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Musculoskeletal Block > Arthritis and some myopathies > Flashcards

Arthritis and some myopathies Flashcards

1
Q

Define Neuromyotonia

A

A autoimmune disease involving antibodies which act against K+ ion channels. It results in hyperexcitability and therefore prolonged skeletal muscle contraction.

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2
Q

Identify two anticonvulsant treatments of Myotonia

A

Carbamazapine, Phenytoin

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3
Q

Lambert Eaton Myasthenic Syndrome (LEMS) is associated with what condition?

A

Small cell bronchial carcinoma

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4
Q

LEMS is associated with the defective release of what neurotransmitter?

A

ACh

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5
Q

LEMS can have autoimmune causes- Identify which channels are effected in this case

A

Ca2+ channels

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6
Q

Identify two types of drug used in the treatment of LEMS.

A

anticholinesterases

potassium channel blockers

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7
Q

Identify the cardinal sign of LEMS.

A

proximal muscle weakness with some absent tendon reflexes

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8
Q

identify the cardinal signs of Myasthenia gravis

A

weakness and fatigability in proximal limbs, ocular and bulbar muscles

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9
Q

What is targeted by autoantibodies in the autoimmune disorder Myasthenia Gravis

A

ACh receptor protein

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10
Q

Identify two types of drugs used to treat MG and an example of each

A

anticholinesterases- Pyridostigmine, edrophonium

Immunosuppressants- azathioprine

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11
Q

What bacteria produces Botulinum toxin? How does it effect ACh release?

A

Clostridium Botulinum

irreversibly inhibits ACh release

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12
Q

How do curare like compounds effect the amplitude of epp?

A

They reduce it below the threshold for an AP by being competitive antagonists to AChRs

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13
Q

10% of myasthenia gravis is caused by ____ ______ while 90% is idiopathic

A

thymic tumours

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14
Q

Describe the pathophysiology of myasthenia gravis

A

CD4+ T cells activated by AChRs expressed on thymic cells leading to autoreactive B cell stimulation thus the generation of auto-IgG antibodies for AChRs. AChRs are thus destroyed by the antibodies. The muscle end plate also becomes damaged

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15
Q

Identify the two main tests for Myasthenia Gravis

A

Auto-IgG antibodies in the serum

repetitive nerve stimulation- the responses gradually decrease

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16
Q

90% of osteomyelitis is caused by what pathogen?

A

Staphlococcus but also salmonella and H. Influenzae

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17
Q

Osteomyelitis occurs due to ____________ spread to the vascular ___________.

A

haematogenous

metaphysis

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18
Q

identify two of the conditions in which setting osteomyelitis is found

A

type 2 diabetes

Chronic skin ulceration ( from venous insufficiency)

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19
Q

_____________ osteomyelitis occurs due to haematogenous spread from the lungs/the GI tract. The __________ are often involved and may collapse and form abscesses

A

haematogenous

vertebrae

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20
Q

identify four symptoms of osteomyelitis

A

localized bone pain, fever, tenderness, erythema

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21
Q

which organism is the main cause of septic arthritis?

A

Staph. Aureus

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22
Q

in young/previously healthy patients identify how septic arthritis would present

A

red, hot, erythematous, swollen, agonizing pain, held immobile by muscle spasm.
in elderly/immunosuppressed/RA patients may be more insidious with few systemic symptoms

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23
Q

to investigate septic arthritis you would 1. aspirate the joint/get a _______ culture 2. _________ the joint 3. provide __________ 4. administer IV _________.

A

blood
immobilise
physiotherapy
antibiotics

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24
Q

What is the difference between primary and secondary osteoarthritis?

A

Primary-idiopathic and with old age

Secondary- due to predisposing conditions

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25
Q

Pathogenesis of OA:
Initial ________ _________ damage leading to surface __________ and ulceration. This causes further ________ loss putting more stress on the bones leading to ____________ and cysts. In the worst case __________ would form which are abnormal sclerotic projections of subchondral bone and they are visible on X-rays..

A 
articular cartilage
fibrillation
cartilage
microfractures
osteophytes
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26
Q

explain the effect of inflammatory cytokines on OA pathogenesis.

A

The stimulation of macrophages and T cells by trauma of joints etc leads to the release of pro-inflammatory cytokines resulting in a disturbance to the cartilage turnover rate leading to articular cartilage degeneration.

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27
Q

identify 5 predisposing risk factors for OA

A 
obesity
gender- more common in women
trauma
sport/occupation
genetic predisposition
secondary causes: RA, gout, spondyloarthritis, septic arthritis
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28
Q

Identify 3 symptoms of OA

A

joint pain upon movement and/or weight bearing
functional limitation
short lived morning joint stiffness

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29
Q

identify 5 signs of OA

A 
crepitus
reduced movement
joint effusion
muscle wasting/ bony instability
bone enlargement
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30
Q

Identify the most commonly affected sites of OA

A 
cervical spine
lumbar spine
interphalangeal joints
hip joint
knee joint
ankle
great toe metatarsal
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31
Q

identify 5 possible investigations of OA

A

X-ray- shows progressive disease and is initial test
blood tests
arthroscopy- early injury
aspiration of synovial fluid
MRI-early injury- shows soft tissue involvement

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32
Q

Identify some non-pharmacological treatments of OA

A 
lose weight
physiotherapy
walking aid
hydrotherapy
suitable footwear
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33
Q

Identify the various treatments of OA

A 
paracetamol
topical then oral NSAIDs
capsaicin
opioids last resort
glucocorticoid injections
replacement arthroplasty
resurfacing surgery
34
Q

What are the nodes exhibited in OA of the PIPs and DIPs called

A

PIP- Bouchard’s nodes

DIP- Heberden’s node’s

35
Q

Knee OA is associated with what other deformities?

A

Bakers cyst

Varus/valgus deformities

36
Q

Which joints are commonly affected in the early stages of RA?

A 
MCP
PIP
MTP
wrist
elbows
shoulders
knees
ankles
37
Q

RA is a chronic ____________ rheumatic disease. patients generally develop chronic ____________ polyarthritis and _________ inflammation.

A

inflammatory
symmetrical
systemic

38
Q

what is the most common age of onset of RA?

A

30 to 50but also may present in early childhood (rare) or late old age

39
Q

what are the three main type of inflammatory arthritis?

what characterises inflammatory arthritis

A

RA, spondyloarthritis, crystal arthritis

synovial inflammation

40
Q

What is the main identifying symptom of inflammatory arthritides? What is typically found raised in a blood sample?

A

Pain and stiffness worst in the morning and lasting several hours + improves with activity.
Raised ESR and CRP

41
Q

The presence of certain Haplotypes of __________ _____________ __________ increases susceptibility to RA.

A

Human Leukocyte Antigens

42
Q

Immunology of RA:
Genetic and environmental factors lead to the _____________ of self antigens (ACPA). This is detected by B and T cells. this leads to the triggering of of osteoclasts, _________ and __________ _________ combining to cause joint damage.

A

citrullination
macrophages
synovial fibroblasts

43
Q

What is citrullination?

A

the reaction for converting the amino acid arginine to citrulline.

44
Q

In RA the synovium greatly ___________ causing swelling around joints and tendons and proliferation of the synovium into folds and fronds. _________ of __________ cells occurs. The hyperplastic synovium spreads from joint margins to the _______ surface leading to ________ formation which damages the underlying cartilage by blocking its normal route for _________. angiogenesis also occurs. the proliferation of fibroblasts of the synovium along the course of blood vessels to the epiphysal bone where it causes erosions.

A 
thickens
proliferation
inflammatory
cartilage
pannus
nutrition
45
Q

identify four early symptoms of RA

A

pain and stiffness of joints in morning
monoarthritis- knee/shoulder
carpal tunnel syndrome
sleep disturbance and fatigue

46
Q

Identify the typical signs of early RA

A 
tenosynovitis signs- 
warm, tender, swollen joints
limited movement
muscle wasting
deformities-swan neck, Boutonniere, ulnar deviation
47
Q

Identify two complications of RA

A

septic arthritis

amyloidosis

48
Q

What results in the Boutonniere and swan neck deformity in RA?

A

B- fixed flexion of PIP

SN- fixed hyperextension of PIP

49
Q

identify some non-articular manifestations of RA

A 
tenosynovitis- leads to trigger finger
subcutaneous nodules around joints
osteoporosis
vasculitis
lungs- pleural disease, bronchiectasis, bronchiolitis, interstitial lung disease, nodules
Cardio risk factor
neuropathies e.g. carpal tunnel syndrome
dry mouth and eyes
amyloidosis
anaemia
felty's syndrome- splenomegaly and neutropenia
50
Q

What are the main investigations for RA

A

Blood count- anaemia, ESR and CRP raised
serology- ACPA positive
X-rays, ultrasound, MRI
Aspiration if effusion

51
Q

Identify the three main clinical features of AS.

A

back pain
buttock pain- either one or both. pain and stiffness worst in the morning, relieved by exercise
retention of lumbar lordosis during spinal flexion

52
Q

Which test is used to identify retention of lumbar lordosis during spinal flexion?

A

Schober’s test

53
Q

What are the two main non-spinal complications of AS?

A

costochondritis- anterior chest pain

anterior uveitis

54
Q

identify 3 tests and expected findings for AS.

A

bloods- raised ESR and CRP
Genes- HLA-B27 positive- adds weight but not diagnostic as is common gene
X-ray- bamboo spine- due to fusion of spinal facet joints, sacroiliac joints lose definition due to erosions and sclerosis.

55
Q

Name 5 types of spondyloarthritis

A 
ankylosing spondylitis
psoriatic arthritis
reactive arthritis
enteropathic arthritis
post-dysenteric reactive arthritis
56
Q

Name the 5 possible patterns of psoriatic arthritis

A 
mono/oligoarthritis
spondylitis
symmetrical polyarthritis (like RA)
DIP arthritis- most common, dactylitis is characteristic of condition
Arthritis mutilans
57
Q

What is dactylitis?

A

Where an entire finger or toe is swollen

58
Q

What percentage of psoriasis patients have psoriatic arthritis?

A

10%

59
Q

state three organisms that cause reactive arthritis

A

shigella
ureaplasma
chlamydia

60
Q

what is the typical presentation of reactive arthritis?

A

asymmetrical lower limb arthritis occuring days/weeks after infection

61
Q

identify three causes of the increasing incidence of gout

A

changing diets- high saturated fat and fructose containing drinks
alcohol misuse
co-morbidities that promote hyperuricaemia

62
Q

Gout is more common in ____ than in ____ because serum _____ _____ levels are higher in ____ than in _______.

A 
men
women
uric acid
men
women
63
Q

____ ____ is the product of endogenous and dietary ______ metabolism in humans. The SUA depends on the balance between ______ synthesis and the elimination of _______ by the _______ (66%) and the _________ (33%).

A 
uric acid
purine
purine
urate
kidneys
intestine
64
Q

90% of gout is due to what problem? the remaining 10 % is due to what problem?

A

90- impaired renal excretion

10- increased uric acid production

65
Q

identify the 5 possible presentations of gout

A 
asymptomatic
acute gout- OFTEN REPEATS
chronic interval gout
chronic polyarticular tophaceous gout- RARE
urate renal stone
66
Q

What is the typical presentation of gout?

A

Sudden onset of agonizing pain, swelling, redness, of the first MTP joint (great toe). 25% of cases a different joint

67
Q

Why is the big toe the target of gout?

A

coolest part of body and thus uric acid crystals most likely to form here.

68
Q

the clinical picture/ rapid response to NSAIDS/colchicine is normally diagnostic of gout. what other tests may you do?

A

SUA measured- raised above 600 micromoles/litre
joint fluid microscopy
signs of renal impairment.

69
Q

What 4 drugs can be used in the initial treatment of acute gout?

A

naproxen
diclofenac
colchicine
corticosteroids

70
Q

What dietary advice is given for gout?

A

avoid alcohol, carbonated drinks

reduce total calorie/cholesterol intake

71
Q

in Gout patients what is the main drug used to reduce and maintain SUA levels below 360 micro-moles/litre?

A

Allopurinol

72
Q

What is allopurinol?

A

A xanthine oxidase inhibitor used to reduce SUA levels of gout patients

73
Q

What drug is used in patients who cannot tolerate allopurinol?

A

febuxostat

74
Q

What characterises chronic tophaceous gout?

A

Sodium urate deposits in skin and around joints (tophi) on ear, fingers and achilles tendon. Also chronic joint pain

75
Q

Tophaceous gout is associated with _____ ___________ and/or the long-term use of _________.

A

renal impairment

diuretics

76
Q

when is pegloticase used in gout patients?

A

if patients are undergoing chemotherapy

if patients suffer from refractory tophaceous gout

77
Q

What does CPPD stand for? what has it also been named?

A

Calcium Pyrophosphate dihydrate deposition arthropathy

pseudogout

78
Q

The presence of Calcium pyrophosphate dehydrate crystals in hyaline and fibrocartilage is the most common cause of ________ ______________.

A

cartilage calcification

79
Q

List the three most common forms of inflammatory arthritis

A

Rheumatoid arthritis
ankylosing spondylitis
CPPD

80
Q

In which two ways is a diagnosis of CPPD deduced?

A

CPP crystals in joint fluid

cartilage calcification on xray

81
Q

Treatments for symptom control in CPPD is similar to that in OA and gout. What two different treatments may be shown?

A

aspiration of joint- pain relief

injection of corticosteroid

82
Q

Apart from sodium urate and calcium pyrophosphate dehydrate what other crystals result in arthropathy?

A

Basic Calcium Phosphate

Musculoskeletal Block (10 decks)

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