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Phase 2a Ru > MSK > Flashcards

MSK Flashcards

1
Q

What is the functional unit of bone

A

Osteon

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2
Q

Describe the structure of an osteon

A

Concentric lamellae (like tree trunk) and central haversion canals

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3
Q

What is the organic and inorganic of bone made from

A

Hydroxyapatite (Ca2(PO4)3)- for stiffness
Type 1 collagen- Elasticity

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4
Q

How many oesteons does 1 haversion canal supply

A

1 longitudinal

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5
Q

What is the most common arthertirits

A

Oesteoarthiritis

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6
Q

What are risk factors for osteoarthritis

A

50+, women, obesity, occupation/ sports, genetic

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7
Q

What gene gives you a predispostion for oestoarthritis

A

COL2A1

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8
Q

What is the pathology of osteoarthritis

A

Imbalance in cartilage breakdown > repair. Increase of chondrocyte metalloproteinase secretion which degrades collagen + causes cysts. Bone attempts to overcoem this with T1 collagen and you get abnormal bony growths + remodelling

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9
Q

What are the abnormal bony growths known as in osteoarthritis

A

Osteophytes

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10
Q

What are Sx of oesteoarthritis

A

Transient morning pain <30 min, worse as day goes on
Bouchard+ Hebderen nodes
Asymmetrical, hard non inflamed joints
Typically in most stressed joints (base of thumb, hip/knee)
No extra articular symptoms

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11
Q

What do you see on XR in osteoarthritis

A

LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

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12
Q

What is managemnt of osteoarthirits

A

Lifestyle changes
NSIADS for pain relief
Last resort:- surgery (osteoplasty)

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13
Q

In which joints does osteoplasty work very well in

A

Hip and knee

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14
Q

RF for rhematoid arthiritis

A

Women 30-50, smoking, HLA DR4/ HLA DR1

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15
Q

What amino acid change occurs in rheumatoid arthritis

A

Arginine to citrulline in T2 collagen

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16
Q

Pain throughout day in rheumatoid arthrits

A

Worse in morning eases as day goes on

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17
Q

What hand deformities do you see in rheumatoid arthritis

A

Boutonniere, Swan neck, Z thumb, ulnar finger deviation

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18
Q

What join is often spared in rheumatoid arthritis

A

DIP

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19
Q

Other than hand deformities, articular Sx of rheumatoid arthritis

A

Symmetrical, hot inflamed joints
MC in hand wrist feet
Bakers cyst

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20
Q

What is a Bakers Cyst

A

Popliteal synovial sac buldge

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21
Q

Extra-articular Sx of rheumatoid arthritis (complications)

A

PE, Pulmonary fibrosis
Episcleritis, keratoconjunctivitis sicca (dry eyes)
Spinal cord compression
CKD
Rheumatoid skin nodes

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22
Q

What do blood tests show in rheumatoid arthritis

A

Raised ESR/ CRP
Normocytic normochromic anaemia

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23
Q

What does serology show in rheumatoid arthritis

A

+antiCCP(80%)
+RF (70%)

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24
Q

What does XR show in rheumatoid arthritis

A

LESS
Loss of joint space
Eroded bone
Soft tissue swelling
Soft bones (osteopenia)

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25
Q

What treatment is given in rheumatoid arthritis (not pain management)

A

DMARD:- Methotrexate
Biologies:- 1st- TNF-alpha inhibitor- infliximab
2nd- B cell inhibitor (CD20 target)- Rituximab

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26
Q

RF for Gout

A

Purine-rich foods (meat, seafood, Beer), CKD, Diuretics
Dairy can be Anti Gout

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27
Q

How do monosodium urate crystals form

A

Purines into Uric acid (by xanthine oxidase) then uric acid into monosodium urate

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28
Q

Why does CKD cause gout

A

Kidneys excrete Uric Acid

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29
Q

Sx of GOUT

A

Monoarticular typically big toe. Sudden onset severe swollen red toe

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30
Q

Dx of GOUT

A

Joint aspiration; Negatively birefringent needle-shaped crystal under light microscopy

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31
Q

Prevention of GOUT treatment

A

Allopurinol

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32
Q

Treatment for GOUT

A

Diet change
NSAIDS 1st line then consider colchicine then consider Steroid Injection

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33
Q

What are pseudogout crystals made of

A

Calcium phosphate

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34
Q

RF for Pseudogout

A

Elderly female, diabetes, metabolic disease, OA

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35
Q

DEXA scan T score interpretation

A

0-1= normal
1-2.5= osteopenia
>2.5 = osteoporosis

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36
Q

RF for oesteoporosis

A

SHATTERED
Steroids
Hyperthyroid/ hyperparathyroidism
Alcohol + smoking
Thin
Testosterone low
Early menopause
Renal/ liver failure
Erosive + inflammatory disease
DMT1 or malabsorption

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37
Q

Dx of Osteoporosis

A

DEXA scan (Dual-energy SR Absorptiometry)

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38
Q

What is used for a fracture risk assessment tool

A

FRAX score

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39
Q

Treatment for Osteoporosis

A

1st:- Bisphosphonates
2nd:- mAB denosumab

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40
Q

What type of hypersensitivity reaction is SLE

A

T3

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41
Q

RF for SLE

A

Female, HLAB8/DR2/DR3, drugs
Afro Caribbean, 20-40

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42
Q

Pathology of SLE

A

Impaired apoptotic debris presented to TH2

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43
Q

Sx of SLE

A

Butterfly rash + photosensitivity
Glomerulonephritis (nephritic syndrome)
Seizures + Psychosis
Mout Ulcers
Anaemia
Joint pain, Raynaurds, Pyrexia

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44
Q

What do blood test show in SLE

A

Anemia, Raised ESR normal CRP
Decreased c3 + c4

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45
Q

What does urine dipstick show in SLE

A

+++Haematuria, ++proteinuria (Nephritic syndrome)

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46
Q

What is the serology of SLE (sensitive and specific)

A

ANA Abs (99%) very sensitive
Anti-dsDNA Abs + anti smith very specific

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47
Q

What antibody in SLE is used to monitor the progression

A

Anti dsDNA

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48
Q

Treatment for SLE

A

Lifestyle changes (less sunlight)
Corticosteroids (main)
Hydroxychloroquine
NSAIDS
Try to taper off drugs so only hydroxychloroquine once stable

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49
Q

What is used to treat severe SLE

A

Azathiopines

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50
Q

What is antiphospholipid syndrome

A

An autoimmune disorder in which the immune system mistakenly produces antibodies against normal proteins in the blood
Characterised by thrombosis, recurrent miscarrge

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51
Q

What is primary vs secondary antiphospholipid syndrome

A

Primary is idiopathic
Secondary to other disease (SLE)

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52
Q

Sx of antiphospholipid

A

CLOTs
Coagulopathy
Livedo Reticularis (Purple discolouration of skin)
Obstetric issues (miscarriages)
Thrombocytopenia
Risk arterial (Stoke, MI+ DVT)

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53
Q

What antibodies are present in antiphospholipid syndrome

A

Anti-cardiolipin antibodies (IgG/M)
Anti beta 2 glycoprotein-1 antibodies

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54
Q

1st line treatment for antiphospholipid syndrome if they’ve had a thrombosis

A

Warfarin
Long term if they’ve had a thrombosis

If preggo give aspirin+ heparin

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55
Q

What is the prophylactic treatment given in Antiphospholipid syndrome

A

Aspirin

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56
Q

What is Sjogren syndrome

A

Autoimmune exocrine dysfunction can be primary or secondary
Affects moisture producing glands

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57
Q

RF for Sjogrens syndrome

A

Female, fHx, 40-50, HLAB8/ DR3

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58
Q

Sx of Sjogrens Syndrome

A

Dry eyes (keratoconjunctivitis)
Dry Mouth (Xerostomia)
Dry vagina

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59
Q

What test is used in the diagnosis of Sjogddrens syndrome

A

Schimer test:- Induce tears + place filter paper under eyes. In Sjogrens syndrome tears travel less than 10mm (should be 20mm)

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60
Q

What is the serology of Sjogren’s syndrome

A

Anti-Ro Ab
Anti LA Ab

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61
Q

What is the treatment for Sjogren’s Syndrome

A

Artificial Tears, salvia + lubricant for sexual activity

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62
Q

What cancer does Sjordens syndrome directly increase the risk of

A

Lymphoma

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63
Q

What is most common type of Scleroderma

A

Limited cutaneous scleroderma (CREST)

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64
Q

What are Sx of Scleroderma

A

Calcinosis (Ca deposits in SC tissue)- Renal failure
Raynauds (digit ischemia due to sudden vasospasm
Esophageal dysmotility (stricture)
Sclerodactyly (local skin thickening or tightening on fingers/ toes)
Telepgientaria (Spider veins) risk of pul Htn

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65
Q

What antibody is present in scleroderma

A

Anti Centromere Antibodies (ACAs)

66
Q

What is fibromyalgia

A

MSK equivalent of IBS
Chronic widespread MSK pain for 3+ months w/ all other causes ruled out

67
Q

RF for fibromyalgia

A

Females, depression, stress, poor, 60+

68
Q

Sx of Fibromyalgia

A

Fatigue, Sleep disturbance, Morning stiffness, Esp back + kneck stiffness + pain

69
Q

Dx of Fibromyalgia

A

Pain in 11/18 regions palpated

70
Q

Treatment for fibromyalgia

A

Educate patient, physiotherapy
Antidepressants + CBT if severe

71
Q

What is polymyalgia rheumatic

A

Large vessel vasculitis presenting as chronic pain syndrome

72
Q

Dx of Polymyalgia rheumatica

A

Raised ESR + CRP

73
Q

Treatment for polymyalgia rheumatica

A

Oral prednisolone

74
Q

Are primary or secondary bone tumours more common

A

Secondary

75
Q

What is most common primary bone malignancy and what disease is it assoiated with

A

Osteosarcoma associated with pagets (15-19 y/o patient)

76
Q

Where does osteosarcoma metastasis too

A

Lung

77
Q

What is XR appearance in osteosarcoma

A

Sunburst

78
Q

What is an Ewing sarcoma

A

Cancer of mesenchymal stem cells of bone

79
Q

Which secondary bone cancers are osteolytic vs osteosclerotic

A

Osteolytic:- Breast + Lungs
Osteosclerotic:- Prostate, Thyroid, RCC

80
Q

General Sx of bone tumours

A

Local severe pain is worst at night
Weight loss, fatigue, fever, malaise

81
Q

What imaging can be used to show bone tumours before XR

A

Skeletal isotope scan

82
Q

Treatment for bone tumours

A

Chemo/ radio therapy
Bisphosphinates

83
Q

What do bloods/ U&Es show in bone tumour

A

Raised ALP/ESR/CRP, hypercalcemia

84
Q

What is osteomalacia

A

Defective bone mineralisation due to Vit D deficiency so lack of calcium and phosphate

85
Q

What is osteomalacia known as before epiphyseal fusion

A

Rickets

86
Q

What can cause osteomalacia

A

HyperPTH
Vitamin D deficiency, malabsorption reduced intake
CKD/ renal failure
Liver Failure
Anticonvulsant drugs

87
Q

Why does CKD/ renal failure decrease Vit D production?

A

Kidney 25-hydroxy vit D to 1,25 dihydroxy Vit D

88
Q

Why does Liver failure reduce Vit D

A

Liver does cholecalciferol into 25-hydroxyvit d

89
Q

Why does anticonvulsants decrease Vit D

A

Increase CYP450 metabolism of Vit D

90
Q

Sx of osteomalacia

A

Fractures, proximal weakness + difficulty weight bearing

91
Q

Sx of rickets

A

Skeletal deformities; Knocked knees + bowed legs
Wide Epiphyses

92
Q

Diagnostic investigation for Osteomalacia

A

BM biopsy; Incomplete mineralisation

93
Q

Blood in osteomalacia show hypocalcemia, raised PTH, decreased serum Ca but what is the best marker

A

Decreased 25(OH)D

94
Q

Treatment for osteomalacia

A

Vit D replacement (Calcitrol) + increase dietary intake

95
Q

What is Pagets disease of bone

A

Excessive activity of both osteoblasts and clasts leads to excessive turnover of bone. Exessive turnover is not coordinated leading to areas of high density (sclerosis) and low density (lysis).
Leads to lsrge and mishaoedn bones

96
Q

Which group most at risk from pagets

A

Female 40+

97
Q

Sx of Pagets disease of bone

A

Bone pain
Bone deformities; bowed tibia
Nerve compression of CN8:- deafness
Hydrocephalus; blockage of sylvian duct

98
Q

What do you see on XR in pagets

A

Osteoporosis circumscripta; describes well-defined osteolytic lesions
Cotton wool skull; due to areas of lysis + sclerosis
V-shaped defects in the long bones; V sphaped osteolytic bone lesions within healthy bone

99
Q

How are ALP, Ca and phosphate affected in pagets diseases

A

Raised ALP, normal calcium and phosphate

100
Q

What can be used to monitor disease progression in pagets

A

Urine hydroxyproline; protein constituent of bone collagen

101
Q

Treatment for Pagets

A

Bisphosphonates
NSAIDS for pain relief

102
Q

What inheritance pattern is Marfan’s

A

Autosomal dominant

103
Q

What does marfans cause

A

Decrease in connective tissue tensile strength due to mutation in gene coding for fibrilin

104
Q

Sx of marfanss

A

‘Marfans Body Habitus’; Tall + thin, long fingers, arachnodactyly, pectus excavatum or carinatum
Aortic complications; Aortic regurg, AAA, AD

105
Q

Dx of Marfan’s

A

Clinical Px + FBN-1 mutation

106
Q

Classical presentation for GCA

A

50+ Caucasian female with unilateral temple headache, jaw claudication +/- vision change
temporal scalp tenderness

107
Q

Which branches lead to the specific symtpoms seen in GCA

A

Temporal:- scalp tenderness
Vision:- Ophthalmic
Jaw:- Facial

108
Q

1st line investigation for GCA

A

ESR will be raised

109
Q

Diagnostic investigation for GCA

A

Temporal artery biopsy (take big chunk as patchy skip lesions)

110
Q

Describe inflammation seen in GCA

A

Granulomatous inflammation of media + intima

111
Q

Treatment for GCA

A

Corticosteroids (prednisolone)

112
Q

Complications of GCA

A

Sudden painless vision loss in one eye (optic neuropathy)
Temporary amaurosis fugax
May be permanent if not delt with ASAP

113
Q

How to treat sudden vison loss in GCA

A

High dose IV Methylyprednisolone

114
Q

Who is more at risk from Polyarteritis Nodosa
Males or females

A

Males

115
Q

What viral infection is polyarteritis nodosa associated with

A

HepB

116
Q

Sx of polyarteritis nodosa

A

Severe systemic Sx
Mononeuritis multiplex
GI bleeds
CKD/ AKI
Skin SC nodules + haemorrhage

117
Q

What do you see on a CT angiogram in polyarteritis nodosa

A

Beads on a string (microaneurysms)

118
Q

Other than CT angiogram, what other test do ou perform in polyarteritis nodosa

A

Biopsy e.g. kidney
See necrotising vasculitis

119
Q

Treatment for polyarteritis nodosa

A

Corticosteroids
Control htn: ACE-i
Hep B treatment after corticosteroids

120
Q

What gene are spondyloarthropathies associated with

A

HLAB27

121
Q

General features of spondyloarthropathies

A

SPINEAHCE
Sausage fingers
Proasisis
Inflammatory back pain
NSAIDs good response
Enthesitis
Arthritis
Chrons or colitis
HLA B27
Eyes; uveitis

122
Q

What is the pathology of ankylosing spondylitis

A

Syndesmophytes (vertical abnormal bony growths) replace spinal bone damaged by inflammation make spine less mobile

123
Q

Sx of ankylosing spondylitis

A

Young make with progressively worsening back stiffness. Worse in morning better w/ exercise
Anterior uveitis
Entheirits
Dacytlitis
Lumbar lordosis

124
Q

What tests lumbar flexion

A

Schober test (<20cm in Ankylosing Spondylitis)

125
Q

What does XR show of ankylosing spondylitis

A

Bamboo spine + sacroiliitis + syndesmophytes

126
Q

What imaging is the best screening tool for ankylosing spond

A

MRI as shows sacroiliitis before XR

127
Q

Treatment for Ankylos Spond

A

NSAIDs to help symptoms (+ exercise)
DMARD (tnf-alpha-blocker) to improve disease such as infliximab

128
Q

What % of patients with psoriasis develop psoriatic arthritis

A

10-20%

129
Q

Sx of Psoaritic arthritis

A

Moderate; Inflamed DIP joints + nail dystrophy, dactylitis and enthesitis
Psoriatic rash on skin
Severe; Arthritis mutilans= pencil in cup deformity; Osteolysis of bone = progressive shortening and fingers telescope in on themselves

130
Q

Treatment for psoariatic arthritis

A

NSAIDs for symptoms (steroid injection if severe)
DMARD (methotrexate) if fials anti TNF (inflixumab)
If fails IL 12+ 23 inhibitor

131
Q

What is used to screen patients with psoriasis for psoriatic arthritis

A

Psoriasis Epidemiological Screening Tool

132
Q

What is reactive arthritis?

A

Sterile synovitis in reaction to a distant infection infection

133
Q

What usually causes reactive arthritis

A

GI or STI infection

134
Q

What organisms in gastroenteritis can cause reactive arthritis

A

C. Jejuni, Salmonella, Shigella

135
Q

What STI infections can cause reactive arthritis

A

C. Trachamatis MC
N. Gonorrhoea

136
Q

Sx of reactive arthritis

A

Reiters Traid
Cant see, cant pee, cant climb a tree
Uveitis, urethritis, Arthritis

137
Q

What does a joint aspirate show in Reactive arthritis

A

Now organism growth
Plane polarised light microscopy is negative for crystal arthropathy

138
Q

Treatment for reactive arthritis

A

NSAIDs + steroid injection for symptoms
Mostly single attack but if not Methotrexate then Inflixumab if it doesn’t work

139
Q

What are the seronegative spondyloarthropathies

A

Ankylosing spondylitis
Reactive Arthritis
Psoriatic Arthritis

140
Q

What is the most common cause of Septic arthritis?

A

Staph Aureus

141
Q

What than S. Aureas what organisms can cause septic arthritis

A

H. Influenza, E. Coli/ Pseudomonas

142
Q

RF for septic Arthritis

A

IVDU, Immunosuppression, Recent surgery, Trauma, Prosthetic joints + inflammatory joint disease

143
Q

What organism are prosthetic joints at risk of infection from

A

Staph epidermidis

144
Q

Investigation for septic arthritis

A

Urgent joint aspirate and ID causative organism

145
Q

Treatment for septic arthritis

A

Joint aspirate (drainage) then empirical Abx
Flucloxacillin (gram -ve)
Vancomycin (MRSA)
IM ceftriaxone + azithromycin (Gonorrhoea)
Stop methotrexate + inflicumab
Double prednisolone dose
NSAIDs for analgesia

146
Q

What is osteomyelitis

A

Acutely inflamed infected bone marrow

147
Q

What is the most common cause of osteomyelitis in children vs adults?

A

Haematgenous in children

Local in adults

148
Q

Most common cause of osteomyelitis

A

S. Aureus
Salmonella in sickle cell patients

149
Q

RF for osteomyelitis

A

IVDU, Immunosuppression, PVD, DM, Sickle cell, Inflammatory arthritis, trauma

150
Q

What acute bone changes occur in osteomyelitis

A

Inflammation and bone oedema

151
Q

What chronic bone changes occur in osteomyelitis

A

Sequestra:- Necrotic bone embeded in pus
Involucrum:- thick sclerotic bone placed around sequestra to compensate for support

152
Q

Sx of osteomyelitis

A

Acutely; Dull bony pain + hot swollen area +/- joint. Worse with movement
Chronic; + deep ulcers (sequestra)

153
Q

Investigations to carry out in osteomyelitis

A

BM biopsy + culture
XR= osteopenia MRI (after XR)= bone marrow oedema (MRI best for diagnosis)
Raised ESR/ CRP

154
Q

Treatment for Osteomyelitis

A

Immobilise + Abx
6 weeks Flucoxacillin + Fusidic acid 2 weeks

155
Q

What Abx to treat salmonella

A

Flucoxacillin

156
Q

Vancomycin vs Teiocoplannin

A

Teiocplannin is longer lasting but has worse side effects (GI upset + pruritis)

157
Q

What is a Charcot joint

A

Damage to sensory nerves due to diabetic neuropathy
Causes progressive degeneration of weih=ght bearing joint + bony destruction. Often affects foot
DDx for osteomyelitis

158
Q

What do you see on XR of a patient with Ewings sarcoma

A

Lytic bone lesions
Onion skin apearnce

159
Q

What does XR show in patient with chondrosarcoma

A

Popcorn calcification

160
Q

What is first-line treatment for neuropathic pain

A

Amitriptyline

161
Q

Treatment for pseudo gout

A

NSAIDs, can use colchicine or

Phase 2a Ru (10 decks)

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