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Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What does the anterior pituitary gland release?

A

FSH

LH

ACTH (adrenocorticotropic hormone)

TSH

Prolactin

GH

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2
Q

What does the posterior pituitary release?

A

Oxytoxin

ADH

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3
Q

What are the components of the Thyroid axis?

A

TRH (from hypothalamus)

TSH

T3/T4 (triiodothyronine / thyroxine)

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4
Q

What are the components of the adrenal axis?

A

Diurnal variation (peak at early morning)

CRH (corticotrophin release hormone)

ACTH

Cortisol (from adrenal gland - stress hormone)

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5
Q

What are the actions of cortisol in the body?

A
  • Inhibits immune system
  • Inhibits bone formation
  • Raises blood glucose
  • Increases alertness
  • Increases metabolism
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6
Q

What are the components of the growth hormone axis?

A

GHRH (somatostatin inhibits, ghrelin promotes)

GH

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

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7
Q

What is the action of growth hormone?

A
  • Stimulates muscle growth
  • Increases bone density
  • Stimulates cell regeneration and reproduction
  • Stimulates growth of internal organs
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8
Q

When is PTH released?

A

Low serum calcium and low magnesium (and high serum phosphate) to increase calcium resorption

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9
Q

What does PTH do?

A

Increases activity and number of osteoclasts in the bone, causing resorption into the blood, increasing serum calcium.

Stimulates an increase in calcium reabsoption in the kidneys

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10
Q

What is the additional function of PTH?

A

Stimulates the kidneys to convert vitamin D3 into calcitriol (active form of vit D) which promotes calcium absoption from food in small intestine

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11
Q

Where is Renin secreted from?

A

Juxtaglomerular cells in the afferent and efferent arterioles in kidbey (sense blood pressure - secrete less if BP is high)

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12
Q

What is the role of renin?

A

Enzyme converts angiotensinogen (from liver) into angiotension I

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13
Q

What are the two actions of angiotention II?

A

Acts on blood vessels to vasoconstrict and stimulates the release of aldosterone form adrenal glands

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14
Q

What does aldosterone result in?

A

Acts on nephrons to increase sodium reabsorption in distal tubules, potassium secretion in distal tubules and hydrogen secretion from collecting ducts

Hypernatraemia

Hypokalaemia

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15
Q

What is Cushing’s syndrome vs Cushing’s disease?

A

Syndrome = signs & symptoms after prolonged elevated cortisol

Disease = pituitary adenoma secreting excessive ACTH

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16
Q

What is the causality between Cushings disease and Cushing syndrome?

A

Disease can cause syndrome but syndrome isnt always caused by disease

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17
Q

What are the features of Cushing’s syndrome?

A

Moon face

Central obesity

Abdo striae

Buffalo hump

Proximal limb muscle wasting

Hypertension

Cardiac hypertrophy

Hyperglycaemia

Insomnia

Osteoporosis

Easy brusing

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18
Q

What are the other effects of high level of stress hormone?

A

Hypertension

Cardiac hypertrophy

Hyperglycaemia (type 2 diabetes)

Depression

Insomnia

Osteoporosis

Easy bruising / poor skin healing

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19
Q

What are some causes of Cushing’s syndrome?

A
  • Exogenuos steroids
  • Cushings Disease
  • Adrenal adenoma (not pituitary)
  • Paraneoplastic cushings
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20
Q

What is the most common cause of paraneoplastic Cushings?

A

SCLC (excess ACTH from cancer)

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21
Q

What is the choice of test for Cushing’s?

A

Dexamethasone Suppression Test

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22
Q

How does the dexamethasone suppression test work?

A

Patient is given low dose of dexamethosone (synthetic glucocorticoid steroid) at night and cortisol/ACTH is measured in the morning to see if its been suppressed

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23
Q

In the high dose Dexamathasone Suppression test (8mg vs 1mg - done if low dose test abnormal) what is the difference between Cushing’s Disease and an Adrenal Adenoma?

A

Cushing’s disease still shows some response to negative feedback whereas Adrenal Adenomas do not (however ACTH is supressed)

In ectopic ACTH neither cortisol or ACTH will be supressed

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24
Q

Complete the following:

A
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25
Q

What is the other investigation for Cushing’s?

A

24 hour urinary free cortisol (doesn’t indicate underlying cause and cumbersome)

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26
Q

What is the imaging of choice for Cushing’s syndrome?

What will blood tests show?

A

MRI brain for pituitary adenomas

Chest CT for small cell lung cancer

Abdo CT for adrenal tumours

Bloods

FBC (raised WCC) and electrolytes (potassium may be low if aldosterone also secreted by adrenal adenoma)

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27
Q

What is the treatment of Cushing’s?

A

Trans-sphenoidal surgery for pituitary adenoma

Surgical removal of adrenal tumour / tumour producing ectopic ACTH

If surgical removal of cause not possible then can remove both adrenal glands and give replacement steroids for life

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28
Q

What hormones are particularily lacking in adrenal insufficiency?

A

Cortisol and aldosterone

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29
Q

What is Addison’s disease?

A

Specific condition where the adrenal glands have been damaged resulting in a reduction of cortisol and aldosterone (mainly autoimmune cause)

Aka primary adrenal insufficiency

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30
Q

What is secondary adrenal insufficiency commonly due to?

A

Inadequate ACTH resulting in low cortisol

E.g. from sugery to remove pituitary tumour, infection, loss of blood, radiotherapy

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31
Q

What is Sheehan’s syndrome?

A

Massive blood loss during childbirth leading to pituitary gland necrosis (causes secondary adrenal insufficiency)

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32
Q

What is teritary adrenal insufficiency?

A

Inadequate CRH released by the hypothalamus usually the result of the patient being on long term steroids (more than 3 weeks) causing suppression of the hypothalamus.

When steroids are stopped then hypothalamus doesn’t ‘wake up’ quick enough, so steroids shouldnt be stopped abruptly

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33
Q

What are some symptoms of adrenal insufficiency?

A
  • Fatigue
  • Nausea
  • Cramps
  • Abdo pain
  • Reduced libido
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34
Q

What are some signs of adrenal insufficiency?

A

Bronze skin due to ACTH stimulating melanocytes to produce melanin

Postural hypotension

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35
Q

What are some investigations for adrenal insufficiency?

A

Hyponatraemia (key clue)

Hyperkalaemia

Early morning cortisol (often falsely normal)

SHORT SYNACTHEN TEST (for diagnosis)

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36
Q

What antibodies are present for autoimmune Addison’s?

A

Adrenal cortex antibodies and 21-hydroxylase antibodies

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37
Q

What imaging can be used for Adrenal insufficency?

A

CT/MRI for adrenal tumour, haemorrhage

MRI pituitary for further info about pituitary

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38
Q

What are the ACTH levels in primary adrenal failure and secondary adrenal failure?

A

Primary = ACTH high

Secondary = ACTH low

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39
Q

What is the short syntacthen test ?

A

Give patient synacthen (synthetic ACTH) in morning

Blood cortisol measured at baseline, 30 mins, 60 mins after.

Should rise, if not (at least double) then primary adrenal insufficiency (Addison’s disease)

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40
Q

What is the treatment for adrenal insufficiency?

A

Hydrocortisone is a glucocorticoid to replace cortidol

Fludrocortisone is a mineralcorticoid to replace aldosterone

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41
Q

What are patients with adrenal insifficiency given in addition?

A

Steroid card and emergency ID tag (indicate they are dependent on steroids)

Doses doubles during acute illness

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42
Q

How do patients with Addisonian crisis present (acute presentation of severe addisons)?

A
  • Reduced consciousness
  • Hypotension
  • Hypoglycaemia, hyponatraemia, hyperkalaemia
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43
Q

When can an Addison’s crisis occur?

A

Long term steroids stopped abruptly

Infection

Trauma

Other acute illness

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44
Q

What are the management options for a patient with an Addisonian Crisis?

A
  • Intensive monitoring if unwell
  • Parenteral steroids (IV hydrocortisone 100mg stat then 100mg every 6 hours)
  • IV fluid resuscitation
  • Correct hypoglycaemia
  • Monitor U&Es
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45
Q

What are the TFTs in hyperthyroidism?

A

TSH is suppressed so low TSH, apart from in pituitary adenoma which secretes TSH

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46
Q

How are the TFTs in hypothyroidism?

A

TSH is high (exception is pituitary/hypothamic cause when TSH will be low)

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47
Q

Label the following:

A
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48
Q

What antibodies are present in Grave’s and Hashimoto’s disease?

A

anti-TPO (antithyroid peroxidase) antibodies

anti-thyroglobulin antibodies (limited use as present in normal individuals)

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49
Q

What antibodies are present in Grave’s disease?

A

TSH receptor antibodies

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50
Q

What imaging is available for thyroid problems?

A

Thyroid ultrasound - diagnose thyroid nodules, and for biopsy guide (distinguish between cystic and solid nodules)

Radioisotope scans - for hyperthyroidism and thyroid cancers (diffuse uptake of iodine in Graves, focal is adenomas/toxic multinodular goitre, ‘cold’ aka abnormally low is thyroid cancer) gamma camera is used to detect gamma rays from radioactive iodine

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51
Q

What is Graves’ disease?

A

Autoimmune condition where TSH receptor antibodies (mimic TSH) cause a primary hyperthyroidism

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52
Q

What is toxic multinodular goitre (Plummer’s disease)?

A

Nodules develop on the gland acting independently of the normal feedback system and continuously produce excessive thyroid hormone

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53
Q

When is exopthalmos seen?

A

Grave’s disease

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54
Q

What is pretibial myxoedema?

A

Specific to Grave’s disease where there are deposits of mucin under the skin and on the anterior aspect of the leg - discoloured, wavy, oedematous appearance of the skin over this area (reaction to the TSH receptor antibodies)

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55
Q

What are some causes of hyperthyroid?

A

Grave’s disease

Toxic multinodular goitre

Solitary toxic thryoid nodule

Thyroiditis (e.g. De Quervain’s, Hashimoto’s, postpartum and drug-induced thyroiditis)

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56
Q

What are some universal features of hyperthyroidism?

A
  • Anxiety and irritabilty
  • Sweating and heat intolerance
  • Tachycardia
  • Weight loss
  • Fatigue
  • Losse stools
  • Sexual dysfunction
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57
Q

What are some unique features of Grave’s disease?

A
  • Diffuse Goitre (without nodules)
  • Graves eye disease
  • Exopthalmos
  • Myxoedema
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58
Q

What are some unique features of toxic multinodular goitre?

A
  • Goitre with firm nodules
  • Most patients >50
  • Second most common form of thyrotoxicosis (after Graves’)
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59
Q

What is a single abnomal thyroid nodule called?

A

Adenoma (benign - treated with surgical removal)

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60
Q

What is De Quervain’s Thyroiditis?

A

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

Hyperthyroid phase followed by a hypothyroid phase as the TSH levels fall due to negative

Self limiting condition and supportive treatment is with NSAIDs for pain and beta-blockers for symptoms

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61
Q

What is a Thyroid Storm?

A

Rare presentation of hyperthyroidism‘thyrotoxicosis crisis’

Severe presentation of hyperthyroidism with pyrexia, tachycardia and delerium (requires admission)

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62
Q

What is the first line antithyroid drug?

A

Carbimazole - remission is usually achieved in 18 months of treatment

Titration block = careful titration for normal levels

Block and replace = blocks all production and patient take levothyroxine

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63
Q

What are the other treatments for hyperthyroidism?

A

Propylthiouracil - second line used in similar way to carbimazole (small risk of severe hepatic reaction)

Radioactive iodine treatment - (drinking single dose of radioactive iodine) radiation destroys the thyroid cells - can be left hypothyroid after and require levothyroxine replacement

Beta blockers (blocks adrenaline symptoms - propanolol is non selective so works everywhere)

Surgery (thyroidectomy) - requires levothyroxine for life

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64
Q

What are the ‘rules’ for radioactive iodine treatment?

A
  • Patient must not be pregnant to allowed to get pregnancy in 6 months
  • No close contact with children/pregnant women 3 weeks after
  • Limit contact with anyone for several days after
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65
Q

What are some causes of hypothyroidism?

A

Hashimoto’s Thyroititis (anti-TPO and antithyroglobulin antibodies - with goitre followed by atrophy of thyroid gland)

Iodine deficiency

Secondary to treatment of hyperthyroidism (carbimazole, propylthiouracil, radioactive iodine, thyroid surgery)

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66
Q

What medications can inhibit the production of thyroid hormones?

A

Lithium

Amiodarone

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67
Q

What are some central causes (secondary) hypothyroidism?

A

Pituitary gland fails to produce enough TSH (associated with lack of ACTH) - hypopituitarism:

  • Tumours
  • Infection
  • Vascular (e.g. Sheehan syndrome)
  • Radiation
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68
Q

How do patients with hypothyroidism present?

A
  • Weight gain
  • Fatigue
  • Dry skin
  • Coarse hair
  • Fluid retention (oedema, ascites)
  • Heavy / irregular periods
  • Constipation
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69
Q

What is the management of hypothyroidism?

A

Levothyroxine (synthetic T4) which is metabolised to T3 in the body

Initially measure monthly until stable then less frequently until symptomatic

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70
Q

What does the body want to keep blood glucose between?

A

4.4 and 6.1

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71
Q

Where is Insulin made?

A

Beta cells in the Islets of Langerhans in the pancreas

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72
Q

How does insulin reduce blood sugar?

A

Causes cells in the body to absorb glucose and causes formation of glycogen stores (in muscle and liver)

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73
Q

Where it glucagon made?

A

Alpha cells in the Islets of Langerhans in the pancreas

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74
Q

What does Glycogen do?

A

Tells the liver to break down stored glycogen into glucose (glycogenolysis)

Also promotes gluconeogenesis

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75
Q

What is Ketogenesis?

A

When there is insufficient glucose and glycogen stores are depleted the liver takes fatty acids and turns them into ketones

They are water soluble fatty acids which can be used as fuel (can cross BBB)

76
Q

How can ketone levels be measured?

A

“Dipstick”

In blood using a ketone meter

Ketosis = acetone smell on breath

77
Q

What happens in T1DM and why?

A

Pancreas stops being able to produce insulin, clause unclear may be genetic or triggered by viruses e.g. Coxsackie B virus and enterovirus

78
Q

What does diabetic ketoacidosis result in?

A

Metabolic acidosis which is life threatening

79
Q

What happens in T1DM ketoacidosis?

A

Over production of ketone acids causes metabolic acidosis

80
Q

Why does dehydration occur in T1DM?

A

Glucose in the urine draws water out with it (osmotic diuresis) causing polyuria and polydipsia

81
Q

Why does T1DM result in a potassium imbalance?

A

Serum potassium = normal but total body potassium is low because of no stores

When insulin is started all potassium is driven into cells causign severe hypokalaemia very quickly

82
Q

How does DKA present?

A
  • Hyperglycaemia
  • Dehydration
  • Ketosis
  • Metabolic acidosis
  • Potassium imbalance
83
Q

How does a patient present with DKA?

A
  • Polyuria
  • Polypdipsia
  • N&V
  • Acetone smell on breath
  • Dehydration
  • Altered conciousness
84
Q

How is DKA diagnosed?

A
  • Hyperglycaemia >11
  • Ketosis >3
  • Acidosis <7.3
85
Q

What is the treatment for DKA?

A

FIG-PICK

Fluids - IV fluid resus with normal saline (1 litre stat, 4 litres with K+ over 12 hrs)

Insulin - e.g. Act rapid

Glucose - monitor and add dextrose (if below 14 mmol / L)

Potassium - monitor and correct (infused at no more than 10 mmol / hr)

Infection - treat any infection

Chart - fluid balance

Ketones - monitor blood ketone

Establish on normal subcut regime prior to stopping insulin

86
Q

What is the long term management of T1DM?

A
  • Sub cut insulin regimes
  • Monitor dietary carb intake
  • Monitor blood sugar levels on waking
  • Monitoring for complications
87
Q

How is insulin usually prescribed?

A

Combi of background - long acting

and

Short acting (30 mins before meal)

88
Q

What can injecting at the same spot be called?

A

“lipodystrophy” - sub cut fat hardens, patients are told to cycle their injecting spots

89
Q

What are some short term complications of T1DM?

A

Hyperglycaemia (and DKA)

Hypoglycaemia

90
Q

What are the symptoms of hypoglycaemia?

A

Tremor

Sweating

Irritability

Dizziness

Pallor

(reduced consciousness, coma and death)

91
Q

How is hypoglycaemia treated?

A

Rapid acting glucose e.g. lucozade and slower acting e.g. biscuits

If severe = IV dextrose and IM glucagon

92
Q

What are some long term complications of T1DM?

A
  • Damage to endothelial cells of blood vessels (leaky / unable to regenerate)
  • High sugar levels causes suppression of the immune system providing optimal environment for infectious organisms to thrive
93
Q

What are some macrovascular complications of T1DM?

A
  • Coronary artery disease
  • Peripheral ischaemia and ‘diabetic foot’
  • Stroke
  • Hypertension
94
Q

What are some microvascular complications of T1DM?

A

Peripheral neuropathy

Retinopathy

Kidney disease, particularly glomerulosclerosis

95
Q

What are some infection related complications of T1DM?

A

Urinary Tract Infections

Pneumonia

Skin and soft tissue infections

Fungal infections, particularly oral and vaginal candidiasis

96
Q

How is T1DM monitored?

A

HbA1c every 3-6 months (glycated Hb - how much glucose attached)

Capillary blood glucose

Flash glucose monitoring (sensor measures glucose levels of interstitial fluid - lag of 5 mins - need “reader” to swipe over sensor - sensor needs replacing every 2 weeks)

97
Q

Who normally gets diabetes (due to beta cells getting fatigued)?

A

Asian, Black

Male

Elderly >40

Obese

Those with lack of exercise

98
Q

What are the non-modifiable and modifiable risk factors for T2DM?

A

Non-modifiable:

  • Older age
  • Ethnicity (black, chinese, south asian)
  • FH

Modifiable:

  • Obesity
  • Sedentary lifestyles
  • High carb (refined) diet
99
Q

What’s a normal HbA1c?

A

<48 mmol/L

100
Q

How long does a HbA1c look at?

101
Q

What is the diet advice to diabetics?

A

​Low glycaemic and high fibre diet

Veg and oily fish

102
Q

How would type 2 diabetes present?

A

Fatigue

Polydipsia and polyuria

Unintentional weight loss

Opportunistic infections

Slow healing

Glucose in urine (on dipstick)

103
Q

What’s normal capillary blood glucose?

104
Q

How is OGTT done?

A

Take baseline blood sugar before breakfast

Then measure 2 hours after sugary drink

105
Q

WhaWhat is HbA1c for pre-diabetes (heading towards T2DM but don’t fit diabetic diagnostic criteria)?

A

42-47 (48 for diabetes)

106
Q

What is the random blood glucose/OGTT for diabetes?

107
Q

What is the fasting blood glucose for diabetes?

108
Q

What is the management of diabetes?

A

Educate (its curable - e.g. DiRECT study - put on 800 calories per day and remission)

Diet advice - veg and oily fish, low glycaemic, high fibre diet

Other risk factors - exercise and weight loss, stop smoking, optimise treatment for other illnesses e.g. HTN, hyperlipaemia, CVD

109
Q

What complications would you look for in diabetes?

A

Retinopathy

Kidney disease

Diabetic foot

110
Q

What is the HbA1c target for metformin treatment and further?

A

48 (new T2DM) and 53 (moved beyond metformin)

111
Q

What are the 2nd line treatments after metformin?

A

Any of:

Sulfonylurea

DPP-4 inhibitor

SGLT-2 inhibitor

Pioglitazone

112
Q

What is the 3rd line treatment for diabetes?

A

Metformin and 2 second line drugs

OR

Metformin and insulin

113
Q

How does metformin (biguanide) exert its action?

A

Increases insulin sensitivity

Decrease liver production of glucose

“weight neutral”

114
Q

Does metformin have an effect on weight?

115
Q

What are some side effects of metformin?

A

Lactic acidosis

Diarrhoea and abdo pain

Does NOT typically cause hypoglycaemia

116
Q

How does pioglitazone work?

A

Same as metformin (increases insulin sensitivity / decreases liver production of glucose)

117
Q

What are some side effects of pioglitazone?

A

Weight gain

Fluid retention

Anaemia

Heart failure

Bladder cancer

NOT HYPOGLYCAEMIA

118
Q

Name a sulfonylureas?

A

Gliclazide

119
Q

How do sulfonylureas work?

A

Stimulate insulin release from pancreas

120
Q

What are some side effects of sulphonureas?

A

Weight gain

HYPOGLYCAEMIA (only one)

Myocardial Infarction (and CVD when used as monotherapy)

121
Q

What does GLP-1 (an incretin) do?

A

Increase insulin secretion

Slows GI tract

Inhibits glucagon production

122
Q

How does a DPP4 (enzyme which breaks down GLP-1) inhibitors work?

A

Inhibits breakdown of GLP-1

123
Q

Name a DPP-4 inhibitor?

A

Sitagliptin

124
Q

What a side effect DPP-4 inhibitor?

A

(P)ancreatitis

GI upset

Symptoms of upper respiratory tract infection

125
Q

What is the most common GLP-1 mimetic?

A

Exenatide (given as subcut injection twice a day / once weekly in modifiable form)

126
Q

What are some side effects of GLP-1 mimetic?

A

GI upset

Weight LOSS

Dizziness

127
Q

Name a SGLT-2 inhibitor?

A

End with -gliflozin e.g. dapagliflozin, empagliflozin, canagliflozin

128
Q

How do SGLT-2 inhibitors work?

A

Block SGLT-2 transporter in proximal tubules of kidneys (usually reabsorbs glucose from urine)

129
Q

What are some side effects of SGLT-2 inhibitors?

A

Glucoseuria (increased UTIs)

Weight LOSS

DKA

130
Q

Name an rapid-acting insulins?

How long do they last?

A

Novorapid

Humalog

Apidra

10 mins - 4 hours

131
Q

When do rapid-acting insulins start work?

A

10 mins to 4 hours

132
Q

Name a short acting insulin?

A

Actrapid

Humulin S

133
Q

When do short acting insulins work?

A

30mins - 8 hours

134
Q

Name an intermediate insulin?

A

Humulin I

Insulatard

135
Q

When do intermediate insulins work?

A

1 hours to 16 hours

136
Q

Name a long acting insulin?

A

Degludec (lasts over 40 hours)

Levemir

Lantus

137
Q

When do long acting insulins work?

A

1 hour - 24

138
Q

What are some causes of GH excess?

A

Pituitary adenoma

Lung cancer secreting GHRH

139
Q

How does acromegaly present?

A

Headaches, bitemporal hemianopia

Overgrowth of tissue: frontal bossing, large nose, large tongue “macroglossia”, large hands and feet, large jaw

140
Q

What organ dysfunction can GH excess cause?

A

Hypertrophic heart

Hypertension

Type 2 diabetes

Colorectal cancer

141
Q

What are the investigations for suspected acromegaly?

A

IGF-1 inital screening (GH not useful - fluctuates)

OGTT whilst measuring GH

MRI brain for pituitary tumour

Refer to opthalmology

142
Q

What are the treatment options for acromegaly?

A

Transphenoidal surgery to remove pituitary tumour

Medication

143
Q

What medications are available for acromegaly?

A

Pegvisomant (GH antagonist given subcut and daily)

Somatostatin analogues (ocreotide)

Dopamine agonist to block GH release (bromocriptine)

144
Q

Which cells of the parathyroid gland release PTH?

A

Chief cells

145
Q

How does PTH act to raise blood calcium?

A
  • Increases osteoclast activity
  • Increases absoption of calcium from gut/kidneys
  • Increases vitamin D activity
146
Q

What are the symptoms of hypercalcaemia?

A

Stones, bones, groans, moans

Renal stones

Painful bones

Abdo groans (constipation, nausea and vomiting)

Psychiatric moans (fatigue, depression, psychosis)

147
Q

How does secondary hyperparathyroidism come about? How is it treated?

A

Insufficient vitamin D/chronic renal failure leading to low absorption of calcium from the intestines, kidneys and bones causing hypocalcaemia - low calcium in blood

PTH responds by raising

Correct vit D deficiency or perform renal transplant to treat failure

148
Q

What is tertiary hyperparathyroidism?

A

When the cause of 2ndary hyperparathyroidism is treated then the PTH remains inappropriately high - due to parathyroid gland hyperplasia and treated with surgery

149
Q

What is primary hyperaldosteronism? (Conn’s syndrome)

A

Adrenal glands produce too much aldosterone (renin will be low)

150
Q

What can cause primary hyperaldosteronism?

A
  • Adrenal adenoma
  • Adrenal hyperplasia
  • Familial hyperaldosteronism
  • Adrenal carcinoma (rare)
151
Q

What is secondary hyperaldosteronism?

A

Excessive renin stimulates the adrenal glands to produce more aldosterone

152
Q

What can cause secondary hyperaldoseronism?

A

Renal artery stenosis

Renal artery obstruction

Heart failure

153
Q

When is Renal Artery Stenosis typically a result of?

A

Atherosclerosis

154
Q

How can the diagnosis of renal artery stenosis be confirmed?

A

Doppler ultrasound

CT angiogram

MRA (magnetic resonance angiography)

155
Q

What are the investigations for hyperaldosteronism?

A

Renin/aldosterone levels

High aldosterone: Low renin = primary

High aldosterone : High renin = secondary

156
Q

What are some other investigations related to the effect of aldosterone?

A

Blood pressure (hypertension)

Serum electrolytes (hypokalaemia)

Blood gas (alkalosis)

157
Q

What investigations can be done for the cause of hyperaldosteronism?

A

CT/MRI to look for adrenal tumour

Renal doppler ultrasound / CT angiogram for RAS

158
Q

What is the management for hyperaldosteronism?

A

Aldosterone antagonist: Eplerenone, spironolactone

Treat underlying cause: Remove of adenoma, percutaneous renal artery angioplasty via femoral artery for RAS

159
Q

What is ADH also known as?

A

Vasopressin

160
Q

What is the result of excessive ADH?

A

Excessive water reabsorption in the collecting ducts cauing dilution of sodium in the blood

161
Q

What is the result of SIADH?

A

Euvolaemic hyponatraemia (urine becomes more concentrated as less water is excreted = high urine osmolality / high urine sodium)

162
Q

What happens to the urine in SIADH?

A

Urine is more concentrated as less water is passed out so there is:

“high urine osmolality”

“high urine sodium”

163
Q

What are the symptoms of SIADH?

A

- Headache

- Fatigue

- Muscle aches and cramps

- Confusion

- Severe hyponatraemia causes seizures and reduced consciousness

164
Q

What are some causes of SIADH?

A
  • Post op from major surgery
  • Infection (atypical pneumonia)
  • Head injury
  • Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs)
  • Malignancy e.g. SCLC
  • Meningitis
165
Q

How is SIADH diagnosed?

A

Diagnosis of exclusion

  • U&Es = hyponatraemia
  • Urine sodium and osmolality will be high
166
Q

How can other causes of hyponatraemia be rulled out?

A
  • Negative short synacthen test to exclude adrenal insufficiency
  • No history of diuretic use
  • No diarrhoea, vomiting/burns
  • No excessibe water intake
  • No CKD / AKD
167
Q

How can a cause for SIADH be established?

A

CXR as first line for pneumonia, lung abscess, lung cancer

168
Q

Why should sodium in hyponatraemia be corrected slowly?

A

Due to risk of central pontine myelinolysis

169
Q

What are the management steps of SIADH?

A

Treat cause (typically medications)

Fluid restriction (to 500ml - 1 litre)

Tolvaptan - ADH receptor blocker

Demeclocycline is a tetracycline abx that inhibits ADH (used prior to development of vaptans)

170
Q

What is central pontine myelinolysis?

A

Due to rapid correction of hyponatraemia

Long standing hyponatraemia causes brain to reduce solutes to prevent oedema - rapidly correcing causes brain cells to burst as water rapidly moves out, presenting:

First phase (due to electrolyte imbalance) headache, nausea and vomiting

Seconds phase (due to demyelination) spastic quadriparesis, cognitive/behavioural changes

171
Q

What is diabetes insipidus?

A

Lack of ADH or lack of a response (classified as nephrogenic / cranial)

172
Q

What is primary polydipsia?

A

Patient has a normally functioning ADH system but they are drinking excessive water leading to excessive urine production don’t have diabetes insipidus

173
Q

What is nephrogenic diabetes insipidus?

A

Collecting ducts in the kidneys do not respond to ADH, caused by:

  • Drugs e.g. lithium
  • Intrinsic kidney disease
  • Electrolyte disturbance (hypokalaemia / hypercalcaemia)
174
Q

What is cranial diabetes insipidus?

A

Hypothalamus doesn’t produce ADH for pituitary gland to secrete

Idiopathic or caused by:

  • Brain tumours
  • Brain malformations
  • Head injury
  • Brain Infections e.g. meningitis, encephalitis
175
Q

How does diabetes insipidus present?

A

Polyuria

Polydispsia

Dehydration

Postural hypotension

Hypernatraemia

176
Q

What is the test of choice for diagnosing diabetes insipidus?

A

Water deprivation test

Initial fluid deprevation (8 hours) then urine osmolality is measured, synthetic ADH (desmopressin) is given and 8 hours later urine osmolality is measured again

In cranial diabetes insipidus the kidneys will respond and urine osmolality will rise

In nephrogenic diabetes insipidus patient is unable to respond to ADH - urine osmolality will be low and remain low

177
Q

Label the following:

178
Q

How is diabetes insipidus managed?

A

Desmopressin (synthetic ADH) used in:

Cranial diabetes insipidus to replace ADH and nephrogenic diabetes insipidus in higher doses

179
Q

Where is adrenaline produced?

A

Chromaffin cells of the adrenal glands in adrenal medulla

180
Q

What type of hormone is adrenaline?

A

Catecholamine

181
Q

What is a phaeochromocytoma?

A

Tumour of the chromaffin cells secreting unregulated and excessive adrenaline

182
Q

How is a phaeochromocytoma diagnosed?

A

24 hour urine catecholamines

Plasma free metanephrines (break down product of adrenaline - has longer half life as adrenaline only lasts few mins so fluctuates)

183
Q

How does a phaeochromocytoma present?

A
  • Anxiety
  • Sweating
  • Headache
  • HTN
  • Palpitations, paroxysmal AF
184
Q

What is the management of a phaeochromocytoma?

A

Alpha blockers (phenoxybenzamine)

Beta blockers

Adrenalectomy

Symptoms need controlling medically before surgery

Medicine (12 decks)

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