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pharmacology 2 > drugs for arthritis > Flashcards

drugs for arthritis Flashcards

1
Q

how is inflammation caused?

A

release of various chemicals at the site of injury including histamine, bradykinin, prostaglandins which are activated by bradykinin

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2
Q

what is the action of bradykinin?

A

local vasodilation stimulation of nerve ending causing pain arachidonic acid release - this is precursor to prostaglandins, leuotrienes and thromboxanes

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3
Q

what is the first step in takling inflammation?

A

block production of inflammatory mediators → prostaglandins can sensitive afferent C fibres to bradykinin

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4
Q

how could prostaglandins be inhibited to treat inflammation?

A

Non -Steroidal Anti Inflammatory drugs (NSAIDs)

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5
Q

describe the roles of the COX 1 and 2 enzyme in inflammation

A

COX 1 - always produced - has protective effect, converts arachidonic acid into prostaglandinsCOX 2 - responsible for pain and inflammation - active at site of traum/injury

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6
Q

how do NSAIDs reduce inflammation?

A

block COX 1 and 2 - blocks many signs/symptoms of inflammation

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7
Q

why is it important to block COX 1 and 2 to reduce inflammation?

A

COX 1 and 2 activate convertion of arachidonic acid to prostaglandins (PGs) PGs increase sensitivity of nociceptors to other stimuli

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8
Q

name the three pharmacological actions of NSAIDs

A

antipyretic analgesic - relieves pain ass. with production of PGs anti - inflammatory - reduces oedema, sensitisation of nociceptors and musculoskeletal pain

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9
Q

what are the side effects of NSAIDs?

A
  • in chronic treatment - high dose, prolonged use indigestion diarrhoea nausea/vomiting gastric bleeding and ulceration
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10
Q

what do NSAIDs inhibit and why does this cause gastric bleeding and ulceration?

A

PG1 and PG2 → these produce mucus and HCO3 secretion, reduced acid secretion and increased blood flow to stomach

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11
Q

how can the side effects of NSAIDs be reduced?

A

develop drugs which only inhibit COX 2 enteric coating of tablets give drugs with protective agent prodrugs

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12
Q

name 2 drugs which only inhibit COX 2

A

celecoxib etoricoxib

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13
Q

name 2 drugs with a protective agent which reduce the side effects of NSAIDs

A

misoprostol (PGE1 analogue) omeprazole (H+ pump inhibitor)

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14
Q

name 3 NSAIDs prodrugs

A

sulindac nabumetone fenbufen

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15
Q

what is aspirin an example of?

A

NSAIDs

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16
Q

what is aspirin effectice for?

A

mild pain and fever

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17
Q

name 5 NSAIDS

A 
aspirin
ibuprofen
diclofenac
melexicam
indomethacin
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18
Q

is paracetamol an NSAID?

A

no

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19
Q

describe the pros and cons of paracetamol

A

pros - antipyrexic, analgesic

cons - not anti inflammmatory

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20
Q

how does paracetamol work?

A

supresses prostaglandin production

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21
Q

name two drugs which have potential benefits for treating osteoarthritis

A

strontium ranelate

glucosamine sulphate

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22
Q

what does strontium ranelate do?

A

promotes osteoblast differentiation / inhibits osteoclast activity

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23
Q

name the classes of drugs which are used to treat rheumatoid arthitis

A

Corticosteriods
immunosupressants
disease modifying anti-rheumatoid drugs (DMARDS)
anticytokines

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24
Q

describe the actions of glucocorticoids

A

metabolic effects
anti inflammatory
immunosuppressive

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25
Q

name 2 Corticosteriods which has mixed gluco and mineralocorticoid actions. what is the duration of action?

A

prednisolone
predisone
intermediate 12–36hrs

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26
Q

name 4 Corticosteriods which have just glucocorticoid actions. what is the duration of action?

A 
dexamethasone
bethamethosone
bedomethosone
budesonide
long 36-55hrs
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27
Q

name a Corticosteriods which has mainly mineralocorticoid actions.

A

fludrocortisone

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28
Q

name 2 short acting Corticosteriods

A

cortisone
hydrocortisone
1-12hrs

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29
Q

name the corticosteroids most likely to be used in rheumatoid arthritis

A

beclomethosone
budesonide
prednisolone

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30
Q

describe the mechanism of glucocorticoids in rheumatic arthritis

A

reduces transcription of pro-inflammatory cytokines (eg. IL-2)
reduces circulating lymphocytes
inhibits phosphodipase A2 which reduces release of anahioddonic acid thus reducing circulating PGs
increase synthesis of anti-iunflammatory proteins (eg. protese inhibitors)

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31
Q

what are DMARDS

A

disease modifying anti-rheumatoid drugs = group of drugs with unrelated structure

32
Q

which DMARD is the first drug of choice in RA?

A

sulfasalazine

33
Q

what is sulfasalazine a complex of?

A

salicylate (NSAID) and sulphonamide (antibiotic)

34
Q

what is the mechanism of action of sulfasazine?

A

acts by scavenging free radials produced by neutrophils

35
Q

what are free radicals?

A

reactive chemicals that kill bacteria - over production destroys surrounding tissue

36
Q

what does sulfasazine achieve in RA?

A

causes remission of ‘active’ RA

37
Q

what are the side effects of sulfasazine

A

GI upset
headache
skin reaction
leukopenis (reduced WC count)

38
Q

what is penicillamine?

A

a DMARD

39
Q

how is penicillamine produced?

A

hydrolysis of penicillin

40
Q

what is the mechanism of action of penicillamine?

A

lowers generation of IL-1 and reduces fibroblast proliferation thus reducing immune response

41
Q

how is penicillamine administered?

A

oral - takes weeks to work

42
Q

what are the side effects of penicillamine?

A 
rashes
stomatitis
anorexia
taste disturbance
fever
N&V
43
Q

what should penicillamine not be given with?

A

gold compound

44
Q

what are gold compounds and what are they used for?

A

DMARDS - RA

45
Q

name 2 gold compounds used in RA

A 
sodium aurthiomalate (deep IM)
auranofin (oral)
46
Q

what is the mechanism of action of auranofin?

A

inhibits production of IL-1 and TNF-a

reduces pain and swelling

47
Q

what are the side effects of gold compounds?

A 
skin rashes
flu symptoms
mouth ulcers
blood disorders
severe: encephalopathy, peripheral neuropathy
48
Q

what are antimalarial in relation to RA treatment?

A

DMARD

49
Q

name 2 antimalarial used in RA treatment

A

choloquine

hydroxychoroquine

50
Q

what are the actions of antimalarial in treating RA?

A

increase pH of intracellular vacuoles which interferes with antigen presenting
induces apoptosis in T-lymphocytes

51
Q

when are antimalarial used in RA treatment?

A

when other treatments fail

52
Q

what are the side effects of antimalarial?

A

N&V
dizziness
blurring of vision
screening needed

53
Q

What are anticytokine drugs used to treat?

A

RA

54
Q

what are anticytokines?

A

engineered recombinant antibodies - v. expensive so restricted to patient that don’t respond to DMARDS

55
Q

name 3 anticytokines which target TNF

A

adalimab
entenercept
infliximab

56
Q

name 3 anticytokines which target leukocyte receptors

A

rituximab
abatacept
natalizumab

57
Q

what is the mechanism of action of tocilizumab

A

blocks IL-6 receptors which disrupts immune signalling

58
Q

what other drug can anticytokines be given with?

A

methotrexate (an immunosuppressant)

59
Q

name 5 immunosuppressant’s used to treat RA

A 
ciclosporin
azathioprine
methotrexate
leflunomide
cyclophosphamide
60
Q

why is immunosuppression useful in RA?

A

RA is an autoimmune disease

61
Q

what is the mechanism of action of ciclosporin?

A

inhibits IL-2 gene transcription

reduces t-cell proliferation

62
Q

how is ciclosporin administered?

A

poorly absorbed orally - special formulations

63
Q

what are the side effects of ciclosporin?

A 
accumulation in high conc. in some tissues
nephrotoxicity
hepatotoxicity
hypertension
N&V, gum hypertrophy, GI probs
64
Q

in what phase of the immune response does azathioprine target cells?

A

induction phase thus depresses cell and antibody mediated immune reactions

65
Q

what is the mechanism of action of azathioprine?

A

cytotoxic - interferes with purine metabolism thus reducing DNA synthesis

66
Q

what is the main specific effect of azathioprine in treating RA?

A

suppression of bone marrow which reduces RBC and WBC production

67
Q

what is methotrexate and what does it treat?

A

immunosuppressant - RA

68
Q

what is the mechanism of action of methotrexate?

A

folic acid antagonist - inhibits DNA synthesis
blocks growth and differentiation of rapidly dividing cells
inhibits T-cell activation

69
Q

what are the side effects of methotrexate?

A

poss. blood abnormalities
liver cirrhosis
folate def.

70
Q

what is leflunomide and what does it treat?

A

immunosuppressant - RA

71
Q

what is the mechanisms of action of leflunomide?

A

inhibits pyrimidine synthesis

specific inhibitor of activated T cells

72
Q

how is leflunomide administered and how long does it last?

A

orally - long t half life (14-18 days)

73
Q

what are the side effects of leflunomide?

A

diahorroea
alopecia
increased liver enzymes - risk of hepatotoxicity

74
Q

what is cyclophosphamide and what does it treat?

A

immunosuppressant- RA

75
Q

what is the mechanism of action of cyclophosphamide?

A

increases cross linking of DNA

76
Q

cyclophosphamide is a PRODRUG when administered orally where is it activated and into which other drugs?

A

liver

phoshoramide mustard & acrolein

77
Q

what can occur when administering acrolein and how is this avoided?

A

haemorrhagic cystitis

large volume of fluid given

pharmacology 2 (11 decks)

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