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PDA Block 2 > Adrenal Steroids > Flashcards

Adrenal Steroids Flashcards

1
Q

How does the rate of secretion of steroids relate to the rate of synthesis

A

steroids are not stored. They are synthesized when they are needed. Therefore the rate of secretion is equal to the rate of synthesis

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2
Q

Describe the creation of aldosterone including where does it take place

A
  • Aldosterone is created in the zona glomerulosa of the adrenal gland
  • cholesterol → pregnenolone → desoxycorticosterone →aldosterone
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3
Q

Describe the production of cortisol including where it takes place

A

It takes place in the Zona fasciculata and reticularis

cholesterol → pregnenolone → desoxycortisol→ cortisol

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4
Q

What is the synthesis of cortisol controlled by

A

ACTH:Adrenocorticotropic hormone

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5
Q

What is the synthesis of Aldosterone controlled by

A

Angiotensin II and plasma K

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6
Q

Describe how adrenergic steroids are found

A

90% are bound to plasma proteins or albumin

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7
Q

How are adrenergic steroids inactivated and where

A

they are inactivated in the liver by

  1. Reduction of A ring
  2. sulfate conjugation
  3. Glucuronide conjugation
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8
Q

What adrenergic steroid structure would increase glucocorticoid activity and reduce mineralo- corticoid activity.

A

A 1,2-double bond and 16- substitution

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9
Q

What structures on an adrenergic steroid are necessary for function

A

Structures necessary for activity include 4,5-double bond, 3-ketone, 11-hydroxyl, 17-hydroxyl, 21-hydroxyl

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10
Q

Describe the mechanism of action of glucocorticoids

A
  1. glucocorticoid (that is probably bound to plasma protein or albumin) bind to a cytosolic steroid receptor
  2. translocated to the nucleus
  3. Stimulates transcription of mRNA
  4. stimulates mRNA directed protein synthesis
  5. proteins mediate glucocorticoid effect
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11
Q

describe the physiological effects of the glucocorticoids on Carbohydrate and protein metabolism

A
  • Mediated by Glucocorticoid receptor
  • Enhances liver gluconeogenesis from protein
  • Stimulates amino acid mobilization (skeletal muscle, skin, etc.)
  • Increases plasma glucose (bc GCs decrease uptake of glucose into tissues which increase plasma concentrations of glucose and liver concentration of glycogen)
  • Increases liver glycogen
  • Increases urinary nitrogen excretion
  • Reduces peripheral glucose utilization
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12
Q

describe the physiological effects of the glucocorticoids on Lipid metabolism

A
  • redistribution of fat (moon face, buffalo hump)

- stimulates release of fatty acids from adipose tissue

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13
Q

describe the physiological effects of the glucocorticoids on Mineral and electrolyte metabolism

A
  • mediated mineralocorticoid receptor in kidney
  • Cortisol = Aldosterone&raquo_space; Cortisone meaning that cortisol and aldosterone have equal affinity to the glucocorticoid receptor, but most cortisol is converted to cortisone via the enzyme 11B-hydroxysteroid dehydrogenase and cortisone does not bind to the mineralocorticoid receptor
  • therefore aldosterone is primarily responsible for the mineralocorticoid receptor mediated effects
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14
Q

The Mineralocorticoid receptor induces it effects via transcriptional activation. What are these effects

A
  • increased Na reabsorption
  • increased K and H ion excretion
  • Responsible for cardiovascular effects - hypertension
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15
Q

Effects of adrenal steroids on the CNS

A

-sleepiness, lability of mood

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16
Q

Effects of adrenal steroid on immune system

specifically discuss how they impact cell traffic or accumulation

A

General
-Mediated through NFkB pathway. Steroids decrease amount of inflammatory cells at the inflammatory site
-steroids reduce access of cells to target tissues
1. Lymphocytopenia and monocytopenia - redistribution of
cells out of vascular space
2. Prevent neutrophil adherence to endothelium
3. Inhibit action of chemotactic factors

17
Q

What immune cells do steroids change function in

A
  1. Macrophages
  2. B Lymphocytes (although nothing specific in notes about how)
  3. T Lymphocytes
18
Q

How do steroids influence macrophage function

A

a) Inhibits antigen processing
b) Inhibit binding to Fc receptors
c) Inhibit synthesis and release of IL-1

19
Q

how do steroids influence T-lymphocyte function

A

a) Interfere with macrophage antigen processing
b) Interfere with actions of lymphokines - IL-2, macrophage migration inhibitory factor, macrophage aggregating factor, monocyte chemotactic factor and lymphotoxin
c) Absence of IL-1 prevents activation
d) Reduces IL-2 synthesis

20
Q

Describe the relationship between IkBa and NFkB and Glucocorticoids

A

when NFkB is bound to IkBa it is inactive. When the immune system is stimulated it causes IkBa to dissociate from NFkB and that is how it allows NFkB to cause its downstream transcriptive effect.

BUT GCs bind to their receptor and then translocate to the nucleus and upregulates transcription of IFkB which binds to NFkB inhibiting the immune response

21
Q

Describe how glucocorticoids have an anti-inflammatory effect

A

-Inhibits signs and symptoms of inflammation by inhibiting
immune system
-Inhibits arachidonic acid release so synthesis of prostaglandins and leukotrienes is reduced.
-Inhibits induction of cyclooxygenase-2 by cytokines. (remember COX2 is primarily associated w inflammation and it converts AA to prostaglandins

22
Q

What are the 4 therapeutic principles of steroid therapy

A

-Therapeutic dose is variable and may change with therapy. (necessary dose may change as therapy progresses) Reevaluate frequently.

-therapy has lethal potential.
A single dose is usually without harmful effects. Prolonged

  • Use is not etiological or curative in most cases. Palliative or symptomatic therapy.
  • Abrupt discontinuation may be life-threatening due to adrenal -insufficiency. (bc it takes the anterior pituitary gland to begin making ACTH again, and it takes even longer for the adrenal gland to recognize that ACTH fully and begin producing cortisol again after taking cortisol for a while)
23
Q

What is the major use of glucocorticoid therapy

A

replacement therapy for adrenal insufficiency

24
Q

Uses of Adrenocortical Steroids

A

a. Adrenal insufficiency - steroid replacement therapy
b. Rheumatoid arthritis - use only in progressive disease in combination with salicylates, gold salts, and physical therapy.
c. Osteoarthritis - given into joint for acute inflammation.
d. Allergic diseases - hay fever, serum sickness, drug reaction, anaphylaxis, bronchial asthma.
e. Inflammatory diseases of eye, ear, skin, etc. Used locally. (bc you only want glucocorticoid activity not mineralocorticoid, so you use it locally to try to acheive this)
f. Cerebral edema.
g. Shock - questionable value.
h. Miscellaneous - organ transplantation, thrombocytopenia, liver diseases, collagen diseases, renal diseases, etc.

25
Q

Name five steroid drugs

A

a. Cortisol
b. Dexamethasone (Decadron®)
c. Prednisolone
d. Fludrocortisone (Florinef®)
e. Aldosterone

26
Q

What two things lead to steroid toxicity

A

rapid withdrawal or prolonged therapy

27
Q

What does rapid withdrawal of steroids lead to

A

Acute adrenal insufficiency occurs. Salt wasting and

cardiovascular collapse.

28
Q

What does two things can prolonged steroid therapy lead to

A
  1. Suppression of pituitary - adrenal function

2. Cushings syndrome

29
Q

Describe how prolonged steroid therapy can lead to suppression of pituitary-adrenal function

A

1) Related to dose and duration of therapy (Large doses for period longer than 2 weeks).
2) May last for periods longer than 12 mo.
3) Reduce dosage slowly.

30
Q

What are six symptoms of cushings syndrome and what are they mostly all associated with

A

-they are mostly all associated with the increased mobilization of proteins that steroids cause

1) Moon face and Buffalo hump.
2) Poor wound healing.
3) Thin skin.
4) Hypertension.
5) Thin extremities.
6) Striae.

31
Q

Name two glucocorticoid synthesis inhibitors

A
  1. Aminoglutethimide

2. Metyrapone****

32
Q

Metyrapone

A

synthesis inhibitor of glucocorticoids

-Blocks 11-beta hydroxylation so synthesis is stopped at 11-
desoxycortisol.

  • 11-Desoxycortisol does not inhibit ACTH release so plasma ACTH levels increase. (normally cortisol via a negative feedback loop with the anterior pituitary gland inhibits release of ACTH. But this drug stops the cortisol production pathway at the step 11-deoxycortisol. This intermediate has no effect on ACTH production by the anterior pituitary gland so the anterior pituitary continues to produce ACTH without inhibition)
  • ACTH stimulates synthesis and excretion of 17-hydroxycorticoids as 11-desoxycortisol.
  • this is used as a diagnostic test bc you shoudl expect to find an increase in 11-deoxycortisol in the urine
33
Q

Name the Antagonist drugs

A
  1. Mifepristone
  2. Spironolactone (Aldactone®) Eplerenone (Inspra™)
  3. Drospirenone
34
Q

Mifepristone

how does it work and what is it used for

A

a. Competitive antagonist at progesterone and glucocorticoid receptor
b. Termination of pregnancy
c. Treat Cushing Disease

35
Q

Spironolactone (Aldactone®) Eplerenone (Inspra™)

how does it work and what is it used for

A

a. Competitive antagonists at mineralocorticoid receptor
b. Diuretics
c. Treat Hypertension
d. Cardiac hypertrophy and heart failure

36
Q

Drospirenone

how does it work and what is it used for

A

a. Progesterone receptor agonist
1. Used with estrogen to suppress ovulation
2. Used with estrogen as hormone replacement therapy in post-menopausal women

b. Mineralocorticoid receptor antagonist
1. Diuretic
2. Antagonizes the salt retaining effects of estrogen

c. Androgen receptor antagonist

37
Q

Drospirenone can be both an agonist and an antagonist explain please

A

it is a progesterone agonist and a mineralocorticoid antagonist

PDA Block 2 (13 decks)

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