MST Week 1 (the Broken Arm) Flashcards
What are the 3 flexors of the arm (BBC)
1) biceps brachii
2) brachialis (greatest amount of flexion force)
3) coracobrachialis (flexes and adducts arm not forearm)
What is the biceps brachii
Simple flexor when elbow is extended but more powerful when the elbow approaches 90
But with forearm in pronation: biceps is a very powerful supinator
Boundaries and contents of the cubical fossa
Boundaries
Superiorly: imaginary line connecting the lateral and medial epicondyles
Medically: pronation teres
Laterally: brachioradials
Contents:
Terminal part of brachial artery, start of radial and ulnar arteries, median nerve, radial nerve (superficial and deep branches)
Flexor muscles of the forearm
1st layer: pronator teres, flexor carpi radialis, palmaris longus, flexor carpi ulnaris
Intermediate layer: flexor digitorium superficialis
Deep (3rd) layer: flexor digitroum profundus, flexor pollicis longus, pronator quadratus
Structures in the anterior arm
The 2 heads of biceps brachii mm and its distal attachment, the brachialis and coracobrachialis mm, motor and sensory parts of the musculocutaenous n, brachial a and its bifurcation
What is compartment syndrome
Increased pressure within any fixed volume space can result in compartment syndrome
- intracompartmental pressure may exceed the capillary perfusion pressure of 25-30 mmHg - will result in temporary or permanent damage
What is the Gleno-humeral joint
Spheroidal head of humerus articulates with pear shaped glenoid fossa of the scapula. This ball and socket joint has striking incongruency (head 4x>socket)
Most common shoulder problems
Dislocation
Rotator cuff injury
Frozen shoulder
Fracture
Arthritis
What happens in frozen shoulder / adhesive capsulitis
The normally very flexible elastic joint capsule becomes inflamed and eventually contracted.
Severely painful and restrictive
Arteriovenous fistula for haemodialysis
Haemodialysis fistulas are surgically created communications between the native artery and vein in an upper extremity.
The access that is created can be routinely used for haemodialysis 2-5 times per week
Order of preference for arteriovenous fistula placement
1) radial - cephalic
2) brachiocephalic
3) braciobasic
Common flexor-pronator attachment
- pronator teres (humeral head)
- flexor carpi radialis
- flexor carpi ulnaris (humeral head)
- palmaris longus
- flex digit superficialis (humeral head)
Common extensor - supinator attachment
- anconeus
- supinator
- extensor digitorum
- extensor digiti minimi
- extensor carpi ulnaris
- extensor carpi radialis brevis
What are muscles of the arm enclosed by
Circumferential fascia
What is the elbow joint complex
Compound joint of 3 separate articulations within the same capsule
Humeroradial joint aka radiocapitellar joint (shallow ball and socket = hinge / pivot joint)
Humeroulnar joint (hinge)
Proximal radioulnar joint (pivot)
What can go wrong with the elbow joint
Dislocation / fracture Osteoarthritis Epicondylitis Olecraon bursitis Distal biceps tendon rupture
3 main mechanisms of injury to the elbow
Valgus forces
Posterior translocation
Posterolateral rotation
What is carpal tunnel syndrome
Compression of the median nerve in the carpal tunnel (most common nerve compression syndrome overall)
What is cartilage
Specialised connective tissue with a support function (often the shock absorbers of the body, can be tough or flexible depending on composition of matrix)
Cells: chondrocytes
Matrix: type II collagen and proteoglycans + others depending on type of cartilage
(Avascular)
Describe cartilage cells
Derived from embryonic mesenchyme (spindle) - clusters of chondroblasts (rounded) surrounded by a layer of perichondrium (mesenchyme derived fibroelastic cells and collagen)
Growth of cartilage is by interstitial and appositional growth
After matrix deposition cells become less active and become maintaining cells (chondrocytes)
What are proteoglycan aggregates
Proteoglycan monomers attached to a molecule of hyaluronin. Hydrophilic. Provides compressive strength: flexible cushioned surface
What do proteoglycans contain
Contain numerous glycosaminoglycans attached to a core protein
Woven with collagen to form an elastic and compressible structure
What are the different types of cartilage
Hyaline: type II collagen only- smooth glistening (glassy) articulates surfaces
Elastic: type II collagen + elastin
Fibrocartilage: type II and type I collagen strong
How does hyaline cartilage act in joints
- resists compression due to the elasticity and stiffness of proteoglycans
- tensile strength due to collagen and hydrogel ground substance
- most is avascular: limits repair and regeneration
- nutrition is by diffusion: limits thickness
- articular surfaces of joint has no perichondrium- no source of new chondroblasts
- cartilage atrophy is reversible but it takes a long time
Function of bone
Structurally strong- mechanical support and protection
- reservoir for calcium and phosphate in the body
- supports haematopoiesis - bone marrow
- composed of cells and extracellular matrix
- matrix must be strong enough to support the body, yet light enough to be moved: max strength; low weight
- cells produce, mediate, maintain and remodel the matrix
Describe bone organisation
Dense outer shell: compact bone
Inner spongy / cancellous bone arranged in interconnecting trabeculae with spaces for bone marrow
What is trabecular bone
Reduces weight
Provides space for marrow
Struts are arranged to provide maximum resistances to stress
Found in wrists, vertebrae, femoral neck
What is osteoporosis
Thinning of both cortical and trabecular bone, but thinned trabeculae are prone to fracture
Ie FOOSH, hip fracture, dowager hump
What are the 2 parts of the bone matrix
Organic (osteoid): produced by osteoblasts, collagen type I, tensile and compressive strength, non collagenous proteins mediate mineral deposition
Inorganic : calcium phosphate, deposited in the organic matrix, 66% of the dry weight of bone, hardness
What is brittle bone disease
Congenital disease
Defective collagen chain disrupts structure of triple helix
Fragile skeleton
Many types with a range of clinical outcomes: type II fatal in utero or perinatal. Type I increased childhood fractures
Describe bone cells
- Derived from mesenchymal stem cells
- differentiate into osteoprogenitor cells or chondroblasts
- osteoprogenitor cells differentiate into osteoblasts
- osteoblasts: lays down organic bone matrix
- and mediates mineralisation of osteoid
- osteoblasts becomes osteocytes when surrounded by mineralised bone
- osteocyte: maintains matrix
How does osteoid become mineralised
Osteoblasts secrete collagen and matrix vesicles
Matrix vesicles contain enzymes and proteins to control availability of calcium and phosphate so that mineral is precipitated
Immature: woven bone, haphazard fibre arrangement, mechanically weak- foetal development / fracture repair
Mature: lamellar bone: remodelled woven bone- regular parallel collagen, strong: all adult bone
What are osteocytes
Mature osteocytes- surrounded by mineralised matrix
Long cytoplasmic processes connecting to each other and osteoblasts (gap junctions)
- in lacunae surrounded by extracellular bone fluid that allows nutrient diffusion through the bony channels
- connected to osteoblasts and osteoclasts
What are osteoclasts
Exist to destroy bone
- bone resorting cell
- phagocytic cell from monocyte macrophage cell line
- multinucleate mobile cell which attaches to bone surface and resorbs bone leaving a pit behind (howships lacuna)
They work with osteoblasts to regulate bone turnover and remodelling
How do osteoclasts destroy bone
Large multinucleate cells
- actin clear zone and integrins adheres it to the bone surface. Ruffled border increases surface area of the cell
- mineral is dissolved by acids. Outside the cell due to low pH
- lysosomal enzymes resorb organic matrix
- number and function affected by PTH and calcitonin
- oestrogen also reduces activity-menopause
How is bone remodelled
Constantly through the coordinated actions of osteoblasts, cytes and clasts to adjust to stresses and strains. Affects density, orientation and responds to micro fractures and wear and tear - keeps bone healthy
How can bone turnover increase
Change in function (onset of walking)
New demands (running, tennis, jumping)
Repair of fractures
Disease eg pagets
What is osteopetrosis
Rare group of inherited conditions
Reduced osteoclastic activity: defective bone remodelling
- osteoclasts cannot excrete H+ ions to dissolve bone mineral (needs H+ for the acidic environment)
- dense bone but brittle and easily fractured
- clinical effects: fractures, spinal nerve compression, and recurrrent infection
- bone marrow transplant to provide healthy osteoclasts precursors can be effective
Describe relationship between osteoblasts and osteoclasts
PTH (parathyroid hormone) stimulates bone resorption by osteoclasts
Receptors for PTH are located on osteoblasts
- osteoclast precursors have RANK receptors on their cell membranes
- osteoblasts have the ligand for this receptor on their cell membranes RANKL
- PTH upregulates RANKL which binds to RANK and stimulates the differentiation of osteoclasts
- osteoblasts also produce osteoprotegrin which prevents resorption by binding to RANKL
- the ratio of RANKL: osteoprotegin determine bone resorption
What is osteoporosis
Loss of bone mass: mineralisation of bone is normal
- due to disuse, hormones and low peak bone mass
Describe the steps of endochondral ossification
1) chondrocytes at the centre of the growing cartilage model enlarge and then die as the matrix calcifies
2) newly derived osteoblasts cover the shaft of the cartilage in a thin layer of bone
3) blood vessels penetrate the cartilage. New osteoblasts form a primary ossification centre
4) the bone of the shaft thickens and the cartilage near each epiphysis is replaced by shafts of bone
5) blood vessels invade the epiphyses and osteoblasts form secondary centres of ossification
What is achondroplasia
Congenital bone disease: dwarfism
Caused by mutation on the fibroblast growth factor receptor 3: activation
-activation of FGFR3 inhibits chondrocyte proliferation: affects growth plates
They are disorganised and hypoplastic: long bone growth is stunted.
Lordosis (back), bowed legs and stunted extremities (especially proximal)
What is metabolic bone disease
Results from an imbalance between bone formation and resorption 4 main diseases: - osteoporosis - rickets and osteomalacia - Paget’s disease - hyperparathyroidism
What is osteomalacia
Lack of vit D leads to inadequate mineralisation of bone- weak and soft. Osteoid is normal. Bowing of bones and bone pain
What is Paget’s disease
Overactive osteoclasts. These destroy bone and result in osteoblasts responding by laying down bone rapidly - immature woven bone. Therefore bone mass is increased but it is weak. Metabolic consequences due to energy demands of the disease
What is hyperparathyroidism
Increased osteoclast activity as a result of increased levels of PTH due to renal disease or tumour. Destruction of cortical and trabecular bone. Inadequare compensation by osteoblasts leads to loss of bone mass and fracture risk
How do limbs arise from paraxial mesoderm (ie somites)
Dermatome gives rise to connective tissue of the dermis.
Myotome gives rise to limb muscles
How do limbs arise from lateral plate mesoderm
Bones of upper and lower limb
Blood vessels
Connective tissue (except for that of the dermis)
Where are sensory nerve elements derived from
Neural crest
At what stage do limbs grow and pattern
Initial growth and patterning of the limbs occurs during weeks 4-8
Limb buds appear at about 4 weeks
Much of the basic structures (bones and muscle groups) are established by 8 weeks. After 8 weeks the limb elements just increase in size
What is proximo-distal growth and patterning
Limb outgrowth initiated by the apical ectodermal ridge (AER) at the tip of the limb buds and proceeds from proximal to distal
What are HOX genes
Group of related genes that specify regions of the body plan of an embryo
HOX proteins encode and specify the characteristics of ‘position’
How is anterior posterior patterning established
By the zone of polarising activity on the posterior side of the limb (ie the little finger side)
What is anterior - posterior patterning
Loss of the ZPA results in loss of posterior elements
Upregulation of ZPA signals results in additional posterior elements (eg polydactyly on hypothenar side of hand)
Duplication of the ZPA results in duplication of posterior elements (eg little fingers on both sides of the thumb)
How do the digit rays separate
They are initially interconnected by tissue but then regress via apoptosis to produce separate digits.
Apoptosis of interdigital tissue is dependent on BMP signaling within the interdigital tissue under the influence of Shh from the ZPA
What happens if the process of separation of digit rays is disrupted
Can result in syndactyly and more often affects digits 3, 4 and or 5
How do limb bones develop via endochondral ossification
Blood vessels invaded the model and osteoblasts localise and proliferate only at the epiphyses
Chondrocytes nearest the shaft undergo hypertrophy, become calcified and undergo apoptosis
Growth of the long bones continues into early adulthood. This is maintained by FGF signalling to cause proliferation of chondrocytes in the growth plates
Describe the development of body musculature
Derived from paraxial mesoderm (somites)
- sclerotome, which develops into vertebral and rib bones
- myotome which develops into muscle
- dermatome which develops into dermal connective tissue
What is the myotome divided into
Primaxial myotome: adjacent to neural tube - affected by signalling factors from the neural tube to generate muscle precursors with limited migratory potential
Abaxial myotome: ventrolateral myoblasts- respond to signals from the adjacent lateral plate mesoderm and ectoderm to give rise to a migratory population
What does the primaxial myotome form
- epaxial muscles (epimere) of the back (innervated by dorsal rami)
- Hypaxial muscles (hypomere) of the body wall
What is spondyloepiphyseal dysplasia congenita
Rare disorder of bone growth that results in dwarfism
Affects the bones of the spine and the ends of bones
Often causes problems with vision and hearing
Signs and symptoms are similar to but milder than achondrogenesis type II and hypochondrogenesis
What is Amelia
Absence of an entire limb eg early loss of FGF signalling
What is meromelia
Absence of part of a limb eg later or partial loss of FGF signalling
What is phocomelia
Short, poorly formed limb eg partial loss of FGF or HOX disruption
What is adactyly
Absence of digits eg even later loss of FGF
What is ectrodactyly
Lobster claw deformity (FGF variant of adactyly - middle digit is lost)
What is polydactyly
Extra digits (disruption - usually upregulation- of Shh pathway)
What is syndactyly
Fusion of digits (BMP or Shh disruption)
What is holt-oram syndrome
TBX5 mutations
Characterised by upper limb abnormalities and heart defects
- all types of limb defects affecting the upper limb have been observed including absent digits, polydactyly, syndactyly,, absent radius and hypoplasia of any of the limb bones
What is osteogenesis imperfecta
Characterised by shortening, bowing and hypomineralisation of the long bones of the limbs
Dominant mutations in the COL1A1 or COL1A2 genes involved in production of type I collagen
- can result in fractures
- several types of osteogenesis imperfecta occur
What is muscle protein balance
Synthesis = degradation
Determined by nitrogen balance, stable isotope tracer determinations of protein turnover.
Negative muscle protein balance = protein degradation
Positive muscle protein balance = protein synthesis
What happens during human immobilisation
Muscle protein synthesis declines
Muscle protein breakdown probably increases but not to anywhere near the same extent as the decrease in muscle protein synthesis
Define insulin resistance
The diminished ability of skeletal muscle to increase blood glucose disposal in response to elevated blood glucose and insulin concentrations
Describe muscle mass rehabilitation
Muscle protein synthesis increases dramatically with exercise. The mechanism for this increase in muscle mass during rehabilitation.ligation appears to be at least partly attributable to increased phosphorylation of the Akt/mTOR pathway
Muscle protein breakdown appears to be inhibited by the instigation of rehabilitation exercise following immobilisation
There is potential for nutritional and pharmacological intervention to facilitate muscle mass restoration following immobilisation induced atrophy by stimulating muscle protein synthesis
What happens to glucose uptake with increasing exercise intensity
The higher the intensity of the exercise the higher the skeletal muscle glucose uptake
Duration of exercise also plays a role as low intensity for a long time may = high intensity for a short time
Effect of inflammation on muscle wasting
Inflammation increases muscle wasting (can be profound in severe cases eg sepsis)
What is muscle wasting acheived by
Acheived by the marked inhibition of muscle protein synthesis and increase in muscle protein breakdown
Causes of fracture
Force- load going through bone is too high on a single cycle for a bone to take
Repeated low energy injuries to the same bone- gradually chips away
Loss of resistance - associated with osteoporosis
Complications of plaster
Pressure sores
Respiratory complications
Clots
Muscle wasting
Skin tears (skin traction)
Pin sire infection (skeletal traction)
Define trauma
The transfer of kinetic energy above the physiological limit of the recipient
