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MBChB 1 > Limbs and Back > Flashcards

Limbs and Back Flashcards

1
Q

Which type of cartilage is found in the knees and hip joints?

A

Articular

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2
Q

What is the main cell type found in cartilage?

A

Chondrocytes

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3
Q

What percentage of the tendon is composed of cells?

A

20%

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4
Q

Shoulder pain and the inability to externally rotate the arm indicates what?

A

Injury of the infraspinatous

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5
Q

What are the three phases of tendon healing?

A

I-R-R

  1. Inflammation
  2. Repair
  3. Remodelling
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6
Q

What is the innervation and function of the Latissimus dorsi?

(Superficial group back muscle)

A
  1. Thoracodorsal Nerve

Adducts, extends, medially rotates the arm.

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7
Q

What is the innervation and function of the Levator scapulae?

(Superficial group back muscle)

A

Dorsal Scapular Nerve and C3-C5.

Elevates the scapula.

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8
Q

What is the innervation and function of the Rhomboudeus Major?

(Superficial group back muscle)

A

Dorsal Scapular Nerve

Rotates and retracts the scapula.

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9
Q

What is the innervation and function of the Rhomboudeus Minor?

(Superficial group back muscle)

A

Dorsal Scapular Nerve

Rotates and retracts the scapula.

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10
Q

What is the innervation and function of the Trapezius?

Superficial group back muscle

A

Elevates and rotates the scapula during abduction of the arm above horizontal.

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11
Q

What is the structure of the brachial plexus?

A

“Rugby Teams Drink Cold Beer”

  1. Roots
  2. Trunks
  3. Divisions
  4. Cords
  5. Branches
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12
Q

Name the tarsal bones of the foot.

A

“Tiger Cubs Need MILC”

  1. Talus
  2. Calcaneus
  3. Navicular
  4. Medial Cuneiform
  5. Intermediate Cuneiform
  6. Lateral Cuneiform
  7. Cuboid
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13
Q

What bones form the “true ankle”? What movements does it allow?

A

Tib/Fib and Talus.

Dorsi and Plantar Flexion.

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14
Q

What bones form the “Sub-Talar Joint”? What movements does it allow?

A

Talus and the Calcaneus.

Inversion and eversion.

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15
Q

Name the contents of the Cubital Fossa (lateral to medial)

A

“Really Need Beer To Be At My Nicest”

  1. Radial Nerve
  2. Biceps Tendon
  3. Brachial Artery
  4. Median Nerve
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16
Q

Name the contents of the Femoral Triangle (lateral to medial)

A

“NAVEL”

  1. Nerve, Femoral
  2. Artery, Femoral
  3. Vein, Femoral
  4. Empty Space
  5. Lymph, Deep Inguinal
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17
Q

What are the major landmarks of the Scapula?

A
  1. Acromial Process
  2. Coracoid Process
  3. Scapula Notch
  4. Superior, Inferior, Lateral, Medial Borders
  5. Neck
  6. Body
  7. Supraspinatous Fossa
  8. Infraspinatous Fossa
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18
Q

What are the muscles of the Rotator Cuff?

A

“TISS”

  1. Teres Minor
  2. Infraspinatous
  3. Supraspinatous
  4. Subscapularis
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19
Q

Describe the structure and functions of tendons

A

Composition:

  1. Water 80%
  2. Solids 20%
    - collagen (I & III), Elastin.

Dense and regularly arranged structures that transmit force and load generated by muscles.

Fibroblasts are the principle cell type. Attach muscle to bone to allow articulation.

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20
Q

What nerves arise from the terminal branches of the Brachial Plexus?

A

Four.

  1. Musculocutaneous (Lateral Cord)
  2. Median (Lateral and Medial)
  3. Radial (Posterior)
  4. Ulnar (Medial)
  5. Axillary (Posterior)
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21
Q

What nerves branch off the Brachial Plexus?

A

Seven.

  1. Long Thoracic
  2. Dorsal Scapular Nerve
  3. Suprascapular Nerve
  4. Pectoral Nerves
  5. Auxillary Nerve
  6. Thoracodorsal Nerve
  7. Medial Cutaneous Nerves
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22
Q

Watch a Brachial Plexus tutorial on YouTube.

OR

Draw the bracial plexus.

A

Go.

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23
Q

Describe 4 x-ray features of Osteoarthritis

A
  1. Loss of joint space/ joint space narrowing
  2. Subchondral Bone Lesions - bone hardens and becomes more white on X-Ray.
  3. Osteophyte formation
  4. Subchondral Cysts
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24
Q

Describe the pathophysiology of Osteoarthritis.

A

Increase in water content in the ECM

Decreased proteoglycan synthesis

Decrease in size of aggrecan/ hyaluronic acid.

Degrading articular cartilage

Inflammation and cytokine release

Erosion due to bone-bone contact

Osteophytes, subchondral lesions and cysts form.

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25
Q

Describe indirect fracture healing.

A
  1. 8 hours. Haematoma forms. Acute inflammatory response takes place.
  2. 3 weeks. Soft callous forms from fibrocartilage.
  3. 4 months. The hard callous forms as osteoblasts lay down woven calcified bone. The callous is re-vascularised.
  4. Remodelling. Osteoclasts work with osteoblasts to form compact bone.
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26
Q

Summarise articular cartilage and osteoarthritis

A
  1. Cartilage is Hyaline. 20% chondrocytes, 80% matrix.
  • Type II collagen
  • Avascular and Aneural
  • Hyaluronic acid chains

Load transmission with low friction.

  1. Homeostasis and Healing.
    - enzymes
    - must breach subchondral bone
  2. Treatments
    - physio
    - medical (drugs)
    - surgical
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27
Q

What does the Axillary Nerve go onto innervate?

A

Deltoid and Teres Minor

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28
Q

What does the Musculocutaneous Nerve go onto innervate?

A

Anterior compartment of the arm.

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29
Q

What does the Median Nerve go onto innervate?

A

Anterior compartment of the forearm and hand. (Mainly the forearm)

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30
Q

What does the Ulnar Nerve go onto innervate?

A

Anterior compartment of the forearm and hand. (Mainly the hand)

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31
Q

What does the radial nerve go onto innervate?

A

Posterior compartment of the arm and forearm.

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32
Q

Which muscles can rotate the arm laterally?

A

Infraspinatous and Teres Minor.

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33
Q

What is the name of the gap located between the Teres Major and Minor, Humerus, and long head of the triceps, through which the axillary nerve travels?

A

Quadrangular Space

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34
Q

What cells are found in bone?

A
  1. Osteogenic cells.
    - unspecialised cells originating from the mesenchyme. “Osteoprogenitor cells”. Mature into osteoblasts.
  2. Osteoblasts.
    - “building” cells. Lay down bone (osteoid), ossification. Initiate mineralisation.
  3. Osteocytes
    - set in bone mineral. Maintains bone metabolism. Mature osteoblasts. Communication maintained by projections through lacunae tight junctions. Arrange in osteons.
  4. Osteoclasts.
    - “clear”/ resorbs bone. Derived from macrophages. Multi-nucleated. Marked by a ruffled border. Lots of lysosomes.
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35
Q

What are the main components of bone?

A

Two main groups.

  1. Organic - TENSILE STRENGTH
    - 95% Type I Collagen
    - rich in proteoglycans.
    - osteocalin, osteopontins and bone sialoprotein.
  2. Inorganic - COMPRESSIVE STRENGTH
    - 75% of bone
    - hydroxyapatite.
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36
Q

Describe the gross anatomy/ structure of bone.

A

Compact/ cortical bone.

  • Dense
  • organised in haversian systems (calcified rings called lamelae)
  • branches called volksman canals
  • vascularised through nutrient foramen

Trabecular bone.

  • not arranged in circular structures. Forms a lattice/ mesh.
  • in line with mechanical stress
  • reduction of weight
  • accommodates bone marrow
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37
Q

List the functions of calcium.

A
  1. Major compenent of ossious tissue.
  2. Central role in homeostasis
  3. Muscle contraction
  4. Cell-Cell adhesion
  5. Neural excitability
  6. Intracellular communication
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38
Q

How is calcium distributed in the body?

A
  1. Free calcium - 47%
  2. Bound calcium - 47%
  3. “Complexed” calcium - 6%
  • Clinically, measured as total calcium, or free alone. Only free calcium is clinically relevant.
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39
Q

What is the main site of calcium absorption?

A

The jejunum.

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40
Q

What regulates calcium absorption?

A

Calcitriol. Mediates the synthesis of calcium binding proteins.

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41
Q

What is the role of Calcitriol?

A

“Active Vitamin D”

Calcium homeostasis. Synthesised in the skin, or can be ingested.

42
Q

What is the role of Parathyroid Hormone in Calcium homeostasis?

A

Acts on the Ascending Loop of Henle and the Distal Convoluted Tubule to reabsorb Calcium.

It also increases OsteaCLAST activity and indirectly increases Calcitriol synthesis.

43
Q

What is the role of Calcitonin in Calcium homeostasis?

A

Secreted by Parafollicular Cells of the thyroid gland, inhibiting OsteoCLAST activity.

Decreases plasma calcium.

Antagonistic to PTH, only really seen in “Calcium Stress”

44
Q

Define Osteoporosis

A

A lower than normal bone density and quality leading to increased risk of bone breaks.

45
Q

What are the two causes of Osteoporosis?

A

Primary “Idiotpathic”/ age related/ previous injury

Seconday, a co-morbidity.

46
Q

What is the largest contributing risk factor for Osteoporosis?

A

Post “consolidation” stage of bone development. Age. Female sex.

47
Q

What are the measurements of bone density given by a DEXA scan?

A
  1. Normal >-1 Sd
  2. Osteopenia -1 - -2.5 Sd
  3. Osteoporosis -
48
Q

Describe the RANK/ RANKL pathway.

A

RANKL found on Osteoblasts. Ligate with RANKR on Osteoclasts. RANK/RANL ligation encourages Osteoclast survival and activity.

OPG binds RANKL, while oestrogen inhibits RANKL expression. Osteoclasts are modulated.

49
Q

A defect in what receptor causes Achondroplasia?

A

Fibroblast Growth Factor Receptor 3 (FGFR3)

  • A Receptor Tyrosine Kinase (RTK) Enzyme Linked Receptor.
50
Q

When is Tendonosis commonly seen?

A

Acute: post injury.

Chronic: With age, or post injury with poor rehab.

Degenerative without physio. Repair cannot keep up with use.

51
Q

What are the types of tendon tear?

A

Full and Partial.

52
Q

What is the repair process of tendons? Briefly describe each step.

A

I-R-R

Inflammation - 0-7 Days

Migration of inflammatory cells. Granulation tissue forms, necrotic tissue is cleared. Haematoma is formed.

Repair - 3 - 60 Days
Tenocytes (a type of fibroblast) lays down mesh like Type III collagen.
4 weeks the tendon callus is formed, Type I collagen is formed. Vascular growth.

Remodelling - 28-180 days.

Cross linking of collagen to restore tensile strength.

53
Q

Name the three muscle fibres types.

A
  1. Type I - Slow Oxidative
  2. Type IIa - Intermediate
  3. Type IIb - Fast Glycolytic

Recruited under Henman’s Principle.

54
Q

Describe Type I muscle fibres.

A
  1. Slow Oxidative
  2. Red in colour (Vascularised)
  3. Slow contractile speed - allows for fine movements
  4. High resistance to fatigue - sh*t ton of mitochondria.
  5. Lower levels of ATPase activity.
  6. Less muscle fibres per motor unit (Henman’s Principle). Allows for finer movement.
55
Q

Describe Type IIa muscle fibres

A
  1. Intermediate/ Fast Oxidative + Glycolytic
  2. Smack bang in the middle of the other two fibres.
  3. Also red.
  4. High Myosin ATPase activity - high contractile speed.
  5. The SR delivers more Calcium
  6. More muscle fibres per motor unit (Henman’s Principle)
56
Q

Describe Type IIb muscle fibres

A
  1. Fast Glycolytic
  2. White - think chickens. Fast AF.
  3. Low resistance to fatigue
  4. SR delivers loads of calcium
  5. Really high concentrations of muscle fibres per motor unit. So much power.
57
Q

What are the body energy stores?

A
  1. Carbs - (sugars). Stored as glycogen.
  2. Fats - energy dense. Gram for gram x4 richer than sh*tty carbs. Utilised in Lipolysis.
  3. Proteins - minor store. Hard times. Converted to glucose with poor energy yield. Releases nitrates - it’s removal uses ATP.
58
Q

How is energy provided?

A
  1. . Creatine Phosphate - Phosphorylates ADP. Good stuff.
    - Lohmanns Reaction ADP + H + CrP = ATP + Cr

(wtf happens to the H+ tho?)
You get tired when this runs out.

  1. Oxidative Phosphorylation (Aerobic Glycolysis)

Standard. Pyruvate - Krebs, ETC - 28 ATPs.

  1. Anaerobic Glycolysis

The aim is to provide Pyruvic Acid. Not long term. Lactate produced.

59
Q

Define Central Fatigue

A

The loss of excitability of the motor cortex.

Provides the perception of fatigue.

60
Q

Define Peripheral Fatigue

A

Failure of excitation - contraction coupling.

depletion of ATP at cross bridges

61
Q

An excess of what ion in the T-Tubules reduces excitability of muscle?

A

Potassium.

62
Q

What are the two phases of resistance training?

A
  1. Neural Phase
    - Increased recruitment of Motor Units. Excitability increases, co-ordination improves.
  2. Hypertrophic Phase
    - Development of new muscle fibres. Fibril split.
63
Q

What changes are seen in endurance training?

A

Cardiovascular changes. Capacity goes up.

Increase in capillaries.

Increase in Mitochondria in Type I fibres.

64
Q

Summarise the generic synovial joint.

A

Main anatomy:

  1. Articular cartilage
  2. Articular capsule
  3. Synovial membrane

Salient points:

  1. Chondrocytes: 5%
  2. ECM: 95%
  3. Type II collagen
  4. Avascular and aneural
  5. Hyaluronic acid chains
  6. Inflammation - Repair - Remodel
65
Q

Describe synovial fluid

A

A viscous, non-newtonian fluid. Low friction, shock absorption, load bearing, carriage of nutrients, drainage of waste.

Contains macrophages.

66
Q

What cell types make up the synovial membrane.

A

Macrophages like synovial cells.

Type A: filter the fluid

Type B: Secrete ECM

67
Q

Describe the articular capsule

A

Envelopes the joint, with two layers.

A membrane (ECM secreting) and a fibrous (structural) layer.

68
Q

Describe synovial bursa

A

Fluid filled cushions. Protects movement.

69
Q

Describe meniscii.

A

Crescent shaped. Fibrocartilaginous. Structure and padding.

70
Q

What is the articular disc?

A

Similar to the meniscus. Padding and structural support.

71
Q

What is a ligament?

A

Fibrous tissue that connects bone-bone. Also aids in joint stability/ direction of locomotion.

72
Q

Define Rheumatoid Arthritis.

A

A systemic autoimmune (Type III, but this is debatable) disease, and a major contributor to inflammatory joint disease.

73
Q

What are the risk factors for Rheumatoid Arthritis?

A

Mostly idiopathic but associated with:

  1. “Genetic disposition”
  2. Female sex
  3. Smoking
  4. Gingivitis
  5. Hypothesised cross reaction with genuine pathogen.
74
Q

What are the principle pathological changes seen in seen in Rheumatoid Arthritis?

A
  1. Activated macrophages secrete TNF-A, IL-1, IL-6 and start a typical immune response.
  2. Synoviocytes activate and secrete RANKL.
  3. Osteoclasts increase in activity.
  4. Protease concentration increases, which degrades cartilage.
  5. Synoviocytes can migrate, causing symmetrical presentation.
  6. M.Øs sensitise CD4+ cells (via MHC-II) to auto-antibody. (Production of IgM is called Rheumatoid Factor, IgG is anti-CCP).
75
Q

What is Rheumatoid Factor?

A

An IgM molecule that recognises auto-antibody to cause R.A. Binds to Fc IgG to form immune complexes. (Hence the Type III hypersensitivity).

76
Q

What is anti-citrinulated protein antibody (Anti-CCP)?

A

Targets citrinulated proteins such as fibrin and fillagrin.

77
Q

What are the three phases of R.A degeneration of joints?

A
  1. Rheumatoid synovium
  2. Articular Cartilage Destruction
  3. Focal destruction of bone
78
Q

What are examples of extra-articular effects of R.A?

A
  1. Skin nodules
  2. Anaemia (hepcidin)
  3. Atherosclerosis (stroke, M.I, Angina)
  4. CNS neuropathy
  5. MSK (Osteopenia, secondary fractures.)
79
Q

What are the treatments of R.A?

A
  1. NSAIDS and analgesia
  2. DMARDS - Methotrexate.
  3. Corticosteroids
  4. Anti-TNF-A therapy.
  5. Surgery
80
Q

List methods of cell-cell signalling.

A
  1. Intracrine. By the cell for the cell inside the cell. (FGF-11)
  2. Autocrine. By the cell, for the cell, leaves the cell, back to the cell (own receptors). (IGF-1)
  3. Juxtacrine. Cell-cell contact dependant. (Lamanin)
  4. Paracrine. Target cell is close by. (EGF)
  5. Endocrine. Target cell is far away. (Oestrogen).
  6. Neuronal. Signal follows a nerve body, neurotransmitters cause the final effect.
81
Q

Briefly describe GPCR and name an example.

A
  1. Ligand binds extracellular domain.
  2. Conformational change propagates through 7 transmembrane domains (serpentine structure) causing conformational change.
  3. Alpha subunit of the GPCR exchanges GDP for GTP.
  4. Subunit dissociates to regulate down-stream proteins.
  5. Signal is transduced to secondary messengers.

Example: Adrenaline and Cyclic AMP.

82
Q

Briefly describe Enzyme Linked Receptors with an example.

A

Example is: FGFR-3. A receptor tyrosine kinase.

  1. Exist as monomers, function as dimers.
  2. Ligand dimerises the monomers.
  3. Dimer is auto-phosphorylated
  4. Phospho-tyrosine residues form in the cytosol.
  5. These residues form binding sites for intracellular proteins.
83
Q

Briefly describe Ligand-Gated Ion Channels.

A
  1. Multimeric structure, form a pore.
  2. Ligand causes conformational change.
  3. The central pore opens.
  4. Ions diffuse passively.
  5. Shape is maintained when ligand is bound.

Example is ACh-R.

84
Q

What is an example oncogene?

A

BCR-ABL. Codes for an “Always on” RTK. Chronic Myeloid Leukaemia.

85
Q

What is an example Tumour Suppressor Gene?

A

Retinoblastoma. Binds E2F to halt cell cycle.

86
Q

What are two mechanisms by which stem cells maintain their population?

A
  1. Obligatory asymmetric replication.

2. Stochastic differentiation

87
Q

What layer of the trilaminar disc does the skeletal system arise?

A

The Mesoderm

88
Q

In which week does gastrulation occur?

A

Week 3

89
Q

The PNS arises from what layer of the trilaminar disc?

A

The Ectoderm

90
Q

Define Somite

A

Somites are bilaterally paired blocks of paraxial mesoderm which form during the somatogenesis stage of development.

91
Q

Define paraxial mesoderm

A

Mesoderm that goes onto form somites, either side of the neural tube.

92
Q

Define intermediate mesoderm

A

The second layer of mesoderm that forms the Genito-urinary tract.

93
Q

Define Lateral Plate Mesoderm

A

The third layer of the mesoderm that forms the parietal and visceral layers, cardiac and smooth muscle.

94
Q

What three gene families regulate mesoderm differentiation.

A
  1. Notch
  2. Wnt
  3. FGF
95
Q

What mediates the median hinge in neurulation?

A

BMP and SHH.

This fold occurs by default.

96
Q

What mediates the dorsal-lateral hinge in neurulation?

A

BMP-2, this inhibits D-L folding at the cranial end of the neural tube.

(SHH, inhibits noggin, which promotes BMP-2, which inhibits Doris-lateral hinge point).

97
Q

What does a lack of SHH in the cranial end of the neural tube cause?

A

Ancephaly.

98
Q

SHH in excess at the caudal region of the neural tube causes what?

A

Spina Bifida.

99
Q

What are the layers of the epiphyseal growth plate?

A
  1. Resting
  2. Proliferative
  3. Hypertrophic
  4. Zone of calcified cartilage
100
Q

What does a mutated FGFR3 gene code for?

A

A dimerised “always on” RTK. Inhibits the differentiated on chondrocytes, which causes achondroplasia.

101
Q

What are the steps of endochondral bone growth?

There are six.

A
  1. Development of the cartilaginous model
  2. Growth of the cartilaginous model
  3. Development of the primary ossification centre
  4. Development of the medullary cavity.
  5. Development of secondary ossification centres
  6. Formation of articular (hyaline) cartilage and the physis.

MBChB 1 (3 decks)

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