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Hayders Phase 2A > MSK > Flashcards

MSK Flashcards

1
Q

prevalence of rheumatoid arthritis

A

1% prevalence

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2
Q

Risk factors and age affected of RA

A

40 - 60 YO
Female
family history
other autoimmune conditions

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3
Q

what is rheumatoid arthritis

A

chronic autoimmune inflammatory conditon

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4
Q

Typical presenation of RA

A

Slow onset
Symmetrical peripheral polyarthropathy
pain and stiffness in small joints, MetaCarpoPhalangeal MCP, metatarsophalangeal MTP, distal and proximal interphalangeal, DIP, PIP
pain is significantly worst in the morning and gets better throughout day, worst after rest.
knees hips elbows shoulders, less common
responds to NSAIDS

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5
Q

signs of RA

A

bony swelling. swelling in synovium of dip pip MCP MTP, often symmetrical
tenosynovitis (tendon stiffness) or bursitis (inflammation of bursa)
Rheumatoid nodules- nodules under skin, near joints. painless
Ulnar deviation
boutonniere
swan neck deformity
muscle wasting

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6
Q

X ray signs of RA

A 
soft tissue swelling
periarticular bone thinning, osteopenia 
joint space narrowing 
bony erosions
JOES
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7
Q

histological finding of RA

A

Pannus

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8
Q

extra articular effects / complications of RA

A 
Pericarditis
pleural effusion
pericardial effusion 
nerve entrapment 
dry eyes 
anemia 
septic arthritis
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9
Q

diagnosis and investigations of RA

A

Serology- Anti CCP diagnostic, also find rheumatoid factor and anti nuclear antibodies
Bloods- ESR CRP and anemia
x ray

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10
Q

diagnostic criteria of RA

A

Small joint involvement
serology present
increase in acute phase proteins, and inflammatory markers, ESR, CRP
chronic duration

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11
Q

early signs of RA

A

fatigue malaise swelling,

pain of inflammatory nature

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12
Q

management for RA

A

first start with symptomatic management of pain - NSAIDS
once pain managed start on DMARD within 3 months
treat flare ups of RA
surgery for entrapment complications
monitor complications
physio

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13
Q

How to treat RA flare ups

A

steroids, Intra Articular methylprednisolone or Dexamethasone.

or oral prednisolone not for long term use

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14
Q

What is a DMARD

A

Disease modifying antirheumatic drugs, steroid sparing drugs, cytokine inhibition to reduce inflammation Methotrexate
used to induce remission then dropped down to maintain remission
sulfasalazine, hydroxychloroquine

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15
Q

other than methotrexate, what other DMARDs are available

A

sulfasalazine

hydoxychoroquines

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16
Q

what is used to treat RA after DMARDs,

A

biological agents
B cell depletion rituximab
TNF alpha inhibition - infliximab

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17
Q

Further management and managing complications of RA

A

DEXA scan for Osteoporosis
control CVA risk, since having constantly increased CRP can form atheromas
refer to physio - manage activities of daily living
joint hip replacement

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18
Q

osteoarthritis prevalence

A

commonest joint disorder
50% of those over 65 are symptomatic
80% show X ray signs

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19
Q

osteoarthritis risk factor

A 
Age biggest one
trauma
obesity 
occupation 
female 
genetic predisposition 
previous joint involvement or arthropathy
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20
Q

pathophysiology of OA

A

Loss of cartilage
disordered bone repair
has an inflammatory component

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21
Q

clinical features of OA

A

hip and knee most commonly effected
not always symptomatic but may show on X ray
can have flare ups with increased CRP and ESR

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22
Q

symptoms of OA

A

Joint pain is presenting complaint, hips or knees. gets worst as use throughout day. worst in mornings and after rest
doesn’t get better with NSAIDS
joint stiffness
loss of function

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23
Q

signs of OA

A 
joint instability 
crepitus 
alteration of gait
boney swelling (effusion, synovitis)
joint tenderness
 cracking
limited range of movement
Heberden's nodes - DIP swelling 
Bouchard's nodes - pip swelling
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24
Q

Investigations for OA

A 
Serology ANA RF Anti CCP -VE
 ESR CRP normal
CRP may be elevated
X Ray of OA 
aspiration of fluid if its present
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25
Q

X Ray finding of OA

A 
LOSS
loss of joint space 
osteophytes 
subchondral cyst
subchondral sclerosis
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26
Q

Conservative Management of OA

A

Conservative, education, weight loss, physio and exercise. walking aids. insoles hot or cold packs

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27
Q

pharmacological management for OA

A

paracetamol and topical NSAIDS, or gel.
if painful joint effusion- corticosteroid injections
subtype inflammatory RA- DMARDs

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28
Q

Surgical management of OA

A

arthroplasty, knee or hip replacemnt

arthroscopy for loose body fragments

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29
Q

what are the 2 types of Crystal arthropathy and their composition

A

Gout: uric acid
Pseudogout: Calcium phosphate

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30
Q

presentation of acute gout

A

severely inflamed , Red Hot Swollen Painful,
monoarthropathy,
usually MTP of big toe

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31
Q

Investigation of gout

A

Joint fluid aspirate is gold standard.
polarised light microscopy
need to exclude septic arthritis

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32
Q

what do the results of polarised light microscopy indicated

A

-Ve birefringent needle - uric acid

weakly +ve birefringent needles - pseudogout, Calcium phosphate

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33
Q

what can cause gout attack

A

high uric acid, consumption of high purine food. dehydration or diuretics
suddenly stopping medication
alcohol shellfish
hereditary

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34
Q

treatment of acute gout

A

NSAIDs, or colchicine

can use intraocular steroid injections

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35
Q

prevention of gout attack

treatment of chronic gout

A 
educations on what can precipitate gout and how to avoid it 
avoid low dose aspire 
avoid alcohol, long fast, 
loss weight 
xanthine oxidase inhibitor-allopurinol
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36
Q

treatment of chronic gout

A 
educations on what can precipitate gout and how to avoid it 
avoid low dose aspire 
avoid alcohol, long fast, 
loss weight 
xanthine oxidase inhibitor-allopurinol 
use NSAIDs or Colchicine
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37
Q

X ray changes on chronic gout

A

Punched out cortex

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38
Q

calcium pyrophosphate deposition / pseudogout features

presentation, where and what triggers it

A

similar to gout presentation but more common in larger joints like- MCP, Wrist knee ankle
triggered by trauma or unprovoked

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39
Q

calcium pyrophosphate deposition / pseudogout management

A

NSAIDs or colchicine
intra-articular steroid injection
joint aspirate

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40
Q

association of pseudogout CPPD

A

Haemochromatosis, hyperparathyroidism

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41
Q

associations for gout

A

DM, hypertension, heart or renal diseae

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42
Q

features of chronic gout

A

excess uric acid deposition throughout forming tophi

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43
Q

Prevalence of gout

A

commonest cause of arthritis in men <40 YO

1%

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44
Q

what type of collagen is in cartilage

A

type 2 collagen

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45
Q

osteoporosis pathophysiology

A

Systemic skeletal disease caused by reduced bone mineral density. osteoclasts breakdown bone
osteoblasts build up bone
osteoporosis is increased osteoclasts and reduced osteoblasts

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46
Q

causes risk factors and associations for osteoporosis

A

Age, increased time the bone remodeling isn’t as well
post menopause, oestrogen Inhibits osteoclast activity
long term glucocorticoids- increase bone resorption
cushing’s disease
hyperparathyroidism
Hyperthyroidism
Inflammatory conditions - RA, IBD, due to increased cytokines and inflammation causing increased resorption
reduced skeletal loading, bed bound for ages
family history

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47
Q

first sign/ symptom of osteoporosis

A 
usually the fracture, 
vertebre - not due to trauma, picking something up 
hip
knee
in order of likeness
writs ankle etc
48
Q

Investigations for osteoporosis

A

DEXA scan - dual energy X Ray absorption - mesures bome mineral denisty and generates a T Score

49
Q

Diagnostic criteria for osteoporosis

A

T-Score> - 1 normal
T-Score= -1 - -2.5 osteopenia
T-Score

50
Q

investigation used to assess likelihood of sustaining a hip fracture in next 10 years

A

FRAX

51
Q

Treatment conservative for Osteoporosis

A 
physio exercises (weight bearing), walking aids prevent falls. 
stop smoking and reduce alcohol less than 3 units a week.
52
Q

Pharmacological treatment for Osteoporosis

A

Vitamin D and calcium ADCAL.
antiresorptives- Bisphosphonates, reduce osteoclast activity.
Alendronic acid

potentially HRT

anabolic - PTH analogues teriparatide

53
Q

what are the side effects of HRT

A

increased risk of breast cancer, stroke and CV disease

54
Q

what is polymyalgia rheumatica

A

Large cell vasculatis, causing sudden onset of severe pain in shoulders and neck stiffness. worst in morning and comes from 30 mintes to hours. usually patients over 50
CRP and ESR elevated

55
Q

what does “sudden onset of sevre pain in shoulders and neck stiffness, lasting 30 mins to hours in over 50 YO patients suggest

A

Polymyalgia rheumatica

56
Q

what is giant cell artheritis and what does it affect

A

LArge cell vasculitis of inflammatory granulomatus arteries affecting aorta but also Extra cranial branches of carotid arteries.

57
Q

Epidemiology of GCA

A

assosiated with PMR in 50%. always over 55

commonly in women

58
Q

Symptoms of GCA

A

Jaw claudication
facial pain
headache
WORST symptom- temporary blindness or visual loss in one eye

59
Q

signs of GCA

A

Temporal artery tenderness

scalp tenderness

60
Q

investigations of GCA

A

bloods, CRP and ESR

Temporal Artery Biopsy - diagnostic

61
Q

Diagnoses of GCA

A 
over 50 YO
new headache 
temporal artery biopsy (shows granulomatous inflammation) (individually diagnostic)
high ESR
Temporal artery tenderness
62
Q

Treatment for GCA

A

corticosteroids for 2 years, prednisolone
considerer DMARDs
DEXA scan, Adcal and potentially bisphosphonates

63
Q

what is betchets disease

A

Vasculities of the whole body

ANCA positive

64
Q

what is goodpastures syndrome

A

pulmonary vasculitis

ANCA positive

65
Q

what is fibromyalgia

A

long term condition causing widespread body pain

66
Q

Prevalence and epidemiology of fibromyalgia

A

4% 10F=M

Female, middle aged, divorced, low household income

67
Q

symptoms of fibromyalgia

A

wise spread pain, muscle stiffness, insomnia and difficulty sleeping, fatigue, extreme tiredness, sensitivity to pain

68
Q

signs of fibromyalgia

A

signs of tenderness

no signs of inflammation

69
Q

Investigations of fibromyalgia

A

all tests return negative

exclude RA Myeloma Infection PMR

70
Q

association of fibromyalgia

A

IBS, Chronic fatigue, Headache

71
Q

Managment of Fibromyalgis

A

Talking therapy, couciling CBT
Analgeisa and analgesic ladder, Tramadol
antidepressants may help amitriptyline
SSRI dont work too well

72
Q

what is systemic lupus erythematosus

A

Autoimmune connective tissue disorer

73
Q

pathophysiology of SLE

A

disease causes inflammation which causes scarring of tissue leading to organ failure. most commonly skin, joints kidney, lungs, blood cells
antibody mediated immune response

74
Q

epidemiology of SLE

A

0.2% prevalnce.

14-64 age group with commonest 20-40 onset

75
Q

clinical features of SLE and tissue commonly effected

A 
relapsing remitting illness. most patients suffer fatigue, fever, arthralgia and skin problems (facial lupus rash)
affects skin
lungs 
joints 
heart
kidney
76
Q

SLE, clinical features of skin

A

Commonest and often earliest sign of SLE
Erythema (Malar) rash, photosensitive rash
purpura and urticaria, discoid rash (commonest rash)
alopecia
raynaud’s phenomenon

77
Q

SLE, clinical features of lungs

A

Pleurisy, pleurisy

78
Q

SLE, clinical features of joints

A

arthralgia, symmetrical, non erosive

79
Q

SLE, clinical features of heart

A

Pericarditis, Pericardial effusion, increased risk of clotting
hypertension

80
Q

SLE, clinical features of kidney

A

glomerulonephritis, can develop into haematuria and proteinuria

81
Q

Investigations and diagnosis of SLE

A

FBC: Anemia, thrombocytopenia, neutropenia, lymphopenia (basically everything is low)
ESR, CRP high
serology: ANA +ve, anti DsDNA (diagnostic)

Other tests (help assess severity)
U and E - elevated 
Dipstick - haematuria 
CXR - effusion
ECG - pericarditis
82
Q

4 results that can make you suspect SLE

A 
Presence of ANA
Presence of anti DsDNA 
Arthritis/ arthralgia 
Discoid Rash 
renal dysfunction
83
Q

Different rashes in SLE

A

Malar rash (erythema) malar means cheek, erythema means redness
Discord Rash
Photosensitive rash

84
Q

Management of SLE
Conservative
maintenance
Flare ups

A

normal management - Hydroxychloroquine (anti-Malarial) +NSAIDs. if not managed use methotrexate or steroids

Flare ups- Corticosteroids or prednisone + NSAIDs, Topical steroids

Conservative, educate on smoking cessation diet exercise and Photosensitive rash, Screen major organ damage.

85
Q

what is seronegative spondyloarthropathy
different types
Epidemiology

A

a group of related inflammatory conditions which affect spine and peripheral joints and are limited by HLA genes.
they are seronegative so test -ve for RF, ANti CCP
presents in younger populations and is more limited than RA

spondylosing ankylosis
psoriatic arthritis
reactive arthritis

86
Q

what is Ankylosing Spondylosis

A

chronic inflammatory disorder of spine and sacroiliac joints

87
Q

epidemiology of ankylosing spondylosis

A

1% prevalence
affects men more
average onset is <30 YO
often presents early teens to twenties

88
Q

Clinical features of Ankylosing spondylosis

A 
gradual onset of lower back pain
worse at night 
stiff in morning
relieved by exercise 
pain radiating from sacroiliac joint to buttocks and hips
chronic back pain
89
Q

diagnostic criteria for ankylosing spondylosis

A 
chronic back pain, under 50 YO. has 3 of the following:
morning stiffness
worst at night- wakes them up
alternating buttocks pain 
back pain improves with exercise
90
Q

what is the name of the connective tissue between tendon or ligament and bone

A

enthesis

91
Q

othey symptoms of ankylosing spondylosis

A

inflammatory back pain
enthesitis
Dyspnoea, due to costochondritis
IBDs

92
Q

complications of AS

A 
Kyphosis 
osetoporosis 
chostochondritis 
enthesis 
iritis
93
Q

Investigation of AS

A

any inflammatory back pain, sacroilliac XRay showing sacrolillitis
ultrasound shows enthesis
FBC, CRP and ESR
HLA B27

94
Q

Management of AS

A

conservative, physio exercise, preventative exercise.

drugs- NSAIDs when requires + PPI
if severe- Intra Articular steroids
if enthsis, TNF A blocker- infliximab

surgery, Hip replacement if needed

95
Q

Prognosis of AS

A

80% lead normal life just on exercise regime and NSAIDs

96
Q

what is psoriatic arthritis

A

a type of seronegative spondyloarthritis

less severe than RA

97
Q

Presentation of psoriatic arthritis

A 
symmetrical polyarthropathy 
commonly affecting DIP
synovitis 
joint pain and stiffness 
Dactylitis
80% of the time has finger nail changes (  
40% of the time associated with psoriasis 
scalp tenderness or scalp problems
98
Q

nail changes in psoriatic arthritis

A 
brittle nails
white spots (leukonychia)
onycholysis (finger nail separating from bed) 
Pitting (commonest sign)
splinter haemorrhage
99
Q

Investigations of psoriatic arthritis

A

X RAY- shows bone erosions in DIP, pencil in cup deformity
CRP elevated
Seronegative
synovial fluid aspirate

100
Q

Treatment of Psoriatic arthritis

A

NSAIDs and analgesia
if more severe use DMARDs or Infliximab
intra articular steroid injections for flare up

101
Q

what is Reactive arthritis

A

arthritis that develops after infection, typically 4 weeks

usually dysentery or GU Infection

102
Q

what causes reactive arthritis

A

GU infection like chlamydia

dysentery salmonella shigella

103
Q

Presentation of reactive arthritis

A 
systemic features like fever 
axial or peripheral arthritis 
peripheral asymmetric polyarthritis (typically larger joints of lower limbs)
enthesitis
nail dystrophy 
dactylitis  
conjunctivitis
skin rash and balantitis
104
Q

Investigations of Reactive Arthritis

A

cultures- stool and GU, usually -ve due to RA happening after infection
esr and CRP increased
Rf and ANA serology -ve
xray shows enthesitis

105
Q

Management of Reactive arthritis

A

NSAIDs,
Intra Articular steroids
DMARDs

106
Q

What is sepric arthritis

A

Infection in the synovium of the joint, either via direct or via blood

107
Q

septic arthrtits presentation and which joints

A

Red Hot Swollen Painful. similar presentation to crystal arthropathy
Most commonly affects knee 50% of cases

108
Q

causes of septic arthritis

A

staph aureus, streptococci, neisseria gonococcus

gram -ve in Immunosuppressed or older patients
gets in via infection, post surgery , immunosuppressed TB, Infected Skin, Indwelling IV lines

109
Q

epidemiology of septic arthritis and risk factors

A 
commoner in RA and pre existing joint conditions 
immunocompromised 
DM
prosthetic joint replacement 
IVDU
over 80 YO
recent surgery
110
Q

Investigation of septic arthritis

A

Joint asperation for Microscopy and cultures

CRP Xray maybe normal may be elevated or shows degeneration

111
Q

Management of septic arthritis

A

start IV antibiotic immediately
use IV vancomycin (gram +ve) or Cefotaxime (gram -ve)
+joint aspirate

112
Q

what is osteomyelitis and what causes it

A

Inflammation of a bone due to an infectious agents commonly Staph aureus

113
Q

what can cause osteomyelitis

A

s aures or group B streptococci

recent open fracture or orthopaedic surgery. also immunocompromised or very young. IVDU

114
Q

osteomyelitis presentation

A 
non specific pain at infection site
malaise and fatigue 
local inflammation 
fever 
presence of risk factors, Scars indicating surgery or fracture
115
Q

osteomyelitis investigation

A

ESR CRP and WCC are raised
Xray will show osteomyelitis, bone destruction
can have MRI - which is very helpful

116
Q

management of osteomyelitis

A

High dose antibiotics

consider surgery if chronic (bone is dead)

Hayders Phase 2A (10 decks)

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