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Endocrinology Flashcards

1
Q

At what eGFR is metformin contraindicated?

A

<30

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2
Q

What is phaeochromocytoma?

A

A rare catecholamine secreting tumour of the adrenal medulla

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3
Q

What are the two parts of the adrenal gland?

A

Outer cortex

Inner adrenal medulla

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4
Q

What does the adrenal cortex produce?

A

Mineralocorticoids - e.g. aldosterone
Glucocorticoids - mainly cortisol
Androgens - mainly dehydroepiandrosterone (DHEA) and testosterone

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5
Q

Where is ACTH made/secreted from?

A

Anterior pituitary gland

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6
Q

What does the adrenal medulla produce?

A

Catecholamines - e.g. adrenaline, noradrenaline and dopamine.

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7
Q

Describe the HPA axis

A

Hypothalamus produces CRH
CRH activates the anterior pituitary
Ant. pituitary releases ACTH which stimulates the cortex of the medulla

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8
Q

What is Cushing’s syndrome?

A

This is a disorder in which the body produces too much cortisol (glucocorticoid)

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9
Q

What is more common, exogenous or endogenous Cushing’s?

A

Exogenous is far more common

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10
Q

What is an exogenous cause of Cushing’s?

A

Steroid therapy e.g. for eczema, asthma, RA etc

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11
Q

How can we split endogenous causes of Cushing’s?

A

ACTH dependent

ACTH independent

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12
Q

What are some ACTH dependent causes of Cushing’s?

A

Cushing’s disease (80%) - pituitary tumour secreting ACTH resulting in adrenal hyperplasia
Ectopic ACTH production (5-10%) - e.g. small cell lung cancer

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13
Q

What are some ACTH independent causes of Cushing’s syndrome?

A

Adrenal adenoma
Adrenal carcinoma
Carney complex
Micronodular adrenal dysplasia

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14
Q

What are signs/symptoms of Cushing’s syndrome?

A 
Central obesity (but thin arms/legs)
Round moon-like face
Fat deposition above collar bone, behind neck
Thin skin
Muscle weakness
High BP
High blood sugar
Reduced libido/ED
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15
Q

What are some causes of pseudo-Cushing’s?

A

Alcohol excess

Severe depression

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16
Q

How can we differentiate pseudo-cushing’s from cushing’s?

A

Insulin stress test

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17
Q

What might you see on an ABG in Cushing’s?

A

A hypokalaemic metabolic alkalosis

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18
Q

What two tests do we commonly do to diagnose Cushing’s?

A

Overnight dexamethasone suppression test (most sensitive)

24 hr urinary free cortisol

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19
Q

Dexamethasone suppression results interpretation

A

Cortisol not suppressed by low dose - Cushing’s syndrome

Suppressed by high dose - Cushing’s disease (pituitary adenoma)
Not suppressed by low or high dose - ectopic ACTH syndrome likely
High dose suppresses ACTH but not cortisol - adrenal tumour

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20
Q

What is primary adrenal failure?

A

Atrophy/destruction of the adrenal gland

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21
Q

What is secondary adrenal failure?

A

Inadequate ACTH production

Most commonly from acute steroid withdrawal

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22
Q

Symptoms/features of primary adrenal failure?

A 
Lethargy
Weakness
Anorexia
Nausea + vomiting
Weight loss
Hyperpigmentation (particularly palmar creases)
Loss of pubic hair
Hypotension (hypovolaemic shock is commonly how acute adrenal insufficiency presents)
Hypoglycaemia
Hyponatraemia
Hyperkalaemia
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23
Q

Is ACTH high or low in primary adrenal failure?

A

High

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24
Q

What is the common cause of primary adrenal failure?

A

Addison’s disease - autoimmune destruction of the adrenal glands

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25
Q

What is reduced in adrenal failure?

A

Cortisol (and aldosterone)

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26
Q

How can we temporarily lower cortisol before surgery/other curative treatment for cushing’s syndrome?

A

Metyrapone (inhib. cortisol synth.) or ketoconazole (p450 inhibition)

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27
Q

What is Addison’s disease associated with?

A

Vitiligo
Premature ovarian failure
Hypothyroidism
Female gender

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28
Q

What is the mechanism of pathology in secondary adrenal failure?

A

Chronic steroid use lowers ACTH levels
This causes adrenal cortex atrophy
If suddenly stopped can provoke adrenal failure

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29
Q

How do we investigate adrenal failure?

A

Short synacthen test (measure cortisol, give them ACTH and then measure cortisol again)
Can also measure adrenal autoantibidoies (e.g. anti-21-hydroxylase)

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30
Q

How do we manage adrenal failure?

A

Chronic
Hydrocortisone (20mg/day), double during infection
Can give fludrocortisone as well but only in primary adrenal failure (because then mineralocorticoids are affected as well)

Acute
Medical emergency - resus + hydrocortisone
Address precipitating factor (e.g. infection)

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31
Q

What is congenital adrenal hyperplasia?

A

A group of autosomal recessive disorders that affect adrenal steroid biosynthesis

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32
Q

Is ACTH high or low in congenital adrenal hyperplasia?

A

ACTH is high in response to low cortisol levels

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33
Q

What can high ACTH cause in female infants?

A

Adrenal androgens that may virilise them

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34
Q

What deficiencies cause congenital adrenal hyperplasia?

A

21-hydroxylase (90%)
11-beta hydroxylase (5%)
17-hydroxylase (v. rare)

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35
Q

Features of congenital adrenal hyperplasia?

A

Virilization of female genitalia
Precocious puberty in males
Salt losing crisis

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36
Q

Treatment of CAH?

A

Dexamethasone (I think)

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37
Q

What is Conn’s syndrome and what does it cause?

A

Benign adrenal adenoma causing primary hyperaldosteronism

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38
Q

Features of hyperaldosteronism

A

HTN
Hypokalaemia (muscle weakness)
Alkalosis

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39
Q

How to diagnose hyperaldosteronism?

A

Aldosterone/reniin ratio (should show high aldosterone levels alongside low renin levels - due to negative feedback from sodium retention by aldosterone)
CT

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40
Q

How do we treat hyperladosteronism?

A 
Surgical removal
Aldosterone antagonist (e.g. spironolactone)
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41
Q

What are features of phaeochromocytoma?

A 
Usually episodic, brought on by exercise etc.)
HTN (90%)
Headaches
Palpitations
Sweating
Anxiety
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42
Q

How do we test for phaeochromocytoma?

A

24 hour urinary collection of metanephrines (metabolites of catecholamines)
MRI

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43
Q

Treatment of phaeochromocytoma?

A

Initial:
Alpha blockade - phenoxybenzamine
Beta blockade - propanolol

Definitive:
Adrenalectomy

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44
Q

What is Addisonian crisis?

A

A severe adrenal insufficiency that is life threatening

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45
Q

What causes Addisonian crisis?

A

Sepsis/surgery exacerbating the chronic insufficiency from Addison’s/hypopituitarism
Adrenal haemorrhage (e.g. Waterhouse-Friderichsen syndrome)
Steroid withdrawal

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46
Q

How do we manage addisonian crisis?

A

Hydrocortisone (100mg im/iv), then continue 6 hourly till patient is stable
1 litre normal saline infused over 30-60 mins (or with dextrose)
Oral replacement after 24 hours, reduced to maintenance after 3 days

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47
Q

What are features of addisonian crisis?

A 
Sudden penetrating pain in legs/lower back/abdomen
Confusion/psychosis, slurred speech
Severe lethargy
Convulsions
Fever
Hyperkalaemia
Hypercalcaemia
Hypot./hypon./hypogly.
Syncope
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48
Q

Control of thyroid hormone secretion

A

Hypothalamus produces thyrotropin-releasing hormone (TRH)
TRH stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH)
TSH stimulates the thyroid to release thyroxine (T4) and triiodothyronine (T3)

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49
Q

What do T3/T4 do?

A

They act on a wide variety of tissues helping the regulation of energy sources, protein synthesis and also affects their sensitivity to other hormones

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50
Q

Which is active, T3 or T4?

A

T3. T4 is converted peripherally into T3 which is 4x more potent.
T3 is less tightly bound than T4 to plasma proteins

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51
Q

How do we classify hypothyroidism?

A

Primary - problem with the thyroid itself
Secondary - problem with the pituitary gland
Congenital

52
Q

What are causes of primary hypothyroidism?

A 
Hashimoto's thyroiditis (most common)
Subacute thyroiditis (De Quervain's)
Iodine deficiency
Drug therapy (e.g. lithium, carbimazole, amiodarone)
53
Q

What are causes of secondary hypothyroidism?

A

Pituitary failure
Down’s
Turner’s
Coeliac’s

54
Q

What are features of hypothyroidism?

A 
Weight gain
Lethargy
Cold intolerance
Dry, cold skin
Constipation
Menorrhagia
Decreased deep tendon reflexes
55
Q

What is hashimoto’s thyroiditis?

A

Autoimmune disease causing hypothyroidism, it is the most common cause of hypothyroidism

56
Q

Features of hashimoto’s thyroiditis

A

Associated with T1DM, Addison’s/pernicious anaemia
Can cause transient thyrotoxicosis in the acute phase
5-10 times more common in women

57
Q

What is de Quervain’s thyroiditis?

A

Hypothyroidism that is usually triggered by a viral infection, it presents with a painful goitre/fever, and it causes a raised ESR

58
Q

What is Riedel’s thyroiditis?

A

When fibrous tissue replaces the normal thyroid parenchyma

It causes a painless goitre

59
Q

What are the TSH and free T4 levels in Hashimoto’s thyroiditis?

A

High TSH

Low T4

60
Q

What is the TSH and T4 in secondary hypothyroidism?

A

Both are low

61
Q

What would you see in TSH/T4 if compliance with thyroxine was bad?

A

High TSH
Normal T4

(Patient with poor compliance may just be taking thyroxine in the days before their blood test)

62
Q

Which autoantibodies should be tested for in thyroid disorders?

A

Anti-thyroid peroxidase (anti-TPO)
TSH receptor antibodies
Thyroglobulin antibodies

TSH receptor antibodies are almost always present in Grave’s disease
Anti-TPO antibodies are almost always present in Hashimoto’s

63
Q

What is subclinical hypothyroidism?

A

Where TSH is high and T4 is normal, basically they are on their way to developing hypothyroidism but still have normal thyroxine

64
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (25mcg if cardiac disease/over 50 as well, 50-100mcg otherwise)

65
Q

Levothyroxine management of hypothyroid

A

Test thyroid function 8-12 weeks after levothyroxine change
Normal TSH of 0.5-2.5
If pregnant, levothyroxine should be increased by 25-50mcg

66
Q

What are side effects of thyroxine?

A

Reduced bone mineral density
AF
Worsening of angina
Hyperthyroid

67
Q

Symptoms of thyrotoxicosis?

A 
Weight loss
Heat intolerance
Palpitations (tachycardia)
Diarrhoea
Oligomenorrhoea
Anxiety
Tremor
68
Q

What are causes of thyrotoxicosis?

A

Graves’ disease
Toxic nodular goitre
Acute phase of de Quervain’s thyroiditis/Hashimoto’s
Amiodarone therapy

69
Q

What do you see on investigation in thyrotoxicosis?

A

TSH down

T3/T4 up

70
Q

What are features of graves’ disease not present in other causes of thyrotoxicosis?

A

Exophthalmos
Ophthalmoplegia
Pretibial myxoedema
Thyroid acropachy

71
Q

What is myxoedema?

A

A dermatological change commonly seen in severe hypothyroidism. Mucopolysaccharides are deposited in the dermis resulting in swelling of the area

72
Q

What is pretibial myxoedema?

A

Myxoedema of the lower limb, seen in Graves’ disease

73
Q

What is the pathophysiology of thyroid eye disease?

A

Caused by an autoimmune response against an autoantigen (maybe TSH receptor?) causing retro-orbital inflammation

74
Q

How can you prevent thyroid eye disease?

A

Smoking prevention

Radioiodine treatment can increase the inflammatory symptoms of thyroid eye disease

75
Q

What is exophthalmos?

A

Bulging of the eye anteriorly (usually bilaterally in Graves’) due to abnormal connective tissue deposition in the orbit/extraocular muscles

76
Q

How do we treat thyroid eye disease?

A

Topical lubricants
Steroids
Radiotherapy
Surgery

77
Q

What is ophthalmoplegia?

A

Paralysis of the muscles within the eye/surrounding the eye

78
Q

What are the features of thyroid eye disease?

A

Exophthalmos
Conjunctival oedema
Optic disc swelling
Ophthalmoplegia

79
Q

What is the treatment of Graves’ disease?

A

Anti-thyroid drugs:
Carbimazole
Radioiodine treatment (can make thyroid eye disease worse)

80
Q

What are the two ways you can give carbimazole in Graves’?

A

Anti-thyroid drug titration

Block and replace

81
Q

What is the concerning side-effect of carbimazole therapy?

A

Agranulocytosis

82
Q

What is thyroid storm?

A

A rare, life-threatening complication of thyrotoxicosis

83
Q

What causes thyroid storm?

A 
Usually has a precipitating event:
Surgery
Trauma
Infection
Acute iodine overload (e.g. from CT contrast)
84
Q

Clinical features of thyroid storm?

A 
Fever >38.5
Tachycardia
Confusion/agitation
Nausea and vomiting
HTN
Heart failure
Abnormal liver function (jaundice?)
85
Q

How do we manage thyroid storm?

A

Paracetamol
Treat precipitating event
Beta blockers (IV propanolol)
Propylthiouracil/methimazole (anti-thyroid drugs)
Dexamethasone (blocks T4 conversion to T3)

86
Q

What are the parathyroid glands?

A

Four tiny glands located in the neck that control the body’s calcium levels
They do this via secretion of parathyroid hormone

87
Q

How does PTH affect calcium?

A

3 ways:
Stimulates osteoblasts (and osteoclasts indirectly) to break down and release calcium
Stimulates GI calcium absorption by activating vitamin D
Promotes calcium conservation at the kidineys

88
Q

What does PTH do to phosphate levels?

A

PTH is the major regulator of serum phosphate concentrations via the kidney. It inhibits its reabsorption and thus lowers the levels of phosphate

89
Q

What are the features of hypercalcaemia?

A

‘bones, stones, abdominal groans and psychic moans’:

Polydipsia, polyuria
Peptic ulceration/constipation/pancreatitis
Renal stones
Depression
HTN
90
Q

What are the findings in hyperparathyroidism investigations?

A

Raised calcium
Low phosphate
PTH may be raised
Pepperpot skull is characteristic on x-ray

91
Q

Primary vs secondary hyperparathyroidism?

A

Primary:
Proliferation of chief cells in the parathyroid
Secondary:
Renal disease resulting in calcium loss/vit. D deficiency can result in compensation from the parathyroid (hypertrophy to synthesise more PTH)

92
Q

Treatment of primary hyperparathyroidism?

A

Total parathyroidectomy

Medical: Cinacalcet

93
Q

What is the main cause of primary hyperparathyroidism?

A

80% are caused by a parathyroid adenoma

94
Q

What is an adenoma?

A

A benign proliferation of glandular tissue

95
Q

Primary hypoparathyroidism

A

Decreased PTH secretion
Can be caused by things like thyroid surgery
You get a low calcium and high phosphate

96
Q

What are the symptoms of hypoparathyroidism?

A 
Symptoms of hypocalcaemia:
Tetany (muscle twitching/cramping/spasm)
Perioral paraesthesia
Trousseau's sign (carpal spasm)
Chvostek's sign (tapping over parotid causes facial muscles to twitch)
ECG: prolonged QT interval
Chronic: depression/cataracts
97
Q

What is pseudohypoparathyroidism?

A

Where the target cells are insensitive to PTH
This is due to an abnormality in a G protein
You get low calcium, high phosphate and high PTH

98
Q

How do we treat hypoparathyroidism?

A

Alfacalcidol

99
Q

What does the anterior pituitary produce?

A 
ACTH
Growth hormone
Luteinising hormone and FSH
Prolactin
TSH
100
Q

What does the posterior pituitary store and release (originally produced in hypothalamus)?

A

ADH (vasopressin)

Oxytocin

101
Q

What does the intermediate pituitary gland produce?

A

Melanocyte-stimulating hormone

102
Q

What is acromegaly

A

A condition caused by an excess of growth hormone secondary to a pituitary adenoma in 95% of cases

103
Q

What are the features of acromegaly

A 
Coarse facial appearance
Spade like hands
Large shoe size
Large tongue
Prognathism (outward jaw)
Excess sweating/oily skin
Pituitary tumour features (headache, bitemporal hemianopia)
Raised prolactin
104
Q

What are complications of acromegaly

A

HTN
Diabetes
Cardiomyopathy
Colorectal cancer

105
Q

How do we investigate acromegaly

A

Serum IGF-1 levels + OGTT

In normal patients growth hormone is suppressed to <2, there’s no suppression in acromegaly

106
Q

How do we manage acromegaly?

A

Trans-sphenoidal surgery is first line

Dopamine agonists (bromocriptine)

Somatostatin analogue (directly inhibits growth hormone release) - octreotide

107
Q

What is a prolactinoma?

A

A tumour of the pituitary gland which produces high levels of prolactin

108
Q

Features of hyperprolactinaemia

A

Infertility
Decreased sex drive
Bone loss

Women:
Vaginal dryness
Irregular periods
Production of milk when not pregnant/nursing

Men:
ED
Breast enlargement
Decreased muscle mass/body hair

109
Q

How to diagnose hyperprolactinaemia?

A

Blood test
Thyroid tests too (rule out hypothyroidism as cause)
Pregnancy test

MRI head for prolactinoma

110
Q

Treatment for hyperprolactinaemia

A

Surgery for tumour
Bromocriptine and cabergoline reduce prolactin production
Radiation

111
Q

Causes of high prolactin

A 
Prolactinoma
Hypothyroidism
Chest wall injuries/shingles
Chronic liver/kidney disease
Drugs
112
Q

What causes hypopituitarism?

A 
Tumours in or near the pituitary gland
Radiation treatment for a tumour
Chemo
Brain surgery
Traumatic bain injury
TB/meningitis
113
Q

Symptoms of hypopituitarism?

A 
Stomach pain, decreased appetite, nausea and vomiting, constipation
Excessive thirst/urination
Fatigue/weakness
Anaemia
Headache/dizziness
114
Q

How do we treat hypopituitarism?

A

Replacement of the missing hormones

Surgery to remove the tumour

115
Q

What type of adenoma causes hypopituitarism?

A

Macroadenomas

116
Q

How do we classify pituitary tumours?

A

By size:
Microadenoma - <1cm in diameter
Macroadenoma >1cm in diameter

Hormone status:
e.g. prolactinoma

117
Q

What type of hemianopia can we get in pituitary adenomas with mass effect?

A

Bitemporal hemianopia due to compression of the optic chiasm

118
Q

How do you investigate pituitary tumours?

A

Pituitary blood profile (prolactin, TFTs, ACTH, GH and FSH/LH)
Visual field testing
MRI brain with contrast

119
Q

What is diabetes insipidus?

A

A disorder characterised by lack of ADH/or insensitivity to ADH

120
Q

What are causes of cranial DI?

A

Idiopathic
Head injury
Pituitary surgery
Haemochromatosis

121
Q

What are causes of nephrogenic DI?

A

Genetic (vasopressin receptor affected - aquaporin 2 channel)
Tubulo-interstitial disease - obstruction/pyelonephritis, sickle-cell

122
Q

What are features of DI?

A

Polyuria

Polydipsia

123
Q

What is the difference between cranial and nephrogenic DI?

A

Deficiency to produce ADH (cranial)

Insensitivity to ADH (nephro)

124
Q

What are investigation findings in DI?

A

Urine osmolality of >700 excludes DI

Water deprivation test

125
Q

How do we treat DI?

A

Thiazides, low salt/protein diet (nephrogenic)

Desmopressin (cranial)

126
Q

What is Nelson’s syndrome?

A

This is where, say you removed the adrenal gland, that you then get zero negative feedback to the pituitary. It keeps producing ACTH and hypertrophies.

Symptoms include discolouration of skin, visual disturbance, headache

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