Case 9 Flashcards

Question

describe what causes muscular contraction (power stroke)?

Answer 1

1. the hydrolysation of ATP into ADP and inorganic phosphate allows the myosin head to return to the resting position 2. ADP + Pi are bound to myosin as myosin head attaches to actin 3. ADP + Pi release causes head to change position and actin filament to move 4. binding of ATP causes myosin head to detach from the actin filament - Attached state -> ATP binds to myosin head, causing the dissociation of the actin-myosin complex -> - Released state -> ATP is hydrolysed, causing myosin heads to return to their resting conformation -> - Cocked state -> a cross-bridge forms and the myosin head binds to a new position on actin -> - Cross-bridge state -> phosphate is released – myosin heads change conformation, resulting in the power stroke – the filaments slide past each other -> - Power-stroke state -> ADP is released -> - Attached state

Answer 2

 H & I bands shorten |  A bands stay the same size

Answer 3

Summation occurs in two ways:  By increasing the number of motor units contracting simultaneously, which is called multiple fibre summation.  By increasing the frequency of contraction, which is called frequency summation and can lead to tetanisation (sustained muscle contraction?).

Answer 4

* As the synaptic activity driving a motor neuron pool progressively increases, low threshold S motor units are recruited first, then FR motor units, and finally, at the highest levels of activity, the FF motor units. * As a result, this systematic relationship has come to be known as the size principle.

Answer 5

The different motor units are driven asynchronously (not occuring at the same time) by the spinal cord, so contraction alternates among motor units one after the other, thus providing smooth contraction even at low frequencies of nerve signals.

Answer 6

• Isometric muscle contraction – when the muscle does not shorten during contraction. The length of the muscle remains unchanged.  E.g. pushing against a wall. • Isotonic muscle contraction – when the length of the muscle shortens but the tension on the muscle remains constant throughout the contraction. • Concentric muscle contraction – in the direction of contraction of a muscle (towards origin of muscle). • Eccentric muscle contraction – in the opposite direction of contraction of a muscle (towards insertion of muscle). isotonic contractions are either concentric (working muscle shortens) or eccentric (working muscle lengthens) Muscles contract better at their optimum length – most of our muscles are maintained within this optimum range most of the time Contraction is stronger and faster the closer the muscle initial length is to the optimum length

Answer 7

 Interaction of actin and myosin filaments during contraction.  Pumping of Ca2+ from the sarcoplasm back into the sarcoplasmic reticulum after contraction.  Restoration of the intracellular ionic environment after muscle contraction because of the actions of the Na+/K+ pump.

Answer 8

Oxidative phosphorylation |  This type of phosphorylation is an aerobic process in which ATP is liberated from fats, carbohydrates, and protein.

Answer 9

Anaerobic glycolysis  This causes the breakdown of glucose to lactate and pyruvate with the release of energy.  This energy is used to convert ADP to ATP.  ATP is generated at double the rate of oxidative phosphorylation.  This is predominant in type II muscle fibres that have few mitochondria but many glycogen granules.  This is only an intermediate-term source of energy, because lactate and pyruvate accumulate in the cell.

Answer 10

• Creatine phosphokinase  Phosphocreatine contains high-energy phosphate bonds, which can be used to phosphorylate ADP to ATP by the enzyme creatine kinase.  It is located in the Z line. • Myokinase  The enzyme myokinase catalyses the transfer of a phosphate group from one ADP molecule to another to form ATP and the by-product adenosine monophosphate (AMP).  This is known as the ‘last gasp’ of short-term energy stores.

Answer 11

* Occurs in slow twitch and intermediate type of fibres. * Reduction of O2 into H20 using electrons from NADH and FADH2. * Occurs on the inner mitochondrial membrane. * Explained by the principle of the chemiosmotic theory. * Involves a series of “downhill” electron transfers – exergonic. * Energy used to drive protons through the inner membrane. * Transmembrane chemical + electrical difference drives ATP synthesis. - 38 ATP molecules produced per molecules of glucose - But quite a slow process – plentiful but slow

Answer 12

* Occurs in fast twitch type of fibres. * Direct formation of ATP by phosphorylation of ADP. * Produced by reaction with high free energy. * These reactions do not require oxygen, therefore, it is important in tissues short of oxygen (e.g. skeletal muscles). - Produces 2 ATP molecules - Limited supply of ATP but fast

Answer 13

* In normal muscular contraction, glucose is converted into pyruvate and then CO2. * This requires ATP via oxidative phosphorylation. * There is plentiful ATP but the process is slow. * In intense muscular contraction, glycogen in converted into glucose and then lactate. * This requires ATP via substrate level phosphorylation. * There is limited ATP but the process is fast. * Oxygen and nutrient supply is rate limiting. • Muscle glycogen reserves are finite and lactate is a problem.  Oxygen is used by liver to produce glucose from lactate – Cori Cycle. • But muscle still needs a rapid method to produce ATP from ADP.  ATP and creatine are produced from ADP and Phosphocreatine via the enzyme creatine kinase.

Answer 14

muscle hypertrophy results from an increase in the number of actin and myosin filaments in each muscle fibre increase in size of fibres? • Along with the increasing size of myofibrils, the enzyme systems that provide energy also increase. This is especially true of the enzymes for glycolysis, allowing rapid supply of energy during short-term forceful muscle contraction.

Answer 15

The rate of synthesis of muscle contractile proteins is far greater when hypertrophy is developing. In turn, some of the myofibrils themselves have been observed to split within hypertrophying muscle to form new myofibrils. hyperplasia = increase in number of fibres

Answer 16

 When a muscle remains unused for many weeks, the rate of degradation of the contractile proteins is more rapid than the rate of replacement.  Therefore, muscle atrophy occurs.  The pathway that appears to account for much of the protein degradation in a muscle undergoing atrophy is the ATP-dependent ubiquitin-proteasome pathway.  Proteasomes degrade damaged or unneeded proteins by proteolysis.  Ubiquitin is a regulatory protein that labels which cells will be targeted for proteasomal degradation.

Answer 17

 When muscles are stretched to greater than normal length, new sarcomeres are eventually added at the ends of the muscle fibres, where they attach to the tendons.  This increases the length of muscles.

Answer 18

* Loss of innervation to a muscle results in atrophy. * After about 2 months, proteasome degradation begins to occur, causing further muscle wastage. * If the muscle is once again innervated, then there can be full recovery within 3 months. • In the final stage of denervation atrophy, most of muscle fibres are destroyed and replaced by fibrous and fatty tissue.  This fibrous tissue has a tendency to continue shortening for many months, which is called contracture. • The fibres that do remain are composed of a long cell membrane with many muscle cell nuclei but with few or no contractile properties and little or no capability of regenerating myofibrils if a nerve does regrow.

Answer 19

* When some but not all nerve fibres to a muscle are destroyed, the remaining nerve fibres branch off to form new axons that then innervate many of the paralyzed muscle fibres. * This causes large motor units called Macromotor units. * This decreases the fineness of control one has over the muscles but does allow the muscles to regain varying degrees of strength.

Answer 20

Exercise can increase muscle mitochondrial biogenesis (i.e. gives more mitochondria per muscle cell).  This is probably via Ca2+ signalling pathways in the cell as well as via a chronic imbalance of ATP demand versus ATP production by mitochondria which causes activation of signalling protein kinases. - Acute exercise initiates higher levels of mRNA, as observed during the recovery period following exercise - The protein products of the mRNA are imported into pre-existing mitochondria, or be incorporated into multi-subunit complexes of the respiratory electron transfer chain - The result is the expansion of the mitochondrial network within muscle cells and the capacity for aerobic ATP provision - The chain of events becomes impaired with chronic inactivity and aging, which leads to a reduced muscle aerobic capacity and an increased tendency for apoptosis (driven by cytochrome-c leakage from the mitochondria) - The resumption or retention of an active lifestyle can ameliorate this, improve endurance, and help maintain muscle mass in older age

Answer 21

AMPK – adenosine monophosphate-activated protein kinase:  This enzyme plays a role in cellular energy homeostasis.  This is the ‘fuel gauge of the cell’.  During a bout of exercise, AMPK activity increases while the muscle cell experiences metabolic stress brought about by an extreme cellular demand for ATP.  Upon activation, AMPK increases cellular energy levels by inhibiting anabolic energy consuming pathways (fatty acid synthesis, protein synthesis, etc.) and stimulating energy producing, catabolic pathways (fatty acid oxidation, glucose transport, etc.). AMPK + AMP -> AMPK-P = important in slow twitch muscle AMP -> IMP +NH3 = important in fast twitch muscle

Answer 22

 Skeletal muscle atrophy causes a drop in:  Protein levels, fibre diameter, force production, and fatigue resistance.  A reduction in protein synthesis coupled with increased protein degradation pathways contribute to muscle loss due to disuse.  Proteolytic pathways (ubiquitin-proteasome, lysosomal, and calpain) are involved in muscle atrophy.  Transcription factor NF-κB and myostatin are important cell signallers for muscle cell atrophy. Lack of exercise leads to increase in these factors in muscle.

Answer 23

one cycle of swing and stance by one limb

Answer 24

1. Heel strike (initial contact) – Gluteus maximus and Tibialis anterior 2. Loading response (foot flat) – Quadriceps femoris 3. Midstance – Soleus and gastrocnemius (together known as Triceps surae) 4. Terminal stance (heel off) – Soleus and gastrocnemius (Triceps surae)

Answer 25

The swing phase begins after push off when the toes leave the ground and ends when the heel strikes the ground. 1. Preswing (toe off) – Rectus femoris 2. Initial and Midswing – Iliopsoas and rectus femoris 3. Terminal swing – Hamstrings, Tibialis anterior and Ankle dorsiflexers

Answer 26

3. Terminal swing – Hamstrings, Tibialis anterior and Ankle dorsiflexers • The swing phase occupies approximately 40% of the walking cycle and the stance phase, 60%. • The stance phase is longer because it features a period of double support as the weight is being transferred from one leg to the other.  In running, there is no period of double support.

Answer 27

Most of the change in cycle time is due to shortening the stance phase; the swing phase remains relatively constant over a wide range of locomotor speeds.

Answer 28

local circuits in the spinal cord called central pattern generators

Answer 29

- apraxic gait - waddling gait - crossing over/scissoring gait - parkinsonian - hemiplegic - cerebellar ataxia - sensory ataxia

Answer 30

- Problem with cortical integration – frontal lobe damage (e.g. hydrocephalus, infarction). - Acquired walking skills become disorganized. - Shuffling small steps (marche a petit pas) may be seen here. - Patient usually has small-stepping, broad-based gait. - Patient almost seems to have forgotten how to walk.

Answer 31

- Muscle / hip disease. | - Patient bends their pelvis forward and walks with a waddle.

Answer 32

- Caused by bilateral spasticity. - Patient may walk stiffly on toe. - Patient has problems turning.

Answer 33

- Small paces, slow and shuffling gait (similar to marche a petit pas) - Stooped posture, reduced arm swing usually unilateral. - Tremor may increase on walking. - Basal ganglia dysfunction.

Answer 34

- Unilateral upper motor neuron lesion - caused by MS or stroke - Classically patient has a flexed upper limb and extended lower limb on the affected side. - To move the affected limb patient has to circumduct the leg

Answer 35

- Broad-based gait, patient may sway from side to side, possibly fall - Patient may appear drunk. - Due to cerebellar lesion.

Answer 36

- Patient over flexes hip, lifts knee high and slaps foot down on walking - This can occur in a patient with peripheral neuropathy (bilateral) or a common peroneal nerve lesion (unilateral) - form of ataxia (loss of coordination) caused not by cerebellar dysfunction but by loss of sensory input into the control of movement

Answer 37

- vision - proprioception - vestibular sense

Answer 38

• Ask the subject to stand with their feet together without support, first with their eyes open and then with their eyes closed. • Closing the eyes eliminates vision.  If the proprioception and vestibular pathways are intact the subject will not sway.  If patient sways - Romberg positive.  If the subject sways with their eyes closed this indicted a defect in their proprioception pathways.  If the patient starts to sway with their eyes open or closed, this indicates a cerebellar lesion.

Answer 39

* A fracture occurring in normal bone that has been subject to excessive and repeated trauma resulting in cumulative microscopic fractures. * Over time, these microfractures exceed the capacity of the normal healing process, resulting in the development of a macrofracture. * Patients are usually long distance runners, ballet dancers, footballers, and others who undergo regular intensive training. * Pain, localised tenderness, and swelling gradually develop. * Initially x-rays are normal, but a bone scan or MRI will usually allow diagnosis to be made. • Treatment – protected weight bearing, rest, cross-training, and (less common) surgery.

Answer 40

a surgical device that exerts external forces on part of the body to support joints or correcting deformity

Answer 41

* The hinged ankle foot orthosis (H.A.F.O) is a moulded plastic splint to stabilize the foot and ankle. * It may allow full up and down movement of the foot or it may have a system that will restrict the amount of ankle movement. * The orthotist will take a cast of the ankle to have one made specifically for the patient to meet their clinical needs. • Different foot lengths are available, some finishing behind the ball of the foot, whilst others will have a full foot to toe end.

Answer 42

* These are bony projections that occur at the sites of cartilage degeneration or destruction near joints and intervertebral discs. * They are usually shaped like a rose-thorn.

Answer 43

* Osteophytes form because of the increase in damaged joint’s surface area. * This is most common from the onset of arthritis. * Osteophytes limit joint movement and typically cause pain. • Osteophyte formation is related to sequential and consequential changes in bone formation that is due to aging, degeneration, mechanical instability, and disease.

Answer 44

• One of the most common knee injuries is an ACL sprain/tear. • Athletes who participate in high demand sports are more likely to injure it.  Higher incidence in females than males  This may be due to:  Physical conditioning  Muscular strength  Neuromuscular control  Pelvis size – females have wider hips and so working their legs will cause the vastus lateralis to develop more than the vastus medialis, thus pulling the patella laterally and causing the tear in the ligament.  Lower extremity (leg) alignment  Increased looseness in ligaments  Effects of oestrogen on ligament properties • Surgery may be required to regain full function of knee. • This will depend on several factors such as:  Severity of injury  Activity level • Damage to other structures in the knee are secondary:  Articular cartilage  Meniscus  Other ligaments

Answer 45

femur, tibia, patella • The kneecap sits in front of the joint to provide protection.

Answer 46

 Collateral ligaments  Medial  Lateral - These control the sideways motion of the knee and brace it against unusual movement.  Cruciate ligament  Anterior – runs diagonally in middle of knee and prevents tibia from sliding out in front of femur as well as providing rotational stability of the knee  Posterior o These are found inside the knee joint o They cross each other to form an "X" o These control the back and forth motion of the knee.

Answer 47

* Changing direction rapidly * Stopping suddenly * Slowing down while running * Landing from jump incorrectly * Direct contact or collision (football tackle)

Answer 48

• Pain with swelling:  Within 24 hours knee swells.  Swelling and pain may resolve on its own.  However, if sports are resumed, the knee will be unstable and there’s risk of further damage to the cushioning cartilage (meniscus). • Loss of full range motion. • Tenderness along joint line. • Discomfort while walking.

Answer 49

A physical examination as well as an X-ray and MRI scan will be carried out:  Physical examination – doctor will compare injured knee with non-injured knee.  X-ray – although this will not show any injury to ACL, it can show whether the injury is associated with a broken bone.  MRI – shows images of soft tissues – ACL.

Answer 50

Nonsurgical: - Bracing  This protects the knee from instability.  Crutches may also be given to keep prevent weight on your leg. - Physical therapy  As the swelling goes down rehabilitation program is started.  Specific exercises will restore function to knee and strengthen the leg muscles that support it.  First, returning motion to the joint and surrounding muscles is prioritised.  This is followed by strengthening program designed to protect the new ligament.  The final phase is aimed at a functional return tailored for the athlete's sport. Surgical: - Rebuilding the ligament  Most ACL tears cannot be sutured back together - to surgically repair the ACL and restore knee stability, the ligament must be reconstructed.  The doctor will replace the torn ligament with a tissue graft.  This graft acts as a scaffolding for a new ligament to grow on.  It may take up to 6 months for recovery.

Answer 51

Female athlete triad is a syndrome of 3 interrelated conditions which include:  Eating disorders (low energy availability)  Menstrual Dysfunction (Amenorrhoea)  Decreased bone mineral density (osteoporosis/ osteopenia) * This is seen in females participating in sports that emphasise leanness or low body weight. * The triad is a serious illness with lifelong health consequences and can potentially be fatal. * Suffering from one element predisposes to suffering from the other 2 as well.

Answer 52

``` • Clinical symptoms include:  Disordered eating and fatigue  Noticeable weight loss  Increased healing time from injuries  Increased incidence of bone fracture  Cessation of menses • Affected females may also struggle with low self-esteem and depression. ``` • Signs include:  Restrictive eating but not meeting the clinical criteria for an eating disorder.  Subtle menstrual disturbances such as a change in menstrual cycle length, anovulation, or luteal phase defects, but not yet have developed complete amenorrhea.  Athlete's bone density may decrease, but may not yet have dropped below her age-matched normal range.

Answer 53

• Energy is taken in through food consumption and our bodies expend energy through normal functioning as well as through exercise. • In the case of the triad, low energy availability may be due to:  Eating disorders - low caloric intake  Excess exercise and same food intake  Increase energy expenditure while also eating less • Having low dietary energy from excessive exercise and/or dietary restrictions leaves too little energy for the body to carry out normal functions such as maintaining a regular menstrual cycle or healthy bone density.

Answer 54

 Primary amenorrhoea, which is the absence of menstruation by the age of 16.  Secondary amenorrhoea, which is the absence of menstruation for 3 months in a woman who has previously had cycles.

Answer 55

 Polycystic ovary syndrome, where the ovaries don’t release the egg (ovulate).  The hypothalamus stops producing GnRH (needed in menstruation).  This can be triggered by excessive weight loss and exercise as well as stress.  Abnormally high levels of prolactin (hyperprolactinaemia).  Premature ovarian failure, when to ovaries stop working before menopause. * Weight fluctuations from dietary restrictions and/or excessive exercise affect the hypothalamus’s output of gonadotropic hormones. * Gonadotropic hormones stimulate growth of the gonads and the secretion of sex hormones. * These gonadotropic hormones play a role in stimulating oestrogen release from the ovaries. * Without oestrogen release, the menstrual cycle is disrupted. • Exercising intensely and not eating enough calories can lead to decreases in oestrogen:  The hormone that helps to regulate the menstrual cycle.  As a result, a female's periods may become irregular or stop altogether.

Answer 56

• This is a skeletal disorder characterised by compromised bone strength predisposing a person to an increased risk of fracture. • Low oestrogen levels + poor nutrition, especially low Ca2+ intake, can lead to osteoporosis  This condition may lead to stress fractures and other injuries. * With oestrogen deficiency, the osteoclasts live longer and resorb more bone. * As osteoclasts break down bone, patients see a loss of bone mineral density. * Low bone mineral density renders bones more brittle and hence susceptible to fracture. * Athletes are active and their bones must endure mechanical stress which means the likelihood of experiencing bone fracture is particularly high. • In terms of diet, a deficiency in the intake of calcium or vitamin D further exacerbates the problem of weak bones.

Answer 57

* This is described as pain along the inner edge of the shinbone (tibia). * They are a common injury affecting athletes who engage in running sports or other forms of physical activity. * Most prevalent lower leg injury. * It is characterised by general pain in the lower region of the leg between the knee and ankle. * They are caused by repeated trauma to the connective muscle tissue surrounding the tibia.

Answer 58

Pronation occurs when the ankle bone moves downward and towards the middle to create a more stable point of contact with the ground:  i.e. the ankle rolls inwards so that more of the arch has contact with the ground.  This abnormal movement causes muscles to fatigue more quickly and unable to absorb any shock from the foot hitting the ground.  Over-pronation is the common cause for shin splints and action should be taken to offset the biomechanical irregularity.

Answer 59

* Pain associated with shin splints is caused from a disruption of Sharpey's fibres that connect the medial soleus fascia through the periosteum of the tibia where it inserts into the bone. * With repetitive stress, impact forces fatigue the soleus and create repeated tibial bending. * The impact is worsened by running uphill, downhill, on uneven terrain or on hard surfaces. * Improper footwear, including worn-out shoes can also contribute to shin splints. * Treatments include resting, applying ice to shin to reduce (increase?) blood flow, elevation of legs reducing swelling and pain killers/anti-inflammatory.

Answer 60

• Characteristics of individuals  Certain individuals have characteristics that make them susceptible to placebo effects.  Characteristics include emotional dependency, extroversion, neurosis, being introverted and being highly suggestible. • Characteristics of the treatment  This depends on the effectiveness of the placebo effect in the actual process involved in the placebo treatment.  For example, larger pill size, 2 pills instead of 1 and surgery have shown to be more effective in eliciting a change. • Characteristics of the health professional  The kind of professional administering the placebo may determine the degree of placebo effect.

Answer 61

* An examination of the processes involved in the interactions between patients, the treatment and the health professionals. * There are mechanisms to understand this multidimensional process: - Experimenter bias  This refers to the impact that the experimenter’s expectations can have on the outcome of a study.  I.e. the doctors expect me to get better. - Patient expectations  Suggests that most patients experience spontaneous recovery following illness as most illnesses go through periods of spontaneous change and that patients attribute these changes to the treatment. - Reporting error  Patients expect to show improvement following medical intervention, want to please doctor and therefore show inaccurate reporting by suggesting that they are getting better, even when their symptoms remain unchanged.  Doctors have also shown to report errors because they would like to see improvement in patients. - Conditioning effects  Patients associate certain factors with recovery and an improvement in their symptoms.  The conditioning theory states that the unconditioned stimulus (treatment) would usually be associated with an unconditioned response (recovery).  However, if this unconditioned stimulus (treatment) is paired with a conditioned stimulus (e.g. hospital, a white coat), the conditioned stimulus can itself elicit a conditioned response (recovery, the placebo effect). - Anxiety reduction  Placebos decrease anxiety and pain reduction, thus helping the patient to recover.  Relating this to the gate control theory, anxiety reduction may close the gate and reduce pain, whereas increased anxiety may open the gate and increase pain.  Placebos may decrease anxiety by empowering the individual and encouraging them to feel that they are in control of their pain.

Answer 62

* Placebos increase endorphin (opiate) release – the brain’s natural painkillers – which therefore decreases pain. * Evidence has been shown through the dependence, withdrawal and tolerance nature of placebos which is very similar to heroin; it also causes increased opiate release. * Placebos work because the patient and the health professionals expect them to work. * This emphasises the role of expectations and regards placebo effects as an interaction between individuals and between individuals and their environment. • Cognitive dissonance theory  Cognitive dissonance is the mental stress or discomfort experienced by an individual who holds two or more contradictory beliefs, ideas, or values at the same time, or is confronted by new information that conflicts with existing beliefs, ideas, or values. (e.g. your parents tell you at a young age that kids with blue eyes = bad, as you grow, you find out that they are just like you and so they aren’t bad at all……you experience cognitive dissonance as you are confronted with two contradictory views)  Cognitive dissonance leads to either a change in behaviour (you start playing with kids with blue eyes) or a change in attitude (you ignore kids with blue eyes).  This theory argues that faith healing has lasted and homeopathic medicines are still used because they work.  This is because time, effort and money is put into them and if they were readily available, they would not be as effective.  Investment is needed and an individual needs to:  Justify their behaviour.  See themselves as rational and in control.  Leon Festinger's theory of cognitive dissonance focuses on how humans strive for internal consistency.  When inconsistency (dissonance) is experienced, individuals tend to become psychologically uncomfortable and they are motivated to attempt to reduce this dissonance, as well as actively avoiding situations and information which are likely to increase it.  This leads to a placebo effect – “this treatment will work because I have put time and money into it” (this is a change in attitude with regards to treatment) • The theory is supported by the following:  It can explain all placebo effects, not just pain.  It does not require patient expectations, but choice.  It suggests the individual needing commitment to the medical procedure such as investment. • Problems with this theory are:  Unconscious regulating mechanisms are not explained.  The theory has only been tested on acute pain in labs – not in real life.  Subjects have been provided with money and persuaded to justify behaviour which may have led to their increased anxiety and therefore pain perception.  Therefore, according to cognitive dissonance theory, dissonance can be resolved by the placebo having an effect on the individual’s health status by activating unconscious regulating mechanisms.

Answer 63

Health beliefs • For a placebo to have an effect, the individual needs to have a belief that the intervention will be effective. • For example, taking a placebo as a prescribed pill will be more effective, as it is a traditional medical intervention, than a placebo in the form of herbal medicine which will only be effective if the patient believes in alternative medicines. • Patients’ beliefs may themselves be a mechanism for explaining placebo effects such as having a direct effect on health through physiological changes, or an indirect effect via behavioural change. Illness Cognition • For a placebo to have an effect, the individual needs to hold particular beliefs about their illness. • If an individual believes that their illness has a medical cause then a placebo in the form of a pill would be effective.

Answer 64

* A doctor may need to believe in the intervention for it to have an effect. * Theories of health professionals’ health beliefs and their role in doctor–patient communication illustrate a useful emphasis on interaction rather than individual characteristics.

Answer 65

* If an individual believes that they have taken something or behaved in a way that may promote good health, they may also change other health-related behaviours (e.g. smoking, drinking, exercise), which may also improve their health. * The choice to take a medication may itself be seen as a health-related behaviour, and may be predicted by theories of behaviour and behaviour change.

Answer 66

* If placebos have an effect either directly (physiological change) or indirectly (behaviour change) then this is in parallel with theories of stress. * Placebos may function by reducing any stress caused by illness. * If an individual has taken control of their illness (perceived control) this may reduce the stress response, reducing any effects this stress may have on the illness.

Answer 67

* Placebo-induced pain reduction may be mediated either by physiological changes, such as opiate release, or by anxiety reduction (gate control theory) which suggests that the experience of pain is a result of an interaction between psychological (beliefs, anxiety) and physiological (opiates) processes. * Placebo-induced pain reduction may also be mediated by patient expectations and previous experience about the efficacy of the treatment intervention.

Answer 68

* In this, the physician presents all options and the patient makes his/her own choice. * The physician provides expert knowledge only and makes no recommendations.

Answer 69

* The physician explains all the option and also makes a recommendation. * The physicians must base their recommendations on the patient’s values rather than on their own. * This can require time and advanced communication skills. * When a patient asks the physician what he/she should do, the physician mist consider the patient’s perspective and ensure he/she is neither intentionally nor unintentionally coercive.

Answer 70

* Greenstick fracture – incomplete fracture – the broken bone is not completely separated * Stable fracture – the broken ends of the bone line up and are barely out of place * Open, compound fracture – the skin may be pierced by the bone or by a blow that breaks the skin at them time of the fracture – the bone may or may not be visible in the wound * Transverse fracture – has a horizontal fracture line * Oblique fracture – has an angled pattern * Spiral fracture – the break spirals around the bone; common in a twisting injury * Comminuted fracture – the bone shatters into three or more pieces * Compression – the bone is crushed, causing the broken bone to be wider or flatter in appearance * Segmental – the same bone is fractured in two places, so there is a ‘floating’ segment of bone

Answer 71

* Patellofemoral pain syndrome is a broad term used to describe pain in the front of the knee and around the patella * Sometimes called ‘runner’s knee’ * Symptoms are often relieved with conservative treatment, such as changes in activity levels or a therapeutic exercise programme * Occurs when nerves sense pain in the soft tissues and bone around the patella * It’s thought to be a result of stress on the joint between your patella and your thigh Causes: • Overuse -vigorous physical activities that put repeated stress on the knee -also caused by a sudden change in physical activity • Patellar malalignment -caused by abnormal tracking of the patella in the trochlear groove -the patella is pushed out to one side of the groove when the knee is bent -this abnormality may cause increased pressure between the back of the patella and the trochlear, irritating soft tissues

Answer 72

• Common term used to describe any of several conditions that cause pain around the patella • These conditions include: anterior knee pain syndrome, patellofemoral malalignment, chondromalacia patella, and iliotibial band syndrome • Running is a common cause, but any activity that repeatedly stresses the knee joint can cause the disorder • More common in women than men, particularly middle age women • Overweight individuals are especially prone • The hallmark of runner’s knee is a dull, aching pain around or behind the patella, especially where it meets the lower part of the femur • Other symptoms include swelling and popping or grinding in the knee • May be caused by irritation of the soft tissues or lining of the knee, worn or torn cartilage, or strained tendons • Any of following can contribute: - Overuse - Trauma to patella - Misalignment of patella - Completely or partial dislocation of patella - Flat feet - Weak or tight thigh muscles - Inadequate stretching before exercise - Arthritis - Fractured patella

Answer 73

SNAREs (anchors in the vesicle membrane) = synaptobrevin, synaptotagmin t-SNAREs (target membrane) = syntaxin, SNAP-25 - Long-endings that zipper together BOTULINUM TOXIN (BOTOX) - Enzymatically cleaves synaptobrevin (a SNARE protein involved in formation of the SNARE complexes) –> disrupts vesicle release -> muscles relax - Disrupts SNARE (mediate vesicle fusion with their target membrane) complex formation - Therapeutic application for cerebral palsy TETANUS - Neurotoxin produced by Costridium tetani in the soil - Spreads through extracellular fluid and enters nervous system at NMJs – spreads retrogradely into CNS - Cleaves synaptobrevin - Particularly active on inhibitory neurons = no inhibition of motor neurons

Answer 74

- Specialised regions of the presynaptic terminal where vesicle release occurs - These areas are complex and dynamic - Main components: Ca2+ channel (Cac), Bruchpilot (Brp)

Answer 75

- Acetylcholine release - Binds to receptor (ligand-gated - ionotropic) - Opens receptor - Sodium moves into cell down concentration and electro-gradient - Small change in membrane potential which activates voltage-gated sodium channels in the membrane - They allow considerably more sodium in - Which is enough to start an action potential in the muscle - Action potential travels around muscle fibre at high speed - Depolarisation around muscle - Voltage-gated calcium channels open in response -> calcium-induce calcium release - Calcium coming in acts on sarcoplasmic reticulum, where calcium floods out

Answer 76

- Neurotransmitter at the mammalian NMJ - Choline source = extracellular fluid - Synthesis = ChAT (choline acetyltransferase) (one step) - Choline + acetyl CoA –> ACh -> choline + acetic acid - Cholinergic neurons = muscle and certain circuits in the PNS and CNS

Answer 77

Type: ionotropic (form an ion channel pore) Signal: increase cations (Na+) Effect: excitatory ‘FAST’ Type: metabotropic (indirectly linked with ion channels on the plasma membrane through signal transduction mechanisms, often G proteins, e.g. G protein-coupled receptors) Signal: influences K+ permeability Effect: mixed ‘SLOW’ Nicotinic receptor – ionotropic Muscarinic receptor – metabotropic

Answer 78

nACh receptor antagonist (weak and reversible) | - used as muscle relaxant

Answer 79

- Physically (and psychologically) able to meet the demands of your environment - Two basic kinds of fitness: - ‘health-related’ - ‘skill-related’ (usually task specific)

Answer 80

Stage 1: food breakdown, gut - Breakdown of large macro-molecules to simple subunits (amino acids, simple sugars e.g. glucose, fatty acids and glycerol) Stage 2: glycolysis, absence of O2, cell cytoplasm - Breakdown of simple subunits of acetyl CoA accompanied by production of limited ATP and NADH Stage 3: aerobic respiration, cell mitochondria - Complete oxidation of acetyl CoA to H2O and CO2 involves production of much NADH, which yields much ATP via electron transport

Answer 81

Type II > 80% - sprinters | Type I >60% - long-distance runners

Answer 82

- Uses oxygen and fuel stores to provide energy - For prolonged low to moderate intensity work - Training load: stead-state exercise 30 minutes or longer - Training improves oxygen transport from lungs to active muscles and removal of waste products

Answer 83

- No oxygen requirements – produces lactate - Energy for short, sharp bursts of high intensity work (1-2 minutes) - Training load: high intensity for about 2 minutes, incomplete rest + reps - Improved ability to generate energy quickly and without oxygen, helps sustain high-intensity exercise due to improved tolerance and buffering/removal of muscle acid build-up

Answer 84

- No oxygen requirements – no lactate production - Uses creatine phosphate (phosphocreatine) to rapidly regenerate ATP from ADP - Immediate high energy supply for a few seconds - Training load: high intensity sprint interval for about 5-10 seconds, complete rest and re-charge + a few reps - Improved ability and capacity to perform short-term maximal efforts

Answer 85

- Stimulus – produces fatigue - Compensation – recovery period – depends on what energy system using - System recovers to be more efficient – have over compensation - So, if you completely recovery and start training again, you can train them but not over fatigue them Different training loads have different effects on the athlete’s recovery - Training too easy you overcompensate slightly - Training adequate you overcompensate a good amount - Training too hard you don’t overcompensate Principle of progressive overload – optimal improvement

Answer 86

- Common marker of aerobic endurance ability is VO2 max - The rate of volume of oxygen consumption while working at maximum capacity ml O2/kg/min - Thought to indicate innate ability to perform endurance sport - Bad news is that can only be improved by no more than 15% with endurance training (individually variable) - Men have higher VO2 max than women generally VO2 MAX AT ALTITUDE - 10% fall in VO2 max for every 1000m above 1200m - If Everest was 20-50m higher, no human could reach the top without supplementary oxygen - Best mountaineers do not have exceptional VO2 max at sea level

Answer 87

measuring ability to utilise oxygen

Answer 88

those who have the greatest capacity to use oxygen

Answer 89

- Anaerobic threshold – when a small increase in oxygen consumption causes a big increase in CO2 production - Appears to be where patients move from using their mitochondrial energy pathways to their glycolytic energy pathways - Olympic athletes have a high aerobic threshold, they can go a long way before they start producing much more CO2

Answer 90

- Actin: 40kD (kilodalton – measure of mass) globular protein that associates to form filaments. It is the major component of the thin filaments. - Tropomyosin: thin filament structural component binding to actin - Myosin: 200kD globular head coupled to long coiled-coil tail. Plus two 20kD light chains. Binds and hydrolyses ATP, undergoing a conformational change in the head. - Troponins: globular proteins. Troponin I binds to actin & troponin-T, and inhibits the actin-myosin interaction unless calcium is bound to troponin-C - Alpha-actinin: cross-links actin filaments at the sarcomere Z-line/disks - Titin: very long filamentous protein, links Z-lines to M-lines - Myomesins: bind to titin – generate hexagonal packing of thick filaments - Vinculin: binds to alpha-actinin - Cap-Z: caps the +ends of actin filaments at the Z-disk/line - Tropomodulin: caps the -ends of the thin filaments - Desmin: links together adjacent myofibrils at the Z-disk/line - Dystrophin: links actin filaments to the muscle cell outer membrane (mutates or absent in Duchenne Muscular Dystrophy) - Nebulin: determines the length of the thin filaments

Answer 91

- Slow twitch or slow oxidative fibres - Slow contraction speed (governed by a low myosin ATPase rate) - These fibres allow steady activity and are resistant to depletion of energy reserves - The motor neurone will have a constant low firing frequency - These cells are designed for good supply of nutrients, having a high surface area- to- volume ratio and good access to nearby blood capillaries - They also have abundant mitochondria (ATP generation) and myoglobin (oxygen capture and storage) and for this reason have a reddish colour and can sustain aerobic metabolism using fat as a source of energy for long periods - Typical or marathon runners

Answer 92

- Fast oxidative-glycolytic fibres - General-purpose type which are similar in most respects to slow twitch fibres - They have a faster contraction speed and a higher myosin ATPase activity than type I - They are still relatively resistant to fatigue and adapted to a good supply of energy sources, but will utilise glucose as well as fats - They are more expensive to operate than type I and can be co-opted when needed, e.g. in a final burst of speed for the line - Their motor neurones characteristically show bursts of activity, but intermittently - Common in footballers

Answer 93

- Fast twitch- or fast glycolytic fibres - They have the highest myosin ATPase activity - They are specialised for short maximal force efforts and easily become short of energy - These cells are not adapted for efficient exchange of nutrients and waste products, with low surface area to volume ratio (cells are larger) and with limited blood supply - They have a paler colour because they contain fewer mitochondria and less myoglobin - They can generate ATP by substrate-level phosphorylation (glucose -> lactic acid) - These types of fibres predominate in a sprinter’s muscles - Their motor neurones transmit occasional bursts of very high frequency impulses

Answer 94

fast twitch fibres in neck muscles to make rapidly his position to balance pall – precision movements are done by the fast twitch muscles The type of skeletal muscle fibre involved in the eyeblink reflex is type 2B

Answer 95

slow twitch fibres

Answer 96

- Muscle glycogen reserves are finite and increase lactate concentration is a problem - Oxygen is used by liver to produce glucose from lactate -> Cori Cycle - Liver ATP used to synthesise glucose (gluconeogenesis)

Answer 97

- ATP-PCr system used most at beginning - Glycolysis then increases when this used up - Then aerobic phosphorylation in creases over time, as glycolysis decreases

Answer 98

FAs, ketones, glucose -> CO2 = light activity Muscle glycogen -> lactate = heavy activity ADP + Pi -> ATP, phosphocreatine -> creatine = intense activity

Answer 99

ADP represents the ‘last gasp’ of the short-term energy stores ADP + ADP – (myokinase)> ATP + AMP - When ADP levels rise in the muscle cells, myokinase can produce one bit more ATP

Answer 100

- ATP in muscle already: 6.8 kJ - Creatine phosphate in muscle: 14 kJ - Muscle glycogen (-> lactate): 200 kJ - Muscle glycogen (-> CO2): 2500 kJ - Liver glycogen (-> CO2): 570 kJ - All fats (-> CO2): 120,000 kJ

Answer 101

- Sprinting is powered by ATP, creatine phosphate and glycolysis - Longer distance running requires oxidative phosphorylation (mitochondria)

Answer 102

- involved in appetite and fat deposition | - may also operate via the AMPK signalling pathway

Answer 103

Target systems: - Decrease protein synthesis rate - Increase protein degradation rate ``` Triggers & signals: - Akt - mTORr - p70S6kinase - 4E-BP1 (all above lead to decrease protein synthesis rate) - Glucocorticoids - Myostatin - NF-kappaB - Reactive oxygen species (above can target both systems) ```

Answer 104

skeletal and cardiac

Answer 105

Less calcium = not much contraction | More calcium = potential for contraction

Answer 106

- Muscle unit – muscle fibres innervated by a single motor neurone - Motor unit – muscle unit plus its motor neurone - Motor neurone pool – collection of neurones innervating a single muscle - A motor neurone innervates one set of muscle fibres - A pool consists of many motor neurones, each of which innervates a motor unit within the muscle

Answer 107

- Fine control – few muscle fibres per motor unit - Coarse control – many muscle fibres per motor unit - typically, a muscle is controlled by about 100 motor neurones – cell bodies in the spinal cord (or brain stem) - each motor neurone controls 100-1000 muscle fibres scattered over the muscle - Muscle fibres can be changed by patterns of motor neurone activity and absolute levels of activity

Answer 108

Two mechanisms: 1. Recruitment of motor units 2. Firing rate of motor units Short-term of increasing exercise it’s the nervous system that has to get used to recruiting more fibres, then long-term you get changes in firing

Answer 109

Tendon tap -> stretch muscle -> stimulate muscle spindles

Answer 110

UMN: - spastic (persistent spasms) - hypertonia - hyperreflexia LMN: - flaccid (muscle loses innervation) - hypotonia - hyporeflexia