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eLCRS - 엔도 > Endo 8: Therapeutic Use of Adrenal Steroids > Flashcards

Endo 8: Therapeutic Use of Adrenal Steroids Flashcards

1
Q

Zona glomerulosa produces

A

aldosterone

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2
Q

Zona fasciculata produces

A

cortisol

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3
Q

zona reticularis produces

A

androgens + oestrogens

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4
Q

NOTE: Adrenal sex steroid = also under control of ACTH
BUT
aldosterone = not under control of ACTH

A

-

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5
Q

Describe the process of aldosterone release :

A
  • aldosterone release = stimulated by Renin-Angiotensin System (RAS)
  • Renin converts Angiotensinogen –> AT I
  • ACE converts AT I –> AT II
  • AT II stimulates release of aldosterone from adrenal cortex
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6
Q

What 4 things triggers release of aldosterone?

A
  1. hyperkalaemia
  2. hyponatraemia
  3. drop in renal blood flow
  4. beta-1 adrenoreceptor stimulation
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7
Q

Why is aldosterone production important?

A
  • promotes Na+ retention + K+ loss

- for salt balance

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8
Q

What are the 2 types of corticosteroid receptors?

A
  • Glucocorticoid Receptors (GR)

- Mineralocorticoid Receptors (MR)

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9
Q

Compare between GR + MR

A

GR

  • wide distribution
  • is selective for glucocorticoids
  • has low affinity for cortisol

MR

  • has discrete distribution (only in kidney)
  • doesn’t distinguish btw aldosterone + cortisol
  • has high affinity for cortisol
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10
Q

How does 11B-hydroxysteroid dehydrogenase protect MRs from cortisol?

A
  • MR doestndistinguish btw aldosterone + cortisol
  • -> and this can lead to problems as cortisol can stimulate the MR
  • 11B hydroxysteroid deactivates cortisol
  • and so prevents MR from being stimulated
  • cortisone = inactive –> can’t stimulate MR
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11
Q

drug receptor selectivity

Binds with GR / MR / Both

a) hydrocortisone
b) Prednisolone
c) Dexamethasone
d) fludrocortisone

A

hydrocortisone

  • -> binds with glucocorticoid
  • -> mineralocorticoid activity - at high doses

Prednisolone

  • -> binds with glucocorticoid
  • -> mineralocorticoid activity WEAK

Dexamethasone
–> only GR

fludrocortisone
–> only MR

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12
Q

Describe the pharmacokinetics of corticosteroids

A
  • all the drugs can be given orally

- or in some cases parenteral IV (hydrocortisone/dexamethasone)

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13
Q

Describe the distribution of corticosteroids

A
  • they bind to plasma proteins
    (CBG + Albumin)
  • hydrocortisone = 90-95% bound
  • prednisone = less bound
  • dexamethasone + fludrocortisone = even less bound
  • fludrocortisone = only bound to albumin
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14
Q

Breakdown / metabolism of corticosteroid =

A

Breakdown / metabolism of corticosteroid = hepatic

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15
Q

Excretion of corticosteroid get excreted via ___ and ____

A

Excretion of corticosteroid get excreted via bile and urine

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16
Q

Hydrocortisone + Fludrocortisone

half-life:
duration of action:

A

Hydrocortisone + Fludrocortisone

half-life: 1 hour
duration of action: 8 hours

17
Q

Prednisolone

duration of action:

A

Prednisolone

duration of action: 12 hours

18
Q

Dexamethasone

duration of action:

A

Dexamethasone

duration of action: 40 hours

19
Q

arrange the corticosteroid in order of shortest –> longest half life:

dexamethasone, fludrocortisone, prednisolone, hydrocortisone

A

shortest:
1. hydrocortisone + fludrocortisone

  1. prednisone
  2. dexamethasone.
    Longest
20
Q

In what cases / conditions would you give corticosteroid replacement therapy?

A
  • primary adrenocortical failure
  • secondary adrenocortical failure
  • acute adrenocortical failure
  • congenital adrenal hyperplasia
  • Iatrogenic adrenocortical failure
21
Q

Primary adrenocortical failure may be due to 2 reasons:

A
  1. addison’s disease

2. chronic adrenal insufficiency

22
Q

What happens in primary adrenocortical failure?

A
  • adrenal cortex = not working

- so you can’t make any of the hormones

23
Q

How would you treat primary adrenocortical failure?

A
  • patients need cortisol replacement + aldosterone

- hydrocortisone or fludrocortisone = given orally

24
Q

Secondary Adrenocortical Failure is due to:

A
  • ACTH deficiency
  • adrenal gland = ok
    but adenohypophysis isn’t working properly
25
Q

What’s the difference between patients with addison’s disease and vs secondary adrenocortical failure?

A
  • secondary adrenocortical failure patients have NORMAL aldosterone production

–> because RAS is still functioning properly

26
Q

How would you treat secondary adrenocortical failure?

A
  • give oral hydrocortisone
27
Q

What is acute adrenocortical failure?

A
  • addisonian crisis
28
Q

How would you deal with addison ian crisis?

A
  1. give IV saline
    - -> because they lack aldosterone
    - -> need to replace lost salt
    - -> restore circulating volume _ improve blood pressure
  2. then give high dose hydrocortisone (IV/IM every 6 hrs)
    - 11BHSD is overwhelmed
  3. if hypoglycaemic –> give 5% dextrose
29
Q

What is congenital adrenal hyperplasia (CAH) ?

A

congenital adrenal hyperplasia (CAH) = congenital lack of enzymes needed for adrenal steroid synthesis.

–> usually due to absence of 21-hydroxylase
BUT
- adrenal androgen production = normal

30
Q

What happens in CAH?

A
  • you can’t make cortisol
  • so there is no -ve feed back on ACTH
  • so ACTH level = high (to try and make more cortisol)
  • so there is a build up of the precursor before the step with 21 hydroxylase

easily measurable precursor = 17a-hydroxyprogesterone

31
Q

What is the consequence of CAH?

A

in boys: precocious puberty
in girls: virilisation

women: hirsutism / acne

32
Q

How would you treat CAH

A
  • replace cortisol–> dexamethasone 1/day or hydrocortisone 2-3/day
  • suppress ACTH –> (and thus adrenal androgen production)
  • replace aldosterone in salt wasting forms –> fludrocortisone
33
Q

What are methods of monitoring therapy for CAH?

A

Measure:
- 17 OH progesterone levels (precursor build up)

Perform clinical assessment of:

  • patient may be Cushingoid (if GC dose = too high)
  • patient may show Hirsutism (if GC dose = too low + ACTH has risen)
34
Q

When should you increase the glucocorticoid dosage?

A
  • in minor illness

- in prep for surgery (hydrocortisone)

35
Q

What must you tell a patient with adrenocortical failure?

A
  • they should carry a steroid alert card + wear a MedicAlert bracelet
36
Q

cortisol binds to both

why does this not cause a problem?

A

GR + MR(aldosterone receptors)

- but not a problem because cortisol inactivates very quickly to the form that can’t bind to the MR

37
Q

aldosterone binds only to

A

MR

38
Q

what converts cortisol into its inactive form?

A

11B- dehydroxysteroid dehydrogenase 2

39
Q

why might cortisol binding to both receptors be a problem for those suffering from cushing’s

A

enzyme that converts cortisol to inactive form is overwhelmed so some cortisol start binding to MR –> acts like aldosterone –> you get hypertension

eLCRS - 엔도 (20 decks)

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