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Medical school finals > MSK + Rheumatology > Flashcards

MSK + Rheumatology Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the pathogenesis of osteoarthritis

A

Cartilage loss with accompanying periarticular bone response. Inflammation of articular and periarticular structures leading to disordered repair
Progressive destruction, more cartilage destruction than can be compensated for, focal erosion of cartilage and disordered repair (death of chondrocytes) - fibrillated and fissured
Weaker cartilage causes microfractures and cysts on bone, attempted repair causes sclerotic subchondral bone and joint margins to become calcified (osteophytes)

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2
Q

What is the presentation of osteoarthritis including on Xray

A

Onset is progressive, pain is relieved by rest/ worse with movement, transient (<30m) morning stiffness
Radiological: (LOSS) loss of joint space, osteophytes, subchondral sclerosis + subchondral cysts; abnormal bone contours
Joints involved: distal interphalangeal (not RA), carpometacarpal, metatarsophalangeal, weight bearing joints - feet, knee, hips, spine
Hands: bouchard’s (pip) and heberden’s (dip) nodes

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3
Q

How is osteoarthritis diagnosed

A

Clinical diagnosis
X rays. MRI can be used if spinal and affecting cord, something else suspected. Joint fluid analysis (rule out)
Bloods: CRP + ESR, RF, anti CCP

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4
Q

How is osteoarthritis managed

A

Non medical: activity (strength), weight loss, footwear, walking aids, orthoses, occupational therapy
Topical NSAIDs FL, paracetamol + topical, oral NSAID + PPI, weak opioids / intra articular steroid if necessary. Rarer DMARDs
Surgery: arthroplasty (knee or hip) if uncontrolled pain, significant limit of function, age considered; only indication for arthroscopy is knee locking due to loose body. Also osteotomy and fusion (ankle + foot)

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5
Q

What is the pathogenesis of rheumatoid arthritis

A

Primarily a synovial disease, chemoattractants are produced in the joint, recruiting circulating inflammatory cells. Overproduction of TNF-alpha leads to synovitis and joint destruction
Synovium proliferates (also new blood vessels) and expands over the cartilage, subsequently weakening by taking its nutrition

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6
Q

How does rheumatoid arthritis present

A

Slowly progressive (>6w), symmetrical, multiple joints, swollen warm + tender, stiff in morning (>1h), cold exacerbates, movement limitation and muscle wasting
Small joints first: metacarpophalangeal, proximal interphalangeal (DIPs not involved), metatarsophalangeal; larger joints (no spine): wrists, elbows, shoulders, knees, ankles
Hand defects: z shaped thumb, swan neck (hyperextended PIP + flexed DIP), boutonniere (flexed PIP + hyperextended DIP), ulnar deviation (fingers at MCP)
Systematic: weight loss, fever, fatigue, dry eyes + mouth, skin nodules, rashes + ulcers, raynaud’s

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7
Q

How is rheumatoid arthritis diagnosed, how does it present on Xray

A

Clinical diagnosis by rheumatologist, confirmed by tests
Rheumatoid factor blood test - positive in 70% but not specific. Positive anti ccp 96% specific but positive in ~70%. Raised ESR + CRP but normal in 40%
X ray, ultrasound, MRI: tissue swelling then joint erosion and space narrowing
LESS: loss of joint space, erosions, soft tissue swelling, see-through bones (osteopenia)
SPADES: soft tissue swelling, periarticular osteoporosis, absent osteophytes, deformity, erosions (late), subluxation (late)

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8
Q

How is rheumatoid arthritis managed

A

Lifestyle: smoking cessation, reduce weight, exercise

Early DMARD: low disease activity: hydroxychloroquine (weakest, least SEs), sulfasalazine; methotrexate (+ folic acid), leflunomide

Pregnancy: steroid, sulfasalazine / hydroxychloroquine

Short term oral steroids can be used for flares, NSAID for pain + PPI

Biological (very expensive): TNF inhibitors - etanercept FL, infliximab, slow/ halt erosion, stimulates osteoclast, risk of infection/ hypersensitivity

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9
Q

What is the pathogenesis of gout and pseudogout

A

Gout: purines (from diet and natural production) → (xanthine / xanthine oxidase) uric acid → kidneys
Hyperuricaemia - monosodium urate crystals (20% chance of gout), deposition in joints (previous trauma and lower temperatures), trigger intracellular inflammation
Also lack of excretion: renal impairment, thiazide diuretics

Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue

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10
Q

What is the presentation of gout and pseudogout

A

Acute gout: sudden onset, agonising pain, swelling, redness. Usually one joint (first metatarsophalangeal) but sometimes poly. Can be exacerbated by food, alcohol, cold, trauma
Chronic (rare): elderly on long term diuretics in renal failure

Pseudo: Knees > wrists&raquo_space; shoulders > ankles > elbows

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11
Q

How is gout investigated

A

Joint fluid aspiration and microscopy (needle shaped crystals that are negatively birefringent), exclude septic arthritis (synovial WBC >2*10^9)
Serum uric acid raised, US, dual energy CT, X ray
Routine bloods (raised WCC, check renal function), inflammatory markers

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12
Q

How is gout managed

A

Acute: NSAIDs, colchicine (targets uric acid crystallisation, toxic in high doses), steroids
2nd line: interleukin inhibitor anakinra / canakinumab

Chronic: allopurinol inhibits FL (xanthine oxidase inhibitor) (may trigger an attack, wait 3 weeks after episode), febuxostat SL (less uric acid) as well as NSAIDs + colchicine / steroid
weight loss, avoid alcohol/ purine rich food, dairy helps. Treatment for at 3-6m
Monitor with serum uric acid

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13
Q

What are the risk factors for gout

A

High alcohol (beer most), purine rich foods (red meat, seafood), high fructose, high fat, low dose aspirin, thiazide diuretics
Diabetes, ischaemic heart disease, hypertension, nonalcoholic fatty liver, proliferative blood disorder
Men over 40, increases in post menopausal women

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14
Q

What is the pathogenesis of osteoporosis

A

Naturally lose bone mass / mineralisation with age/ loss of oestrogen restriction both cause higher turnover: (predominantly) cancellous bone lost, not enough mineralisation, microarchitectural disruption
Oestrogen deficiency: increased osteoclasts, premature arrest of osteoblast activity
Age: decrease in trabecular thickness (preferentially strengthens vertically)

Can also be exacerbated by low calcium / vit D, steriods, chronic diseases (CKD, hyperthyroidism)

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15
Q

How is osteoporosis investigated

A

Dual energy X ray absorptiometry (DEXA) gold standard - area, bone mineral density, density, T score; enough for diagnosis
T score (bone density standard deviation from mean of young and healthy): > -1 healthy, -1 > -2.5 osteopenia, < -2.5 osteoporosis
Z score is standard deviations from the average for their sex, age, ethnicity
Fracture risk assessment tool, FRAX: age, sex, BMI, previous fracture, parental fractured hip, current smoking, steroids, RA, secondary osteoporosis, alcohol (>3 units / day), femoral neck BMD
Also X ray / quantitative CT / US, bloods (calcium (+ albumin), phosphate, alkaline phosphatase, creatinine, vit D, parathyroid)

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16
Q

How is osteoporosis managed

A

Lifestyle: alcohol + smoking, weight bearing exercise, calcium + vitamin D diet/ supplements
Bisphosphonate FL (alendronic acid), hormone replacement therapy, denosumab (women) / teriparatide (men)

(Bisphosphonate, high affinity to hydroxyapatite → eaten by osteoclasts and kills. Denosumab, monoclonal antibody that inhibits RANK ligand. Teriparatide (PTH analogue) increases osteoblast activity, more available calcium
Risk of reflux + oesophageal erosion - empty stomach with full glass, sit upright for 30m. Also risk of osteonecrosis of jaw / femoral neck / external auditory canal)

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17
Q

What are the risk factors for osteoporosis

A

SHATTERED: steroids, hyper(para)thyroidism, alcohol + tobacco, thin, testeosterone decreased, early menopause, renal + liver failure, erosive + inflammatory disease

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18
Q

Describe seronegative axial spondyloarthopies

A

Group of overlapping conditions that are associated with HLA-B27 share certain features. Psoriatic, enteropathic, reactive, undifferentiated, ankylosing spondylitis

SPINEACHE: sausage fingers (dactylitis), psoriasis, inflamed back (axial involvement), NSAIDs response, enthesitis (tendon attachment), arthritis, Crohn’s/ colitis, HLA B27, eyes (uveitis, iritis)

19
Q

Describe the presentations of the different seronegative spondyloarthopathies

A

Ankylosing spondylitis: episodic inflammation of sacroiliac joint, pain to hips/ buttocks, progressive loss of spinal movement as it fuses and new bone forms, causes severe hunchback
Psoriatic: closely resembles RA (small joints, symmetrical, hands), most common pattern is distal interphalangeal only. Can have arthritis mutilans - destructive loss of architecture (floppy fingers)
Reactive: inflammation triggered by infection, 2d-2w following infection, asymmetrical, lower limbs
Enteropathic like reactive, reflects disease activity (IBD etc)

20
Q

What are the 5 key associations with ankylosing spondylitis

A

5 As: anterior uveitis, aortic regurgitation, AV block, apical lung fibrosis, anaemia of chronic disease

21
Q

How is ankylosing sponylitis investigated

A

Bloods: HLA-B27, ESR + CRP, RF, anti-ccp.
Xray, joint aspiration / US
Psoriatic increased risk of metabolic syndrome: lipids, glucose, uric acid
Xray: bamboo spine (late), squaring of vertebral bodies, subchondral sclerosis, bone growth / ossification of ligaments / discs / joints, fusion of sacroiliac / facet / costovertebral joints

22
Q

How is ankylosing spnodylitis managed

A

Axial: high dose NSAIDs (+PPI), paracetamol / codeine
Resistant to NSAIDs: etanercept (anti-TNF), secukinumab (IL-17 inhibitor)
Peripheral arthritis: methotrexate/ sulfasalazine, DMARD fails - etanercept, oral / injection steroid
Enthesitis: steroid injections, dactylitis - etanercept
Stop smoking, exercise, physio

23
Q

What is the presentation of septic arthritis

A

Acute presentation: swollen, red, inflamed, warm, reduced ROM. also fever, chills, rigours
90% monoarthritis, large joints: knee > hip > shoulder
If suspected treat as septic arthritis until proven otherwise
History of infection or joint replacement

24
Q

How is septic arthritis managed

A

Joint aspiration first, gram staining, crystal microscopy, culture and antibiotic sensitivity
Empirical IV Abx until sensitivities known
Abx given for 4-6w, flucloxacillin / clindamycin
Prosthetic joint no aspiration, straight to surgery
Paracetamol / ibuprofen

25
Q

What is the pathogenesis of osteomyelitits and the most common pathogen

A

Infection needs to enter bone
Direct inoculation, trauma, surgery - poly or monomicrobial
Contiguous spread from adjacent soft tissue + joints (more common in children) - poly or mono
Haematogenous spread, in children affects long bones, in adults vertebrae (each the most vascularised, vertebrae increase with age) - difficult so usually mono

Most common: staph aureus, coag-neg staph, aerobic gram negative bacilli
Salmonella in sickle cell, serratia marcescens in IV drug (clavicle/ pelvis)

26
Q

Describe the presentation and investigations for osteomyelitis

A

Onset of several days, dull/ nonspecific pain at site, aggravated with movement, fever, inflammation, tenderness, erythema
Chronic: draining sinus tracts, ulcers, non healing fractures, sinus tracts

Bloods: FBC, ESR + CRP, culture
X ray FL/ MRI GS, bone biopsy (benefits vs cost if sick)

27
Q

How is osteomyelitis treated

A

Sepsis 6, follow local protocol
IV flucloxacillin (vancomycin) - switch to sensitive, analgesia, immobilise limb
MRSA high prevalence - vancomycin FL, suspected pseudomonas - piperacillin/tazobactam
Surgical debridement of infected tissue. Native vertebral infection to spinal surgeons

28
Q

What is the presentation of SLE

A

Most common presentation is a rash - malar (butterfly), photosensitive, discoid

Systemic: fatigue, weight loss, fever, arthralgia (like RA), myalgia

Inflammation / AI: oral ulcers, alopecia, Raynaud’s, pleuritis, pericarditis, lymphadenopathy, thrombosis, splenomegaly

Lupus nephritis is usually subclinical at start of disease: hypertension, oedema

29
Q

What is the pathophysiology of SLE

A

Relapsing and remitting, chronic inflammation, caused mainly by antinuclear antibodies (ANA) against proteins in the nucleus. Anti DsDNA present in around 50% but highly specific

30
Q

How is SLE investigated

A

Test for antibodies: antinuclear antibodies (ANA) (not specific, cheap, 95% positive), anti double stranded DNA antibody (highly specific, positive in 60%)
Bloods: FBC, activated partial thromboplastin (clotting), U+Es, ESR + CRP
ESR is raised but CRP is normal = systemic inflammation
FBC - check for leukopenia
Urinalysis for renal involvement in all, CXR + ECG if cardiopulmonary symptoms

31
Q

How is SLE managed

A

Lifestyle: diet (CV risk), smoking cessation, sun protection, exercise, psychological therapy
Hydroxychloroquine FL, NSAIDs, steroids or azathioprine
More severe: DMARDs (methotrexate, mycophenolate), tacrolimus, biologics (rituximab, belimumab)

32
Q

Describe macrophage activation syndrome

A

Potentially life threatening complication of rheumatic diseases, especially systemic JIA and SLE. Excessive and uncontrolled activation of macrophages and T cells producing a cytokine storm and phagocytosis of blood cells.

Fever, pantocytopaenia, heaptosplenomegaly + liver dysfunction, hyperferritinaemia, coagulopathy

Treat with IV prednisolone and ciclosporin

33
Q

Describe Paget’s disease

A

Focal disorder of bone remodelling, increased resorption followed by formation of weaker bone
Unknown aetiology, latent infection / family history common
60-80% asymptomatic, bone + joint pain, deformities (bowed tibias, skull changes), nerve compression - deafness (C8), paraparesis
Increased serum alkaline phosphatase but normal calcium and phosphate (increased turnover), X ray
Bisphosphonates, NSAIDs, monitor

34
Q

Describe osteomalacia

A

Poor mineralisation due to a lack of calcium/ vitamin D leading to soft bone

Dull aching pain (most commonly in lower back, pelvis, hips, legs, ribs), may be worse at night, decreased muscle tone and leg weakness - slow, waddling gait
Rickets: growth retardation, knocked knees and bowed legs, muscular spasms

35
Q

What are the two types of systemic sclerosis and how do they present

A

2 patterns: limited cutaneous and diffuse cutaneous;
LC = CREST syndrome: calcinosis, Raynaud’s, esophageal dysmotility, sclerodactyly, telangiectasia
DC: CREST + organ involvement, cardiovascular (HTN, coronary artery disease), lung (pulmonary hypertension + fibrosis), kidney (scleroderma renal crisis)

Presentation: scleroderma (hardened, tightened skin), sclerodactyly (tight skin affects ROM), telangiectasia, calcinosis (calcium deposits on skin), reflux, oesophagitis / chest pain, Raynaud’s
Diffuse: dry cough, SOB; renal crisis: severe HTN

36
Q

How is systemic sclerosis investigated and managed

A

Investigations: autoantibodies, FBC (normocytic anaemia), inflam markers, U+Es, hand Xray
ANA non specific in 90%; also Anti-centromere = limited, Anti-Scl-70 = diffuse

Treatment with DMARDs (methotrexate) and biologics (rituximab). Raynaud’s - nifedipine, reflux - lansoprazole, GI upset - metoclopramide, HTN - ACE, pulmonary HTN - bosentan
Avoid smoking, gentle skin stretching, regular emollients, avoid cold, physio, occupational therapy

37
Q

Describe dermato/polymyositis, investigations and treatment

A

Autoimmune conditions causing proximal muscle inflammation and weakness. Can be caused by infection, cancer (paraneoplastic), slight genetic association (HLA)
Presentation: gradual onset + symmetrical + proximal muscle weakness (difficulty standing, stairs), myalgia
Dermato also involves characteristic skin changes - Gottron papules on hands and heliotrope rash on eyelids, periorbital oedema, photosensitive erythematous rash
Diagnosis: creatinine kinase key investigation, clinical features. Also Autoantibodies, EMG, MRI, muscle biopsy
Anti-Jo-1 associated with poly
Steroids FL, immunosuppression (methotrexate, azathioprine), IVIg, biologics (infliximab, etanercept). Managed by rheumatologist, assessed for underlying cancer

38
Q

Describe antiphospholipid syndrome, presentation, investigations and management

A

Autoimmune disorder, antibodies target phospholipids on cell surfaces and phospholipid binding proteins involved in the clotting process, inflammation and thrombosis
3 antibodies: lupus anticoagulant, anticardiolipin Abs, Anti-beta-2 glycoprotein 1 Abs
Associated strongly with SLE, also livedo racemosa (purple reticular rash), nonbacterial endocarditis, thrombocytopenia

Presentation is only recurrent VTE / arterial thrombosis / pregnancy issues
Diagnosis clinical with persistent presence of antibodies

Mx: long term warfarin (INR 2-3), enoxaparin + aspirin used in pregnancy

39
Q

What is the pathogenesis and presentation of Sjogren’s

A

Autoimmune condition affecting the exocrine glands - notably lacrimal and salivary. Antibodies anti-Ro (SS-A) and anti-La (SS-B). 50% develop extraglandular involvement
Secondary occurs following other AI conditions: RA, SLE
Complications: keratoconjunctivitis sicca, corneal ulcers; oral candida infections; vaginal candida, sexual dysfunction

Presentation: sicca (dry eyes and mouth) + saliva gland enlargement, dyspareunia, dry skin, dysphagia, otitis media, pulmonary infection
Extraglandular: vasculitis (purpura, urticaria), arthritis, dental caries, glomerulonephritis, peripheral neuropathy

40
Q

How is Sjogren’s diagnosed and managed

A

Schirmer test (filter paper under lower eyelid, measure diffusion after 5m, <10mm), saliva gland biopsy, bloods: antibodies, raised ESR + normal CRP, FBC
Symptomatic management: artificial tears + saliva, vaginal lube, pilocarpine, hydroxychloroquine for arthritis
Pilocarpine stimulates muscarinic receptors - increasing saliva and lacrimal secretion

41
Q

Describe the presentation, diagnosis, management of polymyalgia rheumatica

A

Presentation: rapid onset of symptoms, pain and stiffness of shoulders / neck / pelvic girdle. Worse in the morning (45m to resolve) / after inactivity, interferes with sleep
Systemic: weight loss, fatigue, low grade fever, carpal tunnel syndrome, peripheral oedema
Clinical diagnosis + response to steroids. Before steroids to rule out: FBC, U+E, LFT, calcium, serum protein electrophoresis, TFTs, creatinine kinase, RF, urine dipstick
15mg prednisolone daily - dramatic improvement after a week, slowly reduce for 1-2y
Long term steroids - don’t STOP: don’t stop abruptly, sick day rules, treatment card, osteoporosis prevention (bisphosphonates + calcium + vit D), PPI

42
Q

Describe the presentation, diagnosis, management of giant cell arteritis

A

Presentation: unilateral headache + scalp tenderness, jaw claudication, blurred vision, loss of vision
Prodromal features: malaise, weight loss, fever
Associate: polymyalgia rheumatica, carpal tunnel syndrome, peripheral oedema
3 of 5 diagnostic criteria: >50y, new headache, temporal artery abnormality (tender, decreased pulse), elevated ESR (>50mm per hour), abnormal biopsy
Biopsy and duplex US or temporal artery
40-60mg prednisolone or 500-1000mg of methylprednisolone if eye / jaw symptoms; weaned over 1-2y
Aspirin, PPI, bisphosphonates + calcium + vit D

43
Q

Describe the presentation, diagnosis and management of Ehler-Danlos

A

Hypermobile EDS most common and least severe, soft and stretchy skin
Classical: remarkably stretchy skin (soft and velvety), severe hypermobility, joint pain, abnormal wound healing, lumps over pressure points, prone to hernias
Vascular: most severe, vessels prone to rupture, thin + translucent skin, GI perforation, spontaneous pneumothorax
Kyphoscoliotic: hypotonia as infant, kyphoscoliosis as they grow, significant hypermobility, only recessive
Other symptoms: easy bruising, bleeding, chronic pain + fatigue, autonomic dysfunction, IBS, menorrhagia, premature rupture of membranes, urinary incontinence
Beighton score for hypermobility, clinical diagnosis + genetics
No cure, physio + occupational therapy, moderating activity, psychology

44
Q

Describe the presentation and management of Behcet’s

A

Main features are oral and genital ulcers: >3/y, painful, sharply circumscribed, red halo, 2-4w
Also: erythema nodosum, papules / pustules like acne, anterior / posterior uveitis, retinal vasculitis, retinal thrombosis, stiffness + arthralgia, GI ulcers, aseptic meningitis, cerebral venous thrombosis, aneurysms, DVT + budd-chiari

Topical + systemic steroids, colchicine, topical anaesthetics, azathioprine / infliximab

Medical school finals (13 decks)

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