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I2 > Drugs > Flashcards

Drugs Flashcards

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

A

reduced prostanoid synthesis

23
Q

anti-nociceptive

A

desensitization of nociceptors…NSAIDs help to block pain

24
Q

antipyretic

A

block hypothalamic triggers for fever

25
Q

antithrombotic

A

inhibition of platelet aggregation (decrease TXA2)

mostly use aspirin…81mg-325mg/day

26
Q

fetal circulation

A

closure of patent ductus

prostaglandins are important for maintaining the ductus arteriosus

27
Q

clinical use of NSAIDs vs GCs

A

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
Q

COX isozyme distribution

A

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
Q

COX selectivity

A

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
Q

aspirin and its interaction with COX

A

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
Q

side effects of cox selective drugs

A

COX1 selective: ulceration; other GI complications

COX2 selective: thrombotic event, CHF/HTN, other CV complications

32
Q

best nsaid for viral infection

A

acetiminophen; avoid aspirin and salicylates in pediatric patients

33
Q

approved NSAIDs

A

cox2: celecoxib
cox1: aspirin, ibuprofen, indomethacin, ketorolac, naproxen, meloxicam

34
Q

celecoxib

A

only cox2 inhibitor on market

35
Q

aspirin

A

cox1 inhibitor; irreversible and covalent inhibitor; low-dose cardioprotective dosing

not typically used at higher anti-inflammatory dosing

36
Q

ibuprofen

A

most common; cox1 inhibitor

37
Q

ketorolac

A

cox1 inhibitor; used for post-operative pain; high risk of GI ulceration

limit use to 5 days per prescriber labeling

IV

38
Q

meloxicam

A

cox1 inhibitor (relative COX-2 selectivity); convenient once daily dosing; use for chronic NSAID therapy

39
Q

dosing for anti-inflammatory vs analgestic effect for ibuprofen and naproxen

A

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
Q

complications of NSAID use with methotrexate

A

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
Q

complications of NSAID use with methotrexate

A

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
Q

acetaminophen

A

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
Q

general effects of cortisol

A

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
Q

general effects of cortisol

A

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
Q

GC high dose short term use side effects

A 
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
Q

gc long term use side effects

A 
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
Q

mineralcorticoid effects

A

hydrocortisone > prednisone > dexamethasone

more potent glucocorticoid = less minearlocorticoid effect

fludrocortisone is potent minearlocorticoid

48
Q

dosing of GC

A

try to replicate normal circadian levels

2/3 in am and 1/3 at 4 pm

49
Q

drug interactions with GC

A

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
Q

ipilimumab

A

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
Q

abatacept

A

Ig-CTLA-4

intercepts the B7…so it binds to the B7 on APCs which means that the T cell cannot be activated

52
Q

Nivolumab

A

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
Q

Sipleucel-T

A

dendritic cell vaccine

cells incubated with PAP

prostate cancer

I2 (7 decks)

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