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Physiology & Science: Therapeutics > Glucocorticoids > Flashcards

Glucocorticoids Flashcards

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1
Q

What are the two types of corticosteroids?

A
  • Glucocorticoids (eg. cortisol)
  • Mineralocorticoids (eg. aldosterone)

Both synthesised and released from adrenal cortex

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2
Q

In regards to the corticosteroids, what is meant by the ‘salt and sugar’ hormones?

A
  1. Glucocorticoids:
    • ‘sugar’ hormone, for carbohydrate + protein metabolism
    • potent anti-inflammatory / immunosuppressant
  2. Mineralocorticoids:
    • ‘salt’ hormone, controls electrolyte + H2O in kidney
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3
Q

How is cortisol released?

A
  • Stimulus = stress (eg extreme exercise)
  • Hypothalamus stimulated -> CRH release (from PVN)
  • CRH acts on anterior pituitary
  • ACTH secreted from anterior pituitary
  • Acts on adrenal gland to secrete cortisol
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4
Q

What are the physiological actions of cortisol?

A
  • Regulates glucose (blood sugar) levels
  • Increases fat in the body
  • Helps to defend body against infection
  • Helps body respond to stress
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5
Q

What stimulates/controls release of aldosterone?

A

Decreased sodium or inc potassium in blood / decreased blood volume/BP -> stimulation of kidneys -> renin -> RAAS cascade -> ang II formed -> vasoconstriction -> bring up BP

Ang II also stimulates production of aldosterone from adrenal cortex + that will regulate how much water is retained. Sodium and water reabsorption increases, so increases blood volume.

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6
Q

Which hormone has an inhibitory effect on the adrenal cortex, therefore inhibiting release of aldosterone?

A
  • Atrial natirueretic peptide (ANP)
  • Inhibits zona glomerulosa of adrenal cortex
  • This is in response to increased BP/BV so aim is to decrease BP by decreasing aldosterone secretion
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7
Q

Can cortisol bind to the same receptor that aldosterone binds to? What can this lead to?

A

Yes, cortisol + aldosterone have equal affinity for the mineralocortiocid (AT1) receptor. So high levels of cortisol -> BP will go up, by mimicking aldosterone action.

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8
Q

What are the metabolic actions/effects of glucocorticoids?

A
  • Breakdown of protein + fats (muscle wasting, etc)
  • Decreased glucose usage + increased gluconeogenesis
  • Tendency to hyperglycaemia and increased glycogen storage
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9
Q

What effect do glucocorticoids have on the cardiovascular system?

A

Decrease in both microvascular permeability and vasodilatation

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10
Q

What changes occur in the CNS as a result of glucocorticoids?

A

Mood changes, linked with changes in memory/stress

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11
Q

What effect do glucocorticoids have on the hypothalamic-pituitary-adrenal axis?

A

Negative feedback on anterior pituitary and hypothalamus

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12
Q

Why go glucocorticoids decrease microvascular fluid exudation?

A

As they reduce influx of cells to areas of inflammation

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13
Q

Which enzyme expression do glucocorticoids decrease in order to bring about anti-inflammatory effects?

A
  • COX-2
  • Reduced levels of eicosanoids
  • Decreased levels of cytokines + complement levels
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14
Q

What are the decreased functions of inflammatory effector cells brought about by glucocorticoids?

A
  • Inhibition of cell migration + mediator release
  • Reduced clonal expansion of T + B cells
  • Reduced in chronic inflammatory events
  • NB healing + repair inhibited
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15
Q

What are the cellular effects of inhaled corticosteroids?

A

Also reduce movement and activity of chemotactic cells

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16
Q

Where is the glucocorticoid receptor?

A

Found intracellularly in almost all tissues

17
Q

How do glucocorticoids bind to their receptor and what happens after this? (just talk about cellular mechanisms, not the biological effects)

A
  • Glucocorticoids enter cells through passive diffusion
  • Form complex with GCR (receptor protein) in cytoplasm
  • GCR dissociates HSP (heat shock protein)
  • Glucocorticoid-GCR complex translocated to nucleus
  • Can bind to specific regulatory components in nucleus
  • Expression of genes can be both increased or decreased
  • ~1% of genome is steroid-sensitive
18
Q

What are the biological effects induced by glucocorticoids binding to its receptor?

A
  • increased hepatic gluconeogenesis
  • increased lipolysis
  • muscle catabolism
  • inhibition of peripheral glucose uptake in muscle + adipose
19
Q

How does NF-kB play a key role in the activation of inflammatory response genes?

A
  • Resting cells - NF-kB in cytoplasm associated with inhibitory protein IkB
  • Inflammatory cytokines -> activate IKK
  • IKK phosphorylates IkB
  • IkB then ubiquinated + degraded by proteasome
  • Freeing NF-kB to migrate into nucleus + activate gene expression
20
Q

Glucocorticoids induce inhibition of NF-kB (IkB-a), what does this lead to?

A

Increased expression of anti-inflammatory proteins:

  • Inc B2 adrenergic receptors; inc lipocortin which decreases AAs/eicosanoids
  • Levels of some anti-inf cytokines go up: IL-10, IL-12

Decreased expression of pro-inflammatory cytokines:

  • Decrease cytokine production (eg TNF-a, IL-1b); endothelin-1
21
Q

What actions will dexamethasone have?

A
  • Glucocorticoid agonist
  • Anti-inflammatory actions
  • Inhibition of leukocyte infiltration at site of inflammation
  • Interference in function of mediators of inflammatory repsonse
  • Suppression of humoral immune responses
  • Reduction in oedeoma + scar tissue

All thought to be done by Phospholipase A2 inhibitory proteins, lipocortins, which control biosynthesis of potent mediators of inflammation such as prostaglandins + leukotrienes.

22
Q

What are therapeutic uses of glucocorticoids?

A
  • Adrenal insufficiency or failure (Addison’s Disease) - congenital or drug-induced, treatment requires combined GC + MC
  • Treatment of inflammation - asthma, rhinitis, skin disorders, sports injuries, reduction of cerebral oedema in patients w brain tumors
  • Immunosuppression - inhibit graft v host reaction in tissue transplantation
23
Q

Give examples of glucocorticoids/drugs

A
  • Hydrocrotisone
  • Prednisolone
  • Dexamethasone
  • Betamethasone
  • Beclomethasone
24
Q

What are the comparative effects of NSAIDs and glucocorticoids on Eicosanoid biosynthesis?

A
  • Glucocorticoids inhibit formation of arachidonic acid (by decreased PLA2)
  • Glucocorticoids also decrease expression of COX-2
  • NSAIDs decrease activity of COX-2 - thus only inhibiting the prostaglandin/thromboxane formation pathway, whereas glucocorticoids will inhibit all eicosanoids forming
25
Q

Name an endogenous mineralocorticoid

A
  • Aldosterone
  • Secretion controlled by renin-angiotensin system + ACTH
26
Q

Where are mineralocorticoid receptors found?

A
  • Only in few places
  • Kidney, colon, bladder
27
Q

What does aldosterone do?

A

Increases Na+ retention in distal tubules of kidney

  • stimulates Na+/H+ exchanger via aldosterone receptors
  • enters cells + up-regulates Na+-permeable epithelial Na channels in cell membrane
  • enters cells + stimulates up-reg of basolateral Na+/K+ ATPase pump
  • also causes H2O retention, loss of K+ and H+

Low Na+ plasma levels increase aldosterone by directly activating adrenal gland + stimulating RAAS to produce Ang II

28
Q

What are therapeutic uses of mineralocorticoids?

A
  • Adrenal insufficiency (eg Addison’s)
  • Electrolyte disorders (cerebral salt wasting)
  • Orthostatic/postural hypotension (failure of baroreceptor reflex)
29
Q

Name an example of a mineralocorticoid drug

A

Fludrocortisone

30
Q

What are side effects of corticosteroids?

A

Cushing’s-like syndrome

  • Euphoria
  • Buffalo hump
  • Round face with red cheeks
  • Thinning skin
  • Thin arms + legs, muscle wasting
  • Increased abdominal fat
  • Poor wound healing

Others: opportunistic infection, osteoporosis, gastric ulcers, growth suppression, behavioural/repro problems

Physiology & Science: Therapeutics (6 decks)

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