The document discusses the neurobiology of stress. It defines stress and outlines the key components of the stress response including activation of the HPA axis and sympathetic nervous system. This leads to release of stress hormones like cortisol and catecholamines. Prolonged stress can sensitize brain circuits and increase vulnerability to mental health issues. Genetics also influence individual stress responses. Psychoneuroimmunology explores bidirectional communication between the brain, behavior and immune system in stress.
The diagnostic assessment and treatment and treatment planning in psychiatry is a dynamic process that integrates the biological, psychological, social, and behavioral paradigms to develop a plan of action that provides a rational for the types of interventions employed to sustain the therapeutic alliance and relieve suffering.
The diagnostic assessment and treatment and treatment planning in psychiatry is a dynamic process that integrates the biological, psychological, social, and behavioral paradigms to develop a plan of action that provides a rational for the types of interventions employed to sustain the therapeutic alliance and relieve suffering.
This is a presentation made on stress and related problems related to physiological aspects of it. It also explains General Adaption Syndrome i.e our bodies response to stressor hormone like Oxytocin and cortisol in basic 3 stages, also some of the sympathetic and parasympathetic functions. It gives you general idea about the "Stress curve" .
This is a presentation made on stress and related problems related to physiological aspects of it. It also explains General Adaption Syndrome i.e our bodies response to stressor hormone like Oxytocin and cortisol in basic 3 stages, also some of the sympathetic and parasympathetic functions. It gives you general idea about the "Stress curve" .
Stress is the body’s physical and psychological response to a specific demand made of us or to an event in our life. In some cases it motivates and encourages us to complete a task we find difficult so that we can take pride in ourselves and what we achieve.
Stress is the body’s physical and psychological response to a specific demand made of us or to an event in our life. In some cases it motivates and encourages us to complete a task we find difficult so that we can take pride in ourselves and what we achieve.
lecture 27 from a college level introduction to psychology course taught Fall 2011 by Brian J. Piper, Ph.D. (psy391@gmail.com) at Willamette University, Seyle
Stress can be defined as any type of change that causes physical, emotional or psychological strain. Stress is your body's response to anything that requires attention or action. Everyone experiences stress to some degree. The way you respond to stress, however, make a big difference to your overall well-being.
GERO 508 Spring 2021
Week 2
The Mind & Body Connection
Timothy Lu Office Hours: By Appointment Email: [email protected]
Dr Paul Nash CPsychol, AFBPsS, FHEA
Office: GERO 231E
Office Hours: Thurs 09.00-12.00
(OR AGREED APPOINTMENT)
Email: [email protected]
Gillian Fennell
Email: [email protected]
Questions about assessments?
2
The session in brief
Biological – What is stress?
Biological consequences of stress
Biological models of stress
Measuring biological stress
What does stress look like?
The meaning of sex
Psychological approaches to stress
Environmental approaches to stress
Specific models of stress
Bio-Psycho-Social models of stress
Measuring psychological components of stress
3
What forms can stress take?
4
Stress – The overview
Actual Stress
- See a predator / See a car coming towards you
5
Perceived Stress
- In a situation where something may or may not happen
Which do you think happens with humans? Why?
Humans exhibit the anticipatory stress response, well done us!! Turn on stress response for psychological reasons
- memory, emotions, thoughts
NOT what stress was designed for which leads to potential for chronic stress
Essentially the aim of the stress response is to return us to the homeostatic equilibrium we are in.
Acute or Chronic?
6
The meaning of sex
7
Fight or Flight
Tend and Befriend
Evolutionary
Protection of self and offspring
Nurturing offspring under stressful situation
Protect from harm (tend)
Create / join social groups to maximize resource and protection (befriend)
Evolutionary
Protection of self
Fight a stressor
Escape a stressor
Short lived
Few mins – Alive or dead
Most research based on males until the tend / befriend hypothesis produced. Mainly due to different cyclical variation in hormones and endocrine responses making research with women less predictable.
Not the whole story and we have biological and psychological differences later in the course!
Stress – The psychological approach
8
Stress as a response
The ways in which we respond to a stressor
Storm and stress approach
Coping & resilience
Effects of prolonged stress
Stress as a stimulus
Views stress as a significant life event or change that demands response, adjustment, or adaptation
Sees change as inherently stressful
Stress is dealt with uniformly across populations
Illness outcome thresholds are uniform
Stress as a transaction
Stress is a product of the human – environment transaction
Hardiness, resilience, locus of control and self-efficacy are important constructs
Duration of transaction (Episodic, Acute, Chronic)
Environmental stressors
9
Suboptimal environmental conditions pose demands that may exceed an individuals ability to cope
The imbalance between environmental demands and response capabilities is called…..?
…Stress
Environmental stressors include:
Chronic
Noise when living by a freeway
Acute
Noise when in a tunnel
Which is more ...
Stress is very important word of our daily life. In a simple word, it is our response to real or imagined challenges or threats. • Stress influences human biology, physiology, behavior, emotion and cognitive process.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. Definition of stress
Stress is defined as an internal state which can be caused by physical demands on body (disease condition,
exercise, extreme of temperatures etc) or by environmental and social situations which are evaluated as
potentially harmful, un-contrallable, or exceeding our resource for coping.
Introduction to psychology morgan and king
The physical, environmental and social cause of stress state are termed as stressors.
Stress arises when individuals perceive that they cannot adequately cope with the demands being made on
them or with threats to their well-being.” ..Lazarus, R.S. (1966).
stress is any uncomfortable "emotional experience accompanied by predictable biochemical, physiological
and behavioral changes.“
APA
3. According to Seyle…….physiological response of the body to external stressors.
Cox (1975) considers that stress involves external stimuli, the physiological
response to these stimuli, and psychological processes that mediate between
stimulus and response. The psychological processes involve differences between
individuals in their perception of the environmental demands and their own
capacity to cope with them.
4. Stress is a physical, mental, or emotional factor that causes bodily or mental tension.
Stresses can be external (from the environment, psychological, or social situations) or internal
(illness, or from a medical procedure)…. Medical dictionary
A hallmark of the stress response is the activation of the ANS and HPA axis
The organism needs the normal stress hormone response to survive, and inadequate or
excessive adrenocortical and autonomic function is deleterious for health and survival.
5. Human beings are prone to prolonged periods of elevated activity of the same systems which
help us survive more acute challenges.
This prolonged elevation may be due to anxiety; to constant exposure to adverse
environments, and interpersonal conflict; and to changes in life-style and health-related
behaviors that result from being under chronic stress.
Brain - key organ of the stress response because it determines what is threatening and,
therefore stressful and also controls the behavioral and physiological responses to
potentially stressful experiences
6. HISTORY
For centuries, physicians and patients have made the association between
adverse life events and illness.
The links between emotion and sudden cardiac death have been repeatedly noted
in sources as diverse as the Bible, anthropology, and clinical experience.
William Harvey in the 17th century and William Osler in the 19th century
frequently alluded to the relationship between adverse life events and illness
onset.
Many contemporary cultures regard illness as the outcome of being out of balance
with the environment.
7. HISTORY
The term stress was coined by Hans Selye (1907 to 1982), who observed that
many highly diverse ways of perturbing the organism resulted in common
physiological responses.
Selye invoked the adrenocortical system as the crucial responder to stressful
stimulation.
He observed that any novelty or perturbation of the system was associated with
an elevation of adrenocortical activity.
8. HISTORY
Walter Cannon (1871 to 1945): Cannon methodically investigated the other great
pathway of stressful responses, the sympathetic nervous system.
Cannon also focused on more immediate or short-term responses to stressors.
9. Stressors
The physical, environmental and social cause of stress state are termed as stressors.
Usually fall into one or more of:
1. Traumatic events outside the usual range of human experience
2. Uncontrollable events
3. Unpredictable events
4. Events that challenge the limits of our capabilities & self-concept
5. Internal conflicts
10. Natural disasters (e.g., flood, earthquake)
Disasters caused by human activity (e.g., war, terrorism, nuclear accident)
Catastrophic accidents (e.g., car/plane crash)
Physical assaults (e.g., rape/physical assault)
Traumatic Events Outside the Usual Range of Human Experience
12. Unpredictable Events
Predictability helps to reduce stress, e.g.,:
Hurricane/flood warnings
Knowing that a loved one will die
Noise pollution on bonfire night
Unpredictable jobs (e.g., A&E) are considered very stressful
13. Finals exams are a good example:
a) they challenge the limits of our intellectual capabilities.
b) they carry the possibility of failure.
Internal Conflicts
Highly Challenging Events
Incompatible beliefs or courses of action, e.g., smoking behaviour
Everyday Hassles
These can accumulate and create an overall feeling of stress that we can’t blame on one thing
14. WHAT ARE THE COMMON CAUSES OF STRESS IN OUR FAMILY
LIFE
?
RELATIONAL STRESSORS:- EXPECTATIONS
INTOLERANCE / IMPATIENCE
MALADJUSTMENT / INCOMPATIBILITY
PERCEPTUAL DIFFERENCES
FINANCIAL STRESSORS:--
INCOME-EXPENSE MISMATCH.
UNFORESEEN/EMERGENT EXPENSES.
UNPLANNED EXPENSES.
FINANCIAL BLUNDERS.
CLASS COMPETITION
MAJOR LIFE EVENTS
• MARRIAGE
• CHILD BIRTH
• DIVORCE
• DEATH IN FAMILY
• SERIOUS ILLNESS
• RETIREMENT
15. WHAT ARE THE COMMON CAUSES OF STRESS IN OUR
WORK LIFE
Occupational
– Everyday stressors
– Role conflict
– Role ambiguity
– Role over and under load
Quantitative and qualitative
– Ethical dilemmas
– Career development
WORK RELATED STRESS
• DEADLINES
• ROLE AMBIGUITY
• WORK OVERLOAD
• LACK OF RECOGNITION AND RESPECT
• LACK OF SUPPORT AND COMMUNICATION
• LACK OF PARTICIPATION IN DECISIONS
• FEELING OF ‘HAVING NO OPTIONS’
• OFFICE POLITICS
• LACK OF INFORMATION & RESOURCES
• EXCESSIVE TIME SPENT AWAY FROM HOME
16. ARE THERE ANY OTHER FACTORS WHICH INCREASE
STRESS
CHEMICAL AND ENVIRONMENTAL FACTORS WHICH MAY INCREASE STRESS
EXCESSIVE TEA OR COFFEE .
EXCESSIVE SUGAR INTAKE.
TOO MUCH OF SALT / SPICES.
SMOKING AND ALCOHOL.
NOISE AND OVERCROWDING.
17. Stress Responses
STRESS
Behavioural response
Sleep disturbance
Use of alcohol/drugs
Absenteeism
Aggression
Emotional
Fear/anxiety
Anger/irritability
Crying spells
Feeling of guilt, Greif
and hopelessness
Withdrawal/feeling of
abandonment
Depression
Numbness
Cognitive
Confusion
Difficulty concentration/attention skills
Difficulty in decision making/creativity
Memory problems
Slowing of thought processes
Rapid speech/pressure of speech
Frequent Negative thoughts
Biochemical
Increased metabolic rate
Altered hormone levels
(adrenaline, cortisol, ACTH)
Altered endorphin levels
Physiological
Higher blood pressure
Rapid shallow breathing
Increased heart rate
Dilation of pupils
Muscle tension
Dry mouth
Physical
Nausea
Sweating/Chills
Fatigue
Hyperventilation/dizziness
Increased heart rate (heart attack)/high blood pressure
Tremors/shakiness/muscle rigidity
Headaches and irritable bowel syndrome
Increased substance use/nicotine use/caffeine
Sleep difficulties/nightmares
19. Stress and the environment: how much
stress is too much stress?
In many ways the body is built for the purpose of handling stress, and in fact a certain amount of “stress
load” on bones, muscles, and brain is necessary for growth and optimal functioning and can even be
associated with developing resilience to future stressors
Resilence is depend on heterogeneous combination of coping behaviour of indidual, individuals' defensive
behaviors, information-seeking behaviors, affiliative behaviors, and all-round problem-solving behaviors.
20. Development of resilience
Development of stress resilience. In a healthy individual, stress can cause a temporary activation of circuits which is resolved when the stressor is removed. As
shown here, when the circuit is unprovoked, no symptoms are produced. In the presence of a stressor such as emotional trauma, the circuit is provoked yet able to
compensate for the effects of the stressor. By its ability to process the information load from the environment, it can avoid producing symptoms. When the stressor
is withdrawn, the circuit returns to baseline functioning. Individuals exposed to this type of short-term stress may even develop resilience to stress, whereby
exposure to future stressors provokes the circuit but does not result in symptoms
21. Development of Stress Sensitization
However, certain types of stress such as child abuse can sensitize brain circuits and render them vulnerable
rather than resilient to future stressors
Prolonged activation of circuits due to repeated exposure to
stressors can lead to a condition known as “stress sensitization,”
in which circuits not only become overly activated but remain
overly activated even when the stressor is withdrawn.
22. For patients with such vulnerable brain circuits who then become exposed to multiple life stressors as adults, the result can be
the development of depression.
Many studies in fact confirm that in women abused as children, depression can be found up to four times more often than in
never-abused women.
Progression from Stress Sensitization to Depression
23. Stress and vulnerability genes: born fearful?
The l (long allele) genotype of SERT is a more resilient
genotype, with less amygdala reactivity to fearful faces, less
likelihood of breaking down into a major depressive episode
when exposed to multiple life stressors, as well as more
likelihood of responding to or tolerating SSRIs/SNRIs if you
do develop a depressive episode
For those with the s (short allele) genotype of SERT,
they are more likely to develop an affective disorder
when exposed to multiple life stressors and may
have more hippocampal atrophy, more cognitive
symptoms, and less responsiveness or tolerance to
SSRI/SNRI treatment.
24. A functional polymorphism in the promoter region of the serotonin transporter (5-HT T) gene was
found to moderate the influence of stressful life events on depression. Individuals with one or two
copies of the short allele of the 5-HT T promoter polymorphism exhibited more depressive
symptoms, diagnosable depression, and suicidality in relation to stressful life events than
individuals homozygous for the long allele.
Similar observations have been made concerning genetics of the dopamine system in response to
stress .
stressful life events were associated with depressive symptoms only in subjects bearing the A2/A2
genotype of the DRD2 gene.
26. Physiologic Responses to Stressors
The body's reaction to a stressor (be it real, symbolic, or imagined) is to initiate a set of responses that seek to diminish
the impact of the stressor.
A stressor disrupts an organism's equilibrium, and the stress response consists of the initiation of physiologic
adjustments that seek to react to the stressor, bring about an adaptive response and restoring homeostasis
Neurotransmitter Responses to Stress
Endocrine Responses to Stress
Immune changes to stress (Psychoneuroimmunology)
– Biological Connections between the CNS and Immune System
– Behavioral and Psychological Influences on Immunity
– Cytokine Influences on the CNS and Behavior
– Sleep, Cytokines, and Immunity
– Clinical Implications of Psychoneuroimmunology and the Cytokine–Brain Link
27. Neurotransmitter Responses to Stress
Stressors of many kinds activate noradrenergic systems in the brain (most notably in the locus
coeruleus) and cause the release of catecholamines from the autonomic nervous system
Stressors also activate serotonergic systems in the brain as evidenced by increased serotonin (5-
HT) turnover
Stress also has the effect of increasing dopaminergic neurotransmission in mesoprefrontal
pathway.
amino acid and peptidergic neurotransmitters are also intricately involved in the stress response
28. Endocrine Responses to Stress
HPA AXIS:-
In response to stress, CRH is secreted from the hypothalamus
into the hypophysial-pituitary-portal system. CRH acts at the
anterior pituitary to trigger release of adrenocorticotrophic
hormone (ACTH).
Once ACTH is released, it acts at the adrenal cortex to stimulate
the synthesis and release of glucocorticoids.
Glucocorticoids themselves have myriad effects within the body,
but their actions can be summarized in the very short term as
promoting energy utilization, increasing cardiovascular activity
(in the service of the flight-or-fight response), and inhibiting
functions such as growth, reproduction, and immunity.
32. Immune changes to stress (Psychoneuroimmunology)
Immune system is also a key player in stress physiology.
There are numerous bidirectional interactions between brain, behavior, and the immune system, and
these interactions are studied in the field of psychoneuroimmunology.
The immune system provides the body's defense against invading external pathogens such as viruses and
bacteria and from abnormal internal cells such as tumors.
33. Psychoneuroimmunology
Psychoneuroimmunology discuss the following headings
1. Biological Connections between the CNS and Immune System
2. Behavioral and Psychological Influences on Immunity
3. Cytokine Influences on the CNS and Behavior
4. Sleep, Cytokines, and Immunity
5. Clinical Implications of Psychoneuroimmunology and the Cytokine–Brain Link
34. Biological Connections between the CNS and Immune System
Model of human psychoneuroimmunology interactions and clinical implications. The model depicts the bidirectional interactions between
the brain and the immune system, and the clinical implications of immune alterations due to stress, depression, or sleep disturbance.
35.
36.
37. Biological Connections between the CNS and Immune System
The CNS and the immune system are linked by two major physiological systems, the HPA and the autonomic nervous
system composed of sympathetic and parasympathetic branches.
Autonomic Nervous System
The sympathetic nervous system (SNS) is a network of nerve cells running from the brainstem down the spinal cord and out into the
body to contact a wide variety of organs including organs where the immune system cells develop and respond to pathogens
Sympathetic release of norepinephrine and neuropeptide Y, together with receptor binding of these neurotransmitters by immune
cells, serves as the signal in this hard-wired connection between the brain and the immune system
In addition, sympathetic nerves penetrate into the adrenal gland and cause the release of epinephrine into the bloodstream, which
circulates to immune cells as another sympathetic regulatory signal.
sympathetic activation can also shunt some immune system cells out of circulating blood and into lymphoid organs (e.g., spleen),
while recruiting other types of immune cells into circulation (e.g., natural killer [NK] cells).
In general, SNS activation can reduce the immune system's ability to destroy pathogens that live inside cells (e.g., viruses) via
decreases of innate and cellular immune responses, while sparing or enhancing the humoral immune response to pathogens that live
outside cells (e.g., bacteria).
Together, these observations are a cornerstone for understanding fundamental, neuroanatomic signaling between the autonomic
nervous and immune systems.
38. Neuroendocrine Axis
The other way in which the brain can communicate with the immune system is via the HPA system.
Cortisol exerts influence on the actions of various cells involved in an immune response by suppressing
the cellular immune response
cortisol can also prompt some immune cells to move out from circulating blood into lymphoid organs or
peripheral tissues such as the skin.
It is important to note that immune cells can produce neuroendocrine peptides (e.g., endorphin, ACTH),
which suggests that the brain, neuroendocrine axis, and immune system use the same molecular signals
to communicate with one another.
39. Behavioral and Psychological Influences on Immunity
Acute stress and immunity-
Acute laboratory stressors (e.g., mental arithmetic) produce profound and rapid changes
in the immune system due to the redistribution of immunoregulatory cells from
lymphoid organs such as the spleen into the vascular space.
acute stressors elicit decreases in cellular immune responses and increases in markers of
inflammation (e.g., IL-6), which are thought to be mediated by release of sympathetic
neurotransmitters and β-adrenergic receptor activation.
among depressed patients, acute psychological stress leads to exaggerated increases of
inflammatory cytokine activity and greater activation of the inflammatory signaling
pathway, nuclear transcription factor-κB.
Depressed patients with more severe sleep disturbance may also be at greater risk for
elevated levels of IL-6 and other proinflammatory markers because acute sleep loss has
also been shown to induce increases in cellular and genomic markers of inflammation,
which are also mediated by nuclear transcription factor-κB.
40. Chronic Stress, Depression and Immunity
Chronic or naturalistic stressors such as bereavement or caregiving, as well as depression, are
associated with reliable decreases of cellular and innate immunity, along with increases in
proinflammatory cytokine activity, due possibly to a downregulation of glucocorticoid receptor signaling.
Genetic variation in the expression of proinflammatory cytokines may play a role, as stress-induced
increases of plasma-C-reactive protein is reported to occur only in stressed persons who have the A
allele of TNF-α 308 G/A polymorphism.
Disease-specific immune measures has received recent attention, and both depressed and stressed
persons show declines of cellular response to varicella zoster virus (i.e., shingles) and impairments in
responses to vaccines including influenza, pneumococcal, and hepatitis B.
.
41. Chronic Stress, Depression and Immunity
Heterogeneity in the effects of stress and depression on immunity can be accounted for by factors
such as age, gender, ethnicity, health behaviors (e.g., smoking, alcohol consumption) and coping
Depressed patients who have comorbidity for alcohol abuse or tobacco smoking show exaggerated
declines of natural and cellular immune responses.
Personal characteristics such as coping and personality (e.g., positive affect), which moderate
neuroendocrine and sympathetic activity, also contribute to individual differences of immune
responses to psychological stress as well as vaccine responses.
42. Cytokine Influences on the CNS and Behavior
Considerable recent research has focused on how these cytokines signal the brain, given their large
molecular size and inability to cross readily the blood–brain barrier.
It is now known that IL-1 and possibly other inflammatory cytokines communicate with the brain by
stimulating peripheral, afferent nerves such as the vagus.
Immune activation leads to changes of peripheral physiology and behaviors that are similar to a stress
response.
With peripheral immune activation, there is an induction of a pituitary–adrenal response and autonomic
activity via central release of CRH.
Coincident with these physiological changes, animals show reductions in activity, exploration of novel
objects, social interactions, food and water intake, and sexual behaviors, a response pattern that has become
known as sickness behaviors.
43.
44. Human studies have begun to reveal links between peripheral cytokines and behavioral changes.
Associations between cytokines and sleep have recently been extended to measures of daytime
fatigue.
For example, in cancer survivors, persistent fatigue is associated with elevated levels of
circulating and cellular markers of inflammation.
Large doses of cytokines, given as immunotherapy for cancer or hepatitis C, frequently induce
sickness behaviors and depressive symptoms, which can be attenuated by pretreatment with
antidepressant medications.
Interestingly, cytokine-induced activation of the HPA axis may represent a risk marker for
depression. Physiological activation of the immune system with the release of proinflammatory
cytokines leads to increases of depressed mood and anxiety and decreases of memory functions.
Studies using functional magnetic resonance imaging (fMRI) have found that high-dose interferon-α induces significant
activation in the dorsal part of the anterior cingulate cortex, a brain region involved in conflict monitoring and cognitive
control during cognitive tasks with high demand
45. Sleep, Cytokines, and Immunity
Disordered sleep and loss of sleep are thought to adversely affect resistance to infectious disease and alter
inflammatory disease progression.
In humans, normal sleep is associated with a redistribution of circulating lymphocyte subsets, increases of
NK activity, IL-2, IL-6, and the transsignaling IL-6 receptor agonist (IL-6R), and a relative shift toward
Th1 cytokine expression, which is independent of circadian processes
Conversely, sleep deprivation suppresses NK activity and IL-2 production and induces decreases in
specific antibody production to infectious challenge (e.g., vaccination to influenza or hepatitis B virus).
decreases of sleep continuity or increases of rapid eye movement (REM) sleep are associated with
increases in the nocturnal and daytime expression of IL-6, possibly with consequences for daytime fatigue
Expression of the anti-inflammatory cytokine IL-10 prior to sleep predicts amounts of delta sleep during
the nocturnal period
47. Clinical Implications of Psychoneuroimmunology and the Cytokine–Brain Link
(continued……..)
Rheumatoid arthritis.
the presence of depression in rheumatoid arthritis patients undergoing stress is associated with
exaggerated increases of IL-6, a biomarker predictive of disease progression.
Conversely, administration of a psychological intervention that decreases emotional distress
produced improvements in clinician-rated disease activity in rheumatoid arthritis patients and in
patients with psoriasis.
48. Structural changes of brain
(animal studies)
The Hippocampus
The Hippocampus is the brain structure primarily responsible for learning and memory
Within the Hippocampus, is the dentate gyrus, a structure which seems to play a role in the
memory of sequences of events
It has high plasticity and is constantly producing new neurons, even throughout adult life.
Certain types of acute stress and many chronic stressors suppress neurogenesis or cell survival in
the dentate gyrus.
CA3 pyramidal cells undergo a reversible remodeling of their dendrites in chronic stress.
chronic stress causes retraction and simplification of dendrites in the CA3 region of the
hippocampus.
49. These structural changes are mediated by adrenal steroids it also involves interactions
with neurochemical systems in the hippocampus, including serotonin, endogenous
opioids, calcium currents, GABA-benzodiazepine receptors, and excitatory amino acids.
Structural changes cause impairments in memory and learning.
The effects of chronic stress on both morphology and learning disappeared within 1–2 wk
after cessation of the stress suggesting that it serves an adaptive function and does not
constitute “damage.
50. Prefrontal Cortex
Acute and repeated stress caused dendritic shortening in medial prefrontal cortex
Remodeling in PFC result in impairment in attention, extinction of a fear.
51. Stress and Amygdala
Both acute and chronic stress produce dendritic growth in neurons in the amygdala.
The results of include:
– ◦Increases anxiety
– ◦Increased aggression
52. Chronic stress
In animal research, chronic stress causes atrophy of neurons in the hippocampus and prefrontal cortex and
Hypertrophy of neurons in the amygdala Results:
◦Decreased learning and memory
◦Increased anxiety and aggression
The results from animal studies are mirrored in humans through a loss of hippocampalvolume and an
increase in amygdalavolume in MRI studies
PET scans also demonstrate altered patterns of activity in the related brain areas during stress
53. Stress and Psychiatric Illness
Stress and Psychotic Disorders
Affective Disorders
Anxiety Disorders (other than PTSD)
Posttraumatic Stress Disorder
Substance abuse
54. Stress and Psychotic Disorders
There is little reason to suspect that stress plays a role in the pathogenesis of schizophrenia.
Most current etiological theories of schizophrenia focus on genetic and prenatal environmental factors, or a
combination thereof.
There is, however, ample evidence that adverse life events and stressful social or familial milieu play an
important role in determining the course of illness in general and episodes of relapse in particular
Chronic interpersonal stress, “expressed emotion,” poverty, homelessness, and criminal victimization, are
an important risk factors for relapse in schizophrenia
Combined with evidence that schizophrenia renders the individual more susceptible and sensitive to the
negative effects of even minor stressors, it is obvious that stress plays a major role in the course of
schizophrenia
psychosocial interventions to enhance schizophrenic patients' ability to cope with stressful events
55. Affective Disorders
Stress and depression
Stress, BDNF, and brain atrophy in depression
Normally, BDNF sustains the viability of brain neurons , but under stress, the gene for BDNF may be repressed .
56.
57. BDNF promotes the growth and development of immature neurons, including monoaminergic neurons, enhances the
survival and function of
adult neurons, and helps maintain synaptic connections. Because BDNF is
important for neuronal survival, decreased levels may contribute to cell atrophy. In some cases, low levels of BDNF may
even cause cell loss.
58. Stress can lower 5HT levels and can acutely increase, then chronically deplete, both NE and DA.
These monoamine neurotransmitter changes together with deficient amounts of BDNF may lead to atrophy
and possible apoptosis of vulnerable neurons in the hippocampus and other brain areas such as prefrontal
cortex .
A concept of the hippocampal atrophy that has been reported in association with chronic stress and with
both major depression and various anxiety disorders, especially PTSD, Fortunately, some of this neuronal
loss may be reversible.
That is, restoration of monoamine-related signal transduction cascades by antidepressants can increase
BDNF and other trophic factors and potentially restore lost synapses.
In some brain areas such as the hippocampus, not only can synapses potentially be restored, but it is
possible that some lost neurons might even be replaced by neurogenesis.
59.
60. Neurons from the hippocampal area and amygdala normally suppress the hypothalamic–pituitary–
adrenal (HPA) axis, so if stress causes hippocampal and amygdala neurons to atrophy, with loss of
their inhibitory input to the hypothalamus, this could lead to overactivity of the HPA axis
61. In depression, abnormalities of the HPA axis have long been reported, including elevated glucocorticoid levels and
insensitivity of the HPA axis to feedback inhibition.
Some evidence suggests that glucocorticoids at high levels could even be toxic to neurons and contribute to their atrophy
under chronic stress.
Novel antidepressant treatments are in testing that target corticotropin-releasing factor1 (CRF-1) receptors, vasopressin
1B receptors, and glucocorticoid receptors , in an attempt to halt and even reverse these HPA abnormalities in
depression and other stress-related psychiatric illnesses.
62. There is a fundamental similarity between the neuroendocrine effects of stress on humans and
the neuroendocrine abnormalities in major depression. For over 30 years major depression has
been recognized as associated with overactivity of the HPA axis, as inferred by elevated
cerebrospinal CRH levels, increased plasma cortisol and corticotropin (ACTH) levels, increased
urinary free cortisol, increased cerebrospinal fluid cortisol, as well as cortisol resistance to
dexamethasone suppression. There is also evidence that some features of psychotic depression, in
particular, may be mediated by hypercortisolemia
63. Anxiety Disorders (other than PTSD)
Panic disorder frequently has its onset or recrudescence in the context of stressful life events. In
particular, there is evidence to suggest that either interpersonal conflict or serious illness (in a
significant other) may trigger the onset of panic disorder in susceptible individuals
In terms of the effects of early life stressors, there is growing evidence that certain adverse early
life events, such as sexual or physical abuse, may be risk factors for the later development of panic
disorder, particularly in women.
64. Stress and trauma related disorders
DSM-5 recognizes the existence of a group of disorders that are, by definition,
stress-related.
It includes PTSD, acute stress disorder, adjustment disorder, reactive attachment
disorder and disinhibited social engagement disorder.
Acute stress disorder has its onset after particularly traumatic (often life-
threatening) events, such as violent assault or serious accidents, and is denoted
by the presence of prominent dissociative symptoms (e.g., derealization,
numbing).
65. When acute stress disorder occurs after trauma, it identifies a subset of
individuals who are at several fold increased risk for the subsequent development
of PTSD (and major depression).
Any life-threatening event, however common can be considered sufficiently
traumatic that it is capable of eliciting PTSD.
The neuroendocrine profile of patients with PTSD is not what one might expect to
see after chronic stress, ie it is associated with hypocortisolism.
66. Substance use
Stress clearly play a role in acquisition, maintenance, and relapse with drug of
abuse.
Studies in human drug addicts have shown that drug desire can be elicited with
stressors and that this stress-induced response predicts relapse.
Stress-induced dopamine release in the NAc correlates temporally with relapse to
heroin seeking, and stress-induced relapse is partially attenuated by
pretreatment with dopamine antagonists
67. The Underlying Mechanisms...
There are two types of instinctive stress response that are important to
understand stress and stress management.
1. Fight-or-Flight
2. General Adaptation Syndrome
3. The way that we think and interpret the situations in which we find
ourselves.
69. The “General Adaptation Syndrome”
Hans Seyle ( 1956 ) proposed an integrative model for the stress response, known as the “General
Adaptation Syndrome” (GAS).
The GAS is a tri-phasic phenomenon.
Phases of G.A.S.
– Alarm reaction – mobilize resources
– Resistance reaction – cope with stress
– Exhaustion – deplete reserves
70. Alarm Reaction
Immediate response to stress triggers the sympathetic nervous system “fight or flight” through the
hypothalamus
The “flight, fight, or freeze” response which causes you to ready for physical activity
Mobilizes the body for immediate physical activity
Short-lived
When the threat or stressor is identified or realized, the body starts to respond and is in a state of alarm.
During this stage, the locus coeruleus/sympathetic nervous system is activated and catecholamines such as
adrenaline are being produced, hence the fight-or-flight response. The result is: increased muscular tonus,
increased blood pressure due to peripheral vasoconstriction and tachycardia, and increased glucose in
blood. There is also some activation of the HPA axis, producing glucocorticoids (cortisol, aka the S-hormone
or stress-hormone).
71. Resistance Reaction
If stress persists longer than a few hours then the resistance reaction is initiated
Prepares the body for long term protection, slow to start but longer lasting
The hypothalamus triggers the pituitary gland to secrete hormones that will
allow the body to continue to survive the stress until homeostasis is returned
72. Resistance Reaction
Overall goal is to:
– Maintain blood pressure and volume
– Increase ATP production
– Prevent water loss
– Prevent inflammation from causing tissue damage
Maintained by ADH, aldosterone, cortisol, growth hormone, and thyroid
hormones
73. Prolonged exposure to stress hormones:
– Depresses cartilage and bone formation
– Depresses the immune system- infections
– Promote changes in cardiovascular, neural, muscular and gastrointestinal function
(usually due to hypokalemia – potassium deficiency)
Cardiac arrhythmias
Muscle wasting
Fatigue, concentration loss, irritability
Prolonged and Excessive Levels of Stress Hormones
74. Exhaustion Phase
Exhaustion Phase:- If the resistance reaction fails to overcome the stress eventually the body reserves
are exhausted and the resistance reaction cannot be sustained.
In this stage, the body’s capacity to respond to both continuous and new stressors has been seriously
compromised.
The adrenal cortex cannot produce aldosterone and cortisol
“Link between the breakdown of the hormonal adaptation mechanism and fatal diseases” Hans Selye
– Results in illness or death
– Cancer, heart disease, depression, hypertension, diabetes
Recovery stage follows when the system’s compensation mechanisms have successfully overcome the stressor effect
(or have completely eliminated the factor which caused the stress). The high glucose, fat and aminoacid levels in
blood prove useful for anabolic reactions, restoration of homeostasis and regeneration of cells.
75. Yerkes–Dodson law
The Yerkes–Dodson law is an empirical relationship between arousal and performance, originally developed
by psychologists Robert M. Yerkes and John Dillingham Dodson in 1908. The law dictates that performance
increases with physiological or mental arousal, but only up to a point. When levels of arousal become too
high, performance decreases. The process is often illustrated graphically as a bell-shaped curve which
increases and then decreases with higher levels of arousal.