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Pharmacology 2 > Steroids > Flashcards

Steroids Flashcards

1
Q

Where are steroid hormones primarily synthesized?

A

Adrenal Cortex-adrenocorticoids

Ovaries and testes-Sex steroids

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2
Q

What is steroid secretion controlled by?

A

Peptides secreted from the hypothalamus and pituitary

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3
Q

What are the effects of glucocorticoids?

A

Modulation of carbohydrate metabolism by increasing levels of glycogen in the liver and blood glucose, stimulate immune system (initial), immune suppression and cells death (prolonged)

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4
Q

When does basal rhythmic secretion of glucocorticoids increase?

A

During periods of stress

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5
Q

What are the effects of mineralcorticoids?

A

Promots Na uptake, modulates K transport, control of water reabsorption

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6
Q

When are mineralcorticoids secreted?

A

Only during periods of stress

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7
Q

Secretion of what is essential for life?

A

Cortisol

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8
Q

What occurs in the evening?

A

Hypothalamic activation releases corticotropin releasing hormone which stimulates the pituitary to make ACTH which stimulates the adrenal gland to make cortisol

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9
Q

At what time of day are corticosteroid levels the highest?

A

The morning

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10
Q

What occurs during stress?

A

Stress gives a bigger stimulation of the limbic system, causing more CRH, more ACTH and thus more cortisol. It also stimulates inflammaory and immune systems which releases interleukins with stimulates CRH and ACTH

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11
Q

What is the negative feedback loop in the case of stress?

A

Cortisol has negative feedback on the hypothalamus, pituitary and inflammatory and immune systems to prevent secretion of CRH and ACTH

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12
Q

What happens if you take long term steroids?

A

Your ability to produce endogenous steroids is compromised, thus your ability to combat stress in reduced.
Prolongation of treatment increases the incidence of disabling or life threatening effects

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13
Q

What is the major building block in glucocorticoid synthesis?

A

Cholesterol

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14
Q

What increases cortisol levels in the body?

A

Stress, hypothydroidsim and liver disease

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15
Q

What does corticosteroid-binding globulin (CBG) do?

A

Binds about 90% of the circulating cortisol, inactivating it. Can reach a point of saturation, increasing free cortisol levels
Only free or loosely bound to albumin are available to work.

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16
Q

What increases CBG levels?

A

Pregnancy, estrogen administration, hyperthyroidism

17
Q

What decreases CBG levels?

A

Hypothyroidism, genetic defects in synthesis and protein deficiency states

18
Q

What do synthetic corticosteroids bind to?

A

Those like dexamethasone are largely bound to albumin rather than CBG

19
Q

How do the steroids work on the cell?

A

Cross the cell membrane and bind to the glucocorticoid receptor which is transported by HSP90 proteins to the nucleus. The steroids dimerize, move into the nucleus and binds to the glucocorticoid response element which increases transcription of anti-inflammatory proteins.

20
Q

How do NF-kB activating signals work on the cell?

A

The signals bind to the receptor on the cell. Proteins (p65 and p50) dissociate from the receptor and bind to response elements to inhibit steroid binding to the element and prevent transcription of pro-inflammatory proteins
No pre-mRNA

21
Q

What causes decreased transcription?

A

Inflammatory cytokines, chemokines, inflammatory enzymes, inflammatory proteins, mediator receptors, adhesion molecules

22
Q

What accounts for the more rapid effects of glucocorticoids?

A

Non-genomic activation of anti-inflammatory proteins

23
Q

Which topical corticosteroids are used for dermatologic use?

A

Ultra high potency: Clobetasol
High: Desoximetasone, Amcinonide
Medium: Betamethasone, Triamcinolone
Low: Desonide, Hydrocortisone

24
Q

How can the vehicle of topical corticosteroids affect its potency?

A

Ointments have higher potency than cream or lotions

25
Q

What are the side effects of topical corticosteroids?

A

Local side effects (striae, skin atrophy)

Higher potency formulations can cause systemic side effects if used on large areas and/or prolonged periods

26
Q

What are the metabolic effects of glucocorticoids?

A

Stimulates gluconeogenesis and glycogen synthesis (destabilize rapidly), stimulate release amino acids in the course of muscle catabolism, increase glucose, insulin release, decrease glucose uptake, increase lipolysis and lipogenesis

27
Q

What are the catabolic and anti-anabolic effects of glucocorticoids?

A

Decreased muscle mass, weakness and thinning of skin, decreased wound healing
Osteoprorosis in Cushing’s syndrome
Reduce growth of children

28
Q

What are the anti-inflammatory effects of glucocorticoids?

A

Affects peripheral leukocytes and their suppressive effects on inflammatory cytokines, chemokines, mediators of inflammation
Increase neutrophils, decrease lymphocytes (B and T), monocytes, eosinophils, basophils
Inhibits phospholipase A2 (PG, platelet activating factor), COX-2 (PG)
Vasoconstriction, decreased capillary permeability

29
Q

What are the immunosuppressive effects of glucocorticoids?

A

Downregulates T-cell proliferation, inhibits T-cell activation, downregulation of plasma cells (all secondary to decreased cytokines)
Inhibits inflammatory cell migration, inhibits antigen phagocytosis by macrophages, suppression of antibody production, inhibits functions of tissue macrophages

30
Q

How long does it take for the anti-inflammatory and immunosupressive effects to begin?

A

After 1 dose of glucocorticoids

31
Q

What are some other effects of glucocorticoids?

A

Slowing of alpha rhythm (depression), behavioural disturbances (insomnia, euphoria), peptic ulcers, increased fat redistribution of body (puffy face, buffalo hump), increased red blood cells and platelets and production of fetal surfactant near term

32
Q

How is the dose of exogenous glucocorticoids determined?

A

Determined by trial and error, must exceed endogenous levels

A few days of usage is unlikely to produce harmful effects

33
Q

Are corticosteroids a specific treatment? Why?

A

No, not curative either.
Pathological processes continue, clinical manifestations suppressed
Primarily useful where host response causes disease manifestations

34
Q

What happens when you abruptly stop prolonged high dose treatment?

A

May induce adrenal insufficiency serious enough to be life threatening

35
Q

What are exogenous glucocorticoids used for?

A

Shock, cerebral edema, increased intracranial pressure, allergies, arthritis, asthma, rheumatic carditis, renal disease, collagen disease, ulcerative colitis, Crohn’s Disease, organ transplants, anemias, oral ulcerations, fetal lung maturation

36
Q

What are the adverse effects of glucocorticoids?

A

Decreased resistance to infections, CNS effects, hyperglycemia, electrolyte imbalance, suppression of growth, peptic ulcer, increased increased intraocular pressure, cataracts, suppression of pituitary-adrenal function, muscle weakness and atrophy, acne, hirsutism, hypertension

37
Q

What should be monitored with corticosteroid use?

A

Blood glucose, blood pressure

Pharmacology 2 (23 decks)

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