Phrm 2011 Arthritis And Gout

Front 1

arthropathy

Back 1

pathology of the joints

Front 2

arthritis

Back 2

inflammatino of joints

Front 3

rheumatism

Back 3

pain joints + muscles

Front 4

non-drug therapy for rheumatic diseases

Back 4

rest, controlled exercise, emotional & social support, OT, indiviualised, health care team approach.

Front 5

rheumatoid arthritis

Back 5

inflammatory disease
1-3%
age 30-50
women 6:1
significant morbidity and mortality
decreases life expectancy

Front 6

pathophysiology of rheumatoid arthritis

Back 6

autoimmune response
activates compliment system
chemotaxis and phagocytosis
release of inflammatory mediators (PG, enzymes)
vasoactive substances (PG) increase blood flow and blood vessel permeability leading to redness, swelling, heat and pain.

Front 7

how is pannus formation achieved

Back 7

inflammation and autoimmune in rheumatoid arthritis causes damage which the body tries to repair and leads to pannus formations (erosion of joints)

Front 8

why must we treat RA hard and fast

Back 8

joint errosion within 2 years

Front 9

treatment (traditional)

Back 9

start with dose of NSAIDs +steroids(alleviate symptoms), followed with dose DMARDs/SAARDs (slow acting), to slow down progression(considered at early stage in course of disease & continued till lasting remission/toxicity
finally cytotoxics (cancer treatment) dose as a last resort.

may need to add antidepressents.

Front 10

treatment (modern)

Back 10

turn pyramid upside down

start with small dose cytotoxins to start hard and fast (start stronger to better prevent progression), then move to dose DMARDs (toxicity compared with NSAIDs not overly different), finally NSAIDs and steriods.


may need to add antidepressant/anxiolytic.

Front 11

NSAIDs in RA

Back 11

use only to treat flare up initially because se

can use paracetamol instead

Front 12

DMARDS in RA

Back 12

slow progression

can exacerbate exisiting conditions.

Front 13

cytotoxins in RA

Back 13

small doses have few side effects

Front 14

initial therapy for rheumatoid arthritis

Back 14

methotrexate (ONE A WEEK)
with
folic acid

Front 15

corticosteroids in RA

Back 15

predinsone prednisolone

anti-inflammatory, immunosuppressive

modify messenger RNA -> decreased arachdonic acid production -> less PG, LKT

short term use only
se profile - growth problems, glucose intolerance (diabetes), osteoporosis

Front 16

methotrexate in RA

Back 16

cytotoxin

once weekly

folic acid analogue (why given with fa to limit se but on different day so dont oppose actions) inhibits DNA synthesis -> decreased inflammatory cells

se: anorexia, nausea, fever, skin rash, liver function, mouth ulcers, pneumonia

folic acid limits se

Front 17

antimalarials in RA

Back 17

hydroxycholorquin
binds to DNA to inhibit lymphocyte function

works on immune response

se: GIT, rash, hair bleaching, occular problems, peripheral neuopathy, leucopenia.

monitor visual tests

Front 18

sulphasalazine in RA

Back 18

antibacterial

moa: decreases synovial angiogenesis, decrease lymphocytes

se: nausea, skin rashes, LFT, blood dyscasias, discolouration of body secreations.
monitor FBC

Front 19

other agents in RA

Back 19

azathioprine, cyclophosphamide (cytotoxins, large se, used as last resort), can increase cancer risk, CPS = haemorrhagic cystitis & immunosuppression

cyclosporin (immunomodulation, increased cancer risk, used in organ transplants)

D-penicillamine (modulates macrophages etc, not used alot, autoimmune distubances)

gold compounds
oral -auranofin
injectable (more se; skin rashes, blood dyscrasias, peripheral neuopathy, pneumonia, aplastic anemia)

Front 20

bDMARDS in RA

Back 20

costly
not used often
opposes pro-inflammatory cytokines
SE: URTIs, UTI, headache, nausea, cough, skin rash etc.
serious risk of developing cancer of lymphoma or MS.

Front 21

Combination therapy in RA

Back 21

MTX + SALA + HCQ
(after MTX mono or as initial therapy, not more toxic)
MTX + LEF
MTX + CYC (cyclosporin)
MTX + bDMARDS (more effective)

Front 22

osteoarthritis

Back 22

occurs in most people over 65yo

risk factors: obese, hereditary, osteoporosis (loss of BMD due to Ca2+), hypermobility, smoking repetitve use.

Front 23

osteoarthritis treatment

Back 23

reduce pain, increase mobility and quality of life

main treatment is paracetamol
can give NSAIDS or steriod injections where inflammation is present.
regular treatment.

Front 24

systemic lupus erythematosus

Back 24

butterfly skin rash, autoimmune, multisystem, fever, fatigue, arthritis, exacerbations and remissions

Front 25

gout

Back 25

uric acid salt or crystals in and around joints or soft tissue.

Front 26

uric acid

Back 26

normal end product of the degradation of purine compounds

Front 27

hyperuricemia

Back 27

underlying metabolic disorder often causing gout

Front 28

primary gout

Back 28

inborn defect in metabolism of uric acid or inherited defects of renal tubular secretions of urate

Front 29

secondary gout

Back 29

acquired disorders that result in increased turnover of nucleic acids by defects in renal excretion of uric acid salts, and by the effects of certain drugs

e.g. chemotherapy

Front 30

epidemiology of gout

Back 30

2.1 million
males more than females
occurs more >50yrs

Front 31

overproduction vs underexcretion

Back 31

overproduction (genetic, 10%)
underexcretion (90%, decreased tubular secretion, increased tubular reabsorbtion, dimished uric acid filtration)

Front 32

pathogenesis

Back 32

urate crystals stimulate release of inflammatory mediators in synovial cells and phagocytes.

chronic gouty inflammation is assoicated with cytokine driven synovial proliferation , cartilage loss and bone erosion.

Front 33

diagnosising gout

Back 33

microscopy

crystals

needle shaped crystals

Front 34

presenting symptoms of gout
systemic, musculoskeletal, skin, GU

Back 34

systemic - fever, chills and malaise
musculoskeletal: monoarticular joint pain
skin: warmth, erythema, tenseness of skin overlying joint
GU: renal colic with renal calculi formation

Front 35

treatment goals for gout

Back 35

reduce pain and inflammation, reduce chance of further attack and complications, reduce flare up,

Front 36

non pharmacological treatments

Back 36

ice packs, immobilsation of joint, alcohol avoidance, dietary modification

Front 37

treatment for acute gout

Back 37

should spontaneously subide in about a week
use NSAIDs
or colchicine
or if ineffective corticosteriods

then reduce risks
if attacks continue it may be chronic :(

e.g. indomethacin
colchicine (give until attacks settle or sign of toxicity)

Front 38

intercritical gout

Back 38

asymptomatic period between attacks

institute urate-lowering therapy with apropriate prophylaxis to avoid an acute exacerbation

Front 39

urate lowering therapy

Back 39

allopurinol AND
colchicine AND/OR
indomethacin

Front 40

chronic gout

Back 40

difficult to treat (no asymptomatic period)
patients may be unwiling to take allopurinol
resolve inflammation (NSAID, colchicine or corticosteriods)

same treatment

Front 41

other gout treatments
other than allopurinol, colchicine and intomethacine

Back 41

corticosteriods (NSAIDs not tolerated) - prednisone.

intra-articular injections with steriods (large joints, elderly patients) - triamcinolone, dexamethasone with lignocaine.

Front 42

new gout treatment

Back 42

febuxostat

inhibits xanthine oxidase
similar reduction in gout flares