Endocrine Flashcards
explain the pathophys of acromegaly
too much GH
most commonly caused by benign pituitary adenoma
can be caused by ectopic secretion of GH or GHRH by lung/pancreatic cancer
what are the symptoms and signs of acromegaly
coarse facial features (large nose etc.) large hands and feet (inc. ring and shoe size) macroglossia, prognathism, skull bossing wide interdental spaces headache arthritis excessive sweating, oily skin raised prolactin - galactorrhoea bitemporal hemianopia
what condition is acromegaly associated with
MEN1
what conditions does acromegaly cause
HTN
diabetes
cardiomyopathy
colorectal cancer
what investigations for acromegaly
IGF1 levels
if equivocal/raised - confirm with OGTT
Glucose should suppress GH levels. If not - acromegaly
MRI pituitary - pit. tumour
refer to ophthalmology for visual field testing
what treatment for acromegaly
transsphenoidal resection of pituitary adenoma
if ectopic - resection of cancer
- somatostatin analogues - octreotide
- pegvisomant OD SC GH antagonist
- dopamine agonist to block GH release (bromocriptine)
what is addison’s disease
primary adrenal insufficiency
lack of cortisol and aldosterone
how does addison’s disease present
- fatigue, weakness, anorexia
- dizziness, myalgia, arthralgia
- hyperpigmentation (esp. in palmar creases)
- vitiligo
- weight loss
- abdominal cramps, N+V, diarrhoea, constipation
- salt craving
what investigations for addison’s disease
FBC, UE - hyponatremia hyperkalaemia
short synACTHen test - measure cortisol before and 30mins after
if cortisol increases after administration of synACTHen, then NOT addison’s
what electrolyte abnormalities in addison’s disease and what ABG findings
hyponatraemia
hyperkalaemia
hypoglycaemia
metabolic acidosis
how is addison’s disease treated
- hydrocortisone (to replace cortisol) and fludrocortisone (to replace aldosterone)
- patients should be given an ID tag and be counselled on importance of not missing doses
- double steroid dose in illness
what is an addisonian crisis and what can cause this
life-threatening lack of glucocorticoids during stressful situations - surgery, sepsis.
caused by
- sepsis/surgery exacerbating chronic insufficiency as in addison’s disease/hypopituitarism
- adrenal haemorrhage e.g. waterhouse-friedrichsen syndrome in meningococcal septicaemia
- steroid withdrawal
what symptoms/signs of addisonian crisis
- reduced consciousness
- hypotension
- fever
- hypoglycaemia hyponatraemia hyperkalemia
- patient appears very unwell
how is addisonian crisis treated
- IV hydrocortisone 100mg then every 6 hours
- IV fluid resus (1L saline over 30-60 minutes)
- monitoring electrolytes and fluid balance
what is secondary adrenal insufficiency
lack of ACTH due to pituitary insufficiency
therefore lack of cortisol production by adrenal glands
adrenal glands atrophy due to understimulation
what can cause secondary adrenal insufficiency
surgery to remove pituitary
sheehan’s syndrome
radiotherapy damage to pituitary
how is secondary adrenal insufficiency diagnosed
ACTH levels
what are the ACTH dependent causes of cushing’s syndrome
- cushing’s disease (pit. adenoma secreting ACTH)
- ectopic ACTH production (small cell lung cancer)
what are the ACTH independent causes of cushing’s syndrome
iatrogenic (steroid use)
adrenal adenoma/carcinoma
McCune-Albright syndrome, carney complex
what are the symptoms/signs of cushing’s
- weight gain - truncal obesity
- moon shaped face
- buffalo hump
- proximal myopathy
- striae, bruising, acne thin skin
- gonadal dysfunction (irregular menses, ED)
- HTN
- diabetes
- depression, insomnia
- Osteoporosis
- prone to infection, poor healing
what investigations for cushing’s
Low-dose dexamethasone suppression test
if Cushing’s syndrome - 9am cortisol will not be suppressed
if low dose dex suppression test shows cushing’s, what next investigation
high dose dex suppression test to determine cause of cushing’s syndrome
what results would you expect in high dose dex test in cushing’s disease
cushing’s disease is pit. adenoma
high dose dex would suppress ACTH and cortisol would also be suppressed
both cortisol and ACTH suppressed
what results would you expect in high dose dex in adrenal adenoma
high dose dex would suppress ACTH, but cortisol would not be suppressed
ACTH suppressed, high cortisol
what results would you expect in high dose dex in ectopic ACTH from cancer
high dose dex doesnt suppress ACTH. no cortisol suppression
unsuppressed ACTH and unsuppressed cortisol
what ABG would you find in cushing’s syndrome
hypokalaemic metabolic alkalosis
what alternative to dex suppression investigation
24 hr urinary free cortisol
what other investigations should you do in cushing’s
FBC - WCC
U+E - hypokalaemia
CT chest - lung cancer
CT abdo - adrenal tumours
what treatment for cushing’s syndrome
transsphenoidal if cushing’s disease (pit adenoma)
surgical resection of lung/adrenal tumour
bilateral adrenal resection and replacement hormones for life
what symptoms of diabetes insipidus
polyuria
polydipsia
postural hypotension
what investigations in diabetes insipidus
U+E - hypernatraemia
low urine osmolality
high serum osmolality
what diagnostic investigation for diabetes insipidus and what results
water deprivation test/desmopressin stimulation test
urine osmolality increases in response to desmopressin = cranial diabetes insipidus
urine osmolality does not respond to desmopressin = nephrogenic diabetes insipidus
primary polydipsia - urine osmolality high after 8 hours water deprivation
how is diabetes insipidus managed
desmopressin
higher doses required in nephrogenic
what are the causes of cranial diabetes insipidus
idiopathic head injury tumour, malformation surgery, radiotherapy infection - meningitis, TB, encephalitis
what causes of nephrogenic diabetes insipidus
- drugs - lithium
- genetic (mutation in AVPR2 on x-chromosome)
- electrolyte abnormalities - hyperCa, hypoK
- intrinsic kidney disease
explain the pathophys behind type 1 diabetes
autoimmune destruction of beta cells in islets of langerhans in pancrease
decreased/no insulin production
high glucose levels in blood, little entering cells
- polydipsia
- polyuria
- weight loss
- DKA
- secondary enuresis in previously continent child
- recurrent infections
what is t1dm associated with
HLA DR3/4
- coeliac
- thyroid
what investigations in patient with suspected T1dm
FBC U+E fasting and random plasma glucose urine dip - ketones and glucose blood cultures if suspected infection C-peptide levels (low in t1dm) diabetes-specific autoantibodies
what are the diabetes specific autoantibodies
- anti-GAD (glutamic acid decarboxylase)
- Islet cell antibodies
- insulin auto-antibodies
- insulinoma associated 2 antibodies
what are the fasting and random plasma glucose thresholds for t1dm
fasting >=7
random >=11 (or after 75mg OGTT)
must be demonstrated on two separate occasions
how is t1dm managed
insulin regime (basal-bolus) basal - long acting insulin glargine in evenings bolus - actrapid TDS before meals
what target hba1c for t1dm and how often should this be monitored
how often should BMs be monitored
48, every 3-6 months
monitor BMs at least 4x a day
what are the short term complications of t1dm
hypoglycaemia
hyperglycaemia and DKA
what symptoms of hypoglycaemia in t1dm
hunger sweating dizziness pallour tremor irritability
how is t1dm hypoglycaemia treated
IV dextrose and IM glucagon
orally - lucozade (rapid acting glucose) and biscuits (long acting carbs)
how is hyperglycaemia (not yet DKA level) treated in t1dm
increase insulin
alter insulin regime
explain the pathophys of DKA
uncontrolled lipolysis generates free fatty acids that are converted to ketone bodies
what precipitates DKA
infection
myocardial infarction
missed insulin dose
how does DKA present
- abdominal pain, nausea, vomiting
- polyuria and polydipsia
- dehydration and hypotension
- altered consciousness
- Kussmaul breathing
- acetone, pear drop smelling breath
what are the diagnostic criteria for DKA
- acidosis (pH <7.3)
- ketosis (serum >3mmol/L)
- hyperglycaemia >11mmol/L
- bicarb low (<15)
how is DKA managed
- IV fluid resus with normal saline
- IV insulin fixed rate (0.1 unit/kg/hour)
- when glucose <15mmol, start 5% dextrose infusion
- continue long-acting insulin and stop short-acting insulin
what are some important points to note for the management of DKA
- correct dehydration slowly over 48 hours, faster could increase risk of cerebral oedema
- add potassium to fluids and monitor serum potassium closely
- treat underlying triggers - infection
what are the thresholds for resolution of DKA
pH>7.3
ketonaemia <0.6mmol
bicarb >15mmol`
by how many hours should ketonaemia and acidosis have resolved
24 hours. if not, senior review from specialist
what complications of DKA
- AKI
- gastric stasis
- thromboembolism
- arrhythmias due to hyperkalaemia/iatrogenic hypokalaemia
- iatrogenic: cerebral oedema, hypoglycaemia, hypokalaemia
- acute respiratory distress syndrome
how would cerebral oedema present in DKA
monitor GCS:
visual disturbance headache nausea, vomiting altered behaviour bradycardia changes to consciousness
how would cerebral oedema be treated
slow the fluid infusion rate
hypertonic saline
IV mannitol
what are the causes of hypoglycaemia
- Insulinoma
- Over-administration of insulin
- Liver failure
- Addison’s disease
- Alcohol
- Nesidioblastosis
what symptoms of hypoglycaemia
- shaking
- sweating
- hunger
- nausea
- anxiety
Neuroglycopaenic:
- confusion
- dizziness
- headache
- weakness
- convulsions
- coma
how should hypoglycaemia be treated
- Oral glucose 10-20g
- IM glucagon
- IV 20% glucose through large vein
what are the features of de Quervain’s thyroiditis
- viral infection
- fever
- neck pain and tenderness
- dysphagia
- hyperthyroidism features (diarrhoea, tachy, weight loss, heat intolerance etc)
RAISED ESR
how is de Quervain’s thyroiditis treated
NSAIDs for thyroid pain and propranolol for the hyperthyroidism stage to manage symptoms
what features are specific to graves disease
- thyroid acropachy
- soft tissue swelling of bones and feet
- new periosteal bone formation
- digital clubbing
- thyroid eye disease (bilateral exophthalmos, ophthalmoplegia)
- pretibial myxoedema
what antibodies can be found in graves disease
- TSH receptor antibodies
- anti TPO antibodies
what would thyroid scintigraphy show in graves disease
diffuse homogenous increased uptake of radioactive iodine
what events can precipitate a thyroid storm
- thyroid surgery
- trauma
- infection
- acute iodine load - CT contrast media
what features of thyroid storm
- fever
- tachycardia
- confusion/delirium
- nausea vomiting
- hypertension
- heart failure
- liver failure - jaundice
how is thyroid storm treated
- A-E resuscitation
- symptomatic - paracetamol
- IV propranolol
- IV propylthiouracil
- Lugol’s iodine
- dexamethasone to block conversion of T4 to T3
what treatment for graves disease
initiated by specialist
- carbimazole - agranulocytosis
- propylthiouracil
- radioiodine, thyroidectomy
- propranolol to block adrenaline effects while awaiting specialist treatment
what is the pathophys behind thyroid eye disease
- autoimmune response to TSH receptor antibodies
- retro-orbital inflammation
what are the features of thyroid eye disease
- exophthalmos
- conjunctival oedema
- ophthalmoplegia
- eyelids fail to close fully - dry, sore eyes
- risk of exposure keratitis
what treatment for thyroid eye disease
- topical lubricants to reduce risk of exposure keratitis
- steroids
- radiotherapy
- surgery
