SECOND YEAR MEDICINE

MUSCULOSKELETAL SYSTEM

2012

School of Medicine

musculoskeletal system
year 2 bmbs 2012
coordinator // ian gibbins@flinders.edu.au

aims of the MSS block teaching staff suggested texts and sources of information notes for practical classes information for examinations past exam feedback student art

page 2 page 3 page 4 page 6 page 64 page 110

aims of the musculoskeletal system block...

The overall aim of this component of Knowledge of Health and Illness 2 is for you to understand the normal structure and function of the musculoskeletal system, and some of the more common pathological changes that affect it. The specific things you need to learn in this subtopic are listed in the learning objectives for each week and supplemented by material in this course booklet. However, the core material includes: *** the normal microscopic and macroscopic structure of bones and joints as they relate to their functions, radiological appearance, and surface features. Macroscopic features include major structural landmarks, ligaments, joint capsules, synovial cavities, intra-articular discs, normal ranges of movement. Microscopic features include the various cells of bone, cartilage, synovial membrane and skeletal connective tissues, their functional relationships, development and usual patterns of turnover. the normal metabolic activity of bone and cartilage; its control by hormones and physical activity ; the ways it can be disrupted in common pathological conditions, including osteoporosis, osteopaenia, inflammation, infection and fractures; recognition of different conditions affecting bone and cartilage metabolism; and common treatments for these conditions. common conditions, including rheumatoid arthritis, osteoarthritis and gout that lead to pathological and degenerative changes in joints, their causes, pathophysiology, functional consequences, recognition, and usual treatments. the normal structure and function of the major muscles of the body, including their actions in day-to-day activities, such as grasping and manipulating objects, locomotion, and posture; how the muscles relate to each other and their skeletal attachments; the roles of agonists and antagonists in controlling movements around joints; the roles of concentric and eccentric contractions in motility and load bearing; the most common ways in which muscles are damaged. recognition and identification of major skeletal and muscular elements in surface anatomy, gross anatomy and radiology; simple tests of dysfunction or injury; radiological identification of common degenerative changes and injuries to the skeleton. the main peripheral nerve and vascular supplies to the muscle groups, and the functional consequences of lesions to these nerves.

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The assessment for MSS tests your knowledge and understanding of some aspect of each of these core areas.

teaching staff
Although Ian Gibbins has ended up doing a substantial amount of the MSS block, several other people are involved in teaching or preparation of the material. If you need assistance in anything, your best first port of call is Ian, who will be able to direct you to the best person, if he cannot help you directly. The best way of getting any of these people, including Ian, outside class time is by email or via their departmental office. The following people have important input into the course, although others will be involved at various stages. Co-ordinator: Ian Gibbins, Anatomy & Histology, Room 6E121, ext. 65271 Malcolm Smith, Clinical Immunology Malcolm will cover inflammatory joint disease. Kathy Knights, Clinical Pharmacology Kathy covers most of the pharmacology relevant to MSS. John Slavotinek, Medical Imaging We introduce a lot of radiology via the prac classes, but John provides critical clinical medical imaging insight.

suggested texts and sources of information

Unfortunately, there is no single text that includes all the material we cover in MSS. On the other hand, much of it can be found in standard texts. For example, all of the core anatomy and histology, including bone formation, is in any decent text you happen to have access to. Any physiology text will fill you in on how muscles contract and how neuromuscular transmission works. Similarly, the pathology and underlying pathophysiology of MSS conditions and their treatments can be found in any textbook of medicine and the recommended pathology texts (eg Robbins). Orthopaedics, radiology and neurology texts also provide valuable information. The major difficulty in trying to learn about the MSS is getting a good idea of the functional stuff: ie how the various muscle groups work in day-to-day life, how they are co-ordinated, and what happens when they go wrong ... Most anatomy texts are 100% accurate when they describe the bones, joints, and which muscles are where. However, they usually have been woefully inadequate when it comes to explaining how the muscles work (ie what they actually do). A valuable exception is the following (smallish) text: Jenkins DB (2008) Hollinsheads Functional Anatomy of the Limbs and Back 9th ed. WB Saunders. Nevertheless, the latest edition (5th) of Moore's anatomy text and the 2nd edition of Gray's Anatomy for Students have pretty good functional material now. For the clinical testing end of things look at: Apley AG, Solomon L (2001) Physical examination in Orthopaedics. Arnold. and Aids to the Examination of the Peripheral Nervous System 4th ed Elsevier Saunders

More detail can be found in: Solomon L, Warwick DJ, Nayagam S (2005) Apleys Concise System of Orthopaedics and Fractures 3rd ed. Hodder Arnold In general, the functions of the MSS are often better described in texts for biomechanics and sports medicine (eg Oatis CA, 2009 Kinesiology: the mechanics and pathomechanics of human movement, 2nd ed, LWW). Overall, much of the relevant information is very scattered and usually you will not have time to look up all this material in detail. That is what the lectures are for - in most cases, the lecture before the practical class will put the anatomy, radiology, etc, into a functional and clinical context.

So what should you do to quickly get on top of things? Recent developments in cognitive neuroscience and its application to learning help us understand why it so hard to learn something like functional anatomy. On one hand, there is all the structure - where things are, how they are related to each other spatially, how the structure interacts with function. This information is largely in the visuo-spatial domain. Then there are all the names of everything, and descriptions of which things connect to what, and knowledge of what happens when things go wrong. This information is largely in the verbal domain. Visuo-spatial information is hard to learn from text. You have to experience it! This means you need to physically explore the material, to literally get a feel for how structures relate to each other. It means you have to use your own body (or that of friend...) to see how different muscles really work, either alone or in combination with others. You need to use devices like anatomy colouring books, or do your own diagrams, to test your spatial knowledge. The colouring books are really good! Photocopy the pages and colour them in different ways depending on the context: eg: according to the innervation according to their function according to their attachments... So how do you link all this with the text? The old tricks of rote learning by recitation actually work! Saying the names of structures and you explore or recount them spatially really helps to assign the names to structures and vice versa. Ultimately, you can string all these domains of information together to explain how you carry out apparently simple day-to-day activities, and then imagine and describe what would be different in the face of various injuries or pathologies. In 2010-2011, Ian and Catherine Truman, Artist-in-Residence in Anatomy & Histology, had a Teaching and Learning Innovation Grant and an Australian Network for Art & Technology Grant to study how students interact with the various materials we use in teaching MSS to develop an internal representation of the body. We found out a lot about how you use the anatomy teaching space and which things matter most to you in understanding how the MSS works. We have used this knowledge to continue improving the classes.

exams
You need to pass a written exam to pass MSS. The format of the MSS exam and the way it is marked are different from other components of KHI. To see what the exams are like, have a look at the section at the end of this book, where previous exams, their sample answers and analysis of what your predecessors did right or wrong is presented. The pass-fail criteria, which are different to previous exams you have done in KHI, also are explained there. In addition, the practical components (ie structure-function, radiology, etc) of MSS will be examined in the final Anatomy practical exam, along with neuroanatomy and any thing else that you have done during the year.

notes for practical classes and lectures

A large amount of the content of MSS subtopic is based on functional anatomy and much of the teaching is based on practical classes. The notes for the classes are included here. There also are notes on related areas for which we do not have specific prac classes or lectures these are for your reference. The information in the notes, and the answers to the questions therein take you a long way to defining what you need to know for the functional anatomy part of the course... Additional notes for some sessions may be put on FLO separately.

mini-cases and mini-case feedback sessions

Each week, in addition to the main case, there will be a set of mini-cases, that illustrate specific aspects of MSS dysfunction relevant to the week. They will tend to get more complex as we move through the course. We will run half-class sessions in the Anatomy Teaching area, when we will go through with you what these mini-cases are showing you, using whatever teaching resources we have. You should use these sessions as an important way to build up and refine your knowledge. The better prepared you are for these sessions, the more you will get out of them. We will run them in a pretty informal way, so there should be plenty of time for you to ask questions and get some answers. Most importantly, the mini-cases model the exam question format very closely... In particular, they encourage you to practise applying basic MSS knowledge to new clinical situations.

web-based resources
There are now many web-based resources that can help you through MSS, but there are a lot of crappy ones too. We will try to put up-dated links to some of the better ones on the GEMP/MSS area. Wherever we can, we will also put our own resources on the MSS site (eg movies, notes etc). If you find a site or resource that seems to be particularly good, please let us know!

biomechanics of the musculoskeletal system

A few biomechanical principles go a long way in helping us to understand how the musculoskeletal system works. You dont need to know this material explicitly (ie there wont be an exam question on it!!) but it really does help to have some idea of mechanical advantage... 1. Levers A lever is defined as "a rigid bar which can rotate around a fixed point when a force is applied to overcome a resistance". To define any particular lever, we must therefore define: the applied force (Fa) the resistance force (Fr) the point of rotation, known as the "fulcrum" The relative location of these features along the length of the lever identifies the type (or class) of lever. a) First class lever The fulcrum lies between the points of the applied force and the resistance force, e.g. a see-saw or a crow-bar: Examples in your body include nodding your head and extending your elbow. b) Second class lever The point of resistance lies between the fulcrum and the point of the applied force, e.g. a wheelbarrow or a bottle-opener:

Examples of second class levers in your body are a bit tricky to find. One potential example is raising up on your toes, where the fulcrum is your toes, the resistance force is your body weight running down through your ankles, and the applied force is being exerted by your calf muscles plantar flexing via your Achilles tendon. However, some experts believe that the forces are not really set up like this... If you hold something relatively heavy (eg. an anatomy text) with your arm extended and abducted, and then lower your arm slowly against gravity, the fulcrum of the movement is your shoulder, the applied force is gravity and the resistance force comes from your deltoid muscle which is contracting eccentrically - voila! A second class lever... c) Third class lever The point of the applied force lies between the fulcrum and the point of resistance, e.g. a spring closing a door:

Most examples of flexing a joint involve third class levers eg biceps brachii flexing the elbow joint, or hamstrings flexing the knee.

2.

Mechanical advantage For any lever to be balanced around its fulcrum, (the distance from the point of the applied force to the fulcrum) x (the size of the applied force) = (the distance from the point of the resistance force to the fulcrum) x (the size of the resistance force). These distances are known as the "force arm" (FA) and the "resistance arm" (RA), respectively. Thus, the previous statement can be written: Fa x FA = Fr x RA where Fa is the applied force and Fr is the resistance force. It should be clear that to keep balance, if Fa decreases, for example, then FA must increase to keep the equation (and the lever!) balanced. This is the "see-saw principle" whereby an overweight adult car can balance a see-saw with a small child on the other end. If you think about it, you should be able to find numerous examples of this principle in operation all around you. If you don't understand it, then get out a ruler, some lumps of chewing gum or other sticky, weighty substance and try it out for yourself! "Mechanical advantage" (MA) is the ratio of the force arm to the resistance arm: MA = FA / RA The greater this ratio, the more efficient the lever will be. In other words, less applied force will be required to move against a given resistance, or alternatively, the same applied force will shift a greater resistance. This is why you use a long crowbar for heaving blocks of concrete and just an old screw driver to open a tin of paint. Increasing MA requires the force arm to move through a large distance compared with the resistance arm. This results in a slow movement of the resistance arm but with relatively great force, equivalent to the low gears on a car or bicycle (think how much you have to pedal to move not very far up a steep hill...). Conversely, decreasing MA means that the force arm moves through a relatively small distance compared with the resistance arm, producing a more rapid movement of the resistance arm at the cost of decreased force generation (high gear is great for cruising, but try a standing start in top...). How is the musculoskeletal system adapted to take advantage of these properties of MA? What limits are set on the optimisation of MA for speed or strength in our bodies? How have these problems been solved in other types of animals?

3.

Pulleys Pulleys allow muscles to pull around corners. Where are some pulleys in your body? They also allow muscles to be situated quite a distance from the parts of the body they are moving. Why is this an advantage?

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Kinematic chains Many simple levers can combine together to produce a wide range of movements at the periphery of a limb. If one end of a chain of levers is fixed and the other end is free, then you have an "open" kinematic chain. Your arm is a good example. Compare the amount of space you can outline just by moving your finger (and nothing else). Now start moving your wrist, then your elbow, your shoulder, your waist. What's happening?? You have probably noticed by now that in an open kinematic chain, you can move any link in the chain without necessarily changing the positions of the other ones relative to each other. Clever, eh? What is the situation when both ends of the chain are fixed? This is a "closed" kinematic chain. Your arm is still a good example. Try doing a push up moving just your elbows, without any movement at your shoulder joints. What's happening now??

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Stress and strain All of the foregoing assumes that bones are inflexible rods. This is not really true. Application of an external force to a solid object will tend to deform it in some way. For example, if you apply a compressive force along the long axis of a long bone, it will tend to become shorter and broader. The measured differences in dimension are called "strains". Strain can also be developed in an object like a bone by tensile (stretching), torsional (twisting) or bending forces. "Stress" is the measure of the forces set up in a particular directions in the bone to resist the strain deformation. Elastic and plastic behaviour As the strains on a material increase, so do the stresses. If a material returns to its original state once the strains are removed, then it is "elastic". This means that the stresses fall to zero when the strains are zero. However, if excessive strains are applied, a material may "yield" and begin to deform without any further increase in stress. In this case, when the deforming force is removed, the stress will fall to zero before the strain does and the material will be deformed permanently: this is "plastic" behaviour. (Why do you think substances like polyethylene and PVC are called plastics?). A material that shows little plastic deformation is "brittle", whereas one with a reasonable amount of plastic deformation is regarded as being "tough". In living bones, the degree of brittleness or toughness is determined by the relative amount of mineralisation of the organic bone matrix. Tougher bones are less mineralised making them more flexible and less likely to be broken. The microscopic structure of bone is organised in such a way to provide a compromise between resistance to bending (why is this so important?) and resistance to breaking.

6.

7.

Hollow bones Why are the shafts of long bones shaped like hollow cylinders? Why is tubular steel or aluminium used so much in making things? Consider a lateral bending force applied to a cylinder. What stresses and strains will be set up in the cylinder? Which parts will be under tension? Which part will be under compression? What will be happening in the middle of the cylinder? How thick do the walls of the cylinder need to be?

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BONES & JOINTS

This is some background information that will be useful for most of the classes. Sooner or later, we will answer all the questions raised in this section... Most of the bones you will see in the museum are dried bones containing only their mineralised content. In life they also contain large amounts of organic material including the all the various cell type that form, maintain and remodel the living bone. Living bones also contain large amounts of collagen and associated proteoglycans - they provide tensile strength and elasticity to the bones. Finally, living bone tissue has a rich supply of blood vessels and nerves, including those in the membranes covering the inner and outer surfaces of the bone (endosteum and periosteum, respectively). If you look carefully at dry bone, you will see many small holes (foramina) where blood vessels run through the compact bone. What would a bone be like if it contained only organic components? Have a look in the museum at the bone tied in a knot.... Bones respond to loading by growing thicker. Conversely, lack of load bearing will lead to loss of bone mass. You can see this most clearly in jaw bones that have lost some teeth - look in the museum cabinet. >> What sorts of forces are generated by biting and chewing? Much of the shape of the bones is determined by the attachments for muscles and ligaments, and for load bearing at joints. >> Why are bones commonly enlarged at points of muscle attachments? Most bones have an outer (cortical) layer of dense compact bone. The inner parts of the bone are made of thin interconnecting rods and spars called trabeculae. The orientation of the trabeculae tend to become aligned in parallel and perpendicular to the directions of the forces set up in the bones under normal loading conditions. Have a look at the museum specimens of bones that have been cut longitudinally so that the trabecular structure is revealed. Many bones, especially the long bones are hollow, and the spaces are filled with blood forming tissue and fat, which tends to predominate in older people. >> Why are the long bones hollow?

Joints are connections of the skeleton between any of its rigid (bony) components. On the basis of the type of tissue applied between two bones joints can be fibrous (syndesmosis), cartilaginous (synchondrosis) or synovial (true joints). In some places, adjacent bones ossify together to form a synostosis. You need to know the composition of synovial joints, their functional classification and the possible range of movements in various joints of the body.

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Fibrous joints In these joints, the bones are joined by collagen fibres that have great tensile strength. a. Sutures - connections between the bones of the skull. Sutures are designed to prevent movement between the bones of the skull. >> Look carefully at the complex interlocking connections between the bones of the roof of the skull. Are all the joints in the skull like this? b. Ligamentous connections - tibiofibular syndesmosis, interosseous membranes of arm and leg and long ligaments of vertebral column. These joints usually allow some degree of twisting to take place between one bone and the next, while ensuring that the two bones do not spread apart from each other under loading. Cartilaginous joints In these joints, the bones are joined via a bridge of cartilage. a. b. Temporary cartilaginous connections - epiphyseal cartilages; these form as part of the development of many bones. They allow the bones to elongate whilst they are in use. Permanent cartilaginous connections - pubic symphysis; This is the somewhat flexible fibrocartilage (cartilage rich in collagen) that joins one half of the pelvis with the other half ventrally. During childbirth, the cartilage softens and allows the pelvis to spread more widely to enlarge the birth canal.

True (synovial) joints These are joints we usually think of. In most cases, the joints allow at least some movement between the apposing bones. The amount of movement in these joints depends on many factors, including the shapes of the bones and their articular surfaces; the strength, length, and orientation of the ligaments surrounding the joint, and the organisation of the muscles around the joint. Synovial joints consist of several components that contribute to their function: articular surface and cartilage: the articular surface of the bone is covered with a layer of hyaline cartilage that is very smooth macroscopically, although is somewhat roughened microscopically by a surface lattice of collagen fibres. The cartilage helps to protect the articular surfaces of the bones. When it is damaged, osteoarthritis can develop. joint capsule: synovial joints are enclosed in a capsule of connective tissue that encloses the joint cavity. In many cases, parts of the capsule are thickened to form ligaments. The overall tightness or looseness of the joint capsule can contribute to the amount of movement that can occur at the joint. articular cavity: this is the actual space between the bones forming the joint. Sometimes, several bones can contribute to a joint complex in a single articular cavity. synovial fluid: joints are lubricated by the remarkable properties of synovial fluid. It is secreted by the synovial membrane that lines most of the joint capsule. The fluid contains complex

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mucopolysaccharides (glycosaminoglycans) that provide viscosity and lubrication. During exercise, synovial fluid is absorbed into the articular cartilage, providing further protection for the joint. The fluid is non-newtonian, meaning that the further it is compressed, the more it resists further compression. This is an ideal property for a load bearing lubricant. ligaments: the bones articulating at synovial joints are held together by ligaments made of collagen. They play a major role in determining the range of movements at a joint. In some cases, they may be inside the joint capsule (eg the cruciate ligaments of the knee). intra-articular disc: some synovial joints contain disc-like structures made of fibrocartilage. Usually these joints have a wide range of movement, but are not strictly load bearing. It is most likely that the intra-articular discs help to spread the synovial fluid in a large joint with a loose capsule. Types of synovial joints They can be classified according to the axes of movement : (i) Uniaxial eg interphalangeal (finger joints) Biaxial eg wrist, joint between finger and metacarpals of hand. Multiaxial eg hip, shoulder.

or according to shape: (ii) Plane eg between vertebrae Hinge eg elbow, between humerus and ulnar Pivot eg between atlas and axis (1st and 2nd vertebra of the neck) Saddle eg at base of 1st metatarsal (base of thumb) Ellipsoid ( = condyloid) eg between metacarpals and phalanges (finger bones) Ball and socket eg shoulder, hip.

Further Considerations >> What factors restrict or reduce the range of movements? >> You already may have experienced how painful joints can become. A very rich nerve supply goes to joints, in particular to the articular capsule and to adjacent soft tissue, although the articular cartilage itself is not innervated. Different classes of sensory nerve fibres convey pain sensation and proprioceptive sensation from the joints. The latter type of sensory fibres are important for the normal neural control of movements of the joints. >> Imagine what it would be like if any of your joints were immobilised. Try not moving your shoulder, elbow, metacarpophalangeal joints, hip, knee, ankle ... as you go about to perform some day to day activities. >> What does it really mean to be "double-jointed"?

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SKULL AND JAWS

In this practical you will investigate the bony structure of the head and neck, the muscles of facial expression. 1. THE SKULL The skull provides a case for the brain (cranial cavity), cavities for organs of special senses (orbital cavity; external, middle and inner ear). It also forms the nasal cavity and the bony framework of the mouth (oral cavity). i. On the dry skull identify the following bones: frontal*, occipital, sphenoid and ethmoid bones (single) parietal and temporal bones (paired) These bones provide a base and covering for the brain vomer (single) maxilla, palatine, zygomatic, lacrimal nasal bones (paired), mandible, These bones form the facial skeleton and jaws. The fissures you can see between some of the bones are specialised joints called sutures. What is their structure? Identify the three major sutures. * The frontal bone develops from two centres of ossification which are separated by the metopic (or frontal) suture in fetal and infant skulls. This suture normally fuses and becomes invisible by the age of 6 years. ii. In the cranial cavity of the dry skull: Identify the anterior, middle and posterior cranial fossae and establish the position of the following structures in these fossae. The nerves and blood vessels associated with each of these structures are given in brackets. a. Anterior cranial fossa: cribriform plate (olfactory nerve)

b. Middle cranial fossa: hypophysial fossa (pituitary gland) optic canal (optic nerve, ophthalmic artery) carotid groove (internal carotid artery) round foramen (maxillary nerve) oval foramen (mandibular nerve) spinous foramen (meningeal artery) superior and inferior orbital fissures (nerves to extraocular muscles and branches of trigeminal nerve) c. Posterior cranial fossa foramen magnum hypoglossal canal

(medulla of the brain) (hypoglossal nerve)

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jugular foramen (internal jugular vein) transverse and sigmoid sulci (dural sinuses of the same name) internal acoustic meatus (facial and vestibulocochlear nerves) d. Petrous part of the temporal bone (internal ear) Tympanic part of the temporal bone (external acoustic meatus)

iii. Surface anatomy Identify the following palpable landmarks of the skull on yourself or on another student: external occipital protuberance zygomatic arch supraorbital margins glabella (ridge above the nose) mastoid process mandible (angle, mental protuberance, head) temporal bone nasal bones

3. Orbital cavity Identify the bones forming the medial, lateral, superior and inferior walls of the orbital cavity. >> Which canals or foramina connect the orbital cavity to the nasal cavity and the middle cranial fossa?

4. Nasal cavity Identify the bones forming the medial and lateral walls, the roof and the floor of the nasal cavity. Establish through which the canal or foramen the nasal cavity connects with the: i. orbital cavity ii. oral cavity iii. anterior cerebral fossa iv. paranasal sinuses Identify the locations of the paranasal sinuses in sectional material of the head. >> What air cavities other than the paranasal sinuses are found in the skull? >> What is the function of the sinuses?

5. Oral cavity and temporomandibular joint The bony framework of the oral cavity includes: maxilla, mandible and the hard palate. The teeth are accommodated in the maxilla (upper jaw) and the mandible (lower jaw).

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a. Identify the bones forming the hard palate. The hard palate separates the nasal cavity from the oral cavity. >> What advantage is there in this arrangement? b. Identify the following landmarks on the mandible: i. base, angle, arch and head ii. mandibular notch, coronoid process and condylar process iii. mandibular foramen, mandibular canal and mental protuberance

The mandible articulates with the skull through the temporomandibular joint. Study the construction of the temporomandibular joint on the dry skull and on the wet specimen. Characterise the temporomandibular joint in anatomical terms and in terms of the type of movements occurring at this joint. - anatomy - movements - ligaments - articular capsule Test on yourself what movements are possible at the temporomandibular joint. >> How does it work?

6. MUSCLES OF THE FACE Identify the muscles of facial expression around the mouth, eye and nose. Familiarise yourself with the position and function of the following muscles on the prosections: orbicularis oculi orbicularis oris levator labii superioris depressor labii buccinator zygomaticus risorius depressor anguli oris frontalis and occipitalis nasalis platysma (around the eyes) (around the mouth) (extending upwards from the upper lip) (extending down from the lower lip) (the muscle of the cheek) (from the corner of the mouth to the zygomatic arch) (from the coner of the mouth across the cheek) (from the corner of the mouth down towards the mandible) (on the forehead and over the occipital region posteriorly) (bridge of the nose) (extends from lower border of the mandible to the deep fascia over pectoralis major and the anterior deltoid)

>> What is unusual about these muscles?

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The muscles of facial expression are second pharyngeal arch derivatives and are innervated by the facial nerve (7th cranial nerve). Find the exit of the facial nerve on the skull (stylomastoid foramen) from where it courses through the parotid gland towards the facial muscles. Within the substance of the parotid gland, the nerve splits up into the following branches: temporal zygomatic buccal mandibular cervical (frontalis) (frontalis, orbicularis oculi) (buccinator, orbicularis oris, levator labii superioris) (orbicularis oris) (platysma)

Identify the muscles of mastication (all innervated by the mandibular branch of the trigeminal nerve, the 5th cranial nerve): masseter temporalis medial and lateral pterygoids >> What are the actions of these muscles on the lower jaw? >> Which way does the temporomandibular joint move as the lower jaw is depressed or elevated by these muscles? Some of the suprahyoid muscles (muscles of the neck), mostly the digastricus muscle also participate in the movement of the temporomandibular joint. >> How? What are the attachments and the actions of these muscles? Muscle masseter temporalis medial pterygoid lateral pterygoid Attachments Action

Identify the course of the mandibular division of trigeminal nerve which carries motor fibres via the oval foramen to the muscles of mastication.

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Problems to Consider: >> How can a blow on the vault of the skull injure the underlying brain without fracturing the bone? >> Why are fractures of the middle cranial fossa common? >> Compare the skull of a neonate with that of the adult. (There are examples of neonatal skulls in the Anatomy Museum). Why are they different? >> Why does dislocation of the jaw (temporomandibular joint) occur relatively frequently? What is the most effective way of reduction? >> What are the most common consequences of facial nerve injury? >> What differences would there be in our skull and jaw muscles if we were primarily carnivores? ... or herbivores? >> Why do we have movable eyebrows?

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BONES AND JOINTS OF THE UPPER LIMB

The bones and joints of the upper limb down to the wrist will be studied in this practical class. The skeleton of the upper limb is attached to the skeleton of the trunk via the shoulder (or pectoral) girdle. Overall, the upper limb and the shoulder girdle is well adapted for both strength and flexibility. In particular, they are adapted for taking large tensile loads (as when hanging from your arms, or carrying heavy objects) - this is a direct evolutionary link with our arboreal primate ancestors. 1. BONES OF THE UPPER LIMB The skeleton of the upper limb includes the shoulder girdle (clavicle and scapula) and the bones of the arm (humerus) and forearm (radius and ulna). Identify the following bones on the skeleton, on X-rays and on yourselves: clavicle, scapula, humerus, radius, ulna. On the articulated skeleton and on X-rays and, where possible, on yourself, note their characteristic features . . . what is attached to each of them?

Clavicle The clavicle is the only direct skeletal attachment between the upper limb and the trunk. Identify the acromial and sternal ends of the clavicle. The bone has a double curve in the horizontal plane. >> How can you distinguish a left clavicle from a right clavicle? >> Where is the weakest area in the bone? Scapula The scapula is a highly mobile element of the shoulder girdle, with several large muscles attached to it. Identify and name its: 3 angles 3 borders 2 processes 2 surfaces Spine and fossae >> Which parts of the scapula can you feel on yourself? >> Much of the scapula is very thin, yet it is rarely fractured. Why?

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Humerus The humerus is the bone of the upper arm (brachium). It is a strong, hollow long bone, with easily identifiable features on it marking muscle attachments. Identify the following: Head Neck - anatomical and surgical Greater and lesser tuberosities (tubercles) Bicipital groove (intertubercular groove) Shaft and the deltoid tuberosity Radial or spiral groove Medial and lateral epicondyles Trochlea Capitulum of the humerus Radial, coronoid and olecranon fossae >> Why is the proximal end of the shaft called the surgical neck?

Ulna The ulna is the medial bone of the forearm (when in anatomical position). It is the load bearing bone of the elbow joint. Identify the: Olecranon Process Trochlear notch of the olecranon process Coronoid process Radial notch Styloid process Capitulum of ulna (=distal head) Note the position of the olecranon with reference to the medial and lateral epicondyles of the humerus during flexion and extension of the elbow joint

Radius The radius is the lateral bone of the forearm (when in anatomical position). It is the load bearing bone of the wrist joint. Identify the: Head Neck Bicipital tuberosity (radial tuberosity) Interosseous border Styloid process Ulnar notch

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2. JOINTS OF THE UPPER LIMB Study the following joints with respect to: - the bones forming the articulation - the type of articulation and shape of the articular surfaces - ligamentous or bony factors strengthening or stabilising the articulation - movements and the factors limiting them A. Shoulder girdle (i) Joints formed by the clavicle The clavicle is important as a brace that keeps the shoulder joint far enough laterally to allow movements of the arm. At its ends, it forms the acromioclavicular and sternoclavicular joints, which provide the only bony connection between the upper limb and the trunk. Note the costoclavicular, coracoclavicular and acromioclavicular ligaments which prevent dislocation of the clavicle against forces transmitted from the arm through the scapula to the clavicle. >> What movements take place at the joint between the clavicle and the manubrium of the sternum (the sternoclavicular joint)? >> What movements take place at the joint between the clavicle and the acromion of the scapula (the acromioclavicular joint? >> What is the relationship between movements at proximal and distal ends of the clavicle? Where is the fulcrum for these movements?

(ii) Shoulder (glenohumeral) joint Movements of this joint occur about 3 different axes, i.e. it is a multiaxial, ball and socket joint. Establish its range of: - flexion-extension - abduction-adduction - rotation The combination of flexion-extension and abduction-adduction results in circumduction, when the arm outlines the surface of a cone, the apex of the cone being the shoulder joint. >> What features of the shoulder joint contribute to its mobility? >> Compare the size of the articular surface of the glenoid fossa and the of the humeral head. How does the discrepancy in size affect range of motion?

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>> How do the articular surfaces of the shoulder joint move with respect to each other? >> What structures contribute to stability of the shoulder joint anteriorly, superiorly, posteriorly and inferiorly? >> In which direction is the shoulder most likely to dislocate? Why? >> Which nerves are at risk when a shoulder dislocates?

(iii) Movements of the scapula The scapula is highly mobile. Any movement of the scapula is associated with movement of the acromioclavicular and the sternoclavicular joints. >> What range of movements can the scapula undertake? >> What contributes to the spatial stability of the scapula? >> How do the joints of the shoulder complex move when the arm is abducted to a horizontal position and to an overhead position? Try to work this out on yourselves.

B. Elbow complex The elbow is basically a load bearing hinge joint, but it also contributes to the pronation / supination movements. Identify the joints of the elbow complex and determine the movements and the range of movement at each articulation. Consider the distal as well as the proximal radioulnar joint. >> Which of these articulations are enclosed within the capsule of the elbow joint? >> What is the angle between the ulnar and the humerus, when the elbow is fully extended? >> In which position is the elbow most stable? Why? >> In what direction does the elbow most commonly dislocate? Why? >> In posterior dislocation of the elbow, which important nerve could be at risk?

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>> Why is dislocation of the radius at the proximal radioulnar joint more common in young children than in adults? >> What happens at the proximal and distal radioulnar joints and at the humeroradial joint during pronation and supination? How does the radius move in relation to the ulna? >> Which is the more powerful movement: pronation or supination? Why? Further Considerations >> Try scratching your right elbow with your right hand. Imagine what it would be like if your left arm were paralysed. >> Compare the length of the upper arm with the length of the forearm? How well would you manage if the forearm was half the length of the upper arm or vice versa? >> How do the movements at each joint of the upper limb combine to maximise flexibility?

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MUSCLES AND MOVEMENTS OF THE SHOULDER & ELBOW

Most of the time, the shoulders and elbows do not move by themselves (when do they?) - usually, the movements at these joints are generated and controlled by the muscles that cross them. Muscles come in all shapes and sizes and you will see many different forms in this class. Once again, the muscles do not normally move by themselves - they are controlled by the somatic motor pathways of the nervous system along with the various forms of sensory feedback coming from tension and position receptors in the joints, ligaments and muscles themselves. Today, we will just look at the major anatomical arrangements of the nerves controlling the shoulder and upper limb. 1. Muscles of the upper limb traditionally are divided into two main groups, namely: **** Shoulder muscles **** Muscles of the freely moving limb (although some of these muscles do cross the shoulder joint...) Muscles of the shoulder a. Extrinsic muscles: Extending between the vertebral column or ribs and the scapula Trapezius Rhomboids Serratus anterior Levator scapulae Pectoralis minor Extending from the trunk to the humerus Latissimus dorsi Pectoralis major b. Intrinsic muscles: Extending between scapula and humerus Deltoid Subscapularis Supraspinatus Infraspinatus Teres minor Teres major >> Which of these muscles form the rotator cuff of the shoulder joint? >> What are the functions of the rotator cuff muscles?

2.

c.

Identify the muscle groups elevating, depressing, rotating, protracting and retracting the scapula.

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Remember that some apparently simple movements of the scapula require the action of more than one muscle group. d. Identify the muscles which act on the glenohumeral joint as flexors, extensors, abductors, adductors, lateral and medial rotators. >> How often do these movements occur simply, ie by themselves? >> How do the sites of their attachments to bones determine the movements generated by the muscles? >> What specialisations of the bones increase the efficiency of these movements? >> Think carefully about the actions of muscles in the real world - for example, how can the deltoid, traditionally identified as an abductor, control adduction?

e.

>> How do muscles acting on the scapula and muscles acting at the glenohumeral joint work together in generating co-ordinated movements of the shoulder? Note that muscles that usually cause movements at the shoulder joint can do other things as well. In particular, remember that muscles exert forces at both ends! Consider the pectoralis major, for example... what happens when you fix the ends of your arms (eg by leaning on them) and then contract the pectoralis major? Hint: why do you fix the ends of your arms when you are puffing?

f.

*************************************************************************** time out - - - eccentric muscle contractions Usually, when a muscles contracts and exerts a force, the muscle shortens in length. This is called a concentric contraction, and is the usual way we think about muscles working. However, muscles also can exert a force as they lengthen - this is called an eccentric contraction. Eccentric contractions are surprisingly common - you will see more about them when we look at walking later in the course and often go on at the same time as a concentric contraction of an opposing muscle. When might this happen? It turns out that muscles tend to expend more energy when they are contracting eccentrically than when they are contracting concentrically. They also are more likely to tear during an eccentric contraction. Why this is so is not clear - at least partially because it is not entirely clear what is happening at a molecular level under these conditions... However, one of the big problems is trying to anticipate what is going to happen next when an external force (due to gravity, movement of the body itself or whatever) is being applied. ***************************************************************************

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3.

Muscles of the Arm The muscles of the arm (ie brachium) are mostly involved with flexing and extending the elbow: Flexors: Biceps brachii (the brachii is important - there is another biceps in your lower limb!) Brachialis [NOTE: there is another elbow flexor, brachoradialis, that is found in the forearm - more about this later] Extensor: Triceps Identify the position and attachments of these muscles, the joints they act upon and the range of movement they cause whilst contracting. >> What is the difference in the functions of the brachialis and biceps brachii in flexing the elbow? How do these differences relate to their distal attachments? >> Why do the proximal heads of biceps brachii and the long head of triceps cross the shoulder joint? Another muscle also is present in the arm, namely the coracobrachialis. It goes from the coracoid process to the humerus and has an important role on stabilising the shoulder joint, especially when it is moving whilst loaded under tension. It is not involved in moving the elbow. Remember that the elbow also is flexed by another muscle that is in the dorsal compartment of the forearm, known as brachioradialis. We will see more about its relations in a later class.

*************************************************************************** time out - - - length-tension curves If you plot out the relationship between the force generated by a contracting muscle and its length, you usually will get a bell shaped curve. In other words, if the muscle is stretched too much, the force development will decrease; and if the muscle is shortened too much, the force development also will decrease. Thus, there is an optimal length at which the muscle will develop maximal contractile force. At a molecular level, this corresponds fairly well to the region of maximum overlap between the actin-containing thin filaments and the myosin-containing thick filaments, so that there is the maximum number of cross-bridges to generate contractile force. (If you want to know more about these matters, look up any decent physiology textbook.) Throughout the musculo-skeletal system, muscle attachments to bones tend to be set so that the maximal mechanical advantage at a joint is achieved at a point where the length of muscles matches their peak force production. ***************************************************************************

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4.

Brachial plexus

Dont worry if you dont get time to look at all this material in this class - there will be a review session later when you can have another go. The brachial plexus is formed from the ventral rami of spinal nerves C5 to T1. It extends from the neck into the axilla and supplies the muscles of the upper limb. The plexus is a developmental device that ensures that the spinal nerves connect with the appropriate muscles of the upper limb as it grows from the limb bud. It should be noted right at the start that the posterior cord of the brachial plexus supplies all extensor muscles in the morphological posterior aspect of the limb distal to the axilla (armpit). The flexor muscles are supplied by the medial and lateral cords. More of this later. In the brachial plexus: a. b. The five ventral rami sometimes are termed the "roots" of the brachial plexus. The five ventral rami combine into 3 trunks: Upper ( = superior) Middle Lower ( = inferior) c. d. : : : from rami C5 and C6 from rami C7 from rami C8 and T1

Each of the three trunks splits into an anterior and posterior division. The divisions recombine into 3 cords. Lateral cord Medial cord Posterior cord : : : from anterior divisions of the upper and middle trunks from anterior division of the lower trunk from the posterior divisions of all three trunks.

e.

The cords then give rise to the main nerves of the upper limb: Musculocutaneous nerve Ulnar nerve Radial nerve Axillary nerve (= circumflex) Median nerve : : : : : from the lateral cord from the medial cord from the posterior cord from the posterior cord from the lateral and medial cords

>> From which segments are each of these nerves derived?

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f.

The brachial plexus also gives rise to nerves supplying the pectoral muscles and muscles of the shoulder region. Identify the origin, course and target of each of the following nerves: Nerve Dorsal scapular Suprascapular Long thoracic Medial pectoral Lateral pectoral Thoracodorsal Subscapular Axillary Origin Muscle

>> Where, and under what circumstances, might some of these nerves be injured? g. Note that the nerves derived from the brachial plexus contain various combinations of somatic motor fibres, autonomic fibres and sensory fibres. We will look more carefully at the distal target of these nerves in a subsequent class.

h.

What are relationships of the brachial plexus (especially the cords) to the axillary artery?

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wrists, hands and fingers

In this class, we will look at the structure of the wrist, hand and fingers, and the muscles that move them. Many of these muscles are not in the hand itself, but in the forearm, with some of the muscles having their proximal attachments at the humerus. In trying to understand and learn the roles of the various muscles in generating the movements of the hands, it is easiest to think of the muscles as making up a series of natural groups. These groups are defined by the position of the muscles, their actions, and their innervation. 1. a. Bones and joints Wrist: 8 carpal bones are arranged in 2 rows. The proximal row articulates with the radius to form the radio-carpal joint. This joint acts as an ellipsoid or condyloid joint allowing flexion, extension, abduction, adduction and circumduction. The carpal bones are separated from the ulnar by a fibrocartilage disk. - proximal row of carpals = scaphoid, lunate, triquetral, pisiform - distal row of carpals = trapezium, trapezoid, capitate, hamate >> Which movement of the wrist has greater range: abduction (radial deviation) or adduction (ulnar deviation)? What is the anatomical reason for this? Why would this difference have evolved? >> The scaphoid is commonly fractured in young adults falling on outstretched hands. Why does this sometimes result in a surprisingly troublesome injury? >> Which bones make up the carpal tunnel? >> The pisiform is not really part of the main carpal bone series, but is a sesamoid bone. Which tendon is it associated with?

b.

Hand:

5 metacarpal bones each having a base, a shaft and a head. 3 phalanges for each of the fingers but only 2 for the thumb.

Joints:

For each of the following joints, identify: a. bones forming the articulation b. type of articulation c. ligaments strengthening or stabilising the articulation d. movements of the articulation and their range Intercarpal joints: Mid-carpal joints: Irregular surfaces, permitted. little movement is

i. ii.

Between bones of proximal and distal rows, slight displacement only during forced flexion and extension.

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iii.

Common carpometacarpal joints:

Because of irregular articular surfaces and tight ligaments they are largely nonmovable, except for: Saddle joint, critical in allowing flexible movements of the thumb, as in : Opposition-reposition Abduction-adduction Circumduction

1st carpometacarpal joint:

The flexibility of the first carpometacarpal joint is essential allowing the opposition of the tip of the thumb against the ends of the other fingers in a wide variety of precision and power movements. >> How much movement is there at the 5th carpometacarpal joint? Why?

iv.

Metacarpophalangeal joint:

Condyloid joints, important in the gripping movements of the hand. - extension-flexion - abduction-adduction - circumduction - passive rotation

>> How does the degree of flexion and extension at these joints affect their range of abduction-adduction? >> Why is there so much passive rotation at these joints?

v.

Interphalangeal joints:

These articulations are hinge joints, allowing only flexion and extension.

>> If you look at these joints carefully, you can see that they are really a kind of double condyloid joint - how does this arrangement restrict their range of movements? >> The proximal interphalangeal joints have wider range of flexion-extension than the distal joints. How does this interact with the way we grip things?

Study the radiological anatomy of the hand and compare the articulated bony hand with X-ray pictures. Match up the features on the skeleton and radiographs with the bony features on your own hands.

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*************************************************************************** revision time out - - - types of joints Joints can be classified functionally according to their shape or according to the types of movements they allow. Obviously, the two characteristics are related. A typical classification is: degrees of freedom 1 - uniaxial type hinge bicondyloid axle condyloid (=ellipsoid) movements flexion-extension flexion-extension rotation flexion-extension abduction-adduction circumduction

2 - biaxial

3 - multiaxial

ball and socket flexion-extension abduction-adduction circumduction rotation saddle flexion-extension abduction-adduction circumduction rotation

Of course, the exact range of movement is determined not only by the joint itself, but the ligaments and muscles crossing the joint. You should be able to think up examples of each of these joint types. *************************************************************************** 2. Muscles of the forearm

The muscles of the forearm are classified initially into two main groups: - those on the flexor aspect = anterior or ventral compartment - those on the extensor aspect = posterior or dorsal compartment Each compartment is arranged in a series of layers. On both sides of the forearm, the most superficial muscles move the wrist. Most of the remaining muscles move the fingers and thumb. Most of the extensors have a common attachment to the lateral epicondyle of the humerus, whilst most of the flexors have a common attachment to the medial epicondyle of the humerus. The forearm muscles attach to bones in the wrist and digits via long tendons, which are held in place by bands of connective tissue called retinacula on each aspect of the wrist. The tendons are surrounded by synovial sheaths which provide lubrication as the tendons move to and fro deep to the retinacula.

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The muscles of the forearm include many muscles that move the fingers and thumb. These muscles comprise the extrinsic hand muscles.

a.

Muscles of the flexor aspect of the forearm Majority arise from the medial epicondyle of the humerus and pass across both the elbow and wrist joints to gain insertion upon the metacarpals or the phalanges. These muscles can be divided into three layers: i. Superficial: pronator teres flexor carpi radialis palmaris longus flexor carpi ulnaris flexor digitorum superficialis flexor digitorum profundus flexor pollicis longus pronator quadratus

ii. iii.

Intermediate: Deep:

The tendons of the finger flexors pass into the hand via the carpal tunnel and share a common synovial sheath in the tunnel. Note carefully the locations and distal attachments of the superficial and deep finger flexors: - the superficial flexors attach to the middle phalanx of each finger, and are mostly involved in precision movements of the fingers; - the deep flexors attach to the distal phalanx of each finger and are mostly involved in power movements of the fingers. >> How is this arrangement achieved? >> To see the difference between these muscles working, look at the flexor side of your wrist whilst wriggling your fingers compared with making a tightly clenched fist. >> Why are these muscles so long?

b.

Muscles of the extensor aspect of the forearm Many of these muscles have a proximal attachment to the lateral epicondyle of the humerus. They form two layers: i. Superficial: brachioradialis (an elbow flexor !!!) extensor carpi radialis longus

32

extensor carpi radialis brevis extensor digitorum extensor digiti minimi extensor carpi ulnaris All the superficial extensor muscles have a proximal attachment to the lateral epicondyle of the humerus. ii. Deep: supinator abductor pollicis longus extensor pollicis brevis extensor pollicis longus extensor indicis

The extensor muscle tendons, on the dorsum of the hand run in 6 compartments, each with its own synovial sheath, set from radial to ulnar in the following order: - Abductor pollicis longus and extensor pollicis brevis - Extensor carpi radialis longus and brevis - Extensor pollicis longus - Extensor digitorum and extensor indicis - Extensor digiti minimi - Extensor carpi ulnaris The tendons of the finger extensors end in a broad expansion over the distal ends of the fingers, called the extensor hood, expansion, or sheath. >> Look at the extensor compartment of your forearm while you are making a tightly clenched fist. Which muscles are contracting on the extensor side? Why? >> Why would you have an extra extensor muscle each for the index finger and for the little finger? >> Where is the anatomical snuff box? Why do you need to know? 3. Intrinsic muscles of the hand

The intrinsic muscles of the hand mostly are involved in precision movements of the thumb and fingers. The only muscles causing abduction and adduction of the fingers are intrinsic to the hand. The intrinsic hand muscles are arranged in 3 groups (their names describe their function) a. Thenar - moving the thumb: abductor pollicis brevis flexor pollicis brevis opponens pollicis adductor pollicis (part of this muscle is really a palmar interosseus muscle, in the mesothenar group)

33

b.

Mesothenar - associated with all the digits dorsal interossei - abduct digits II, III, IV palmar interossei - adduct digits II,IV,V (and thumb, as part of adductor pollicis) lumbricals - flex the metacarpophalangeal joint and extend the inter-phalangeal joints of the fingers (not the thumb) Hypothenar - moving the little finger abductor digiti minimi flexor digiti minimi opponens digiti minimi

c.

Note that the hypothenar muscles form a mirror image of the thenar muscles, and do more or less the same things. >> The lumbricals (earthworms) are odd in that they run between the tendons of two other muscles, namely flexor digitorum profundus and extensor digitorum. They work together with these muscles to cause flexion of the metacarpophalangeal joints and extension at the interphalangeal joints. How? 4. Innervation Learning the basic innervation of the forearm and hand muscles is easy: - three named nerves derived from the brachial plexus are involved: radial nerve median nerve ulnar nerve. - all of the muscles in the posterior compartment are innervated by the radial nerve, no matter what they do. - none of the intrinsic muscles of the hand is innervated by the radial nerve. - most of the forearm flexors are innervated by the median nerve. - the forearm flexors that not are innervated by the median nerve are innervated by the ulnar nerve - they are flexor carpi ulnaris and the ulnar half of flexor digitorum profundus, past which the ulnar nerve runs. Easy! - the thenar muscles are innervated mostly by the median nerve. - the hypothenar muscles are innervated by the ulnar nerve (which runs down the little finger side of the forearm - easy!). - the interosseus muscles are innervated by the ulnar nerve, including the bit of adductor pollicis that is really a palmar interosseus. - the lumbricals on the ulnar side of the hand (digits IV and V) are innervated by the ulnar nerve, the other two are innervated by the median nerve (what else could it be?)

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*************************************************************************** time out - - - power v precision: motor units How do we control the force, speed and precision of movement of our fingers? Many things are involved, especially in the CNS. But the basic building blocks of this control can be seen in the periphery. For any individual muscle fibre, the speed of contraction is inversely related to the applied load: the greater the load, the slower the contraction, and vice versa. However, the real trick lies in the way in which the motor neurons are connected up to the muscle fibres. Each motor neuron and the muscle fibres it innervates comprise a motor unit. Some motor neurons innervate only a few muscle fibres (as small as 2 or 3), forming a small motor unit, whilst other motor neurons innervate many muscle fibres (up to several hundred), forming a large motor unit. Fine control is achieved by activating small motor units, whilst coarse control mostly involves large motor units. When a graded increase in force or speed of muscle contraction is required, smaller motor units are recruited first, followed by larger and larger motor units. The level of activation of motor units required for a particular movement under a particular load is determined initially by feedback (from proprioreceptors and tension receptors etc) and then, after repetition, by experience. Part of training or practice in co-ordination or strength skills involves learning to use the minimum number of appropriate motor units to do the required task. Some of the smallest motor units in the body are in the intrinsic muscles of the hands. In skilled manual tasks, individual small motor units may be recruited as required. ***************************************************************************

35

pelvis and hip joint

The pelvis and hip joints of humans are adapted to allow efficient bipedal locomotion, whilst at the same time allowing for the birth of large-brained babies. This means that there is a trade-off in the design of the pelvis, since efficient bipedal locomotion requires the hip joints to be as close to the midline as possible (why??), while big-brained babies require as large a pelvis as possible. Many of the special features of the pelvis are related to the distribution of loads generated during weightbearing exercise, such as walking, running and jumping. 1. The bony pelvis is formed by the two hip bones and the sacrum. The space in and above the bony pelvis is the pelvic cavity. The linea terminals subdivides it to the upper greater pelvis and lower true pelvis. The hip bone, during fetal life and in babies, is composed of three bones, the ilium, ischium, and pubis. They are fused together at the acetabulum. In many animals, these three components of the pelvis remain separate from each other. The shape of the pelvis helps align the muscles of the hip joint to maximise their mechanical advantages during standing and locomotion. It also provides support and protection for the abdominal and pelvic organs in our upright posture. Note that the pelvis effectively consists of a series of arches diverging away from the acetabulum. First, identify the principal named parts of the hip-bone. Place the hip-bone from a halfskeleton alongside a living model, and identify the following bony landmarks both on the bone and the model (You can use yourself as the model..!!): iliac crest anterior superior iliac spine anterior inferior iliac spine pubic tubercle ischial tuberosity posterior superior iliac spine centre of sacroiliac joint 3. a. The intact pelvis has a superior aperture (linea terminalis), a cavity and an inferior aperture. The latter is formed by the pubis, ischium and the sacrum together with the sacrospinous and sacrotuberous ligaments. The inferior aperture or pelvic outlet is supported by the perineal muscles (levator ani and urogenital diaphragm). Compare the dimensions of the three parts (inlet, cavity and outlet). Position the articulated pelvis alongside the living model, in the standing and sitting positions. >> How does the orientation of the pelvis and the palpable features of the hip-bone change when we sit down? >> What happens to the pelvis when you slouch forward while sitting down? >> How is the weight of the body transmitted from the vertebral column to the floor in the two cases?

2.

b.

36

4.

Look at the shape of the sacrum (formed by the fusion of 5 sacral vertebrae) and note how it is slotted between the two hip-bones. Two displacements of the sacrum must be prevented: - downward displacement of the whole sacrum. - forward rotation of the upper part of the sacrum, with backwards rotation of the caudal part, pivoting around the sacro-iliac joints. There are two main sets of ligaments preventing these displacements: - the short sacro-iliac ligaments; - the sacrospinous and the sacrotuberous ligaments >> Where are these ligaments? >> Which movements do they prevent?

5.

The hip joint is formed by the head of the femur and the acetabulum. It is a deep ball and socket joint, with three degrees of freedom of movement allowing: - flexion / extension - abduction / adduction - circumduction - medial and lateral rotations The acetabulum is deepened somewhat by a rim of fibrocartilage, the acetabular labrum. The joint capsule is thickened and reinforced by three strong ligaments: iliofemoral, pubofemoral and ischiofemoral ligaments. >> How do the ligaments restrict the possible movements and stabilize the joint? >> Is the hip more or less stable than the shoulder? Why? >> In particular, look at the role of the iliofemoral ligament in supporting the body weight during quiet standing.

6.

The hip joint is surrounded by strong sets of muscles that act to generate and control the movements of the hip joint. Many of these muscles run from the pelvis to the proximal end of the femur, and are similar in arrangement and function to the corresponding muscles of the shoulder. Use the prosected specimens to identify the following muscles associated with the hip joint. All of them attach to the proximal parts of the femur. Examine both their proximal and distal attachments in order to see how they work in generating the movements of the hip. ilio-psoas internal obturator external obturator piriformis quadratus femoris flexor lateral rotator * lateral rotator * abductor * adductor *

37

gluteus minimus gluteus medius gluteus maximus

medial rotator, abductor # medial rotator, abductor # extensor, lateral rotator #

* These muscles are somewhat similar to the rotator cuff muscles of the shoulder in their arrangement and functions. Their main function probably is to provide dynamic stability to the hip joint during a wide range of movements. The lateral rotators play an important role in keeping the feet pointing forward during walking. # The gluteal muscles as a group have some similarities in arrangement and function to the deltoid muscle of the shoulder. The gluteus medius and minimus muscles have a vital role in walking, contracting on the same side as the leg supporting the body weight. Here they abduct to stop the body falling toward the unsupported side as the free leg takes a forward stride. They also generate a medial rotation from the supported side to swing the pelvis forward. There also are several other muscle groups that generate movements of the hip joint: they mostly form the muscles of the thigh. Most of them also have actions at the knee joint. They include: adductors hamstrings rectus femoris adduct hip extend hip, flex knee flex hip, extend knee

We will look at these muscles and their functions more fully in a subsequent class... 7. a. The muscles of the pelvis and lower limb are innervated by nerves arising from the lumbosacral plexus. Lumbar plexus The lumbar plexus is formed from the ventral rami of L1 - L3 and the superior part of L4. It gives rise to two main nerves, the obturator and the femoral nerves, which supply muscles of the lower limb. On the prosected specimens, observe the formation of the obturator and femoral nerves from the lumbar plexus and follow their path through the pelvis and its associated structures. >> The lumbar plexus also gives rise to the ilioinguinal and iliohypogastric nerves. What muscles do they supply? b. Sacral plexus The sacral plexus is formed from the ventral rami of the inferior part of L4 and L5 - S4. The largest nerve derived from this plexus is the sciatic nerve, which in turn forms two major branches, the common peroneal and tibial nerves. Also derived from the sacral plexus are the superior and inferior gluteal nerves. On the prosected specimens, trace the origin and path of the sciatic nerve through the pelvis and its associated structures. >> What are their relations to the muscles of the hip and the foramina of the pelvis?

38

Further Problems >> Why is the hip usually dislocated backwards? >> Consider the consequences of the anatomical construction of the pelvis, especially the dimensions of the inlet and outlet, during delivery of a baby. >> What soft tissue injuries would you expect to find associated with pelvic fractures? >> How can a dancer or a gymnast produce such extreme movements of the hip joint? >> Stand upright beside a wall, touching it, but not leaning against it. Now try to abduct the leg on the side away from the wall. What is going on?

39

BONES AND JOINTS OF THE LOWER LIMB

In this class, you will be dealing with the individual bones and joints of the lower limb, including the foot. Overall, the plan of the bones and muscles of the lower limb is similar to that of the upper limb, but with obvious modifications associated with weight bearing and bipedal locomotion. 1. Identify the following features of the lower limb bones on dry bones, on wet specimens, and, where possible, their surface markings on yourself: Femur (thigh bone) head, neck, greater and lesser trochanters, inter-trochanteric line, shaft, medial and lateral epicondyle, intercondylar fossa, patellar surface, popliteal surface, medial and lateral condyles

The femur is angled inwards towards the midline to bring the lower part of the limb closer to the centre of gravity. >> Why is this important for efficient walking and running? >> Why is the femur curved in the anterior-posterior plane? Patella (knee cap) Tibia (shin bone) medial and lateral condyles, intercondylar eminence, medial and lateral intercondylar tubercles, tibial tuberosity, shaft, medial malleolus, fibular notch

>> The tibia is most commonly broken distally. Why? Fibula head, lateral malleolus

The fibula is attached to the tibia proximally by the proximal tibiofibular joint (a gliding synovial joint) and distally by the tibiofibular syndesmosis, a peculiar fibrous joint. Most of the shaft is joined to the shaft of the tibia by a strong interosseus membrane. Tarsals (ankle) talus, calcaneus (heel bone), navicular, cuboid and three cuneiforms base, head, shaft (x5)

Metatarsals (foot)

The tarsals and the metatarsals combine to form the arches of the foot. More about this below... Digits (toes) proximal, middle and distal phalanges for digits II-V; proximal and distal phalanges for digit I (big toe = hallux)

40

2.

Joints of the lower limb You should be familiar with the following items on each of the principal joints: a. b. c. d. The articular surfaces of the component bones The nature of the articular capsule (slack or taut, thin or thick etc) The ligaments reinforcing the joint The movements occurring at the joint and their normal range.

Hip joint Revise the features contributing to the unique construction of the hip joint that allows relatively free movement with the combination of admirable stability. Knee The knee is a complex modified hinge joint. It main movements are flexion and extension, although there is a reasonable amount of rotation possible when the knee is flexed. There normally is no adduction or abduction. The joint has to bear very large loads during locomotion, and the articular surfaces are greatly expanded to accommodate these loads. Indeed, the articular surface of the femur is much greater than that of the tibia, so that there is considerable gliding of the joint surfaces past each other during flexion and extension. The mobility of the joint is controlled largely by four ligaments: the anterior and posterior cruciate ligaments and the medial (tibial) and lateral (fibular) collateral ligaments. Nevertheless, much of the strength of the joint comes from the muscles that cross it. a. The cruciate ligaments act together to maintain contact and alignment of the femur and tibia during the flexion-extension cycle. The anterior cruciate prevents hyperextension, whilst the posterior cruciate is under more tension during flexion of the knee. However, because the way they cross over each other, the ligaments are relatively taut throughout the flexion-extension cycle, and, together with the collateral ligaments, they help to fix the axis of movement of the joint. Identify the cruciate ligaments in the wet specimens and observe their interactions during the flexion-extension cycle. Note that the cruciate ligaments lie within the joint capsule but are outside the synovial cavity. >> How do the cruciate ligaments interact to "lock in" the fully extended knee? >> Under what conditions are you most likely to damage the anterior or the posterior cruciate ligament? b. The tibial (medial) and fibular (lateral) collateral ligaments are formed from thickenings of the joint capsule. Their main function is to prevent abduction and adduction of the knee joint. >> The medial collateral ligament is more likely to be damaged than the lateral collateral ligament. Why? c. The knee joint contains two large intra-articular fibrocartilage disks, or menisci, that project into the synovial cavity from the joint capsule. The lateral meniscus is

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more free to move than the medial meniscus, which is tied to the medial collateral ligament. Both menisci are tied to the tibia and each other by the transverse ligament. The function of the menisci is still not really understood - they probably do not absorb much load themselves - rather, they probably help spread the synovial fluid over the large articular surfaces of the joint, especially over the femur. >> When are the menisci most likely to be damaged? >> Why is the medial meniscus more likely to be the one that is damaged? d. The knee has a very large and complex synovial cavity with out-pocketings (bursae) between the patella and the femur that extends proximal and distal to the patella itself. The extent of the synovial cavity is not the same as the joint capsule. >> What is the functional significance of the supra- and infrapatellar bursae? e. The patella is really a sesamoid bone within the tendon of the quadriceps muscle. It helps to protect the anterior aspect of the knee joint and increases the mechanical advantage of the quadriceps. >> Compound fracture of the patella is quite common, with poor prospect for healing. Why? Ankle (talocrural joint) The ankle also is a modified hinge joint. It allows flexion (towards the sole of the foot = plantar flexion) and extension (towards the top of the foot = dorsiflexion). The joint is formed proximally by the medial malleolus of the tibia and the lateral malleolus of the fibula, and distally by the talus, which is the only bone of the foot to articulate with the leg. Because of the shape of the talus, which is wider anteriorly than posteriorly, the ankle is much more stable in the dorsiflexed position than in the plantarflexed position. The talocrural joint is strengthened by the medial and lateral collateral ligaments of the ankle. They run from the malleoli to the tarsal bones. >> Under what conditions are the collateral ligaments of the ankle most likely to be damaged? >> How does the range of movements at the talocrural joint compare with that of the radiocarpal joint? Intertarsal joints The joints between the tarsal bones allow the foot to change shape and orientation so that maximum contact is maintained with the ground during a variety of movements over a range of terrains. Eversion means turning the foot outwards, so that the plantar surface (sole) tends to face laterally. The opposite movement is inversion, so that the plantar surface turns to face more medially.

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The movements of inversion and eversion of the foot occur at three of the intertarsal joints: Subtalar joint Talocalcaneonavicular joint Calcaneocuboid joint The last two constitute the transverse or midtarsal joint. If you make the inversion-eversion movement with your toes and ankle strongly dorsiflexed, then the movement is taking place almost entirely at the subtalar joint, with the axis of the movement running almost longitudinally down the foot. If you move your foot from a fully everted position to a fully inverted position with your ankle and toes strongly plantarflexed, you also will be moving at the transverse tarsal joint, which more-or-less flexes and twists during the movement, allowing a greater degree of inversion to occur. Identify on the dry and wet specimens and on yourself, how these movements of inversion and eversion take place.

>> What types of movements occur between each of the tarsal bones themselves? The tarsometatarsal and the metatarsophalangeal joints are similar in shape and function to the carpometacarpal and metacarpophalangeal joints of the hand. The metatarsophalangeal joints allow flexion-extension, abduction-adduction and circumduction, just as in the hands. In the foot the axis for abduction-adduction is centred on the second digit (not the third as in the hand). Arches of the foot The human foot is characterised by its arches: the lateral and medial longitudinal arches and the transverse arch. The highest point of the arches is the apex of the medial longitudinal arch (instep) which corresponds to the talus. During quiet standing, weight is supported evenly by the heels and the distal ends of the metatarsals. During walking, weight is transferred forward from the heel, along the lateral longitudinal arch, and then medially across the transverse arch to the big toe. The medial longitudinal arch flexes and absorbs some of the impact forces setup during the transfer of weight in the walking cycle. Both the bones and ligaments of the foot are important in maintaining the longitudinal and transverse plantar arches: -- The bones lock together like the blocks in a stone arch (especially across the transverse arch); -- They are held together by a series of short strong ligaments on both their dorsal and plantar surfaces. -- The ends of the arches are tied by the plantar aponeurosis that underlies the skin of the foot. -- The longitudinal arches are supported on the plantar side by strong longitudinal ligaments. -- The plantar calcaneonavicular ligament contains elastin, which helps support the talus at the apex of the medial longitudinal arch, while allowing it absorb and spring back from deforming forces generated during weight bearing.

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-- During activity, the intrinsic and extrinsic muscles of the foot help to provide dynamic support for the arches, but during quiet standing, the ligaments do it all. Define the components of the arches: Medial longitudinal arch Lateral longitudinal arch Transverse arch

>> How much energy does you foot absorb (and give back to you by elastic recoil) compared with fabulously expensive sports shoes?

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MUSCLES AND MOVEMENTS OF THE LOWER LIMB

During quiet standing, very few muscles are used to support the body weight. However, once we start walking, all of the muscles of the lower limb are used at least once in the walking cycle. During running, the muscles are used very efficiently, with the tendons and muscles themselves storing and releasing a lot of energy as elastic deformation. The best way to understand about how these muscles work is to think of them as functional groups, rather than individual muscles with individual actions.

1.

Hip and Gluteal Region You have already examined the muscles of this region in the class on the pelvic girdle. Revise the locations and actions of these muscles in standing, walking and climbing. In addition, note the location of the tensor fasciae latae muscle which applies longitudinal tension to the ilio-tibial tract. It helps to support the pelvis along with the gluteus medius and minimus muscles, and is very important is stabilising the knee in almost any position from fully flexed to fully extended.

2.

Thigh Muscles In the thigh, there are three distinct sets of muscles, forming anterior, posterior and medial groups. a. Anterior group These muscles mostly are united into one large powerful muscle, the quadriceps femoris. This muscle has four components: rectus femoris vastus medialis vastus lateralis vastus intermedius - flex hip, extend knee - extend knee - extend knee - extend knee

All the components of the muscle join into a common tendon which contain the patella and attaches distally to the tibial tuberosity. On the prosections, look carefully at the orientation of the muscle fibres in each part of quadriceps. Why are they arranged the way they are?

Running across the anterior aspect of the quadriceps is sartorius. It is able to flex both the hip and the knee joints. How? Its name means belonging to a tailor. What characteristic action of the lower limb does it contribute to?

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b.

Posterior group These are also known as the "hamstrings" (why?) and contain three muscles: - biceps femoris - semimembranosus - semitendinosus (lateral) (medial, deep) (medial, superficial)

All of them share a common proximal attachment at the ischial tuberosity, and they extend to attach to the tibia or fibula just distal to the knee. Thus, they extend the hip and flex the knee, but have difficulty doing both at once. As in many of the muscles of the lower limb, they do much of their work eccentrically, acting to slow the forward movement of the limb prior to the heel making contact with the ground. Identify the distal tendons of these muscles on yourself. >> Why are the hamstrings torn to frequently? >> Why are they so long? >> What is meant by a torn muscle?

c.

Medial group These muscles all adduct the thigh. Identify the size, location and attachments of the following muscles: - pectineus - gracilis - adductor longus - adductor brevis - adductor magnus These muscles act together in a similar way to the pectoralis major and latissimus dorsi muscles acting on the upper limb: ie, they pull the lower limbs back towards the midline from wherever they have been. This means that they are active during nearly every phase of the walking cycle. Make sure you understand why... >> Sporting types often refer to pulling a groin muscle. What muscles are they talking about? Why do they get injured?

3.

Leg muscles The muscles of the (anatomical) leg are grouped into three compartments separated by strong fasciae. These muscles are similar in their overall arrangement to the forearm muscles. Here they mostly flex and extend the ankle and toes. Remind yourself why the muscle mass is concentrated as proximally as possible within the limbs.

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a.

Anterior (extensor) compartment tibialis anterior extensor hallucis longus extensor digitorum longus

- extends (dorsiflexes) ankle - extends big toe - extends digits

Determine the surface markings of these muscles and their tendons on yourself. Note that as the tendons pass to the foot, they are held in place by extensor retinacula at the ankle. >> When are these muscles likely to be active? Work it out for yourself by watching your feet as you walk around bare-footed... b. Lateral (peroneal) compartment fibularis / peroneus longus - everts and plantarflexes ankle and helps support the arches during locomotion fibularis / peroneus brevis - everts the foot Determine the surface markings of these muscles and trace the course of their tendons. It is easy to see them if your try to evert your foot against some resistance. c. Posterior (flexor) compartment These muscles all flex (plantarflex) the ankle and toes. As the tendons pass to the foot, they are held in place by flexor retinacula at the ankle. This compartment is sub-divided into a superficial and a deep component. Superficial: triceps surae = gastrocnemius and soleus - plantarflex ankle

Identify their surface markings and their common attachment to the calcaneal (Achilles) tendon. Deep: tibialis posterior flexor digitorum longus flexor hallucis longus - flex ankle, support arch - flex toes - flex big toe

These are important and powerful muscles that provide the force for pushing off from the ankles and toes during walking running and jumping. The tendons of these muscles also are important in storing a large amount of elastic energy which can be regained during the rebound phase of running. >> What are their functions during quiet standing?

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4.

Intrinsic muscles of the foot The intrinsic muscles of the foot are arranged in three functional groups, similar to those in the hand: Thenar Mesothenar Hypothenar (medial group for big toe) (central group) (lateral group for fifth digit)

They mostly act to change the shape of the foot, the positions of the toes, and some (eg the lumbricals, quadratus plantae) also modify the actions of some extrinsic muscles. These muscles form 4 main layers beneath the plantar aponeurosis First layer: (most superficial) Second layer: Third layer: abductor hallucis flexor digitorum brevis abductor digiti minimi quadratus plantae (= flexor accessorius) lumbricals (four) flexor hallucis brevis adductor hallucis (oblique and transverse heads) flexor digiti minimi brevis interossei (4 dorsal = abduct, 3 plantar = adduct)

Fourth layer: (deepest)

Identify these muscles on the prosected specimens and plastic models. Which of them can you see working in your own feet?

5.

Motor innervation of the lower limb The lower limb is innervated by nerves arising from the lumbosacral plexus. Sciatic nerve -> muscles in posterior compartment of thigh eg hamstrings -> branches = tibial nerve -> posterior leg muscles -> medial & lateral plantar nerves of foot = common peroneal nerve -> branches = deep peroneal nerve -> anterior leg mm = superficial peroneal nerve -> lateral leg mm Femoral nerve -> muscles in anterior compartment of thigh eg quadriceps. Obturator nerve -> muscles in medial compartment of thigh eg adductors. (except...... femoral n -> pectineus, usually; sciatic n -> posterior part of adductor magnus)

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6.

Summary of walking When you take a step (leading with the right leg, in this example): a The gluteus medius and minimus muscles on the side supporting your weight (here, the left side) contract. They abduct the pelvis, raising it slightly on the opposite side (the right side, where the leg is swinging forward). They also medially rotate the pelvis, swinging the non-weight bearing (right) side forward. b The (right) leg that is stepping forward is flexed at the hip by the quadriceps and the iliopsoas, and at the knee by the hamstrings. The ankle and toes are dorsiflexed by tibialis anterior and the toe extensors to help stop them dragging along the ground. The swinging (right) leg is rotated laterally by the deep muscles of the hip. This ensures that the foot is facing forward in the direction of movement when it hits the ground. Prior to heel strike, the hamstrings on the forward swinging (right) leg start to contract eccentrically to slow the leg down. At heelstrike, the ankle and toes are dorsiflexed and stabilised by the anterior muscles of the shin. They contract eccentrically to control the transfer of weight from the heel to the rest of the foot. Weight is transferred to the leading (right) foot by contraction of the plantar flexors of the weight-bearing (left) leg. The quadriceps on the right side contracts eccentrically to stop the right knee flexing under the newly applied body weight. The hamstrings extend the hip on the leading (right) side. ... and the adductors on both sides contract to bring the body over the leading (right) foot. Then the process is repeated on the other side as the (left) leg leads off. Got it? Try it for yourself. Work out where the muscle groups are on your own legs, and then slowly walk through the sequence while watching what is happening at your hips, knees, ankles and toes... The whole sequence normally takes less than a second!

d e

f g h i j

During steady walking and running, the legs develop considerable momentum as they swing forward. Much of the activity of the leg muscles is to control these ballistic movements, generally using eccentric contractions to oppose their "normal" actions. This is part of the reason why your muscles get tired and sore after walking down hill.

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Further Problems to Consider >> >> >> >> >> >> What are the consequences of common peroneal nerve injury (e.g. when the bumper of a car hits the lateral aspect of the knee?) Sit on a chair with your back straight and your feet flat on the floor. Try to stand up without leaning forward. What's going on? What structural deformation would lead to flat foot (pes planus)? Consider the consequences of not being able to invert and evert your feet in running, walking over rough ground, skiing, surfing, playing tennis ...... Why is flexor hallucis longus such a large muscle? We usually walk with our legs more-or-less straight when they are in contact with the ground, but with our knees bent during ground contact when running. Why?

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VERTEBRAL COLUMN AND MUSCLES OF THE TRUNK

The vertebral column is the flexible axis of the body and is composed of vertebrae, intervertebral discs and ligaments. 1. Study the parts of a typical vertebra first and identify the following structures on it: a. b. c. d. e. f. body arch (pedicles and laminae) spinous, transverse and articular processes vertebral foramen intervertebral foramina between two adjacent vertebrae the articular surfaces

2. Look carefully at the articulated vertebral column Identify the cervical, thoracic, lumbar, sacral and coccygeal regions of the vertebral column. >> How many vertebrae are there in each region? >> How do the vertebrae of each region differ? The vertebral column has four curvatures in the sagittal plane: Establish the two anterior convexities (lordosis) in the cervical and lumbar regions and the two posterior convexities (kyphosis) in the thoracic and sacral regions. You may also notice very slight lateral curvatures. If they are exaggerated with apparent accompanying rotation, the deformity is termed scoliosis. 3. The atlas and the axis Study the 1st (atlas) and 2nd (axis) vertebrae in detail. Since they take part in the formation of the occipital-vertebral joint, their structure is different from other cervical vertebrae. a. On the atlas (C1) identify: i. The anterior and posterior arch and the vertebral foramen. ii. The lateral masses and articular surfaces. The atlas articulates with the occipital bone of the skull through its superior articular facets and with the axis through the inferior facets. iii. Transverse process and transverse foramen. b. On the axis (C2) identify i. The body and the dens (odontoid process which represents the detached body of the atlas). ii. Spinous, articular and transverse processes and transverse foramen iii. Arch and vertebral foramen.

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4. Radiology Identify all the above mentioned parts of the vertebrae on lateral and antero-posterior radiographs. >> Can you see any other components of the vertebral column on radiographs?

5. Surface anatomy Establish, on yourself or another student, which vertebrae can be readily palpated. >> Which part of the vertebra is felt in each case?

6. Joints of the vertebral column Except for the first two cervical vertebrae, the fused vertebrae of the sacrum and the coccyx, the vertebrae articulate with each other via fibrocartilaginous joints (the intervertebral discs between the bodies) and synovial joints (between the articular processes). a. Fibrocartilaginous joints (intervertebral discs). Hyaline cartilage covers the upper and lower surfaces of the vertebral bodies. Between these surfaces identify the intervertebral disc. The disc is subjected to a combination of compression, bending and torsional forces. It bears and distributes loads and restrains excessive movement. It has two components: i. The annulus fibrosus composed of fibrocartilage. Collagen fibre bundles in a crisscross arrangement withstand high bending and torsional loads. ii. The nucleus pulposus is a gelatinous mass located within the annulus fibrosus. It contains hydrophilic glycosaminoglycans. The glycosaminoglycans content diminishes with age. The nucleus pulposus acts hydrostatically to distribute pressure throughout the disc. >> Measure your height first thing in the morning and last thing at night. Does your height change during the day? If it has changed, what can you attribute this to? >> Other than allowing movement, what other functions does the disc have? b. Facet joints (apophysial joints) Identify the joints between the superior articular facets of a vertebra and the inferior facets of the adjacent superior vertebra. These are plane type synovial joints. 7. Ligaments of the vertebral column Six ligaments reinforce the intervertebral joints. On the wet specimens identify i. the anterior longitudinal ligament, a dense band on the anterior surface of the vertebral bodies extending from C2 to the sacrum. ii. the posterior longitudinal ligament on the posterior surface of the vertebral bodies within the vertebral canal from C2 to the sacrum.

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iii. the ligamentum flavum, a thick elastic ligament which connects the lamina of adjacent vertebrae. iv. the interspinous ligament connecting the lower border of the spinous process of the vertebra above with the upper border of the spinous process below. v. the intertransverse ligament connecting the transverse processes of adjacent vertebrae. vi. the supraspinous ligaments between the tips of adjacent vertebrae. 8. Movements of the vertebral column. Limited movement occurs between the adjacent vertebrae. However, the compound effect of movement at several intervertebral joints produces a large range of movement. >> Determine the possible movements of the vertebral column on yourself or on another student and list them. >> Which part of the vertebral column is the most mobile? >> How does movement in the thoracic region compare with that in the cervical and lumbar regions? What structures promote and restrict movement in each region? Tilting and rotation occur at the fibrocartilaginous joints. Compare the height of the disc in relation to its anteroposterior and the mediolateral diameter in the cervical, thoracic and lumbar regions. >> How does disc height relate to the amount of movement that can occur? >> What happens to the disc during extension, flexion, lateral flexion and rotation? Tilting and gliding occur at the facet joints. Note the orientation of the articular surfaces of these joints in the cervical region the thoracic and lumbar regions. >> What effect does the orientation of the facets have on movement? >> How do the ligaments of the vertebral column influence its movements? >> What effect do the articulations between the ribs and the vertebra have on the mobility of the vertebral column? >> How does the pelvis contribute to the range of movement of the spine? 9. The atlanto-occipital and atlanto-axial joints The occipital bone, the first and the second cervical vertebrae move together as a multiaxial occipitovertebral joint with limited degree of movement. a. Note the shape of the superior articular facets of the atlas and compare their shape with that of the occipital condyles on the skull. >> What sort of movement occurs at the atlanto-occipital joint?

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b. The atlas articulates with the axis via two lateral (facet) joints and a median pivot joint between the dens of the axis and the osteo-ligamentous ring formed by the arch of the atlas and a transverse ligament. c. Many ligaments contribute to stability of these joints. i. the tectorial membrane between the body of the axis and the occipital bone is a continuation of the posterior longitudinal ligament. ii. the transverse ligament between the lateral masses of the atlas holds the dens of the axis in place. iii. the apical ligament extends from the tip of the dens to the occipital bone. iv. The anterior atlanto-occipital ligament is an extension of the anterior longitudinal ligament. v. Alar ligaments between the dens and the occipital bone limit rotation. >> At which of the above joints does nodding (flexion and extension) and lateral flexion occur? >> Where does rotation occur? d. Movements at the atlanto-occipital and atlanto-axial joints are generated by a complex of small deep muscles. They include: i. rectus capitis posterior major and minor ii. obliquus capitis superior and inferior >> What do these muscles do? 10. Muscles which act on the vertebral column As a rule the flexors are placed anteriorly, extensors and lateral flexors posteriorly, or laterally and the rotators obliquely in relation to the vertebral column. a. Flexors (prevertebral muscles) situated anterior to the vertebral column: i. the longus colli (capitis and cervicis) in the cervical and upper thoracic regions; ii. the psoas in the lumbar region. iii. rectus abdominis of the abdomen. This muscle extends between the xiphoid process and pubic tubercle. Along its course 3 or 4 tendinous intersections are present. These intersections extend across the entire thickness of the muscle. >> What importance do they play in the proper functioning of the muscle? >> What is the function of the rectus sheath? Name the aponeuroses forming the anterior and posterior walls of the rectus sheath. Note that the tendinous intersections of rectus abdominis are firmly attached to the rectus sheath. Determine the location of the arcuate line (of Douglas) and the linea alba.

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b. Extensors (postvertebral muscles) situated posterior to the vertebral column: i. superficial muscles: - splenius capitis and cervicis. Note these muscles are deep to the extrinsic muscles, trapezius, latissimus dorsi, levator scapulae and the rhomboids which move the upper limb. The upper fibres of trapezius assist in extension of the vertebral column. ii. intermediate muscles: - bands of muscles, the sacrospinalis or erector spinae, extending from the pelvis to the skull. (You do not need to learn the names of the individual bands). iii. deep muscles: - semispinalis extending from T10 to the occipital bone - rotatores running from transverse process of a vertebra to the base of the spinous process of the vertebra above. iv. quadratus lumborum extending from the 12th rib to the iliac crest and the iliolumbar ligament. c. Lateral flexors and rotators: Rotation is usually combined with some degree of lateral flexion. i. the extensor muscles acting unilaterally ii. multifidius in the groove on each side of the spinous processes extending from the sacrum to the axis iii. external oblique and internal oblique muscles of the anterior abdominal wall. Notice the origin and the course of the muscle fibres in each of these muscles. They insert into the aponeurosis of the muscle which forms the linea alba in the mid line. (The third and deepest abdominal muscle, transversus abdominis, is not involve in movement of the vertebral column but assists in supporting the loaded spine when lifting heavy objects.) iv. The intercostal muscles contribute to rotation.

11. Nerve supply to muscles acting on the vertebral column a. Postvertebral muscles are supplied by the dorsal rami of the corresponding segmental nerves. Each muscle (because they are long, flat substantial muscles) has a multisegmental nerve supply. b. Abdominal muscles are supplied by intercostal nerves 7 to 12, the ilioinguinal and the iliohypogastric nerves. c. Quadratus lumborum is supplied by the 12th intercostal and first lumbar nerves.

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12. Inguinal canal Study the boundary of the canal, its anterior and posterior walls, roof, and floor and finally the position of the superficial and deep inguinal rings. Anterior wall - aponeurosis of external oblique. Superior wall - lower margin of internal oblique. Posterior wall - transversalis fascia Inferior wall - inguinal ligament >> How long is the canal? >> What are the contents of the inguinal canal in the female and in the male? Problems to Consider: >> Why do fractures of the spine most commonly involve T12, L1 and L2. >> Dislocation or fracture of cervical vertebrae frequently occur in motor-car or aeroplane crashes why? What are the consequences of such injuries? >> The annulus fibrosus may rupture most commonly at L1 - L5, allowing the nucleus pulposus to protrude posteriorly into the vertebral canal (prolapsed intervertebral disc). What symptoms might this condition cause? >> What is the function of the muscles of the back when you are standing? >> Compare the mechanisms of direct and indirect inguinal hernia. >> What implications does the arrangement of the fibres of the external oblique, the internal oblique and the tranversus abdominis and the structure of the rectus sheath have for abdominal surgery? >> Why do you hold your breath when you lift a heavy load? Reminder Many of the muscles you have looked at today and in previous classes (including practical sessions last year!) are involved in respiration. inspiration diaphragm pectoralis major erector spinae quadratus lumborum sternocleidomastoid scalenes intercostals rotatores expiration abdominal muscles intercostals

>> How do each of these muscles contribute to respiratory movements?

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CARTILAGE
1. a specialised form of connective tissue comprised of "chondrocytes" which synthesise an amorphous, firm gel-like matrix. Properties * * * * * high tensile strength resilience and elasticity avascular and aneuronal capacity for continued rapid growth poor regenerative abilities

2.

Types of cartilage Hyaline cartilage: nose, larynx, trachea ventral ends of the ribs articular surfaces of synovial joints "model" for most developing bones ears, external auditory canal epiglottis parts of the larynx intervertebral discs pubic symphysis lining of tendon grooves attachments of some tendons to bones intra-articular discs Eustachian tube

Elastic cartilage:

Fibrocartilage:

3.

Embryology - origins from * neural crest * sclerotome * lateral plate mesoderm * interstitial growth (most of matrix) * appositional growth (perichondrium)

- two types of cartilage growth:

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4.

Matrix composition Hyaline cartilage: * * type II collagen embedded glycosaminoglycan matrix in highly hydrated

basophilic matrix around chondrocytes

Elastic cartilage:

similar to hyaline cartilage but penetrated by meshwork of elastin

Fibrocartilage:

transitional between cartilage and dense connective tissue * * * * sparse matrix with large bundles of type I collagen acidophilic always in association with other connective tissues no true perichondrium

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BONE AND BONE FORMATION

Bone is a specialised connective tissue, its main distinguishable feature is that the interstitial part contains inorganic components in the form of calcium hydroxyapatite crystal deposition. The outer and inner surfaces of the bone are covered with periosteum and endosteum, respectively, which contain blood vessels, nerves, and cells capable of making and remodelling bone. Composition: i. ii. iii. iv. Structure: osteocytes, maintain the bone osteoblasts, form new bone, some resorption osteoclasts, resorb bone during remodelling connective tissue fibres, mostly collagen, provide elastic strength amorphous ground substance, mostly glycosaminoglycans inorganic components, mostly crystalline calcium hydroxyapatite cells:

The histological and functional unit of most bone tissue is the Haversian system ( = osteon). The centre of the unit is the Haversian canal which accommodates blood vessels and some nerves and is surrounded by concentrically arranged lamellae of bone matrix. The alternating orientation of collagen fibres in concentric lamellae gives much of the elastic strength to bone. The osteocytes sit within spaces (lacunae) in the matrix. Osteocytes communicate with each other via thin processes and gap junctions which lie in tiny canals running more or less radially through the matrix (canaliculi). In living bone, there is a continuous formation and reformation of the Haversian systems. This process, known as remodelling, also is important in fracture healing, when the callus formed in the initial stages of healing is remodelled to mature bone.

Bone formation is commonly described as being as intramembranous or endochondral, but really the bone formation process itself is the same in each case. The difference is that intramembranous ossification starts directly from connective tissue, whereas in endochondral ossification the bone forms from a cartilage model precursor. In both cases, osteoprogenitor cells differentiate into osteoblasts and lay down a dense meshwork of connective tissues fibres containing mostly collagen, known as osteoid, to form a woven bone precursor. The osteoid becomes mineralised (primary spongiosa), but it is still not proper bone. Osteoclasts begin to resorb the osteoid as it is remodelled into new bone by osteoblasts and osteocytes. In endochondral ossification, this process happens first in a region around the shaft of a long bone, for example, followed by the ends (epiphyses) as the cartilage model becomes invaded by blood vessels. The cartilage calcifies and breaks down, as osteoid is laid down around it. This osteoid then develops into bone. The epiphyseal plate persists as a specialised region of cartilage formation and subsequent ossification that allows the bones to continue to grow longitudinally whilst in use. The shaft of the bone increases in thickness by appositional growth from cells in the periosteum. The mechanism of bone healing and fracture repair is similar to normal remodelling and growth. Around the site of damage osteoblasts proliferate and make a callus of woven bone that is ossified and remodelled, initially as trabeculae, but eventually as compact bone following the lines of maximum loading.

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The balance between bone formation and resorption in remodelling is determined by many factors, including: Parathyroid hormone (PTH): decreased blood calcium -> increased PTH secretion from parathyroid glands -> activation of receptors on osteoblasts, which then release osteoclast stimulation factor -> increased resorptive activity of osteoclasts -> calcium returned to blood. NB: PTH also increases blood calcium by - increasing calcium resorption from glomerular filtrate in proximal tubules of kidney; - increasing formation of metabolite of vitamin D (calcitriol) -> increased absorption of calcium from the small intestine. Calcitonin: high blood calcium -> release of calcitonin from C-cells of thyroid -> activation of receptors on osteoclasts -> decreased bone resorption. Vitamin D: deficiency -> excessive production of osteoid compared with mineralised matrix -> rickets in children, osteomalacia in adults. Growth hormone: increase -> growth of epiphyseal plates; excess -> acromegaly; deficiency -> dwarfism. Oestrogens, androgens: receptors on osteoblasts increase bone formation compared with resorption; contribute to closure of epiphyseal plates during puberty; excess in childhood / early puberty may -> precocious sexual maturity accompanied by dwarfism. Vitamin C: decrease -> decreased ability to produce and maintain connective tissue matrix -> deficient collagen production -> deficient bone matrix -> scurvy. Vitamin A: - decrease -> slowed rate of growth and remodelling; - increase -> loss of cartilage production -> early obliteration of epiphyseal plates. Thyroid hormone: increase -> increased collagen turnover -> increase in osteoid and bone resorption.

****

A really important factor in increasing bone formation and decreasing resorption is mechanical loading, although the underlying mechanisms still are not well understood. The loading can come either from forces applied directly to the bone, as in weight bearing, or more indirectly, by the load exerted on the bones by the muscles attaching to them.

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****

Over the last few years, there have been great advances made in understanding the molecular interactions regulating bone metabolism, including the control of differentiation of osteoblasts and osteocytes, as well as the regulation of the mineralisation processes. As a result of this research, there are likely to be a whole new range of therapeutic strategies to deal with metabolic bone disease.

HISTOLOGY OF BONE TISSUE

On the following histological slides identify the cellular (osteocytes, osteoblasts, osteoclasts) and extracellular (lamellae) components of bone tissue. Notice the three dimensional arrangement of the elements in a long bone in relation to the Haversian (running longitudinally) and Volkmann's (right angles to its long axis) canals. Determine the position of the periosteum and endosteum. From your observations, complete the following table: Osteoblast Position Shape Size Distinguishable Character Staining reaction Relative frequency Osteocyte Osteoclast

Slide 5A: Decalcified bone, transverse section (Pig fibula; H & E) Identify the Haversian canals and the lamellae arranged concentrically around them. Relate the position of osteocytes to the Haversian canal and the lamellae. >> Where is the periosteum? What does it contain? >> How are lamellae arranged beneath the periosteum? >> How do oxygen and nutrients reach the osteocytes in compact bone? >> Is collagen present in bone? How could you demonstrate the presence of collagen? >> Where would you expect most of the inorganic components of bone to be deposited?

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Slide 8A: Ground bone, transverse section (unstained) >> What component/s of the bone tissue can you see now? >> Are all the Haversian systems (osteons) complete? If not, what has happened to those that are incomplete? Skull, transverse section Slide 6A: Slide 18: Sheep, H & E Cat, H & E

>> How are the lamellae arranged? Examine carefully the relations between the collagen and bone tissue in the suture included in the section on slide 6A. Developing membrane bone Slide 7A: Slide 17: Fetal skull, H & E Young cat skull, Masson trichrome

Identify osteoblasts, osteocytes and osteoclasts. >> Where can you find osteoclasts most frequently? Why? >> How does growth in size of a membrane bone take place? Slide 9A: Developing long bone (H & E) Look first at the cartilage adjacent to the area of new bone formation. Make a labelled sketch to illustrate the principal characteristics of cartilage in this zone. >> What elements preserve the structural continuity between bone and cartilage? Spicules of calcifying matrix are arranged between the rows of cartilage cells. >> How are osteoblasts and osteoclasts distributed around the spicules? Compare the mechanisms of membranous and chondrogenic bone formation. During the practical class the ultrastructure of bone will also be demonstrated.

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Questions to consider >> What is the function of collagen in bone? >> What are the similarities and differences in bone formation resorption remodelling? >> How do stress and weightless conditions influence the fine structure of the bone? >> What is the rate of bone turnover under normal conditions osteoporosis osteomalacia?

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information for examinations

In 2012, we will assess MSS in the same way as the last several years, to take full advantage of the pass-fail environment and to make the assessment of MSS as simple as possible for staff and students alike. Our aim is to create a less threatening exam environment, so you can concentrate on learning what you really have to know, while still giving us a chance to find if you do actually know it (that is our responsibility to the profession!) and if you can apply that knowledge in a meaningful way. You need to accept two important things about exams - they are stressful, and, if you know your work, you will never have enough time to answer the questions in the way you would ideally like. As such, exams test your ability to access and apply your knowledge under conditions that are largely outside your control. This is a very good model for real life! There will be very many occasions when you must provide information accurately and in the appropriate context and detail, perhaps whilst being seriously stressed out. Job interviews... explaining a medical condition to an emotional patient... presenting a case report for your colleagues or for publication... and so on... So, stressed out? Not enough time? Better start getting used to it!!

The written exam

It should be obvious from looking at previous exam papers that we usually test pretty much the same core knowledge base each year. The questions cover material that comes straight out of the learning objectives of the cases with an emphasis that matches that given in the lectures, pracs etc... The questions are introduced by mini-cases similar to those we have used from week to week of the course. Some of the mini-cases may be based upon presentation of conditions that may not have been covered explicitly in the course. However, all the new information you need to answer the questions is provided in the exam - this means that with a bit of luck, you might even learn something in the exam... For each case there will be a more-or-less generic set of questions for you to consider, along the lines of: what is going on? how do you know? what mechanisms underlie the pathophysiology? what might you do about it? what is the likely outcome? It is possible that one or more of the weekly minicases might turn up in some form on the exam... if you think you recognise one, be careful: the presentation may have been changed to suit the exam format. So don't think that learning the answers to the minicases off rote is a short cut to instant exam success. As in previous years, we will determine if you pass or fail the exam by the number of questions you pass. The exam will have 10 equally-weighted questions; you will need to pass 7 of them to pass the exam. Each questions is marked according to a three-point scale as follows: A = a clear pass, given the exam conditions B = borderline C = clearly unsatisfactory A clear pass means that you have effectively got the answer completely right: youve covered everything and have not made any mistakes. Just getting half of the key items is not enough. You cannot compensate a bad failing question by doing really well on another. A borderline answer might be one that is incomplete (ie no mistakes but not answering everything) or one that contains a mixture

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of correct and incorrect statements. A failing answer is one the has not provided the core information required, either by leaving this material out or by getting it wrong. Any papers that are near the borderline will be checked again and any questions on these papers that had been scored at borderline level will be remarked so that a decision will be forced as to whether the answer passed or failed. Then the number of passed and failed questions will be tallied up to confirm an overall pass or fail for the paper. If you clearly pass the paper overall, any borderline grades are not rechecked. This process works very well and is very efficient. There is no evidence at all to believe that anyone has been or will be disadvantaged by this marking method. If this seems tough, it is, in the sense that the pass criterion is set high. But hundreds of students have done really well on this exam over recent years and there is no reason to expect you cannot join them! This level of knowledge reflects what clinicians expect of you in third year.

The practical exam

This is the second part of your anatomy assessment, making up 67% of the total marks for this part of KHI. The MSS component is a straightforward structure-recognition exam: ie. what is it? what does it do? where does it go? what attaches to it? etc etc . There also will be some neuroanatomy and perhaps some questions from material studied earlier in the year The preparations are the usual ones we use for teaching, and include prosections, pots, dry bones, radiographs etc. We do not have a special set of exam specimens! You will need to get 65% overall to pass the anatomy practical component of KHI. Previous years results have shown that this score represents the minimum level of competence you require in functional anatomy, especially for MSS. Any papers near the borderline will be remarked. You may be reassured that generations of students before you have worried themselves half to death about the prac exam, but usually have done extremely well at it. The details of the prac exam organisation will be given to you closer to the time...

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FLINDERS UNIVERSITY ADELAIDE AUSTRALIA

SCHOOL OF MEDICINE

AUGUST EXAMINATIONS 2011

SECOND YEAR BMBS

MMED8202 INTRODUCTION TO CLINICAL PERFORMANCE

MUSCULOSKELETAL SYSTEM { with sample answers }

TIME: 1 hour and 30 minutes (90 minutes)

MARKING SCHEME:

Each question will be marked to a pass/fail set of criteria. To pass the exam, you must pass seven (7) of the ten (10) questions. All questions are weighted equally.

OVERALL COMMENTS ON RESULTS:

The class did very well on the written exam this year. As in 2010, you had to get the answer to a question pretty much completely right to get a clear pass on it. Most people achieved clear passes most questions, thereby easily passing the exam overall. This is a great outcome! Nevertheless, the questions on the ankle and hands were not so well done: although few of you failed these questions outright, not many got clear passes either... The prac exam was done very well overall, with a class average of 65/80. Nine of you got Gold Stars: effectively full marks for the exam = 10/10 on the written exam and > 70/80 for the prac. Well done! Another big bunch made up the peloton, not far behind... See comments on individual questions for more info...

Bob The Brat Ng crashes his high-performance motorcycle during his first heat in the Black Buffalo Extreme Sports Showdown leading to severe dislocation of his talo-crural joint and a spiral fracture of his distal fibula. Also, his medial malleolus is avulsed. As part of his treatment, his fibula is pinned and his leg is placed in cast.
Question 1. What features normally contribute to the stability and strength of the talo-crural joint? How do other joints in the ankle contribute to overall mobility of the foot? What potential risk does the leg cast pose for the future stability of his ankle?

(9 mins) Source: Week 5 minicases / main pracs

Answer: Talo-crural joint stability = strong collateral ligaments limit ab/adduction. Joint more stable in dorsiflexion when wider anterior part of talus is tightly held by medial and lateral malleoli (tibia and fibula). Additional stability by muscles crossing joint eg soleus / tibialis anterior control anterior / posterior sway during standing. Other joints: subtalar joint (talus -> calcaneus) => inversion / eversion (inversion by tibialis anterior / posterior; eversion by fibularis longus / brevis); transverse tarsal joint => more inversion/eversion + flexion/extension. Risk of cast => pressure on common fibular (= peroneal) nerve could lead to its damage => loss of innervation to anterior and lateral compartments => foot-drop = loss of dorsiflexion and eversion. Comment: 50/121 clear passes I hope I dont get a sore ankle and have to be treated by most of you... this question was done pretty badly overall! Very few of you answered the second part well, either with regard to subtalar / transverse tarsal joints or the inversion / eversion movements.

Bobs manager, Knobby Knox, aged 62, hobbles down to the track to help collect Bobs damaged motorcycle. He complains to anyone wholl listen that he needs a new hip joint, as soon as he pays off the other one. Kills me every time I bend over... he informs a bystander.
Knobbys history reveals that he has osteoarthritis in his hips. Already, he has had one total hip replacement.
Question 2. Briefly discuss the pathogenesis of osteoarthritis. How would osteoarthritis interfere with the normal range of movement at the hip? What are the main longer-term risks for Knobby subsequent to a total hip replacement?

(9 mins) Source: Weeks 4 & 5 main cases

Answer: Osteoarthriitis = abnormal loading on normal articular cartilage OR normal loading on abnormal cartilage. In either case, primarily a disease / disorder of the articular cartilage. Once triggered (injury / idiopathic), chondrocytes => increased secretion of matrix metalloproteinases => breakdown of extracellular matrix => more hydrated, reduced strength, exposure of articular collagen fibres => fibrillation => increased friction => more wear & tear => more breakdown => subchondral bone sclerosis and breakdown => exposure of subarticular bone => eburnation => pain, osteophyte

formation, secondary inflammtion & synovitis => more cartilage and bone loss => cycle continues... Reduced RoM of hip due mostly to pain; at extreme limits may be due to osteophyte impingement. Secondary inflammation could contribute to joint stiffness. Long term risks of hip replacement = relatively few; fracture distal to femoral implant after a fall; loosening of implant (after 10-15 years). [ Infection is a risk but likely to appear within 6 months; however, prosthesis could be long-term site for haematogenous spread. DVTs = short-term risk. ] Comment: 108/121 clear passes Well done overall. Some of you seemed to get sidetracked by the original Eva Kominski case and talked about risk of avascular necrosis of the femoral head, which is irrelevant here, since its gone as a result of the prosthesis...

The bystander, Maria Scarpantoni, aged 43, tells Knobby to stop complaining. But she declines to help, since her own hands are severely deformed: her fingers seem stiff, shortened, deviated to the little finger side, and her knuckles are very swollen. Been like this for years, she mutters, and the drug theyre giving me now helps, but it makes me feel awful... Maria clearly has rheumatoid arthritis, probably an early onset form, given her age.
Question 3. How does rheumatoid arthritis lead to deformation of the hands? What structural changes would you expect to see on a plain radiograph of Marias hands? Which drug is she most likely to be receiving, given her description? How does it work?

(9 mins) Source: Week 3 main case

Answer: RA -> degeneration of joints (initially MCP joints) via chronically inflamed synovial membrane / invasive pannus -> loss of articular cartilage + weakened ligaments => increased joint instability => subluxation / ulnar deviation due to pull of extrinsic forearm muscles. Apparent swelling of knuckles (MCP joints) due to combination of subluxation and inflammation. Apparent shortening of fingers due to subluxation of MCP joints. Plain radiographs => subluxed MCP joints with ulnar deviation (subluxation seen as overlapping profiles of proximal phalanges and distal metacarpals; articular surfaces of MCP joints => probably eroded with underlying sclerosis and surrounding osteophytes [ if subluxed, then joint space would not be present at all... ]. With this level of RA, would look out for degeneration of carpal / radiocarpal / IP joints. Drug could be any of a range of DMARDs, since many have nauseating side effects; at this level of disease progression, most likely would be methotrexate (inhibit T-cell proliferation and production of cytokines probably via DNA synthesis inhibition, perhaps in combination with a TNFa inhibitor. Both drugs generate malaise and nausea as side effects. [ NSAIDs much less likely to make people feel awful... ] Comment: 104/121 clear passes Quite well answered by most people. Many of you seemed to forget or overlook the obvious feature of the presentation: her fingers seem shortened ... and knuckles are very swollen. This is a classic appearance due to subluxation of the MCP joints. This was often mentioned in general as a feature of RA, but a surprising number of people negelected to mention this in the radiological appearance.

After the semi-finals of the MegaPipe Freestyle Skateboard competition, a fight breaks out between defending champion, M-Fix Smith, aged 28, and popular young challenger, Ahmed Khan, aged 19. Following a vicious exchange of heavy punches, both skaters are hurt. M-Fix has a severe pain in his hand proximal to his index finger. The pain is worse when he forms a power grip or when tension is applied to his index finder, consistent with a fracture of the second metacarpal.
Question 4. Compare the mechanisms of a power grip and a precision grip. What are the main muscle groups used in each grip? Why does forming a power grip cause pain in this case?

(9 mins) Source: Week 3 main case and minicases

Answer: Precision grip = holding object between thumb and tips of fingers, nearly always involves opposition of thumb. Finger movements controlled mainly by superficial finger flexors (fl. dig. superficialis; ending on middle phalanx) working together with lumbrical and interossei (fingers) and the thenar muscles (thumb). Deep finger flexors (fl. dig. profundus, ending on distal phalanx) used to flex DIP. Power grip = holding object tightly against flexed fingers and palm, thumb may or may not flex across the object. Main muscle here is fl.dig. profundus. Requires co-activation of wrist extensors (ext. carpi ulnaris / radialis) to keep wrist stable. [ flexion of MCP => help lock knuckles to stop forced abduction ] Pain during the power grip is due to compression of the fractured metacarpal as a result of contraction of the fl.dig. profundus; pulling on the index finger -> tension across the fracture -> pain, either from the fracture itself or the damaged perisoteum. Comment: 54/121 clear passes Another functional anatomy question not very well done by many people. If you didnt mention the function of the thumb in the precision grip, you couldnt get a clear pass on the question: its essential!! A lot of people considered that the finger extensors were co-activated with the flexors in a powergrip: this is not so only the wrist extensors are involved; furthermore, the wrist flexors are not involved either, contrary to the suggestions in many answers. This should have been a relatively simple answer: all you needed to do was to make a fist or look at your hand holding a pen and describe what you see... if so, you would not have made these types of errors...

M-Fix almost certainly broke his metacarpal when he punched Ahmed in the mouth. Ahmed has had several lower jaw teeth knocked out, his mandible is fractured, and he is in considerable pain. He will need to have his jaw wired.
Question 5. Discuss the process of bone healing after a fracture. How does wiring help? If Ahmeds teeth are not replaced, what will happen to his jaw? Why? Which nerve is responsible for transmitting pain from his injury?

(9 mins)

Source: Week 1 minicases + week 4 main case, week 6 revision sessions

Answer: Bone healing = bleeding from fracture -> haematoma / fibrin clot -> debirsi cleaned up by macrophages -> callus -> proliferation of osteoprogenitor cells / osteoblasts, sometimes with chondroblasts -> osteoid -> calcification -> woven bone -> remodelling (osteoclasts and osteoblasts) -> increased density and alignment with loading forces. Wiring keeps fractured surfaces applied to each other => prevent movement => maximise chance of callus forming and healing quickly with minimal subsequent remodelling. Long-term loss of teeth => loss of mandibular bone mass around roots due to loss of loading (increased activity of osteoclasts cf osteoblasts in these areas). Pain due to inferior alveolar nerve (mandibular = third branch of trigeminal nerve). Comment: 99/121 clear passes Very well done overall. However, quite a few of you mistakenly thought the pain came from a branch of the facial nerve (it doesnt).

While shifting equipment around to set up the start of the Ultra-XS marathon crosscountry cycling event, Scotty Maclaren feels a sudden severe pain in his back. It is worse if he twists or bends to the right, when it is accompanied by shooting pins-and-needles down his right lower limb. Scotty is 49 years old, 182cm tall and weighs 103kg. Subsequent investigation reveals a prolapsed disc in his lower back.
Question 6. Discuss the structure and function of the inter-vertebral discs. What causes intra-vertebral discs to rupture or prolapse? How does the prolapsed disc lead to unilateral pain in the back and pins-and-needles in the lower limb? How could the pain associated with a prolapsed disc be distinguished from pain arising from a strained back muscle? (9 mins)

Source: Week 6 main case and minicases

Answer: IV discs = central nucleus polposus (jelly-like) surrounded by tough annulus fibrosus (fibrocartilage and concentric rings of criss-crossed collagen fibres). [ attached to bodies of vertebrae via layer of hyaline cartilage ]. Function = act as shock absorbers between adjacent vertebrae; also increase range of movement between vertebrae => larger from superior to inferior spinal levels. Prolapse = rupture of annulus fibrosus due to excessive [compressive] loading +/- structural weakness (eg due to age) => nucleus pulposus protrudes, most commonly -> posterior. Pins & needles => direct [mild] pressure on roots of spinal nerve => sensation mapped to territory of that nerve. Pain from disc prolapse usually unilateral, relieved by leaning to one side (releases pressure of prolapse on [inflamed] nerve root cf muscle strain -> pain leaning both ways => concentric or eccentric loading -> pain. Femoral / sciatic nerve stretch tests give pain due to root inflammation from prolapsed disc, not very likely for a pulled muscle.

Comment: 117/121 clear passes Also very well done by just about everyone.

The carnage continues on the BMX HyperStunt cycle track. Professional BMX cyclist, Jonty Wiedersheim, 31 years old, misjudges his landing from a large jump when he is distracted by a photographers flash. He flips over the handle-bars and falls heavily on his outstretched arm. He knows immediately that he has an anterior dislocation of his shoulder, having done so several times previously.
Question 7. Discuss the main features providing a combination of strength and mobility to the shoulder. Why is the shoulder dislocated anteriorly in this case? How might the previous shoulder injuries that Jonty has suffered contribute to this one?

(9 mins) Source: Week 2 main case

Answer: Mobility = wide RoM at glenohumeral joint due to shallow ball-and-socket + loose joint capsule; total RoM increased by mobility of scapula (via A-C joint and sterno-clavicualr joints) Strength = mostly muscular: rotator cuff + deltoid at glenohumeral joint itself; scapula -> trunk muscles for overall strength = trapezius, serratus anterior (+ rhomboids, levator scapulae, pec minor), especially for abduction / elevation / retraction. Anterior dislocation: outstretched arm => abducted, extended, externally rotated => head of humerus anterior and inferior in glenohumeral joint; joint capsule weakest inferior where there is no rotator cuff; once dislocated, spasm of pec major holds it there. Previous dislocations-> damage to joint capsule and supporting ligaments -> more loose than normal => even less support. Comment: 83/121 clear passes Reasonably well done by most people, although many didnt mention the role of the scapula in increasing the mobility and strength of the shoulder. Many people said that the anterior dislocation was because the joint capsule was least strong anteriorly, but it is actually the inferior part of the capsule that is not reinforced by anything (no ligaments or rotator cuff). The main reason for going anterior is the line of force from the fall, combined with the absence of any bony protection such as the coracoacromial arch.

During the final of the SuperCross ExOrbital MonsterJump competition, a stunt goes horribly wrong and the riders motor-bike careens into the crowd. Mrs Doreen OLaughlin, 72 year old sister-in-law of Knobby Knox, breaks her left distal radius and ulna when she is knocked to the ground during the chaos. Not again... she moans. Her history reveals that this is third fracture she has sustained in the last 6 years and that she has a moderate level of osteoporosis.
Question 8. Discuss the factors that lead to the development of osteoporosis in later life. What can be done to minimise the risk of osteoporotic fractures?

(9 mins)

Source: Week 4 main case + week 3 minicases

Answer: Major factors = reduced Vitamin D levels via diet / intestinal absorption / exposure to sunlight / renal or liver disease => increased PTH => increased bone resorption; decreased oestrogen levels, especially post-menopausal; decreased loading of bones due to reduced exercise; age-related reduced ability of osteoprogenitor cells to produce osteoblasts / osteocytes. All processes lead to increased osteoclast activity cf osteoblast activity -> net loss of bone mass, especially trabecular bone. Minimise risk of fracture by: >> building and maintaining high peak bone density early in life via weight-bearing exercise, good diet (sufficient Vit D and Ca) and maintaining good BMI. >> if already osteoporotic, consider disease modifying drugs, eg bisphosphonate; check endocrine function re PTH, Vit D metabolism, thyroid status. >> life-style issues to minimise chances of falls, eg no loose carpets, rugs, powercords, good lighting, handrails if necessary for steps, etc. Comment: 106/121 clear passes Well done overall. However, Im not sure how much weight-bearing exercise a 72 year old would be able to do and how long it would take to build up bone mass, as some of you thought might help..

Back at the MegaPipe Skateboard competition, former womens champion, Missy Jackster, aged 24, junks a big aerial move, lands very heavily, and badly hurts her knee, taking her out of the competition. Subsequent testing of her knee indicates an anterior drawer sign, and abnormal instability in response to attempted abduction of the knee.
Question 9. What factors contribute to the stability of the knee during a range of activities from quiet standing to running or landing from a jump? What has been damaged in this accident? How do you know? Once the knee has been repaired, what could Missy Jackster do to minimise re-occurrence of the injury? (9 mins)

Source: Week 5 main case + minicases

Answer: Stability in standing = cruciate ligaments, especially anterior cruciate in full extension (knee screwed home) pulling across posterior cruciate; lateral stability via medial and lateral collateral ligaments. Few if any muscles required. Running / landing from a jump => muscles take much loading, including quadriceps (eccentric), tensor fascia lata (lateral), gracilis + sartorious medially; possibly also gastrocnemius + hamstrings. Accident => torn ACL shown by anterior drawer sign, and probably medial collateral also damaged shown by abduction instability. [ Possible secondary damage to menisci and / or articular cartilage, but no evidence from presentation... ] Minimise future injury by strengthening muscles crossing joint, especially quadriceps via non-weightbearing exercise. Use a knee brace or strapping to support knee. Give up high risk sport.

Comment: 102/121 clear passes Well done overall.

At the Black Buffalo Extreme Sports Showdown Presentation Dinner, Bilby Gronitz, aged 47, special guest presenter and former BMX star, falls off the stage whilst guzzling a bottle of champagne. He lands on his upper back and hits his head against the wall. Although shaken, he doesnt appear badly hurt. However, two days later his neck is stiff and sore, especially when he extends or rotates his head. The pain is relieved to a reasonable degree by aspirin.
Question 10. What are the skeletal mechanisms that allow flexion-extension and rotation of the head? Which main muscle groups are involved in generating these movements? Why would Mr Gronitz feel stiff in the neck two days after his accident?

(9 mins) Source: Week 6 practical class and minicases + Week 2 main case
Answer: Flexion / extension: atlas-occipital condyles => gentle flexion / extension; further flexion / extension involve all cervical vertebrae. Rotation => atlanto-axial joint => atlas rotates around dens (=odontoid process) of axis; further rotation via other cervical vertebrae. Extension via splenius capitis / semispinalis capitis. Flexion via gravity + longus capitis / cervicis (for neck) Rotation via ipsilateral splenius + contralateral sternocleidomastoid Subtle adjustments of head position via deep muscles, including rectus capitis major / minor + and inferior / superior obliques. [ Sternocleidomastoid extends at atlanto-occipital joint, flexes lower cervical joints. ] Stiffness due to mild muscle tearing of extensors / rotators due to forced flexion at impact of fall. Relief via aspirin => pain mostly due to inflammation associated with minor injury. Pain two days later common after stretch-induced (including eccentric) injury. Comment: 96/121 clear passes Well done overall. Nearly everyone got the clue that if aspirin helped the stiffness a couple of days after the fall, it was probably due to soft tissue damage and associated inflammation (eg pulled muscle, ligaments), but not a broken bone...

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END OF EXAMINATION

AUGUST EXAMINATIONS 2010

SECOND YEAR BMBS

MMED 8220A/B KNOWLEDGE OF HEALTH & ILLNESS 2A/B

MUSCULOSKELETAL SYSTEM {with sample answers}

TIME: 1 hour and 30 minutes (90 minutes) MATERIALS ALLOWED IN THE EXAMINATION ROOM:
None

INSTRUCTIONS TO CANDIDATES:
1. 2. Write your student number on each examination booklet. Start answers to each question on a new page.

MARKING SCHEME:
Each question will be marked to a pass/fail set of criteria. To pass the exam, you must pass seven (7) of the ten (10) questions. All questions are weighted equally.

You are encouraged to make use of diagrams in your answers.

While setting up the public address system for the Big Day on Park Green Music Festival, Steve The Crunch Hobbs, aged 47, 196 cm tall and weighing 122 kg, felt a sudden severe pain in his lower back as he bent forward to pick up a heavy speaker box.
Question 1. Discuss the most likely causes of the Mr Hobbs back pain. How could you distinguish between them? How could Mr Hobbs reduce his risk of developing back pain in the first place?

(9 mins)

A. Source: main case, week 6. Most likely causes: pulled muscle / ligament; prolapsed disc; Less likely, but possible: avulsed vertebral spine / transverse process; collapsed vertebra due to cancer (eg multiple myeloma) Distinguish by testing pain on movements: muscles will hurt on any movement due to concentric / eccentric contractions; probably painful on palpation. Disc prolapse most likely to cause pain on bending in a particular direction, relieved by bending in opposite direction. Test possible nerve involvement with femoral / sciatic nerve stretch tets. Avulsed spine / transverse process detected by tapping vertebral spines. Vertebral body collapse may be painful to touch, probably need radiology. Osteporotic collapse of the vertebral body is possible but unlikely due to age and gender of the patient. Reduce risk by good lifting practice: bend knees and keep back straight with centre of gravity through lumbar vertebrae => much less loading on back muscles (erector spinae, quadratus lumborum). Holding breath (usually automatic) helps to spread load to abdominal muscles. In the workplace, a good idea to get assistance or use some device to help lifting heavy items. In lifestyle, reduce weight to reduce loading on back. Comment: Very well done by just about everyone. Some answers failed to provide a decent test to distinguish between the possibilities you suggested.

During the performance by electro-prog-punk band I Did It for Sid, die-hard fan, Doreen Summerhayes, aged 23, fell heavily while crowd-surfing and badly hurt her forearm. In the First Aid tent, examination revealed a so-called dinner fork deformity, such that her wrist and hand appeared to be shifted dorsally to the rest of her forearm. The hand also was deviated radially with the wrist somewhat supinated in relation to the forearm. She was sent to hospital with a suspected broken radius.
Question 2. Why is Ms Summerhayes hand displaced in this injury? If she had not broken her radius, what other injuries to her upper limb might she had suffered in her fall? Discuss the normal mechanism of pronation and supination of the forearm. How do these actions contribute to overall functions of the upper limb? (9 mins)

A. Source: main case, week 3; mini-cases, week 2 and week 3. Most likely injury = fracture of the distal radius (Colles fracture). Hand is displaced because it is attached to radius at the radio-carpal joint. Direction of displacement mostly due to pull of muscles unopposed by radius.

Other possible injuries include fractured scaphoid, proximal ulna (maybe with elbow dislocation), distal humerus, shoulder dislocation, fractured clavicle. Which one happens depends mainly on the angle of the fall and the position of the upper limb. Pronation-supination occurs at the proximal and distal radio-ulnar joints: proximal = pivot joint where head of radius is held against ulnar (radial notch) by the annular ligament; distal = radius rotates around end of ulna, taking the radio-carpal joint (and hand) with it. Radius and ulna are parallel when supine; pronation => radius rolls over ulna. Muscles: pronation = pronator teres and quadratus; supination = supinator and biceps brachii => much stronger. Pronation-supination => increase range of movement of hand: most daily tasks difficult or impossible with out it! Position of forearm pronation-supination determines recruitment of elbow flexors (eg brachoradialis at mid-position; biceps at supine). Comment: Generally well done.
Around sunset, Francesca, an iconic folk singer from the 1960s, now aged 72, performed some of her famous songs, accompanied on guitar by her grandson. She explained to the audience that she has not been able to play guitar herself for many years due to painful arthritis which has progressively crippled her fingers and hands. Holding up her hands, she showed the audience her badly deformed and swollen knuckles. Her fingers appeared shortened and deviated to the ulnar side.
Question 3. Francesca most probably has rheumatoid arthritis. If so, how would rheumatoid arthritis interfere with her ability to play a guitar? What structural changes would contribute to her impaired function? Briefly discuss the possible sources of pain in her hands. How might the pain be treated? (9 mins)

A. Source: main case, week 3. RA would interfere with guitar playing by reducing movements of fingers: eg subluxed MCP joints, perhaps also PIP joints; reduced range of motion due to altered joint structure, stiffness due to inflammation, and pain; also reduced movement and pain in wrist => more difficulty in holding / playing guitar. As well as joint subluxation, articular cartilage would be eroded; subchondral cysts => pain and reduced range of movement of joints even if not subluxed. Possible ligament / tendon destruction further reduces mobility. If wrist is involved, carpal tunnel syndrome could involve median nerve => decreased sensation, motor weakness with intrinsic hand muscles (thenar, 1st two lumbricals) and inflammatory pain. Pain could arise from joint damage, inflammation, nerve inflammation. Apart from analgesia, try to treat cause => reduce inflammation via NSAIDs, coriticosteroids, DMARDS, eg methotrexate, TNFa blockers; test for median nerve involvement and carpal tunnel release. Comment: Generally well done. Some answers neglected to relate the condition to the presentation.

Roger Baleena, a 36 year-old camera operator, was preparing to video-record the evening sessions of the Festival, when he tripped on a cable and fell 5 metres from a scaffolding tower. He landed hard on his knees with his hips flexed. He was in considerable pain from his right hip, which remained flexed, adducted and internally rotated. His right lower limb appeared to be shorter than his left limb.
Question 4. Mr Baleena clearly has damaged his hip. What is his most likely injury? How has this happened? Briefly discuss the major features that contribute to stability and load bearing of the hip joint. How is hip joint be protected from injury in a controlled landing from a jump? (9 mins)

A. Source: mini-case, week 4 Most likely injury = posterior dislocation of femur (fractured neck not so likely given age of patient, nature of fall, and direction of rotation: internal not external, as usually the case with fractured NoF). Hip joint is generally strong and well supported but is most susceptible to posterior dislocation due to high-force impact on distal femur when the hip is flexed and ligaments are least taut. Stability of the hip due to deep acetablum, enhanced by acetabular labrum, encloses most of spherical head of femur. Strong joint capsule, reinforced by strong ligaments: iliofemoral / ischiofemoral / pubofemoral. Iliofemoral lig limits extension and takes most of the load of quiet standing (with centre of gravity behind the joint). Muscles crossing the joint (ilio-psoas, rectus femoris, hamstrings) take a lot of loading off hip when landing from a jump via eccentric contractions. Total load to hip is reduced by eccentric contractions of muscles around knee (quadriceps) and ankle (gastrocnemius / soleus; tibialis posterior; probably peroneus (fibularis) longus and brevis). Comment: generally well done. Some people tried to argue the case for a fracture rather than dislocation, but used wrong info to do so (eg actions of muscles). Most people got the importance of eccentric contractions of muscles crossing the ankle and knee in unloading the hip, but you had to mention the muscle groups (at least) by name.
Nicolette van Ostenliederhoek, sensational 18 year-old bass player and vocalist for The Rainy Day Sunshine Orchestra, appeared on stage with her lower leg in a cast. She said that she had broken both bones in her lower leg whilst skiing in New Zealand a few weeks previously.
Question 5. Discuss the process of bone healing after a fracture. How does remodelling correct for any misalignment in the re-united bones? Under what conditions might a fractured bone not heal properly?

(9 mins)

A. Source: mini-cases, weeks 4 and 5; revision session, week 6 Bone healing after a fracture: Clot (haematoma) forms around broken ends of bones => fibrin => callus => proliferation of osteoprogenitor cells (osteoblasts) and maybe chondroblasts => lay down osteoid => mineralisation to woven bone => remodelled by osteoclasts => mature bone.

Abnormal loading on misaligned bone leads to selective remodelling by osteoclasts and osteoblasts: new bone formation enhanced on one side (usually concave surface, under compression) and bone resorption enhanced on opposite side (usually convex surface, under tension). Loading may be sensed by piezoelectric effects. Bone may not heal properly if: ends are not apposed; ends keep moving relative to each other; infection or other source of inflammation at the fracture site; blood supply to bone interrupted by fracture (=> avascular necrosis); there is serious metabolic bone disease (eg osteoporosis). Comment: Generally well done. You needed to get at least three of the reasons for failed fracture healing to get a clear pass.
Unfortunately, the set by psychometal-Goth band, Blood Type Black was cancelled when their 32-year old lead singer, Jim-Bob Schultz, was sent to hospital with a fractured skull. According to television reports, he had been hit in the head by an amplifier thrown during an off-stage fight with the bands lead guitarist, Bob The Scalpel Hunt.
Question 6. Briefly discuss the structural features that contribute to the overall strength of the skull? Which areas of the skull are most likely to be damaged as a result of heavy direct impact? How can fractures of the skull lead to soft tissue damage? Which soft tissues are most at risk? (9 mins)

A. Source: main case, week 1 Strength of the skull: strongly interlocking immovable sutures between most of the flat bones; dome shape helps to distribute force of impact (bones somewhat elastic, helped by diploic structure) Direct impact => depression fracture at point of impact (especially over maxillary / frontal sinuses; impact to face => le Fort type fractures => mobile face; impact to dome of skull => (countre-coup) fracture to base of skull opposite impact point. Weak areas at thinner bones, eg temporal bone around pterion; nasal bones, ethmoid. Skull fractures => soft tissue damage by dislocation of skull pieces => tearing of soft tissue; pieces of bone can embed in soft tissue (eg in brain); fracture edges themselves could sever soft tissues, eg meninges, blood vessels, cranial nerves Tissues at risk include meninges (eg at cribriform plate), blood vessels (eg venous sinuses draining brain; middle meningeal artery benath pterion), cranial nerves, eyes (eg fractures around orbit), ear drum (eg fractures in tympanic bone), and brain itself, either by impact or consequences of subarachnoid or epidural bleeding. Comment: This question was done terribly! Many people did not answer it at all, and most answers did not much anything sensible to say about sites of skull or soft tissue damage. This outcome is surprising given that all these issues were explicitly addressed in the first main case where the patient suffered a wide range of head injuries affecting his skull and soft tissues (brain, meninges, blood vessels) following a motor vehicle accident...

In a change of pace for the Festival, radical hip-hop artist, Q-tox, teamed up with the infamous juggling-acrobatic-harmony quartet, The Blue Ivories. As part of their act, one member of The Blue Ivories lifted another member high overhead, supporting her with only one hand, while Q-tox rhymed and mixed beats.
Question 7. Explain the movements of the shoulder and associated structures when lifting a heavy load overhead. How do movements at the various joints of the shoulder girdle contribute to the overall lifting action? Which muscle groups are involved? What kinds of injuries could impair or limit ones ability to lift a load overhead? (9 mins)

A. Source: main case, week 2 Lifting a heavy load => abduction / upward rotation of the scapula as well as flexion / abduction at the glenohumeral joint. During the initial lift, the scapula also may be retracted. This is necessary since abduction at glenohumeral joint is about 120 degrees: full lift (eg 180 degrees abduction) requires 60 degrees abduction of scapula. Movement of the scapula requires movement at sternoclavicular and acromioclavicular joints (about 30 degrees each). Main muscles in moving the scapula during lifting are trapezius (abduction, retraction, elevation) and serratus anterior (abduction, stabilisation), helped by levator scapulae (elevation) and rhomboids (retraction). Abduction at glenohumeral joint = supraspinatus and deltoid. Flexion during initiation of lifting a load = pectoralis major (upper fibres) and anterior deltoid. Lifting impaired by nerve damage: most common => to serratus anterior (long thoracic n) or trapezius (accessory n) or deltoid (axillary n). Inflammation of subacromial bursa => pain during abduction => may limit lifting. Muscle strains, inflammation of glenohumeral, A-C, S-C joints (eg over use, sprain, arthritis), joint pain (typically osteoarthritis in these joints). Comment: Generally very well done. Most of you understood the coordinated movements of the glenohumeral joint and the scapula. Many of you noted (correctly!) that this type of lifting involves flexion of the shoulder as well as abduction. Given the wording of the question you didnt need to talk about muscles in the forearm or back also involved in picking up a heavy load.
Former manager of the Blue Ivories, Albert Aardvark Henry, aged 37, recently was eliminated from a national television cooking competition after he attempted a dish showcasing the health benefits of smoked salmon souffl with sashimi tuna and grilled mushroom jam, all good sources of vitamin D.
Question 8. Discuss the role of vitamin D metabolism in the regulation of bone density. How can alterations in vitamin D metabolism contribute to the development of osteoporosis during ageing? What can be done to minimise the risk of developing osteoporosis in later life? (9 mins)

A. Source: main case, week 4. Vitamin D => required for net increase in bone formation / preservation of bone mass. Synthesised in skin via sunlight (UV) or gained from diet as D3, converted to 25-OH-D3 in liver then to 1,25-OH2-D3 in kidney => increase gut absorption of calcium; increased

movement of calcium from osteoblasts to osteoclasts. Synthesis of 1,25-OH2-D3 enhanced by PTH in response to low blood Ca2+. Vitamin D probably also directly stimulates turn over of both osteoclasts and osteoblasts, and is essential for the normal mineralisation of bone. Vitamin D works synergistically with oestrogen in maintaining bone mass. Aging => possibility of less GIT absorption, less sunlight exposure, combined with decreased oestrogen / androgen and reduced weight-bearing activity => overall tendency for reduced bone mass. By itself, vitamin D deficiency => osteomalacia. But if low vitamin D results in low blood calcium, PTH levels rise, activating osteoclasts via actions on osteoblasts, and this is what leads to osteoporosis. Vitamin D effectively cannot be stored => need to keep up dietary intake and some sun exposure; dietary calcium supplements can help if Ca2+ levels are low (but check for malabsorption...). Best prevention of OP is to build up peak bone mass by middle age => maintained weight bearing exercise => increased mass of trabecular and cortical bone. Comment: Well done by many, but many others didnt really identify the difference between the role of vitamin D deficits in osteomalacia compared with osteoporosis (which was the question): you really had to mention the link between vitamin D and PTH or oestrogen to get a clear pass on this question.
The members of the once influential Reggae-and-Western dance band, Ska Rodeo, reformed especially for the Festival. Their drummer, Simon Ellis, now aged 54, also was a semi-professional footballer until he gave up the game when he was 32, after recurrent injuries to the cruciate ligaments and intra-articular disks of his right knee. Now he can only play drums for relatively short periods before the pain in his knee becomes too severe to continue. He often complains of grating in his knee, even if he is not playing drums.
Question 9. Simon Ellis has the outward signs of osteoarthritis in his knee. Briefly discuss the pathogenesis of osteoarthritis. Why does Mr Ellis knee grate? How might previous knee injuries have contributed to the development of osteoarthritis in Mr Ellis? If you took a plain radiograph of his knee, what would you expect to see? (9 mins)

A. Source: main case, week 5. OA = abnormal loading on normal cartilage / normal loading on abnormal cartilage. Articular cartilage breaks down by physical damage or metabolic dysfunction. Chondrocytes => increased secretion of matrix metalloproteinases => breakdown of extracellular matrix => more hydrated, reduced strength, exposure of articular collagen fibres => fibrillation => increased friction => more wear & tear => more breakdown => subchondral bone sclerosis and breakdown => exposure of subarticular bone => eburnation => pain, osteophyte formation, secondary inflammtion & synovitis => more cartilage and bone loss => cycle continues... Knee grating could be pieces of articular cartilage or intra-articular disc fragments; possibly small bony fragments if very severe OA with eburnation (continuous pain => may be at this stage).

Torn mensici => increased risk of OA, due to reduced ability to lubricate properly (by spreading synovial fluid); damaged ligaments => abnormal loading patterns => abnormal wear of articular cartilage. (articular cartilage also may have been damaged in original knee injury => fibrous repair => further damage). Plain radiograph => reduced joint space (due to articular cartilage loss); subchondral sclerosis (hyperdense bone) and maybe cysts (areas of bone loss) beneath areas of wear; osteophytes around margin of joint; mal-alignment if severe eburnation. Comment: generally very well done. Some forgot the radiological findings...

After the Festival concluded, an intoxicated patron, known to her friends simply as Marz stepped out onto the road without looking and was hit on the lateral side of the right leg by a car. Luckily the car was not moving fast. Nevertheless, Marz suffered a fracture of the proximal end of the fibula which was set in plaster. Three weeks later, with her limb still in a cast, Marz complained of numbness in her right shin and foot.
Question 10. What structures are at risk with a fracture of the proximal end of the fibula? Why has Marz developed numbness in her lower leg? If nothing is done to remediate the situation, what would be the long term consequences for her lower limb function and mobility? Explain your answer.

(9 mins)

A. Source: mini-case, week 5. Structures at risk = mainly the common peroneal (fibular) nerve. Numbness could be due to initial impact on nerve; broken fibula compressing / damaging nerve; pressure of cast putting pressure on the nerve. From the presentation, the last is most likely. Common peroneal / fibular nerve => lateral compartment (peroneus / fibularis longus and brevis) via superficial branch; anterior compartment (tibailis anterior, ext hallucis longus, ext dig longus) via deep branch. Loss of whole nerve => loss of eversion and dorsiflexion => "footdrop". Functionally, need to lift foot higher off ground during walking to prevent toes dragging on ground (eg more hip abduction contra-laterally; more knee flexion ipsilaterally => high stepping gait); lose function of tib ant to control weight transfer from heel across arches of foot via eccentric contractions => foot tends to slap down. Reduced of support of arches via tib ant and fibularis mm during running / jumping. Reduced postural stability via same mm in quiet standing. Reduced ankle stability (no lateral support) via fibularis mm (concentric = eversion; eccentric control inversion). Comment: Very well done overall.

FLINDERS UNIVERSITY ADELAIDE AUSTRALIA

SCHOOL OF MEDICINE

AUGUST EXAMINATIONS 2009

SECOND YEAR BMBS

MMED 8220A/B KNOWLEDGE OF HEALTH & ILLNESS 2A/B

MUSCULOSKELETAL SYSTEM
TIME: 1 hour and 30 minutes (90 minutes) MATERIALS ALLOWED IN THE EXAMINATION ROOM: INSTRUCTIONS TO CANDIDATES:
1. 2. Write your student number on each examination booklet AND the attached marking slip. Start answers to each question on a new page.
None

MARKING SCHEME:

Each question will be marked to a pass/fail set of criteria. To pass the exam, you must pass seven (7) of the ten (10) questions. All questions are weighted equally.

This examination is in 2 sections: Section A and Section B, which are weighted equally. Section A Short Answer Questions (Questions 1-5) Suggested time: 45 minutes Section B Short Answer Questions (Questions 6-10) Suggested time: 45 minutes

You are encouraged to make use of diagrams in your answers.

SECTION A
Suggested writing time: 45 minutes
Robert The Rat Johnson, a 42 year old member of a well-known criminal family, was stabbed repeatedly in the torso after a fight in a nightclub. Although his wounds were not life-threatening and healed well overall, he cannot fully abduct his right arm. When asked to push his flexed right arm against resistance, his right scapula shows a characteristic winged appearance.
Question 1. Discuss the muscle groups that provide mobility and strength to the shoulder. What is the mechanism of arm abduction? What has happened to Mr Johnson? Why is his scapula winged? (9 mins)

Answer: [cf Bridges case, mini-cases ]

Three muscle groups -> strength and mobility: : trunk to humerus = pec major; lat dorsi => adduction, bringing arms back to anatomical position from anywhere in space [pec maj more from behind; lat dorsi more from in front] : trunk to scapula = serratus anterior, trapezius mostly for strength and additional range of motion during abduction; [also rhomboids => retraction of scapula; pec minor => stabilise; adduction of scapula against resistance] : scapula to humerus = deltoid => abduction; rotator cuff [=supraspinatus => initiate abduction; infraspinatus, teres minor => lat rotation; subscapularis => med rotation]; teres major => adductor. All can work eccentrically to stabilise shoulder position [other scapula to humerus = coracobrachialis => stabilise glenohumeral joint; biceps, long head of triceps => probably help stabilise joint too] Abduction of the arm requires abduction at glenohumeral joint; initiated by supraspinatus, then powered by deltoid. But only about 120 degrees of abduction available there [ due to bony constraints ]. Rest of abduction (about 60 degrees) achieved by upward rotation of scapula mostly via serratus anterior & trapezius. [ movements occur at acromio-clavicular and sterno-clavicular joints ] Mr Johnsons long thoracic nerve has been severed => loss of function of serratus anterior => winging when trying to abduct or elevate upper limb.

Comment: Generally well done. Most of you realised that the scapula needs to move for full abduction, although some of you suggested some novel muscle actions to do so. Most of you got that the injury was something to do with serratus anterior. The stabbing could have damaged the muscle rather than the long thoracic nerve, so if you said this, you got the points.

In a subsequent interview with the police, Mr Johnson claims the fight started when his 72 year old mother was accused of being a witch. Just because she lost all her teeth 25 years ago, and shes hunched over something terrible since she turned 60 says Johnson, shes no witch, shes an old sweetheart. Police medical files (from another recent incident) confirm significant reduction in the

bone mass of her mandible and bone density in the bodies of her vertebrae.
Question 2. Explain the skeletal changes you would predict to accompany the altered appearance of Mr Johnsons mother as she aged? What features do they have in common? (9 mins)

Answer: [cf Kominski case, minicases ] Facial changes: as a result of losing her teeth, reduced bone mass of the jaws (mandible and probably maxilla) is due to lack of load bearing via the teeth.
Hunchback: reduced bone density of the bodies of her vertebrae => osteoporosis => reduced levels of cortical and trabecular bone => reduced load bearing capacity => collapse under loading [due to body weight and daily activities] => exaggerated thoracic kyphosis. Features in common: in each case, osteoclast activity exceeds osteoblast activity; in each case, the microscopic structure of the bone (ie its mineralisation) would be fundamentally normal. In the jaws, the lack of loading drives the balance towards net bone resorption [maybe via piezoelectric effects in the bone matrix ]. In the back, osteoporotic degeneration is most likely due to post menopausal decreases in oestrogen. [Oestrogen inhibits osteoclast proliferation and activation, and promotes activity of osteoblasts]. At 72 years old, it is possible that the osteoporosis also could be due in part to vitamin D deficits, perhaps due to diet, poor absorption, inadequate exposure to sunlight, or associated with renal disease. [Conceivably, there also could be osteoporotic changes in the jaws which would make the bone loss following tooth loss more severe...]

Comment: Generally well done the presentation was a combination of cases or minicases we explicitly discussed in class. A few of you thought that the hunched back was due to prolonged bad posture, and didnt comment on the likelihood of osteoporosis: this is not very likely. The owner of the nightclub, 64 year old James Cobber McCracken, complained that he had tried to stop the fight by throwing a fire-extinguisher at the combatants. However, as he told reporters, With all the rheumatism in my hands, I could hardly pick the thing up. Television news footage that night focussed on his knuckles, which were deformed and swollen. His fingers appear shortened and deviated to the ulnar side.
Question 3. Presumably Mr McCracken has rheumatoid arthritis. If so, how would the arthritis interfere with his ability to pick up a fire extinguisher (which weighs several kilograms)? What structural changes would be responsible for his impaired function? What would you expect to see on a radiograph of his hands? (9 mins)

Answer: [cf ORiordan case, minicases ] RA => reduced ability to pick up fire extinguisher due to: : reduced flexion at MCP joints due to erosion, subluxation, tendon displacement depending on the level of disease progression; : pain in joints due to inflammation associated with RA : if RA has progressed to include wrist, pain in wrist joints [due to compressive loads] would reduce effectiveness of finger flexors; may involve synovial sheaths in carpal tunnel => pain and reduced range of motion; inflammation and possible carpal bone collapse => carpal tunnel syndrome

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due to pressure on median nerve => pain, reduced sensory feedback from fingers, joints : since the extinguisher weighs several kg, Cobber would need to recruit his deep finger flexors (fl dig prof) for a power grip, which would exacerbate all the features above. Radiographs: damage mainly to MCP joints => reduced joint space, some subluxation, ulnar deviation, subchondral sclerosis, bone erosions or cysts around perimeter of joint, possible osteophytes; if RA more advanced, then similar observations for joints between carpal bones and perhaps radio-carpal joint.

Comment: This question was a straight re-write of the presentation of RA in the ORiordan case. It was a bit surprising that more of you didnt do better on this question. If you just listed a whole lot of generic factors associated with RA without relating them to the presentation, you did not pass the question. One of the television camera operators, Cherie-Marie Schwartz, aged 29 and a competitive netballer, slipped and fell down some steps when filming outside the nightclub. She felt intense pain in her right knee which had been reconstructed after a netball injury three years previously. Although she had extensive physiotherapy following the surgery, the knee still felt weak sometimes, and showed a modest anterior drawer sign.
Question 4. Compare the features that provide structural stability to the knee during quiet standing and more vigorous activity such as carrying a load up and down steps. What was the most likely injury that Ms Schwartz suffered when playing netball? Why would her knee still feel weak three years after the reconstructive surgery? (9 mins)

Answer: [cf Latimer case; minicases] Stability during quiet standing: mostly ligaments = ACL, PCL, lateral and medial collaterals. Centre of gravity runs anterior to knee, forces it into extension and most load is taken by ACL which limits extension. During activity, additional support from muscles crossing knee [up to about 25% of strength ]. Most important = quadriceps anteriorly; tensor fascia lata laterally; sartorius and gracilis medially; hamstrings posteriorly. [ these muscles often work eccentrically to support knee under loading ].
Anterior drawer sign => she probably ruptured her ACL [ presumably due to hyper-extension ]. Weakness probably due to poor healing of ligaments. If anterior drawer sign is present, then this is evidence that the ACL has healed at a longer length than normal. This deficit is corrected only slowly if at all.

Comment: Well done overall, although some of you mixed up the functions of the collateral ligaments. If you didnt give a reasonably good account of the role of the muscles in providing dynamic support for the knee, it was hard to pass the question. After several hours of unhelpful interviews with witnesses of the nightclub fight, the detective in charge of the case, Broderick Van Noorden, aged 51,184 cm tall, weighing 121 kg, hypertensive and borderline diabetic, complains to his workmates that he has a dreadful pain in his lower back. Must be the cheap chairs they give us these days, he mutters.
Question 5. Discuss the most common causes of lower back pain in middle aged adults. How could you distinguish between them? How could you reduce the risk of back pain developing in the first place?

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(9 mins) Answer: [cf Tonetti case, minicases] Sources of back pain: muscle strain / damage; ligament damage [could be associated with avulsion of attachments to vertebrae]; intervertebral disk prolapse => pain from the prolapse, or via pressure on spinal nerve; osteoporotic degeneration => bone pain, pressure on nerves; osteoarthritis => joint pain, osteophytes => inflammation, pressure on nerves; inflammatory joint disease of vertebrae; osteomyelitis; osteosarcoma.
Examination => flex / extend / lateral flexion => source of pain = first pass distinction between muscular or discs [ usually muscular give pain bending both ways cf discs only one side ]; tap vertebral spines for bone damage; sciatic / femoral nerve stretch tests for root inflammation; bone scans for OP [DEXA]; CT for OA or other degenerative disease; perhaps MRI for osteomyelitis, osteosarcoma. Reduce risk: => good lifting practice; reduced body weight; increased fitness; [ reduce diabetes => reduced risk of microvascular disease and perhaps consequential bone degeneration ]. If OP, then adjustments to diet, VitD intake if necessary.

Comment: Given that this question comes straight out of the presentation of the Matt Tonetti case, it was not done well overall. Most of you gave a couple of potential causes, a cursory differentiation of them, and then a decent list of suggestions to prevent injury. However, if you managed this without any errors, you squeaked a pass on the question. Three weeks after the nightclub incident, a male aged about 25 years, referring to himself only as Dog, presents to a regional hospital with an extremely painful wrist. He says he must have hurt it playing football. Examination reveals that dorsiflexion, radial deviation or generating a power grip all produce pain in the region of the anatomical snuffbox. X-rays reveal a line of reduced density across the mid-section of the scaphoid bone.
Question 6. Discuss the process of bone healing after a fracture. Under what conditions might a fractured bone not heal properly? What is the likely outcome of this case? How will the outcome affect the function of the wrist in the future? (9 mins)

Answer: [cf ORiordan and Kominski cases, minicases] Process of bone healing is not very different from basic bone formation. After the break, a clot forms between the fractured ends of the bone [bones are heavily vascularised], and the gap between the fractured surfaces is spanned by fibrin (assuming the bone has been set so that the fractured surfaces abut). The fibrin clot is invaded by mesenchymal stem cells including osteoblasts [probably derived from nearby periosteum] => a callus. In some cases, chondroblasts appear first [probably also from the periosteal stem cells]. Osteoblasts form osteoid and then woven bone to bridge the fracture via the callus. [if chondrocytes have made cartilage, the osteoblasts will use this cartilage as a model and eventually replace it ]. Then remodelling, involving osteoclasts and osteoblasts, will realign the repaired bone with the loading forces if it has been set out of alignment.
Healing may not occur if: : the fractured ends are not set adjacent to each other. : the blood supply to the bone is compromised (=> avascular necrosis) : the bone is badly osteoporotic [other factors that impair healing are concurrent infection and inflammation, no matter what the cause ]

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Fracture of the scaphoid can lead to avascular necrosis. If the scaphoid had been broken 3 weeks previously, and the fracture is still evident on X-ray, then the chances of avascular necrosis are high. If so, the movements of the wrist will be compromised mainly due to pain, especially during loading in a power grip or during radial deviation.

While Dog is being treated in the regional hospital, his mother calls the police, reporting him missing. Aged 67, she is 157 cm tall, weighs 88 kg, and only recently gave up smoking. She now is awaiting hip replacement surgery due to severe osteoarthritic degeneration of the hip joint.
Question 7. Discuss the pathogenesis of osteoarthritis. What specific features would you expect to see in advanced osteoarthritis of the hip joint? How would hip mobility be affected by the arthritis? (9 mins)

Answer: [cf Kominski and Latimer cases and minicases] OA can be a result of abnormal articular cartilage and normal loading, or normal cartilage and abnormal loading => can be caused by injury or it can be idiopathic. In either case, the primary defect is in the biochemical composition of the matrix of the articular hyaline cartilage. Normally highly hydrated matrix of glycoproteins / proteoglycans [mostly chondroitin sulphate and hyaluronic acid along with collagen type II; matrix = avascular, aneuronal, low metabolic activity]. During pathogenesis of OA, over activity of matrix metalloproteinases => breakdown of articular cartilage => fibrillation => reduced ability to act as smoothly lubricated surface => further wear and breakdown, made worse by continued use. Eventually the articular cartilage breaks down totally and exposes subchondral bone surfaces leading to erosion and eburnation. Subsequent bone pathology includes subarticular scelerosis and osteophytes. There may be secondary inflammation of the joint.
In the hip, expect to see reduced joint space between head of femur and acetabulum; possibly osteophytes around rim of acetabulum and neck of femur. Hip mobility reduced by pain and potentially reduced range of movement due to osteophytes.

Called in by the police for further questioning, Robert The Rat Johnson now admits that he started the nightclub fight with Dog. The fight was over a woman known as Two Faced Jane, whose face had been severely cut by a broken beer glass many years previously. The police photograph clearly shows a deep scar running from behind her eye, across her cheek, down to the angle of her jaw. Much of this side of her face remains expressionless.
Question 8. Which main muscle groups contribute to facial expression? Why has Jane lost expression on one side of her face? What other problems is she likely to have developed as a result of the injury? Is her ability to eat and drink likely to have been affected? Explain. (9 mins)

Answer: [cf Justin Mills and minicases] Muscles of facial expression include groups associated with forehead (eg frontalis, corrugator supercilii), nose (eg nasalis), orbit (eg orbicularis orbis / oculi), cheeks (eg buccinator), mouth (egorbicularis oris, zygomaticus, risorius, levator / depressor labii), and chin (eg mentalis, platysma).
Janes scar suggests her facial nerve has been severed.

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Other problems might include dry eyes (inability to blink properly [although tear production should still be normal]), problems with speech due to impaired ability to move lips properly on one side, increased risk of tooth decay on affected side due to paralysis of buccinator and reduced ability to move food scraps from lateral region of mouth. Chewing and biting will be OK, since muscles of mastication [masseter => chewing, temporalis => biting, pterygoids => grinding] innervated by [mandibular branch of] trigeminal nerve. However, impaired actions of orbicularis oris and buccinator => increased chance of drooling. Swallowing is OK no damage to nerves to these muscles [mostly CN IX]

Despite Mr Johnsons confession and unwillingness to press charges, the police search for Dog to charge him with attempted murder. During an ensuing car chase through the outer suburbs, Dog hits a 17 year old girl riding a bicycle. She was wearing a helmet and seemed at first not to be seriously hurt. However, she reported a severe pain in her neck, and she felt as though her head was about to fall off. X-rays revealed a fracture at the base of the odontoid process of the axis with some dislocation of the atlanto-axial joint. She was treated with a halo brace that immobilized the joint and she made a full recovery.
Question 9. How do movements at the atlanto-axial and atlanto-occiptal joints contribute to the orientation of the head? How is the position of the head normally set and stabilised? What would have been the most probable outcome if the cyclists odontoid process had become dislocated rather than fractured?

(9 mins) Answer: [cf Justin MIlls case and minicases] Atlanto-occipital joints => gentle nodding [via pair ellipsoid / condyloid joints] = flexion /extension Atlanto-axial joints => gentle rotation to left / right [via dens / odontoid process held in place by transverse ligament]
Position of the head is set by complex of muscles [centre of gravity of the head lies in front of the atlanto-occipital joint => tend to flex with gravity] : support via sternocleidomastoid, splenius capitus, erector spinae. Turn to one side via contralateral sternocleidomastoid and ipsilateral splenius and erector spinae. Precise setting of head position by deep small muscles assocaited with atlas and axis [rectus capitus major / minor; superior / inferior obliques] Flexion via longus capitus, gravity. Dislocation of the odontoid process => probably tear into adjacent spinal cord / brain stem => fatal.

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Many years later, Broderick Van Noorden, Robert The Rat Johnson and a character known even to his mother as Dog are sharing a drink in the bar they bought together after securing a lucrative deal with up and coming television producer Cherie-Marie Schwartz. They are watching their grandchildren play around the barbeque. When one of them falls off a chair, with little apparent lasting injury, Broderick remarks Its amazing how tough those kids seem to be ...
Question 10. How do the different components of bone contribute to its strength? Why do childrens bones seem to be tougher than those of adults? In other words, why do childrens bones resist fracture better than adult bones? Conversely, which features of childrens bones could lead to permanent impairment if damaged prior to maturity? (9 mins)

Answer: [cf minicases]

Compressive strength and hardness due to the mineral component = calcium hydroxyapatite. Tensile strength and toughness / elasticity = organic component = collagen [type I] [Collagen matrix provides the structural framework for bone calcification eg in osteons / Haversian systems ] Childrens bones have higher proportion of collagen => somewhat more flexible => less likely to fracture completely => Greenstick fracture. [very young children - babies - still have significant regions of cartilaginous skeleton that is much more flexible that bone] Childrens bone have epiphyseal plates => continued longitudinal growth via ongoing proliferation of cartilage and replacement by osteogenesis in the growth plate. If growth plates are damaged, any further longitudinal growth of the bones is prevented.

END OF EXAMINATION

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feedback on mss exam 2008

THE PROCESS: This was the fourth year in which we used a pure pass / fail criterion-based marking system for MSS. The sample answers were generated by Ian using realistic time constraints: ie each sample answer was initially written in 9 minutes. A few of them were edited subsequently to take into account some of the alternative ways of answering that some of you came up with that we considered were appropriate. In order to clearly pass any question, you had to get nearly all of the key points in the sample answers. This sounds tough, but by setting the standards this high, we can be sure that when we say youve passed, we can be confident that you really do know the material. If you did not show a clear pass on the question it was usually scored as a borderline. Fails were reserved for badly incomplete or erroneous answers. You had to get clear passes on 7 of the 10 questions to pass the exam. Any paper that did not reach this criterion on the first marking was looked at again and each borderline question was re-marked by both Sue and Ian, until it was clear that the paper was an overall pass or fail. THE ANALYSIS: Overall, we were very pleased by the quality of the answers this year. Several questions were pretty well fully answered by nearly the whole class (1, 5, 7, 10), but others (2, 3, 4, 6) were not clearly passed by something like 1/3 of the class. Question 5 was on last years exam; questions 4, 9 and 10 were closely based either on minicases or a main case. As a class, it seems you got arthritis pretty well, but struggled more with bone metabolism. A bit of a surprise really, given the time we spent on it... 18 of you got clear passes on all ten questions, with another 30 getting 9 clear passes and a borderline on just one question. At the other end of the scale, 20 papers did not get 7 clear passes on the first marking, but got there after borderline answers were re-marked by both Sue and Ian. The practical exam was done very well, with an average mark of 33/40! A few of you got nearly full marks.

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FLINDERS UNIVERSITY ADELAIDE AUSTRALIA

SCHOOL OF MEDICINE
\

AUGUST EXAMINATIONS 2008 SECOND YEAR BMBS

KNOWLEDGE OF HEALTH & ILLNESS

MUSCULOSKELETAL SYSTEM
TIME:
1 hour 30 minutes
None

MATERIALS ALLOWED IN THE EXAMINATION ROOM: INSTRUCTIONS TO CANDIDATES:

Write your student number on each examination booklet AND the attached marking slip. Start answers to each question on a new page.

MARKING SCHEME:
Each question will be marked to a pass/fail set of criteria. To pass the exam, you must pass seven (7) of the ten (10) questions. All questions are weighted equally. This examination is in 2 sections: Section A and Section B, which are weighted equally. Section A Section B Questions 1-5 (Suggested time 45 minutes) Answer these 5 questions in the answer booklets marked Section A Questions 6-10 (Suggested time 45 minutes) Answer these 5 questions in the answer booklets marked Section B

You are encouraged to make use of diagrams in your answers. 91

Jimmy Macclesthwaite, aged 54 years, complains of pain in his shoulder which is worse at night and particularly bad during activities such as putting on a jacket. The shoulder looks normal but is tender to touch just below the anterior margin of the acromion. When asked to abduct his upper limb, he reports aggravated pain as the limb traverses an arc between 60 and 120 degrees, which is relieved somewhat by externally rotating his humerus prior to abduction. Radiology shows an obvious osteophyte extending from the underside of the acromio-clavicular joint towards the subacromial bursa. There also is some sclerosis of the adjacent acromion. This presentation is consistent with an impingement syndrome leading to painful arc.
Question 1. Osteophytes are commonly associated with joint damage, especially in osteoarthritis and related conditions. How does the progression of osteoarthritis lead to the development of osteophytes? How can they influence joint function? How can you determine the degree of development of osteophytes?

[9 mins]
Answer: Abnormal loading on articular surfaces => osteoblasts respond to increase bone mass in response.
Abnormal loading due to erosion of articular cartilage : subsequent to damage or idiopathic => eburnation and exposure of bone surface [ osteoblasts try to respond to load but matrix continues to erode away ] [ excessive loading leads to sclerosis of subchondral bone: may be due to microvascular damage ] If they become large enough, osteophytes could reduce joint function by reducing range of motion (ie bone to bone contact in joint, eg at shoulder, hip, thumb CMC joint, vertebrae). Also could interfere with ligaments / joint capsule. Degree of development of osteophytes often can be tested by surface examination eg at knee. Also range of motion, but ultimate test is radiography (plain film usually enough but may need specific angles to get best view)

Comment: Clear passes = 84% of answers This question was generally done very well. Not many of you mentioned surface examination as a method to determine osteophyte development. Surprising, since this was a feature of the Peter Latimer case of osteoarthritis in the knee.
Question 2. How do the muscles of the shoulder interact to abduct the upper limb? How does the acromioclavicular joint contribute to the total range of motion? Why would external rotation of the humerus facilitate pain-free abduction in Mr Macclesthwaites case?

[9 mins]
Answer: Abduction requires movement of both scapula => also move clavicle => elevation / abduction at sterno-clavicular and acromio-clavicular joints and humerus at gleno-humeral joint
180 degree abduction => about 60 degrees due to scapula; about half of this at a-c joint. Full range of abduction requires muscles to abduct scapula (mostly trapezius and serratus anterior) and humerus at gleno-humeral joint = initially by supraspinatus and then deltoid.

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[ Supraspinatus still shortens as deltoid contract => pressure on bursa => painful arc ] External rotation helps here by: :: helping to move greater tuberosity away from subacromial osteophyte :: helps to keep supraspinatus stretched so its less likely to bunch up against site of subacromial inflammation.

Comment: clear passes = 67% of answers This question was the least well done overall: nearly 1/3 of you didnt get a clear pass for it. Many of you didnt clearly identify the role of supraspinatus or the movement of the scapula in abduction of the upper limb. Painful arc is a common condition of the shoulder and the question is testing your ability to apply your knowledge of the mechanics of the shoulder complex to one of many ways this condition can develop.
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Marco LaPaglia, aged 5 years old, presents with severe genu valgum (knock-knees) and enlarged epiphyseal plates, including those at the ankles, knees, wrists and costochondral junctions. He also has hypophosphataemia with excess urinary phosphate, consistent with hypophosphataemic vitamin D-refractory rickets associated with renal tubular dysfunction. He is treated successfully with oral phosphates and 1,25-dihydroxyvitamin D3.
Question 3. Briefly describe how epiphyseal plates contribute to bone growth. How could impaired phosphate metabolism lead to enlarged epiphyseal plates and abnormally shaped lower limbs? Why would vitamin D help in recovery from rickets?

[9 mins]
Answer: Epiphyseal plates are the main way that long bones increase in length. Main part of plate is hyaline cartilage [ derived from original cartilage model of the bone ]
The plate is made up of a series of zones: proliferating chodrocytes / hypertrophic chondrocytes / degenerating chondrocytes + calcified matrix / osteoblasts form osteoid + woven bone over cartilage remnants / new bone rapidly remodelled by nearby osteoclasts / osteoclasts also remove calcified cartilage matrix / whole ossification process driven in part by microvascular development. Once epiphyseal plates close, no further longitudinal growth of bone can occur. Rickets = inadequate ossification of bone / formation of bone matrix due to either inadequate activity of osteoblasts or, more usually, inability to properly calcify the matrix that they make. In this case, the lack of phosphate (due to renal dysfunction) is responsible for the lack of ossification (bone matrix = calcium hydroxyapatite = phosphate salt). However, the cartilage keeps proliferating in the epiphyseal plates, so they enlarge without forming new bone. The larger cartilaginous parts of the limbs => increased propensity to deformity under weight-bearing / load. High levels of Vit D upregulate osteoblast activity and, together with phosphate supplement, facilitate proper calcification of the bone matrix.

Comment: clear passes = 69% of answers Again nearly 1/3 of you didnt get a clear pass on this question. Despite the time spent in histology pracs and the thursday mini-case sessions on the underlying biology of bone and its formation from cartilage models, a lot of you did not really get the process of endochondral ossification in the epiphyseal plate. However, although we had not discussed the role of phosphate in bone metabolism in a lot of detail, most of you did a good job of interpreting the bone metabolism defect here.

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Question 4. Compare the features that contribute to the stability of the knees during load-bearing in quiet standing and a strenuous activity such as running or landing from a jump. When are the ligaments of the knee most heavily loaded?

[9 mins]
Answer:
Standing: Stability mostly due to ligaments when knee fully extended: ACL main load bearing [ but it pulls across PCL to help take load and lock articular surfaces together; locking due to shapes of articular surfaces ] In full knee extension, both collateral ligaments are also taut and prevent any ab / adduction. No muscles required to support knee in quiet standing [ as long as centre of gravity runs anterior to joint ] Running / landing from a jump: Ligaments still very important, but now muscles take a lot of the load. Tensor fascia lata provides dynamic support laterally at all positions of knee Gracilis, sartorius, medial hamstrings provide dynamic support medially. Quadriceps => strong support in all positions, mostly via eccentric contractions at foot fall. [ maybe some additional support by gastrocnemius and hamstrings ] Ligaments are most loaded during hyperextension loads (ACL) or when the flexed knee is twisted (ACL + MCL); load on lateral knee (abduction force) => loading of MCL [ bonus point: of course, you can decrease load on knees by absorbing the load elsewhere eg by landing on your toes from a jump, much of the impact forces are absorbed by eccentric contractions of the posterior calf muscles ]

Comment: clear passes = 73% of answers Done fairly well by most of you, but a lot did not get the functions of the cruciate ligaments correct: they get damaged a lot, and you need to know when and why and how!
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Martha Mills, a well-liked 38-year old PBL tutor, felt a severe pain in her back while lifting a couple of full shopping bags into the back of her car. She was unable to straighten her back, and felt additional pain radiating through her lower right leg. Two days later the pains were still present. CT scans revealed a prolapsed disc between the 4th and 5th lumbar vertebrae.
Question 5. What is the normal function of an intervertebral disc? How does it work? What happens when a disc prolapses? How could this lead to pain in Marthas lower leg?

[9 mins]
Answer: Main function of intervertebral disc is to act as shock absorber between adjacent vertebrae. Also acts to allow some degree of movement between the vertebrae.
Disc consists of jelly-like core = nucleus polposus, made of highly hydrated glycoprotein matrix, so mostly = water. Outer layer = annulus fibrosus = fibrocartilage with concentric bands of collagen fibres; each layer of collagen runs in an opposite direction (similar to cross-ply tyre). Core of the disc is largely incompressible, as long as outer layers hold => resists compressive forces,

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typically generated during flexion / lateral flexion. Prolapse occurs when the annulus fibrosus ruptures leading to expulsion / protrusion of the nucleus polposus when loaded. This generates pain due to tissue damage in the disc itself, associated inflammation affecting nearby tissues, such as longitudinal ligaments of vertebrae. Pain in leg could be due to inflammation spreading to sheath of nearby spinal nerve roots; pressure from disc on the nerves with associated inflammation; potentially also could be segmentally referred pain from the disc and surrounding tissue.

Comment: clear passes = 96% of answers Most of you got this question very well. The same question (with a different person) was on last years exam.
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Wilson Svendt, aged 25, has developed psoriatic arthritis. In addition to a scaling itchy rash around his umbilicus, elbows and forearms, the distal interphalangeal joints of his fingers are painful and swollen. He recalls his father had a similar condition, which ended up with his fingers and toes becoming severely deformed. Blood tests show that Wilson is negative for rheumatoid factor. His doctor explains that the swelling is likely to be due to inflammation of the attachments of tendons to the bones at the ends of his fingers as well as synovitis of the nearby joints. If left untreated, the inflammation may lead to total destruction of the affected joints, which probably is what happened to his father.
Question 6. Which tendons are likely to be involved in this case? What are the functions of the corresponding muscles in the control of the fingers? How do other muscles contribute to the movements of the fingers? Which, if any, of these movements might be affected in Wilsons case?

[9 mins]
Answer: Tendons = fl dig profundus, that end on distal phalanx; [ as disease advances and inflammation spreads down common flexor tendon sheath, fl dig sup could be involved as middle phalanx becomes damaged around DIP joint; also possible for extensor hood / sheath to be involved => finger extensors ]
FDP = only flexor of DIP joint; main function as finger flexor in power grip [ can work with FDS and lumbricals to set IP joint angles in complex precision movements ] FDS = flex PIP joint; important in precision movements. FDP and FDP both flex at MCP joints. Lumbricals flex at MCP and extend at IP joints => set angles in precision movements. Extension via ext dig, ext dig ind, ext dig min. Abduction / adduction via palmar and dorsal interossei, respectively, at MCP joints. Hypothenar & thenar muscles for little finger & thumb fine positioning including opposition. In this case, power grip likely to be most severely affected due to FDP damage; precision may be affected as inflammation spreads to affect FDS, extensors, lumbricals...

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Comment: clear passes = 72% of answers Most of you got a more or less complete list of muscles working the fingers. However, many of you (about of the class...) forgot to mention which ones would be most affected in this case. If you didnt do this, you only got a borderline grade for this question on first marking.
NB: the superficial and deep flexor tendons share a synovial sheath in each finger, but except for the little finger, these sheaths do not connect to the large common flexor sheath in the palm and carpal tunnel, so inflammation could not get directly from the region of the DIPs to the carpal tunnel, unless it came via the little finger. So no points for going on about carpal tunnel syndrome unless you mentioned the little finger connection. Question 7. Given that psoriatic arthritis has many features in common with rheumatoid arthritis, what would you expect to see in radiographs of Wilsons fingers? How would you explain the pathogenesis of the damage to the fingers? Why might the fingers end up being so badly deformed?

[9 mins]
Answer: Radiology: loss of joint space at DIPs; perhaps adjacent sclerosis and cysts / osteopaenia / osteoporosis / erosions; maybe small osteophytes around margins of damaged joint; more advanced => possible subluxation; ultimately total destruction of joint tissue.
Pathogenesis: inflammation in synovium - probably triggered by autoimmune response => release of cytokines, especially IL-1, IL-6, TNF-alpha, => activation of osteoclasts => damage to articular cartilage and resorption of adjacent bone. In this case, also inflammation of tendon attachments to bone (as stated in question) and distal tendon sheaths (= synovial sheaths around flexor tendons). Inflammation of synovial sheaths => swelling and pain => reduced movement at joint; inflammation at attachment of tendons to bone => they may detach => total loss of function of FDP. Extreme deformation: inflammatory process proceeds unchecked, with rampant cytokine production and osteoclast activity; as well as tendons pulling away from joints, joint capsules and associated ligaments (normally very tight) become damaged => subluxation of joints as muscles pull in abnormal ways; if inflammation proceeds to middle phalanx (highly likely), then FDS and its tendons also could be involved => head towards total loss of flexor function. In any case, there would be pain from the DIPs that would limit activity. [ might predict that overall alignment would depend on involvement or not of finger extensors: if they are not as affected as much as flexors, then they could pull distal phalanges way out of alignment. ]

Comment: clear passes = 96% of answers Very well done by nearly everyone! A few of you just went on about RA without noticing the information in the question that told you that this is psoriatic arthritis. Thus, there is no involvement of the MCP joints (at least at this stage) and there is no Rh factor...
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Georgette Pascoe, a 32 year old medical graduate, is on her first visit to the United States. When crossing a small side street in a Mid West town, she looks to the right, then left, then right again for traffic and seeing nothing, steps into the path of a slowly moving car. She is hit on the lateral side of her left leg, fracturing the upper part of her fibula. Several weeks later, after her plaster is removed, she can neither dorsiflex nor strongly evert her left ankle.
Question 8. What has happened to Georgette? How will her gait be affected? Why? What changes would you

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predict in her ability to balance on her damaged leg?

[9 mins]
Answer: She has damaged her common peroneal / fibular nerve (superficial branch to lateral compartment muscles = peroneus / fibularis longus and brevis => eversion; deep branch to anterior compartment muscles = tib ant, ext dig longus, ext hall long => dorsiflexion). Could be due to initial impact or piece of fractured fibula or the cast was too tight.
During walking, she will show footdrop ( = dragging toes) as non-supported leg swings forward due to loss of dorsiflexion of ankle and toes, ankle also likely to be turned inward (inverted) to some degree. To avoid this, she may develop a high-stepping or wide-swing gait. At heel-strike, foot will clap down, due to loss of eccentric contractions of dorsiflexors that take load of impact and transfer weight from heel to forefoot via the longitudinal and transverse arches of the foot. [ this will make running more difficult due to difficulty in absorbing / transferring impact forces at ankle to foot ] Balance on injured leg would be more difficult => normally postural adjustments made by anterior compartment muscles vs posterior compartment (eg soleus) to adjust for posterior / anterior sway respectively; lateral sway more difficult to control due to loss of everters (fibularis / peroneus muscles) and one inverter (tib ant). [ Standing with ankle as dorsiflexed as possible would minimise sway due to wide part of talus held tight in talo-crural joint. ]

Comment: clear passes = 76% of answers Generally well done. A lot of you got all of this. If you didnt mention the names of the muscles supplied by each nerve and their functions, you only got a borderline. Several of you mentioned only the extensors or the evertors and forgot the others. In case you thought this question seemed familiar, this question was taken straight from one of the mini-cases...
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Felicity Brownstein, aged 4, complains of severe pain in the proximal end of her tibia, which is extremely sensitive to gentle touch. She shows malaise and has a fever. She has the remnants of a large abrasion on her shin following a fall about 2 weeks earlier. Scans with technetium-99 phosphonate show areas of increased activity around the cortical region of the proximal tibia. Plain Xrays reveal areas of rarefaction surrounded by bands of sclerotic bone in the same region of the tibia. Almost certainly, Felicity has developed osteomyelitis following haematogenous spread from her shin abrasion. She will be treated with antibiotics.
Question 9. How would you explain these findings? Why is there both rarefaction and sclerosis of the bone? Why is the bone so painful? Why has it taken two weeks for this condition to develop?

[9 mins]
Answer: Technetium scan => increased metabolic activity of bone: in this case both increased osteoblast and osteoclast activity. Osteoblast activity main contributor to scan due to phosphate uptake into new bone matrix. Inflammation associated with infection => increased osteoclast activity driven by cytokine cascade (especially IL-1, IL-6, TNF alpha) => localised bone resorption, especially around sites of infection; surrounding areas => increased osteoblast activity, but abnormal calcification / vascularisation => scelerotic bone (ie higher than usual density bone matrix, but as a precursor to subsequent degeneration).
Bone is painful because it is innervated by pain fibres (C-fibre nociceptors)! Mostly in the periosteum,

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but also in endosteum and within bone matrix. Inflammation associated with infection => increased sensitivity and activation of nociceptors. [ changed bone matrix associated with site of infection / inflammation may change loading => increase pain due to abnormal loading ] [ peptides released from nociceptors may alter bone metabolism themselves and contribute to changed bone matrix in region of infection / inflammation ] Bone infection usually takes a long while to develop due to small pockets of bacteria lodging in areas of low blood flow within bone; they grow slowly and are initially out of reach of the blood borne immune system cells. Micro-organisms may reside in complex extracellular matrix of bone similar to biofilm environment. It also takes while for the infection to develop to a level that results in symptoms within the bone.

Comment: clear passes = 80% of answers This question takes up LOs from the Eva Kominski case and several of the minicases. It was very well done by most of the class, with nearly everyone getting all the key points.

You may remember Mr Drewer. He is having trouble chewing his food: he has no difficulty in opening or closing his mouth or moving his jaw from side to side, but food accumulates between his teeth and his cheek on the right side. Investigations reveal a malignant tumor of the parotid gland. When it is removed, the upper three branches of the facial nerve were unavoidably severed.
Question 10. How do you explain Mr Drewers initial presentation? Why are only some movements associated with his eating affected? What changes can Mr Drewer expect as a result of the surgery?

[9 mins]
Answer: Initial tumor development puts pressure on branch of facial nerve (CN VII) to buccinator muscle (buccal branch) => difficulty in moving food out of cheek, especially space beside lower jaw. Jaw muscles for chewing (temporalis, masseter, pterygoids) still OK since they are innervated by trigeminal nerve (maxillary / 3rd branch). Upper three branches of facial nerve = temporal, zygomatic and buccal.
Loss of temporal branch function will affect the frontalis m. which raises the eyebrows and furrows the brow when frowning and the orbicularis occuli m. which circles the eye and closes it. Mr Drewer will be unable to close his eye and the lower lid of the eye may droop. Impaired blinking may lead to corneal ulceration. The zygomatic branch supplies the levator labii superioris alaeque nasi m.(raises the upper lip and flares the nose), labii superioris m (raises the upper lip), levator anguli oris and zygomaticus ms. (raise the angle of the mouth). He will be unable to smile / sneer/ pout on that side. He will also have difficulty eating without dribbling, and may have some speech difficulties. The buccal branch supplies buccinator m. and the muscle around the mouth (orbicularis oris m.). In addition to having difficulty with chewing he will not be able to purse his lips as in whistling or be able to blow. The corner of his mouth will sag on the affected side. Again high chance of dribbling and speech difficulty due to impaired lip motility.

Comment: clear passes = 88% of answers Very well done by most of the class. This was one of the minicases we worked through in class.
A few of you said that the upper part of the facial muscles would still be OK, due to the bilateral supply: the bilateral contribution to the facial nerve is in the CNS: here we are talking about a

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peripheral lesion which is unilateral. The facial nerve supply of the lacrimal gland (parasympathetic) and tongue (sensory) takes different peripheral routes and are not affected here. ----------------------------------------------------------------------------------------------------------------------------

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feedback on mss exam 2007

THE PROCESS: This was the third year in which we used a pure pass / fail criterion based marking system for MSS. The sample answers were generated by Ian using realistic time constraints: ie each sample answer was initially written in 9 minutes. A few of them were edited subsequently to take into account some of the acceptable alternative ways of answering that some of you came up with. In order to clearly pass any question, you had to get nearly all of the key points in the sample answers. This sounds tough, but by setting the standards this high, we can be sure that when we say youve passed, we can be confident that you really do know the material. If you did not show a clear pass on the question it was usually scored as a borderline. Fails were reserved for badly incomplete or erroneous answers. You had to get clear passes on 7 of the 10 questions to pass the exam. Any paper that did not reach this criterion on the first marking was looked at again and each borderline question was re-marked by both Sue and Ian, until it was clear that the paper was an overall pass or fail. THE ANALYSIS: Overall, we were somewhat disappointed by the quality of the answers this year. Neverhtelss. some of you did really well right across the paper. Two of the questions should have been familiar to you: question 3 asked about a set of actions that were a key element of the Mary ORiordan case; and question 8 was an extension of one of the mini-cases that we spent quite a bit of time working through in one of the thursday sessions. Nevertheless, neither of these questions was done very well. Part A and Part B of the written paper were matched: in each part there was a question about bone metabolism, joint pathology, upper limb function, lower limb function, and the axial skeleton / trunk. One question in each pair was somewhat more straight forward than the other. In general, you did the questions with a higher component straight recall better than those where you had to interpret the question a little more carefully and synthesise an answer from what you know. This suggests that many of you did not really come to grips with notions of how things work. There is a statistical analysis of these outcomes following the sample answers. Many of you gave us the impression that you had not carefully read the question. For example, in each question, we told you what the presenting complaint was: you didnt need to try to come up with a diagnosis - and those of you who did, usually got it wrong...

100

FLINDERS UNIVERSITY ADELAIDE AUSTRALIA

SCHOOL OF MEDICINE

AUGUST EXAMINATIONS 2007 SECOND YEAR BMBS

KNOWLEDGE OF HEALTH & ILLNESS

MUSCULOSKELETAL SYSTEM
TIME:
1 hour 30 minutes
None

MATERIALS ALLOWED IN THE EXAMINATION ROOM: INSTRUCTIONS TO CANDIDATES:

Write your student number on each examination booklet AND the attached marking slip. Start answers to each question on a new page.

MARKING SCHEME:
Each question will be marked to a pass/fail set of criteria. To pass the exam, you must pass seven (7) of the ten (10) questions. All questions are weighted equally. This examination is in 2 sections: Section A and Section B, which are weighted equally. Section A Section B Questions 1-5 (Suggested time 45 minutes) Answer these 5 questions in the answer booklets marked Section A Questions 6-10 (Suggested time 45 minutes) Answer these 5 questions in the answer booklets marked Section B

You are encouraged to make use of diagrams in your answers.

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SECTION A
weighted equally)

(allow 45 minutes to answer this section; all questions are

Walter Smithson, aged 47, has been battling alcoholism for more than 20 years. He reports increasingly severe pain and stiffening in his right hip that suddenly has become even worse. Radiographic investigation reveals collapse and marked sclerosis of the head of the femur with adjacent areas of rarefaction. This appearance is consistent with avascular necrosis due to microvascular disease associated with prolonged alcoholism.
Question 1. How do you explain these abnormalities in the appearance and strength of Mr Smithsons femur? Why has the head of the femur collapsed? How would you treat the problem with his hip? Explain your rationale.

[9 mins]
ANSWER: Normal bone is highly vascularised: strong link between microvasculature and microscopic structure of the bone in that each osteon / Haversian system has a blood vessel / capillary running inside the Haversian canal. The blood vessels provide nutrients to the bone cells, and interact with them in the regulation of bone metabolism (eg: remodelling of bone must include remodelling of the microvasculature; calcium moves between the bone matrix and the circulation). If the microvasculature is compromised, so is bone metabolism and bone structure. Initial response is an attempt by bone to recover / repair leading to sclerosis (like bone scarring): hyperdense, but not very strong. Then, ischaemic / sclerotic bone collapses and degenerates, leading to reduced bone density. Increased resorption also could be a consequence of an inflammatory reaction to the necrosis. Head of the femur experiences very high loads during normal activity: probably collapsed at point of contact between head of femur and acetabulum. Pain due mostly to bone damage; possible osteoarthritic degeneration and inflammation around joint secondary to on-going ischaemic damage to bone. Most likely treatment is hemi-arthroplasty (ie replace head of femur). (bone cannot recover in face of ongoing ischaemia). Depending on level of any associated osteoarthritic damage to joint, may require total replacement. Try to manage alcohol abuse, in attempt to prevent further vascular disease, including risk of DVTs after surgery. Consider dietary deficit in vitamin D secondary to alcoholism. COMMENT: Overall, this question was not done very well. Many of you commented about the poor blood supply to the neck of the femur, which is true and certainly contributes to worsening the problem. However, very few of you made the straightforward connection between the necessity for a functional microcirculation in the bone, and the maintenance of normal bone function. Remember: every osteon / Haversian system has a blood vessel within that is essential for providing nutrients to the bone cells, and is an critical part of the remodelling process... A lot of you didnt mention the sclerosis at all (it featured in at least two of the mini-cases). It was hard to pass the question clearly if you didnt answer the last part: what you could do about Mr Smithsons condition... Question 2. What features limit the movement of a healthy hip joint? How do they contribute to the stability and load bearing capabilities of the hip? What are the most common reasons for failure of the joint?

[9 mins]

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ANSWER: Overall stability provided by deep ball and socket structure (head of femur to acetabulum, deepened by acetabular labrum, and stabilised by tight joint capsule). Extension limited by ligaments of joint capsule: iliofemoral / ischiofemoral / pubofemoral, Flexion limited by hamstrings when knees are extended; by rest of body when knees flexed. Abduction limited by contact between greater trochanter and rim of acetabulum; range extended by lateral rotation which moves greater trochanter out of the way. Adduction limited by other limb and ligaments. During quiet standing with hip extended, most of the load is taken by iliofemoral ligament (tightened by centre of gravity going behind the hip joint). [Some postural stability provided by iliopsoas, quadratus lumborum, and erector spinae.] Hip joint failure: - avascular necrosis: vascular disease, fractured neck of femur - osteoarthritis: wear and tear, idiopathic disease - posterior dislocation when flexed (following impact onto knees) - osteoporosis, leading to fractured neck of femur, collapsed femoral head - consequences of developmental dysplasia COMMENT: The question was mainly about the limits to hip joint movement... many of you went off talking about all the muscles that move the hip without addressing the limits to movement: if this is all you talked about, it was hard to pass the question. The stabilisation of the sacro-iliac joint, while important to the strength of the pelvis, it not part of the hip joint... --------------------------------------------------------------------------------------------------------------------------

Mrs Millie OToole, aged 72, has had considerable pain and stiffness in the muscles of her shoulders and pelvic region for the preceding 6 weeks. Picking up even light objects has become difficult. Her ESR (erythrocyte sedimentation rate) is abnormally high. Suspecting polymyalgia rheumatica, an inflammatory condition affecting muscles, her doctor prescribes prednisolone, and two days later, her pain and stiffness have regressed significantly .
Question 3. Briefly describe the muscles and their actions involved in picking up a light object, such as a piece of clothing on the floor. Why would Mrs OTooles shoulder stiffness impair this activity?

[9 mins]
ANSWER: Starting at the hand: picking up light object requires precision grip: - flex fingers with flexor digitorum superficialis (attach to middle phalanx) in combination with lumbricals to set angles of MCP / IP joints (the object is light so not much call on fl. dig. profundus) - thumb position set by thenar muscles (flexor pollicis brevis, opponens pollicis, adductor pollicis) and flexor pollicis longus. - wrist position set by flexor carpi radialis & ulnaris, extensor carpi radialis & ulnaris; may be some setting of pronation / supination position using pronator teres & quadratus / supinator. - elbow flexion mostly by brachialis; may be also brachoradialis depending on pronation / supination position and weight of object. - overall position of arm set by position of shoulder using rotator cuff and deltoid. Also serratus

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anterior, pectoralis minor, rhomboids position shoulder and provide strength for the lift. Almost any movement of the upper limb requires movement of the scapula as well as the gleno-humeral joint. Therefore, inflammation and pain in any of these muscles would generate stiffness and reduced strength / mobility. COMMENT: This question was almost exactly the same situation as seen in the Mary ORiordan case, where she had a problem in picking up her kettle. Despite this, many of you could not give a precise description of a sequence of muscle actions involved in picking up a light object, and very few of you mentioned the simple point that if you move your arm, you nearly always move the shoulder in some way. Some of you took a cue from the question stem and decided to focus on the muscles of the shoulders, back and hips. This was OK, but you still had to get them correct: lots of eccentric contractions going on to hold the body against gravity, eg erector spinae, , hamstrings at hips, quadriceps acting at knees, triceps surae (mostly soleus) at ankle. Another strange track that some of you took was to speculate on the cause of the shoulder stiffness, and went on to talk about various ideas of arthritis etc. But the question told you that the problem was muscle stiffness... there was no need to consider anything else. So no credit for doing so. --------------------------------------------------------------------------------------------------------------------------

Shoulder pain and impaired function also can be caused by generalised rheumatoid arthritis. Some improvement may be obtained by operative synovectomy (ie, surgical removal of some of the synovium) of the glenohumeral joint.
Question 4. What changes would you expect to see in a plain radiograph of the glenohumeral joint affected by severe rheumatoid arthritis? Explain your predictions. Why would removing some of the synovium improve joint function?

[9 mins]
ANSWER: Serious RA of a large joint would include: - loss of joint space due to erosion of the articular cartilage (inflammation from enlarged pannus derived from synovial membrane). - degeneration of bone under joint surfaces (subchondral cysts) seen as regions of sclerosis adjacent to areas of reduced bone density; - probably further osteoporosis of bone adjacent to joint due to on-going inflammation promoting osteoclast activity over osteoblast activity. - possible osteophytes around margins of joint in response to damaged articular bone and secondary osteoarthritic changes. - possible misalignment of joint due to damaged / degenerated joint surfaces / glenoid labrum; also possible involvement of tendons near joint (eg. long head of biceps) Shoulder joint has a large loose capsule, lined with synovial membrane; removing some of this will reduce amount of inflamed synovium and thereby reduce total joint inflammation and help slow down or prevent further damage to the joint from the RA. Reduced swelling etc also would help increase joint mobility if the articular damage has not gone too far. COMMENT: This question was well done overall. Some of you fell into the trap of forgetting that the question was about the shoulder, not the hands or feet... --------------------------------------------------------------------------------------------------------------------------

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Frank Fittler (known to his associates as Freaky), aged 35, felt a severe pain in his back while lifting a bag of fertilizer destined for his hydroponic herb garden. He was unable to straighten his back, and felt additional pain radiating through his lower right leg. Two days later the pains were still present. CT scans revealed a prolapsed disc between the 4th and 5th lumbar vertebrae.
Question 5. What is the normal function of an intervertebral disc? How does it work? What happens when a disc prolapses? How could this lead to pain in Freaky Franks lower leg?

[9 mins]
ANSWER: Main function of intervertebral disc is to act as shock absorber between adjacent vertebrae. Also acts to allow some degree of movement between the vertebrae. Disc consists of jelly-like core = nucleus polposus, made of highly hydrated glycoprotein matrix, so mostly = water. Outer layer = annulus fibrosus = fibrocartilage with concentric bands of collagen fibres; each layer of collagen runs in an opposite direction (similar to cross-ply tyre). Core of the disc is largely incompressible, as long as outer layers hold => resists compressive forces, typically generated during flexion / lateral flexion. Prolapse occurs when the annulus fibrosus ruptures leading to expulsion / protrusion of the nucleus polposus when loaded. This generates pain due to tissue damage in the disc itself, associated inflammation affecting nearby tissues, such as longitudinal ligaments of vertebrae. Pain in leg could be due to inflammation spreading to sheath of nearby spinal nerve roots; pressure from disc on the nerves with associated inflammation; potentially also could be segmentally referred pain from the disc and surrounding tissue. COMMENT: This question was well done by most of you. Some of you did an excellent job of explaining the various options for generating the radiating pain. A few of you didnt seem to notice that the questions told you the level at which the prolapse occurred and headed off into other areas of the vertebral column... -------------------------------------------------------------------------------------------------------------------------

As a teenager, Helen Vander fell down some stairs and badly broke her ankle. She went on to play basketball semi-professionally, and during her playing career, she severely sprained the same ankle on several occasions. Now, aged 53, she has severe degenerative arthritis of talo-crural and subtarsal joints. It is likely the ankle will need to be treated by arthrodesis (surgical fusion of the joints).
Question 6. Briefly discuss the normal pathogenesis of osteoarthritis? How can injury to a joint pre-dispose it to developing osteoarthritis?

[9 mins]
ANSWER: OA can be idiopathic or as a result of injury to the articular cartilage. Initial damage associated with eburnation or fibrillation of the cartilage. Collagen fibres just below articular surface of cartilage start to fray as matrix breaks down; matrix metalloproteinases increase activity leading to hydration and degeneration of matrix. All this leads to reduced ability to act as lubricating / load bearing surface => further wear => further damage and so on.

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As articular cartilage degenerates further, small pieces may flake off into joint => clicks and crepitations; further wears gets down to subchondral bone, leading to more pain, reduced joint function. Continued wear / abnormal loading on bone may lead to formation of osteophytes around joint margins. Secondary inflammation may contribute to pain, swelling, osteoporosis around joint. Injury to cartilage not well repaired. Hyaline cartilage tends to be replaced by fbrous connective tissue => reduced / impaired lubrication properties => predisposed to further degenerative change. COMMENT: Quite a few of you mixed up the involvement of chondrocytes and osteocytes iin the pathogenesis of the bone abnormalities. Question 7. Compare how the ankle and foot absorb the loading forces generated by quiet standing, walking and landing from a jump. What are the relative contributions of the skeleton, ligaments and muscles in each case?

[9 mins]
ANSWER: Quiet standing: load taken by bones and ligaments holding them together. Ankle tends to be dorsiflexed, which is more stable (held together by collateral ligaments). Longitudinal arches of feet supported by longitudinal ligaments (eg plantar calcaneo-navicular; spring ligament); talus supported as top of arch (keystone) by sustentaculum tali of calcaneus. Transverse arches supported by wedge-shaped cuneiforms and proximal ends of metatarsals, held together by ligaments. Walking: at heel-strike, tibialis anterior contacts eccentrically to transfer load from heel to front of foot. Loading in foot mostly taken by the bone of the arched. Landing from a jump: landing on toes => posterior calf muscles (esp. gastrocnemius) contract eccentrically to absorb load; tibialis posterior; fibularis (=peroneus) longus help support arches and contract eccentrically to absorb impact forces / loads. COMMENT: A common error here was confusing the eccentric and concentric contractions of the muscles around the ankle: if you land from a jump onto your toes, the posterior compartment (plantar-flexors) work eccentrically; if you place you weight onto your heels as in normal walking, then the anterior compartment (dorsiflexors = extensors) work eccentrically. --------------------------------------------------------------------------------------------------------------------------

You may remember Mrs McGuiness, who was suffering from Pagets disease. One consequence of the disease was that her skull showed areas of low bone density (osteoporosis) adjacent to areas of high bone density (osteosclerosis) accompanying a net increase in apparent thickness of her skull. Her disease is now being treated with bisphosphonates that inhibit osteoclast activity.
Question 8. Briefly discuss the main factors that contribute to the maintenance of normal bone density in healthy people. How would inhibition of osteoclast activity slow the progression of Mrs Guiness disease?

[9 mins]
ANSWER: Bone density depends on maintaining proper balance between osteoblast and osteoclast activity: regulated by levels of oestrogen / vitamin D / parathyroid hormone / weight-bearing exercise.

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Oestrogen promotes activity of osteoblasts and inhibits activity of osteoclasts (inhibits formation of osteoclasts from precursor cells; promotes apoptosis of osteoclasts). PTH levels increase in response to low blood calcium levels; promotes osteoclast activity via receptors on osteobalsts; also promotes calcium retention by kidneys. Vitamin D required to maintain bone mineralisation; activates both osteoblasts and osteoclasts; activated osteoclasts release calcium to be used by nearby osteoblasts. Cytokines (eg IL-1, IL-6, TNFalpha) generated by inflammation around joints or bone infection activate osteoclasts => localised reduction in bone density Overall bone mass maintained / increased by weight-bearing exercise (sensor may be piezo-electric effects); peak bone mass probably achieved in most people as young adult / early middle-age; bone loss proceeds from there. Inhibition of osteoclasts will lead to reduction of bone loss in Pagets disease; likely to help break cycle of out-of-control feedback between osteoclasts and osteoblasts => reduces rampant remodelling. ----------------------------------------------------------------------------------------------------------------------------

Kane LeMont, aged 19, fell into an alcoholic stupor after a night of heavy drinking with his mates. He had passed out in a kitchen chair with his right arm draped over the back of the chair. When he finally awoke several hours later, he realised that he could not move his arm properly and got taken to hospital. Examination revealed compression damage to the posterior cord of his brachial plexus.
Question 9. How would this injury affect the function of Kanes upper limb? Which muscle groups and actions would be affected? If the lesion to the brachial plexus did not recover, how could you maximise the remaining function in his limb?

[9 mins]
ANSWER: Posterior cord continues on as radial nerve => loss of function to all extensor compartment => - no active elbow extension (triceps; could use gravity and elbow flexors eccentrically) - brachoradialis inactive => reduced elbow flexion strength, especially in mid supine/prone position - no extension of wrist (extensor carpi ulnaris / radialis) and weakened ulnar / radial deviation (only flexors available) - impaired power grip due to inability to hold wrist steady - loss of finger extension => reduced fine control of fingers (must rely on lumbricals interacting with flexors) Function improved by providing a wrist splint / support to prevent passive flexion => more power grip strength; more stability at wrist for precision movements. COMMENT: Many of you didnt really define very well which muscles at which joints would be affected by the lesion. Also, its important to get the names of the nerves correct: the one that goes around the neck of the humerus is the axillary nerve, not the axial or ax-anything else... ----------------------------------------------------------------------------------------------------------------------------

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Jody-Louise Heffernan, aged 17, was knocked off her bicycle by a car. She went over the handle bars and landed on the back of her head and neck. She was wearing a helmet and was lucky not to be more seriously injured. However, she had a severe pain in her neck, and she felt as though her head was about to fall off. X-rays revealed a fracture at the base of the odontoid process of the axis with some dislocation of the atlanto-axial joint. She was treated with a halo brace that immobilised the joint and she made a full recovery.
Question 10. How do movements at the atlanto-axial and atlanto-occiptal joints contribute to the orientation of the head? How does the rest of the cervical spine contribute to the full range of movements of the head? What would have been the most probable outcome if Jody-Louises odontoid process had become dislocated rather than fractured?

[9 mins]
ANSWER: Atlanto-occipital joint (C1 => occipital condyles of skull) => gentle flexion / extension (ie nodding) Atlanto-axial joint (C1 => C2) => gentle rotation from side to side (ie shaking head); atlas rotates around the odontoid process (= dens) of axis; held in place by transverse ligament. [Position of head at these joints controlled by vestibular and visual inputs via brain stem motor pathways] Facets of cervical vertebrae oriented more or less in transverse plane (+ flexible intervertebral discs; small spinous processes) => some movement in nearly every direction: flexion / extension; rotation; lateral flexion. Contribute to more extreme movements of head and neck (eg turning to look behind). Dislocation of the odontoid process => tear / rupture of transverse ligament => highly likely that it would spear into brainstem / cervical spinal cord => almost certainly fatal. COMMENT: You really needed to use correct anatomical terminology here: you are training to be professionals...

END OF EXAMINATION ************************************

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mss written exam 2007

---------------------------------------------------------------------------------------------------------------------Q1. bone metabolism* Q2. lower limb Q3. upper limb* Q4. joint disease* Q5. axial Q6. joint disease Q7. lower limb* Q8. bone metabolism Q9. upper limb / nerves Q10. axial* 13 14 19 30323 + 14 20 + 14 27 22 40 + 16 7 15 24 30 20 29 49 59 38 79 + 81 + 74 + 51 58 52 44 18 12 10 9 19 15 9 515 20

fail

borderline

pass

strong pass

----------------------------------------------------------------------------------------------------------------------

OVERALL

12

23

59

13

---------------------------------------------------------------------------------------------------------------------* bold questions non-bold questions = require synthesis = mostly recall

bold numbers = significant deviation from overall pattern: + => more than expected - => less than expected

---------------------------------------------------------------------------------------------------------------------recall questions synthesis questions 9% 14% 18% 25% 61% 49% 12% 12%

fail

borderline

pass

strong pass

----------------------------------------------------------------------------------------------------------------------

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and now a bit of art ....

ODE TO A KNIGHT-IN-GA
by Simon Marrable, Paul Lambert, Shona Charlton & Chris Brampton Year 2 BMBS 2001 reprinted here by permission of the authors {published originally in placebo november 2001}

Twas a strange time in August When I came to this land, A place of head And of arm And of foot And of hand. Here I found a problem Of a muscular kind And a problem with brains But pay that no mind. We picked up some dead bits And flopped them around, Delved superficious And skimmed past profound. Is this rectus of longus? Or brevis supine? Does it adduct my leg? Or hold up my spine? What say you Prof Gibbo? To this problem of mine. Id look in a book But I dont have the time. Well he looked at me strangely And said Youll be fine As he pulled up a corpse And told me this rhyme. Its a body you see just how it goes. Dont fret about latin or coracoid crows. Learn whats important And the questions I pose. But dont forget thumbs And opposable toes. Now longus is long

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And rectus is straight. Brevis is short But may help your gait. Quadratus is square And vastus is great, Frontalis is one And biceps are eight. Find a pec Now a lat Now a quad And an ab... No not over there Did you not attend lab? Now you see, Sartorius helps when sowing up suits, Though sitting cross leggeds A pain in the glutes; It also is known for sartorial splendour, This rotator of legs And inner knee bender. Your knowledge seems little Your future looks grim, But tell a good story And Ill pass you on a whim. Just remember my words And learn what you see. And make sure you know Your arse from your knee.

***************************

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