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- Sit upstairs – done in prac room - declaration – Will be rec - 4 stations (2 VIVA / 2 OSCE) Can you explain the function of this physiological process and...

- Sit upstairs – done in prac room - declaration – Will be rec - 4 stations (2 VIVA / 2 OSCE) Can you explain the function of this physiological process and name the key structures? Period of turn around…→ then progress on to practical How does the process the occur ? Additional time?? Discuss how pathology or age - elated change affect this physiological process? Negatively impact? Discuss the role of this process in a given pathology or age related change? Score based on performance based on each individual section.. → This is where most prompting come froms REMEMBER MIGHT ANSWER BETTER IN CERTAIN SCETIONS THAN OTHERS Can you explain the function of this physiological process and name the key structures? How does the process occur? Discuss how pathology or age-related change affects this physiological process?  Can you explain the function of this physiological process and name the key structures? Soft tissue response to injury injury to any soft tissue (muscle ligaments tendons and facia) it is split into 4 phases 1. Bleeding 2. inflammation 3. proliferation 4.remodelling How does the process the occur ? Bleeding at time of the injury / trauma starts when blood leaks out of the body, blood vessels constrict to restrict the blood flow. Within seconds platelets adhere to sub endothelium surface - Last approx. =4-6 hours There is a Great vascularity of soft tissue. 60s → firbin mesh begins to form and blood is transformed form liquid to gel = clot/ thrombus keeping platletes within wound – can cause complications if it comes off through circulatory system (stroke) Inflammation Essential process of bodies natural healing Onset- almost immediately after injury, peaks 2-3 days gradually resolves over next few weeks The chemical mediators cytokines initiate 2 processes: → Create the swelling , heat , pain and redness Vascular = incl vasodilation and inc vascular permeability = fluid is moving across tissue layers and is leaky Chemical = phagocytes and neutrophils attracted: initiate clear up - bacteria and damaged cells is removed. Proliferation Starts 3-7 days after injury ongoing between 2-6 months Focus on tissue repair and forming new collagen – wound rebuilding phase Collagen type 3- fine Angiogenesis occurs fibrous connective Fibroblast activity & collagen synthesis (type 3) (support/filtration) Granulation tissue - scar tissue ( we can influence how it lays) – should be pink/red Type 1 – found in Remodelling bones/tendons/ Starts 3-6 weeks after injury ongoing for months – years organs -strength Collagen maturation type 3 -> type 1 (improving tensile strength ) enzymes help this – unorganised and thick – scar? Collagen realignment (increasing structural integrity) Reduction in vascularity ( tissue metabolic rate reduces) Discuss how pathology or age - elated change affect this physiological process? Discuss the role of this process in a given pathology or age related change? The grading systems used for classifying ankle sprains focuses on a single ligament: Grade I represents slight stretching and damage to fibers of the ligament, Grade II represents partial tear of the ligament, Grade III represents complete rupture of the ligament Charexteristics Lateral Ligaments (most commonly injured): - Swelling and bruising around the ankle. Anterior Talofibular Ligament (ATFL): Most frequently sprained. Reduced range of motion (ROM). Calcaneofibular Ligament (CFL). Difficulty or inability to weight-bear (depending on severity). Posterior Talofibular Ligament (PTFL). balance, potential initial bruising haematoma and swelling (link to phases of healing) PEACE AND LOVE 1. bleeding 2.Infalmation 3. proliferation 4. Remodelling.  Week One - Inflammation and Healing: tissue response to damage – vascular and cellular response to injury Can you explain the function of this physiological process and name the key structures? Inflammation and tissue response to damage - Signs of inflammation – redness, heat, swelling, pain Function is to trap microbes, toxins or forein material & begin Tissue repair. How does the process the occur ? Vascular Phase In the vascular phase, small blood vessels adjacent to the injury dilate (vasodilatation) and blood flow to the area increases. The endothelial cells initially swell, then contract to increase the space between them, thereby increasing the permeability of the vascular barrier. This process is regulated by chemical mediators → Histamine THIS enables fluids to move into extracellular spaces from the vascular space, resulting in oedema. The formation of increased tissue fluid acts as a medium for which inflammatory proteins can migrate through. It may also help to remove pathogens and cell debris in the area through lymphatic drainage. Cellular Phase The predominant cell of acute inflammation is the neutrophil. They are attracted to the site of injury by the presence of chemotaxins, the mediators released into the blood immediately after the damage. The migration of neutrophils occurs in four stages: Margination – cells line up against the endothelium Rolling – close contact with and roll along the endothelium Adhesion – connecting to the endothelial wall Emigration – cells move through the vessel wall to the affected area Once in the region, neutrophils recognise the foreign body and begin phagocytosis, the process whereby the pathogen foreign body is engulfed and contained with a phagosome. The phagosome is then destroyed via oxygen-independent or oxygen-dependent mechanisms. Discuss how pathology or age - elated change affect this physiological process? – ANKLE SPRAIN The grading systems used for classifying ankle sprains focuses on a single ligament: Grade I represents slight stretching and damage to fibers of the ligament, Grade II represents partial tear of the ligament, Grade III represents complete rupture of the ligament Charexteristics Lateral Ligaments (most commonly injured): - Swelling and bruising around the ankle. Anterior Talofibular Ligament (ATFL): Most frequently sprained. Reduced range of motion (ROM). Calcaneofibular Ligament (CFL). Difficulty or inability to weight-bear (depending on severity). Posterior Talofibular Ligament (PTFL). balance, potential initial bruising haematoma and swelling (link to phases of healing) 1. bleeding 2.Infalmation 3. proliferation 4. Remodelling. PEACE AND LOVE  Can you explain the function of this physiological process and name the key structures? Week One - Bone structure & function: bone remodelling Healthy bone remodeling occurs at many simultaneous sites throughout the body where cycle bone is experiencing growth, mechanical stress, microfractures, or breaks. About 20% of all bone tissue is replaced annually by the remodeling process. There are five phases in the bone remodeling process: ACTIVATION, RESORPTION, REVERSAL, FORMATION, and MINERALISATION. The total process takes about 4 to 8 months, and occurs continually throughout our lives How does the process the occur ? ACTIVATION 1. pre-osteoclasts are attracted to the remodeling sites. 2. Pre-osteoclasts fuse to form multinucleated osteoclasts Resorption 1. Osteoclasts. Dig out cavity, called a resorption pit in spongey bone or burrow a tunnel in compact bone 2. Calcium can be realeased into the blood for use in various body functions 3. Osteoclasts disappear Reversal 1. mesenchymal stem cells, pre-cursors to osteoblasts appear along the burrow pit where… Discuss how pathology or age - elated change affect this physiological process? - #NOF (Fractured neck of femur) 2. Proliferate (increase In numbers) and differentiate into pre osteoblasts then.. Formation #NOF is usually graded 1. Mature into osteoblasts at the surface of the site and release ostoid at the site, Stage 1: incomplete fracture line or impacted fracture forming new soft non-mineralised matrix Stage 2: complete fracture line, non-displaced 2. The new site matrix is mineralised with calcim and phosphorus -> remains dormant Stage 3: complete fracture line, partial displacement until next cycle Stage 4: complete fracture line, complete displacement Neck of femur fractures can be intracapsular (proximal to the intertrochanteric line) or extracapsular (below the intertrochanteric line). Intracapsular fractures complications have a high risk of avascular necrosis of the femoral head and non-union of the fracture Avascular Necrosis (AVN): When a fracture occurs it will go through 1. Haematoma 2. inflammation 3. Soft callus 4. hard callus 5. remodelling Disruption of blood supply 1. Haematoma – when fracture occurs there will be bleeding locally – this creates a fibrin blood clot to the femoral head, 2. Inflamation – stem cells migrate to the fracture and form the granulation tissue and releases growth factors that helps in healing the fracture and untie the especially in displaced fracture together. intracapsular fractures. 3. Soft callus will occur within 2 weeks – the amount of callus correlates with the immobilization The stiffer the immobilisation the less amount of callus = flexible Non-Union: Poor healing fixation wil result in endochondral ossification (abundant callus) due to insufficient stability SECONDARY AND PRIMARY BONE HEALING? or blood supply. Deep Vein Thrombosis Primary bone healing – find absolute stability when bone is fixed with plates and it’s called Haversian remodelling or intramembranous healing type 1 collagen (DVT): Due to immobilization Secondary bone healing – occurs when the fixation is not ridgid eg. CAST/ ROD and there will be endochondral ossification post-injury or surgery. 4. Hard callus – collagen changes from type 2 to type 1 Post-Traumatic Arthritis: 5. Remodelling – begins early and continues for many years after #. Woven bone will be replaced by stronger laminar bone and the fracture healing will be complete Following joint damage. with the continuation of the medullary canal. → this is influenced by wolff’s law ( bone is affected by stress)  Week One - Tendon structure & function: tendon and ligament stress strain curve Can you explain the function of this physiological process and name the key structures? this describes the mechanics of the collagen fibers within the tendons and ligaments – both of these can stretch but there are limits to how much they can stretch and their elasticity. Strain = how much force is being used to put tension on a particular fibre (external) Stress = The force applied to a material per unit area. Stress can be caused by pressure, stretch, shear, or torque. Stress is measured in pascals How does the process the occur ? 1.Toe region: this is where “stretching out” or "un-crimping" of crimped tendon fibrils occurs from mechanically loading the tendon up to 2% strain. This region is responsible for nonlinear stress/strain curve, because the slope of the toe region is not linear. 2.Linear region: this is the physiological upper limit of tendon strain whereby the collagen fibrils orient themselves in the direction of tensile mechanical load and begin to stretch. The tendon deforms in a linear fashion due to the inter-molecular sliding of collagen triple helices. If strain is less than 4%, the tendon will return to its original length when unloaded, therefore this portion is elastic and reversible and the slope of the curve represents the Young's modulus. 3.Yield and failure region/ rupture : this is where the tendon stretches beyond its physiological limit and intramolecular cross-links between collagen fibres fail. If micro-failure continues to accumulate, stiffness is reduced and the tendon begins to fail, resulting in irreversible plastic deformation. If the tendon stretches beyond 8-10% of its original length, macroscopic failure soon follows. Tendons also have viscoelastic properties→ the relationship between stress and strain for a tendon is not constant but depends on the time of displacement or load. Tendons at low strain rates tend to absorb more mechanical energy but are less effective in carrying mechanical loads. However, tendons become stiffer and more effective in transmitting large muscular loads to bone at high strain ratesDiscuss how pathology or age - elated change Discuss Discuss thepathology how role of thisorprocess in a given age - elated pathology change or age affect this related change? physiological process? – ANKLE SPRAIN affect this physiological process? The grading systems used for classifying ankle sprains focuses on a single ligament: Grade I represents slight stretching and damage to fibers of the ligament, Grade II represents partial tear of the ligament, Grade III represents complete rupture of the ligament Charexteristics Lateral Ligaments (most commonly injured): - Swelling and bruising around the ankle. Anterior Talofibular Ligament (ATFL): Most frequently sprained. Reduced range of motion (ROM). Calcaneofibular Ligament (CFL). Difficulty or inability to weight-bear (depending on severity). Posterior Talofibular Ligament (PTFL). balance, potential initial bruising haematoma and swelling (link to phases of healing) 1. bleeding 2.Infalmation 3. proliferation 4. Remodelling. PEACE AND LOVE  Week Two - Motor Unit: muscle contraction Can you explain the function of this physiological process and name the key structures? This shows the motor unit comprised of muscle fibre and nerve fibre. This shows the contraction and relaxation cycle of muscle tissues. This diagram shows how neurotransmitters affect the action potential of a nerve enabling the sliding filament theory of actin and myosin to occur for optimal contractions. How does the process the occur ? A motor unit is comprised of a nerve fibre and a muscle fibre. At this point you will find the axon terminal of a motor neuron → this has neurotransmitter of acetylcholine. At the muscle fibre it contains many myofibrils and mitochondria which provide ATP. The muscle fibre has a membrane called the sarcolemma which holds many ion channel receptors. Once an action potential arrives at the terminal of a motor neuron it will cause neurotransmitters containing acetylcholine to diffuse across the synaptic cleft binding to receptors within the sarcolemma. At this point sodium ions are able to come inside and the voltage gated channels open causing an Action potential travelling across the sarcolemma down the T TUBULE. While this is happening → enzymes within the synaptic cleft destroy the remaining acetylcholine inhibiting another action potential from happening unless more is released from motor neuron. The muscle AP traveling along T-tubule enables more calcium ion channels to open. Ca+ within the sarcoplasmic reticulum (SR) Flood into the sarcoplasm where Ca+ can bind to troponin on the thin filament exposing actin. Alongside this are the thick filaments which contain myosin, on the thick filament there are actin binding sites and ATP binding sites. The binding here causes tension and contraction – where thin filaments are pulled towards centre of the sarcomere. This is known as the sliding filament theory where each filament slides pulling z disks closer. Ca+ is then actively transported using ATP to restore low levels of Ca+ in sarcoplasm. Enabling the tropin-myotroposin compex to slide back to relaxed state as the myosin and actin binding sites are blocked. Discuss how pathology or age - elated change affect this physiological process? Discuss the role of this process in a given pathology or age related change? Following a stroke or a cerebral vascular accident – CVA there can be damage to the primary motor cortex (M1). This will then cause disruption to the nerve transition producing positive and negative motor functions affecting muscle contraction. NEGATIVE - If the M1 is damaged less/ no signals are sent down the motor pathway to the– aplpha motor neuron = resulting in the muscles being less innervated causing muscle weakness and low tone. The repeated lack of Action potential at the neuromuscular junction over time can then cause muscle atrophy as the muscles are not contracting and therefore weakness occurs. POSITIVE - A Normally in the spinal cord there are lots of motor signals coming down the corticospinal tract to the aplpha motor neuron. When these signals are reduced you initially see the negative features of low tone, loss of dexterity and weakness. However, overtime the alpha motor neuron can become sensitised causing it to produce exaggerated responses to muscle stretch. Which then contributes to the positive symptoms of high tone / spasticity / clonus at the ankle. This would trigger more ACh triggering a contraction This is velocity depended and known as neural factors Week Two - Motor Unit: sliding filament theory Can you explain the function of this physiological process and name the key structures? - sliding filament theory Sarcomere: The basic unit of muscle contraction, bordered by Z-lines. Actin (Thin Filament): Protein filaments attached to the Z-line. Myosin (Thick Filament): Protein filaments with heads that interact with actin. Tropomyosin and Troponin: Regulatory proteins on actin that control access for myosin binding. ATP: The energy molecule required for muscle contraction How does the process the occur ? 1. An action potential arrives from the motor neurones at the muscle fibres. 2. The action potential triggers the release of calcium ions to enter the sarcoplasm from the sarcoplasmic reticulum. 3. The calcium ions bind to the troponin which causes the troponin to change shape. 4. The change of shape of the troponin results in the actin binding sites being opened. 5. When myosin heads are bound to ATP they want to attach to the actin binding sites. 6. When the myosin attaches to the actin binding sites cross bridges are formed and the ATP is hydrolysed into ADP. 7. The myosin heads rotate and pull the actin towards the centre of the sarcomere and release the ADP known as the power stroke. 8. The crossbridge then de attaches from the actin when it binds to an ATP molecule. 9. The ATP is then hydrolysed which causes the myosin to re-cock into position. 10. This cycle is then continued if there are enough calcium ions present in the sarcoplasm and there is sufficient ATP available Discuss the role of this process in a given pathology or age related change? When a stroke occurs in the primary motor cortex the brain is unable to send signals down the corticospinal tract due to the damage caused by the stroke. This stops or reduces the signals that reach the alpha motor neurone which reduces the ability for it to be activated. The reduction in activation of the alpha motor neurone leads to less action potentials being sent down the lower motor neurones to the muscle. This reduces the occurrence of the sliding filament theory as muscle contractions only begins when action potentials reach the muscular junction causing calcium ions to enters the sarcoplasm and binds to troponin on actin. This results in low tone and muscles being weak and floppy. However, over time the alpha motor neurone can undergo neuroplastic changes which results in the hypersensitivity of the alpha motor neurone which leads to a greater number of action potentials being sent to the muscles down the lower motor neurones. This may result in the muscles being contracted more due to this hypersensitivity as the action potentials will stimulate calcium to enter the sarcoplasm allowing a greater base muscle tone and results in a greater resistance caused by high levels of spasticity. The increased activity of alpha motor neurone can also cause exaggerated movements caused by the spasticity due to uncontrolled contractions.  Can you explain the function of this physiological process and name the key structures? - Week Three - Physiology of balance: vestibular system static labyrinth that is responsible for gravity and linear movement Key features, otoliths, otolithic membrane, utricle and saccule, cilia How does the process the occur ? 1.The tips of the cilia are embedded in the otolithic membrane membrane is weighted down with protein calcium carbonate granules called otoliths. otiliths add to the weight and inertia of the membrane and enhance the sense of gravity and motion 2. When the head is erect, the otolithic membrane bears directly down on the cilia and simulation is minimal - when the head is tiled, otolithic membrane sags and bends stereo-cilia and kinocilium which opens or closes channels in the cilia that release or do not release neurotransmitters which go to the cerebellum 3. Any orientation of the head causes a combination of stimulation to the utricles and saccules in both ears brain (floculonodular lobe in the cerebellum) interprets head orientation by comparing inputs to each other and other inputs from the eyes and stretch receptors the brain can detect where the head is tilted or the body is tipping movement can then be corrected in the cerebellum and sent efferently to muscles to complete correction. Balance motor signals are sent down the vestibulospinal tract and inervates muscles ipsilaterally – alters muscle activity in neck and antigravity muscles in response to head Discuss the role of this process in a given pathology or age related change? movements Parkinson’s Disease PD distrusts the basal ganglia function which influences motor control and reflexes, causing the integration of vestibular input and postural adjustment to be affected, increasing the likelihood of falls PD causes rigidity, bradykinesia and stooped posture which may cause vestibular dysfunction and make it difficult to respond to changes in the environment overall, PD affects cognition and the ability to integrate sensory inputs (including information format the vestibular system, Rutherford impairing balance and coordination  Areas involved in motor control – Week Four – Basal ganglion – initatiing and stopping movement cerebellum – co-ordination and balance / feedback to correct movements Motor Pathway: motor-sensory integration for a motor skill Spinal cord –transport of motor(decending efferent tracts) / sensory (acending afferent tracts During the course of an action, feedback is compared against a standard to enable an action to be carried out as planned. CLOSED LOOP SYSTEM Two components:- Feedforward (motor plan Feedback: Information from sensory system indicates status to CNS which makes corrections to the ongoing movement. How does the process the occur ? - The sensory information is received through the receptors throughout the body. Eg. Nociceptors / Thermoreceptors / Mechanoreceptors → Meissner corpuscles The sensory information then travels from the receptor through the sensory neurones and the dorsal horn off the spine. This information then travels up the posterior column in the spine. - At the top of the spine/posterior column the sensory neurone synapses with the interneuron. The interneuron then travels through up to the brain through the thalamus (sensory co- ordination center) and into the primary somatosensory cortex where the information is then received and then processed. Here is the sensory homunculus map M1 (motor homunculus) areas with greater dexterity have greater representation There are three motor pathways coming down 1.Corticospinal tract (voluntary) 2. reticulospinal tract (tone) 3. Vestibulospinal tract (balance) The decision on movement then occurs in the primary motor cortex where the movement pattern travels down the upper motor neurones down the tracts. The information then is received by the by the alpha motor neurone at the anterior horn of the spine. The alpha motor neurone then sends impulses down the lower motor neurones to the muscles. Gamma motor neurons = muscle spindles – monitor amount of stress/ stretch ensuring normal sensitivity. The impulse then reaches a synapse within the neuromuscular junction where the action potential travels reaches the muscles to result in a muscular contraction Stroke – CVA – UPPER MOTOR NEURON SYNDROME eg. Damage to left side of the brain will affect motor control on right side of the body. This is due to the crossing over in the dorsal horn Will experience Neg- symptoms (low tone, weakness, loss of dexterity) this is due to a lack of signals coming down the Corticospinal tract – lack of neural drive – Tone Reticulospinal tract Positive signs – High tone (spacticity) Hyper-reflexia(eggagerated reflex - Alpha motor neuron has become hypersensitive – disinhibition of alpha motor neuron = High tone and spacticity Will also experience sensory losses at somatosensory cortex damage – altered light touch, proprioception temperature and pain sensation Intergrative – reduced co-ordination and balance ATAXIA = cerebellum damage / vestibular system makes postural adjustments altering spinal tone via veticulospinal tract. Spinocerebellar tract and vestibulo-spinal tract Parkinson's disease → Parkinson's is a neurological condition caused by degeneration of dopamine producing cells of the substantia nigra in the basal ganglia → This is because the dopamine is used in the direct which pathway as dopamine excites the striatum to excite the Gpi which inhibits the thalamus which excites the cerebral cortex for movement so with no dopamine being produced neither pathway can be activated. This causes people with Parkinson’s to struggle to initiate, maintain or stop movements. Bradykinesia which is the slowness of movement and freezing. Muscle rigidity is caused by Parkinsons due to the muscle tone being turned upwards which causes resistance at all speeds of passive movement Another motor symptom is tremor at rest which may be caused by the indirect pathway being unable to fire signals to prevent the unwanted movement.  Can you explain the function of this physiological process and name the key structures? Week four – Synaptic Transmission - shows a neuromuscular junction the synaptic transmition between neurons called a synapse separated by the synaptic cleft. How does the process the occur ? - presynaptic neuron generates an action potential along its myelinated axon towards the presynaptic junction Neurotransmitter molecules are made from precursors bby the influence of enzymes. Neurotransmitters are stored within the synaptic vesicles. 1. The AP will reach the axon terminal 2. Voltage gated Ca2+ channels are opened which signals the vesicles. 3. Positivley charged calcium ions enable the synaptic vesicles with the neurotransmitters inside to fuse with the cell membrane 4. Neurotransmitters are released into the synaptic cleft via Exocytosis 5. On the adjacent postsynaptic cleft they bind with the auto receptors which inhibit further neurotransmitter realease. 6. Neurotransmitters also bind to neurotransmitter receptor sites on post synaptic membrane --> this opens the ion gated channels. 7. At this point depending on which neurotransmitter binds to which specific receptor site either - Increase the likely hood that the post synaptic membrane will become activated and generate an action potential EXCITORY SYNAPSE – depolarisation – Na+ enter - Decrease the chance of an AP being produced INHBITORY SYNAPSE – hyperpolarisation – Cl- enter Discuss how pathology or age - elated change affect this physiological process? Discuss the role of this process in a given pathology or age related change? → Parkinson's is a neurological condition caused by degeneration of dopamine producing cells of the substantia nigra in the basal ganglia. As dopamine is a neurotransmitter – lack of this dosent enable AP to be generated.. → This is because the dopamine is used in the direct which pathway as dopamine excites the striatum to excite the Gpi which inhibits the thalamus which excites the cerebral cortex for movement so with no dopamine being produced neither pathway can be activated. This causes people with Parkinson’s to struggle to initiate, maintain or stop movements. → Bradykinesia which is the slowness of movement and freezing. These are caused by reductions in the ability of the direct pathway which initiates and maintains movement. → Muscle rigidity is caused by Parkinsons due to the muscle tone being turned upwards which causes resistance at all speeds of passive movementAnother motor symptom is tremor at rest which may be caused by the indirect pathway being unable to fire signals to prevent the unwanted movement. Week Five - Sensory Pathway: perception of fine-touch and proprioception Can you explain the function of this physiological process and name the key structures? 1. The somatosensory system detects sensation in the skin, joints, muscles and fascia and relay this information to the brain. Stimuli - fine touch, vibration, pressure and proprioception How does the process the occur ? - The sensory information is received through the receptors throughout the body. Eg. Nociceptors / Thermoreceptors / Mechanoreceptors → Meissner corpuscles The sensory information then travels from the receptor through the sensory neurones and the dorsal horn off the spine. There are three main sensory tracts 1. Posterior column and 2. Spinothalamic tract light touch/ pressure/ proprioception( body is in space). Go up spine and is CONTRALATERAL. This information then travels up the posterior column in the spine. - At the top of the spine/posterior column the sensory neurone synapses with the interneuron. The interneuron then travels through up to the brain, Will go through thalamus (sensory co-ordination center) and into the primary somatosensory cortex terminate in (S1) ( s1 )Has a sensory map =sensory homunculous The homunculus looks different from the body because body parts that require more precise movements, like the hands and mouth, are given more brain area. 3. Spinocerebellar tract - main carrier impulses for proprioception. Has two division anterior and posterior Impulses stay on the same side of the body – ipsilateral. Impulses go to the cerebellum which is important for co-ordination and balance Discuss how pathology or age - elated change affect this physiological process? Stroke → Depends on what area of the brain has been damaged it will present differently Eg. Sensory signals are detected in receptors which travel through the peripheral nervous system to the spinal cords - Signals travel through those three main sensory tracts Damage to S1 - parietal lobe – if the S1 is damaged it is unable to properly process info leading to alteration in the senses of light touch proprioception pressure pain and temp. Hypoesthesia: Reduced sensitivity to touch or temperature. This can cause numbness in the limbs, making it difficult to notice pressure from tight clothing or shoes. Hyperesthesia: Increased sensitivity to stimuli, such as touch, taste, or hearing. This can make it difficult to be in crowded places or watch television. Can also experience visual disturbances called hemi-anopia – Dysaesthesia or paraesthesia: Unusual sensations on the skin or in the limbs, such as tingling or pins and needles half blindness in each eye - Damage to cerebellum = unconscious proprioception - balance / co-ordination problems on the same side of the body (ipsilateral)  Cerebral Cortex DIRECT Supplementary motor area, somatosensory cortex PATHWAY SN modulates (dopamine) striatum GPe SN Striatum inhibits the GPi STN Less GPi inhibition of the thalamus Thalamus excites the cortex Cerebral Cortex Primary motor area (M1) Thalamus Cerebral cortex, cerebellum  Can you explain the function of this physiological process and name the key structures? Week four – Basal Ganglia: Motor loop (direct pathway) this shows the direct neural pathway in the basal ganglia of the CNS that helps initiate and carry out voluntary movement. This direct pathway is an excitory pathway that is modulated by dopamine. The basal ganglia is important in motor planning and co-ordination of movements → The aim of the direct pathway is to excite the motor cortex to increase motor activity --- turning OFF the area which causes inhibition Cerebral Cortex DIRECT Supplementary motor area, somatosensory cortex How does the process the occur ? PATHWAY → when you want to complete a voluntary movement the plan starts in the cerebral cortex and SN projects into the Striatum. modulates → Substantia nigra modulates dopamine production towards direct pathway (dopamine) striatum → Striatum sends inhibitory neurons towards the Globus Pallidus Internus (Gpi) – this results in less inhibition of the thalamus. GPe SN → This disinhibition of thalamic control enables the thalamus to excite the Cerebral Cortex and the Striatum primary motor area(M1) where movement occurs. → This system functions on a positive feedback system inhibits the GPi Discuss how pathology or age - elated change affect this physiological process? Discuss the role of this process in a given pathology or age related change? STN Less GPi → Parkinson's disease inhibition of → Parkinson's is a neurological condition caused by degeneration of dopamine producing cells of the thalamus the substantia nigra in the basal ganglia → This is because the dopamine is used in the direct which pathway as dopamine excites the Thalamus excites striatum to excite the Gpi which inhibits the thalamus which excites the cerebral cortex for the cortex movement so with no dopamine being produced neither pathway can be activated. This causes Cerebral Cortex Primary motor area (M1) Thalamus people with Parkinson’s to struggle to initiate, maintain or stop movements. Cerebral cortex, → Bradykinesia which is the slowness of movement and freezing. These are caused by reductions cerebellum in the ability of the direct pathway which initiates and maintains movement  Can you explain the function of this physiological process and name the key structures? Week Five - Muscle spindles: Muscle spindles provide proprioceptive information about the length the muscle is in, changes in that muscle’s length and the velocity of the change in length. They do this by monitoring muscle stretch and changes in the amount of stretch on the muscle and the information is used to help with protection and for muscle tone. How does the process the occur ? - Muscle spindles are small diameter striated muscle fibres (intrafusal) enclosed in a capsule which lies parallel to the main extrafusal muscle fibres. These intrafusal fibers are called nuclear bag and nuclear chain fibres. -The outer 2/3s of the muscle fiber are striated and contractile but the middle 1/3 are non-striated and non-contractile. -Sensory innervation comes from the type 1a afferent neurons which detects stretch and velocity which wrap in an annulo-spiral direction around the nuclear bag and nuclear chain fibres. -There are also type 11 fibres which flower spray onto the nuclear bag and nuclear chain fibres. The type 11 fibres only detect length. -These fibres send their sensory information to the alpha motor neuron in the spine, the primary somatosensory cortex in the parietal lobe and the cerebellum. -The sensory information causes the muscle to either contract or relax which also changes the shape of the muscle spindle. -Gamma motor neurons are efferent – come from the anterior horn of the spinal cord and supply the contractile outer regions of the muscle spindles intrafusal fibres. This allows the muscle spindles to change shape back to their optimum length when the muscle changes in length ready to respond to another contraction or stretch. This is known as alpha gamma coactivation.  Week Five - Spinal reflexes: phasic stretch reflex phasic stretch reflex This is a quick active reflex that occurs when the muscle is at rest. It is stereotypical/ fast and predictable. It is also uncocious / cerebral cortex is not involved. It is ispilateral That stretches the muscle spindles With the muscles that sets off sensory neurons to spinal cord and alpha motor neuron enabling c contraction. This enables us to relive stretch/ stress on a muscle - The muscle is at rest – 1. stretching – hammer stretches the patella tendon stretching the quadriceps muscle this is a passive movement 2. This sets the muscle spindle sensory receptiors tot send off a signal along the 1a sensory neuron (excited) 3. This arrives at the posterior part of spinal cord 4. Synapses with integrating center on the motor neuron as a direct mono-synaptic reflex of quads 5. Signal to the quads to contract - alpha motor neuron = extrafusal muscles fibers to contract Gamma motor neuron providing signals for contractile ends of intrafusisle fibers to contacts 6. We will see a kicking movement. 7.At the same time the interneuron – on the intergrating center it will send an inhibition to the antagonistic muscle (hamstrings) so they relax at the same time of contraction. Stroke – CVA – UPPER MOTOR NEURON SYNDROME eg. Damage to left side of the brain will affect motor control on right side of the body. This is due to the crossing over in the dorsal horn Will experience Neg- symptoms (low tone, weakness, loss of dexterity) this is due to a lack of signals coming down the Corticospinal tract – lack of neural drive – Tone Reticulospinal tract Positive signs – High tone (spacticity) Hyper-reflexia(eggagerated reflex - Alpha motor neuron has become hypersensitive – disinhibition of alpha motor neuron = High tone and spacticity Will also experience sensory losses at somatosensory cortex damage – altered light touch, proprioception temperature and pain sensation Intergrative – reduced co-ordination and balance Parkinson's disease → Parkinson's is a neurological condition caused by degeneration of dopamine producing cells of the substantia nigra in the basal ganglia → This is because the dopamine is used in the direct which pathway as dopamine excites the striatum to excite the Gpi which inhibits the thalamus which excites the cerebral cortex for movement so with no dopamine being produced neither pathway can be activated. This causes people with Parkinson’s to struggle to initiate, maintain or stop movements. Bradykinesia which is the slowness of movement and freezing. Muscle rigidity is caused by Parkinsons due to the muscle tone being turned upwards which causes resistance at all speeds of passive movementAnother motor symptom is tremor at rest which may be caused by the indirect pathway being unable to fire signals to prevent the unwanted movement.  Week Six - Respiratory System: gas exchange at respiratory membrane Can you explain the function of this physiological process and name the key structures? this shows the structure of the alveoli in the lungs. There are millions that sit in the lungs and are responsible for gas exchange for respiration during inhalation and exhalation. In this process gas moves down a pressure graidient from atmospheric air into the bloodstream so it can be used by our tissues. HIGH PP --> LOW PP How does the process the occur ? air passes through mouth → trachea→ two main bronchi → bronchioles → alveoli where gas exchange occurs In the alvoli are made up of a single layered epithelium where gas can easily diffuse across. There is a large surface area of them. Moist = increases rate of diffusion The alvoli are covered by a system of capillaries with being supplied by the pulmonary artery and leaving through the pulmonary vien. In the alveoli are lined with Type I and Type II pneumocytes which sit on a basement membrane. Type II cells are cuboidal and secrete surfactant – a lipoprotein – which helps to prevent the alveolus from collapsing, especially on expiration. Type I cells are structural., they are flat, thin squamous cells which promote diffusion of respiratory gases. These line 90% of an alveolus. The respiratory membrane is the membrane that oxygen and carbon dioxide diffuse across during the process of gaseous exchange from the alveolus to pulmonary capillary or vice versa. When Heamaglobin reaches capillary wall it has given up the majority of o2 to the tissues and after inhalation alveoli are o2 rich creating an concentration gradient. HIGH PP --> LOW PP Expiration → There is a high conc of Carbon dioxide HIGH PP --> LOW PP. co2 is transported through plasma AND in the blood as bicarbonate, the bicarbonate reacts with hydrogen in blood and forms co2 and water. Here it can diffuse across the cell wall via diffiusion and osmosis entering the alveolus. → Co2 can also disassociate with haemoglobin into the alvolius Inhalation O2 enters the alvoli and can be transported via dissolving in plasma OR bind to haemoglobin to form oxyheamoglobin to be transported in the blood Discuss how pathology or age - elated change affect this physiological process? → COPD Chronic obstructive lung disease is an umbrella term that includes asthma, chronic bronchitis, emphysema. This can be characterised progressive airflow limitation on pulmonary ventilation. Furthermore, tissue scaring within the respiratory tract due to chronic inflammation leading to airway narrowing and decreased lung recoil. Lung compliance is reduced making it harder to increase lung volume. → Airway narrowing increase resistance and decreasing airflow these combined features decrease the gas exchange at the alvoli. → Excessive mucus/ sputum can clog bronchioles → Damage to Alveoli (Emphysema): 3.Hyperinflation and Trapping of Air: - Alveoli walls lose elasticity, leading to the destruction of alveolar walls. - Trapped air due to narrowed airways causes lungs to overinflate. - Reduces surface area for gas exchange, causing hypoxemia (low blood oxygen). - Results in difficulty exhaling completely, dyspnea (breathlessness), and limited activity tolerance.  Can you explain the function of this physiological process and name the key structures? Week Six – Lung Volumes: Pulmonary Ventilation → This shows the mechanism of breathing depicting the pulmonary ventilation phases of inspiration and expiration. It also shows the difference in lung volumes throughout these phases.. When discussing pulmonary ventilation its important to remember that gases travel from an area of high pressure to an area of low pressure. This is happening between atmospheric pressure / intrapulmonary pressure and interpleural pressure. How does the process the occur ? At rest the Atmospheric pressure is equal to intrapulmonary pressure = 760mmHg = relative 0 The intrapleural pressure is usually negative acting as suction to keep lungs inflated stopping lung collapse. Pulmonary ventilation is achieved by the rhythmically changing the volume Of the thoracic cavity Inspiration The diaphragm and the external intercostal muscles contract expanding the thoracic Cavity and the lungs. This increase in volume causes a decrease in pressure, causing Atmospheric air to flow in. Air (O2) will flow into the lungs from an area of high p to an area of low p. Furthermore, the warming of the inhaled air further inflating the lungs Alvoli inflate with o2 providing o2 to blood. Inspiration requires muscle contraction therefore energy expenditure whereas… Expiration = During quiet breathing passive process The diaphragm returns to its original position and muscles relax, thoracic and lung volumes Decrease while pressures increase → pushing air out. This relies on the elasticity of the lungs and ribcage. – alvoli deflate In deep breathing this is an active process requiring additional muscles to produce larger changes in thoracic volume. Resistance to airflow exists within the lung tissues and the airways In these healthy lungs we can observe high compliance and low resistance to air flow. Contralateral ventilation/ Discuss how pathology or age - elated change affect this physiological process? Discuss the role of this process in a given pathology or age related change? → COPD Chronic obstructive lung disease is an umbrella term that includes asthma, chronic bronchitis, emphysema. This can be characterised progressive airflow limitation on pulmonary ventilation. Furthermore, tissue scaring within the respiratory tract due to chronic inflammation leading to airway narrowing and decreased lung recoil. Lung compliance is reduced making it harder to increase lung volume. → Airway narrowing increase resistance and decreasing airflow these combined features decrease the gas exchange at the alvoli. → Excessive mucus/ sputum can clog bronchioles → Due to r3educed elastic nature of tissue air can get trapped within alvoli and do not deflate like normal lungs this makes it harder to inhale.  Week Seven - The vascular system: structure and function of blood vessels Can you explain the function of this physiological process and name the key structures? - this shows the vascular system which is comprised off Arteries distribute blood to tissues and organs —> arterioles Arterioles respond to nerve activity —> constrict / dilation offering resistance to blood flow go smaller —> capillaries where transport of substance occurs Venules —> vein →back to heart Pulmonary system → heart & lungs Systemic system -> heart and body tissues How does the process the occur ? Arteries are larger and thicker blood vessels with more smooth muscle and elastic tissue to allow for high pressure blood to be transported around the body- primarily carry oxygenated blood away from the heart towards soft tissu Capilleries are single cell thickness of endothelial cells. Their aim is to allow the easy diffusion of air, nutrients and waste products into and out of the tissues/blood. Veins - take blood back to the heart. Has a similar 3 layered structure to the arteries, but are generally thinner with less smooth muscle & elastic tissue. They also contain valves to help prevent backflow. - Primary carry deoxygenated blood from tissues towards heart Blood vessles are split into 3 layers of tissue. Lined with endothelial cells Tunica: Externa, Media & Intima Tunica Intima - innermost layer, prevents blood clots (via smooth lining). Surround the blood, regulate blood pressure. Tunica Media - thicker in artery. Smooth muscle w/ elastic tissues. Contracts and relaxes to allow vasodilation and vasocontriction, to control blood flow. Tunica Externa - outer layer provides structure and support. Supplies the tissues w/ nutrients & nerve supply Discuss how pathology or age - elated change affect this physiological process? - Atherosclerosis → build up of substances is the key cause of coronary heart disease and can cause stroke. Atherosclerosis Causes Stenosis within the lumen → reduces blood flow to the heart muscle – myocardial ischemia further causing an imbalance of tissue oxygen supply and demand Before sevre cases we want to reduce risk factors eg. Smoking / diet / increase PA/ loose weight and overall increase contractile forces of blood flow, but …… If stenosis >70% medical management is required to improve efficiency STENT – less invasive – expand lumen using ballon and catheter CABG – Coronary artery bypass grafting grafting a vein over the top of blocked/ narrowed arteries to improve blood flow back to the heart. Can be taken from vein/ artiery of synthetic.. Need to them monitor.. ECG – arthymia, Atrial fibrillation, BP and output.. Watch for occulusion/ thrombus/ embolius / sepsis