Mind Map Gallery Stress and Disease
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Stress and Disease
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Edited at 2020-09-28 11:47:11
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Stress and Disease
Neuroendocrine Regulation
Neuroendocrine Regulation
SNS: Is aroused during the stress responseCauses the adrenal gland medulla to release catecholamines
Hypothalamic CRH stimulates the pituitary gland to release a variety of hormones
Posterior pituitary gland: Antidiuretic hormone and oxytocin
Anterior pituitary gland: Prolactin, endorphins, growth hormone (GH), and adrenocorticotropic hormone (ACTH), which stimulate the adrenal gland cortex to release cortisol
Catecholamines - Bound to albumin
Mimic sympathetic stimulation
Released from chromaffin cells of the adrenal medulla
Large amounts of norepinephrineSmall amounts of epinephrine
Noreprinephrine
Peripherial vasoconstriction - Raises Blood Pressure
Dilates Pupils
Piloerection - hairs stand up
Sweaty arm pits, palms
Epinephrine
Acts on Several organs - Metabolized quicklyMetabolic Regulation Decreased insulin = Decreased glucose uptakePromoting Gluconeogenesis and glycogenolysis in Liver
Cardiac action: Increases myocardial contractility (Inotropic effect)Increases Heart rateVasodilation =Increased venous return = increased cardiac output/blood pressure and oxygenation
Receptor Binding Types
α-adrenergic receptors (α1 and α2)
β-adrenergic receptors (β1 and β2)
Epinephrine: Binds and activates both α- and β-adrenergic receptorsNorepinephrine: Binds primarily to α-adrenergic receptors
Glucocorticoid
Cortisol activated by ACTH
Stimulates gluconeogenesis
Elevates the blood glucose level
Has a protein anabolic effect in the liver and a catabolic effect in other tissues
Is lipolytic in some areas of the body and lipogenic in others
Is a powerful antiinflammatory or immunosuppressive agent
Causes poor wound healing and an increased susceptibility to infection
Metabolic syndrome and the pathogenesis of obesity
Development of diabetes is secondary to cortisol-induced obesity
Chronic cortisol excess = lipogenesis in the abdomen, trunk, face, resulting in central obesity
Cortisol and the Immune System
T1 helper activity supressed
T2 activity is stimulated
T1 to T2 shift. (T1 decreases and T2 increases)
Systemic responses may decrease innate immunity enhancing adaptive immunity
Local responses can produce pro-inflammatory activities
Cortisol and the Immune System Effects
A patient will have stress and release cortisol
Increases protein synthesis in the liver (Anabolic action)
Promotes gastric secretions
Suppresses immune function and reduces inflammation
Reduces fibroblasts at wound sites and slows wound healing
Stress, Personality, Coping, and Illness
A stressor for one person may not be a stressor for another
Psychologic distress
General state of unpleasant arousal after life events that result in physiologic, emotional, cognitive, and behavior changes
Coping
Is managing stressful demands and challenges that are appraised as taxing or exceeding the resources of the person.
May be adaptive or maladaptive
Stress and the Immune System
Prolactin, Oxytocin, Testosterone
Prolactin
Pituitary gland
Anterior pituitary gland
Lactation and breast development
Oxytocin
HypothalamusOrgasm
Posterior pituitary gland
Released during child-birth and lactation.Has antistress properties. Reduces HPA activity
Testosterone
TestesAdrenal glands
Leydig cells
Regulates libido and male secondary sex characteristics.Decreases after stressful stimuli
Somatotropin (Growth Hormone)
Produced by:Anterior PituitaryMononuclear Phagocytic cells
Functions:Affects protein, lipid, and carbohydrate metabolism.Counters the effects of insulinEnhances immune function
Endorphins and Enkephalins
These are proteins in the brain that have pain relieving action
Causing insensitivity to painincreased feeling of excitement, pos well-being, even euphoria (runners high)
Hormones of the Female Reproductive System
Cortisol suppresses the release of luteinizing hormone, estradiol, and progesterone
Stress suppresses the hypothalamic gonadotropin-releasing hormone
Estrogen stimulates the HPA axis
Leptin inhibits the HPA axis - maybe decrease food intake
Other Hormones
Neuropeptide Y (NPY): Sympathetic neurotransmitter
NPY is a stress mediator
NPY is a growth factor for many cells
implicated in atherosclerosis and tissue remodeling
Other hormones can influence the stress and immune responses
Some may suppress or enhance the immunity responseResponse is dependent upon the concentration and length of exposure, the target cell, and the specific immune function studied
Concepts of Stress
Causes psychologic and physical responses. Defined as interactional/transactional (How we interact, perceive, experience stress). Demand of stress may exceed coping abilities resulting in disturbed thinking, emotions or behaviors that are maladaptive and adversely effect wellness.
Reactive response involves psychologic stressorsAnticipatory response anticipates a disruption in homeostasisConditional response associates a stimulus with danger may cause posttraumatic stress disorder (PTSD) or phobias
Can precipitate diseaseCardiac diseaseCan worsen an existing diseaseIrritable bowel diseaseAsthmaAutoimmune diseasesHuman immunodeficiency virus (HIV) progression
PTSD - in response to a memory
Historical Background - Dr. Hans Selye
Dr. Selve worked to discover a new sex hormone
Injected ovarian extracts into rats
Dr. Selve witnessedEnlargement of the adrenal cortexThymic atrophyDevelopment of bleeding ulcers in the stomach and duodenal liningWitnessed these changes with many agents and called these stimuli stressors
Dr Selve termed - GAS - General Adaptation Syndrome
GAS has 3 Stages
Alarm stage - Arousal of body defenses—fight or flight. Triggers hypothalamic-pituitary-adrenal (HPA) axis
Stage of resistance or adaptation. Mobilization that contributes to fight or flight. Begins with the actions of adrenal hormones. Cortisol, epinephrine, and norepinephrine
Stage of exhaustion (Allostatic overload)Breakdown of compensatory mechanisms - May lead to diseaseOnly happens if stress continues without adaptation
Psychoneuroimmunologic Mediators (PNI)Of Stress
Defined as: Conscious interactions from the brain, spinal cord, bodies defense
Stressors elicit a response of the Nervous & Endocrine systems (Pain, Trauma, Malnutrition, Excitement, Drugs, Surgery an many others)
Stress Response
Starts with the central nervous system and the endocrine system
Corticotropin-releasing hormone (CRH) is released from the hypothalamus
CRH is also peripherally released at inflammatory sites
May be perceived as real threat
Norepinephrine promotes arousal, increased vigilance, increased anxiety, and other protective emotional responses
Central Stress Response
Major Stress Hormones
Glucocorticoids from the adrenal cortex in response to adrenocorticotropic hormone (ACTH) from the pituitary gland
Parasympathetic System
Balances the SNS (Opposes Catechloamine)Influences adaptation or maladaptation to stress
Allostasis
Adaptive Physiological response to stress - Chronic or Disregulated long term exaggerated response can lead to disease
Allostatic Load - cumulative (genetic, lifestyle, behavioral)
Allostatic Overload - PNS decreases restraint of SNS prolonging inflammatory response. The brain is influential in determining when overload occures
Many immune-related conditions and diseases are associated with stress.Stress and negative emotions increase levels of pro-inflammatory cytokines, providing a possible link among stress, immune function, and disease. Stress-induced immune changes affect immune cell functions.
decreased natural killer cell
Stress-induced immune changes cause
cause impaired B cell function
increased risk for infection
decrease in melatonin
Aging and Stress
Excitability changes in the limbic system and hypothalamus
Increased catecholamines, antidiuretic hormone (ADH), ACTH, and cortisol
Decreased testosterone, thyroxine, and other hormones
Alterations of opioid peptides
Immunodepression
Alterations in lipoproteins
Hypercoagulation of the blood
Free radical damage of cells
Development of stress reactions
Lower adaptive reserve and coping mechanisms