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Medicine 2 > MST Week 1 (the Broken Arm) > Flashcards

MST Week 1 (the Broken Arm) Flashcards

1
Q

What are the 3 flexors of the arm (BBC)

A

1) biceps brachii
2) brachialis (greatest amount of flexion force)
3) coracobrachialis (flexes and adducts arm not forearm)

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2
Q

What is the biceps brachii

A

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

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3
Q

Boundaries and contents of the cubical fossa

A

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)

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4
Q

Flexor muscles of the forearm

A

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

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5
Q

Structures in the anterior arm

A

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

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6
Q

What is compartment syndrome

A

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
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7
Q

What is the Gleno-humeral joint

A

Spheroidal head of humerus articulates with pear shaped glenoid fossa of the scapula. This ball and socket joint has striking incongruency (head 4x>socket)

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8
Q

Most common shoulder problems

A

Dislocation

Rotator cuff injury

Frozen shoulder

Fracture

Arthritis

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9
Q

What happens in frozen shoulder / adhesive capsulitis

A

The normally very flexible elastic joint capsule becomes inflamed and eventually contracted.

Severely painful and restrictive

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10
Q

Arteriovenous fistula for haemodialysis

A

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

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11
Q

Order of preference for arteriovenous fistula placement

A

1) radial - cephalic
2) brachiocephalic
3) braciobasic

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12
Q

Common flexor-pronator attachment

A
  • pronator teres (humeral head)
  • flexor carpi radialis
  • flexor carpi ulnaris (humeral head)
  • palmaris longus
  • flex digit superficialis (humeral head)
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13
Q

Common extensor - supinator attachment

A
  • anconeus
  • supinator
  • extensor digitorum
  • extensor digiti minimi
  • extensor carpi ulnaris
  • extensor carpi radialis brevis
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14
Q

What are muscles of the arm enclosed by

A

Circumferential fascia

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15
Q

What is the elbow joint complex

A

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)

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16
Q

What can go wrong with the elbow joint

A 
Dislocation / fracture 
Osteoarthritis 
Epicondylitis 
Olecraon bursitis 
Distal biceps tendon rupture
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17
Q

3 main mechanisms of injury to the elbow

A

Valgus forces

Posterior translocation

Posterolateral rotation

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18
Q

What is carpal tunnel syndrome

A

Compression of the median nerve in the carpal tunnel (most common nerve compression syndrome overall)

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19
Q

What is cartilage

A

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)

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20
Q

Describe cartilage cells

A

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)

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21
Q

What are proteoglycan aggregates

A

Proteoglycan monomers attached to a molecule of hyaluronin. Hydrophilic. Provides compressive strength: flexible cushioned surface

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22
Q

What do proteoglycans contain

A

Contain numerous glycosaminoglycans attached to a core protein

Woven with collagen to form an elastic and compressible structure

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23
Q

What are the different types of cartilage

A

Hyaline: type II collagen only- smooth glistening (glassy) articulates surfaces

Elastic: type II collagen + elastin

Fibrocartilage: type II and type I collagen strong

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24
Q

How does hyaline cartilage act in joints

A
  • 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
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25
Q

Function of bone

A

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
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26
Q

Describe bone organisation

A

Dense outer shell: compact bone

Inner spongy / cancellous bone arranged in interconnecting trabeculae with spaces for bone marrow

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27
Q

What is trabecular bone

A

Reduces weight

Provides space for marrow

Struts are arranged to provide maximum resistances to stress

Found in wrists, vertebrae, femoral neck

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28
Q

What is osteoporosis

A

Thinning of both cortical and trabecular bone, but thinned trabeculae are prone to fracture

Ie FOOSH, hip fracture, dowager hump

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29
Q

What are the 2 parts of the bone matrix

A

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

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30
Q

What is brittle bone disease

A

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

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31
Q

Describe bone cells

A
  • 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
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32
Q

How does osteoid become mineralised

A

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

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33
Q

What are osteocytes

A

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
34
Q

What are osteoclasts

A

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

35
Q

How do osteoclasts destroy bone

A

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
36
Q

How is bone remodelled

A

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

37
Q

How can bone turnover increase

A

Change in function (onset of walking)

New demands (running, tennis, jumping)

Repair of fractures

Disease eg pagets

38
Q

What is osteopetrosis

A

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
39
Q

Describe relationship between osteoblasts and osteoclasts

A

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

40
Q

What is osteoporosis

A

Loss of bone mass: mineralisation of bone is normal

  • due to disuse, hormones and low peak bone mass
41
Q

Describe the steps of endochondral ossification

A

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

42
Q

What is achondroplasia

A

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)

43
Q

What is metabolic bone disease

A 
Results from an imbalance between bone formation and resorption 
4 main diseases: 
- osteoporosis 
- rickets and osteomalacia 
- Paget’s disease 
- hyperparathyroidism
44
Q

What is osteomalacia

A

Lack of vit D leads to inadequate mineralisation of bone- weak and soft. Osteoid is normal. Bowing of bones and bone pain

45
Q

What is Paget’s disease

A

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

46
Q

What is hyperparathyroidism

A

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

47
Q

How do limbs arise from paraxial mesoderm (ie somites)

A

Dermatome gives rise to connective tissue of the dermis.

Myotome gives rise to limb muscles

48
Q

How do limbs arise from lateral plate mesoderm

A

Bones of upper and lower limb

Blood vessels

Connective tissue (except for that of the dermis)

49
Q

Where are sensory nerve elements derived from

A

Neural crest

50
Q

At what stage do limbs grow and pattern

A

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

51
Q

What is proximo-distal growth and patterning

A

Limb outgrowth initiated by the apical ectodermal ridge (AER) at the tip of the limb buds and proceeds from proximal to distal

52
Q

What are HOX genes

A

Group of related genes that specify regions of the body plan of an embryo

HOX proteins encode and specify the characteristics of ‘position’

53
Q

How is anterior posterior patterning established

A

By the zone of polarising activity on the posterior side of the limb (ie the little finger side)

54
Q

What is anterior - posterior patterning

A

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)

55
Q

How do the digit rays separate

A

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

56
Q

What happens if the process of separation of digit rays is disrupted

A

Can result in syndactyly and more often affects digits 3, 4 and or 5

57
Q

How do limb bones develop via endochondral ossification

A

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

58
Q

Describe the development of body musculature

A

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
59
Q

What is the myotome divided into

A

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

60
Q

What does the primaxial myotome form

A
  • epaxial muscles (epimere) of the back (innervated by dorsal rami)
  • Hypaxial muscles (hypomere) of the body wall
61
Q

What is spondyloepiphyseal dysplasia congenita

A

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

62
Q

What is Amelia

A

Absence of an entire limb eg early loss of FGF signalling

63
Q

What is meromelia

A

Absence of part of a limb eg later or partial loss of FGF signalling

64
Q

What is phocomelia

A

Short, poorly formed limb eg partial loss of FGF or HOX disruption

65
Q

What is adactyly

A

Absence of digits eg even later loss of FGF

66
Q

What is ectrodactyly

A

Lobster claw deformity (FGF variant of adactyly - middle digit is lost)

67
Q

What is polydactyly

A

Extra digits (disruption - usually upregulation- of Shh pathway)

68
Q

What is syndactyly

A

Fusion of digits (BMP or Shh disruption)

69
Q

What is holt-oram syndrome

A

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
70
Q

What is osteogenesis imperfecta

A

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
71
Q

What is muscle protein balance

A

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

72
Q

What happens during human immobilisation

A

Muscle protein synthesis declines

Muscle protein breakdown probably increases but not to anywhere near the same extent as the decrease in muscle protein synthesis

73
Q

Define insulin resistance

A

The diminished ability of skeletal muscle to increase blood glucose disposal in response to elevated blood glucose and insulin concentrations

74
Q

Describe muscle mass rehabilitation

A

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

75
Q

What happens to glucose uptake with increasing exercise intensity

A

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

76
Q

Effect of inflammation on muscle wasting

A

Inflammation increases muscle wasting (can be profound in severe cases eg sepsis)

77
Q

What is muscle wasting acheived by

A

Acheived by the marked inhibition of muscle protein synthesis and increase in muscle protein breakdown

78
Q

Causes of fracture

A

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

79
Q

Complications of plaster

A

Pressure sores

Respiratory complications

Clots

Muscle wasting

Skin tears (skin traction)

Pin sire infection (skeletal traction)

80
Q

Define trauma

A

The transfer of kinetic energy above the physiological limit of the recipient

Medicine 2 (16 decks)

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