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FINALS REVISION > Endocrine > Flashcards

Endocrine Flashcards

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
Q

what results would you expect in high dose dex in ectopic ACTH from cancer

A

high dose dex doesnt suppress ACTH. no cortisol suppression

unsuppressed ACTH and unsuppressed cortisol

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26
Q

what ABG would you find in cushing’s syndrome

A

hypokalaemic metabolic alkalosis

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27
Q

what alternative to dex suppression investigation

A

24 hr urinary free cortisol

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28
Q

what other investigations should you do in cushing’s

A

FBC - WCC
U+E - hypokalaemia
CT chest - lung cancer
CT abdo - adrenal tumours

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29
Q

what treatment for cushing’s syndrome

A

transsphenoidal if cushing’s disease (pit adenoma)
surgical resection of lung/adrenal tumour
bilateral adrenal resection and replacement hormones for life

30
Q

what symptoms of diabetes insipidus

A

polyuria
polydipsia
postural hypotension

31
Q

what investigations in diabetes insipidus

A

U+E - hypernatraemia
low urine osmolality
high serum osmolality

32
Q

what diagnostic investigation for diabetes insipidus and what results

A

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
Q

how is diabetes insipidus managed

A

desmopressin

higher doses required in nephrogenic

34
Q

what are the causes of cranial diabetes insipidus

A 
idiopathic
head injury
tumour, malformation
surgery, radiotherapy
infection - meningitis, TB, encephalitis
35
Q

what causes of nephrogenic diabetes insipidus

A
  • drugs - lithium
  • genetic (mutation in AVPR2 on x-chromosome)
  • electrolyte abnormalities - hyperCa, hypoK
  • intrinsic kidney disease
36
Q

explain the pathophys behind type 1 diabetes

A

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
Q

what is t1dm associated with

A

HLA DR3/4

  • coeliac
  • thyroid
38
Q

what investigations in patient with suspected T1dm

A 
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
Q

what are the diabetes specific autoantibodies

A
  • anti-GAD (glutamic acid decarboxylase)
  • Islet cell antibodies
  • insulin auto-antibodies
  • insulinoma associated 2 antibodies
40
Q

what are the fasting and random plasma glucose thresholds for t1dm

A

fasting >=7
random >=11 (or after 75mg OGTT)

must be demonstrated on two separate occasions

41
Q

how is t1dm managed

A 
insulin regime (basal-bolus)
basal - long acting insulin glargine in evenings
bolus - actrapid TDS before meals
42
Q

what target hba1c for t1dm and how often should this be monitored
how often should BMs be monitored

A

48, every 3-6 months

monitor BMs at least 4x a day

43
Q

what are the short term complications of t1dm

A

hypoglycaemia

hyperglycaemia and DKA

44
Q

what symptoms of hypoglycaemia in t1dm

A 
hunger
sweating
dizziness
pallour
tremor
irritability
45
Q

how is t1dm hypoglycaemia treated

A

IV dextrose and IM glucagon

orally - lucozade (rapid acting glucose) and biscuits (long acting carbs)

46
Q

how is hyperglycaemia (not yet DKA level) treated in t1dm

A

increase insulin

alter insulin regime

47
Q

explain the pathophys of DKA

A

uncontrolled lipolysis generates free fatty acids that are converted to ketone bodies

48
Q

what precipitates DKA

A

infection
myocardial infarction
missed insulin dose

49
Q

how does DKA present

A
  • abdominal pain, nausea, vomiting
  • polyuria and polydipsia
  • dehydration and hypotension
  • altered consciousness
  • Kussmaul breathing
  • acetone, pear drop smelling breath
50
Q

what are the diagnostic criteria for DKA

A
  • acidosis (pH <7.3)
  • ketosis (serum >3mmol/L)
  • hyperglycaemia >11mmol/L
  • bicarb low (<15)
51
Q

how is DKA managed

A
  • 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
Q

what are some important points to note for the management of DKA

A
  • 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
Q

what are the thresholds for resolution of DKA

A

pH>7.3
ketonaemia <0.6mmol
bicarb >15mmol`

54
Q

by how many hours should ketonaemia and acidosis have resolved

A

24 hours. if not, senior review from specialist

55
Q

what complications of DKA

A
  • AKI
  • gastric stasis
  • thromboembolism
  • arrhythmias due to hyperkalaemia/iatrogenic hypokalaemia
  • iatrogenic: cerebral oedema, hypoglycaemia, hypokalaemia
  • acute respiratory distress syndrome
56
Q

how would cerebral oedema present in DKA

A

monitor GCS:

visual disturbance
headache
nausea, vomiting
altered behaviour
bradycardia
changes to consciousness
57
Q

how would cerebral oedema be treated

A

slow the fluid infusion rate
hypertonic saline
IV mannitol

58
Q

what are the causes of hypoglycaemia

A
  • Insulinoma
  • Over-administration of insulin
  • Liver failure
  • Addison’s disease
  • Alcohol
  • Nesidioblastosis
59
Q

what symptoms of hypoglycaemia

A
  • shaking
  • sweating
  • hunger
  • nausea
  • anxiety

Neuroglycopaenic:

  • confusion
  • dizziness
  • headache
  • weakness
  • convulsions
  • coma
60
Q

how should hypoglycaemia be treated

A
  • Oral glucose 10-20g
  • IM glucagon
  • IV 20% glucose through large vein
61
Q

what are the features of de Quervain’s thyroiditis

A
  • viral infection
  • fever
  • neck pain and tenderness
  • dysphagia
  • hyperthyroidism features (diarrhoea, tachy, weight loss, heat intolerance etc)

RAISED ESR

62
Q

how is de Quervain’s thyroiditis treated

A

NSAIDs for thyroid pain and propranolol for the hyperthyroidism stage to manage symptoms

63
Q

what features are specific to graves disease

A
  • thyroid acropachy
    • soft tissue swelling of bones and feet
    • new periosteal bone formation
    • digital clubbing
  • thyroid eye disease (bilateral exophthalmos, ophthalmoplegia)
  • pretibial myxoedema
64
Q

what antibodies can be found in graves disease

A
  • TSH receptor antibodies

- anti TPO antibodies

65
Q

what would thyroid scintigraphy show in graves disease

A

diffuse homogenous increased uptake of radioactive iodine

66
Q

what events can precipitate a thyroid storm

A
  • thyroid surgery
  • trauma
  • infection
  • acute iodine load - CT contrast media
67
Q

what features of thyroid storm

A
  • fever
  • tachycardia
  • confusion/delirium
  • nausea vomiting
  • hypertension
  • heart failure
  • liver failure - jaundice
68
Q

how is thyroid storm treated

A
  • A-E resuscitation
  • symptomatic - paracetamol
  • IV propranolol
  • IV propylthiouracil
  • Lugol’s iodine
  • dexamethasone to block conversion of T4 to T3
69
Q

what treatment for graves disease

A

initiated by specialist

  • carbimazole - agranulocytosis
  • propylthiouracil
  • radioiodine, thyroidectomy
  • propranolol to block adrenaline effects while awaiting specialist treatment
70
Q

what is the pathophys behind thyroid eye disease

A
  • autoimmune response to TSH receptor antibodies

- retro-orbital inflammation

71
Q

what are the features of thyroid eye disease

A
  • exophthalmos
  • conjunctival oedema
  • ophthalmoplegia
  • eyelids fail to close fully - dry, sore eyes
    • risk of exposure keratitis
72
Q

what treatment for thyroid eye disease

A
  • topical lubricants to reduce risk of exposure keratitis
  • steroids
  • radiotherapy
  • surgery

FINALS REVISION (17 decks)

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