Sensory Physiology Flashcards
Explain the difference between unencapsulated and encapsulated nerve endings?
The main difference between unencapsulated nerve endings and encapsulated nerve endings lies in their structure and function:
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Unencapsulated Nerve Endings:
- Also known as free nerve endings, these nerve endings lack specialized structures surrounding them.
- They are distributed throughout various tissues and organs, including the skin, epithelia, and connective tissues.
- Unencapsulated nerve endings are responsible for detecting stimuli such as pain, temperature, and light touch.
- Examples include Merkel cells associated with light touch and Meissner’s corpuscles associated with touch sensation.
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Encapsulated Nerve Endings:
- Encapsulated nerve endings are surrounded by specialized connective tissue structures that enhance their sensitivity to specific stimuli.
- These structures can vary in complexity and include structures like corpuscles, bulbs, or capsules.
- Encapsulated nerve endings are responsible for detecting more specialized sensations such as pressure, vibration, and proprioception (awareness of body position and movement).
- Examples include Pacinian corpuscles sensitive to deep pressure and vibration,
Ruffini endings sensitive to skin stretch, and
Golgi tendon organs sensitive to changes in muscle tension.
In summary, unencapsulated nerve endings are simple nerve endings dispersed throughout tissues, responsible for detecting general stimuli, while encapsulated nerve endings are surrounded by specialized structures that enhance their sensitivity to specific types of stimuli.
What is hyperventilation? Its mechanism?
Hyperventilation is a breathing pattern characterized by rapid, deep breaths that result in excessive ventilation of the lungs, leading to a decrease in the carbon dioxide (CO2) levels in the blood. It can occur voluntarily or involuntarily and may be associated with various physiological and psychological factors.
The mechanism of hyperventilation involves changes in the levels of gases, particularly oxygen (O2) and carbon dioxide (CO2), in the blood and tissues. Here’s how it typically occurs:
- Increased Ventilation: During hyperventilation, there is an increase in the rate and depth of breathing. This results in more air entering the lungs with each breath, leading to greater oxygen intake and carbon dioxide elimination.
- Decreased CO2 Levels: The rapid exhalation of CO2 from the lungs during hyperventilation leads to a decrease in the partial pressure of CO2 (PaCO2) in the blood. CO2 is a waste product of cellular metabolism, and its levels in the blood are tightly regulated by the body’s respiratory system.
- Respiratory Alkalosis: The decrease in PaCO2 causes a shift in the body’s acid-base balance, leading to respiratory alkalosis. Alkalosis refers to a higher-than-normal pH level in the blood, resulting from decreased CO2 levels. This can affect various physiological processes in the body, including the function of enzymes and the delivery of oxygen to tissues.
- Symptoms: Hyperventilation can cause a variety of symptoms, including dizziness, lightheadedness, tingling or numbness in the extremities (paresthesia), chest discomfort, palpitations, and feelings of breathlessness. These symptoms are often due to changes in blood pH and altered oxygen delivery to tissues.
- Triggering Factors: Hyperventilation can be triggered by various factors, including anxiety, stress, panic attacks, pain, fever, certain medications, high altitudes, and metabolic conditions such as diabetic ketoacidosis.
While hyperventilation is usually a temporary and self-limiting phenomenon, persistent or severe hyperventilation may require medical evaluation and management. Treatment may involve addressing the underlying cause, managing symptoms, and, in some cases, breathing techniques to restore normal breathing patterns and correct imbalances in blood gases.
What are the modalities of sensations?
, here are the modalities of sensation along with their respective sensory receptors:
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Mechanoreception: Sensory receptors include:
- Mechanoreceptors: Detect mechanical stimuli such as pressure, touch, vibration, and proprioception.
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Thermoreception: Sensory receptors include:
- Thermoreceptors: Detect changes in temperature, responding to heat and cold stimuli.
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Nociception: Sensory receptors include:
- Nociceptors (pain receptors): Detect noxious stimuli such as extreme heat or cold, mechanical pressure, and chemical irritants.
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Chemoreception: Sensory receptors include:
- Taste buds: Detect chemicals in food, allowing for the perception of taste.
- Olfactory receptors: Detect odor molecules in the air, allowing for the perception of smell.
- Chemoreceptors in the blood: Detect changes in blood chemistry and gas levels, regulating physiological processes such as respiration.
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Photoreception: Sensory receptors include:
- Photoreceptors (rods and cones) in the retina: Detect light stimuli, allowing for the perception of visual images and vision.
These modalities of sensation enable organisms to perceive and respond to various stimuli from the environment and within the body, contributing to sensory experiences and behaviors.
What are prostaglandins? Origin? Their function?
Prostaglandins are a group of hormone-like substances that are derived from fatty acids and have a wide range of effects on the body. They are produced by almost all tissues in the body and play important roles in various physiological processes, including inflammation, pain sensation, fever, blood clotting, and regulation of blood pressure.
Here are some key points about prostaglandins:
- Chemical Structure: Prostaglandins are lipid compounds that are derived from arachidonic acid, a type of fatty acid found in cell membranes. They are synthesized locally in cells from arachidonic acid through enzymatic reactions involving cyclooxygenase (COX) enzymes.
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Physiological Effects: Prostaglandins exert their effects by binding to specific receptors on the surface of target cells, known as prostaglandin receptors. Depending on the specific receptors activated and the tissue involved, prostaglandins can have diverse effects on various physiological processes:
- Inflammation: Prostaglandins promote inflammation by causing vasodilation (widening of blood vessels), increasing vascular permeability, and sensitizing pain receptors, leading to redness, swelling, heat, and pain at the site of injury or infection.
- Pain Sensation: Prostaglandins sensitize pain receptors (nociceptors) in response to tissue damage or inflammation, contributing to the perception of pain.
- Fever
Why pain receptors show no adapatation?
Pain receptors, also known as nociceptors, do not exhibit adaptation in the same way as other sensory receptors because their primary function is to alert the body to potentially harmful or damaging stimuli. Unlike other sensory receptors that may adapt or become less sensitive to continuous stimulation over time, nociceptors remain highly responsive to noxious stimuli to ensure that the body can rapidly detect and respond to threats to its well-being.
What is referred pain? Its basis?
Referred pain is when you feel discomfort or pain in an area of the body that is different from the actual source of the pain. It occurs because the nervous system can sometimes misinterpret signals from internal organs or deep structures and perceive the sensation as coming from a different location.
The basis of referred pain lies in the shared neural pathways in the nervous system. Different regions of the body may share nerve pathways that converge on the same spinal cord segments. When an organ or deep structure is experiencing pain or dysfunction, the sensory signals travel through these shared pathways and may be interpreted by the brain as coming from a different area that shares those neural connections.
For example, a heart attack can cause pain in the left arm or jaw because the nerves from these areas share pathways with those from the heart. Similarly, issues with the diaphragm can cause shoulder pain because both the diaphragm and shoulder share nerve pathways.
Stimulation of which area can cause sensation of pain?
The periaqueductal gray (PAG) area is a region of gray matter located around the cerebral aqueduct in the midbrain. It plays a crucial role in modulating pain perception and response.
The PAG is involved in both pain modulation and analgesia (pain relief). It receives input from various areas of the brain, including the hypothalamus, amygdala, and prefrontal cortex, as well as from descending pathways from the brainstem. When the PAG is activated, it can either inhibit or facilitate pain signals traveling through the spinal cord.
One of the ways the PAG modulates pain is through its connections with the descending pain modulation pathways, such as the periventricular gray matter and the rostroventral medulla. These pathways can inhibit the transmission of pain signals in the spinal cord, leading to analgesia.
Additionally, the PAG is involved in the modulation of emotional responses to pain, such as fear and anxiety, through its connections with the amygdala and other limbic structures.
Overall, the periaqueductal gray area is a critical component of the brain’s pain modulation system, playing a key role in regulating both the perception and response to painful stimuli.
What is post-tetanic facilitation?
Post-tetanic facilitation is a phenomenon observed in neurons and synapses whereby a brief period of high-frequency stimulation (tetanic stimulation) leads to a temporary enhancement of synaptic transmission.
During tetanic stimulation, the presynaptic neuron releases neurotransmitters at a high frequency, causing a buildup of calcium ions in the presynaptic terminal. This increase in calcium concentration can lead to the mobilization of additional synaptic vesicles containing neurotransmitters, priming them for release.
After the tetanic stimulation ceases, the increased availability of synaptic vesicles persists for a short period, resulting in an enhanced response to subsequent stimuli. This enhanced synaptic transmission is known as post-tetanic facilitation and can lead to increased synaptic efficacy and neuronal excitability.
Post-tetanic facilitation is believed to be one of the mechanisms underlying short-term synaptic plasticity, which is the ability of synapses to undergo rapid changes in efficacy in response to neuronal activity. It allows neurons to dynamically adjust their synaptic strength in response to changes in their activity patterns.
Sure! Imagine you have a doorbell. When you press it many times really quickly, it becomes more sensitive for a short while. Even if you press it lightly after that, it will ring louder. That’s like post-tetanic facilitation. The neurons in your brain get extra ready to send messages to each other after a lot of activity, so they become more responsive for a little bit.
What is herpes zoster disorder?
Herpes zoster, commonly known as shingles, is a viral infection caused by the varicella-zoster virus, which also causes chickenpox. After a person recovers from chickenpox, the virus remains dormant in the nerve tissue near the spinal cord and brain.
In some cases, the virus can reactivate later in life, typically due to factors such as aging, stress, or a weakened immune system. When the virus reactivates, it travels along the nerve fibers to the skin, causing a painful rash that usually appears as a band or stripe on one side of the body.
The rash is characterized by fluid-filled blisters that crust over as they heal. In addition to the rash, shingles can cause symptoms such as itching, burning, tingling, and sensitivity to touch. Some individuals may also experience fever, headache, fatigue, and general malaise.
Shingles is contagious, but it does not spread through casual contact. However, the fluid from the blisters contains the varicella-zoster virus, and direct contact with the rash can cause chickenpox in someone who has not been previously infected or vaccinated against the virus.
Treatment for shingles typically involves antiviral medications to reduce the severity and duration of the outbreak, as well as medications to help manage pain and discomfort. Additionally, vaccines are available to help prevent shingles and reduce the risk of complications associated with the infection.
What is lateral medullary syndrome?
Lateral medullary syndrome, also known as Wallenberg syndrome, is a neurological condition caused by damage to the lateral part of the medulla oblongata, which is the lower part of the brainstem. This damage typically occurs due to a blockage or interruption of blood flow in the vertebral or posterior inferior cerebellar arteries.
The syndrome presents with a variety of symptoms, which may include:
- Ipsilateral facial pain and temperature loss: Loss of sensation of pain and temperature on the same side of the face as the lesion.
- Contralateral body pain and temperature loss: Loss of sensation of pain and temperature on the opposite side of the body from the lesion.
- Horner syndrome: A combination of symptoms, including drooping of the eyelid (ptosis), constriction of the pupil (miosis), and decreased sweating on one side of the face.
- Dysphagia (difficulty swallowing)
- Hoarseness or dysphonia (difficulty speaking)
- Nystagmus (involuntary eye movements)
- Vertigo (dizziness)
- Ataxia (loss of coordination)
The specific symptoms experienced by an individual with lateral medullary syndrome depend on the location and extent of the damage to the medulla oblongata.
The most common cause of lateral medullary syndrome is a blockage or occlusion of the vertebral or posterior inferior cerebellar arteries, usually due to a blood clot (thrombus) or an embolus (a clot that has traveled from another location). Other less common causes include vertebral artery dissection, arteritis (inflammation of the arteries), and tumor compression of the blood vessels. Additionally, trauma or injury to the medulla oblongata can also lead to lateral medullary syndrome.
What is brown sequard syndrome?
Brown-Séquard syndrome is a neurological condition characterized by a specific pattern of neurological deficits resulting from damage to one half of the spinal cord, usually caused by trauma such as a stabbing or gunshot wound, tumor, or spinal cord injury.
The hallmark features of Brown-Séquard syndrome include:
- Ipsilateral (same side) loss of motor function and proprioception (awareness of body position) below the level of the lesion due to damage to the corticospinal tracts and posterior columns on the same side.
- Contralateral (opposite side) loss of pain and temperature sensation below the level of the lesion due to damage to the spinothalamic tracts on the opposite side.
In other words, the person typically experiences paralysis and loss of sensation on one side of the body below the level of the injury, along with loss of pain and temperature sensation on the opposite side of the body.
Other possible symptoms of Brown-Séquard syndrome may include muscle weakness, spasticity, hyperreflexia (exaggerated reflexes), and urinary and bowel dysfunction, depending on the level and severity of the spinal cord injury.
Treatment for Brown-Séquard syndrome focuses on stabilizing the spine and managing symptoms. Rehabilitation may also be necessary to improve function and quality of life. Prognosis varies depending on the extent of the spinal cord injury and the individual’s response to treatment and rehabilitation.
Difference between lateral medullary syndrome and brown sequard syndrome?
Lateral medullary syndrome (Wallenberg syndrome) and Brown-Séquard syndrome are both neurological conditions, but they affect different parts of the nervous system and have distinct symptoms.
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Affected Area of the Spinal Cord/Brainstem:
- Lateral medullary syndrome: It results from damage to the lateral part of the medulla oblongata, which is in the brainstem.
- Brown-Séquard syndrome: It occurs due to damage to one half of the spinal cord, usually caused by trauma or injury.
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Symptoms:
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Lateral medullary syndrome: Symptoms typically include ipsilateral facial pain and temperature loss,
contralateral body pain and temperature loss, Horner syndrome, dysphagia, hoarseness, nystagmus, vertigo, and ataxia.
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Lateral medullary syndrome: Symptoms typically include ipsilateral facial pain and temperature loss,
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Causes:
- Lateral medullary syndrome: It is usually caused by a blockage or interruption of blood flow in the vertebral or posterior inferior cerebellar arteries.
- Brown-Séquard syndrome: It is typically caused by trauma such as a stabbing or gunshot wound, tumor, or spinal cord injury.
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Prognosis and Treatment:
- Prognosis and treatment depend on the underlying cause, extent of damage, and individual factors in both syndromes. Treatment often involves stabilizing the spine, managing symptoms, and rehabilitation.
In summary, while both syndromes involve neurological deficits, they arise from different areas of the nervous system, have distinct symptoms, and are caused by different mechanisms.
Where are the pain receptors NOT present?
Pain receptors, also known as nociceptors, are specialized nerve endings that detect painful stimuli. While nociceptors are found throughout the body, there are certain areas where they are less or not present. These areas include:
- The brain: The brain itself does not contain nociceptors, so it cannot feel pain. However, pain can be perceived in the brain when signals from nociceptors in other parts of the body are transmitted and interpreted by the brain.
- The inner organs (viscera): While there are pain receptors in the walls of hollow organs such as the gastrointestinal tract, bladder, and uterus, the innermost layers of these organs lack nociceptors. Therefore, injuries or damage to these deeper layers may not be felt as acutely as injuries to the outer layers or adjacent tissues.
- Certain areas of the skin: Some areas of the skin, such as the hair follicles and the epidermis (outermost layer), have fewer nociceptors compared to other areas. As a result, injuries or stimuli in these areas may be less painful compared to areas with a higher density of nociceptors, such as the fingertips or lips.
It’s important to note that while certain areas may have fewer nociceptors, the perception of pain can still occur through various mechanisms, including referred pain or neural pathways that amplify or dampen pain signals.
What is IPSP or inhibitory Post synaptic potential? Its basis?
An inhibitory postsynaptic potential (IPSP) is a temporary decrease in the electrical potential of a neuron’s membrane potential, making it less likely to generate an action potential. IPSPs occur when neurotransmitters released from presynaptic neurons bind to receptors on the postsynaptic neuron and cause inhibitory effects.
The basis of an IPSP lies in the neurotransmitter-receptor interaction at the synapse. When an inhibitory neurotransmitter, such as gamma-aminobutyric acid (GABA) or glycine, binds to its specific receptors on the postsynaptic neuron, it opens ion channels that allow negatively charged ions (such as chloride ions) to enter the neuron or positively charged ions (such as potassium ions) to leave the neuron. This results in hyperpolarization of the postsynaptic neuron, meaning that the inside of the neuron becomes more negative compared to the outside.
The hyperpolarization caused by an IPSP makes it more difficult for the postsynaptic neuron to reach the threshold for generating an action potential, thereby inhibiting neuronal activity. IPSPs act as a balancing mechanism in neural circuits, counteracting the excitatory effects of excitatory postsynaptic potentials (EPSPs) and helping regulate the overall level of neuronal activity in the brain.
Think of an IPSP as a “chill out” signal for a neuron. When it receives this signal, it becomes less likely to fire or send messages to other neurons. This happens because certain chemicals tell the neuron to take a break by making it more negative inside, which makes it harder for the neuron to get excited and fire off a message.
Spatial summation vs temporal summation??
Temporal summation and spatial summation are both mechanisms by which the strength and frequency of synaptic inputs determine whether a neuron will generate an action potential (nerve impulse) or not. However, they operate in different ways:
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Temporal Summation:
- Temporal summation refers to the cumulative effect of multiple signals arriving at a synapse in rapid succession over a short period of time.
- In temporal summation, a single presynaptic neuron repeatedly releases neurotransmitters onto the same postsynaptic neuron within a short time frame.
- Each individual signal (or EPSP - excitatory postsynaptic potential) may not be strong enough to trigger an action potential on its own. However, if these signals arrive close together in time, they can add up or “summate” to reach the threshold for triggering an action potential.
- Temporal summation occurs over time, involving repeated stimulation of a single synapse.
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Spatial Summation:
- Spatial summation refers to the integration of signals from multiple presynaptic neurons that synapse onto the same postsynaptic neuron at different locations on its dendrites and cell body.
- In spatial summation, multiple presynaptic neurons simultaneously release neurotransmitters onto the postsynaptic neuron, but at different synapses.
- Each individual signal (or EPSP) from the different synapses may not be strong enough to trigger an action potential on its own. However, when multiple EPSPs occur simultaneously and are spatially close together on the postsynaptic neuron, they can add up or “summate” to reach the threshold for triggering an action potential.
- Spatial summation occurs at the same time, involving simultaneous stimulation of multiple synapses.
In summary, the main difference between temporal and spatial summation lies in the timing and location of the synaptic inputs: temporal summation involves repeated signals from a single synapse over time, while spatial summation involves simultaneous signals from multiple synapses at different locations on the postsynaptic neuron. Both mechanisms allow neurons to integrate and process information from multiple sources to determine whether to generate an action potential.
