msk

Question 1

Explain Soft tissue injury ATFL/ CFL and the prevalence of this kind of injury

Answer 1

lateral ligaments of the ankle that resist inversion. 70% of the population have experienced ankle injuries. ATFL is the most common.

Question 2

signs and symptoms of ATFL/CFL

Tests for the ATFL/CFL

Answer 2

Clinical signs: pain during inversion - swelling.

Talar tilt test and anterior drawer on the ankle.

Question 3

NICE guidelines for rehabilitation of the ATFL/ CFL

Answer 3

PRICE - dependant on grade- 1, 2 or 3. first 48–72 hours following injury

Start active mobilization and flexibility (range of motion) exercises as soon as tolerated without excessive pain.

Question 4

Lateral Epicondylitis definition

Answer 4

Inflammation, pain and tenderness in the medial epicondyle of the humerus at the common extensor tendon (radialis and brevis) failure of the musculotendinious attachment. Repercussions stress has been an implicated factor and overuse of the tennis backhand hence (TENNIS ELBOW)

Question 5

Symptoms of lateral epicondylitis

Answer 5

Pain at distal and lateral epicondyle. Pain can radiate distally or proximally. Pain may be felt when opening a door knob or gripping and resisted extension

Question 6

Functional limitations of lateral epicondylitis?

Answer 6

Inability to lift, carry, type or use a mouse on the affected side or squeezing

Question 7

Medial Epicondylitis Treatment

Answer 7

Initial treatment: ~rest and avoid repetitive movements - brace may be worn to reduce forearm extension/splint set at neutral. rehab: decrease pain with ultrasound, electrical stimulation and education of repetitive stress.

When the patient is pain-free a program is implemented to improve strength and endurance of the wrist extensions and stretching. However this must be monitored so that the muscles are strengthened and without itself causing an overuse situation.

Wrist extension/flexion exercises/stretching and hammer pronations

Question 8

Lateral Epicondylitis Treatment (when pain free)

Answer 8

When pain free - start with static exercises then progress to resistance exercises (emphaisis on the eccentric phase), therabands, light weights and manual self resistance may be used

Question 9

OA of the hip definition

Answer 9

Degenerative joint disease (femoral acetabular joint) hip trauma is associated with unilateral OA. OA is also associated by bilateral OA (4-8x BW mechanical force through the joint). 3-6% in white population and lower in Black, Asians & Indian but twice as common in women. Breakdown of cartilage compromising the femoralacetabular articulation. Degeneratition of the joint capusle, subchondral bone, synovial fluid/membrane and narrowing of the joint space.

Question 10

The causes of Hip OA ?

Answer 10

Idiopathic (primary) o. Occupation heavy lifting and the use of stairs can cause ‘wear and tear’ and

secondary would be a result of hip trauma

Question 11

Symptoms of hip OA

Answer 11

Hip pain and stiffness and ‘groin pain’ with referrer pain as far down as the medial knee. It is worse with weight bearing rotational loading and may feel relieved with rest. Advanced OA may be painful at rest though

Question 12

Physical examination of OA

Answer 12

Characterised by a a limp, decreases single limb stance time on painful limb. Decreased stride length. Reduced ROM (esp internal rotation indicates hip rather than spine) . Hip abductor weakness with Trendelenburg gait. FABER test - buttock pain is Sacroiliac joint and groin is infra-articular hip

Question 13

Functional limitations of Hip OA

Answer 13

Reduced weight bearing, running, climbing stairs, getting on shoes and socks and use of upper limb from sit to stand

Question 14

Pathophysiology of OA

Answer 14

Osteoarthritis is traditionally thought of as a ‘wear and tear’ disease which occurs as we age. However, recent research suggests otherwise.

The pathogenesis of OA involves a degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage and the inflammatory cells in the surrounding tissues.

The release of enzymes from these cells break down collagen and proteoglycans, destroying the articular cartilage. The exposure of the underlying subchondral bone results in sclerosis, followed by reactive remodelling changes that lead to the formation of osteophytes and subchondral bone cysts. The joint space is progressively lost over time.

Question 15

Definition of Adhesive capsulitis?

Answer 15

It is idiopathic, progressive and painful and occurs over 1-2 years. Painful phase, freezing phase and thawing (resolution phase), usually affects women 50+ involving the non- dominant shoulder. Primary cause is unknown but secondary causes diabetes, hyperthyroidism, breast cancer and autoimmune disease.

Question 16

Pathophysiology of frozen shoulder

Answer 16

Synovitis (inflamed synovial membrane) due to cytokines. Depending on the stage when it’s assessed. The painful phase is the capsular thickening and reduces synovial fluid, thinking of the rotator cuff tendons. Reducing glenohumeral joint space.

Question 17

Symptoms of frozen shoulder/adhesive capsulitis ?

Answer 17

Painful phase: gradual onset at pain/ worse at night- exacerbated by overhead activities. Freezing: increases pain and reduced ROM Thawing: decrease in pain & increase in pain free ROM.

Question 18

Presentation examination of frozen shoulder

Answer 18

Pain stage: reduction in both passive/active ROM painful external rotation & abduction followed by an increase loss of flexion. Reduced glenohumeral glide- same symptoms of shoulder OA

Question 19

Treatment or frozen shoulder

Answer 19

Initial: RICE to reduce pain and inflammation while increasing shoulder ROM. Home exercise program: pendulum, deltoid stretch, arm overheads, hand behind back stretch. 15% of patients report permanent loss of function

Question 20

Total knee R|eplacement definition

Answer 20

Arthroplasty is reconstruction of the joint by artifical replacement of diseased, damaged or ankylosed (stiff) joint. 90% of the cases are due to arthritis.

Question 21

Knee replacement pathophysiology ?

Answer 21

athroplasty or ‘knee resurfacing’ cartilage and some underlying bone are removed, (PREPARE), metal implants are used to recreate the surface of femur and tibia and a spacer is put in (cartilage) to create a smooth surface.

Question 22

Exercises for TKR post-op

Answer 22

knee mobility to encourage flexion/extension to avoid contractures, weight bearing (gravity is resistance) with walking aid. Pain for 2 weeks (sutures for 10-14 days then removed)

Question 23

Post Op Rehab Total Knee Replacement

Answer 23

Quad/hamstring strengthening, gait retraining, ADL (stairs and walking with aid)

Question 24

contraindications to TKR

Answer 24

Morbid obesity, bone infections, knee sepsis, severe vascular dysfunction

relative contraindications- osteomylotiis

Question 25

Weeks 1-4 rehab TKR

Answer 25

low resistance dynamic exercises, ADL tasks are independent, electrical stimulation of the quads

Question 26

Weeks 4-8 TKR rehab

Answer 26

open and closed chain actvities and return to light/meduim activities. Explosive activites are NOT advised

Question 27

Total hip replacement definition

Answer 27

TKR arthroplasty is the artifical replacement of the proximal femur and acetabulum. cut through TFL and glute min/med then disloate the hip, severe femoral head and replace acetanbulum and femoral head with polyethylene and titanium

Question 28

Causes for THR

Answer 28

Osteoarthritis (90%), avascular necrosis, degenerative join disease, infecion of the joint

Question 29

physical examination of THR

Answer 29

Altered gait (Trendelenburg sign), hip, knee and back pain, decline in ADL, functional activities Sit to stand, Hip flexor contracture (Thomas test).

Question 30

Risks of patients post-op THP/TKR

Answer 30

DVT, PE, on warfarin (vitamin K antagonist), sciatic nerve damage, dislocation, Myocardical Infarction (heart attack)

Question 31

4 stages of fracture repair

Answer 31

1. Heamatoma
2. Fibrocartilaninous callus
3. Bony callus
4. Bone remodelling

Question 32

Describe stage 1 of fracture repair

Answer 32

Heamatoma formation: blood cells tear/break so they clot heamatoma, inflammed days 1-5

Question 33

Stage 2: fibrocartilaginous Callus

Answer 33

Soft callus - capillaries grow into the heamotoma - stem cells recruited. fibroblasts secrete collagen to connect muscle to bone. Osteoblasts build bone. Chondroblasts secrete cartliage matrix days: 5-11

Question 34

Stage 3: Bony Callus - 3-4

Answer 34

Cartliaginious callus begins ossification as the fibrocartilaginious callus converts to a bony callus spongy bone 3-4 weeks

Question 35

fourth stage of bone remodelling

Answer 35

Bone remodelling: osteoblast and osteoclast remodelling callus is replaced with bone and substancial remodelling of vascular 6 weeks+

Question 36

Sub-Acrominal impingement ‘impingement sign’ defintion

Answer 36

Non-traumatic, unilateral shoulder pain, that causes pain around the acromion. The inflammed rotator cuff muscles (supraspintus) become ‘impinged’ in the narrow sub-acromial space by coracoclavicular ligament, coracoid process, long head of biceps & subacromial bursa

Question 37

Causes of Impingement syndrome ‘rotator cuff tendonopathy’

Answer 37

The rotator cuff tendons are squeezed in the narrow junction causing inflammation by overuse, weak by disuse, muscular imbalances or degeneration from the aging prcoess.

Question 38

Pathphysiology of ‘impingment syndrome’

Answer 38

chronic rotator cuff tendinopathy and weak scapulathorasic stabilisors affects how the humerus on the glenoid fossa. impingment in forward flexion impinges on the anterior suprspinatus - chronic inflammation causes oseocyte ‘hooking’ on the acromion and can cause tears

Question 39

signs and symptoms of ‘shoulder impingment’

Answer 39

Pain in over head reaching, referred pain in the deltiod, abduction about 70-120 degress (90 degrees), pain when lifting, arm weakness.

Question 40

testing the rotator cuffs

Answer 40

Painful Arc Test- 70-90 degrees, infraspinatus/teres minor (external rotation), lift off test (subscapularis), Hawkins-kenedy/ Empty can test (Supraspinatus).

Question 41

treatment of ‘impingment syndrome’

Answer 41

initial gentle, passive prolonged stretching restore ROM, Educate of correct posture (kyphosis), protracted shoulders, scapula stabilisor exercises, wall push up, shrugs, rows, for propriocpetion closed chain/ then open chain rotator cuff exercises

Question 42

Frozen shoulder pathophysiology

Answer 42

Painful and progressive restrictive active and passive glenohumeral range of motion. Fibrosis and Synovitis of the joint capsule, stiffness. Particularly external rotation.

Question 43

Defintion of adhesive capsulitis ?

Answer 43

Painful and progressive restrictive active and passive glenohumeral range of motion. Fibrosis and Synovitis of the joint capsule, stiffness. Particularly external rotation.

Question 44

Adhesive capsulitis causes/etiology

Answer 44

Primary: idiopathic

Secondary: thyroid (hyper/hypo), diabetes, heart disease, parkinson’s, as a result of other trauma, stroke, broken arm etc. woman 50+

Question 45

frozen shoulder red flags

Answer 45

diabetes, stroke, thyroid disorder, metastatic disease,

Question 46

Examining the difference between adhesive capsulitis and frozen shoulder ?

Answer 46

Rotator cuff tears will have will have pain but you will be able to passively move while, adhesive capsulitis will be stiff while active and passive.

Question 47

Static Stretching definition

Answer 47

A stretch is improving flexibility and ROM around a joint which decreases the risk of injury. A low force, long duration elongation of the muscle. The effect is that it decreases joint stiffness, extensibility of connective tissue, returns neuromuscular balance and reduces joint pain.

Question 48

Mechanism of static stretching ?

Answer 48

As you elongate (stretch) the muscle fibres (sarcomere) actin and myosin are less cross bridged so they don’t overlap as much in the myofilament. This tension allows the collagen fibres to realign disorganised fibres. This realignment helps in rehab of scar tissue.

Question 49

Proprioceptors Golgi tendon organs ? Muscle spindles ?

Answer 49

Golgi tendon organs = ‘tension’ tensile load mechanoreceptors Muscle spindles = detect changes in length ‘ stretch detectors’

Question 50

Contraindications to stretching

Answer 50

Infection, vascular injury, excessive pain, hard end feel, acute inflammation (Heamatoma), post fracture before fully healed, joint instability dislocation.

Question 51

What are tendons made from in tendinitis

Answer 51

Collagen - tough, flexible and strong are healthy tendons. In Medial/lateral epicondylitis there is increase microtears and colleges disorientation. This causes fibrovasular scar tissue and granulation tissue in the tendon. Increase proteoglycan content and (Failure of the musculotendinous attachment with resultant fibroplasia/tendinosis).

Question 52

Differential diagnosis for epicondylitis

Answer 52

Elbow OA, Fractures, nerve damage radial/posterior interosseous nerve

Question 53

Intervertebral disc lesion definition

Answer 53

Degeneration of the anatomical structures of L4-5 and S1 (these are under the most compressive loads while we are active). 90% of adults have lumbar degenerative disease over the age of 60. As we age we lose proteogylcan within the intervertebral disc. This results in a loss of osmotic pressure, dehydration and breakdown of the outer ring (annulus fibrous ) and the nucleus polpus leaks, leading to loss of disc height,

Question 54

Pathophysiology of intervertebral disc lesion

Answer 54

Degenerative with age. Proteogylcan reduction causes dehydration and loss of osmotic pressure degenerates the annulus fibrosis. This leads to loss of joint height and the nucleus polpus leaking out and pressing on the sciatic nerve causing an inflammatory response.

Question 55

Symptoms of intervertebral disc lesion?

Answer 55

Chronic lower back pain, stiffness, pain radiating down the lower limbs (sciatic nerve), spasms, RED Flags (saddle anaesthesia, bladder as bowel dysfunction) Cauda Equina Syndrome. Flexion and extension limited ROM. Slump test and straight leg raise.

Question 56

rehab for intervertebral disc lesion

Answer 56

Pelvic stability strengthening exercises. Mobility and stretching in flexion and extension Education on posture and appropriate lifting technique and lifestyle activity. Dynamic lumbar stabilisation Plank, lateral plank, glute bridge, knee to chest stretch, hamstring stretch too

Question 57

Frozen shoulder presentation

Answer 57

Patients in the initial (freezing) stage of frozen shoulder syndrome (FSS) will describe the following: Insidious onset of vague, dull pain at the deltoid insertion. Pain with shoulder movement. Nagging pain at night, with sleep deprivation and the inability to sleep on the affected side

Question 58

Tendinopathy continuum (disorganised collagen formation)

Answer 58

Reactive tendinopathy: Non-inflammatory proliferation response this increases production of proteoglycan & collagen. Thickens tendons and increases stiffness. Tendon disrepair - load continues then you get an increase in proteoglycan and as a result of increased cellular water content and blood vessels in the matrix and collagen formation is disorganised. Collagen type 1 is replaced by thinner type 3 collagen and is unable to resist tensile force as effectively.

Question 59

The stages of tendinopathy ?

Answer 59

Reactive- tendinopathy - non- inflammatory proliferation response. Stiffness and thickening (reversible). Tendon Dysrepair - collagen disorganisation and proteoglycan increase in size Tendon degeneration - type 1 to type 3 thinner collagen (weaker) to tensile forces and failure of musculoskeletal attachment and fibrotic changes (irreversible).

Question 60

3 signs of frozen shoulder

Answer 60

>Can’t sleep at night > pain in deltoid tuberosity > reduction in passive and active ROM

Question 61

Pathology of adhesive capsulitis

Answer 61

Cytokine response mast cell (regulate fibroblast proliferation) and macrophage response affects the glenohumeral capsule and coracohumeral ligament and the rotor interval causes inflammatory changes causing proliferation fibrosis,

Question 62

Teach active exercises for glute min/med activation

Answer 62

Single leg squat/deadlift (isometric work) Side plank bridge (progress leg raise at same time) Stepper on one leg eccentric lowering (progress with weight) concentric and eccentric muscle actions Side lying ABDuction (progress with resistance band)

Question 63

Precautions and contraindications to stretching

Answer 63

Age of subject, fracture newly healed, osteoporosis (other bone disease), hemotoma, joint integrity, hyper mobility, open wounds, contractures that promote mobility

Question 64

The underlying pathology of OA and how it affects the range of movement

Answer 64

OA will decrease the range of movement due to pain and osteophyte formation (bone spurs) and loss of joint space. They will have pain while sitting to standing using stairs etc. They will have decreased synovial fluid and increased viscosity. They will slowly reduce in quad strength and have reduced internal rotation at the knee.

Question 65

stages of ligament repair

Answer 65

The inflammatory phase follows trauma to collagen fibres and lasts for 3-5 days, depending on the severity of the injury. Chemicals are released which produce pain, and there is bleeding in the tissues. This, together with fluid from damaged cells, produces swelling within the joint, putting pressure on nerve endings and causing more pain.

The repair phase is mediated by blood clotting over the damaged tissue. Blood platelets form a mesh to initiate healing. Also present in the blood clot are fibroblast cells, which proliferate and begin to lay down Type 3 (immature) collagen tissue, between 3-21 days after the injury. The use of electrotherapy in this phase has been shown to encourage fibroblast activity that ultimately provides a structurally stronger ligament.

The remodelling phase follows the repair phase and can last for up to a year. It involves maturation of collagen tissue from Type 3 to Type 1 and realignment of collagen tissue. When it is first laid down, the collagen tissue is haphazard and does not possess a lot of tensile strength. The ligament gradually becomes stronger through being subjected to controlled strain in a functional pattern, which aligns the fibres in a longitudinal fashion. Physiotherapy, in the form of controlled exercises progressing to functional activity, aid this process of remodelling

Question 66

What is proprioception ?

Answer 66

Proprioception results from sensory receptors in your nervous system and body. Most of these receptors are located in your muscles, joints, and tendons.

When you move, the receptors send detailed messages to your brain about your positions and actions. Your brain processes these messages and works with your vision, nervous system, and vestibular system to create your perception of where your body is and how you’re moving.

Question 67

How Does PNF work ?

Answer 67

The PNF techniques of ‘hold–relax’ and ‘contract–relax’ are specifically used to increase the range of movement. The principle of hold–relax is to achieve maximal relaxation in the tight muscle group that is limiting the movement by using the maximal relaxation achieved after a maximal contraction. During the technique the limb is taken to the end of available ROM and the patient is instructed to ‘hold’ the position whilst the physiotherapist applies measured resistance to build up a maximal isometric contraction in the muscle group that requires lengthening. Following this maximal contraction the instruction to relax is given whilst the limb is fully supported to allow maximal relaxation. The limb is then taken to the new end of ROM and the technique repeated.

Question 68

Pathology of contract relax PNF stretch

Answer 68

Contract–relax works on the principle of reciprocal inhibition, whereby a maximal contraction is built up in the antagonistic muscle group to produce relaxation in the tight muscle group.

Other PNF techniques are also useful to increase ROM, the facilitatory nature of PNF can help to move into new ROM and PNF is also effective in muscle strengthening.

Question 69

Soft tissue repair Healing

Answer 69

Acute inflammatory response 0-2 days - neutrophils, mast cells (histamine), macrophages engulf cellular debris.

Profilertation Phase 2 days to 21 days (3 weeks). where disorganised scar tissue is formed - fibroplasia and granulation- fibroblast - collagen, elastin, proteoglycans lay down type 3 collage rather then type 1.

remodelling phase - beings half way way through the proliferation phase 21 days to a year. loading should start taking place