Rheumatology Flashcards

Question

Indications of 'plain X-ray' in back pain

Answer 1

* Suspected vertebral compression fractures * OA (Osteroarthritis) * Degenerative _disc_ disease

Answer 2

If metastatic disease is suspected

Answer 3

* Routine biochemistry * CBC *(= haematology)* * ESR * CRP (to screen for sepsis and inﬂammatory disease) * Protein and urinary electrophoresis \>\>\> for myeloma * HLA-B27 status \>\>\> in IBP * PSA \>\>\> for prostate carcinoma

Answer 4

* _Progressive_ spinal stenosis * Spinal cord compression _with_ nerve root compression

Answer 5

* **Education** is important in mechanical back pain. Eemphasise \>\>\> * It is self-limiting condition * Exercise is helpful (rather than damaging) * Regular **Analgesia and/or NSAIDs** (may be required) \>\>\> to improve mobility + to facilitate exercise. * **Return to work** and normal activity (ASAP) * Bed rest is NOT helpful \>\>\> may increase the risk of chronic disability. * If a return to normal activities has not been achieved by 6 weeks \>\>\> refer for **physical therapy** * **Low-dose tricyclic antidepressant** \>\>\> may help pain, sleep and mood. Other occasional treatment modalities \>\>\> * Epidural and facet joint injection * Traction * Lumbar supports *(though there is limited RCT evidence to support their use)* * Malignant disease, osteoporosis, Paget’s disease and SpAs \>\>\>\>\> speciﬁc treatment of the underlying condition. * Surgery is required in less than 1% of patients with low back pain

Answer 6

* The prevalence rises progressively with age * At some point of life \>\>\> 45% of all people develop knee OA and 25% hip OA * Although some are asymptomatic \>\>\>\>\> the lifetime risk of having a total hip or knee replacement for OA in someone aged 50 is about 11% for women and 8% for men in the UK. * There are major ethnic differences in susceptibility: * The prevalence of hip OA is lower in Africa, China, Japan and the Indian subcontinent than in European countries, and that of knee OA is higher. * Higher prevalence of knee OA in the Indian subcontinent and East Asia might be accounted for _by squatting._

Answer 7

**Genetics** • Skeletal dysplasias • Polygenic inheritance (in most cases \> polygenic; several genetic variants of small effects) * Heritability of OA ranges from \>\>\> * *_Knee \> 43%_* * *_Hip \> 60%_* * *_Hand \> 65%_* * OA can, however, be a component of _multiple epiphyseal dysplasias_ \>\>\>\>\> caused by mutations in the genes that encode components of _cartilage matrix._ **Developmental abnormalities (/structural abnormalities) Cause:**presumably due to \>\>\> abnormal load distribution across the joint • _Developmental dysplasia_ of the hip • _Slipped femoral epiphysis_ \>\>\> these are associated with a high risk of OA (Similar mechanisms probably explain the increased risk of OA in patients with limb deformity secondary to Paget’s disease of bone) **Repetitive loading (due to 'biomechanical factors')** • Farmers \>\>\> hip OA • Miners \>\>\> knee OA • Elite or pofessional athelets \>\>\> knee or ankle OA **Adverse biomechanics (who have had destabilising injuries)** • Meniscectomy • Ligament rupture • Paget’s disease **Obesity** (strong association) * Particularly hip \>\>\> thought to be,partly due to \>\>\> * biomechanical factors * (also play a role) _cytokines_ released from adipose tissue **Trauma Hormonal**(_Oestrogen_ appears to play a role) • Oestrogen deficiency • Aromatase inhibitors *(for therapy of breast cancer)* \>\>\> flare of OA symptoms **Neutral factor:** Participation in recreational sport \>\>\> does not increase risk significantly **Protective factor:** HRT; \>\>\> women who use HRT have lower rates of OA

Answer 8

* **Defining feature of OA:** degenation of articular cartilage * **Normally,** chondrocytes are terminally differentiated cells * **In OA** \>\>\> chondrocytes start dividing to produce \>\>\> "nests of metabolically active cells" * **Initially,** matrix components are produced by these cells (at an increased rate) * **At the same time** \>\>\> accelerated degradation of the major structural components of cartilage matrix, including _aggrecan_ _and type II collagen_ * **Eventually,** the concentration of aggrecan in cartilage matrix falls \>\>\> makes the cartilage vulnerable to load-bearing injury \>\>\> fissuring of the cartilage surface (‘fibrillation’) then occurs \>\>\> leading to \>\> * the development of deep vertical clefts * localised chondrocyte death * decreased cartilage thickness. ## Footnote \>\>\>This is initially focal \>\>\> mainly targeting the maximum load-bearing part of the joint \>\>\> But eventually \> large parts of the cartilage surface are damaged \>\>\> in the abnormal cartilage, _c__alcium pyrophosphate and basic calcium phosphate crystals_ often become deposited

Answer 9

degenation of articular cartilage

Answer 10

Abnormalities in subchondral bone \>\>\> * sclerotic * the site of subchondral cysts

Answer 11

At the joint margin \>\>\> fibrocartilage is produced \>\>\> undergoes endochondral ossification \>\> form osteophytes

Answer 12

* Bone remodelling + cartilage thinning \>\>\> slowly alter the shape of the OA joint \>\>\> _increasing its surface area._ * Homeostatic mechanism operative in OA \>\>\> causes \> enlargement of the failing joint \>\>\> to spread the mechanical load over a greater surface area.

Answer 13

* Higher BMD values (at sites distant from the joint) + particularly, associated with osteophyte formation. * Patients with OA are partially protected from developing osteoporosis and vice versa. * Why: the genetic factors that predispose to osteoporosis might be protective for OA.

Answer 14

* in OA \>\>\> the synovium is often **hyperplastic** * It may be the site of **inflammatory change** * But to a much lesser extent than in RA &other inflammatory arthropathies. * **Osteochondral bodies** commonly occur within the synovium, reflecting \>\>\> * chondroid metaplasia or * secondary uptake and growth of damaged cartilage fragments

Answer 15

Outer capsule also thickens and contracts \>\>\> usually retaining the stability of the remodelling joint.

Answer 16

Around the joints \>\>\> wasting of muscles + non-specific type II fibre atrophy

Answer 17

* *Main presenting symptoms:** joint pain + functional restriction * *Characteristic distribution:** the hips, knees, PIP and _DIP_ joints of the hands, neck and lumbar spine **Pain** * **Onset**: insidious \>\>\> over months or years * **Nature:** Variable or intermittent nature over time (‘good days, bad days’) * **Mainly related to/increased by** \>\>\> movement and weight-bearing * **Releived by** \>\>\> Rest * _Only brief (\<15 mins) morning stiffness and brief (\<5 mins) ‘gelling’ after rest_ * _Usually only one or a few joints painful_ **Clinical signs** * **Restricted movement** * For many people, functional restriction of the hands, knees or hips is an equal, if not greater, problem than pain * **Coarse crepitus:** _Palpable, sometimes audible_ * **Bony swelling** (_Around joint margins_) * **Tenderness** (_Joint-line or periarticular_) * **Deformity** (usually _without instability_) * **Muscle weakness and wasting** * *Mild or absent synovitis* * The clinical findings _vary according to severity_ but are *principally* *those of joint damage.*

Answer 18

The causes of pain in OA are not completely understood but may relate to \>\>\> * _increased pressure_ in **subchondral bone** (mainly causing _night pain)_ * **Trabecular** _microfractures_ * **Capsular** _distension_ * **Synovium** \>\>\> _Low-grade synovitis_ * Bursitis (may also be) * Enthesopathy (Secondary to altered joint mechanics) (may also be)

Answer 19

Rough articular surfaces

Answer 20

due to capsular thickening or blocking by osteophyte

Answer 21

The correlation between the presence of structural change (as assessed by imaging, and symptoms such as pain and disability) **Varies markedly according to site.** The correlation \>\>\> * **Stronger at the hip (than that of knee)** * **Poor at small joints** This suggests that \>\>\> the risk factors for pain and disability may differ from those for structural change. \>\>\>\> for example \>\>\> * **At the knee,** \>\>\>\>\> reduced quadriceps muscle strength + adverse psychosocial factors (anxiety, depression) \>\>\>\> correlate more strongly with pain and disability [[than the degree of radiographic change]] * _Radiological evidence_ of OA is _very common in middle-aged_ _and older people_ * The disease may coexist with other conditions, \>\>\> so it is important to remember that \>\>\> pain in a patient with OA may be due to another cause.

Answer 22

* **Age:** Peak onset in the middle age * **Sex:** Marked female preponderance * **Genetics:** Strong genetic predisposition; * the daughter of an affected mother has a 1 in 3 chance of developing nodal OA herself. * **In hand:** * Polyarticular \>\>\> finger interphalangeal joint OA * Heberden’s (± Bouchard’s) nodes * _Good functional outcome for hands_ * Predisposition to OA at other joints, _especially knees_

Answer 23

Some patients are _asymptomatic_ ..... whereas, others \>\>\> **From 40 years onwards** \>\>\> at **one or more PIP and DIP joints** of the hands \>\>\> _pain +_ _stiffness + swelling_ \>\>\> gradually, these develop _posterolateral swellings_ *on each side of the* *_extensor tendon_* \>\>\> which slowly _enlarge + harden_ \>\> become **Heber**_d_**en’s (**_D_**IP)** and **Bouchard’s (PIP)** nodes. Typically, **Each joint** \>\>\> goes through *_a phase of episodic symptoms_* *_(1–5 years)_* \>\>\> while _the node evolves and OA develops_ \>\>\> **Once OA** **is fully established** \>\>\> * *Symptoms may subside + hand function often remains good* * Due to _osteophyte_ formation \>\>\> affected _joints are enlarged_ * characteristic lateral deviation (often showed) \>\>\> reflecting the asymmetric focal cartilage loss of OA

Answer 24

Involvement of the first CMC joint is also common, leading to \>\>\> * Pain on trying to open bottles and jars * Functional impairment Clinically, it may be detected by \>\>\> * The presence of crepitus on joint movement, and * Squaring of the thumb base

Answer 25

At the knee, OA principally targets \>\>\> * the patello-femoral compartment * the medial tibio-femoral compartments But eventually spreads \>\>\> to affect the whole of the joint It may be \>\>\> * Part of generalised nodal OA or isolated OA * Most patients have bilateral and symmetrical involvement.

Answer 26

Trauma \>\>\> may cause unilateral OA

Answer 27

* **Localised pain** \>\>\> in the anterior or medial aspect of the knee and upper tibia. * **Patello-femoral pain** \>\>\> (usually) worse going up and down stairs or inclines. * **If posterior** **knee pain** \>\>\> suggests \>\>\> the presence of a complicating popliteal cyst (Baker’s cyst). * Difficulties in tasks, such as: * Prolonged walking * Rising from a chair * Getting in or out of a car * Bending to put on shoes and socks

Answer 28

* **Gait:** A jerky, asymmetric (antalgic) gait + less time weightbearing on the painful side * **Deformity:** * Varus * Valgus (less commonly) * (and/or) fixed flexion deformity * **Tenderness:** * Joint-line and/or periarticular tenderness (_secondary anserine bursitis + medial ligament enthesopathy_) \>\>\> causing tenderness of the _upper medial tibia_ * **Weakness and wasting** of the _quadriceps muscle_ * **Restricted flexion and extension** + **coarse crepitus** * **Bony swelling** _around the joint line_ * **In knee OA \>\>\> CPPD crystal deposition is common** * *This may result in** \>\>\> more _overt inflammatory component (stiffness, effusions)_ + _super-added acute attacks of synovitis_ \>\>\> which may be associated with \>\>\> *more rapid radiographic and clinical progression*

Answer 29

* A **Plain X-ray of the affected joint** \>\> often will show one or more typical features of OA * **For hip** \>\>\> Do *_non-weight beraing_*_X-ray pelvis PA view_ * **For knee** \>\>\> Do *_stan_**_ding_*_X__-ray knee AP view_ \>\>\> to assess \>\>\> tibio-femoral cartilage loss * A _flexed skyline view_ \>\>\> to assess patello-femoral involvement. * **For spine** \>\>\> _Plain X-ray spine_ * If suspected spinal stenosis or nerve root compression \>\>\> _Do MRI_ * Routine biochemistry: normal * CBC/haematology: normal * Autoantibody tests: usually normal * Acute phase response: moderate * Synovial fluid (aspirated from an affected joint) * _viscous_ * _A low cell count_

Answer 30

**Importance:** It is of value in **assessing the severity of structural change** \>\>\> which is _helpful if joint replacement surgery is being considered._

Answer 31

In hand: * **Joint space narrowing** affecting the **_PIP and DIP_** * In some OA-affected joints \>\>\> typical \> **Articular subchondral and ‘gullwing’ appearances** * **Osteophyte formation**

Answer 32

In knee: * **Advanced OA** \>\>\> _almost_ _complete loss of joint space_ \>\>\> *affecting both compartments* * _Sclerosis of subchondral bone_ * **In severe patello-femoral OA** \>\>\> _almost complete loss of joint space_ + _lateral displacement of the patella_ * **If marked medial tibio-femoral OA** \>\>\>\>\> typical _varus_ knee deformity

Answer 33

**In hip:** * Superior joint space narrowing * Subchondral sclerosis * Osteophytes * Cysts

Answer 34

**In spine:** * Disc narrowing * Osteophytes * Osteosclerosis *_at the apophyseal joints_* * Cervical spondylosis

Answer 35

* If unexplained early-onset OA \>\>\> **Do additional investigation**: _Guided by the suspected underlying condition._ * **In acromegaly** \>\>\> X-ray shows: * Dysplasia or * Vascular necrosis * _Widening_ of joint spaces * **In haemochromatosis** \>\>\> X-ray shows * Multiple cysts * Chondrocalcinosis * _MCP joint_ involvement in haemochromatosis * **In neuropathic joints** \>\>\> X-ray shows * Disorganised architecture

Answer 36

* A common form of **inflammatory arthritis** * It occurs **throughout the world** and in **all ethnic groups** * **Chronic disease** * Characterised by a ***_clinical course of exacerbations and remissions_*** * _A complex disease \>\>\> both genetic and environmental components_

Answer 37

* **Age:** Peak onset = _30-50_ years, _although occurs in all age groups_ * **Sex:** Female: Male ratio = _3:1_ (_Female has more_ ratio than male) * **Prevalence in the UK** = _1%_ (= 1 in 100 = 1000 in 100,000) * **Prevalence in Europe & in the Indian subcontinent** = _0.8-1.0%_ * **Prevalence in the south-east Asia** = _0.4% (lower)_ * **Prevalence in Pima Indians** = _5% (highest in the world)_ * Some ethnic differences e.g. *_High in Native Americans_*

Answer 38

**HLA-DR4** (especially _Felty’s syndrome_) The strongest association is with variants in the HLA region. Recent studies have shown that \>\>\> the association with HLA is determined by \>\>\> * Variations in 3 amino acids in the _HLA-DRβ1 molecule_ *(positions 11, 71 and 74)* * _Single variants HLA-B_ *(at position 9)* * _HLA-DPβ1_ *(at position 9)* The non-HLA loci generally lie within or close to genes involved in regulating the immune response.

Answer 39

**TNF (Tumour necrosis factor)** ## Footnote *So, anti-TNF is given in RA treatment*

Answer 40

The importance of genetic factors is demonstrated by \>\>\> * **H****igher concordance**of RA in ***_monozygotic (12–15%)_*** compared with *_dizygotic twins (3%)_* * **increased frequency** of disease in the **first-degree relatives** * _Nearly 100 loci_ *that are associated with the risk of developing RA (detected by genome wide association studies)*

Answer 41

* **Infection** * In a _genetically susceptible host_ \>\>\> through processes like _citrullination_ \>\>\> _modify host proteins_ \>\>\> _triggers autoimmunity_ \>\>\> becomes immunogenic * NO single specific pathogen has been identified * **Cigaretter smoking** * Associated with *_more severe disease_* * *_Reduced responsiveness to treatment_*

Answer 42

* **infiltration of the synovial membrane with \>\>\>** * CD4+ T -lymphocytes *(interacts with other cells of the synovium)* * B lymphocytes *(interacts with other cells of the synovium)* * Plasma cells * Dendritic cells * Macrophages * \>\>\> **Lymphoid follicles form within the synovial membrane** \>\>\> in which T- and B-cell interactions occur \>\>\> causing \> 1. Activation of T cells \>\>\> to produce _cytokines (+)_ 2. Activation of B cells \>\>\> to produce _autoantibodies, (including RF and ACPA)_ * **The** **Positive feedback loop:** * T cells produce _TNF_ and _interferon gamma (IFN-γ)_ \>\>\> they activate synovial macrophages * Macrophages produce several _pro-inflammatory_ _cytokines_, including \>\>\> _TNF, IL-1 and IL-6_ \>\>\> which act on synovial fibroblasts \>\> produce further cytokines \>\>\> set up a positive feedback loop * **Synovial fibroblasts proliferate,** causing \>\>\> synovial hypertrophy \>\>\> producing _matrix metalloproteinases +_ _the proteinase ADAMTS-5_ \>\>\> which degrade soft tissues and cartilage. * **Within ithe inflammed** **synovium** \>\>\> _Prostaglandins and nitric oxide_ produced \>\>\> cause \> vasodilatation \>\> swelling + pain. * **Systemic release of _IL-6_** triggers production of acute phase proteins by the liver. * **At the joint margin** \>\>\> the inflamed synovium (pannus) \>\>\> directly invades bone and cartilage \>\> cause joint erosions. * A **key pathogenic factor in bone erosions and** **periarticular osteoporosis** is osteoclast activation, stimulated by \<\<\< * the production of _M-CSF by synovial cells_ and _RANKL by activated_ _T cells_ * New blood-vessel formation (**angiogenesis)** **occurs** \>\>\> causing \> the inflamed synovium to become \>\>\> highly vascular * Within these blood vessels \>\>\> pro-inflammatory cytokines \>\>\> activate endothelial cells \>\>\> support recruitment of yet more leucocytes \>\>\> perpetuate the inflammatory process. * **Later,** fibrous or bony ankylosis may occur. * **Adjacent miscles to inflamed joints** \>\>\> atrophy + (may be) infiltrated with lymphocytes \>\>\> leads to \>\>\> progressive biomechanical dysfunction \>\>\> may further amplify destruction * **Rheumatoid nodules** occur in patients _who are RF or ACPA_ _positive_ \>\>\> primarily affect extensor tendons. * They consist of \>\>\> * A central area of fibrinoid material * Surrounded by a palisade of proliferating mononuclear cells. * **Granulomatous lesions** may occur in \>\>\> the pleura, lung, pericardium and sclera.

Answer 43

* Small joints of the hands **_(PIP, MCP)_** * **_Feet_** and **_wrists_** * **_Large joints_** * ***Symmetrical involvement (= arthritis)***

Answer 44

* Pain * Joint _swelling_ _(_*commonly* _of PIP, MCP or wrist joints)_ * Soft tissue _swelling_ * Morning stiffness \>1 hour

Answer 45

* Swelling * Tenderness * *Erythema is unusual* *_(Erythema suggests Co-existent sepsis)_*

Answer 46

**“Proximal muscle stiffness”** mimicking \>\>\> *_polymyalgia rheumatica_*

Answer 47

**Proteus mirabilis** is a _(G-ve rod)_, causes **UTI** → *predisposes susceptible patients to RA*

Answer 48

* It is M**ainly chronic** disease * *Sometimes* RA has \>\>\> An acute onset + severe early morning stiffness + polyarthritis + pitting oedema. (This occurs more commonly in old age) * *Occasionally* \>\>\> the onset is palindromic + with relapsing and remitting episodes of pain, stiffness and swelling (that last for only a few hours or days)

Answer 49

**When they develop:** _Long-standing uncontrolled_ disease in _older people_ *Although these have become less common over recent years with more aggressive management in young age* * **Ulnar deviation** *of the fingers* * **Swan neck** _deformity_ * **Boutonnière or ‘button hole’** _deformity_ * **Z** _deformity_ *of the thumb* * _Dorsal subluxation of the ulna_ *at the distal radio-ulnar joint* (may be) \>\>\> contribute to **Rupture of the fourth and fifth extensor tendons.** * If _nodules_ in the *flexor tendon sheaths* \>\>\> **Triggering of fingers**

Answer 50

* *When they develop:** _Long-standing_ _uncontrolled disease_ in _older people_ * Although these have become less common over recent years with more aggressive management in the young age* * **Subluxation of the MTP joints** *(meta-tarso-phalangeal joints) of the feet* \>\>\> (may result) in **‘cock-up’ toe** deformities, causing: * **Pain on weight-bearing** _on *the exposed MTP heads*_ * Development of **secondary adventitious bursae and callosities** * *_In the hind foot_* \>\>\> **damage to the ankle and subtalar joints** \>\>\> **valgus** deformity o**f the calcaneus** * Associated with **loss of the longitudinal arch (flat foot)** \<\<\< **due to rupture of the tibialis posterior tendon** * *In patients with _knee synovitis_* \>\>\> **Popliteal (Baker’s) cysts** may occur * Here, synovial fluid communicates with the cyst but is prevented from returning to the joint by a valve-like mechanism (NOT specific to RA) * _Rupture may be induced by knee flexion \>\>\> leading to \>\> calf pain + swelling \>\>\> may mimic a deep venous thrombosis (DVT)._

Answer 51

* PIP, MCP, Wrist \>\>\> Rheumatoid arthritis * DIP \>\>\> Osteoarthritis, Psoriatic arthritis * Base of the thumb \>\>\> Osteoarthritis

Answer 52

Target population: 1. Patient with **At least 1 joint with clinical synovitis** 2. Patient with **synovitis**, **_not explained by any other disease_**

Answer 53

**Diagnosis by scale:** * Add score of categories A to D: If score ≥ 6/10 \>\>\> Dx: Rheumatoid arthritis * *For not missing any criteria \>\>\> Check through the criteria (from high score to low score) (= 5 to 0, 3 to 0, 1 to 0)*

Answer 54

* Fever * Susceptibility to infection * Weight loss * Fatigue * Anorexia

Answer 55

*(above downwards)* * Bronchiolitis obliterans * Pulmonary fibrosis → *often _asymptomatic_; sometimes, risk is increased by _anti-TNF therapy_* * Pulmonary nodules * Methotrexate pneumonitis (A complication of drug therapy) * Fibrosing alveolitis * Pleural effusion * Pleurisy * Caplan's syndrome \>\>\> massive fibrotic nodules (= pneumoconiosis) (due to occupational coal dust exposure) * Infection (possibly atypical) secondary to immunosuppression

Answer 56

RA patients have an increased risk of IHD * IHD (Ischaemic Heart Disease) *(more common)* * Pericarditis * Myocarditis * Endocarditis * Conduction defects * Coronary vasculitis * Granulomatous aortitis * Rare: heart block, cardiomyopathy, coronary artery occlusion, aortic regurgitation

Answer 57

* Cervical cord _compression_ * _Compression neuropathies_ * Peripheral _neuropathy_ * Mononeuritis multiplex

Answer 58

Depression

Answer 59

Fron to back * **Keratoconjunctivitis sicca *(most common)*** → _d__ry, burning, gritty eyes_ * Cause: Secondary Sjogren’s syndrome * **Episcleritis** → redness * **Scleritis** → redness + pain → *uncommon, but most serious sight-threatening* * If so → urgent refer to ophthalmology, artificial tear, antibiotics * **Keratitis** (peripheral ulcerative keratitis) → redness + pain → uncommon, but most serious sight-threatening * **Corneal ulceration** * **Steroid-induced cataracts** * **Scleromalacia** * **Chloroquine retinopathy**

Answer 60

* **Osteoporosis (more common)** * Muscle-wasting *(Cause:* *systemic inflammation + reduced activity)* * Tenosynovitis * Bursitis

Answer 61

* Digital _arteritis_ * Visceral _arteritis_ * *Ulcers* * *Pyoderma gangrenosum* * Mononeuritis multiplex

Answer 62

* Anaemia *_(Due to NSAID induced GI blood loss → iron deficiency → microcytic anaemia)_* * Thrombocytosis * Eosinophilia * **In active disease → normochromic normocytic anaemia + thrombocytosis**

Answer 63

* **Felty's syndrome** (*_RA + splenomegaly + low white cell count/ neutropaenia)_* * **Splenomegaly** * **Localised or generalised lymphadenopathy** can occur in patients with _active disease_ * But **persistent lymphadenopathy** → may indicate \>\>\> the _development of lymphoma_ \>\>\> more common in _long-standing RA_

Answer 64

* **Subcutaneous nodules** * Sinuses * Fistula

Answer 65

Amyloidosis

Answer 66

* Patient with **_long-standing_ _seropositive_ _erosive_ disease** * *Occasionally.* They can occur *_At presentation (especially In men)_* * ***Most are due to*** * ***_Serositis_*** * ***_Granuloma_*** * ***_Nodule formation_*** * ***_Vasculitis_***

Answer 67

Almost exclusively in RF or ACPA positive patients

Answer 68

Extensor tendons

Answer 69

* *Frequently* **asymptomatic** * *_Some_ may be complicated by \>\>\>* **ulceration and secondary infection**

Answer 70

This is *uncommon* but *may occur in **seropositive patients.*** **The presentation is with →** * **systemic symptoms, such as** * fatigue * fever * nail-fold infarcts * **Rarely,** * cutaneous ulceration * skin necrosis * mesenteric, renal or coronary artery occlusion (may occur)

Answer 71

A combination of \>\>\> conventional risk factors, such as: * High cholesterol * Smoking * High BP (HTN) * Low physical activity * _NSAIDs_ * _Glucocorticoids_ * *The effects of inflammatory cytokines on vascular endothelium*

Answer 72

Subluxation of the cervical spine

Answer 73

At the _atlanto-axial joint_ or at _subaxial level_

Answer 74

Course: Due to **erosion of the transverse ligament** *_posterior to the odontoid peg._* \>\> **atlanto-axial subluxation** →can lead to \>\>\> **cord compression** OR ***_following minor trauma/manipulation → sudden death_***

Answer 75

* Suspect if – **paraesthesia or electric shock in the arms** * **Insidious onset** * **Subtle loss of function**→ may _initially be attributed to active disease_ ## Footnote In patients with _extensive joint disease_ → _reflexes and power can be difficult to assess; *Therefore, sensory and upper motor signs are most important*_

Answer 76

Urgently refer to neurosurgery → stabilisation and fixation

Answer 77

Hypertrophied synovium or Joint subluxation

Answer 78

* *The most common:** median nerve compression → present as: bilateral carpal tunnel syndrome * *others:** ulnar nerve (at elbow or wrist), lateral popliteal nerve (at fibular head)

Answer 79

Entrapment of **posterior tibial nerve** in the _flexor retinaculum_ → tarsal tunnel syndrome → *_burning, tingling and numbness*_ in the _*distal soles and toes_*

Answer 80

* ***_Asymptomatic;_*** *but may be –* * **Pleural pain** * **Pericardial pain** * **Breathlessness** * *Pericardial effusion (rare)* * *Constrictive pericarditis (rare)*

Answer 81

If RA is poorly controlled

Answer 82

* _Albumin:_ very low * _Creatinine:_ high * **_Protein_**uria (may be as nephrotic syndrome) * Hepatomegaly * Small joint Arthropathy * *Fatigue* * *Weight loss* * _Peripheral_ oedema * _Peripheral_ neuropathy

Answer 83

_*Extracellular* accumulation_ of **AA fibrils** _within tissue and organs_ (due to **acute phase reactant, serum amyloid A)**

Answer 84

* **Age of onset:** _50-70_years * **Sex:** _Female_ \> Male * **Race:** _Caucasians_ \> Black * **Long standing RA** * **Deforming** + but **inactive disease** * **RF seropositive**

Answer 85

* **_Splenomegaly (MAIN)_** * **_Lymphadenopathy_** * *_Weight loss_* * _Skin pigmentation_ * _Keratoconjunctivitis sicca_ * *Vasculitis, leg ulcers* * *Recurrent infections* * *Nodules*

Answer 86

* Normochromic, normocytic anaemia *(Like active RA)* * Neutropenia (MAIN) * Thrombocytopenia * Impaired T- and B-cell immunity * Abnormal liver function

Answer 87

Anti-CCP antibodies (= Anti-cyclic citrullinated peptide antibody = ACPA)

Answer 88

test for anti-CCP antibodies → if it’s positive → Dx: RA

Answer 89

* **IOC:** Anti-CCP antibodies (= Anti-cyclic citrullinated peptide antibody = ACPA) * Rheumatoid factor (RF) * NICE recommendation: If suspected RA + but, rheumatoid factor negative → test for anti-CCP antibodies → if it’s positive → Dx: RA * X-ray of the joints

Answer 90

* Clinical criteria * ESR and CRP → raised *(but normal level do NOT exclude RA, especially if few joints are involved)* * USG or MRI * Not routinely required * *_Indication:_* _clinical uncertainty about the presence of →synovitis_ * Anti-CCP (NICE recommended IOC) * RF

Answer 91

* Pain (visual analogue scale) * Early morning stiffness (minutes) * _Joint_ tenderness * _Joint_ swelling * *DAS28 score* * *_ESR_* * *_CRP_*

Answer 92

* X-rays * Functional assessment

Answer 93

* FBC (Full blood count) * Urine R/E (Urinalysis) * Urea and creatinine * Liver function tests (LFT) * Chest X-ray

Answer 94

* Sensitivity = 70-80% (similar to RF) * Means, among the ‘Patients with RA’ → ACPA & RF can detect 70-80% of them * Specificity = 90-95% (higher than RF)

Answer 95

* Detectable up to 10 years before the development of RA * Play a key role in the future RA → allows early detection of patients \>\>\> suitable for “aggressive anti-TNF therapy”.

Answer 96

Circulating Ab (usually IgM) which reacts with Fc portion of patient’s own IgG

Answer 97

* Rose-waaler test: → sharp red cell agglutination * Latex agglutination

Answer 98

* Sensitivity: 70% (these are also positive for ACPA) * Less specific than ACPA

Answer 99

* Rheumatoid arthritis (70%) * Sjogren’s syndrome (100%) * Felty’s syndrome (100%) * Infective endocarditis (50%) * SLE (20-30%) * Systemic sclerosis (30%) * General population: 5% * Rarely: TB, leprosy, HBV, EBV

Answer 100

* Loss of joint space *(seen in both RA and osteoarthritis)* * Juxta-articular osteoporosis * Soft-tissue swelling * Usually normal hand, wrist, feet

Answer 101

* Periarticular erosions (osteopenia and osteoporosis) (periarticular osteoporosis and marginal joint erosions) * Subluxation of joint

Answer 102

Assessment of → **painful joints** → to determine \>\>\> if any _significant structural damage_

Answer 103

Lateral X-rays (taken in flexion and extension) + MRI

Answer 104

Ultrasound (may require)

Answer 105

To assess \>\>\> the need of: * Disease activity * Response to treatment * Need for biological therapy

Answer 106

Count **_“the number”_** of **_“swollen and tender joints”_** in the _upper limbs and knees_ \>\>\> combine this with \>\>\> the _ESR_ **+** the _patient’s assessment of the activity of their arthritis_ *(on a visual analogue scale**: where, 0 indicates no symptoms and 100 the worst symptoms possible)* → enter into a calculator *(online)* → generate a numerical score. **Interpretation:** The higher the value → the more active the disease

Answer 107

* **Old prior diagnosed RA** _improves (may remission)_ in pregnancy * Often has a _flare after delivery_ (or _often first presents post-partum)_ * *Why:** *_immunosuppression in pregnancy + hormonal changes_*

Answer 108

* **If early RA or poorly controlled (= unstable)** **RA**→ defer conception until disease is stable * **Stop methotrexate _(at least) 3 months before_ pregnancy** * **Stop Leflunomide _(at least) 24 months before_ pregnancy**

Answer 109

* **Analgesic of choice:** Paracetamol * **Contraindicated** → _NSAIDs_ * NSAIDs & selective COX-2 inhibitors → can be used _up to 32weeks_ of pregnancy *(Davidson says _upto*_ _*20 weeks_)* * _NASIDs can cause early closure of ductus arteriosus_

Answer 110

* Can be used **to control disease flares** * **Risks of:** *_Hypertension, glucose intolerance, osteoporosis_* * *Short-term glucocorticoids is safe in lower dose in pregnancy* * *If needed* → **TOC:** **Low –dose prednisolone**

Answer 111

* Sulfasalazine _(1st line)_ * Hydroxychloroquine (_1st line)_ * Azathioprine _(2nd line)_ ## Footnote **SHA**

Answer 112

* Methotrexate *(also C.I in breast-feeding)* * Leflunomide *(also C.I in breast-feeding)* * Cyclophosphamide *(also C.I in breast-feeding)* * Mycophenolate * Gold

Answer 113

* *Limited experience* * *May be _relatively safe_ during pregnancy* * **The main theoretical risk** → _immunosuppression in the neonate_ * *Except for** → **_Certolizumab_** → *_crosses the placenta in negligible amounts._*

Answer 114

* **First line:** Sulfasalazine or Hydroxychloroquine (Safe in pregnancy) * **Second line:** Azathioprine (If first line fails to control * Before Azathioprine → check TMPT deficiency * **Oral analgesic of choice** in pregnancy: Paracetamol * Short-term glucocorticoids (Low –dose prednisolone) is safe in lower dose in pregnancy * In obstetric anaesthesia of RA patient → check the risks of atlanto-axial subluxation

Answer 115

* Methotrexate * Leflunomide * Cyclophosphamide

Rheumatology Flashcards

(143 cards)