Pharmacology of pain 3 ; NSAIDS/DMARDS Flashcards by Jenna Dymond

paracetemol, aspirin, naproxen are examples of which type of drug?

a. NSAIDS
b. DMARDS
c. opiods

a.NSAIDS

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High doses of NSAIDS can be toxic to what organ?

a. kidney
b. liver
c. heart
d. lungs

b.liver

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signs of inflammation

a. pain,redness, heat, swollen, loss of function
b. pain, deformity, bruising
c. pain,heat,redness

a.pain,redness, heat, swollen, loss of function

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what are NSAIDS used to treat?

a. inflammation,fever,pain,muscle injury,sprains,fractures
b. fever, pain, muscle injury, sprains , fractures
c. inflammation,fever,pain,muscle injury,sprains,fractures, infection

inflammation, fever,pain, muscle injury, sprains ,factures

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which drug has this mechanism of action?
inhibition of the COX 1 and 2 , lowers levels of prostoglandins (cox converts arachadonic acid to prostoglandins)

aNSAIDS

b. DMARDS
c. Opiods

a. NSAIDS

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what enzymes are inhibited by NSAIDS

a. COX1
b. COX 1 and 2
c. COX 2 and COX 3

b.COX 1 and COX 2

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What is the role of cox 1 and 2 that NSAIDS inhibit?

a. convert prostoglandins to arachadonic acid
b. convert arachadonic acid to prostoglandins

b.convert arachadonic acid to prostoglandins

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which drugs lower arachdonic acid level by inhibiting lipocortin? (higher up chain)

a.NSAIDS
bAnalgesics
c.corticosteroids
d.paracetemol

c.corticosteroids

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what do prostaglandins do?

a. cause swelling, pain , vasodilation
b. cause swelling, pain and vasoconstriction
c. cause swelling pain and bleeding

a. swelling, pain (bradykinin mediated nociception), vasodilation

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which enzyme is purposely inhibited to reduce inflammation

a. cox 1
b. lipocortin
c. cox 2

cox 2

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what is the role of cox 1

a. platelet aggregation, regulation of kidney blood flow, protection of the gastric mucosa
b. expressed in inflammatory cells to activate them

a. platelet aggregation
regulation of kidney blood flow
protection of gastric mucosa

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what does cox 2 do ?

a. platelet aggregation, regulation of kidney blood flow, protection of the gastric mucosa
b. expressed in inflammatory cells to activate them

b. in response to mediators it activates inflammatory cells, expressed in inflammatory cells

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which cox enzyme is found all over the body

a. 1
b. 2

a.1

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blocking which enzyme gives side effects of NSAIDS

a. cox 1
b. cox 2
c. cox 1 and 2

a.cox 1

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which cells have high cox 2

a. eiosinophils and baso
b. neutor and baso
c. eiosin and neutro

a.eiosinophils and baso

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which of these are the correct set of properties for NSAIDS?

a. antibiotic, anti pyretic
b. anti inflammatory, analgesic, anti pyretic
c. anti inflammatory, analgesic
d. analgesic, anti pyretic

b.anti inflammatory , analgesic and anti pyretic (fever)

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main side effects of what drug include gastric irritation

compromised renal blood flow
increased bleeding
increase risk of MI

a. opiods
b. DMARDS
c. corticosteroids
d. NSAIDS

d. NSAIDS

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Why are NSAIDS anti inflam?

a. inhibition of COX 1
b. inhibition of COX2
c. inhibition of dihydrooroate dehydrogenase
d. inhibition of dihydrofolate reductase

a.inhibition of cox 2

decreased prostoglandins
decreased blood flow
decreased pain
decreased swelling

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patient with inflam arthiritis which drug most useful?

a. NSAID
b. opiod
c. corticosteroid

a. NSAIDS

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NSAIDS do not affect…

a. pain
b. cause of inflammation
c. inflammation
d. fever

b.cause of inflammation

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drug used for ora facial pain
post op pain
bone metasteses in cancer
inflam arthiritis

a. DMARDS
b. NSAIDS
c. corticosteroids
d. simple analgesics

b.NSAIDS

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how do NSAIDS reduce pain?

a. Decreased prostaglandins, reduced bradykinin nociception
b. decreased prostaglandins, decreased blood flow, decreased swelling
c. decreased prostaglandin production in the hypothalamus, vasodilation and sweating decreased temp

a. decreased prostaglandins, reduced bradykinin nociception

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in what conditions are NSAIDS used to reduce pain?

arthiritis, muscle pain, toothace, postpartum pain, cancer metastasus in bone pain and headaches

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how do NSAIDS reduce fever?

c. decreased prostaglandin production in the hypothalamus, vasodilation and sweating to decrease temp

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how do NSAIDS have their anti pyretic effect? a. Decreased prostaglandins, reduced bradykinin nociception b. decreased prostaglandins, decreased blood flow, decreased swelling c. decreased prostaglandin production in the hypothalamus, vasodilation and sweating (COX 3)decreased temp d. .release of endotoxins , increased IL-1 from macrophages , increased prostaglandins in hypothalamus via COX

decreased PG production in hypothalamus, vasodilation and sweating (COX3) decreased temp *no effect on normal body temp

which enzyme is indicated in sweating a. cox 1 b. cox 2 c. cox 3

c.cox 3

how does aspirin have anti platelet effect? a. Decreased prostaglandins, reduced bradykinin nociception b. decreased prostaglandins, decreased blood flow, decreased swelling c. decreased prostaglandin production in the hypothalamus, vasodilation and sweating decreased temp d. inhibition of cox 1

d, COX 1 inhibition

what is aspirin used for? a.stroke prevention, MI prevention, unstable angina ,DVT prevention b. reducing pain in arthritis, muscle pain, toothache, dysmenorrhea postpartum pain, cancer metastasis in bone pain c.reducing fever

a. stroke prevention MI prevention unstable angina DVT prevention

why are there a lot of side effects of NSAIDS? a. inhibit cox 2 b. inhibit cox 1 c. reduce prostaglandin levels

b.inhibit housekeeping cox 1

3 main side effects of nsaids

GI disturbances, adverse renal effects, liver toxicity

GI effects of NSAIDS?

perforations, ulcers, bleeds , diarrhoea, nausea, constipation, vomiting

who are most affected by GI effects of NSAIDS a. young people b. pregnant women c. elderly taking long term NSAIDS for arthiritis d. people with chronic hypertension

c.elderly taking long term NSAIDS for arthiritis

how do NSAIDS have adverse affects on the GI? a. inhibit cox 1 which generates PGE2/PGI2 THIS STIMULATES MUCUS Production and inhibits acid secretion from parietal cells in the stomach b. Decreased prostaglandins, reduced bradykinin nociception c. decreased prostaglandins, decreased blood flow, decreased swelling d. decreased prostaglandin production in the hypothalamus, vasodilation and sweating decreased temp

a. inhibit cox 1 which generates PGE2/PGI2 THIS STIMULATES MUCUS Production and inhibits acid secretion from parietal cells in the stomach

what is often prescribed with NSAIDS to protect from GI damage ulcers? a. antibiotics b. PPIs eg omeprazole c. amitriptyline

b.PPIs eg omeprazole

healthy patient taking NSAIDS which adverse effect will they not experience? .A. renal effects b. gi disturbances c. liver toxicity

renal affects

what can NSAIDS cause in patient with compromised renal function? a. chronic renal failure b. acute renal failure c. liver failure

b.acute renal failure

who is not at risk of renal side effects of NSAIDS? a. neonates b. obese c. elderly, d. heart/liver/kidney disease patients

b.obese

what is the cause of the renal side effects of the NSAIDS? a. inhibit cox 1 which generates PGE2/PGI2 THIS STIMULATES MUCUS Production and inhibits acid secretion from parietal cells in the stomach b. COX inhibition, reduced PGE2/PGI2 production , altered renal blood flow as PGE2 causes vasodilation

b.COX inhibition, reduced PGE2/PGI2 production , altered renal blood flow as PGE2 causes vasodilation

how does the renal side effect of NSAIDS cause hypertension? a. Na + excretion b. Na+ secretion c. K+ excretion d. Na+ retention

d. Na+ retention

what type of drug is amitriptyline? a. opiod b. NSAID c. tricyclic anti depressant d. DMARD

c. tricyclic anti depressant

how does amitriptyline work? a. inhibits cox 2 , reduced prostaglandins, vasodilation and reduced swelling b. inhibits cox 2, reduced prostaglandins , reduced bradykinin regulated nociception c. reduced release of prostaglandins from the hypothalamus ,vasodilation, sweating d. blocks reuptake of noradrenaline and 5HT (serotonin) , remains in synapse

d. blocks reuptake of noradrenaline and 5HT (serotonin) , remains in synapse

what is amitriptyline often used for as NSAIDS are inneffective? a. ora facial pain b. arthirits c. back pain d. tootache

back pain as it targets spinal nerves

when could NSAIDS be used? a. patient with peptic ulcer disease b. patient with GI bleeding c. patient on anticoagulants d. obese patient

d. obese patient

In which of these groups can NSAIDS be used with caution? a. patients with peptic ulcer disease,GI bleeding, anticoagulants b. patients with renal impairment pregnancy (3rd trimester) previous history of allergic reactions eg asthma c. pregnancy and avoid conception for 3 months after d. pregnancy, breastfeeding and premenopausal women

b. renal impairment pregnancy (3rd trimester) previous history of allergic reactions eg asthma

what effect do NSAIDS have in the 3rd trimester? a. neural tube defects b. closure of the ductus arteriousus in utero c. cushings syndrome d. increased risk of premature birth

b. closure of ductus arteriosus in utero

what do DMARDS do?

decrease the severity of the condition decrease number of swollen joints reduce pain score decrease serum IgG

what is methotrexate? a. DMARD b. NSAID c. opiod

DMARD folic acid antagonist immunosurpressant

why should methotrexate not be given to pregnant women? a. can cause in utero closure of the ductus arteriosus b. folic acid antagonist so could cause neural tube defects

b. folic acid antagonist | could cause neural l tube defects spina bifida in baby

what enzyme does methotrexate inhibit? a. dihydroorate dehydrogenase b. cox 1 and cox 2 c. dihydrofolate reductase

c. dihydrofolate reductase

How does methotrexate agonise folic acid and act as an immunosurpressant?

inhibits dihydrofolate reductase accumulation of AMP and adenosine which surpresses inflammation surpression of neutrophils macrophagesdc and lymphocytes effect on DHFR inhibits proliferation of immune inflammatory cells

what drug is used as first line for rheumatoid arthiritis? a. amitriptyline b. methotrexate d. paracetemol e. leflunomide

b. methotrexate

how is methotrexate given? a. oral b. IV c. IM d. oral/IV

d. oral / iv

what is the onset of action of methotrexate? a. 6 weeks b. 4 weeks

a.6 weeks

side effects of methotrexate? a. GI damage, neural tube defects b. GI disturbamces, renal blood flow disturbances, liver toxicity c. anaemia, hepatoxicity, diarrohea, nausea

b. GI damage | neural tube defects

contraindications for methatrexate? a. obesity and hypertension b. pregnancy and 3 months post drug contraception d. pregnancy third trimester, patients with history of GI bleeding, on anticoagulants, with peptic ulcer disease , renal impairment, heart failure

b.avoid in pregnancy and avoid contraception for 3 months post

how long does it take for methotrexate to be removed from system? a. 2 years b. 4 weeks c. 6 weeks d. 3 months

d.3 months

what does leflunomide inhibit? a. dihydroorate dehydrogenase b. cox 1 and cox 2 c. dihydrofolate reductase

a.dihydroorate dehydrogenase | so inhibits activated lymphocytes

what is the mechanism of action of leflunomide? a. inhibits cox 2 , reduced prostaglandins, vasodilation and reduced swelling b. inhibits cox 2, reduced prostaglandins , reduced bradykinin regulated nociception c. reduced release of prostaglandins from the hypothalamus ,vasodilation, sweating d. blocks reuptake of noradrenaline and 5HT (serotonin) , remains in synapse e.inhibits dihydroorate dehydrogenase, blocks pyrimidine production blocks clonal expansion of t cells

e. inhibits dihydroorate dehydrogenase, blocks pyrimidine production blocks clonal expansion of t cells

how is leflunomide taken? a. IV b. IM c. Oral

c. orally

main side effects of leflunomide a. renal blood flow impairment, GI disturbances, liver toxicity b.anaemia , hepatotoxicity,diarrohea nausea c.blood disorders, liver cirrhosis, nephotoxicity , GIT damage , neural tube defects

b. anaemia hepatotoxicity diarrohea nausea

onset of action of leflunomide a. 6 weeks b. 4 weeks

b. 4 weeks

time to remove leflunomide from body? a. 2 years b. 3 months c. 3 years

a.2 years

``` avoid leflunomide in .. \a.elderly b. patients with renal impairment c. hypertensive patients d.premenopausal women ```

d. premenopausal women

what is given to patients who dont respond to methotrexate? a. amitriptyline b. Opiods c. leflunomide d. NSAIDS

C. leflunomide

how does 10-15 grams of paracetemol have fatal hepatotoxicity? a. inhibits cox enzymes causing reduced prostaglandin release b. depletion of glutathione and accumulation of toxic intermediates c. blocks reuptake of noradrenaline d. inhibit dihydrofolate causing accumulation of AMP and adenosine and surpression of neutrophils, macrophages and lymphocytes

b. depletion of glutathione and accumulation of toxic intermediates

what is the correct set of side effects associated with NSAIDS? a. anaemia , hepatoxicity, diarrohea, nausea b. GI irritation, compromised renal blood flow, increased bleeding, increased risk of MI c. Cushings syndrome

GI irritation, compromised renal blood flow, increased bleeding, increased risk of MI

patient on anti inflammatory drug for rheumatoid arthirits, they have returned to gp with complaints of diarrohea and constipation , investigations later show renal failure which drug is this patient most likely to be taking ? A.NSAIDS B.DMARDS C.corticosteroids D.opiods

a.NSAIDS

how do bacteria induce fever a. Decreased prostaglandins, reduced bradykinin nociception b. decreased prostaglandins, decreased blood flow, decreased swelling c. decreased prostaglandin production in the hypothalamus, vasodilation and sweating decreased temp d. .release of endotoxins , increased IL-1 from macrophages , increased prostaglandins in hypothalamus via COX 2/3

d..release of endotoxins , increased IL-1 from macrophages , increased prostaglandins in hypothalamus via COX

what is the role of cox 1 in the GI tract? a. generating PGE2/PGI2 that stimulate mucus production and inhibit acid secretion from the parietal cells b. inhibiting PGE2/PGI2 that stimulate mucus production and inhibit acid secretion from the parietal cells

a.generating PGE2/PGI2 that stimulate mucus production and inhibit acid secretion from the parietal cells

which metabolite of paracetemol is toxic at the liver? a. glutathione b. cysteine c. NAPQI d. NAC

C.NAPQI

what does dihydrocolate reductase do? a. allows for RNA and DNA production and so proliferation of immune inflammatory cells b. protection of gastric mucosa, platelet aggregation, renal blood flow regulation c. converts arachadonic acid to prostaglandins d. activates inflammatory cells

a.allows for RNA and DNA production and so proliferation of immune inflammatory cells

main side effects of lmethotrexate a. renal blood flow impairment, GI disturbances, liver toxicity b.anaemia , hepatotoxicity,diarrohea nausea c.blood disorders, liver cirrhosis, nephotoxicity , GIT damage , neural tube defects

c.blood disorders, liver cirrhosis,

Which DMARD needs blood monitoring? aAmitriptyline b. methotrexate c. leflunomide

c.leflunomide

what drugs can be used after two DMARDS have been tried? a. NSAIDS b. opiods c. biological DMARDS

c.biological DMARDS

what type of drug is infliximab? a. NSAID b. biological DMARD c. opiod d. simple analgesic e. DMARD

b.Biological DMARD | monoclonal antibody against TNFa- tumour necrosis factor antibody

what drug can be used for rheumatoid arthiritis and crohns? a. methotrexate b. infliximab c. leflunomide d. amitriptyline

b.infliximab

if methotrexate cannot be used due to contraindications what is used as monotherapy? a. methotrexate b. infliximab c. leflunomide d. amitriptyline e. etanercept

e.etanercept

what drug is infliximab used in combination with? a. methotrexate b. infliximab c. leflunomide d. amitriptyline

a.methotrexate

first line drug for rapid pain relief? a. opiod b. NSAID c. DMARD

b.NSAID

How long for effects of DMARDS? a. 2 weeks b. 2 hours c. immediate d. 5 weeks

d.5 weeks