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WEEK 10 SEM 4 > Glucocorticoids > Flashcards

Glucocorticoids Flashcards

1
Q

What are corticosteroid?

A

group name given to glucorticoids (eg cortisol) and minrealcorticoids (eg aldosterone)

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2
Q

What metabolism is glucorticoid involved in?

A

carbohydrate and protein

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3
Q

What are mineralcorticoids involved in?

A

H2O and electrolyte balance in kidney

can increase blood pressure

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4
Q

How is cortisol released?

A

times of stress
hypothalamus releases CRH (corticotrophin releasing hormone)
ACTH (adrenocorticotrophic hormone) is released from anterior pitutary

stimulates adrenal gland
cortisol released

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5
Q

What effects does cortisol have?

A

glucose levels regulation
inhibit insulin release
defends against infection
help respond to stress

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6
Q

What effects do glucocorticoids have?

A

Metabolic
Cardiovascular
CNS
Hormonal regulation

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7
Q

What are the metabolic effects of glucocoritcoids?

A
  • promote breakdown of proteins and fats into glucose (gluconeogenesis)= leads to muscle wasting
  • lesss glucose usage
  • tendency for the body to go into a hyperglycaemic state = also increase glycogen storage
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8
Q

What are the cardiovascular effects of glucocorticoids?

A
  • decrease both microvascular permeability and vasodilation = get hypertension if use glucocorticoids chronically
  • INCREASE IN BLOOD VOLUME AND PRESSURE
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9
Q

How do glucocorticoids lead to an increase in blood pressure?

A

glucocorticoids have an affinity to the aldosterone receptor

aldosterone= water retention by activating ENAC in collecting duct and upregulating Na+/K+ pumps

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10
Q

How do glucocorticoids affect the CNS?

A

cortisol- mood changes

euphoria, memory and stress changes

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11
Q

What are that antiinflammatory effects of glucocorticoids?

A

decrease microvascular and fluid exudation
decrease inflammatory mediators and cytokines
decrease function of inflammatory effector cells

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12
Q

What does phospholipase A2 do?

A

in lipid metabolism pathway

produces arachidonic acid

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13
Q

What happens if you inhibit Phospholipase A2?

A

inhibits the production of arachidonic acid

SOlipoxygenase cannot produce leukotriene B4 which is a chemoattractant (attracts immune cells)

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14
Q

What do glucocorticoids decrease the expression of (in terms of inflammation)?

A

COX2-so less prostaglandins
inhibit cell migration and mediator release
reduce the clonal expansion of T and B cells that occurs after antigen recognition
Reduce chronic inflammatory responses

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15
Q

What is complement involved in?

A

Involved in opsonization (allowing macrophages to see foreign bodies), increasing vascular permeability, and lysis of foreign cell

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16
Q

When is renin released?

A

decreased Na+, or increase K+ in the blood

=decreased blood volume and pressure

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17
Q

Renin converts angiotensinogen to angiotensin II. What does this work on?

A

angiotensin II works on the zona glomerulosa of the adrenal cortex

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18
Q

Where is aldosterone released from?

A

adrenal cortex

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19
Q

How does aldosterone work in the kidneys?

A
  • increase in ENAC channels (which reabsorb Na+ from the urine) in the collecting duct of the renal tubule
  • this also leads to an increase in Na+/K+ pump which further promotes Na+ to move into the blood
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20
Q

When the blood volume is high, what is released to lower the blood volume?

A

heart produces atrial natriuretic peptide which inhibits the RAAS and restores the blood pressure

21
Q

What does the enzyme 11beta hydroxysteroid dehydrogenase type 1 do?

A

deactivates cortisol to cortisone and so cortisol cannot act on the kidneys

22
Q

Why is the enzyme 11beta hydroxysteroid dehydrogenase type 1 important?

A
  1. cortisol has an affinity for the mineralocorticoid receptor in the kidneys
  2. enzyme 11beta hydroxysteroid dehydrogenase type 1 deactivates cortisol to cortisone and so cortisol cannot act on the kidneys
  3. when a person has excess cortisol (eg cushing’s), the enzyme gets saturated and can lead to problems such as hypertension and hypokalaemia
23
Q

What are glucorticoids?

24
Q

Why is it good that glucocorticoids are lipids?

A

can easily diffuse into cell

25
Once a glucocorticoid diffuses into a cell, what does it bind to?
glucocorticoid receptor | receptors found all around the body
26
What does the glucocorticoid receptor have with it?
bound to chaperone molecule which has immunophilin associated with it
27
What can the glucocorticoid receptor complex do?
translocate into nucleus- attach to promoter region of genes prevent gene activation by other transcription factors induce Ikappa-Balpha
28
What does the glucocorticoid receptor complex prevent?
prevent AP-1 and NK kappaB from activating COX2, phospholipase A2, IL1, ICAM-1 (cell surface receptor), IL8, eotaxin, I kappa Balpha
29
What is eotaxin?
chemoattractant- recruits eosinophils
30
What does IKappa-Balpha do?
causes NF-kappaB repression (represses the transcription factor called NF-kappaB)
31
What is NF-Kappa B?
pro-inflammatory transcription factor
32
What does IKappa-Balpha do?
in cytoplasm Ikappa-Balpha is bound to NF-kappaB which does not allow NF-kappaB to enter the nucleus and lead to transcription of inflammatory genes
33
What does IL1beta and TNF alpha do?
when IL1beta and TNF alpha act on their receptor in a cell, it activates something called the IkappaB kinase (IKK)
34
What does Ikappa B kinase do?
IkappaB kinase phosphorylates the Ikappa-Balpha on the NF-kappaB leads to degradation of IkappaBalpha by ubiquitin ligase complexes now the NF-kappaB is free to enter the nucleus and transcribe inflammatory genes
35
What are the actions of glucocorticoid receptor complex?
increase beta 2 adrenergic receptors- cause bronchodilation- important for asthmatics increased lipocortin which is important in bringing about resolution in inflammation by decreasing arachidonic acid levels and eicosanoids the levels of some anti-inflammatory genes and cytokines go up like IL10 and IL12 there is decreased expression of pro inflammatory proteins such as TNF alpha, IL1beta, and endothelin-1
36
What happens when corticosteroids are inhaled?
less cytokines released from T helper cells less cytokines produced by macrophages less number of dendritic cells less cytokine release by epithelial cells
37
What are examples of synthetic glucorticoids?
hydrocortisone, prednisolone, dexamethasone, betamethasone, beclomethasone
38
How does aldosterone act in the kidneys?
increases Na+ retention in distal tubules of the kidney stimulates the Na+/H+ exchanger via the aldosterone receptors up regulates the Na+ permeable (ENaC) channels in the cell membrane stimulates the up regulates the basolateral Na+/K+ ATPase pump
39
What is CRH released into?
median eminence of the pituitary gland
40
Where in the adrenal cortex is CRH released from?
zona fasciulata
41
Explain the RAAS system:
low Na+, low renal blood flow trigger juxtaglomerular cells of the kidney to release renin. This converts angiotensinogen to angiotensin I. ACE then converts ang I to ang II in the lung. Ang II has a no. of effects including stimulating release of aldosterone.
42
Where is CRH released from?
paraventricular nucleus (PVN) of the hypothalamus
43
What are the roles of cortisol?
``` normal metabolism maintains blood sugar levels provides resistance to stress anti-inflammatory agent regulation of fluid balance in the body. mobilises fatty acids from fat cells helps to maintain blood pressure. ↑breakdown of proteins into amino acids (except in liver cells). . ```
44
What happens if you have high CRH?
low WBCs antibody formation = so overall less immunity This is a very important therapeutic property of glucocorticoids: ↓ inflammatory response which suppresses immunity.
45
How do glucorticoids switch gene expression on/off?
1) Interaction of steroid/receptor with promoter regions - these gene promoters have ‘glucocorticoid response elements’ (GREs) and occupancy of GREs turn on/off certain genes 2) Steroid/receptor complexes PREVENT gene activation by other transcription factors - e.g. AP-1, NFkB: transcription factors involved in switching on COX-2; PLA2, IL-1, ICAM-1, IL-8, eotaxin, IκB-α, etc. 3) Induction of IB (inhibitor of NF-κB) which causes NF-κB repression
46
What are the therapeutic uses of glucocorticoids?
-Adrenal insufficiency or failure (Addison’s disease) congenital or drug-induced treatment requires combined GC and MC - Treatment of inflammation asthma, rhinitis, skin disorders, sports injuries, reduction of cerebral oedema in patients with brain tumours -Immunosuppression inhibit graft v host reaction in tissue transplantation
47
What are examples of glucocorticoids?
Hydrocortisone, prednisolone, dexamethasone, betamethasone, beclomethasone
48
What are the therapeutic uses of mineralcorticoids?
Adrenal insufficiency e.g. Addison’s disease ``` Orthostatic hypotension (postural hypotension) Failure of baroreceptor reflex ``` Electrolyte disorders - cerebral salt wasting

WEEK 10 SEM 4 (8 decks)

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