Steroids Flashcards

1
Q

What are the main types of steroids?

A

Glucocorticoids
Mineralocorticoids
Androgens

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2
Q

What are the steroids secreted by?

A

The adrenal cortex

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3
Q

Where are mineralocorticoids secreted?

A

Zona glomerulosa of the adrenal cortex

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4
Q

Where are glucocorticoids secreted?

A

Zona fasciculata of the adrenal cortex

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5
Q

Where are adrenal androgens secreted?

A

Zona Reticularis of the adrenal cortex

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6
Q

Why are the boundaries between the different types of steroids not absolute?

A

Synthesised from cholesterol
Additionally, they are also all highly aromatic structures
Due to the steroids having similar structures boundaries are not absolute

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7
Q

Give some examples of glucocorticoids

A

Corticosterone

Hydrocortisone (Cortisol)

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8
Q

What are the effects of glucocorticoids?

A

Metabolism.

Negative feedback loops

Anti-inflammatory and immunosuppressive.

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9
Q

What are the metabolic effects of glucocorticoids?

A

Elevated glucose levels.
Inhibition of protein synthesis (wasting of muscle)
Redistribution of fats
Negative balance of calcium as there is an increased in calcium secretion and decrease in calcium absorption.

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10
Q

What effect does glucocorticoids have on the hypothalamus and pituitary glands?

A

Hypothalamus releases CRF which stimulates the pituitary gland to release ACTH into the blood.
When these are in the blood it releases steroids which negatively feedback to the hypothalamus and the pituitary gland to inhibit the release of CRF and ACTH.

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11
Q

What are the anti-inflammatory and immunosuppressive effects of glucocorticoids?

A

Anti-inflammatory:
Reduce redness, swelling and pain (early)
Wound healing, proliferation (late)

Immunosuppressive:
Suppress function of immune cells.

steroids impact both stages of inflammation where as NSAIDs only effect the early
stage

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12
Q

What is the mechanism of action of glucocorticoids?

A
  1. Steroid binds to nuclear receptor in cytosol – remember steroids are hydrophobic!
  2. Translocation of receptor to nucleus
  3. Receptor act as transcription factor → binds to DNA to initiate lipocortin production
  4. Also trans represses IL1/TNF-alpha activation
  5. Lipocortin then inhibits PLA2 thereby inhibiting PG synthesis
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13
Q

What is the function of lipocortin?

A

Inhibits phospholipase A2 and therefore when steroids are present, this leads to reduced prostaglandin and leukotrienes synthesis.

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14
Q

What are some uses of steroids as drugs?

A

Replacement therapy (underactive adrenal cortex)
Anti-inflammatory
Immunosuppressive
Emesis

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15
Q

What would the anti-inflammatory effects of steroids be used to treat?

A

Severe asthma (inhaler beclomethasone)
Severe arthritis
Skin disorders

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16
Q

What are the immunosuppressive effects of steroids used to treat?

A

Organ transplant recipients

17
Q

What are the emesis effects of steroids used to treat?

A

Synergy with 5-HT R antagonists after chemotherapy is used to treat cancers.

18
Q

What are the main steroid drugs?

A

Cortisone and hydrocortisone (replacement therapy)

prednisolone (Fairly selective)

Dexamethasone (highly selective)

19
Q

What are some side effects to steroids?

A

Suppressed response to infection/injury
Atrophy of adrenal cortex
Disrupted metabolism (iatrogenic crushing syndrome)

20
Q

Why does a steroid work as a 5-HT R antagonist?

A

When anti cancer drugs are taken (such as cisplatin) the mucosa stops dividing rapidly and therefore the deeper layers of the gut start to get damaged.
The inflammatory response in the gut causes enterochromaffin cells to release 5-HT into the blood.
5-HT goes to the brain where it activates 5-HT3 receptors in the brain triggering the emetic reflex.
Therefore 5-HT receptor antagonist prevents the action of 5-HT on the brain and therefore reduces the emetic effects.