Physiology Exam 2 Learning Objectives PDF

Cardiac stuff will be on the exam but Arterial/vascular stuff will not be. There will be a little bit of the laws (Ohm’s, Starling, etc) that spills over into Exam 2 but it will show up more on Exam 3. Exam review on 07/24/2024 around 5:30, TBD. Note that there are some Module 5...

Cardiac stuff will be on the exam but Arterial/vascular stuff will not be. There will be a little bit of the laws (Ohm’s, Starling, etc) that spills over into Exam 2 but it will show up more on Exam 3. Exam review on 07/24/2024 around 5:30, TBD. Note that there are some Module 5 items (up to number 8) that we will be responsible for that are really spill-over from Module 4, see the course announcement. The Exam covers module 3, 4, and the first eight points of module 5. Emphasis from 4-5 will be on cardiac stuff more than vessel stuff. Cellular and Molecular Basis for Medical Physiology Weekly Objectives: Physiology Module 3 1. Explain the role played by soma, dendrites, axon, and initial segment in impulse generation and conduction. Soma is the cell body of a neuron and contains the nucleus. Dendrites receive signals from other neurons and transmit them towards the soma (EPSP or IPSP (Post-Synaptic Potential)). The axon carries signals away from the soma. The initial segment of the axon is where the action potential is initiated. 2. Explain the basis for the resting membrane potential of a neuron and the effect of hyperkalemia and hypokalemia on the resting potential. The resting membrane potential is based on the differential distribution of ions across the neuron’s membrane, maintained by the sodium-potassium pump (-90mV). Hyperkalemia (high potassium levels) can depolarize the resting potential, making neurons more likely to fire. Hypokalemia (low potassium levels) can hyperpolarize the resting potential, making neurons less likely to fire. 3. Explain the ionic fluxes that occur during an action potential. During an action potential, there is a rapid influx of sodium ions followed by an efflux of potassium ions. This causes a rapid change in membrane potential. Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  [Board Review Series] Linda S. Costanzo - Physiology (2018, LWW).pdf - Google Drive https://canvas.south.edu/courses/44314/files/9288662/download?download_frd=1 4. Compare and contrast how unmyelinated and myelinated neurons propagate impulses. Unmyelinated neurons propagate impulses through continuous conduction, which is slow. ○ [Board Review Series] Linda S. Costanzo - Physiology (2018, LWW).pdf - Google Drive Myelinated neurons propagate impulses through saltatory conduction, which is faster due to the action potential ‘jumping’ between nodes of Ranvier. ○ Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  5. Compare the conduction velocity and other properties of different types of sensory and motor nerve fibers. Sensory nerve fibers (afferent) carry signals from sensory receptors to the CNS. Motor nerve fibers (efferent) carry signals from the CNS to muscles or glands. Different types of fibers have different conduction velocities, diameters, and levels of myelination. See the paragraph at the end of this doc that breaks down the differences specifically and lists each of the 3 types of sensory fibers and the 5 types of motor fibers. In summary, the conduction velocity of both sensory and motor nerve fibers is largely determined by their diameter and whether they are myelinated. Larger, myelinated fibers conduct signals faster than smaller, unmyelinated fibers. The type of information transmitted also differs between sensory and motor fibers, as well as among different types of fibers within these categories. 6. Compare the functions of the various types of glia found in the nervous system. Glia are non-neuronal cells in the nervous system. Types include astrocytes (support and repair), oligodendrocytes (form myelin in the CNS), Schwann cells (form myelin in the PNS), and microglia (immune defense). 7. Identify neuropathologies related to dysfunction of myelin proteins or the loss of myelin. Neuropathologies related to myelin include multiple sclerosis (loss of myelin in the CNS) and Guillain-Barré syndrome (loss of myelin in the PNS). ○ https://canvas.south.edu/courses/44314/files/9288662/download?dow nload_frd=1 8. Describe the function of neurotrophins. Neurotrophins are a family of proteins that induce the survival, development, and function of neurons. 9. Differentiate the major classes of muscle in the body. The body has three types of muscle: skeletal (voluntary movement), cardiac (heart contraction), and smooth (involuntary movement in organs). Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  10. Describe the molecular and electrical makeup of muscle cell excitation–contraction coupling. Excitation-contraction coupling is the process where an action potential triggers a muscle cell to contract. This involves the release of calcium ions. ○ https://canvas.south.edu/courses/44314/files/9288841/download?wrap =1 11. Define elements of the sarcomere that underlie striated muscle contraction. A sarcomere is the basic unit of striated muscle tissue. It consists of overlapping thick (myosin) and thin (actin with troponin and tropomyosin) filaments. Contraction occurs when these filaments slide past each other in a process called cross-bridging. ○ Module 3: Video Lecture (Atlanta): DPT6150_G00_32_24 - Human Physiology (south.edu) 12. Differentiate the role(s) for Ca2+ in skeletal, cardiac, and smooth muscle contraction. Ca2+ plays a crucial role in the contraction of all muscle types. It binds to troponin, causing a conformational change that allows myosin to bind to actin and initiate contraction. 13. Describe the major location and functional components of a neuron-to-neuron synapse. A neuron-to-neuron synapse typically consists of a presynaptic neuron, a synaptic cleft, and a postsynaptic neuron. Neurotransmitters released from the presynaptic neuron cross the synaptic cleft and bind to receptors on the postsynaptic neuron, influencing its activity. Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  ○ 14. Contrast the ionic fluxes responsible for the fast and slow excitatory and inhibitory postsynaptic potentials. Fast excitatory and inhibitory postsynaptic potentials are mediated by ionotropic receptors and involve rapid ionic fluxes. Slow postsynaptic potentials are mediated by metabotropic receptors and involve G-protein-coupled second messenger systems. 15. Compare and contrast the terms temporal summation and spatial summation and their role in action potential generation in a postsynaptic neuron. Temporal summation is the addition of successive neural signals within a short period of time. Spatial summation is the addition of simultaneous signals from multiple neurons. Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  ○ 2.11 The Physiology of Neurons - Part 2 16. Explain postsynaptic inhibition, presynaptic inhibition, and presynaptic facilitation. Postsynaptic inhibition is when an inhibitory presynaptic neuron reduces the effect of the main excitatory neuron. Presynaptic inhibition is when an inhibitory neuron suppresses the release of a neurotransmitter from the presynaptic neuron. Presynaptic facilitation is when an excitatory neuron enhances the effect of the main excitatory neuron. ○ 2.6 Excitation-Contraction Coupling.pdf: DPT6150_G00_32_24 - Human Physiology (south.edu) 17. Identify the components of the neuromuscular junction and the sequence of events that leads to a propagated action potential in the skeletal muscle fiber. The neuromuscular junction is where a motor neuron communicates with a muscle fiber. It includes the presynaptic motor neuron, the synaptic cleft, and the postsynaptic muscle Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  fiber. An action potential in the motor neuron triggers the release of acetylcholine, which binds to receptors on the muscle fiber, leading to muscle contraction. ○ [Board Review Series] Linda S. Costanzo - Physiology (2018, LWW).pdf - Google Drive 18. Explain how autonomic neurons communicate with their effector organs at a neuroeffector junction. Autonomic neurons communicate with their effector organs via neurotransmitters. The sympathetic nervous system typically uses norepinephrine, while the parasympathetic nervous system uses acetylcholine. 19. Define denervation hypersensitivity. Denervation hypersensitivity is when a post-synaptic cell becomes more sensitive to neurotransmitters following the loss of innervation. Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  ○ https://youtu.be/TvfuKDI_Hfs via Module 3: Video Lecture (Atlanta): DPT6150_G00_32_24 - Human Physiology (south.edu) 20. Describe some pathologies associated with dysfunction at the neuromuscular junction. Myasthenia gravis and Lambert-Eaton syndrome are examples of pathologies associated with dysfunction at the neuromuscular junction. 21. List the major types of neurotransmitters and neuromodulators that are broadly characterized as small-molecule transmitters, large-molecule transmitters, and gas transmitters. Small-molecule transmitters include amino acids (like GABA and glutamate) and monoamines (like dopamine and serotonin). Large-molecule transmitters include neuropeptides like endorphins. Gas transmitters include nitric oxide. 22. Summarize the five common steps involved in the biosynthesis, release, action, and removal from the synaptic cleft of the major small-molecule and large-molecule neurotransmitters. The steps involved in neurotransmission are: synthesis of the neurotransmitter, storage in vesicles, release into the synaptic cleft, binding to postsynaptic receptors, and removal from the synaptic cleft. 23. Compare the actions initiated by binding of a neurotransmitter to an ionotropic (ligand-gated) versus metabotropic (G-protein-coupled, GPCR) receptor and identify the second messengers involved in mediating the actions of neurotransmitters that act on GPCRs. Ionotropic receptors are ligand-gated ion channels that open quickly upon neurotransmitter binding, leading to fast synaptic responses. Metabotropic receptors are G-protein-coupled receptors that initiate a cascade of intracellular events, leading to slower and longer-lasting synaptic responses. 24. Describe the major distribution of the various types of receptors that mediate the functional responses of the common neurotransmitters: amino acids (glutamate and GABA),acetylcholine, monoamines (norepinephrine, epinephrine, dopamine, and serotonin), and opioid peptides. Different neurotransmitters have different distributions of receptors. For example, GABA receptors are widespread in the brain, while dopamine receptors are more concentrated in certain areas like the striatum. 25. List receptor antagonists for each of the common neurotransmitters. Cardiac Output = Stroke Volume x Heart Rate (CO=SV HR) Frank-Starling Jv=Kf[(Pc-Pi)-(𝛑c-𝛑i)]  Receptor antagonists include drugs like naloxone (for opioid receptors), atropine (for muscarinic acetylcholine receptors), and propranolol (for beta adrenergic receptors). 26. Describe the role of nitric oxide and carbon monoxide (CO) in modulating synaptic transmission. Nitric oxide and carbon monoxide are gas neurotransmitters that can modulate synaptic transmission by acting as retrograde messengers, diffusing back to the presynaptic neuron to influence neurotransmitter release. 27. Provide examples of how neurotransmitter dysfunction contributes to some neuropathological disorders. Neurotransmitter dysfunction can contribute to disorders like Parkinson’s disease (dopamine deficiency), depression (serotonin and/or norepinephrine deficiency), and schizophrenia (dopamine hyperactivity in certain brain regions). From