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I2 > Drugs > Flashcards

Drugs Flashcards

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1
Q

DMARDs

A

RA
Disease modifying anti-rheumatic drugs

immunosuppressive agents with goal of inducing/maintaining remission - all oral

methotrexate, leflunomide, sulfasalazine, hydroxychloroquine, azathiopurine

“My Lucky Sister Has Arthritis”

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2
Q

Biologics

A

RA
newer, made by molecular biologic techniques

targets cytokines, T cell activation and depletion of B cells

Anakinra, TNF inhibitors (etanercept, adalimumab, certolizumab, golimumab, infliximab), Abatacept, Tocilizumab, Tofacitinib, Rituximab

ATATTR (ATT totally rules)

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3
Q

TNF inhibitors

A

RA
pro-inflammatory cytokine
produced by macrophages
reduces joint inflammation and damage to joints

Etanercept (Enbrel): subcutaneous; binds TNF and blocks its interaction with receptors

Adalimumab (Humira): subcutaneous; human monoclonal antibody directed against TNF

Certolizumab (Cimzia): subcutaneous; Fab fragment of a humanized monoclonal antibody directed against TNF

Golimumab (Simponi): subcutaneous; human monoclonal antibody directed against TNF

Infliximab (Remicade): infusion; chimeric monoclonal antibody directed against TNF

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4
Q

methotrexate

A

first line treatment; give folic acid to prevent side effects

RA
increases adenosine release from cells which can dampen cellular inflammation

inhibits dihydrofolate reductase (why need to give folate)

side effects: oral ulcers, nausea, cytopenias, liver toxicity

NOT FOR PREG. WOMEN -> induces abortions

dose: 15-25mg/week

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5
Q

leflunomide

A

RA
inhibits pyrimidine synthesis which leads to reduction of lymphocytes

is a pro-drug; enterohepatocyte circulation leads to long half life

side effects: diarrhea, cytopenias, liver toxicity

DO NOT GIVE TO PREG WOMEN

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6
Q

sulfasalazine

A

RA
sulfapyridine is active moiety; mechanism of action not known

side effects: rash, GI upset, hepatotoxicity, cytopenias

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7
Q

hydroxychloroquine

A

RA
mildest; also used for SLE

inhibits activity of TLRs and acidification of lysosomes ultimately interfering with antigen processing

side effects: rare retinal toxicity

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8
Q

azathiopurine

A

RA
pruine synthesis inhibitor

not often used due to side effects: cytopenias, rash, GI upset, pancreatitis

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9
Q

Etanercept (Enbrel)

A

RA
subcutaneous; binds TNF and blocks its interaction with receptors - is a fusion protein of TNF receptor linked to Fc portion of IgG

The only TNF that is not a monoclonal antibody

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10
Q

Adalimumab (Humira)

A

RA

subcutaneous; human monoclonal antibody directed against TNF

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11
Q

Certolizumab (Cimzia)

A

RA

subcutaneous; Fab fragment of a humanized monoclonal antibody directed against TNF

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12
Q

Golimumab (Simponi)

A

RA

subcutaneous; human monoclonal antibody directed against TNF

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13
Q

Infliximab (Remicade)

A

RA

infusion; chimeric monoclonal antibody directed against TNF

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14
Q

Anakinra

A

RA
antagonist of IL-1 receptor

does not work very well but is FDA approved

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15
Q

Abatacept

A

RA
Binds CD90/86 on APCs blocking the interaction of CD28 between APCs and T cells

blocks the costimulation of T cells -> blocks T cell activation which are the center cells of pathogenesis

prevents joint damage and inflammation; short and long term benefits

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16
Q

Tocilizumab

A

RA
humanized monoclonal antibody targeting IL-6 receptor

reduces inflammation and joint damage -> helps to prevent natural history of RA

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17
Q

Rituximab

A

RA
monoclonal antibody directed against CD20 antigen on B lymphocytes -> depletes B cells but NOT existing plasma cells

also works for B cell cancers

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18
Q

Tofacitinib

A

RA
inhibits JAK enzymes, which prevents cytokine/growth factor mediated gene expression and intracellular activity of immune cells

target synthetic DMARD

oral

totally different pathway that is early in the disease pathogenesis

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19
Q

triple therapy

A

for RA: methotrexate, sulfasalazine, hydroxychloroquine

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20
Q

NSAIDs vs Glucocorticoids

A

NSAIDs: block cyclooxygenase (COX)…very specific

GC: block phospholipase A2 (PLA2) and some can affect COX

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21
Q

what is the molecular path to inflammation?

A

phospholipids (cell membrane) —- phospholipase A2 (PLA2) —> Arachidonic Acid —– cyclooxygenase (COX) —-> prostaglandin H2 (PGH2), which are pro-inflammation mediators

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22
Q

anti-inflammatory goals

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A

reduced prostanoid synthesis

23
Q

anti-nociceptive

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A

desensitization of nociceptors…NSAIDs help to block pain

24
Q

antipyretic

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A

block hypothalamic triggers for fever

25
antithrombotic
inhibition of platelet aggregation (decrease TXA2) mostly use aspirin...81mg-325mg/day
26
fetal circulation
closure of patent ductus prostaglandins are important for maintaining the ductus arteriosus
27
clinical use of NSAIDs vs GCs
NSAIDs: inflammation, pain, fevers, migraines, dysmenorrhea (menstrual cramping), to close the patent ductus arteriosus, cardioprotection (aspirin), flushing (mast cell degranulation) GCs: immune reaction-related inflammation, acute and chronic autoimmune disease (low doses), organ transplantation (high doses), modulates inflammation and immune function, but has serious side effects with chronic use
28
COX isozyme distribution
COX1: GI tract mostly...esophagus, stomach, intestines, liver, pancreas, kidney and platelets; constitutively expressed COX2: brain, kidney, bone, pancreas, female reproductive tract, vascular endothelium; induced esp in inflammatory conditions
29
COX selectivity
COX1: homeostatic functions - selective, irreversible inhibition of COX1 is basis for cardioprotective effects of low-dose Aspirin; promotes vasoconstriction and platelet aggregation COX2: inflammation - selective inhibition of COX-2 results in an increase in risk of CV death; promotes vasodilation and inhibits platelet aggregation most of COX1 have some affinity for COX2, but since COX2 has a hydrophobic binding pocket not all of COX2 will work for COX1
30
aspirin and its interaction with COX
aspirin reacts with serine residues on COX1 and COX2 so it actually irreversibly inhibits the enzyme by adding an acetyl group via a covalent bond NSAIDs and aspirin will compete for the COX bonding site and aspirin will win. so give aspirin before NSAID so as to gain the cardiac prevention effects and still get the pain reliever thought that naproxen may be least likely NSAID to compete with aspirin
31
side effects of cox selective drugs
COX1 selective: ulceration; other GI complications COX2 selective: thrombotic event, CHF/HTN, other CV complications
32
best nsaid for viral infection
acetiminophen; avoid aspirin and salicylates in pediatric patients
33
approved NSAIDs
cox2: celecoxib cox1: aspirin, ibuprofen, indomethacin, ketorolac, naproxen, meloxicam
34
celecoxib
only cox2 inhibitor on market
35
aspirin
cox1 inhibitor; irreversible and covalent inhibitor; low-dose cardioprotective dosing not typically used at higher anti-inflammatory dosing
36
ibuprofen
most common; cox1 inhibitor
37
ketorolac
cox1 inhibitor; used for post-operative pain; high risk of GI ulceration limit use to 5 days per prescriber labeling IV
38
meloxicam
cox1 inhibitor (relative COX-2 selectivity); convenient once daily dosing; use for chronic NSAID therapy
39
dosing for anti-inflammatory vs analgestic effect for ibuprofen and naproxen
ibuprofen 1. anti-inflammatory: 2400-3600 mg/day 2. analgestic: 1200-1600 mg/day naproxen 1. anti-inflammatory: 1000 mg/day 2. analgestic: 440 mg/day
40
complications of NSAID use with methotrexate
with high doses of methotrexate in combination of NSAIDs, the kidneys cannot secrete the methotrexate so can use NSAIDs with RA treatment but not for cancer treatment IF methotrexate is being used
41
complications of NSAID use with methotrexate
with high doses of methotrexate in combination of NSAIDs, the kidneys cannot secrete the methotrexate so can use NSAIDs with RA treatment but not for cancer treatment IF methotrexate is being used
42
acetaminophen
NOT and NSAID reduce fever and help with mild pain be cause of use with ethanol -> can get hepatotoxicity with overdose or high daily doses (> 4 g/day) once damage is done it is irreversible
43
general effects of cortisol
genomic: upregulate genes involved in inflammation (can cross into nucleus very easily non-genomic: interact with other signaling pathways: inhibits NF-kB, IL-1, MAPK and Annexin I (activates Annexin I which inhibits activation of AA metabolism)
44
general effects of cortisol
genomic: upregulate genes involved in inflammation (can cross into nucleus very easily non-genomic: interact with other signaling pathways: inhibits NF-kB, IL-1, MAPK and Annexin I (activates Annexin I which inhibits activation of AA metabolism)
45
GC high dose short term use side effects
``` hyperglycemia NA+/H2O retention hypertension insomnia, behavioral changes WBC increase with L shift (increased bands, decreased other WBCs) increased appetite and weight gain gastritis, GI bleed, pancreatitis ```
46
gc long term use side effects
``` cushing's syndrome (moon face/buffalo hump...fat redistribution) potential addisonian crisis with stress increased risk of infection impaired wound healing, acne, thinning of skin cataracts, glaucoma osteoporosis growth impairment mscle weakness withdrawal: myalgia, athralgia, malaise ```
47
mineralcorticoid effects
hydrocortisone > prednisone > dexamethasone more potent glucocorticoid = less minearlocorticoid effect fludrocortisone is potent minearlocorticoid
48
dosing of GC
try to replicate normal circadian levels 2/3 in am and 1/3 at 4 pm
49
drug interactions with GC
susceptible to drug-drug interactions through CYP3A4 (ie they inhibit CYP3A4) proton pump inhibitors (omeprazole) or histamine-2 receptor antagonists in high doses (famotidine) may reduce GI side effects
50
ipilimumab
anti-CTLA-4 so binds to CTLA-4, thus inactivating it so that B7 can bind to CD28 and turn on the T cells use for cancer, metastatic carcinoma
51
abatacept
Ig-CTLA-4 intercepts the B7...so it binds to the B7 on APCs which means that the T cell cannot be activated
52
Nivolumab
anti-PD-1 blocks tolerance -> PD-1 is an inhibitory co-receptor on T cells...blocking PD-1 means keeping the t cell turned on melanoma
53
Sipleucel-T
dendritic cell vaccine cells incubated with PAP prostate cancer

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