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Endocrinology Flashcards

1
Q

Describe the aetiology of hyperthyroidism

A

Grave’s disease
Nodular thyroid disease
Iodine excess
Exogenous thyroid hormone
Thyroid carcinoma

Secondary causes:
-TSH secreting pituitary tumour
-Thyroid hormone resistance

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2
Q

Describe the pathophysiology of Grave’s disease

A

Autoimmune thyroiditis caused by the production of TSH receptor stimulating antibodies

These stimulate the thyroid to produce more T3/T4

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3
Q

Describe the presentation of hyperthyroidism

A

Heat intolerance and sweating

Hyperactivity/irritability/altered mood

Palpitations

Weight loss with increased appetite

Fatigue and weakness

Fine tremor

Muscle weakness and wasting

Pretibial myxoedema

Diffuse, symmetrical goitre

Hyperreflexia

Monorrhagia

AF

Palmar erythema

Sinus tachycardia

Eyelid retraction, peri-orbital oedema, proptosis (opthalmopathy)

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4
Q

Give the presentation of thyrotoxic storm

A

Marked fever

Seizures

Vomiting

Diarrhoea

Jaundice

Death

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5
Q

Give the management of thyrotoxic storm

A

Propranolol

Corticosteroids

Carbimazole (anti-thyroid)

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6
Q

Give the investigations for hyperthyroidism

A

TFTs:
-Primary: low TSH, high T3/T4
-Secondary: high TSH, high T3/T4

TSH receptor antibodies - diagnostic for Grave’s

Radionucleide scan (Tc-99m) - diffuse widespread uptake in Grave’s

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7
Q

Describe the management of hyperthyroidism

A

Propranolol - for symptoms

Carbimazole/propylthiouracil - anti-thyroid - decrease output of T3/T4

Block and replace: high dose carbimazole + levothyroxine

Subtotal thyroidectomy: once euthyroid

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8
Q

Describe the management of hyperthyroidism in pregnancy

A

First trimester - propylthiouracil
Second and third trimester - carbimazole

Monitor fetal heartbeat (carbimazole may have effect on fetus)

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9
Q

Describe the aetiology of a toxic multinodular goitre

A

Common in older women and associated with increased iodine uptake. Strong link with amiodarone (contains iodine)

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10
Q

Describe thyroiditis

A

Autoimmune destruction of the thyroid resulting in the release of the thyroxine within

Causes a brief thyrotoxicosis, followed by a transient period of hypothyroidism

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11
Q

Describe De Quervain’s Thyroiditis

A

AKA subacute thyroiditis

4 phases:
1. Painful goitre, hyperthyroidism
2. Euthyroid
3. Hypothyroidism
4. Normal thyroid structure and function

Investigation: reduced uptake of I-131

Management: self-limiting, aspirin and NSAIDs for pain

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12
Q

Give two causes of pituitary space occupying lesions

A

Prolactinoma

Craniopharyngioma

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13
Q

Describe the pathophysiology of hyperprolactinaemia

A

Prolactin mainly controlled by tonic inhibition by hypothalamic dopamine.

Prolactin acts to induce lactation but also has inhibitory effect on GnRH secretion and the action of LH.

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14
Q

Describe the presentation of hyperprolactinoma

A

Galactorrhoea

Oligo/amenorrhoea

Reduced libido

Gynaecomastia

Subfertility

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15
Q

Give the investigations for prolactinoma

A

Serum prolactin raised

MRI head - pituitary prolactinoma

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16
Q

Describe the management of prolactinoma

A

1st line: dopamine agonist (e.g. cabergoline/bromocriptine) - DO NOT USE ROPINIROLE, this is D2 selective and therefore mostly effective in Parkinson’s

2nd line: trans-sphenoidal surgery

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17
Q

Describe the pathophysiology of acromegaly

A

Excess growth hormone, usually due to a GH secreting pituitary adenoma

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18
Q

Describe the presentation of acromegaly

A

Prominent supraorbital ridge

Large tongue

Spade-like hands and feet

Tall stature

Menstrual irregularities

Galactorrhoea

Visual field defects (due to pituitary adenoma compressing optic chiasm)

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19
Q

Describe the investigations for acromegaly

A

Insulin-like growth factor-1 (IGF-1) levels + OGTT (if GH not suppressed by glucose then diagnose acromegaly)

MRI head

Pituitary function testing

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20
Q

Describe the management of acromegaly

A

1st line: trans-sphenoidal surgery + radiotherapy

2nd line: somatostatin analogue (e.g. octreotide) +/- dopamine agonist

3rd line: GH antagonist (e.g. pegvisomant)

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21
Q

Why is OGTT used in the diagnosis of acromegaly?

A

GH is suppressed by hyperglycaemia, but would not be suppressed by hyperglycaemia in acromegaly due to the underlying pituitary adenoma

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22
Q

Why are dopamine agonists used in the management of acromegaly?

A

Dopamine inhibits GH secretion

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23
Q

Describe Cushing’s syndrome

A

Clinical state of increased free-circulating glucocorticoid

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24
Q

Describe the aetiology of Cushing’s syndrome

A

Exogenous use (most common)

ACTH-producing pituitary tumour (Cushing’s disease)

Adrenal adenoma

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25
Q

Describe the presentation of Cushing’s syndrome

A

“Moon face”

Buffalo hump

Central obesity

Proximal muscle wasting

Abdominal striae

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26
Q

Describe the pathophysiology of Cushing’s disease

A

ACTH hypersecretion from the anterior pituitary resulting in excess glucocorticoid (cortisol) production (usually due to pituitary tumour)

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27
Q

Describe the presentation of Cushing’s disease

A

Cushing’s syndrome:
-“Moon face”
-Buffalo hump
-Central obesity
-Proximal muscle wasting
-Abdominal striae

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28
Q

Describe the investigations for Cushing’s disease

A

Aim to demonstrate inappropriate cortisol secretion which is not suppressed by exogenous steroids

48 hour low-dose dexamethasone suppression test (gold standard)

24 hour urinary cortisol/ACTH levels

Adrenal/pituitary MRI

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29
Q

Describe the management of Cushing’s disease

A

TSS - MUST CONTROL CORTISOL FIRST (usually with metyrapone)

Bilateral adrenalectomy (if treatment resistant)

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30
Q

How does metyrapone work?

A

It is an 11-beta-hydroxylase inhibitor

11-beta-hydroxylase normally acts to convert 11-deoxycortisol to cortisol

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31
Q

Define Nelson’s syndrome

A

Formation of an ACTH-secreting pituitary adenoma following bilateral adrenalectomy

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32
Q

Describe the management of Nelson’s syndrome

A

TSS with prior cortisol control

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33
Q

Describe the pathophysiology of pituitary apoplexy

A

Rapid loss of pituitary function due to a bleed into the gland or an impaired vascular supply

Vascular impairment may occur as a result of a rapidly expanding tumour or a massive haemorrhage in childbirth (Sheehan’s syndrome)

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34
Q

Describe the presentation and management of pituitary apoplexy

A

Severe headache, double-vision and visual field restriction

Management: hormone replacement

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35
Q

Describe empty-sella syndrome

A

All or most of the sella is devoid of pituitary tissue

Gland is normally flattened against the fossa wall and has normal function

Usually diagnosed incidentally but may be a sign of raised ICP

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36
Q

Describe the aetiology of primary hyperparathyroidism

A

Solitary adenoma

Parathyroid hyperplasia

Carcinoma

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37
Q

Describe the investigations for primary hyperparathyroidism

A

Raised serum calcium

Low serum phosphate

Raised PTH (may be inappropriately normal)

Hand and skull XR - osteolysis in phalanges and “pepper-pot” skull

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38
Q

Describe the presentation of hyperparathyroidism

A

Classically elderly lady with an unquenchable thirst and a raised PTH

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39
Q

Describe the management of primary hyperparathyroidism

A

Total parathyroidectomy - GOLD STANDARD

Cinacalcet (calcium mimetic) v- reduced PTH secretion

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40
Q

Why does primary hyperparathyroidism present with unquenchable thirst?

A

Causes a reversible nephrogenic diabetes insipidus due to degredation of aquaporin-2 channels, leading to dehydration

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41
Q

Describe the pathophysiology of secondary hyperparathyroidism

A

Physiological compensatory hypertrophy of the parathyroid glands in response to hypocalcaemia

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42
Q

Describe the aetiology of secondary hyperparathyroidism

A

CKD and vit. D deficiency

Failing kidneys do not convert enough Vit. D to it’s active metabolite or excrete enough phosphate

This results in the formation of insoluble CaPO4 - removing calcium from the circulation

PTH therefore rises but calcium remains low

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43
Q

Describe the management of secondary hyperparathyroidism

A

Treat underlying cause, reduce dietary phosphate, Vit. D supplementation

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44
Q

Describe the pathophysiology of tertiary hyperparathyroidism

A

Autonomous increased release of PTH whilst in a hypercalcaemic state following longstanding secondary hyperparathyroidism - common in CKD

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45
Q

Describe the management of tertiary hyperpararthyroidism

A

Parathyroidectomy

Would see raised calcium and phosphate on bloods

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46
Q

Describe the pathophysiology of hungry bone syndrome

A

High pre-op PTH provides constant osteoclast stimulation

This creates a constant hypercalcaemic state due to bone demineralisation

Parathyroidectomy causes sudden drop in PTH and osteoclast activity subsequently diminishes quickly.

Bones rapidly remineralise with rapid depletion of serum calcium phosphate stores

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47
Q

Describe the management of hungry bone syndrome

A

Calcium supplementation and PTH replacement

48
Q

Describe the pathophysiology and management of primary hypoparathyroidism

A

Decreased PTH secretion resulting in a low calcium and high phosphate

Management: alfacalcidol

49
Q

Describe the pathophysiology and presentation of pseudo-hypoparathyroidism

A

End-organ resistance to PTH due to mutation in PTH-G gene

Presentation:
-Low IQ
-Short stature
-Shortened 4th/5th metacarpals
-Low calcium, high phosphate

50
Q

Describe the investigations and anagement for pseudo-hypoparathyroidism

A

cAMP and phosphate levels following PTH infusion - in hypoparathyroidism they would both increase

Management: calcium/vit. D supplementation

51
Q

Describe the hormones produced by the adrenal cortex

A

Steroid hormones! (mineralocorticoids, glucocorticoids, androgens)

Zona glomerulosa: aldosterone (m)
Zona fasciculata: cortisol (g)
Zona reticularis: androstenedione

52
Q

Describe the hormones produced by the adrenal medulla

A

Adrenaline!

53
Q

Describe the pathophysiology of Addison’s disease

A

Primary hypoadrenalism with destruction of the entire adrenal cortex, resulting in reduced steroid hormone production

Reduced cortisol drives increased CRH and ACTH

54
Q

Describe the aetiology of Addison’s disease

A

Autoimmune

55
Q

Describe the presentation of Addison’s disease

A

Addisonian adrenal destruction works from outside in:

First: zona glomerulosa - low aldosterone - hypotension, hyponatraemia, hyperkalaemia, salt craving

Second: zona fasciculata - low cortisol - tiredness, immunocompromised, hypermigmented, abdo pain

Third: zona reticularis - low androgen - reduced libido, loss of pubic/axillary hair

56
Q

Describe the investigations for Addison’s disease

A

Short synacthen test - stimulates adrenal glands to produce cortisol and tests how they respond

57
Q

Describe the management of Addison’s disease

A

Steroid replacement: PO hydrocortisone

In extreme exercise or if ill, double dose!

58
Q

Describe the pathophysiology of congenital adrenal hyperplasia

A

Autosomal recessive deficiency of 21-hydroxylase (normally in cortisol synthesis pathway) causing an increased testosterone

Leads to reduced cortisol and subsequently increased ACTH - hyperstimulating the adrenals and causing hyperplasia

59
Q

Describe the presentation of congenital adrenal hyperplasia

A

Sexual ambiguity

Adrenal failure

Hirsutism

60
Q

Describe the investigations for congenital adrenal hyperplasia

A

Adrenocortical profile before and after ACTH administration

61
Q

Describe the management of congenital adrenal hyperplasia

A

Steroid replacement

62
Q

Describe the pathophysiology of primary hyperaldosteronism

A

5-10% of cases of HTN

Disorder of the adrenal cortex leading to excessive aldosterone production, commonly due to bilateral adrenal hyperplasia

Causes sodium retention, hypertension and hypokalaemia

63
Q

Describe the pathophysiology of Conn’s syndrome

A

Adrenal adenoma causing a primary hyperaldosteronism - presents as HTN +/- hypokalaemia

64
Q

Describe the pathophysiology of secondary hyperaldosteronism

A

Renal artery stenosis causing renin excess

65
Q

Describe the investigations for primary hyperaldosteronism

A

Aldosterone:renin - shows high aldosterone and low renin

CT abdo

Adrenal vein sampling

66
Q

Describe the management of primary hyperaldosteronism

A

Adenoma –> surgical resection

Hyperplasia –> aldosterone receptor blocker (e.g. spironolactone). If not tolerated may use CCB to control HTN (do not use ACEi, ARB or beta blocker)

67
Q

How does renal artery stenosis cause increased renin secretion?

A

Causes reduced renal perfusion, stimulating juxtaglomerular cells to release renin.

They are “tricked” into thinking the BP is low

68
Q

Why can ACEi and ARBs not be used in the management of hyperaldosteronism?

A

Block constriction of efferent glomerular vessels - those with renal artery stenosis rely on this to maintain GFR.

69
Q

Describe the diagnostic criteria for DKA

A

Glucose > 11
pH < 7.3
Bicarb < 15
Ketones > 3 (or urine ketones ++)

70
Q

Describe the causes of DKA

A

Infection

MI

Missed insulin doses

71
Q

Describe the presentation of DKA

A

Abdo pain

Thirst, polyuria, dehydration

Kussmaul respiration - fast, deep breaths in an attempt to blow off CO2

Ketotic breath (pear drops)

72
Q

Describe the management of DKA

A

FLUIDS - normal saline regime. If hypotensive give 500ml boluses first

INSULIN - fixed rate IV insulin 0.1 units/kg/hr, plus K+!

73
Q

Define the resolution criteria for DKA

A

pH > 7.3

Ketones < 0.6 AND bicarb > 15

Should resolve within 24 hours

74
Q

Describe the aetiology of thyroid storm

A

Stress

Infection

Surgery

75
Q

Describe the presentation of thyroid storm

A

Rapid deterioration in hyperthyroidism

Hyperpyrexia
Severe tachycardia
Restlessness
Cardiac failure
Liver dysfunction

76
Q

Describe the management of thyroid storm

A

IV propranolol - controls HR and failure

Carbimazole - anti-thyroid
Potassium iodide
Corticosteroids (e.g. hydrocortisone)

77
Q

Describe thyrotoxic cardiomyopathy

A

Ischaemic changes on ECG

Resolves completely once the patient is euthyroid

78
Q

Describe the pathophysiology of Addisonian crisis

A

Severe hypotension and dehydration caused by illness or trauma

Hypovolaemic shock
Vomiting
Fever
Abdo pain

79
Q

Give the management of Addisonian crisis

A

IV hydrocortisone

IV fluids

80
Q

Describe myxoedema

A

Accumulation of mucopolysaccharides in the SC tissue

81
Q

Describe myxoedema coma

A

Seen in hypothyroidism

Extreme version of myxoedema in which patients have hypothermia, cardiac failure, hypoventilation, hyponatraemia, hypoglycaemia, psychosis

82
Q

Describe the management of myxoedema coma

A

IV levothyroxine

IV hydrocortisone

83
Q

Describe the aetiology of hypercalcaemia

A

Most commonly in palliative care!

Hyperparathyroidism or bone mets

84
Q

Describe the presentation of hypercalcaemia

A

“Stones, bones, groans and psychic moans”:
Renal stones
Bone pain
Abdo pain
Depression

Polydipsia, polyuria, dehydration, pancreatitis

85
Q

Describe the management of hypercalcaemia

A

IV fluids and bisphosphonates

Treat underlying cause

86
Q

Give 1 important side effect of carbimazole

A

Agranulocytosis

87
Q

What is the minimum HbA1c for diagnosis of T2DM

A

48

88
Q

Give 1 condition which cause gynaecomastia

A

Goserelin - GnRH agonist used in the management of prostate cancer

89
Q

What is the most common thyroid cancer?

A

Papillary (70%) - seen in young females and has excellent prognosis

90
Q

What is the second most common thyroid cancer?

A

Follicular

91
Q

What is the management of thyroid cancer?

A

total thyroidectomy
followed by radioiodine (I-131) to kill residual cells
yearly thyroglobulin levels to detect early recurrent disease

92
Q

Which drug may cause psychosis?

A

Steroids

93
Q

Describe the aetiology of hypothyroidism

A

Primary:
-Autoimmune - e.g. Hashimoto’s thyroiditis, atrophic thyroiditis
-Congenital
-Iodine deficiency

Secondary:
-Hypopituitarism
-Post-surgery

94
Q

Describe the epidemiology of hypothyroidism

A

Much more common in women

Mean age of onset = 60

Classically middle aged women

95
Q

Which hormone is released by the hypothalamus which forms a part of the hypothalamic-pituitary-axis?

A

Thyrotropin releasing hormone

96
Q

Which hormone is released by the anterior pituitary which forms a part of the hypothalamic-pituitary-axis?

A

Thyroid stimulating hormone

97
Q

Which hormone is released by the thyroid which forms a part of the hypothalamic-pituitary-axis?

A

T3 and T4

(only 25% of circulating \T3 is produced by the thyroid, the rest is produced from T4 in peripheral tissues)

98
Q

Describe the pathophysiology of primary hypothyroidism

A

Thyroid unable to produce sufficient T3/T4 despite a high TSH

99
Q

Describe the pathophysiology of secondary hypothyroidism

A

Insufficient TSH produced by the anterior pituitary, so the thyroid produced less T3/T4

OR

Thyroid has been removed/damaged during surgery

100
Q

Describe the pathophysiology of atrophic thyroiditis

A

T-cell mediated auto-reactive cytotoxicity to follicular cells

DOES NOT PRODUCE A GOITRE!

101
Q

Describe the pathophysiology of Hashimoto’s thyroiditis

A

Autoimmune hypothyroidism

Thyroid attacked by T-cells resulting in lymphocyte infiltration and fibrosis - resulting in a GOITRE

Very high levels of thyroid peroxidase antibodies, resulting in insufficient iodide for T3/T4 production

May be initial transient hyperthyroidism followed by period of hypothyroidism

102
Q

Describe the pathophysiology of post-partum thyroiditis

A

May involve hypo- or hyper-thyroid pathology

Usually seen transiently after pregnancy

B-HCG acts on TSH receptors, including to induce the production of more T3/T4, resulting in hyperthyroidism

Usually self-limiting

103
Q

Describe myxoedema

A

Skin and tissue disorder associated with hypothyroidism

Skin and subcutaneous tissue thickening due to accumulation of mucopolysaccharides in the subcutaneous tissue, resulting in a “coarse” appearance

104
Q

Describe the presentation of hypothyroidism

A

Puffy eyes

Dry skin

Overweight

Dry, brittle, unmanageable hair

Thin hair, loss of eyebrows

Deep voice

Goitre (Hashimoto’s)

Pretibial myxoedema

Cold intolerance

Fatigue/tiredness/malaise/headache

Poor memory/slow thoughts/depression

Bradycardia/peripheral oedema/hypertension/decreased exercise tolerance

Poor libido/infertility/oligomenorrhoea/menorrhagia

105
Q

Describe the TFT results in primary hypothyroidism

A

High TSH

Low T4

106
Q

Describe the TFT results in subclinical hypothyroidism

A

High TSH

Normal T4

107
Q

Describe the TFT results in secondary hypothyroidism

A

Normal/low TSH

Low T4

108
Q

Describe the TFT results in primary hyperthyroidism

A

Low TSH

High T4

109
Q

Describe the TFT results in subclinical hyperthyroidism

A

Low TSH

Normal T4

110
Q

Describe the confirmatory investigation for autoimmune hypothyroidism

A

TPO antibodies

(also do FBC due to risk of B12 deficiency of autoimmune cause, e.g. pernicious anaemia, atrophic gastritis)

111
Q

Give the management of hypothyroidism

A

Levothyroxine - oral T4 supplementation

112
Q

Give the management of hypothyroidism in pregnancy

A

Levothyroxine - if already taking then increase dose by 25%

Low TSH in mother can lead to cognitive impairment in the child

113
Q

Describe the management of depression in hypothyroidism

A

Levothyroxine! Depression will usually resolve within a few weeks of starting levothyroxine

114
Q

What ABG findings are seen in Addisonian crisis?

A

hyperkalaemic metabolic acidosis

115
Q

Describe the TFT findings in sick euthyroid syndrome

A

In sick euthyroid syndrome it is often said that everything (TSH, thyroxine and T3) is low. In the majority of cases however the TSH level is within the normal range (inappropriately normal given the low thyroxine and T3).

Sick euthyroid is where there are decreased values but no underlying pathology - associated with stress (e.g. acute illness)

116
Q

What can result in a falsely high HbA1c?

A

Splenectomy

Finals (11 decks)

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