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whats the endogenous glucocorticosteroid
cortisol
cardinal inflammatory responses
rubor - increased permeability - fluid release into tissues
dolor - systemic response
tumor - increased permeability
calor - capillary widening - increased blood flow
glucocorticosteroids effect on body
innate immunity
adaptive immunity
anti tumor immunity
can NSAID impact all 4 cardinal signs?
no
glucocorticosteroids can tho
HPA axis
hypothalamus
corticotropin releasing factor (CRF) —> stimulates anterior pituitary to secrete adrenocorticotropin (ACTH)
anterior pituitary
secretes ACTH
gives:
glucocorticoids = anti inflammatory and immunosuppression
mineralocorticoids = salt and water retaining
INCREASES BP, sometimes IOP
sex hormones
aldosterone secretion (not asking ? specifically on )
regulated by angiotensin
renin in plasma released by kidney in response to blood sodium levels
zona fasciculata
where endogenous glucocorticoids are released
in cortex of adrenal gland
regulated by AC
zona reticularis
adrenal androgens
zona glomerulosa
mineral corticoids
medulla of adrenal gland
catecholamines
what do glucocorticosteroids inhibit
phospholipase A2
anti inflammatory effects of glucocorticosteroids
inflammatory responses decreased
cardinal symptoms dec
inhibition of phospholipase A2
lymphocytopenia induced
decreases WBC - immunosuppression
inh of chemotaxis
prostaglandin synthesis inh
NSAID work here too
suppression of
edema
capillary dilation
scar formation
wound healing
could make an infection worse in the eye
manifestations are supressed
UNDERLYING CAUSE REMAINS
ophthalmic steroids drugs
prednisolone
difluprednate
dexamethasone
fluorometholone (FML)
loteprednol
rimexolone
soft steroids
soft steroids
good anti inflammatory actions w less impact on IOP
side effects less intense
what are the soft steroids
loteprednol
fluorometholone
rimexolone
ocular side effects of steroids
posterior subcapsular cataract
no sig reduce in VA
after long term topical/systemic use
glaucoma
LESS LIKELY W LOTEPREDNOL, RIMEXOLONE, FML
IOP elevation is reversible after discontinuation
secondary infections
bacterial, viral, fungal
retardation of corneal ep healing
INH OF WOUND HEALING
is high dose short period of time or low dose long period of tie worse
low dose long period of time
what does the steroid respone impact
outflow of aq humor
mech of posterior subcapsular cataract
changes w lens fibers and proteins
Corresponds with duration of treatment
More likely with oral steroids; less likely with Lotemax (ester)
ocular physiologic effects of retina
dec retinal oxygen consumption
increase glycogen content
vasoconstriction/ dec in capillary pressure near fovea
CSCR/ICSC (idiopathic CSC)
central serous chorioretinopathy
serous blood vessels leaks out of BV
SYMPATHOMIMETICS CAN ALSO CAUSE THIS
body secretes more cortisol when scared
anterior segment side effects
Delayed wound healing (epithelium)
Risk of infection
Glaucoma (Ocular hypertension aka IOP spike)
Posterior subcapsular cataract
posterior segment side effects
CSCR (central serous chorioretinopathy)
are corticosteroid side effects dose dependent
YES
after how many days must you taper a systemic steroid
high dose
and/or greater than 14 days of treatment
systemic side effects of steroids (9)
adrenal insufficiency
less likely w drops
cushings syndrome
most often w long term steroids
muscle atrophy
redistribution of body fat
purple stretch marks
peptic ulceration
TAKE THESE W FOOD
TAKE NSAIDS W FOOD TOO
osteoporosis
hypertension
most systemic steroids have low salt adn water retention but its not 0
inh of growth
skeletal maturation
children
diabetes
these will put someone close to diabetes into diabetes
activation of infection
supression of immuen response
delayed wound healing
glucocorticoids phys effect
carbohydrate/protein metabolism
inc glucose production
inc blood sugar level
DM pt
liber glycogen storage inc
lipid metabolism
redistribution of body fat
back of neck hump
moon face
lost from extremities
CNS
mood changes