Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Musculoskeletal Block > Arthritis and some myopathies > Flashcards

Arthritis and some myopathies Flashcards

(82 cards)

Start Studying
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Identify two anticonvulsant treatments of Myotonia

A

Carbamazapine, Phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

Small cell bronchial carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

LEMS is associated with the defective release of what neurotransmitter?

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Ca2+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

anticholinesterases

potassium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Identify the cardinal sign of LEMS.

A

proximal muscle weakness with some absent tendon reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

identify the cardinal signs of Myasthenia gravis

A

weakness and fatigability in proximal limbs, ocular and bulbar muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is targeted by autoantibodies in the autoimmune disorder Myasthenia Gravis

A

ACh receptor protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

anticholinesterases- Pyridostigmine, edrophonium

Immunosuppressants- azathioprine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Clostridium Botulinum

irreversibly inhibits ACh release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

thymic tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Identify the two main tests for Myasthenia Gravis

A

Auto-IgG antibodies in the serum

repetitive nerve stimulation- the responses gradually decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

90% of osteomyelitis is caused by what pathogen?

A

Staphlococcus but also salmonella and H. Influenzae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Osteomyelitis occurs due to ____________ spread to the vascular ___________.

A

haematogenous

metaphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

identify two of the conditions in which setting osteomyelitis is found

A

type 2 diabetes

Chronic skin ulceration ( from venous insufficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

identify four symptoms of osteomyelitis

A

localized bone pain, fever, tenderness, erythema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which organism is the main cause of septic arthritis?

A

Staph. Aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the difference between primary and secondary osteoarthritis?

A

Primary-idiopathic and with old age

Secondary- due to predisposing conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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..
``` articular cartilage fibrillation cartilage microfractures osteophytes ```
26
explain the effect of inflammatory cytokines on OA pathogenesis.
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.
27
identify 5 predisposing risk factors for OA
``` obesity gender- more common in women trauma sport/occupation genetic predisposition secondary causes: RA, gout, spondyloarthritis, septic arthritis ```
28
Identify 3 symptoms of OA
joint pain upon movement and/or weight bearing functional limitation short lived morning joint stiffness
29
identify 5 signs of OA
``` crepitus reduced movement joint effusion muscle wasting/ bony instability bone enlargement ```
30
Identify the most commonly affected sites of OA
``` cervical spine lumbar spine interphalangeal joints hip joint knee joint ankle great toe metatarsal ```
31
identify 5 possible investigations of OA
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
32
Identify some non-pharmacological treatments of OA
``` lose weight physiotherapy walking aid hydrotherapy suitable footwear ```
33
Identify the various treatments of OA
``` paracetamol topical then oral NSAIDs capsaicin opioids last resort glucocorticoid injections replacement arthroplasty resurfacing surgery ```
34
What are the nodes exhibited in OA of the PIPs and DIPs called
PIP- Bouchard's nodes | DIP- Heberden's node's
35
Knee OA is associated with what other deformities?
Bakers cyst | Varus/valgus deformities
36
Which joints are commonly affected in the early stages of RA?
``` MCP PIP MTP wrist elbows shoulders knees ankles ```
37
RA is a chronic ____________ rheumatic disease. patients generally develop chronic ____________ polyarthritis and _________ inflammation.
inflammatory symmetrical systemic
38
what is the most common age of onset of RA?
30 to 50but also may present in early childhood (rare) or late old age
39
what are the three main type of inflammatory arthritis? | what characterises inflammatory arthritis
RA, spondyloarthritis, crystal arthritis | synovial inflammation
40
What is the main identifying symptom of inflammatory arthritides? What is typically found raised in a blood sample?
Pain and stiffness worst in the morning and lasting several hours + improves with activity. Raised ESR and CRP
41
The presence of certain Haplotypes of __________ _____________ __________ increases susceptibility to RA.
Human Leukocyte Antigens
42
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.
citrullination macrophages synovial fibroblasts
43
What is citrullination?
the reaction for converting the amino acid arginine to citrulline.
44
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.
``` thickens proliferation inflammatory cartilage pannus nutrition ```
45
identify four early symptoms of RA
pain and stiffness of joints in morning monoarthritis- knee/shoulder carpal tunnel syndrome sleep disturbance and fatigue
46
Identify the typical signs of early RA
``` tenosynovitis signs- warm, tender, swollen joints limited movement muscle wasting deformities-swan neck, Boutonniere, ulnar deviation ```
47
Identify two complications of RA
septic arthritis | amyloidosis
48
What results in the Boutonniere and swan neck deformity in RA?
B- fixed flexion of PIP | SN- fixed hyperextension of PIP
49
identify some non-articular manifestations of RA
``` 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
What are the main investigations for RA
Blood count- anaemia, ESR and CRP raised serology- ACPA positive X-rays, ultrasound, MRI Aspiration if effusion
51
Identify the three main clinical features of AS.
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
Which test is used to identify retention of lumbar lordosis during spinal flexion?
Schober's test
53
What are the two main non-spinal complications of AS?
costochondritis- anterior chest pain | anterior uveitis
54
identify 3 tests and expected findings for AS.
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
Name 5 types of spondyloarthritis
``` ankylosing spondylitis psoriatic arthritis reactive arthritis enteropathic arthritis post-dysenteric reactive arthritis ```
56
Name the 5 possible patterns of psoriatic arthritis
``` mono/oligoarthritis spondylitis symmetrical polyarthritis (like RA) DIP arthritis- most common, dactylitis is characteristic of condition Arthritis mutilans ```
57
What is dactylitis?
Where an entire finger or toe is swollen
58
What percentage of psoriasis patients have psoriatic arthritis?
10%
59
state three organisms that cause reactive arthritis
shigella ureaplasma chlamydia
60
what is the typical presentation of reactive arthritis?
asymmetrical lower limb arthritis occuring days/weeks after infection
61
identify three causes of the increasing incidence of gout
changing diets- high saturated fat and fructose containing drinks alcohol misuse co-morbidities that promote hyperuricaemia
62
Gout is more common in ____ than in ____ because serum _____ _____ levels are higher in ____ than in _______.
``` men women uric acid men women ```
63
____ ____ 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%).
``` uric acid purine purine urate kidneys intestine ```
64
90% of gout is due to what problem? the remaining 10 % is due to what problem?
90- impaired renal excretion | 10- increased uric acid production
65
identify the 5 possible presentations of gout
``` asymptomatic acute gout- OFTEN REPEATS chronic interval gout chronic polyarticular tophaceous gout- RARE urate renal stone ```
66
What is the typical presentation of gout?
Sudden onset of agonizing pain, swelling, redness, of the first MTP joint (great toe). 25% of cases a different joint
67
Why is the big toe the target of gout?
coolest part of body and thus uric acid crystals most likely to form here.
68
the clinical picture/ rapid response to NSAIDS/colchicine is normally diagnostic of gout. what other tests may you do?
SUA measured- raised above 600 micromoles/litre joint fluid microscopy signs of renal impairment.
69
What 4 drugs can be used in the initial treatment of acute gout?
naproxen diclofenac colchicine corticosteroids
70
What dietary advice is given for gout?
avoid alcohol, carbonated drinks | reduce total calorie/cholesterol intake
71
in Gout patients what is the main drug used to reduce and maintain SUA levels below 360 micro-moles/litre?
Allopurinol
72
What is allopurinol?
A xanthine oxidase inhibitor used to reduce SUA levels of gout patients
73
What drug is used in patients who cannot tolerate allopurinol?
febuxostat
74
What characterises chronic tophaceous gout?
Sodium urate deposits in skin and around joints (tophi) on ear, fingers and achilles tendon. Also chronic joint pain
75
Tophaceous gout is associated with _____ ___________ and/or the long-term use of _________.
renal impairment | diuretics
76
when is pegloticase used in gout patients?
if patients are undergoing chemotherapy | if patients suffer from refractory tophaceous gout
77
What does CPPD stand for? what has it also been named?
Calcium Pyrophosphate dihydrate deposition arthropathy | pseudogout
78
The presence of Calcium pyrophosphate dehydrate crystals in hyaline and fibrocartilage is the most common cause of ________ ______________.
cartilage calcification
79
List the three most common forms of inflammatory arthritis
Rheumatoid arthritis ankylosing spondylitis CPPD
80
In which two ways is a diagnosis of CPPD deduced?
CPP crystals in joint fluid | cartilage calcification on xray
81
Treatments for symptom control in CPPD is similar to that in OA and gout. What two different treatments may be shown?
aspiration of joint- pain relief | injection of corticosteroid
82
Apart from sodium urate and calcium pyrophosphate dehydrate what other crystals result in arthropathy?
Basic Calcium Phosphate

Musculoskeletal Block (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions