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Final Year > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is released by the anterior pituitary gland?

A

TSH
ACTH
FSH and LH
GH
Prolactin

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2
Q

Which hormones are released by the posterior pituitary?

A

Oxytocin
ADH

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3
Q

Outline the thyroid axis

A

Hypothalamus releases thyrotropin-releasing hormone (TRH)
TRH stimulates anterior pituitary to release TSH
TSH stimulates thyroid gland to release T3 and T4

Hypothalamus and anterior pituitary respond to T3 and T4 by supressing release of TRH and TSH- Lowers T3 and 4

Low T3 and T4 offer less suppression of TRH and TSH- Increases T3 and T4

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4
Q

Outline the adrenal axis

A

Cortisol secreted by 2 adrenal glands (sit above kidneys)
Hypothalamus controls release of cortisol- Released in pulses throughout day and in response to stressful stimulus- Diurnal variation- Peaks early morning, lowest in evening

Hypothalamus releases corticotropin-releasing hormone (CRH)- Stimulates anterior pituitary to release ACTH- Stimulates adrenal glands to release cortisol

Cortisol sensed by hypothalamus and anterior pituitary- Suppresses release of CRH and ACTH- Lowers cortisol

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5
Q

What are the actions of cortisol on the body?

A

Increases alertness
Inhibits immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism

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6
Q

Outline the growth hormone axis

A

Hypothalamus produces GHRH- Stimulates anterior pituitary to release GH- Stimulates release of IGF-1 from liver

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7
Q

What is the function 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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8
Q

Outline parathyroid axis

A

PTH released from 4 parathyroid glands (in thyroid gland) in response to low calcium level in blood
PTH also released in response to low Mg or low phosphate level
Role of PTH is to increase serum calcium conc.
When serum calcium high- Suppresses release of PTH to reduce serum calcium

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9
Q

What is the role of PTH?

A

Increases activity and number of osteoclasts in bone- Causing reabsorption from bone into blood- Increases calcium conc.
Stimulates calcium reabsorption in kidneys- Less calcium excreted in urine
Stimulates kidneys to convert Vit D3 into calcitriol- Active form of Vit D- Promotes calcium absorption from food in intestine

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10
Q

Outline the Renin-Angiotensin-Aldosterone System (RAAS)

A

Renin (enzyme) secreted by juxtaglomerular cells in afferent arterioles in kidney- Sense BP- Secrete more renin in response to low BP, and less renin in repose to high BP
Renin converts angiotensinogen (released by liver) into angiotensin I
Angiotensin I converts to angiotensin II in lungs with help of angiotensin-converting enzyme (ACE)
Angiotensin II causes vasoconstriction- Increases BP- Stimulates release of aldosterone from adrenal glands- Promotes hypertrophy of myocytes
Sodium reabsorbed in kidneys, water follows by osmosis- Increased intravascular volume and BP

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11
Q

What is the role of aldosterone?

A

Mineralocorticoid steroid hormone
Act on nephrons in kidneys
Increases sodium reabsorption in distal tubule
Increases potassium secretion from distal tubule
Increases hydrogen secretion from collecting ducts

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12
Q

What is the link between RAAS and ACE inhibitors/ARBs?

A

Blocking action of ACE-i or ARBs- Reduce activity of angiotensin II, reducing vasoconstriction/cardiac remodelling/secretion of aldosterone
Reduced aldosterone leads to reduced sodium reabsorption in kidneys and less water retention
Reduced potassium secretion means meds can cause hyperkalaemia (raised potassium)

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13
Q

What happens to TSH, T3 and T4 in primary hyperthyroidism?

A

TSH- Low
T3 and T4- High

Thyroid behaves abnormally and produces excessive thyroid hormones
TSH suppressed by high T3 and T4, causing low TSH level

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14
Q

What happens to TSH, T3 and T4 in secondary hyperthyroidism?

A

TSH- High
T3 and T4- High

Pituitary behaves abnormally- Produces excessive TSH (eg: Pituitary adenoma)- Stimulates thyroid gland to produce excessive thyroid hormones

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15
Q

What happens to TSH, T3 and T4 in primary hypothyroidism?

A

TSH- High
T3 and T4- Low

Thyroid behaves abnormally and produces inadequate thyroid hormones- Negative feedback absent- Increased production of TSH

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16
Q

What happens to TSH, T3 and T4 in secondary hypoparathyroidism?

A

TSH- Low
T3 and T4- Low

Pituitary behaves abnormally and produces inadequate TSH (eg: After surgical removal of pituitary)
Under stimulation of thyroid gland and insufficient thyroid hormone

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17
Q

What are anti-thyroid peroxidase antibodies?

A

Anti-TPO
Antibodies against thyroid gland
Most relevant thyroid autoantibody in AI thyroid disease
Present in Grave’s disease and Hashimoto’s thyroiditis

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18
Q

What are Anti-thyroglobulin antibodies?

A

Anti-Tg
Antibodies against thyroglobulin
Can be present in normal individuals w/o thyroid pathology
Raised- Grave’s disease, Hashimoto’s thyroiditis, thyroid cancer

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19
Q

What are TSH receptor antibodies?

A

Autoantibodies that mimic TSH, bind to TSH receptor and stimulate thyroid hormone release
Cause Grave’s disease

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20
Q

Outline imaging associated with thyroid

A

US thyroid- Diagnose thyroid nodules and distinguish between cystic and solid nodules, guide biopsy of thyroid lesion
Radioisotope scans

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21
Q

Outline radioisotope scans of thyroid

A

Investigate hyperthyroidism and thyroid cancers- Radioactive iodine given orally/IV and travels to thyroid and taken up by cells
Iodine used by thyroid cells to produce thyroid hormones
More active thyroid cells- Faster radioactive iodine taken up
Gamma camera detects gamma rays- More gamma rays emitted from an area, more radioactive iodine taken up

Diffuse high uptake- Grave’s disease
Focal high uptake- Toxic multinodular goitre and adenomas
‘Cold’ areas (abnormally low uptake)- Can indicate thyroid cancers

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22
Q

What is thyrotoxicosis?

A

Effects of abnormal and excessive quantity of thyroid hormones in body

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23
Q

What is subclinical hyperthyroidism?

A

T3 and T4 normal, TSH supressed
May be absent or mild symptoms

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24
Q

What is Grave’s disease?

A

AI condition
TSH receptor antibodies cause primary hyperthyroidism
TSH receptor antibodies stimulate TSH receptors on thyroid
Most common cause hyperthyroidism

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25
Q

What is a Toxic multinodular goitre?

A

Plummer’s disease
Nodules develop on thyroid gland- Unregulated by thyroid axis and continuously produce excessive thyroid hormones
Most common in >50y
Nodules may be palpable within swollen thyroid gland

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26
Q

What is exophthalmos?

A

Proptosis
Bulging of eyes caused by Grave’s disease
Inflammation, swelling and hypertrophy of tissue behind eyeballs
Caused by TSH receptor antibodies

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27
Q

What is pretibial myxoedema?

A

Caused by deposits of glycosaminoglycans under skin on anterior aspect of leg
Gives skin discoloured/waxy/oedematous appearance
Specific to Grave’s disease- Reaction to TSH receptor antibodies

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28
Q

What is a goitre?

A

Neck lump caused by swelling of thyroid gland

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29
Q

What are the causes of hyperthyroidism?

A

Grave’s disease
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre

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30
Q

What are the causes of thyroiditis?

A

Often causes initial period of hyperthyroidism followed by hypothyroidism

De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug induced thyroiditis

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31
Q

Outline presentation of hyperthyroidism

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination

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32
Q

What are the specific features of Grave’s disease?

A

Specific features relate to presence of TSH receptor antibodies

Diffuse goitre (w/o nodules)
Grave’s eye disease- Including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)

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33
Q

What is a solitary toxic thyroid nodule?

A

Single abnormal thyroid nodule acts alone to release excessive thyroid hormone
Nodules usually benign adenomas
Treat- Surgical removal of nodule

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34
Q

Outline De Quervain’s thyroiditis

A

Condition causing temporary inflammation of thyroid gland
3 phases:
Thyrotoxicosis
Hypothyroidism
Return to normal

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35
Q

Outline the initial thyrotoxic phase of De Quervain’s thyroiditis

A

Excessive thyroid hormones
Thyroid swelling and tenderness
Flu-like illness (fever, aches, fatigue)
Raised inflammatory markers (CRP and ESR)

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36
Q

Outline management of De Quervain’s thyroiditis

A

NSAIDs- For pain and inflammation
BBs- For symptoms of hyperthyroidism
Levothyroxine- For symptoms of hyperthyroidism

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37
Q

What is a thyroid storm?

A

Rare presentation of hyperthyroidism
Thyrotoxic crisis
Severe- Fever, tachycardia, delirium
Can be life-threatening- Admit for monitoring
Treat as any other presentation of thyrotoxicosis- May also need fluid resuscitation, anti-arrhythmic meds and BBs

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38
Q

Outline management of hyperthyroidism

A

Carbimazole- 1st line anti-thyroid drug
Propylthiouracil- 2nd line anti-thyroid drug
Radioactive iodine treatment
Beta blockers
Surgery- Definitive

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39
Q

Outline the role of carbimazole in hyperthyroidism

A

1st line
Take for 12-18mths
Once normal TH level (within 4-8wks)- Continue on maintenance carbimazole and either:
- Titrate carbimazole to maintain normal levels
- Higher dose carbimazole blocks all production and levothyroxine added and titrated to effect

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40
Q

What is a risk of patients taking carbimazole?

A

Risk of developing acute pancreatitis
(severe epigastric pain radiating to back)

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41
Q

Outline the role of propylthiouracil in hyperthyroidism

A

2nd line
Used similar way to carbimazole
Small risk of severe liver reactions, including death- Carbimazole proferred

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42
Q

What is a side effect of both carbimazole and propylthiouracil?

A

Agranulocytosis with dangerously low WBCs
Vulnerable to severe infections
Sore throat= Key presentation- Need urgent FBC and aggressive treatment of infections

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43
Q

Outline radioactive treatment of hyperthyroidism

A

Drink single dose radioactive iodine
Thyroid gland takes this up, emitted radiation destroys proportion of thyroid cells- Decrease in thyroid hormone production
Remission can take 6mths, after which thyroid is often underactive- May require long term levothyroxine

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44
Q

What are the strict rules of radioactive iodine treatment of hyperthyroidism?

A

Women must not be pregnant/breastfeeding and must not get pregnant within 6mths treatment
Men must not father children within 4mths treatment
Limit contact with people after dose, particularly children and pregnant women

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45
Q

Outline the role of beta blockers in hyperthyroidism

A

Propanolol
Blocks adrenalin-related symptoms of hyperthyroidism
Control symptoms, don’t treat the condition
Particularly useful in thyroid storm

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46
Q

Outline surgery for hyperthyroidism

A

Definitive
Remove thyroid gland or toxic nodules
Requires life-long levothyroxine

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47
Q

List causes of primary hypothyroidism

A

Hashimoto’s thyroiditis
Iodine deficiency
Treatments for hyperthyroidism
Lithium
Amiodarone

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48
Q

What is Hashimoto’s thyroiditis?

A

Most common cause of hypothyroidism in ‘developed world’
AI condition
Causes inflammation of thyroid gland
Associated with anti-TPO antibodies and anti-Tg antibodies

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49
Q

What effect does iodine deficiency have on thyroid?

A

Causes primary hypothyroidism
Most common cause of hypothyroidism in ‘developing world’

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50
Q

What effect does lithium have on the thyroid?

A

Inhibits production of thyroid hormone
Can cause goitre and hypothyroidism

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51
Q

How does amiodarone affect the thyroid?

A

Interferes with thyroid production and metabolism
Can cause hypothyroidism or thyrotoxicosis

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52
Q

List causes of secondary hypothyroidism

A

Associated with lack of pituitary hormones, such as ACTH (hypopituitarism)

Tumours (eg: Pituitary adenoma)
Surgery to pituitary
Radiotherapy
Sheehan’s syndrome (major post-partum haemorrhage causes avascular necrosis of pituitary gland)
Trauma

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53
Q

Outline presentation of hypothyroidism

A

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

Iodine deficiency- Goitre
Hashimoto’s thyroiditis- Initially goitre, then atrophy of thyroid gland

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54
Q

Outline management of hypothyroidism

A

Oral levothyroxine (synthetic T4, metabolises to T3 in body)
Dose titrated based on TSH level, initially every 4wks

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55
Q

How is levothyroxine titrated?

A

Based on TSH level every 4wks
High TSH- Levothyroxine too low- Increase dose
Low TSH- Levothyroxine too high- Reduce dose

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56
Q

What is Cushing’s syndrome?

A

Features of prolonged high levels of glucocorticoids in body

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57
Q

What are the two groups of corticosteroid hormones?

A

Glucocorticoids- Cortisol (produced by adrenal glands)
Mineralocorticoids- Aldosterone

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58
Q

What is Cushing’s disease?

A

Pituitary adenoma secreting excessive adrenocorticotropic hormone (ACTH)- Stimulates excessive cortisol release from adrenal glands

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59
Q

List causes of Cushing’s syndrome

A

Cushing’s disease (Pituitary adenoma)
Adrenal adenoma (adrenal tumour secreting excess cortisol)
Paraneoplastic syndrome
Prolonged use exogenous corticosteroids (prednisolone/dexamethasone)

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60
Q

List features of Cushing’s syndrome

A

Round face (moon face)
Central obesity
Abdominal striae (stretch marks)
Enlarged fat pad on upper back (buffalo hump)
Proximal limb muscle wasting (difficulty standing from sitting position w/o using their arms)
Male pattern facial hair in women (hirsutism)
Easy bruising and poor skin healing

Hyperpigmentation of skin in patients with Cushing’s disease (due to high ACTH)

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61
Q

What are the metabolic effects of Cushing’s syndrome?

A

HTN
Cardiac hypertrophy
T2D
Dyslipidaemia (raised cholesterol and triglycerides)
Osteoporosis

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62
Q

What are the potential mental health effects of Cushing’s syndrome?

A

Anxiety
Depression
Insomnia
Rarely psychosis

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63
Q

What is paraneoplastic Cushing’s syndrome?

A

ACTH released from tumour somewhere other than pituitary gland (ectopic ACTH)
Small cell lung cancer most common
Ectopic ACTH stimulates excessive cortisol release from adrenal glands

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64
Q

Why does ACTH cause skin pigmentation?

A

Stimulates melanocytes in skin to produce melanin
Sign on Cushing’s disease or primary adrenal insufficiency

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65
Q

Outline treatment of Cushing’s syndrome

A

Trans-sphenoidal (through nose) removal of pituitary adenoma
Surgical removal of adrenal tumour
Surgical removal of tumour producing ectopic ACTH (small cell lung cancer)
Surgically remove both adrenal glands- Life long steroid replacement therapy

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66
Q

What is Nelson’s syndrome?

A

Development of ACTH-producing pituitary tumour after surgical removal of both adrenal glands due to lack of cortisol and negative feedback
Causes skin pigmentation, bitemporal hemianopia and lack of other pituitary hormones

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67
Q

What is the role of metyrapone?

A

Reduces production of cortisol in adrenals and occasionally used in treating Cushing’s

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68
Q

Outline dexamethasone suppression tests

A

Diagnose Cushing’s syndrome (don’t diagnose Cushing’s caused by exogenous steroids)
Normal response to dexamethasone- Suppressed cortisol
Lack of cortisol suppression in response to dexamethasone- Cushing’s syndrome

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69
Q

What is the effect of dexamethasone on the body?

A

Suppresses cortisol due to negative feedback

Causes negative feedback on hypothalamus- Reduces CRH output
Causes negative feedback on pituitary- Reduces ACTH output
Lower CRH and ACTH levels- Results in low cortisol output by adrenal glands

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70
Q

Outline low-dose overnight dexamethasone suppression test

A

Screening to exclude Cushing’s syndrome
1mg given at night, cortisol checked at 9am
Normal- Cortisol suppressed
Failure to suppress- Suggests Cushing’s syndrome- Further assessment required

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71
Q

Outline low-dose 48h dexamethasone suppression test

A

Used in suspected Cushing’s syndrome
0.5mg dexamethasone given every 6h for 8 doses- Start at 9am on first day
Check dose at 9am on day 1 (before 1st dose), and 9am day 3
Normal- Cortisol level day 3 suppressed
Failure to suppress cortisol- Cushing’s syndrome indicated- Further assessment required

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72
Q

Outline high-dose overnight dexamethasone suppression test

A

Same as low-dose test- Use 2mg per dose instead of 0.5mg
Higher dose is enough to suppress cortisol in Cushing’s syndrome caused by pituitary adenoma (Cushing’s disease)- But not when caused by adrenal adenoma or ectopic ACTH

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73
Q

What are the results of the low dose dexamethasone suppression test?

A

Normal- Low
Adrenal adenoma- Not suppressed
Pituitary adenoma- Not suppressed
Ectopic ACTH- Not suppressed

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74
Q

What are the results of the high dose dexamethasone suppression test?

A

Normal- Low
Adrenal adenoma- Not suppressed
Pituitary adenoma- Low
Ectopic ACTH- Not suppressed

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75
Q

What are the results of the ACTH dexamethasone suppression test?

A

Normal- Normal
Adrenal adenoma- Low
Pituitary adenoma- High
Ectopic ACTH- High

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76
Q

What is hyperaldosteronism?

A

High levels of aldosterone

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77
Q

What is Conn’s syndrome?

A

Adrenal adenoma producing too much aldosterone

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78
Q

What is the key presenting feature of hyperaldosteronism?

A

Present in 5-10% of patients with HTN

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79
Q

What are the non-specific symptoms of hyperaldosteronism?

A

HTN
Headaches
Muscle weakness
Fatigue

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80
Q

Outline primary hyperaldosteronism

A

Adrenal glands directly responsible for producing too much aldosteronism
Serum renin low as high BP suppressed it

Adrenals may produce too much aldosterone

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81
Q

Why may adrenals produce too much aldosterone in primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia- Most common
Adrenal adenoma- Secretes aldosterone (Conn’s syndrome)
Familial hyperaldosteronism (rare)

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82
Q

Outline secondary hyperaldosteronism

A

Caused by excessive renin stimulating release of excessive aldosterone
Excessive renin released due to disproportionately lower BP in kidneys

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83
Q

Why would excessive renin be released to cause secondary hyperaldosteronism?

A

Disproportionately low BP in kidneys:
Renal artery stenosis (usually due to atherosclerosis)
HF
Liver cirrhosis and ascites

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84
Q

How is renal artery stenosis confirmed?

A

Doppler US
CT angiogram
MRA

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85
Q

Outline investigations of hyperaldosteronism

A

Screening- Aldosterone-to-renin (ARR)
HTN
Hypokalaemia
Alkalosis
CT/MRI- Adrenal tumour or adrenal hyperplasia
Renal artery imaging- Renal artery stenosis (Doppler/CT angiogram/MRA)
Adrenal vein sampling

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86
Q

Outline aldosterone-to-renin ratio (ARR)

A

Primary hyperaldosteronism- High aldosterone, low renin
Secondary hyperaldosteronism- High aldosterone, high renin

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87
Q

Outline management of hyperaldosteronism

A

Eplerenone
Spironolactone
Surgical removal- Adrenal adenoma
Percutaneous renal artery angioplasty via femoral artery- Renal artery stenosis

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88
Q

What is the most common cause of secondary HTN?

A

Hyperaldosteronism

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89
Q

What is adrenal insufficiency?

A

Adrenal glands don’t produce enough steroid hormones (cortisol and aldosterone)

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90
Q

Outline primary adrenal insufficiency

A

Addison’s disease
Adrenal glands damaged- Reduced cortisol and aldosterone secretion
Autoimmune

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91
Q

Outline secondary adrenal insufficiency

A

Inadequate adrenocorticotropic hormone (ACTH) and lack of stimulation of adrenal glands- Low cortisol
Result of loss or damage to pituitary gland

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92
Q

List causes of secondary adrenal insufficiency

A

Tumours (eg: Pituitary adenoma)
Surgery to pituitary
Radiotherapy
Sheehan’s syndrome
Trauma

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93
Q

Outline tertiary adrenal insufficiency

A

Inadequate corticotropin-releasing hormone (CRH) release by hypothalamus
Usually result of taking long term oral steroids (for >3wks), causing suppression of hypothalamus
If exogenous steroids suddenly withdrawn- Hypothalamus doesn’t wake up fast enough- Steroids not adequately produced

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94
Q

Outline symptoms of adrenal insufficiency

A

Fatigue
Muscle weakness
Muscle cramps
Dizziness and fainting
Thirst and craving salt
Weight loss
Abdo pain
Depression
Reduced libido

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95
Q

Outline signs of adrenal insufficiency

A

Bronze hyperpigmentation- Particularly in creases- Caused by excessive ACTH stimulating melanocytes to produce melanin
Hypotension (particularly postural)

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96
Q

Outline investigations of adrenal insufficiency

A

*Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Raised creatinine and urea- Dehydration
Hypercalcaemia

Early morning cortisol may have a role- Often falsely normal

Short synacthen test

ACTH measured directly

Autoantibodies- In AI adrenal insufficiency

CT/MRI of adrenal glands
MRI of pituitary

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97
Q

Outline measurements of ACTH in adrenal insufficiency

A

Primary adrenal insufficiency- High ACTH- Pituitary producing lots ACTH w/o negative feedback in absence of cortisol

Secondary adrenal failure- ACTH low

98
Q

Which autoantibodies are present in AI adrenal insufficiency?

A

Adrenal cortex antibodies
21-hydroxylase antibodies

99
Q

Outline short Synacthen test

A

ACTH stimulation test
Give dose of synacthen in morning
Measure blood cortisol before then 30mins and 60mins after dose

Healthy adrenal glands- Cortisol should at least double

Failure to double:
Primary adrenal insufficiency (Addison’s disease)
Very sig. adrenal atrophy after prolonged absence ACTH in secondary adrenal insufficiency

100
Q

Outline management of adrenal insufficiency

A

Replace and titrate steroids
Hydrocortisone (glucocorticoid)- Replace cortisol
Fludrocortisone (mineralocorticoid)- Replace aldosterone
Give steroid card, ID tag and emergency letter
Double dose in acute illness

Train close contacts to give IM hydrocortisone in emergency

101
Q

How may a patient present in an adrenal crisis?

A

Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

May be initial presentation of adrenal insufficiency or triggered by infection/trauma/acute illness

102
Q

What is an adrenal crisis?

A

Addisonian crisis
Acute presentation of severe adrenal insufficiency
Absence of steroid hormones leads to life-threatening emergency

103
Q

Outline management of adrenal crisis

A

ABCDE
IM/IV hydrocortisone
IV fluids
Correct hypoglycaemia (eg: IV dextrose)
Careful monitoring of electrolytes and fluid balance

104
Q

What is type 1 diabetes?

A

Pancreas can’t produce adequate insulin
Cells of body can’t absorb glucose from blood
Causes hyperglycaemia
Cause unclear- Coxsackie B and enterovirus may trigger it

105
Q

What is the classic triad of hyperglycaemia?

A

Polyuria
Polydipsia
Weight loss

In T1D- May present with diabetic ketoacidosis

106
Q

What is normal levels of blood glucose between?

A

4.4-6.1 mmol/L

107
Q

Outline the role of insulin

A

Produced by beta cells in Islets of Langerhans in pancreas
Causes cells in body to absorb glucose from blood and causes muscle and liver cells to absorb glucose from blood and store as glycogen (glycogenesis)

108
Q

Outline role of glucagon

A

Produced by alpha cells in Islets of Langerhans in pancreas
Catabolic hormone (breakdown hormone)
Released in response to low blood sugar levels and stress- Works to increase blood sugar levels
Tells liver to breakdown stored glycogen and release into blood as glucose- Glycogenolysis
Tells liver to convert proteins and fats into glucose- Gluconeogenesis

109
Q

Outline ketogenesis

A

Occurs when insufficient glucose supply and glycogen stores exhausted- Prolonged fasting
Liver takes fatty acids and converts them to ketones

110
Q

Outline some of the features of ketones

A

Water-soluble fatty acids
Can cross blood-brain barrier and used by brain
Kidneys buffer ketones in healthy people
In T1D- Hyperglycaemic ketosis- Life-threatening metabolic acidosis- DKA

111
Q

How are ketones measured?

A

Urine dipstick test
In breath using ketone meter

112
Q

Outline pathophysiology of diabetic ketoacidosis

A

Consequence of inadequate insulin
W/o insulin- Body’s cells don’t recognise glucose
Liver produces ketones as fuel
Initially kidneys produce bicarbonate to counter ketone acids
Over time blood becomes acidotic

113
Q

List the most common scenarios for diabetic ketoacidosis to occur

A

Initial presentation of type 1 diabetes
Existing T1D who is unwell with eg: Infection
Existing T1D not adhering to insulin regime

114
Q

What are the 3 key features of diabetic ketoacidosis?

A

Ketoacidosis
Dehydration
Potassium imbalance

115
Q

Outline dehydration in DKA

A

Hyperglycaemia overwhelms kidneys, glucose leaks into urine
Urine draws out water by osmotic diuresis
Polyuria- Severe dehydration- Polydipsia

116
Q

Outline potassium imbalance in DKA

A

Insulin normally drives potassium into cells
W/o insulin- potassium not added and stored in cells
Serum potassium can be high/normal- Kidneys balance blood potassium with potassium excreted in urine
Total body potassium low
With treatment of insulin- Severe hypokalaemia very quickly- Fatal arrhythmias

117
Q

What does the pathophysiology of DKA lead to?

A

Hyperglycaemia
Dehydration
Ketosis
Metabolic acidosis (low bicarbonate)
Potassium imbalance

118
Q

List symptoms of DKA

A

Polyuria
Polydipsia
Nausea and vomiting
Acetone smell on breath
Dehydration
Weight loss
Hypotension
Altered consciousness

119
Q

How is DKA diagnosed?

A

Hyperglycaemia- >11mmol/L
Ketosis- Blood ketones >3mmol/L
Acidosis- pH <7.3

120
Q

Outline treatment of DKA

A

Fluid resuscitation first- Correct dehydration/electrolyte disturbance/acidosis
Follow with insulin infusion- Cells start taking up glucose and stop producing ketones

F- Fluids- IV fluid resuscitation with normal saline (1L in 1st h, then 1L every 2h)
I- Insulin- Fixed rate insulin infusion (Actrapid at 0.1U/kg/h)
G- Glucose- Closely monitor and add glucose infusion when <14mmol/L
P- Potassium- Add potassium to IV fluids and monitor closely
I- Infection- Treat
C- Chart fluid balance
K- Ketones- Monitor blood ketones, pH and bicarbonate

121
Q

What should the patient have before insulin and fluid infusions stopped in DKA management?

A

Ketosis and acidosis resolved
Eating and drinking
Started regular SC insulin

122
Q

What are the key complications of DKA treatments?

A

Hypoglycaemia
Hypokalaemia
Cerebral oedema
Pulmonary oedema- Secondary to fluid overload or ARDS

123
Q

What are the autoantibodies in T1D?

A

Anti-islet cell antibodies
Anti-GAD antibodies
Anti-insulin antibodies

124
Q

What is serum C-peptide a measure of?

A

Insulin production
Low with low insulin production
High with high insulin production

125
Q

Outline long-term management of T1D

A

SC insulin
Monitor dietary carbohydrate intake
Monitor blood sugar waking/each meal/before bed
Monitor and manage complications

126
Q

Outline basal-bolus regime of T1D management

A

Combination of:
Background, long-acting insulin injected once daily
Short-acting insulin injected 30mins before carbs

127
Q

Why should diabetics not inject insulin in the same spot?

A

Causes lipodystrophy
SC fat hardens- Insulin not absorbed properly

128
Q

Outline insulin pump use in T1D

A

Continuously infuse insulin at different rates to control blood sugars
Pushes insulin through cannula- Replaced every 2-3d- Insertion sites rotated to prevent lipodystrophy

129
Q

What are the advantages of insulin pumps?

A

Better blood glucose control
More flexibility with eating
Less injections

130
Q

What are the disadvantages of insulin pumps?

A

Difficulties learning to use pump
Having it attached at all times
Blockages in infusion set
Small risk of infection

131
Q

What are the different types of insulin pump?

A

Tethered- Replaceable infusion sets and insulin
Patch- Sit directly on skin- When run out of insulin, entire patch replaced

132
Q

What is the role of a pancreas transplant in T1D?

A

Implant donor pancreas to produce insulin
Original pancreas left in place to produce digestive enzymes
Reserved for patients with severe hypoglycaemic episodes and those also having kidney transplants

133
Q

What is the role of Islet transplantation in T1D?

A

Insert donor islet cells into patient’s liver
Produce insulin

134
Q

Outline monitoring of T1D

A

HbA1c- Every 3-6mths
Capillary blood glucose- Finger prick test- Immediate result
Flash glucose monitors
Continuous glucose monitors

135
Q

Outline HbA1c in T1D

A

Measures glycated Hb- How much glucose is attached to Hb molecule
Reflects average glucose level over previous 2-3mths
Measured every 3-6mths

136
Q

What are flash glucose monitors?

A

Sensor on skin that measures glucose level of interstitial fluid in SC tissue
5min lag behind blood glucose

137
Q

What are continuous blood glucose monitors?

A

Sensor on skin monitors level of glucose in interstitial fluid

138
Q

What is a closed loop system in T1D?

A

Artificial pancreas
Combination of continuous glucose monitor and insulin pump
Automatically adjust insulin based on glucose readings

139
Q

What are the short-term complications of T1D?

A

Hypoglycaemia
Hyperglycaemia (and DKA)

140
Q

How is hypoglycaemia managed?

A

Initially with rapid-acting glucose (sugary drink) then slower-acting carbs (toast)
Severe- IV dextrose and IM glucagon

141
Q

What are the symptoms of hypoglycaemia?

A

Hunger
Tremor
Sweating
Irritability
Dizziness
Pallor

Severe:
Reduced consciousness
Coma
Death

142
Q

What are the macrovascular complications of T1D?

A

Coronary artery disease
Peripheral ischaemia- Poor skin healing and diabetic foot ulcers
Stroke
HTN

143
Q

What are the microvascular complications of T1D?

A

Peripheral neuropathy
Retinopathy
Kidney disease- Glomerulosclerosis

144
Q

What are the infection-related complications of T1D?

A

UTIs
Pneumonia
Skin and soft tissue infections- Particularly feet
Fungal infections- Oral and vaginal candidiasis

145
Q

Why do complications of T1D occur?

A

Chronic high blood glucose levels cause damage to endothelial cells of blood vessels
Vessels leaky and unable to regenerate
High glucose causes immune system dysfunction and optimal environment for infectious organisms to thrive

146
Q

What is type 2 diabetes?

A

Combination of insulin resistance and reduced insulin production

147
Q

Outline pathology of T2D

A

Repeated exposure to glucose and insulin- Body resistant to effects of insulin
Pancreas becomes fatigued and damaged- Insulin output reduced
Chronic hyperglycaemia- Microvascular/macrovascular/infectious complications

148
Q

List the modifiable risk factors of T2D

A

Obesity
Sedentary lifestyle
High carb diet

149
Q

List non-modifiable risk factors of T2D

A

Older age
Ethnicity- Black African, South Asian
Family history

150
Q

Outline presentation of T2D

A

Tiredness
Polyuria and polydipsia
Unintentional weight loss
Opportunistic infections (oral thrush)
Slow wound healing
Glucose in urine
Acanthosis nigricans- Thickening and darkening of skin (velvety)- In neck/axilla/groin- Associated with insulin resistance

151
Q

What is pre-diabetes?

A

HbA1c 42-47mmol/L

152
Q

Outline diagnosis of T2D

A

HbA1c >48mmol/mol
Sample typically repeated after 1mth

153
Q

Outline management of T2D

A

Low-glycaemic index, high fibre diet
Exercise
Weight loss
Antidiabetic drugs
Monitoring and managing complications

154
Q

What are the treatment targets for T2D?

A

New T2D- 48mmol/mol
Patients on >1 antidiabetic meds- 53mmol/mol

Measure HbA1c every 3-6mths

155
Q

Outline medical management of T2D

A

1st line- Metformin

2nd line- Sulfonylurea, pioglitazone, DPP-4 inhibitor, SGLT-2 inhibitor

3rd line- Triple therapy with metformin and 2 of second line drugs or insulin therapy

If triple therapy fails and BMI >35kg/m2- GLP-1 mimetic (liraglutide)

156
Q

Outline metformin

A

Biguanide
Increases insulin sensitivity and decreases glucose production by liver
Does not cause weight gain or hypoglycaemia

157
Q

What are the SEs of metformin?

A

GI symptoms- Pain, nausea and diarrhoea
Lactic acidosis (secondary to AKI)

DOES NOT CAUSE Weight gain or hypoglycaemia

158
Q

List examples of SGLT-2 inhibitors

A

Empagliflozin, canagliflozin, dapagliflozin, ertugliflozin

159
Q

Outline SGLT-2 Inhibitors

A

Protein found in proximal tubules of kidneys- Acts to reabsorb glucose from urine back into blood- blocked by SGLT2 Inhibitor
Cause more glucose to be excreted in urine
Lowers HbA1c- Reduce BP, leads to weight loss and improves HF
Reduce risk of CVD

160
Q

List SEs of SGLT-2 inhibitors

A

Glycosuria
Increased urine output and frequency
Genital and UTIs
Weight loss
DKA
Lower-limb amputation may be more common in patients on canagliflozin
Fournier’s gangrene

Can cause hypoglycaemia if used with insulin or sulfonylureas

161
Q

Which SLGT-2 inhibitors are also licensed for HF?

A

Empagliflozin and dapagliflozin

162
Q

Which SGLT-2 inhibitors are also used for CKD?

A

Dapagliflozin

163
Q

What are the SEs of pioglitazone?

A

Weight gain
HF
Increased risk bone fractures
Small increase in risk of bladder cancer

164
Q

What is the role of pioglitazone in T2D?

A

Increases insulin sensitivity and decreases liver production of glucose

Doesn’t typically cause hypoglycaemia

165
Q

What are the SEs of sulfonylureas?

A

Weight gain
Hypoglycaemia

166
Q

What is an example of a sulfonylurea and how does it work?

A

Gliclazide
Stimulate insulin release from pancreas

167
Q

What is a hyperosmolar hyperglycaemic state?

A

Rare but potentially fatal complication of T2D
Hyperosmolality (water loss leads to very conc. blood)
Hyperglycaemia
Absence of ketones (distinguishes it from ketoacidosis)

MEDICAL EMERGENCY

168
Q

How does hyperosmolar hyperglycaemic state present?

A

Polyuria
Polydipsia
Weight loss
Dehydration
Tachycardia
Hypotension
Confusion

169
Q

How is hyperosmolar hyperglycaemic state managed?

A

High mortality
Involve seniors early
IV fluids and careful monitoring

170
Q

What are incretins?

A

Hormones produced by GI tract
Secreted in response to large meals to reduce blood sugar:

Increasing insulin secretion
Inhibiting glucose production
Slowing absorption by GI tract

Eg: GLP-1
Inhibited by DPP-4

171
Q

What are the SEs of DPP-4 inhibitors?

A

Headaches
Low risk of acute pancreatitis

172
Q

How do DPP-4 inhibitors treat T2D?

A

Block DPP-4
Allow increased incretin activity

DO NOT cause hypoglycaemia

173
Q

Give examples of DPP-4 inhibitors

A

Sitagliptin and alogliptin

174
Q

What are the SEs of GLP-1 mimetics?

A

Reduced appetite
Weight loss
GI symptoms- Discomfort, nausea and diarrhoea

175
Q

How do GLP-1 mimetics treat diabetes?

A

Given as SC injections
Exenatide and liraglutide

Liraglutide also used for weight loss in non-diabetic obese patients

176
Q

Outline use of NovoRapid

A

Rapid-acting insulin
Works after 10mins and lasts 4h

177
Q

Outline use of Actrapid

A

Short-acting insulin
Works after 30mins and lasts 8h

178
Q

Outline use of Humulin I

A

Intermediate-acting insulins
Start working in 1h and last 16h

178
Q

Outline use of combinations insulins

A

Contain rapid-acting and intermediate-acting insulin
Humalog or Novomix

179
Q

Outline use of Levemir and Lantus

A

Long-acting insulin
Start working in 1h and last 24h

179
Q

What are the key complications of T2D?

A

Infections (periodontitis/thrush/infected ulcers)
Diabetic retinopathy
Peripheral neuropathy
Autonomic neuropathy
CKD
Diabetic foot
Gastroparesis (slow emptying of stomach)
Hyperosmolar hyperglycaemic state

180
Q

List the 4 options for neuropathic pain in T2D

A

Amitriptyline- TCA
Duloxetine- SNRI antidepressant
Gabapentin- Anticonvulsant
Pregabalin- Anticonvulsant

181
Q

What is the 1st line treatment of HTN in patients with T2D?

A

ACE-Is

182
Q

What is the management of HTN in T2D with CKD?

A

ACR >3mg/mmol- ACE-Is
ACR >30mg/mmol- SGLT-2 inhibitor

183
Q

What is a treatment of erectile dysfunction?

A

Phosphodiesterase-5 inhibitor- Sildenafil or tadalafil

184
Q

Which medications may be used for gastroparesis?

A

Prokinetic drugs- Domperidone or metoclopramide
Slow emptying of stomach
Use with caution due to cardiac SEs

185
Q

What is acromegaly?

A

Result of excessive GH

186
Q

Outline pathophysiology of acromegaly

A

GH produced by anterior pituitary
Most common cause unregulated GH- Pituitary adenoma- Can be microscopic/significantly sized tumour- Compresses local structures
Rarely secondary to cancer (lung or pancreatic)- Secretes ectopic GHRH or GH- Paraneoplastic syndrome

187
Q

Outline association between pituitary adenoma and optic chiasm

A

Optic chiasm just above pituitary gland
Optic nerve from eyes cross over to opposite side of head before travelling to visual cortex in occipital lobe
Pituitary tumour can compress this- Bitemporal hemianopia- Loss of outer half of vision in both eyes

188
Q

Outline presentation of space-occupying pituitary tumour

A

Headaches
Visual field defect (bitemporal hemianopia)

189
Q

Outline presentation of excess GH

A

Prominent forehead and brow (frontal bossing)
Coarse, sweaty skin
Large nose
Large tongue (macroglossia)
Large hands and feet
Large protruding jaw (prognathism)

190
Q

What are the additional features of acromegaly?

A

Hypertrophic heart
HTN
T2D
Carpal tunnel syndrome
Arthritis
Colorectal cancer

191
Q

Outline investigations of acromegaly

A

IGF-1 tested on blood sample- Indicates GH level and raised in acromegaly- Unreliable as fluctuates through the day
GH suppression test- 75g glucose drink with GH tested at baseline and 2h following drink- Failure to suppress GH indicates acromegaly
MRI pituitary- Pituitary adenoma

192
Q

Outline management of pituitary tumour causing acromegaly

A

Trans-sphenoidal surgery (through nose and sphenoid bone)
Radiotherapy
Pegvisomant- GH receptor antagonist daily by SC injection
Somatostatin analogues (octreotide)- Block GH release
Dopamine agonists (bromocriptine)- Block GH release

193
Q

What is somatostatin?

A

GH-inhibiting hormone
Normally secreted by brain, GI tract and pancreas
Blocks GH release from pituitary gland
Can be used in acromegaly

194
Q

How does dopamine work in acromegaly?

A

Inhibitory effect on GH release
Weaker than somatostatin

195
Q

Outline basic pathology of hyperparathyroidism

A

4 parathyroid glands in corners of thyroid gland
Chief cells in parathyroid glands produce PTH in response to hypocalcaemia

196
Q

How does PTH raise blood calcium?

A

Increasing osteoclast activity in bones (reabsorb calcium from bones)
Increasing calcium reabsorption in kidneys (less calcium lost in urine)
Increasing Vit D activity- Increased calcium absorption in intestines

197
Q

How does Vit D affect calcium levels in the blood?

A

Raises blood calcium levels
Increases calcium absorption from intestines
PTH acts on Vit D to convert it to its active form

198
Q

What are the symptoms of hypercalcaemia?

A

Stone, bones, groans, moans

Kidney stones
Painful bones
Abdo groans (constipation, nausea and vomiting)
Psychiatric moans (fatigue, depression, psychosis)

199
Q

Outline primary hyperparathyroidism causes, PTH and calcium

A

Cause- Tumour
PTH- High
Calcium- High

200
Q

Outline secondary hyperparathyroidism causes, PTH and calcium

A

Cause- Low Vit D or CKD
PTH- High
Calcium- Low/normal

201
Q

Outline tertiary hyperparathyroidism causes, PTH and calcium

A

Cause- Hyperplasia
PTH- High
Calcium- High

202
Q

Outline primary hyperparathyroidism

A

Caused by uncontrolled PTH production by tumour of parathyroid glands
Leads to raised calcium
Treat- Remove tumour surgically

203
Q

Outline secondary hyperparathyroidism

A

Insufficient Vit D or CKD reduces calcium absorption from intestines/kidneys/bones
Results in hypocalcaemia
Parathyroid glands react to low serum calcium by excreting more PTH
Serum calcium- Low/normal
PTH- High
Treat- Correct Vit D deficiency or CKD

204
Q

Outline tertiary hyperparathyroidism

A

Secondary hyperparathyroidism continues for extended period after which underlying cause is treated
Hyperplasia of parathyroid glands occurs as a adapt to producing higher baseline level of PTH
An absence of previous pathology- High PTH level leads to inappropriately high absorption of calcium in intestines/kidneys/bones- Hypercalcaemia
Treat- Surgically removing part of parathyroid tissue to return PTH to normal level

205
Q

What is Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)?

A

Increased release of ADH from posterior pituitary
Increases water reabsorption from urine, diluting blood and leading to hyponatraemia

206
Q

Outline pathophysiology of SIADH

A

ADH (vasopressin) produced in hypothalamus and secreted by posterior pituitary gland
ADH stimulates water reabsorption from collecting ducts in kidneys

207
Q

What are the 2 potential sources of too much ADH?

A

Increased secretion by posterior pituitary
Ectopic ADH- Most commonly small cell lung cancer

208
Q

What does excessive ADH result in?

A

Increased water reabsorption in collecting ducts, diluting blood
Excess water reduces sodium conc. (hyponatraemia)
SIADH results in euvolaemic hyponatraemia
Urine becomes more conc. as kidneys excrete less water

209
Q

What happens to urine osmolality and sodium in SIADH?

A

High urine osmolality
High urine sodium

210
Q

Outline presentation of SIADH

A

Hyponatraemia
May be asymptomatic
Headache
Fatigue
Muscle aches and cramps
Confusion

Severe hyponatraemia- Seizures, reduced consciousness

211
Q

List causes of SIADH

A

Post-operative after major surgery
Lung infection- Atypical pneumonia and lung abscess
Brain pathologies- Head injury, stroke, ICH, meningitis
Meds- SSRIs, carbamazepine
Malignancy- Small cell lung cancer
HIV

212
Q

What are the clinical features of SIADH?

A

Euvolaemia
Hyponatraemia
Low serum osmolality
High urine sodium
High urine osmolality

213
Q

What are the other causes of hyponatraemia in SIADH needing to be excluded?

A

Short synacthen test- Exclude adrenal insufficiency
No history of diuretic use
No diarrhoea/vomiting/burns/fistula/excessive sweating
No excessive water intake
No CKD or AKI
No HF or liver disease

214
Q

What is primary polydipsia?

A

Excessive water consumption with no underlying cause
Dilutes blood and urine
Causes euvolaemic hyponatraemia
Low sodium and urine osmolality

215
Q

Outline investigations of SIADH

A

Chest XRAY to assess pneumonia, lung abscess and lung cancer
Check for recent SSRI/chest infection/recent major surgery
No clear cause- Look for malignancy- CT thorax/abdomen/pelvis and MRI head

216
Q

Outline management of SIADH

A

Admit if symptomatic/severe
Treat underlying cause
Fluid restriction- Limit to 750-1000ml/d
Vasopressin receptor antagonists (eg: Tolvaptan)- Block ADH receptors- Can cause rapid rise in sodium

Correct sodium slowly- Prevent osmotic demyelination- Sodium conc. shouldn’t change >10mmol/L in 24h

217
Q

What is osmotic demyelination syndrome?

A

Central pontine myelinolysis (CPM)
Complication of long-term severe hyponatraemia (<120mmol/L) being treated too quickly

218
Q

Outline pathophysiology of Osmotic demyelination syndrome

A

Severe hyponatraemia treated too quickly
Blood sodium conc. drops- Water moves by osmosis across BBB into brain- Brain swells
Brain adapts by reducing solutes in brain cells so water balanced across BBB and brain doesn’t become oedematous
1st phase- Due to electrolyte imbalance- Presents as encephalopathic and confused, headache, vomiting, seizures- Symptoms resolve before onset of 2nd phase
2nd phase- Due to demyelination of neurones, particularly in pons- Occurs a few days after rapid correction of sodium- Present with spastic quadriparesis, pseudobulbar palsy and cognitive/behavioural changes- Significant risk of death

219
Q

Outline treatment of osmotic demyelination syndrome

A

Prevention essential
Treatment supportive once demyelination occurs
Some patients make clinical improvement, but most have neurological deficit

220
Q

Why does diabetes insipidus occur?

A

Lack of ADH (cranial diabetes insipidus)
Lack of response to ADH (nephrogenic diabetes insipidus)

221
Q

What is the role of ADH?

A

Stimulates water reabsorption from collecting ducts in kidneys
Makes urine more concentrated

222
Q

Where is ADH produced?

A

In the hypothalamus
Secreted by posterior pituitary

223
Q

Outline nephrogenic diabetes insipidus

A

Collecting ducts of kidneys don’t respond to ADH

224
Q

What are the causes of nephrogenic diabetes insipidus?

A

Idiopathic
Meds- Lithium
Genetic mutation in ADH receptor gene (X-linked recessive)
Hypercalcaemia
Hypokalaemia
PKD

225
Q

What is cranial diabetes insipidus?

A

Hypothalamus doesn’t produce ADH

226
Q

What are the causes of cranial diabetes insipidus?

A

Idiopathic
Brain tumour
Brain injury
Brain surgery
Brain infections (meningitis/encephalitis)
Genetic mutation in ADH gene (autosomal dominant)
Wolfram syndrome

227
Q

What is Wolfram syndrome?

A

Cause of cranial diabetes insipidus
Genetic condition
Causes optic atrophy, deafness and diabetes mellitus

228
Q

Outline presentation of diabetes insipidus

A

Polyuria
Polydipsia
Dehydration
Postural hypotension

229
Q

Outline investigations of diabetes insipidus

A

Low urine osmolality (lots of water diluting urine)
High/normal serum osmolality (water loss may be balanced by increased intake)
>3L on 24h urine collection

Water deprivation test- Diagnosis

230
Q

What is the water deprivation test?

A

Diagnose diabetes insipidus
Desmopressin stimulation test

Patient avoids all fluids for up to 8h before test- Urine osmolality measured
If urine osmolality low- Synthetic ADH (desmopressin) given- Urine osmolality measured over 2-4h following

High urine osmolality after water deprivation rules out diabetes insipidus
Primary polydipsia- Water deprivation causes high urine osmolality- No desmopressin given
Cranial diabetes insipidus- Lacks ADH- Urine osmolality remains low- Give desmopressin- Urine osmolality high
Nephrogenic diabetes insipidus- Patient unable to respond to ADH- Urine osmolality low before and after desmopressin

231
Q

Outline management of diabetes insipidus

A

Treat underlying cause
Cranial diabetes insipidus- Desmopressin (synthetic ADH)- Monitor serum sodium (risk of hyponatraemia)
Nephrogenic diabetes insipidus- Drink plenty, high-dose desmopressin, thiazide diuretics, NSAIDs

232
Q

What is phaeochromocytoma?

A

Tumour of adrenal glands that secretes unregulated and excessive amounts catecholamines (adrenaline)

233
Q

Outline pathophysiology of phaeochromocytoma

A

Adrenaline produced by chromaffin cells in medulla of adrenal glands
Phaeochromocytoma- Tumour of chromaffin cells- Secretes unregulated and excessive amounts of adrenaline

234
Q

What is adrenaline?

A

Catecholamine hormone- Stimulates sympathetic nervous system
Responsible for fight/flight response

235
Q

Which conditions are phaeochromocytomas more common in?

A

Multiple endocrine neoplasia type 2 (MEN 2)
Neurofibromatosis type 1
Von Hippel-Lindau disease

236
Q

What is the 10% rule associated with phaeochromocytomas?

A

10% bilateral
10% cancerous
10% outside adrenal gland

237
Q

Outline presentation of phaeochromocytoma

A

Intermittent symptoms- Depends on when tumour is secreting adrenaline
Anxiety
Sweating
Headache
Tremor
Palpitations
HTN
Tachycardia

238
Q

Outline investigations of phaeochromocytoma

A

Initial:
Plasma free metanephrines
24h urine catecholamines
CT/MRI- Tumour
Genetic testing

239
Q

Outline management of phaeochromocytoma

A

Alpha blockers (eg: Phenoxybenzamine or doxazosin)
Beta blockers- Only when established on alpha blocker
Surgical removal

Final Year (14 decks)

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