MSK Flashcards

1
Q
  • Provide examples of synarthroses, diarthroses and amphiarthroses
A

Synarthroses or fibrous joints
are joints where adjacent bones are directly connected by fibrous connective tissue. There is no synovial cavity.
Examples include:
- an interlocking suture line between adjacent bones (e.g. skull). Sutures consists of strong fibrous tissue between skull bones e.g. sagittal suture
- Syndesmoses which consist of a fibrous ligament or membrane connecting bones e.g. interosseous membrane between the radius and ulna (technically amphiarthroses as some degree of motion is permitted)
- Gomphoses which consists of periodontal ligaments tethering teeth onto sockets e.g. roots of teeth in sockets of mandible

Amphiarthroses or cartilaginous joints
can be defined by the presence of cartilage, either hyaline or fibro-, between articulating bones. There is no synovial joint cavity.
- synchrondrosis or primary cartilaginous joints are connected by hyaline cartilage. Some are temporary e.g. epiphyseal plate, first sternocostal joint, or permanent e.g. costochrondral joints. Immovable.
- symphysis or secondary cartilaginous joints are joined by fibrocartilage e.g. pubic symphysis, interbody joints between vertebral bodies and intervertebral discs. Movable.

Synovial or Diarthrodial Joints
are freely movable, but limited by surrounding joint capsule, ligaments and muscles.
Many examples: knee/hinge, shoulder/ball and socket etc

  • Types: Hinge, Ball and socket, Saddle (as well as ellipsoid/condyloid, pivot, plane)
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2
Q
  • Provide an example of a ball-and-socket, hinge, pivot, condyloid, saddle, and plane joint
A
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3
Q
  • Describe the function of menisci/labrum/bursae and provide an example of each
A

Menisci:
pads of fibrocartilage ^[[[Histology Lecture 4]]]. Discs allow bones of different shapes to fit better, thus increasing the joint’s stability

e.g. of knee

Labrum:
a fibrocartilaginous ring which deepens the articular surface of a bone, increasing the surface area available for articulation and thus improving joint stability

e.g. in GH joint

Bursa:
sac-like structures, found between bones and adjacent structures (skin, tendons, muscle ligaments, or fibrous capsules). Bursae work to reduce friction between moving parts

e.g. supra and prepatellar bursae

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4
Q
  • Distinguish between types of cartilage
A
  • Articular or hyaline cartilage – e.g. found in synovial joints, cartilaginous. Appears blue or glue microscopically
  • Fibrocartilage – attaches tendons and ligaments to bone. Appears white microscopically
  • Elastic cartilage – auricles ^[think ear and elastic], nose, epiglottis, trachea. Appears yellow.
  • Fibroelastic cartilage – intervertebral discs and intraarticular menisci (load bearing and shock absorption). Appears yellow microscopically
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5
Q
  • Discuss the components of ground substance (PGs and collagen)
A

Proteoglycans
- Components of the ground substance.
- Secreted by chondrocytes
- Among collagen fibrils
- 15-40% of dry weight
- Hydrophilic - this means it attracts the water within the synovial fluid, giving the cartilage its resilient properties, permitting shock absorption (note in osteoarthritis the cartilage becomes ‘dried out’)
- Core protein plus side chains of glycosaminoglycans
- Chondroitin and keratin sulphate
- Attach to hyaluronic acid filaments (aggregation)

Collagen
- Collagen is produced by fibroblasts, as well as chondroblasts and osteoblasts
- 28 types, 90% is type 1.
- All collagen types are composed of three alpha polypeptide chains arranged like a three stranded rope

  • Type 1 - skin, fascia, tendon, ligament, bone. (It is this, within the ground substance of the bone ECM (osteoid) that becomes mineralised)
  • Type 2 – all forms of cartilage.
  • Type 3 - in association with type 1, found in skin, artery, uterus
  • Type 4 - basement membrane
  • Type 5- placenta, blood vessels
  • Determines the tensile strength of tissues
  • Provides a framework
  • Limits movement of other tissue components
  • Induces platelet aggregation and clot formation
  • Regulates hydroxyapatite deposition in bone (Hydroxyapatite deposition on collagen fibres confers hardness. Recall that deposition occurs in the first few days but can take months to complete calcification)
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6
Q
  • Distinguish ligaments and tendons
A

Ligament
- Dense collagenous structure linking bone to bone.
- Similar to a tendon (more collagen)
- Rows of fibroblasts within extracellular matrix of mainly type 1 collagen fibres.
- Elastin allows stretch, allowing an extra degree of movement e.g. rotation at knee joint, otherwise known to be a hinge joint (uniaxial motion)
- Deformation curve gives it a crimped appearance
- Function: Prevent excessive movement.
- Injury to the ligament is termed a sprain.

Tendon

  • Dense collagenous structure linking muscle to bone.
  • Collagen fibrils embedded in ground substance
  • A matrix of PGs, GAGs, structural glycoproteins…
  • More collagen (65-75% of dry mass) and less ground substance than ligaments.
  • 86% type I collagen, some elastin (2% dry mass) ^[less stretchy than ligaments]
  • Very linear collagen fibre arrangement - thus no stress strain relationship as with ligaments
  • Fibroblasts (tenocytes) in parallel rows between collagen bundles, synthesise collagen, elastin, PGs, and GAGs
  • Carries tensile forces. ^[Think Tendon, Think Tension]
  • Main injuries: tear or degeneration.
  • Tendonopathy not tendonitis.
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7
Q
  • Describe paratenon, epitenon, enthesis
A

Paratenon and Epitenon
- Paratenon – loose, areolar connective tissue around tendons.
- Type 1 and 3 collagen fibres, elastic fibrils and synovial cells
- Permits free movement of the tendon against surrounding structures
- Epitenon – fine connective tissue sheath covering the tendon.
- Injury – peritendonitis.

Enthesis
- Attachment of tendon to bone.
- Four zones
1. Tendon or ligament, whose collagen bundles continue into…
2. Fibrocartilage, which separates from…
3. Mineralised fibrocartilage
4. Bone
- Common site of disease in spondyloarthropathies (cause of lower back pain, j.o.interest = sacroiliac)

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8
Q

HII

  • Discuss the main upper limb muscles (Action, attachments, innervation)
A

Key upper limb muscles
There are three main muscles that are of high clinical importance.
- deltoid
- attachments: the deltoid has a wide origin (lateral third anterior clavicle, acromion process, spine of scapula posterior border) inserted into deltoid tuberosity of humerus
- movements: abduction of the humerus – although it needs rotator cuff to function correctly (otherwise would simply elevate, rotator cuff holds humeral head down)
- innervation: axillary nerve, supplying it from posterior to anterior ^[susceptible to palsy with dislocation of humeral head as it wraps around it to supply deltoid]
- vascularisation: posterior circumflex humeral artery
- triceps
- features
- three heads: long, lateral, medial
- long: infraglenoid tubercle of the scapula (or inferior glenoid lip)
- lateral: posterior aspect of the humerus, superior to the radial groove (or superior lip)
- medial: posterior aspect of humerus, inferior to the radial groove on the shaft. Medial head is deep.
- attachments: inserts into posterior surface of olecranon process of ulna
- movements: elbow extension
- innervation: radial nerve
- vascularisation: deep brachial artery
- biceps
- features: long head (from glenoid labrum, arises intra-articularly), short head (from coracoid process)
- attachments: inserts into the radial tuberosity
- movements: elbow flexor and supinator
- innervation: musculocutaneous nerve
- vascularisation: muscular branches of brachial artery
- note: long head is highly susceptible to injury as it sits in bicipital groove
- pectoralis major
- attachments: from the chest wall (clavicle and sternocostal) to the lateral lip of the bicipital groove
- movements: adduction and flexion of humerus (also medially rotates the glenohumeral joint). The clavicular head flexes the glenohumeral joint and the sternocostal head extends the glenohumeral joint from the flexed position
- innervation: lateral and medial pectoral nerves supplying the two heads
- vascularisation: several (thoraco-acromial - pectoral branch, internal thoracic artery — perforating branches…)

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9
Q

HII

  • Discuss the muscles of the forearm, and intrinsic muscles of the hand (as above)

action attachments innervation

A

go to forearm and hand deck

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10
Q

HII

  • List and describe the joints of the shoulder
A
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11
Q

HII

  • Describe the key ligaments of the shoulder
A

Two key ligaments is the coracoclavicular ligament, which has a conoid and trapezoid component; and the glenohumeral ligament, whose inferior component is the prime stabiliser of the shoulder joint. A full list is included below:
- glenohumeral ligament: divided into superior middle and inferior. Middle and inferior prevent shoulder dislocation as most dislocations are anterio-inferior. tighten with extremes of movement preventing further translation. inferior glenohumeral ligament is the prime stabiliser of the shoulder
- coracohumeral ligament:
- coracoacromial ligament:
- coracoclavicular ligament:
- acromioclavicular ligament:
- long head of biceps tendon:

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12
Q

HII

  • Describe the key ligaments of the elbow, and key ligament/s of the wrist and fingers
A

There are three main ligaments that support the elbow joint: the ulnar collateral ligament, radial collateral ligament and annular ligament.

The medial collateral ligament has three bands:
- anterior (strong)
- posterior (weaker)
- oblique
The MCL is crucial for combatting valgus stress. The anterior band of MCL is especially crucial for this.

The annular ligament runs around the radial head from the anterior and the posterior margin of the radial notch, to approximate the radial head to the radial notch and enclose the radial circumference. It encircles 80% of the radial head and functions to maintain the relationship between the head of the radius and the humerus and ulna.

Function:
- Holding the proximal radius against the ulna as it fits strongly around the radial head,
- It permits for free rotation of radial head as it’s internal surface is lined with cartilage.

Note that the radial is synonymous with the lateral collateral ligament. Similarly the ulnar is synonymous with the medial collateral ligament.

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13
Q
  • Describe the innervation and vascular supply of the upper and lower limb
A

Upper limb

Nerves of the upper limb
The major peripheral nerves that innervate the upper limb are the:

  • Axillary
  • Radial
  • Musculocutaneous
  • Median
  • Ulnar

Innervation of upper limb muscles

  • Musculocutaneous nerve: all anterior arm compartment muscles
  • Median nerve: anterior forerarm compartment muscles exceptflexor carpi ulnaris muscle andmedial half of flexor digitorum profundus
  • Ulnar nerve: intrinsic muscles of the hand, except for the thenar muscles and two lateral lumbrical muscles,
  • Radial nerve: posterior arem and forearm compartment muscles
  • Axillary nerve: deltoid and teres minor muscles

Sensory innervation of the upper limb

  • Musculocutaneous nerve: skin on anterolateral forearm
  • Median nerve: skin on palmar surface of the lateral three and one-half digits
  • Ulnar nerve: skin on medial one and one-half digits
  • Radial nerve: skin on posterior surface of forearm and dorsolateral surface of hand
  • Axillary nerve: skin on lateral arm

Blood supply of the upper limb
## Arteries

The major arteries include the:

  • Subclavian
  • Axillary
  • Brachial, continuing axillary
    • Radial
    • Ulnar
  • Palmar arches

The deep veins accompany the arteries of the same name.

The superficial veins empty into the dorsal venous network on the posterior hand over the metacarpal bones.

The cephalic vein originates from the lateral side of the dorsal venous network and travels through the lateral forearm and arm before emptying into the axillary vein.

The basilic vein originates from the medial side of the dorsal venous network and passes into the dorsomedial aspect of the forearm. It pierces the deep fascia in the middle of the arm to become the axillary vein.

Lower limb
## Blood supply
As the external iliac artery passes under the inguinal ligament, it becomes the femoral artery.

The femoral artery passes through the femoral triangle between the femoral vein and femoral nerve. At the apex of the femoral triangle it enters the adductor canal (deep to the sartorius muscle) and then passes through the adductor hiatus of the adductor magnus muscle where it enters the popliteal fossa and becomes the popliteal artery. The popliteal artery lies deep to the tibial nerve and popliteal vein in the popliteal fossa.

  • From the popliteal artery
  • Five geniculate branches – middle, and medial and lateral superior and inferior geniculate arteries
  • Superiors curve around the femoral condyles proximal to the epicondyles
  • Inferiors course around the margins of the tibial plateau, passing under the collateral ligaments
  • Anastomoses around the knee joint
  • Middle and inferior arteries supply the menisci, the outer ¼ of which are vascular.

Nerve Supply

  • Three sources
    • Sciatic nerve – branches from tibial and common peroneal nerves
    • Femoral nerves – branches travelling via the vastus muscles
    • Obturator nerve – small nerve from posterior division, accompanies femoral artery to popliteal fossa ^[relevant in paeds: knee looks fine]
      • May explain referral of hip pain to the knee
  • Popliteal artery is a continuation of the femoral artery
  • Below the knee it divides into the anterior and posterior tibial arteries
  • The posterior tibial artery follows the course of the tibial nerve and
    supplies the posterior muscles of the leg.
  • It passes behind the medial malleolus and passes to the plantar
    aspect of the foot
  • Forms the medial and lateral plantar arteries which supply the
    plantar structures
  • Below the bifurcation of the popliteal artery the peroneal artery
    arises
  • This passes across the back of the interossesos membrane and
    descends on the lateral aspect of the leg to supply the lateral
    muscles
  • The bifurcation of the popliteal artery gives rise to the anterior tibial
    artery
  • This passes anteriorly between the tibia and fibula across the upper
    margin of the interosseous membrane and courses down the
    anterior surface of this structure.
  • It supplies the muscles of the anterior compartment of the leg (TA,
    EHL, EDL)
  • Reaches the dorsum of the foot as the dorsalis pedis artery
  • Terminal branches are the dorsal metatarsal and dorsal digital
    arteries

Nerve supply
* The main nerve to the lower leg and foot, the tibial nerve is a
continuation of the sciatic nerve.
* It enters the lower leg between the two heads of the gastrocnemius and passes deep to the soleus to enter the posterior compartment of the leg.
* The tibial nerve supplies the gastrocnemius, soleus, and the three muscles whose tendons pass behind the medial malleolus (tibialis posterior, FHL, FDL) – plantar flexors.
* Posterior tibial nerve divides into the medial and lateral plantar
nerve and sends a branch to the calcaneus

  • The other division of the sciatic nerve, the common peroneal nerve arises above the knee joint.
  • After passing behind the head of the fibula it wraps around the neck of the fibula and divides near here into the superficial and deep peroneal nerves.
  • The superficial peroneal nerve descends adjacent to the fibula to supply peroneus longus and brevis (everters of the foot)
  • The deep peroneal nerve supplies the dorsiflexors of the ankle
    (anterior compartment – tibialis anterior, extensor digitorum longus, extensor hallucis longus)
  • It ends supplying extensor digitorum brevis
  • It supplies a small area of sensation between the first two toes on the dorsum of the foot
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14
Q
  • Identify the key features of the scapula, clavicle, humerus, radius and ulna/pelvis, tibia, fibula (Alternatively label an Xray)
A

Key features:

Tthe key features of the clavicle are:
- sternal end or the medial end- viewable both superiorly and inferiorly. Note that the sternal end is more flat.
- acromial end or the lateral end- viewable both superiorly and inferiorly. The acromial end is more likely to be dislocated.
- body or shaft
- conoid tubercle
- trapezoid line
- impression for costoclavicular ligament

Scapula
The scapula is a large flat bone.
Key features include:
- Body
- Spine, which terminates in the acromion laterally
- Coracoid process (coracobrachialis, pectoralis minor and short head of biceps originate here)
- Acromion, which is important because deltoid muscle attaches here, and rotator cuff muscles pass underneath. The narrowed subacromial space or downward sloping acromion pinches the cuff during elevation (see below for [[#Rotator cuff (mightily important)]])
- Glenoid cavity, articular surface with humerus
- Subscapular fossa
- Supraspinous fossa
- Infraspinous fossa
- Superior angle
- Inferior angle
- Medial border
- Lateral border

Humerus
is a long bone, and the only bone of the upper arm.
It has several key features, including:
- head
- anatomical neck, and surgical neck: note that these two terms are NOT synonymous. Anatomical neck rings around the articular surface, and separates rough humerus from smooth articular surface. Surgical neck is common site of fracture
- greater and lesser tuberosity. Note that the greater tuberosity is more lateral to the lesser tuberosity when viewed anteriorly. The lesser tuberosity is not visible at all posteriorly.
- supraspinous, infraspinous and teres minor (off rotator cuff) insert onto greater tuberosity
- subscapularis inserts onto lesser tuberosity
- bicipital groove: the long head of the biceps runs through here. Other muscles attach to the lateral lip, medial lip and floor
- lateral lip: pectoralis major
- medial lip: teres major
- floor: latissimus dorsi
- shaft
- deltoid tuberosity
- olecranon fossa
- coronoid fossa
- capitulum
- trochlea
- medial epicondyle
- lateral epicondyle

Radius
Key features of the radius include:
- head: The discoid head of the radius articulates superiorly with the capitulum of the humerus, contributing to the formation of the elbow joint. At the same time, the head of the radius also articulates with the ulna forming the proximal radioulnar joint. In this joint, the circumference of the head of the radius is situated on the radial notch of ulna.
- neck
- radial tuberosity/biceps tuberosity: where biceps inserts
- styloid process: The lateral aspect of the distal radius forms a ridge and terminates distally as the radial styloid process.
- ulnar notch: The distal end of the radius widens to form three smooth, concave surfaces. The medial aspect of the distal radius forms a concavity known as the ulnar notch, which articulates with the distal ulna.

Ulna
Key features of the ulna include:
- olecranon
- trochlear notch
- coronoid process: Projecting anteriorly from the proximal portion of the ulna is the coronoid process. The coronoid process aids in stabilizing the elbow joint and preventing hyperflexion of the forearm.
- head: The distal end of the ulna tapers to form the disc-like head of the ulna. The head of the ulna does not articulate with the carpal bones and is therefore not a component of the wrist joint
- radial notch
- ulnar tuberosity: Inferior to the coronoid process is the tuberosity of ulna, which functions as an attachment point for the brachialis muscle.
- styloid process: Projecting from the head of the ulna is a small bony protrusion known as the styloid process of ulna.

ILIUM
- superior portion of hip
- Large wing like, or fan shaped Ala
- Key features include: Iliac crest ,tubercle, four spines ASIS AIIS, PSIS, PIIS
- Like the scapula, it has flat surfaces for muscle origin
- Main weight bearer along with ischium
- Another key feature is the iliopubic eminence is junction with pubic bone

  • the gluteal Surface has three lines separating gluteus max, med and min
  • Tensor Fascia sits between ASIS and tubercle
  • Reflected head of Rectus femoris sits above acetabulum
  • ASIS is a point of attachment for Inguinal lig , Sartorius
  • AIIS is a point of attachment for Straight head RF and iliofemoral lig

Pubis
- Smallest Section of the Hip
- Forms anterior inferior section of the acetabulum.
- Upper surface of body is the pubic crest which terminates laterally at the pubic tubercle
- Key features include: Superior and inferior pubic rami, pubic tubercle, obturator foramen
- Pubis and ischium border the obturator foramen
- obturator foramen is covered in a membrane, is a site of muscle attachment
- Body is quadrilateral
- Projected Laterally as Superior Ramus, joining Ilium and Ischium at Acetabulum and Inferiorly as Inferior Ramus, fuses with Ischial Ramus
- Symphysis medially located, coated with fibrocartilage, secondary cartilaginous joint ^[enables expansion during delivery for infant head]
- Upper border Body is convex
- Laterally is pubic tubercle
- 2 ridges go out laterally, upper sharp, pectineal line continues into Arcuate line
- Below this is Obturator crest, Nerve ( on Bone ) and Vessels below, over the obturator foramen

Ischium
- L shaped bone, upper portion “Body”, joins with Ilium and Pubis at acetabulum, extends down to ischial tuberosity, for sitting and Hamstrings, and lower medial, thinner bar , ischial ramus, joins the pubic ramus to enclose the Obturator foramen
- Key features: ischial tuberosity and ramus, spine
- Tuberosity has oval upper and crest below
- Hamstrings attached oval area Semimembranosus laterally and Semitendinosis and Biceps medially
- Spine of Ischium , extends medially to separate the Greater and Lesser sciatic notches

Femur
- articulates with hip at aceatbulum
- Key features include: head, neck, greater and lesser trochanter, intertrochanteric crest, shaft, linea aspera, gluteal tuberosity, patellar surface, lateral and medial epicondyles, lateral and medial condyles,

Tibia
- Major weight transmission
- Forms most of the ankle (talo-crural) joint
- Medial malleolus extends one third the way down the talus
- Medial malleolus is anterior to the lateral
- Inferior articular surface is rectangular
- Tibial tuberosity
- Medial and lateral condyles
- Shaft
- Articulates with talus and fibula
- Origin of deltoid ligament, on medial aspect, very strong

Fibula
- Lateral side of the leg, parallel with the tibia
- No or very little weight transmission
- Forms part of the ankle (talo-crural) joint
- Lateral malleolus extends more inferiorly by 1cm
- Lateral malleolus is posterior to the medial
- Head and shaft
- Articulates with the lateral surface of the talus and tibia
- Origin of important ligaments – anterior and posterior talo-fibular, calcaneo-fibular, anterior inferior tibio-fibular

See notes for X-ray

NOTE: ignores knee

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15
Q
  • Name carpal and tarsal bones
A

self explanatory

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16
Q

Label this Xray of the lower leg

A
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17
Q

Label this Xray of the shoulder

A
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18
Q

Discuss micro and macro features of osteosarcoma

A

Compared to normal bone, osteosarcoma shows:
- Architecture: crowded/more cellular
- Cytology: Tumour cells often ‘spindle’ shaped, hyperchromatic, variable
- Pathognomonic feature = production of neoplastic osteoid/ matrix (appears pink due to lack of mineralisation)
- Often scanty, irregular/’lace-like’ & does not mineralize normally
- Tumor cells may also show predominantly fibrosarcomatous or chondrosarcomatous differentiation

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19
Q

HII

  • Identify common pathologies associated with carpal bones
A

Scaphoid fractures
- Scaphoid within the wrist minimal soft tissue attachment
- Limited blood supply
- Retrograde supply to proximal pole
- Difficult to diagnose
- Easily missed: not very painful
- Develops avascular necrosis and arthritis untreated
- May require internal fixation

Lunate avascular necrosis
also known as Keinboch’s disease. Occurs spontaneously in 30-40 year old males.

Other issues include the trapezium developing arthritis, , arthritis developing in the junction between the pisiform and triquetral bones, hook of hamate issue causing tendon rupture.

Scapholunate ligament can tear:
- Fall or twisting Injury
- Sprained or weak wrist
- Clunk or pop with activity, weak wrist
- Predictable arthritic pattern
- Needs repair

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20
Q

HII

  • Identify NoF fracture; describe blood supply to femoral neck and how different fractures that interfere with blood supply
A
  • note: intracapsular fractures e.g. subcapital and transcervical will jeopardise the vascular supply of the head as it is retrograde ^[similar to scaphoid bone]
    • blood supply is two-fold
      • interosseous, travelling up to the head (retrograde intramedullary vessels): not affected by intracapsular fractures
      • travels through capsule around neck to the head (medial and lateral circumflex femoral arteries )

n.b. intra-capsular and extra-capsular fx will both cut off the intramedullary retrograde supply.
BUT, only intra-capsular fx will cut off the medial femoral circumflex artery.

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21
Q

HII

  • What is Trendelenburg gait and what causes it?
A
  • occurs if medius and minimus fail to fire, as they work to stabilise and keep pelvis level when opposite leg is raised
  • result is opposite end drops
  • causes include: loss of hip abductors, L5 radiculopathy, polio, detachment of abductors, fracture or operation on greater trochanter
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22
Q
  • Describe the innervation (SENSORY AND MOTOR) and vascular supply of the upper limb
A

Innervation of upper limb muscles
Musculocutaneous nerve: all anterior arm compartment muscles
Median nerve: anterior forerarm compartment muscles except flexor carpi ulnaris muscle and medial half of flexor digitorum profundus
Ulnar nerve: intrinsic muscles of the hand, except for the thenar muscles and two lateral lumbrical muscles,
Radial nerve: posterior arem and forearm compartment muscles
Axillary nerve: deltoid and teres minor muscles

Sensory innervation of the upper limb

Musculocutaneous nerve: skin on anterolateral forearm
Median nerve: skin on palmar surface of the lateral three and one-half digits
Ulnar nerve: skin on medial one and one-half digits
Radial nerve: skin on posterior surface of forearm and dorsolateral surface of hand
Axillary nerve: skin on lateral arm

Vascular:

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23
Q

HII

  • Label hip muscles and briefly describe their attachements, action and innervation
A

SEE Hip deck (gluteal muscles)

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24
Q

HII

  • Label thigh muscles (Anterior and posterior) and briefly describe their function/Lis t and describe their function and innervation
A

See thigh deck

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25
Q

HII

  • List muscles of lower leg: anterior, posterior, lateral compartments. Their attachments, innervation and action
A

See lower limb deck

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26
Q
  • Describe how nerve of the lower limb arise from the sciatic nerve

links to popliteal

A

The sciatic nerve arises in the lumbosacral region. It descends through the posterior aspect of the thigh. Before entering the popliteal fossa, the nerve terminates by splitting into two large terminal branches: the tibial nerve and common fibular (peroneal nerve). Note that peroneal splits again into superficial and depp peroneal nerves.

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27
Q

LAbel Knee HII

  • Label knee structures. What does ACL do? What does meniscus do?
A

Role of ACL:

  • Prevents anterior translation of the tibia on a fixed femur
  • FFAATT
  • Controls rotation
  • From the area between the posterior ends of the menisci
  • Passes forwards, medially, and upwards
  • To antero-lateral surface of medial condyle of the femur
    Note mechanism of ACL injury: non-contact injuries e.g. landings. Recurrent collapses of the knee increase the risk of osteoarthritis.

Role of meniscus:

  • semilunar Cartilages
  • Medial and lateral
  • Crescentic pieces of fibrocartilage
  • Lateral meniscus is a fuller crescent
  • Attached to the periphery of the articular surfaces of the lateral and medial tibial condyles by the adjacent deep parts of the capsule – the coronary ligaments.
  • Thick at the periphery, thin inner edges (wedge in cross-section)
  • Upper femoral surface is concave
  • Lower tibial surface is flat
  • Improve congruence of joint surfaces
  • Guide movement
  • Shock absorption
    Mechanism of injury to menisci: semi-flexed, weight-bearing, and twist
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28
Q
  • List the typical vertebrae features, and specific features of cervical, thoracic and lumbar vertebrae/**distinguish between cervical thoracic and lumbar vertebrae
A

Common features to all vertebrae include (from anterior to posterior):
- vertebral body and foramen
- pedicle
- transverse process
- articular processes
- lamina
- spinous process

Cervical vertebrae
There are seven cervical vertebrae. They are the smallest of the vertebrae.

They are characterised by:
- an uncus on either side of the vertebral body (anterior side)
- a bifid spinous process (with exceptions…C7 may not bifurcate)
- transverse foramina, in each transverse process. Through here, vertebral arteries travel to the brain
- **a triangular vertebral foramen
- **articular processes are ‘open’ ( ..allows x movement. See physiopedia)

There are several features that distinguish thoracic vertebrae:
- **spinous processes are oriented obliquely, inferiorly and posteriorly
- **articular processes are ‘reading the book’ ( ..allows x movement. See physiopedia)
- **circular vertebral foramen
- demi facets, one superior and one inferior, on either end of the vertebral body
- the demi facets articulate with the heads of two different ribs to form the costovertebral joints-
– e.g. at T2, the head of rib 2 articulates with the superior demi facet of T2, and the head of rib 3 articulates with the inferior demi facet of T2
- costal facet on the transverse process which articulates with the shaft of the rib of the same number e.g. costal facet of T2 articulates with shaft of rib 2

Special characteristics include:
- kidney shaped vertebral bodies
- **triangle shaped vertebral foramen
- shorter spinous processes c.v. thoracic vertebrae and do not extend inferiorly
- **articular processes ‘close the book’ ( ..allows x movement. See physiopedia)

Atlas
or C1. It articulates with the occiput and C2.

It has NO:
- vertebral body
- spinous process

It has:
- lateral masses, with oval-shaped superior articular facets (articulating with occipital condyles) and inferior articular facets (articulating with C2) connected by…
- anterior arch, which has a facet for articulating with the dens of the axis, which is secured by the transverse ligament of the atlas (see below)
- posterior arch, which has a groove for the vertebral artery and C1 spinal nerve

Axis
or C2, which articulates with C1 and C3.
Its most characteristic feature is the dens, in addition to the general features of the typical cervical vertebrae.

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29
Q
  • How do the vertebrae facilitate or disallow movement?
A

Intervertebral joints
Vertebrae will articulate with each other via two types of joints
#### Facet (zygapophysial) joints
Facet joints are synovial plane joints, between the superior articular facets of the inferior vertebra and the inferior articular facets of the superior vertebra.
It works to guide and limit movements between vertebrae.

As synovial plane joints, the facet joints are composed of:
- hyaline articular cartilage which lines the facet surfaces of the superior and inferior articular processes
- synovial joint cavity between the articular surfaces which contains synovial fluid
- fibrous capsule, surrounding the joint, and lined by synovial membrane
- except for the anterior fibrous capsule, which is formed by the ligamentum flavum

The articular surfaces glide in a multitude of directions, which collectively produce movement in the spine of all planes:
- flexion and extension
- right and left lateral flexion
- right and left rotation

Interbody joints
Interbody joints sit between the vertebral bodies and intervertebral discs.
It is a cartilaginous symphysis.
Interbody joints connect the vertebrae anteriorly, to enable movement.
The disc is also involved in:
- weight-bearing
- shock absorption
- load distribution

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30
Q
  • Describe the surface anatomy of the shoulder/elbow/hand/KNEE/foot
A

Shoulder:
At the acromion, one can palpate the acromion itself, the acromioclavicular joint, and scapular spine.
Humeral head and GT, bicipital groove can also be palpated.

Elbow:
- lateral epicondyle
- medial epicondyle
- olecranon
- radial head
- wrist:
- radial styloid
- lister’s tubercle: EPL runs around it to thumb
- ulnar styloid

Hand:
- DIPS, PIPS, MCPs
- extensor tendons
- snuffbox
- pisiform
- radial and ulnar tubercles

Knee:
- patella
- tibial tuberosity
- quadriceps tendon
- patellar tendon
- medial and lateral joint lines

Foot:
- lateral malleolus
- medial malleolus
- edl tendons
- ehl tendon
- tibialis anterior tendon
- 5th MT base
- calcaneal tendon

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31
Q
  • **Identify the different parts of the brachial plexus, and some significant branches of the plexus
A

The brachial plexus can be divided into roots, trunks, divisions and cords. It provides motor and sensory innervation to the upper limb structures.

It is formed by the ventral rami of C5-T1 spinal nerves .

The plexus originates in the neck and then passes laterally and inferiorly over the first rib to enter the axilla. As it crosses the first rib, the brachial plexus is located with the axillary artery between the anterior and middle scalene muscles. This is where the roots can be found.

Trunks emerge in the posterior triangle of the neck. C5 and C6 merge to form one trunk, C7 is its own trunk, and C8 and T1 merge to form a trunk.
Divisions emerge behind the clavicle. Each trunk forms an anterior and posterior divisions.
Cords emerge in the axilla.

Three cords emerge:
- lateral: which is formed from the merging of the anterior divisions from upper and middle trunks
- posterior: which is formed from the merging of the three posterior divisions
- medial: which is formed from the merging of anterior division from lower trunk

  • Axillary and radial nerves from the posterior cord - innervate posterior muscles and skin
  • Musculocutaneous, median and ulnar nerves from the medial and lateral cords - innervation anterior muscles and skin
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32
Q

HII

  • What forms the ulnar nerve (from brachial plexus)? What forms the medial nerve? The radial nerve?
A
  • Axillary and radial nerves from the posterior cord - innervate posterior muscles and skin
  • Musculocutaneous, median and ulnar nerves from the medial and lateral cords - innervation anterior muscles and skin
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33
Q
  • List and describe the ligaments of the spinal cord
A

There are five main ligaments of the spine:
- the anterior longitudinal ligament which connects the anterior vertebral bodies and intervertebral discs up to the anterior tubercle of C1. The anterior atlanto-occipital membrane then connects the anterior tubercle of C1 to the occiput.
- the posterior longitudinal ligament which connects the posterior aspects of the vertebral bodies and intervertebral discs up to the C2 vertebral body. The tectorial membrane then connects C2 to the occiput
- the ligamentum flavum which is composed of elastic tissue and connects the laminae of adjacent vertebrae up to the posterior arch of C1. The posterior atlanto-occipital membrane connects the posterior arch of C1 and the occiput
- the interspinous ligament which connects adjacent spinous processes
- the supraspinous ligament which connects the tips of the spinous processes up to the C7 spinous process. It forms astrong broad ligament extending between theC7 spinous process and external occipital protuberance known as the ligamentum nuchaeand isan important site of muscle attachment

  • transverse ligament, which is a strong thick horizontal band that passesbehind the dens of C2 as itattaches betweenthe lateral masses of C1.
    • It is essential to maintaining the stability of the median atlanto-axial joint by preventing posterior displacement of the dens and anterior displacement of C1.
  • Alar ligaments, which extend betweenthe sides of the dens andthe lateral margins of the foramen magnum.
    • The alar ligaments prevent excessive rotation of the atlanto-axial joints.

  • anterior longitudinal ligament = limits hyperextension of spine
  • posterior longitudinal ligament = limits hyperflexion of spine; prevents posterior herniation of IVD
  • ligamentum flavum = limits separation of laminae to prevent hyperflexion of spine
  • interspinous ligament = prevents separation of spinous processes during flexion; resisting hyperflexion
  • supraspinous = prevents separation of spinous processes during flexion; resisting hyperflexion
  • transverse = resists separation of vertebral bodies?, in order to resist or limit flexion
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34
Q
  • Describe the (relevant) layers of anterior and posterior spinal cord muscles
A

Posterior muscles

Layer 1
- latissimus dorsi
- function
- glenohumeral joint: extension, adduction, and medial rotation
- innervation: thoracodorsal nerve (C6 - C8 ventral rami)
- trapezius
- function
- scapula: elevation, depression, rotation and retraction
- head and neck: extension and lateral flexion
- innervation: CN XI, and C3-4 ventral rami
#### Layer 2
- levator scapulae
- function
- scapula: elevation and rotation
- neck: extension and lateral flexion
- innervation
- dorsal scapular nerve (C4,5); C3-C4 ventral rami
- rhomboids
- function
- scapula: retraction
- innervation
- dorsal scapular nerve (C4,5)

Layer 4
- splenius capitis and cervicis
- function
- head and neck: extension, lateral flexion and ipsilateral rotation
- innervation
- dorsal rami (capitis: C3 and C4?, cervicis: ‘lower cervical nerves’; c5-8?)
#### Layer 5
- erector spinae (iliocostalis, longissimus, spinalis)
- function
- spine: extension and lateral flexion
- innervation
- dorsal rami (C1-L5)


### Anterior muscles

Layer 1
- sternocleidomastoid
- function
- head and neck: flexion, lateral flexion and contralateral rotation
- atlanto-occipital joints: extension
- innervation
- CN XI; C2-3/4 ventral rami
##### Layer 2
- scalenes (anterior, middle and posterior)
- function
- neck: flexion, lateral flexion and rotation
- innervation
- ventral rami (C3-8?)

Deep head and neck (aka Layer 3)
- Longus capitis and colli

Superficial lumbar
- rectus abdominis, external oblique, internal oblique and transversus abdominis
- function: flexion, lateral flexion and rotation
- innervation: ventral rami

Deep lumbar
- psoas major
- function
- lumbar spine: flexion and lateral flexion
- hip joint: flexion
- innervation: ventral rami (L1-4, plus femoral nerve branches?)
- quadratus lumborum
- function
- lumbar spine: lateral flexion
- innervation: ventral rami (L12, S1-5?)

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35
Q

HII

  • List the muscles in the six extensor compartments, and pathology associated with the extensor compartment
A

Extensor Tendons
- Wrist has 6 extensor compartments
- Extensor Retinaculum covers the tendons
- Prevents Bowstringing of the tendons
- Improved mechanical advantage
- Tendons are susceptible to compression friction or attrition rupture within the compartments

Extensor tendons: compartments
1. Abductor Pollicis Longus and Extensor Pollicus Brevus
2. Extensor Carpi Radialis Longus and Brevus
3. Extensor Pollicis Longus
4. Extensor Digitorum Longus and Extensor indicis Proprius
5. Extensor Digiti Minimi
6. Extensor Carpi Ulnaris

De Quervain’s Tendonitis
- Common Cause of radial wrist pain
- Over use or narrow compartment
- Treatment : Rest, Physio, stretching NSAID gel, Injection with Steroid
- Surgery if resistant

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36
Q
  • What is wrist drop? What nerves are involved?
A

Wrist drop is caused by damage to the radial nerve, which travels down the arm and controls the movement of the triceps muscle at the back of the upper arm, because of several conditions. This nerve controls the backward bend of wrists and helps with the movement and sensation of the wrist and fingers.

The wrist and the fingers cannot extend at the metacarpophalangeal joints. The wrist remains partially flexed due to an opposing action of flexor muscles of the forearm. As a result, the extensor muscles in the posterior compartment remain paralyzed.

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37
Q

- List the contents of the carpal tunnel

A

The contents of the carpal tunnel are as follows:
- 4 Profundus tendons
- 4 superficialis tendons
- flexor pollicis longus
- median nerve
Carpal bones make up the walls and the floor. The tunnel was roofed by the flexor retinaculum.

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38
Q

**- What pathology is associated with CT? How does it occur? List risk factors, presentation and treatment

A
  • Median nerve compression due to either reduced volume or increase in the size of structures passing through the carpal tunnel
  • Intermittent paraesthesia median nerve distribution
  • Wasting of thenar muscle when severe and longstanding
  • Many causes including over use, pregnancy, gigantism, SLE, other inflammatory conditions
  • rest ice strtch
  • CS and NSAIDs
  • Splint
  • CT surgery
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39
Q

- What are the common extensor and flexor origin? List ligaments/muscles/nerves (as they apply) that attach to the common extensor origin and common flexor origin

A

Tendons attach around the elbow at two sites:
- common extensor origin: CEO - a blend of muscles whose tendons attach to the lateral epicondyle
- ECRB
- EDC
- ECU
- EDM

  • common flexor origin: CFO - a blend of muscles whose tendons attach to the medial epicondyle
    - Pronator Teres
    - Flexor Carpi Radialis
    - Flexor Digitorum Superficialis
    - Palmaris Longus
    - Flexor Carpi Ulnaris
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40
Q

- Describe pathology associated with CFO and CEO?

A
  • # clinicallyrelevant : tennis elbow, or lateral epicondylitis
        - Damage to the tendinous insertion common wrist and finger extensors
        - Pain and tenderness at common extensor origin and Lateral epicondyle
        - Pain with wrist and finger extension
        - Treated with rest and stretching, physiotherapy and cortisone injection
        - Rarely requires surgery to cut tendon
    • common flexor origin: CFO - a blend of muscles whose tendons attach to the medial epicondyle
      • Pronator Teres
      • Flexor Carpi Radialis
      • Flexor Digitorum Superficialis
      • Palmaris Longus
      • Flexor Carpi Ulnaris
      • # clinicallyrelevant : golfer’s elbow or medial epicondylitis
        • damage to the tendinous insertion common wrist and finger flexors
        • pain and tenderness at common flexor origin and medial epicondyle
        • pain with wrist and finger flexion
        • treated with rest and stretching, physiotherapy and cortisone injection
        • rarely requires surgery
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41
Q

- What are the rotator cuff muscles, their attachments and actions, and innervation?

A

There are four muscles that comprise the rotator cuff:
- subscapularis: which originates from the whole anterior surface of the scapula and inserts on the lesser tuberosity. Subscapularis* medially rotates the glenohumeral joint. It is suppliedby the upper & lower subscapular nerves.
- supraspinatus: originates from the supraspinatus fossa and inserts on the greater tuberosity. Supraspinatus* intitiates and assists deltoid with abduction of the glenohumeral joint. Innervated by the suprascapular nerve
- infraspinatus: originate from the infraspinatus fossa and inserts on the greater tuberosity. Infraspinatus* laterally rotates the glenohumeral joint.It is innervated by the suprascapular nerve.
- teres minor: originates from the inferior angle of the scapula and inserts on the greater tuberosity. Teres minor* laterally rotates the glenohumeral joint.It is innervated by the axillary nerve.
The tendons of supraspinatus, infraspinatus and teres minor blend together at the greater tuberosity.

All of the rotator cuff muscles function to stabilise the glenohumeral joint.
The rotator cuff muscles hold down the humeral head while the deltoid abducts the arm. Without the rotator cuff muscles the deltoid would pull the head upwards.
They are actually head depressors — holds down the head while the deltoid abducts the humerus.
The rotator cuff also has a role in internal and external rotation.

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42
Q
  • List some examples of rotator cuff disease, and broad examples of management
A

The rotator cuff is commonly compressed.
This leads to bursitis, and partial and full thickness tears, with pain and limited movement.

Treatment involves rest and restriction of overhead activity.
It also involves:
- anti-inflammatory medications
- physio
- cortisone injection

Sometimes surgery is required:
- arthroscopic decompression, open acromioplasty
- repair of the rotator cuff

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43
Q

- Patient presents with loss of sensation to dorsum of foot and foot is inverted and plantarflexed at rest. Loss of eversion and dorsiflexion. Which nerve is likely to be involved?

A

Deep peroneal is responsible for dorsiflexion and eversion
Foot eversion is coordinated by superficial peroneal.
Superficial nerve innervates most of dorsal surface.
Deep peroneal only innervates region betweebig and index toe.

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44
Q

- List the key nerves supplying the lower limb and list one or two muscles innervated by these nerves

A

Nerves of lower limb

The major peripheral nerves that innervate the lower limb are the:

  1. Femoral
  2. Obturator
  3. Sciatic. The sciatic nerve is composed of the:
  • Common Peroneal (Fibular) - Superficial Peroneal (Fibular) and Deep Peroneal (Fibular) nerves
  • Tibial nerve

Innervation of lower limb muscles

Femoral nerve: anterior thigh compartment muscles

Obturator nerve: medial thigh compartment muscles

Sciatic nerve: posterior thigh compartment muscles

  • Superficial Peroneal (Fibular) nerve: lateral leg compartment muscles
  • Deep Peroneal (Fibular) nerve: anterior leg compartment muscles
  • Tibial nerve: posterior leg compartment muscles
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45
Q

- What structures form the sciatic foramen? What structures travel through? How can we avoid injecting the sciatic nerve?

A

Sciatic Foramen
- Greater and lesser sciatic notches
- Converted to Foramen by ligaments
- Sacrospinous converts Greater
- Sacrotuberous ligament converts Lesser

Ligaments and Greater Sciatic Foramen
- Sciatic Nerve, with nerve to Quadratus Femorus deep to it, lies on the ischium, one third of the way up from the ischial tuberosity to PSIS
- Sciatic Nerve can be located at the top of thigh, just medial to midpoint of GT and Ischial tuberosity ^[important NOT to inject here, instead superiorlateralquadrant]
- Pudendal nerve lies on the ligament, medial to spine
- Internal Pudendal vessels, cross the tip
- Nerve to obturator internus lies on the base of the spine
- Piriformis exits through greater foramen, sciatic nerve can be located inferior to Piriformis
- Lesser Sciatic Notch
- Obturator Internus muscle and Pudendal Vessels

List of nerves at greater sciatic notch
* 7 nerves:
* Sciatic Nerve
* Superior Gluteal Nerve
* Inferior Gluteal Nerve
* Pudendal Nerve
* Posterior Femoral Cutaneous Nerve
* Nerve to Quadratus Femoris
* Nerve to Obturator Internus
* 3 Vessel Sets:
* Superior Gluteal Artery & Vein
* Inferior Gluteal Artery & vein
* Internal Pudendal Artery & vein
* 1 Muscle:
* **Piriformis

List of nerves at lesser sciatic notch
* 2 nerves:
* Pudendal Nerve
* Nerve to Obturator Internus
* 1 Vessel Set:
* Internal Pudendal Artery & vein
* 1 Muscle:
* Obturator Internus

Upper right quadrant is site of injection

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46
Q

- Identify the content and borders of the femoral triangle

A

Femoral Triangle
- Borders
- Inguinal Ligament is base, lateral border Sartorius and medial border adductor Longus ^[this means sartorius is NOT part of the triangle, but adductor longus is]
- Floor
- Iliacus, Psoas (or iliopsoas), Pectineus, and Adductor Longus
- Contents
- Lateral to medial: Femoral nerve, artery and vein

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47
Q

- Identify the contents and borders of the popliteal fossa

A

The popliteal fossa
is the space behind the knee

Above – medial – semitendonosis and semimembranosus
Above – lateral – biceps femoris
Below – medial and lateral heads of gastrocnemius
Roof – fascia lata
Floor – popliteal surface of femur, capsule of the knee joint (oblique popliteal ligament), popliteus muscle

Contents of the popliteal fossa
Common peroneal nerve – branch of sciatic nerve- lateral, medial to biceps tendon, runs behind head of fibula.
- Tibial nerve – branch of sciatic nerve – more central, passes deep to gastrocnemius, sensory branch is the sural nerve
- Popliteal artery – from the hiatus in adductor magnus to the fibrous arch in soleus, deepest of the neurovascular structures, superiorly medial to the sciatic nerve. This will branch into peroneal; anterior and posterior tibial arteries
- popliteal vein
- sciatic nerve- which branches briefly before hand to give rise to tibial and common peroneal

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48
Q

- Describe acetabular dysplasia, and the spectrum of instability

A

Acetabular Dysplasia
- USUALLY The normal hip has good cover of the femoral head by the acetabulum
- This helps bear the weight and distribute it evenly
- **Acetabulardysplasiais characterised by anacetabulumwherein theload bearingsurface isless horizontaland the head of thefemurisless well covered**
- Acetabular angle can be measured
- Changes in angle can indicate dysplasia to subluxation and full dislocation
- dysplasia in adults, subluxation more of a paediatric issue

49
Q
  • List the joints that make up the knee and ankle joints
A

Knee

  • Two distal joint surfaces – anterior patello-femoral, inferior tibio-femoral ^[note that there is no direct contact between fibia and femur]
  • Patello-femoral – femur
    • Patellar groove or trochlea
    • Distally the groove becomes the intercondylar notch
    • Saddle shaped, asymmetrical
    • Lateral face larger and more convex than the medial face
    • Lined with articular cartilage
  • Tibio-femoral – femur
    • Flattened anteriorly, curved posteriorly
    • Two condyles separated by a deep U-shaped notch, the intercondylar fossa
    • Two articular surfaces- medial and lateral
    • Two surfaces arch up towards each other and are separated by two bony spines – intercondylar eminence.
    • Covered by articular cartilage 3-4cm thick.
    • Vaguely triangular with a rounded base and sharper but still rounded inferior point.
    • The “extensor mechanism” – quadriceps - quadriceps tendon – patella –patella tendon – tibial tuberosity. ^[i.e. patella sites within quadriceps tendon] ^[note also that patella tendon may be interchanged with patellar ligament]
    • Posterior surface is wedge shaped with three facets.
    • Lateral facet is longer
    • Median ridge orientated in the long axis separates the medial and lateral facets
    • “Odd” facet – along the medial border of patella
    • Thick articular cartilage: 6-7x the weight of the body is applied on patella during 90 degrees squat, so it protects against stress on patella
    • Glides in the trochlea of the femur

Ankle
- Talo-crural
- a synovial joint that connects the bones of the leg, the fibula and tibia, with the talus of the foot
- main action of the ankle joint is to allow dorsiflexion and plantar flexion of the foot, as well as some degree of pronation and supination with subtalar and midtarsal joints.
- The joint also acts as a shock absorber as the heel strikes the ground during the first phases of gait.
- Subtalar joint
- the talus and calcaneus
- the joint is classed structurally as a synovial joint, and functionally as a plane synovial joint
- chief site within the foot for generation of eversion and inversion movements

50
Q

HII

  • Describe pathology associated with structures surrounding the knee joint
A

Baker’s cyst:

POPLITEAL BURSA – BAKER’S CYST
A synovial cyst in the popliteal fossa. Occurs when bursa distends.
Can be confused with an aneurysm

ACL tear:
mechanism of ACL injury: non-contact injuries e.g. landings. Recurrent collapses of the knee increase the risk of osteoarthritis. Signs include popping, severe pain and inabiliy to continue activity, rapid swelling, loss of ROM.

PCL tear: rarer than ACL. a posteriorly directed force on the anterior aspect of the proximal tibia with the knee flexed

Meniscal tear: catching / locking - think of the meniscus as a horizontal, circular, twisting circle.

MCL/LCL tear: valgus / varus stress test - think of how a lateral/medial blow can easily rip something that is vertically situated.

51
Q
  • List the key ligaments of the knee joint and describe their roles

also provide examples of what could go wrong

A

see pathology question

52
Q

HII

  • List the key ligaments of the ankle and describe their function and associated common pathology
A

Syndesmosis
- Holds the tibia and fibula together
- Anterior and posterior inferior tibio-fibular ligaments and interosseous membrane

Lateral Ankle (sprained ankle)
- Anterior talo-fibular ligament (neck of talus to fibula): first to damage in sprain (mechanism of damage is inversion with plantarflexion) ^[there is a posterior equivalent but it is rarely damaged]
- Calcaneofibular ligament (calcaneus to fibula) - next in line of damage
- Posterior talo-fibular ligament (body of talus to fibula) ^[also anterior inferior tibio-fibular important]

Medial ankle
- Deltoid ligament
- Shaped like a delta
- Medial malleolus to navicular, sustentaculum tali and posterior aspect of talus
- Four bands
- Complete tears are rare

Inversion injury: ATaloFL
Eversion: deltoid and A/PTibioFL

note also bifurcate

Bifurcate ligament
* Origin - the upper part of the calcaneus
* Insertion – both the cuboid and navicular
* May lead to avulsion fracture in inversion injuries of the ankle
Traction can produce a fracture that is easily missed.

53
Q
  • Taking a history e.g. for joint pain
A

Consider red flags

Acute or acute on chronic situations
- Swelling, erythema (flushing of skin, may be hot to touch), marked reduction in range of motion – infection or inflammation (e.g. sepsis, gout)
- Systemic features in the absence of trauma – infection or inflammation
- Rapid swelling of a joint following trauma – haemarthrosis
- Pain and/or abnormal sensation with loss of power or altered reflexes - radiculopathy ^[usually at the exit foramen or lateral recess] (compression of nerve by spinal process)

Chronic or persistent alterations
- Unusually severe pain, swelling, temperature change, cyanosis/pallor and immobility in a limb or part thereof, often following a minor injury – complex regional pain syndrome.
- Diffuse limb pain in the absence of other signs – somatic referred pain
- Pain and/or abnormal sensation with loss of power or altered reflexes - radiculopathy
- Persistent localized pain uninfluenced by posture or movement – bone disease ^[n.b. soft tissue would be influenced by posture or movement]

If Traumatic
- Mechanism of injury?
- Direct – extrinsic force
- Indirect – intrinsic force
- Lever
- Also: describe what happened to you

If Spontaneous
- Onset
- Duration
- Intensity
- Fluctuations
- Timing: Nocturnal? Morning stiffness?
- Varying factors/movement – at rest, with movement, weight bearing.

Site
- Joint
- Non-joint
- bone
- soft tissue
- referred
- diffuse
- radiation
- Multiple sites?
- Distribution?

54
Q
  • Dx for joint pain e.g. of hands
A
  • gout: e.g. 1st MTP, knee, MCP - ‘initially’ asymmetrical monoarthritis
  • RA: symmetrical polyarthritis - wrists, MCP, PIP NO DIP NO CMC
  • PsA: asymmetrical poly/oligoarthritis - DIP, spinal, large joints (Shoulder, knee)
  • AS: stiffening spine: mainly lumbosacral and neck; less heel knee, shoulder; virtually all SI
  • OA:weightbearing, PIP, DIP, 1st CMC; spares wrist and MCP; asymmetrical polyarthritis
55
Q
  • Steps of physical exam: shoulder, hand and elbow, knee, foot, spine, hip
A

Rapid recall and check KSG

56
Q

- Label bones of wrist and hand XR frontal

A
57
Q

- Label bones of wrist and hand XR oblique/lateral

A
58
Q
  • Label bones of foot XR
A

Lateral:
- tibia
- fibula
- lateral/medial malleolus
- talus
- calcaneum
- cuboid
- navicular
- 5th MT base

Frontal:
- phalanges
- metatarsals
- cuneiforms: lateral, intermediate, middle
- cuboid
- navicular
- talus
- calcaneus
- tibia
- fibula

Medial view:
- phalanges
- metatarsals
- cuneiforms
- navicular
- cuboid
- talus
- calcaneus

59
Q
  • Identify wrist fracture XR
A

Scaphoid wrist fracture
Risk of avascular necrosis due to retrograde blood supply

60
Q

HII

  • Label XR pelvis
A

see question below

61
Q
  • Label knee XR
A

see question below

62
Q

- Label spine MRI and identify exiting/transiting nerves

A
63
Q

- Label spine MRI, identify types of disc bulge

degrees etc

A

> 90 is disc bulge
<90 is protrusion

64
Q

- Identify NoF fracture; comment on effect on vascular supply

A
  • note: intracapsular fractures e.g. subcapital and transcervical will jeopardise the vascular supply of the head as it is retrograde ^[similar to scaphoid bone]
    • blood supply is two-fold
      • interosseous, travelling up to the head (retrograde intramedullary vessels): not affected by intracapsular fractures
      • travels through capsule around neck to the head (medial and lateral circumflex femoral arteries )

n.b. intra-capsular and extra-capsular (inter or sub trochanteric) fx will both cut off the intramedullary retrograde supply.
BUT, only intra-capsular fx will cut off the medial femoral circumflex artery.

65
Q

- Describe the role of inflammation in SLE

A

PATHOPHYSIOLOGY
An interplay of genetic factors and environmental factors can trigger the inflammatory process.
Inflammatory process engages the innate and adaptive immune systems.
These interacting roles of innate and adaptive immunity allow the production of autoantibodies, acute tissue inflammation, and damage. Dendritic cells, macrophages, and B cells are involved in innate immunity, whilst subsets of T and B lymphocytes are involved with adaptive immunity. B cells are certainly central players in the pathogenesis. Loss of self-tolerance in B cell development contributes to the development of autoimmunity. B cells also play a key role in T cell activation and contribute to the production of inflammatory cytokines.

These autoantibodies are pathogenic and cause organ damage by immune complex deposition, complement, and neutrophil activation, altering cell function leading to apoptosis and cytokine production.

66
Q

- List and describe some examples of autoimmune MSK conditions associated with HLA polymorphisms

A
  • Rheumatoid arthritis
    • MHC class II
  • HLA DRB1 0401/0404 (HLA DR4)
  • Spondylarthritis
    • MHC class I
  • Strong association with HLA B27
  • Systemic lupus erythematosus
    • MHC class II
  • Polymyositis
    • MHC class II
67
Q
  • Distinguish between central and peripheral tolerance
A
  • Central tolerance.
    • Developing lymphocytes encounter antigen in the primary/central lymphoid organs.
  • Deletion
    - Editing
    - Site of Action
    - Thymus
    - Bone marrow
  • Peripheral tolerance.
    • Mature lymphocytes encounter antigen in secondary lymphoid organs.
    • anergy, Treg, deletion
68
Q

- Describe lab findings in RA/SLE

A

RA:
- elevated erythrocyte sedimentation rate (ESR, also known as sed rate) or C-reactive protein (CRP) level
- Rheumatoid factor (RF): Not all people with RA test positive for RF; some people test positive for RF but never develop the disease; and some people test positive but have another disease.
- Anti-cyclic citrullinated peptide antibody (anti-CCP)

SLE:
- ANA
- anti-dsDNA
- anti-Sm
- anti-Ro/La

69
Q

- Define osteoarthritis

A

OA is now considered as a partly inflammatory whole-joint disease that affects various anatomical structures in and around the joint capsule. These include muscle, ligaments, entheses, synovial tissue, and the sub-chondral bone.

70
Q

**- Define osteoporosis, list some risk factors, distinguish between osteoporosis and osteomalacia

A

Osteoporosis:

  • Fragility of bone causing increased risk of fracture
  • WHO Classification: BMD T score < -2.5 defined as osteoporosis

Risk factors:
inadequate amounts of dietary calcium.
low vitamin D levels.
cigarette smoking or alcohol intake of more than two standard drinks per day.
lack of physical activity.
early menopause (before the age of 45)
loss of menstrual period if it is associated with reduced production of oestrogen

Osteoporosis vs osteomalacia:

Osteopenia/Osteoporosis
- Bone matrix normally mineralised but there is less bone (osteopenia not < 2.5)

Osteomalacia
- When there is insufficient Calcium and Phosphate to mineralise newly formed osteoid. Bone is softer and liable to bend, deform or fracture

71
Q

**- Describe the pathogenesis of osteoporosis

A

background:
- OC resorption over 3 weeks
- OB activation and bone formation over 3 months

Key point - underpinning osteoporosis pathogenesis
- - Remodelling imbalance
- Resorption cavities deeper and more frequent, resulting in perforations
- Cavities incompletely filled, resulting in…
- Progressive loss of trabecular bone due to increased osteoclastogenesis

Osteoblast and osteoclast communication
- Receptor activator of nuclear factor kappa B (NFkB) RANK, RANK ligand system and OPG (Osteoprotegrin) involved in OB-OC communication
- OC maturation dependent on RANK and RANKL interaction (RANKL on OB, stromal cells)
- OPG and RANKL compete. OPG is the decoy, keeps OC stimulation in check
- Estrogen may exert antiresorptive effect on bone by stimulating OPG expression in OB
- Antibodies to RANKL (Denosumab) now available for osteoporosis

Osteoblast regulation
- LDL receptor – related protein 5 (LRP5) is modulator of OB function.
- Co receptor of series of OB stimulating proteins operating through Wnt signalling pathway.
- Frizzled and LRP5 bind to Wnt, activating bone formation

Sclerostin
- Sclerostin antagonizes Wnt signaling by occupying Wnt coreceptors LRP5/6 and preventing their binding to Wnt ligands, which inhibits downstream canonical Wnt signaling.— inhibiting bone formation?

72
Q

**- Describe how osteoporosis is investigated and diagnosed

A

Diagnosis of Osteoporosis
- Early diagnosis now possible before fracture occurs
- Osteoporosis is defined in relation to degree to which bone mineral density is reduced
- T score (number of standard deviations from the young normal mean) – used to make diagnosis
- Z score (number of standard deviation from age matched mean) – gives a clue as to whether secondary cause is indicated
- Osteoporosis is defined as T score below –2.5

BMD
- Spine (L1-4 or L2-4)
- Predicts spine fracture
- Useful for monitoring – treatment changes are largest
- Trabecular bone
- Note: Osteophytes can cause falsely high bone density results
- Hip (Femoral neck, intertrochanteric, trochanteric)
- Femoral neck or total hip
- Predictive of fracture risk hip and spine
- Cortical bone

T scores and Z scores
- T score – measured BMD compared with mean value for young healthy population. T score is number of standard deviation below or above this average. Used for diagnosis of osteoporosis
- Z score – the measured BMD (g/cm2) compared with mean value for age and sex and race matched population. Useful to determine if a secondary cause exists for OP

BMD
- 1994 benchmark for diagnosis of Osteoporosis
- Good predictor of fracture
- As good as, if not better, than ability to predict heart disease from blood cholesterol and to predict stroke from blood pressure
- Note: severe osteoporosis= -2.5 or less, plus fracture

Bone Mineral Density

Advantages
- Quick and easy
- Minimal radiation exposure
- Widely used in clinical trials
- WHO classification based on DEXA
- Good correlation with risk of fracture

Limitations
- Mineral content across a specific area not taking depth into consideration
- Does not provide full assessment of bone strength (microarchitecture, bone turnover)
- Vary between instruments (therefore do follow-up densities in the same clinic if possible)

FRAX Tool –WHO Fracture Risk Assessment Tool
- Clinical risk factors as well as bone mineral density (BMD) at the femoral neck.
- FRAX® tool is computer-driven
- FRAX® algorithms give the 10-year probability of fracture. The output is a 10-year probability of hip fracture and the 10-year probability of a major osteoporotic fracture (clinical spine, forearm, hip or shoulder fracture).
- 10 yr probability >20% in MOP and >3% for Hip # - consideration for treatment
- Avoids possibility of overtreating someone with bone density low alone, with low probability of fracture

73
Q

**- Describe prevention for osteoporosis

A

Prevention strategies
- Attain Best Peak Bone Density
- Good Calcium Intake
- Exercise
- Avoid smoking, excessive alcohol
- Minimise drugs that can influence BMD adversely

74
Q
  • Distinguish between primary and secondary osteoporosis
A
  • Osteoporosis unassociated with other diseases – Primary Osteoporosis
  • Osteoporosis associated with other diseases – Secondary Osteoporosis
75
Q

**- Detail some treatments and lifestyle changes for osteoporosis (aka management)

A

Pharmacological management
- Antiresorptives – 1st line agents
- Bisphosphonates
- SERMS
- RANK Ligand inhibitor
- Calcitriol
- Anabolic Agents – 2nd line
- Parathyroid Hormone
- Antisclerostin Ab
- Dual Agents
- Strontium Ralenate

Non-Pharmacological treatment
- Weight Bearing Exercises
- Adequate Calcium 800mg – 1200mg/day
- Vitamin D intake
- Avoid Risk Factors –smoking, alcohol

76
Q

**- Compare and contrast RA and OA: clinical features, joint distribution, extra-articular manifestations and systemic features

A

OA:
Frequency:
- most common
- commonly affect older people
- over 55 has greater prevalence in women

Pathogenesis:
1. Mechanical damage to joint + metainflammatory systemic state
2. Degeneration of cartilage → inflammatory response
3. Chondrocytes release matrix metalloproteinases → kill chondrocytes & destroy cartilage
ECM
4. Progressive loss of cartilage
* Release of cartilage and bone breakdown products into the joint cavity triggers
synovitis (can also precede cartilage destruction w/ hypercholesterolaemia,
metainflammatory state)
Associated with:
* Major risk factors: obesity, joint overuse, untreated ligament injury

Presentation:
* Slow, progressive disorder w/ pain in weight-bearing joints after use (eg, at the end of the
day), improving with rest; morning stiffness <30mins)
* Asymmetric joint involvement
o Hands: 1st CMC, DIPs (Heberden’s nodes)
o Other: 1st MTP, hip, knees, spine (cervical & lumbar)
o Bony swelling (no inflammation)
* No systemic symptoms

Investigations (+ findings):
* X-ray: osteophytes, joint space narrowing, subchondral sclerosis (+/- cysts)
* Arthrocentesis: non-inflammatory
* Bloods: rheumatoid factor (-ve), anti-CCP antibodies (-ve), ESR & CRP (normal)
Management:
* Lifestyle: education, physical therapy (strengthen quads for knee OA), weight loss, orthotics,
walking aids, heat
* Pharm: oral NSAIDs, intra-articular corticosteroids (for flare-ups)
* Surgical: joint replacement

RA:
Frequency: second most common, occurs in young people with family history, greater prevalence in womenn

Pathogenesis:
1. Autoimmune response against synovium
o Synovium expresses peptidyl-arginine deaminase (arginine residues → citrulline)
o Citrulline recognised as foreign antigen, activating CD4+ T-cells → activation of B
cells (autoantibodies) & macrophages (TNF-α → inflammation)
2. Inflammation → formation of pannus (granulation tissue)
3. Pannus invades of cartilage and bone → progressive destruction
4. Autoantibodies (anti-CCP, & RF) are produced → inflammation
* RF is an IgM antibody against Fc portion of IgG (can aid in removing autoantibodies)

Associated with:
* Genetics: HLA-DR4; smoking

Presentation:
* Pain, swelling, & morning stiffness (>1hr), improving with use
* Symmetric joint involvement
o Hands: MCP, PIP (not DIP)
o Arthritis in 3 or more areas
o Synovial +/- bony swelling (inflammation, hot/red)
* Systemic symptoms (fever, fatigue, weight loss)
* Extraarticular manifestations: rheumatoid nodules (subcutaneous & lungs), interstitial lung
disease, pericarditis, pleuritis, anaemia, neutropenia, scleritis, vasculitis

Investigations (+ findings):
* X-ray: joint space narrowing, erosions, osteopenia (+ soft tissue swelling)
* Arthrocentesis: inflammatory (↑WBC)
* Bloods: rheumatoid factor (+ve), anti-CCP antibodies (+ve), ESR & CRP (elevated), anaemia of
chronic disease (normocytic), thrombocytosis
Management:
* Lifestyle: education, physical therapy
* Pharm: NSAIDs (pain) & corticosteroids (inflammation, often used in combination), DMARDs
(csDMARD/methotrexate → bDMARDs → tsDMARDs/JAK inhibitors)

77
Q

**- Differences in radiological findings for SLE, RA, OA, gout

A

OA: Characterized by osteophyte formation, non-uniform narrowing within joints, and progressive worsening.
- distribution: Hips, Knees, 1 st MTP, L4/5, C5/6, DIPs, PIPs, 1 st CMC
- non-uniform narrowing within joints, and progressive worsening
- juxta-articular sclerosis
- symmetric: although one side can be worse than the other

RA:Affects the synovium, leading to uniform narrowing within joints, bone resorption, juxta-articular osteopenia, and erosions.

  • disease of synovium
  • exhibits erosions (visible as dark holes or dots)
  • will show erosions at lateral edge of joint (juxta-articular osteopaenia): ends look chewed
  • joint space still preserved (uniform narrowing within joint)
  • resorbs bone
  • degeneration (laxity of joints) with progression of disease

SLE: soft tissue swelling, normal joint spaces, swan neck/boutonniere, subluxation, hallux valgus,

Gout:
which can be distinguished from RA by overhanging edge, soft tissue swelling, and involvement of DIPs.
- Dense soft tissue swelling
- Erosions with sclerotic margins distant to the joint space
- Incidental calcific arteriopathy
- Bone density preserved on either side of the joint
- indicated by demographics (ethnicity), hx (genetics, alcohol consumption, systemic disease)

78
Q

**- Distinguish between gout and non-gout, including clinical features and lab findings

A

Gout: common in men over 40, women over 55
Frequency:
Associated with:
* Renal impairment
* Diabetes, hypertension, obesity, dyslipidaemia, hyperuricaemia
Frequency:
Associated with:
* Hyperparathyroidism
* Hemochromatosis (↑Fe)
Pathogenesis:
1. Gout: hyperuricaemia (serum >0.4mmol/L) → monosodium urate (MSU) deposition/formation in joint space
o 90% due to underexcretion (purine metabolism → uric acid) & 10% overproduction
3. Macrophages (via Pattern Recognition Receptors) detect & phagocytose crystalline deposits in joints → NLRP3 inflammasome forms → inflammatory cascade mediated by
IL-1
* Neutrophils invade joint and bind crystals via neutrophil extracellular traps (NETs)

Presentation:
* Asymmetric mono-, oligo- or polyarthritis
* Inflamed: swollen, red, painful & loss of movement (esp. 1st MTPJ/podagra)
* Precipitants for acute attack: large meal in purines (red meat, seafood), trauma,
surgery, infection, dehydration, diuresis, or alcohol consumption
* Chronic/interval: tophus formation (external ear, olecranon bursa or calcaneal
tendon)

Investigations (+ findings):
* X-ray: erosions w/ overhanging sclerotic margins, normal joint space, soft tissue
tophi
* Arthrocentesis: inflammatory (↑WBC, cloudy & yellow), MSU crystals (brightly
birefringent, needle-shaped & yellow)
Management:
* Lifestyle: diet changes, weight loss
* Acute Pharm: NSAIDs, glucocorticoids & colchicine
* Chronic pharm (>2 acute attacks): xanthine oxidase inhibitors (allopurinol,
febuxostat)

Pseudo-gout:
Frequency: over 50 years and equal between genders
Associated with:
* Hyperparathyroidism
* Hemochromatosis (↑Fe)

Pathogenesis:
2. CPPD: deposition of calcium pyrophosphate crystals within joint space.
3. Macrophages (via Pattern Recognition Receptors) detect & phagocytose crystalline deposits in joints → NLRP3 inflammasome forms → inflammatory cascade mediated by
IL-1
* Neutrophils invade joint and bind crystals via neutrophil extracellular traps (NETs)

Presentation:
* Mono- or oligoarthritis
* Inflamed: pain, swelling (esp. knee)

Investigations (+ findings):
* X-ray: cartilage calcification
* Arthrocentesis: inflammatory (↑WBC, cloudy & yellow), CPPD crystals (positive
birefringent, rhomboidal/rectangular shape & blue)
Management:
* Acute episode mostly self-limiting (5-7days)
* Pharm: NSAIDs, glucocorticoids, colchicine
* Joint aspiration
* Treat any underlying metabolic condition

79
Q
  • Provide some examples and features of seronegative arthritis
A

seronegative spondyloarthropathies: psoriatic,
ankylosing spondylitis

Spondylarthritis

Types and Characteristics
- Reactive arthritis e.g. after STI
- Psoriatic arthritis
- Arthritis related to inflammatory bowel disease
- Ankylosing spondylitis
- M:F ratio 2-3:1 for AS
- Onset usually in 3rd decade of life
- Strong association with HLA B27

Association between Spondylarthritis and HLA-B27

Disease and HLA-B27 Frequency
Note that there is variation in frequency across ethnic populations, e.g. over-represented in European populations.
- Ankylosing spondylitis: > 90%
- Undifferentiated spondyloarthropathy: 70%
- Reactive arthritis: 30-70%
- Psoriatic arthritis: 40-50%
- Iritis: 50%
- Cardiac manifestations: >80%

Clinical features
(some)
- peripheral enthesitis
- dactylitis
- skin psoriasis
- peripheral ulceration
- peripheral inflammatory arthritis
- extra-articular manifestations: skin psoriasis, anterior uveitis and conjunctivitis

80
Q
  • What is the serum uric acid level above which it will precipitate into tissue? What are some causes of this?
A
  • Uric acid - end product of purine metabolism and is present in the serum and tissues in the form of monosodium urate.
  • Serum uric acid levels higher than 0.40 mmol/L monosodium urate supersaturates the serum and precipitates into tissues.
  • Elevated levels of uric acid do not necessarily translate into clinical disease.
  • An acute gouty attack occurs when monosodium urate crystals are released or form de novo in the joint space.
  • Trauma, surgery, infections, or initiation of medications such as allopurinol or diuretic agents can abruptly alter uric acid levels and incite an attack of gout.

Gout Risk Factors

  • Hyperuricemia
  • Male sex if younger than 60 years
  • Obesity
  • High-purine diet (e.g., red meat, shellfish)
  • Alcohol (esp. beer and spirits) and high-fructose drinks
  • Medications (esp. thiazide diuretics or cyclosporine)
  • Renal insufficiency
  • Lead exposure
  • Organ transplantation
  • Specific diseases (e.g., hypertension, diabetes, hyperlipidemia, hematologic malignant conditions)
  • Genetic risk factors
81
Q
  • Briefly describe reactive and septic arthritis
A

Reactive arthritis:
Frequency:
* Commonly affects 20-40yr olds
* More common in men & Caucasians
Pathogenesis:
Arthritis developing soon after or during an infection elsewhere in the body, but in
which microorganisms cannot not be recovered from the joint
Associated with:
* Recent infections: chlamydia, salmonella, campylobacter
* Genetics: HLA-B27 (along with other seronegative spondyloarthropathies: psoriatic,
ankylosing spondylitis & inflammatory bowel disease)
Presentation
* Acute, asymmetric oligoarthritiis
* Affects large joints
* Triad: conjunctivitis, urethritis (non-gonococcal, e.g.,), arthritis

Investigations (+ findings):
* X-ray: ill-defined erosions, bone proliferation, enthesopathy
* Bloods: ESR & CRP (usually elevated), HLA-B27 (+ve)
* Arthrocentesis: inflammatory (elevated WBCs, yellow colour)
Management:
* Pharm: NSAIDs, antibiotics for infection

Septic arthritis:
Frequency:
* Uncommon but more likely in elderly
Pathogenesis:
Acute arthritis due to an active infection in a joint, commonly bacterial from
hematogenous seeding.
Associated with:
* Most common causes: S. Aureus, Streptococcus, and Neisseria gonorrhoeae
Presentation:
* Abrupt monoarticular pain w/ swelling (+redness, heat)
* Knee involved in 50% of cases

Investigations (+ findings):
* X-ray: usually normal joints, joint effusion & swelling, destruction of articular
cartilage
* Arthrocentesis: bacteria (S. Aureus, gonorrhoea, strep), very high WBC & PMNs,
purulent/yellow, ↑viscosity
Management:
* Pharm: antibiotics
* Aspiration, drainage (+/- debridement) to prevent irreversible joint damage
Complications: osteomyelitis, chronic pain, irreversible joint damage, sepsis

82
Q
  • What are some conditions associated with gout?
A

hypertension, diabetes, hyperlipidemia, hematologic malignant conditions

83
Q

- What is SLE? What is thought to be the cause?

A

DEFINITION
A chronic autoimmune disease, characterized by multisystem clinical manifestations, as the complex pathogenesis can cause inflammation of any organ. The key pathogenesis relates to a dysfunctional immune system that results in overproduction of autoantibodies usually against cell nuclei, deposition of antibodies into tissues and complement activation and induction of chronic inflammation, ultimately culminating in end-organ damage and dysfunction.

PATHOPHYSIOLOGY
An interplay of genetic factors and environmental factors can trigger the inflammatory process.
Inflammatory process engages the innate and adaptive immune systems.
These interacting roles of innate and adaptive immunity allow the production of autoantibodies, acute tissue inflammation, and damage. Dendritic cells, macrophages, and B cells are involved in innate immunity, whilst subsets of T and B lymphocytes are involved with adaptive immunity. B cells are certainly central players in the pathogenesis. Loss of self-tolerance in B cell development contributes to the development of autoimmunity. B cells also play a key role in T cell activation and contribute to the production of inflammatory cytokines.

84
Q

- Outline the non-pharmacological and pharmacological management of SLE

A

The general principles include monitoring disease activity e.g. via autoantibodies and clinical signs (Aim remission (SLEDAI REM<2, LDA 2-4)), preventing flares of disease but not treating serology alone, preventing damage (15-20% irreversible organ dysfunction 1st 2 years, 40-50% in 5 years), limiting steroid use and tapering off ASAP, and using antimalarial drugs (hydroxychloroquine) at all stages.

Additional needs include monitoring for adverse therapy side effects & treating infection, osteoporosis, monitoring for & treating co-existent vascular risk factors (BP, lipids, smoking), if associated hypocomplementemia – pneumococcal immunization, if thromboembolism-anticoagulation with aspirin, warfarin, heparins, NOACs; photo-protective measures (Sunscreen creams, hat, long-sleeve clothing, Vit D), care with contraception and timing of family issues, and education on disease, diet, exercise.

Antimalarial Drugs - Emphasis on Hydroxychloroquine (Plaquenil)
- Direct immunomodulatory effects have resulted in its use in Rheumatoid Arthritis, Primary Sjogren’s Syndrome, SLE, and Antiphospholipid Syndrome.
- In SLE, should be used in most patients during the entire course of the disease, particularly useful for skin and joint manifestations. Immunomodulatory capacity also prevents disease flares, promotes long-term survival in SLE, controls autoimmune disease activity during pregnancies without evidence of fetotoxic or embryonic effects, can delay or prevent organ damage, and has antithrombotic effects in SLE. Helps successful tapering corticosteroids.
- For this and other inflammatory rheumatic diseases, can also reduce rates of atherosclerosis, improve hyperglycemia, and protect against infections

Skin & Musculoskeletal Treatment

Other Immunosuppressive Drugs

85
Q

- Describe the diagnostic criteria for SLE

A
  • Expansion on neuropsych manifestations
  • Haematology and immunological criteria are expanded
  • Need 4 or more criteria with at least **1 clinical +1 **immunological laboratory criteria EXCEPT WHEN Biopsy-proven lupus nephritis
  • Criteria are cumulative and need not be present concurrently
86
Q

- Distinguish between the presentation of gout and RA

A
  • Symmetrical polyarthritis in small joints of hands and feet - whereas gout involves monoarticular and rarely oligo arthritis. Not likely symmetrical
  • Hand involvement more likely than in gout- 1st MTP classic finding
  • Subcutaneous nodules - similar to tophi in gout– lower extremities and ear helix
  • X-ray: soft-tissue swelling, diffuse joint space-narrowing (in a joint), marginal erosions of small joints, symmetrical multiple joint involvement
  • Usually osteopenic without signs of repair
  • gout subsides in 3 to 14 days post treatment, RA does not

clarify with lecturer

87
Q

- Discuss the synovial fluid findings of gout

A

Crystal Analysis

  • MSU crystals are more easily detected than CPPD crystals.
  • CPPD crystals have a rhomboidal or rectangular shape and have positive birefringence.
  • Compared to MSU crystals birefringence is weaker, and some CPPD crystals may not appear birefringent.
    • A birefringent CPPD crystal appears blue.
  • MSU crystals are brightly birefringent and needle-shaped; MSU crystals appear yellow.
88
Q

- Discuss the benefits of exercise, discuss some papers to this effect (signposted in Kieran’s lecture)

A
89
Q

- Discuss OA risk factors, pathogenesis

A

see combined

90
Q

- Discuss OA management

A

see combined

91
Q

- Describe the ladder of treatment for RA (DMARDs lecture)

A

Phase I treatment
- MTX, and if not, leflunomide or sulfasalazine ^[used more than HCQ due to efficacy in reducing radiological damage]
- may be used in conjunction with short-term steroids

Phase II
Move to biologics or alternative csDMARD depending on prognostic factors.

92
Q

- Describe the pathology of fracture healing and detail the timeline, and list factors that complicate fracture healing

A
  1. Reactive phase:
    * Haematoma formation (hrs - 3 days): haemorrhaging and clot forms in medullary cavity and surrounding soft tissue
    * Inflammation (<48hrs-10 days): vasodilation, increased permeability & inflammatory cell infiltration, releasing cytokine and recruiting mesenchymal stem cells; clot is reabsorbed
    * Granulation tissue formation (2-12 days): neovascularisation and fibrovascular primitive connective tissue forms (composed of fibroblasts, mesenchymal cells, and
    inflammatory cells/macrophages) around the ends of the fracture
  2. Reparative phase: soft callus begins as fibrocartilaginous tissue (new connective tissue, microscopic blood vessels, cartilage) and woven
    bone that then becomes spongy bone.
    * Soft callus formation (1 week-months): fibroblasts and osteoblasts influx, producing fibrocartilaginous tissue (soft callus) that bridges the fracture site
    * Hard callus formation (1 week– months): endochondral ossification converts soft callus to hard callus of woven bone. With adequate immobilisation, gradual connection of bone
    filaments to woven bones supports strengthening of bone
    * Ossification (2 weeks – months): Mineralisation of bone matrix converts hard callus to lamella bone, uniting fracture and forming new haversian system
  3. Remodelling phase:
    * Bone remodelling (months to years): hard callus/new lamella bone is progressively remodelled to restore normal bone contour

Factors:

Conditions that interfere with fracture healing
- Poor blood supply to fractured area; could lead to avascular or aseptic necrosis
- Poor immobilization of the fracture site may cause misalignment or deformity
- Infection – more common with open fractures

Local Anatomic Factors That Influence Fracture Healing
- Soft tissue injury
- Interruption of local blood supply
- Interposition of soft tissue at fracture site
- Bone death caused by radiation, thermal or chemical burns or infection

Systemic Factors That Decrease Fracture Healing
- Malnutrition
- Reduces activity and proliferation of osteochondral cells
- Decreased callus formation
- Smoking
- Cigarette smoke inhibits osteoblasts
- Nicotine causes vasoconstriction diminishing blood flow at the fracture site
- Diabetes Mellitus
- Associated with collagen defects including decreased collagen content, defective cross-linking and alterations in collagen subtype ratios
- Anti-Inflammatory Medications
- Cause (at least a temporary) reduction in bone healing

93
Q

- List systemic and local factors that can impact fracture healing

A

Conditions that interfere with fracture healing
- Poor blood supply to fractured area; could lead to avascular or aseptic necrosis
- Poor immobilization of the fracture site may cause misalignment or deformity
- Infection – more common with open fractures

Local Anatomic Factors That Influence Fracture Healing
- Soft tissue injury
- Interruption of local blood supply
- Interposition of soft tissue at fracture site
- Bone death caused by radiation, thermal or chemical burns or infection

Systemic Factors That Decrease Fracture Healing
- Malnutrition
- Reduces activity and proliferation of osteochondral cells
- Decreased callus formation
- Smoking
- Cigarette smoke inhibits osteoblasts
- Nicotine causes vasoconstriction diminishing blood flow at the fracture site
- Diabetes Mellitus
- Associated with collagen defects including decreased collagen content, defective cross-linking and alterations in collagen subtype ratios
- Anti-Inflammatory Medications
- Cause (at least a temporary) reduction in bone healing

94
Q

- Distinguish between woven and lamellar bone

A
  • Bone exists in 2 main forms
    • Lamellar bone: Regular parallel bands of collagen arranged in sheets. Replaces woven bone in development by undergoing remodelling to have collagen fibres in parallel. Lamellar bone is mature bone, and is found in two types: compact and cancellous
    • Woven Bone: Immature form with randomly arranged collagen fibres in osteoid. Remodelled to form lamellar bone. Found in
      • Foetal bone development. If not foetal, then produced when osteoid is rapidly produced e.g. …
      • Healing fracture
      • or a developmental disease e.g. Paget’s disease of bone
95
Q
  • What are the cells found in bone?
A

Cells
- Osteoblasts: which synthesise matrix components e.g. osteoid, as well as mediating mineralisation.
- Osteocytes: which are resting or inactive osteoblasts trapped within formed or mature bone
- Osteoclasts: which are responsible for the resorption of bone, which itself comprises two steps: erosion and remodelling

96
Q
  • What types of collagen are found in bone? Hyaline cartilage?
A

Collagen in bone is 1
Collagen in hyaline cartilage is 2

  • Type 1 - skin, fascia, tendon, ligament, bone. (It is this, within the ground substance of the bone ECM (osteoid) that becomes mineralised)
  • Type 2 – all forms of cartilage.
  • Type 3 - in association with type 1, found in skin, artery, uterus
  • Type 4 - basement membrane
  • Type 5- placenta, blood vessels
97
Q
  • What are the differences between intramembranous ossification and endochondral ossification?
A

In intramembranous ossification, bone develops directly from sheets of mesenchymal connective tissue. In endochondral ossification, bone develops by replacing hyaline cartilage. Activity in the epiphyseal plate enables bones to grow in length (this is interstitial growth).

98
Q
  • Distinguish between the two main types of sarcoma
A

Osteosarcoma

Definition
- Malignant tumour differentiating towards osteoblasts, with production of osteoid/bone

Epidemiology
- Most common bone sarcoma (35%)
- M:F = 2:1
- Usually in children/adolescents (during maximal bone growth); also in older adults

Etiology
- Most cases = Unknown
- Patients with retinoblastoma (Rb) gene mutations = several hundred-fold greater incidence
- Associated with conditions of high bone turnover, such as Paget’s disease and fibrous dysplasia of bone, also if prior radiotherapy or bone necrosis
- Older adults with osteosarcoma often have one of these predisposing conditions (= ‘secondary’ osteosarcoma)

Clinical Features
- Metaphysis (most often distal femur, proximal tibia)
- Localized pain and swelling or pathological fracture
- ~10-20% of patients have pulmonary metastases at diagnosis

Investigations for Diagnosis and Staging

  • Imaging:
    • XR
    • CT: cortical irregularities/fracture sites/mineralisation
    • MRI: extension into soft tissue/marrow/joint space
    • PET scan: assess primary lesion; detect metastases elsewhere
    • Radionuclide bone scan.
  • Biochemistry: Elevated ALP ^[indicates osteoblast activity] + LDH ^[indicates high cell turnover].
  • Biopsy: Core or open (incisional) biopsy preferred - core limits risk of recurrence; FNA is inappropriate due to loss of architectural information.

Osteosarcoma features
Compared to normal bone, osteosarcoma shows:
- Architecture: crowded/more cellular
- Cytology: Tumour cells often ‘spindle’ shaped, hyperchromatic, variable
- Pathognomonic feature = production of neoplastic osteoid/ matrix (appears pink due to lack of mineralisation)
- Often scanty, irregular/’lace-like’ & does not mineralize normally
- Tumor cells may also show predominantly fibrosarcomatous or chondrosarcomatous differentiation

Treatment
- Combination of neoadjuvant (ie pre-surgical) chemotherapy, surgery and adjuvant (ie post-surgery) chemotherapy
- Complete excision with negative margins (within a specialist sarcoma unit)
- Adjuvant treatment may include radiotherapy

Prognosis
- Depends on stage and response to neoadjuvant treatment:
- Tumour necrosis of ≥ 90% has a > 90% disease free survival
- < 90% necrosis has < 50% survival
- Overall 5-year survival with current treatment, 60-70%

Well-differentiated Liposarcoma (WDLPS)

Definition: Locally aggressive mesenchymal neoplasm with mature adipocytes and stromal cells showing focal nuclear atypia.

Epidemiology: Most common form of liposarcoma, affecting middle-aged to elderly adults.
- extremely rare in childhood
- Sex: M = F

Etiology: Unknown.
Molecularly characterized by ring or giant marker / rod chromosomes, with amplification of several genes including MDM2.

Clinical Features:

  • Location:
    - Deep thigh or other proximal limbs, retroperitoneum, trunk, spermatic cord, mediastinum
    - May also arise in subcutaneous tissue; rarely in skin (‘atypical lipomatous tumour’)
    - Less frequent in head/neck area
  • Slow-growing, painless, deep-seated mass
  • Retroperitoneal tumours may only be discovered after attaining significant growth (> 20 cm)

Investigations for Diagnosis and Staging:
- MRI preferred for imaging.
- Biopsy: Core, incisional, or excisional; FNA inappropriate.

Treatment:
- Complete excision with negative margins often curative
- Surgical debulking for large, multifocal retroperitoneal/intra-abdominal tumours
- May require partial or complete resection of intraabdominal organs

Prognosis: Behaviour depends on location.
- Superficial locations more surgically amenable – can resect with negative margins
- In skin it’s called an ‘atypical lipomatous tumour’ (ALT)
- Deep locations (eg retroperitoneum) more difficult to resect – often recur locally – and can undergo ‘de-differentiation’ and subsequently metastasise
- No metastatic potential unless dedifferentiation is present

99
Q
  • Explain how sarcomas are graded
A

Based on Combination of Three Features:
1. Tumour Differentiation: (1, 2, or 3 points based on how closely it resembles normal tissue)
2. Mitotic Count: (1, 2, or 3 points based on how many mitoses per 10 high power fields)
3. Tumour Necrosis: (0, 1, or 2 points if no necrosis, <50% or >50% necrosis)

  • Grade = Sum total of scores for differentiation, mitotic count, and necrosis
    • 2-3 points = Grade 1 (low grade)
    • 4-5 points = Grade 2 (intermediate grade)
    • 6-8 points = Grade 3 (high grade)
100
Q

Compare and contrast sarcoma and carcinoma

A
  • Sarcoma
    • Arises from connective tissues (e.g., bone, cartilage, muscle, fat, nerve)
    • Rare
    • Usually haematogenous spread
    • Mostly affects children/young adults
  • Carcinoma
    • Arises from epithelial tissues (e.g., lung, breast, prostate, colon, skin)
    • Common
    • Usually lymphatic spread
    • Mostly affects people >50
101
Q

Discuss macro and micro features of WDLPS

A

Image of liposarcoma
![[Pasted image 20240216190134.png]]
- Well-circumscribed, lobular
- Cream/tan/grey, homogeneous cut surface
- Appears to arise from fat and bulge into muscle
- Thickened fibrous bands may be evident
- Fat necrosis may be seen in larger tumours (not pictured. Looks very pale yellow)

Lipomyosarcoma: microscopy
Compared to normal fat, liposarcoma shows:
- Significant variation in size and shape of adipocytes
- Focal nuclear hyperchromasia and mild atypia
- Thickened, irregular fibrous bands/septa
- Often contain atypical spindle shaped cells
- Lipoblasts may be seen
* Multivacuolated
* Nucleus indented by the vacuoles
- Significant nuclear pleomorphism/atypia absent

102
Q
  • Discuss Neoplasms of UMP
A
  • Some bone tumours are difficult to classify as benign or malignant (e.g., Giant Cell Tumour is locally aggressive and sometimes metastasizes) i.e. intermediate
103
Q
  • Discuss osteosarcoma
A

Definition
- Malignant tumour differentiating towards osteoblasts, with production of osteoid/bone

Epidemiology
- Most common bone sarcoma (35%)
- M:F = 2:1
- Usually in children/adolescents (during maximal bone growth); also in older adults

Etiology
- Most cases = Unknown
- Patients with retinoblastoma (Rb) gene mutations = several hundred-fold greater incidence
- Associated with conditions of high bone turnover, such as Paget’s disease and fibrous dysplasia of bone, also if prior radiotherapy or bone necrosis
- Older adults with osteosarcoma often have one of these predisposing conditions (= ‘secondary’ osteosarcoma)

Clinical Features
- Metaphysis (most often distal femur, proximal tibia)
- Localized pain and swelling or pathological fracture
- ~10-20% of patients have pulmonary metastases at diagnosis

Investigations for Diagnosis and Staging

  • Imaging:
    • XR
    • CT: cortical irregularities/fracture sites/mineralisation
    • MRI: extension into soft tissue/marrow/joint space
    • PET scan: assess primary lesion; detect metastases elsewhere
    • Radionuclide bone scan.
  • Biochemistry: Elevated ALP ^[indicates osteoblast activity] + LDH ^[indicates high cell turnover].
  • Biopsy: Core or open (incisional) biopsy preferred - core limits risk of recurrence; FNA is inappropriate due to loss of architectural information.
104
Q
  • Discuss liposarcoma
A

Well-differentiated Liposarcoma (WDLPS)

Definition: Locally aggressive mesenchymal neoplasm with mature adipocytes and stromal cells showing focal nuclear atypia.

Epidemiology: Most common form of liposarcoma, affecting middle-aged to elderly adults.
- extremely rare in childhood
- Sex: M = F

Etiology: Unknown.
Molecularly characterized by ring or giant marker / rod chromosomes, with amplification of several genes including MDM2.

Clinical Features:

  • Location:
    - Deep thigh or other proximal limbs, retroperitoneum, trunk, spermatic cord, mediastinum
    - May also arise in subcutaneous tissue; rarely in skin (‘atypical lipomatous tumour’)
    - Less frequent in head/neck area
  • Slow-growing, painless, deep-seated mass
  • Retroperitoneal tumours may only be discovered after attaining significant growth (> 20 cm)

Investigations for Diagnosis and Staging:
- MRI preferred for imaging.
- Biopsy: Core, incisional, or excisional; FNA inappropriate.

Treatment:
- Complete excision with negative margins often curative
- Surgical debulking for large, multifocal retroperitoneal/intra-abdominal tumours
- May require partial or complete resection of intraabdominal organs

Prognosis: Behaviour depends on location.
- Superficial locations more surgically amenable – can resect with negative margins
- In skin it’s called an ‘atypical lipomatous tumour’ (ALT)
- Deep locations (eg retroperitoneum) more difficult to resect – often recur locally – and can undergo ‘de-differentiation’ and subsequently metastasise
- No metastatic potential unless dedifferentiation is present

105
Q

- Provide two examples of NSAIDs, detail their MoA, SEs, role in therapy, precuations and/or contraindications

A
  • ibuprofen
  • naproxen
  • diclofenac
  • indomethacin
  • piroxicam
  • NSAIDs work by inhibiting COX-1 and COX-2 enzymes
  • COX-1 are expressed in most tissues and platelets, primarily involved in tissue homeostasis, and responsible for producing prostaglandins involved in renal blood flow autoregulation, and platelet aggregation (1)
  • COX-2 is induced in many inflammatory cells, and is responsible for prostinoid mediators of inflammation; activated by IL-1, TNHa, and other inflammatory cytokines
  • They appear on the second step of the WHO ladder, and are considered simple analgesia

Antipyretic effects:
Temperature balance is regulated by hypothalamus,
NSAIDs rest this control returning it to normal point when fever is present
Do not alter normal temperature
Achieved by inhibition of prostaglandin production in the hypothalamus

Analgesic effects:
Used for mild to moderate pain caused my inflammation or tissue damage
Peripherally ↓ prostaglandin production that sensitise receptors to inflammatory mediators

SEs:
- related to inhibition of COX-1 and COX-2
- CV: Rise in blood pressure, fluid retention, myocardial infarct, stroke (caution advised for patients with cardiovascular disease)
- GI: Upper abdominal pain, gastric erosions, peptic ulcers, oesophageal ulcers, GI bleeding, perforation. (Relative risk varies between different NSAIDs and is dose related). Selective COX-2 have less (but not none) GI complications. If a NSAID must be used and there is concern about GI bleed a proton pump inhibitor (PPI) may be co-prescribed to prevent (or atleast reduce the risk) of GI complications.

Of the NSAIDs, Diclofenac and Ibuprofen appear to have the lowest risk of GI complications (and are commonly used in practice)
- Renal: Renal impairment (risk is increased in elderly, perioperatively, pre-existing renal disease and coadministration with ACEI and diuretics (triple whammy) or co-administration with other nephrotoxic medications should be considered before prescribing.
- Skin:
Erythematous reactions
Urticaria
Photosensitivity
Stevens-Johnson Syndrome (rare)

  • Lungs
    Aspirin-sensitive asthma (5% of asthmatics)
    Bronchospasm (does not occur with coxibs)
  • Liver: NSAIDs should NOT be prescribed to patients with severe hepatic impairment!!

Precautions:
- if given with paracetamol should use a lower dose of NSAID
- triple whammy
- Low dose aspirin is not used for pain (high doses can be used in some conditions such as Migraine)

Unsafe in children due to risk of Reye Syndrome

Most commonly used as an antiplatelet for cardiovascular and neurological indications. - Do not stop low dose aspirin when using a NSAID (as the antiplatelet effect of NSAIDs is less reliable than low dose aspirin)

106
Q

- Discuss bDMARDs, their MoA, indications, side effects, provide some examples, and explain why they are not first line drugs

A
  • Abatacept=Interruption 2nd T cell costimulation signal
  • Tocilizimab=IL-6 cytokine receptor inhibitor
  • Rituximab=B cell blocker(CD 20 monoclonal antibody)
  • JAK inhibitors tofacitinib, baracitinib, upadacitinib

Abatacept, Tocilizimab, Rituximab, JAKs Cautions
- Same as TNF-inhibitors for prescreening and exclusions
- Discontinue Rx if a patient develops serious infection (more likely if on steroids, over 65 years –perhaps etanercept, abatacept, rituximab less infection risk)
- Monitor immunoglobulin levels for those on rituximab
- Monitor full blood count(especially neutrophils), liver function and lipids for those on tocilizimab
- Vaccination against influenza and pneumococcus all RA patients. Ideally also herpes zoster vaccine pre starting boDMARDs and tsDMARDs
- Avoid JAK inhibitors if significant clot and vascular history

All in RA
All seronegative except tocilizumab, rituximab, anakinra, abatacept.

Contraindications:
Current infections (TB, hepatitis, HIV)
Exposure to serious infections (hepatitis, HIV)
Malignancy (breast cancer)
Multiple Sclerosis
HF

SEs:
Infections
Rash, itch
Headache
Auto-Ab
Psoriasis, eczema
Blood dyscrasia
Malignancies
Demyelination
Interstitial lung disease
Vasculitis
HF

Note: rituximab requires Ig monotrong, certolizumab-pegol is safe for pregnancy, and tocilizumab needs monitoring of LFT, FBC, WCC

107
Q
  • What is the role of corticosteroids in rheumatic disease? What are some side effects?
A

Part of conservative management
Indicated for multiple:
- short term relief OA
- first line acute gout attack along with NSAIDs or colchicine
- optional part of phase I for RA
- De Q tendonitis
-

Not first line and not ongoing due to side effects:
- avascular necrosis of bone
- osteoporosis
- tendonopathies

108
Q

- Discuss azathioprine/cyclophosphamide/cyclosporin/tacrolimus/mycophenolate mofetil/rituximab: administration/MoA and indications, side effects, contraindications and monitoring/toxicity

A

Go straight to Immsupp deck

109
Q

- Provide examples of csDMARDs, their MoA, indications, side effects, any contraindications

A

Names:
Methotrexate
Sulfasalazin
Hydroxychloroquine
Leflunomide,
Cyclosporine

MTX:
Antimetabolite
Folic acid analogue which binds to dihydrofolate reductase enzyme & antagonises folic acid. As folic acid is essential to DNA synthesis, MTX impairs cell division , reduces monocytic cell growth & induces apoptosis
Has cytotoxic and immunosuppressant activity
Common first choice drug for RA

ADVEs: heptox, myelotox, pulmo tox; synergistic BM, liver and pulmo tox with leflunomide; contrad in pregnancy

Monitring: FBC and LFTs, renal function

Once a week therapy. Consideration for implications for compliance
Co-administration of folic acid (not on the same day as methotrexate) reduces GI adverse effects and hepatotxicity


Leflu
Anti metabolite
Inhibits pyrimidine synthesis by competitively blocking dihydro-orotate dehydrogenase and thus inhibiting activated lymphocytes.
It has immunosuppressive, immunomodulating and antiproliferative properties. Also has uricosuric effects.

  • hep, myelo, pulmo tox and BP
  • synergistic BM, liver, lung with MTX
  • monitoring: FBC, LFT, BP (Renal function)

CONTRAINDICATED IN PREGNANCY

Washout procedure

  • Due to long half-life of active metabolite, if cessation of leflunomide is required (particularly due to adverse effects or unexpected pregnancy etc) a washout may be required

Sulf

May act by scavenging the toxic oxygen metabolites produced by neutrophils
Anti-inflammatory and immunosuppressant - usually used if methotrexate is not required first line eg if the patient has low-grade inflammation, few affected joints and no indicators of poor prognosis.

hep, myelotox; hypersensitivity

Monitor: FBC, LFT (renal function)

Reversible decrease in sperm count has been reported (but safe in female pregnancies)

HCQ
Inhibits the release of lysosomal enzymes, PML chemotaxis, IL-1 release and the action of phospholipase A2 -> ↓ formation of inflammatory mediators
Monotherapy with hydroxychloroquine may be used if the patient has low-grade inflammation, few affected joints and no indicators of poor prognosis (and therefore doesn’t require methotrexate).

  • advEs: retinopathy and GIT
  • monitor: eye exam, renal and LFTs, FBC
  • ONTRAINDICATED IN PREGNANCY
    Monitoring : check complete blood count, renal and hepatic function at baseline
    • may take approximately 2–6 months of treatment before benefit is seen
      Ocular toxicity:
    • Blurred vision is common.
    • Corneal changes (eg oedema, opacities) occur infrequently, are transient or reversible and may cause effects such as blurred vision and halos.
    • Retinopathy is related to daily dose and duration of treatment. Retinal toxicity can lead to vision loss. Damage is irreversible and may progress after stopping hydroxychloroquine.
    • Baseline and regular ophthalmological examination required.
110
Q

- Provide examples of anti-resorptive agents, their MoA, indications, side effects, any contraindications

A

SERM and calcitriol
S:
Antiresorptive
Acts on estrogen receptors andindicated in post-menopausal osteoporosis

  • Acts on estrogen receptors in bone and not in the breast tissue
    Improves boen density and reduces vertebral bone fractures
  • Evidence of improved bone density
  • Evidence for reduced fracture at vertebral site

Calcitriol:
- antiresorptive
indication: osteoporosis
- improves bone density but does not reduce bone fractures

Bisphosphonates:
Bisphosphonate molecules attach to osteoclasts where they disrupt bone resorption
Post-menopausal osteoporosis
Male osteoporosis
Corticosteroid induced osteoporosis
Osteoporosis – primary prevention

Side effects:
GI upset and osteonecrosis of jaw; atypical fractures

EXTRA:
- poor compliance: Weekly medications, Risendronate now monthly, IV Zolendronic Acid – annual infusion
- 50% compliance for orals
- improves bone density
reduced compact and trabecular bone fractures

e.g.s alendronate risendronate

111
Q

- Provide examples of anabolic agnets, their MoA, indications, side effects, any contraindications

A

Anabolic
MoA:PTH homolog. Intermittent exposure activates osteoblasts.

  • Chronically elevated PTH will deplete bone stores.
  • Intermittent exposure to PTH - activate osteoblasts more than osteoclasts. -
  • Once-daily injections of teriparatide have a net effect of stimulating new bone formation leading to increased bone mineral density.

Indications:Post-menopausal osteoporosis

Side effects/name: Sarcoma if used for longer then 18 months

Teriparatide

112
Q

- Provide an example of a dual agent, its MoA, indications, side effects and any other relevant information

A

Strontium Ralenate

Dissociates bone remodelling – increases bone formation. Induces preosteoblasts. Inhibits osteoclast formation.

SEs: Hypertension, PH and CVA, Thrombosis

Extra: Reduces compact and trabecular bone fractures.

113
Q

Describe hip fractures and their relative severity

A

Pelvic Fractures ^[imp]
- fractures of superior and inferior rami are stable, can be treated conservatively

  • similarly, fractures of the iliac wing, although high energy, can also be managed conservatively
  • by contrast, disruption of sacroiliac joint (and pubic symphysis is more serious)
  • The most serious of these is a pelvic diastasis, with risk of rupture of retroperitoneal veins, bleeding, and haemodynamic instability. MUST BE CLOSED ^[Open book fracture_(anterior + posterior pelvic ring fracture)_ ]: “superiorlateralquadrant
    -
114
Q

Describe psoas abscess

A

Infection within psoas major can cause irritability and infection can be transmitted to hip joint

Psoas major abscess can lead to septic arthritis of the hip joint

115
Q

Label this Xray of the elbow

A
116
Q

Label this Xray of the pelvis

A
117
Q

Label this Xray of the knee

A
118
Q

Describe the sensory innervation of the lower limb

A
  • obturator nerve: L2-4 – medial thigh
  • lateral femoral cutaneous nerve – anterolateral thigh
  • femoral nerve – anteromedial thigh
  • sural – posterolateral leg (from sciatic -> tibial)
  • saphenous – branch of femoral: medial leg and foot
  • deep peroneal – first web space
  • superficial peroneal – dorsum of foot and anterolateral leg (from sciatic)
  • tibial – plantar foot (via sciatic)
  • common peroneal – lateral knee