Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > MSK/ Rheumatology/ Orthopaedic Surgery > Flashcards

MSK/ Rheumatology/ Orthopaedic Surgery Flashcards

1
Q

Outline DDX for acute back pain.

A

IV DISC = degeneration, herniation
MUSCLE = strain, sprain
ARTHRITIS = OA, RA, ankylosing spondylitis
OSTEOPOROSIS/ FRACTURE
CANCER = primary, metastatic
INFECTION = septic arthritis, osteomyelitis, abscess (epidural, paraspinal)
VISCERAL =
AAA
Renal
GIT = pancreatitis, gallbladder, perforation
Endometriosis, PID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List red flags for acute back pain.

A 
VITAL SIGNS = abnormal
SYSTEMIC FX = fevers, chills, night sweats, unintentional weight loss
PATIENT FX = age > 50 years
PRESENTING COMPLAINT FX = 
Worse with rest or lying down
Night pain, esp. waking from sleep
assoc. with bladder/bowel dysfunction
PMH/PSH =
Cancer
Immunosuppression
Osteoporosis
Significant major trauma
IVDU
Current bacterial infection
MEDS/ALLERGIES:
corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline treatment of acute low back pain w/o red flag features.

A

Conservative management.
EDUCATION = will likely resolve within 4 wks with conservative management, investigations are not required.
BE AS ACTIVE AS POSSIBLE
HEAT
SIMPLE ANALGESIA = paracetamol +/- NSAIDs
PHYSIO may be beneficial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the aetiology of osteoporosis?

A

(1) Failure to attain normal peak bone mass.
- genetic causes: e.g. gene polymorphisms - RANKL, oestrogen receptor, IGF1
- environmental: calcium deficiency, immobility, growth hormone deficiency
(2) Uncoupling of bone resorption and bone formation.
- Lack of oestrogen (post-menopausal) –> increased RANKL expression –> increased osteoclasts (increased differentiation, activity and longer lifespan) and decreased osteoblasts.
- Secondary causes:
Endocrine: Cushing, hyperparathyroidism, hyperthyroidism
GIT: coeliac, IBD
Chronic disease
Deficiencies: vitamin D, calcium
Drugs: corticosteroids, aromatase inhibitors, anti-androgen therapy in men (e.g. for tx of prostate ca)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the pathologic features of osteoporosis?

A

Loss of bone mass

Loss of trabeculae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the indications for DEXA?

A
  • all women 65+ years
  • post-menopausal women <65 with risk factors for fracture
  • history of fragility fracture
  • starting corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain your approach to treatment of osteoporosis.

A

(1) LIFESTYLE:
- weight-bearing exercise
- calcium and vitamin D supplementation if dietary intake not sufficient (daily intake 800 IU vit D and 1g calcium).
- smoking cessation
- healthy body weight
- healthy alcohol intake
- reduce risk of falls: correct vision, balance disorders, medication reconciliation (prevent polypharmacy, sedating drugs etc.), OT to address trip hazards etc.
(2) MEDICATION: bisphosphonates, denosumab, teriparatide
Begin pharmacotherapy if T score of -2.5 or osteopenia with high risk of fracture (using FRAX calculator)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

BISPHOSPHONATES

A

Alendronate, risendronate are oral
Zolendronic acid is IV
MOA: synthetic analogue of pyrophosphate –> incorporated into bone –> inhibition of osteoclasts
USE: Treatment of osteoporosis & fracture prevention; hypercalcemia
Risendronate,
PRECAUTIONS:
Osteonecrosis of jaw - dental assessment and procedures before starting bisphosphonate.
UE:
GIT: N&V, oesophagitis/gastritis, erosions and ulcers
Bone pain
Atypical femoral fracture
Flu-like symptoms for 1-2 days after IV bisphosphonates.
MONITOR: CMP
Ensure adequate calcium and Vit D intake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TERIPARATIDE

A

MOA: teriparatide is a PTH analogue –> promotes bone formation by increasing osteoblast activity (only anabolic therapy for osteoporosis)
USES: osteoporosis
CI: hyperparathyroidism, hypercalcaemia
Given SC daily
Lifetime max use of 24 months due to risk of osteosarcoma.
Monitor CMP
Ensure adequate calcium and vit D intake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

DENOSUMAB (PROLIA)

A

MOA: antibody to RANKL –> binds to RANKL –> prevent activation of RANK –> decreased osteoclast formation and activity.
USE: osteoporosis, hypercalcemia
Given SC every 6 months. Must not miss dose –> increased fracture risk.
Monitor CMP.
Ensure adequate calcium and vit D intake. CI if hypocalcaemic as can decrease serum calcium further.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Explain the pathophysiology of rickets and osteomalacia.

A

Defect in mineralisation of bone.
If occurring in childhood –> rickets
If occurring after epiphyseal plate closure –> osteomalacia.
Occurs due to:
VITAMIN D DEFICIENCY = the MOST COMMON cause of osteomalacia
(1) Decreased sunlight exposure –>
- sunscreen
- skin covered by clothing/veil etc.
- dark skin pigmentation
- insufficient time outdoors
(2) Insufficient activation of vitamin D –>
- CKD
- anticonvulsants affect production of vitamin D (affect the production of 25-hydroxy-vitamin D in the liver)
(3) Inadequate dietary intake of vit D
INADEQUATE CALCIUM OR PHOSPHATE INTAKE
(1) Inadequate dietary intake of Ca or PO4
(2) Malabsorption - e.g. CF, coeliac disease
(3) Paraneoplastic syndrome - tumour producing FGF-23

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Compare and contrast CMP, vit D, ALP and PTH levels in osteoporosis, osteomalacia/rickets and Paget’s disease.

A

OSTEOPOROSIS: usually normal
OSTEOMALCIA/RICKETS: low Ca and low PO4, low vit D, high ALP, high PTH
PAGET’s DISEASE: high ALP, otherwise normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the main causes of raised ALP?

A

Alkaline phosphatase elevation is most commonly caused by LIVER or BONE disease.
LIVER = mainly cholestasis
BONE = increased bone formation - primarily Paget’s disease (can be raised by metabolic bone disease e.g. osteomalacia, osteoporosis, and bone tumours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline the metabolism of vitamin D.

A

7-dehydro-cholesterol in skin –> converted into pre-vitamin D by UVB light –>
OR dietary vitamin D (mainly dairy, also eggs, fish, fortified cereals)
–>
in the liver are converted by 25-hydroxy-vitamin D –> in the kidney the enzyme 1-alpha-hydroxylase produces 1,25-hydroxy-vitamin D.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What factors affect the activity of 1-alpha-hydroxylase in the kidney?

A

PTH and low phosphate –> increase enzyme activity

FGF-23, calcium and vitamin D –> decrease enzyme activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the functions of vitamin D?

A

GIT –> increase calcium and phosphate absorption.
KIDNEY –> increase calcium reabsorption + increase phosphate excretion in urine
BONE –> complex actions, stimulates osteoclasts (by stimulating production of RANKL by osteoblasts) + provides calcium for mineralisation.

17
Q

Explain the cause and risk factors of gout.

A

HYPERURICAEMIA
Uric acid is an end product of purine metabolism

Can occur due to:
1. INCREASED URIC ACID PRODUCTION
- High cell turnover:
Tumour lysis syndrome
Haemolytic anaemia
Psoriasis
- Diet rich in purines
Red meat
Seafood
Beer
  1. DECREASED URIC ACID EXCRETION
    Loop and thiazide diuretics
    CKD
  2. INBORN ERROR OF METABOLISM

When ECF becomes supersaturated with uric acid –> intra-articular uric crystal precipitation –> phagocytosis by neutrophils –> release of inflammatory mediators –> acute joint inflammation.

An acute attack can be triggered by:
Sudden increase in uric acid - e.g. large meal
Physiological stress - e.g. trauma, surgery
Dehydration

Repeat attacks can lead to tophi - commonly deposited in bone (elbows, knees) and soft tissues (pinna of ear, Achilles tendon sheath)

18
Q

How would you diagnose gout?

A

Presumptive diagnosis is made clinically.

Serum uric acid often elevated, but not diagnostic (can be normal in acute gout, and can be elevated w/o gout).
Raised WBC and ESR are typically elevated

Definitive diagnosis is by aspiration of joint fluid.

Shows NEGATIVELY birefringent,
NEEDLE-SHAPED, MONOSODIUM URATE crystals. + Inflammation present (WBCs > 2000/uL and >50% neutrophils) w/ NEGATIVE gram stain and culture

Imaging:
- Not used for dx of acute attacks - does not exclude septic arthritis, but can be supportive if synovial fluid analysis CI
- Shows: BONE EROSION with SCLEROTIC RIM and OVERHANDING EDGE - i.e. PUNCHED OUT.
Joint space is preserved.

19
Q

DDX of acute monoarticular joint inflammation.

A 
Septic arthritis
Gout
Pseudogout
Trauma
Bursitis
Psoriatic arthritis
20
Q

How would you treat gout?

A
  • DRSABCD, VITALS, LOC, STABLE/UNSTABLE?
  • Exclude septic arthritis/ trauma
  • Treat acute attack:
    LIFESTYLE: Rest and ice
    PHARMACOLOGIC: NSAIDs, colchicine, corticosteroid (either systemic or intra-articular)
    Most effective when started within first 24 hours.
    –> these meds do not address hyperuricaemia
  • Treat recurrent gout to prevent further acute attacks and tophi (indicated when >2 attacks/year, presence of tophi, XR changes showing destructive joint disease, patient preference due to disabling attacks)

LIFESTYLE: limit purine intake, . limit alcohol intake, weight loss/ maintain healthy weight, increase fluid intake

PHARMACOLOGIC: need to lower urate –>
1ST line: Xanthine oxidase inhibitors –> prevent metabolism of xanthine to uric acid

  • Allopurinol –> Allopurinol worsens an acute attack of gout!!! DO NOT USE WITHIN 2 WEEKS OF ACUTE FLAIR
  • Febuxostat

2ND line: uricosurics –> inhibit uric acid reabsorption in proximal convoluted tubule –> enhance renal clearance of uric acid
- Probenecid
UE: uric acid kidney stones

21
Q

COLCHICINE

A

MOA:
Bines to tubulin –> stabilises tubulin –> inhibits microtubule polymerization –> inhibits neutrophil function –> less phagocytosis of urate crystals –> reduced inflammation

USE: to treat acute attack of gout

UE:
GIT most common - diarrhoea, N&V, abdo pain
Narrow therapeutic window –> dose to treat gout is similar to dose that causes GI upset

22
Q

What findings do you see on analysis of joint fluid in pseudogout?

A 
Weakly POSTIIVELY birefringent
RHOMBOID-shaped
CALCIUM PYROPHOSPHATE DIHYDRATE crystals
\+ inflammation (raised WBCs with >50% neutrophils)
NEGATIVE gram stain and culture
23
Q

How would you treat pseudogout?

A
  • DRSABCD, VITALS, LOC, STABLE/UNSTABLE?
  • Exclude septic arthritis/ trauma
  • Treat acute attack (as for gout)
    If monoarticular –> intraarticular steroid injection

If polyarticular –> NSAIDs, colchicine or systemic steroids

For recurrent acute attacks –>

  • Prophylactic colchicine
  • Treat any underling metabolic disease

For chronic ongoing symptoms –>

  • Anti-inflammatory: NSAIDs, colchicine, low dose prednisone
  • Analgesia: paracetamol
24
Q

Explain the cause and risk factors of pseudogout.

A

AGE > 60 is the strongest factor.
Previous joint injury (unclear mechanism)
Underlying metabolic disease:
- Hyperparathyroidism
- Haemochromatosis
- Hypo-magnesium
–> if recurrent or chronic attacks of pseudogout, investigate for an underlying cause (CMP, iron studies)

These factors –> CPP crystals deposit into articular cartilage (chondrocalcinosis) –> crystals can enter joint space –> inflammation.

25
Q

Explain the pathogenesis of rheumatoid arthritis.

A

Combination of genetic and environmental factors.
Genetic - family history increases risk, many loci identified including PTPN22 and PADI genes.

Environment -
Smoking –> expression of peptidylarginine deiminase by alveolar macrophages –> citrullination of proteins –> novel antigens stimulate immune response –>

PLUS gingivitis –> P. gingivalis also expresses peptidylarginine deiminase –> novel antigen –> immune response –>

(1) production of anti-citrullinated protein antibodies
(2) activation of T cells –> stimulates of synovial macrophages –> inflammatory cytokines produced –> joint inflammation, activation of MMPs (destroy ECM), stimulates of osteoclasts (bone destruction).
(3) activation of synovium with angiogenesis, hyperplasia –> forms pannus and destroys joint.

26
Q

List symptoms and signs of rheumatoid arthritis.

A

SYMPTOMS

  • Chronicity: greater than 6 wks of symptoms
  • Prolonged early morning stiffness > 30 min
  • Loss of function
  • Joint pain
  • Swelling
  • Systemic symptoms: weight loss, fatigue, fever
SIGNS:
LOOK - 
- Symmetrical polyarthritis
- Involves typical joints: MCP and PIP (not DIP!), MTP, elbow, shoulder, ankle, knee, c spine
- Swelling
- Erythema
- Joint deformities: Swan neck, Boutonniere, ulnar deviation of fingers, volar subluxation, Z thumb
FEEL - 
- Tender
- Warm
- Feels 'boggy' from effusion (not bony)
MOVE - 
- Limited ROM
27
Q

RA is a systemic disease. List systemic features.

A
  • Fatigue
  • Weight loss
  • Fever

Muscles, Bones and Joints –>

  • Osteopenia and osteoporosis
  • Muscle wasting and weakness
  • Rheumatoid nodules - commonly on olecranon
  • Carpal tunnel

Neurological –>
- Mononeuritis multiplex - asymmetrical sensory and motor neuropathy in at least 2 separate areas (commonly foot drop and wrist drop)

Cardiovascular –>

  • Vasculitis –> rash (palpable purpura, ulceration, splinter haemorrhages)
  • Coronary artery disease risk
  • Pericarditis

Respiratory –>

  • Interstitial lung disease
  • Pleuritis

Haem –>

  • Felty’s syndrome: triad of RA, splenomegaly and neutropenia
  • Anaemia of chronic disease

Eyes –>

  • Scleritis
  • Episcleritis
  • Uveitis
28
Q

Explain your approach to diagnosis of RA.

A

History and examination

Lab tests -

  • RF: antibody (IgM) against IgG - NOT SPECIFIC (found in up to 10% of healthy people), but when pre-test probability is high has a high PPV - i.e. if a patient with inflammatory arthritis has RF –> they likely have RA.
    RF also gives prognostic information - if +, more aggressive disease and more likely extra-articular manifestations.
  • Anti-CCP antibodies: more specific than RF, also useful prognostically
  • FBC often abnormal: anaemia, thrombocytosis
  • ESR and CRP typically elevated

Can consider:

  • ANA, anti-dsDNA and anti-Smith for SLE
  • Uric acid for gout
IMAGING:
Obtain XR - diagnostic and for baseline and monitoring 
- SYMMETRICAL NARROWING
- SUBCHONDRAL EROSIONS
- PERIARTICULAR OSTEOPENIA
- SOFT TISSUE SWELLING

Consider synovial fluid analysis.

29
Q

How would you treat RA?

A

SUPPORTIVE CARE

  • MODERATE EXERCISE improves joint function and ROM (not intensive - can worsen large joint disease), can be combined with PHYSIOTHERAPY to provide a regimen of ROM exercises
  • OT: assistive devices
  • PSYCHOLOGIST
  • SUPPORT GROUP
  • HEALTHY DIET: Mediterranean diet, certain spices (e.g. ginger), antioxidants and probiotics can reduce disease activity

PHARMACOTHERAPY
Initial treatment =
Begin DMARD ASAP
- Usually methotrexate (if CI, consider sulfasalazine or leflunomide) used
+/- short course of low-dose corticosteroid (used for rapid symptom control - because DMARDs have a delayed effect)
+/- NSAIDs for analgesia - no disease-modifying properties

If insufficient response –>

  • Add second DMARD or
  • Add biologic - usually TNF-a inhibitor

SURGERY

  • May be required if severe joint disease and uncontrolled pain
  • Joint replacement

REGULAR FOLLOW-UP/ MONITORING

  • Refer to rheumatologist
  • Use a validated scoring system to rate disease activity at regular intervals

MANAGE COMORBIDITIES:

  • CVD risk –> because increased risk of CAD ensure risk factors are controlled
  • Osteoporosis risk - can occur as part of RA, or due to steroid treatment
  • MOOD disorders - ask about mood, psychology/psychiatry
30
Q

List the complications of fracture.

A 
EARLY, LOCAL
- Vascular injury, haemorrhage, shock
- Nerve injury
- Infection
- Compartment syndrome
- Avascular necrosis
EARLY, GENERAL
- Fat embolism
- Immobilisation --> DVT, PE
LATE, LOCAL
- Non-union
- Malunion
- OA
- Complex regional pain syndrome
LATE, GENERAL
- Atelectasis --> pneumonia
- Immobilisation --> deconditioning, loss of independence, nursing home
31
Q

Outline your general approach to fracture management.

A
  1. Clinical assessment
    HX - AMPLE: allergies, medications, PMH, last meal, events surrounding injury (mechanism)
    EXAM - Inspection, gentle palpation, neurovascular exam (neuro: motor, sensation; vascular: warmth, pulses, capillary refill)
  2. Imaging
    2 views at 90 degrees
    2 limbs (compare both sides)
    2 joints (above and below the suspected break)
    2 time points (for bones susceptible to avascular necrosis)
  3. Analgesia
  4. Definitive treatment
    Reduction –> fixation –> immobilisation
    May involve surgery
    - Orthopaedic consult
    - Prepare for surgery: NBM, IV cannula, bloods, consent
    Before casting, need to splint until soft tissue swelling resolves
    Be sure to check fit of splint/cast – do NOT compromise neurovascular status (e.g. too tight), do NOT compromise soft tissues (adequate padding, not rubbing)
    XR again once reduced to ensure correct positioning
    • for open fractures
      - Antibiotics
      - Tetanus prophylaxis
      - Prompt irrigation and debridement
  6. Immobilised? = DVT prophylaxis
  7. Patient education -
    - Safety netting - when to return to ED
  8. Arrange follow-up
    - If more imaging is needed, to remove cast, for physiotherapy/ rehabilitation etc.
32
Q

Describe the blood supply to the head of the femur.

A

The supply is mainly from the medial and lateral circumflex arteries, branches of the femoral a.

A small amount of blood is supplied in the artery that accompanies the ligament of the head of the femur (branch of the obturator a.) - this is INADEQUATE to supply the femoral head if the circumflex arteries are damaged –> avascular necrosis

33
Q

What fractures would you be worried about after fall onto an outstretched hand?

A

Scaphoid fracture

Distal radial fracture (Colles)

34
Q

What are the clinical features of a hip fracture?

A
  • Pain
  • Unable to weight bear
  • Shortened and externally rotated leg
  • Possible soft tissue injury/ bruising
35
Q

What are the clinical features of a scaphoid fracture/ how would you examine for a scaphoid fracture?

A
  • Hx of fall onto outstretched hand
  • On examination –>
    Pain on palpation of the anatomical snuffbox
    Pain when compressing in the axial direction through the first MCP (push thumb into wrist)
36
Q

How would you investigate a suspected scaphoid fracture?

A

XR - best initial test
But 25% of scaphoid fracture are initially undetectable on XR.

If initial XR is negative, but clinical suspicion remains –> either:

  1. Immobilise with a cast and repeat XR in 2 weeks
  2. Wrist MRI

Medicine (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions