Physiology and Autonomic System Overview

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Questions and Answers

The main chemical trigger for pH control is ______ in arterial blood.

CO2

Olfactory receptor neurons are free nerve endings connected to unmyelinated ______.

axons

The axons from tufted and mitral cells form the olfactory ______ which transmits information to the olfactory cortex.

tract

The entorhinal cortex is involved in the association of ______ and related memories.

smells Signup and view all the answers

Baroreceptors sense volume change via pressure ______.

detection Signup and view all the answers

The drive for action seeks a way to restore balance to a bodily system or function with goals of survival and ______.

reproduction Signup and view all the answers

The autonomic system creates situations favorable to restoring ______ balance.

homeostatic Signup and view all the answers

The ______ nervous system generates energy for action to remedy a deficit.

sympathetic Signup and view all the answers

The parasympathetic nervous system uses resources to create energy stores and sets many system ______ states.

tonic Signup and view all the answers

The ultimate aim of the autonomic system is to return to homeostatic ______.

equilibrium Signup and view all the answers

Basic physiological needs promote immediate ______ and thriving.

survival Signup and view all the answers

Hunger and thirst are examples of basic physiological ______.

needs Signup and view all the answers

Emotions and memories deeply influence behaviors related to both physiological and psychological ______.

needs Signup and view all the answers

Facial expression scales are the preferred medium for ______ populations.

pediatric Signup and view all the answers

Single nucleotide polymorphisms (SNP) can alter the function of the Mu (μ) ______ receptor.

opioid Signup and view all the answers

Pre-existing chronic pain states can predispose to less controlled ______ pain.

acute Signup and view all the answers

Individual differences in endogenous opioid functionality affect the response to ______ opioid therapy.

exogenous Signup and view all the answers

Differential opioid receptor physiology in men and women can alter exogenous opioid ______.

efficacy Signup and view all the answers

Areflexia or moderated ______ is discussed in the context of assessment.

reflexia Signup and view all the answers

Peripheral interventions can block signal ______, preventing pain transmission.

transduction Signup and view all the answers

Spinal interventions aim to prevent ______ and plasticity/windup.

hypersensitivity Signup and view all the answers

Cortisol controls electrolyte balance primarily by regulating Na+ and H2O retention, excretion of ______ and protons.

K+ Signup and view all the answers

Cortisol usually functions as a negative feedback loop to modulate the release of ______/ACTH.

CRH Signup and view all the answers

The adrenal medulla releases ______ and norepinephrine.

epinephrine Signup and view all the answers

Sustained HPA Axis Response can occur in relation to perioperative ______.

stress Signup and view all the answers

Injured tissues trigger an inflammatory response characterized by redness (rubor), heat, and ______.

swelling Signup and view all the answers

Histamine causes the 'triple flare of Lewis', which includes ______, heat, and swelling.

redness Signup and view all the answers

The adrenal gland as a whole functions as a stress ______.

transducer Signup and view all the answers

The sympathetic nervous system is initiated by the release of epinephrine and ______.

norepinephrine Signup and view all the answers

Cortisol has immunosuppressive properties and is often used ______ for its effects.

systemically Signup and view all the answers

The preganglionic sympathetic neurons exert direct control over the ______ medulla.

adrenal Signup and view all the answers

The combination of all of this causes pain but is functionally intended to deal with the ______.

injury Signup and view all the answers

To initiate healing, an inflammatory response must then quickly ______.

follow Signup and view all the answers

Histamine leads to increased ______ flow into the injured tissue.

blood Signup and view all the answers

Injured cells immediately release ______ acid.

arachidonic Signup and view all the answers

The extent of the overall response is mediated by the magnitude, invasiveness, and duration of the ______ procedure.

surgical Signup and view all the answers

The worst offenders for an intense stress response are major open vascular and ______ surgery.

abdominal Signup and view all the answers

The stress response can be needed but should be controlled for best results in ______.

M&M Signup and view all the answers

All the body's homeostatic mechanisms are intended for time-limited ______.

interventions Signup and view all the answers

SNS is strongly activated leading to adrenal medullary positive ______ feedback.

feedback Signup and view all the answers

Epinephrine release reinforces the SNS activation and mobilizes ______ and fat stores.

CHO Signup and view all the answers

Intracranial invasion with a medical device has a reported mortality of greater than ______%

64 Signup and view all the answers

Severe craniofacial trauma may complicate the insertion of ______ or a nasopharyngeal airway.

NGT Signup and view all the answers

The medial temporal lobe is critical for ______ processing.

memory Signup and view all the answers

A key area involved in transforming short-term memory into long-term memory is the ______.

hippocampus Signup and view all the answers

The ______ bodies are thought to integrate memory and emotions.

mammillary Signup and view all the answers

______ memory involves conscious recollection of specific facts or occurrences.

Declarative Signup and view all the answers

Bilateral damage to the medial temporal lobes can result in ______ amnesia.

anterograde Signup and view all the answers

The ______ is considered the seat of emotions and survival motivation.

amygdala Signup and view all the answers

Sensory information reaches the amygdala through the ______ terminalis.

stria Signup and view all the answers

Klüver Bucy syndrome is associated with bilateral lesions in the ______.

amygdala Signup and view all the answers

Wernicke-Korsakoff syndrome is often caused by severe and sustained deficiency of ______.

thiamine Signup and view all the answers

Chronic Wernicke-Korsakoff syndrome can lead to difficulties with ______ function.

executive Signup and view all the answers

Anterograde amnesia presents a deficit in ______ new memories.

forming Signup and view all the answers

Patients with Alzheimer’s disease often experience ______ amnesia as the disease progresses.

retrograde Signup and view all the answers

The basal forebrain is involved in cholinergic projections related to ______ function.

memory Signup and view all the answers

Study Notes

NSG 7430/7204 Week 8 Lecture 1

Weekly objectives include Drives and Emotions, Limbic System Functional A&P, Limbic System Dysfunction, Sleep & Wakefulness, Hypothalamic Pituitary Adrenal (HPA) Axis, and The Stress Response.
The Limbic System is a complex set of structures that bridge the neocortex and hypothalamus, involved with multiple functions
The Limbic System has many areas, including the insular lobe, association cortices, basal nuclei, prefrontal cortex, and diencephalon.
The Limbic System is involved in the stress response, homeostatic balance, emotion, and memory.
The Hypothalamus is part of the diencephalon, and controls the pituitary gland and related functions (0.3% of total brain mass)
Outside physiological limits, biochemistry does not function optimally, and includes examples shown like temperature, blood glucose concentrations, and oxygenation levels.
Drives are physiological needs that create a desire for action for survival and reproduction.

Homeostasis

Homeostasis is the physiological body's set interthreshold ranges, essential to normal biochemical function.
Body parameters like temperature, blood pH, blood pressure, and others need to remain within these ranges for optimal bodily function.

Weekly Objectives Week 8 Lecture 2

Drives and Emotions
Limbic System Functional A&P
Limbic System Dysfunction
Sleep & Wakefulness
Hypothalamic Pituitary Adrenal (HPA) Axis
The Stress Response

Weekly Objectives Week 9 Lecture 1

Functional A&P of the Sensory System
Nociception Pathways
Acute Pain Epidemiology & Impact
Acute Pain Interventions
Selected Pathophysiology: Risk Factors for Acute Pain Persistence/Transformation

Weekly Objectives Week 9 Lecture 2

Functional A&P of the Sensory System
Review
Nociception Pathways
Acute Pain: Nociceptive Physiology and Interventions
Selected Pathophysiology: Risk Factors for Acute Pain Persistence/Transformation

Neurobiology: Pain Pathways & Interventions

Overview of pain pathways and interventions.
Peripheral mechanisms
Spinal mechanisms
Supraspinal mechanisms
Targeted interventions

Peripheral Pain Physiology - Nociceptors

Nociceptors are free nerve endings that detect noxious stimuli.
Nociceptors convert (transform/transduce) the energy of noxious stimuli into an electrochemical signal.
Analgesic targets include receptors and the transmission of neuronal fibers to the spinal cord.

Primary Somatosensory Afferent Neuronal Fibers

A-beta fibers transmit pain response for touch and pressure (non-noxious).
A-delta fibers transmit noxious mechanical stimuli and sub-noxious temperature stimuli.
C fibers transmit noxious stimuli, including heat, mechanical, and chemical.

Fiber Summary - Anterolateral Pathway Reference

The classic lateral spinothalamic pathway uses non-myelinated C fibers and thinly myelinated A delta fibers for transmitting pain, temperature, and other sensations
The posterior column-medial lemniscus pathway serves thicker, faster myelinated fibers (A-beta and other similar fibers) for transmitting touch, vibration, and proprioception.

Primary Afferent Neurochemistry Targets

TRP Vanilloid Type 1 Channels (TRPV1) are pain receptors for capsaicin and heat.
Voltage-gated Nat and K+ channels initiate and transmit nociception.
Voltage-gated Ca2+ channels are a target for pain management.
G-coupled protein receptors modulate inflammatory mediators, such as CGRP, bradykinin, and prostaglandins (excitatory) and opioids, and adrenergic agonists (inhibitory).

Primary Nociceptive Peripheral Afferent Physiology

When exposed to noxious stimuli, nociceptors initiate a chain reaction that includes the release of various chemicals by damaged cells.
Release of chemical mediators causes the "triple response of Lewis" (flare, wheal, and hyperalgesia).

Primary Peripheral Afferent – Facilitory Modulation

Nociceptors that have been stimulated can release neuromodulatory proteins to trigger the recruitment of additional nociceptors (that are typically silent under normal conditions).
These released neuromodulatory proteins (e.g., substance P, neurokinin A, CGRP, and neurotrophins) are involved in facilitating nociception.

Consequences of Peripheral Neuronal Sensitization

Decreased threshold and latency
Increased frequency response
Increased receptive field plus overlap
After-discharges
Increase in excitatory nociceptive transmission within the SC
Recruitment of further neurons
Increased neurotransmitter release locally and upstream

Spinal Nociceptive Mechanisms

Nociceptors transmit pain signals through the dorsal horn, via Rexed's laminae.
Glutamate is the primary neurotransmitter involved.
GABA and glycine are inhibitory neurotransmitters.
The substantia gelatinosa in laminae II plays a crucial role in modulating nociception.

Spinal Cord Cascade-Facilitory Modulation

C-fibers can trigger release of excitatory neurotransmitters (glutamate and substance P).
Activation of certain channels (e.g., Na+) can increase the temporal and spatial summation of noxious stimuli.
This leads to neuronal sensitization and the development of persistent pain conditions.

Spinal Cord Synapse Receptors

Key excitatory receptors: Glutamate (NMDA, AMPA, kainate, mGluR), substance P.
Key inhibitory receptors: GABA, glycine, serotonin (5-HT).
Alpha2-adrenergic and opioid receptors also play a significant role

Glutamate

Continued nociceptor activity leads to prolonged glutamate release.
Increased activity of NMDA, AMPA, and mGluR receptors.
Calcium influx into secondary afferent neurons.
Long-term sensitization through mechanisms like NO and prostaglandins.
Chronic inflammation and opioid tolerance are linked to NMDA receptor activation.

Sequence of NMDA Receptor Activation

Removal of Mg2+ block.
Calcium influx.
Neurotransmitter release.
Activation and/or production of intracellular second messengers.
Facilitation of pathway transmission.
Gene transcription in the cell's nucleus.
Increased responsiveness.
Production of arachidonic acid (AA) metabolites.

sP Receptor Activation

Excitatory amino acid cascade is activated in spinal cord and peripheral afferents.
NK-1 receptors are crucial for mediating peripheral and spinal neuronal sensitivity involved in visceral sensations.
Ongoing nociceptor activity is maintained throughout the body from the periphery to the SC.

Supraspinal Mechanisms

Pain is perceived and localized via supraspinal structures (e.g., the reticular formation, hypothalamus, midbrain and others).
Descending pathways for pain modulation originate from higher brain centers (the limbic system, prefrontal cortex)
The pathways involve neurotransmitters like glutamate, 5-HT, endogenous opioids, norepinephrine, cannabinoids, GABA, and glycine to modulate nociceptive transmission.

Double-edged Sword

Divergent pain signaling to important areas by the central nervous system is modulated (inhibited) by descending inhibitory pathways.
Glutamate and other excitatory transmitters involved.
Serotonin and other neurotransmitters crucial in pain modulation.

Supraspinal Descending Inhibition

Brain and other structures modulate the nociceptive transmission.
Cortical structures (e.g., PFC, insula, anterior cingulate cortex, amygdala); associated with descending inhibition of pain.
Subcortical structures like the midbrain PAG, pontine parabrachial complex and locus coeruleus, medulla (RVM), and SC interneurons involved.

Global Actions- Main Pathway Descending Inhibition

The PAG is stimulated by ascending pain signals and other inputs
PAG activates structures in the parabrachial and RVM nuclei.
RVM raphe nuclei is the final relay for descending inhibitory influence.
Inhibitory neurotransmitters release in the spinal cord.

Nociceptive Modulation

Excitatory amino acids (glutamate and aspartate) and substance-P initiate a cascade in response to nociceptive transmission
Descending pathways from the brain can help inhibit this cascade, involving neurotransmitters such as GABA, glycine, and opioids.

Overview of Chronic Pain (CP) Conceptual Summary

Persisting noxious stimuli can contribute to chronic pain through peripheral and central sensitization.
Central structures (spinal cord, brainstem, midbrain) and cortical structures (limbic system, prefrontal cortex).
Induction of central plasticity (particularly affecting WDR neurons in spinal cord) is involved.
Chronic pain can lead to structural changes in the CNS and peripheral nervous system after prolonged stimuli
Psychological mechanisms may contribute to the development or maintenance of chronic pain.

Special Issues in Chronic Pain Rx

Opioid prescribing practices.
The shift from an endorsement of widespread opioid use to a more cautious approach.
The role of evidence-based medicine in guiding treatment decisions.

Sobering Facts - Substance Use

High number of opioid-related deaths.
Opioids strongly linked with addiction.
Synthetic opioids play a sizable role in overdose deaths.

Things to Ponder...

America's significant role in global opioid consumption.
Responsibility of providers and pharmaceutical companies.

Evaluation of Potential CP Patient

Multifactorial evaluation including a thorough medical, surgical, social, and family history (including current and past medications).
In addition to the history, a focused neurological exam is important to assess any potential neurological involvement, including pain symptoms over time.

Common Diagnostics

Blood tests to evaluate organ function (e.g., renal and liver function, thyroid function)
Drug screens and other chemical assays.
Imaging techniques (e.g., X-rays, CT scans, MRIs).

Specific Neuro Diagnostics

Electromyography (EMG) and nerve conduction studies (NCS) to evaluate nerve dysfunction.

Thermography

Detects heat via infrared energy emitted by body surfaces.

Chronic Pain Team Members

An interdisciplinary approach is crucial for effective management of chronic pain.

Persistence of Acute Pain

Estimates for prevalence of chronic pain in various procedures.

CP ~ Preoperative Risk Stratification

Clinical risk factors that can predict chronic pain after surgical procedures or trauma

CP ~ Pre-incisional Risk Stratification

High-dose opioid use is a potential trigger for OIH (opioid-induced hyperalgesia).
Interventions aimed at preventing CNS plasticity induction and neuronal sensitization are essential.

CP ~ Postoperative Risk Stratification

Early and significant pain is a risk factor
Patients with neurotoxic chemo exposure more at risk.
Alteration of immune function can cause hyperalgesia and increase pain severity.

Gabapentin and Pregabalin

Effective, in some cases, as preemptive pain management agents, particularly for neuropathic pain.
Work on inhibiting various neurotransmitters, including GABA (inhibitory) and others, acting presynaptically and postsynaptically within the SC and/or other CNS sites

Postoperative CP Risk Mitigation

Effective anesthetic and analgesia methods for postoperative pain management.
Multimodal strategies; including analgesics, nerve blocks, and continuous wound infiltration, to prevent or mitigate the development of prolonged pain.
Considerations: specific regional or neuraxial approaches that may decrease the amount of opioid use for managing pain

Balanced, Preemptive Multimodal Analgesia

Modalities that act on diverse pain pathways, increasing efficacy and reducing risks.
Initiating interventions before the actual surgical procedure.
Preventing prolonged noxious stimuli or at least most excessive periods.

Clinical Example (C-section Protocol)

Example steps of anesthetic and pain management regimen for a C-section.
Use of various drugs and techniques that are utilized for management.

Selected Pain Syndromes

General descriptions of pain syndromes.
Emphasis on treatment and management issues.

Entrapment Syndromes

Entrapment of nerves where they go through a narrow passage or proximity with other structures can cause various symptoms (often lasting pain, numbness).
Diagnoses usually rely on nerve conduction testing and imaging methods, and sometimes require surgical intervention
Treatment involves addressing inflammation, immobilization, and potentially surgical decompression of affected tissues.

Myofascial Pain Syndromes

Defined trigger points within muscle groups.
Treatment involves medication, therapy (massage, PT).

Typical Presentation of Lumbar Radiculopathies

Symptom presentation as it relates to the affected spinal nerve root.
Associated weakness and reflexes, including pain, depending on the level of injury or lesion

Diabetic Peripheral Neuropathy

Issues with nerve structure and blood vessel health.
Diagnosis relies on symptom reports and nerve conduction tests
Treatment options focus on mitigating complications and improving nerve health.

Complex Regional Pain Syndromes

Pain syndromes with autonomic involvement, especially hyperalgesia and allodynia..
Characterized by intense, prolonged pain, often with autonomic symptoms and reduced range of motion..
Treatment options emphasize sympathetic nerve blocks, various pharmacological measures, and physiotherapy.

Headaches- Sinus, Cluster, Tension/Migraine

Descriptions of the types of headaches, including their characteristics, etiology and associated complications
Identification, and management strategies including medication, and other specialized care

Sphenopalantine Ganglion Block

Description of the anatomical area and procedure.
Indications, and complications.

Other Techniques, Radical Treatment Options

Various newer interventional and surgical techniques that are used in the management of chronic pain or complicated pain.

Interdisciplinary Modalities/Team Members

Multidisciplinary approach to chronic pain management
Team members and roles should be incorporated

What matters in Anesthesia?

Key considerations when treating patients expected to have various pain syndromes.

Opioid Minimization vs. Opioid-Free

Importance of recognizing the effects of chronic opioid exposure to patients.

Opioid Efficacy

Opioid efficacy can vary due to many factors, including patient responses to the drugs, how they are administered, and prior conditions.
Risk factors for dependence and aberrant medication usage.

Opioids Use in Oncology Care

The use of opioids in cancer treatment for pain relief is complex, due to a combination of immune system effects, and other tumor-related changes.

Chronic Opioid Use

Repeated opioid use leads to structural changes in the CNS, and sometimes to worsening pain sensations.
Mechanisms of how opioids lead to increased pain symptoms and sensitivity

OIH(Opioid Induced Hyperalgesia)

This is a significant side effect of opioids that can lead to increased pain sensations as a consequence of extended use in some patients.

Diagnosis & Treatment of Chronic Pain

Multifactorial evaluations are essential.
This includes neurological, imaging, and blood tests, along with determining psychological and social factors impacting pain.

Pain Assessment

Various pain scales can be used for evaluating and addressing patient needs
Non-verbal communication should be evaluated when determining the effectiveness and safety of treatment.

Individualizing Pain Regimens

Tailoring opioid and other analgesic treatments to individual pain responses to enhance efficacy.
Individual differences in pain perception and management needs should be considered.
Genetic and gender influences on opioid responses, effectiveness, and efficacy

Overall Chronic Pain Pathogenesis

Sustained/prolonged nociceptive neuronal plasticity is involved.
Peripheral and central sensitization factors influence the persistence/development of chronic pain.

Chronic Pain AP&P

Nociceptive and neuropathic types of chronic pain, including hyperalgesia and allodynia.

Peripheral Sensitization

Release of various substances due to nerve damage/inflammation including histamine and others that amplify pain
Mediated by histamine, serotonin, bradykinin, prostaglandins and other chemicals within the periphery, and some neurotransmitters into the nervous spinal cord.

Central Sensitization

WDR(wide dynamic range) neurons are key
Activation of these neurons can be triggered by many substances that cause an increase in pain perception, including glutamate and others.
These substances lead to prolonged glutamate and other neurotransmitter release in the spinal cord.

Glutamatergic Facilitation

Prolonged glutamate release due to chronic nociceptor activity leads to cellular changes.
These changes can cause widespread, long-lasting pain sensitization that amplifies pain sensation throughout the body

Inhibitory Modulation in the SC, Segmental and Supraspinal Descending Inhibition

Methods of pain modulation, including mechanisms of how different substances inhibit neuronal pathways or pain transmission.

CP Conceptual Summary

Summary of the various mechanisms, factors, and considerations of chronic pain sensitization, induction and/or maintenance

Pain Syndromes

Descriptions of various pain syndromes, including specific symptoms patterns.

Opioid Prescribing

Historical opioid use and its implications.

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Description

This quiz covers key concepts in physiology, focusing on the autonomic nervous system and its role in maintaining homeostasis. Questions explore pH control, sensory receptors, and the brain's involvement in physiological functions. Test your understanding of how the body strives for balance and survival.