Glucocorticoids

Question 1

Glucocorticoids MOA:

Answer 1

Modulate the production of regulatory proteins, rather than the activity of signaling pathways.
Bind receptors on the cytoplasm located on the INSIDE of the cell, which converts them to an active form.

Question 2

The 2 Major Clinical Applications of Glucocorticoids

Answer 2

Ability to suppress the immune response

Ability to suppress the inflammatory response

Question 3

What are the 3 specific mechanisms of glucocorticoids?

Answer 3

1) Inhibit synthesis of chemical mediators (prostaglandins, leukotrienes, histamine)
- the inflammatory mediators
2) Suppress infiltration of phagocytes
3) Suppress proliferation of lymphocytes
- the immune response of inflammation

Question 4

Short-term vs. Long-term Glucocorticoid therapy:

Answer 4

Short-term: 2-3 weeks

Long-term: > 3 weeks

Question 5

Patients on long-term glucocorticoid therapy are considered:

Answer 5

IMMUNOCOMPROMISED

Question 6

Name the 9 diseases that glucocorticoids are used for:

Answer 6

1) RA (autoimmune)
2) SLE (autoimmune)
3) Tendonitis (inflammation)
4) N/V
5) Organ transplant
6) Asthma
7) Cancer
8) Preterm infants (to avoid RDS; lung maturation)
9) Drug allergy

Question 7

Glucocorticoids & Hyperglycemia:

Answer 7

Promote gluconeogenesis
Reduce peripheral glucose utilization & uptake into muscle and adipose cells
CAN RESULT IN sDM w/ LT therapy
Intervention: monitor glucose AC/PC
insulin administration if indicated

Question 8

Glucocorticoids & Fluid and Electrolytes:

Answer 8

Due to mineralocorticoid activity –> results in Na+ & H2O retention, and K+ loss
Intervention:
-monitor electrolytes and provide replacement as necessary
-watch for early signs of hypokalemia (muscle cramps)

Question 9

Glucocorticoids & Iatrogenic Cushing’s Syndrome (Cushingoid Syndrom)

Answer 9

LT therapy results in Sxs that mimic the presentation of Cushing’s Syndrome

Question 10

S/S of Iatrogenic Cushing’s Syndrome:

Answer 10

Most common:

-hyperglycemia, F&E imbalance, osteoporosis, muscle weakness, “pot belly,” “moon-face,” “buffalo hump.”

Question 11

Glucocorticoids & Osteoporosis

Answer 11

LT therapy results in LOSS in bone density
-suppress bone formation, accelerate bone resorption, decrease intestinal Ca2+ absorption (causes PTH to mobilize Ca2+ from bone)
Interventions: DexaScans, increase intake of Ca2+ and VitD

Question 12

Glucocorticoids & Skin Integrity

Answer 12

LT therapy or High-doses lead to thinned skin and capillary fragility
-Can result in purpura, loss of IV sites, and infection

Question 13

Glucocorticoids & Psychological Disturbances

Answer 13

More common with high-dose, ST therapy, but can occur with LT therapy
60% –> psychological disturbances (insomnia, hyperactivity, mood changes, mania)
6% –> Steroid Psychosis (hallucinations, delirium, suicidal tendencies)

Question 14

Glucocorticoids & PUD

Answer 14

Inhibit prostaglandins that protect the GI mucosa
Interventions:
-administer w/ food or milk
-avoid concurrent use w/ NSAIDs

Question 15

Glucocorticoids & Vaccines

Answer 15

immunosuppressant, resulting in decreased immune response (Aby production) to vaccines

Question 16

Glucocorticoids & Withdrawal

Answer 16

LT therapy can cause Adrenal Insufficiency

NEED TO WEAN!

Question 17

S/S of Adrenal Insufficiency

Answer 17

Hypotension, Hypoglycemia, Myalgia, Arthralgia, fatigue

Question 18

Glucocorticoids & Once-a-Day Dosing

Answer 18

Most common prescription type for LT therapy

-Give before 9 am WITH FOOD

Question 19

Glucocorticoids & Alternate-day Dosing

Answer 19

Allows the adrenal glands to maintain functionality, while still receiving corticosteroid’s therapeutic effects
Helps to reduce LT therapy ADRs

Question 20

Glucocorticoid Drug Types (names)

Answer 20

Prednisone
Methylprednisolone (Solumedrol)
Inhaled/Intranasal types