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Endocrinology Flashcards

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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
Describe the presentation of Cushing's syndrome
"Moon face" Buffalo hump Central obesity Proximal muscle wasting Abdominal striae
26
Describe the pathophysiology of Cushing's disease
ACTH hypersecretion from the anterior pituitary resulting in excess glucocorticoid (cortisol) production (usually due to pituitary tumour)
27
Describe the presentation of Cushing's disease
Cushing's syndrome: -"Moon face" -Buffalo hump -Central obesity -Proximal muscle wasting -Abdominal striae
28
Describe the investigations for Cushing's disease
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
29
Describe the management of Cushing's disease
TSS - MUST CONTROL CORTISOL FIRST (usually with metyrapone) Bilateral adrenalectomy (if treatment resistant)
30
How does metyrapone work?
It is an 11-beta-hydroxylase inhibitor 11-beta-hydroxylase normally acts to convert 11-deoxycortisol to cortisol
31
Define Nelson's syndrome
Formation of an ACTH-secreting pituitary adenoma following bilateral adrenalectomy
32
Describe the management of Nelson's syndrome
TSS with prior cortisol control
33
Describe the pathophysiology of pituitary apoplexy
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)
34
Describe the presentation and management of pituitary apoplexy
Severe headache, double-vision and visual field restriction Management: hormone replacement
35
Describe empty-sella syndrome
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
36
Describe the aetiology of primary hyperparathyroidism
Solitary adenoma Parathyroid hyperplasia Carcinoma
37
Describe the investigations for primary hyperparathyroidism
Raised serum calcium Low serum phosphate Raised PTH (may be inappropriately normal) Hand and skull XR - osteolysis in phalanges and "pepper-pot" skull
38
Describe the presentation of hyperparathyroidism
Classically elderly lady with an unquenchable thirst and a raised PTH
39
Describe the management of primary hyperparathyroidism
Total parathyroidectomy - GOLD STANDARD Cinacalcet (calcium mimetic) v- reduced PTH secretion
40
Why does primary hyperparathyroidism present with unquenchable thirst?
Causes a reversible nephrogenic diabetes insipidus due to degredation of aquaporin-2 channels, leading to dehydration
41
Describe the pathophysiology of secondary hyperparathyroidism
Physiological compensatory hypertrophy of the parathyroid glands in response to hypocalcaemia
42
Describe the aetiology of secondary hyperparathyroidism
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
43
Describe the management of secondary hyperparathyroidism
Treat underlying cause, reduce dietary phosphate, Vit. D supplementation
44
Describe the pathophysiology of tertiary hyperparathyroidism
Autonomous increased release of PTH whilst in a hypercalcaemic state following longstanding secondary hyperparathyroidism - common in CKD
45
Describe the management of tertiary hyperpararthyroidism
Parathyroidectomy Would see raised calcium and phosphate on bloods
46
Describe the pathophysiology of hungry bone syndrome
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
47
Describe the management of hungry bone syndrome
Calcium supplementation and PTH replacement
48
Describe the pathophysiology and management of primary hypoparathyroidism
Decreased PTH secretion resulting in a low calcium and high phosphate Management: alfacalcidol
49
Describe the pathophysiology and presentation of pseudo-hypoparathyroidism
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
Describe the investigations and anagement for pseudo-hypoparathyroidism
cAMP and phosphate levels following PTH infusion - in hypoparathyroidism they would both increase Management: calcium/vit. D supplementation
51
Describe the hormones produced by the adrenal cortex
Steroid hormones! (mineralocorticoids, glucocorticoids, androgens) Zona glomerulosa: aldosterone (m) Zona fasciculata: cortisol (g) Zona reticularis: androstenedione
52
Describe the hormones produced by the adrenal medulla
Adrenaline!
53
Describe the pathophysiology of Addison's disease
Primary hypoadrenalism with destruction of the entire adrenal cortex, resulting in reduced steroid hormone production Reduced cortisol drives increased CRH and ACTH
54
Describe the aetiology of Addison's disease
Autoimmune
55
Describe the presentation of Addison's disease
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
Describe the investigations for Addison's disease
Short synacthen test - stimulates adrenal glands to produce cortisol and tests how they respond
57
Describe the management of Addison's disease
Steroid replacement: PO hydrocortisone In extreme exercise or if ill, double dose!
58
Describe the pathophysiology of congenital adrenal hyperplasia
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
Describe the presentation of congenital adrenal hyperplasia
Sexual ambiguity Adrenal failure Hirsutism
60
Describe the investigations for congenital adrenal hyperplasia
Adrenocortical profile before and after ACTH administration
61
Describe the management of congenital adrenal hyperplasia
Steroid replacement
62
Describe the pathophysiology of primary hyperaldosteronism
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
Describe the pathophysiology of Conn's syndrome
Adrenal adenoma causing a primary hyperaldosteronism - presents as HTN +/- hypokalaemia
64
Describe the pathophysiology of secondary hyperaldosteronism
Renal artery stenosis causing renin excess
65
Describe the investigations for primary hyperaldosteronism
Aldosterone:renin - shows high aldosterone and low renin CT abdo Adrenal vein sampling
66
Describe the management of primary hyperaldosteronism
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
How does renal artery stenosis cause increased renin secretion?
Causes reduced renal perfusion, stimulating juxtaglomerular cells to release renin. They are "tricked" into thinking the BP is low
68
Why can ACEi and ARBs not be used in the management of hyperaldosteronism?
Block constriction of efferent glomerular vessels - those with renal artery stenosis rely on this to maintain GFR.
69
Describe the diagnostic criteria for DKA
Glucose > 11 pH < 7.3 Bicarb < 15 Ketones > 3 (or urine ketones ++)
70
Describe the causes of DKA
Infection MI Missed insulin doses
71
Describe the presentation of DKA
Abdo pain Thirst, polyuria, dehydration Kussmaul respiration - fast, deep breaths in an attempt to blow off CO2 Ketotic breath (pear drops)
72
Describe the management of DKA
FLUIDS - normal saline regime. If hypotensive give 500ml boluses first INSULIN - fixed rate IV insulin 0.1 units/kg/hr, plus K+!
73
Define the resolution criteria for DKA
pH > 7.3 Ketones < 0.6 AND bicarb > 15 Should resolve within 24 hours
74
Describe the aetiology of thyroid storm
Stress Infection Surgery
75
Describe the presentation of thyroid storm
Rapid deterioration in hyperthyroidism Hyperpyrexia Severe tachycardia Restlessness Cardiac failure Liver dysfunction
76
Describe the management of thyroid storm
IV propranolol - controls HR and failure Carbimazole - anti-thyroid Potassium iodide Corticosteroids (e.g. hydrocortisone)
77
Describe thyrotoxic cardiomyopathy
Ischaemic changes on ECG Resolves completely once the patient is euthyroid
78
Describe the pathophysiology of Addisonian crisis
Severe hypotension and dehydration caused by illness or trauma Hypovolaemic shock Vomiting Fever Abdo pain
79
Give the management of Addisonian crisis
IV hydrocortisone IV fluids
80
Describe myxoedema
Accumulation of mucopolysaccharides in the SC tissue
81
Describe myxoedema coma
Seen in hypothyroidism Extreme version of myxoedema in which patients have hypothermia, cardiac failure, hypoventilation, hyponatraemia, hypoglycaemia, psychosis
82
Describe the management of myxoedema coma
IV levothyroxine IV hydrocortisone
83
Describe the aetiology of hypercalcaemia
Most commonly in palliative care! Hyperparathyroidism or bone mets
84
Describe the presentation of hypercalcaemia
"Stones, bones, groans and psychic moans": Renal stones Bone pain Abdo pain Depression Polydipsia, polyuria, dehydration, pancreatitis
85
Describe the management of hypercalcaemia
IV fluids and bisphosphonates Treat underlying cause
86
Give 1 important side effect of carbimazole
Agranulocytosis
87
What is the minimum HbA1c for diagnosis of T2DM
48
88
Give 1 condition which cause gynaecomastia
Goserelin - GnRH agonist used in the management of prostate cancer
89
What is the most common thyroid cancer?
Papillary (70%) - seen in young females and has excellent prognosis
90
What is the second most common thyroid cancer?
Follicular
91
What is the management of thyroid cancer?
total thyroidectomy followed by radioiodine (I-131) to kill residual cells yearly thyroglobulin levels to detect early recurrent disease
92
Which drug may cause psychosis?
Steroids
93
Describe the aetiology of hypothyroidism
Primary: -Autoimmune - e.g. Hashimoto's thyroiditis, atrophic thyroiditis -Congenital -Iodine deficiency Secondary: -Hypopituitarism -Post-surgery
94
Describe the epidemiology of hypothyroidism
Much more common in women Mean age of onset = 60 Classically middle aged women
95
Which hormone is released by the hypothalamus which forms a part of the hypothalamic-pituitary-axis?
Thyrotropin releasing hormone
96
Which hormone is released by the anterior pituitary which forms a part of the hypothalamic-pituitary-axis?
Thyroid stimulating hormone
97
Which hormone is released by the thyroid which forms a part of the hypothalamic-pituitary-axis?
T3 and T4 (only 25% of circulating \T3 is produced by the thyroid, the rest is produced from T4 in peripheral tissues)
98
Describe the pathophysiology of primary hypothyroidism
Thyroid unable to produce sufficient T3/T4 despite a high TSH
99
Describe the pathophysiology of secondary hypothyroidism
Insufficient TSH produced by the anterior pituitary, so the thyroid produced less T3/T4 OR Thyroid has been removed/damaged during surgery
100
Describe the pathophysiology of atrophic thyroiditis
T-cell mediated auto-reactive cytotoxicity to follicular cells DOES NOT PRODUCE A GOITRE!
101
Describe the pathophysiology of Hashimoto's thyroiditis
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
Describe the pathophysiology of post-partum thyroiditis
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
Describe myxoedema
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
Describe the presentation of hypothyroidism
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
Describe the TFT results in primary hypothyroidism
High TSH Low T4
106
Describe the TFT results in subclinical hypothyroidism
High TSH Normal T4
107
Describe the TFT results in secondary hypothyroidism
Normal/low TSH Low T4
108
Describe the TFT results in primary hyperthyroidism
Low TSH High T4
109
Describe the TFT results in subclinical hyperthyroidism
Low TSH Normal T4
110
Describe the confirmatory investigation for autoimmune hypothyroidism
TPO antibodies (also do FBC due to risk of B12 deficiency of autoimmune cause, e.g. pernicious anaemia, atrophic gastritis)
111
Give the management of hypothyroidism
Levothyroxine - oral T4 supplementation
112
Give the management of hypothyroidism in pregnancy
Levothyroxine - if already taking then increase dose by 25% Low TSH in mother can lead to cognitive impairment in the child
113
Describe the management of depression in hypothyroidism
Levothyroxine! Depression will usually resolve within a few weeks of starting levothyroxine
114
What ABG findings are seen in Addisonian crisis?
hyperkalaemic metabolic acidosis
115
Describe the TFT findings in sick euthyroid syndrome
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
What can result in a falsely high HbA1c?
Splenectomy

Finals (11 decks)

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