steroid drug chart + adrenal review questions

PoP II

which glucocorticoids are most potent

betamethasone and dexamethasone (0.75)

what is the relative potency of methylprednisolone and triamcinolone

4

what is the relative potency of prednisolone and prednisone

5

what is the relative potency of hydrocortisone

20

what is the relative potency of cortisone

25

what is the generic name for Decadron

dexamethasone

what is the generic name for Medrol

methylprednisolone

what is the generic name for Solumedrol

methylprednisolone

what is the generic name for Millipred

prednisolone

what is the generic name for Orapred

prednisolone

what is the generic name for Prelone

prednisolone

what is the generic name for Solu-cortef

hydrocortisone

what is the generic name for Cortef

hydrocortisone

what are some indications for glucocorticoids

acute exacerbation of COPD or asthma, inflammatory disease states, autoimmune disorders, etc.

what is the active form of the prodrug cortisone

cortisol

what is the active form of the prodrug prednisone

prednisolone

where are cortisone and prednisone activated

liver (hepatic activation)

which glucocorticoids have the shortest duration of action

cortisone and hydrocortisone

which glucocorticoids have the longest duration of action

dexamethasone and betamethasone

how can you prolong the duration of action of glucocorticoids

IM administration

what are two contraindications for glucocorticoids

use with caution in fungal infection

avoid with live attenuated vaccines

what are two precautions for glucocorticoids

glaucoma

activation of latent infection

what can happen when glucocorticoids and diuretics are taken together

combined hypokalemia

which glucocorticoids are most like mineralcorticoids

cortisone and hydrocortisone

what are some acute side effects of glucocorticoids

increased appetite and weight gain, Na/water retention, hypokalemia, CNS, indigestion, hypertension, hyperglycemia, immunosuppression, impaired wound healing, acne, myopathy

what are chronic side effects of glucocorticoids

cushing syndrome, dermal thinning, bruising, diabetes, glaucoma, cataracts, amenorrhea, growth retardation, acne, pancreatitis, GI bleed/esophagitis/ulcers, osteoporosis, hirsutisim, immunosuppression

which glucocorticoid is most commonly prescribed in pediatrics

prednisolone

how should glucocorticoids be taken to minimize stomach upset/GI effects

take with food

at what time should glucocorticoids being taken for replacement of endogenous steroids be given

7-8 AM to mimic diurnal cortisol

how long can a large dose of glucocorticoids be given

10-14 days

why should glucocorticoids taken longer than 14 days be tapered

to minimize HPA axis suppression

which glucocorticoids are given in premature labor and fetal distress

betamethasone or dexamethasone

why are glucocorticoids given in premature labor or fetal distress

to promote surfactant production

what are some signs and symptoms of withdrawal/acute adrenal insufficiency

N/V, abdominal pain, dehydration, hyponatremia, hyperkalemia, weakness, lethargy, hypotension

what type of corticosteroid is fludrocortisone

mineralocorticoids

what is the generic name for Florinef

fludrocortisone

what is the indication for fludrocortisone

Addison’s disease to treat hyponatremia

which corticosteroid has no anti-inflammatory effect

fludrocortisone

what does fludrocortisone do

impacts serum sodium/potassium (aldosterone like)

what is a precaution for fludrocortisone

liver dysfunction

what are common side effects of fludrocortisone

sodium/water retention, hypokalemia, hyperglycemia, myopathy

what are serious adverse effects of fludrocortisone

congestive heart failure, hypercortisolism

what is the body’s basal rate of secretion for cortisol

10 mg/day

what is the rate of cortisol secretion when the body is under physiological stress

250 mg/day

what are the preferred agents for replacement of deficiency

hydrocortisone 25 mg or prednisone 5 mg

what is the preferred agent for acute adrenal insufficiency

hydrocortisone 200-300 mg/day

what are the main components of the neuroendocrine system

hypothalamus → pituitary gland → target organ/tissue

what are the key functions of the neuroendocrine system

create and release hormones that regulate growth, development, metabolism, and homeostasis

what is the function of the anterior pituitary gland

synthesis and release of hormones in response to hormones from the hypothalamus

what is the function of the posterior pituitary

hormones synthesized in the hypothalamus are transported and stored for release

what are the similarities between the anterior and posterior pituitary

both are encased by the sphenoid bond and both release peptide hormones

how does the hypothalamo-hypohyseal-target gland axis (HPT) function

hypothalamus is stimulated → specific releasing hormone travels to anterior pituitary → tropic hormone released from pituitary → reaches target cell

what are the four different releasing hormones

growth hormone releasing hormone (GHRH), thyrotropin releasing hormone (TRH), gonadotropin releasing hormone (GnRH), and corticotropin releasing hormone (CRH)

what does the release of growth hormone releasing hormone stimulate

growth hormone

what does the release of thyrotropin releasing hormone stimulate

thyroid stimulating hormone (TSH) and prolactin

what does the release of gonadotropin-releasing hormone stimulate

follicle stimulating hormone (FSH) and lutenizing hormone (LH)

what does the release of corticotropin releasing hormone stimulate

adrenocorticotropic hormone (ACTH) and melanocyte stimulating hormone (MSH)

what two hormones inhibit growth hormone and thyroid stimulating hormone

growth hormone inhibiting hormone of somatostatin

what hormone inhibits prolactin and melanocyte stimulating hormone

prolactin inhibiting hormone

what are the key effects of growth hormone

works with IGF1 from the liver to promote growth and broadly modulates metabolism — overall a very broad effect in most cells

what are the key effects of TSH

stimulates thyroxine (T4 and some T3) release from follicular cells in thyroid gland

what are the key effects of FSH

development of follicular/sertoli cells, ovaries/testes

what are the key effects of LH

ovulation in the ovaries and testosterone in the testes

what is the key effect of prolactin

milk in the mammary glands

what are the key effects of ACTH

synthesis and release of glucocorticoids (cortisol) and androgens

what are the key effects of melanocyte stimulating hormone

increases pigmentation through melanocytes in skin and hair

what two hormones are made in the hypothalamus and transported/released from the posterior pituitary

anti-diuretic hormone (ADH/AVP) and oxytocin

what is the HPA axis

hypothalamus → pituitary → adrenal cortex

what is the primary effector hormone released from the HPA axis

cortisol

what other hormones are released from the adrenal gland

corticosteroids, aldosterone, testosterone, DHEA, epinephrine

how does the HPA axis work

CRH released from hypothalamus → stimulates release of adrenocorticotropic hormone (ACTH) → cortisol released from adrenal cortex → target organs/tissues

where does cortisol work

glucocorticoid receptors in every cell in the body

what induces cortisol release

physiological stress

when are cortisol levels highest and lowest

highest — morning

lowest — evening

what is proopiomelanocortin

precursor protein made in the hypothalamus

what products are released from proopiomelanocortin

adrenocorticotropic hormone, melanocyte stimulating hormone, enkephalins, and endorphins

what is the primary mineralocorticoid and where is it produced

aldosterone — produced in zona glomerulosa

how is aldosterone regulated

by angiotensin II and serum K+ levels

what is aldosterone’s primary function

regulate electrocytes, sodium retention, potassium secretion

what is the primary glucocorticoid and where is it produced

cortisol — produced in the zona fasiculata

what primarily controls cortisol

adrenocorticotropic hormone

what is cortisol’s primary function

metabolism (mobilizing energy substrates) during fasting, immunomodulation, anti-inflammatory

how does corticotropin-releasing hormone act on corticotrophs in the anterior pituitary

binds to Gs protein receptor → stimulates release of ACTH from granules and increases proopiomelanocortin synthesis

how does ACTH act on adrenal cortical cells

increases uptake of cholesterol and regulates initial steps of cortisol synthesis (cholesterol desmolase and 17 a-hydroxylase)

how are cortical hormones transported throughout the body

transcortin (glucocorticoids and aldosterone) and serum albumin (aldosterone only) binding

how are the cortical hormones removed from the body

degraded in the liver and conjugated to glucuronic acid → excreted through bile/feces or urine

how does cortisol work

binds to glucocorticoid receptor on cell → receptor-hormone complex binds to glucocorticoid response elements on DNA to change gene and protein expression → many effects on cells with respect to metabolism

what role does cortisol play during the first few days of fasting

uses carbohydrates and converts protein to glucose through gluconeogensis and uses glycogen stores

what role does cortisol play in long-term fasting

fat metabolism increases, tissues use fatty acids, and the brain uses ketones for energy

what are the key effects of cortisol on carbohydrate metabolism

increases liver enzymes needed for conversion of amino acids to glucose, increases amino acid release from muscles, and causes cells to use less glucose for energy by decreasing glycolysis and increasing insulin resistance

what are the key effects of cortisol on lipid metabolism

lipolysis (mobilize fat from peripheral sites), beta-oxidation of fatty acids, specific forms of obesity (central obesity, buffalo hump, moon face)

what are the key effects of cortisol on protein metabolism

increased protein breakdown (catabolism), decreased protein synthesis, muscle weakness, and protein conversion to glucose in the liver

what are the key mediators for inflammation

histamine, bradykinin, proteolytic enzymes, prostaglandins, and leukotrienes

what are the effects of key mediators for inflammation

vascular effects — increase in blood flow, increase in capillary permeability, swelling, heat, redness, and infiltration of neutrophils and macrophages

what effect does cortisol have on inflammation

activates lipocortin gene → inhibits PLA2 → inhibits prostaglandin and leukotriene synthesis → reduce WBC activity

also decreases T and B cells, decreases capillary leakiness, and reduces release of IL1 from white blood cells

what effect does cortisol have on allergies

it has no effect on mast cell degranulation (what triggers body’s response) but does prevent subsequent inflammation

what is the rate limiting step in adrenocortical hormone synthesis

conversion of cholesterol to pregnenolone via adenylyl cyclase to protein kinase A

how is cortisol release regulated

negative feedback to decrease CRH and ACTH

what is Conn’s syndrome

tumor derived from zona glomerulosa cells that causes retention of sodium and loss of potassium

where is aldosterone released

from zona glomerulosa cells