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PPT year 4 > masterclass 1: MSK and rheumatology > Flashcards

masterclass 1: MSK and rheumatology Flashcards

1
Q

what does antalgic mean

A

to avoid pain - limp

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2
Q

what might you see on xray of osteoathritis of the hip

A 
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchodnral cysts
Femoral deformation
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3
Q

non pharmacological options for osteoathritis management

A

weight loss if obese/overweight; physiotherapy; appropriate footwear; heat/cool packs; pacing; psychological support; assistive devices; joint supports

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4
Q

pain management ladder for osteoporosis

A

paracetamol/topical NSAID
swap topical for oral NSAID
weak opioid

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5
Q

example of a weak opioid

A

codein

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6
Q

adjuct treatment for osteoathritis

A

capsaicin cream

intraarticular joint injections

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7
Q

how does capsaicin work

A

reduces the amount of substance P

defunctionalization of nociceptor fibers by inducing a topical hypersensitivity reaction on the skin

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8
Q

what is the prostoglandin pathway

A

tissue injury = arachadonic acid = cox 1 and cox 2

cox 2 = inflammatory prostoglandins

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9
Q

what do NSAIDs inhibit

A

cox

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10
Q

other than prostoglandins what does arachadonic acid produce

A

thromboxanes

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11
Q

what is the role of cox 1

A

regulation of homeostatic processes, such as renal and gastric blood flow, gastric cytoprotection and platelet aggregation

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12
Q

when is cox 2 expressed

A

after stimulation by a inflammatory process

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13
Q

what do cox 2 prostaglandins do

A

inflammatory/painful process, through vasodilation, increasing vascular permeability and sensitisation of nerve fibres to inflammatory mediators

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14
Q

what are the actions of NSAIDs

A

analgesic
antiinflammatory
anti pyretic

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15
Q

side effects of NSAIDs

A 
GI disturbance 
Renal insufficiency
Salt/water retention
Hyponatraemia/hyperkalaemia 
Cardiovascular effects
Hypersensitivity reactions
Headaches/dizziness
Skin reactions
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16
Q

what GI distrubance does NSAIDs give

A

nausea, dyspepsia, gastric irritation, gastric ulceration

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17
Q

why do NSAIDs give GI disturbance

A

inhibition of mucosal production of COX-1 generated prostaglandins

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18
Q

can you avoid GI disturbance

A

no, you can reduce it but it can still be absorbed into the gastric mucosa

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19
Q

in the kidneys why are the cox enzymes important

A

important for maintaining renal blood flow

have a direct effect on the tubules = naturesis

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20
Q

what is naturesis

A

excretion of sodium in the urine

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21
Q

what thrombotic events do NSAIDs increase the risk of

A

MI/stroke

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22
Q

which NSAIDs are particular worry for MI and stroke

A

diclofenac and high dose ibuprofen

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23
Q

name a drug that is more active on cox 2 than 1

A

celecoxib

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24
Q

name a drug that is more active on cox 1 than 2

A

aspirin

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25
Q

what do you need to think about when giving NSAID

A

gastroprotection

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26
Q

how can you do gastro protection with NSAIDs

A

take with food
PPI
consider cox 2 selective

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27
Q

what is the risk with cox 2 inhibitors

A

increases the risk of MI

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28
Q

when do you refer people to surgery with osteoarthritis

A

if they have joint symptoms which reduce their quality of life, non surgery treatments dont work

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29
Q

pain and swelling in a knee over a day DDX

A 
pseudogout
septic arthritis
cellulitis
busitis
OA
haemachromatosis
trauma
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30
Q

risk factors for pseudogout

A

alcohol
HTN
diuretics
male

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31
Q

how do you exclude septic athiritis

A

normal CRP is not enough

need joint aspiration

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32
Q

what will synovial fluid analysis show on gout

A

negative birefringent, needle-shaped crystals, monosodium urate

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33
Q

what does uric acid come from

A

catabolism of purines

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34
Q

why doyou get a high uric acid

A

over production or decreased renal excretion

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35
Q

what is deposited in tissues in gout

A

monosodium urate crystals = tophus

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36
Q

what do the tophi do

A

shed crystals into the synovial fluid = an inflammatory response

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37
Q

pseudogout synovial fluid analysis

A

positive birefringent, rhomboid/rectangular shaped crystals, calcium pyrophosphate

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38
Q

name some drugs that increase the risk of gout

A

diuretics, cytotoxic drugs, aspirin, ciclosporin/tacolimus, levodopa citalopram, lansoprazole, salbutamol, clenil

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39
Q

non pharmacological options for gout

A

rest, elevate, ice
avoid trauma
analgesia

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40
Q

what are the first line medications for gout

A

colchicine

NSAIDs

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41
Q

what condition may NSAIDs exacerbate

A

asthma

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42
Q

how do SSRI and NSAID interact

A

increase the risk of bleeding

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43
Q

what are the actions of colchicine in gout

A

Reduced production of TNF alpha
Inhibits production of chemotaxins
Disrupts assembly of microtubules in neutrophil leucocytes
Inhibit release of enzymes and free radicals by neutrophils

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44
Q

what produces TNF alpha

A

macrophages

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45
Q

what does TNF alpha do

A

priming of neutrophil leucocytes

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46
Q

what do chemotaxins do

A

attracting leucocytes to inflamed tissues

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47
Q

what happens if the microtubules in neutrophils dont work

A

impairing adhesion to endothelial cells

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48
Q

what do enzyme free radicals do in a joint

A

damage it

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49
Q

when do you give colchicine

A

gout

familial Mediterranean fever

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50
Q

what are the side effects of colchicine

A 
GI disturbances
Blood disorders
GI haemorrhage 
Hepatic/renal impairment
Myopathy
rash
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51
Q

prophylaxis therapy for gout

A

allopurinol

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52
Q

what is familial Mediterranean fever

A

autosomal recessive inflammatory disease

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53
Q

how does familial Mediterranean fever present

A

fever with attacks of inflammation

e.g. peritonitis, joint pain, pleuritis

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54
Q

contraindications for colchicine

A

pregnancy

blood disorders

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55
Q

what are some drugs that interact with colchicine

A 
Macrolides
Anti-virals/fungals
CCB	
Grapefruit juice
statins
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56
Q

why cant you have colchicine and lipid lowering therapy

A

myopathy

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57
Q

what is the interaction between colchicine and macrolide

A

increased toxicity

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58
Q

what is the interaction between colchicine and antifungal

A

increased toxicity

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59
Q

what is the interaction between colchicine and CCB

A

increased toxicity

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60
Q

what is the interaction between colchicine and grapefuit juice

A

increased toxicity

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61
Q

describe when to take colchicine

A

1-2 days after the attck
2-4 times a day
3-6 days

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62
Q

lifestyle advice for gout

A 
weight loss
red meat/seafood stop
cut down on alcohol
hydration
smoking cessation
lowfat dairy products
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63
Q

when after an attack of gout would you measure someones blood to think about the risk

A

4-6 weeks after

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64
Q

how does allopurinol work for gout

A

xanthine oxidase inhibitor which catalyses two of the step to get from purines to uric acid

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65
Q

what levels rise if you give allopurinol and is this an issue

A

xanthine and hypoxanthine

no they cant form crystals and they are soluble in water

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66
Q

Signs on x ray of OA x5

A 
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
Femoral deformation
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67
Q

criteria for clinical diagnosis x3

A

45 and over
has activity-related joint pain - develops over months/years
no morning stiffness longer than 30 mins

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68
Q

analgesia ladder for OA

A

paracetamol/topical NSAID
oral NSAID
weak opioids such as codeine

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69
Q

adjuct therapy for OA

A

Topical capsaicin cream

Intra-articular steroid injections

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70
Q

where would you use Topical capsaicin cream x2

A

hand/knee

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71
Q

NSAID inihibit

A

COX enzymes

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72
Q

what two things do COX enzymes produce

A

prostaglandins/thromboxanes

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73
Q

what do prostaglandins/thromboxanes begin as

A

arachidonic acid

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74
Q

COX 1 house keeping role x3

A

renal and gastric blood flow
gastric cytoprotection
platelet aggregation

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75
Q

when is COX 2 expressed

A

only after stimulation by an inflammatory process

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76
Q

how do the products of COX 2 contribute to inflammation x3

A

vasodilation
increasing vascular permeability
sensitisation of nerve fibres to inflammatory mediators

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77
Q

3 actions of NSAIDs

A

anti-inflammatory, analgesic and antipyretic

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78
Q

Selective COX-2 inhibitors x3

A

Celecoxib, etoricoxib, parecoxib

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79
Q

whats good about selective COX 2

A

less likely to cause GI side effects

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80
Q

risk of COX 2 inhibitors

A

myocardial infarction

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81
Q

NSAID affect on electrolytes x2

A

Hyponatraemia/hyperkalaemia

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82
Q

NSAID affect on kidney x2

A

Renal insufficiency

Salt/water retention

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83
Q

NSAID affect on the head x2

A

Headaches/dizziness

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84
Q

why does NSAID cause GI disturbance

A

inhibition of mucosal production of COX-1 generated prostaglandins

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85
Q

hwo does NSAIDs get into the gastric mucosa x2

A

direct absorption from the gastric lumen but also by systemic delivery

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86
Q

NSAIDs alternative route and GI side effects

A

dosent make a difference - NSAIDs delivered systemically

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87
Q

what to prescribe alongside NSAIDs for gastric

A

PPI

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88
Q

what vascular affects do NSAIDs have on kidneys

A

afferent dilatation

89
Q

NSAIDs direct affect on kidney

A

promoting natriuresis

90
Q

what can NSAID induced salt and water retention exacerbate x2

A

HTN

CCF

91
Q

prostoglandins affect on ADH

A

antagonise

92
Q

unopposed ADH action =

A

dilutional hyponatraemia

93
Q

why do you get hyperkalaemia with NSAIDs

A

less renin is produced because less prostoglandins = hypoaldosterone = less potassium excreted

94
Q

affect of prostoglandin on renin

A

= release

95
Q

diclofenac increases the risk of what x2

A

MI/stroke

96
Q

GI contraindications for NSAIDs

A

GI bleeding/ulceration

97
Q

failure of which organs is a contraindication for NSAIDs

A

Severe heart failure

Severe renal impairment

98
Q

infection contraindication for NSAIDs

A

varicellar zoster infection

99
Q

pregnancy and NSAIDS

A

Avoid 3rd trimester of pregnancy

100
Q

3 cautions for NSAIDs

A

Crohn’s disease, ischaemic heart disease and elderly

101
Q

SSRI and NSAID risk

A

increase the risk of bleeding

102
Q

NSAIDs and asthma

A

can excacerbate

103
Q

NSAIDs interactions (not bloody obvious ones) x6

A 
Bisphosphonates
Steroids
Methotrexate
ACEi
Diuretics 
Cephalosporins
104
Q

do cephlasporins kill bacteria

A

yes

105
Q

common cephlasporins

A

cefuroxime and ceftriaxone

106
Q

moa of cephlasporins

A

disrupt the synthesis of the peptidoglycan layer of cell wall

107
Q

risk factors for crystal athropathy x4

A

male
diuretic use
alcohol intake
HTN

108
Q

common location for pseudogout

A

knee

109
Q

measuring urate in gout

A

unhelpful in the acute - better to measure after 4-6 weeks

110
Q

how to exclude septic athritis

A

urgent joint aspiration

111
Q

acute gout aspiration findings x3

A

negative birefringent, needle-shaped crystals, monosodium urate

112
Q

where does uric acid come from

A

catabolism of purines

113
Q

precursers of uric acid

A

xanthine and hypoxanthine

114
Q

what do monosodium urate crystals for when deposited in tissue

A

tophi

115
Q

how can the tophi be harmful

A

shed crystals into the synovial membrane or joint cartilage, triggering a painful inflammatory response

116
Q

drug risk factors for gout x6

A 
Diuretics
cytotoxic drugs
aspirin
ciclosporin
tacolimus
levodopa
117
Q

first line drugs for acute gout x2

A

NSAID or colchicine

118
Q

Lifestyle advice for gout x7

A 
Weight loss
reduction in alcohol 
reduction red meat/seafood consumption
keep hydrated
regular exercise
use low fat dairy products
smoking cessation
119
Q

first line ULT

A

Allopurinol

120
Q

when to start ULT

A

after the attack has resolved

121
Q

colchicine overall affect

A

Prevention of activation, migration and action of neutrophils within the joint space

122
Q

colchicine affect on TNF alpha

A

reduction

123
Q

TNF alpha reduction affect on the inflammatory process

A

inhibits priming of neutrophil leukocytes

124
Q

who produces TNF alpha

A

macrophages

125
Q

what C does colchicine reduce

A

chemotaxins

126
Q

colchicine structure affect on neutrophils

A

Disrupts assembly of microtubules

127
Q

what does disrupted microtubules mean for neutrophils

A

impaired adhesion to endothelial cells

128
Q

how does colchicine stop damage to the joint

A

Inhibit release of enzymes and free radicals

129
Q

colchicine indications x2

A

Gout

Familial Mediterranean fever

130
Q

what is FMF

A

genetic disorder = recurrent episodes of fever and abdomen, chest, or joint pain

131
Q

6 side effects of colchicine

A 
GI disturbances
Blood disorders
GI haemorrhage 
Hepatic/renal impairment
Myopathy
132
Q

when to give colchicine

A

acute flare up and prophylaxis when starting ULT

133
Q

2 contraindications for colchicine

A

Blood disorders

Pregnancy - tera

134
Q

what drugs interact to increase the risk of colchicine toxicity x5

A

Macrolides
Anti-virals/fungals
CCB
Grapefruit juice

135
Q

what other drugs are contraindicated with colchicine

A

lipid lowering therapy e.g. fibrates and statins

136
Q

colchicine ineraction with LLT

A

increased risk of myopathy

137
Q

how long to take colchicine for

A

1-2 days after the attack has resolved

138
Q

pain relief time scale colchicine

A

starts by 18 hours and reaches max at 48 hours

139
Q

colchicine dose

A

500 micrograms 2-4 times a day

140
Q

colchicine max amount

A

6mg per course so use is restricted to 3-6 days

141
Q

macrolides end in

A

mycin

142
Q

how do macrolides work

A

preventing peptidyltransferase from adding the growing peptide attached to tRNA to the next amino acid as well as inhibiting ribosomal translation

143
Q

allopurinol moa

A

Xanthine oxidase inhibitor

144
Q

allopurinol affect on uric acid

A

lowers it

145
Q

what does allopurinol increase

A

xanthine and hypoxanthine

146
Q

what do high levels of xanthine and hypoxanthine mean

A

nothing they are more soluble in water and dont cystalise

147
Q

3 indications for allopurinol

A

Gout
Uric acid and calcium oxalate renal stones
Hyperuricemia associated with chemotherapy

148
Q

when to and not to use allopurinol in gout

A

dont use in the acute phase but can continue if gout develops

149
Q

what to encourage with allopurinol

A

fluids

150
Q

what to give when starting allopurinol

A

colchicine and NSAIDs

151
Q

how long to cover gout with NSAID and colchicine

A

1 month

152
Q

4 side effects of allopurinol

A

GI disturbances
Rash
Blood disorders
Hypersensitivity reactions

153
Q

amoxicillin allopurinol interaction

A

rash

154
Q

allopurinol and ACEi interaction

A

leucopenia

155
Q

allopurinol and azathiopurine interaction

A

toxicity

156
Q

allopurinol and bendrofluromethiazide interaction

A

hypersensitivity

157
Q

allopurinol interaction with warfarin

A

increased anticoagulant effect

158
Q

what to do if someone gets a rash with allopurinol

A

stop and reintroduce gradually if mild

159
Q

why is there a risk of toxicity with mercaptopurine and allopurinol

A

mercaptopurine is metabolised by xantine oxidase - same with azathiopurine

160
Q

how to monitor treatment with allopurinol

A

Check serum uric acid level and renal function every 4 weeks until within target range and then annually thereafter

161
Q

what is the uric acid aim for people who suffer gout

A

<300 micromol/l

162
Q

what to do if someone is still having gout with allopurinol treatment x5

A 
compliance?
increase the dose?
Review any trigger factors?
advance prescription of treatment for future attacks
referral to secondary care
163
Q

gout trigger factors

A

such as medication (for example diuretics), trauma, diet, weight gain, and excess alcohol consumption

164
Q

complication of tophi

A

secondary infection

165
Q

RA diagnosis features

A

clinical diagnosis - investigations are part of assessment and to rule out other things

166
Q

when to urgently refer someone for RA

A

small joints of hand/feet affected
more than one joint affected
delay of over 3 months between onset and seeking advice

167
Q

3 good tests for diagnosing RA

A

RF
Anti-CCP
X-ray of hands and feet

168
Q

which test is better RF or ACCP

A

ACCP

169
Q

what to look for on RA xray

A 
soft tissue swelling
peri-articular osteopenia
loss of joint space
erosion
deformity
170
Q

RA FBC

A

NNanaemia

reactive thrombocytosis

171
Q

ESR, CRP and PV in RA

A

usually raised - can be normal

172
Q

other tests to do in RA and why

A

U&E and LFT – in preparation of drug therapies

173
Q

5 drugs that affect the immune process

A

Hydroxychloroquine, Methotrexate, Azathioprine, Ciclosporin, Leflunomide.

174
Q

3 drugs that affect the disease process

A

Gold, Penicillamine, Sulfasalazine

175
Q

DMARDs onset of action

A

takes 3 months

176
Q

firstline for new RA

A

monotherapy using methotrexate, leflunomide or sulfasalazine

177
Q

mild or palindromic RA management

A

hydroxychloroquine

178
Q

what to use as bridge while DMARD starts to work on RA

A

steroids

179
Q

what to do after first line for RA

A

increase dose

add another DMARD

180
Q

Sulphasalazine metabolite

A

5-ASA

181
Q

5 side effects of sulphasalazine

A 
GI disturbances
Orange secretions
Pancreatitis
Blood disorders
Hepato/renal toxicity
182
Q

sulphasalazine affect on sperm

A

Reversible oligospermia

183
Q

sulphasalazine interaction

A

Reduces absorption of digoxin

184
Q

contraindication for sulphasalazine

A

Salicylate allergy

185
Q

Tumour necrosis factor inhibitors x4

A

Infliximab, adalimumab, entanercept, golimumab

186
Q

Anti-IL1 therapy

A

Anakinra

187
Q

Anti-CD20 therapy

A

Rituximab

188
Q

Anti-IL6 receptor therapy

A

Tocilizumab

189
Q

T-cell co-stimulator modulator

A

Abatacept

190
Q

when to start biologics for RA

A

in addition to steroids, two trials of six months of DMARD monotherapy or combination therapy (at least one including methotrexate) should fail to control symptoms/prevent disease progression

191
Q

when to stop biologic

A

no adequate response six months after starting

192
Q

Infliximab moa

A

Monoclonal antibody which inhibits TNF-α

193
Q

infliximab contraindications

A

Severe infections

Heart failure

194
Q

infliximab administartion

A

intravenous injection

195
Q

infliximab schedule

A

initially 2-4 weekly and then every 2 months

196
Q

infliximab and vaccines

A

Patients should be up-to-date with immunisations before initiating treatment

197
Q

infliximab and TB

A

Assess for active and latent TB and treat accordingly, advising patients to attend if develops symptoms of TB

198
Q

infliximab and contraception

A

Contraception is required for up to 6 months after last dose

199
Q

infliximab monitoring

A

Monitor for reactivation of hepatitis B

Periodic skin examination for non-melanoma skin cancer

200
Q

methotrexate moa

A

Dihydrofolate reductase enzyme inhibitor

201
Q

methotrexate indications

A

Rheumatoid arthritis
Cancer therapy
Crohn’s disease

202
Q

methotrexate route

A

Oral once a week (mild/moderate)

IM/SC once a week (severe)

203
Q

methotrexate contraindications

A 
Active infection
Ascites
Pleural effusion
Severe renal impairment
Teratogenic in pregnancy
204
Q

methotrexate interaction with antibiotics

A

Trimethoprim/Co-trimoxazole - severe bone marrow depression

205
Q

methotrexate and NSAIDs

A

= toxicity

206
Q

why is methotrexate contraindicated with ascites or pleural effusion

A

Risk of further accumulation of ascites/pleural effusion

207
Q

when to discontinue methotrexate and why

A

Stomatitis - may be first sign of GI toxicity

208
Q

methotrexate lung side effects

A

pneumonitis and pulmonary fibrosis

209
Q

methotrexate co prescribe

A

folic acid

210
Q

methotrexate and vaccines

A

avoid live vaccines
annual flu jab
pneumoccocal vaccine at the start of treatment and every 5-10 years.

211
Q

folic acid cycle

A

Folic acid becomes tetrahydrofolic acid (THF) and is converted to dihydrofolic acid (DHF)

212
Q

whats dihydrofolate reductase for

A

converts DHF back to THF, allowing it to be re-used

213
Q

signs of blood disorders

A

sore throat, bruising, mouth ulcers

214
Q

signs of heptatoxicity

A

abdominal pain, N+V, dark urine

215
Q

which vaccines are live

A

MMR, yellow fever, typhoid

216
Q

how does FA help with wethotrexate

A

prevent mucositis and myelosuppression

217
Q

monitoring in methotrexate

A

FBC, renal function and LFTs every 2 weeks until on stable dose for 6 weeks

218
Q

methotrexate when the dose is stable

A

Monthly FBC, renal function and LFTs for 3 months

Maintenance

219
Q

methotrexate maintenance monitoring

A

FBC, renal function and LFTs at least every 12 weeks

PPT year 4 (7 decks)

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