pharmacology part 2 Flashcards
besides NSAIDS, steroids, and immunosuppressants, name 4 other drugs that can be used to treat arthritis pain
capsaicin
tramadol
opioids
duloxetine
what is capsaicin and how does it work
it will burn first. member of vanilloid family
binds and desensitizes TRPV1 receptor and depletes substance P
TRVP1 is stimulated by heat and physical abrasion
where can capsaicin NOT be applied
to mucous membranes
capsaicin desensitizes _____ and depletes __________
desensitizes TRVP1 and depletes substance P (pain neurotransmitter)
what is tramadol and how does it work
a less potent opioid
a mu-opiod receptor agonist
suppresses serotonin and NE mediated pain
how is duloxetine used to treat pain in arthritis patients
SNRI – minimizes the perception of pain
direct SEROTONIN agonist at halluninator receptor
what is a MAJOR concern of taking high dose corticosteroids
the risk for unusual and dangerous infections that should normally be fought off easily
which has more side effects - inhaled corticosteroids or topical?
what about IV?
topical is least
then inhaled
then IV
true or false
corticosteroids are highly lipophilic
true
where does steroid-receptor binding occur
in the cytoplasm (highly lipophilic)
how do steroids have a ____ effect**
catabolic
protein is lost and fat is redistributed
steroids increase the synthesis of ____ which inhibits _________**
increase synthesis of lipocortin (annexin) which inhibits PLA2
TRUE OR FALSE
steroids inhibit the synthesis of NFKB
true
this is the “on” signal for inflammation
true or false
steroids increase the production of eicosanoids
FALSE
decrease
these are prostaglandins – responsible for inflammation
what is IKKB and what do steroids do to it
the INHIBITOR of NFKB
steroids increase the synthesis of this, thus having an anti inflammatory effect
True or false
steroids increase the synthesis of IL10
TRUE
it has anti inflammatory properties – gives an off signal for inflammation to stop
how do steroids affect the cell cycle
inhibit it
this causes increase in apoptosis, especially of immune cells
note – he said specifcally to know MOA of steroids and wrote all this down
so study it bitch
what do steroids do to IL-1
repress
true or false
steroids enhance immune cell activity
FALSE - repress, including macrophages which are resident WBC that protect us
this is why more prone to infections
corticosteroids are __________ regulators
transcriptional
where does the steroid-receptor complex bind
to HREs (promoter regions)
true or false
steroids DECREASE adhesion molecules like iCAM and vCAM
true
name 3 things that steroids increase
lipocortin (annexin)
IL-10
IKKB
true or false
steroids reduce apoptosis
false
increase
what helps corticosteroids to meet their receptor in the cytoplasm and bind to the correct gene in the nucleus
chaperones (heat shock proteins)
what is the inflammatory “on” signal
NFKB
what is the endogenous inhibitor of NFKB and what drugs increase this inhibitor’s synthesis
IKKB
steroids
do corticosteroids have any effect on B cells?
no. only at VERY HIGH doses they are inhibited
in general, macrophages are inhibited by corticosteroids
what is an exception
they increase phagocytosis of apoptotic cells
true or false
corticosteroids cause both innate and adaptive immunity to decrease
true
long term use of corticosteroids can cause what?
psychosis
if you take off cold turkey, patient is permanently psychotic
what is one general ADR for steroids
risk of infection bc decreased immunity
how are steroids a concern in pts with HTN
can make htn worse through sodium retention
they act as partial aldosterone agonists
what is lipodistrophy
aka fat redistribution - ADR of corticosterouds
typically fat in concentrated in the upper back
how can corticosteroids affect the skin
dermatitis - skin may bruise or crack when moved gently
name an ADR that is UNIQUE to corticosteroids***
hypokalemic metabolic alkalosis
body pH elevated
what is a concern that parents often have with children taking corticosteroids
decreased growth hormone - worried that it will stunt growth
however, this is really no often phsyiologically observed – if you have lower levels to begin with then it may be a problem
how can CS’s affect the GI
peptic ulcer disease, GERD bc no prostaglandins in stomach
when is adrenal suppression a concern when taking corticosteroids
if using long term and not tapering off
how can CS affect the bones
osteoporosis, osteopenia, osteomalacia
true or false
corticosteroids can cause diabetic like syndrome
true because of increased cortisol - an antagonist to insulin
how can CS affect the eyes
glaucoma and cataracts
what are DMARDS
disease modifying antirheumatic drugs
*******what does methotrexate inhibit
dihydrofolate reductase
what are 2 different uses of methotrexate? how can you tell the difference just by looking at prescription
anticancer and for RA
high dose (roughly 200mg and above per week) is anticancer
low dose (roughly 20mg and below) is RA
in a nutshell, what does methotrexate do
inhibits dihydrofolate reductase
messes up immune cells and causes rapidly proliferating cells to die
interfere with nucleic acid synthesis and this DNA/RNA synthesis
does methotrexate increase or decrease apoptosis
increase
as mentioned, methotrexate is most toxic to rapidly proliferating tissues
with this knowledge, name some ADRs/side effects of methotrexate
watery or bloody diarrhea - GI mucosal cells rapidly proliferate
alopecia - hair loss
-anorexia - bc insult to GI
anemia - decreased RBC and WBC. hemapoeitic tissues affected
decreased gamatogenesis (sperm production)
how can methotrexate affect the kidney
acute tubular necrosis, renal failire, glomerular sclerosis
methotrexate ______ uric acid
what is the result of this
increases
gout flares
SJS/ Toxic epidermal necrolysis are _____ reactions.
a _____ like attack on the _______ occurs
cutaneous reactions (inflammatory/immune reactions)
an autoimmune like attack on the replicating layer of the skin occurs
name 4 drugs that most commonly cause SJS
bactrim
carbamazepine
phenytoin
nevirapine
