glucocorticoids

Question 1

adrenal gland components

Answer 1

• adrenal cortex: secrete glucocorticoids and mineralocorticoids
• adrenal medulla: epinephrine and norepinephrine

anterior pituitary ACTH stimulates glucocorticoids release
- mainly cortisol
- drugs given mimic cortisol

Question 2

glucocorticoids physiology

Answer 2

• promote glucose availability - protein metabolism
• fat metabolism
• cardiovascular: support SNS activity on blood vessels

Question 3

over secretion of glucocorticoids

Answer 3

cushing syndrome

Question 4

under secretion of glucocorticoids

Answer 4

addison’s disease (autoimmune of adrenal cortex)

Question 5

glucocorticoids example

Answer 5

• prednisone: drug of choice of oral glucocorticoids for anti-inflammatory purposes and hormone replacement
• prednisolone
• cortisone
• dexamethasone

all mimic cortisol

dose for hormone replacement much lower than dose for immunosuppressant

Question 6

glucocorticoids given by:

Answer 6

• inhalation: asthma/COPD
• nasally: rhinitis, prevent recurrence of polyps
• topically: inflammation of eye, ear, skin
• systemic (IV, PO): hormone replacement and immunosuppression

Question 7

glucocorticoids moa

Answer 7

alter gene expression of many proteins
- physiological doses (low: hormone replacement)
- pharmacological doses (high: inmunosupresion)

glucocorticoids help control inflammatory and immune responses
- cytokines (IL-2), COX, inhibit immune cell proliferation

Question 8

glucocorticoids indications

Answer 8

• adrenocortical deficiency (addison’s disease): lifelong replacement therapy
• anti-inflammatory/immune suppression: COPD, asthma, organ transplant, GI diseases, dermatological diseases

Question 9

glucocorticoids contraindications

Answer 9

serious infections ongoing
- systemic fungal infections
- body cannot fight

Question 10

glucocorticoids cautions

Answer 10

• GI issues: provoke PUD, reflux, gastritis
• high doses increase glucose levels in plasma: diabetes mellitus
• CV: HTN, HF, renal impairment, pregnancy

Question 11

glucocorticoids AE

Answer 11

mimic cushing’s syndrome
- moon face
- buffalo hump (fat deposit on neck)
- abdominal fat
- thin arms and legs
- stria (red markings)

CV: HF, edema, HTN
CNS: convulsions, headache, vertigo, mood swings, nervousness, insomnia, steroid psychosis
endocrine: growth suppression, cushings, menstrual irregularities, carb intolerance, hyperglycemia
GI: ulcers, perforation, distension, pancreatitis
Integumentary: skin thinning
musculoskeletal: muscle weakness, loss of muscle mass

Question 12

AE depends on dosage

Answer 12

replacement therapy doses do not produce cushing’s syndrome

higher doses for inflammation or immune suppression major AE are more common (must have shorter term use)

Question 13

replacement therapy

Answer 13

lifelong treatment may need to increase dosage in times of stress
- infections, surgery, traumas
- simulating what happens physiologically
- 3x3 rule: three times usual dose for 3 days

Question 14

immunosuppressant therapy

Answer 14

drug inhibits physiological control of cortisol secretions
- reduced/absent ACTH and CRH
- negative feedback

• leads to cortex atrophy (nonfunctional)
• tapering of doses when coming off drugs allow adrenal cortex to recover
• inhibition on ant pit reduced step by step, ACTH levels rise, stimulate adrenal cortex so it is functional, produce natural cortisol again

Question 15

client implication

Answer 15

sudden discontinuation of glucocarticoids can precipitate an adrenal crisis
- adrenal gland cannot make glucocorticoids
- abdominal pain
- low BP, dehydration (shock, fatal)
- N&V
- extreme fatigue
- confusion, convulsions

taper doses before drug is discontinued

Question 16

client implications cont

Answer 16

take at the same time every day (usually morning with food)
- replicate normal secretion pattern

caution with NSAID use (no PG to protect)
- stomach ulcers

• inhaled: rinse mouth to prevent fungal infections
• avoid contact with people with infections, report symptoms (immune suppression)