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Endocrine II DF > Adrenal Corticosteroid drugs DSA > Flashcards

Adrenal Corticosteroid drugs DSA Flashcards

1
Q

mineralcorticoids

A

fludrocortisone

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2
Q

short to medium acting glucocorticoids

A 
hydrocortisone
cortisone
prednisone
prednisolone
methyprednisolone
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3
Q

intermediate acting glucocorticoids

A

triamcinolone

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4
Q

long acting glucocorticoids

A

DBs go long

betametasone
dexametasone

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5
Q

steroid syntheis inhibitors

A

aminoglutethimide
ketoconazole
metyrapone
mitotane

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6
Q

glucocorticoid antagonist

A

mifepristone

my pristine body doesn’t need sugar

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7
Q

steroid hormones are transported by what

cortisol bound to ___ considered ___

A

protein carriers bc they are hydrophobic

  • transcortin or CBG
  • rest loosely bound to albumin
  • albumin bound cortisol should be considered free
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8
Q

when is transcortin and CBG high

low?

A

pregnancy

low in liver failure

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9
Q

half life of cortisol is increased in what pts

A

pts with liver disease

hypothyroid pts

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10
Q

direct effects of mineralocorticoids on CV system:

1) effects on gene expression
2) aldosterone excess causes

A 
gene expression:
NAPDH reductase-->oxidative stress
collagen, TGFB--> fibrosis
IL-6, CAM-->inflammation
PAI-1-->inhibition of fibrinolysis, blood clotting

Cat NIP

2) aldosterone excess:
- cardiac fibrosis and hypertophry
- vascular remodeling and inflammation

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11
Q

glucocorticoid effects

A

transactivation: effect on carb, lipid, protein metab

transrepression mech: GR-ligand complex binds other txn factor complexes and suppresses gene txn
-NF-Kb, AP-1 = anti-inflamm, immunosupp, anti growhth

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12
Q

what receptor may be responsible for glucocorticoid resistance

A

GR beta

-no ligand binding, inactive

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13
Q

11B-HSD type 2 role

A

converts cortisol into inactive cortisone so cannot bind MR
-this is how aldosterone gets effect bc aldost and cortisol bind MR with same affinity but more cortisol is produced daily

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14
Q

what tissues does 11B-HSD type 2 convert cortisol to cortisone

A

renal tubular epithelium
salivary glands
sweat glands
colon epithelium

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15
Q

inhibtion of 11B-HSD type 2 results in

A

hypertension and edema with excess MR stim by cortisol

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16
Q

what may inhibit 11B-HSD2

A

glycyrrhizin (licorice root extract)

carbenoxolone

17
Q

glucocorticoid effect on carb metabolism

3 enzymes
transporter
development of what

A

increase PEPC–>increased gluconeogenesis

increased glucose 6 phosphatase = more glucose in circulation

increased glycogen synthase

decreased GLUT4

development of hyperglycemia

18
Q

glucocorticoid effect on lipid metabolism

A

promote stimulation of HSL

increasedd FFA and glycerol into gluconeogenic pathway

increased insulin secretion

increase fat deposition and chane in fat distribution

19
Q

glucocorticoids in skeletal muscle

A

suppressed protein synthesis will lead to myopathy and muscle wasting

20
Q

gluocorticoids and phospholipase A2 and COX

A

decrease production

= less prostaglandins and leukotriens

21
Q

glucocorticoids on CVS

A

increased Epi and ?Ne
increased HR and CO
increased BP
residual mineralocorticoid activity (Na+/H20+ retention)

22
Q

glucocorticoids on GI

A

decreased gastroprotective prostaglandins
decrease immune response H pylori
increase gastric acid and pepsin secretion

23
Q

glucocort on CNS

A

insomnia
irritanility
euprhoia then depression
decreased libido in males

24
Q

glucocort in bones/growth

A

decreased intest absorption calcium
increase osteoclast activity (osteoporis)
growth retardation in children

25
Q

glucocort in skin

A

dfragile and thin skin with stretch marks

26
Q

treatment addisons

A

hydrocortisone and fludrocortisone

27
Q

cataracts, peptic ulcers, glaucoma in what steroid

A

glucocortioids

28
Q

a prodrug activated by esterases present in bronchial epithelial cells; systemically absoerbed active drug bound to serum proteins

A

ciclesonide

29
Q

pt populations in which systemic glucocorticoids administration is problematic

A 
immunocompromidsed
diabetics
pts with infections
pts with peptic ulcer
pts with CV conditions
pts with psychiatric condistions
pts with osteoporosis
children
30
Q

aminoglutethimide MOA

  • indication
  • side effects
A

blocks conversion of cholesterol to pregnenolone
reduces all steroid hormones

adrenocortical cancer

drowsiness
GI upset

31
Q

ketocanzole

MOA
indication
AE

A

p450 inhibition, reduces adrenal and sex hormones

prostate cancer
antifungal
cushing syndrome
stops androgenic hair loss

PACH of keys

hepatotox and gynecomastia in males

32
Q

metyrapone

MOA
indication
AE

A

inhibtion of steroid 11 hydroxylation
stops cortisol and corticosterone

cushing syndrome (only drug for this in pregnancy) (tyra banks pregnant)

accumulation 11 deoxycortisol = increased aldosterone = more sodium and water retention
-also increased androgens = hirsutism in women
GI upset
dizziness

33
Q

mitotane

MOA
indication
AE

A

sodium and calcium ionophore
PKC and AC inhibitor
cytotoxic action on adrenal cortex

adrenal carcinoma

depression, somnolence
GI upset
rashes

too tan gets rashes, GI problems bc he eats, and depression from eating too much/being fat

34
Q

mifepristone

MOA
indications
AE

A

glucocorticoid receptor antagonist
stabilizes hsp90-GR complex in cytosol, no nuclear translocation
-progest receptor antagonist

endogenous cushings
anti progest action for termination intrauterine preg

dizziness
GI upset
fatigue

35
Q

spirnonolactone MOA
indications
side effects

A

aldosterone receptor antagonist
also antagonist at androgen receptors

primary hyperaldost
hirsutism in women
diuretic for HF and HTN

hyperkalemia
gynecomastia and impotence in men
menstrual abnormalty in women

36
Q

eplerenone
MOA
indications
side effects

A

antag of aldosterone at mineralocorticoid receptors
lower affinity for androgen recept than spironolact

HTN
HF

hyperkalemia

Endocrine II DF (7 decks)

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