Pathophysiology Test 2 Notes
Pathophysiology Test 2 Notes BIOL 3123
Popular in Pathophysiology
Popular in Biology
This 27 page Class Notes was uploaded by Hope Gulley on Sunday August 16, 2015. The Class Notes belongs to BIOL 3123 at Auburn University taught by Dr. Davonya Person in Spring 2015. Since its upload, it has received 61 views. For similar materials see Pathophysiology in Biology at Auburn University.
Reviews for Pathophysiology Test 2 Notes
Report this Material
What is Karma?
Karma is the currency of StudySoup.
You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!
Date Created: 08/16/15
E Closer Look at Neurotransmitters synthesis of Ach Epi and Norepi 1 Ach a synthesized in axon terminal cytoplasm of cholinergic fibers b stored in synaptic vesicles c after use broken down into acetate and choline by acetvlcholinesterase Achase a don t want to destroy want to recycle 2 Epinephrine and Norepinephrine a synthesis begins in axonal terminal cytoplasm of adrenergic fibers b dopamine is then stored inside synaptic vesicles i within vesicles there is further modification ii within 20 of the vesicles c in the adrenal medulla steps are the same EXCEPT 80 of the vesicles produce epinephrine d ie e epinephrine and norepinephrine are removed in the following ways i reuptake and recycling in adrenergic axonal terminals for NT released from actual neuron ii diffusion and dilution into surrounding body uids iii destruction by enzymes from postganglionic fiberin axon terminals monoamine oxidase from bloodstream in tissues catecholomethvl transferase F Pharmacology 1 Cholinergic Drugs cholinergic receptor a parasympathomimetics i only work at the level muscarinic receptor agonists only place where these are located are on effector organs ii induce a parasympathetic visceral response iii ex Pilocarpine a used to treat dryness of mouth increases saliva production in salivary glands b works with M3 receptor on our salivary glands c because its mechanism of action is to stimulate muscarinic receptor can have stimulation of any muscarinic receptor d could be used to slow the HR b acetylcholinesterase inhibitors i General mechanism is to enhance response to Ach by preventing its breakdown ii Ach half life is extended and it will be around longer so receptor can be more vigorously stimulated iii Don t bind to receptors iv Prevent chemical breakdown of Ach no interaction with receptor v Neither agonist or antagonists because they aren t binding to a receptor vi ex Neostigmine works at the NMJ a tx for Myasthenia Gravis an autoimmune disease whereby the body destroys a portion of the N2 receptors on skeletal muscle Fewer N2 muscle contraction is less efficient Increase Ach remaining receptors are stimulated more often to alleviate symptoms Enhance function of N1 N2 M1 M2 M3 receptors stimulates any cholinergic receptor Any cholinergic receptor is going to have a greater response NOT BINDING TO THESE RECEPTORS THOUGH preventing Achesterase from breaking down Ach c anticholinergics i cholinergic receptor antagonists bind to receptors but block their functioning ii ex Atropine selective muscarinic receptor antagonist gt ulcer tx decreases GI tract glandular secretion 0 especially hydrochloric acid production from chief cells 0 M3 receptor blocked gt allergy tx decreases activity of mucous glands at bronchioles 0 M3 receptor being blocked gt preoperative medication decreases salivary gland activity 0 M3 blocked gt GENERAL MECHANISM OF ACTION OF ATROPINE BLOCK MUSCARINIC RECEPTOR gt Based on mechanism of action atropine could be used to increase HR blocks parasympathetic response increase HR 0 Parasympathetic would normally decrease HR iii ex Scopalamine selective muscarinic receptor antagonist gt Tx for motion sickness blocks action of Ach at vestibulocerebellum preventing signals from being sent to emetic re ex emesisvomiting center in hypothalamus 0 M1 receptor stimulated M1 receptors in nervous system 0 Based on mechanism of action scopolamine could be used to treat an ulcer iv ex dtubocurare DTC selectively blocks N2 receptor antagonist gt potent muscle relaxant gt skeletal muscle gt won t be used to treat an ulcer because that would need to stimulated an M3 receptor gt MECHANISM OF ACTION SELECTIVELY BLOCK N2 RECEPTOR Adrenergic Drugs epinephrine and norepinephrine sympathetic NS weep a sympathomimetics i adrenergic receptor agonists ii induce sympathetic response iii Two types a direct acting directly bind to and stimulate adrenergic receptors 0 ex Yutopar selective beta2 receptor agonist I can t stimulate B1 receptor 0 tx in high risk pregnancies to prevent premature labor decreases contractility of uterine smooth muscle 0 Beta 2 cause relaxation of smooth muscle 0 Based on mech Of action yutopar can stimulate any beta 2 0 ex Neosynephrine selective alphal receptor agonist 0 based on mech Of action can stimulate any Alpha 1 receptor 0 tx for congestion causes vasoconstriction of blood vessels serving nasal mucous glands decreases blood ow and therefore glandular activity 0 alpha 1 aren t directly on gland O constrict blood ow decrease in Whatever gland happens to secrete b indirect acting acts at axonal terminals of adrenergic postganglionic fibers to induce exocytosis of epinephrine and norepinephrine i don t directly bind 0 ex Ephedrine not selective 0 tx for hypotension stimulation of betal receptors increases HR which yields an increase in CO and an increase in BP 0 can be used as Central Nervous System stimulant via stimulation of alpha2 I ex stimulate reticular formations O can be used as bronchodilator via stimulation of beta2 smooth muscle surrounding bronchioles increases blood ow 0 appetite suppressant via stimulation of beta2 in satiety center of hypothalamus b svmpatholvtics 1 adrenergic receptor antagonists they bind to Whatever receptor they are specific for and block sympathetic response ii ex Priscoline selective alphal receptor antagonist gt tx for pulmonary hypertension induces vasodilation of pulmonary blood vessels 0 stimulate it vasoconstriction block it vasodilation iii ex Propranolol selective betal and beta2 antagonist BOTH gt tx for hypertension used to decrease heart rate and therefore CO and BP 0 Beta 1 receptor gt tx for migraines decreases vasodilation of blood vessels in pia mater 0 decrease relaxation of smooth muscle if you block it less vasodilation less relaxation 0 increase in blood ow due to extreme vasodilation V Introduction to the Nervous System A Characteristics 1 one of the two main control systems a endocrine is the other using hormones gt takes longer to go into affect 2 communication is via electrical signals a action potentials electrical signals 3 this system performs 3 general functions a receives stimuli from sensory receptors associated with sensory neurons via an afferent pathway heads to the brain CNS b processes sensory input via intemeurons and decides on an appropriate response 99 c sends information regarding response to effector organs muscles skeletal cardiac smooth glands through motor neurons via an efferent pathway picture on board B Organization of the Nervous System 1 Central Nervous Svstem CNS a includes the brain and spinal cord ONLY not the nerves b CNS is an integrating center same thing as analysis have an organized motor response 2 Peripheral Nervous Svstem PNS a neural tissue outside CNS ie cranial and spinal nerves 12 cranial all originate in CNS but have to reach out to all the different tissues gt even if it is extending just a little bit or extending a lot it s a nerve and is part of the PNS b relays input to CNS and relays output to effector organs gt sensory neurons afferent pathwav part of PNS gt motor neurons effector part of PNS c divisions gt Afferent Division 0 Sensory 0 Not further divided gt Efferent Division 0 Motor 0 Divided into two more branches I Somatic I Concerned with only skeletal muscle I Autonomic I Concerned with cardiac muscle and glands 0 Divided into two more branches 0 Sympathetic I Always does what is in the best interest of a fight or ight response I Increases HR C Cell types 1 Neurons I Decreases digestive function 0 Parasympathetic I rest and digest function I Decrease HR I Increases digestive function a functional cell of the NS b brain alone has 100 billion c initiates APs OR generate APs d propagates APs propagate reproduce and spread all down the neuron to get it to the end of the axon and so the neuron can communicate with others continuous APs generated down the axon not just one AP e releases neurotransmittersneurohormones that carry messages to postsynaptic structures neuron muscle gland f anatomy picture on board gt AP generated down axon remains the same strength The terminals release the same strength AP Soma cell body contains nucleus and all other organelles Dendrites receive incoming signals via surface receptors known as the input zones because of receiving function Axon Hillock on axon Initiates the AP by adding together the incoming stimuli Because of this function the hillock is known as the trigger zone Axon also called the nerve fiber This is where the AP is propagated Starts at axon hillock and is carried all the way down Because of this function the axon is known as the conducting zone Axon Collateral branches of the distal end of the axon Axon terminals ends of axon collaterals Release neurotransmitterneurohormone to other cells Because of function the axon terminals are known as the output zone Allows neuron to send the signal along to other cells by releasing chemicals Myelin Sheath lipid insulator Function is to speed the conduction of AP More myelinthe faster that AP will be spread from hillock to terminalsthe faster the chemicals will be transmitted to other cells More myelin the more axon the AP can skip gt Nodes of Ranvier bare axonal spaces between the myelin Allows for salutatory salterto jump conduction g collection of cell bodies within CNS m gt not related to the nucleus h collection of cell bodies outside of CNS ie in PNS W gt we can have cells that are not related to brain or spine i the larger the axon diameter gt the more stimulation needed to reach threshold from rest gt the faster the speed of AP conduction gt the smaller the axon diameter the less stimulation and the slower the speed of conduction because there is less resistance to the ow of electricity j classi cation of fibers based on degree of myelination and diameter gt A FIBERS Further divided into Alpha Beta Gamma and Delta fibers order of conductivity fastest 9 slowest 1 Even the ADelta fiber is faster than B or C fibers AFibers are the fastest conductors 1 Means that these fibers are heavily myelinated 2 Diameter is large faster it is able to spread action potential gt B FIBERS Intermediate conduction Moderately myelinated Medium diameter A Delta is faster than a B Fiber has more myelin gt C FIBERS Slowest conductors Unmyelinated but some do have myelin but are lightly myelinated small diameter k two types of neuronal communication gt Excitatory response of postsynaptic structure Post svnaptic structure A structure that comes after the synapse space that exists between the 2 structures Hypopolarization 1 We want the membrane to become more positive this is done by the cell becoming less negative gt 1 neuronal structural types gt gt gt E a Moving sodium down it s concentration gradient INTO cell in ux b OR CALCIUM in ux on the dendrite c Via Ion channel linked receptors In ux results in Intracellular positivity Membrane moving closer to threshold Excitability of the membrane more likely or less likely to generate an AP Bringing a membrane closer to threshold creating intracellular positivity is going to make it hyperexcitable membranemore likely to generate AP a ONLY IN MEMBRANE NOT WHOLE CELL Inhibitog response of postsynaptic structure NHNT that bound to that specific dendrite is going to send inhibitory response Hyperpolarization 1 Not the one that is in AP 2 Means becoming more negative than the membrane is at rest more separation of charges 3 What causes hyperpolarization a Potassium ef ux out of cell b Chloride ion Cl in ux 4 Intracellular negativity 5 Signal indicates moving further from threshold 6 Less likely to generate AP 7 Hypoexcitable membrane EPSP Excitatory Post Synaptic Potential associate with excitatory response IPSP Inhibitory Post Synaptic Potential associate with inhibitory response multipolar many dendrites and one axon most abundant type motor neurons efferent signals and intemeurons confined completely to CNS bipolar 1 axon and 1 dendrite coming from the cell body rarest type olfactory mucosa nose and m of the eye senso neurons 1 dendrite can branch but initially comes from 1 dendrite unipolar one axon from the cell body that branches into 2 processes 1 Central Process that goes to the CNS carrying out motor information 2 Peripheral Process which has receptive endings that extend to the periphery how you get sensory neuron coming into cell afferent information coming into cell most sensory neurons 2 processes peripheral process sensory endings afferent going in ECMS going to nervous system B MIDBRAIN 1 Mesencephalon a corpora quadrigemina gt 4 body gt Four raised hillocks on the superior aspect of the brain stem Superior Colliculi visual re ex center you see something out of the comer of your eye and automatically turn and look at it Inferior Colliculi auditory re ex center you hear something and automatically turn to see what it was C HINDBRAIN 1 Composed of 2 parts Metencephalon amp myencephalon 2 Metencephalon 2 parts cerebellum and pons a w gt 2 largest portion of the brain wavy bumpy section gt arbor vetae gt 3 functional areas Vestibulocerebellum i In charge of Maintenance of balance and control of eye movement Spinocerebellum i Coordination of skilled voluntary movements 1 Piano playing 2 Intricateprecise types of movements ii Ensuring accurate timing of various motormuscle functions or activity 1 Coordination of arms and legs working in harmony synergy iii Aids in proprioception iv Works with the parietal lobe for proprioception Cerebrocerebellum i Provides input to the motor cortex in cerebral cortx 1 Cerbreal cortex Motor cortex amp sensory cortex 2 Motor frontal lobe 3 Sensory parietal lobe b ons gt conduction pathway for impulses traveling between the brain and spinal cord because anything that goes to and from the brain has to go through the spinal cord 3 Myelencephalon medulla oblongata MO a MO gt control of respiration houses the Dorsal Respiratory Group and the Ventral Respiratory Group i centers are in control of inhalation and exhalation patterns gt control of cardiovascular function Two houses vagal and vasomotor center i these control HR amp blood pressure negative feedback mechanism control of BP gt modification of GI tract function involves secretion of digestive enzymes mucous uids etc and motility of food from one organ to the next i SI to LI Stomach to SI etc D Reticular formation 1 A network of nuclei scattered throughout the brain reticular formation is not in one specific area 2 Maintains a state of awareness and mental arousal keeping you mentally alert and aware of what is going on a Not unconscious vs conscious 3 Functioning greatly impaired by many classes of drugs alcohol narcotics general anesthetics E Limbic System 1 Ring of neural tissue running through the thalamus hypothalamus and cerebrum 2 Main function is the control of emotional behavior a Functionally connected with the hypothalamus therefore Limbic System output can have autonomic manifestations physical changes changes in body temperature appetite GI tract movements heart rate hormonal pulses affect female cycle or a man s seX drive etc 3 Target tissue of antipsychotic and antidepressant drugs most are going to have to do with reuptake or recycling of NTN T that control emotional behavior a Serotonin NT that s associated with emotional behavior that can be affected by antidepressant or antipsychotic F Spinal Cord 1 Functional Anatomy White matter axons coming out myelin is lipid like so it makes it white Grey matter clusters of cell bodies a Dorsal Root gt bring bers of sensoryafferent mostly unipolar neurons to the CNS b Dorsal Root Ganglion gt cluster of unipolar neuron cell bodies c Dorsal Horn gt contains cell bodies on interneurons function in integration what is the sensory information how many different places does it need to go and what area of the brain does it need to communicate with Remember that intemeurons are confined to CNS i Axon and Soma only in spinal cord or going to the brain d m gt contains cell bodies of autonomic efferentmotor neurons serve viscera gt autonomic bers carried out to effector organ cardiac muscle smooth muscle or glands e Ventral Horn gt contains cell bodies of somatic efferentmotor fibers serve skeletal muscle f Ventral Root gt motorefferent fibers from Lateral and Ventral horns exit the spinal cord here going to effectors gt going to carry info to cardiac muscle smooth muscle skeletal muscle and glands gt path to get to PNS G CNS Pathways 1 Ascending Pathways sensory information entering dorsal root of spinal cord BRINGING TO CNS a Dorsal Column Svstem gt involved in touch sensations requiring precise localization and extreme distinctions in intensity This means that whatever stimulus has come in you know exactly what part of body has been stimulated and how strong vigorous that stimulus is gt very fast transmission gt large diameter A fibers gt A alpha and A beta fibers b Spinothalamic Pathway gt Pain reception thalamus thermal sensations crude touch not knowing what part of body was stimulated pressure gt Thalamus gt Slow type C bers c Spinocerebellar Pathwav gt Primarily propicoception gt Part of brain affected parietal lobe and spinal cerebellum 2 Integrative Pathways process afferent information from different areas and determines efferent output WITHIN CNS a Cortico pontile cerebellar gt informs cerebellum of intended muscle movement to cause smooth and coordinated movement b Dentata thalamocortical gt Smoothes out communication between cerebellum and motor cortex and to the right degree 3 Descending Pathways motor information leaving the ventral root of spinal cord CARRYING INFO FROM CNS TO EFFECTORS a PM gt Responsible for rapid and fine muscle movement from the cortex gt Fibers cross over in the medulla Fibers from right side go to left and vice cerse Control is contralateral b Extrapyramidal gt Functioning is the same gt Responsible for rapid and fine muscle movements from the corteX gt Same function as Pyramidal but control is ipsilateral not contralateral Do not cross over left side goes to left right goes to right side of body 0 Min 31 gt Ensures motor movements are as intended from corteX Want to move right arm make sure right arm moves H Protection of the CNS 1 Meninges a fibrous coverings around the brain and spinal cord b Three gt Dura Mater OUTERMOST Outermost first mode of contact Made of dense fibrous connective tissue Continuous with the periosteum of the cranium and vertebral column Periosteum outer connective tissue membrane of bone i Peri outside surrounding ii End inside gt Arachnoid Mater Middle layer Subarachnoid space i Passageway for ow of cerebral spinal uid ii Has arachnoid villi extensions of tissue that help to absorb CSF for recvcling bc CSF is not constantly made 1 Ependymal uid gt Pia Mater Innermost layer Made of very thin connective tissue Adheres to Peaks and valleys GNS Socci and Gyri Highly vascularized i Lots of blood vessels ii Helps to supply nutrients to ependymal cells that are in brain cavity ff 7 a g 1 i quotma rq l ark Hl r uf l il Lilli 51 391 xiiiquot 1 r I Eryn L x r39 339 Iquot F quotI quot I l l t A Foramen of Monroe a Connects the 157211d ventricle to the 3rd B Aqueducts of SylviusSylvi a Connects the 3rd ventricle to the 4th C Foramen of Magendie a Connects the 4th ventricle to the central canal of the spinal cord SC D Foramen of Luschka a Connects the 4th ventricle to the subarachnoid space 2 Cerebral Spinal Fluid CSF see fig 55 pg 138 and 56 pg 140 a not tested on overall figure b shock absorber for CNS c produced by extensions of pia mater called choroid plexuses d uid travels through four brain cavities called ventricles gt lined by ependymal cells gt connected by channelsaqueducts 3 Blood Brain Barrier Read page 140143 A highly selective blood brain barrier H CNS Pathologies 1 Epilepsy a disruption of the brain s internal electrical balance b Etiology development of a focus discrete area of hyperexcitable closer to threshold neurons due to brain damage at birth metabolic disorders tumors infectious disease most cases are idiopathic A don t know why c stimulation started because of hyperexcitable neurons shouldn t be signaled in the first place d unregulated electrical activity started by the focus quickly spreads to surrounding cells and can result in a seizure usually selflimiting stimulation and response of inhibitory neurons stops hyperexcitable focus from firing ending seizure e Treatment TX surgery tumor 2 Meningitis a b Dilantin hyperpolarizes focal neurons by increasing Na ef uX andor increasing GABA release A B Bringing the neurons further away from threshold to stop them form ring Increase working of NaK pump gt Kick Na out of cell Increase GABA release inhibitory NT keeps hyperexcitable neurons where they need to be Does it make them tired gt NO Drug cocktail keeps them normally functioning In ammation of the pia and arachnoid mater 2 meninges Etiology Bacterial viral Caused by Streptococcus pneumonie or Neisseria meningitides Bacteria replicate and lyse in CSF releasing endotoxins The immune system responds by endotoxins via an in ammatory response Steps of response that make bacterial meningitis so severe a Neutrophils type of white blood cells bind to and damage endothelial cells specialized epithelial cell of CV system making up Blood Brain Barrier protects neurons and neural tissue from everything that is circulating in peripheral blood vessels trying to get to endotoxins b Allows the entry of pathogens blood cells and albumin into CSF i All of these extra things entering the CSF auses CSF to thicken amp meninges to swell c Swollen tissue can press on cranial nerves which nerves depends on which meninges are swollen causing damage amp can also block arachnoid villi from absorbingrecycling CSF gt signssymptoms feverchills headache stiff neck nauseavomiting photophobia light gt findings increase in neutrophils positive bacterial culture increased albumin in CSF gt Tx antibiotics kill bacteria decrease endotoxins corticosteroids anti in ammatory drugs bring down in ammation V VV V gt very similar to bacterial but less severe gt usually caused by common intestinal viruses eX Enterovirus via direct or indirect contact with fecal matter gt signssymptoms similar to bacterial when present gt findings increase in T lymphocytes WBC specific for increasing in number in viral infection NO increase in albumin in CSF no neutrophils gt Tx none can t kill a virus it s already dead a Less severe because less damage to nervous tissue 3 Hydrocephalus a abnormal increase in CSF within the ventricular spaces of the brain b etiology noncommunicating gt obstruction in ventricular system prevents CSF from reaching arachnoid villi gt CSF is not communicating with villi because it can t reach it tumor in ammation communicating gt CSF reaches villi but villi are not affective with reabsorption abilities are impaired too few villi formed during fetal development post infective scarring of villi c symptomssigns prominent forehead distended scalp veins mental deterioration convulsions d Tx shunting procedures to provide alternate route for return of CSF to venous system if there is a blockage direct CSF to right vein 4 Alzheimer s a Reading assignment pages 164167 Concentrate on Underlying Pathology 5 Multiple Sclerosis a demyelinating disease of the CNS b etiology immunemediated in ammatory response autoimmune disease c cells of immune system recognize myelin as being form 1 could be from past diagnosis of shingles or herpes d causes formation of sclerotic plaques scar tissue throughout the white matter axons coming from cell bodies lying in gray matter results in decreased conduction of electrical impulses andor complete conduction blocks depends on how severe the destruction of the myelin is A axon hillock to axon terminal B Nodes of Ranvier d Signssymptoms Decreased visual field eye sight first sign PT will recognize Difficulty with speech Difficulty in swallowing decreased muscle strength Decrease in balance and coordination happens later on down the road Fatigue is the 2nd most common problem to be combined with eye sight e Tx antiin ammatory agents both taken in cocktails Interferon Beta helps immune system recognize selfcells Can try to prevent further damage Cyclosporine is an immunosuppressive drug suppress immune system as a whole NO CURE PROGRESSIVE DISEASE degree can vary greatly can be in a wheelchair can die can go into remission 2 Neuroglia a support cells of the NS do NOT produce or conduct Action Potentials b completely in charge of taking care of the neurons c 5 types gt VI Central Nervous System A FOREBRAIN Astrocytes most abundant guides neuronal placement during fetal development tells neurons where to go located close to capillaries to assist in nutrient transfer to neurons absorbs excess K in ECF surrounding neurons 0 by absorbing excess K in ECF helps maintain RMP 0 would alter how excitable cell is helps form neural scar tissue 0 process called Gliosis 0 neurons can t be regenerated so make scar tissue helps form Blood Brain Barrier 0 BBBspecial system of capillaries that keeps certain things from coming into contact with our CNS and neurons Oligodendrocytes wrap around neuronal axons in the CNS to form myelin sheath SALTATORY CONDUCTION Microglia phagocytic cells that clean up cellular debris after cell damage infection or cell death phagocytosiscell eating 0 Engulf another cell and has special enzymes to break down Ependymal Cells line cavities of brain and spinal cord contribute to cerebral spinal uid production have cilia that help distribute CSF 0 cilia hair like particles from the plasma membrane that wave back and forth to propel things towards other things Schwann Cells wrap around neuronal axons in the PNS to form myelin sheath do the same thing as oligodendrocytes 1 Telencephalon composed of the cerebral cortex corpus callosum a cerebral cortex cerebrum gt gt gt largest portion 80 of brain mass diVided into left and right hemispheres comprised of 4 lobes each with a distinct set of functions FRONTAL LOBE 0 Analysis and control of motor output 0 Efferent signals being sent from this area of the brain 0 Control is called contralateral control of motor output from one side to another left cerebral hemisphere controls right side of body and vice versa 0 Speaking ability controlled here PARIETAL LOBE 0 Analysis of sensory input contralateral 0 Responsible for determining location and intensity of stimuli I What part of body it is coming from and how vigorous that stimuli is 0 Aids in Proprioception Awareness of the body s position in space allows for a certain amount of coordination TEMPORAL LOBE 0 Hearing 0 Receives and processes auditory stimulus 0 Aids in speech organization 0 Responsible for storage of short term information I Some needs to be converted to long term memory 0 Conversion of short term to long term memory OCCIPITAL LOBE 0 Receives and processes vision info I Why severe injury to back of head can affect your sight b corpus callosum gt gt gt neural pathway that connects L and R hemispheres for functional integration in the middle of the cerebral hemisphere halfmoon shape contralateral control way for info from one side to get to the other side 2 Diencephalon includes the thalamus and hypothalamus a thalamus gt V VVVV sends incoming sensoryafferent signals to the proper brain area seen signals sent to occipital heard signals sent to temporal lobe if necessary amplifies information integrates emotional behavior actions representative of what emotions you feel receptive area for pain 0 nociceptors b hypothalamus gt collection of nuclei cell bodies in the CNS that act to integrate and control several physiologic parameters control monitoring of uids and electrolytes Via osmoreceptors control of temperature I sweat shiver initiated here control of food intake and satiety 39 Beta 2 receptors amphetamines Endocrine control of the anterior and posterior secretory activity VII Peripheral Nervous System Efferent A Comprised of 1 Somatic Nervous Systemmotor neurons that innervate skeletal muscle 2 Autonomic Nervous System concerns our viscera motor neurons that innervate smooth muscle cardiac muscle and glands viscera controlled autonomically a Sympathetic Nervous System gt Concerned With energetic functions things that expend energy increase in HR and decrease in digestive functions gt fight or ight b Parasympathetic Nervous System gt Concerned With vegetative functions decrease in HR increase in digestive functions gt Rest and digest B Diagrams 1 Somatic Nervous System 2 Autonomic Nervous System 2 neuron chain a Parasympathetic Division a Long preganglionic in sacral region of SC i Origin 1 Oculomotor III 2 Facial VII 3 Glossopharyngeal IX 4 VagusX b Short Postganglionic i Origin 1 Terminal ganglia close to or in the effector organ C Cholinergic Stimulation Parasympathetic 1 Cholinergic Fibers a Ach releasing gt all somatic motor neurons gt all autonomic preganglionic neurons gt all parasympathetic postganglionic neurons b Ach released from somatic motor neurons and WW ALWAYS has an excitatory effect on target tissues c Ach released from parasympathetic postganglionic fibers can have an excitatory or inhibitory effect depending on the target tissue 2 Cholinergic Receptors CholinergicNicotinicN2 general to specific a Stimulated by ACh b Two subtypes gt Nicotinic N 0 At autonomic ganglia on the cell bodies on postganglionic fibers in both sympathetic And parasympathetic 39 N1 0 When stimulated ALWAYS causes the release of NT from postganglionic ber 0 At neuromuscular junction NMJ skeletal tissue N2 receptor I Stimulation always causes depolarization of skeletal tissue 0 Heart or skeletal muscle 0 Both are excitatory effects gt Muscarinic M 0 On viscera 0 On cardiac and smooth muscle and glands I M1 receptors 0 On neural tissue I M3 receptors 0 Pupil constriction via contraction of iris circular muscle M3 receptors 0 Increases secretory activity of glands 0 Increases motility of gut smooth muscle 0 Constriction of bronchial smooth muscle 0 Decrease in air ow I M2 receptors 0 Decrease in heart rate 0 Innervate erectile tissue vasodilation of blood vessels erection in both male penis and female clitoris I Increase blood ow D Sympathetic Division a Short Preganglionic fiber i Origin 1 Lateral horn of SC a Specifically T1L2 thoracolumbar region b Long Postganglionic fiber i Origin 1 Sympathetic ganglion chain a Close to SC 2 Collateral ganglion a Halfway between spinal cord and effector organ E Adrenergic Stimulation Sympathetic 1 Adrenergic fibers a Release epinephrine and norepinephrine gt Sympathetic postganglionic fibers b Neurotransmitters can have an excitatory or inhibitory effect on the target tissue 2 Adrenergic receptors a Stimulated by epinephrine and norepinephrine b On cardiac muscle smooth muscle and glands c 4 Classes gt Alpha 1 symbol used x O Stimulation of alpha 1 causes contraction of smooth muscle 0 Smooth muscle locations I Sphincters in GI tract I Inhibits forward movement of food I Blood Vessel walls specifically serving viscera I Decrease blood ow I Slows down digestive activity I Radial Muscle of the Iris I Causes pupil dilation I Accessory sex glands in male I Organs that produce semen I With stimulation causes ejaculation gt Alpha 2 0 Once epi and norepinephrine attach Block postganglionic parasympathetic fiber from releasing ACh I In GI Tract I Blocks release of Ach from parasympathetic postganglionic fibers I Decreases contractilitymotility of gut smooth muscle I Inhibits parasympathetic response and inhibit forward movement of food I Inhibits insulin release from pancreas gt Beta1symbol used B 0 Mostly on the heart I Increase in HR 0 Adipose tissue fat tissue I Stimulation promotes lipolysis fat breakdown I Burns fatamphetamines 0 On kidneys I Promotes release of renin hormone form kidneys that results in increase in blood volume and therefore blood pressure gt Beta 2 0 When stimulated causes smooth muscle to relax O In GI tract I Decreases contractility therefore relax the muscle I By decreasing the contractility also inhibits forwards movement of food 0 Bronchioles I Allows bronchodilation I Increases air ow I Promotes glucagon release from pancreas I Glucagon is the antagonistic hormone to insulin 0 Breaks down glycogen I Glycogen breakdown from liver I Glycogen storage form of glucose O Insulin beta cells and glucagon alpha cells comes from pancreas and goes to the liver Why glycogen is 3 Adrenal Medulla a Part of the adrenal gland a Has two parts cortex and medulla that release two different things b Has N1 receptors on the adrenal medulla Which are stimulated by Ach from sympathetic preganglionic fibers don t really have a post ganglion c This stimulation causes release of epinephrine and norepinephrine into the bloodstream systemWide sympathetic response that has been released from the adrenal medulla a The adrenal gland is not haVing a sympathetic response It s causing organs to have a sympathetic response by releasing epinephrine or norepinephrine A B C D SKELETAL MUSCLE The Sarcomere 1 functional unit smallest part of a whole thing of skeletal muscle a therefore in this case the sasrcomere is the smallest part that contracts 2 muscle contraction sarcomere shortens Fig 89 3 muscle relaxation sarcomere lengthens Fig 89 4 composed of two types of protein myofilaments CONTRACTILE PROTEINS a Actin thin filament Fig 820 i Globular actin Gactin gt pearls of necklace gt grouped to form a helical strand gt has a binding site for myosin which is covered up when the muscle is relaxed ii Tropomyosin gt wraps around Gactin to provide stability string of the pearl necklack iii Troponin gt 3 polypeptide complex TnI binds to Gactin TnT anchors tropomyosin to Gactin TnC binds Ca2 ions b Myosin thick lament Fig 85 i each molecule has two tails made of entwined polypeptide chains ii each molecule also has two heads possessing two binding sites each gt one binds actin gt one binds an ATP molecule this binding site has ATPase activity meaning it is capable of enzymatically cleaving ATP to yield the energy needed for contraction ADP Pu energy iii the heads are hinged where they join the tails allowing for the ratcheting mechanism in the contractile process Membrane System Fig 810 1 Sarcoplasmic Reticulum a network of interconnected tubules surrounding each sarcomere b regulates intracellular Ca2 levels i releases stored Ca2 from terminal cistemae also known as lateral m in order to begin contractile process 2 Transverse Tubules Ttubules a invagination of the sarcolemma muscle cell membrane b runs between the terminal cistemae forming a tria 1 Ttubule plus 2 lateral sacs c quickly transmits the action potential AP deep into the muscle cell d the action potential signals the release of Ca2 from adjacent terminal cistemae Contractile thsiologv in a Motor Unit Fig 812 a Motor Unit is a motor neuron and all the muscle fibers it innervates a AP travels down the axon of the motor neuron and causes the in ux of Ca2 into axonal terminals Ca2 induces the exocytosis of E into the neuromuscular junction 0 Ach travels across the synapse and binds N2 receptors on skeletal muscle d this causes chemicallygated Na channels to open in response to the binding of the chemical ach allowing Na in ux into the sarcolemma e an AP is initiated and travels down the Ttubules E Rigor Mortis the AP causes the release of Ca2 from the terminal cisternae the Ca2 diffuses into the sarcomere a calcium coming from lateral sac without calcium it will not contract binds to the m of troponin causing a shape change in the actin molecule which uncovers the binding site for myosin Fig 87 actin and myosin bind together and under the energy of ATP the myosin head ratchets forward a pull actin towards the center of the sarcomere steps hj Fig 813 a new ATP molecule binds and allows the detachment of actin and myosin a need ATP for ratcheting and deattachment of myosin and reattchment to the next actin the new ATP molecule is cleaved and the myosin reattaches to actin at a distal location and ratchets again steps hj repeat until the muscle has fully contracted ie the sarcomere shortens for relaxation to occur an ATPdependent Ca2 pump removes Ca2 from the sarcomere pumping it back into the lateral sacs allowing troponin and tropomyosin to recover myosin s binding site and actin and myosin to detach They remain detached until another AP is sent down the motor neuron 1 ATP production stops therefore actin and myosin cannot detach and Ca2 cannot be removed form the sarcomere The muscle is temporarily in a suspended state of contraction Hence the slang term stiff for the deceased 2 Can estimate time of death 3 Caused by normal protein breakdown F Sources of ATP for Muscle Mechanisms 1 Glycolysis a b C anaerobic respiration does not use oxygen not very efficient breaks down 1 molecule of glucose to form only 1 molecules and pyruvic acid important Glucose92 ATP pyruvic acid 2 Oxidative Phosphorylation a b 9amp9 aerobic respiration requires oxygen pyruvic acid formed in glycolysis is fed into the m cm and produces a net yield count the rst 2 from glycolysis of 36 ATP 2 from glycolysis and 34 from Krebs Cycle 36 from oxidative phosphorylation pyruvic acid is fed into Kreb s cycle which creates 34 ATP 34 ATP from Oxidative Phosphorylation So add 2 ATP from glycolysis and the 34 ATP from the Krebbs36 many ATP molecules are produced but it s a slow process due to the number of steps involved 3 Creatine PhosphatePhosphocreatine a b 0 Immediate source of ATP a high energy molecule stored in muscle tissue rst energy storehouse utilized for contraction creatine phosphate ADP 9 creatine ATP reaction takes place in the presence of creatine kinase an enzyme that transfers the phosphate group from creatine to ADP not gonna get much ATP here IX Pathologv Muscular Dvstrophv 1 k 6 Xlinked recessive disorder recessive gene for the disease is on the X chromosome affecting the gene that codes for the protein dystrophin a this protein is necessary for maintaining the integrity of muscle cell membranes b muscle cells atrophy or deteriorate without it due to the dying of cells as the disease progresses skeletal muscle becomes replaced with more and more fat and connective tissue PSEUDOHYPERTROPHY going to look like its get bigger but its not with muscle cells death eventually occurs mostly due to fibrosis excessive scar tissue formation leading to hard unyielding tissue of cardiac respiratory and smooth muscle Pseudohypertrophy and fibrosis are two different things 2 classes of the disease a Duchenne s 50 of all cases early childhood onset usually fatal during 2 decade of life b Becker s 50 onset between ages 5 and 15 usually fatal by age 50 Diagnosis a analysis of serum levels of creatine kinase damaged muscle cells loserelease this enzyme monitoring cell injury b DNA analysis showing defective gene 7 Treatment a no cure b mostly aimed at stalling deformities stretching of muscle or splinting limbs 0 great precautions taken to avoid respiratory infections
Are you sure you want to buy this material for
You're already Subscribed!
Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'