masterclass 1: MSK and rheumatology Flashcards
(219 cards)
1
Q
what does antalgic mean
A
to avoid pain - limp
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
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
4
Q
pain management ladder for osteoporosis
A
paracetamol/topical NSAID
swap topical for oral NSAID
weak opioid
5
Q
example of a weak opioid
A
codein
6
Q
adjuct treatment for osteoathritis
A
capsaicin cream
intraarticular joint injections
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
8
Q
what is the prostoglandin pathway
A
tissue injury = arachadonic acid = cox 1 and cox 2
cox 2 = inflammatory prostoglandins
9
Q
what do NSAIDs inhibit
A
cox
10
Q
other than prostoglandins what does arachadonic acid produce
A
thromboxanes
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
12
Q
when is cox 2 expressed
A
after stimulation by a inflammatory process
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
14
Q
what are the actions of NSAIDs
A
analgesic
antiinflammatory
anti pyretic
15
Q
side effects of NSAIDs
A
GI disturbance Renal insufficiency Salt/water retention Hyponatraemia/hyperkalaemia Cardiovascular effects Hypersensitivity reactions Headaches/dizziness Skin reactions
16
Q
what GI distrubance does NSAIDs give
A
nausea, dyspepsia, gastric irritation, gastric ulceration
17
Q
why do NSAIDs give GI disturbance
A
inhibition of mucosal production of COX-1 generated prostaglandins
18
Q
can you avoid GI disturbance
A
no, you can reduce it but it can still be absorbed into the gastric mucosa
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
20
Q
what is naturesis
A
excretion of sodium in the urine
21
Q
what thrombotic events do NSAIDs increase the risk of
A
MI/stroke
22
Q
which NSAIDs are particular worry for MI and stroke
A
diclofenac and high dose ibuprofen
23
Q
name a drug that is more active on cox 2 than 1
A
celecoxib
24
Q
name a drug that is more active on cox 1 than 2
A
aspirin
25
what do you need to think about when giving NSAID
gastroprotection
26
how can you do gastro protection with NSAIDs
take with food
PPI
consider cox 2 selective
27
what is the risk with cox 2 inhibitors
increases the risk of MI
28
when do you refer people to surgery with osteoarthritis
if they have joint symptoms which reduce their quality of life, non surgery treatments dont work
29
pain and swelling in a knee over a day DDX
```
pseudogout
septic arthritis
cellulitis
busitis
OA
haemachromatosis
trauma
```
30
risk factors for pseudogout
alcohol
HTN
diuretics
male
31
how do you exclude septic athiritis
normal CRP is not enough
| need joint aspiration
32
what will synovial fluid analysis show on gout
negative birefringent, needle-shaped crystals, monosodium urate
33
what does uric acid come from
catabolism of purines
34
why doyou get a high uric acid
over production or decreased renal excretion
35
what is deposited in tissues in gout
monosodium urate crystals = tophus
36
what do the tophi do
shed crystals into the synovial fluid = an inflammatory response
37
pseudogout synovial fluid analysis
positive birefringent, rhomboid/rectangular shaped crystals, calcium pyrophosphate
38
name some drugs that increase the risk of gout
diuretics, cytotoxic drugs, aspirin, ciclosporin/tacolimus, levodopa citalopram, lansoprazole, salbutamol, clenil
39
non pharmacological options for gout
rest, elevate, ice
avoid trauma
analgesia
40
what are the first line medications for gout
colchicine
| NSAIDs
41
what condition may NSAIDs exacerbate
asthma
42
how do SSRI and NSAID interact
increase the risk of bleeding
43
what are the actions of colchicine in gout
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
44
what produces TNF alpha
macrophages
45
what does TNF alpha do
priming of neutrophil leucocytes
46
what do chemotaxins do
attracting leucocytes to inflamed tissues
47
what happens if the microtubules in neutrophils dont work
impairing adhesion to endothelial cells
48
what do enzyme free radicals do in a joint
damage it
49
when do you give colchicine
gout
| familial Mediterranean fever
50
what are the side effects of colchicine
```
GI disturbances
Blood disorders
GI haemorrhage
Hepatic/renal impairment
Myopathy
rash
```
51
prophylaxis therapy for gout
allopurinol
52
what is familial Mediterranean fever
autosomal recessive inflammatory disease
53
how does familial Mediterranean fever present
fever with attacks of inflammation
| e.g. peritonitis, joint pain, pleuritis
54
contraindications for colchicine
pregnancy
| blood disorders
55
what are some drugs that interact with colchicine
```
Macrolides
Anti-virals/fungals
CCB
Grapefruit juice
statins
```
56
why cant you have colchicine and lipid lowering therapy
myopathy
57
what is the interaction between colchicine and macrolide
increased toxicity
58
what is the interaction between colchicine and antifungal
increased toxicity
59
what is the interaction between colchicine and CCB
increased toxicity
60
what is the interaction between colchicine and grapefuit juice
increased toxicity
61
describe when to take colchicine
1-2 days after the attck
2-4 times a day
3-6 days
62
lifestyle advice for gout
```
weight loss
red meat/seafood stop
cut down on alcohol
hydration
smoking cessation
lowfat dairy products
```
63
when after an attack of gout would you measure someones blood to think about the risk
4-6 weeks after
64
how does allopurinol work for gout
xanthine oxidase inhibitor which catalyses two of the step to get from purines to uric acid
65
what levels rise if you give allopurinol and is this an issue
xanthine and hypoxanthine
| no they cant form crystals and they are soluble in water
66
Signs on x ray of OA x5
```
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
Femoral deformation
```
67
criteria for clinical diagnosis x3
45 and over
has activity-related joint pain - develops over months/years
no morning stiffness longer than 30 mins
68
analgesia ladder for OA
paracetamol/topical NSAID
oral NSAID
weak opioids such as codeine
69
adjuct therapy for OA
Topical capsaicin cream
| Intra-articular steroid injections
70
where would you use Topical capsaicin cream x2
hand/knee
71
NSAID inihibit
COX enzymes
72
what two things do COX enzymes produce
prostaglandins/thromboxanes
73
what do prostaglandins/thromboxanes begin as
arachidonic acid
74
COX 1 house keeping role x3
renal and gastric blood flow
gastric cytoprotection
platelet aggregation
75
when is COX 2 expressed
only after stimulation by an inflammatory process
76
how do the products of COX 2 contribute to inflammation x3
vasodilation
increasing vascular permeability
sensitisation of nerve fibres to inflammatory mediators
77
3 actions of NSAIDs
anti-inflammatory, analgesic and antipyretic
78
Selective COX-2 inhibitors x3
Celecoxib, etoricoxib, parecoxib
79
whats good about selective COX 2
less likely to cause GI side effects
80
risk of COX 2 inhibitors
myocardial infarction
81
NSAID affect on electrolytes x2
Hyponatraemia/hyperkalaemia
82
NSAID affect on kidney x2
Renal insufficiency
| Salt/water retention
83
NSAID affect on the head x2
Headaches/dizziness
84
why does NSAID cause GI disturbance
inhibition of mucosal production of COX-1 generated prostaglandins
85
hwo does NSAIDs get into the gastric mucosa x2
direct absorption from the gastric lumen but also by systemic delivery
86
NSAIDs alternative route and GI side effects
dosent make a difference - NSAIDs delivered systemically
87
what to prescribe alongside NSAIDs for gastric
PPI
88
what vascular affects do NSAIDs have on kidneys
afferent dilatation
89
NSAIDs direct affect on kidney
promoting natriuresis
90
what can NSAID induced salt and water retention exacerbate x2
HTN
| CCF
91
prostoglandins affect on ADH
antagonise
92
unopposed ADH action =
dilutional hyponatraemia
93
why do you get hyperkalaemia with NSAIDs
less renin is produced because less prostoglandins = hypoaldosterone = less potassium excreted
94
affect of prostoglandin on renin
= release
95
diclofenac increases the risk of what x2
MI/stroke
96
GI contraindications for NSAIDs
GI bleeding/ulceration
97
failure of which organs is a contraindication for NSAIDs
Severe heart failure
| Severe renal impairment
98
infection contraindication for NSAIDs
varicellar zoster infection
99
pregnancy and NSAIDS
Avoid 3rd trimester of pregnancy
100
3 cautions for NSAIDs
Crohn’s disease, ischaemic heart disease and elderly
101
SSRI and NSAID risk
increase the risk of bleeding
102
NSAIDs and asthma
can excacerbate
103
NSAIDs interactions (not bloody obvious ones) x6
```
Bisphosphonates
Steroids
Methotrexate
ACEi
Diuretics
Cephalosporins
```
104
do cephlasporins kill bacteria
yes
105
common cephlasporins
cefuroxime and ceftriaxone
106
moa of cephlasporins
disrupt the synthesis of the peptidoglycan layer of cell wall
107
risk factors for crystal athropathy x4
male
diuretic use
alcohol intake
HTN
108
common location for pseudogout
knee
109
measuring urate in gout
unhelpful in the acute - better to measure after 4-6 weeks
110
how to exclude septic athritis
urgent joint aspiration
111
acute gout aspiration findings x3
negative birefringent, needle-shaped crystals, monosodium urate
112
where does uric acid come from
catabolism of purines
113
precursers of uric acid
xanthine and hypoxanthine
114
what do monosodium urate crystals for when deposited in tissue
tophi
115
how can the tophi be harmful
shed crystals into the synovial membrane or joint cartilage, triggering a painful inflammatory response
116
drug risk factors for gout x6
```
Diuretics
cytotoxic drugs
aspirin
ciclosporin
tacolimus
levodopa
```
117
first line drugs for acute gout x2
NSAID or colchicine
118
Lifestyle advice for gout x7
```
Weight loss
reduction in alcohol
reduction red meat/seafood consumption
keep hydrated
regular exercise
use low fat dairy products
smoking cessation
```
119
first line ULT
Allopurinol
120
when to start ULT
after the attack has resolved
121
colchicine overall affect
Prevention of activation, migration and action of neutrophils within the joint space
122
colchicine affect on TNF alpha
reduction
123
TNF alpha reduction affect on the inflammatory process
inhibits priming of neutrophil leukocytes
124
who produces TNF alpha
macrophages
125
what C does colchicine reduce
chemotaxins
126
colchicine structure affect on neutrophils
Disrupts assembly of microtubules
127
what does disrupted microtubules mean for neutrophils
impaired adhesion to endothelial cells
128
how does colchicine stop damage to the joint
Inhibit release of enzymes and free radicals
129
colchicine indications x2
Gout
| Familial Mediterranean fever
130
what is FMF
genetic disorder = recurrent episodes of fever and abdomen, chest, or joint pain
131
6 side effects of colchicine
```
GI disturbances
Blood disorders
GI haemorrhage
Hepatic/renal impairment
Myopathy
```
132
when to give colchicine
acute flare up and prophylaxis when starting ULT
133
2 contraindications for colchicine
Blood disorders
| Pregnancy - tera
134
what drugs interact to increase the risk of colchicine toxicity x5
Macrolides
Anti-virals/fungals
CCB
Grapefruit juice
135
what other drugs are contraindicated with colchicine
lipid lowering therapy e.g. fibrates and statins
136
colchicine ineraction with LLT
increased risk of myopathy
137
how long to take colchicine for
1-2 days after the attack has resolved
138
pain relief time scale colchicine
starts by 18 hours and reaches max at 48 hours
139
colchicine dose
500 micrograms 2-4 times a day
140
colchicine max amount
6mg per course so use is restricted to 3-6 days
141
macrolides end in
mycin
142
how do macrolides work
preventing peptidyltransferase from adding the growing peptide attached to tRNA to the next amino acid as well as inhibiting ribosomal translation
143
allopurinol moa
Xanthine oxidase inhibitor
144
allopurinol affect on uric acid
lowers it
145
what does allopurinol increase
xanthine and hypoxanthine
146
what do high levels of xanthine and hypoxanthine mean
nothing they are more soluble in water and dont cystalise
147
3 indications for allopurinol
Gout
Uric acid and calcium oxalate renal stones
Hyperuricemia associated with chemotherapy
148
when to and not to use allopurinol in gout
dont use in the acute phase but can continue if gout develops
149
what to encourage with allopurinol
fluids
150
what to give when starting allopurinol
colchicine and NSAIDs
151
how long to cover gout with NSAID and colchicine
1 month
152
4 side effects of allopurinol
GI disturbances
Rash
Blood disorders
Hypersensitivity reactions
153
amoxicillin allopurinol interaction
rash
154
allopurinol and ACEi interaction
leucopenia
155
allopurinol and azathiopurine interaction
toxicity
156
allopurinol and bendrofluromethiazide interaction
hypersensitivity
157
allopurinol interaction with warfarin
increased anticoagulant effect
158
what to do if someone gets a rash with allopurinol
stop and reintroduce gradually if mild
159
why is there a risk of toxicity with mercaptopurine and allopurinol
mercaptopurine is metabolised by xantine oxidase - same with azathiopurine
160
how to monitor treatment with allopurinol
Check serum uric acid level and renal function every 4 weeks until within target range and then annually thereafter
161
what is the uric acid aim for people who suffer gout
<300 micromol/l
162
what to do if someone is still having gout with allopurinol treatment x5
```
compliance?
increase the dose?
Review any trigger factors?
advance prescription of treatment for future attacks
referral to secondary care
```
163
gout trigger factors
such as medication (for example diuretics), trauma, diet, weight gain, and excess alcohol consumption
164
complication of tophi
secondary infection
165
RA diagnosis features
clinical diagnosis - investigations are part of assessment and to rule out other things
166
when to urgently refer someone for RA
small joints of hand/feet affected
more than one joint affected
delay of over 3 months between onset and seeking advice
167
3 good tests for diagnosing RA
RF
Anti-CCP
X-ray of hands and feet
168
which test is better RF or ACCP
ACCP
169
what to look for on RA xray
```
soft tissue swelling
peri-articular osteopenia
loss of joint space
erosion
deformity
```
170
RA FBC
NNanaemia
| reactive thrombocytosis
171
ESR, CRP and PV in RA
usually raised - can be normal
172
other tests to do in RA and why
U&E and LFT – in preparation of drug therapies
173
5 drugs that affect the immune process
Hydroxychloroquine, Methotrexate, Azathioprine, Ciclosporin, Leflunomide.
174
3 drugs that affect the disease process
Gold, Penicillamine, Sulfasalazine
175
DMARDs onset of action
takes 3 months
176
firstline for new RA
monotherapy using methotrexate, leflunomide or sulfasalazine
177
mild or palindromic RA management
hydroxychloroquine
178
what to use as bridge while DMARD starts to work on RA
steroids
179
what to do after first line for RA
increase dose
| add another DMARD
180
Sulphasalazine metabolite
5-ASA
181
5 side effects of sulphasalazine
```
GI disturbances
Orange secretions
Pancreatitis
Blood disorders
Hepato/renal toxicity
```
182
sulphasalazine affect on sperm
Reversible oligospermia
183
sulphasalazine interaction
Reduces absorption of digoxin
184
contraindication for sulphasalazine
Salicylate allergy
185
Tumour necrosis factor inhibitors x4
Infliximab, adalimumab, entanercept, golimumab
186
Anti-IL1 therapy
Anakinra
187
Anti-CD20 therapy
Rituximab
188
Anti-IL6 receptor therapy
Tocilizumab
189
T-cell co-stimulator modulator
Abatacept
190
when to start biologics for RA
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
when to stop biologic
no adequate response six months after starting
192
Infliximab moa
Monoclonal antibody which inhibits TNF-α
193
infliximab contraindications
Severe infections
| Heart failure
194
infliximab administartion
intravenous injection
195
infliximab schedule
initially 2-4 weekly and then every 2 months
196
infliximab and vaccines
Patients should be up-to-date with immunisations before initiating treatment
197
infliximab and TB
Assess for active and latent TB and treat accordingly, advising patients to attend if develops symptoms of TB
198
infliximab and contraception
Contraception is required for up to 6 months after last dose
199
infliximab monitoring
Monitor for reactivation of hepatitis B
| Periodic skin examination for non-melanoma skin cancer
200
methotrexate moa
Dihydrofolate reductase enzyme inhibitor
201
methotrexate indications
Rheumatoid arthritis
Cancer therapy
Crohn’s disease
202
methotrexate route
Oral once a week (mild/moderate)
| IM/SC once a week (severe)
203
methotrexate contraindications
```
Active infection
Ascites
Pleural effusion
Severe renal impairment
Teratogenic in pregnancy
```
204
methotrexate interaction with antibiotics
Trimethoprim/Co-trimoxazole - severe bone marrow depression
205
methotrexate and NSAIDs
= toxicity
206
why is methotrexate contraindicated with ascites or pleural effusion
Risk of further accumulation of ascites/pleural effusion
207
when to discontinue methotrexate and why
Stomatitis - may be first sign of GI toxicity
208
methotrexate lung side effects
pneumonitis and pulmonary fibrosis
209
methotrexate co prescribe
folic acid
210
methotrexate and vaccines
avoid live vaccines
annual flu jab
pneumoccocal vaccine at the start of treatment and every 5-10 years.
211
folic acid cycle
Folic acid becomes tetrahydrofolic acid (THF) and is converted to dihydrofolic acid (DHF)
212
whats dihydrofolate reductase for
converts DHF back to THF, allowing it to be re-used
213
signs of blood disorders
sore throat, bruising, mouth ulcers
214
signs of heptatoxicity
abdominal pain, N+V, dark urine
215
which vaccines are live
MMR, yellow fever, typhoid
216
how does FA help with wethotrexate
prevent mucositis and myelosuppression
217
monitoring in methotrexate
FBC, renal function and LFTs every 2 weeks until on stable dose for 6 weeks
218
methotrexate when the dose is stable
Monthly FBC, renal function and LFTs for 3 months
| Maintenance
219
methotrexate maintenance monitoring
FBC, renal function and LFTs at least every 12 weeks
