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2021 Pre-registration > Chapter 10: Musculoskeletal system > Flashcards

Chapter 10: Musculoskeletal system Flashcards

1
Q

What happens in arthritis?

A

The immune system attacks the synovial fluid which results in pain, inflammation and stiffness

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2
Q

Three different types of arthritis?

A

Osteoarthritis
Rheumatoid arthiritis
Spondyloarthritis

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3
Q

What happens in osteoarthritis?

A

cartilage degenerates faster than chondrocytes can repair - essentially wear and tear

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4
Q

Signs and symptoms of osteoarthritis?

A 
Pain
Inflammation
'bony' - bones pop out
Stiffness
Crackling of bones
Tender
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5
Q

Lifestyle measures to help OA?

A

Reduce weight
exercise
reduce strain on joints
suitable footwear

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6
Q

OA commonly affects…

A

More in women than men

- affects knees, hands, hips

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7
Q

Treatment for OA?

A

1) paracetamol
2) NSAIDS / capsaicin 0.0025% cream QDS
3) Opioids

Note: if patient is on aspirin 75mg, give opioids before NSAIDs

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8
Q

What is not recommended for OA treatment?

A

Rubefacients and glucosamine - only for symptomatic relief

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9
Q

Which injections can be given intra-articularly in OA?

A
  • corticosteroid injections: temp benefit especially if there is also tissue inflammation
  • sodium hyaluranote injections in synovial fluid, reduces pain in 1-6mths but increases risk of knee inflammation
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10
Q

Methotrexate interactions?

A

1) Antivirals e.g. aciclovir/alcohol/antifungals/ceftriaxone/carbamazepine: hepatoxicity
2) Aciclovir/trimethoprim/ciclosporin/NSAIDs - nephrotoxic
3) penicillins/quinolones - increased toxicity
4) Bleomycin - myelosuppression and thromboembolism risk
5) Aminophylline: decreased clearance and increased levels
6) live vaccine e.g. yellow fever - life threatening infections

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11
Q

Compare OA and RA

A

OA is generally not inflammatory. OA is not relieved by exercise like RA - symptoms could worsen

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12
Q

What is RA?

A

Chronic inflammatory disease that causes persistent inflammation (mainly of small joints of hands/feet)

  • immune system attacks synovial fluid
  • pain and prolonged stiffness that is even worse at rest
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13
Q

Why is it critical to identify and treat RA early?

A

It can progress to other organs such as lungs, heart and eyes

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14
Q

Symptoms of RA?

A

Pain (particularly at rest often relieved with exercise), stiffness, inflammation
Fatigue
Muscle ache
weight loss

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15
Q

Pain from an inflammatory condition is _____

A

Worse at rest and better with exercise. Pain from a mechanical problem e.g. OA - is better with rest and worse with activity

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16
Q

Refer all patients suspected with ________ due to risks of RA progession

A

persistent inflammation

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17
Q

Diagnosis of RA includes:

A
  • observation of inflammation (particularly hands)
  • inflammatory markers e.g. CRP and ESR
  • duration around 6 weeks of persistent inflammation
  • Rheumatoid factor/anti-CCP
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18
Q

Treatment for RA (based on NICE)?

A

1) DMARDS: methotrexate, leflunomaide, sulfasalazine (take 2-3mths to work) so bridge with steroids
2) Mild DMARD: hydroxychloroquine - visual acuity and nightmares
3) Monoclonal antibodies/TNF-a inhibitors: adalimumab, etanercept, tocilizumab, infliximab
4) surgery
5) pain-relief: NSAIDS/cox-2 inhibitors but GI adv effects so co-prescribe PPI if suitable

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19
Q

What side effects are particularly prominent in those with monoclonal antibodies?

A

Immunosuppression - increased risk of infections

Can reactivate dormant infections such as TB/Hep B

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20
Q

Caution with hydroxochloroquine?

A

Monitor retnipathy - if long term tx do a baseline eye test and another within 6-12mths

> 5yrs tx: annual eye test
<5yrs + risk factors e.g. tamoxifen, impaired renal func, dose >5mg/kg/day: do annual eye test

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21
Q

Hydroxychloroquine and overdose.

A

Very hard to treat. Presents with arrhythmias and convulsions

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22
Q

What can be used for juvenile idiopathic arthritis?

A

methotrexate

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23
Q

MHRA warning for tocilizumab used in RA?

A

Serious liver injury, may require liver transplantation

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24
Q

Notable side-effects of methotrexate?

A
  • Mouth ulcers and mucositis
  • Liver toxicity
  • Pulmonary fibrosis
  • Bone marrow suppression and leukopenia (low white blood cells)
  • It is teratogenic (harmful to pregnancy) and needs to be avoided prior to conception in mothers and fathers
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25
Q

Notable side-effects of leflunomide?

A

Mouth ulcers and mucositis
Increased blood pressure
Rashes
Peripheral neuropathy
Liver toxicity
Bone marrow suppression and leukopenia (low white blood cells)
It is teratogenic (harmful to pregnancy) and needs to be avoided prior to conception in mothers and fathers

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26
Q

Notable side-effects of sulfasalazine?

A

Temporary male infertility (reduced sperm count)

Bone marrow suppression

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27
Q

Notable side-effects of hydroxychloroquine?

A

Nightmares
Reduced visual acuity (macular toxicity)
Liver toxicity
Skin pigmentation

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28
Q

Notable side-effects of Anti-TNF drugs?

A

vulnerability to severe infections and sepsis

Reactivation of TB and hepatitis B

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29
Q

Notable side-effects of rituximab?

A 
Vulnerability to severe infections and sepsis
Night sweats
Thrombocytopenia (low platelets)
Peripheral neuropathy
Liver and lung toxicity
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30
Q

Key SE of RA treatmenet?

A

Methotrexate: pulmonary fibrosis
Leflunomide: Hypertension and peripheral neuropathy
Sulfasalazine: Male infertility (reduces sperm count)
Hydroxychloroquine: Nightmares and reduced visual acuity
Anti-TNF medications: Reactivation of TB or hepatitis B
Rituximab: Night sweats and thrombocytopenia

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31
Q

What is the antidote for methotrexate?

A

Folinic acid

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32
Q

Talk about methotrexate dosing.

A

Once weekly (same day every week)

Take folic acid 24-48hrs after day of methotrexateto reduce side-effects and toxicity

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33
Q

Woman of child-bearing age is given methotrexate for RA, what do you advise?

A

Effective contraception during and 6months after (even if a man) - is teratogenic

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34
Q

What OTC remedies should be avoided with methotrexate?

A

Nsaids/aspirin: risk of blood dysrasias

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35
Q

What medication can increase the risk of MTX toxicity?

A

Theo/Amino-phylline, quinolones, penicillin

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36
Q

Which vaccine should be avoided with MTX?

A

Live vaccines e.g. yellow fever as increases risk of serious infections

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37
Q

Which group of NSAIDS pose the lowest risk of GI SE/Toxicity?

A

Coxibs

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38
Q

How long does it take NSAIDS to work?

A

pain relief: 1st dose
analgesia: 1 week
anti-inflammatory: 3 weeks

^if inapp response, choose another NSAID

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39
Q

What NSAIDS have the highest risk of GI toxicity?

A

ketoprofen / piroxicam

medium: diclofenac and naproxen

40
Q

What NSAIDS have the lowest risk of GI toxicity?

A

ibuprofen

41
Q

Above what daily dose of NSAIDS is there an increased risk of CVS effects e.g. risk of MI/stroke/HF

A

> 2.4g

42
Q

Side-effects of NSAIDs?

A

bronchospasm - avoid is asthma
hypersensitivity - NSAIDS/aspirin previous allergies
photosensitivity - use SPF esp with ketoprofen
nephrotoxic: caution in renal imp and avoid during sick days

fluid and sodium retention so avoid in heart failure

43
Q

How would you prevent GI SE of NSAIDS?

A

Add PPI
Take with food
not for anyone who is actively bleeding

44
Q

Can NSAIDS be used in pregnancy?

A

No. Especially not in 3rd trimester due to induction of labour and pulmonary hypertension

45
Q

Interactions with NSAIDs?

A

1) Aki: ace/ard/tacrolimus/ciclosporin/diuretics
2) bleeding - warfarin, DOAC, heparin
3) reduced renal function
4) hyperkalaemia: ace/arb/ald antag/potassium sparing
5) convulsions: quinolones

46
Q

First line treatment for acute attacks of gout?

A

1) NSAIDS - diclofenac, eterocoxib, indometacin, ketoprofen, naproxen

47
Q

Alternative treatment for acute gout attacks if NSAIDs are not tolerated?

A

Alt: Colchicine (max 12mg per course - due to risk of toxicity with higher doses)

48
Q

Benefits of using colchicine?

A

Can be used in heart failure (as doesnt cause fluid retention) and in those using anti-coagulants

49
Q

In those who cannot tolerate NSAIDS and colchicine for gout, what is an option?

A

Oral or parenteral corticosteroids

50
Q

Long-term treatment for gout should be initiated after ______

A

1-2 weeks of the gout as it can trigger an attack

51
Q

Long-term gout treatment is controlled by ______

A

NSAIDS (if tolerated) and colchicine for a minimum of one month

52
Q

How would prophylactic treatment for gout be managed if a patient has an attack whilst on preventative treatment?

A

Continue with therapy and treat attack separately

53
Q

Is allopurinol suitable in those with renal impairment?

A

Yes

54
Q

Particular SE of allopurinol?

A

Rash

55
Q

Can aspirin be used for gout?

A

No

56
Q

What medication apart from colchicine can be used for treatment of gout?

A

Febuxostat

Rasburicase - mainly in haem/cancer pts

57
Q

With enzyme ______ the dose of colchicine should be reduced by _________

A

inhibitors (sickfaces.com)

Reduce dose by 50-75% (75% if potent)

58
Q

Which drug requires a dose reduction to 1/4 with allopurinol?

A

Azathioprine

59
Q

Max dose of allopurinol daily?

A

100mg

60
Q

CALS with allopurinol?

A

Do not stop taking unless doctor tells you to stop

Take with food/after meal

Take with a full glass of water

61
Q

Ensure adequate _____ whilst on gout medication

A

adequate fluid intake

62
Q

Febuxostat MHRA warnings?

A
  • not for those with a hx of cardiac disease as increased risk of CVS death
  • serious hypersensitivity reactions - SJS
63
Q

After starting Febuxostat how long should prophylactic NSAIDS or colchine be continued for and why?

A

6 months to prevent gout attacks

64
Q

Indication for rasburicase?

A

prophylaxis and treatment for hyperuricaemia before and after starting chemotherapy - v.expensive 200-300 pounds

65
Q

Rasburicase contra-indication?

A

G6PD deficiency

66
Q

Rasburicase SE?

A

Monitor for hypersensitivity

67
Q

Rasburicase storage requirement and strength?

A

Keep in fridge
1.5mg/5ml
Dose 200mg/kg upto 7 days and then go back down to allopurinol or febuxostat

68
Q

What is myasthenia gravis?

A

Muscle weakness that occurs due to ache receptor blockade by ach antibodies at neuromuscular junction (autoimmune) and linked to thymoma (thymus cancer)

Increased activity = less effective stimulation

69
Q

Symptoms of myasthenia gravis?

A

diplopia
droopy eyes
unilateral arm weakness

tests: ct/mri of thymus gland and ach-receptor antibodies

70
Q

1st line for myasthenia gravis?

A

anticholinesterase inhibitors e.g. neostigmine (effect for 4hrs max 180mg daily) and pyridostigmine (slow but longer MOA) - STOPP criteria
(increase ach levels by inhibiting the enzyme that breaks down ach - allowing for more receptor occupancy)

71
Q

2nd line for m.gravis?

A

Corticosteroids (suppress antibody production) and if want to wean then use immunosuppressants like azathioprine

72
Q

Which surgery can relieve M.gravis even if there is no tumour?

A

Thymectomy - linked to this gland

73
Q

If someone with myasthenia gravis had a respiratory infection, what would you be concerned about?

A

Can trigger a myasthenic crisis where lung muscles are unable to contract effectively so pt may need o2 and/or bipap

74
Q

AntiCHOLINESTERASE, muscuranic side-effects?

A

Dribbling
Increases GI motility - diarrhoea
bradycardia - KEY esp if HR <60bpm
increased sweating

75
Q

Baclofen can be used in muscle spasms. What are the major side-effects?

A

Sedation
Muscular hypotonia
- as depresses CNS

Hence dantrolene is drug of choice as acts directly on skeletal muscle

76
Q

Signs of overdose for acetylcholinesterase? Why is this a concern

A 
Ex. bradycardia
Ex. drooling
Diarrhoea
Heart block
arrhythmias 
hypotension
agitation
ex. dreaming
weakness
( and can lead to paralysis )
77
Q

What is used for nocturnal leg cramps?

A

Quinine but not routinely used unless it causes disruption to sleep as toxic - helps around 25% patients

78
Q

How often should quinine treatment be reviewed to ensure it is still suitable and prevent toxicity?

A

every 3 months

79
Q

How long could quinine take to work?

A

4 weeks

80
Q

What is sciatica?

A

neuropathic pain due to prolonged compression of lumbosacral nerve - can undergo spinal decompression

81
Q

Selective inhibition of _______ = less GI SE

A

COX 2

82
Q

Which NSAID can be given OD?

A

piroxicam as long MOA

83
Q

Which NSAIDS increase the risk of MI/STROKE?

A

Cox-2 selectives e.g. celecoxib but reduced GI SE

84
Q

NSAID can cause deterioration of renal function particularly in those with an egfr>…

A

EGFR<50ml/min

85
Q

Which non-selective NSAID has the lowest risk of GI SE?

A

ibuprofen (not high dose)

86
Q

Ways to reduce symptoms like dyspepsia in those taking NSAIDS?

A

With milk/food

Enteric-coated formulation

87
Q

Which lifestyle habit interacts with NSAIDS and what is the consequence?

A

Alcohol (not moderate) but those that heavy drink/alcohol dependance = increased risk of GI haemmorhage and AKI

88
Q

With which drug should the dose of celecoxib be halved?

A

Fluconazole

89
Q

Do NSAIDS affect fertility?

A

long term use = reduced fertility (stops when treatment stops)

90
Q

Counselling points for topical NSAIDS?

A

photosensitivty
wash hands after use
excess usage can cause systemic SE

91
Q

NSAID Poisoning treatment?

A

Activated charcoal

92
Q

Signs of NSAID toxicity?

A

tinnitus
epigastric pain
n/v

93
Q

Ibuprofen suspension comes in what strength?

A

100mg/5ml

94
Q

Ibuprofen child dosing:

A

1-2months: 5mg/kg TDS/QDS

3-5months: 2.5ml TDS

6-11months: 2.5ml TDS/QDS

1yrs to 3yrs: 5ml TDS

4yrs to 6yrs: 7.5ml TDS

7yrs to 9yrs: 10ml TDS

10-11yrs: 10-15ml TDS

12+: 15-20ml TDS/QDS

95
Q

Mefenamic acid in overdose can cause _____

A

convulsions

96
Q

Intra-articular steroid injections can be given for RA. What is the maximum number of times this can be given in a year?

A

4 times

97
Q

Significant SE of hydrocortisone intra articular?

A

Myocardial rupture (if used after recent mi)

2021 Pre-registration (15 decks)

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