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Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

List the hormones released by the anterior pituitary gland

A

Thyroid stimulating hormone

Adrenocorticotropic hormone (ACTH)

Follicle stimulating hormone (FSH) and Luteinising hormone (LH)

Growth hormone (GH)

Prolactin

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2
Q

List the hormones released by the posterior pituitary gland

A

Oxytocin

Antidiuretic hormone (ADH)

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3
Q

What stimulates anterior pituitary to release TSH

A

Thyrotropin releasing hormone (TRH)

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4
Q

When does cortisol peak

A

In the morning

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5
Q

When is cortisol at its lowest

A

Late in the evening

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6
Q

List the actions of cortisol on the body

A

Inhibits the immune system

Inhibits bone formation

Raises blood glucose

Increases metabolism

Increases alertness

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7
Q

What does growth hormone stimulate the release of?

A

Insulin like growth factor 1 (IGF-1) from the liver

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8
Q

What are the actions of growth hormone

A

Stimulates muscle growth

Increases bone density and strength

Stimulates cell regeneration and reproduction

Stimulates growth of internal organs

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9
Q

What is parathyroid hormone released in response to

A

Low calcium
Low magnesium
High serum phosphate

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10
Q

What is the role of parathyroid hormone

A

Increase the serum calcium

Increases osteoclast activity - increases calcium reabsorption

Increases calcium reabsorption in kidney

Stimulates kidney to metabolise vitamin D into its active form calcitriol that promotes calcium absorption from the small intestine

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11
Q

What is renin

A

Released when there is low blood pressure

Enzyme that converts angiotensinogen into angiotensin 1

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12
Q

What happens to angiotensin 1

A

Converted into angiotensin 2 in lung by enzyme ACE

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13
Q

What does angiotensin 2 do?

A

Causes vasoconstriction
Increased BP
Aldosterone from adrenal glands

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14
Q

What does aldosterone do?

A

Mineralocorticoid steroid hormone which acts on the nephrons in the kidney to

  • Increase sodium reabsorption from distal tubule - increase intravascular volume and increases BP
  • Increase potassium secretion from distal tubule
  • Increase hydrogen secretion from the collecting ducts
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15
Q

What is Cushing’s syndrome

A

Signs and symptoms thaqt develop after prolonged abnormal elevation of cortisol

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16
Q

What is Cushings disease

A

Pituitary adenoma secretes excessive ACTH

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17
Q

List some features of Cushings syndrome

A
  • Round moon face
  • Central obesity
  • Abdominal striae
  • Buffalo hump
  • Proximal limb muscle wasting
  • HTN
  • Cardiac hypertrophy
  • Hyperglycaemia
  • Depression
  • Insomnia
  • Osteoporosis
  • Easy bruising and poor skin healing
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18
Q

List some causes of Cushing’s syndrome

A

Exogenous steroids (prednisolone/glucocorticoids)

Cushing’s disease

Adrenal adenoma

Paraneoplastic Cushing’s - excess ACTH released from a cancer somewhere else - most common is small cell lung cancer causing ectopic ACTH

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19
Q

Describe the dexamethasone suppression test

A

Diagnose Cushing’s syndrome

Initially giving low dose test, if normal then Cushing’s excluded. If test is abnormal then high dose performed to distinguish cause

Dose of dexamethasone at night and their cortisol and ACTH is measured in the morning - find out if dexamethasone suppresses normal morning spike

Low dose - 1mg dexamethasone - dexamethasone suppresses release of cortisol is normal response. When cortisol not suppressed this is an abnormal result

High dose - 8mg, Cushings disease, pituitary shows response to negative feedback and this is enough the suppress the cortisol. Where there is adrenal adenoma the cortisol is not suppressed by ACTH is. Where there is ectopic ACTH, neither cortiosl or ACTH suppressed.

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20
Q

What is an alternative method of diagnosing Cushing syndrome to the dexamethasone suppression test?

A

24 hr urinary free cortisol

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21
Q

What investigations should be carried out if Cushing’s is suspected

A

Dexamethasone suppression test or 24hr urinary free cortisol

FBC - raised WCC

U&Es - potassium may be low if aldosterone also secreted by adrenal adenoma

MRI brain - pituitary adenoma

Chest CT - Small cell lung cancer

Abdominal CT - adrenal tumour

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22
Q

Describe the management of Cushing’s

A

Trans-sphenoidal removal of pituitary tumour

Surgical removal of adrenal tumour

Surgical removal of tumour producing ectopic ACTH

If surgical removal not possible, give replacement steroid hormones

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23
Q

What acid-base picture would be consistent with Cushing’s syndrome

A

Hypokalaemic metabolic alkalosis

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24
Q

What is adrenal insufficiency

A

Where the adrenal glands do not produce enough steroid hormones - cortisol and aldosterone

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25
Q

What is primary adrenal insufficiency

A

Addison’s disease
- Adrenal glands have been damaged resulting in reduced aldosterone and cortisol production
Autoimmune

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26
Q

What is secondary adrenal insufficiency

A

Low ACTH stimulating the adrenal gland - surgery, infection, loss of blood flow or radiotherapy or Sheehan’s (blood loss during childbirth causing pituitary necrosis)

Pituitary problem

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27
Q

What is tertiary adrenal insufficiency

A

Inadequate CRH release by hypothalamus

Long term oral steroids >3weeks causing suppression of the hypothalamus and when steroids stopped the body doesn’t start producing its own steroids

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28
Q

List the symptoms of adrenal insufficiency

A 
Fatigue 
Nausea 
Cramps
Abdominal pain
Reduced libido
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29
Q

List some signs of adrenal insufficiency

A

Bronze hyperpigmentation to skin - ACTH stimulates melanocytes to produce more melanin

Hypotension -postural

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30
Q

List the investigations for adrenal insufficiecy

A

U&Es - hyponatraemia, hyperkalaemia

Early morning cortisol - often falsy normal

Short synacthen test - diagnose adrenla insufficiency

ACTH - primary adrenal failure, ACTH high as pituitary tryung hard to stimulate the adrenal glands without any negative feedback in the absocence of cortisol. In secodnary the ACTH is low

Adrenal autoantiboides - adrenal cortex antbides and 21-hydroxylase antibodies

CT/MRI adrenals or pituitary

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31
Q

Describe the short synacthen test

A

Adrenal insufficiency

Morning

Give synacthen (synthetic ACTH) and measure blood cortisol baseline, 30 and 60 mins. Should double in healthy individual. Failure of cortisol to rise indicates primary adrenal insufficiency

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32
Q

Describe the treatment of adrenal insufficiency

A

Hydrocortisone - glucocorticoid and used to replace cortisol

Fludricortisone - mineralococrticoid and used to replace aldosterone

Steroid card and emergeny ID tag - steroid dependent and important doses are not missed, doses are doubled during illness to match normal steroid response to illness

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33
Q

Describe Addisonian crisis

A

Severe Addisons where the abscence of steroid hormones leads to life threatening presentation

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia
Patients can be very unwell

1st presentation of triggered by ilnness/ truama or sudden withdrawal of steroid

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34
Q

Describe the management of Addisonian crisis

A

Intensive monitoring
Parenteral steroid - IV hydrocortisone 100mg stat then 100mg every 6 hrs
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of fluid and electrolytes

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35
Q

How are the steroids given throughout the day in Addison’s

A

Hydrocortisone dose is split with the majority given in the first half of the days

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36
Q

Describe how Addison’s patients should adjust their steroids during illness

A

Double the glucocorticoid dose

Keep the mineralocorticoid (fludrocortisone) dose the same

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37
Q

Describe the thyroid results in hyperthyroidism

A

Low TSH and High T3 and T4

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38
Q

Describe the thyroid results in primary hypothyroidism

A

High TSH

Low T3 and T4

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39
Q

Describe the thyroid results in secondary hypothyroidism

A

Low TSH

Low T3 and 4

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40
Q

Give a cause of secondary hypothyroidism

A

Pituitary or hypothalamic cause

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41
Q

Which antibodies are present in Graves and Hashimotos thyroiditis

A

Antithyroid peroxidase (Anti-TPO) antibodies

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42
Q

Which antibodies are specific to Graves disease

A

TSH receptor antibodies

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43
Q

Describe some investigations for thyroid disease

A

Ultasound

Biopsy

Radioisotope scan - hyperthyroidism and thyroid cancer - the greater activity, the more radioisotope
Diffuse high uptake - Graves
Focal high uptake - toxic multinodular goitre and adenoma
Cold areas - cancer

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44
Q

Describe primary hyperthyroidism

A

Thyroid pathology

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45
Q

Describe secondary hyperthyroidism

A

Pituitary or hypothalamus pathology

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46
Q

What is thyrotoxicosis

A

Abnormal and excessive thyroid hormone

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47
Q

Describe Graves disease

A

Autoimmune condition

Antibodies to TSH receptor

Mimic TSH and stimulate TSH receptors on the thyroid

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48
Q

Describe toxic multinodular goitre (Plummers disease)

A

Nodules develop on the thyroid gland act indenpendently of the normal feedbkac system and continously produce excessive thyroid hormone

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49
Q

What is exopthakmos

A

Buldging of the eyeball due to graves disease

Inflammation and hypertroophy of tissue behind eyeball

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50
Q

What is pretibial myxoedema

A

Derm condition - deposits of mucin under the anterior aspect of the leg
Discoloured, waxy and oedematous appearance to the skin over this area
Specific reaction to the TSH receptor antibodies

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51
Q

List some causes of hyperthyroidism

A

Graves disease
Toxic multinodular goitre
Solitary toxic thyroid nodule
Thyroiditis

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52
Q

List the universal features of hyperthyroidism

A

Anxiety and irritability

Sweating and heat intolerance

Tachycardia

Weight loss

Fatigue

Frequent loose stools

Sexual dysfunction

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53
Q

List some unique features of Graves disease

A

Diffuse goitre
Graves eye disease
Bilateral exopthalmos
Pretibial myxoedema

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54
Q

List some unique features of toxic multinodular goitrew

A

Goitre with nodules

> 50 yo

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55
Q

Describe solitary thyroid nodule

A

Benign adenoma

Surgical removal

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56
Q

Describe De Quervains thyroiditis

A

Viral infection - fever, neck pain, tenderness, dysphagia and features of hyperthyroidism

There is a hyperthyroid phase followed by a hypothyroid phase as the TSH levels fall due to negative feedback

Symptomatic treatment with NSAIDs and beta blockers

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57
Q

Describe thyroid storm

A

Severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium

Supportive care and treatment of comlications such as AF

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58
Q

Describe management of hyperthyroidism

A

Carbimazole is 1st line

  • Titration block
  • Block and replace - block production then take levothyroxine

Propylthiouracil is 2nd line

Radioactive iodine - single drink which destroys proportion of the thyroid cells - remission takes 6 months and patient may be hypothyroid after

Beta blockers - propranolol is non selective

Surgery - post thyroidectomy patients will need to take levothyroxine replacement for life

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59
Q

How long does carbimazole take to produce a normal thyroid level

A

4-8 weeks

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60
Q

What is a complication of propylthiouracil

A

Hepatic reaction

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61
Q

What are some rules of radioactive iodine

A

Must not be pregnant and not allowed to get pregnant within 6 months

Avoid close contact with pregnant women and children for 3 weeks

Limit contact for several days

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62
Q

Describe hashimotos thyroiditis

A

Autoimmune inflammation of the thyroid gland associated with Antithyroid peroxidase anti-TPO antibodies and antithyroglobulin antibodies

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63
Q

List some causes of hypothyroidism

A

Hashimotos thyroiditis

Iodine deficiency

Secondary to hyperthyroid treatment

Lithium - inhibits thyroid hormone production

Amiodarone - interferes with thyroid hormone production and metabolism

Central causes (hypopituarism) - less TSH - tumour, infection, vascular (Sheehan syndrome), radiation

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64
Q

Describe the presenation of hypothyroidism

A 
Weight gain 
Fatigue
Dry skin 
Coarse hair and hair loss
Fluid retnetion -oedema, pleural effusion, ascites
Heavy or irregular periods
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65
Q

Describe the investigations for hypothyroidism

A

TFTs

66
Q

Describe the TFT result of primary hypothyroidism

A

Low T3 and T4, High TSH

67
Q

Describe the TFT result of secondary hypothyroidism

A

Low T3 and T4

Low TSH

68
Q

Describe the management of hypothyroidism

A

Oral levothyroxine

Titrate until TSH levels are normal

69
Q

Describe Type 1 diabetes

A

Pancreas stops producing insulin

70
Q

Which viruses may be implicated in T1DM

A

Coxsackie B and enterovirus

71
Q

What is the ideal blood glucose range

A

4.4-6.1

72
Q

How does insulin reduce blood sugar level

A

Cells absorb glucose from blood

Muscles and liver absorb glucose from blood and store it as glycogen

73
Q

Describe the action of glucagon

A

Catabolic hormone which breaks down glycogen into glucose - glycogenolysis

Tells liver to convert protein and fat into glucose - gluconeogenesis

74
Q

Describe ketogeneies

A

When insufficient glucose supply

Fatty acids converted to ketones

Cross blood brain barrier

75
Q

Describe the pathophysiology of diabetic ketoacidosis

A

Not producing insulin themselves and not injecting adequate insulin to compensate

Ketoacidosis - glucose can not enter the cells so body thinks it is staving, higher glucose, higher ketones.

Kidneys produce bicarbonate to counteract the ketones however eventually can not compensate and person becomes acidotic

Dehydration - hyperglycaemia - osmotic diuresis - polyuria and dehydration, stimulates thirst centre in the brain resulting in polydipsia

Insulin usually drives potassium into cells however without it the serum potassium can be normal or high and potassium is excreted in the urine however total body potassium is low as none in the cells - hypokalaemia - arrythmia

76
Q

Describe how people in DKA present

A

Hyperglycaemia

Dehydration - poluruia and polydipsia, dehydration and hypotension

Ketosis - Acetone smell to breath

Metabolic acidosis

Potassium imbalance

Altered consciousness

Symptoms of underlying trigger

Nausea and vomiting

77
Q

Describe management of DKA

A

Fluid resuscitation

Insulin infusion

Dextrose and potassium eventually

Look for infection

Chart fluid balance

Ketones- monitor

Establish the patient on their normal SC insulin prior to stopping insulin and fluid infusion

78
Q

How is DKA diagnosed

A

Check with local guidelines

Hyperglycaemia (glucose >11)
Ketosis (ketones >3)
Acidosis (pH <7.3)

79
Q

How fast can potassium be infused at

A

<10mmol/L/hr

80
Q

Describe the long term management of type 1 diabetes

A

SC insulin regimes
Monitor carb intake
Monitor blood sugar levels on waking, each meal and before bed
Monitor and manage complications

81
Q

What can injecting insulin at the same spot cause

A

lipodystrophy - sc fat hardens and insulin not absorbed properly

82
Q

What are some short term complications of T1DM

A

Hypoglycaemia
Hyperglycaemia
DKA

83
Q

What are some long term complications of T1DM

A 
Coronary artery disease 
Peripheral ischaemia - ulcers, diabetic foot
Stroke
HTN
Peripheral neuropathy 
Retinopathy 
Glomerulosclerosis
UTI, pneumonia, candida
84
Q

What monitoring is done in T1DM

A

HbA1c - glycated Hb - how much glucose attached to the Hb - average glucose level over past 3 months. Measured every 3-6months to see their long term control

Capillary blood glucose

Flash glucose monitoring - sensor on skin measuring glucose level of interstitial fluid, lag time of 5mins

85
Q

Describe the pathophysiology of T2DM

A

Repeated exposure to glucose and insulin makes the cells more resistant to the effects of insulin - more and more insulin to produce a response from the cells and get them to take up and use glucose

Overtime the pancreas becomes fatigues and damaged so produce less insulin

Chronic hyperglycaemia and micro/macrovascular complications

86
Q

List some risk factors of T2DM

A

Old age
Ethnicity - black, chinese, south asian
FH

Modifiable - obesity, sedentary lifestyle, high carbohydrates

87
Q

Describe the presentation of T2DM

A 
Fatigue 
Polyuria and polydipsia 
Unintentional weight loss
Opportunistic infection
Slow healing
Glucose in urine
88
Q

Describe the oral glucose tolerance test

A

Performed in morning prior to breakfast - fasting plasma glucose result, give 75g glucose drink then measure plasma glucose 2hrs later

89
Q

What is pre-diabetes

A

Indication the patient is heading towards diabetes
HbA1c 42-47 mmol/mol

Impaired fasting glucose (6.1-6.9)

Impaired glucose tolerance 7.8-11.1 on an OHGTT

90
Q

Describe T2DM diagnostic criteria

A

HbA1C >48
Random glucose >11
Fasting glucose >7
OGTT 2hr result >11

91
Q

Describe the management of T2DM

A

Dietary modification - veg and oily fish, low glycaemic index food, high fibre, low carbohydrate

Exercise and weight loss

Stop smoking

Optimise treatment for other illness

Monitor for complications - diabetic retinopathy, kidney disease, diabetic foot

92
Q

Describe the medical management of T2DM

A

Metformin - 1st line

2nd line - add sulphonyurea, pioglitazone, DPP-4i or SGLT2i

3rd line - triple therapy with metformin and 2 second line drugs combined or metformin plus insulin

93
Q

List some notable side effects of metformin

A

Diarrhoea and abdominal pain

Lactic acidosis

94
Q

How does metformin work

A

Increases sensitivity to insulin and decreases liver production of glucose

95
Q

How does pioglitazone work

A

Increases insulin sensitivity and decreases liver production of glucose

96
Q

List some notable side effects of pioglitazone

A 
Weight gain 
Fluid retention 
Anaemia
Heart failure 
Extended use may increase risk of bladder cancer
97
Q

How does sulfonylurea work

A

Stimulate insulin release from pancreas

98
Q

List some notable side effects of sulfonylureas

A

Weight gain
Hypoglycaemia
Increased risk of CVD and MI as a monotherapy

99
Q

List some rapid acting insulins

A

Novorapid
Humalog
Apidra

100
Q

List some short acting insulins

A

Actrapid
Humulin S
Insuman rapid

101
Q

List the intermediate acting insulins

A

Insulatard
Humalin I
Insuman basal

102
Q

List some long acting insulins

A

Lantus
Levemir
Degludec

103
Q

What are incretins

A

Hormones normally secreted by GI tract after eating a large meal

Increase insulin secretion
Inhibit glucagon production
Slow absorption by GI tract

104
Q

What are some symptoms of Sitagliptin (DPP-4 inhibitors)

A

GI tract upset
Symptoms of URTI
Pancreatitis

105
Q

What is acromegaly

A

Excessive growth hormone

106
Q

What causes acromegaly

A

Pituitary adenoma

Secondary to other cancer - ectopic growth hormone releasing hormone or growth hormone

107
Q

What visual disturbance is associated with pituitary tumours

A

Bitemporal hemianopia - loss of the outer half of vision of both eyes

108
Q

Describe the presentation of acromegaly

A 
Headaches 
Visual field defect
Prominent forehead and brow
Large nose, tongue, hands and feet, protruding jaw 
Arthritis from imbalanced growth of joints 
Hypertrophic heart
Hypertension
T2DM
 Colorectal cancer 
Development of new skin tags
Profuse sweating
109
Q

List the investigations for acromegaly

A

Insulin like growth factor 1 (IGF-1) - initial screening test (raised)

Oral glucose tolerance test whilst measuring growth hormone (high glucose normally suppresses growth hormone)

MRI brain for the pituitary tumour

Refer to ophthalmology for formal visual field testing

110
Q

Describe the treatment of acromegaly

A

Trans-spehnoidal removal of pituitary tumour

If ectopic hormones from pancreatic or lung cancer - surgical removal of these cancers

Medication

  • Pegvisomant (GH antagonist given SC and daily)
  • Somatostatin analogues (block GH release) - ocreotide
  • Dopamine agonists - block GH release (bromocriptine)
  • Somatostatin - growth hormone inhibiting hormone - normally secreted in the brain, GI tract, pancreas - blocks GGH release from pituitary
  • Dopamine also has inhibitory effect on GH release
111
Q

How does parathyroid hormone raise blood calcium

A

Increase osteoclast activity in bone (reabsorbing Ca from bones)

Increasing calcium absorption from the gut

Increasing calcium absorption from the kidney

Increasing vitamin D activity - increase calcium absorption from intestines

112
Q

What are the symptoms of hypercalcaemia

A

Renal stones

Painful bones

Abdominal groans - constipation, nausea, vomiting

Psychiatric moans - fatigue, depression and psychosis

113
Q

What is primary hyperparathyroidism caused by

A

Uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid glands

114
Q

What does primary hyperparathyroidism lead to

A

hypercalcaemia - abnormally high level of calcium in the blood

115
Q

How is primary hyperparathyroidism treated

A

Surgically removing the tumour

116
Q

What is secondary hyperparathyroidism

A

Where insufficient vitamin D or chronic renal failure leads to low absoprtion of calcium from intestine, kidneys and bones and causes hypocalcaemia, the parathyroid glands react to the low serum calcium by excreting more parathyroid hormone. Hyperplasia occurs in the parathyroid glands. The serum calcium begins to become low or normal but parathyroid hormone will be high

117
Q

How is secondary hyperparathyroidism treated

A

Vitamin D

Renal transplant

118
Q

What is tertiary hyperparathyroidism

A

When secondary hyperparathyroidism occurs for a long time. Hyperplasia of the glands. The baseline parathyroid hormone increases dramatically. High absorption of calcium and causes hypercalcaemia

119
Q

How is tertiary hyperparathyroidism treated

A

Surgically remove some of the parathyroid tissue

120
Q

Describe the renin, angiotensin aldosterone system

A

Juxtaglomerular cells in afferent arteriole in the kidney sense blood pressure in these vessels. When they sense a low blood pressure in the arteriole they secrete a hormone called renin. This liver secretes a protein called angiotensinogen which is converted to angiotensin 1 by renin. Angiotensin 1 becomes angiotensin 2 when converted by ACE in the lungs. Angiotensin 2 causes release of aldosterone in adrenal glands

121
Q

What does aldosterone do to the kidney

A

Increase sodium reabsorption from the distal tubule

Increase potassium secretion from the distal tubule

Increase hydrogen secretion from the collecting duct

122
Q

What is primary hyperaldosteronism

A

Conn’s syndrome

Too much aldosterone produced from the adrenal glands

Serum renin will be low as it is suppressed by the high blood pressure

Adrenal adenoma - secreting aldosterone
Bilateral adrenal hyperplasia
Familial hyperaldosteronism type 1 and 2
Adrenal carcinoma

123
Q

Describe secondary hyperaldosteronism

A

Excessive renin stimulating adrenal glands to produce more aldosterone - serum renin will be high

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

124
Q

List some causes of secondary hyperaldosteronism

A
  • renal artery stenosis
  • Renal artery obstruction
  • Heart failure
125
Q

Describe renal artery stenosis

A

Narrowing of the artery suppling the kidney

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. Confirm with Doppler US, CT angiogram or magnetic resonance angiography

126
Q

List the investigations for hyperaldosteronism

A

Renin/aldosterone ratio

BP

Serum electrolytes (hypokalaemia)

Blood gas analysis (alkalosis)

CT/MRI

Renal doppler US, CT angiogram or MRA for renal artery stenosis or obstruction

127
Q

Describe the management of hyperaldosteronism

A

Eplerenone
Spironolactone
Remove the adenoma
Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis

128
Q

What does a high aldosterone and low renin indicate

A

Primary hyperaldosteronism

129
Q

What does a high aldosterone and high renin indicate

A

Secondary hyperaldosteronism

130
Q

What does ADH normally do

A

Stimulate water reabsorption in the collecting duct

131
Q

What electrolyte imbalance occurs in SIADH

A

Hyponatraemia

132
Q

What happens to the fluid balance in SIADH

A

Euvolaemic

133
Q

What happens to the urine in SIADH

A

High urine osmolarity
High urine sodium
More concentrated

134
Q

List the symptoms of SIADh

A 
Headache
Fatigue
Muscle aches and cramps
Confusion 
Severe - seizure and reduced GCS
135
Q

List some causes of SIADh

A

Post op
Infection - atypical pneumonia and lung abscess
Head injury
Medication - thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs
Malignancy
Meningitis

136
Q

How do you diagnose SIADH

A

Dianosis of exclusion
Euvolaemic hyponatraemia

Exclude excessive water intake
No history of diuretic use
Negative synacthen test to exclude adrenal insufficiecny
No diarrhoea, vomiting, burns, fistula or excessive sweating
No CKD or AKI

137
Q

How do you establish the cause of SIADH

A

Medications
CXR - pneumonia or lung cancer
Malignancy - CT CAP and MRI brain

138
Q

How is SIADH managed

A

Treat the cause

Fluid restriction - concentrates blood and increases sodium concentration

Tolvaptans - ADH receptor blockers and cause rapid rise in sodium

Demeclocycline - rarely used now - ADH inhibitotion

139
Q

Why is sodium corrected slowkly

A

Prevent central pontine myelinosis

140
Q

How fast should sodium be corrected in hyponatraemia

A

<10mmol/L per 24hrs

141
Q

What is central pontine myelinolysis

A

Osmotic demylination
Comliation of severe hyponatraemia being treated too quickly
Brain cells swell
1st phase - encephalopathic and confused and headache or nausea and vomiting
Second phase - spastic quadriparesis, pseudobulbar palsy, cognitive behavioural changes, risk of death

142
Q

What is diabetes inspidus

A

Lack of ADH

143
Q

What are the two types of DI

A

Nephrogenic

Cranial

144
Q

What is an important differential for DI

A

Primary polydipsia

145
Q

Describe nephrogenic diabetes insipidus

A

Collecting ducts not responding to ADH

146
Q

What can casue nephrogenic DI

A

Drugs - lithium
Mutations in AVPR2 gene on X chromosome coding for ADH receptor
Intrinsic kidney disease
Electrolyte disturbance - hypokalaemia and hypercalcaemia

147
Q

Describe cranial diabetes insipidus

A

Hypothalamus does not produce ADH for the pituitary gland to secrete

148
Q

What can cause cranial DI

A 
Brain tumour
Head injury 
Brain malformation
Brain infection 
Brain surgery or radiotherapy
149
Q

Describe the presentation of diabetes insipidus

A 
Polyuria
Polydipsia 
Dehydration
Postural hypotension 
Hypernatremia
150
Q

How is diabetes insipidus investigated

A

Low urine osmolarity - low concentration of solute in urine

High serum osmolarity

Water deprivation test

151
Q

Describe the water deprivation test/desmopressin stimulation test

A

Avoid fluid for 8hrs before

Measure urine osmolarity and synthetic ADH (desmopressin) is given

8 hrs later urine osmolarity measured again

Cranial DI - urine osmolarity will be high as kidney able to respond to the fake ADH

Nephrogenic DI - urine osmolarity will be low initially and remain low

Primary polydipsia - high urine osmolarity before and after desmopressin

152
Q

Describe the management of diabetes insipidus

A

Cranial - replace ADH - desmopressin

Nephrogenic diabetes insipidus - higher doses desmopressin under close monitoring

153
Q

Where is adrenaline produced

A

Adrenal medulla chromaffin cells

154
Q

What is a pheochromocytoma

A

Tumour of chromaffin cells secreting lots of adrenaline

155
Q

What are the signs and symptoms of pheochromocytoma

A

Bursts of adrenaline - more settled periods

156
Q

Which genetic condition is associated with pheochromocytoma

A

MEN2

157
Q

Describe the 10% rule in pheochromocytoma

A

10% cancerous
10% bilateral
10% outside adrenal gland

158
Q

How is phaeochromocytoma diagnosed

A

24hr urine catecholamines

Plasma free metanepherines longer half life than adrenaline which varies in the response due to the bursts of adrenaline

159
Q

Describe the presentation of phaeochromocytoma

A 
Anxiety
Sweating 
Headache 
HTN 
Palpitations, tachycardia, paroxysmal AF
160
Q

Describe the management of phaeochromocytoma

A

Alpha blockers
Beta blockers once established on alpha blockers
Adrenalectomy - control symptoms before surgery

Finals (18 decks)

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