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PMCOL 200 Final > adrenocorticosteroids > Flashcards

adrenocorticosteroids Flashcards

1
Q

Where are the 2 adrenal glands located in relation to the kidney?

a) beside
b) in front
c) below
d) behind

A

a) beside

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2
Q

What are the 2 main divisions/layers of the adrenal gland? Which one is the innermost layer?

A

1) cortex

2) medulla (innermost)

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3
Q

What are the 2 main hormones that the adrenal medulla produces?

A

1) adrenaline

2) catecholamines/AA hormones

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4
Q

What are the 3 zones/layers of the adrenal cortex?

A

1) zona glomerulosa
2) zona fasciculata
3) zona reticularis

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5
Q

The adrenal cortex produces ____________ hormones.

A

steroid

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6
Q

What is the common precursor for all adrenal steroid hormones?

A

cholesterol

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7
Q

What are the 3 types of steroid hormones produced by the adrenal cortex? For each type of steroid hormone, provide: function, adrenal cortex zone that produces it, example hormone.

(hint: salt, sugar, sex)

A

1) mineralocorticoids (salt)
- salt balance
- zona glomerulosa
- aldosterone

2) glucocorticoids (sugar)
- metabolic and immune effects
- zona fasciculata
- cortisol

3) androgens (sex)
- act as precursor for strong androgens (testosterone) and estrogens
- zona reticularis
- DHEA (precursor androgen)

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8
Q

What is the HPA axis? (i.e. what does it stand for?)

A

hypothalamus-pituitary-adrenal axis

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9
Q

What response does the HPA axis control?

a) glucocorticoid response
b) mineralocorticoid response

A

a) glucocorticoid response

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10
Q

HPA axis controls release of ________ from the zona ________.

A

cortisol, zona fasciculata

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11
Q

in order of release from the hypothalamus –> anterior pituitary –> adrenal cortex, which is correct (HPA axis)?

a) CRH –> ACTH –> cortisol
b) cortisol –> ACTH –> CRH
c) ACTH –> CRH –> cortisol
d) cortisol –> CRH –> ACTH

A

a) CRH –> ACTH –> cortisol

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12
Q

Does cortisol exert positive or negative feedback on CRH and ACTH?

A

negative feedback

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13
Q

What is the function of cortisol?

A

immunosuppression

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14
Q

What response does the RAAS system control?

a) glucocorticoid response
b) mineralocorticoid response

A

b) mineralocorticoid response

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15
Q

What does RAAS stand for? (hint: which hormone does this system release?)

A

renin-angiotensin-aldosterone system

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16
Q

What is the primary role of RAAS?

A

control blood pressure and blood volume

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17
Q

what is the primary target organ of aldosterone?

A

kidneys

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18
Q

Aldosterone promotes _______ and ________ reabsorption and ________ excretion.

A

Na+ and H2O reabsorption

K+ excretion

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19
Q

What are the 4 steps of steroid hormone action?

A

1) hormone binds to unliganded receptor in complex with Hsp90 in CYTOPLASM
2) hormone dissociates from Hsp + is transported to nucleus
3) dimerized receptors interact with DNA and influence TRANSCRIPTION of TARGET GENES
4) GRE - glucocorticoid receptor/response element

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20
Q

What are the 2 key targets of GR (glucocorticosteroid response/receptor) binding?

A

lipocortin and COX-2

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21
Q

TRUE or FALSE: a given steroid has different affinities for either the glucocorticoid receptor or the mineralocorticoid receptor.

A

TRUE - steroids lie on a spectrum where one end represents high affinity to glucocorticoid receptor binding and the other end represents high affinity to mineralocorticoid receptor binding

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22
Q

TRUE or FALSE: Cortisol can act on both the glucocorticoid receptor and the mineralocorticoid receptor, but it has a higher affinity for the glucocorticoid receptor.

A

FALSE - cortisol has EQUAL AFFINITY for both GC and MC receptors

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23
Q

What enzyme is responsible for activating cortisol IN VIVO? what is the precursor of cortisol in vivo?

A

enzyme: 11-beta-hydroxysteroid dehydrogenase, type 1

cortisone –enzyme–> cortisol
ketone –enzyme–> hydroxyl

24
Q

Explain why, even though cortisol has a 1:1 affinity for GC and MC receptors, it has weak MC effects IN VIVO?

A

kidney cells (MC targets) produce 11-beta-hydroxysteroid dehydrogenase, type 2, which DEACTIVATES cortisol

i.e. cortisol –enzyme–> cortisone

25
Q

What is the difference between 11-beta-hydroxysteroid dehydrogenase, type 1 and type 2?

A

type 1: cortisone –> cortisol

type 2: cortisol –> cortisone

26
Q

Which is the active form?

a) prednisone
b) prednisolone

A

b) prednisolone

27
Q

Which one is more widely used (oral/injection)?

a) prednisone
b) prednisolone

A

a) prednisone

28
Q

Which one has a strong topical effect?

a) prednisone
b) prednisolone

A

b) prednisolone

29
Q

What is the structural difference between prednisone and prednisolone?

A 
prednisone = ketone
prednisolone = hydroxyl
30
Q

1) TRUE or FALSE: prednisone is significantly metabolized by the liver and GC target tissues in order to become prednisolone.
2) What is the term used for this metabolism of a drug by the liver to become an active form of the drug?

A

1) TRUE

2) first pass metabolism

31
Q

Pseudohyperaldosteronism is caused by licorice overdose. Explain how this works.

A
  • licorice contains an inhibitor of the an 11-beta-hydroxysteroid dehydrogenase, type 2 inhibitor (remember: type 2 inhibits cortisol binding to MC receptors)
  • this allows glucocorticoids like cortisol to bind to aldosterone target tissues (e.g. kidney), which is the WRONG EFFECT of cortisol IN VIVO
  • aldosterone increases Na and H2O reabsorption
  • reabsorption of Na and H2O results in high blood pressure
32
Q

What is the genetic disease that results in pseudohyperaldosteronism? what causes this genetic disease?

A

apparent mineralocorticoid excess

caused by mutation in 11-beta-hydroxysteroid dehydrogenase, type 2 gene

33
Q

What is the overall metabolic effect of glucocorticoids?

a) catabolic
b) anabolic

A

a) catabolic

34
Q

Do glucocorticoids increase or decrease circulating glucose?

35
Q

TRUE or FALSE: glucocorticoids lead to fat deposition in limbs but fat breakdown in the trunk.

A

FALSE - GC –> fat deposition in trunk + fat breakdown in limbs

36
Q

Glucocorticoids cause a/an ___________ of muscle and bone mass in _________.

a) loss; the trunk
b) loss; the limbs
c) gain; the trunk
d) gain; the limbs

A

b) loss; the limbs

37
Q

What is one term (2 words) that summarize the effects of fat/lipid balance as a result of glucocorticoid action?

A

“skinny fat”

38
Q

What are the 2 key mechanisms in glucocorticoid anti-inflammatory effects?

A

1) glucocorticoids inhibit AA generation
2) glucocorticoids inhibit prostanoid synthesis

note: these mechanisms cause DOWNSTREAM effects on inflammatory reactions

39
Q

In the anti-inflammatory mechanism, glucocorticoids cause _______ suppression.

a) COX-1
b) COX-2
c) COX-1 and COX-2

A

b) COX-2 suppression

40
Q

Explain the mechanism of glucocorticoids in COX-2 suppression. (hint: what does COX-2 do?)

A
  • COX-2 = inflammatory mediator
  • COX-2 metabolizes arachidonic acid to prostanoids
  • glucocorticoid suppresses TRANSCRIPTION of COX-2 GENE –> suppression of COX-2 expression on the PROTEIN levels
41
Q

TRUE or FALSE: Glucocorticoid regulation of COX-2 involves direct receptor antagonism.

A

FALSE - glucocorticoids suppress COX-2 gene expression

42
Q

Why does lipocortin induction by glucocorticoid receptor activation result in anti-inflammatory effects? (i.e. explain the mechanism)

A
  • lipocortin has annexin A which has 2 anti-inflammatory roles:
    1) direct effects on leukocytes –> inhibit tissue infiltration
    2) suppression of phospholipase A2 (PLA2) activity –> prevent AA generation –> suppress generation of prostanoids
43
Q

what is another name for lipocortins? why?

A

annexins –> lipocortins are characterized by annexin repeats

44
Q

What causes Addison’s disease?

a) insufficient adrenocorticosteroids (GC and MC)
b) excess adrenocorticosteroids (GC and MC)

A

a) insufficient adrenocorticosteroids

45
Q

what are the 4 symptoms of Addison’s disease?

A

1) fatigue
2) salt imbalance
3) sugar imbalance
4) skin discoloration

46
Q

What drug is used to treat Addison’s disease?

A

HYDROCORTISONE

47
Q

Cushing’s syndrome is caused by:

a) insufficient adrenocorticosteroids (GC and MC)
b) excess adrenocorticosteroids (GC and MC)
c) excessive cortisol
d) insufficient cortisol

A

c) excessive cortisol

48
Q

What are the 4 causes of Cushing’s syndrome?

A

1) adrenal tumor (cortisol-producing)
2) pituitary tumor (ACTH-producing)
3) drug induced
4) ectopic tumor (ACTH-producing)

49
Q

What are the 3 symptoms of Cushing’s syndrome?

A

1) round face
2) fat deposition in trunk
3) muscle loss, osteoporosis (protein and bone catabolism)

50
Q

What is the treatment for Cushing’s Syndrome?

A
  • resect adrenal or pituitary tumor

- follow with gradual adjustment towards maintenance dose of CORTISOL

51
Q

What are the main therapeutic effects of glucocorticoids?

A

1) anti-inflammatory
2) immunosuppressive
3) treat asthma
4) treat hematologic disorders

52
Q

What is the metabolic side effects of glucocorticoids?

A

hyperglycemia

53
Q

What is immunosuppressive side effects of glucocorticoids?

A

latent infections can emerge

54
Q

What is the catabolic side effect of glucocorticoids?

A

osteoporosis and muscle wasting

55
Q

what is the anti-inflammatory side effect of glucocorticoids?

A

slow wound healing and ulceration

56
Q

TRUE or FALSE: glucocorticoids may lead to hypotension and psychosis.

A

FALSE - HYPERtension and psychosis

57
Q

Why do you need to use tapering when stopping the long-term use of glucocorticoids? (i.e. what does abruptly stopping the use of GC lead to?)

A
  • abruptly stopping GC –> Addison-like symptoms
  • this is due to negative feedback of GC administration on CRH and ACTH production
  • if you stop abruptly, body does not have time to readjust
  • therefore. tapering is necessary

PMCOL 200 Final (11 decks)

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