Physio Reinforce Concepts Pt10 PDF
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Dr. Kiran C. Patel College of Osteopathic Medicine
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Summary
This document covers various concepts in physiology, including action potentials, types of transport, water volumes, the autonomic nervous system (ANS) and its applications, and skeletal muscle. It provides a detailed explanation of these biological processes.
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Action Potentials Neurons live at their resting membrane potential, which is maintained by the Na+/K+ ATPase(3Na out, 2K in) When a neuron is stimulated to the point it reaches threshold, Na channels open -> Na influx and depolarization occurs. Depolarization is ALL OR NOTHING. Action Potentials trav...
Action Potentials Neurons live at their resting membrane potential, which is maintained by the Na+/K+ ATPase(3Na out, 2K in) When a neuron is stimulated to the point it reaches threshold, Na channels open -> Na influx and depolarization occurs. Depolarization is ALL OR NOTHING. Action Potentials travel via active propagation. There is constant velocity, and constant amplitude(the signal is as strong at the end of the tract as it is at the start). In repolarization positively charged K leaves the cell, bringing membrane potential back towards normal resting, more K+ exits than needed, causing afterhyperpolarization Timed summation: one neuron sending small stimulatory signals in rapid succession, to the point the postsynaptic neuron reaches threshold Spatial Summation: Multiple neurons sending small stimulatory signals to one postsynaptic neuron, bringing it to threshold If all channels have their inactivation gates closed, there is no possibility for an action potential, this is the absolute refractory period. If some channels have their inactivation gate close, while others have it open, an action potential could potentially be sent. This is the relative refractory period, and there is a higher likelihood of reaching threshold if more Na channels have their inactivation gates open. Types of transport Passive: diffusion which can be simple(without help) or facilitated(with help of a carrier protein/channel). Passive transport is solute moving from high concentration to low concentration, requiring NO ENERGY Active transport can be primary or secondary, but always low concentration to high concentration ● ● Primary active: ATP is directly broken down to bring molecules against their gradient(Na+/K+ ATPase) Secondary active: Utilizes the ion gradient made by an ATPase, pairing the transport of one molecule down its gradient with the transport of another molecule against its gradient (Na+/Glucose symporter) Diffusion is mediated by multiple factors: Membrane thickness, Membrane area, Fick’s Law: Membrane permeability x Concentration gradient, Size and Polarity of the molecule ● A small, nonpolar molecule with a large concentration gradient will diffuse across a large thin membrane the fastest Types of transport proteins: Membrane Pores, Gated Ion Channels, Carriers, Pumps and ATPases for primary active transport, Symporters and Antiporters for secondary active transport Water Volumes 60-40-20 Rule: 60% of total body weight is water(50% in women) 40% of total body weight is intracellular water 20% of total body weight is extracellular water ● 25 % of extracellular fluid is plasma, the other 75% is interstitium Isotonic: intracellular and extracellular osmolarities match Hypertonic: high extracellular osmolarity, water efflux from the cell causing it to lose volume and shrivel Hypotonic: low extracellular osmolarity, water influx into cell causing swelling and potential lysis Approach to volume shift problems: The question will alter the Extracellular fluid(either volume, osmolarity or both) and we have to determine how it affects the ICF Osmotic pressure is the pulling force solutes have on water, and water flows either intracellularly or extracellularly until osmolarities are balanced ANS Receptors Remember parasympathetic and sympathetic have reciprocal, antagonistic functions. CNS increases one and simultaneously decreases the other ANS Applications ANS on arterioles Sympathetic dominates the input on blood vessels, with a combination of Alpha1 and Beta2 receptors Beta2 has higher affinity for EPI, at low circulating EPI levels B2 causes vasodilation of vessels to skeletal muscle(increases flow to muscles we use when running from tiger) Alpha1 responds to NorEpi and high concentration EPI, A1 causes vasoconstriction (lowering blood flow to muscles not in use when running from tiger) ANS on skin- vessels with only alpha1 Vasodilation in cutaneous tissue during exercise is due to lack of sympathetic input Vasodilation engorges Arterio-venous shunts, helps reduce temperature Skeletal Muscle The functional unit of skeletal muscle is the sarcomere, which contracts z line to z line. Nerves input onto skeletal muscle, and their synapse is the Neuromuscular junction(NMJ) Excitation-contraction steps: 1. 2. 3. 4. 5. 6. 7. Ach released from motor neuron binds Nm receptor, Na influx depolarizes the membrane Membrane depolarization travels down the T tubules, induces conformation change in calcium releasing dihydropyridine receptors (DHPR) DHPRs couple to ryanodine receptors type 1 (RYR1) on the sarcoplasmic reticulum(SR), calcium is released into cell Calcium binds troponin c(TnC), induces confirmation changes in TnT, and TnI, freeing tropomyosin from its attachment to actin As tropomyosin disassociates from actin, myosin binding sites are exposed on actin Myosin walks along actin via the cross bridging cycle a. ATP binds myosin(this atp-myosin complex has low affinity for actin) this is muscle relaxation b. ATP hydrolysis(adp-pi-myosin complex undergoes a confirmation change to extend myosin neck) c. ADP-Pi-Myosin binds actin weakly d. Pi ejection(ADP-myosin has strong affinity to actin) e. Powerstroke, flexing of the myosin neck slides the filaments along one another f. ADP releases, filaments do not relax until another ATP binds Reuptake of Calcium back into the SR by the SERCA pump, minimal Calcium loss by cell via Ca-ATPase or Na-Ca exchanger Myasthenia Gravis: autoimmune disorder where antibodies bind Ach receptors at NMJ,Repetitive stimulation decreases strength Lambert Eaton: autoimmune disorder where antibodies bind Ca2+ channels on motor neuron terminal. No calcium influx results in no Ach release into NMJ. stronger with repetitive motor neuron stimulation Muscle Contraction and Motor Units Motor unit: All the muscle fibers innervated by a single neuron. Varying number of muscle fibers per neuron, motor units with a small amount of fibers are intended for precise, fine motion, large motor units are for power. Small motor units are recruited first If muscle tension>stress resistance, this is concentric contraction(muscle is tense, and shortening) If muscle tension<stress resistance, this is eccentric contraction(muscle is tense, and lengthening) If muscle tension=stress resistance, this is isometric contraction(muscle is tense, but not changing length) Muscle spindles live in the belly of a muscle, and are stretch receptors that respond to rapid lengthening of muscle, send this information to CNS where the efferent response is a muscle contraction. Rapid lengthening can strain a muscle, the muscle spindle initiates the contractile reflex to protect against injury. Golgi tendon organs are mechanoreceptors in the tendon of a muscle. They send the CNS information regarding the tensile load being applied to the tendon. If muscle tension is too high, to the point the muscle attachment could be injured, the GTO signals to relax the muscle and prevent injury. Type 1: slow twitch, OXIDATIVE PHOSPHORYLATION, high mitochondria, high blood supply(red fibers), hard to fatigue ex. Marathon, erector spinae Type 2a: fast twitch, intermediate oxidative phosphorylation, medium blood supply(pink), 1 minute-30 minutes of contraction potential ex. Crossfit Type 2b: fast twitch, GLYCOLYSIS, low blood supply(white fibers), low mitochondria, high power output, easy to fatigue, 1 minute or less ex. 100m dash