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Y3 medicine > Endocrinology > Flashcards

Endocrinology Flashcards

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1
Q

Primary hypothyroidism

A

Low levels of blood thyroid hormone due to destruction of the thyroid gland
Causes:
- Autoimmune – Hashimoto’s thyroiditis (thyroid peroxidase antibodies)
- Iodine deficiency
- Drugs – amiodarone, lithium
- Surgery, radiotherapy

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2
Q

Secondary hypothyroidism

A

Decreased activity of the thyroid caused by failure of the pituitary gland
Causes:
- Tumours
- Surgery
- Radiotherapy
- Sheehan’s syndrome – postpartum hypopituitarism caused by necrosis of the pituitary gland
- Trauma

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3
Q

Hypothyroidism symptoms and signs

A

Symptoms – weight gain, cold intolerance, fatigue, constipation, hoarse voice, low mood +/- depression, dry & thin hair, dry skin, menorrhagia
Signs – bradycardia, thickening of skin and puffiness around the eyes (myxoedema)

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4
Q

Hypothyroidism investigations

A

TFTs – low T3 and T4, elevated TSH
Thyroid antibodies – anti-TPO
USS of thyroid
Other – FBC, B12 and folate, serum lipids, HbA1c, coeliac serology

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5
Q

Hypothyroidism TFT results

A

Primary hypothyroidism – thyroid gland, high TSH, low T3 & T4
Secondary hypothyroidism – pituitary gland, low TSH, low T3 & T4

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6
Q

Hypothyroidism management

A

Levothyroxine (T4)

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7
Q

Hypothyroidism monitoring

A

TSH
- Elevated: under-replacement, poor compliance, malabsorption
- Suppressed: over-replacement (increased risk of AF and osteoporosis)
If symptomatic despite treatment, investigate for non-thyroid pathology

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8
Q

Hyperthyroidism causes

A

Autoimmune – grave’s disease
Nodular thyroid disease – solitary toxic thyroid nodule or toxic multinodular goitre
Thyroiditis – De Quervain’s thyroiditis, postpartum thyroiditis, drug-induced thyroiditis (amiodarone, lithium)
Follicular thyroid cancer
TSH-secreting pituitary adenoma
Exogenous – iodine excess, levothyroxine

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9
Q

Hyperthyroidism symptoms and signs (+ specific to Graves)

A

Symptoms – weight loss with increased appetite, insomnia, irritability, anxiety, heat intolerance, diarrhoea, amenorrhoea, reduced libido, hair loss
Signs – tachycardia, palpitations, tremor, palmar erythema
Graves – exophthalmos (proptosis), lid retraction and chemosis (eye irritation), goitre, pretibial myxoedema, thyroid acropachy (hand swelling and finger clubbing)

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10
Q

Hyperthyroidism investigations

A

TFTs – low TSH, high T3 & T4
Thyroid antibodies – TSH receptor antibodies
USS thyroid gland
Thyroid scintigraphy – radioactive iodine/technetium uptake can determine cause
- Overall increase in Graves
- Only in nodules for nodular causes
- Absent in thyroiditis

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11
Q

Hyperthyroidism TFT results

A

Hyperthyroidism (all other causes) – high T3 & T4 and low TSH
Pituitary adenoma – high T3 & T4 and high TSH

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12
Q

Hyperthyroidism management

A

Medical – carbimazole, propylthiouracil, reduce synthesis of T3 & T4, can take 4-6 weeks to feel effect
- Can causes agranulocytosis (severe form of neutropenia) -> if unexplained fever/sore throat request urgent blood for pancytopenia (deficiency of red cells, white cells and platelets)
Beta-blockers may also be used to control symptoms
Definitive treatment – radioactive iodine (single dose): contraindicated in pregnancy and commonly causes hypothyroidism, thyroidectomy: complications of bleeding, infection, recurrent laryngeal nerve damage, hypothyroidism

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13
Q

Parathyroid gland

A

Chief cells – secrete PTH
Oxyphil cells – purpose unknown, increase in number with age
PTH actions – increase calcium levels in the body
1) Increased bone resorption – PTH acts directly on bone, induce osteoclast activity
2) Increased reabsorption in the kidney – increases absorption of calcium from loop of Henle & distal tubules & increases rate of phosphate excretion to prevent calcium phosphate stones
3) Vitamin D synthesis – stimulates formation of vitamin D -> increases absorption of calcium from the gut

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14
Q

Hyperparathyroidism types

A

Primary – uncontrolled PTH production by a tumour of parathyroid glands (malignant and benign)/hyperplasia of glands
Secondary – insufficient vitamin D/CKD reduces calcium absorption from intestines, kidneys and bones -> compensatory to a prolonged hypocalcaemia
Tertiary – development of parathyroid hyperplasia after secondary hyperparathyroidism occurs for an extended period of time & underlying cause is left untreated
Malignant – some tumours produce PTHrP

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15
Q

Hyperparathyroidism symptoms and signs

A

Reflective of hypercalcaemia & raised PTH
Stones – renal calculi
Bones – fragility fractures, bone pain
Moans – mood disturbances, depression, fatigue, psychosis, confusion
Groans – abdominal pain, N&V, constipation, pancreatitis
Polyuria, polydipsia, fatigue, insomnia, dehydration, HTN

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16
Q

Hyperparathyroidism investigations

A

Bloods – ALP (raised), vitamin D (deficiency in secondary), U&Es (secondary), decreased phosphate (unless in renal failure) PTH (elevated in all causes except malignant), serum calcium (increased in all except secondary)
Imaging – DXA scan for osteopenic & osteoporotic changes, USS to identify abnormal parathyroid glands

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17
Q

Hyperparathyroidism management

A

Treat underlying cause
Primary: mild – monitor, increase fluids, vit D supplementation, if symptomatic or Ca2+ > 2.85mmol/L – parathyroidectomy, cinacalcet – calcimimetic (lowers serum calcium & PTH), consider bisphosphonates for bone protection
Secondary: vit D supplementation, UV exposure, calcium, CKD -> reduce phosphate intake & consider phosphate binders
Tertiary: cinacalcet & parathyroidectomy
Malignant: treatment of malignancy, bisphosphonates & cinacalcet

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18
Q

Parathyroidectomy complications

A

Hypoparathyroidism
Hypocalcaemia
Recurrence
Recurrent laryngeal nerve palsy

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19
Q

Hypoparathyroidism types

A

Primary – gland failure (autoimmune), congenital (Di George syndrome)
Secondary – radiation, surgery, hypomagnesaemia (Mg required for PTH secretion)
Pseudohypoparathyroidism – failure of target cells to respond to PTH, genetic cause, short stature, round face, calcified basal ganglia, short metacarpals (4th and 5th)
Pseudopseudohypoparathyroidism – same as pseudo but with normal biochemistry

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20
Q

Hypoparathyroidism investigations

A

Serum calcium decreased
PTH
- Decreased in primary and secondary
- Increased in pseudohypoparathyroidism
- Normal in pseudopseudohypoparathyroidism
ALP normal or increased
ECG - prolonged QT interval indicated severe, life-threatening hypocalcaemia
Bloods - magnesium, vitamin D, phosphate, creatinine

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21
Q

Hypoparathyroidism symptoms and signs

A

Hypocalcaemia - muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light-headedness, arrhythmias – tachycardias, constipation- ileus, rhabdomyolysis
Symptoms of underlying cause

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22
Q

Hypoparathyroidism management

A

Management – calcium supplementation & calcitriol (synthetic vitamin D)
If hypomagnesaemia – oral or IV magnesium

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23
Q

Central (cranial) diabetes insipidus

A

Lack of ADH
- Idiopathic (most common)
- Tumours - primary (hypothalamic), secondary (lung, leukaemia, lymphoma)
- Trauma to the head - temporary if distal to pituitary stalk
- Neurosurgery (hypophysectomy)
- Hypopituitarism
- Infection - meningitis, TB, abscess
- Infiltration - sarcoidosis, histiocytosis

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24
Q

Nephrogenic diabetes insipidus

A

Lack of response to ADH
- Inherited - defect in the gene for the ADH receptor
- Metabolic - hypokalaemia, hypercalcaemia
- Drugs - lithium
- Tubulo-interstitial disease - obstruction, pyelonephritis, chronic renal disease

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25
Diabetes insipidus symptoms and signs
Polyuria - large volumes of dilute urine Polydipsia Nocturia Dehydration Symptoms of hypernatraemia - Fatigue, weakness, irritability, nausea and vomiting, fever, thirst, confusion Postural hypotension
26
Primary polydipsia
Patient has normally functioning ADH system Drinks excessive amounts of water, leading to excessive urine production Not diabetes insipidus
27
Diabetes insipidus investigations
Bloods - U&Es, Ca2+, glucose (+HbA1c) Urine dipstick - exclude DM, evidence of renal disease MRI head Test pituitary function Serum osmolality - high, >295 mOsmol/Kg Urine osmolality - low, <300 mOsmol/Kg, excluded if >600 mOsmol/Kg or double serum osmolality Urine volume >3L/24 hrs
28
Water deprivation test
Deprive patients of fluids for 8 hrs or until 3% loss of body weight Measure serum osmolality, urine volume and osmolality hourly If urine osmolality >600 mOsmol/Kg and serum osmolality <300 mOsmol/Kg, DI excluded as the condition causes inappropriately dilute urine Patient is then given synthetic ADH (desmopressin) to differentiate between cranial and nephrogenic DI
29
Water deprivation results (urine osmolality)
Primary polydipsia – high after water deprivation Cranial DI – low after water deprivation, high after desmopressin Nephrogenic DI – low after water deprivation, low after desmopressin
30
Diabetes insipidus management
Cranial DI - Give desmopressin intranasally, orally, sublingually or parenterally - If acute - desmopressin first line and consider oral/IV fluids - Monitor serum sodium levels as risk of hyponatraemia with desmopressin Nephrogenic - Treat the cause - Drink according to thirst to manage water loss - If persists, bendroflumethiazide - NSAIDs - lower urine volume and plasma Na+ by inhibiting prostaglandin release - Low salt, low protein diet If hypernatraemic - Oral/IV fluids, 5% dextrose infusion
31
SIADH causes
Malignancy - SCLC, pancreas, prostate, thymus, lymphoma CNS disorders - Meningoencephalitis, abscess, stroke, subarachnoid or subdural haemorrhage, head injury, neurosurgery, vasculitis, SLE, Guillain-Barre Chest disease - TB, pneumonia, abscess, aspergillosis Drugs - Opiates, psychotropics, SSRIs, cytotoxics Other - Post-operative, porphyria, major abdominal or thoracic injury, HIV
32
SIADH symptoms and signs
May be asymptomatic or present with non-specific symptoms Confusion Nausea Irritability Later - seizures and coma NO oedema Symptoms of hyponatraemia - Lethargy, anorexia, headache, weakness, reduced GCS, hyporeflexia
33
SIADH investigations
Diagnosis of exclusion Urine osmolality - high, >100 mOsmol/Kg, urine Na+ - high, >20/30 mmol/L Serum osmolality - low, <260 mOsmol/Kg, serum Na+ - low, <125 mmol/L If no cause for SIADH is found, cross-sectional imaging or bowel investigation may be required to find any underlying malignancy TFTs - hypothyroidism can cause increased ADH release ACTH - hyponatraemia in Addison’s disease presents in the same way (cortisol deficiency causes increase in ADH activity)
34
SIADH management
Treatment of the underlying cause Fluid restriction - 1-1.5L per day (poorly tolerated) If intolerant to fluid restriction - Sodium chloride tablets with furosemide - increase urine output and improve serum Na+ levels (monitoring of serum K+ levels) Correction of hyponatraemia - Slowly 8-10 mmol/L/day, prevent osmotic demyelination syndrome/cerebral pontine myelinolysis Vasopressin receptor antagonists - tolvaptan (short period of time, not in patients with liver injury) Demeclocycline - tetracycline Abx, causes an iatrogenic nephrogenic DI by inhibiting ADH
35
Adrenal insufficiency symptoms and signs
Fatigue, muscle weakness and cramping Dizziness and fainting - postural hypotension Thirst and craving salt Weight loss, abdominal pain, N&V Depression Reduced libido Hyperpigmentation of the skin creases (increased ACTH causes increased melanin) Loss of pubic and axillary hair Hypoglycaemia Crisis – reduced consciousness, confusion, hypotension (shock), pyrexia, N&V
36
Adrenal insufficiency types
Primary – destruction/dysfunction of the adrenal cortex - Addison’s disease - Infection, infiltration (when antibody -ve) Secondary – reduction in ACTH release - Hypopituitarism, isolated deficiency (ACTH), following brain injury, stopping long term steroids Tertiary – reduction in CRH - Following chronic glucocorticoid steroid use
37
Adrenal insufficiency investigations
9am cortisol - low ACTH concentration - high (low in secondary and tertiary) ACTH stimulation/Synacthen test - when morning cortisol doesn’t give definitive result - Synthetic ACTH given, cortisol measured before and 30 and 60 mins after the dose - Cortisol level should at least double, failure indicates adrenal insufficiency Hyponatraemia, hyperkalaemia, hypoglycaemia Anaemia Raised creatinine and urea Imaging - CT, MRI of adrenals if suspecting structural pathology, MRI pituitary if underlying pituitary pathology Adrenal antibodies Elevated renin levels, low aldosterone levels
38
Adrenal insufficiency management
Lifelong glucocorticoid and mineralocorticoid steroid replacement - Hydrocortisone - cortisol (sometimes low dose prednisolone is used) - Fludrocortisone - aldosterone Can offer androgen replacement to premenopausal women with low libido
39
Steroid sick day rules
Instruct patients to double their glucocorticoid doses in times of illness and to continue with this until the illness resolves May need IV or IM doses during a surgery or cases of prolonged vomiting or diarrhoea Patients should also carry a steroid emergency card and are encouraged to wear medical alert jewellery
40
Adrenal crisis management
IV fluids – dehydration & hypotension IV hydrocortisone IV dextrose infusion for hypoglycaemia
41
Cushing’s syndrome symptoms and signs
Round face (moon face), red face (plethora), central obesity, abdominal striae (purple), “Buffalo hump” - enlarged fat pad on the upper back Proximal limb muscle wasting Hirsutism Easy bruising and poor skin healing, hyperpigmentation of the skin (ACTH dependent) Depression, lethargy, irritability Gonadal dysfunction - erectile dysfunction, irregular menses Osteoporosis If malignant cause - weight loss
42
Cushing’s syndrome causes
ACTH dependant (high ACTH) - Cushing’s disease - pituitary adenoma secreting excessive ACTH - Ectopic ACTH production - SCLC, carcinoid tumours ACTH independent (low ACTH) - Iatrogenic - exogenous steroids - Adrenal adenoma/hyperplasia (+ carcinoma rarely) - secretes excess cortisol (no dexamethasone suppression)
43
Cushing’s syndrome investigations
Plasma ACTH Dexamethasone suppression test 24 hr urinary free cortisol (elevated) Late-night salivary cortisol (elevated) CRH stimulation - pituitary source if cortisol rises Pregnancy testing in women of reproductive age Imaging - pituitary MRI, adrenal CT, CT chest, abdo, pelvis, MRI chest Inferior petrosal sinus blood sampling - pituitary lesions
44
Adrenal adenoma investigations results (Cushing’s)
Low dose test – not suppressed High dose test – not suppressed ACTH – low
45
Pituitary adenoma investigations results (Cushing’s)
Low dose test - not suppressed High dose test – low ACTH – high
46
Ectopic ACTH investigations results (Cushing’s)
Low dose test – not suppressed High dose test - not suppressed ACTH – high
47
Cushing’s syndrome management
Iatrogenic - stop medications Cushing’s disease - removal of pituitary adenoma (trans-sphenoidal), bilateral adrenalectomy if source not located or recurrence post-op, consider post-op PTH and/or cortisol replacement Adrenal - adrenalectomy + permanent post surgical corticosteroid replacement therapy Ectopic - treatment of tumour, resection if located and no spread, radiotherapy Metyrapone, ketoconazole and fluconazole decrease cortisol
48
Hyperaldosteronism types
Primary hyperaldosteronism – cause is from adrenal gland directly - Serum renin will be low as the hypertension suppresses it - Causes: bilateral adrenal hyperplasia, adrenal adenoma secreting aldosterone (Conn’s syndrome), familial (rare) Secondary hyperaldosteronism - caused by excessive renin stimulating release of aldosterone - Usually due to disproportionately lower blood pressure in the kidneys - Renal artery stenosis, heart failure, liver cirrhosis
49
Hyperaldosteronism investigations
Bloods - U&Es, aldosterone:renin ratio - High aldosterone, low renin - primary - High aldosterone, high renin - secondary CT, MRI - adrenal tumour or hyperplasia Renal artery doppler, CT angiogram, MR angiography - renal artery stenosis
50
Hyperaldosteronism management
Aldosterone antagonists - spironolactone, eplerenone Treat underlying cause - surgical resection, renal artery angioplasty
51
Phaeochromocytoma
Tumour of the adrenal medulla (chromaffin cells) that secretes unregulated and excessive catecholamines (adrenaline)
52
Phaeochromocytoma symptoms and signs
Anxiety, sweating, headache, tremor, palpitations, hypertension, tachycardia If untreated: hypertensive crisis, encephalopathy, hyperglycaemia, pulmonary oedema, cardiac arrhythmias
53
Phaeochromocytoma investigations
24 hr metanephrines (metabolites of catecholamines) Plasma metanephrines CT/MRI of adrenals to locate tumour
54
Phaeochromocytoma management
Surgical excision of the tumour Alpha +/- beta blockers for hypertension control, make sure to give alpha blocker first (and beta blockers cover tachycardia) High sodium diet due to volume loss
55
Hyperprolactinemia symptoms and signs
Amenorrhoea or oligomenorrhoea Infertility Galactorrhoea Decreased libido Weight gain Dry vagina Erectile dysfunction, decreased facial hair in males
56
Hyperprolactinaemia causes
Pregnancy, breastfeeding PCOS Pituitary tumours - prolactinomas Drugs - metoclopramide, haloperidol, methyldopa, antipsychotics Renal failure, primary hypothyroidism
57
Hyperprolactinaemia investigations and management
Prolactin levels, pregnancy test, TFTs, U&Es MRI pituitary - lesions Management - Prolactinomas (benign tumour of pituitary gland) treated with dopamine agonists - cabergoline or bromocriptine - If visual disturbances or raised ICP - may need surgical resection, though many decrease in size with dopamine antagonists
58
Acromegaly symptoms and signs
Increased size of hands and feet, coarse facial features - frontal bossing of the forehead, protrusion of the chin and widely spaced teeth Soft tissue swelling - enlargement of the tongue and soft palate (snoring and sleep apnoea), puffiness of hands (carpal tunnel syndrome) Acroparaesthesia (numbness in extremities), headaches, sweating, decreased libido If pituitary tumour - bitemporal hemianopia may be present Increased risks - cardiovascular disease, colorectal cancer, arthritis, T2DM, thyroid cancer
59
Acromegaly causes
GH secreting pituitary tumours Ectopic GH secretion - lung or pancreatic tumours Excess GHRH - hypothalamic tumours
60
Acromegaly investigations
IGF-1 - cannot test GH directly as fluctuates through the day and with physiological states OGTT (oral glucose tolerance test) - serum GH measured before and after dose, in acromegaly, GH not suppressed GHRH levels - hypothalamic cause MRI brain - pituitary lesions CT chest, abdo, pelvis - ectopic causes Investigate for complications - ECG, echo, glucose etc.
61
Acromegaly management
Surgery - trans-sphenoidal removal of pituitary tumours, or other for other tumours Medical - Somatostatin analogues (octreotide) - Dopamine agonists (bromocriptine) - Growth hormone receptor antagonist Radiotherapy

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