PBL of MSK

PBL Day 2
1. Causes of Shortness of Breath (Dyspnoea)
Pulmonary

Obstructive lung diseases

Asthma Bronchitis Chronic obstructive pulmonary disease Cystic fibrosis Emphysema Hookworm disease Contagious

Diseases of lung parenchyma and pleura

Other causes

Anthrax through inhalation of Bacillus anthracis Pneumonia Fibrosing alveolitis Atelectasis Hypersensitivity pneumonitis Interstitial lung disease Lung cancer Pleural effusion Pneumoconiosis Pneumothorax Non-cardiogenic pulmonary edema or acute respiratory distress syndrome Sarcoidosis

Non-contagious

Pulmonary vascular diseases Acute or recurrent pulmonary emboli Pulmonary hypertension, primary or secondary Pulmonary veno-occlusive disease Superior vena cava syndrome

Obstruction of the airway

Cancer of the larynx or pharynx Empty nose syndrome Pulmonary aspiration Epiglottitis Laryngeal edema Vocal cord dysfunction Lesion of the phrenic nerve Polycystic liver disease Tumor in the diaphragm Ankylosing spondylitis Broken ribs

Immobilization of the diaphragm

Restriction of the chest volume

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Kyphosis of the spine Obesity Pectus excavatum Scoliosis Aortic dissection Cardiomyopathy Congenital heart disease CREST syndrome Heart failure Ischaemic heart disease Malignant hypertension Pericardium disorders, including:

Disorders of the cardiovascular system

Other

Cardiac tamponade Constrictive pericarditis Pericardial effusion

Pulmonary edema Pulmonary embolism Pulmonary hypertension Valvular heart disease Anemia Hypothyroidism Adrenal insufficiency Metabolic acidosis Sepsis Leukemia Holocarboxylase synthetase deficiency Amyotrophic lateral sclerosis Guillain-Barr syndrome Multiple sclerosis Myasthenia gravis Parsonage Turner syndrome Eaton-Lambert syndrome Chronic fatigue syndrome Anxiety disorders and panic attacks Fentanyl Carbon monoxide poisoning Pregnancy
[3]

Disorders of the blood and metabolism

Disorders affecting breathing nerves and muscles

Psychological conditions Medications

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2. Causes of Scoliosis
Scoliosis is a lateral (toward the side) curvature in the normally straight vertical line of the spine. When viewed from the side, the spine should show a mild roundness in the upper back and shows a degree of swayback (inward curvature) in the lower back. When a person with a normal spine is viewed from the front or back, the spine appears to be straight. When a person with scoliosis is viewed from the front or back, the spine appears to be curved.

Causes Idiopathic scoliosis (unknown cause) - in about 80% of cases the cause is unknown. Neuromuscular conditions - these are conditions that affect the nerves and muscles. About 20% of scoliosis cases are caused by neuromuscular conditions, such as cerebral palsy or muscular dystrophy. In such cases the child may not be able to walk to stay upright, further preventing the spins from growing properly. Degenerative scoliosis. This may result from traumatic (from an injury or illness) bone collapse, previous major back surgery, or osteoporosis (thining of the bones). Congenital scoliosis (present at birth) - this is rare and occurs because of the bones in the spine developing abnormally when the fetus is developing in the uterus (womb). Genes - The first gene associated with adolescent idiopathic scoliosis was identified by scientists at the RIKEN Center for Integrative Medical Sciences in Japan. The gene - GPR126 - is involved in the growth and development of the spine during the early years of a human's life. Their finding was published in the journal Nature Genetics. Leg length - if one leg is longer than the other the individual may develop scoliosis. Other causes - bad posture, using backpacks or satchels, and exercise may also cause scoliosis. Although rare, scoliosis can also develop as part of a pattern of symptoms called a syndrome. This is known as syndromic scoliosis. Conditions that can cause syndromic scoliosis include: o Marfan syndrome a disorder of the connective tissues inherited by a child from their parents

PBL of MSK o Rett syndrome a genetic disorder, usually affecting females, which causes severe physical and mental disability These conditions are usually diagnosed at a young age and children with them are often monitored for problems such as scoliosis.

3. Anatomy of the Calf Muscles 4. Causes of Enlarged Calf Muscles

People who are into sports activities, generally are more prone to be affected by swollen or tight calf muscles. Sports where stretching is a necessity, may increase calf pain leading to swollen calf muscles which include running, crossing hurdles, basketball etc. Calf muscle pain may also be caused due to overexertion, fatigue and cold weather. Deep vein thrombosis (DVT), a type of blood clotting disorder in the veins, is another reason that causes swelling on calf muscle. A torn calf muscle, caused by any strenuous activity will ultimately lead to swelling and a feeling of soreness in the muscles. Compartment syndrome is a condition where the nerves or blood vessels in the muscle tissue restrict the flow of blood and nutrients. It occurs after injury, repetitive activity like running or even surgery. Lack of adequate minerals like magnesium or calcium can lead to calf muscle strain. Incorrect postures like leaning your weight forward can cause undue stress on the calf muscles causing them to swell. Most of the time, people engage in hyperpronation, or abnormal foot motion while walking or rolling their feet, consciously or unconsciously, that may constantly strain the calf muscles. Charley Horse, a condition where a person experiences sudden and knotty spasm in the calf muscle, caused by hormonal imbalance is also a reason for calf muscle swelling. Muscular dystrophy: Kids with MD often develop enlarged calf muscles (called calf pseudohypertrophy) as muscle tissue is destroyed and replaced by fat. Bruise

5. Causes of Contractures of Elbow Joint and Achilles Tendon

A muscle contracture is a permanent shortening of a muscle[1] or joint.[2] It is usually in response to prolonged hypertonic spasticity in a concentrated muscle area, such as is seen in the tightest muscles of people with conditions like spastic cerebral palsy. Contractures are essentially muscles or tendons that have remained too tight for too long, thus becoming shorter. Once they occur they cannot be stretched or exercised away; they must be released with orthopedic surgery. Most of the physical therapy, occupational therapy, and other exercise regimens targeted towards people with spasticity focuses on trying to prevent contractures from happening in the first place. Contractures can also be due to ischemia, as in Volkmann's contracture. Excessive matrix metalloproteinase and myofibroblast accumulation in the wound margins can result in contracture.

PBL of MSK Elbow Joint There are numerous and varied inciting events ultimately resulting in a stiff elbow that can be broadly categorized as either traumatic or atraumatic. Trauma, burns, and head injury are known causes of elbow contractures that are directly proportional to the severity of the insult [64]. Elbow surgery involves controlled trauma to the tissues and may be complicated by postoperative stiffness. Atraumatic causes of elbow stiffness include osteoarthritis and inflammatory arthritis, post-septic arthritis, multiple hemarthroses in hemophiliacs, and congenital contractures found in arthrogryposis and congenital radial head dislocation. Stiffness and contractures of the elbow result in loss of motion and difficulty performing activities of daily living Pathophysiology o causes of elbow stiffness and contractures include trauma surgery arthritis cerebral palsy traumatic brain injury burns congenital conditions arthrogryposis congenital radial head dislocation o pathoanatomy intrinsic causes joint incongruity synovitis loose bodies intra-articular fractures osteochondritis dissecans post-traumatic arthritis extrinsic causes formation of eschar following a burn heterotopic ossification adhesions/contraction of the capsule myositis ossificans ligament contractures Achilles Tendon Achilles tendon contracture is a shortening of the Achilles tendon (tendon calcaneus or heel cord), which causes foot pain and strain, with limited ankle dorsiflexion Causes Achilles tendon contracture may reflect a congenital structural anomaly or a muscular reaction to chronic poor posture, especially in women who wear high-heeled shoes and joggers who land on the

PBL of MSK balls of their feet instead of their heels. Other causes include paralytic conditions of the legs, such as poliomyelitis and cerebral palsy. Signs and symptoms Sharp, spasmodic pain during dorsiflexion of the foot characterizes the reflex type of Achilles tendon contracture. In footdrop (fixed equinus), contracture of the flexor foot muscle prevents placing the heel on the ground.

6. Degrees of Muscle Strength and Causes of its Reduction

Muscle Strength Scale Major skeletal muscles can be functionally assessed for their strength. Muscles are evaluated individually with comparison to that of the same muscle on the opposite side of the body. Muscle strength can be monitored over time to follow progression or remission of disease. Findings normal motor power able to overcome gravity and significant resistance but strength not quite normal able to overcome gravity and moderate resistance able to overcome gravity and mild resistance able to overcome gravity but not resistance unable to overcome the force of gravity but able to move in the plane of the supported extremity flicker movements only total paralysis Grade 5 4++ 4+ 4 3 2 1 0

Reduction Muscle weakness can be classified as either "true" or "perceived" based on its cause. True muscle weakness (or neuromuscular weakness) describes a condition where the force exerted by the muscles is less than would be expected, for example muscular dystrophy. Perceived muscle weakness (or non-neuromuscular weakness) describes a condition where a person feels more effort than normal is required to exert a given amount of force but actual muscle strength is normal, for example chronic fatigue syndrome. In some conditions, such as myasthenia gravis muscle strength is normal when resting, but true weakness occurs after the muscle has been subjected to exercise. This is also true for some cases of chronic fatigue syndrome, where objective post-exertion muscle weakness with delayed recovery time has been measured and is a feature of some of the published definitions. Neuromuscular fatigue can be classified as either "central" or "peripheral" depending on its cause. Central muscle fatigue manifests as an overall sense of energy deprivation, while peripheral muscle fatigue manifests as a local, muscle-specific inability to do work. Neuromuscular fatigue Nerves control the contraction of muscles by determining the number, sequence, and force of muscular contraction. When a nerve experiences synaptic fatigue it becomes unable to stimulate the

PBL of MSK muscle that it innervates. Most movements require a force far below what a muscle could potentially generate, and barring pathology, neuromuscular fatigue is seldom an issue. For extremely powerful contractions that are close to the upper limit of a muscle's ability to generate force, neuromuscular fatigue can become a limiting factor in untrained individuals. In novice strength trainers, the muscle's ability to generate force is most strongly limited by nerves ability to sustain a high-frequency signal. After an extended period of maximum contraction, the nerves signal reduces in frequency and the force generated by the contraction diminishes. There is no sensation of pain or discomfort, the muscle appears to simply stop listening and gradually cease to move, often lengthening. As there is insufficient stress on the muscles and tendons, there will often be no delayed onset muscle soreness following the workout. Part of the process of strength training is increasing the nerve's ability to generate sustained, high frequency signals which allow a muscle to contract with their greatest force. It is this "neural training" that causes several weeks worth of rapid gains in strength, which level off once the nerve is generating maximum contractions and the muscle reaches its physiological limit. Past this point, training effects increase muscular strength through myofibrillar or sarcoplasmic hypertrophy and metabolic fatigue becomes the factor limiting contractile force. Central fatigue Central fatigue is a reduction in the neural drive or nerve-based motor command to working muscles that results in a decline in the force output.[13][14][15] It has been suggested that the reduced neural drive during exercise may be a protective mechanism to prevent organ failure if the work was continued at the same intensity.[16][17] There has been a great deal of interest in the role of serotonergic pathways for several years because its concentration in the brain increases with motor activity.[18][19][20] During motor activity, serotonin released in synapses that contact motoneurons promotes muscle contraction.[21] During high level of motor activity, the amount of serotonin released increases and a spillover occurs. Serotonin binds to extrasynaptic receptors located on the axon initial segment of motoneurons with the result that nerve impulse initiation and thereby muscle contraction are inhibited.[22] Peripheral muscle fatigue Peripheral muscle fatigue during physical work is an inability for the body to supply sufficient energy or other metabolites to the contracting muscles to meet the increased energy demand. This is the most common case of physical fatigueaffecting a national[where?] average of 72% of adults in the work force in 2002. This causes contractile dysfunction that manifests in the eventual reduction or lack of ability of a single muscle or local group of muscles to do work. The insufficiency of energy, i.e. sub-optimal aerobic metabolism, generally results in the accumulation of lactic acid and other acidic anaerobic metabolic by-products in the muscle, causing the stereotypical burning sensation of local muscle fatigue, though recent studies have indicated otherwise, actually finding that lactic acid is a source of energy.[23] The fundamental difference between the peripheral and central theories of muscle fatigue is that the peripheral model of muscle fatigue assumes failure at one or more sites in the chain that initiates muscle contraction. Peripheral regulation therefore depends on the localized metabolic chemical conditions of the local muscle affected, whereas the central model of muscle fatigue is an integrated mechanism that works to preserve the integrity of the system by initiating muscle fatigue through

PBL of MSK muscle derecruitment, based on collective feedback from the periphery, before cellular or organ failure occurs. Therefore the feedback that is read by this central regulator could include chemical and mechanical as well as cognitive cues. The significance of each of these factors will depend on the nature of the fatigue-inducing work that is being performed. Though not universally used, "metabolic fatigue" is a common alternative term for peripheral muscle weakness, because of the reduction in contractile force due to the direct or indirect effects of the reduction of substrates or accumulation of metabolites within the muscle fiber. This can occur through a simple lack of energy to fuel contraction, or through interference with the ability of Ca2+ to stimulate actin and myosin to contract. Lactic acid hypothesis It was once believed that lactic acid build-up was the cause of muscle fatigue.[24] The assumption was lactic acid had a "pickling" effect on muscles, inhibiting their ability to contract. The impact of lactic acid on performance is now uncertain, it may assist or hinder muscle fatigue. Produced as a by-product of fermentation, lactic acid can increase intracellular acidity of muscles. This can lower the sensitivity of contractile apparatus to calcium ions (Ca2+) but also has the effect of increasing cytoplasmic Ca2+ concentration through an inhibition of the chemical pump that actively transports calcium out of the cell. This counters inhibiting effects of potassium ions (K+) on muscular action potentials. Lactic acid also has a negating effect on the chloride ions in the muscles, reducing their inhibition of contraction and leaving K+ as the only restricting influence on muscle contractions, though the effects of potassium are much less than if there were no lactic acid to remove the chloride ions. Ultimately, it is uncertain if lactic acid reduces fatigue through increased intracellular calcium or increases fatigue through reduced sensitivity of contractile proteins to Ca2+.

7. What are the Muscle Stretch Reflexes

The stretch reflex (myotatic reflex) is a muscle contraction in response to stretching within the muscle. It is a monosynaptic reflex which provides automatic regulation of skeletal muscle length. When a muscle lengthens, the muscle spindle is stretched and its nerve activity increases. This increases alpha motor neuron activity, causing the muscle fibers to contract and thus resist the stretching. A secondary set of neurons also causes the opposing muscle to relax. The reflex functions to maintain the muscle at a constant length. Gamma motoneurons regulate how sensitive the stretch reflex is by tightening or relaxing the fibers within the spindle. There are several theories as to what may trigger gamma motoneurons to increase the reflex's sensitivity. For example, gamma co-activation might keep the spindles taut when a muscle is contracted, preserving their stretch-sensitivity even as the muscle fibers become shorter. Otherwise the spindles would become slack and the reflex would cease to function. This reflex has the shortest latency of all spinal reflexes including the Golgi tendon reflex and reflexes mediated by pain and cutaneous receptors. Examples A person standing upright begins to lean to one side. The postural muscles that are closely connected to the vertebral column on the side will stretch. Because of this, stretch receptors in those muscles contract to correct posture.

PBL of MSK Other examples (followed by involved spinal nerves) are responses to stretch created by a blow upon a muscle tendon: Jaw jerk reflex (CN V) Biceps reflex C5/C6 Brachioradialis reflex C6 Extensor digitorum reflex C6/C7 Triceps reflex C7/C8 Patellar reflex L2-L4 (knee-jerk) Ankle jerk reflex S1/S2 Another example is the group of fibers in the calf muscle, which synapse with motor neurons supplying muscle fibers in the same muscle. A sudden stretch, such as tapping the Achilles' tendon, causes a reflex contraction in the muscle as the spindles sense the stretch and send an action potential to the motor neurons which then cause the muscle to contract; this particular reflex causes a contraction in the soleus-gastrocnemius group of muscles. Like the patellar reflex, this reflex can be enhanced by the Jendrassik maneuver. There are basically four types of muscle fibers. This includes the slow twitch (ST) fibers, which are slow contracting and slow to fatigue. The fast twitch muscle fibers are sub-divided into several subclasses and include fibers that are fast contracting and resistant to fatigue (FRF), fast contracting but more easily fatigued (FEF), and fast contracting fast fatiguing white fibers (FFF). Grading of stretch reflexes upon tapping muscle tendon Grade 0 1+ 2+ 3+ 4+ Response no response slight but definitely present response brisk response very brisk response clonus Significance always abnormal may or may not be normal normal may or may not be normal always abnormal

The clasp-knife response is a stretch reflex with a rapid decrease in resistance when attempting to flex a joint. It is one of the characteristic responses of an upper motor neuron lesion.