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Pharm Exam 5 > Adrenal Agents > Flashcards

Adrenal Agents Flashcards

1
Q

Adrenal cortex produces?

A

CORTICOSTEROIDS

  • mineralocorticoids (Aldosterone)
  • glucocorticoids (hydrocortisone)
  • androgens
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2
Q

Adrenal medulla produces?

A

CATECHOLAMINES

  • E
  • NE
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3
Q

Mineralocorticoid (aldosterone) actions:

A
  • inc Na reabsorption at renal collecting tubule –> regulates blood pressure
  • Inc excretion of K
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4
Q

GLucocorticoids (cortisol/hydrocortisone) actions:

A
  • restore homeostasis after exposure to physical/emotional stresses
  • inc blood glucose levels + other metabolic effects
  • works with E and NE responses
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5
Q

Androgens actions

A

(dehydroepiandrosterone (DHEA) and androstenedione)

  • weak -converted to testosterone
  • major source of female androgens
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6
Q

Major drug target enzymes in corticosteroid synthesis?

A
  • Cholesterol desmolase
  • 17alpha-hydroxylase
  • 11beta-hydroxylase
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7
Q
  • What is signal for inc steroid synthesis by adrenals?

- Exact effects on adrenals?

A

-inc corticotropin releasing hormone (CRH) from hypothalamus –> inc adrenal corticotropic hormone (ACTH) from anterior pituitary –> stimulates steroid synthesis by adrenals

  • increased import of cholesterol
  • inc transcription of cholesterol desmolase and other enzymes involved in steroid synthesis
  • growth of adrenal cortex
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8
Q

Role of hypothalamus in hypothalamus-pituitary-adrenal (HPA) axis?

A

-inc corticotropin releasing hormone (CRH) from hypothalamus

(–> inc adrenal corticotropic hormone (ACTH) from anterior pituitary –> stimulates steroid synthesis by adrenals)

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9
Q

Role of anterior pituitary in hypothalamus-pituitary-adrenal (HPA) axis?

A

-CRH binds G-proteins on anterior pit = rapid release of preformed ACTH and slow inc in synth of ACTH precurson

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10
Q

Role of adrenal cortex in hypothalamus-pituitary-adrenal (HPA) axis?

A
  • ACTH binds G-protein (GPCR), melanocortin 2 receptor (MC2R) on surface of adrenals
  • inc steroidogenic enzyme expression and synthesis + secretion of cortical steroids (++CORTISOL AND ++ADRENAL ANDROGENS)
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11
Q

ACTH and aldosterone synthesis?

A

(ACTH give base synthesis of aldosterone. aldosterone synthesis by adrenal cortex stimulated by angiotensin2 more so)

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12
Q

What is the feedback control in hypothalamus-pituitary-adrenal axis?

A

Circulating cortisol neg inhibits ant pit and hypothalamus

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13
Q

How do cortcosteroids exert their effect on cell?

A
  • bind glucocorticoid receptor or mineralocorticoid receptor in the cytoplasm
  • go to nucleus to increase or decrease trascription
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14
Q

How do cortisol and aldosterone regulate if cortisol levels are usually way hgiher than aldosterone?

A

-enzyme type 2 isoform of 11beta-hydroxysteroid dehydrogenase converts cortisol to cortisone with does not bind the mineralocorticoid receptor so aldosterone can have its efefct to

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15
Q

Side effects of high glucocorticoids on the nervous system?

A

psychiatric disorders

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16
Q

Side effects of high glucocorticoids on the cardiovascular system?

A

cardiovascular disease

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17
Q

Side effects of high glucocorticoids on the musculoskeletal system?

A

osteoporosis

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18
Q

Side effects of high glucocorticoids on the visual system?

A

glaucoma

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19
Q

Side effects of high glucocorticoids on glucose and liver metabolism?

A

obesity and hyperglycemia

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20
Q

Side effects of high glucocorticoids on the reproductive system?

A

gonadal virtzation

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21
Q

What is the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-hydroxylase type 2 - 11beta-HSD2) used for?

A

converts cortisol to cortisone with does not bind the mineralocorticoid receptor so aldosterone can have its effect to regulate since cortisol levels are so much higher it gives aldo a chance

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22
Q

Physiological effect/Uses of glucocorticoids on the nervous system?

A
  • physiological homestasis

- response to stressors

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23
Q

Physiological effects/Uses of glucocorticoids on the cardiovascular system?

A
  • anti-inflammatory
  • cardiomyocyte survival
  • homeostasis of blood pressure and vascular tone
  • ant-angigenesis
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24
Q

Physiological effects/Uses of glucocorticoids on the immune system:

A
  • suppression of proinflammatory cytokines

- regulation of immune cell maturation, migration, and apoptosis

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25
Q

Physiological effects/Uses of glucocorticoids on the musculoskeletal system?

A
  • anti-inflammatory
  • muscle anabolism and catabolism
  • insulin resistance
  • osteoblast apoptosis
  • osteoclastogenesis
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26
Q

Physiological effects/Uses of glucocorticoids on the visual system

A
  • anti-inflammatory
  • anti-angiogenesis
  • photoreceptor survival
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27
Q

Physiological effects/Uses of glucocorticoids on the respiratory system?

A

-suppression of cytokines, chemokines, and cell adhesion molecules

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28
Q

Physiological effects/Uses of glucocorticoids on glucose and liver metabolism?

A
  • glucose regulation

- lipid homeostasis

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29
Q

Physiological effects/Uses of glucocorticoids on the reproductive system

A
  • gonadal function in males and females

- fetal organ development and maturation

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30
Q

Physiological effects/Uses of glucocorticoids on the integumentary system?

A
  • anti-inflammatory
  • delayed wound healing
  • regulate epithelial integrity
31
Q

Glucocorticoids on development of a fetus?

A

-in babies who are going to be premies the glucocorticoids are given to speed up development of the lungs

32
Q

Cortisol and E/NE functions?

A
  • cortisol inc glycogen synthesis in the liver so that there can be increase glycogenolysis induced by E/NE (inc blood glucose)
  • cortisol ==> ++ upreg of receptors for E/NE (vascular tone reg - potentially hypotension if low cortisol levels)
  • cortisol inc expression of enzyme that converts NE into E in adrenal medulla
33
Q
  • Mineralocorticoid vs glucocorticoid use?

- mineralocorticoid fludrocortisone + a GC is used for?

A
  • glucocorticoids for almost anything while mineralos for replacement therapy
  • replacement therapy in adrenal insufficiency
34
Q

MOA for anti-inflammatory effects of corticosteroids?

A

1) inh of phospholipase A2 > dec production of lipd mediators (PG, leukotrienes, platelet activating factor)
2) Inh COX induction > dec PG synthesis
3) inh NO synthase induction > dec NO production
4) inh cytokine production > suppress cell-mediated inflam
5) inh mast cell activity and #s > fewer mast cell inflam mediators (his and 5HT)
6) vasoconstriction > dec local blood flow

35
Q

glucocorticoid effect on neurtrophils:

A

inc blood count

36
Q

glucocorticoid effect on macrophages and monocytes:

A

dec number and activity

37
Q

glucocorticoid effect on lymphocytes

A

dec blood count

38
Q

glucocorticoid effect on eosinophils

A

dec blood count

39
Q

glucocorticoid effect on basophils

A

dec blood count

40
Q

which corticosteroid is used as a mineralocorticoid?

A

Fludrocortisone

41
Q

Which corticosteroid as the most salt retaining potnecy?

A

fludrocortisone - mineralocorticoids retain salt

42
Q

Which glucocorticoids are pro-drugs?

Which enzyme converts?

A

cortisone –> cortisol
prednisone –> prednisolone

11beta- HSD type 1

43
Q

Topical gucocorticoid

-uses/effects?

A
  • reduce inflam and inh immune function for skin disorders (atopic dermatitis, psoriasis…etc)
  • antiproliferative qualities
  • MANY DIFFERENT POTENCIES
44
Q

Topical Corticosteroid side effects:

A
  • atrophy
  • acne
  • enhanced fungal infection
  • retard wound healing
  • contact dermatitis
  • glaucoma
  • cataracts

Systemic side-effects: hyopothalamus pit adrenal axis suppression; cushings syndrome; growth retardation

45
Q

Topical corticosteroid therapy principles:

A
  • start with low potency to try to control disease
  • avoid prolonged use –> use low potency if you have to
  • low potency on face (thin skin)
  • high potency on palms and soles (thicker skin)
  • do not use high potency in children - high surface area to body mass ratio
  • alternate day application to avoid tachyphylaxis (diminished benefit)
46
Q

How are glucocorticoids transported through the blood?

A

90% bound to albumin or corticosteroid binding protein (CBP) –> remaining unbound is ACTIVE FRACTION

47
Q

glucocorticoids in people with liver issues?

A

-they have low serum proteins ==> less steroids will be bound = need to give smaller doses

48
Q

Glucocorticoid metabolism and excretion?

A

liver met and kidney excretion

49
Q

Glucocorticoid drug interaction-

  • dec effects of steroid?
  • inc effects of steroid?
A
  • DEC-drugs that inc expression of P450s in liver should be avoided or youre going to lose effective therapeutic level of drug (barbs, carbamazepines, rafampin)
  • INC-drugs like estrogens and androgens compete for metabolism so INC active level of drug in circulation
50
Q

How do glucocorticoids increase Na retention and inc K secretion?

A

When they bind to mineralocorticoid receptors in renal collecting duct

51
Q

Glucocorticoid drug interacion-

-what happens with NSAIDS?

A

-inc risk of stomach ulcers

52
Q

Glucocorticoid drug interacion-

-glucocorticoids reduce effects of which types of drugs?

A
  • hypoglycemics
  • BP meds
  • glaucoma meds
53
Q

Adverse effects - glucocorticoids

-2 weeks or less of therapy:

A
  • even with high doses not major AEs
  • insomnia
  • hypomania
  • *-acute peptic ulcers
54
Q

Adverse effects - glucocorticoids

-more than 2 weeks of therapy:

A
  • iatrogenic Cushings
  • metabolic
  • myopathy
  • mast bacterial infections
  • sodium and fluid retention (11beta-HSD2 saturated)
  • hgih BP
  • *-HPA axis suppression (for up to 12 mo after stopping)
  • *-gastric acid and pepsin production (large doses) == + peptic ulcers
  • *-OSTEOPOROSIS - stim bone reabsorption inc osteoclast activity
55
Q

How to take a patient off of glucocorticoids?

A

must taper off slowly! - helps HPA axis come back online and other stuff..?

56
Q

Primary adrenal insufficiency

  • other name for disease?
  • most common cause US vs OUS
  • what is it/what happens?
  • tx?
A

-Addison’s disease
-US=autoimmune vs OUS=TB
-deficiency in cortisol, aldosterone and androgens
-ACTH and CRH are elevated bc no negative feedback
==> hypotension bc unresponsiveness of vascular smooth muscle to catecholamines
-TX= oral cortisol and fludrocortisone

57
Q

Secondary adrenal insufficiency

  • cause?
  • describe types?
  • what is Tx?
A

1) pituitary disease or hypothalamic disorders
2) a) pituitary
- decrease ACTH levels –> decreased cortisol levels (CRH levels inc bc dec cortisol induced neg feedback at hypothalamus) == basically pituitary is broken so hypothalamus pumps out CRH
b) hypothalamic disorder
- decrease CRH production –> dec ACTH and cortisol == bascially hypothalamus is broken so CRH is down and pituitary isnt making ACTH bc its not getting an CRH
* -oral cortisol NO NEED FOR FLUDROCORTISONE bc aldosterone levels are normal*

58
Q

Do Primary or secondary adrenal insufficiency patients have normal aldosterone levels?

A

-Secondary have normal aldosterone levels = dont need fludrocortisone bc Na and K levels are ok-ish

59
Q

Congenital adrenal hyperplasia

  • what is the issue?
  • what happens?
  • tx?
A

-most common issue is 21-hydroxylase deficiency
=dec cortisol and aldosterone
=inc ACTH (hyperplasia of adrenal cortex)
=inc androgens (build up of products is shunted toward testosterone production since aldosterone and cortisol production is broken) leading to virilization (sex changes due to hormones)
-tx: oral cortisol and fludrocortisone if needed

60
Q

21-hydroxylase

  • what does this enzyme do?
  • what does def cause? disease name?
A
  • important step in both aldosterone AND cortisol production
  • disease is called congenital adrenal hyperplasia = build up of mineralocorticoid (aldosterone product) and glucocorticoid (cortisol product) intermediates that get shunted to testosterone production
61
Q

21-hydroxylase deficiency - what does baby have?

A

-usually a female with male genetalia

62
Q

Dosing of glucocorticoids?

A

follow circadean pattern of body as with normal corticoid peaks and decreases .. so 2/3 dose given in morning and 1/3 dose given in afternoon

63
Q

Cushings syndrome

  • -what happens?
  • -causes?
  • affected indiv/issues?
A
  • 1) chronic glucocorticoid excess
  • 2) -chronic glucocorticoid therpy
  • pituitary tumor with ACTH secretion
  • extopic hypersection of ACTH by non pit tumor
  • adrenal tumor with inc cortisol secretion
    3) -adbominal and shoulder/back fat = buffalo hump
  • moon face - lipids in the face
  • thinning of the skin
  • poor wound healing
64
Q

Lab studies for Pit hypersecretion tumor

A

DEC CRH
INC ACTH

  • pit tumor secretes a lot of ACTH
  • ACTH stim adrenal cortex to make cortisol
  • cortisol feedbacks to hypothalamus so low CRH levels
65
Q

Lab studies for adrenal adenoma

A

DEC CRH
DEC ACTH

  • adrenal cortex tumor secretes a lot of corticoids
  • feedback to hypothal and pituitary to stop making CRH and ACTH
66
Q

Lab studies Ectopic ACTH production

A
  • DEC CRH
  • INC ACTH
  • some tumor somewhere secretes ACTH = more corticoids from adrenals
  • feedback to hypothal and pit to stop making CRH and ACTH (but ACTH is still being made elsewhere)
67
Q

Adrenocorticosteroid synthesis inhibitors-name the drugos:

A
  • aminolutethimide
  • metyrapone
  • ketoconazole
68
Q

Aminoglutethimide

  • type?
  • MOA?
  • tx for?
A
  • adrenocorticosteroid synthesis inh
  • blocks conversion of cholesterol to pregnenolone (first step of mineralo, gluco-corticoid and androgen synthesis
  • tx adrenocortal tumors and cushings syndrome
69
Q

Ketoconazole

  • type?
  • MOA?
  • used for?
  • AE?
A
  • adrenocorticosteroid synthesis inh – ANTIFUNGAL
  • inh 17alpha hydroxylase and 11beta hydroxylase at high levels (so conversion steps btw minceralos and glucocorts and glucocorts and androgens)
  • used to tx cushings syndrome
  • LIVER TOX
70
Q

Metyrapone

  • type?
  • MOA?
  • used for?
  • AE?
A
  • adrenocorticosteroid synthesis inh
  • selectvie 11beta-hydroxylase inh (final step to make aldosterone and cortisol)
  • for cushings syndrome
  • build up of androgens and 11beta-deoxycorticosterone
  • salt and water retention (HTN)
71
Q

Mifepristone

  • type?
  • high dose use?
  • other use?
A
  • glucocorticoid receptor antagonist - ONLY AT HIGH DOSES
  • anti progestin effects = terminate prego
  • tx inoperable patients with ectopic ACTH secretion or adrenal carcinoma
72
Q

Mineralocorticoid receptor antagonist?

A
  • spironolactone

- eplerenone

73
Q

Spironolactone

  • type? MOA?
  • uses?
  • AEs?
A

1) Mineralocorticoid receptor antagonist (ALSO ANDROGEN RECEPTOR ANTAGONIST)
2) *tx primary aldosteronism (adrenal cortex adenoma that secretes aldosterone)
- diuretic for HTN
- hirsutism in women (bc androgen receptor antagonist)
3) hyperkalemia - cardiac arrhythmias
- gynecomastia, skin rash, menstrual issues, GI issues

74
Q

Eplerenone

  • type?
  • uses?
  • AE?
A

1) Mineralocorticoid receptor antagonist (DOES NOT HIT ANDROGEN RECEPTOR)
2) Tx HTN
3) mild hyperkalemia

Pharm Exam 5 (10 decks)

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