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Therapeutics 2 > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

Describe how mineralocorticoid synthesis is regulated.

A

Aldosterone synthesis is not regulated by the HPA axis, unlike cortisol. Aldosterone synthesis is regulated by the renin-angiotensin-aldosterone system, one of the end results of which is aldosterone production.

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2
Q

Glucocorticoids upregulate the gluconeogenic enzyme ________ and the anti-inflammatory enzyme __________.

A

PEP carboxykinase, lipocortin 1

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3
Q

Name a mechanism other than eicosanoid synthesis suppression by which glucocorticoids suppress inflammation.

A

binding to and preventing NFkB from binding to DNA

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4
Q

Outline the RAS system, including significant hormones, enzymes, and organs.

A

It begins with the liver, which releases angiotensinogen. This is converted by renin (released by the kidneys) to angiotensin I. ACE in the lungs converts angiotensin I to angiotensin II. Angiotensin II has several effects, one of which is on the adrenal glands, where it stimulates aldosterone release.

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5
Q

Describe the physiologic effects of glucocorticoids on the liver.

A

(1) increased gluconeogenesis

(2) increased glycogen synthesis

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6
Q

What are the effects of glucocorticoids on muscle tissue?

A

(1) decreased sensitivity to insulin
(2) decreased protein synthesis
(3) promoting of protein degradation

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7
Q

What are the effects of glucocorticoids on adipose tissue?

A

(1) breakdown of fatty acids

(2) decreased sensitivity to insulin

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8
Q

How is the immune system affected by glucocorticoids?

A

(1) inflammation suppression via blocking of eicosanoid synthesis
(2) immunosuppression by cytokine synthesis suppression

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9
Q

What is Addison’s disease?

A

hypoadrenalism; by some mechanism the body’s ability to synthesize or release glucocorticoids has been compromised. The body cannot handle stress.

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10
Q

Addison’s disease symptoms

A

extreme weakness, mental depression, N/V/anorexia, anemia, hyperpigmentation of skin, hypotension

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11
Q

Which symptoms of Addison’s disease are unique to primary Addison’s?

A

hyperpigmentation of the skin and hypotension

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12
Q

How are (1) CRH (2) ACTH (3) cortisol and (4) aldosterone levels affected by (a) primary (b) secondary and (c) tertiary Addison’s disease?

A 
1a&b: elevated
1c: decreased
2a: elevated
2b: decreased
2c: decreased
3a,b,&c: decreased
4a: decreased
4b&c: unaffected
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13
Q

What is Cushing’s disease?

A

hyperadrenalism

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14
Q

What are the potential causes of Cushing’s disease?

A

(1) excess exogenous glucocorticoids (drugs)
(2) adrenal carcinoma
(3) ectopic production of ACTH via some bodily tumor
(4) pituitary tumor

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15
Q

symptoms of Cushing’s disease

A

(1) increased protein synthesis
(2) increased BG
(3) osteoporosis
(4) opportunistic infections form immunosuppression

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16
Q

How are (1) CRH (2) ACTH and (3) cortisol levels affected in (a) adrenal (b) pituitary and (c) ectopic Cushing’s disease?

A

1a,b,&c: decreased
2a: decreased
2b&c: elevated
3a,b,&c: elevated

17
Q

A lack of 17-alpha hydroxylation strictly in the adrenal cortex results in _____ disease. Because it is only in the adrenal cortex, __________ will develop normally, but levels of ______ will still be low.

A

Conn’s, sex organs, cortisol

18
Q

What symptoms would suggest Conn’s syndrome to a practitioner?

A

(1) hypernatremia
(2) alkalosis
(3) polyuria (increased salt in blood causes increased thirst)
(4) hypertension

19
Q

The ideal glucocorticoid will maximize _________ activity while minimizing _________ activity.

A

anti-inflammatory, mineralocorticoid

20
Q

What structural elements are required for glucocorticoid activity?

A

(1) 4,5-double bond
(2) 3 ketone
(3) 11-beta hydroxyl
(4) 17-alpha hydroxyl

21
Q

What structural elements are required for mineralocorticoid activity?

A

(1) 4,5-double bond
(2) 3 ketone
hydroxyls not required/less important

22
Q

Explain why topical cortisone is not effective, but systemic cortisone is.

A

Cortisone is inactive and requires activation in the liver by 11-beta hydroxysteroid dehydrogenase. If applied topically, this activation will never take place.

23
Q

Name some commonly used glucocorticoids in each class (short, intermediate, and long acting)

A

short: hydrocortisone, cortisone
intermediate: prednisone, prednisolone, methylprednisolone, triamcinolone
long: beta/dexa

24
Q

Which glucocorticoid has a greatly enhanced mineralocorticoid activity and is used in mineralocorticoid replacement therapy? What structural element is responsible for this?

A

the 9-alpha fluoro group of fludrocortisone adds some GC activity, but even more MC activity

25
Q

What structural modification has been made to prednisone and prednisolone that increase their GC activity? By how much does it do this?

A

An extra double bond between C1&2, GC activity enhance about 4 times and MC reduced to 0.25

26
Q

Methylprednisolone has an extra methyl group at carbon __. What effect does this have on GC an MC activity?

A

6, GC increased to 5x, MC almost 0

27
Q

The methyl group at carbon __ in dexa/betamethasone increases GC activity to ___ times that of hydrocortisone.

A

16, 25

28
Q

Modification of the hydroxyl group at carbon ___ to a(n) ______ allows for control of the absorption/length of action of glucocorticoids.

A

21, ester

29
Q

Describe the effect of conjugating the hydroxyl with an acetate/butyrate, succinate, and phosphate group at carbon 21.

A

acetate/butyrate: increases lipophilicity and prolongs duration of action

succinate: slows hydrolysis
phosphate: increases solubility to enhance drug delivery, suitable for IM or IV injection in emergency situations

30
Q

What structural modifications are most common to topical GCs? Why is this?

A

halogenation, addition of acetonide ring or esterification at C17

increases lipophilicity to aid in absorption

31
Q

Substitution with what halogen at what carbon is commonly employed to increase topical anti-inflammatory activity?

A

chlorine at C21

32
Q

Give examples of some 21-chlorocorticoids.

A

clobetasol, halobetasol, halcinonide

33
Q

Give two examples of medium potency topical steroids.

A

fluticasone propionate, mometasone furoate

34
Q

Inhaled corticosteroids must have high lipophilicity, but solubility is not as important because _________?

A

poorly soluble inhaled glucocorticoids are acceptable because the microcrystals that form can sit in the airways and slowly be absorbed into the airways.

35
Q

What are some adverse effects associated with glucocorticoid therapy?

A

(1) crossover mineralocorticoid activity-increased BP and edema
(2) steroid myopathy
(3) osteoporosis
(4) increased BG
(5) fat redistribution
(6) reduced long bone growth in children
(7) adrenal insufficiency upon withdrawal (Addisonian crisis)

Therapeutics 2 (9 decks)

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