PHYSIOLOGY EXAM REVISION MODULE ONE Sensory Pathways    Information from our environment being picked up by our receptors

in the periphery of our body Information is sent by afferent fibers. Provide an internal representation of the outside world

MODALITY Vision Audition Smell Taste Somatic (Touch, Propriception, pain, thermal)       

STIMULUS Light Sound Chemical Chemical Mechanical, thermal, noxious

RECEPTOR TYPES Photoreceptor Mechanoreceptor Chemoreceptor Chemoreceptor Mechanoreceptor, Thermoreceptor, Nociceptor, Propriceptor

Detect  Process  Perceive COMPOUND SENSATIONS – some sensations that we perceive but don’t have receptors for, occurs when two or more stimuli come together example, Wetness and flavor. SENSATION – sensory information that reaches our level of consciousness PERCEPTION – understanding what the sensation means What we perceive is not necessarily what is occurring THREE LEVELS OF PROCESSING = a physical stimulus  stimulus is transducted to a message of impulses  a response CLASSES OF SENSORY RECEPTORS o MECHANORECEPTORS – Stretch, pressure o THERMORECEPTORS – Cold, Warmth o CHEMORECEPTORS – Binding of chemicals o PHOTORECEPTORS – Light wavelengths o NOCICEPTORS – Pain, tissue damage, extreme heat and cold TWO WAYS FOR RECEPTORS TO BE STIMULATED o Stimulus directly causes receptor potential on neuronal surface o Stimulus first affects receptor cell then neurotransmitter will be sent to afferent neuron SENSORY RECEPTORS o Stimulus specific o Graded potentials SENSORY UNIT – A single afferent neuron and all of its receptor endings – all receptors in a sensory unit are the same

Sensory Transduction    Action potentials are just impulses that are all the same – how to get an AP to being able to perceive the stimulus when the only thing carrying the information is an AP CODING – interpreting the stimulus in different ways INTENSITY CODING o You can’t get different sizes of action potentials due to the ALL OR NONE PRINCIPLE o You can have different frequencies of action potentials  high stim strength, high receptor potential  Number of receptors activated and the number of afferent neurons activated  Big stimulus activate and recruit more receptors and more neurons. o RECRUITMENT – big stimulus can lead to recruiting extra sensory endings MODALITY CODING o Modality is the type of stimulus and sub-modality is the sub-type example, taste is a modality and sour is a submodality.

LABELLED-LINE CODING – the most common way – different receptors respond to different stimuli, the labeled line pathway comes in when the information transmitted to the CNS from our periphery go through separate pathway  Example – all pain will travel down a pain pathway o PATTERN CODE – Less common used in taste – carried on the same nerve but with a different pattern of Action potentials LOCATION CODING o Where is it coming from? o ACUITY – how precisely we can pick where a stimulus is being applied to the body or where it is coming from, determined by;  Size of the receptive field  Receptive field – the area in which a nerve can pick up stimuli from  Recpetive endings are most dense at the centre of a receptive field  Small number of receptors with large receptive field = LOW acuity  Large number of receptors with small receptive field = HIGH acuity  Density of sensory units  Overlap in receptive fields  Stimulus would be detected by more than one neuron  Frequency of AP’s would be greatest at the neuron in the middle  Lateral inhibition  Don’t want too many action potentials and overlap  Sharpens the information travelling to the CNS  Information that is coming from the receptor that is triggered the most inhibits the action potentials travelling in the sensory neurons nearby o SENSORY HOMUNCULUS – Primary somatosensory cortex – also have a labeled line for location, carried on a separate pathway and end up on separate parts of the brain  Shows which parts of the cortex correspond to different parts of the body  Larger parts are parts of the body with higher sensory information coming in o DESCENDING PATHWAYS  Prevent constant influx of information coming from parts of the body that are not very usuful  Information from descending pathways decide whether or not the stimulus detected by sensory neurons is able to travel up pathways, done in two ways. o Affect the post synaptic neuron o Synapses with afferent fiber prevents AP at junction end of sensory neuron DURATION CODING o How long is the stimulus being applied for o TONIC – slowly adapting  When we constantly need to know about a stimulus o PHASIC – Rapidly adapting  Good at telling about changes o Receptor adapt by no longer responding to pattern of action potentials o

Somatosensory Pathways     Carry information from our body wall that we’re conscious of Ascending pathways – towards brain From thalamus  particular part of cortex that processes the information – info from left of body to right side of brain and vice versa BASIC STOPS IN PATHWAY o Spinal cord  Brainstem  Thalamus  Specific sensory areas of cortex o Everything goes to thalamus before being redirected out. ANTEROLATERAL PATHWAY – carries pain, temperature, crude touch, tickle, pressure information

o CROSSES OVER AT LEVEL OF SPINAL CORD AND TRAVEL ON OPP SIDE DORSAL COLUMN PATHWAY o Receptors enter spinal cord stays on the same side  enters dorsal column  travels up spinal cord  synapses at brain stem travels to thalamus and synapses again then travels to somatosensory cortex o Heirachy  Stimulus  sensory afferent activity (afferent pathways)  awareness (thalamus)  discrimination (primary sensory cortex)  meaning (association cortex). o Sclera – outer white part of the eye – fibrous.  Mechanical anchor for the muscles moving your eye around – the muscles used for focusing the eye are also attached to the sclera o Choroid – the intermediate tunic  The vascular section.  Aqueous – anterior. Neural and pigmented The eye is hollow – humours provide the eye with shape o TWO HUMOURS.  RODS – light and dark  CONES – colour – 3 types – red. move similar to water due to water having a very low refractive index. blood vessels supplying the eye anchored to the choroid  Extends into the iris  All the muscles that control the shape of the lens also attach to the choroid o Retina – the inner tunic  Holds the photoreceptors that we detect the light with and the neural layer which turns light into an electrical signal  Two layers. Receptors come in and enter the spinal cord then synapse with the 2 nd order neuron (IMMEDIATELY CROSSES OVER) then at the anterolateral column  travels up to the thalamus where it synapses with 3rd order neuron which takes it to somatosensory cortex. when light hits directed to the lens  Vitreous – posterior. green and blue o First part of light hits the retina photoreceptors inner layer o MACULA LUTEA – area of most cones o FOVEA CENTRALIS – highest concentration of cones o Rods found in the periphery o Optic disc – region where the nerves innervating the eye are found and blood supply of the eye. Opp is Macula Sparing GLAUCOMA – Distorts nerve fibers and blocks AP propagation REFRACTION – lens shape is the same but the angle that the light is coming in is different ACCOMMODATION – accommodate for the different distances that the light is coming in by changing the shape of the lens o Close – round Far – Flattened            . Cornea refracts light slightly inwards towards the lens If iris is opened enough that light is let in refract a little bit  focused onto the fovea centralis MACULA DEGENERATION – loss of central vision – the light hitting the macula doesn’t pass because there are no photoreceptors – the macula has degenerated. has to be clear so light can pass through needs to be thicker to maintain size and shape of the eye. Visual  Has three layers. Optical component – directs light rays to retina Neural Component – converts light to a neural stimulus THE LENS – posterior to the cornea and is anchored by the ciliary bodies from the choroid o Focus an image on the photoreceptors by changing shape RETINAL ORGANIZATION – outer layer contains photoreceptors – inner neural layer contains bipolar and ganglion cells o Two types of photoreceptors.

    CILIARY CONTRACTION o Zonular fibers – don’t contract – they’re suspension ligaments – hold the lens o Ciliary muscles contract the muscle to round the lens and relax the muscle to flatten the lens o DISTANT VISION – ciliary muscle relaxed and zonular fibers are flattened o CLOSE – clilary muscle contracted and zonular fibers are loose NEAR-SIGHTED – the focal distance is shorter than retina – the initial refraction is happening to where the light comes together o Lens shape change FAR SIGHTED – the focal point is beyond the retina AUTONOMIC CONTROL OF THE EYE o Sympathetic and parasympathetic nerves control pupil size and accommodation o Ciliary Muscles – increased parasympathetic = constriction (ROUND LENS)  Increased sympathetic = dilation (FLATTENED LENS) o Iris – increased parasympathetic = constriction and increased sympathetic = dilation Photoreception  DARK o CyclicGMP binds to Cgmp Na+ channels causing an influx of sodium o Cell is depolarized LIGHT o Cis-rhodopsin is changed to trans rhodopsin o Transducin is activated o Activation of phosphodiesterase (breaks down cyclic GMP) o Decreased cyclic GMP o Cyclic GMP doesn’t bind to Na+ channels o Photoreceptor no longer depolarized Colour vision – three different forms of opsin sensitive to various wavelengths   Light/Dark Adaptation     When rods are hit by light the opsin is activated but is burnt out quickly  don’t use rods during the day – so use cones because less sensitive to light – using less opsin When its dark rely less on cones and start to depend on rods DARK ADAPTATION – During the day light breaks down opsin rods – rods are burnt. in the dark have to wait for opsin in rods to regenerate  why it takes a while to see in the night time LIGHT ADAPTATION – Bright light hitting rods causing high opsin activation and huge decrease in cyclic GMP prevents release of glutamate o Opsin is broken down very quickly – very white due to rods black/white Neural Pathways of Vision     Retina has millions of photoreceptors Fovea is almost a 1:1 cone: ganglion Away from fovea there is more convergence of cones to ganglion – less rods more cones RECEPTIVE FIELD o Ganglion cell and the photoreceptors that activate it o Bipolar cell is a graded potential  action potential starts in the ganglion ON AND OFF CENTRES – refers to bipolar cells o Shining a light on the receptor leads to depolarization of bipolar cell  leads to an AP in the ganglion cell o Shining a light in the surrounding cells leads to hyperpolarization of bipolar cell – Dark turn self off ON PATHWAY o Photoreceptors depolarized in the absence of light rays (high cyclic GMP) o Light hyperpolarizes photoreceptor cell o Decreased glutamate released onto bipolar cell   .

    o Bipolar cell depolarizes and releases more excitatory NT o Ganglion cell depolarized and generates more action potentials OFF PATHWAY o Photoreceptor is depolarized in the absence of light rays o Light hyperpolarizes photoreceptor cell o Decreased glutamate onto bipolar cell o Bipolar cell hyperpolarizes and releases less excitatory NT o Gnaglion cell hyperpolarizes and generates fewer Aps Two types of bipolar cells on/off Determined by the type of glutamate receptor Increases viual acuity Visual Fields   Left side of vision hits the back right hand side of retina Right side of vision hits the back left hand side of retina   Outer parts of vision goes through optic chiasm Everything goes through LGN Visual Association Pathways  DORSAL – HOW AND WHERE o Spatial recognition o Short term memory o Hand-eye coordination VENTRAL – WHAT o Object recognition o Long term memory  Motor Pathways  Sensory and motor systems rely on each other .

hands.        Need sensory information to guide our movements by providing information on what’s occurring and also by giving fee dback Sensory Input  Primary Sensory Area  Higher Sensory Area  Association Areas  Higher Motor Areas  Primary Motor Cortex  Motor Output Allows for three different types of movements o VOLUNTARY MOVEMENTS – complex movements. HEIRACHY OF MOTOR CONTROL o Higher levels – association cortex  PLANNING – WHAT? o Middle Levels – cerebellum. thalamus. usually goal directed and can be learned and improved o REFLEX RESPONSES – very simple movements. PREMOTOR AREA. no time to correct errors. basal ganglia  PROGRAMMING – HOW? o Lower Levels – Spinal cord. finger therefore more motor units and a larger part of homunculus\ Basal Nuclei and Cerebellum        Regulate and modify the motor program coming from the motor cortex Very important in motor control Middle level of hierarchy Basal Nuclei – a number of structures which are directly linked through pathways Thalamus – relay center where everything that enters the basal nuclei enters the thalamus before it sends it back to where it came from Motor Control – a process of restricting output to get a sustained controlled motor response need to restrict the output BASAL NUCLEI o Sole responsibility of the basal nuclei is to inhibit unwanted movement o Important in converting what you want to do. brain stem. motor cortex  EXECUTION – ACTION Motivational system is the limbic system Motor Programs – patterns of learned movement stored in the brain Cerebral Cortex     Interested in PRIMARY MOTOR CORTEX. using information from memory and past experience. rapid responses o RHYTHMIC MOTOR PATTERNS – where you see overlap between voluntary and reflex movements  Voluntary when we decide to start and end but reflex when in between CONTRACTING AND RELAXING MUSLCES o Three major things to consider  TIMING – occurring in the right sequence  POSTURAL ADJUSTMENTS – maintaining balance  MECHANICAL ARRANGEMENTS – constant sensory information coming in SENSORY INFORMATION AND MOTOR CONTROL o Internal and external information essential for planning and refining movements o Feedback – need constant sensory input to make sure you’re doing what you want to do and correct any errors o Feed Forward – less time for feedback. wrists. Anticipating. muscle. can have some voluntary control but not a lot. SUPPLEMENTARY MOTOR CORTEX Primary Motor Cortex – voluntary motor movement Pre Motor Area – preparation of movement. has a role in initiating movements Supplementary Motor Cortex – coming up with the order of sequence we need for the movement Motor Homunculus    How many motor units come from these cortical areas How precise are the movements we can make in the different areas of the body Need more precise movements from face. to actually doing it o Converts planning of the movement into programming .

 INTERNAL CUES – generated from thought where thought is the stimulus Decides what behavious is most likely to be correct  Cortex sending information to the basal nuclei of what we want the body to do  Basal nuclei decides the appropriateness can REINFORCE (direct) or SUPPRESS (indirect)  REINFORCE – Removal of an inhibitory effect causes increased firing of thalamic neurons to motor cortex o IMPAIRMENT OF BASAL GANGLIA  Tremors seen at rest  Involuntary movement  No Movement  Impairment is opposite side of lesion  Parkinson disease CEREBELLUM o Error control device – ongoing modification of motor plans o Receives both input from motor cortex and spinal cord o Coordination o Lesion is on same side as impairment o OPEN LOOP  Ensures that doing a movement you are aware of your environment o CLOSED LOOP  What you’re about to do to what is actually happening. Gamma motor neurons become important o Gamma and alpha co activation – alpha motor neurons contract muscle at the same time as an action potential from gamma motor unit got o intrafusal fibers to contract  Maintains tension in spindle to maintain response to shortening TENSION MONITORING SYSTEM o Tension in tendons is different to muscle belly o Golgi tendon organs on tendons to measure tension     Descending Motor Pathways  PYRAMIDAL TRACT/ CORTICOSPINAL o Allow for innervation of fingers and hands o Fine movement o Cortex  decussate at brain stem  synapse at spinal cord o Fast and fine skilled movements EXTRAPYRAMIDIAL TRACT/ BRAINSTEM PATHWAY o Starts at the brainstem  don’t decussate  go to muscles and muscle groups o Used for big movements o Balance and posture.  Information from sensory also feeds into cerebellum and makes sure that whats intended and what actually matches o o Motor Neurons     Directly innervate skeletal muscle Extrafusal muscle fiber – the one that contracts – innervated by alpha motor neurons Intrafusal muscle fibers innervated by gamma motor neurons o Important in detecting muscle stretch To monitor the length of muscles need muscle spindle – made up of intrafusal fibers in very close alignment with stretch receptors o Can tell us when muscle is contracting or relaxing Extrafusal fibers doing the work of contraction run in parallel to intrafusal fibers Extrafusal fibers contract and so will intrafusal Extrafusal innervated muscle shortens. intrafusal also shorten – tension decreases and stretch receptors will no longer respond. coarse limb movements  .

 UPPER AND LOWER MOTOR NEURONS o Upper Motor Neurons – Originate in the motor region of cerebral cortex  Connects the brain to level of spinal cord o Lower Motor Neurons – Cause contraction – from spinal cord to muscle Wernicke’s and Broca’s Aphasia  WERNICKE’S APHASIA – comprehension of language o Difficulty understanding written or spoken word o Fluent but incomprehensible speech BROCA’S APHASIA – Articulation of language o Damage – difficulty in expressing thoughts in written or spoken language  .

protecting further structures.have no gas exchange does not get to lungs to participate in gas exchange RESPIRATORY ZONE o ALVEOLI – Contain three types of cells  Simple Squamous Epithelium – wall  Macrophages – keep air clean – last mechanism of protection  Surfactant secreting cells – Lowers surface tension o Lots of capillaries surrounding alveoli very close interaction  INSPIRE – Alveoli expand  EXSPIRE – Alveoli recoil o Alveoli have elastic properties due to being surrounding by elastic walls o Alveoli are interconnected by pores so air flow can move between them o PNEUMONIA – walls become thicker due to producing fluid – inhibits respiration o EMPHYSEMA – walls break down  Lose ability of respiration o SURFACTANT – diffusion does not occur sufficiently across a dry surface therefore alveolar cells lined with water – Very thin layer of water to allow diffusion  Water has very strong attractive properties – limit to expand during inspiration  Surfactant weakens water bonds reducing surface tension allowing expansion of alveoli            . also has the ability to produce mucous by lining cells to also trap particles Nasal cavity has cartilaginous plates that project lateral called nasal conchii create a turbulence to flow of air this slows the movement of air down o Heavily vascularized for warmth  To prevent cold air from constricting smooth muscle of the air ways – keeps airways always dilated Breathing from the mouth is more beneficial when you’re exercising due to large aperture  to move large volumes of air Pharynx has many immune cells Larynx – makes sure food and water don’t enter the trachea NOSE  PHARYNX  LARYNX  TRACHEA  BRONCHII  BRONCHIOLES  ALEVOLI Just dorsal to the trachea is the oesophagus – there is no cartilaginous ring in the posterior part of the trachea because it would restrict the movement of food through the esophagus Internal wall of the conducting zone is made of ciliated columnar epithelial cells embedded inside is goblet cells which are mucous producing and trap any particles that have made it through the nasal cavity o Cilia of the cells push these particles up towards the pharynx BRONCHII – divides into 23 branches continue to branch – become smaller and no more cartilaginous rings Where bronchii lose cartilage they are bronchioles get smaller and smaller Terminal part ALVEOLI – Round to increase surface area for gas exchange CONDUCTING ZONE o Nasal Cavity  Pharynx  Larynx  Bronchi  Bronchioles o Known as DEAD SPACE – VOLUME OF 150 Ml.MODULE 2 Respiration Functional Anatomy           Respiratory system brings in O2 and eliminates CO2 Lungs – generation of O2 into the body but more importantly the removal of CO2 ELIMINATION OF CO2!!! Inspiration – inhalation – air moves into the lungs Exspiration – exhalation – air moves out of the lungs RESPIRATION – exchange of gases between two compartments VENTILATION – Breathing Starts at nasal cavity and mouth – preferred option being the nose Nose and nasal cavities have coarse hairs which are able to trap matter.

relies on lung elasticity and surface tension INSPIRATION o Requires the contraction of skeletal muscles  DIAPHRAGM AND EXTERNAL INTERCOSTALS  Contraction of external intercostals causes the elevation of rib cage  Contraction of diaphragm moves inferiorly  Increasing the volume of the thorax EXSPIRATION o Relaxation of the external intercostals and diaphragm – thorax gets smaller and lungs recoil Lungs are indirectly attached to the thorax THORACIC CAVITY – contains lungs and heart o Where the body has cavities there are membranes lining the cavities – SEROUS MEMBRANES o For thorax PLEURAL MEMBRANE o The attachment to lung to thoracic through pleural membranes THE PLEURA o Like a fluid filled balloon o PARIETAL PLEURA – the pleura attached to thoracic wall and diaphragm o VISCERAL PLEURA – the pleura attached to lungs o Changing volume of the thorax will physically change the volume of lungs because they are attached to the pleural membrane o Penetrating the pleura causes the lungs to collapse because air gets in o Pleura must be filled with fluid due to not being compressable o Keeps lungs inflated o Negative pressure acts like a suction keeping the lungs firmly attached to pleura o Negative pressure due to.  Surface tension want to shrink alveoli because water wants to get closer together – want to reduce the volume of lungs  Elastic always want to shrink to become smaller  OPPOSING FORCES – Thoracic wall wants to move out and lungs want to move in – pulling the fluid in opposite direction causing a negative pressure PRESSURE AND VOLUME RELATIONSHIPS o BOYLES LAW – Less volume = more pressure and vice versa o INSPIRATION – Contract intercostals and diaphragm – lung volume increase therefore pressure decreases and air comes in o EXSPIRATION – Relaxation of intercostal and diaphragm – lung volume decreases and pressure increases therefore air moves out FORCED INSPIRATION AND EXSPIRATION o To take in bigger breath more muscles start to work these further lift up the ribs cage and really expand the volume of the thorax o DEEP BREATHING – for forced expiration requires internal intercostals and abdominals Volume of air brought into lungs then pushed out of the lungs is about 500Ml Air stops moving into the lungs when pressure is equal and expiration will start Intrapleural fluid pressure does not change during the inspiratory cycle Intraplueral pressure is largest (most negative) when thorax is biggest because the lung is trying to recoil and is strongest there pull on fluid is greatest RESPIRATORY VOLUMES o TIDAL VOLUME – amount of inhaled or exhaled air per breath in resting conditions – 500Ml o INSPIRATORY RESERVE VOLUME – amount of air that can be forcefully inhaled after tidal volume – 3100Ml . Lung Mechanics     Helps prevent alveoli from collapsing            Process of ventilation is all about changes in pressure ACTIVE PROCESS – requires energy. often requires neural input Expiration doesn’t require energy.

no physiological change to bind and transport O2 o Sharp increase is a safety mechanism so you can off load higher amounts of O2 o Only when you get to Po2 <60 that haemoglobin saturation drops off not very sensitive to changes in Pco2 o <60 comprimised dramatically o Offload 250mL of O2 to tissues every minute whilst resting approx. 1L of O2 in blood at any one time  .   o EXSPIRATORY RESERVE VOLUME – Amount of air that can be forcefully exhaled after tidal volume – 1200Ml RESPIRATORY CAPACITIES o TOTAL LUNG CAPACITY – 6000Ml o VITAL CAPACITY – 4800Ml the maximum amount of air that can be inspired or exspired PULMONARY VENTILATION = TIDAL VOLUME x FREQUENCY OF BREATHS (7000 = 500 x 14) ALVEOLAR VENTILATION = (TIDAL VOLUME – DEAD SPACE) x FREQUENCY (4900 = (500 – 150) x 14) Gas Exchange    Pulmonary respiration – respiration that occurs between the alveoli and the pulmonary capillaries o Oxygen to capillaries and carbon dioxide to alveoli Systemic Respiration – the diffusion of gases in the cells of the body o Oxygen to cells and carbon dioxide to the capillaries FICK’S EQUATION o Relates to the rate of diffusion and rate of respiration o Reliant on a number of variables  Surface area  Big concentration gradient the greater the rate of diffusion  Diffusion stops at equilibrium  Oxygen is far less soluble than carbon dioxide   ATMOSPHERIC GASES o Partial Pressure – the part of the total pressure that the gas contributes  pO 2 = 160 pCO 2 = 0. least important gas is humidified – evaporate some of the liquid on the way to the lung  MIXING OLD AND NEW – not all the air you breath enter the alveoli (dead space) breathing out the air in the dead space will be the first air that enters the lung when you inhale again  First 150ml is stale air and 350ml is fresh air o pO 2 = 100mmHg pCO 2 = 40mmHg Breathing more deeply increases pO 2 HYPOVENTILATION – insufficient ventilation – reduction in respiration rapid drop in oxygen very rapid increase in carbon dioxide    Gas Transportation      O2 and CO2 can take on different forms Oxygen particularly and carbon dioxide to some degree is not soluble in liquid Transporting oxygen around the body two options – physically dissolved or bound to haemoglobin Oxygen particularly is not soluble Haemoglobin – contains heme groups – iron forms the basis of heme group – oxygen binds to this iron o Four oxygen can bind to a single haemoglobin o When haemoglobin is fully oxygenated = Oxyhaemoglobin o Binding to oxygen is fully reversible OXYGEN HAEMOGLOBIN DISSOCIATION CURVE o pO 2 100 approx 99% fullysaturated o If Po2 drops from 100 to 80 the saturation is still 97% .3 ALVEOLAR PRESSURES o Partial pressure of O2 in alveoli is lower than the atmosphere and CO2 partial pressure is higher o Partial pressures of gas’ in our lungs and alveoli are different from the atmosphere due to – HUMIDIFICATION.

otherwise the cell will become depolarized o A lot of H+ . CARBON DIOXIDE TRANSPORT o Has three ways of being transported around the body  More dissolved than oxygen because of higher solubility  CO2 does not bind to the heme groups of haemoglobin but binds to the globin part  Not in competition with oxygen  Haemoglobin without O2 though will have a high affinity for CO2 to carry it to lungs  Majority of CO2 is converted to HCO3 if CO2  CO2 + H2O = H2CO3 = H+ + HCO3 o Nearly all CO2 in our blood comes from our tissues o Bicarbonate is a negative ion therefore RBS exchange bicarbonate fro Cl.might become acidic – need buffers to remove Respiration Control    Basic rhythm of breathing controlled by brainstem Exspiration is passive and doesn’t require nerve signals MEDULLA OBLANGATE AND PONS o Particularly pons o Respiratory centres – nerve cells – set rhythm by initiating inspiration o Phrenic nerve – connects brainstem to diaphragm there are also intercostal nerves o Exspiration duration is generally longer than inspiration o Increase ventilation increase inspiration and contract muscles more forcefully CHEMORECEPTORS o Change basic pattern of breathing o Sensitive to partial pressure of carbon dioxide. oxygen and pH o Changes detected by chemoreceptors central and peripheral feed forward into respiratory centre o Change pattern of breathing o CENTRAL CHEMORECEPTORS  Located in the medulla of brain – next to respiratory centres for quick control  Change the way you breathe  Monitor pH with fluid surrounding brain  MAIN RECEPTORS  Associated with CARBON DIOXIDE  Carbon dioxide combines with water to form carbonic acid – very unstable dissociates to form H+ and bicarbonate  Increase CO2 caused by increase in metabolism also insufficient alveolar ventilation – can’t get rid of CO2  Increased H+ and bicarb – changes Ph  Decreases ph more acidic  CO2 that travels to brain and crosses to CBS isn’t buffered therefore changes in ph  Stimulate central chemoreceptors  Increase ventilation o PERIPHERAL CHEMORECEPTORS  Aortic arch and carotid artery  Respond to oxygen  Respond to large changes in Po2  Renal  FUNCTIONS OF THE RENAL FUNCTIONS o Regulation of water and electrolyte balance o Hydrogen ion regulation o Excretion of wastes o Regulation of arterial blood pressure .

o Keeps plasma at a pH of 7.4 Anatomy of Urinary System       Kidneys get a large percentage of cardiac output Blood enters the kidney through the renal artery and blood exits the kidney through the renal vein Kidneys filter plasma and form urine – travels down ureter’s and are stored in the bladder Kidney’s lie behind the abdominal cavity Fat surrounds the kidneys  important to kidney function – holds up the kidneys Distinct layers inside the kidney o Renal Cortex o Renal Medulla o Pelvis Blood comes into the kidneys and feeds onto functional unit NEPHRONS – forms urine and drains into renal pelvis into ureter  bladder  The Nephron   Structural and functional units that carry out processes that form urine TWO MAJOR STRUCTURES o GLOMERULUS – bed of capillaries where filtration is occurring o RENAL TUBULE – begin as bowman’s capsule             Not all fluid flowing into capillaries is filtered. only 20% at any one time remaining 80% goes straight back out by efferent arteriole Fluid from plasma cross over from capillaries into glomerular capsule of bowman’s capsule Filtrate is 180 Ml Glomerulas supplies blood by an afferent arteriole Renal corpuscle forms a plasma called filtrate Filtration barrier ensures filtrate is free of cells and proteins Filtrate leaves bowman’s capsule and enters the tubule As filtrate flows through tubule substances are added or removed from filtrate Fluid reaching the end of each nephron combines in collecting ducts Filtrate drains from collecting duct system into renal pelvis and that is continuous with ureter draining that kidney TWO TYPES o CORTICAL – majority of nephrons  Loops of henle don’t penetrate deep into the medulla  Renal corpuscles are in outer cortex o JUXTAMEDULLARY .

   Basic Renal Processes  Renal corpuscle lies close to cortical-medullary region Efferent arterioles become vasa recta Loop of henle plunge into medulla     GLOMERULAR FILTRATION o Filtration of fluid from plasma o Initial filtrate has same composition as plasma but does not contain cells and proteins TUBULAR REABSORPTION o Movement of substances from tubule to peritubular capillary plasma TUBULAR SECRETION o Movement of substances from peritubular capillary to tubule Peritubular run back into vein and to bloodstream Filtering get rid of harmful substances and fine tune what is in the body to keep it at a set point Micturition     Is expelling urine from the bladder Detrusor muscle must contract (autonomic NS) Internal Urethral sphincter must open (autonomic NS) External Urethral sphincter must open (Somatic NS) Renal Blood Flow  Kidney’s receive 1/5 of cardiac output o All blood flows through filtration sites o Only 20% at any one time is being filtered o AFFERENT ARTERIOLE  CAPILLARIES  EFFERENT ARTERIOLE  CAPILLARIES Two determinants of blood flow. Pressure and Resistance o RBF = ΔP/R If either afferent or efferent arterioles constrict – REDUCE RBF If either afferent or efferent arterioles dilate – INCREASE RBF FORMATION OF GLOMERULAR FILTRATE o Renal Corpuscles (Glomerulus and Bowman’s Capsule) o Glomerular Filtration Membrane  Fenestrated capillaries – restricts the movement of large things  All components are negatively charged most proteins are negatively charged therefore you get repulsion  Basement membrane and everything else stops proteins and cells  BARRIER SELECTIVITY BASED ON: molecular size and electrical charge     Glomerular Filtrate Rate   The volume of fluid filtered from the glomeruli into Bowman’s space per unit time FORCES DETERMING NET FILTRATION PRESSURE AND GLOMERULAR FILTRATION RATE o Blood Pressure in Glomerular Capillary – main force driving filtration from plasma to bowman’s space o Also two opposing forces smaller in magnitude oppose filtration  Fluid Pressure in Bowman’s Space – Much lower than blood pressure  Presence of protein in plasma – no protein in bowman’s space – having protein in one compartment and not the others will cause an osmotic gradient o FOUR WAYS TO CHANGE GFR  REDUCE GFR – CONSTRICT AFFERENT ARTERIOLE OR DILATE EFFERENT ARTERIOLE  INCREASE GFR – CONSTRICT EFFERENT ARTERIOLE OR DILATE AFFERNT ARTERIOLE Regulation of GFR .

follows the movement of Na+ Na+/K+ PUMP – ATP is utilized by ligand in basolateral membrane freeing energy to allow for Na+ reabsorption and the secretion of K+ Na+ REABSORPTION o The concentration of Na+ is high in the tubule lumen and low in epithelial membrane so moves to membrane (electrochemical gradient) and then from the basolateral membrane to the interstitial fluid by Na+/K+ pumps o PROXIMAL TUBULE .and H2O      REABSORPTION OF Na+ . Cl.. Cl.and water are reabsorbed back into the blood Most reabsorption takes place in the proximal tubule Reabsorption usually driven by active transport    Reabsorption of Na+ Drives Reabsorption of Other Molecules       Either directly or indirectly sodium is the first thing being reabsorbed. bulk flow to capillary – diffuse through the cytosol o PARACELLULAR – going between cells  tight junction  don’t have to enter the epithelial cells Limited capacity for reabsorption of some molecules  Total Body Balance of NaCl and H2O   Intake of water through food and drink and also produce water in metabolism o Output usually equals input – not just through urine Either reabsorbed by transcellular or paracellular movement o TUBULAR LUMEN  TUBULAR EPITHELIAL CELL (membrane between cell and ICF is BASOLATERAL MEMBRANE)  INTERSTITIAL FLUID  CAPILLARY Pretty much all Na+.passive paracellular or active transcellular process but is coupled with reabsorption of Na+ due to maintaining an electrochemical gradient REABSORPTION OF H2O – by osmosis – paracellular. AUTOREGULATION – keeping GFR relatively constant o Can change various factors.an active transcellular process. can drive reabsorption of other things Sodium reabsorption is an active process ATP is utilized with Na+/K+ pumps to pump Na+ to extracellular fluid When Na+ is reabsorbed an anion is also reabsorbed to maintain the electrochemical gradient Water follows sodium due to osmosis Due to water content decreasing in lumen other solutes also follow Reabsorption of Na+. kidney tries to minimize effects of blood pressure on filtration rate so yo u don’t lose too many salts or water or accumulate too much o Changes the diameter of arterioles to change affect of MAP and GFR o Reduction in GFR you want to maintain water o MYOGENIC MECHANISM – muscles are reacting to change in pressure – if blood pressure is high afferent arterioles would constrict – if BP is low afferent arterioles afferent arterioles will dilate o TUBULOGLOMERULAR FEEDBACK MECHANISM – Directly by macula densa cells of juxtaglomerular apparatus  Macula densa feed back information into the afferent arteriole influencing the contractile state in afferent arterioles  Macula densa cells are salt detectors Tubular Reabsorption  Two ways to get into the interstitial fluid o TRANSCELLULAR – through cells from filtrate tubular lumen through epithelial cells to interstitial fluid. Na/K+-ATPase pumps in basolateral membrane REABSORPTION OF Cl.

aquaporin or paracellular movement  Tubular Reabsorption  PROXIMAL CONVOLUTED TUBULE o Primary reabsorption site o Most solutes are reabsorbed here o All nutrients reabsorbed LOOP OF HENLE o Only part of the nephron where sodium is not coupled with water o Descending limb – ONLY reabsorption of H2O o Getting further down the solute concentration is getting higher o ASCENDING LIMP – reabsorption of solutes NOT H2O due to lack of aquaporins DISTAL CONVOLUTED TUBULE o Most of reabsorption is physiologically regulated – everything prior occurs all the time o Hormones come in to fine tune. ALDOSTERONE and ANTIDIURETIC HORMONE o More water reabsorption filtrate in the collecting ducts via andtidiuretic hormone o ADH increases water reabsorption by increasing the permeability of collecting ducts for water   Regulation of Blood Pressure     Kidneys have baroreceptors that detect the pressure in afferent arteriole supplying the filtration site Baroreceptors are apart of juxtaglomerular cells Juxtaglomerular cells secrete renin Baroreceptors trigger Renin-Angiotensin-Aldosterone system Renin-Angiotensin System   Angiotensin 2 is a vasoconstrictor  constriction of arterioles  high peripheral resistance  increased MAP How it works o Drop in blood pressure triggers juxtaglomerular cells to secrete RENIN o Causes activation of angiotensinogen (circulating enzyme secreted by liver) o Angiotensinogen cleaved by an enzyme to make angiotensin 1 o Angiotensin 1 is converted to angiotensin 2 by angiotensin converting enzyme How is renin secretion triggered? o Decrease in blood pressure from set point o Three mechanisms  Decreased stretch in intrarenal baroreceptors  Decrease NaCl to macula densa cells due to decreased glomerular filtration rate  Renal sympathetic nerves  Long-Term Regulation of BP   Via the control of body Na+ content and therefore plasma volume ALDOSTERONE – secreted by adrenal organ . Occurs through cotransport and countertransport  Cotransport – sodium moves into the cell with an organic molecule  Countertransport – sodium moves in and H+ is moved out o CORTICAL COLLECTING DUCTS – have simple sodium potassium channels moving via diffusion COUPLING OF WATER REABSORPTION TO SODIUM o When sodium is reabsorbed it causes the osmolarity to be higher in the interstitial fluid therefore water follows osmotic gradient o Water follows sodium in almost all cases o For water reabsorption to occur the membrane must be permeable to water – either through  Simple diffusion.

    High plasma levels of angiotensin 2 causes aldosterone to be secreted by the adrenal cortex Aldosterone increases the number of sodium and potassium pumps in the cortical collecting ducts  water follows sodium Increased reabsorption of sodium and water increased plasma volume ANTIDIURETIC HORMONE – to reabsorb more water o Secreted by posterior pituitary gland o Triggered by an increase in osmolarity Renal ECF K+ Regulation         Urinary excretion of K+ is the major mechanism of regulating the body K+ K+ is freely excreted into bowman’s capsule 90% of filtered K+ is reabsorbed in proximal tubule ECF K+ balance achieved by K+ secretion by collecting ducts K+ secretion coupled with the reabsorption of Na+ Aldosterone will increase the secretion of potassium Aldosterone can also be secreted by high potassium concentrations in ECF Hyperldosteronism can lead to a decrease of K+ in plasma Renal H+ Regulation    Kidney’s are the long term regulator of body plasma H+ ions Done by altering bicarbonate levels Normally reabsorb bicarbonate unless Ph is high .

o Receptors can be found on the cell membrane or within the cytosol or nucleus Endocrine system is not physically connected and it controls longer responses   Chemical Classification of Hormones  AMINES – from an amino acid o THYROID HORMONES o CATECHOLAMINES. estrogen. Of hormone circulating. consists of endocrine glands that secrete hormones Main endocrine glands – Hypothalamus.MODULE 3 Endocrine System    Control system of the body. adrenal gland and pancreas Hormone – a chemical messenger that enters the blood and travels to target cells o Target cell – responds to the hormone because it has the receptors specific for hormone changing the cells metabolism and producing a response Not just one receptor in a target cell – contains numerous receptors. pituitary gland. REMOVAL o Fast for water soluble hormones o Slow for lipid soluble molecules o Removal is by excretion or metabolic transformation o LIVER and KIDNEYS most important in removal of hormones   Target Cell Activation   Dependent on blood levels of the hormone The number of receptors on the target cell o UP-REGULATION – target cells form more receptors due to a constant exposure to low concentrations of the hormone o DOWN REGULATION – target cells lose receptors due to a constant exposure to high concentrations of hormone. progesterone. thyroid gland. o Activate receptors on the surface of a cell membrane    . Affinity of the cell for the hormone PERMISSIVENESS – Hormone A must be present for the full effect of hormone B o Example thyroid hormone must be present for epinephrine to have an effect MECHANISM OF WATER SOLUBLE HORMONES o Water soluble hormones are unable to diffuse through the hydrophobic cell membrane and they are also too large to pass through channels. cortisol and aldosterone PEPTIDE – derived from proteins o Most hormones example. Norepinephrine and epinephrine STEROIDS – derived from cholesterol o Produced by the adrenal cortex and gonads o Testosterone. growth hormone and insulin   Hormone Transport and Removal  WATER SOLUBLE HORMONES o Peptide and catecholamine o Dissolve easily in water so are carried freely in plasma LIPID SOLUBLE HORMONES o Steroid and thyroid o Need to be attached to carrier proteins because they aren’t soluble in water o Small amount of the hormone is free in the plasma – only this part can diffuse out of the blood to target cells o Over time protein releases some of the hormone – depends on the hormone and conc.

get a change in metabolism in a target cell o Disorder Categories     HYPERSECRETION – too much hormone secreted HYPOSECRETION – not enough hormone secreted HYPERRESPONSIVENESS – cells has exaggerated effect to binding of hormone HYPORESPONSIVENESS – cells have a lack of response to binding of hormone Hypothalamus and the Pituitary Gland   HYPOTHALAMUS o Controls the pituitary gland HYPOTHALAMUS AND THE ANTERIOR PITUITARY GLAND o Hypothalamus regulates the secretion of anterior pituitary hormones o Neurons within the hypothalamus will synthesize the hormone and secrete into the portal circulation to be taken to the anterior pituitary gland o Ant pit synthesize hormones o Hypothalamus sends inhibitory and excitatory hormones to ant pit to regulate release of hormones o Some hormones only have an active hormone and some only inactivate hormones and some have both o Continuous neural input to hypothalamus from all over the CNS HYPOTHALAMUS AND THE POSTERIOR PITUITARY GLAND o Hypothalamus will synthesize the hormones antidiuretic hormone and oxytocin in neuronal cell bodies o Transported along axons to posterior pituitary where they are stored o Secreted when action potentials reach axon terminal  Growth Hormone   Growth hormone promotes protein synthesis especially in muscle Height determined by bone growth o EPIPHYSEAL GROWTH PLATE – someone who is growing in height made up of dividing cartilage cells that can be formed into bone. Initiate signal transduction which sends out a signal to the membrane causing a sequence of events to occur eventually leading to the response of the cell MECHANISM OF LIPID SOLUBLE HORMONES o Can diffuse through the lipid bilayer membrane o Attaches to receptors in the nucleus or cytosol of a cell o Activates receptors. When growth plate is inactive you can no longer grow GROWTH HORMONE SECRETION o Growth Hormone Releasing Hormone stimulates the release of Growth Hormone from the anterior pituitary gland o Travels in portal circulation o Somatostatin is the inhibiting hormone o Growth hormone acts on the liver and other cells to secrete Insulin Like Growth Factor 1 IGF-1 o Growth hormone also acts on many organs to do protein synthesis. carbohydrate and lipid metabolism EFFECTS OF GROWTH HORMONE o Stimulate protein synthesis in muscle o Promote lipolylsis in adipose tissue o Stimulates Gluconeogenesis o Reduces insulin function Growth hormone usually secreted at night Growth hormone levels highest in adolescents lowest in adults REGULATION OF GH o Most secretion is controlled by negative feedback o High plasma IGF-1 will feedback to anterior pituitary to lower growth hormone secretion or it will work on the hypothalamus to decrease secretion of GHRH and increase SS      .

  o High plasma GH will feedback to hypothalamus HYPERSECRETION OF GROWTH HORMONE o Giantism – occurs while still growing – usually due to benign tumour of the anterior pituitary gland o Acromeagly – occurs once grown HYPOSECRETION o Growth stunt Thyroid Hormone  THYROID HORMONE SECRETION o In the hypothalamus have THYROTROPIN RELEASING HORMONE o Secreted into the blood to anterior pituitary gland o Stimulates secretion of THYROID STIMULATING HORMONE o Targets thyroid gland to secrete THYROID HORMONE (T3 & T4) Lipid soluble molecules – receptor within the cell SYNTHESIS OF THYROID HORMONE o Iodine attached to a tyrosine forming T3 (active form) and T4 (inactive form) o T4 is converted into T3 within the target cells ACTIONS o Most important factor is BASAL METABOLIC RATE  Baseline metabolism  sets the rate of chemical reactions o Growth and Development – needed for normal production of growth hormone. Iodine Deficiency (iodine is the raw material in production of thyroid) OR Autoimmune destruction of the thyroid tissue  Leads to increased plasma levels of thyroid releasing hormone  Causes goiter  Not enough iodine leads to a drop in plasma thyroid hormone causing the negative feedback loop to produce more thyroid stimulating hormone o CONGENITAL HYPOTHYROIDISM  Mental retardation due to poorly developed nervous system o HYPERTHYROIDISM  Too much thyroid hormone  Autoimmune disease where antibody acts like TSH to secrete thyroid hormone  Symptoms – weight loss (increase BMR). increased appetite. important for growth of nervous system in fetus o Cognition in adults o Permissive action  need to be there for epinephrine to work CONTROL OF THYROID FUNCTION o High levels of thyroid hormone in the plasma causes a negative feedback reaction on the hypothalamus to produce less thyrotropin releasing hormone and also on the anterior pituitary to produce less thyroid stimulating hormone. COMPLICATIONS o HYPOTHYROIDISM  Not enough thyroid hormone – has two potential causes. increased sympathetic nervous system (permissiveness)      Cortisol Hormone     Secreted by the adrenal glands – each adrenal gland is composed of a medulla and an outer cortex Secreted by the middle layer of the adrenal cortex Cortisol is a steroid hormone therefore it is lipid soluble SECRETION OF CORTISOL o Hypothalamus secretes Corticotropin releasing hormone stimulating the anterior pituitary to secrete Adrenocorticotropic Hormone leading to the activation of adrenal cortex to secrete cortisol FUNCTIONS o Stress  .

 Protein Catabolism – chronic high levels of cortisol can lead to break down of bone and muscle when normally the tissue should be replaced o Stimulates gluconeogenesis o Stimulates TAG catabolism in adipose tissue o Highest levels are when we first wake up to provide us with fuels o Maintenance of blood pressure c  Cant exert full effect without norepinephrine  When sympathetic NS acts norepinephrine is released and causes contraction of smooth muscle  Decrease diameter and increase resistance of blood vessels causing increased MAP PROBLEMS o HYPOSECRETION – caused by autoimmune attack of adrenal cortex o HYPERSECRETION – cushing’s syndrome – become fat o Pancreatic Hormones         Exocrine and endocrine functions Alpha cells of pancreas secrete glucagon and beta cells secrete insulin High plasma glucose secrete insulin to store glucose as glycogen Low plasma glucose secrete glycogen to breakdown glycogen to glucose Insulin is a peptide hormone and has its receptor on the membrane of a cell Activated GLUT to be on the membrane of a cell TYPE 1 DIABETES o No secretion of insulin due to an autoimmune destruction of beta cells TYPE 2 DIABETES o Decreased cellular sensitivity to insulin have an insulin resistance Gastrointestinal System – just read lecture notes .

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