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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?

A

Lipids

24
Q

Why is it good that glucocorticoids are lipids?

A

can easily diffuse into cell

25
Q

Once a glucocorticoid diffuses into a cell, what does it bind to?

A

glucocorticoid receptor

receptors found all around the body

26
Q

What does the glucocorticoid receptor have with it?

A

bound to chaperone molecule which has immunophilin associated with it

27
Q

What can the glucocorticoid receptor complex do?

A

translocate into nucleus- attach to promoter region of genes
prevent gene activation by other transcription factors
induce Ikappa-Balpha

28
Q

What does the glucocorticoid receptor complex prevent?

A

prevent AP-1 and NK kappaB from activating COX2, phospholipase A2, IL1, ICAM-1 (cell surface receptor), IL8, eotaxin, I kappa Balpha

29
Q

What is eotaxin?

A

chemoattractant- recruits eosinophils

30
Q

What does IKappa-Balpha do?

A

causes NF-kappaB repression (represses the transcription factor called NF-kappaB)

31
Q

What is NF-Kappa B?

A

pro-inflammatory transcription factor

32
Q

What does IKappa-Balpha do?

A

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
Q

What does IL1beta and TNF alpha do?

A

when IL1beta and TNF alpha act on their receptor in a cell, it activates something called the IkappaB kinase (IKK)

34
Q

What does Ikappa B kinase do?

A

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
Q

What are the actions of glucocorticoid receptor complex?

A

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
Q

What happens when corticosteroids are inhaled?

A

less cytokines released from T helper cells
less cytokines produced by macrophages
less number of dendritic cells
less cytokine release by epithelial cells

37
Q

What are examples of synthetic glucorticoids?

A

hydrocortisone, prednisolone, dexamethasone, betamethasone, beclomethasone

38
Q

How does aldosterone act in the kidneys?

A

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
Q

What is CRH released into?

A

median eminence of the pituitary gland

40
Q

Where in the adrenal cortex is CRH released from?

A

zona fasciulata

41
Q

Explain the RAAS system:

A

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
Q

Where is CRH released from?

A

paraventricular nucleus (PVN) of the hypothalamus

43
Q

What are the roles of cortisol?

A 
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
Q

What happens if you have high CRH?

A

low WBCs
antibody formation = so overall less immunity

This is a very important therapeutic property of glucocorticoids: ↓ inflammatory response which suppresses immunity.

45
Q

How do glucorticoids switch gene expression on/off?

A

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
Q

What are the therapeutic uses of glucocorticoids?

A

-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
Q

What are examples of glucocorticoids?

A

Hydrocortisone, prednisolone, dexamethasone, betamethasone, beclomethasone

48
Q

What are the therapeutic uses of mineralcorticoids?

A

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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