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SBT > Glucocorticoids > Flashcards

Glucocorticoids Flashcards

1
Q

What are the two different types of corticosteroids?

A

Glucocorticoids

Mineralocorticoids

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2
Q

How do is cortisol release controlled?

A
  • Stress and extreme exercise can cause the release of CRH by the PVN
  • Acts on anterior pituitary, causing release of ACTH
  • ACTH acts on adrenal cortex to release cortisol
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3
Q

What are cortisol’s effects?

A
  • Promotes normal metabolism
  • inhibits insulin product/ controls blood sugar levels
  • Controls BP
  • Acts as an anti-inflammatory agent
  • Mobilises fatty acids from fat cells
  • Increases gluconeogenesis
  • Helps body respond to stress
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4
Q

How is aldosterone release controlled?

A
  • Renin release causes cleavage of angiotensinogen to angI.
  • ACE in the lungs causes AngI to be converted to AngII
  • AngII acts on zona glomerulosa of adrenal cortex and causes the release of Aldosterone
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5
Q

What can happen if you have too much cortisol?

A
  • Overwhelm the enzyme involved in cortisol metabolism (11b-steroid dehydrogenase)
  • Cortisol then binds to the aldosterone receptor, stimulating its effects -> increasing blood volume -> increased BP
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6
Q

What are the metabolic actions of glucocorticoids?

A
  • Breakdown of protein and fats (muscle wasting etc) - gives disproportionate distribution (buffalo hump, moon face, distended belly)
  • Decreased glucose usage and increased gluconeogenesis
  • Tendency to hyperglycaemia and increased glycogen storage - can lead to diabetes
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7
Q

What are the cardiovascular effects of glucocorticoids?

A

Decrease in both microvascular permeability and vasodilation

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8
Q

What are the CNS effects of glucocorticoids?

A

Mood changes, linked with changes in memory/stress

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9
Q

What are effects do glucocorticoids have on the immune system?

A

Decrease the amount of immune ells such as neutrophils, lymphocytes etc

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10
Q

What are the anti-inflammatory effects of glucocorticoids?

A
  • Decreased microvascular fluid exudation (reduces immune cell chemotaxis)
  • decreased inflammatory mediators and cytokines (less IL-1b and TNFa so less AA, also reduces COX-2, so less eicosanoids, less complement)
  • Decreased function of inflammatory effector cells
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11
Q

What are the cellular effects of inhaled corticosteroids?

A
  • Decreased numbers of eosinophils, t-cell cytokines and mast cells reduces the numbers of harmful mediators they produce
  • less dendritic cells to present antigens
  • less mucus secretion and endothelial cell leakage
  • less cytokines and mediators from epithelial cells
  • Less cytokines from airway smooth muscle, but increased B2 recptors -> relaxation with salbutamol
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12
Q

What is the cellular mechanism of action for glucocorticoids?

A
  • Binds to its receptor in the cytoplasm
  • dissociates HSP
  • Glucocorticoid-receptor complex enters nucleus and binds to regulatory elements in DNA promoters - alters gene expression
  • Coactivators carry out histone acetylation, opening up the chromatin strture, allowing transcription
  • Deacetylation stops the production of mediators
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13
Q

What does NF-kB do?

A
  • Activation of inflammatory response genes
  • In resting cells, NF-kB is inhibited by association with IkB
  • Inflammatory cytokines activate IkB kinase (IKK), phosphorylating IkB on two serine residues
  • IkB is then ubiquitinated and degraded by the proteasome - allowing NF-kB to go to the nucleus and activate gene expression
  • NF-kB has signals telling it where to go to get to the nucleus
  • IkB-alpha proteins can mask these signals, keeping the NF-kB sequestered in the cytoplasm
  • If it cannot go to the nucleus, then DNA transcription wont happen, and so COX-2 and cytokines wont be synthesised
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14
Q

How do glucocorticoids switch gene expression on and off?

A
  • interaction of steroid/receptor with promoter regions - these gene promoters have glucocorticoid response elements (GREs); activation of these turns on/off certain genes (off = damage and inflammation, on = resolution)
  • Steroid receptor complexes can prevent gene activation by other transcription factors - e.g. phosphorylation of IkB -> NFkB activation
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15
Q

What are the therapeutic uses of glucocorticoids?

A
  • Adrenal insuffiiency or failure (Addisons) - congenital or drug-induced; treatment requires combined GC and MC
  • Treatment of inflammation - asthma, rhinits etc
  • Immunosupression - inhibit graft vs host reaction in tissue transplants
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16
Q

Give 5 examples of glucocorticoids

A
  • hydrocortisone
  • prednisolone
  • dexamethasone
  • betamethasone
  • beclomethasone
17
Q

Glucocorticoids vs NSAIDS in eicosanodi biosynthesis

A
  • Glucocorticoids decrease levels of Phospholipase A2 -> decreased AA
  • AA can be metabolised into PGs and TXs or LTs and other lipoxygenase products such as lipoxins
  • Glucocorticoids also decrease expression of COX-2
  • NSAIDs just decrease activity of COX-2
18
Q

Give an example of an endogenous mienralocorticod

A

Aldosterone

19
Q

What does aldosterone do?

A
  • Its secretion is controlled by RAAS and ACTH
  • Increases Na retention in DCT of kidneys
  • Simulates Na/H exchanger via aldosterone receptors
  • Enters cells and upregulates ENaC channels in membrane
  • Enters cells and stimualtes upregulation of basolateral Na/K ATPase
  • Also causes water retention so loss of K and H
20
Q

What are the therapeutic uses of mineralocorticoids?

A
  • Adrenal insufficiency - Addisons
  • Electrolyte disorders - cerebral salt wasting (EC volume depletion due to a renal sodium transport abnormality)
  • Orthostatic (postural) hypotension - failure of baroreceptor reflex
21
Q

Give an example of a therapeutic MC?

A

Fludrocortisone

22
Q

What is the mechanism of cerebral/renal salt wasting?

A

Brain injury leads to increased adrenergic activity, and increased production of natriuretic peptides

  • Causes natriuresis in the kidney
  • Increased adrenergic activity causes increased perfusion pressure and dopamine levels, which also acts on the kidney and causes natriuresis
23
Q

What are the side effects of corticosteroids?

A
  • Cushings
  • Opportunistic infection
  • Osteoporosis
  • Gastric ulceration (inhibits PGE2 synthesis so less mucus and bicarbonate secretion)
  • Growth suppression
  • Behavioural or reproductive problems
24
Q

What is cushings syndrome?

A
  • Abnormally high levels of cortisol
  • Reasons for high cortisol = overuse of corticosteroids/adenoma
  • Symptoms = moon face, upper body weight gain, easily bruised skin
25
Q

What is negative nitrogen balance?

A
  • Associated with burns, serious tissue injuries, fevers, hyperT, wasting diseases and during fasting periods
  • The amount of nitrogen excreted is greater than the amount of nitrogen ingested

SBT (8 decks)

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