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PDA Block 2 > Adrenal Steroids > Flashcards

Adrenal Steroids Flashcards

1
Q

Steroidal Biochemical Pathways:

A
  1. Zona glomerulosa: cholesterol → pregnenolone → desoxycorticosterone → aldosterone
  2. Zona fasciculata and reticularis: cholesterol → pregnenolone → desoxycortisol → cortisol
  3. Zona fasciculata and reticularis: cholesterol → pregnenolone → androstenedione
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2
Q
  • What regulates synthesis of cortisol?
  • What regulates synthesis of aldosterone?
A
  • Corisol: ACTH
  • Alodsterone: angiotensin II and plasma potassium
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3
Q

Steroids are not stored:

A
  • synthesized when needed
  • rate of secretion = rate of synthesis
  • 90% bound in plasma by CBG and albumin
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4
Q

How are steroids inactivated?

A
  • Inactivated in liver:
    1. Reduction of A ring
    2. Sulfate conjugation
    3. Glucuronide conjugation
      • make substances more polar
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5
Q

Describes the basics of this loop:

A
  • Negative feedback loop:
    1. ACTH provides a stimulatory effect on the adrenal gland
    2. Adrenal gland produces cortisol
    3. Cortisol has inhibitory effects on the production of ACTH
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6
Q

What is the Basic Pharmacological Mechanism of Action for Adrenocortical Steroids?

A
  1. Binds to cytosolic steroid receptor
  2. Translocated to nucleus
  3. Stimulates transcription of mRNA
  4. Stimulates mRNA directed protein synthesis
  5. Proteins mediate glucocorticoid effect
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7
Q

How do glucocorticoids effect peripheral carbohydrate and amino acid metabolism?

A

Mediated by Glucocorticoid receptor:

  1. Enhances liver gluconeogenesis from protein
  2. Stimulates amino acid mobilization (skeletal muscle, skin, etc.)
    • cause muscle wasting
  3. Increases plasma glucose
    • cause glycosuria
  4. Increases liver glycogen
  5. Increases urinary nitrogen excretion
  6. Reduces peripheral glucose utilization
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8
Q

How are lipids affected?

A

Lipid metabolism:

  1. Redistribution of body fat
    • moon face, buffalo hump
  2. Stimulates release of fatty acids from adipose tissue
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9
Q

What is the primary effect of mineralcorticoids (MCs)?

A
  1. Increases sodium reabsorption
  2. Increases potassium and hydrogen ion excretion
  3. Responsible for cardiovascular effects - hypertension
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10
Q

When would this situation occur?

Cortisol = Aldosterone >> Cortisone

A
  • When 11-ß hydroxysteroid dehydorgenase is inhibited
    • activates cortisol ⇒ cortisone
  • Inhibitors:
    • certain drugs, foods or pathological states
    • glycyrrhizic acid found in licorice
      • mimics symptoms of excess mineralcorticoids
      • edema, hypokalemia, hypertension
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11
Q

CNS effects:

A
  • sleepiness
  • lability of mood
    • i.e. mood swings
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12
Q

Immune System effects:

Cell traffic/accumulation

A

GC effects:

  • Lymphocytopenia and monocytopenia: redistribution of cells out of vascular space
  • Prevent neutrophil adherence to endothelium
    • via NF-κB
  • Inhibit action of chemotactic factors
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13
Q

Immune System effects:

Cell function

A
  1. 1) Macrophage
    • Inhibits antigen processing
    • Inhibit binding to Fc receptors
    • Inhibit synthesis and release of IL-1
  2. 2) B-Lymphocytes
  3. 3) T-lymphocytes
    • Interfere with macrophage antigen processing
    • Interfere with actions of lymphokines:
      1. IL-2
      2. macrophage MIF
      3. macrophage aggregating factor
      4. monocyte chemotactic factor
      5. lymphotoxin
    • Absence of IL-1 prevents activation
    • Reduces IL-2 synthesis
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14
Q

How do corticosteroids act as anti-inflammatory drugs?

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 COX-2 by cytokines
  • Decrease capillary permeability
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15
Q

What are the therapeutic principles of corticosteroid use?

A
  • Therapeutic dose is variable and may change with therapy.
    • Reevaluate frequently
  • Single dose is usually without harmful effects
    • Prolonged therapy has lethal potential
  • Palliative or symptomatic therapy
    • Use is not etiological or curative in most cases
  • Abrupt discontinuation may be life-threatening
    • adrenal insufficiency
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16
Q

What are the therapeutic uses of corticosteroids?

A
  1. Adrenal insufficiency: steroid replacement therapy
    • Will lose both GCs and MCs
    • therapy must have both GC and MC activity
  2. ​Rheumatoid arthritis: use only in progressive disease
  3. Osteoarthritis: acute inflammation
  4. Allergic diseases: hay fever, serum sickness, drug reaction, anaphylaxis, bronchial asthma
  5. Inflammatory diseases: eye, ear, skin, etc.
    • Used locally
  6. Cerebral edema
  7. Shock
  8. Miscellaneous: organ transplantation, thrombocytopenia, liver diseases, collagen diseases, renal diseases, etc.
17
Q

Cortisol:

  • Anti-inflammtory potency:
  • Action:
A
  • Anti-inflammtory potency: low
  • Action: binds to the mineralcoticoid receptor, which leads to transcriptional activation
    • also can act as a glucocorticoid
18
Q

Dexamethasone (Decadron®):

  • Anti-inflammatory potency:
  • MC potency:
A
  • Anti-inflammatory potency: high
  • MC potency: none
19
Q

Prednisolone:

  • Anti-inflammatory potency:
  • MC potency:
A
  • Anti-inflammatory potency: intermediate
  • MC potency: low
20
Q

Fludrocortisone (Florinef®):

  • Anti-inflammatory potency:
  • MC potency:
A
  • **Anti-inflammatory potency: **high
  • MC potency: high
21
Q

Aldosterone:

  • Anti-inflammatory effects:
A
  • Anti-inflammatory effects: very low
22
Q

What happens during rapid withdrawal?

A
  • Rapid withdrawal: Acute adrenal insufficiency occurs
    • Life threatening
    • Salt wasting and cardiovascular collapse
23
Q

What are the consequences of prolonged corticosteroid therapy?

A
  1. Suppression of pituitary: adrenal function
    • Related to dose and duration of therapy (Large doses for period longer than 2 weeks)
    • May last for periods longer than 12 mo
    • Reduce dosage slowly
  2. Cushings syndrome:
    • Moon face and Buffalo hump
    • Poor wound healing
    • Thin skin
    • Hypertension
    • Thin extremities
    • Striae
24
Q

Adrenal Steroid Synthesis Inhibitors:

A
  1. Aminoglutethimide
  2. Metyrapone
  3. Ketoconazole
25
Q

Metyrapone:

A
  • Blocks 11-beta hydroxylation so synthesis is stopped at 11- desoxycortisol
  • 11-Desoxycortisol does not inhibit ACTH release so plasma ACTH levels increase
    • i.e. does not affect the pituitary gland
  • ACTH stimulates synthesis and excretion of 17-hydroxycorticoids as 11-desoxycortisol
  • Used as diagnostic test
26
Q

Adrenal Steroid Antagonists:

A
  1. Mifepristone
  2. Spironolactone
    Eplerenone
  3. Drospirenone
27
Q

Mifepristone - (RU486)- (Mifeprex™):

A
  • Competitive antagonist at progesterone and glucocorticoid receptor
  • Termination of pregnancy
    • “morning-after pill”
  • Treats Cushing Disease
28
Q

Spironolactone (Aldactone®)
Eplerenone (Inspra™):

A
  1. Competitive antagonists at mineralocorticoid receptor
  2. Diuretics
  3. Treat Hypertension
  4. Cardiac hypertrophy and heart failure
29
Q

Drospirenone:

A
  1. Progesterone receptor agonist
    1. Used with estrogen to suppress ovulation
    2. Used with estrogen as hormone replacement therapy in post-menopausal women
  2. Mineralocorticoid receptor antagonist
    1. Diuretic
    2. Antagonizes the salt retaining effects of estrogen
  3. Androgen receptor antagonist

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