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Endocrine Flashcards

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1
Q

explain the pathophys of acromegaly

A

too much GH
most commonly caused by benign pituitary adenoma

can be caused by ectopic secretion of GH or GHRH by lung/pancreatic cancer

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2
Q

what are the symptoms and signs of acromegaly

A 
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
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3
Q

what condition is acromegaly associated with

A

MEN1

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4
Q

what conditions does acromegaly cause

A

HTN
diabetes
cardiomyopathy
colorectal cancer

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5
Q

what investigations for acromegaly

A

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

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6
Q

what treatment for acromegaly

A

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)
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7
Q

what is addison’s disease

A

primary adrenal insufficiency

lack of cortisol and aldosterone

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8
Q

how does addison’s disease present

A
  • fatigue, weakness, anorexia
  • dizziness, myalgia, arthralgia
  • hyperpigmentation (esp. in palmar creases)
  • vitiligo
  • weight loss
  • abdominal cramps, N+V, diarrhoea, constipation
  • salt craving
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9
Q

what investigations for addison’s disease

A

FBC, UE - hyponatremia hyperkalaemia
short synACTHen test - measure cortisol before and 30mins after
if cortisol increases after administration of synACTHen, then NOT addison’s

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10
Q

what electrolyte abnormalities in addison’s disease and what ABG findings

A

hyponatraemia
hyperkalaemia
hypoglycaemia
metabolic acidosis

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11
Q

how is addison’s disease treated

A
  • 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
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12
Q

what is an addisonian crisis and what can cause this

A

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
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13
Q

what symptoms/signs of addisonian crisis

A
  • reduced consciousness
  • hypotension
  • fever
  • hypoglycaemia hyponatraemia hyperkalemia
  • patient appears very unwell
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14
Q

how is addisonian crisis treated

A
  • IV hydrocortisone 100mg then every 6 hours
  • IV fluid resus (1L saline over 30-60 minutes)
  • monitoring electrolytes and fluid balance
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15
Q

what is secondary adrenal insufficiency

A

lack of ACTH due to pituitary insufficiency
therefore lack of cortisol production by adrenal glands
adrenal glands atrophy due to understimulation

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16
Q

what can cause secondary adrenal insufficiency

A

surgery to remove pituitary
sheehan’s syndrome
radiotherapy damage to pituitary

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17
Q

how is secondary adrenal insufficiency diagnosed

A

ACTH levels

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18
Q

what are the ACTH dependent causes of cushing’s syndrome

A
  • cushing’s disease (pit. adenoma secreting ACTH)

- ectopic ACTH production (small cell lung cancer)

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19
Q

what are the ACTH independent causes of cushing’s syndrome

A

iatrogenic (steroid use)
adrenal adenoma/carcinoma
McCune-Albright syndrome, carney complex

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20
Q

what are the symptoms/signs of cushing’s

A
  • 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
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21
Q

what investigations for cushing’s

A

Low-dose dexamethasone suppression test

if Cushing’s syndrome - 9am cortisol will not be suppressed

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22
Q

if low dose dex suppression test shows cushing’s, what next investigation

A

high dose dex suppression test to determine cause of cushing’s syndrome

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23
Q

what results would you expect in high dose dex test in cushing’s disease

A

cushing’s disease is pit. adenoma

high dose dex would suppress ACTH and cortisol would also be suppressed

both cortisol and ACTH suppressed

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24
Q

what results would you expect in high dose dex in adrenal adenoma

A

high dose dex would suppress ACTH, but cortisol would not be suppressed

ACTH suppressed, high cortisol

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25
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
26
what ABG would you find in cushing's syndrome
hypokalaemic metabolic alkalosis
27
what alternative to dex suppression investigation
24 hr urinary free cortisol
28
what other investigations should you do in cushing's
FBC - WCC U+E - hypokalaemia CT chest - lung cancer CT abdo - adrenal tumours
29
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
30
what symptoms of diabetes insipidus
polyuria polydipsia postural hypotension
31
what investigations in diabetes insipidus
U+E - hypernatraemia low urine osmolality high serum osmolality
32
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
33
how is diabetes insipidus managed
desmopressin | higher doses required in nephrogenic
34
what are the causes of cranial diabetes insipidus
``` idiopathic head injury tumour, malformation surgery, radiotherapy infection - meningitis, TB, encephalitis ```
35
what causes of nephrogenic diabetes insipidus
- drugs - lithium - genetic (mutation in AVPR2 on x-chromosome) - electrolyte abnormalities - hyperCa, hypoK - intrinsic kidney disease
36
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
37
what is t1dm associated with
HLA DR3/4 - coeliac - thyroid
38
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 ```
39
what are the diabetes specific autoantibodies
- anti-GAD (glutamic acid decarboxylase) - Islet cell antibodies - insulin auto-antibodies - insulinoma associated 2 antibodies
40
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
41
how is t1dm managed
``` insulin regime (basal-bolus) basal - long acting insulin glargine in evenings bolus - actrapid TDS before meals ```
42
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
43
what are the short term complications of t1dm
hypoglycaemia | hyperglycaemia and DKA
44
what symptoms of hypoglycaemia in t1dm
``` hunger sweating dizziness pallour tremor irritability ```
45
how is t1dm hypoglycaemia treated
IV dextrose and IM glucagon | orally - lucozade (rapid acting glucose) and biscuits (long acting carbs)
46
how is hyperglycaemia (not yet DKA level) treated in t1dm
increase insulin | alter insulin regime
47
explain the pathophys of DKA
uncontrolled lipolysis generates free fatty acids that are converted to ketone bodies
48
what precipitates DKA
infection myocardial infarction missed insulin dose
49
how does DKA present
- abdominal pain, nausea, vomiting - polyuria and polydipsia - dehydration and hypotension - altered consciousness - Kussmaul breathing - acetone, pear drop smelling breath
50
what are the diagnostic criteria for DKA
- acidosis (pH <7.3) - ketosis (serum >3mmol/L) - hyperglycaemia >11mmol/L - bicarb low (<15)
51
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
52
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
53
what are the thresholds for resolution of DKA
pH>7.3 ketonaemia <0.6mmol bicarb >15mmol`
54
by how many hours should ketonaemia and acidosis have resolved
24 hours. if not, senior review from specialist
55
what complications of DKA
- AKI - gastric stasis - thromboembolism - arrhythmias due to hyperkalaemia/iatrogenic hypokalaemia - iatrogenic: cerebral oedema, hypoglycaemia, hypokalaemia - acute respiratory distress syndrome
56
how would cerebral oedema present in DKA
monitor GCS: ``` visual disturbance headache nausea, vomiting altered behaviour bradycardia changes to consciousness ```
57
how would cerebral oedema be treated
slow the fluid infusion rate hypertonic saline IV mannitol
58
what are the causes of hypoglycaemia
- Insulinoma - Over-administration of insulin - Liver failure - Addison's disease - Alcohol - Nesidioblastosis
59
what symptoms of hypoglycaemia
- shaking - sweating - hunger - nausea - anxiety Neuroglycopaenic: - confusion - dizziness - headache - weakness - convulsions - coma
60
how should hypoglycaemia be treated
- Oral glucose 10-20g - IM glucagon - IV 20% glucose through large vein
61
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
62
how is de Quervain's thyroiditis treated
NSAIDs for thyroid pain and propranolol for the hyperthyroidism stage to manage symptoms
63
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
64
what antibodies can be found in graves disease
- TSH receptor antibodies | - anti TPO antibodies
65
what would thyroid scintigraphy show in graves disease
diffuse homogenous increased uptake of radioactive iodine
66
what events can precipitate a thyroid storm
- thyroid surgery - trauma - infection - acute iodine load - CT contrast media
67
what features of thyroid storm
- fever - tachycardia - confusion/delirium - nausea vomiting - hypertension - heart failure - liver failure - jaundice
68
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
69
what treatment for graves disease
initiated by specialist - carbimazole - agranulocytosis - propylthiouracil - radioiodine, thyroidectomy - propranolol to block adrenaline effects while awaiting specialist treatment
70
what is the pathophys behind thyroid eye disease
- autoimmune response to TSH receptor antibodies | - retro-orbital inflammation
71
what are the features of thyroid eye disease
- exophthalmos - conjunctival oedema - ophthalmoplegia - eyelids fail to close fully - dry, sore eyes - risk of exposure keratitis
72
what treatment for thyroid eye disease
- topical lubricants to reduce risk of exposure keratitis - steroids - radiotherapy - surgery

FINALS REVISION (17 decks)

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