Soft Tissue and MSK Disorder (copy)

What is the predominant collagen in tendons?

Type I collagen (~95% of dry weight), arranged in parallel fibrils.

What is the main function of a tendon?

Transmit tensile force from muscle to bone and store/release elastic energy.

What is the main function of ligaments?

Stabilize bone-to-bone alignment and provide proprioceptive feedback.

What are the four zones of an enthesis?

Dense fibrous tissue → uncalcified fibrocartilage → tidemark/calcified fibrocartilage → subchondral bone.

What is fascial densification?

Increased hyaluronan viscosity that restricts fascial layer gliding and may sensitize nociceptors.

What are the four stages of pain processing?

Transduction → transmission → modulation → perception.

How do A-delta and C fibers differ?

A-delta: thinly myelinated, fast sharp pain; C fibers: unmyelinated, slow dull/burning pain.

Which mediators sensitize peripheral nociceptors?

PGE2, bradykinin, substance P, CGRP, NGF, H+, K+, IL-1β, and TNF-α.

What is central sensitization?

Increased excitability of CNS pain pathways, causing allodynia, secondary hyperalgesia, and expanded referred pain.

What is the gate-control mechanism of pain?

Large A-beta mechanoreceptor input activates enkephalinergic inhibitory spinal interneurons to REDUCE pain transmission.

What treatments can activate gate control?

TENS, massage, heat, and vibration.

Which pathways/mediators support descending pain inhibition?

PAG–RVM/locus coeruleus pathways; endogenous opioids, norepinephrine, serotonin, and GABA.

What are the three major pain phenotypes?

Nociceptive (tissue injury), neuropathic (somatosensory lesion/disease), and nociplastic (altered central nociception without clear tissue/nerve damage).

What is the key difference between tendinitis and tendinosis?

Tendinitis is acute inflammatory; tendinosis is chronic degenerative/angiofibroblastic change.

What are the stages of tendinopathy?

I: pain after activity; II: start-up pain improves with warm-up then returns; III: pain during/after activity limits performance; IV: complete rupture.

What is a core exercise treatment for chronic tendinosis?

Heavy slow eccentric strengthening, typically 3 sets of 15 twice daily for 12 weeks.

Why avoid corticosteroid injection into weight-bearing tendons?

Risk of spontaneous tendon rupture, especially Achilles, patellar, and quadriceps tendons.

Which tendon is commonly affected in lateral epicondylitis?

Extensor carpi radialis brevis (ECRB) origin.

What provocative tests support lateral epicondylitis?

Cozen test and Mill test.

What is preferred initial management for lateral epicondylitis?

Load/ergonomic modification, counterforce strap, eccentric wrist-extensor exercises, and topical NSAID.

Which tissues are involved in medial epicondylitis?

Common flexor-pronator origin, especially pronator teres and flexor carpi radialis.

What should be checked in medial epicondylitis?

Ulnar nerve Tinel sign at the cubital tunnel.

What causes trigger finger?

Thickening/fibrocartilaginous metaplasia of the A1 pulley with impaired tendon gliding.

What are the clinical grades of trigger finger?

I: pain/tenderness; II: catching but actively extends; III: needs passive extension or cannot actively flex; IV: fixed PIP contracture.

What is first-line treatment for trigger finger in early disease?

MCP extension splint, warm soaks, tendon gliding, and topical/oral NSAIDs.

Where is corticosteroid injected for trigger finger?

At the volar MCP/A1 pulley region, into the sheath and outside—not into—the tendon substance.

What causes De Quervain tenosynovitis and what is the key test?

First dorsal compartment APL/EPB stenosing tenosynovitis; positive Finkelstein test.

What is initial treatment for De Quervain tenosynovitis?

Thumb-spica splint, activity modification, and NSAID; injection may target both APL and EPB subcompartments.

What is Dupuytren contracture?

Palmar fibromatosis with pretendinous cords causing progressive finger flexion contracture, often ring then little finger.

What is a positive Hueston tabletop test?

The patient cannot lay the palm flat on a table → Dupuytren contracture sign

Threshold for treatment in Dupuytren contracture?

MCP contracture ≥30° or any PIP contracture ≥15–20° in Huueston table top test

What causes mallet finger?

Terminal extensor tendon avulsion or dorsal distal-phalanx avulsion fracture after forced DIP flexion.

How is a stable mallet finger treated?

Continuous DIP extension splinting for 6–8 weeks, then night splinting for 4 weeks; keep PIP free.

What happens if the DIP flexes during mallet-finger splinting?

The continuous-splinting clock resets to day 0.

What clinical clue suggests olecranon bursitis rather than elbow joint effusion?

Posterior “goose-egg” swelling with relatively preserved passive elbow flexion and extension.

What is the classic presentation of subacromial bursitis?

Painful arc during shoulder abduction, commonly 60°–120°.

What is greater trochanteric pain syndrome associated with?

Lateral hip tenderness, often involving gluteus medius/minimus tendinopathy and bursa.

What is pes anserine bursitis/tendinopathy location?

Posteromedial tibia, about 4–5 cm below the knee joint line.

When should septic bursitis be suspected?

Erythema, fever, or skin abrasion; aspirate fluid for cell count, Gram stain, and culture.

What is the classic symptom of plantar fasciitis?

Sharp medial heel pain with the first steps in the morning or after sitting; it may improve with walking then recur later.

Where is plantar fasciitis tenderness and what test may be positive?

Anteromedial calcaneal tubercle; Windlass test (passive first MTP dorsiflexion).

What is first-line plantar fasciitis management?

Plantar-fascia and calf stretching, heel cup/arch support, night splint, and short-course NSAID if appropriate.

What are key risks of plantar-fascia steroid injection?

Heel fat-pad atrophy and plantar-fascia rupture.

What is the classical Simons–Travell trigger-point hypothesis?

Excess ACh at dysfunctional motor endplates causes sustained sarcomere contraction, capillary compression, hypoxia, and sensitization.

What does the newer protective-response model propose about myofascial trigger points?

They may be an adaptive protective co-contraction in response to strain-repair mismatch, overload, or sensorimotor instability.

Why can trigger points recur after needling alone?

The underlying overload, poor fascial gliding, posture, or motor-control deficit remains unaddressed.

What characterizes an active myofascial trigger point?

Spontaneous pain and familiar referred pain on palpation, often with a taut band/local twitch response.

How does myofascial pain syndrome differ from fibromyalgia?

MPS is regional with taut bands/trigger points; fibromyalgia causes generalized widespread pain without focal taut bands.

Two phases of MPS treatment model

Modulate protection (e.g., needling/manual therapy) then address strain-repair mismatch with graded motor control, stabilizer endurance, ergonomics, and sleep.

What distinguishes CRPS type I from type II?

Type I has no identifiable major nerve injury; type II follows documented major peripheral nerve injury.

What are the Budapest clinical criteria for CRPS?

Disproportionate continuing regional pain; ≥1 symptom in ≥3 of 4 categories and ≥1 sign in ≥2 categories, with no better diagnosis.

What are the four CRPS symptom/sign categories?

Sensory; vasomotor; sudomotor/edema; motor/trophic.

What are typical sensory findings in CRPS?

Allodynia and hyperalgesia.

What are typical vasomotor findings in CRPS?

Temperature asymmetry >1°C and/or skin-color changes.

What are typical sudomotor/edema findings in CRPS?

Sweating asymmetry and non-articular edema.

What are typical motor/trophic findings in CRPS?

Weakness, tremor, dystonia, shiny/thin skin, nail or hair changes, and reduced ROM/contractures.

What are the broad CRPS stages?

Stage I warm/inflammatory (0–3 months); Stage II cool/dystrophic (3–9 months); Stage III cold/atrophic (>9–12 months).

What is a core rehabilitation approach for CRPS?

Graded motor imagery (laterality, explicit motor imagery, mirror therapy), desensitization, and active stress-loading.

What defines fibromyalgia pain distribution?

Generalized pain in ≥4 of 5 body regions for ≥3 months.

What are the 2016 ACR fibromyalgia score thresholds?

WPI ≥7 and SSS ≥5, OR WPI 4–6 and SSS ≥9; symptoms present ≥3 months.

What do WPI and SSS measure in fibromyalgia?

WPI counts painful sites (0–19); SSS grades symptom severity including fatigue, unrefreshing sleep, cognitive symptoms, and somatic symptoms (0–12).

What labs to exclude mimics of fibromyalgia?

ESR/CRP, CBC, TSH, 25-OH vitamin D, and CK.

What is the strongest first-line management foundation for fibromyalgia?

Graded low-impact aerobic/strengthening exercise, CBT, and sleep-hygiene restoration.

Fibromyalgia treatment

Duloxetine, milnacipran, pregabalin, and low-dose amitriptyline or nortriptyline.

Which treatments to AVOID in fibromyalgia?

Strong opioids and systemic corticosteroids; NSAIDs generally lack efficacy for pure nociplastic pain