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FINALS > MSK and Rheumatology > Flashcards

MSK and Rheumatology Flashcards

1
Q

 name the 4 stages of bone repair?

A

Haematoma formation f ibro cartilaginous callus formation bony callus formation bone remodelling

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2
Q

describe what occurs in the first stage of bone repair?

A

A haematoma forms at the injury site macrophages and inflammatory leucocytes move to the damaged area They scavenge debris and kill pathogens they begin producing pro-inflammatory agents that initiate healing

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3
Q

describe what occurs in the second stage of bone repair?

A

After a haematoma is formed and inflammation has begun: cell division growth of new blood vessels, chondrocytes -secrete collagen and proteoglycans creating fibrous cartilage + forms the soft callus

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4
Q

describe what occurs in the third stage of bone repair?

A

Through endochondral ossification and direct bone formation soft callus is replaced by woven bone creating a hard callous around the broken bone

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5
Q

describe what occurs in the fourth stage of bone repair?

A

Over time mechanically strong highly organised cortical bone replaces the weaker disorganised woven bone which makes the hard callus eventually creating normal bone

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6
Q

what is osteoarthritis? Describe pathophysiology

A

A degenerative joint disorder: - from mechanical and biological events - these destabilises the normal cycle of cartilage matrix and subchondral bone - overall : resulting in either reduced formation of bone or increased catabolism of bone

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7
Q

describe the pathophysiology of osteoarthritis?

A
  1. Chondrocytes release enzymes which break down collagen and proteoglycans
  2. destroying the cartilage
  3. this paired with reduced formation of bone exposes the sub control bone
  4. causing sclerosis the disordered remodelling
  5. creates osteophytes and sub- chondral bone cysts
  6. causing a decrease in joint space
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8
Q

which bones does osteoarthritis affect the most?

A

Knees hips hands lumber and C-spine The base of the thumb:where the thumb and wrist join (the trapeziometacarpal [TMC] or carpometacarpal [CMC] joint) The joint closest to the fingertip (the distal interphalangeal [DIP] joint) The middle joint of a finger (the proximal interphalangeal [PIP] joint)

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9
Q

what does the following images show?

A

squaring at the base of thumb

Heberdens nodes at DIP and

Bouchard nodes at PIP

  • osteoarthritis of the hand
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10
Q

what usually causes secondary osteoarthritis?

A

Proceeding injury or trauma repetitive strain

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11
Q

what are some congenital causes of osteoarthritis?

A

Hip dysplasia or inflammatory arthropathies

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12
Q

a patient presents with:

  • pain in the small joints of the hand
  • pain increases with the use
  • sometimes there clunking and stiffness
  • notes some tranient monring stiffness

On examination:

  • some slight swelling of the small joints DIP PIP
  • no signs of redness or tenderness

when asked about pain relief she notes that paracetamol and Ibruprophen were proven help somewhat what is the most likely diagnosis?

A

Osteoarthritis

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13
Q

what are the classic symptoms of degenerative arthritis?

A

Pain increasing with use clicking and clunking of the joints/blocking short lived stiffness symptoms worse in the morning and evening not much swelling around the arthritic joints no signs of clinical inflammation older demographics poorer response to NSAIDs

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14
Q

what does locking in joints affected by arthritis indicate?

A

Involvement of the cartilage such as a tear or loose body

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15
Q

What investigations should you perform in a ? Osteoarthritis ?

A

bloods: CRP and ESR to exclude inflammatory cause if you are suspecting rheumatoid arthritis check for rheumatoid factor and anti-CCP negative results indicate osteoarthritis x-ray of joints

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16
Q

what classic x-ray findings would you see on the joints affected by osteoarthritis?

A

osteophytes joint space narrowing sub control sclerosis and cysts

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17
Q

what is the management of osteoarthritis?

A

Patient education and nonpharmacological measures: weight loss low impact aerobic activity to strengthen muscles pacing of exercise and good footwear thermotherapy with hot or cold patches medical therapy: topical NSAIDs e.g. Dick Cliff Anak analgesia (NSAIDs but be aware in elderly patients and paracetamol make sure to give gastro protection intra-articular corticosteroid injection Surgery: consider joint replacement

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18
Q

what factors would indicate needing joint replacements for osteoarthritis?

A

Patient been offered and tried at least one nonsurgical treatment osteoarthritis having a substantial impact on quality-of-life and symptoms are refractory to nonsurgical treatment refer for surgery before there is prolonged and established functional limitation and severe pain patient specific factors should not be barriers to referral for joint surgery e.g. smoking obesity EDC give all information required to make an informed decision

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19
Q

what is rheumatoid arthritis?

A

A chronic inflammatory condition affecting mainly the small joints of the hands feet which must be treated aggressively

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20
Q

what is the pathophysiology of rheumatoid arthritis?

A

The sign opium becomes inflamed resulting in increased angiogenesis cellular hyperplasia and an influx of inflammatory cells this causes the sign avium to be hyperplastic and hypertrophic

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21
Q

what other characteristic symtpoms of rheumatoid arthritis?

A

Pain which is worse in the morning and eases with use morning cyst stiffness that is prolonged significant swelling over the Sino VM which is hot and red potentially which has a good response to NSAIDs

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22
Q

what features would you find on examination of the hand a patient with rheumatoid arthritis?

A

Rheumatoid nodules over the tendons swan neck deformity boutonieres deformity ulnar deviation

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23
Q

what extra articular features can be present in rheumatoid arthritis?

A

Scleritis+/- uveitis vascular take rashes and purity chest pain these tend to occur in more severe disease

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24
Q

what does the following images show?

A

Rheumatoid nodules over the tendons swan neck deformity boutonieres deformity ulnar deviation - rhaumatoid arthritis

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25
Q

What investigations are necessary for rheumatoid arthritis?

A

Rheumatoid factor and anti-CCP will be positive (either one or both) X-ray ultrasound scan for synovitis of the wrist and fingers

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26
Q

what features are characteristic of rheumatoid arthritis on x-ray?

A

Erosions at joint margins

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27
Q

how quickly should you to start treatment in a patient who presented symptoms of rheumatoid arthritis?

A

within three months of symptoms starting

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28
Q

what treatment is used for rheumatoid arthritis?

A

Diem ARD such as methotrexate or second-line sulfazine then infliximab – biological agents. Glucocorticoids is used as an adjunct to manage flares they are also used during pregnancy when other treatments are contraindicated and at the start of treatment when methotrexate may not have kicked in

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29
Q

what is a seronegative arthritis?

A

An arthritis which is present with rheumatoid symptoms/inflammatory arthritis symptoms but has no serological markers (rheumatoid factor or anti-CCP)

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30
Q

what are some examples of seronegative arthritis?

A

Spondylosis are properties crystalline arthropathy viral arthropathy seronegative rheumatoid arthritis

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31
Q

what is gout?

A

A syndrome characterised by hyperuricaemia and the deposition of urate crystals causing acute attacks of inflammatory arthritis

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32
Q

what joints does gout usually effect?

A

First toe foot ankle knee fingers wrist elbow but can be anywhere in the body

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33
Q

what are the risk factors for gout?

A

male consumption of purines

  • found in :red meats, seafood, alcohol especially port

drugs such as aspirin cyclosporine tracolimus and diuretics

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34
Q

what does the image below show?

A

A tophi - Gout

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35
Q

what is the presentation of gout?

A

The rapid onset of severe pain joint stiffness swelling and joint effusions joint tenderness

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36
Q

how do you diagnose gout?

A

Do atheroscentesis with synovial fluid analysis (athough diagnosis can be clinical)

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37
Q

what would atheroscentesis with sinovial fluid analysis show in gout?

A

strongly negative bi fingant needle shaped crystals under polarised light

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38
Q

apart fromatheroscentesis what other investigations could you perform in gout and what would they show?

A

Ultrasound scan – erosions trophi and double contour lines uric acid levels – are obtained to weeks after the acute attack and are elevated

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39
Q

how do you manage acute gout?

A

NSAIDs (colchisine if nsaids CI or corticosteroids if both CI)

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40
Q

how do you manage a recurrent gout?

A

Allopurinol if recurrence and start 2 – 3 weeks post-attack

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41
Q

what is pseudo-gout?

A

Depositions of calcium phosphate causing both acute and chronic arthritis

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42
Q

what is the presentation of acute pseudo-gout?

A

Mimics normal gout

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43
Q

In what joints does pseudo-gout occur?

A

usually affecting one or more joints of the wrists knees shoulders ankle elbows or hands

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44
Q

What are the risk factors for developing pseudo-gout?

A

Elderly or younger patients with a metabolic condition such as hyperparathyroidism or haemochromatosis

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45
Q

what is the presentation of chronic pseudo-gout?

A

mimics osteoarthritis or rheumatoid arthritis as it has varying levels of inflammation

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46
Q

what would atheroscentesis show for pseudo-gout?

A

bi fringant rhomboid crystals, the fluids are often bloody

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47
Q

what would x-rays show in pseudo-gout?

A

May show cartilage calcification

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48
Q

in a patient with pseudo-gout, especially younger patients, what further investigations should you perform?

A

Check for metabolic abnormalities: serum calcium and serum parathyroid hormone (hyperparathyroidism) iron studies (haemochromatosis) serum magnesium and serum alkaline phosphate

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49
Q

what is the management of mono or oligo articular pseudo-gout?

A

intra-articulate corticosteroids then NSAIDs/colchicine then systemic corticosteroids or joint aspiration

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50
Q

what is the management of poly-articular pseudo-gout?

A

NSAIDs or colchicine then systemic corticosteroids or joint aspiration

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51
Q

how do you define a chronic spinal injury?

A

Progressive or permanent interruption of the conduction causing neurological defects lasting over one year

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52
Q

what usually causes chronic spinal injury?

A

Mechanical trauma compression vascular insult

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53
Q

what are the symptoms of chronic spine injury?

A

motor weakness loss of fine motor skills spasticity and joint contractures paraesthesia numbness hyperreflexia and ankle clonus/ pathological reflexes as well as sphincter abnormalities - constipaton or incontinence or retention, ED, unsteady gait

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54
Q

what investigations are required in chronic spinal injury?

A

MRI shows lesions and a vertebra EMG shows conduction abnormalities urodynamic studies and bladder ultrasound for sphincter function and consider other pathologies which may be causing urinary symptoms

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55
Q

what is the management of progressive spinal-cord injury?

A

Surgical decompression and if there is also gnomic dysregulation remove or treat the stimulus and adjunct vasodilator nifedipine

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56
Q

what are symptoms of autonomic dysreflexia?

A

increase in blood pressure - occurs at T6 lesion usually caused by excess response to a trigger below the lesion such as impaction or blocked catheter

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57
Q

what is the management of stable chronic spine injury?

A

Physiotherapy and supportive care bladder and bowel management pain control

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58
Q

what are acute causes of spinal-cord compression?

A

Trauma or herniation usually in younger patients

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59
Q

What are chronic causes of spinal cord compression?

A

osteoporotic/osteomyelitic in middle group middle-aged patients or malignancy

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60
Q

what are the symptoms of spinal cord compression?

A

Back pain weakness or paraesthesia sensory loss hyperreflexia muscle weakness or wasting

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61
Q

what does hyperreflexia mean in a ? Spinal-cord compression?

A

It is an early sign commonly occurring with malignancy

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62
Q

what word symmetrical sensory loss in spinal-cord compression indicates?

A

Neuropathy

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63
Q

What types spinal-cord compression?

A

Spinal shock completed cord transaction neurogenic shock cauda equina central cord compression

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64
Q

what is spinal shock

A

and initial symptom usually occurring in acute spinal-cord compression where there is loss of reflexes motor paralysis and hyperreflexia these later turn into hyperreflexia and primitive reflexes

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65
Q

what is complete cord transaction?

A

Occurs in severe spinal injury where there are no preserved nerves can be of the C-spine thoracic lumbar sacral or lumbar thoracic

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66
Q

what would occur in complete transaction of the C-spine?

A

Quadriplegia respiratory insufficiency loss of bladder and bowel function anaesthesia and neurogenic shock if very high in the C-spine Horner’s syndrome may occur and respiratory muscles will be involved

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67
Q

what would occur in complete transaction of the thoracic spine?

A

paraparesis and normal functional loss such as bladder and bowel function

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68
Q

what is a neurogenic shock?

A

Occurs in C-spine and high T spine damage - hypotension and bradycardia warm and dry extremities peripheral vasodilation venous pooling pre-prism and low CO

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69
Q

what is cauda equina?

A

Occurs mainly due to disk compressions and stenosis of the spinal-cord has saddle anaesthesia bladder retention and leg weakness usually affecting males 40 to 60

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70
Q

how do you investigate spinal-cord compression?

A

MRI is diagnostic

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71
Q

what is the management of spinal-cord compression?

A

IV corticosteroids unless infection is causing symptoms - decompression surgery and if there is an infective cause add IV antibiotics - plus VDE prophylaxis fluids and PPI

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72
Q

apart from MRI what other Ix could you order for SCC and why?

A

PET scan : Cancer/hypermetabolism FBC, ESR, CRP + Cultures : infections (also CSF analysis)

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73
Q

what is spinal-cord stenosis?

A

a degenerative condition which narrows the spinal canal causing symptoms of neural compression such as cauda equina

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74
Q

what are the causes of spinal-cord stenosis?

A

Facet joint and ligamentous hypertrophy intervertebral disc protrusion

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75
Q

What is the presentation of spinal-cord stenosis?

A

Symptoms of neurological claudication such as leg pain when walking pain and weakness in thighs and calves sensational numbness in lower extremities stupid posture when walking as it relieves the symptoms symptoms relieved also by sitting down pain radiating down legs from compressional L4 – L5 a.k.a. sciatica radiculopathy

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76
Q

can spinal-cord stenosis Turn into cauda equina?

A

yes if left untreated and long-standing

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77
Q

how to diagnose spinal-cord stenosis?

A

MRI

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78
Q

what is the management of spinal stenosis?

A

Surgical decompression of the significant neurological defect or analgesia with short-term bed rest and adding PO corticosteroids

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79
Q

what is scoliosis?

A

Spinal deformity causing abnormal vertical alignment

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80
Q

what are the types of scoliosis?

A

infantile (0 – 3) juvenile (4 – 9) adolescents (>10y)

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81
Q

what can cause scoliosis?

A

Spina bifida poliomyelitis also readable Paul C due to abnormal innovation of muscles intrinsic dysfunctional muscles causing imbalanced forces thus curvature congenital vertebral failure to form

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82
Q

what is the presentation of scoliosis?

A

Postural asymmetry para spinal prominence on bending forward usually no pain and normal neurological exam however sufficient deformity can decrease the racket volume causing shortness of breath and a restrictive pattern as well as right-sided heart failure

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83
Q

how do you investigate scoliosis?

A

X-ray C-spine T spine L spine and hip MRI if there are any neurological findings Scoliometer to used to measure the angle of the spine

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84
Q

what is the management of scoliosis?

A

excersise and physio –> brace and excersise —> surgery + monitoring with x ray every 4-12m depending on growth rate

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85
Q

What are the main causes of lower back pain?

A

Annular tear degenerative disc disease facet joint mediated pain

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86
Q

what makes up an intervertebral disc?

A

a nucleus filled with Fluid and proteoglycans surrounded by an annular disc the nucleus is not innervated but the annulus is by the Sinovertebral nerve

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87
Q

what is an annular tear?

A

An acute event involving trauma to the annular disc and following inflammation causing a sudden and acute pain

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88
Q

what is the pathophysiology of degenerative disc disease?

A

Has both mechanical and genetic factors involving a long-standing inflammation apoptosis and abnormal proteoglycans and collagen and vascular regrowth as well as disordered angiogenesis

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89
Q

what causes facet joint mediated pain?

A

repeated trauma causing pain through the dorsal primary rami nerve

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90
Q

what is vertebral pain syndrome?

A

Pain usually caused by osteoarthritis of the neck causing subsequent myelopathy

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91
Q

what is the presentation of vertebral pain syndrome?

A

Pain in the neck that radiates down to the shoulder ache and discomfort decreased range of motion with no sensory loss or muscle weakness

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92
Q

what should you investigate in vertebral pain of the thoracic spine?

A

do a CT as it can be indicative of cancer metastases causing fractures

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93
Q

what is Perthes disease?

A

A disease of the femoral head composing of necrosis collapse repair and remodelling of the femoral head

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94
Q

what is the pathophysiology of Perthes disease?

A

a singular or multiple vascular events Cause necrosis and collapse of the femoral head there is subsequent revascularisation and remodelling which is in perfect forming a poorly functioning hip and causing pain

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95
Q

who is the typical patient presenting with perthes disease?

A

male aged 4 – 8 years unilateral hip pain

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96
Q

what is the presentation of perthes disease?

A

Young male with a limp and decreased range of motion canal short stature and muscle wasting causing positive Trond Ellenberger test synovitis can be present

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97
Q

what investigations are required for perthes disease?

A

Bilateral hip x-ray – diagnostic ESR and CRP if ?infection and RF is ? RA

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98
Q

what is the management of perthes disease?

A

Encouraging mobilisation and physiotherapy and once arthritis sets in and they are over 12 hip replacement is required once the hip has reached the skeletal maturity

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99
Q

what is haemarthrosis?

A

Bleeding into the joint space causing inflammation of the joints

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100
Q

what typically is the cause of haemarthrosis??

A

haemophilia - either spontaneous or following injury or individuals on warfarin/ other anticoagulants

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101
Q

how do you diagnose haemarthrosis?

A

x-ray and synovial fluid asirate (blood +++)

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102
Q

what is a consequence of recurrent haemarthrosis?

A

arthropathy requiring replacement

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103
Q

what is the management of haemarthrosis?

A

selection of coagulation you can aspirate the joints but this increases rates of infection so it is controversial

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104
Q

what is irritable hip syndrome?

A

also known as a transient synovitis non-specific inflammation with hypertrophy of the sign opium causing effusion of the hip joint affecting young children and is self-limited

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105
Q

what usually is present in the history of transient synovitis of hip?

A

recent history of upper respiratory tract infection

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106
Q

what is the presentation of transient synovitis of hip?

A

Pain which is relieved at rest reduced range of motion pain is better with abduction and external rotation of the hip

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107
Q

what clinical examination is very sensitive for transient synovitis of the hip?

A

Positive log roll test there as in voluntary muscle guarding of the affected limb

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108
Q

what are diagnostic tests of transient synovitis?

A

These are usually only performed if you want to rule out septic arthritis perthese malignancy or osteomyelitis Xray, ESR CRP (both slighlty raised) FBC

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109
Q

what is the management of transient synovitis of the hip?

A

bedrest NSAIDs and paracetamol usually self resolves within a week

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110
Q

what is Tenosynovitis?

A

Tendon irritation manifesting as pain reduced tendon gliding causing locking and clicking

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111
Q

what is the term for Tenosynovitis of the hand/fingers§?

A

trigger finger

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112
Q

what is the presentation of trigger finger?

A

Pain increases with emotion there is painful popping with flexion and extension and a palpable nodule at the level of the metacarpal head

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113
Q

what is the term forTenosynovitis of the wrist?

A

De quervians disease

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114
Q

what is the presentation of De quervians disease?

A

pain increases with motion there is tenderness and swelling on the radial aspect of the wrist

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115
Q

how do you diagnose Tenosynovitis?

A

high resolution ultrasound scan shows a fusion with the tendon sheath thickening

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116
Q

how do you manage Tenosynovitis?

A

NSAIDs and corticosteroid injection with Lidocaine if that fails surgery splinting is used in all types of Tenosynovitis apart from trigger finger

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117
Q

what does the ulnar nerve innervate in the hand?

A

The palmar and dorsal aspects of pinky and ring finger see image below

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118
Q

what does the median nerve innervate in the hand?

A

on the Palomar aspect half of the ring finger middle and index finger as well as most of the thumb, on the dorsal aspect the tips of the thumb index middle and half of the tip of the ring finger - see image below

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119
Q

what does the radial nerve innervate in the hand?

A

the side of the base of the thumb on the Palomar aspect of the hand on the dorsal aspect of the hand the base of the thumb and base of the index and middle finger see image below

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120
Q

what is carpal tunnel syndrome?

A

A collection of signs and symptoms caused by the compression of the median nerve in the carpal tunnel

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121
Q

what type of neuropathy is carpal tunnel?

A

Mono neuropathy

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122
Q

what is the presentation of carpal tunnel syndrome?

A

Numbness and tingling and in more advanced cases can cause weakness and clumsiness of the hand there can be pain but that is not the main symptom usually has a gradual onset

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123
Q

what other risk factors associated with carpal tunnel?

A

Females aged 40 – 60 obesity diabetes pregnancy and repeated strain

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124
Q

when are the symptoms of carpal tunnel worst

A

usually worse at night

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125
Q

are the reflexes affected in carpal tunnel syndrome?

A

No they are normal

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126
Q

what investigations are diagnostic for carpal tunnel syndrome?

A

usually it is a clinical diagnosis however an electromyographic and be used – Shows slowing of the median nerve conduction through the carpal tunnel

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127
Q

what is the management of carpal tunnel syndrome?

A

Wrist splints –> corticosteroid injections and splints —> surgery

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128
Q

what is Dupatrons contracture?

A

an inherited disease of progressive fibrosis of the tissue of the palmar facia

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129
Q

what are risk factors for Dupatrons contracture?

A

males over 40 family history of diabetes mellitus anticonvulsants therapy smoking alcohol trauma

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130
Q

what is the presentation of Dupatrons contracture?

A

difficulties in the fine movements of the hand with limitations in washing face combing her putting hands in pockets Palomar nodule Palomar thickening tethering puckering or pitting there can be pre-tendinous chords causing joint contracture at the MCP or PIP’s

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131
Q

what is the diagnostic test for Dupatrons contracture?

A

ultrasound scan of the hand

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132
Q

what is the management ofDupatrons contracture?

A

No significant functional damage: expectant management with six monthly follow-ups / involvement of MCP < 30°: collagenase injections needle aperneurotomy corticosteroid injections percutaneous fasciotomy/ > 30° involvement or the PIPs involved surgical intervention

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133
Q

What is epicondylitis?

A

A condition characterised by tenderness at the Ethicon dial associated with repeated forearm and elbow activities

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134
Q

what is the name for epicondylitis of the lateral epicholdyl?

A

Tennis elbow

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135
Q

what is the name for epicondylitis of the medial epichondyl?

A

golfers elbow

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136
Q

what is the presentation of tennis elbow?

A

Tenderness slightly distal and anterior to the lateral epicondyle with pain during resisted wrist and digital extension pain during passive flexion with elbow extended

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137
Q

what is the presentation of golfers elbow?

A

Tenderness along the medial elbow distally and anteriorly pain on resisted forearm pronation and wrist flexion

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138
Q

is there any sensory or motor deficit associated with epicondylitis?

A

usually no sensory deficit but grip strength may decrease over time

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139
Q

how do you diagnose epicondylitis?

A

Clinical diagnosis unless there are abnormal features i.e. nerve conduction if there is a sensory deficit

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140
Q

what are differentials for epicondylitis?

A

Cubicle tunnel syndrome osteoarthritis radial tunnel syndrome

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141
Q

what is the management of epicondylitis?

A

Ice and NSAIDs consider using brace/strap if there is no improvement at six weeks give physiotherapy and local anaesthetic ongoing management is surgical

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142
Q

what is osteoporosis?

A

A complex skeletal disease characterised by low bone density micro-architectural defects in bone tissue causing increased bone fragility and susceptibility to fractures

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143
Q

what is the function of osteoclasts?

A

resorption of bone matrix. They create a resorption pits and then cause apoptosis they then signal to osteoblasts

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144
Q

what is the function of osteoblasts?

A

Build bone. Once osteoclasts have signals the osteoblasts synthesised bone matrix this bone matrix then undergoes mineralisation

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145
Q

what factors influence bone remodelling?

A

Interleukins colony-stimulating factors parathyroid hormone activated vitamin D calcitonin and oestrogen

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146
Q

how does parathyroid hormone and vitamin D effect bones?

A

see image

147
Q

what is rank L?

A

expressed by osteoblasts allows for interaction with rank receptors on osteoclasts

148
Q

what is osteoprogenitor?

A

secreted by osteoblasts and inhibits rank held induced activation of rank on osteoclasts

149
Q

what is the function of oestrogen on bone remodelling? What does this mean for postmenopausal women?

A

oestrogen allows for expression of rank L. A decrease in oestrogen means that there is overexpression of rank L meaning that there is increased osteoclast function

150
Q

what are the features of the FRAX score?

A

see image

151
Q

What is a presentation of osteoporosis?

A

Usually asymptomatic until there is a fracture commonly hit all vertebral - vertebral fractures may not be noticed and may present with back pain and kyphosis

152
Q

what is the management of a patient who has a FRAX score < 10 %

A

ensure adequate calcium intake and vitamin D give lifestyle advice such as increase low impact exercise and tips to reduce risk of falls

153
Q

what is the management of patient who has a FRAX score > 10%

A

measure bone mineral density with DEXA scan

154
Q

what should you do with a patient who has a key score of <2.5 and no Hx of hip fracture

A

ensure adequate calcium intake and vitamin D give lifestyle advice such as increase low impact exercise and tips to reduce risk of falls

155
Q

what should you do with a patient who has a T score of >2.5

A

exclude any secondary causes of osteoporosis and commence medical management of osteoporosis (bisphosphonates + calcium and vD)

156
Q

what T score is diagnostic of osteopenia?

A

1-2.5

157
Q

what T score is diagnostic of osteoporosis?

A

>2.5

158
Q

what T score is diagnostic of severe osteoporosis?

A

>2.5 with history of hip fracture

159
Q

apart from the decks of and what other investigations might want to perform in patient with osteoporosis?

A

Wrist hit spine heel x-rays may show osteoporotic fractures and bone metabolic profile as well as PTH thyroid function tests cortisol (cushings) and testosterone (hypogonadism IF PT IS YOUNG MALE)

160
Q

what tests are involved in a bone metabolic profile?

A

alkaline phosphate serum calcium albumin creatinine phosphate vitamin D

161
Q

what would the results be in osteoporosis for a bone metabolic profile?

A

alkaline phosphate (+) serum calcium (- in osteoporosis/malacia but + in hyper PTH) albumin (- in malnutriition) creatinine (CKD causes mineral disorders) phosphate (-) vitamin D (usually normal)

162
Q

what are secondary causes of osteoporosis?

A

Hyperparathyroidism hyperthyroidism Cushing’s disease/Cushing’s syndrome hypogonadism in younger males chronic kidney disease causing mineral disorders

163
Q

what is the management for osteoporosis?

A

Bisphosphonates with calcium and vitamin D supplements (second line use renlofaxine or denusomab or if those CI tetrapartide )

164
Q

how do bisphosphonates work in the management of osteoporosis?

A

Analogues of pyrophosphate which inhibits bone resorption by binding to bone preventing both growth and the dissolution of bone newer bisphosphonate agents have a decreased effect on pacification but still stop restore balance they may also cause osteoblasts to produce inhibitors of osteoclast formation

165
Q

what are side effects of bisphosphonates?

A

Osteonecrosis of the jaw peripheral oedema GI upset oesophageal ulcer if this occurs discontinue oesophagitis if this occurs discontinue eye inflammation and renal impairment

166
Q

what is denusomab and how does it work in osteoporosis?

A

A monoclonal antibody which blogs rank L by binding to it

167
Q

What is ralofexine and how does it work in osteoporosis?

A

Mimics the effects of oestrogen causing an increase in osteoprogenitor and a decrease in osteoclast activity through decreasing rank L

168
Q

What is oosteomalacia?

A

Metabolic bone disease characterised by incomplete mineralisation of the underlying osteo it for a low weighing growth plate closure it adult Ricketts

169
Q

what are the causes of osteomalacia?

A

vitamin D deficiency malabsorption chronic kidney disease kidneys convert vitamin D to activated vitamin D liver disease hypophosphataemia drugs inborn errors of metabolism

170
Q

how does vitamin D deficiency because osteomalacia?

A

from decreased UVB exposure and inadequate dietary intake - reduced activated vitamin D means there is less absorption of calcium which in turn causes bone weakness

171
Q

what diseases can cause malabsorption of vitamin D or calcium?

A

coeliac gastrostomy cystic fibrosis

172
Q

How does kidney disease cause osteomalacia?

A

kidneys convert vitamin D to activated vitamin D

173
Q

How does liver disease cause osteomalacia?

A

liver and bowel disease can cause abnormal vitamin D metabolism

174
Q

How does hypophosphataemia cause osteomalacia?

A

attenuate activation of vitamins D

175
Q

what causes hypophosphataemia?

A

Genetic Ricketts poorly controlled diabetes metabolic acidosis diuretics and alcohol abuse hyperparathyroidism

176
Q

What drugs can cause osteomalacia?

A

first-generation bisphosphonates prolonged PETN dietary fluoride phosphate binders containing aluminium

177
Q

described the physiology of calcium in the body?

A

Parathyroid hormones from the parathyroid glands and calcitonin from thyroid glands regulate serum calcium low serum calcium activates the parathyroid gland to make parathyroid hormone this acts on the bones small intestines and kidneys – increasing intestinal absorption decreasing kidney excretion and increase the release of calcium on the bones when calcium is too high calcitonin inhibits the resorption of calcium and encourages calcium deposit in the bone matrix

178
Q

describe the physiology of vitamin D in the body?

A

UVB or dietary vitamin D is absorbed the liver converts vitamin D2 25 hydroxy vitamin D which is then converted by the kidneys to 125 dihydroxyvitamin D this causes bone mineralisation and calcium absorption

179
Q

What are the symptoms of Osteomalacia?

A

increase in fractures proximal muscle weakness (usually from a decrease in vitamin D) very severe can have a waddling gait from bone pain and proximal myopathy

180
Q

what investigations are required in the diagnosis of osteomalacia??

A

Bone profile (low calcium/or normal low phosphate high alk phos) vitamin D (low) levels para thyroidhormone levels (high due to low calcium) renal liver and thyroid function tests (causes of vitamin D) FBC and iron studies (check for malnutrition) rheumatoid factor ESR and CRP (inflammatory and autoimmune causes)

181
Q

what tests does bone profile include?

A

Calcium Phosphate Albumin Alkaline phosphatase

182
Q

A patient presents with a history of frequent fractures you do a bone profile the calcium is normal the serum phosphate is low out phosphate is high - you also check the parathyroid hormone in vitamin D (high and low respectively) - what is most likely diagnosis?

A

Osteomalacia

183
Q

what is the management of osteomalacia?

A

The calcium and vitamin D supplements phosphate used in inherited or acquired disorders of phosphate wasting or oncogenic causes

184
Q

what is Ricketts?

A

Metabolic bone disorder characterised by defective mineralisation of the episeal growth plate cartilage resulting in stunted growth and abnormalities

185
Q

what are the symptoms of rickets?

A

bone pain from pseudo-fractures or insufficiency fractures growth failure and delayed motor development bony deformities – bowlegged and knees muscle weakness

186
Q

what investigations are required for Ricketts?

A

X-rays of the long bone urinary calcium and phosphate

187
Q

what are the two types of Ricketts?

A

Hypocalcaemia (will have low calcium and high phosphate) and hypophosphataemia (normal calcium and high phosphate)

188
Q

what is the management of rickets?

A

Hypocalcaemia is a medical emergency and is to be treated in hospital ongoing care with calcium and vitamin D supplements +/- phosphate salts if it is vitamin D resistant give high-dose or intra-cavle vitamin D

189
Q

What is the acute management of hypocalcaemia?

A

intravenous (IV) calcium gluconate

190
Q

what is Paget’s disease?

A

chronic bone disorder that is characterised by focal areas of increased bone remodelling resulting in overgrowth of poorly organised bone leading to deformities nerve compressions and pathological fractures

191
Q

what Are the symptoms of pagets disease?

A

mainly asymptomatic symptoms arising from lesion secondary osteoarthritis deformity or pathological fracture or neurogenic symptoms from bony overgrowth is causing impingement

192
Q

what are the most common neurogenic symptoms associated with pagets disease?

A

chronic facial pain hydrocephalus nerve entrapment spinal stenosis

193
Q

why might pagets disease cause heart failure?

A

Increased demand due to increased flow to metabolically active site

194
Q

what investigations are required in pageants disease?

A

Bone profile will show very raised alk Phos, vitamin D (normal differentiates between osteomalacia) liver function tests (differentiate from liver causes of increased alk phos) plain x-ray of long bones

195
Q

What usually raises suspicion of pagets disease?

A

incidental finding of increased alk phos

196
Q

what blood marker is used to monitor the management response of pagets disease?

A

serum procollagen peptides

197
Q

what is the management of pagets disease?

A

asymptomatic: observation regular follow-up patient education and preventative measures – increase calcium and vitamin D symptomatic: bisphosphonates or calcitonin and physiotherapy as well as Occupational Therapy such as frames and spinal braces surgery may be needed for severe deformity or secondary osteoarthritis

198
Q

what are the main methods of management of fractures?

A

Reduction restoring bones and joints to normal position retention maintaining the reduced position until there is been healing and rehabilitation

199
Q

how should you examine an x-ray?

A

Bones cartilage joints and soft tissue in that order

200
Q

what is the most severe complication of major pelvic fractures?

A

exsanguination

201
Q

What are complications of compartment syndrome?

A

Ischaemia myoglobunurea renal failure

202
Q

what is a severe complication of open fractures?

A

Blood loss or osteomyelitis

203
Q

what is a complication of limb injury with vascular injury?

A

Amputation

204
Q

what is a typical presentation of a fracture?

A

Bruising swelling tenderness however incomplete or unique or to fractures will have no swelling

205
Q

what are the two most common fractures of the wrist?

A

fracture of the distal radius or of the scaphoid

206
Q

what usually causes a fracture of the distal radius?

A

Fall on outstretched hand

207
Q

what other fractures are commonly associated with fracture of the radius?

A

ulnar styloid fracture distal ulnar fracture isolated scaphoid fracture

208
Q

patient has a fall on their outstretched hand they noticed a lot of pain on the left side of their wrist near the base of the thumb however on examination it is not very swollen or bruised what is the most likely pathology?

A

scaphoid fracture

209
Q

what severe complication is associated with fracture of long bones?

A

Haemorrhage and fat embolism

210
Q

what is the acute management of a long bone fracture?

A

Fluid resuscitation and control of major haemorrhage box splints analgesia cheque for neurovascular compromise and if present use traction to try and regain neurovascular supply

211
Q

what investigations are always required in open fractures?

A

X-rays full blood count blood type cross and match although these are often used in any severe fracture

212
Q

what is the management of an open fracture?

A

Analgesia debridement covered with antibiotics and tetanus toxoid injection surgery is needed within six hours

213
Q

what is the management of a stress fracture?

A

non-weight-bearing rest and analgesia and retention of position until healing has occurred

214
Q

when word of surgical management be required in stress fractures?

A

In femoral neck fractures or emerald displaced fractures

215
Q

where does the clavicle most commonly fracture?

A

In the middle third of the clavicle

216
Q

what is the most common cause of clavicle fractures?

A

Direct trauma or indirect trauma such as a fall onto the shoulder

217
Q

what is the presentation of a threatened skin injury?

A

Tented tethered non-blanching skin

218
Q

what is a common complication of clavicle fractures?

A

Open Fractures or threatened skin injuries due to the subclavian artery

219
Q

patient has recently fallen onto the shoulder they have pain on the active movement of the arm what fractures could this be?

A

Clavicle sternoclavicular or ACJ joint dislocation x-rays are needed for diagnosis

220
Q

what usually causes fractures of the humorous shaft?

A

High impact injury in the young low impact injury in the elderly

221
Q

what is a common complication of humorous shaft fracture?

A

radial nerve injury

222
Q

how can you check for radial nerve injury?

A

Check sensation all over the dorsal webspace and check for weakness in wrist extension

223
Q

where is the location of the radial nerve on the humerus?

A

Spiral groove

224
Q

in which population group is a supra-chondylar fracture common?

A

paediatrics

225
Q

what is important that you assess in supra chondylar fractures?

A

careful neurovascular assessment of median radial and ulnar nerves as supra chondylar fracture occurs close to neurovascular structures

226
Q

what complications can occur through the elbow dislocation?

A

Ulnar or medial artery damage as well as damage to the brachial artery

227
Q

what is the most common carpal fracture?

A

scaphoid fracture

228
Q

what follow-up is required for scaphoid fracture?

A

x-ray again in one – two weeks as they can be difficult to see so even if the x-rays normal it needs re-imaging

229
Q

who is most at risk of hip fractures?

A

Older people with osteopenia or osteoporosis are low impact falls

230
Q

what can be the source of haemorrhage in pelvic injury?

A

Internal Ilac

231
Q

what is the management of a neck of femur fracture?

A

Analgesia and fast-track to the ward for surgery

232
Q

what is the management of a femoral shaft fracture?

A

Oxygen and IV fluids with analgesia given thermal nerve block and traction splints before surgery

233
Q

how can you commonly differentiate between ligamentous injury of the ankle or an ankle fracture?

A

See image below for the classic bruising pattern of a ligamentous injury

234
Q

what are indications for x-ray of the ankle?

A

Bony tenderness inability to weight bear

235
Q

what is the management of an ankle fracture?

A

ASAP reduction as ankle fractures can cause serious complications due to poor circulation and increased pressure on skin

236
Q

what are the most common foot fractures?

A

calcaneal and 5th metacarpel

237
Q

What Causes calcineal fractures?

A

direct blow from fall from height

238
Q

how does the fracture of the fifth metatarsal present?

A

Present similar to a sprained ankle so it is important to check the fifth metatarsal for local tenderness

239
Q

what is septic arthritis?

A

infection of one or more joints caused by pathogenic inoculation of microbes either directly or through the blood

240
Q

what is the presentation of septic arthritis?

A

Acute onset red-hot swollen and painful joint decreased range of motion pain not better at rest fever usually present

241
Q

what are the most common causes of septic arthritis?

A

Streptococcus or staphylococcus including MRSA gonococcal in sexually active people in elderly and immunocompromised can be gram negatives

242
Q

what is the approach to septic arthritis?

A

Any joint which is red-hot swollen acutely painful with decreased range of motion should be treated as septic arthritis until proven otherwise this is even in the absence of fever and irrespective of microbiology and blood results

243
Q

what investigations are required for septic arthritis?

A

Urgent referral and admission aspiration of joint (ultrasound guidance if the hip) with microscopy Gram stain cultures & over your fluid white cell count blood cultures and inflammatory markers FBC and U+E and LFT for ?sepsis

244
Q

what is the management of septic arthritis?

A

start empirical antibiotics straightaway if caused by a prosthesis then urgent surgery is required joint aspirations may also be performed

245
Q

what is reactive arthritis?

A

An inflammatory arthritis that occurs after exposure to certain GI or GU infections

246
Q

what is the classic triad of reactive arthritis?

A

Post infection arthritis non-gonococcal you with writers and conjunctivitis

247
Q

what pathogens usually cause reactive arthritis?

A

Chlamydia Campylobacter judge tonight Salmonella or Shigella

248
Q

what is the presentation of reactive arthritis?

A

systemic features such as fever peripheral and axial arthritis usually asymmetrical oligo arthritis of the large joints of lower limbs and etethesis ( inflammation of the insertion of the tendon to the bone) + urethritis and conjunctivitis may be presents (classic triad not always there) PLUS Hx of GI or GU infection

249
Q

what does the picture show below

A

blennor rhagicum an uncommon presentation of reactive arthritis

250
Q

what investigations are required for reactive arthritis

A

inflammatory markers swabs from G Utrecht stool cultures screen for differentials: ANA – SLE R or anti-CCP atheroscentesis – gout Plain X may show chronic changes

251
Q

what is the acute management of reactive arthritis?

A

treat any underlying cause arthritis merged with NSAIDs or corticosteroids if it’s severe or poly articular or if there is severe eye disease intra-articular corticosteroids may be used in mono/oligo arthritis

252
Q

what is the correct management of reactive arthritis?

A

sulfalazine DMARD

253
Q

What is osteomyelitis?

A

Inflammatory bone condition caused by an infective organism usually affecting one bone

254
Q

what pathogen usually causes osteomyelitis?

A

Staphylococcus aureus

255
Q

what is the presentation of osteomyelitis?

A

non-specific pain at the site of infection malaise and fatigue and fever local inflammation erythema and swelling decreased range of motion

256
Q

what are risk factors for osteomyelitis?

A

Diabetes will ices especially if the foot ulcers present periodontitis

257
Q

how do you diagnose osteomyelitis?

A

Plain x-ray confirmed with MRI/CT

258
Q

apart from imaging what other tests are useful in osteomyelitis?

A

ESR CRP white cell counts and blood cultures as well as deep microbiological samples which confirms the diagnosis

259
Q

what is the acute management of osteomyelitis?

A

High-dose antibiotics IV broad spectrum and once cultures come back more targeted therapy immobilisation and analgesia surgery is required if there is dead bone or biofilm

260
Q

what does the presence of dead bone or biofilm indicate in osteomyelitis?

A

it is now chronic

261
Q

What is SLE?

A

a chronic multisystem disorder that most commonly affects women in their reproductive years

262
Q

what are some triggers of SLE?

A

Environmental factors such as drugs (sulfasalazine) or viruses such as EBV

263
Q

what is the pathophysiology of SLE?

A

An antigen driven immune-mediated disease with high affinity IgG that bind to double-stranded DNA as well as nuclear proteins causing T cell dysregulation and B-cell dysregulation resulting in an autoimmune response to your own tissues

264
Q

what are the 11 diagnostic criteria is of SLE?

A

malar rash discoid rash photosensitive rash oral/nasopharyngeal ulcers arthritis sclerosis renal disorders neurological disorders haematological disorders immunological disorders ANA positive

265
Q

what does the image below show?

A

malar rash

266
Q

What does the image below show?

A

discoid rash – erythematous and raised rash with adherent ^ Artic scaling and follicular plugging

267
Q

what is the description of the type of arthritis which usually affects patients with SLE?

A

Are the writers of two or more peripheral joints with tenderness and swelling or diffusion commonly affecting the hands

268
Q

what other common consequences of sclerosis in SLE?

A

Pruritus or pericarditis

269
Q

how do you detect renal disorders in SLE?

A

proteinuria red cell casts U+E + creatinine plus renal USS

270
Q

what is the presentation of neurological disorders in SLE?

A

Seizures or psychosis in the absence of any other causes

271
Q

what type of haematological disorder does SLE cause?

A

Haemolytic anaemia is with leukopenia lymphopenia and thrombocytopenia

272
Q

what antibodies are usually present in SLE?

A

ANA anti-DNA auntie Smith anti-phospholipid

273
Q

what does antiphospholipid antibodies cause in patients with SLE?

A

Increased PTT

274
Q

what is the diagnostic criteria for SLE?

A

four out of the 11 symptoms and if ANA is positive it is surely diagnostic

275
Q

how do you manage SLE/ SLE serositis/arthritis?

A

moderate/mild symptoms of arthritis: hydro chloroquine NSAIDs or corticosteroids corticosteroids are given methotrexate plus foaling acid can be added in if necessary to help control symptoms

276
Q

how does management change of lupus nephritis or neuropsychiatric lupus is present?

A

cycloposphamide, mycrophenylate or tacrolimus + corticosteroids are needed

277
Q

what is Raynaud’s disease?

A

vasospasm which causes digits to change colour to white due to lack of blood flow they then turn either red or blue if there is reperfusion or de-oxygenation

278
Q

what can cause secondary Raynauds?

A

scleroderma rheumatoid arthritis SLE’s sjorgens syndrome connective tissue disease atherosclerosis or malignancy

279
Q

how do you diagnose raynauds disease?

A

Clinical investigations only required if you think that Raynaud’s is secondary in order to find the underlying cause

280
Q

what are the symptoms of raynauds disease

A

well demarcated pallet occurring when cold digital pain/discomfort (more typical and secondary) paraesthesia on rewarming dilated capillaries and nail bed (secondary)

281
Q

what is the management of 1ry raynauds disease

A

primary usually doesn’t require any management perhaps only some analgesia - lifestyle advice of keeping warm stopping smoking exercise more and avoiding stress

282
Q

what is the management of secondary raynauds disease?

A

CCB first-line then ace inhibitor or sometimes SSRI or topical GTN spray then alpha blocker for secondary rain old that can cause complications give prostacyclin + or phosphodiesterase - 5 inhibitor

283
Q

what complications can occur secondary to severe secondary raynauds disease?

A

digital ischaemia ulcers and infections

284
Q

what is giant cell arteritis?

A

a granulomatous vasculitis of large and medium-sized arteries

285
Q

what is the pathophysiology of giant cell arteritis?

A

T cells and macrophages are involved in the immune response Affecting the arteries artery releases growth and angiogenic factors in response to the immunological injury ultimately leading to intimal expansion and hyperplasia as well as narrowing of the vessel lumen

286
Q

what is the presentation of giant cell arteritis?

A

The headache at temporal or occipital lobes scalp tenderness claudication of upper extremities and jaw symptoms of poly myalgia rheumatica

287
Q

what findings would you see on examination of giant cell arteritis?

A

Absent temporal artery biopsy bruits abnormal funduscopy - anterior ischaemic optic neuropathy

288
Q

what are complications of giant cell arteritis?

A

Increase risk of cerebrovascular events if untreated can cause anterior ischaemic optic neuropathy leading to visual loss

289
Q

how do you diagnose giant cell arteritis?

A

Have high level of suspicion inflammatory markers should be taken plus full blood counts and liver function tests as haematological malignancy, hepatitis or other types of malignancy can mimic symptoms then urgent temporal artery biopsy

290
Q

what would a temporal artery biopsy show in giant cell arteritis?

A

Granulomatosis

291
Q

what is the management of giant cell arteritis?

A

After you’ve taken the bloods start prednisolone even if the diagnosis is unconfirmed by biopsy this avoids vision loss

292
Q

what is Henloch Schonlein Purpura?

A

the most common childhood vasculitis, a vasculitis affecting small vessels

293
Q

what usually precedes an episode of Henloch Schonlein Purpura?

A

URTI

294
Q

what is the pathophysiology of Henloch Schonlein Purpura?

A

there is deposition of IgA containing immune complexes within the tissues along with C3 and fibrin

295
Q

A child presents with a petechial/purpuric rash name the differentials and how you would differentiate based on symptos?

A

Insert picture

296
Q

charge presents with air a petechial purpuric rash which is non blanching but palpable, they are a febrile, complaining of abdominal pain and arthritis you do a urine dipstick and noticed there is presence of protein and red-cell casts - what is the most likely diagnosis?

A

Henloch Schonlein Purpura

297
Q

How do you diagnose Henloch Schonlein Purpura?

A

clinical diagnosis with your analysis is all that is required however some clinicians may do blood cultures as the appearance is similar to meningococcal infection

298
Q

what is the management of Henloch Schonlein Purpura?

A

and slides unsupportive management unless there is nephritis or severe abdominal pain then give corticosteroids

299
Q

what is polyarteritis nodosa?

A

A necrotising inflammation of medium-sized and small -sized arteries without glimmer you learn of writers or vasculitis in smaller vessels such as arterioles capillaries or venules

300
Q

What can cause polyarteritis nodosa?

A

hepatitis B although this is quite rare since the vaccine so it is usually non-hep B related

301
Q

what makes polyarteritis nodosum different from other vasculitis’?

A

it is not ANCA -positive and does not involve any small vessels

302
Q

what is the presentation of polyarteritis nodosum?

A

myalgia/arthralgia mono neuritis multiplex abdominal pain and renal impairment, ischaemia skin manifestations: leivido reticularis skin ulcers bullus/ vesicular eruptions purpurar/skin infarction

303
Q

what does the image below show?

A

Polyarteritis nodosum

304
Q

what investigations are carried out in Poliarteritis nodosa?

A

FBCLFT complement renal function test inflammatory markers and diagnostic is angiography showing micro aneurysms and vocal narrowing in medium blood vessels

305
Q

Wildwood SBC show anaemia in polyarteritis nodosum?

A

If there is any bleeding in the GI tract

306
Q

how can polyarteritis nodosa because derangements in renal function and liver function?

A

Ischaemic changes or if the liver potentially hepatitis B related

307
Q

wine might complement be decreased in polyarteritis Meadows up

A

due to increased coagulation esp if liver involved

308
Q

when would you take a biopsy in polyarteritis nodosum?

A

If angiography is inconclusive or unavailable biopsy would show focal and segmental transmural necrotising inflammation

309
Q

what is the management of polyarteritis nodosa?

A

If be related: short course of corticosteroids either IV or PO antivirals and plasma exchange if non-hepatitis related: PO corticosteroids + DMARD + cycliphosphomide. Wide (potentially IV corticosteroids if necessary)

310
Q

what is polymyalgia rheumatica?

A

An inflammatory room at a logical syndrome that manifests as pain and morning stiffness involving the neck shoulder girdle pelvic girdle in individuals over 50 years old

311
Q

what is poly myalgia rheumatic are commonly associated with?

A

giant cell arteritis although can occur in isolation

312
Q

What are the symptoms of poly myalgia rheumatic?

A

Acute onset pain which is typically worse in the morning of the neck shoulder girdle pelvic girdle stiffness and constitutional symptoms may be present

313
Q

what investigations might be used in polymyalgia rheumatics?

A

ESR CRP IL – 6 raised but normal tests for differentials + TEST FOR GCA

314
Q

what tests might you perform in a patient with ?Polymyalgia Rheumatica to exclude differentials?

A

Hypothyroidism (thyroid function tests) blood cancers (FBC serum protein electrophoresis) myositis (creatine kinase) ultrasound scan to check for bursitis synovitis ETC

315
Q

what is diagnostic for Polymyalgia rheumatica?

A

Absence of differentials positive GCA is highly indicative and rapid improvement of symptoms on corticosteroids is basically diagnostic

316
Q

what is the management of polymyalgia rheumatica?

A

PO corticosteroids plus calcium vitamin D supplements bisphosphonates are used to maintain bone strength if corticosteroids are required for more than one month

317
Q

why should you perform a chest x-ray before commencing methotrexate?

A

contraindicated in interstitial lung disease

318
Q

what is ankylosing spondylitis?

A

A chronic progressive inflammatory arthropathy leading to spinal fusion

319
Q

what genetic marker is ankylosing spondylitis closely associated with?

A

HLA-B27

320
Q

what is HLA-B27 commonly associated with?

A

I believe the acute anterior uveitis ankylosing spondylitis sero-negative arthropathy is: reactive arthritis and her passing arthritis psoriatic arthritis and aortic insufficiency

321
Q

what is the pathophysiology of ankylosing spondylitis?

A

has inflammation and erosion like rheumatoid arthritis but then has additional ossification causing the fusion of the joints mainly the SSacro Ilac joint and axial joints

322
Q

a patient presents with back pain which has been getting worse for over a month it is worse in the mornings and improves with exercise he notes that NSAIDs help with the pain but recently he has been waking up in the second half of the night because of the pain he has a history of Crohn’s disease – what is the most likely diagnosis?

A

Ankylosing spondylitis

323
Q

what are the symptoms of ankylosing spondylitis

A

: insidious onset worsen mornings improves with exercise resolution pain using NSAIDs and waking up in the second half the night with pain

324
Q

what features would you know on examination in ankylosing spondylitis?

A

loss of lumbar lordosis and flexion tenderness of the sacro-Ilac joint Costo-vertebral and hip joints may also be involved and kyphosis occurs in chronic ankylosing spondylitis

325
Q

if a patient presents the symptoms of? Ankylosing spondylitis that has spanned for more than three months what must you do?

A

specialist referral

326
Q

what is the BASMI score?

A

The Bath ankylosing spondylitis metrology index used to assess the severity and the level of disability of ankylosing spondylitis

327
Q

how do you investigate ankylosing spondylitis?

A

No test is diagnosticbut pelvic x-ray is (sacroilitis) MRI (mainly used if there is strong clinical indication but pelvic x-ray is normal ) x-ray of C, T, L spine HLA-B27 ESR and CRP

328
Q

what is the management of ankylosing spondylitis?

A

Physio and patient education h – telling them that no treatment will cause remission or decrease the rate of joint involvement but NSAIDs and paracetamol can help injure or to killer corticosteroids sulphasalazine for peripheral joint involvement or children with polyarthritis TNF alpha inhibitor pain refractory to other Mx

329
Q

what is antiphospholipid syndrome?

A

the assocuation of Antiphospholipid antibodies with a variety of symptoms caused by thrombosis and pregnancy -related morbidity

330
Q

what is a definition of pregnancy morbidity in antiphospholipid syndrome?

A

loss of three or more embryos before 10 weeks for the loss of one or more after 10 weeks or the premature birth of a normal baby because of eclampsia/pre-eclampsia or placental insufficiency in relation to antiphospholipid antibodies being present

331
Q

what is the diagnostic criteria for antiphospholipid syndrome?

A

Vascular thrombosis or pregnancy morbidity the presence of antiphospholipid antibodies onto or more occasions 12 weeks apart or in general anyone with a thrombotic MRI is presumed to have antiphospholipid syndrome until proven otherwise

332
Q

What can antiphospholipid syndrome occur secondary to?

A

SLE and less commonly sjoirgens, rheumatoid arthritis systemic sclerosis or vasculitis

333
Q

what antibodies should you screen for in? Antiphospholipid syndrome?

A

Lupus anticoagulant anticardiolipin antibodies anti b2 glycoprotein

334
Q

what is the management of antiphospholipid syndrome?

A

Manage acute thrombosis with: LMWH and long-term warfarin with management of risk factors for clotting if pregnant give LMWH during pregnancy anticoag after delivery for 6-8wspecialist obstetric care is required

335
Q

what is the management of catastrophic antiphospholipid syndrome?

A

Low molecular weight heparin with prednisolone and fatal monitoring if pregnant

336
Q

what is sjorgen syndrome?

A

a chronic inflammatory autoimmune disorder characterised by diminished lacrimal gland and the library gland secretion

337
Q

what is sjorgen syndrome commonly associated with?

A

Other autoimmune/perimeter logical diseases such as SLE rheumatoid arthritis and scleroderma but can occur 1ry - less common

338
Q

who is most at risk of developing sjorgens syndrome?

A

female 20 – 30 years or postmenopausal autoimmune disease

339
Q

what is the presentation of sjorgen syndrome?

A

fatigue dry eyes – sensitivity to light and wind dry mouth – dental caries vasculitis commonly causing a rash arthralgia andmyalgia - symptoms lasting over three months

340
Q

what type of arthritis does sjorgen sndrome typically cause?

A

inflammatory arthritis that is noncorrosive characterised by morning stiffness and pain of the small joints of hands and feet

341
Q

what investigations should be performe for sjorgen syndrome?

A

anti-60 Kd and anti LA antibodies schimers test +ve - diminished tear production x-rays of arthritic joints skin biopsy and angiogram if there is vascular tick presentation renal function tests and urinalysis

342
Q

what renal involvement can sjorgens cause?

A

renal tubular acidosis with hypokalaemia and a normal anionic gap

343
Q

what is the management of Sjorgen syndrome related arthritis?

A

NSAIDS and short-term corticosteroids can be given

344
Q

what is the management of Sjorgen syndrome related vasculitis?

A

corticosteroids and is more severe IVIG

345
Q

what is the management of Sjorgen syndrome related renal acidosis?

A

potassium depletion and alkali

346
Q

what is the management of Sjorgen syndrome related neuropathy?

A

IVIG’s

347
Q

what is the management of Sjorgen syndrome related salivary and lacrimal disfunction?

A

artificial tears , salivary substitutes if more severe cholinergic drug like Polycarpine

348
Q

what is systemic sclerosis?

A

A multisystem autoimmune disease characterised by functional and structural abnormalities of small blood vessels fibrosis of the skin and internal organs

349
Q

what are the main features of systemic sclerosis?

A

Vasculopathy fibrosis immune system activation has a strong genetic factors so family history of systemic sclerosis or any other autoimmune disease is relevant

350
Q

What are the musculoskeletal manifestations of systemic sclerosis?

A

Causes symptoms similar to synovitis as well as tendon friction rubs inflammatory like arthritis and calcinosis (localised hard masses at pressure point)

351
Q

what is the pathophysiology of systemic sclerosis?

A

There is inflammation causing swelling as the swelling decreases sclerodactyl occursm causing stiffness

352
Q

what are some vascular manifestations of systemic sclerosis?

A

Reynard disease digital pits and ulcers from poor perfusion can cause heart/renal failure

353
Q

What are the GI manifestations of systemic sclerosis?

A

GOR D dysphasia abdominal distension and constipation from delayed motility and anaemia from chronic GI bleeding

354
Q

what are nerve manifestations of systemic sclerosis?

A

usually causes proximal muscle weakness

355
Q

what are pulmonary manifestations of systemic sclerosis?

A

Interstitial lung disease and pulmonary hypertension

356
Q

what are the main diagnostic factors of systemic sclerosis??

A

Presence of certain antibodies: anti scl 70 or anti topirimase - lung anti rna - renal and skin anti pm/scl and anti am/rnp - myositis

357
Q

how would you assess pulmonary involvement in systemic sclerosis?

A

Pulmonary function tests and chest x-ray echo for pulmonary hypertension

358
Q

how would you assess GI involvement in systemic sclerosis?

A

FBC barium swallow and endoscopy if you think there is GI bleeding

359
Q

how would you assess muscular involvement of systemic sclerosis?

A

Creatine kinase EMG and muscle biopsy

360
Q

what are complications of systemic sclerosis?

A

Renal crisis cardiac tamper Nadia GI bleeding and malfunction skin involvement myopathy synovitis interstitial lung disease and failure pulmonary hypertension pericardial involvement

361
Q

what is compartment syndrome?

A

a pathological condition characterised by the elevated interstitial pressure in a closed superficial compartment resulting in microvascular compromise due to a restriction of capillary blood flow

362
Q

what are the causes of compartment syndrome?

A

fracture compartment haemorrhage direct soft tissue injury direct muscular injury

363
Q

what is the initial management of compartment syndrome?

A

High index of suspicion and early recognition is crucial as unity suspect compartment syndrome do a fasciotomy - if you have immediate access to compartment pressure measurement device then you can check this however do not delay treatment

364
Q

what is the presentation of compartment syndrome?

A

pain pressure pulses this paralysis paraesthesia these indicate arterial ischaemia pain disproportionate to the severity of injury and pain worse on passive stretching - most common syndromes

FINALS (24 decks)

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