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Finals > Endo/ Electrolyte Abnormalities On Ward > Flashcards

Endo/ Electrolyte Abnormalities On Ward Flashcards

1
Q

What is acromegaly?

A

Excess GH secondary to a pituitary adenoma in over 95% of cases
A minority of cases are caused by ectopic GHRH or GH production by tumours.

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2
Q

What are the features of acromgealy?

A

coarse facial appearance, spade-like hands, increase in shoe size
large tongue, prognathism, interdental spaces
excessive sweating and oily skin: caused by sweat gland hypertrophy
features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases → galactorrhoea
6% of patients have MEN-1

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3
Q

What are the complications of acromegaly?

A

hypertension
diabetes (>10%)
cardiomyopathy
colorectal cancer

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4
Q

What features are specific to graves but not other causes of thyrotoxicosis?

A

Eye signs- exopthalmos and ophthalmoplegia
Pretibial myxoedema
Digital clubbing
Soft tissue swelling of the hands an feet
Periosteal new bone formation

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5
Q

What antibodies are associated with graves?

A

TSH receptor stimulating antibodies

Anti thyroid peroxidase antibodies

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6
Q

What are the different types of thyroid cancer?

A 
Papillary (young females- excellent prognosis) 80% 
Follicular 20% 
Medullary 5% 
Anaplastic 1% 
Lymphoma
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7
Q

What are the causes of hpoglycaemia?

A

Insulinoma- increased ratio or proinsulin to insulin
Self administration of insulin/sulphonyureas
Liver failure
Addisons disease
Alcohol

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8
Q

What are the features of hypoglycaemia?

A

blood glucose levels and the severity of symptoms are not always correlated, especially in patients with diabetes.
blood glucose concentrations <3.3 mmol/L cause autonomic symptoms due to the release of glucagon and adrenaline (average frequency in brackets):
Sweating
Shaking
Hunger
Anxiety
Nausea
blood glucose concentrations below <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:
Weakness
Vision changes
Confusion
Dizziness
Severe and uncommon features of hypoglycaemia include:
Convulsion
Coma

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9
Q

What is the treatment of hypoglycaemia?

A

the following guidelines are based on the BNF hypoglycaemia treatment summary.
in the community (for example, diabetes mellitus patients who inject insulin):
Initially, oral glucose 10-20g should be given in liquid, gel or tablet form
Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
in a hospital setting:
If the patient is alert, a quick-acting carbohydrate may be given (as above)
If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
Alternatively, intravenous 20% glucose solution may be given through a large vein

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10
Q

What should you think of in metabolic ketoacidosis with normal or low glucose?

A

Alcoholic ketoacidosis

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11
Q

What way of diagnosing diabetes mellitus should be used in sickle cell patients?

A

OGTT
As sickle cell is associated with increased red cells turnover, this can lead to falsely low HbA1c readings, making this test less reliable for diagnosing diabetes.

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12
Q

What is the diagnostic test for acromegaly?

A

OGTT

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13
Q

What are the causes of osteoporosis?

A 
SHATTERED
S= steroids 
H= hyperparathyroidism 
A= alcohol and smoking 
T= thin (BMI <22) 
F= family history 
T= testosterone deficiency 
E= early menopause 
R= renal/liver failure 
E= erosive/inflammatory bone disease 
D= diabetes
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14
Q

What is the classification of osteoporosis?

A

Normal = T score > or equal to 1SD
Osteopenia= T score -1 to -2.55 SD
Osteoporosis= T score -2.5 SD
Severe osteoporosis = -2.5SD T score + 1 or more fragility fractures

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15
Q

What is the management of osteoporosis?

A

Nutrition
Exercise
Reduce falls if poss
Ensure adequate calcium and vit D

1st line= bisphosphonages - alendronic acid

2nd line= raloxifene

3rd line= teripatide
Denosumab

Review after 5 years of bisphosphonate treatment, if no fractures then remeasure BMD and FRAX

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16
Q

What type of patients cant take bisphosphonates?

A

People with CKD as it is renally excreted

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17
Q

What is an importat SE of raloxifene?

A

VTE

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18
Q

When would you use GLP-1 Mimetics?

A

When triple therapy has not worked
BMI >35 (these drugs cause early satiety and therefore cause weight loss)
Obesity and associated illness
If there BMI <35 with insulin therapy is likely to cause an issue ie: lorry driver

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19
Q

To continue of GLP-1 what should you assess for?

A

At 6 months you should assess for…

3% weight loss
1% HbA1C decrease

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20
Q

What is the diabetic treatment escalation?

A

Initially start them on metformin..
If this doesn’t work then add DPP-4 inhibitor, pioglitazone or sulfonylurea

If still not worked then add in GLP-1 mimetic and insulin

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21
Q

What is cushings syndrome? What are the causes?

A

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

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22
Q

What are the features of cushings syndrome?

A 
Personality changes 
Moon face 
Hyperglycaemia 
NA and fluid retention 
Increase susceptibility to infection 
Thin extremities 
Male: Gynaecomastia 
Fat deposits on face and back of shoulders 
GI distress- increased acid 
Female- amenorrhoea, hirsutism 
Thin skin 
Purple striae 
Bruises and petechiae 
Osteoporosis
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23
Q

What is cushings disease specifically?

A

It means it is being caused by a pituitary problem

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24
Q

What tests do you do for cushings?

A

Firstly you do a low dose dexamethasone test at midnight- 1mg dexamethasone and measure cortisol levels in the morning

Next thing you do if there is still high cortisol levels in the morning…
Look at the ACTH levels
If the ACTH levels are high then we know its either a pituitary tumour or something else secreting ACTH as an ectopic ie: lung cancer

High dose dex- if a pituitary lesion then you should be able to suppress it, you wouldn’t be able to in ectopic.

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25
Q

What are some SES of amiodarone?

A

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

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26
Q

What is a phaeochromocytoma?

A

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

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27
Q

What is associated with medullary cancer?

A

MEN2B syndrome

They will have phaeochromocytomas

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28
Q

What would you expect calcium levels to be in a patient with secondary hyperparathyroidism?

A

Normal or low

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29
Q

What is primary hyperparathyroidism?

A

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

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30
Q

What is secondary hyperparathyroidism?

A

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.

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31
Q

What is tertiary hyperparathyroidism?

A

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

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32
Q

What do people with primary hyperparathyroidism present with?

A

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

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33
Q

When do you operate for primary hyperparatyrlidism?

A

Symptomatic
Osteoporosis and bone disease
Kidney stones
<50 years

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34
Q

What are the causes of cushings syndrome?

A

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

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35
Q

What is addisons disease?

A

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

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36
Q

What is secondary adrenal insufficiency?

A

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)

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37
Q

What type of adrenal insufficiency is associated with long term oral steroid use?

A

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.

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38
Q

What are the symptoms and signs of adrenal insufficiency?

A

Symptoms- fatigue, nausea, cramps, abdo pain, reduced libido

Signs- bronze hyperpigmentation to skin (ACTH stimulates melanocytes to produce melanin)
HYPOTENSION

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39
Q

What investigations do you want to do for addisons disease?

A

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

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40
Q

What does the short synacthen test involve?

A

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).

41
Q

What are the antibodies found in thyroid disease?

A 
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

42
Q

What information can you get from radioisotope scans?

A

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

43
Q

What is the difference between primary and secondary hyperthyroidism?

A

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.

44
Q

What is Graves disease?

A

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.

45
Q

What is a toxic multinodular goitre?

A

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.

46
Q

What are the examination findings in Graves?

A

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

47
Q

What are the unique features of toxic multi nodular goitre?

A

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

48
Q

What is a solitary toxic thyroid nodule?

A

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

49
Q

What is de quervains thyroiditis?

A

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.

50
Q

How do you treat de quervains thyroiditis?

A

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

51
Q

What is a thyroid storm?

A

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.

52
Q

What is the treatment of hyperthyroidism?

A

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.

53
Q

What is the second line anti thyroid drug used for hyperthyroidism?

A

Propylthiouracil

54
Q

What are the strict rules for radioactive iodine

A

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
55
Q

What beta blocker is used in hyperthyroidism?

A

Propanolol

56
Q

What is the surgical option in thyrotoxicosis?

A

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.

57
Q

What are the causes of hypothyroidism?

A

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

58
Q

What are the secondary hypothyroidism?

A

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

59
Q

What are the features of hypothyroid?

A 
Weight gain 
Fatigue 
Dry skin 
Coarse hair and hair loss 
Fluid retention (oedema, pleural effusions, ascites) 
Heavy or irregular periods 
Constipation
60
Q

What are the ix in hypothyroidism?

A

TSH and T3/T4

Primary= T3/T4 low, TSH high

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

61
Q

What is the management of hypothyroidism?

A

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.

62
Q

What is T1DM?

A

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.

63
Q

What are the three things you worry about in DKA?

A

Ketoacidosis
Hyperkalaemia
Dehydration

64
Q

Why are patients in DKA dehydrated?

A

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.

65
Q

What are the presentation of DKA?

A 
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)
66
Q

What are the main principles of management of DKA?

A

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

67
Q

How often do we do HbA1C for diabetics?

A

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.

68
Q

What is the presentation of T2DM?

A 
Fatigue
Polydipsia and polyuria (thirsty and urinating a lot)
Unintentional weight loss
Opportunistic infections
Slow healing
Glucose in urine (on dipstick)
69
Q

How do you diagnose pre diabetes?

A

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

70
Q

How do you diagnose diabetes?

A

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

71
Q

What are the dietary modifications you should advise for T2DM?

A

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

72
Q

What complications should you monitor for in diabetes?

A

Diabetic retinopathy
Kidney diseas
Diabetic foot

73
Q

What are the HbA1c targets for T2DM?

A

48mmol/mol for new type 2 diabetics

53mmol/mol for diabetics that have moved beyond metformin alone

74
Q

How does metformin work and what are the side effects?

A

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

75
Q

How does pioglitazone work and what are the side effects?

A

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

76
Q

What is gliclazide?

What are the SEs?

A

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

77
Q

What is primary hyperaldosteronism?

A

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

78
Q

What are the causes of primary hyperaldosteronism?

A 
An adrenal adenoma secreting aldosterone (most common)
Bilateral adrenal hyperplasia
Familial hyperaldosteronism type 1 and type 2 (rare)
Adrenal carcinoma (rare)
79
Q

What is primary hyperaldosteronism?

A

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:

80
Q

What are the causes of primary hyperaldosteronism (conns)?

A 
An adrenal adenoma secreting aldosterone (most common)
Bilateral adrenal hyperplasia
Familial hyperaldosteronism type 1 and type 2 (rare)
Adrenal carcinoma (rare)
81
Q

What is secondary hyperaldosteronism?

A

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

82
Q

What is renal artery stenosis?

A

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).

83
Q

What are the Ix of hyperaldosteronism?

A

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

84
Q

What is the most common cause of secondary hypotension?

A

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.

85
Q

What is the management of hyperaldosteronism?

A

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

86
Q

What is the pathophysiology of SIADH?

A

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”.

87
Q

What are the symptoms of SIADH?

A 
Headache
Fatigue
Muscle aches and cramps
Confusion
Severe hyponatraemia can cause seizures and reduced consciousness
88
Q

What are the causes of SIADH?

A

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

89
Q

How do you diagnose SIADH?

A

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

90
Q

What are the features of hypocalcaemia?

A

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

91
Q

What is diabetes insipidus?

A

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

92
Q

What is nephrogenic diabetes insipidus?

A

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)

93
Q

What is cranial diabetes insipidus?

A 
This is when the hypothalamus does not produce ADH 
Can be caused by; 
- idiopathic 
- brain tumours 
- head injury 
- meninigitis/encephalitis etc...
94
Q

What is the presentation of diabetes insipidus?

A 
Polyuria 
Polydipsia 
Dehydration 
Postural hypotension 
Hyponatraemia
95
Q

What are the Ix of diabetes insipidus?

A

Low urine osmolality
High serum osmolality
Water deprivation test

96
Q

What is the Ix of choice and management for diabetes insipidus?

A 
Ix= water deprivation test 
management= desmopressin
97
Q

What is a phaechromocytoma?
What does it present with?
How do you diagnose?
How do you manage?

A

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

98
Q

How does parathyroid hormone raise blood calcium?

A

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.

Finals (24 decks)

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