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94 Cards in this Set
- Front
- Back
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t/f
steroids have receptors on the plasma membrane |
f
receptors are inside the cell |
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steroids alter ---- of dna
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transcription
(increase or decrease) |
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steroids alter protein -----
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synthesis
(increase or decrease) |
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what's ligand dependent
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steroids altering transcription
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3 major portions of a receptor
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1. DNA binding portion
2. Ligand binding portion 3. internal activation domain |
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portion of the receptor that binds to the response element
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dna binding portion
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part of the receptor that binds to the steroid
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ligand
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what part of the receptor determines how well they interact w/ DNA
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internal activaton domain
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GR activation or transcription depends on ----- present
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coactivators or corepressors
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GR can also interact w/ otehr --- ------
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transcription factors
other receptors or NFKB |
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what can GR homodimer w/
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itself and other transcriptors
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2 types of receptors for the natural adrenal steroids
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GR
MR |
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cortisol will binds to:
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both MR and GR
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what does cortisol have a higher affinity to:
mr or gr |
MR>GR
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which has a higher capacity to cortisol:
MR or GR |
GR>MR
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what will have a higher saturation of cortisol:
MR or GR |
GR>MR
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which binds to aldosterone
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MR
|
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which has high affinity, low capacity ot cortisol:
mr or gr |
MR
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in vivo normal levels of cortisol do not bind to -- in kidney
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MR
but it will at high doses |
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in vivo, protection of -- by 11bHSD in -----, ---, ------
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MR
kidney, colon, salivary gland |
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what will convert cortisol to cortisone i the kidney, colon, salivary gland
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11bHSD
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where will 11bHSD convert cortisone to cortisol
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other sites, esp: LIVER
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which is water soluable:
cortisone or cortisol |
cortisone
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which receptor will cause Na retention and HTN
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MR
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the liver isoform of 11B HSD will convert:
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cortisone to cortisol
prenissone to prednisolone |
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routes of steroids:
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oral
intraarticular epidural IM IV inhalation |
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systemic effects of steroids depends on:
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route
systemic levels produced (less for inhalation and intra-articular) |
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steroids associated w/ severe -- disease
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liver
(bioconversion of cortisone and prednisone in the liver) |
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--- effects for many synthetic steroids
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CNS
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what can limit uptake into cns
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multi drug resistance transporter: esp cortisol
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what 's used to tx asthma in a pregnant mother
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prednisolone
cuz does not x placenta |
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what's used for antenatal tx of baby
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betamethasone or dexamethasone
will x placenta these drugs will help mature fetal lungs |
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which meds are glucocorticoids
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prednisone
6a methylprednisolone (medrol) 9a fluoro 16a hydroxyprednisone (triamcinolone) 9a fluoro-16a-methylprednisolone (dexamethasone) has more gr activity/potency |
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which meds are MRs
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aldosterone
deoxycorticosterone 9a fluorocortisol has more mr activity/potency |
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short acting gc
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cortisol
cortisone (8-12 hr) |
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intermediate acting gc
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prednisone
methylprednisolone triamcinolone (12-36 hrs) |
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long acting gc
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betamethasone
dexamethasone (>24 hrs) |
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cortisone equivalent to
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hydrocortisone
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prednisolone dose equivalent to
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prednisone
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methylprednisolone does equivalent to
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triamcinolone
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dexamethasone dose equivalent to
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betamethasone
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for replacement
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cortiosol
prednisolone dexamethasone |
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asthma tx
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prednisolone
(inhaled dose: budesonide) |
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for antiinflammatory
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prednisolone
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major pharm action of steroids
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anti-inflammatory: #1
immune suppressive inhibit tissue degradation |
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actions of steroids via:
increase ---- of --- proteins |
transcription
suppressive (immune) |
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actions of steroids via:
decreased transcription of ---, --- proteins |
inflammatory
immunogenic |
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actions of steroids via:
block effects of other agents: |
NFKB
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GR mediated actions:
decrease action of --- cells |
immune
|
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GR-mediated actions:
decrease circulating ----- from circulation to --- -----, -- and ----- |
wbc
lymphoid tissue splen bone marrow |
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GR mediated actions:
will have increased apoptosis of ---- and ---- |
eosinophils
t cells |
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GR mediated actions:
inhibit monocyte-macrophate -- production |
IL
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GR mediated actions:
change balance btw - and --- activity |
Th1
Th2 |
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GR mediated actions:
inhibit ---- form Th1 |
cytokines
|
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GR mediated actions:
stimulate cytokines from |
Th2
|
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which is antiinflammatory:
Th1 or Th2 |
Th2
|
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GR mediated:
inhbit --- production stimulate ---- and ------ these will inhbit -----A2 this will reduce ----- |
prostanoid
lipocortin annexin 1 phospholipase AA (substrate for prostanoid) |
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GR mediated actions: inhibit Prostanoid production
stimulate ----- inhibit NFkB --- activity this will inhibit -------, cox 2 |
IkB
transcriptional cylcooxygenase |
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GR mediated actions: inhibit Prostanoid production
inhibit both --- and -- production |
PG
leukotriene (many nsaids prevent only PG production . . .why they're not good for asthma and why u can use steroids for asthma) |
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nfkb will activate/inactivate inflammatrion
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activate. . .
so when gr binds to nfkb there will be decreased transcription and less inflammation |
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gc actions:
decrease --- stimulated histamine and --- release form mast cells and basophils |
IGE
leukotriene |
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gc actions:
decreased --- action |
macrophage
|
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gc actions: decreased macrophage action:
decreased -- of monocytes and macrophages decreased ----- of monocytes ot macrophages |
chemotaxis
differentation |
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gc actions: decreased macrophage action:
decreased activation of ------ and secretion of ---, ----, and --- ----- |
macrophages
collegenase elastase plasminogen activator (decreased tissue breakdown and clot dissolution) |
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gc actions: decreased macrophage action:
decrease ---, ---, ---- |
IL-1
IL-6 TNF a |
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GC actions
inhibt inflammatory responses in the --- ---- |
endothelial cells
|
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some things that are inhibited in endothelial cells due to GC
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endothelial leukocyte adhesion factor
intracellular adhesion factor prostaglandin IL-1 |
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major net effects of GC
inhibit: -- synthesis inhibt inflammatory ----, -- receptors, ----- proteins inhibit collengenase, -----, --- ------- |
PG
cytokines cytokines receptors chemotactic metalloproteases adhesion factors (GCs almost everywhere) |
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gc used to tx:
ocular --- |
inflammation (not infection)
|
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catabolic se in adipose tissue for gr
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lipolytic enzymes
anti-insulin |
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catabolic se in muslce for gr:
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protein degradation
anti-insulin |
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catabolic se in liver for gr:
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gluoconeogenic
|
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se of gr:
--glycemia |
hyperglycemia
|
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diabetogeic se of gr:
--- wasting possible ---- -- redistribution |
protein (muscle loss, esp in limbs)
myopathy fat (truncal obesity: redistribute calories from proteins to fat) |
|
catabolic se in bones
inhibit ------- in intestine: inhibit -- absorption kidney: increase --- loss |
osteoblasts
ca ca loss |
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se of gc in adults due to catabolic effects in bone
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osteoporosis
veterbral compression fx (buffalo hump) |
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se of gc in adults in kids
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arrest growth in children
|
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--- face is a se of gc
|
moon
|
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cv se of gc
kidney/MR: |
na retention: increase BP
|
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cv se of gc
kidnye/GR |
may mediate K excretion
|
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mr/gr in:
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heart
vasculature brain (contractility, vascular responsiveness, hypertension) |
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cv se of gc:
|
thrombosis
vasculitis dylipidemia |
|
htn more likely w/ which drugs?
why |
hydrocortisone
cortisone due to mr binding: na retention/vol loading |
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synthetic steroids will have increased/decreased cv effects cuz
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decreased
due to decreased MR activity |
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se of gr in eye
|
cataracts
glaucoma |
|
se of gr:
increase susceptibility to ------ poor --- ----- connective tissue: inhibit ----- ---, ----- |
cataracts/glaucoma
infection wound healing inhibit collagen hirutism, acne (if androgen to steroid) |
|
corticosteriods can alter ------
can cause ---- or ------ |
mood
euphoria depression |
|
se of corticosteroids
reduce ----- adrenocortical activity |
endogenous
gr feedback: long term tx suppresses ach and the adrenal |
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brain/pituitary: gr
decrease in --- and --- |
CRF
ACTH |
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chronic use of corticosteroids:
reduce size and repsonsiveness of ----- |
adrenal gland
|
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--- w/ withdrawal
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hypocorticism: addisonian symptoms
|
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addisonian symptoms:
|
hypotension
hypovolemia |
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prevention of suppression of endogenous secretion:
w/ systemic adminstration for short periods or ------- |
alternate day tx
|
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prevention of suppression of endogenous secretion
w/ long term use: |
taper off for drug holiday to allow adrenal to recover from lack of acth
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