Y2 ENDOCRINE PHARMACOLOGY Flashcards

1
Q

main use of corticosteroids?

A
  • suppress inflammation, suppress immune system, replacement therapy.
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2
Q

activation of the renin angiotensin system leads to?

A

angiotensin II production causing vasoconstriction and indirect increase in BP (aldosterone).

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3
Q

renin angiotensin system is activated in response to?

A

aldosterone production

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4
Q

aldosterone production is regulated by?

A

renin angiotensin system and plasma potassium

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5
Q

sodium and water are controlled by?

A
  • mineralocorticoid activity and ADH.
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6
Q

mineralocorticoid receptors are found?

A
  • kidneys, salivary glands, gut and sweat glands.
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7
Q

aldosterone acts on mineralocorticoid receptors to?

A
  • regulate BP
  • balance Na+ and K+
  • regulate ECF volume
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8
Q

management of adrenal insufficiency?

A
  • hydrocortisone (cortisol) 15-30m/day in divided doses to try mimic diurnal variation.
  • fludrocortisone (aldosterone) - carefully monitor BP and K.
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9
Q

adrenal cortex is a major source of?

A

human glucocorticoids - cortisol, mineralocorticoids - aldosterone and androgens.

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10
Q

cortisol/androgen secretion is regulated by?

A

pituitary ACTH secretion by a negative feedback mechanism.

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11
Q

aldosterone regulates?

A

BP and electrolyte excretion

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12
Q

how do you manage phaeochromocytoma medically?

A

full α and β blockade - α before β!!!

  • α: phenoxybenzamine.
  • β: propranolol/ atenolol/ metoprolol.
  • fluid +/or blood replacement.
  • careful anaesthetic assessment.
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13
Q

how do you manage phaeochromocytoma surgically?

A

laparoscopically:

  • total excision when possible.
  • tumour de-bulking where full removal not possible.
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14
Q

management of acute hypercalcaemia?

A
  • fluids 4-6L of 0.9% saline over 24 hours.
  • loop diuretics? once rehydrated (not thiazide)
  • bisphosphonates
  • steroids if sarcoidosis.
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15
Q

management of acute malignant hypercalcaemia?

A
  • chemo e.g. in myeloma
  • fluids 4-6L of 0.9% saline over 24 hours
  • bisphosphonates
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16
Q

what are bisphosphonates?

A

anti-resorptive agents (bone).

They are pyrophosphate analogues that adsorb onto bone within the matrix.

17
Q

examples of bisphosphonates?

A
  • alendronate and risedronate
18
Q

action of bisphosphonates?

A

prevent bone loss at all sites vulnerable to osteoporosis

19
Q

why are bisphonates used?

A

to reduce the risk of hip and spine fracture

20
Q

bisphosphonates are ingested by?

A

osteoclasts to cause cell death - inhibiting bone resorption

21
Q

bisphosphonates allow filling of resorption sites by new bone to increased BMD by?

A

5-8%

22
Q

Bisphosphonates e.g. alendronate and risedronate reduce the risk of fragility fracture by?

A

= 50% in those with post-menopausal osteoporosis.

23
Q

what long term concerns are associated with bisphosphonate therapy?

A
  • osteonecrosis of the jaw.
  • oesophageal carcinoma
  • atypical fractures
24
Q

zoledronic acid is given as?

A
  • a once/year IV infusion for 3 years.

- 5mg in 100ml NaCl ver 15 mins.

25
Q

how many experience an acute phase reaction with 1st infusion of zoledronic acid?

A

1:3

26
Q

how do you manage an acute phase reaction with 1st infusion of zoledronic acid?

A

paracetamol

27
Q

zoledronic acid reduces fracture risk by?

A
  • 70% for vertebral fracture

- 40% for hip fracture

28
Q

what monoclonal antibody targets and binds to RANKL to prevent activation of RANK receptor and thus inhibiting development and activity of osteoclasts?

A

denosumab

decreases bone resorption and increases bone density

29
Q

how is densoumab (monoclonal antibody) administered for osteoporosis?

A

subcut. injection every 6 months

30
Q

side effects of denosumab?

A
  • cellulitis
  • eczema
  • hypocalcaemia (can be fatal)
31
Q

what is teriparatide?

A

a recombinant parathyroid hormone

32
Q

action of teriparatide?

A

stimulates bone growth instead of reducing bone loss.

- anabolic agent

33
Q

when is teriparatide prescribed?

A
  • if <65 yrs with T-score of equal to or less than -4.
  • if T score of 2 fractures.
  • if 55-64y/o with T score less than or equal to -4 + >2 fractures + unsatisfactory response to oral agents
34
Q

how do corticosteroids directly impact bone?

A
  • reduce osteoblast activity and life span
  • suppress replication of osteoblast precursors
  • reduce calcium absorption
35
Q

how do corticosteroids indirectly impact bone?

A
  • inhibit gonadal and adrenal steroid production
36
Q

management of Paget’s

A
  • analgesia

- bisphosphonates if pain doesn’t respond to analgesia

37
Q

management of addisonian crisis?

A

high dose oral hydrocortisone and fludrocortisone