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Dermatology Board Prep > DERM (12) Medical Therapy > Glucocorticoids > Flashcards

Glucocorticoids Flashcards

1
Q

Where is exogenous corticosteroid absorbed?

A

Jejunum

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2
Q

What is the spectrum of glucocorticoid to mineralocorticoid effects for short, intermediate, and long-acting corticosteroids

A

Short: decreased glucocorticoid and increased mineralocorticoid (hydrocortisone and cortisone)

Intermediate: as compared to short, increased glucocorticoid and decreased mineralocorticoid activity Prednisone, prednisolone, methylprednisolone, and triamcinolone)

Long: More increased glucocorticoid and the least amount of mineralocorticoid effect.

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3
Q

What effect does food consumption have on oral steroid absorption?

A

It slows down absorption but does not decrease the amount absorbed

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4
Q

Where in the cell does systemic steroid drugs bind, and where is the effect exerted?

A

Glucocorticoid receptor binds the drug in the cytoplasm, then translocates to the nucleus where it binds to nuclear DNA and affects gene regulation/transcription (acts as a transcription factor)

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5
Q

What is the main carrier protein for systemic steroids, and when drug is bound is it inactive or active?

A

Cortisol-binding globulin is the main protein carrier. When steroids are bound to this they are inactive

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6
Q

What things increase cortisol binding protein (thereby decreasing free corticosteroid fraction)?

A

Estrogen therapy, pregnancy, and hyperthyroidism

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7
Q

What things decrease cortisol binding protein, thereby increasing free corticosteroid fraction?

A

hypothyroidism, liver disease, renal disease, and obesity

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8
Q

What is the enzyme in the liver that converts steroids to active forms?

A

11beta-hydroxysteroid dehydrogenase

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9
Q

What are some examples of inactive/active corticosteroid pairs?

A

Cortisone (inactive) to cortisol (active)

Prednisone to prednisolone (active form)

[The ol indicated that active form]

These are the two systemic active steroids used

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10
Q

Which systemic steroid should be used in a patient with liver disease?

A

Likely prednisolone as it is in its active form

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11
Q

What is the primary alteration that corticosteroids induce to affect immunosuppression and antiinflammatory processes?

A

Mediated via cytokine alteration (decrease proinflammatory cytokines and increase anti-inflammatory cytokines)

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12
Q

What things are decreased in corticosteroid use?

A

NFkappaB signally, AP-1, phospholipase A2, eicosanoids (e.g., leukotrienes, prostaglandins, 12-HETE, and 15-HETE), cox-2, the activity of all types of WBC’s, fibroblast activity and prostaglandin production

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13
Q

What things are increased in corticosteroid use molecularly?

A

Increased IL-10 (down-regulation of cell-mediated immunity), antiinflammatory proteins (vasocortin, lipocortin, vasoregulin), increased apoptosis of lymphocytes and eosinophils

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14
Q

What is a physiologic level of prednisone?

A

5-7.5mg/day

Anything more than this is pharmacologic therapy

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15
Q

What is the conversion of cortisone to cortisol (hydrocortisone), prednisone, prednisolone, methylprednisolone, triamcinolone, dexamethasone, betamethasone?

A

25mg cortisone = 20mg cortisol (hydrocortisone) = 5mg (prednisone/prednisolone)=4mg (methylprednisolone/priamcinolone) = 0.75mg (dexamethasone)=0.6-0.75mg (betamethasone)

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16
Q

If you keep somebody on long-term corticosteroid therapy and induce exogenous adrenal insufficiency is the mineralocorticoid axis affected?

A

No! So it is very rare to get a true Addisonian adrenal crisis with hypotension, coma etc

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17
Q

What is the maximal stress production of endogenous corticosteroid in prednisone equivalents?

A

60mg

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18
Q

When corticosteroid is given, what part of the HPA axis is the fastest and slowest to be suppressed?

A

The hypothalamus is the fastest and the adrenal gland is the slowest

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19
Q

What components of the HPA axis recover first when corticosteroid medications are removed? recover last?

A

Hypthalmus is the quickest to recover, adrenals are the slowest to recover

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20
Q

How long does someone usually have to be on corticosteroid therapy before exogenous adrenal insufficiency is seen?

A

>3 to 4 weeks

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21
Q

What are some risk factors for exogenous adrenal insufficiency?

A

Abrupt cessation (always taper if course is >4weeks)

Major stressor (surgery, trauma, illness)

Divided dosing (BID/TID)

Daily doses given at any time other than morning

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22
Q

What type of corticosteroid dosing can be given to decrease the risk of complications?

A

Every other day dosing decreases the risk of complications including HPA axis suppression, growth suppression, HTN, opportunistic infections and electrolyte disturbances

23
Q

What two corticosteroid complications are not reduced by every other day dosing?

A

Osteoporosis and cataracts

24
Q

What two clinical presentations of exogenous adrenal insufficiency are seen?

A

Steroid withdrawal syndrome (most common): Presents with arthralgias, myalgias, mood changes, headache, fatigue, anorexia, nausea/vomiting. No change in serum cortisol levels but there is decreased intracellular corticosteroid

Adrenal (Addisonian) crisis: Very uncommon. Life-threatening and has sx’s of the withdrawal syndrome above plus hypotension. Decreased levels of cortisol in serum

25
Q

What are some glucose-based side effects of corticosteroids?

A

Hyperglycemia and increased appetite/weight gain (stress hormone, increases gluconeogenesis, increases insulin resistance)

26
Q

What are the lipid effects seen in corticosteroid therapy?

A

Hypertriglyceridemia (careful for pancreatitis), cushingoid changes (lipodystrophy, stores are mobilized and then deposited elsewhere like the face, posterior neck, and central obesity), menstrual irregularities

27
Q

Important pediatric concern with glucocorticoid therapy?

A

Growth impairment (results from decreased growth hormone and IGF-1 production)

This risk can be decreased by every other day dosing

28
Q

What are some bone effects of corticosteroid therapy?

A

Osteoporosis: Risk does not go down with every other day dosing.

Osteonecrosis: proximal femur most common area

Hypocalcemia

29
Q

When does the greatest reduction in bone density occur during corticosteroid therapy?

A

During the first 6 months

30
Q

Who loses the most bone mass and who is at the highest risk for fracture during corticosteroid therapy?

A

Increased fracture risk in post-menopausal women; greatest absolute loss of bone mass in young men as they have the highest baseline bone mass

31
Q

How long does it take for osteonecrosis to occur with glucocorticoid therapy usually?

A

2-3 month courses is when this occurs usually

32
Q

What are some gastrointestinal side effects of corticosteroid therapy?

A

Bowel perforation, peptic ulcer disease (mostly if total dose is >1g), H2 inhibitors or PPI can help, fatty liver changes, esophageal reflux, and nausea/vomiting

33
Q

What are some ocular side effects seen with chronic corticosteroid use?

A

Cataracts (risk not changed with every other day dosing), glaucoma, infections, and refraction changes

34
Q

Psychiatric side effects of glucocorticoid therapy?

A

Psychoisis, hypomania, insomnia, agitations and depression

35
Q

Neurologic side effects of glucocorticoids?

A

Pseudotumor cerebri, seizures, epidural lipomatosis, and peripheral neuropathy

36
Q

Risk of infection with corticosteroid therapy?

A

Increased risk of tuberculosis reactivation, deep fungi, prolonged herpes virus infections, and pneumocystis jiroveci pneumonia

decreased risk with every other day dosing

37
Q

Muscular side effects of corticosteroid therapy?

A

Myopathy (proximal lower extremity > others) and muscular atrophy

38
Q

Cutaneous side effects of corticosteroid therapy?

A

Decreased wound healing, striae, atrophy, telangiectasia, steroid acne, purpura, infections (staph/HSV), telogen effluvium, hirsutism, pustular psoriasis flare upon withdrawal, perioral dermatitis, contact dermatitis, and hypopigmentation

39
Q

Safety of corticosteroids in pregnancy?

A

Category C, likely safe for short courses if needed for severe PUPP or gestational pemphigus

40
Q

What does every other day dosing have a lower side effect profile?

A

The anti-inflammatory effects last longer than the HPA axis inhibition

good for maintenance once acute disease is controlled but systemics are still needed

41
Q

What is the advantage and disadvantage of divided daily doses of corticosteroid?

A

They are more effective, but higher risk of side effect

42
Q

What are the unique side effects to IM corticosteroid?

A

Cold abscesses, subcutaneous fat atrophy, crystal deposition, menstrual irrgularities adn purpura

43
Q

Why do IM corticosteroids lead to greater HPA axis suppression?

A

Levels are constant through the day, so you get the levels present at night/morning

44
Q

How many times per year does Wolverton suggest a IM corticosteroid be used max?

A

For long-acting ones like Kenalog, 3-4x/year max

45
Q

What is the dosing for pulse dose steroids and which corticosteroid is used?

A

Usually Methylprednisolone, 500-1000mg (roughly 10-15mg/kg) given over 60 minutes (at least). This is done for 5 consecutive days

46
Q

What are the indications for pulse dose methylprednisolone?

A

Systemic vasculitis, systemic lupus erythematosus, pyoderma gangrenosum, and bullous pemphigoid

47
Q

What monitoring should be performed during a pulse dose of steroids and why?

A

Cardiac monitoring is recommended: there is a risk for sudden cardiac death, atrial fibrillation

Also, BMP (electrolyte shifts)

Clinically for seizures and anaphylaxis

48
Q

What is the target layer of the skin for intralesional Kenalog?

A

The goal is to inject in the dermis, otherwise can get atrophy more commonly

49
Q

What two patient populations are at high risk of bowel perforation with corticosteroid use?

A

Bowel anastomosis and patients with active diverticulosis

50
Q

What patients are at higher risk for getting the peptic ulcer perforation for systemic corticosteroids?

A

Most likely with adjunctive non-steroidal anti-inflammatory drugs (NSAIDs)s and patients w/ history of peptic ulcer disease.

Consider H2 blocker or PPI if using in someone w/ sx’s or history of PUD

51
Q

After how long on pharmacologic level of therapy with systemic corticosteroids does osteonecrosis become more worrisome?

A

Usually for at least 2-3 months

52
Q

At what point do you implement interventions to prevent bone loss for corticosteroid treatment?

A

Preventative measures to prevent bone demineralization should be instituted in any patient with a plan to be on corticosteroid for longer than 4 weeks.

53
Q

Do betamethasone and dexamethasone need the 11beta hydroxysteroid dehydrogenase enzyme to be active?

A

No, these are active independently from this enzyme

54
Q

What laps can be considered for monitoring in systemic corticosteroid use >1 month?

A

Can consider BMP (potassium), fasting lipids (watch the tri’s), height/weight for children, DEXA scan, TB test/CXR, and MRI of the hip/should/knee if there is pain during long term (>3month) therapy).

DERM (12) Medical Therapy (7 decks)

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