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Introductory Physiology

by: Merle Waelchi MD

Introductory Physiology PSL 250

Marketplace > Michigan State University > Physiology > PSL 250 > Introductory Physiology
Merle Waelchi MD
GPA 3.63

Pat Dillion

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Pat Dillion
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This 83 page Class Notes was uploaded by Merle Waelchi MD on Saturday September 19, 2015. The Class Notes belongs to PSL 250 at Michigan State University taught by Pat Dillion in Fall. Since its upload, it has received 18 views. For similar materials see /class/207335/psl-250-michigan-state-university in Physiology at Michigan State University.


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Date Created: 09/19/15
1822014 Lecture 21 Cardiac Structure and activation Cardiac Muscle Structure cylindrical shaped cells Intercalated disks join cells endtoend Filaments as in skeletal muscle Thin filament activation by Ca binding to Troponin Intercalated disks strong connection between cells Desmosomes for strength Gap junctions for electrical activation Circulatory Flow Circuit Sys LV to aorta to vena cava to RA SA Node the heart beat starts here Fastest role to depolarization into threshold which starts AP In right atrium Has no baseline MP nternodal pathway connects SA and AV Atrial Muscle Right atrium by SA AV node electrical connection between atrium and ventricles Electrical connections from AV to ventricles Delays AP allows ventricular filling to be completed AV block produces arterial and ventricular activation Ventricles AP enters septum first spreads to apex then up to ventricular muscle Bundle of His off of AV node down septum Purkinje Fibers branch off spetum to ventricular muscle Activated by bundle of His through gap junctions Ventricular Muscles Apex cells activated first by purkinje fibers then cell to cell through gap junctions Contraction spreads upwards forcing blood into aorta and pulmonary artery Pacemaker cells autorhythmic no flat baseline Depolarization Na entry to threshold Open Ca channels during AP Neural Influences sympathetic neurons decreases depolarization Opens Ca in atria and ventricles Heart Rate increase in strength and contraction Electrocardiogram shows sum of changes of cardiac AP P wave atrial depolarization start of contraction QRS Completion Ventricular depolarization Sta rt of ventricular contraction Start of aortic filling T wave Ventricle repolarization start of ventricular filling Lecture 22 Cardiac Pumping Cardiac Cycle sequences of contraction and relaxation Diastole relaxed heart time for filling End of diastolic volume quot 130ml When the heart is full depends on age weight and fitness Atrial Systole Contracts firsts completes filling of ventricles Ventricular Systole follows atrial systole Contraction spreads upwards Pressure must be greater than aorta to open aortic valve Aortic Pressure High BP puts greater load on heart Ejected Blood volume 7090ml ejected 65 diastolic Lower heart rate means ejected higher volume Heart Rate Dependence 220 age Max Heart Rate Rates above 180 are dangerous decreasing filling time life threatening Arterial pulse arterial walls expand to hold blood Reloads during diastole creates pulse Little drop in BP throughout arteries Heart Sounds Closing of valves turbulent blood flow creates sound Low AV pressure first 9 then high pressure by aorticpulmonary valves different sound intensities Murmurs nonlaminar flow sounds when valves should be closed Valve Stenosis Valve is stuck Stiff valve small opening Turbulent flow spurts blood through Valve Insufficiency sections of valve don t properly mesh Children with improper valve closures sometimes quotcorrectquot themselves as growth may alter valve alignment Cardiac Output amount of blood pumped Stroke Volume x Heart Rate quot 70ml at 70 bpm 5Lmin Baby has 5L of blood one minute for full circulation Neural Influences Both SV and HR are influences Lecture 23 Arteries Arterioles Blood Vessels 3 layers endothelium vascular smooth muscle Connective tissue capillaries only have endothelium Types of Blood Vessels Arteries arterioles capillaries veins Each has a different function Lymph vessels carry excess filtered fluid Physical Factors some factors constant such as vessel length some factors vary Flow PressureResistance Vessel Radius most important variable factor Resistance quot 1radiusquot4 small constriction causes large increase in resistance low flow small dilation causes large decrease in resistance increased flow short blockages can compensate with increased velocity until Until greater than 80 closed Viscosity thickness of blood Controlled by HEMATOCRIT RBC s in blood 45 in males and 42 in females need a large change to influence blood flow Above about 42 RBC interaction with arteriole walls greatly increases resistance Arterial Conductance High pressure blood enters aorta at 93mm Hg Large arteries expand to hold blood little change in BP 24mm wide Momentum of moving blood carries blood forward to tissues Arterial Pressure systolic P is 120 mm Hg diastolic is 80mm Hg Pulse pressure is systolic diastolic 1208040 mm Hg The mean arterial pressure Diastolic 13PP 80 13 93mmHg Coronary Circulation heart rate dependent low diastole at high HR low filling time and low coronary flow coronary flow only occurs during diastole HRgt 180 decreases cardiac output potential heart failure Atherosclerosis reduce blood flow build up of plaque Multiple stages I LDL low density lipoprotein lays down fatty streak FA ITY STREAK WBC s and fibroblasts overgrow fatty streak CELLULAR OVERGROWTH Calcium infiltration hardens overgrowth hardening of the arteries CALCIFICATION Alcohol Effect reverses the stage 1 from above modest alcohol consumption can solubilize fatty streak can reverse atherosclerosis stage I biophysical effect not receptor effect no alcohol effect on other stages 1 drink per day Arteriolar Flow arterioles branch off arteries 30 microns wide 93mm Hg at artery end Carries blood flow to capillaries 37mmHg at capillary end Arteriole can go either direction Tone Keeps blood vessels partially dilated so you can relax or contract more easily Partial activation with no stimulus Perfusion Control sympathetic neurons metabolites paracrines control arteriole smooth muscle BE adenosine NO Lecture 24 Capillaries Lymph Veins Capillary Blood Flow very slow many capillaries spread flow out and speed Smallest in your brain very tight Capillary Pressure 37mmHg at arteriolar end down to 17mm Hg at venous end Capillary Fluid Exchange Balance of BP forcing fluid out and osmotic pressure from plasma proteins drawing fluid in Fluid moves through capillary pores Filtration moving out dominates at high pressure end anteriolar Reabsorption at venous end lower BP BP lt Osmotic pressure fluid reenters Net fluid sweeps volume around capillary slightly more fluid filtered than reabsorbed Lymph Flow return of excess filtered fluid to circulation Return of Filtered Fluid fluid enters closed ended lymph vessels Lymph nodes are sites of large lymph vessel merger large lymph vessels have valves Vena Cava 0 or negative 5milmin lymph enters the vena cava BP0 at thoracic duct in chest 0 7200 litersday Edema swelling excess filtration broken capillaries low blood pressure starvationalcoholism bacteria presence and destruction draws fluid osmotically parasites filariasis block lymph flow fatal Venous Flow capacitance vessels holds large volume of blood veins Venous Pressure l7mmHg at capillary end to 0 at vena cava during inspiration vessels in thorax may have negative pressure BP needs help getting blood up to the heart Venous Valves prevent backflow every 12 inches in large veins Valves can be demonstrated on veins on back of hand Skeletal Pump muscle contraction squeezes veins forces blood to heart Varicose Veins ruptured valves column of blood slow return comes from standing around clots may form blood bypasses varicosities through other veins Pulmonary Artery blood clot Coronary Heart Attack Corotid Artery left asleep right stroke center feet asleep Lecture 25 Red Blood Cells Platelets Plasma liquid portion of blood water electrolytes metabolites hormones proteins Plasma Proteins Albumin highest amount draws fluid into capillary binds hydrophobic hormones Globulins many subgroupsgamma globulins are ANTIBODIES Fibrinogen final protein for blood clot formation Erythrocytes RBC s carry oxygen and C02 no organelles only in hemoglobin Hb produced in bone marrow RBC s have NO nucleus and NO organelles Production in bone marrow from stem cells 20ml of RBC sday 150ml of bloodday low blood 0 causes release of EPO from kidneys when 0 levels low produce more live for 120 days and get significantly stiffer 1132014 T 39 RBC 39 lose 39 39 Iovertime Rupture in spleen capillaries at 120 days If spleen lost liver ruptures RBCs Adult Hemoglobin 2 alpha and 2 beta chains Each subunit has protein globin with a heme group in the center Each heme has an iron atom at its center Oxygen binds to the iron atom Cooperativity increase bindings at lungs and release tissues Fetal Hemoglobin 2 alpha and 2 gamma chains Higher affinity for oxygen than adult hemoglobin Draws oxygen from maternal blood Replaced by 23 months postnatal Anemias Lack of oxygen altitude Reduced RBCs bleeding no anemia with menses 50ml5 days Reduced delivery circulatory Reduced use cyanide Sickle Cell Anemia Single Hb mutation Low oxygen 9Hb forms stacks changes cell shape Sickled cells hang up on branch points Survival value protection from the malaria parasites lay eggs in RBCs Growing malarial parasites rupture weakened RBC membranes before maturity Iron deficiency Lack of iron decreases amount of Hb Not from using noniron cookware wrong form of iron in cookware Platelets Pinched off parts of megakaryocytes in bone marrow Production megakaryocytes stay in bone marrow Platelets pinch off and enter circulation Spleen kidneys and liver make thrombopoietin ThrP stimulates platelet formation ThrP binds to platelets in blood when platelets low 9 increase free ThrP Activation Activation activated by collagen and other proteins in connective tissue of blood vessels Platelets adhere increase ADP release more P s come and stick Make platelet plug Hemostasis Stoppage of bleeding Vasoconstriction decreased BP at site of cut tone constricts small vessels Platelet plug exposure of collagen 9 platelet sticking 9 ADP positive feedback Prostacyclin from healthy blood vessels blocks platelet adherence Coagulation Blood clotting 2 systems Both lead to fibrinogen soluble 9 fibrin selfadhering Form mesh that traps RBCs etc Intrinsic System inside plasma collagen activiates Cascade needs Ca and all factors in pathways Extrinsic System thromboplastin from damaged tissue starts cascade Merges with intrinsic system halfway down Clot Removal Plasminogen trapped in clot 9 cascade started by collagen 9 Plasmin Plasmin is an enzyme that slowly dissolves a clot over quot 2 weeks Lecture 26 White Blood cells Innate Immunity Cell Types Leukocytes 5 types all have different defense functions Multilobed nuclei ganulocytes neutrophils eosinophils basophils Stained by neutral acid and basic dyes Singlelobed nuclei 0 39 and 39 39 Phagocytes phagocytosis of bacteria and dead cells Order of attack resident macrophages neutrophils new monocyte 9 macrophage migration Neutrophils rapid response move from blood to damaged tissue Diapedesis squeeze through capillary pores attack bacteria Monocytes Macrophages Monocytes move into tissue and become macrophages Resident macrophages wait for bacteria to come During infection vast movement of monocytes into infected area Massive macrophages attack on bacteria Eosinophils produce acids that kill parasites High in GI tract Produce allergic responses Basophils release histamine Histamine causes inflammation Increase blood flow arteriolar dilation Increases pore size allow diapedesis Defense mechanisms Innate nonspecific immunity defense mechanisms not influenced by prior exposure Acquired specific immunity B and T lymphocytes attack specific antigens Inflammation nonspecific response occurs with any infection or injury Chemotaxis chemical signals from damaged areas draw phagocytes Complement system series of 9 plasma factors C1C9 Major bacteria killer Activation by antibodies or by the protein porperdin This is opsonin tags of surface carbohydrates on bacteria Leads to pore formation in bacteria membranes Pore Formation C5C9 can form pores in membrane Very local rapid inactivation Pore allows osmotic lysis Na enters H20 follows cell swells and bursts Ill feeling cause bacterial toxins activation of pain receptors from partially digested protein of dead bacteria Histamine increase Blood Flow brings phagocytes oxygen amino acids Increase capillary permeability opens pores for liquid and diapedesis Interferon cytokine released from virusinfected cells Activated antiviral defenses in cells near virus infected cells Many side effects Natural killer cells NonT lymphocytes No prior exposure needed for activation Activation Lipids and carbs on bacteria tumors transplants and by antibodies on cell surfaces Forms pores by injecting perforin kills by lysis 18314 Lecture 29 Lung Structure Breathing 2 lungs Intake of oxygen let out C02 External Respiration Exchange of gases 02 and C02 between body and environment Internal respiration use of 02 by mitochondria Nonrespiratory Lung Functions Water and heat loss increases venous return acidbase balance speech pathogen defense circulatory modification ACE sense of smell Lung Structure Trachea 9 bronchi 9 bronchioles 9 alveoli gt 20 generations of bronchioles Alveoli are air sacs sites of gas exchange Alveoli 2 types of cells Type Cells epithelial cells quot 1 micron think Separate air from interstitial fluid Type II Cells In alveoli produce surfactant Reduce resistance to alveolar opening Lung Mechanics air flows from high pressure to low pressure Atmospheric ntraalveolar interpleural pressures A 760 at sea leavel 600 at Denver 1 mile up A variable exhale 12 gtatm in hale 12 ltatm P between lungs and the thoracic wall Always 4 mm Hg ltatm Lower pressure keeps lung always inflated o e s aw ressurex o ume cons an B L P V t t Decrease V 9 increase P Increase V 9 Decrease P Tidal volume normal breathing volume Inspiratory reserve volume extra amount you can inspire Expiratory reserve volume extra amount you can expire Inspiration Regular phrenic nerve from medulla sends AP to diaphragm Diaphragm contraction increase thorax volume decrease pressure Decreased pressure causes inspiration Extra inspiration eternal intercostal muscles contract expand thorax Expiration normally passive as diaphragm relaxes volume decreases and pressure increases Extra Expiration Internal intercostal muscles between ribs contract Abdominal muscles contact also Squeeze thorax Compliance ease of lung expansion Normally easy Increase fibrosis asbestosis of lungs decrease compliance Alveolar surface tension adherence of H20 molecules creates surface tension on inside of alveoli Surface tension must be overcome to open alveoli Surfactant several phospholipids mix with water and decrease surface tension Also prevent edema in lungs First made at 36 h week of gestation Glucocorticoids increase surfactant production in premature infants Anatomical dead space Normal tidal volume is 500 ml 150 ml of mouth pharynx trachea bronchi and bronchioles is dead space 350 ml is normal alveolar inflation Long slow breathing minimizes dead space effect Short rapid breathing still must fill 150 ml dead space Lecture 30 Gas exchange Partial Pressures Gas equivalent to concentration Sea level 760 mmHg 600 N2 160 02 C02 3 mmHg Gases independent of one another Air in lungs is water saturated Alveolar air P02 100 mmHg PCOZ 40 Venous blood P02 40 PCOZ 46 Diffusion Across alveolar wall Gases follow partial pressure gradients 0202 enters pulmonary capillaries until P02 is 100 C02 C02 leaves pulmonary capillaries until PC02 is 40 Pulmonary Circulation Lower BP then aorta quot 1520 mmHg Mean Arterial Pressure of pulmonary artery VentilationPerfusion Ratio Ventilation and perfusion normally well matched 8 Areas that have open alveoli get more blood flow As need for gas exchange increases both blood flow and ventilation increase in new lung areas Tissue Gas Exchange reverse of lungs 02 100 mmHg arterial blood loses 02 to 40 mmHg tissue until capillary is 40 mmHg C02 40 mm Hg arterial blood receives C02 from 46 mm Hg tissue until capillary is 46 mm Hg 0xygen Transport 15 carried by dissolved 02 985 carried by binding to hemoglobin OxygenHemoglobin Binding Sigmoid curve cooperative between 4 Hb subunits Plateau Region Steep Region P at lungs all Hb is 02 bound no effect of extra 02 S at tissues fall in P02 unloads 02 At lower P02 even more 02 delivery quotwork hard get oxygen Bohr Effect C02 acid shift Hb02 curve to the right More 02 unloading at give P02 Carbon Monoxide 2 effects Binds HB 200x stronger than 02 less 02 available Never dissociates must lyse RBC to lose C0 Shifts Hb02 curve to left less 02 delivery Hypoxia Low blood 02 Low 02 air high altitude or 02 deprivation High altitude ethnic groups higher Hb even at sea level Sea level ethnic groups low 02 training increases Hb lose when return to sea level Hyperoxia Breathe high 02 no addition Hb binding already full Increased dissolved 02 may decrease breathing rate benefit only psychological Carbon Dioxide Transport 10 dissolved 30 bound to plasma protein and Hb 60 converted to bicarbonate by carbonic anhydrase CA CA catalyzes H2O C02 9 H2CO3 9 HCO3 H Carbonic anhydrase In RBCs Converts C02 9 bicarbonate at tissues as C02 added At lungs reversal bicarbonate 9 C02 then breathed out Hypocapnia Low CO2 Hyperventilation decrease CO2 in blood 9 faint Breathing into bag CO2 increases back to normal Hypercapnia High CO2 increased breathing rate Increase CO2 in blood strongest stimulus for increased respiration Lecture 31 Regulation of Respiriation Lung Diseases Medullary Control Centers Dorsal Respiratory Group DRG rhythmic discharge 9 phrenic nerve 9 diaphragm Initiates normal breathing Ventral Respiratory Group VRG causes increase inspiration expiration Pontine Control Centers Modify medullary Centers Pneumotaxic Center switches off inspiration Apneustic Center prolongs inspiration normally inhibited If PC damaged Hering Breuer reflex from lungs stops inspiration Chemical Control of Respiriation Most powerful controller of rate Increases blood C02 9 increases brain C02 9 increases H and HC03 H in the brain increases DRG rate Peripheral Changes In carotid bodies and aortic bodies increase H or increase CO2 or decrease 02 will increase rate of respiration Little effect in normal range PO2 lt 60 mmHg increases rate no helping in CO poisoning Sleep Apnea Decreased DRG activity or airway obstruction In REM pharyngeal muscles relax and tongue blocks trachea Decreases restful sleep SIDS Sudden infant death syndrome exact cause unknown May be due to congenital DRG problem or cardiac arrhythmia Baby sleeping on back decreases SIDS mother smoking in pregnancy increases SIDS Child abuse may have skewed SIDS statistics Pneumothorax Rupturing thorax air enters intrapleural space Pressure equalizes lung collapses on rupture side Decreased flow on good side Danger of kinking of great veins if opening remains Reclosed normal breathing on good side lung reinflates Asthma Episodic or chronic wheezing tightness in chest Increased morbidity and mortality Airway obstruction Increased mucus production in response blocks airway Reduces flow Inflammation Response to allergies increaseIgE increase mast cell release of histamine and other cytokines Edema decreases air flow Bronchoconstriction Some cytokines are bronchconstrictors Also some cool air and exercise Constriction decrease air flow SRS A Slow Reactive Substance of Anaphylaxis leokotrienes Powerful bronchoconstrictor during allergic attacks Potentially fatal attack Epinephrine Beta 2 Receptors bind Epi relax bronchioles increase air flow Rescue from serious allergic attacks Steroids decrease inflammation 9 side effects significant Emphysema cigarette smoke coal tar most common causes Decreased alphaAntitrypsin Lungs have digestive enzymes for defense Alphaantitrypsin protects lung tissue from digestion Inhibit alphaantitrypsin production and enzyme digest alveoli Decreased number of alveoli and increased size of remaining alveoli Surface area progressive decrease in surface area May need pure 02 to fill Hb Irreversible right heart enlarges and fails Lecture 11 Subcortical Structures Memory Subcortical Structures Structures below cortex that control different functions Basal Nuclei Ready GET SET Go Collection of 5 structures on each side of the brain Below cortex to the sides of the thalamus connected to each other and to the cortex Posture control is not conscious Feedback loops correct posture variations Decreased dopamine linked to Parkinson s Decreased dopamine schizophrenic Thalamus quotGatekeeperquot Sensory info passes through to synapse Receives sensory input from the opposite side About 98 of input blocked from reaching cortex cortical focus allows input through thalamus one time of autism due to lack of thalamic editing Hypothalamus detects but doesn t solve problems Monitors homeostatic functions temperature thirst milk release hunger reproductive urges circadian rhythms and increase in emotional feelings Limbic system Ring of structures underneath cortex of cerebrum Detects emotions and memory formation Hippocampus part of the limbic system where emotions are processed Emotions feelings about things reproductive drive rage fear motivation Can t make emotions go away it just takes time Cortical control doesn t control emotions but controls responses 30114 Neurotransmitters Norepinephrine Dopamine and Seratonin are NTs in the limbic system Altered concentrations of NTs have been 39 Iwith 39 r 39 Anti 39 r use receptors for these NTs Excess dopamine has been linked to Schizophrenia limits LDopa Parkinson s treatment Memory Retention storage and ability to recall information Memory traces sequences of neural activations Declarative Memory Facts events words language rules hippocampus and temporal lobe for storage Procedural memory Unconscious Physical skills habits tasks Cerebellum plays a major role Short Term Memory Seconds to hours alter activity in existing neurons in hippocampus can be erased and replaced Long Term Memory Creation of new synapses and memory traces Makes multiple copies of important memories over years Retain youthful memories as you age Transfer from hippocampus to cortex Working Memory In the PreFrontal Association Cortex Compares newly acquired short term data and stored long term data Determines relevance of new material organizes and prioritizes Amnesia inability to recall REPRESSED MEMORY DOESN T EXIST IN PHYSIOLOGY Retrograde Amnesia Fairly common RA caused by trauma loss of short term memory No long term memory formation of traumatic events Anterograde Amnesia RARE Hippocampal damage Can t for new LT memories No Loss of previous LT memory Memory stuck on day of damage Lecture 12 Cerebellum Sleep Spinal Cord Cerebellum Structure on back of brainstem controls coordinated movements and learned movements Balance maintains balance and controls eye movements Coordination Connected to motor cortex received llmotor plan Afferent input gives current muscle position Coordinated function with quotaimquot ie movement matches motor plan As practice occurs motor cortex parietal lobe and cerebellum take over Planning is reduced initiation of activity is faster and smother input to cortex Input to cortex Brain stem Medulla pons and midbrain Interface between spinal cord and higher brain centers Cranial nerves supply sensory and motor function to head and neck Different center in brainstem control heart rate breathing wakefulness Reticular Activating System RAS Neural net awareness of surroundings Cortical pain auditory visual input Output to cortex and thalamus 9 all cortex Controls consciousnesssleep Sleep Low frequence activity in hypothalamus thalamus 9 sleep Reason needed UNKNOWN EEG Patterns Slow wave patterns in EEG give slow wave sleep its name EEG pattern during REM sleep similar to being awake Slow Wave Sleep 4 stages each progressively deeper over about 75 minute cycle Circadian rhythm 9 Increased adenosine 9 sleep Caffeine block adenosine response Sleep factor muramyl dipeptide strongest molecule that activates any receptor in the body 9 strong sleep inducer Rapid Eye Movement Paradoxical Sleep 15 minutes long at end of slow wave sleep cycle Paradoxical Sleep hard to awaken most likely waken self High visual cortex low frontal high memory areas dreams illogical New synaptic contacts made greater long term memory Will make up for missed REM sleep Spinal Cord neural tissue encased in verbal column Carries Aps between brain and body Grey matter in the middle cell bodies and interneurons White matter on the outside myelinated neuronal tracts Tracts bundles of neural axons that carry Aps Ascending tracts carry APs toward Dorsal Roots Entry points for afferent neurons to the spinal cord Afferent cell bodies are in the dorsal root ganglion Ventral Roots carry efferent APs out of the spinal cord Cell bodies of efferent neurons in the grey matter Reflexes neural responses without the conscious output Reflex Arc from receptor to afferent neuron to CNS to Efferent Neuron to Effector CNS portion may have 1 or more synapses Effectors are musclesglands Monosynaptic Reflex 1 synapse Polysynaptic reflex multiple synapse Withdrawal Reflex polysynaptic reflex Multiple neurons between afferent and motor neurons Prolonged response and feedback Very strong reflex but with potential CNS input Stretch Reflex muscle length information Monosynaptic reflex knee jerk Activation of afferent neuron produces reflex response through synapse to efferent neuron No control by upper CNS Lecture 13 Afferent Nervous System Pain Taste and Smell Sensory receptors Sensation connect and environmental signal to body Transduction the conversion of a stimulus to a physiological signal The brain converts the physiological signal to a perceived sensation Stimulus an environmental signal that binds and changes a receptor Each receptor binds one stimulus best Sensation two kinds Conscious sense touch taste smell hearing seeing and time Unconscious position temperature blood pressure changes Types of receptors all must bind to stimulus modified nerve ending to interact with stimulus Physical physical changes open ion channels changes membrane potential Touch receptors hair cells in ears photoreceptors baroreceptors Chemical taste and smell chemoreceptors chemical binds receptors and opens ions channels Changes membrane potential 422014 Receptor Potentials aka Generatorlocal potentials Depolarization of receptor cells size of potential proportional to size of stimulus Receptor fields vary in size depend on the number of afferent neurons Magnitude More stimulus 9 greater Receptor Potential n receptor cells without Action Potential release of Neurotransmitter is proportional to Receptor potential Frequency Dependence Continuous stimulus 9 larger gradient potentials 9 more actions potentials to CNS Action potential number translated by CNS as size of stimulus Adaptation decreases action potential number despite prolonged stimulus Phasic Receptors adapt over time rate is variable Touch receptors adapt quickly Pain Blood Pressure receptors adapt slowly Taste is Phasic Tonic Receptors Virtually do not adapt few true tonic receptors smell receptors Postural receptors in trunk are near tonic Sensory Specificity Normal stimulus produces a response that the brain interprets Different stimulus needs more strength for a response brain still interprets as quotnormalquot response see quotstarsquot Pain Survival value protection from harm Anticipation of pain activates pain areas and cortex Nociceptors pain receptors chemical and physical Fast pain sharp localized passes quickly Fast myelinated afferents glutamate neurotransmitter Slow pain diffuse dull long lasting Slow unmyelinated afferents substance P neurotransmitter Substance P presence suspected before discovery Neurotransmitter unique to afferent slow pain neurons Opioid Receptors natural analgesics block pain by binding to opioid receptors Activation alters ion channels and membrane EnkephalinsEndorphins types of natural opioids Peptides multiple types different sizes Short half life 25 seconds Morphine effective for hours Chemical senses Molecular binding to receptor Flavor combination of smell and taste Taste Molecules dissolve in saliva and reach taste bud receptors to be tasted Taste buds receptors at taste pore Tight junctions keep saliva away from the rest of taste bud Surrounding epithelial cells 9 basal cells 9 receptor cells Turnover is roughly 10 days for taste buds Neural tracts Sensory neurons send taste information Neurons to thalamus parietal lobe quotwhatquot taste Neurons to limbic system quotlikequot it Taste Receptors Salty Na Sweet organic sugars Acid sour H Bitter basics quinine cations poisons most sensitive receptor Umami glutamate MSG Smell Olfactory mucus membrane on roof of nasal cavity gt 1000 different odor receptors Largest gene family gt1 of human genome Molecules must diffuse through mucus H20 soluble Olfactory Receptors Part of dendrites of olfactory neurons covered by mucus Neurons turn over every few weeks Unusual dendrites as receptors new neurons Olfactory adaptation Unusual Reception primarily tonic Unusual Most adaptation in CNS brain can overcome adaptation Adaptation to one smell does not affect others Lecture 14 VISION Eye designed to receive light and produce electrical signals Cornea clear noncellular front of the eye Light passes through not refracted bent Lens Ciliary body Lens refracts light to focus on retina Ciliary body has muscles parallel to lens Muscles contraction allow lens to round up focus near Muscles relax for distance vision ris opencloses pupil Smooth muscle contractions adjust to light level Aqueous humor between cornea and lens constanct production and drainage Glaucoma Decrease drainage or excess production causes an increase in pressure causing retinal damage Beta blockers decrease production cholinergic agonist increase drainage Vitreous Humor Gellike bulk of eye volume Between lens and retina maintenance of eyeball shape No refraction Retina visual receptors at the back of the eye Multiple cell layers Choroid highly pigmented layer behind retina Absorbs light no reflection no signal Refraction bending light waves Glycoproteins in lens refract light focus it on the retina Retina light passes through bipolar and ganglion cells to reach photoreceptor cells Bipolar and ganglion cells pulled back at fovea Fovea has best color vision dense cone concentration Photoreceptors Rods shades of gray most photoreceptors Cones color receptors fewer overall receptors Rods and cones produce receptor potentials no Action potentials Bipolar cells generate potentials activated by rodscones No Action potentials synapse with ganglion cells Edge effect centersurround onoff effects MAKE edges appear sharp Ganglion cells reach threshold and fire Aps that leave eye for CNS Carry visual information to lateral geniculate part of thalamus 9 cortex Optic nerve bundle of ganglion cell axons Creates blind spots as axons pass through the retina Cortex fills in blond spot with expected image Lateral Geniculate receives information from ganglion cells Edits information to cortex Visual cortex multiple areas in occipital lobe Integrates input of visual perception Relative positions 3D images Accommodation change in lens thickness alters focal point near and far vision Ciliary muscles control focus Presbyopia lens gradually hardens over decades Hardening reduces rounding of lens for near vision At 4045 years old difficulty focusing on near objects Reading glasses bifocals Myopia Hyperopia inability to focus on retina Myopia nearsighted eyeball too long focus in front of retina Hyperopia farsighted eyeball too short focus behind retina Rhodopsin Visual pigment in rod cells Opsin Retinene Combination ofopsin in retinenea dye Vitamin A derivative Light hits retinene and partially splits from opsin bleaching Opsin now active G Protein system recycles makes 14 imagessec System changes membrane potential release Neurotransmitter Retinene rebinds to opsins awaiting new light Color vision 3 different opsins with retinene Shading of retinene limits frequency range Peaks at red also sees yellow green and blue wavelengths Colorblindness One opsin missing more common in males because they only have one x chromosome whereas women have two Can t distinguish certain wavelengths with equal activation of remaining opsins Lecture 15 Hearing and equilibrium Outer Ear Little amplification direction detection Tympanic membrane Eardrum Separates outer and middle ears Vibrates to external air waves Middle ear air filled amplifies sound 20x Ear Bones these 3 bones carry waves from tympanic membrane to oval window Hammer Malleus Anvil incus Stirrup stapes Eustachian Tube Drains middle ear fluid Equalizes air pressure between middle ear and sinuses Normally closed if unopenable tubes needed in eardrum Oval Window membrane that connects middle ear to inner ear nner Ear fluid filed converts sound waves to electrical signals Cochlea Organ of Corti C Spiral shaped tube of inner ear 0 of C part of cochlea that transduces sound to action potentials Waves carried to apex and back to round window Round window absorbs all sounds waves no action potentials Similar to choroid in eye Basilar Membrane vibrates to sound waves shape change over length High frequency at base low frequency at apex Hair cells rest on basilar membrane hairs imbedded in tectorial membrane Tectorial Membrane Much stiffer than basilar membrane less movement When Basilar membrane vibrates imbedded hairs pulled on Hair calls produce graded potential 9 neurotransmitters to afferent neurons Action potentials 9 to CNS auditory nerve Maximum range 20 Hz to 20000 Hz High frequency lost with age Timbre pronounce tambor Overtones allow source destination Type of musical instrument or individual voice Total signal fundamental frequency overtones Amplitude of Sound Height of soundwave higher wave more hair cell movement and more action potentials to brain Deafness Loss of hearing Conductive sound waves don t reach hair cells Wax eardrum damage middle ear bone damage hearing aid helps Amplify sound to vibrate oval window directly Nerve Deafness Damage to hair cells or auditory nerve Need cochlear implant to treat Frequency deafness loud repetitive sounds at one frequency pull out hair cells in one place selective hearing loss Equilibrium Vestibular apparatus detect changes in motion Rotational Acceleration 3 semicircular canals at right angles to one another Fluid filled as fluid lags motions fluid pulls on hair cells Semicircular canals hair cells imbedded in cupula intertia Generates graded potential 99 action potential When hard rotation stops 2530 seconds to reequilibriate Linear acceleration hair cells imbedded in gel with otoliths Acceleration pulls on hair cells Gravity constant 9 MOST tonic signal know the position of the head Utricle Saccule Detect linear acerlation U Horizontal motion S vertical motion Mismatch of signals 9 motion sickness Excess rides or loss space flight Lecture 16 Efferent Nervous System Sympathetic Structure part of the Autonomic nervous system Sympathetic chain ganglia parallel spinal cord mpur from cord medulla hypothalymus No direct corticol control Preganglionic Neurons Short neurons Use Acetylcholine Ach as neurotransmitter to post ganglionic neurons in ganglia Postganglionic Neurons Long neurons Activated by preganglionic neurons Use Norephinephrine NE as neurotransmitter Adrenal medulla behaves like Postg neuron Sympathetic responses respond to emergencies Flightorfight response designed to remove danger Increased blood flow to skeletal muscle and heart Concurrent activation of motor units Decrease activity of digestive and related functions Receptor types adrenergic Receptors All bind norepinephrine from postganglionic neurons Alpha adrenergic receptors Cause increase in tissue activity Alpha 1 9 Increase IP3 9increase Ca release from SR 9increased Ca Alpha 2 9 decrease in cAMP9 decreased Ca pump 9 net increase Ca Beta 1 adrenergic receptors Increase Ca in heart open Ca channels Increase heart activity Beta 2 adrenergic receptors increase cAMP9 increase Ca 9 decrease Ca Decrease blood vessel contraction and decrease lung bronchiole constriction more blood more air Parasymphatic structure Part of autonomic nervous system 2 neuron series all use Ach as Neurotransmitters Cholinergic activation controls daytoday homeostatic maintenance Preganglionic Neurons long neurons spinal cord to organ Synapse at ganglia on organs with postganglionic neurons Postganglionic Neurons short neurons travel from ganglia to cells Parasympathetic responses Decrease in heart rate Increase GI contractions and secretions Increase pancreatic secretions Contracts urinary bladder Relaxes internal anal and urinary sphincters AgonistsAntagonists Pharmeceuticals can mimic or antagonize autonomic nervous system Para increase or decrease digestive activity etc Sym increase blood pressure in shock decrease blood pressure in hypertensions Motor Neurons Alpha motor neurons gets multiple inputs up to 10000 Input from stretch receptors withdrawal reflexes cerebellum learned activities cortex conscious control Both IPSPs and EPSPs to alpha motor neurons threshold PUT IN NOTES FROM TRISH YA DUMB 1822014 Lecture 19 Muscle Metabolism and Control Muscle energy use Progressive use of energy resources Phosphocreatine Supports about 20 seconds of full activity PCr ADP 9 ATP Cr by creatine kinase reaction ATP 9 ADP Pi by myosin ATPase PCr9 Cr Pi net reaction NET REACTION Pi inhibits myosin ATPase MADPPi 9M ADP Pi Glycolysis 10 Rxs quot 2 min of energy use Glucose and glycogen in muscles 9 pyruvate 9 lactate No Oxygen use Oxidative Phosphorylation Krebs and electron transport quot 2 hours of energy support Pyruvate 9 C02 Oxygen used Carbohydrate Loading increases glycogen storage increased by up to 30 Fiber types Variation in fiber type even within same muscle Controlled by motor neuron most muscles are mixed Red Fibers Also called slow oxidative High mitochondria levels slow myosin ATPase slow speed High energy capacity low energy use no fatigue White fibers also called fast glycolytic Few mitochondria fast myosin ATPase fast speed Low energy capacity high energy use easily fatigued Hypertrophy Larger cells not hyperplasia more cells High intensity high force exercise needed for maximum effect Filament Number High intensity exercise causes microdamage to filament Disassembly of tangled filaments increases free myosin and causes pain Free myosin causes increase in expression of filament forming enzymes more filaments bigger cells Young 48 hour cycle 24 disassembly 24 assembly Elderly 72 hour cycle risk T T 39 Filament r optimized by testosterone Females with normal hormones cannot maximize muscle size Atrophy reduction in size of muscle fibers not a loss of numbers of fibers Disuse muscle immobilized loss of filaments easily reversible Denervation Motor neuron damage fiber loses filament Not reversible loss of myotrophic factor from neuron Electrical stimulation cannot prevent atrophy Stretch Reflex muscle length information Monosynaptic reflex knee jerk Activation of afferent neuron produces reflex response No control by upper CNS Muscle Spindles Stretch receptors in muscles Groups of intrafusal fibers in connective tissue ntrafusal fibers Each fiber contains muscle section and stretch receptor section Fibers activate afferent neurons from receptor section fiber Fibers also receive efferent gamma motor neuron to muscle section of fiber Nuclear bag fibers Have larger central portion of receptor Dynamic response Only Detects change of length Highest response when muscle rapidly stretch Decreased response as stretch is sustained Rapid adaptions Nuclear chain fibers Smaller set of receptors parallel to n bag fibers Static response detects fiber length Response proportional to position slow adaptation Gamma motor fibers efferents to intrafusal fibers Contract muscle portions of intrafusal fibers Coactivation Dual activation ofalpha and gamma motor neurons Alpha motor neurons contract muscle fibers Gamma motor neurons contract intrafusal fibers Keeps muscle spindles taut Reciprocal Innervation Inhibitions of paired muscles when stretch reflex occurs Afferent n 9 interneuron 9 IPSP to paired alpha motor neuron Golgi Tendon Organ Muscle force detectors Receptors in tendon afferent input proportional to muscle force At very high forces GTO sends PSPs to alpha motor neurons Protective effect Lecture 20 Smooth Muscle Smooth Muscle Structure Small cell linked by desmosomes no striations Filaments parallel but not in register Filaments Thin filaments actin and tropomyosin no troponin TM in groove no AM blocking Dense Bodies smooth muscle equivalent to 2 lines Anchored to cell membrane also in interior Thin filaments attach here and pull ends of cell Tone Force with no stimulus Ca leaks in and partially activates smooth muscle Important in BP maintenance holding cavity contents Smooth Muscle Contraction different control mechanism than striated muscle Ca also activates Calcium Sources Most come through channels across cell membrane Some small SR released by P3 Myosin Light Chain Kinase Ca activated Adds phosphate to myosin light chains Force Generation MyosinADPPi with MLCP binds action ADP and Pi leave Myosin twists generates force Filaments slide to reduce force This part similar to striated muscle Myosin Light Chain Phosphate MLCPase removes phosphate from myosin light chains Turns off myosin and causes relaxation whenCa is low Latch Removal of Pi from light chain when AM attached decreases M detachment rate discovered by Dr Dillon 10172011 115600 PM Lecture 11 Subcortical Structures 7 Memory gt Subcortical Structures 0 Structures below the cortex that control different function H v w a Collection of 5 structures on each side of brain i Below cortex to the sides of thalamus ii Connected to each other and cortex iii Postural control is nonconscious iv Feedback loops connect posture variations V Decreased dopamine linked to Parkinson s disease a Receives sensory input from the opposite side b Directs and edits input to cerebral cortex c About 98 of input blocked from reaching cortex d Cortical focus allows info through thalamus e One type of autism may be due to lack of thalamus editing Controls homeostatic functions a b Temperature thirst milk release hunger reproductive urges circadian rhythms increases emotional feelings c HT sees what is wrong makes no decisions i Cortex decides what to do gt Limbic System 0 Ring of structures underneath cortex of cerebrum o Detects emotions and memory formation 0 Hippocampus is part of limbic system a Feelings about things Fquot Reproductive drive rage fear motivation c Cortical decisions few connections to cortex i Limited cortical control of emotion d Can t make emotions just go away it takes time distractions e Cortical control is over responses i Limited input of limbic system to motor areas ii No compulsory action a Nonepinephrine dopamine and serotonin are NTs in limbic system b Altered concentrations of NTs have been associated with depression i Antidepresants use receptors for these NTs c Excess dopamine has been linked to Schizophrenia i Limits Ldopa Parkinson s treatment gt Memory 0 Retention storage and ability to recall information 0 Memory traces are sequences of neural activities I Declarative Memory I Facts events words language rules 0 Hippocampus and temporal lobe for storage I Procedural Memory unconscious I Physical skills habits and tasks I Cerebellum plays major role a Seconds to hours b Alter activity in existing neurons in hippocampus c Can be erased and replaced a Creation of new synapses and memory traces b Make multiple copies of important memories over years c Retain youthful memories as you age d Transfer from hippocampus to cortex a In the prefrontal association cortex b Compares newly acquired short term data and long term data c Determine relevance of new material organizes priorities a All amnesia is inability to recall I Retrograde Amnesia Caused by trauma I I Loss of short term memory I No long term memory formation of traumatic events I No long term loss nothing to recall later I Antero grade Amnesia D Hippocampal damage D Can t form new long term memories D Memory stuck on day of damage D Common with strokes Lecture 12 Cerebellum 7 Sleep 7 Spinal Cord gt Cerebellum 0 Structure on back of brainstem 0 Controls coordinated movements and learned movements a Connected to motor cortex receives motor plan b Afferent input gives current muscle position c Coordinates function with aim movement matches motor plan d As practice occurs motor cortex parietal lobe and cerebellum take over e Flaming is reduced initiation of activity is faster and smoother input to cortex a Allows cortex to know current position and movement b Cortex uses this information to plan future movements gt Brain Stem C Medulla pons and midbrain o Interference between spinal cord and higher brain centers 0 Cranial nerves supply sensory and motor functions to head and neck 0 Different centers in brainstem control heart rate breathing wakefulness gt Reticular Activating System 0 Neural net awareness of surroundings o Cortical pain auditory input 0 Output to cortex and thalamus all cortex 0 Controls consciousness and sleep gt Sleep 0 Low frequency activity in hypothalamus and thalamus sleep 0 Reason needed is unknown Slow wave patterns in EEG give slow wave sleep its name EEG pattern during REM sleep similar to being awake 1quot l p 4 stages each progressively deeper over about a 75 minute cycle Circadian rhythm high adenosine 7 sleep Caffeine blocks adenosine response Sleep factor 39 Muramyl dipeptide 7 strong sleep inducer e gt Spinal Cord o Neural tissue encased in verbal column 15 minutes long at end of slow wave sleep cycle Paradoxical Sleep i Hard to awaken most likely waken self High visual cortex low frontal high memory areas 7 dreams illogical New synaptic contacts made greater long term memory Will make up for missed REM sleep 0 Carries APs between brain and body 0 Grey matter in the middle A cell bodies and intemeurons 0 White mater on the outside A myelinated neuronal tracts Bundles of neural axons that carry APs Ascending tracts carry APs toward brain Entry points for afferent neurons to the spinal cord bilateral Afferent cell bodies are in the dorsal root ganglin gt Re exes l Carry efferent APs out of the spinal cord Cell bodies of efferent neurons in the grey matter 0 Neural responses without the conscious output a From receptor to afferent neuron to CNS to Efferent Neuron to Effector b CNS portion may have 1 or more synapses c Effectors are muscles and glands d Monosynaptic Re ex l synapse e Polysynaptic Re ex Multiple synapse f Interactions between afferent and efferent neurons a Polysynaptic re ex b Multiple neurons between afferent and motor neurons c Prolonged response and feedback d Very strong re ex but with potential CNS input l r V 1 n l a Muscle length information b Monosynaptic re ex knee jerk c Activation of afferent neuron produces re ex response through synapse to efferent neuron d No control by upper CNS Lecture 13 Afferent Nervous System 7 Pain 7 Taste Smell gt Sensory Receptors Sensation 0 Connect an environmental signal to body 0 Transduction is the conversion of a stimulus to a physiological signal 0 The brain converts the physiological signal into a perceived sensation gt Stimulus 0 Environmental signal 0 Binds and changes a receptor 7 signal now in body 0 Each receptor binds one stimulus best A Ex Hit in eye with ball 7 you see stars even though there are no stars gt Sensation o Conscious senses 7touch taste smell hear see and time o Unconscious 7 position temperature blood pressure changes gt Types of Receptors 0 Must bind stimulus 7 no dendrites on receptor cells ex Smell o Modified nerve endings to interact with stimulus a Physical changes open ion channels b Changes membrane potential c Touch receptors hair cells in ears photoreceptors baroreceptors a Taste and smell b Chemoreceptors 7 chemical binds receptors and opens ion channels i Changes membrane potential gt Receptor Potential Also called generator potentials local potentials graded potential Depolarization of receptor cells Size of potential proportional to size of stimulus Receptor elds vary in size depends on of afferent neurons 11 Pl a More stimulus greater receptor potential b In receptor cells without AP release of NT proportional to receptor potential a Continuous stimulus leads to larger generator potentials more APs to CNS b AP number translated by CNS as size of stimulus gt Adaptation Decreases AP number despite prolonged stimulus a Adapt overtime 7 rate is variable b Touch receptors adapt quickly c Pain BP receptors adapt slow a Virtually do not adapt b Few true tonic receptors smell gt Sensory Speci city gt Pain Normal stimulus produces a response that the brain interprets Different stimulus needs more strength for a response Brain still interprets as normal response 7 eX see stars Survival value protection from harm Anticipation of pain activates pain areas of cortex Nociceptors 7pain receptors chemical or physical a Sharp localized passes quickly Fast myelinated afferents 7 glutamate NT 31 a Diffuse dull long lasting w unmyelinated afferents 7 substance P NT a Presence suspected before discovery b NT unique to afferent slow pain receptors a Natural analgesics block pain by binding to opioid receptors b Activation alters ion channels and membrane potential A Enkephalins Endorphins I Peptides multiple types different sizes I Short halflife 25sec I Morphine 7 effective for hours gt Chemical Senses 0 Molecular binding to receptors 0 Flavor combination of smell and taste gt Taste 0 Molecules dissolve in saliva and reach taste bud receptors to be tasted a Receptors at taste pore b Tight junctions keep saliva away from rest of taste bud c Surrounding epithelial cells 7 basal cells 7 receptor cells d Turnover 10 days a Sensory neurons sent taste information b Neurons to thalamus 7 parietal lobe i wha taste c Neurons to limbic system i like it a Salty 7 Na b Sweet 7 organic sugars c Acid sour 7 H d Bitter bases quinine 7 cations poisons i Most sensitive receptor e Umami 7 glutamate MSG gt Smell o Olfactory mucus membrane on roof of nasal cavity 0 1000 different odor receptors largest gene family A 1 of human genome molecules must diffuse through mucus H20 soluble and bind to recpetor to activate must be volatile enough to oat to top of cavity l Part of dendrites of olfactory neurons E i Covered in mucus b Neurons turn over every few weeks c Unusual dendrites as receptors i New neurons mitosis a Unusual receptors primarily tonic b Unusual most adaptation in CNS i Brain can overcome adaptation Adaptation to ones smell does not effect others 0 Odors seem less strong after some time 3 1 Lecture 14 Vision gt Structure of the Eye 0 Designed to receive light and produce electrical signals to send to brain to produce 3D image a Clear noncellular front of eye Light passes through not refracted bent Fquot Lens refracts light to focus on retina a b Cilia body has muscles parallel to lens c Muscle contraction allows lens to round up focus near Muscles relax for distance vision 2 1 a Opens closes pupil b Smooth muscle c Contractions adjust to light level a Between cornea and lens i Constant production and drainage b Glaucoma less drainage or excess production 7 high pressure 7 retinal damage c Beta blockers have low production cholinergic agonists have high drainage a b Between lens and retina c Maintenance of eyeball shape d No refraction E Visual receptor at the back of the eye 6 Multiple cell layers a Highly pigmented layer behind retina Fquot Absorbs light 7 no re ection 7 no signal gt Refraction 0 Bending of light waves 0 Glycoproteins in lens refract light and focus it on retina gt Retina 0 Light passes through bipolar and ganglion cells to reach photoreceptor cells 0 Bipolar and ganglion cells pulled back at fovea o Fovea has best color vision D Dense cone concentration a Rods i Shades of grey ii Most photoreceptors b Cones i Color receptors ii Few overall receptors c Rods and cones produce receptor potentials No APs d Both converge on bipolar cells Mr C l ls a Generator potentials activated by rods and cones b No APs i Synapse with ganglion cells c Edge effect centersurround onoff effects W a R ach threshold and re APs the leave eye for CNS b Carry visual information to lateral geniculate part of thalamus 7 cortex gt Optic Nerve 0 Bundle of ganglion cell axons o Creates blind spot as axons pass through retina o Cortex lls in blind spot with expected image Il b Edits information to cortex a Multiple areas in occipital lobe b Integrates output of visual perception c Relative positions 7 3D image gt Accomodation 0 Change in lens thickness alters focal point for near and far vision 0 Ciliary muscles control focus 0 Thin lens far thick close 39j l v w a Lens gradually hardens over decades b Hardening reduces rounding of lens for near vision c At 4050 years old difficulty focusing on near objects d Need reading glasses bifocals u IrHV we a Inability to focus retina b Myopia nearsighted eyeball too long focus in front of retina c Hyperopia farsighted eyeball too short focus behind retina Corrective lenses or laser surgery on cornea 3 1 gt Rhodopsin Visual pigment in rod cells Combination of opsin and retinene Vitamin A derivative 0 Light hits retinene and partially splits it from opsin bleaching o Opsin now active 7 G protein system 7 releases NT from rod proportional to light 0 Retinene rebinds to opsins awaiting new light gt Color Vision 0 3 different opsins with retinene A Shading of retinene limits frequency range 7 peaks at red also sees yellow green and blue wavelengths a One opsin missing b Can t distinguish certain wavelengths with equal activation of remaining opsins Lecture 15 Hearing and Equilibrium gt Outer Ear 0 Little ampli cation 0 Direction detection a Overlapping membranes b Seperates outer and middle ears c Vibrates to external air waves gt Middle Ear 0 Air lled o Ampli es sound 20X a Maileus incus stapes b Hammer anvil stirrup c Carry waves from tympanic membrane to oval window 5 LJL315 juan l y liv a Drains middle ear of uid b Equalizes air pressure between middle ear and sinuses c Normally closed i If unopenable tubes needed in eardrum a Membrane that connects middle ear to inner ear gt Inner Ear o Fluid lled o Converts sound waves to electrical signals l 1 7 130 a Cochlea spinal shaped tube of inner ear b Organ of Corti part of cochlea that transduces sound to APs i Waves carried to apex and back to oval window ii Oval window absorbes all sound waves NO APs I Similar to choroid in eye a 391quot1l n39snle I Vibrates to sound waves I Shape change over length I High frequency to base low frequency at apex I Rest on basilar membrane I Hairs imbedded in tectorial membrane I Less movement I When basilar membrane vibrates imbedded hairs are pulled on I Hair cells produce GP 7 NT to different neurons APs to CNS by auditory nerve gt Frequency of Sound 0 Maximum range A 20 hz to 20000 hz 0 Lose high frequency hearing with age l a Overtones allow source distinction i Type of musical instrument or individual voice b Total signal fundamental frequency and overtunes gt Amplitude of Sound 0 Amplitude of sound 0 Height of sound wave 0 Higher wave more hair cell movement and more APs to brain gt Deafness 0 Loss ofhearing l L ijri4l1JJiiyy Sound waves don t reach hair cells a b Wax eardrum damage middle ear bone damage c Hearing aid helps i Amplify sound to vibrate oval sound directly a Damage to hair cells or auditory nerve b Need cochlear implant to treat c Frequency deafness i Loud repetitive sounds at one frequency pull out hair cells in one place selective hearing loss gt Equilibrium o Vestibular apparatus 0 Detect changes in motion 1139 nil1m m will 91 in 1 1 a 3 semicircular canals at right angles to one another b Fluid lled i As uid lays motion uid pulls hair cells I Hair cells imbedded in cupula I Inertia generates GP 7 AP L 1 E a Hair cells imbedded in gel with otoliths i Acceleration pulls on hair cells ii Gravity constant itonic signal know position of head I Detect linear acceleration I Utricle horizontal motion I Saccule vertical motion I Mismatch of signals 7 motion sickness excess rides or less space ight Lecture 16 Efferent Nervous System gt Sympathetic Structure 0 Part of the autonomic nervous system Sympathetic chain ganglia parallel to spinal cord Input from cord medulla hypothalamus o No direct cortical control 1 Preganglionic Neurons a Short neurons b Use Acetylcholine Ach as NT to postganglionic neurons in ganglia 2 Postganglionic Neurons a Long neurons b Activated by preganglionic neurons c Use norepinephrine NE as NT d Adrenal medulla behaves like postganglionic neuron gt Sympathetic Responses 0 Responds to emergencies l FightorFlight Response a Designed to remove danger b High blood ow to skeletal muscle and heart c Concurrent activation of motor units d Low activity of digestive and related functions 2 Receptor Types a Adrenergic receptors b All bind NE from postganglionic neurons 0 Alpha Adrenergic Receptors I Alpha 1 7 high 1P3 7 high Ca release from sympathetic response 7 high Ca I Alpha 2 7 low cAMP 7 low Ca pump 7 net high Ca 0 Beta 1 Adrenergic Receptors I Increase Ca in heart 7 open Ca channels I Increase in heart activity 0 Beta 2 Adrenergic Receptors I High cAMP 7 high Ca pump 7 low Ca I Low blood vessel contraction and low lung bronchiole construction more blood more air gt Parasympathetic Structure 0 Port of autonomic nervous system 0 Two neuron sites 7 all neurons use Ach as NT 0 Cholinergic activation controls daytoday homeostatic maintenance 1 Preganglionic Neurons a Long neurons i Spinal cord to organ b Synapse at ganglia or organs with postganglionic neurons 2 Postganglionic Neurons a Short neurons i Travel from ganglia to cells gt Parasympathetic Responses 0 Decrease in heart rate 0 Increase GI contractions and secretions 0 Increase pancreatic secretions o Contractions urinary bladder o Relaxes internal anal and urinary sphincters gt AgonistsAntagonists o Pharmaceuticals can mimic or antagonize autonomic NS 0 Parasympathetic higher or lower digestive activity etc o Sympathetic high BP in shock low BP in hypertension gt Motor Neurons 0 Alpha motor neuron gets multiple inputs 7 up to 10000 0 Input from stretch receptors withdrawl re exes cerebellum learned activities cortex conscious control 0 Both IPSPs and EPSPs to alpha motor neurons 7 Threshold 0 1 AP in motor neuron 1 AP in muscle neuron gt Neuromuscular Junction NMJ 0 Motor neuron synapse with skeletal muscle ber cell 0 Motor end plate very large synapse l Acetylcholine Release a Presympathetic AP 7 Ca entry 7 Ach release b Ach binds to receptors on muscle membrane 2 Endplate Potential a EPP is larger than EPSP b Ach binds receptor 7 high Na entry threshold c 1 motor neuron AP leads to 1 muscle AP 3 1 control of motor neuron APs controls nuscle activation 3 Acetylcholinesterase 7 AchE a AchE degrades Ach to choline and acetic acid b Reuptake of choline diffusion away of acetic acid 4 NM Poisons a Inhibit diaphram can t breathe i Black widow spider venom 7 releases all Ach ii Botulinum toxin 7 blocks Ach release iii Curare 7 blocks Ach receptors Lecture 17 Muscle Structure and EC Coupling gt Striated Muscle Structure 0 Skeletal connects to 2 tendons 7 tendons attach to bone 0 Cardiac smaller cells 7 attached endtoend 1 Muscle Fibers a Cell ber b Runs length of muscle in skeletal muscle c Changes size thickness but no mitosis 2 Striations a Lines skeletal and cardiac muscle b Due to laments lined up in register c Filaments overlap 7 overlap more during muscle contractions A Dark and Light Bands I Dark bands contain thick laments may also have thin laments I Light bands only have thin laments NO thick laments B Sarcomere I Unit of contraction zline to zline I Thin laments are anchored to zlines I Thick laments connect to thin laments during contraction I What one sarcomere does all do C Thin Filaments I Actin polymer backbone 7 double stranded helix I Tropomyosin long thin protein polymer runs along actin I Troponin binds to tropomyosin D Thick Filaments I Myosin polymer of lamentous protein I Extension of myosin is crossbridge I Crossbridge head can bind to actin E Ttubules Sarcoplasmic Return I Ttubules invaginations of muscle membranes carry APs into muscle ber interior I Sarcoplasmic Return develops from ER stores Ca I Connected to ttubule by voltage sensitive protein I AP down the ttubule opens Ca channels in the SR Excitation Contraction Coupling 0 Electrical events leading to muscle contraction l Skeletal Actin Potential a Starts at NMJ synapse b NT Ach binds to receptor and opens Na channels and starts AP spread in both directions N Release of Calcium a At ttubule AP travels inward and alters protein in ttubule i Leads to opening Ca channels in SR near ttubulin I Ca released b Ca pumps at far end of SR resequesters i Ca and causes relaxation 3 TroponinCalcium Binding a Ca binds to troponin on thin lament 4 Tropomyosin Shift a Ca bound to troponin causes tropomyosin to shift into actin groove exposing actinmyosin binding site 5 ActinMyosin Binding a Actin and Myosin connect b Myosin already has ATP bound and converted to ADPPi with ADPPi still bound to myosin head A Force Generation I ADPPi released 7 myosin shape changes and head twists leading to force development I No sliding I Pi release is key to force development B Filament Sliding I Filaments slide to decrease force on crossbridge head goes to lowest energy state Force 0 I New ATP binds to myosin and actin is releases D Process repeats as long as Ca is elevated gt Relaxation Cessation of APs stops Ca release from SR Calcium pumps return released Ca to SR Tropomyosin reblocks Actinmyosin binding site Muscle relaxes Lecture 18 Skeletal Mechanics gt Motor Unit 0 Motor neuron and muscle bers it innervates 0 Motor neuron AP activates all the bers in a motor neuron 1 Recruitment a Small motor neurons rst then larger b Allows gradiation of force c Mazimum force requires all motor neurons active simultaneously 2 Asynchronous Recruitment a For submaximal forces rotate activation of all motor neurons b Maintain force cannot simultaneously optimize force and continuous activity gt Twitch 0 Single muscle activation 0 l neural AP 7 1 muscle AP 7 l twitch o submaximal force not enough Ca4 reaches all troponin for full activation gt Tetanus o Summation of all twitches many APs o Enough Ca so that all myosin heads reach actin 0 Max force muscle can produce gt Length Tension Relation 0 L0 muscle length at which maximum force occurs 0 Resting skeletal muscle length is near L0 1 Falloff at Long Lengths a Reduce overlap of thick and thin laments 2 Falloff at Short Lengths a Thick laments compression against zline b Thin laments overlap and interfere with each other c Reduced Ca release gt Force Velocity 0 Heavy loads can only be moved slowly 0 Light loads are moved quickly 1 Inverse Relation a High force load 7 low velocity b Low force load 7 high velocity 2 Stretched Muscles a Stretching before activation windup uses top of LT curve b Better force maintenance c Activating stretch re exes 7re eX contraction of stretched muscle A Power Curve I From FV curve I Power F X V I At F0 P0 At V0 P0 I All others F X V is positive must have maximum I 025 F0 has optimal power output I stretching active muscle can hold 7 15x F0 before yielding I muscles resist being stretched more than the force they can generate Lecture 19 Muscle Metabolism and Control gt Muscle Energy Use 0 Progressive use of energy resources 1 Phosphocreatine a Supports about 20 sec of full activity b PCr ADP 7 ATP Cr by creatine kinase reaction c ATP 7 ADP Pi by myosin ATPase d PCr 7 Cr Pi net reaction e Pi inhibits myosin ATPase i MADPPi 7 M ADP Pi 2 Glycolysis a 10 reactions generates ATP more slowly b c d 72 min of energy use Glucose and glycogen in muscles 7 pyruvate 7 lactate No oxygen use 3 Oxidative Phosphorylation a b 9 D gt Fiber Types Also knows as Krebs Cycle and electron transport system 72 hours of energy support Pyruvate 7 C02 Oxygen used Carbohydrate loading increases glycogen storage increase up to 30 0 Variations in ber type even within same muscle 0 Controlled by motor neuron most muscles are mixed 1 Red Fibers a b C Also called slow oxidative High mitochondria levels 7 slow myosin i ATPase 7 slow speed High energy capacity low energy use 7 no fatigue 2 White Fibers a b C gt Hypertrophy Also called fast glycolytic Few mitochondria 7 fast myosin ATPase 7 fast speed Low energy capacity 7 high energy use 7 easily fatigued 0 Larger cells not hyperplasia more cells 0 High intensity high force exercise needed for maximum effort 1 Filament Number a b C d C High intensity exercise causes microdamage to filaments Disassembly of tangled filaments increases free myosin and causes pain Free myosin causes increase in expression of filament forming enzymes 7 more filaments bigger cells Young 48 hour cycle 24 disassembly 24 assembly Elderly 72 hour cycle 2 Testosterone Dependence a b gt Atrophy Filament production optimized by testosterone Females with normal hormones cannot maximize muscle size 0 Reduction in size of muscle bers 0 Not loss of of bers 1 Disuse a Muscle immobilized 7 loss of laments b Easily reversible 2 Denervation a Motor neuron damage 7 ber loss lament b Mot reversible 7 loss of myotrophic factor from neuron c Electrical stimulation cannot prevent atrophy gt Stretch Re ex Muscle length information Monosynaptic re ex knee jerk Activation of afferent neuron produces re ex response No control by upper CNS 1 Muscle Spindles a Stretch receptors in muscles b Groups of intafusal bers in connective tissue capsule 2 Intrafusal Fibers a Each muscle contains muscle section and stretch receptor section Fquot Fibers activate afferent neurons to CNS from receptor section of ber Fibers also receive efferent gamma motor neuron to muscle section of ber A Nuclear Bag Fibers I Have larger central portion of receptor 0 D Dynamic Response Detects change of length Highest response when muscle rapidly stretched Decreased response as stretch is sustained Rapid adaptation B Nuclear Chain Fibers I Smaller set of receptors parallel to nuclear bag bers D Static Response 0 Detects ber length 0 Response proportional to position 7 slow adaptation C Gamma Motor Fibers I Efferents to intrafusal bers I Contract muscle portions of intrafusal bers D Coactivation 0 Dual activation of alpha and gamma motor neurons 0 Alpha motor neurons contract muscle bers 0 Gamma motor neurons contract intrafusal bers 0 Keeps muscle spindles taut gt Reciprocal Innervation 0 Inhibition of paired muscle When stretch re ex occurs 0 Afferent neuron 7 intemeuron 7 IPSP to paired alpha motor neuron gt Golgi Tendon Organ Muscle force detectors Receptors in tendon 7 afferent input proportional to muscle force At very high forces GTO sends IPSPs to alpha motor neurons Protective effect Lecture 20 Smooth Muscle gt Smooth Muscle Structure 0 Small cells linked by desmosomes o No striations o Filaments parallel but not in register 1 Filaments a Thin laments actin and tropomyosin no troponin b TM in groove no AM blocking 2 Dense Bodies a Smooth muscle equilivent to zlines b Anchored to cell membrane all in interior c Thin laments attach here and pull ends out of cell gt Tone 0 Force with no stimulus o Ca leaks in and partially activates smooth muscle 0 Important in BP maintenance holding cavity contents gt Smooth Muscle Contraction 0 Different control mechanism than striated muscle 0 Ca also activates 1 Calcium Sources a Most through channels across cell membrane b Some small SR released by 1P3 2 Myosin Light Chain Kinase a Ca activated b Adds phosphate to myosin light chains c Activate myosin ATPase for shortening and force 3 Force Generation a MyosinADPPi with MLCP bind actin b Myosin twists generates force c Filaments slide to reduce force d This part similar to striated muscle 4 Myosin Light Chain Phosphatese a MLCPase removes phosphate from myosin light chains b Turns off myosin and causes relaxation when Ca is low gt Latch 0 Removal of Pi from light chain when AM attached decreases M detachment rate 0 Maintains force with little energy use 0 Allows BP maintenance with low energy use allow upright position gt Smooth Muscle Types 0 Vary with function empting cavities or maintaining force 1 Visceral Single Unit SM a If one contracts they all contract b Use APs linked by gap junctions c Phasic activity stomach d Random contractions small interval e Most shorten to empty cavity f Open sodium channel 7 move toward threshold A Neural Effects I Parasympathetic release Ach cause contraction I Sympathetic release NE cause relaxation 2 MultiUnit SM a Each cell is individually active no APs or gap junctions b Get average force large blood vessels eye muscles A Tone I Very important I Small force with latch 7 low energy cost to maintain BP I Force can go up or down from tone level B Neural Effects I Sympathetic receptor dependent I Alpha open Ca channels increase concentration I Beta 2 increase Ca pump activity decrease contraction 10172011 115600 PM Lecture 32 Renal Filtration Reabsorption Renal functions Filter waste from blood Maintain blood volume Maintain blood osmolarity Use filtration reabsorption secretion Nephron functional unit of the kidney Has vascular system and tubular system All but cells and proteins in blood can be filtered Most reabsorbed remainder urine Vascular system 2 capillary system 1 for filtering 1 for reabsorption Afferent arteriole 9 glomerulus filtration 9 efferent arteriole 9peritubular capillaries reabsorption 9venules Tubular system sshaped Bowman s Capsule receives filtrate 9 proximal tubule 9 Loop of Henle9 distal tubule 9 collection duct 9 ureter Variable reabsorption Hormonal control of volume and osmolarity Glomerular Filtration From glomerulus into Bowman s capsule Glomerular capillaries have very wide pores Only cells and proteins are not filtered nulin fructose polymer Filtered not reabsorbed or secreted Used to measure glomerular filtration rate G FR Inject in blood measure in urins proportional to amount of filtrate GFR quot 125 mlmin in a young healthy person 140 of total blood volume HydrostaticOsmotic Pressures H BP force filtrate into Bowman s Capsule OP So much fluid is filtered remaining proteins have higher than normal osmotic pressure Net Lots of filtration Control of GFR Afferent arteriole radius controls entry to glomerulus Afferent arteriole dilation increased GFR Afferent Arteriole Constriction decreases GFR Tubular Reabsorption Must recover most filtrate 125 filtered 124 mlmin rehab 9 1 mlmin urine 144 Lday 125 filtered 123mlmin rehab 9 2 mlmin urine 288 Lday Excess urine loss in diabetes 9 decrease BP 9 shock 9 death Transport Maximum Different carriers for different molecules TM is limit of transport due to limited of carriers Glucosuria 3x more carrier capacity than normal filtered load fG in urine blood must have at least 3x more G than normal Sodium reabsorption controls reabsorption of many other molecules Na pump only on basolateral side of tubular cells Pump Na out create gradient for Na entry into cells ATP needed for energy Tight junctions prevent flow in spaces between cells Caffeine decreases Na reabsorption Cotransport Carriers for Na and cotransported molecule Glucose amino acids bicarbonate Cl are co transported with Na during reabsorption Energy use is Na movement down gradient into cells H20 follow osmotically at proximal tubule Variable H20 reabsorption at distal tubule and collection duct Glucose reabsorption Binds carrier with Na on luminal side to enter tubular cell Separate no Na glucose carrier moves G into interstitial space Proximal Tubular Water Reabsorption 6070 of water reabsorbed in PT 180 Lday filtered quot 1 L of urine variable 500 ml of urine minimum per day to remove toxins Osmotic reabsorption of water follows solutes especially Na Lecture 33 Renal Control Secretion Filtrate Dillution ReninAngiotensin System Maintain BP by increase Na and H20 reabsorption Decrease renal BP 9 release of renin from kidney JG cells Renin is a protease Production of Angiotensin II Renin converts angiotensinogen into angiotensin I Angiotensin Converting Enzyme ACE converts A to A ll ACE is in the walls of lung capillaries Effects of Ang II powerful vasoconstrictor 9 increases BP Causes release of aldosterone from adrenal cortex ACE inhibitors Block production of Ang II Used as treatment for hypertension Few side effects but may produce fetal development problems Tubular Secretion Extra removal from plasma Carriers and pumps move material from tubular cells into filtrate Most secretion is at proximal tubule Organic acids and bases secreted poisons medicines dyes food additives Renal Blood Flow PAH PAH is totally secreted from plasma Appearance in urine proportional to renal blood flow RBF quot 2025 of cardiac output H secretion carbonic anhydrase in tubular cells makes H and HC03 H secreted in both proximal and distal tubules Uses Na H countertransport H into filtrate HC03 9 interstitial fluid net loss of H K Secretion K reabsorbed in exchange for Na in proximal tube The Na pump activity increases tubular cell K which increases its secretion by the proximal tubule cell Since K and H both exchange with Na an increase in the secretion of one decreases secretion of the other Plasma Clearance Measure of the kidney s ability to remove a substance from the plasma It is the volume of plasma from which an amount of material has been removed Glucose has zero clearance Ifa substance is filtered but not secreted or reabsorbed like inulin its plasma clearance is the GFR If a substance is both filtered and secreted its clearance is greater than GFR Ifa substance like PAH is filtered and entirely secreted its plasma clearance is the renal blood flow quot 2025 of Cardiac Output Loop of Henle Creates osmotic gradient in kidney medulla 300 mOsm at cortex 1200 mOsm in deep medulla Filtrate at the end of the LofH is 100 mOsm Plasma is 300 mOsm Countercurrent Multiplication Descending limb of LofH is H20 permeable Ascending limb is H20 impermeable H K Cl pumped out Filtrate entering distal tubule always dilute quot 100 mOsm Collecting Duct Goes from the cortex down from the medulla Always dilute filtrate at cortical end Responds to vasopressin no VP 9 little water reabsorption 9 dilute urine Vasopressin released from posterior pituitary Released when plasma osmolarity is high Causes insertion of aquaporins in CD membrane Aquaporins H20 channels H20 goes through AqP 0smotic pressure of solutes in medulla 1200 mOsm draws water Retain H20 urine up to 1200 mOsm Diabetes nsipidus Either decreases VP production of lack of kidney response bad receptor Excess water loss 9 shock 9 death Need to drink much water to survive Urine Buffering Filtrate pH must be 45 or greater for H to enter filtrate Bicarbonate and phosphate from filtration and ammonia from tubular secretion buffer urine Aldosterone Effects Increases of active Na carrier on luminal side of CD tubular cells This increases Na reabsorption in collection duct H20 follows osmotically K reabsorption is reciprocal to Na Secondary Hypertension Reduced renal artery flow decreases renal BP 9 excess renin 9 increase BP Treat with ACE inhibitors to block Ang II production Diagnosis by determining RBF with PAH Renal Dysfunction Wide glomerular pores 9 protein in urine 9 edema due to low protein Loss of concentratingdiluting loss of nephrons multiple causes Acidosis by eg lack of ammonia reduced H excretion 9 decreases neural function Sodium Dysfunction excess Na retention leads to edema hypertension decreases filtering Excessive aldosterone leads to heart failure Bladder Function storage of urine no changes after leaving kidney Ureter Entry Ureter connects kidney to bladder Ureters pass inside bladder wall at an angle Increased bladder pressure closes ureters prevents backflow Bladder Sphincters around urethra the tube draining the bladder Internal urinary sphincter is smooth muscle involuntary External urinary sphincter is skeletal muscle voluntary Control of Micturition urination Spinal reflex relaxation of internal sphincter when bladder pressure increases Reflex relaxation of external sphincter follows Cortex can overcome reflex relaxation of external sphincter Parasympathetic neurons increase bladder body contraction Pelvic floor descends allowing urine flow Exercise after delivery maintains pelvic floor strength Lecture 35 Fluid Balance Balance concept the ECF is the pool of available material for cells Input comes from ingestion or metabolic production Output occurs from excretion of consumption Balance must occur over the long run with input output Negative Balance output is greater than input Net reduction in pool concentration Positive Balance Input is greater than output Net increases in pool concentration Fluid balance balance of H20 in the body 60 of the body is H20 with adipose tissue causing variation Plasma 90 water soft tissues 7080 bone 22 adipose 10 Intracellular Fluid 23 of total body water K dominated with protein Extracellular Fluid 13 of total body water Na dominated Plasma 20 of ECF with protein Interstitial Fluid 80 ECF no protein Minor ECF Components Relatively small volumes lymph CSF saliva etc ECF Volume Regulation Regulation of volume needed for longterm BP control Changes in BP causes shifts of fluid between plasma and IF Blood Pressure Control Short term a drop in pressure causes Autotransfusion Movement of fluid from IF to plasma to maintain BP Change in baroreceptor activity Long term control of volume is balance of thirstintake and kidney fluid excretion Salt Intake The kidneys need 5g NaClday for fluid loss in sweat feces Intake is 105 g NaClday excess excreted in urine Cl follows Na Salt excretion Kidneys good at elimination Na but inc retention inc BP Must balance 105 gday input Fitness reduces Na content in sweat ReninAngiotensinAldosterone System Long term control of Na excretion controls BO Everyone has their own set point for BP ECF Osmolarity Control Needed to prevent swelling or shrinking of cells Total amount of material in a volume regardless of composition produces its osmolarity Ions Na and K dominate the osmolarity of ICF and IF Other nonpenetrating substances like proteins also contribute to osmolarity Water moves by osmosis if there are differences in ICF and IF Osmolarity Normal ICF and IF osmolarity is 300 mOsm Tonicity The standard for tonicity is not the number of dissolved particles but the behavior of cells in the solution Cells swell in hypnotonic solutions ECF is rarely hypotonic Hypertonicity cells shrink in hypertonic solution gt thank 300 mOsm Dehydration low intake excess loss diabetes Vasopressin Controls osmolarity of urine VP adds aquaporins to collecting ducts to increase reabsorption Water Intake Fluid drinking food intake metabolism add water Balance water loss from lungs skin sweat feces urine Osmoreceptors Receptors in hypothalymus that control VP release Inc osmolarityinc VP release inc H20 retention Dec osmolarity de VP release inc H20 excretion Lecture 36 AcidBase Balance Acids AH acides dissociate into A and H Strong acids like HCI in the stomach completely dissociate Weak acids like H2C03 carbonic acid partially dissociate Bases B can bind to H to become BH The only significant physiological base is ammonia NH3 9 becomes NH4 Amonnia buffers renal filtrate allowing more H excretion pH measure of H in a solution pH logH increases in H cause decreases in pH The average blood pH is 740 average cell pH is about 70 Blood pH below is acidosis Blood pH above 745 is alkalosis Acidosis is far more common Cells will have bigger pH shifts than blood Acidosis Effects Acidosis depresses the neurons especially in the CNS Alkalosis makes neurons hyperexcitable Acidosis in general decrease enzyme activity but a few increase Asidosis causes increased H excretion and therefore decreased K excretion Increased K causes cardiac and neural problems Sources of H small amount in food such as citric acid Most generated in the body carbonic acid from C02 sulfur and phosphoric acids from preoteins Metabolic acids such as lactic acids Control H is controlled in three ways Chemical buffering respiratory control of C02 and renal control of H secretion Buffers different buffers work in different places Buffers work by binding H converting A into AH This removes H from the solution and from pH First line of H defense Extracellular buffering Bicarbonate is the most important ECF buffer HC03 bind H to form H2C03 which dissociates to C02 H20 Hemoglobin in RBCs buffers H produces by C02 Increase venous blood Intracellular buffering Proteins in cells bind H in ICF In some cells especially muscle cells phosphate helps buffer ICF Urine Buffering Phosphate and bicarbonate are dissociated acids that buffer renal filtrate Ammonia is a base that also buffers renal filtrate Respiratory Control of H Second line of defense Works with nonrespiratory sources of H Increased H or increased C02 increase depth and frequency of respiration This reduces C02 in blood reducing H back toward normal Kidney Control of H Third line of H defense Removes H from any nonrenal source in the body H Excretion H ion pumps in the renal tubules secrete H into the filtrate Urine pH is normally 60 but can be as low as 45 AcidBase Imbalances Pathological changes in the control of H result in pH changes These can be compensated by the respiratory and renal systems if not of respiratory or renal origin A system cannot compensate for its own problem renal problems require respiratory compensation respiratory problems require renal compensation Respiratory acidosis Abnormal C02 retention from hypoventilation Lung disease drugs nervemuscle disorders breath holding Renal compensation by increases H secretion Respiratory Alkalosis decreased CO2 by hyperventilation Fearanxiety aspirin poisoning conscious breathing Decreased H secretion or removal of condition Metabolic acidosis most common acidbase disorder Severe diarrhea loss of bicarbonate Excess H production during fat use in diabetics Exercise leading to lactate and H production Kidney failure cannot excrete H or conserve HC03 Metabolic Alkalosis Decrease in H for nonrespiratory reasons Vomiting loses H in vomitus Excess bicarbonate ingestion Decrease respiratoy rate and retain H in kidneys to compensate H retention increases K loss Lecture 37 Cardiovascular Regulation Hypertension Local Control Nonneural factors Decreased P 9 decreased flow 9 homeostatic tissue response 9 increase flow Autoregulation each organ controls local blood flow Metabolic Vasodilators Active tissues produce vasodilators ATP use 9 increase adenosine production Adenosine is a strong vaso dilator active hyperemia Endothelial Factors paracrines released from endothelium affect VSM Nitric Oxide NO Hormonalneural activation Increase NO 9 relaxes VSM 9 increased blood flow Endothelien peptide constricts VSM Decreased flows 9 increase BP Stimulants of E increase gene activity that makes E Baroreceptors Stretch receptors in carotid sinus and aortic arch Changes in BP alter baroreceptor activity Input to Medulla Baroreceptors send neurons to medulla in brain stem Control of vasoconstrictiondilation Cardiovascular Control Center CCC is in medulla CCC controls sympathetic and parasympathetic output Homeostatic short term control of BP Sym decrease BP 9 decrease baroreceptor input 9 increase sympathetic output 9 increase BP heart VSM Para increase BP 9 increase baroreceptor input 9 increase parasym output 9 decrease BP lower HR Resetting Body adjusts to own quotnormalquot BP Adaptation to prolonged BP change occurs over days Hypertension Chronic elevated BP Multiple causes several small changes cause large increase in BP Cardiac effects hypertrophy against increased load diastolic pressure Increased oxygen use heart attack when coronaries constrict With age increases in systolic pressure increase stroke risk Essential Hypertension cause unknown treat symptoms Effective reduces pathology Renal Hypertension Also called secondary hypertension Decrease blood flow to kidney cause increased kidney renin release Renin converts angiotensinogen to angiotensin I A I Angiotensin converting enzyme ACE in lung capillaries Converts A to Angiotensin II Angiotensin II increase BP Angiotensin II is a strong vasoconstrictor and causes aldosterone release from adrenal cortex Aldosterone increase Na reabsorption and H20 reabsorption by kidneys more volume In Pregnancy Placental factor causes vaso constriction Preeclampsia is hypertension during pregnancy Magnesium sulfate treatment lowers BP Drug Treatments Often in combination Varying side effects Diuertics Increases Na excretion lowers blood volume decreases BP ACEInhibitorsBlock 39 ofquot 39 39Itoquot 39 39 u u alphaAdrenergic Receptor Blockers stops sympathetic constriction of VSM blocks NE effects Fewer Ca channels open less Ca entry less force BetaAdrenergic Receptor Blockers blocks NEEpi effects on heart less Ca entry Decreases force of cardiac contractions Calcium Channel Blockers decreases VSM contraction blocks tone Shock very low blood pressure Loss of blood toxic vasodilation Reversible shock can recover from Epinephrine increases BP side effects significant Irreversible shock multiple organ failure due to low BP Death results Lecture 38 Digestion and Absorption The breaking down of food into absorbable units and their absorption Carbohydrate Digestion must be reduced to monosaccharides to be absorbed Complex carbohydrates chains of sugars usually glucose different complex carbs have different links between sugars starch is different than cellulose we cannot digest cellulose sugar in fruit is often monosaccharide fructose or glucose Enzymes produced in the mouth and in pancreas amylase converts starch to disaccharides disaccharides are in wall of small intestines disaccharides convert disaccharides to mono sucrose is converted to glucosefructose Lactose Intolerance lactose is milksugardisaccharide of glucose galactose if no lactose is produced no digestion of lactose bacteria in large intestines use lactose as food source gas diarrhea produced Absorption complete all sugars totally absorbed no diffusion use glucose transporters Sodium Dependence glucose cotransported with Na into epithelial cells transport of glucose from epithelial cells to interstitial fluid uses a nonNa glucose transporter Protein Digestion some in stomach most in small intestine Proenzymes released in protected form acid then pepsin converts pepsinogen into pepsin so pepsin completes its own conversion Peptidases both from pancreas on small intestine wall convert peptides into amino acids some disaccharides and tripeptides absorbed Absorption use amino acid transporters in mucosal wall some use Na Cl or no cotransporter Source of Protein 50 food 25 digestive enzymes 25 mucosal cells no dietary protein in feces Infant Protein Absorption newborns can absorb protein directly until tightjunctions form lgG is colostrum provides protection Lipid Digestion mouth and stomach lipases unimportant pancreatic lipases enter duodenum in active form Lipases convert lipids to absorbable form lipases convert triglycerides into monoglycerides and free fatty acids Micelles bile salts form liver emulsifying MG and FFA and Cholesterol fats diffuse into mucosa at brush border microvilli Absorption MG FFA cros to reform into T6 mucosal cells TG and cholesterol form chylomicrons chylomicrons enter lymph through thoracic duct to blood Portal Vein comes H20 soluble foods directly to liver liver processes and detoxifies foods fatsljlymphlZEloodlEerywhereElliver eventually Electrolyte Absorption salts all H20 solubleD portal vein small intestine has tight junctions salts use carries channels and pumps go through cells Water 2000m Lday ingestion 7000m Lday secretions 200mLday in stool follows other absorption osmotically Sodium most Na enters through cells E gradient form Na pumps on basolated said of mucosa as in kidney some Na entry through leaky tight junctions Potassium K enters down concentration gradient through channels K exchanges for Na lost electrolyte absorbed during diarrhea K loss too fast for K reabsorption active transport of K in colon Bicarbonate huge secretion by pancreas buffers acids in duodenum reabsorbed by concentration gradient in small intestines Vitamins H20 soluble B and C are rapidly absorbed and rapid loss in urine must take B and C daily B12 absorption needs intrinsic factor from stomach Vitamins A D E K are fat soluble DmicellesDEmph Minerals Ca2 3080 absorbed but is vitamin D dependent Ca2 binding protein Ca2 ATPases increase Ca2 entry L39 GI Intro Mouth Esophagus GI Layers Mucosaepithelial cells 39 39 U39 quot 39 muscle 39 plexus quotquot circular longitudinal smooth muscle myenteric plexus Serosaouter epithelial layer produces serosal fluid GI Innervation Plexusesneuronscontrol local contractions longitudinal muscle regulates the propulsion of chime circular muscle milks food secretions Parasympathetic Neurons activate plexuses which increase GI activity sympathetic neurons decrease GI activity Basal Electrical Rhythm variable electrical baselines Ca2 channels open and close Contraction when BER reaches threshold and action potentials occur Migrating Motility Complex Strong contraction migration from stomach to end of small intestines starts at previous meal nears complete digestion clears stomach small intestines in anticipation of next meal GI Hormones release in different areas both upstreamdownstream effects Gastrin from stomach protein strongest stimulus for release increase stomach secretion of acid and pepsinogen increase SI ileocecal valve relaxation Dempties SI initiates mass movement in chat triggers defecation Cholecystokinin CCK secreted by duodenum into blood when fat or protein present causes contraction of gall bladder causes release of pancreatic digestive enzymes inhibits stomach secretions Secretin secreted from duodenum into blood when H in duodenum increased secretion of pancreatic bicarb into pancreatic duct bicarb neutralizes stomach acid in duodenum Mouth little digestion here almost no absorption only some medicine nitroglycerine absorbed by oral m ucosa Secretions bicarb neutralizes acids H20 amalyse lipase mucus to coat food Lysozyme antibacterial enzyme Swallowing deglutination boluses formed coated with mucus voluntary propulsion to pharynx reflex relaxation of upper esophageal sphincter bolus forced into esophagus Esophagus tube to stomach sphincter at each end 59sec transit time to stomach no digestion or absorption Sphincters upper relaxes upon swallowing peristaltic contractions behind bolus force it into stomach lower normally tightly closed relaxes to let bolus in Reflux acid into esophagus through LES loss of neural input most common cause acid imitates esophagusheartburnpotential ulcer Gas in stomach swallowed gas some burped out some absorbed some to colon most colonic gas is bacterial L40 Stomach Pancreas Liver Stomach holds contents kills pathogens starts protein digestion relaxes as food enters and holds up to one liter Structure lining has gastric pits cells produce secretions mucus coats gastric pitsprevents HCI killing cells Secretions pepsinogen HCI separate H and Cl pumps pH 12 mucus gastrin BlZ absorption Motility Peristaltic wave 3min fundus to body to antrum Forces food into antrum crushes bluses there forms chime Chyme is mixture of food and secretions Emptying Pyloric sphincter separates antrum and duodenum Pyloric sphincter squeezes shut as boluses are crushed Only a small amount of chime squirts through Ulcers Open sores in stomach cells exposed to acid Kills cells no mucus covering Histamine Acid 9 damage 9 histamine 9 more acid Positive feedback loop Treatment stop acid secretion neutralize acid H Pylori Bacteria Live in gastric pits gt 50 of all ulcers Hard to get to due to mucus antibodies can kill H Pylori Exocrine Pancreas Secretes bicarbonate solution to neutralize stomach acid Secretes enzyme for digestion Duct System Carries solution to duodenum Duct cells secrete bicarbonate solution Alkaline Secretion Bicarbonate solutionPacreatic Aqueous Alkaline Solution PAAS Almost entirely Na Bicarbonate quot 45 x more bicarbonate than plasma 15 liters or more per day Regulation Increased H lower pH in duodenum causes secretin release into blood Secretin from duodenum causes release of NA Bicarbonate solution PAAS Enzymatic Secretions Preteases released in protected form Lipase and amylase released in active form Pancreas has trypsin inhibitor for protection Regulation Fat or protein in the duodenum causes CCK release CCK causes acinar cells to release enzymes Enzymes carried to duodenum by PAAS Parasympathetic neurons increase enzyme release sightsmell response Liver releases bile into duodenum to emulsify fats Mostly undifferentiated cells 1000 s of metabolic reactions Makes plasma protein Blood supply 2 sources merge at liver sinusoids Hepatic artery supplies oxygenated blood from heart Portal vein carries water soluble foods from SI Bile Salts Major component of bile made by hepatocytes Released into bile canalculi on opposite side from blood Bile salts form micelles 9095 of bile salts reabsorbed at ileum recycled Bilirubin Metabolism Formed from heme of lysed RBCs fat soluble9 circulate bound to albumin Released to liver cells 9 modified to H20 soluble form 9 most to bile 9 feces Some is reabsorbed at the ileum excreted in urine Provided color for both urine and feces Jaundice is a buildup of bilirubin usually liver problem Gall Bladder Function stores bile between meals when Sphincter of Oddi closed CCK relaxes S of O and contracts the GB 9 bile enters duodenum Gall stones calcium bilirubinate some or cholesterol stones most Form in gall bladder with glycoprotein binding Can block S of O gall bladder attack If GB removed bile duct expands to hold bile Lecture 41 Small Intestine and Large intestine Small Intestine primary site ofdigestion and absorption Structure of Small Intestine Duodenum jejunum ileum Many folds increase surface area 600 fold 9 litersday presented 2 food 7 secretions 12 litersday to colon 200 ml in feces Villi folds of SI wall tissue Crypts of Lieberkuhn at base Cells migrate upward die by digestion Cells replaced every 3 days Microvilli Brush border Folds of cell membrane at the tips of villi cells Site of absorption Bound enzymes on surface Enterokinase disaccharidases etc Mucus Secreted with H20 Contains glycoproteins Covers S epithelium in C of L and upwards Protection from digestive enzymes Motility Basic Electrical Rhythm BER higher at duodenum than at ileum Moves chime down S Peristaltic waves of longitudinal smooth mucle Segmentation mixing contractions of circular smooth muscle Malabsorption decreased amino acid absorbance 9 wasting decreased muscle mass Decreased carb and fat absorbance 9 increased stool and gas decreased vitamin absorbance Autoimmune Crohn s and allergic diseases Diarrhea Multiple causes most common S motility gt absorption Loss of H20 and K potentially serious or fatal neuralheart problems Dehydration leads to shock Travel changes in waterelectrolytes kills L bacteria or E Coliother bacteria in food Large Intestine Colon Handles absorption of H20 and Na and some K No nutrient absorption from S some from bacteria Large Intestine Structure SI 9 cecum 9 ascending transverse descending colons 9 rectum 9 anus Internal and external sphincters control anus Appendix closed pouch of lymphoid tissue off cecum Gastrolileal reflex Food in stomach causes relaxation of cecum and allows ileum to empty Gastrin relaxes ileocecal valve Absorption Active transport of Na waters follows FecesFiber Feces is minerals fiber bacteria H20 Bacteria grow even during starvation Fiber is cellulose and related compounds Fiber increases colonic activity decrease colon cancer Bacteria E Coli and other types appear soon after birth Bacteria acquire nutrients from the colon mucosa Introductory Physiology PSL 250 Dr Patrick Dillon 517 884 5040 dillonmsuedu Office hours Wednesdays 101130 2178 BPS James Ba rger TA barger39msuedu Office hours TBA Review Sessions Wednesday evenings Day before tests COME TO REVIEW SESSIONS 830 PM 326 Natural Science What is physiology That is functional anatomy Dynamic process maintaining or moving to a control set point Our body is at a set point a normal position What are the different organizational levels Each level is built on the one smaller than it List is smallest to largest Chemical level Cellular level Tissue level Organ level Body system level Organism level Each level has characteristics the lover one does not Molecules assembly of atoms we don t deal with pure atoms molecules at smallest Major physiological molecules are proteins carbohydrates lipids and nucleic acids these will be talked about very irregularly Cells the basic unit of life Use energy has metabolism carry out some chemical reactions removes waste Made of groupings of molecules Side Note Heart attacks tend to be additive If you have one you are more likely to have another based on the scar tissue that you get from the first Tissues Collection of similar cells with the same local function They will be identical to one another They usually associated with one another and link together Term is used generally ex Lung tissue Organs collections of different tissues carry out distinct function in the body Stomach is there for protection more than digestion Secretes acids to would break down something harmful that would enter in to the rest of your G tract Systems control organs controls major 39 functions Homeostasis main the normal physiological state We have 20 trillion cells Internal environment interstitial fluid liquid around cells Cells are like magnets like cells like similar poles on a magnet don t attract but push apart No cell touches each other Negative Feedback If something stops physiologically in the body your body will respond to positively fix this change to bring the body back to homeeostasis The major reason women out live men is because of low blood pressure side effect of estrogen Our cardiac systems are less likely to wear out because of this Blood pressure example of homeostasis say you have high BP Then you take the meds to lower your BP Your body fights this because it is trying to get the BP back to the original set point Once you are off your body will raise your BP past the set point because it is used to fighting the medicine If your BP gets to high you will have a stroke Knee Jerk reflex when you hit the tendon it stretches quadriceps muscle which causes the contraction They are actually testing the ability of your spinal chord to see how fast you have the reaction Positive feedback rare but important Where your body is at one state and changes you another and stays there forever at that set point Example scab Blood turns to solid covering Stays that way forever Once the wound is healed the scab doesn t go back to fluid but stays solid Ultimate state change Living to dead Parturition medical term for childbirth Lecture 2 Cell Structure Cyto means cell sol means liquid Cytoso Liquid portion high protein content Protein clusters organized enzyme pathways enhance metabolism When proteins they cluster they require a smaller about of liquid to exist Enzymes carry out chemical reactions Proteins with sequential enzymes are often the ones that are linked together In every one of our cell we have mostly 40mgmls per cell Some are as much as 60 mgmls per cell Metabolism thousands of reaction Enzymes protein catalysts Enhance the process towards equilibrium Structural proteins work in energy production enzymes storage and use of carbohydrates Protein synthesis Chains of connected amino acids Structure is determined by genes mRNA from nucleus codes for protein manufacture on ribosomes Ribosomes Combinations of protein and RNA Free ribosomes make proteins for use in cytosol Few or no modifications after production Chaperones help protein folding Look roughly like a snowman Protein needs to retain its specific shape for it to retain its function Example albuminwhite of egg when you cook it Goes from translucent to white Can t go back this is an example of positive feedback Storage Glycogen chains of glucose linked together is the polymer of glucose n muscle for use during contraction n liver to maintain blood glucose between meals because your brain runs purely off of glucose So we need it in between meals Must be constant as well Some in many other tissues Endoplasmic reticulum Inside of the cytoplasm It is a series of tubes made out of membranes But it s all one tube Complex of interconnected membrane tubules Production of exported or organelle proteins Rough ER have ribosomes site of protein synthesis Newly formed protein threaded into ER lumen as it is made New protein moves through this to smooth ER Smooth ER has no ribosomes fat and membrane Produces vesicle that carry new protein to Golgi apparatus Membranes are made here as well as complex lipid molecules 14114 Golgi apparatus a series of flattened membrane tubes that receives vesicles from smooth ER It the site of protein modification Directs vesicles with new protein to specific organelles or cell membrane Also docks proteins on vesicles and destination membrane to ensure proper delivery Protein Modification Proteins in GA have amino acids removed or modified Sugars are added to proteins and modified Proteins only work in specific shapes Most proteins naturally fold into their appropriate shape Chaperones ensure that proteins fold properly Exocytosis a secretory vesicle fuses with the plasma membrane releasing the vesicle contents to the cell exterior The vesicle membrane becomes part of the plasma membrane Vesicles from GA with export proteins merge with the membrane and dump contents An increase in intracellular Ca triggers exocytosis ATP needed ATP is like cell s money The more you have the more you can do It s like when a bubble envelops another The contents then quotexplodequot outwards Lysosomes contain digestive enzymes merge with endocytotic vesicles digest molecules down to usable size proteins to amino acids complex carbohydrates to monosaccharides Endocytosis must occur to balance exocytosis Extra molecules bind receptors and trigger membrane infolding HAS TO OCCUR because of homeostasis Exocytosis makes something bigger by adding some membrane Endocytosis takes back some of the membrane that on the outside of the cell to create a balance Almost all of our cells with carry out both processes Bacteria or dead cells trigger phagocytosis Phagocytosis WBCpseudopods surround prey close around prey lysosome fuses with vesicle releasing enzyme that attack new material inside vesicle Recycles material eaten to be used elsewhere in the body Like Endocytosis Peroxisomes Organelle 4 Cellular equivalent to the liver They carry out all sorts of reactions Contain antioxidants Vit C Vit E do this outside of the cells Destroy oxygen radicals very reactive destroy protein function Radicals molecules with odd extra electron are harmful to us not normal have extra electron that is SUPER reactive Catalyse prevents you from dying from too much oxygen peroxide produces by you Fastest enzyme known Works at 1000000 per second Lecture 3 Energy Production Cytoskeleton ATP quotJ 39 Tu39 39 39 cellular 39 39 of money the Phosphates are highly transferable Manufactured by two processes Glycolosis anaerobic amp Anaerobic Energy Production Glycolosis no oxygen WHAT GOES IN WHAT COMES OUT WHAT IS IT GOOD FOR know this for the reactions Where does this happen In cytoplasm free ATP and cell membrane ATP for ion pumps Produces 2 ATP per glucose without oxygen If you start with glucose there are 9 reactions If you start with glycogen there are 10 reactions Glucose NAD 2 ADP 9 9 reactions 9 NADH 2 pyruvate 2 ATP Goes in 9 Comes out NADH pyruvate 9 NAD lactate produces very quickly produced so that you can recycle the NADH to NAD Mitochondria oval shape like rugby ball they have a double layer Cristae are the folds inside Aerobic Energy Production double membrane structure Outer membrane has large pores only there to hold it together TCA Cycle Citric Acid Cycle first molecule created in it is citric acid Krebs cycle inside of the matrix ofinner membrane Electron transport system part of the inner membrane uses oxygen Pyruvate 9 mitochondria can migrate to mitochondria to help produce more ATP Goes in9 Comes out Pyruvate NAD FAD 9 C02 ATP NADH FADH Fats stored in pairs in adipose tissue divided by 2 into Acetyl CoA which enters TCA cycle Pyruvates from carbs and Fat 9Actyl CoA 9 TCA cycle 39 iai nner quotquot 39 C 39 quot is what makes red meat red and dark meat 1 dark for melectron transport system on inner membrane Oxidative Phosphorylation NADH donates electrons to ETS H follows NAD recycled As e passes H pumped at 3 Cytochromes ATP made on H return Goes In 9 comes out e H oxygen 9 H20 use of inhaled oxygen 253 ATPNADH 152 ATP FADH 30 ATP moleculesglucose molecule Cyanide kills you by blocking access of ATP Vaults octagonal barrel shaped structures maybe involved in transport from the nucleus to the cytoplasm mRNA and ribosomes are possible cargo that go through these Cytoskeleton Intracellular frameworks protein polymer filament of different size and function WE don t have spherical cells but have at least SOME structure 3 kinds of these protein polymers Microtubules microfilament keratin Microtubules Polymers of tubulin works like railroad tracks the street on which transport actually occurs have a and ends cell stabilitytransport along neurons move vesicles organelles and chromosomes Movement Kinesin carries cago along microtubules in direction toward membrane Dynein moves cargo in direction away from the membrane Taxol anticancer drug binds to and stabilizes MTs kills dividing cells Takes 623 years to have a singular molecule of glucose to travel from spinal cord to big toe by pure diffusion Cilia movement looks like a field of waving wheat primarily present in lungs oviducts dynein drives MT twists propels mucus ovum Flagella only present in sperm propel sperm to ovum rotary movement Intermediate filaments Permanent lad bearing filaments in stressed cells skin maintain shape Layers of deadthick skin 13 layers in men 8 in women 7 in men Microfilaments Thin filaments actin polymer Thick filaments myosin polymer Interaction between these are what actually Movement in muscles and WBC Lecture 4 Membrane Structure 16114 Membrane structure Separates Intracellular fluid ICF what s inside cells from Interstitialfluid IF what s outside of cells Physical and chemical barrier Phospholipid molecule Backbone of membranes soaplike Fluidity within membrane as a whole Looks like two tailed lollipop Tails next to tails heads to heads Head of phospholipid molecule negatively charged polar hydrophilic Tail of phospholipid molecule uncharged non polar hydrophobic HydrophobicHydrophilic Fat soluble center of membrane Hydrophobic molecules cross easily Hydrophilic outer sides of membrane Hphils don t cross by diffusion except H20 High water solubility due to small size in comparison to phospholipids they are small So they can kind of squeeze their way inside Cholesterol nterspersed between lipid portions of phospholipids prevents close packing of fatty acid chains create membrane fluidity flexibility forms semicrystaline structure that keeps your skin from popping sit in between phospholipid tails Protein in membranes some mobile some restricted Receptors on outside bind to solute either chemical neurotransmitter hormone drug or ion Some are activated by physical change touch 9activate either channel or enzyme Channels only ions go through proteins channels span membranes open or closed specialized by ion type K Na Ca Cland receptors open channels Enzymes a protein that catalyzes a reaction A 93 some activated by receptors some always active Dockingmarker Acceptors recognize and bind to secretory vesicles sites of exocytosis Carriers quotrevolvingquot more like flex on one side then the other EX ltgtproteins example of you pushing revolving door with a child that s too weak to do so on the other side to ATPase alternate open side 2 types 1 molecules move with gradient 2 cotransport with ion usually Na Use the ion gradient for energy source CarbohydrateProtein Complexes Identify quotselfquot to the immune system Basis for separation of cell into tissues during embryonic development Act like anchors preventing proteins from fully rotatating all the way around They are always on the outside of the cell Limit normal tissue growth to confined regions prevent metastatic cancer ntercellular connections proteins and large structures CAMs Cell adhesion molecules Proteins Anchor cells to other cells or to basal lamina noncellular surface maintain tissue integrity abnormalities occur during metastatic cancer control cell migration Tight Junction block movement between cells create tissue sidedness they are in skin intestines kidneys Allow selective transport molecules must go through cells form a ring around them like plastic holding together a 6 pack connection of these are called kissed sites Desmosomes cellular rivet hold moving cells together skin and heart Gap Junctions Channels between cells ions pass electrical link Electrical signal from one cell activates next cell These are in the Heart GI tract bladder uterus and rectum Lecture 5 Membrane Transport Diffusion across membrane Driven by chemical or electrical gradients Simple diffusion channels and carriers Diffusion goes in all directions Net diffusion will always go from high to low Hydrophobicity how fat soluble something is Fats and gases cross easily Fluiditiy allows 8 micron RBC s to deform through 7 micron capillaries enhance oxygen transport Size small objects pass through more easily than large objects Fick s Law of Diffusion rate of diffusion Q QPAdetaCdetaX MW P permeability hydrophobicity hydrophilicity A area DeltaCdeltaX concentration gradient MW molecular weight size Ion Channels Different types for different ions Nadiffuses in the cell easily Kelectrical gradient wants to go in while chemical outwards Casame as Na Cl allow ions to move by chemicalelectrical gradients Osmosis the diffusion of water water moves from high concentration to low concentration semi permeable membrane allow water to cross but nothing else Pure water has a higher concentration Any llSTUFF in water will make it low concentration This means water will WANT to move towards the less pure water sites 1 Carrier transport protein molecules change shape in membrane and move molecules across energy for transport may come from concentration gradient or ATP Specificity each carrier transports a specific molecule or type of molecule Saturation there are only a limited number of carriers in each cell when all carriers are being used the rate will be at a maximum That is called the Transport maximum Facilitated diffusion no ATP used move down diffusion gradient Molecules bind to one side carriers reorient molecules leave on opposite side more binding on high concentration side movement from high to low concentration 2 Active Transport Use ATP for energy to move ions against their concentration gradient movement from a low to high concentration Ions move from high affinity side to low affinity side At produces the ion gradients across cell membranes NaK ATPase EVER ANIMAL CELL HAS THIS Moves Na out of cells moves K into cells K high inside cells Na is high outside cells creates gradients that allows electrical signaling 3 Secondary Active Transport SAT Carrier has 2 binding sites agonist and Na energy of the Na gradient out to in drives SAT Cotransport agonist in revolving door kid is in same space as you or countertransport agonist out the kid is across from you in the revolving door Na transports some glucose and amino acids in this way in some tissues other ions drive SAT LINING OF DIGESTIVE TRACT has carrier active and secondary active transport 21114 Lecture 6 Membrane potential Voltage Separation of charge All cells have a negative charge inside compared with interstitial fluid The opposite charges line up along the membrane Membrane Potential is always in the mV millivolt range Average cell size 10 microns Resting Membrane Potential Voltage across cell membrane when the cell is not activated 70mV Determined by ion channels K dominates at rest most open channels Some Na contribution few open channels Concentration Na is 150mM in Extracellular Fluid 15mM in Intracellular fluid in muscle K is 5mM in ECF 150mM in ICF in muscle Protein is 0 in ECF and 65 in ICF muscle Most proteins have negative charge The intracellular concentrations of Na K and Protein are different in different cell types Permeability Determined by the number of open channels The number of open K or Na channels determine ion diffusion Different open number in different cell types Produces different resting Membrane potential NaK ATPase This enzyme creates the gradients and restores them after ions diffuse across the membrane this is ion pump activity Equilibrium Potential limits on K and Na What voltage balances chemical gradient Only open channels determine MP 60 70 90mV Na most K K balanced out by the 90 all Few Na all K Diffusion at rest At rest K channels are open K diffuses out Intracellular protein A is trapped in the cell Na channels are mostly closed like Na diffusion PumpLeak Balance There is a balance between pump and diffusion channel activity Since ions will constantly diffuse down their gradients through channels a constant input of ATP energy into ion pumps is needed to maintain the gradients Resting MP changes The membrane potential will change in many cells including nerve and muscle cells The MP always is negative at rest The MP magnitude decreases gets less negative during depolarization The MP increases gets more negative during hyperpolarization Most of the time your brain suppresses itself what signals go through CNS are actually the rare event One type of autism where the thalamus doesn t always quoteditquot f searching in where s waldo they can t focus on one thing Normal people look for redwhite combination This type of autism would be distracted by purpleyellow greenwhite other color combinations They are overloaded with information and just ignore it all to cope Depolarization The membrane potential is less negative as from 70 to 60mV Caused by K channels closingNa channels opening MP moves toward Na equilibrium potential Hyperpolarization the MP gets more negative as from 70 to 80mV Caused by K channels opening Na channels closing MP moves toward K equilibrium potential Graded Potentials Triggered by agonists or by physical force like a pebble in water ripple effect circles around and slowly fades away Action potentials are more like tsunamis Size proportional to the size of the stimulus spreads to the adjacent areas but decays rapidly over time and distance Occurs in many types of cells receptors neurons muscles n neurons and muscle GP needed to reach threshold of Action Potential Lecture 7 Neurons and Action Potential Action Potentials Electrical signal long range in neurons and muscles Activated by graded potentials AP s do not degrade over time and distance like tsunami VoltageGated Channels Will open when membrane reaches particular voltage Usually quot 1520mV above resting potential All vgated channels open together causing action potential Enter inactivated state soon after opening making refractory period The pause Example heart If the heart pumped super super fast then it couldn t get the blood in the heart to pump back out You need the pause in order for effective blood pumping Phases of AP Controlled by different open channels there are 5 stages 5 Stages Depolarization AP spike Repolarization Hyperpolarization and Return to rest Depolarization to Threshold Firing level 1 Chemical or mechanicalgated Na channels open Na enters down gradient tThreshold at t all the vgated Na channels open I39I39X blocks fast vgated Na channels AP Spike 2 These last for 12 milliseconds Since all vgated Na channels open together all Aps in one neuron are identical Na enters Rapid depolarization to 20mV Doesn t reach Na equilibrium potential because some vgated channels also open Repolarization 3 Vgated Na channels close after 12 msec K channels still open K leaves membrane potential falls Hyperpolarization 4 Voltage goes below resting because extra K channels are still open Nearer to 90mV K equilibrium Potential than at rest Return to resting potential 5 Extra K channels close Neural Structure Neuron Receive and pass on signals Nerve is a collection of neurons Dendrites Receive neurotransmitter from other neurons many branches no action potential only graded potential Cell body cell organelles nucleus Axon hillock quotare we there yetquot at beginning of axon high density of Vgated Na channels Action potential starts here Axons Very long carry Action potential away from cell body Speed of AP variableFwith diameter and with myelin the bigger the center is the faster Myelin Node of Ranvier Cells surround axon and wrap layers of membrane Electricity insulates axon prevent electrical loss to IF Interstitial fluid Increase AP speed Node of Ranvier spaces between myelin complete AP circuit AP jumps between Nodes of Ranvier Refractory Period After vgated channels close they are unopenable for a time 30200 msec No new AP s during this time limits AP frequency AP only travel along axon in ONE direction can t go back Frequency of Action Potential All APs are identical in a given cell Information is passed by the frequency not the size of action potentials More APS create a stronger signal input to CNS Lecture 8 Synapses Synaptic structure Neuralneural synapses MOST synapses go through axons and dendrites Presynaptic neuron End of axon also known as synaptic knob terminal button Receive Action Potential down axon Action Potential opens voltage gatedCa channels 23114 Vesicles Contain neurotransmitter Increased Ca triggers merger with cell membrane Neurotransmitter NT dumped into cleft space in between the pre and post synaptic neuron diffuses with postsynaptic membrane quotquot 39 39 diffusel perl 39 Post synaptic Cell Has r 39 for Receptors connected to ion channels When Neurotransmitter binds to reception channels open fromquot r39 neuron Excitatory Postsynaptic Potentials EPSPs NT binds and Na channels open Na enters and causes depolarization One EPSP is not enough to reach threshold Inhibitory Postsynaptic Potentials IPSPs vast majority in brain and spinal chord K or Cl channels opened by Neurotransmitter K leaves or Cl enters down their electrochemical gradient Membrane potential more negative Less likely to reach threshold One synapse one produces either IPSPs or EPSP when it occurs Don ts switch around Also IPSPs and EPSPs are collective can happen at the same time Grand Postsynaptic Potential GPSP Sum ofall the EPSPs and IPSPs They reach threshold and fire AP Most neurons are inhibited by IPSPs most of the time Axon Hillock At the junction of the cell body and the axon High density of vgated Na channels Action potential starts here One way Conductance Neurotransmitter is only releases from presynaptic neuron Receptors only on postsynaptic neuron Information only goes in one direction Temporal summation EPSP form the same neuron close in time are additive they may sum to reach threshold Spatial Summation EPSP from different neurons are additive The sum of these may reach threshold Some neurons receive synapses from 1000 s of other neurons All EPSPs and IPSPs are graded potentials Everything occurs just before the axon hillock Convergence Multiple synapses into a single neuron Anatomical basis for spatial summation Divergence Each axon has many synaptic knobs terminal buttons to other neurons An AP in one neuron delivers neurotransmitter to all its divergent neurons at the same time Lecture 9 ntercellular Communication Communication types Communication between cells over short and long distances Combinations of electrical and chemical activity Paracrines Local hormones released from one cell affect nearby cell Nitric Oxide Important in control of blood flow Neurotransmitters specific each neuron has only one type of neurotransmitter Variable neural cell length NT s work locally as released NT s released by exocytosis synapse cell to cell Neural to neural muscle endocrine cells Rapid removal diffusion digestion reuptake Endocrine Hormones released from endocrine tissues endothelial origin Broad effects hormone released into blood Goes everywhere Effects depends on target cell receptor Neurohormones Released from neurons into the blood Functions as other hormones receptor dependent Hydrophilic Hormones Cannot cross the membrane Rely on membrane receptor activation Membrane proteins produce second messengers Second messangers Made ate membrane internal activation mechanism started by hydrophilic hormone 1st messenger only cells with receptors respond cAMP ATP 9cAMP activated kinases add phosphate to molecules Kinase cascades amplify signals Individualized effects in different cells cGMP GTP 9cGMP activates kinase cAMP and cGMP tend to do the opposite within the cells If cAMP turns something on cGMP turns something off IP3 Causes release of intracellular Ca stores Ca stored in sarcoplasmic reticulum a structure modified from endoplasmic reticulum Calcium Released from internal sarcoplasmic reticulum by IP3 Enters across cell membrane through Ca channels Binds to and alters protein activity Celltocell Ca signal produces coordinated cilia waves exocytosis Gap junctions depolarization causes cardiac and smooth muscle contraction in adjacent cells by opening Ca channels G Proteins timing proteins Bind GTP 9 Increase activity until GTP 9GDP Regulate vesicle movement cytoskeleton growth vision 2nd messengers Hydrophobic Hormones Diffuse easily into cells Need transport molecules in watery environment Steroid thyroid hormone Vit A Vit D Increase protein synthesis by activation genes Widespread actions significant side effects Nuclear Receptors Form interface between hydrophobic hormones and genes Will determine which genes activated by hydrophobic hormones Variations in gene activation in different cells basis for side effects NeuralEndocrine Comparisons Neurons coordinate rapid precise brief responses Electrical activity covers most distance NT diffusion distance small Takes tens of milliseconds Hormones control long duration activity slower responses More complex reactions long duration binding of hormones Takes tens of minutes Lecture 10 Central Nervous System Organization the CNS is the brain and spinal cord The peripheral NS is the nerves that carry information into and out of the CNS Afferent Neurons Afferent carry information into the CNS Both conscious and unconscious information is carried Efferent Neurons Carry information from the CNS to the body pronounced EEEfurent Somatic NS neurons activate the skeletal muscles The Autonomic NS supplies neural input Sympathetic and parasympathetic to most organs The parasympathetic NS oversees daytoday homeostasis The sympathetic NS responds to emergencies nterneurons In the CNS more than 99 of all neurons Perform all the neural functions of the CNS Thinking emotions memory etc Glial Cells nonneural support cells in the CNS capable of mitosis have cancer potential support cells that help carry out neural functions Astrocytes star shaped hold neurons in proper physical position Control neural growth and blood vessel growth in the brain Repair brain injuries from scar tissue Degrade neurotransmitters Oligodendrocytes Form myelin sheaths around axons limit neural growth in CNS Language control connection of sounds and symbols with objects Broca s Area In frontal lobe speech formation Deficit difficult to form words Wernicke s Area In temporal lobe comprehension ofauditoryvisual info Deficit can form sounds but contain no content Don t know what you re saying


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