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Endo II > Corticosteroids DSA > Flashcards

Corticosteroids DSA Flashcards

1
Q

aldosterone

A

mineralocorticoid

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2
Q

cortisol

A

glucocorticoid

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3
Q

CRH

A

corticotropin releasing hormone

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4
Q

ACTH

A

adrenicorticotropic hormone

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5
Q

dexamethasone

A

semisynthetic glucocorticoid

aka decadron

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6
Q

hydrocortisone

A

semisynthetic glucocorticoid

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7
Q

methylprednisolone

A

semisynthetic glucocorticoid

aka medrol

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8
Q

prednisolone

A

semisynthetic glucocorticoid

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9
Q

prednisone

A

semisynthetic glucocorticoid

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10
Q

fludrocortisone

A

mineralocorticoid

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11
Q

zona glomerulosa

A

ANG II receptor

synthesis of aldosterone

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12
Q

zona fasciculata and reticularis

A

17 alpha hydroxylase and 11-beta hydroxylase

regulated by ACTH

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13
Q

POMC

A

precursor protein

forms MSH, ACTH, LPH, and beta endorphin

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14
Q

ACTH MOA

A

GPCR activity

activates synthesis of corticosteroids

mobilization of cholesterol

also - trophic (growth) effect on adrenal cortical cells

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15
Q

diurnal ACTH

A

peak ACTH early in the morning

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16
Q

cortisol negative feedback

A

inhibit release of CRH from hypothalamus

inhibit release of ACTH from pituitary

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17
Q

therapeutic glucocorticoids

A

high doses for long time

-supress HPA axis

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18
Q

stress stimuli

A

injury, hemorrhage, infection, surgery, cold, pain, fear, etc.

can override normal negative feedback
-leading to elevated levels of adrenocortical steroids

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19
Q

cushings syndrome

A

hypercortisol

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20
Q

addisons disease

A

primary adrenocortical insufficiency

T cell mediated autoimmune destruction, infection, infiltration, cancer, b/l TB of adrenals, hemorrhage
-in adrenal cortex

decreased

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21
Q

secondary adrenocortical insufficiency

A

decreased circulating ACTH levels

adrenal atrophy and low levels of glucocorticoids

may be due to prolonged glucocorticoid tx**

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22
Q

ACTH plasma concentration measure

A

immunoradiometric assay

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23
Q

adrenal cortex steroids

A

corticosteroids - gluco and mineralo - 21 carbons

androgens - 19 carbons

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24
Q

type I GR

A

glucocorticoid receptor - GR

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25
Q

type II GR

A

mineralocorticoid receptor - MR

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26
Q

steroid hormone receptor mechanisms

A

in cytoplasm of cells

complexed with heat shock proteins
-dissociate when bind steroid

activated receptor - to nucleus and bind GREs**

GRE site binding - either activates or inhibits transcription of specific genes

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27
Q

cortisol and aldosterone

A

both bind MR with equal affinity

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28
Q

mineralocorticoid specificity

A

tissue specific localization of receptor

enzymatic protection against glucocorticoid excess
-11-beta hydroxysteroid DH inactivates cortisol to cortisone

differential binding of GR and MR to nuclear transcription factors

29
Q

11-beta hydroxysteroid DH

A

inactivates cortisol to cortisone

30
Q

effect of corticosteroids

A

decrease peripheral glucose uptake (anti-insulin)

stimulate protein breakdown and lipolysis

stimulate gluconeogenesis in liver

net effect - elevated blood glucose**

also - redistribution of body fat - moon facies and buffalo hump

31
Q

aldosterone effect

A

enhance reabsorption of Na in kidney distal tubules and collecting ducts

increased K and H secretion in urine

32
Q

excess aldosterone

A

elevated Na expansion of ECF volume, hyponatremia, hyperkalemia, acidosis

33
Q

glucocorticoids and immunosuppression

A

can prevent or suppress inflammation

inhibit production and release of cytokines that normally stimulate proliferation and function of B and T cells

glucocorticoids - suppress IFN, GM-CSF, ILs, TNF, prostaglandins, and leukotrienes

34
Q

IL-1

A

inflammatory cytokine

  • stimulate release of CRH and ACTH
  • increase glucocorticoids
  • which in response inhibit immune/inflammatory response further
35
Q

steroid absorption

A

lipophilic

diffuse across cell membranes

wide volume of distribution

36
Q

steroid transport

A

90% cortisol bound to protein

albumin and corticosteroid binding globulin (CBG

37
Q

transcortin

A

CBG

-corticosteroid binding globulin

38
Q

higher steroid levels

A

binding capacity of CBG and albumin is overwhelmed - much more free state and is more active

39
Q

biological half life

A

used for steroid

because plasma drug concentration does not correlate with time course of bio effects

40
Q

anti-inflammatory effects

A

mediated by same receptor as metabolic effects
-none of glucocorticoid derivatives have selective anti-inflammatory activity without also affecting carb, protein, fat metabolism

41
Q

compounds that are classified as glucocorticoids

A

also have modest but significant mineralocorticoid activity

42
Q

long acting glucocorticoids

A

betamethasone

dexamethasone

43
Q

short acting glucocorticoids

A

cortisol and cortisone

44
Q

intermediate acting glucocorticoids

A

prednisone
prednisolone
methylprednisolone
triamcinolone

45
Q

mineralocortoids

A

corticosterone

fludrocortisone

46
Q

beclomethasone dipropionate

A

inhalation for asthma or COPD

47
Q

toxicity of adrenocortical steroids

A

1 - withdrawal effects

2- continued use of high dose

48
Q

withdrawal of adrenocorticosteroids

A

flare up of underlying disease

acute adrenal insufficiency**

consider this in any patient with high dose over 2 weeks

49
Q

continued use of high dose corticosteroids

A 
suppression of HPA axis
HTN and hypoerglycemia
increased infections
peptic ulcers
myopathy
behavioral changes
cataracts
osteoporosis
osteonecrosis
growth retardation
50
Q

unharmful steroid therapy

A

single dose or short course (1 week)

51
Q

steroid therapy for life-threatening disease

A

initial dose should be large - aimed at achieving rapid control of crisis

no benefit observed - dose doubled or tripled

52
Q

steroid therapy regimens

A

alternate day - to diminish HPA suppression

pulse therapy - for high dose glucocorticoids

53
Q

glucocorticoid therapy

A

palliative

because underlying cause of disease remains

54
Q

glucocorticoids inhibit

A

both early inflammatory processes and later manifestations

55
Q

lipocortins

A

induced by glucocorticoids

-inhibit phospholipase A2 activity and suppress release of lipid mediators from cells

56
Q

rheumatoid arthritis

A

main cytokine - TNF-alpha

tx - glucocorticoids

57
Q

osteoarthritis tx

A

intraarticular joint injections

58
Q

ICS therapy

A

inhaled corticosteroids
-for tx of bronchial asthma

for prophylaxis

59
Q

severe asthma attack tx

A

aggressive treatment with parenteral glucocorticoids

IV methylprednisolone
-followed by oral prednisone

dose tapered gradually

60
Q

tx allergic disease

A

immediate epinephrine tx

glucocorticoids to suppress delayed inflammation

61
Q

tx of ocular diseases

A

topical glucorticoids

may exacerbate glaucoma - increased intraocular eye pressure

may also mask ocular infection - CI in herpes simplex infections

62
Q

CI for glucocorticoids in eye disease

A

herpes simplex infection

mechanical laceration/abrasion - impaired wound healing

63
Q

skin disease tx

A

topical glucocorticoids

-hydrocortisone 1%

64
Q

tx of ulcerative colitis and crohns

A

oral prednisone and enteric coated budesonide

65
Q

cerebral edema tx

A

corticoisteroids useful with parasites and neoplasms

66
Q

mitotane

A

o,p - DDD
-similar to insecticides

selective toxicity for adrenal cortex

used only to treat inoperable adrenal tumors

67
Q

RU-486

A

progesterone receptor antagonist

aka mifepristone

use to terminate early pregnancy

inoperable patients with ectopic ACTH secretion or adrenal cracinoma failed to respond to other tx options

68
Q

spironolactone

A

K-sparing diuretic
-competes for mineraolcorticoid receptor

aldosterone antagonist

effective tx for hyperaldosteronism

Endo II (12 decks)

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