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Y3 medicine > Endocrinology > Flashcards

Endocrinology Flashcards

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
Q

Diabetes insipidus symptoms and signs

A

Polyuria - large volumes of dilute urine
Polydipsia
Nocturia
Dehydration
Symptoms of hypernatraemia
- Fatigue, weakness, irritability, nausea and vomiting, fever, thirst, confusion
Postural hypotension

26
Q

Primary polydipsia

A

Patient has normally functioning ADH system
Drinks excessive amounts of water, leading to excessive urine production
Not diabetes insipidus

27
Q

Diabetes insipidus investigations

A

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
Q

Water deprivation test

A

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
Q

Water deprivation results (urine osmolality)

A

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
Q

Diabetes insipidus management

A

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
Q

SIADH causes

A

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
Q

SIADH symptoms and signs

A

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
Q

SIADH investigations

A

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
Q

SIADH management

A

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
Q

Adrenal insufficiency symptoms and signs

A

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
Q

Adrenal insufficiency types

A

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
Q

Adrenal insufficiency investigations

A

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
Q

Adrenal insufficiency management

A

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
Q

Steroid sick day rules

A

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
Q

Adrenal crisis management

A

IV fluids – dehydration & hypotension
IV hydrocortisone
IV dextrose infusion for hypoglycaemia

41
Q

Cushing’s syndrome symptoms and signs

A

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
Q

Cushing’s syndrome causes

A

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
Q

Cushing’s syndrome investigations

A

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
Q

Adrenal adenoma investigations results (Cushing’s)

A

Low dose test – not suppressed
High dose test – not suppressed
ACTH – low

45
Q

Pituitary adenoma investigations results (Cushing’s)

A

Low dose test - not suppressed
High dose test – low
ACTH – high

46
Q

Ectopic ACTH investigations results (Cushing’s)

A

Low dose test – not suppressed
High dose test - not suppressed
ACTH – high

47
Q

Cushing’s syndrome management

A

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
Q

Hyperaldosteronism types

A

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
Q

Hyperaldosteronism investigations

A

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
Q

Hyperaldosteronism management

A

Aldosterone antagonists - spironolactone, eplerenone
Treat underlying cause - surgical resection, renal artery angioplasty

51
Q

Phaeochromocytoma

A

Tumour of the adrenal medulla (chromaffin cells) that secretes unregulated and excessive catecholamines (adrenaline)

52
Q

Phaeochromocytoma symptoms and signs

A

Anxiety, sweating, headache, tremor, palpitations, hypertension, tachycardia
If untreated: hypertensive crisis, encephalopathy, hyperglycaemia, pulmonary oedema, cardiac arrhythmias

53
Q

Phaeochromocytoma investigations

A

24 hr metanephrines (metabolites of catecholamines)
Plasma metanephrines
CT/MRI of adrenals to locate tumour

54
Q

Phaeochromocytoma management

A

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
Q

Hyperprolactinemia symptoms and signs

A

Amenorrhoea or oligomenorrhoea
Infertility
Galactorrhoea
Decreased libido
Weight gain
Dry vagina
Erectile dysfunction, decreased facial hair in males

56
Q

Hyperprolactinaemia causes

A

Pregnancy, breastfeeding
PCOS
Pituitary tumours - prolactinomas
Drugs - metoclopramide, haloperidol, methyldopa, antipsychotics
Renal failure, primary hypothyroidism

57
Q

Hyperprolactinaemia investigations and management

A

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
Q

Acromegaly symptoms and signs

A

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
Q

Acromegaly causes

A

GH secreting pituitary tumours
Ectopic GH secretion - lung or pancreatic tumours
Excess GHRH - hypothalamic tumours

60
Q

Acromegaly investigations

A

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
Q

Acromegaly management

A

Surgery - trans-sphenoidal removal of pituitary tumours, or other for other tumours
Medical
- Somatostatin analogues (octreotide)
- Dopamine agonists (bromocriptine)
- Growth hormone receptor antagonist
Radiotherapy

Y3 medicine (10 decks)

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