 9

Symptomatic Osteoporosis and bone disease Kidney stones <50 years

Answer 10

Exogenous steroids (in patients on long term high dose steroid medications) Cushing’s Disease (a pituitary adenoma releasing excessive ACTH) Adrenal Adenoma (a hormone secreting adrenal tumour) Paraneoplastic Cushing’s

Answer 11

The specific condition where the adrenal glands have been damaged, resulting in a reduction in the secretion of cortisol and aldosterone. It is also called primary adrenal insufficiency The most common cause is autoimmune

Answer 12

This is a result of inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release This is the result of loss or damage to the pituitary gland This can be due to surgery to remove a pituitary tumour, infection, loss of blood (sheehans)

Answer 13

Long term oral steroids causes suppression of the hypothalamus (CRH), when the exogenous steroids are suddenly withdrawn the hypothalamus does not wake up fast enough and endogenous steroids are not adequately produced. Therefore long term steroids should be tapered slowly to allow time for the adrenal axis to regain normal function.

Answer 14

Symptoms- fatigue, nausea, cramps, abdo pain, reduced libido Signs- bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin) HYPOTENSION

Answer 15

U and Es- hyponatraemia, hyperkalaemia Early morning cortisol although this is often falsely normal Short synacthen test is the test of choice to diagnose adrenal insufficency Adrenal autoantibodies are present in 80% of autoimmune adrenal insuffiency; adrenal cortex antibodies and 21- hydroxylase antibodies CR/MRI for suspected adrenal tumour MRI for suspected pituitary tumour

Answer 16

The short synacthen test is the test of choice for adrenal insufficiency. It is ideally performed in the morning when the adrenal glands are most “fresh”. The test involves giving synacthen, which is synthetic ACTH. The blood cortisol is measured at baseline, 30 and 60 minutes after administration. The synthetic ACTH will stimulate healthy adrenal glands to produce cortisol and the cortisol level should at least double. A failure of cortisol to rise (less than double the baseline) indicates primary adrenal insufficiency (Addison’s disease).

Answer 17

``` Antithyroid peroxidase (anti TPO) antibodies, they are the most relevant thyroid autoantibody in autoimmune thyroid disease Usually present in graves disease and hashimotos thyroiditis ``` Antithyroglobulin antibodies= antibodies against thyroglobulin, limited use because can be present in normal individuals TSH receptor antibodies found in graves

Answer 18

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 19

Primary hyperthyroidism is due to thyroid pathology. It is the thyroid itself that is behaving abnormally and producing excessive thyroid hormone. Secondary hyperthyroidism is the condition where the thyroid is producing excessive thyroid hormone as a result of overstimulation by thyroid stimulating hormone. The pathology is in the hypothalamus or pituitary.

Answer 20

Grave’s disease is an autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism. These TSH receptor antibodies are abnormal antibodies produced by the immune system that mimic TSH and stimulate the TSH receptors on the thyroid. This is the most common cause of hyperthyroidism.

Answer 21

Toxic multinodular goitre (also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thyroid hormone.

Answer 22

Exopthalmos= bulging of the eyeball out of the socket It is due to inflammation, swelling and hypertrophy of the tissue behind thee eyeball that forces the eyeball forward Pretibial myxoedema is a dermatological condition where there are deposits of mucin under the skin on the anterior aspect of the leg (the pre-tibial area). This gives a discoloured, waxy, oedematous appearance to the skin over this area. It is specific to Grave’s disease and is a reaction to the TSH receptor antibodies. Diffuse goitre Graves eye diseas Clubbing, painful finger and toe swelling, periosteal new bone formation

Answer 23

Goitre with firm nodules Most pts are aged over 50 Second most common cause of thyrotoxicosis after graves

Answer 24

This is where a single abnormal thyroid nodule is acting alone to release thyroid hormone Treated with surgical removal of the nodule

Answer 25

Presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism. There is a hyperthyroid phase followed by hypothyroid phase as the TSH level falls due to negative feedback.

Answer 26

Self limiting condition NSAIDS for pain and inflammation Beta blockers for symptomatic relief of hyperthyroidism

Answer 27

Thyroid storm is a rare presentation of hyperthyroidism. It is also known as “thyrotoxic crisis”. It is a more severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium. It requires admission for monitoring and is treated the same way as any other presentation of thyrotoxicosis, although they may need supportive care with fluid resuscitation, anti-arrhythmic medication and beta-blockers.

Answer 28

Carbimazole is the first line anti thyroid drug Usually successful after 4-8 weeks Once the pt has normal thyroid hormone levels they continue on maintenance carbimazole and either The dose is carefully titrated to maintain normal levels (titration block) The dose is sufficient to block all production and the patient takes levothyroxine titrated to effect (block and replace) Complete remission and ability to stop taking carbimazole is usually achieved within 18 months of treatment.

Answer 29

Propylthiouracil

Answer 30

Radioactive iodine involves drinking a single dose of radioactive iodine This is taken up by the thyroid gland and the emitted radiation destroys a proportion of the thyroid cells, this is reduction in functioning cells results in reduce of thyroid hormone production and thus remission. Remission can take up to 6 months Strict rules: - must not be pregnant and are not allowed to get pregnant within 6 months - must avoid close contact with children and pregnant women for 3 weeks - limit contact with anyone for several days after receiving the dose

Answer 31

Propanolol

Answer 32

A definitive option is to surgically remove the whole thyroid or toxic nodules. This effectively stops the production of thyroid hormone, however the patient will be left hypothyroid post thyroidectomy and require levothyroxine replacement for life.

Answer 33

Hashimotos thyroiditis Iodine deficiency Secondary To treatment of hyperthyroidism- carbimazole, propylthiouracil, radioactive iodine, thyroid surgery Medications- lithium inhibits the production of thyroid hormones in the thyroid gland and can cause goitre and hypothyroidism Amiodarone interferes with thyroid hormone production and metabolism, usually causing hypothyroidism but can also cause thyrotoxicosis

Answer 34

This is where the pituitary gland is failing to produce enough TSH This is often associated with lack of other pituitary hormones such as: ACTH Tumours, infection, vascular (Sheehan), radiation

Answer 35

``` Weight gain Fatigue Dry skin Coarse hair and hair loss Fluid retention (oedema, pleural effusions, ascites) Heavy or irregular periods Constipation ```

Answer 36

TSH and T3/T4 Primary= T3/T4 low, TSH high Secondary= T3/T4 and TSH low (pituitary problem)

Answer 37

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. When starting levothyroxine, initially measure TSH levels monthly until stable, then once stable it can be checked less frequently unless they become symptomatic. If the TSH level is high, the dose is too low and needs to be increased. If the TSH is low, the dose is too high and needs to be reduced.

Answer 38

Type 1 diabetes mellitus (T1DM) is a disease where the pancreas stops being able to produce insulin. What causes the pancreas to stop producing insulin is unclear. There may be a genetic component. It may be triggered by certain viruses, such as the Coxsackie B virus and enterovirus. When there is no insulin being produced, the cells of the body cannot take glucose from the blood and use it for fuel. Therefore the cells think the body is being fasted and has no glucose supply. Meanwhile the level of glucose in the blood keeps rising, causing hyperglycaemia.

Answer 39

Ketoacidosis Hyperkalaemia Dehydration

Answer 40

Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes the patient to urinate a lot (polyuria). This results in severe dehydration. The dehydration stimulates the thirst centre to tell the patient to drink lots of water. This excessive thirst is called polydipsia.

Answer 41

``` Polyuria Polydipsia Nausea and vomiting Acetone smell to their breath Dehydration and subsequent hypotension Altered Consciousness They may have symptoms of an underlying trigger (i.e. sepsis) ```

Answer 42

Fluid replacement Most pts with DKA are deplete around 5-8 litres Isotonic saline is used initially even if the pt is severely acidotic. insulin an intravenous infusion should be started at 0.1 unit/kg/hour once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started correction of electrolyte disturbance serum potassium is often high on admission despite total body potassium being low this often falls quickly following treatment with insulin resulting in hypokalaemia potassium may therefore need to be added to the replacement fluids if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required long-acting insulin should be continued, short-acting insulin should be stopped

Answer 43

HbA1c When we check HbA1c we are counting glycated haemoglobin, which is how much glucose is attached to the haemoglobin molecule. This is considered to reflect the average glucose level over the last 3 months because red blood cells have a lifespan of around 3-4 months. We measure it every 3 – 6 months to track progression of the patient’s diabetes and how effective the interventions are. It requires a blood sample sent to the lab, usually red top EDTA bottle.

Answer 44

``` Fatigue Polydipsia and polyuria (thirsty and urinating a lot) Unintentional weight loss Opportunistic infections Slow healing Glucose in urine (on dipstick) ```

Answer 45

HbA1c – 42-47 mmol/mol Impaired fasting glucose – fasting glucose 6.1 – 6.9 mmol/l Impaired glucose tolerance – plasma glucose at 2 hours 7.8 – 11.1 mmol/l on an OGTT

Answer 46

HbA1c > 48 mmol/mol Random Glucose > 11 mmol/l Fasting Glucose > 7 mmol/l OGTT 2 hour result > 11 mmol/l

Answer 47

Vegetables and oily fish Typical advice is low glycaemic, high fibre diet A low carbohydrate may in fact be more effective in treating and preventing diabetes but is not yet mainstream advice

Answer 48

Diabetic retinopathy Kidney diseas Diabetic foot

Answer 49

48mmol/mol for new type 2 diabetics | 53mmol/mol for diabetics that have moved beyond metformin alone

Answer 50

Metformin is a “biguanide”. It increases insulin sensitivity and decreases liver production of glucose. It is considered to be “weight neutral” and does not increase or decrease body weight. Notable Side Effects: Diarrhoea and abdominal pain. This is dose dependent and reducing the dose often resolves the symptoms Lactic acidosis Does NOT typically cause hypoglycaemia

Answer 51

Pioglitazone is a “thiazolidinedione”. It increases insulin sensitivity and decreases liver production of glucose. Notable Side Effects: ``` Weight gain Fluid retention Anaemia Heart failure Extended use may increase the risk of bladder cancer Does NOT typically cause hypoglycaemia ``` Do not use if someone has had heart diseas

Answer 52

The most common sulfonyluria is “gliclazide”. Sulfonylureas stimulate insulin release from the pancreas. Notable Side Effects: Weight gain Hypoglycaemia Increased risk of cardiovascular disease and myocardial infarction when used as monotherapy

Answer 53

Also known as conns, this is where the adrenal glands are directly responsible for producing too much aldosterone Serum renin will be low as it is suppressed by the high blood pressure

Answer 54

``` An adrenal adenoma secreting aldosterone (most common) Bilateral adrenal hyperplasia Familial hyperaldosteronism type 1 and type 2 (rare) Adrenal carcinoma (rare) ```

Answer 55

Also known as conns syndrome Where the adrenal glands are directly responsible for producing too much aldosterone Serum renin will be low as it is suppressed by the high blood pressure. There are several possible reasons for this:

Answer 56

``` An adrenal adenoma secreting aldosterone (most common) Bilateral adrenal hyperplasia Familial hyperaldosteronism type 1 and type 2 (rare) Adrenal carcinoma (rare) ```

Answer 57

Secondary hyperaldosteronism is where excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high. There are several causes of high renin levels and they occur when the blood pressure in the kidneys is disproportionately lower than the blood pressure in the rest of the body: Renal artery stenosis Renal artery obstruction Heart failure

Answer 58

Renal artery stenosis is a narrowing of the artery supplying the kidney. This is usually found in patients with atherosclerosis, as an atherosclerotic plaque causes narrowing of this vessel similar to the narrowing of the coronary arteries found in angina. This can be confirmed with a doppler ultrasound, CT angiogram or magnetic resonance angiography (MRA).

Answer 59

The best screening tool for someone that you suspect has hyperaldosteronism is to check the renin and aldosterone levels and calculate a renin / aldosterone ratio: High aldosterone and low renin indicates primary hyperaldosteronism High aldosterone and high renin indicates secondary hyperaldosteronism Other investigations relating to the effects of aldosterone: ``` Blood pressure (hypertension) Serum electrolytes (hypokalaemia) Blood gas analysis (alkalosis) If a high aldosterone level is found then investigate for the cause: ``` CT / MRI to look for an adrenal tumour Renal doppler ultrasound, CT angiogram or MRA for renal artery stenosis or obstruction

Answer 60

Hyperaldosteronism is worth remembering as the most common cause of secondary hypertension. If you have a patient with a high blood pressure that is not responding to treatment consider screening for hyperaldosteronism with a renin:aldosterone ratio. One clue that could prompt you to test for hyperaldosteronism might be a low potassium however be aware that potassium levels may be normal.

Answer 61

Aldosterone antagonists Eplerenone Spironolactone Treat the underlying cause Surgical removal of adenoma Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis

Answer 62

Anti-diuretic hormone (ADH) is produced in the hypothalamus and secreted by the posterior pituitary gland. It is also known as “vasopressin”. ADH stimulates water reabsorption from the collecting ducts in the kidneys. SIADH is a condition where there is inappropriately large amounts of ADH. This may be the result of the posterior pituitary secreting too much ADH or the ADH may be coming from somewhere else, for example a small cell lung cancer. The excessive ADH results in excessive water reabsorption in the collecting ducts. This water dilutes the sodium in the blood so you end up with a low sodium concentration (hyponatraemia). The excessive water reabsorption is not usually significant enough to cause a fluid overload, therefore you end up with a “euvolaemic hyponatraemia”. The urine becomes more concentrated as less water is excreted by the kidneys therefore patients with SIADH have a “high urine osmolality” and “high urine sodium”.

Answer 63

``` Headache Fatigue Muscle aches and cramps Confusion Severe hyponatraemia can cause seizures and reduced consciousness ```

Answer 64

Post-operative from major surgery Infection, particularly atypical pneumonia and lung abscesses Head injury Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,) Malignancy, particularly small cell lung cancer Meningitis

Answer 65

In a way, SIADH is a diagnosis of exclusion as we do not have a reliable test to directly measure ADH activity. Clinical examination will show euvolaemia. U+Es will show a hyponatraemia. Urine sodium and osmolality will be high. Other causes of hyponatraemia need to be excluded: Negative short synacthen test to exclude adrenal insufficiency No history of diuretic use No diarrhoea, vomiting, burns, fistula or excessive sweating No excessive water intake No chronic kidney disease or acute kidney injury

Answer 66

Tetany- muscle twitching, spasm, cramping perioral paraesthesia if chronic- depression and cataracts ECG- prolonged QT interval

Answer 67

This is either a lack of ADH or a lack of response to ADH This prevents the kidney from being able to concentrate the urine leading to polyuria and polydipsia It can be nephrogenic or cranial

Answer 68

This is where the collecting ducts of the kidneys do not respond to ADH It can be caused by; drugs- lithium Intrinsic kidney disease Electrolyte disturbance (hypokalaemia and hypercalcaemia)

Answer 69

``` This is when the hypothalamus does not produce ADH Can be caused by; - idiopathic - brain tumours - head injury - meninigitis/encephalitis etc... ```

Answer 70

``` Polyuria Polydipsia Dehydration Postural hypotension Hyponatraemia ```

Answer 71

Low urine osmolality High serum osmolality Water deprivation test

Answer 72

``` Ix= water deprivation test management= desmopressin ```

Answer 73

Tumour of the chromaffin cells in the adrenal medulla of the adrenal gland Presentation; - Headache - Anxiety - Sweating - Hypertension - Palpitations Diagnose by 24hr urine catecholamines and plasma free metanephrines Manage with alpha blockers, beta blockers once established on alpha blockers and adrenalectomy

Answer 74

Parathyroid hormone acts to raise blood calcium level by: Increasing osteoclast activity in bones (reabsorbing calcium from bones) Increasing calcium absorption from the gut Increasing calcium absorption from the kidneys Increasing vitamin D activity Vitamin D acts to increase calcium absorption from the intestines. Parathyroid hormone acts on vitamin D to convert it into active forms. So vitamin D and parathyroid hormone act together to raise blood calcium levels.