Endocrine Flashcards
Signs of diabetes mellitus
Polyuria
Polydipsia
weight loss
What are the types of diabetes?
T1DM = an absolute insulin deficiency causes persistent hyperglycaemia. (autoimmune)
T2DM = a combination of insulin resistance/insensitivity and insulin deficiency
Diagnostic criteria for diabetes
Symptomatic:
1. fasting glucose > 7.0 mmol/l
- random glucose > 11.1 mmol/l (or after 75g oral glucose tolerance test)
HbA1c > 48 mmol/mol
4 main ways to check blood glucose
- a finger-prick bedside glucose monitor
- a one-off blood glucose.
- a HbA1c.
- a glucose tolerance test.
Management of T1DM
Insulin
Management of T2DM
- Metformin
- Sulfonylureas, gliptins + pioglitazone
- Insulin
Signs and symptoms of DKA
Common in new diagnosis T1DM:
- abdominal pain
- polyuria, polydipsia, dehydration
- deep hyperventilation
- acetone-smelling breath (‘pear drops’ smell)
When should HbA1c be monitoried for T1DM?
Every 3-6 months
What is the HbA1C targets for T2DM?
Lifestyle = 48
Lifestyle + metformin = 48
Lifestyle + any drug cause hypoglycaemia (sulfonylurea) = 53
Diabetes Mellitus sick day rules
- Increase frequency of blood glucose monitoring to four hourly or more frequently
- Encourage fluid intake aiming for at least 3 litres in 24hrs
- If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake
- It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
- Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis
- Continue taking medication
What is Hashimoto’s thyroiditis
autoimmune disorder of the thyroid gland
typically associated with hypothyroidism although there may be a transient thyrotoxicosis in the acute phase
Clinical features of Hashimoto’s thyroiditis
- hypo sx
- goitre
- anti-TPO and anti-thyroglobulin antibodies
What may trigger thyroid storm
- surgery
- trauma
- infection
- iodine load e.g CT Contrast
Management of thyroid storm
symptomatic tx (paracetemol), treat underlying, beta blockers
- anti-thyroid drugs: e.g. propylthiouracil
- Lugol’s iodine
- dexamethasone (blocks conversion of T3 to T4)
What is Subacute (De Quervain’s) thyroiditis
thought to occur following viral infection and typically presents with hyperthyroidism
Investigations for Subacute (De Quervain’s) thyroiditis
thyroid scintigraphy: globally reduced uptake of iodine-131
Management of Subacute (De Quervain’s) thyroiditis
analgesia, self-limiting
Diagnostic critieria for DKA
- glucose > 11 mmol/l or known diabetes mellitus
- pH < 7.3
- bicarbonate < 15 mmol/l
- ketones > 3 mmol/l or
- urine ketones ++ on dipstick
Management of DKA
- Fluid replacement
- Insulin
- Correction of electrolyte disturbance
- Long-acting insulin
What is hypoglycaemia
blood glucose concentrations <3.3 mmol/L
Symptoms of hypoglycaemia
- Sweating
- Shaking
- Hunger
- Anxiety
- Nausea
- weakness
- vision change
- confusion
- dizziness
Symptoms of severe hypoglycaemia
- convulsion
- coma
Management of hypoglycaemia
- in the community:
- oral glucose 10-20g should be given in liquid, gel or tablet form
- Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
- A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home - in a hospital setting:
- If the patient is alert, a quick-acting carbohydrate may be given (as above)
- If the patient is unconscious or unable to swallow, subcut or IM glucagon
- Alternatively, IV 20% glucose solution through a large vein
Define hypercholesterolaemia
Total cholesterol > 7.5 mmol
Management of hypercholesterolaemia
Familial = high dose statin
Atorvastatin 80 mg
Management of hypertriglyceridaemia
- Statins (e.g atorvastatin 10mg)/Fenofibrates (initially 200mg OD).
- Qrisk score would also be done to determine risk of 10 years cardiac related mortality.
- Weight loss/dietary advice
What is Addison’s disease?
Reduced cortisol + aldosterone produced
Features of Addison’s disease
- lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
- hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension,
- hypoglycaemia
hyponatraemia and hyperkalaemia may be seen - crisis: collapse, shock, pyrexia
Definitive investigation for Addison’s disease
ACTH Test (Short synacthen test)
Other:
9 am Serum Cortisol
1. > 500 nmol/l = Addison’s very unlikely
2. < 100 nmol/l = abnormal
3. 100-500 nmol/l = ACTH stimulation indicated
Management of Addison’s Disease
Combination of:
- hydrocortisone
- fludrocortisone
What is Addison’s crisis?
Acute exacerbation of chronic insufficiency
Causes of Addisonian crisis
- Sepsis or surgery
- adrenal haemorrhage
- steroid withdrawal
Management of Addisonian Crisis
- hydrocortisone 100 mg im or iv
- 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
- continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
- oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
Clinical features of hypothyroidism
- Weight gain
- Lethargy
- Cold intolerance
- dry skin, brittle hair
- constipation
What is the most common cause of hypothyroidism
Hashimoto’s thyroiditis
What are the expected TFT results in primary hypothyroidism
High TSH, Low T4
What are the expected TFT results in Secondary hypothyroidism
Low TSH, Low T4
How is hypothyroidism classified
Primary = problem with thyroid gland itself
Secondary = disorder with pituitary gland
Congenital
Management of hypothyroidism
Levothyroxine
How long after levothyroxine dose change should TFT be repeated?
8-12 weeks
What is the most common cause of thyrotoxicosis
Graves’ disease
Epidemiology of Graves Disease
women 30-50 yo
Clinical signs of Graves disease
- exophthalmos
- pretibial myxoedema
Which antibodies can help distinguish Graves disease from other forms of hyperthryoidism?
TSH Receptor stimulating antibodies
Management of Graves disease
propanolol to control symptoms
carbimazole is uncontrolled with propanolol
What is Graves Disease
autoimmune condition leading to overactive thyroid glands
What is the typical description of a patient with hyperparathyroidism in exam questions?
elderly females with an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level
How do most patients with hyperparathyroidism present?
80% are asymptomatic
Mnemonic used to remember symptomatic features of primary hyperparathyroidism
bones, stones, abdominal groans and psychic moans
What are the expected blood results in primary hyperparathyroidism?
normal or raised PTH
raised Ca , low Phosphate
Characteristic Xray finding of hyperparathyroidism
pepperpot skull
Definitive management of primary hyperparathyroidism
total parathyroidectomy
What may be given to patients with hyperparathyroidism who are not suitable for surgical management
cinacalcet
- a calcimimetic which ‘mimics’ the action of calcium on tissues
What is hyperparathyroidism
condition in which one or more of the parathyroid glands makes too much PTH leading to excess calcium production
Most common cause of hyperparathyroidism
solitary adenoma
What are the expected blood results in secondary hyperparathyroidism?
High PTH
Low/normal Ca, High Phosphate
Cause of secondary hyperparathyroidism
CKD = low calcium = PTH Hyperplasia
What is hypoparathyroidism?
inadequate PTH activity = low calcium, high phosphate
What is Tertiary hyperparathyroidism?
High PTH = normal or high Ca = normal of low Phosphate
HIGH ALP
What is the cause of Tertiary hyperparathyroidism?
ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder
Treatment for Tertiary hyperparathyroidism?
Allow 12 months to elapse following transplant as many cases will resolve
otherwise parathyroidectomy or excision of affected gland
Main sx of hypoparathyroidism
secondary to hypocalcaemia
- Tetany: muscle twitching, cramping, spasm
- perioral paraesthesia
Tx hypoparathyroidism
alfacalcidol
Symptoms of thyroid cancer
- a painless lump in neck
- lymphadenopathy
- unexplained hoarseness that does not get better after a few weeks.
- persistent sore throat
- difficulty swallowing
What is Cushing’s?
Glucocorticoid excess –> increased cortisol
What tests confirm Cushing’s?
1st line = overnight dexamethasone suppression test
In Cushing’s syndrome - you do not have their morning cortisol spike suppressed
24 hr urinary free cortisol
Symptoms of Cushing’s syndrome
- Moon Face”, “buffalo hump”, truncal obesity
- Weight gain
- Gonadal dysfunction (Oligomenorrhea and infertility, decreased libido, hirsutism, erectile dysfunction)
- Mood change - emotional lability, anxiety, depression
- Proximal muscle weakness
- Thirst and polyuria (due to hyperglycaemia)
Interpretation of high-dose dexamethasone test
- Normal Cortisol + Supressed ACTH = Adrenal cause
- Low Cortisol + Low ACTH = Cushing’s disease
- Normal Cortisol + high ACTH = Ectopic ACTH
Management of Cushing’s disease
Depends on underlying cause:
- Cushing’s Disease
- -> surgical removal of pituitary adenoma +/- bilateral adrenalectomy, radiotherapy
- -> exogenous medication (steroids) - Adrenal Adenoma
- -> bilateral adrenalectomy - Adrenal Carcinoma
- -> Adrenalectomy, radiotherapy, chemotherapy - Ectopic ACTH
- -> Surgical removal if tumour located, radiotherapy, chemotherapy
What is Gynaecomastia?
Abnormal amount of breast tissue in males
-> caused by an increased oestrogen: androgen ratio.
Management of Gynaecomastia
- Refer if red flags (unilateral, hard/irregular tissue, fixed mass, pain, axillary LAD)
- Treat underlying cause
- Tamoxifen = pain in acute gynaecomastia
- -> Has anti-oestrogen effect - Possible surgical removal of breast tissue
Causes of hyponatraemia
Sodium depletion
- diuretics
- Addisons disease
- renal failure
- diarrhoea
- vomiting
- burns
Water excess
- secondary hyperaldosteronism
- nephrotic syndrome
Complication of severe hyponatraemia if left untreated
cerebral oedema
What is used to treat acute hyponatraemia with severe symptoms?
Hypertonic saline (NaCl)
Euvolaemic causes of hyponatraemia
- SIADH (impaired water excretion caused by the inability to suppress ADH secretion)
- Hypothyroidism (decreased rate of free water excretion)
Tx of chronic hyponatraemia if hypovolaemic cause
Hypertonic saline (NaCl)
Tx of chronic hyponatraemia if euvolaemic cause
fluid restrict (500-1000ml/day)
- consider demeclocycline
- consider Vasopressin receptor antagonists (Vaptans))
Tx of chronic hyponatraemia if hypervolaemic cause
fluid restrict to 500–1000 mL/day
- consider loop diuretics
- consider Vasopressin receptor antagonists (Vaptans)
When should Vaptans be avoided
hypovolaemic hyponatraemia
- may precipitate hypotension and renal failure
Causes of hypernatraemia
dehydration
osmotic diuresis e.g.
diabetes insipidus
excess IV saline
Complication of rapidly correcting hypernatraemia
cerebral oedema = coma, seizure, death
Treatment of hypovolaemic hypernatraemia
IV Saline
Treatment of hypervolaemic hypernatraemia
diuretics and 5% dextrose
Investigations in hypo/hypernatraemia
- serum osmolality
- serum electrolytes, urea, creatinine, and glucose
Causes of hypomagnasaemia
drugs diuretics PPIs total parenteral nutrition diarrhoea alcohol hypokalaemia hypercalcaemia metabolic disorders
Signs and sx of hypomagnasaemia
similar to hypercalcaemia
- tetany
- seizures
- arrhythmias
Tx of hypomagnasaemia
IV Magnesium
Oral Mg salts if <0.4
Features of hypocalcaemia
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts
ECG finding in hypocalcaemia
prolonged QT interval
What is Trousseau’s sign
sign of hypocalcaemia where carpal spasm occurs if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
Causes of hypocalcaemia
- vitamin D deficiency (osteomalacia)
- CKD
- hypoparathyroidism
- Acute pancreatitis
What might cause falsely low Ca levels
contamination of blood samples with EDTA
Management of acute, severe hypocalcaemia
IV calcium gluconate
ECG finding in hypercalcaemia
shortened QT interval
Sx of hypercalcaemia
‘bones, stones, groans and psychic moans’
2 main causes of hypercalcaemia
Primary hyperparathyroidism
Malignancy
Initial tx of hypercalcaemia
rehydration with normal saline
Which drugs may be used to treat hypercalcaemia
- bisphosphonates
- calcitonin
- Loop diuretics (CAUTION as may worsen electrolyte derangement)
What is Galactorrhoea?
Milky secretion from the breasts , not due to breastfeeding.
Cause of Galactorrhoea
Excess prolactin due to drugs or physiological factors:
- prolactinoma
- pregnancy
- acromegaly
- primary hypothyroidism
- PCOS
Features of excess prolactin
- men: impotence, loss of libido, galactorrhoea
2. women: amenorrhoea, galactorrhoea
Investigations for Galactorrhoea
- Prolactin, TFTs, U&Es, LFTs
+/- hCG
- MRI (prolactinoma)
Management of Galactorrhoea
- Rule out serious pathology – breast cancer
- Treat underlying cause: hypothyroidism, prolactinomas
- If the causes cannot be addressed:
1. Dopamine agonist – bromocriptine or cabergoline
2. Hormone treatment: - -> men = testosterone
- -> women = oestrogen
What is lactose intolerance?
An enzyme deficiency, rather than lactose allergy, which is an IgE-mediated reaction
Symptoms of lactose intolerance
Gas build-up:
- Bloating
- flatulence
- Abdominal discomfort
Acidic and osmotic effects of undigested lactose:
- Loose watery stool
- Perianal itching due to acidic stools
Diagnosis of lactose intolerance
Can be made on clinical features alone
Trial of 2-week period of strict lactose -free diet
No single diagnostic test:
- A lactose tolerance test
- Breath hydrogen test
Management of lactose intolerance
Avoid milk and dairy products
What is Phaeochromocytoma?
Catecholamine-secreting tumour formed by chromaffin cell within the adrenal medulla
–> Catecholamine = norepinephrine epinephrine
Symptoms of Phaeochromocytoma
Triad:
- headaches
- palpitations and tachycardia
- sweating
Other:
- hypertension
- anxiety
Investigations for Phaeochromocytoma
24 hr urinary collection of metanephrines (sensitivity 97%*)
Management of Phaeochromocytoma
Surgery is the definitive management.
Stabilise pt first with:
- alpha-blocker (e.g. phenoxybenzamine), given before a
- beta-blocker (e.g. propranolol)
What is Acromegaly?
Excessive secretion of growth hormone due to pituitary adenoma.
Acromegaly causes an overgrowth of all organ systems, bones, joints and soft tissues.
Features of Acromegaly
- coarse facial appearance, spade-like hands, increase in shoe size
- large tongue, prognathism, interdental spaces
- excessive sweating and oily skin: caused by sweat gland hypertrophy
- features of pituitary tumour = hypopituitarism, headaches, bitemporal hemianopia
- raised prolactin in 1/3 of cases → galactorrhoea
1st line investigation for Acromegaly
Serum IGF-1 levels
Other investigation for Acromegaly
Oral glucose tolerance test:
1. in normal patients GH is suppressed to < 2 mu/L with hyperglycaemia
- in acromegaly there is no suppression of GH
- may also demonstrate impaired glucose tolerance which is associated with acromegaly
Pituitary MRI = pituitary tumour.
1st line treatment for Acromegaly
Trans-sphenoidal surgery
What is Diabetes insipidus?
Either:
1. a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI)
or
- an insensitivity to antidiuretic hormone (nephrogenic DI)
Symptoms of Diabetes insipidus
- Polyuria (dilute urine)
- polydipsia (thirst)
- dehydration
Investigation for Diabetes insipidus
- U&Es (hypernatremia, hyperuricemia)
- Plasma & urine osmolality
- -> high plasma osmolality, low urine osmolality
- -> a urine osmolality of >700 mOsm/kg excludes diabetes insipidus - Water deprivation test - urine abnormally dilute
Management of Diabetes Insipidus
- Find & treat cause (pituitary tumour, metastases, head injury, meningitis, sarcoidosis, inherited)
- Cranial: Desmopressin (synthetic analogue of ADH)
- Nephrogenic: Bendroflumethiazide, low protein, low salt
What is Conn’s syndrome?
Primary hyperaldosteronism
Features of Conn’s syndrome
- hypertension
- hypokalaemia
- -> muscle weakness
1st line investigation in suspected Conn’s syndrome
Plasma aldosterone/renin ratio
- High aldosterone + low renin
Next step after 1st line investigation in Conn’s syndrome
High-resolution CT abdomen + adrenal vein sampling
Management of Conn’s syndrome
- adrenal adenoma: surgery
2. bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
Most common cause of Addison’s
Autoimmune
Causes of hyperkalaemia
- AKI
- Addisons disease
- Rhabdomyolysis
- Drugs
Which drugs cause hyperkalaemia
ACEi, ARB, spironolactone, heparin
ECG changes seen in hyperkalaemia
tall-tented T waves, small P waves, widened QRS
What does untreated hyperkalaemia lead to?
life-threatening arrhythmias
Emergency treatment of severe hyperkalaemia
- IV calcium gluconate: to stabilise the myocardium
- insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
Sx of hyperkalaemia
- muscle weakness
- numbness
- palpitations
- sob
- n&v
Sx of hypokalaemia
- muscle weakness
- hypotonia
What does hypokalaemia predispose patients to?
digoxin toxicity
ECG features of hypokalaemia
U waves, long PR, long QT
Causes of hypokalaemia
- diuretics
- diarrhoea
- vomiting
- excess alcohol
- DKA
- CKD
Management of hypokalaemia
IV Potassium
What is metabolic alkalosis
loss of hydrogen ions or gain of bicarbonate
Main causes of metabolic alkalosis
- vomiting
- diuretics
- hypokalaemia
- primary hyperaldosteronism
- Cushing’s syndrome
What is the normal anion gap
10-18mmol/L
Causes of metabolic acidosis
normal anion gap
- GI (diarrhoea)
- Addisons
raised anion gap
- lactate (shock, sepsis, hypoxia)
- ketone (DKA, alcohol)
- renal failure
Common causes of resp alkalosis
- anxiety = hyperventilation
- PE
- pregnancy
- altitude
- salicylate poisoning
- stroke
- subarrachnoid haemorrhgae
Common causes of resp acidosis
- COPD
- Decompensation in other resp conditions
- sedative drug OD
- neuromuscular disease
What acid-base imbalance is associated with cushing’s syndrome?
Hypokalaemic metabolic alkalosis
