Endocrinology Flashcards

1
Q

Management nephrogenic diabetes insipidus

A

thiazides

low salt and protein diet

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2
Q

Management central diabetes insipidus

A

desmopressin

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3
Q

define cranial diabetes insipidus

A

deficiency of ADH

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4
Q

define nephrogenic diabetes insipidus

A

insensitivity to ADH

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5
Q

Causes of cranial diabetes insipidus

A
  • idiopathic
  • head injury
  • pituitary surgery
  • craniopharyngioma
  • histocytosis X
  • DIDMOAD - DI + DM + Optic atrophy + deafness = Wolfram’s syndrome
  • haemochromatosis
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6
Q

Causes of nephrogenic diabetes insipidus

A
  • genetic
  • electrolytes imbalance (hypercalcaemia, hypokalaemia)
  • drugs (demeclocycline, lithium)
  • tubulo-interstitial disease (obstruction, sickle cell, pyelonephritis)
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7
Q

Fts of diabetes insipidus

A

polyuria

polydipsia

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8
Q

Investigation + result in diabetes insipidus

A
  • high plasma osmolality
  • low urine osmolality (<700)
  • water deprivation test (12hrs no water + vasopressin - if response it is central DI)
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9
Q

1st line management of T2DM

A

diet and lifestyle advice

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10
Q

single drug manaement T2DM

A

metformin

if CI =
- if CVD established/risk orCHF = SGLT-2i
- otherwise = any other

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11
Q

Troubleshooting intolerance to metformin

A
  • titrate up slowly
  • trial MR
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12
Q

When to use GLP-1 mimentic (i.e semaglutide/ozempic)

A

does not achieve HbA1c control on dual drug therapy AND
- BMI >35
- BMI <35 but insulin would have implications/weight loss would benefit comorbidities

AND only continued if reduction of at leasr 11mmol/mol AND weight loss 3% in 6mo

NOT additional to insulin unless under specialist care

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13
Q

when to start 3rd line management T2DM

A

if HbA1c >58mmol/mol + with lifestyle advice and one drug

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14
Q

Second drug management T2DM

A
  • if high risk/established CVD or HF - SGLT-2 inhibitor
    • sulfonylurea if no risk of hypoglycaemia
  • DPP4-i or thiazolidindedione if at risk of hypoglycaemia
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15
Q

target HbA1c if on lifestyle + sulfonylurea

A

53

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16
Q

target HbA1c if on one drug but HbA1c has rised to 58mmol/mol

A

53mmol/mol

17
Q

target HbA1c if on lifestyle + one drug (excluding sulfonylurea)

A

48mmol/mol

18
Q

Typical blood findings seen along with Cushing’s syndrome

A

hypokalaemic metabolic alkalosis (esp a/w ectopic ACTH in SCC)

impaired glucose tolerance

19
Q

3 most common tests used to confirm Cushing’s syndrome

A
  • overnight (low-dose) dexamethasone suppression = most sensitive; positive = no cortisol spike in am
  • 24hr urinary free cortisol (2 measurements)
  • bedtime salivary cortisol 2 measuremetns required)
20
Q

Localizing tests for Cushing’s syndrome
1. fist line test
2. interpretation

A
  1. 9am and midnight plastma ACTH (and cortisol)
  2. ACTH suppressed = non-ACTH dependent cause (i.e adrenal adenoma)
21
Q

Localizing tests for Cushing’s syndrome
1. second line test
2. interpretation

A
  1. High dose dexamethasone supression test
    • cortisol not supp BUT ACTH supp = non-ACTH dependent (o.e adrenal adenoma)
    • cortisol AND ACTH supp = Cushing’s disease (pituitary adenoma)
    • cortisol AND ACTH not supp = ectopic ACTH
22
Q

investigations for suspected Addison’s disease
1. in GP
2.2nd line GP/hospital

A
  1. 9am serum cortisol (if >500 Addison very unlikely)
  2. ACTH simulation (short Synacthen test) = plasma cortsol before and 30 mins after giving Synachen 250ug IM
23
Q

associated electrolyte abnromalities with Addison’s disease (undiagnosed)

A

hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis

24
Q
A