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Pharmacology > Adrenocortical Steroids > Flashcards

Adrenocortical Steroids Flashcards

0
Q

secretes glucocorticoids

A

zona fasciculata

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1
Q

secretes mineralocorticoids

A

zona glomerulosa

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2
Q

secretes the androgens

A

zona reticularis

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3
Q

secretes the catecholamines (norepinephrine, epi)

A

medulla

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4
Q

principal endogenous glucocorticoid substance produced by zona fasciculata is the

A

cortisol

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5
Q

cortisol secretion is regulated by

A

ACTH from the anterior pituitary

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6
Q

circadian rhythm pattern

A

it peaks early morning (before waking up) and after meals

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7
Q

Main mineralocorticoid is _______ which is regulated by Renin- Angiotensin system in response to sodium level and ECF.

A

aldosterone

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8
Q

Main androgen secreted is ____

A

Dehydroepiandrosterone (DHEA)

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9
Q

oral absorption of glucocorticoids

A

Rapidly and completely absorbed

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10
Q

Water soluble esters

A

via IV administration ➡️ high concentrations in tissue fluids

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11
Q

Insoluble esters

A

via IM administration ➡️ slowly absorbed; more prolonged effects

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12
Q

Local administration of glucocorticoids

A

also absorbed (some systemic)

same pharmacokinetic pathways as glucorticoids given systemically

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13
Q

TRANSPORT of glucocorticoids

A

Protein bound

  • 90% to Corticosteroid-Binding Globulin (CBG)
  • albumin (loosely bound)]
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14
Q

are largely bound to albumin rather than CBG.

A

Synthetic corticosteroids such as dexamethasone

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15
Q

CBG is increased in

A

pregnancy, with estrogen administration and in hyperthyroidism

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16
Q

20% of cortisol is converted to this bio inactive form

A

cortisone

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17
Q

more resistant to metabolism➡️longer acting

A

synthetic congeners

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18
Q

urine excretion of glucocorticoids

A

a. (2/3) conjugates of glucuronide and sulfate

b. (1/3) dihydroxy ketone metabolites

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19
Q

a gauge of the response of cortisol to ACTH stimulation/repression when exogenous glucocorticoids are given

A

17-hydroxysteroids

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20
Q

glucocorticoid interaction: responsible for the metabolic effects

A

promoters on target genes

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21
Q

glucocorticoid interaction: responsible for the anti-inflammatory effects

A

repressors on target genes

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22
Q

glucocorticoid interaction: regulate proinflammatory cytokines, growth factors, etc (delayed onset of effects)

A

transcription factors

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23
Q

glucocorticoid classification based on

A
  1. Duration of action
  2. RELATIVE potencies on
    a. Sodium retention
    b. effects on CHO metabolism
    c. anti-inflammatory effects
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24
Q

potency to affect glucose metabolism closely parallel their potency as an anti-inflammatory

A

glucocorticoids

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25
Q

short acting glucocorticoids

A

Hydrocortisone

Cortisone

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26
Q

intermediate acting glucocorticoids

A

Prednisone
Prednisolone
Methylprednisolone
Triamcinolone

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27
Q

long acting glucocorticoids

A

Dexamethasone

Betamethasone

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28
Q

equal anti inflamm and salt retaining activity at 25 mg

A

CORTISONE

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29
Q

equal salt retaining activity and anti inflammatory activity at 20mg

A

HYDROCORTISONE

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30
Q

intermediate acting GC with no salt retaining activity at 4mg

A

TRIAMCINOLONE

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31
Q

intermediate acting GCs with same anti inflamm 4 and same mineralcorticoid 0.8 at dose of 5 mg

A

PREDNISONE

PREDNISOLONE

32
Q

at 0.75 mg dose, have no salt retaining activity and 25 anti inflamm

A

DEXAMETHASONE

BETAMETHASONE

33
Q

SHORT ACTING Half life:

A

8-12 hours

34
Q

pharmacologic preparation of the cortisol

A

hydrocortisone

35
Q

lesser anti-inflammatory and salt retaining activity when compared to Hydrocortisone at standard dose = less potent

A

Cortisone

36
Q

serves as a prodrug of Prednisolone

A

Prednisone

37
Q

addition of methyl group makes it more potent (higher anti- inflammatory activity at a lower dose)

A

Methylprednisolone

38
Q

same as methylprednisone but no salt-retaining activity

A

Triamcinolone

39
Q

very high anti-inflammatory activity at a very low dose

NO salt-retaining activity

A

LONG ACTING

Dexamethasone
Betamethasone

40
Q

Effects of Glucocorticosteroids: PROTEIN METABOLISM

A

a. Accelerates protein degradation causing release of amino acids.
b. Inhibits protein synthesis
c. skin, connective tissue, muscle fibers are mostly affected

41
Q

AE of GCs in relation to protein metab

A

Decrease in muscle mass/strength; weakness

skin becomes thin, fragile, and easily bruised

42
Q

Effects of Glucocorticosteroids: LIPID METABOLISM

A

a. Lipolysis via permissive facilitation of lipolytic hormones leads to increase FFA & glycerol
b. Redistribution of body fat

43
Q

physiologic role of GC in carbohydrate metabolism

A

maintain adequate blood glucose levels especially during the fasting state

44
Q

mechanism of GC. on maintaining glucose level

A

a. Gluconeogenesis: increase serum glucose
b. Glycogen storage in the liver: for rapid mobilization
c. Inhibits glucose uptake and utilization- especially in muscles and adipose tissue

45
Q

AE of Gcs in relation to carb metab

A

hyperglcemia, diabetes mellitus

46
Q

how does GC LIMIT the inflammatory cells at the site of injury/trauma

A

Increasing circulating neutrophils
-neutrophils are released from the bone marrow but are unable to leave the blood vessels (stay in circulation)

Decreasing circulating lymphocytes, monocytes, basophils, eosinophils
-/;?:leave the circulation and move to the lymphoid tissue

47
Q

when GC Inhibits func. of tissue macrophages & Antigen presenting cells

A
  • decrease phagocytosis

- decrease production of cytokines

48
Q

anti inflamm effect of GCs

A

Increasing circulating neutrophils

Decreasing circulating lymphocytes, monocytes, basophils, eosinophils

Inhibits func. of tissue macrophages & Antigen presenting cells

decrease phagocytosis

decrease production of cytokines

Inhibits activation of phospholipase A

decrease prostaglandins, leukotrienes

Decrease expression of COX-2

Suppress mast cell degranulation

49
Q

GC immunosuppressive effects

A

inhibition of:
a. Antigen expression

b. Sensitization of cytotoxic T lymphocytes
c. Primary antibody formation

50
Q

AE of GC in relation to immunosuppression

A

Susceptibility to infection- could be bacterial, viral or fungal infection; common occurrence: reactivation of latent TB

51
Q

GC effects on bone metab

A

Inhibits bone formation by osteoblasts

Inhibit intestinal Ca absorption

Enhance renal excretion of Ca

52
Q

ae of GC in relation to bone metabolism

A

a. Arrest of growth (children)
b. Osteoperosis (adults)
c. Osteonecrosis of femoral head- avascular or asceptic necrosis, disruption of vascular supply to femoral head

53
Q

effect of GC on CNS

A

a. Mood changes: restlessness, mild euphoria, depression, acute psychosis
b. High doses: decrease seizure threshold, caution when used in epileptics (because it can increase occurrence of seizure attacks)

54
Q

PEPTIC ULCER FORMATION effect by GC mechanism

A

suppression of local immune response to H. Pylori

a. Increased gastric acid and pepsin secretion
b. Weakness of mucosal defenses

55
Q

complication of GC to eyes

A

a. Posterior subcapsular cataracts

b. Increased IOP, can lead to glaucoma

56
Q

common effect of discontinuing steroids

A

flare up of underlying disease

57
Q

effect of discontinuing steroids

A

a. flare up of underlying disease
b. steroid withdrawal syndrome
c. symptoms of acute adrenal insufficiency

58
Q

goals of Dexamethasone Suppression Test

A
  1. To diagnose hypercortisolism (Cushing’s syndrome)

2. To distinguish the source of ↑cortisol (if already verified that there is an increase)

59
Q

adrenal disorders where GCs are used

A
  1. Chronic Adrenal Insufficiency (Addison’s disease)
  2. Acute Adrenal Insufficiency
  3. Congenital Adrenal Hyperplasia (CAH)
60
Q

types of chronic adrenal insufficiency

A

a. Primary chronic adrenal insufficiency – adrenal origin

b. Secondary adrenal insufficiency – pituitary or hypothalamic

61
Q

Abrupt withdrawal of steroids especially if used at high doses or prolonged periods

A

Acute Adrenal Insufficiency

62
Q

clinical feature of acute adrenal insufficiency

A

+ +

hypoNa , hyperK , hypotension, circulatory collapse

63
Q

immediate tx for acute adrenal insufficiency

A

IV hydrocortisone, fluid and electrolyte correction

Revert back to maintenance therapy w/ steroids once patient is stabilized

64
Q

blocks the downstream synthesis ➡️ cortisol deficiency. With the block, there will be a deviation to other pathways and this can now lead to excess adrenal androgens ➡️ virilization in female genitalia

A

21-hydroxylase deficiency

65
Q

most common non adrenal use of GCs

A

bone and jt disorders: osteoarthritis, bursitis, tendinitis

66
Q

first line treatment in nephrotic syndrome

A

prednisone

67
Q

GC used To prevent or reduce cerebral edema (can be a result of tumor or after brain surgery)

A

Dexamethasone

68
Q

GC used to
To prevent respiratory distress syndrome in preterm infants
a. Increase rate of alveolar development
b. Stimulates synthesis of surfactant

A

betamethasone, or dexamethasone

69
Q

Most potent endogenous mineralocorticoid

A

aldosterone

70
Q

salt retaining activity is very potent 25 x compared to Hydrocortisone
anti-inflammatory activity 10x that of Hydrocortisone

A

Fludrocortisone

71
Q

Principal Sites of Receptor Activation of Mineralocorticoids

A

a. Distal convoluted tubules

b. Collecting ducts

72
Q

effects of mineralocorticoids

A

Reabsorption – Na , H2O, HCO3

Excretion—K , H

73
Q

adr of mineralocorticoids

A

Hypokalemia – due to excretion of K +

Metabolic alkalosis - due to excretion of H ions

Hypertension - due to reabsorption of Na

74
Q

physiologic role of adrenal androgens in males

A

of little biologic importance; DO NOT stimulate or support MAJOR androgen-dependent pubertal changes

75
Q

physiologic imp of mineralocorticoids in post menopausal women

A

source of estrone

76
Q

pathologic adrenal androgens in prepubertal males

A

cause isosexual precocious puberty

-early development of their secondary sex characteristics

77
Q

pathologic effect of mineralicorticoids in adult and prepubertal female

A

virilizing effects; hirsutism, cyclic acne, anovulation, infertility

78
Q

us of adrenal androgens

A

a. Improved well-being and sexuality

b. Enhanced athletic performance (doping)

Pharmacology (8 decks)

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