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Pathophysiology - UT Houston SON Grad School > Module 3: Topic 1: Stress Adaption > Flashcards

Module 3: Topic 1: Stress Adaption Flashcards

1
Q

What is physiologic stress?

A

A chemical or physical disturbance in the body produced by a change that requires a response. (Hans Selye)

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2
Q

HPA Axis

A

Hypothalamic-Pituitary-Adrenal (HPA) Axis.

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3
Q

What is homeostasis?

A

A balanced physiological and psychological state of an organism, “steady state”.

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4
Q

What is the General Adaptation Syndrome?

A

Nonspecific response to noxious stimuli.

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5
Q

GAS Stages

A
  1. Alarm: CNS aroused and body’s defenses initiated (fight or flight)
  2. Resistance: or adaptation- mobilization contributes to “fight or flight”
  3. Exhaustion: continuous stress causes progressive breakdown of compencompensatory mechanismstations) & homeostatis.
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6
Q

Stress Response

A
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7
Q

HPA Hormonal Release Sequence

A

Stress

|

Hypothalamus → CRH (CorticoTropin Releasing Hormone)

|

CRH → Binds in pituitary receptors → ACTH (Adreno-CorticoTropic Hormone)

|

ACTH travels to adrenal glands → release Glucocorticoid hormones (Cortisol primarily)

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8
Q

When is stress experienced?

A

A person experiences stress when:

Demand exceeds a person’s coping abilities,

resulting in reactions such as:

Cognition disturbances

Emotion

Behavior that can adversely affect well-being.

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9
Q

What is the reactive response?

A

A physiologic response from psychological stress.

(example: stress of taking an exam = initiation of stress response)

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10
Q

What is the anticipatory response?

A

Physiologic responses develop in anticipation of disruption homeostasis.

(example: anxiety about upcoming exam performance = initiation of stress response)

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11
Q

What is a conditional response?

A

Occurs when one learns that specific stimuli are associated with dangers - the anticipation of subsequent encounters produces physiologic stress.

(example: abused child experiences physiologic stress when parent enters the room)

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12
Q

Explain brain process for anticipatory response stress

A
  • Anticipatory responses are LEARNED
  • Controlled by regions of brain’s limbic system
  • Hippocampus, amygdala and prefrontal cortex (assc. with learning and memory)

|

  • For stress response to happen - PVN (paraventricular nucleus) of Hypothalamus must be stimulated.
  • The above limbic structures rarely interact with PVN - so they use intermediary neurons to get response.
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13
Q

HPA vs. Stages

A

Alarm ⇒ stressors triggers hypothalamus and sympathetic nervous system

Resistance ⇒ adrenal hormones: cortisol, norepinephrine, epinephrine

Exhaustion=impaired immune response and chronic disease

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14
Q

What is PTSD response?

A

Memory of traumatic events initiates stress response.

(example: memories of war horrors initiate stress response)

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15
Q

What is psychoneuroimmunology PNI?

A

Study of interaction of:

consciousness (psycho)

+

brain & spinal cord (neuro)

+

body’s defense against infection and abnormal cell division (immunology)

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16
Q

What three areas does corticotropin-releasing hormone affect?

A
  1. Sympathetic nervous system
  2. Pituitary gland
  3. Adrenal gland
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17
Q

Neural Recognition and Response to Real or Predicted Stressors

A
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18
Q

What structures of the CNS begin the stress response?

A

It depends: Percieved vs. Real stressors

Perceived Stressors:

  • Elicit anticipatory response; Limbic system (emotions and cognition) →
  • Indirectly elicits both:
    • endocrine (sensory information enhanced) &
    • central stress response (stimulating LC-Locus Ceruleus –> Norepinephrine (arousal, increased vigilance, anxiety)

Real Stressors:

  • Elicit reactive response; Limbic system OR brain regions receiving sensory info.
  • Info relayed to PVN
  • PVN stimulates LC and both central and endocrine responses
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19
Q

What stress response is related to perceived stressors?

A

Perceived Stressors –> ANTICIPATORY RESPONSE

  • Elicit anticipatory response; Limbic system (emotions and cognition) →
  • Indirectly elicits both:
    • endocrine (sensory information enhanced) &
    • central stress response (stimulating LC-Locus Ceruleus –> Norepinephrine (arousal, increased vigilance, anxiety)
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20
Q

What stress response is related to real stressors?

A

Real Stressors –> REACTIVE RESPONSE

  • Elicit reactive response; Limbic system OR brain regions receiving sensory info.
  • Info relayed to PVN
  • PVN stimulates LC and both central and endocrine responses
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21
Q

What is allostasis?

A

An adaptive physiologic response to stressful events (fight/flight).

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22
Q

What does chronic or dysregulated allostasis lead to?

A

DISEASE

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23
Q

What is allostatic load?

A

Individualized cumulative amounts of stressor that exist in our lives and influence our physiologic responses.

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24
Q

What happens during allostatic overload?

A

The parasympathetic system may decrease its restraining of the sympathetic system, resulting in increased/prolonged inflammatory responses.

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25
Q

What are physiologic brain changes that happen under acute/chronic stress?

A

Some regions of the brain may respond by undergoing:

Structural Remodeling –> behavioral and physiologic responses (cognitive impairment or depression)

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26
Q

What is allostatic overload?

A

Exaggerated pathophysiologic responses to stress.

27
Q

What happens when the sympathetic nervous system is aroused by the stress response?

A

Causes :

  1. Medulla of the adrenal gland to release catecholamines:
  • Epineprhine 80%
  • NORepineprhine 20%
  1. Hypothalamic CRH
  • Posterior-pituitary → ADH & Oxytocin
  • Anterior-pituitary → Prolactin, Endorphins, Growth Hormone & ACTH (adrenocorticotropic hormone)
  1. ACTH → stimulates cortex of Adrenal glands → Cortisol
28
Q

What are two catecholamines produced in the adrenal glands?

A

Epinephrine

and

Norepinephrine

29
Q

What physiologic effects does norepinephrine have?

A
  • Regulates BP by constricting smooth muscle in blood vessels
  • Increases BP during stress
  • Dilates pupils
  • Piloerection (goose bumps)
  • Increase sweat in palms and armpits
  • Effects primarily SNS - very little reaches distal tissue
30
Q

What physiologic effects does Epinephrine have?

A

Short-acting b/c of quick metabolization

  • Causes transient hyperglycemia
  • Decreases glucose uptake in muscles/organs
  • Decreases insulin release in pancreas
  • Principal catecholamine in metabolic regulation
  • Enhances myocardial contractility
  • Increases HR
  • Increase venous return
  • Overall increase in CO and BP
  • Dilates blood vessels in skeletal muscles (allowing more O2 in muscle)
  • Stimulates lipolysis - mobilizing free fatty acids and cholesterol (protecting degradation into bile acids)
  • Aids in Cortisol metabolic actions
    *
31
Q

Physiologic actions of adrenergic receptor: Alpha-1

A

Increased Glycogenolysis

Smooth muscle contraction (blood vessels and GU tract)

32
Q

Physiologic actions of adrenergic receptor: Alpha-2

A

Smooth muscle relaxation (GI)

Smooth muscle contraction (some vascular beds)

Lipolysis inhibition

Renin release inhibition

Platelet aggregation inhibition

Insulin secretion inhibition

33
Q

Physiologic actions of adrenergic receptor: Beta-1

A

Stimulation of lipolysis

Myocardial contraction (increased rate and contractile force)

34
Q

Physiologic actions of adrenergic receptor: Beta-2

A

Increased hepatic gluconeogenesis & glycogenolysis

Increased muscle glycogenolysis

Increased release of insulin, glucagon, and renin

Smooth muscle relaxation (bronchi, blood vessels, GU and GI tract)

35
Q

Physiologic Effects of Cortisol:

Carbohydrate and Lipid Metabolism

A
  • Diminished use/update of glucose
  • Promotes gluconeogenesis
  • Promotes lipolysis
36
Q

Physiologic Effects of Cortisol:

Protein Metabolism

A
  • Increase protein synthesis liver
  • Decreased protein synthesis everywhere else (muscle, lymphoid tissue, adipose, skin and bone)
37
Q

Physiologic Effects of Cortisol:

Anti-inflammatory Effects

(Systemic Effects)

A
  • High levels used in drug therapy to suppress inflammatory response
  • Inhibits Pro-Inflammatory response of many growth factors and cytokines

Over time some may develop tolerance to glucocorticoids - causing increased susceptibility to inflammation and autoimmune disease.

38
Q

Physiologic Effects of Cortisol:

Pro-Inflammatory Effects

(possible local effects)

A
  • Increases pro-inflammatory response
39
Q

Physiologic Effects of Cortisol:

Lipid Metabolism

A
  • Lipolysis in extremities
  • Lipogenesis in face and truck
40
Q

Physiologic Effects of Cortisol:

Immune Effects

A

Medical Treatment:

  • Used at treatment levels = immunosuppressive
  • Suppression of T-cells (Th1 function innate immunity) (at large doses)

Under Stress:

  • Th1 to Th2 Shift
    • Suppress innate Th1 and increase adaptive Th2
  • Locally (vs. systemic effect) - can induce Pro-Inflammatory effects:
    • onset/course of infection
    • auto-immune/inflammatory allergic and neoplastic diseases
41
Q

Physiologic Effects of Cortisol:

Digestive Function

A

Promotes gastric secretions.

42
Q

Physiologic Effects of Cortisol:

Urinary Function

A

Enhances secretion of calcium

43
Q

Physiologic Effects of Cortisol:

Connective Tissue Function

A
  • Decreases healing
    • Decreased proliferation of fibroblasts in connective tissue
44
Q

Physiologic Effects of Cortisol:

Muscle Function

A
  • Maintains normal contractility
  • Maximal work output for skeletal and cardiac muscle
45
Q

Physiologic Effects of Cortisol:

Bone Function

A
  • Decreases bone formation (osteoporosis)
46
Q

Physiologic Effects of Cortisol:

Vascular System / Myocardial Function

A
  • Maintain normal BP
  • Allows for increased response to adrenergic stimulation (arteriole constriction)
  • Optimizes myocardial performance
47
Q

Physiologic Effects of Cortisol:

CNS Function

A
  • Modulates perceptual and emotional functioning
  • Essential for normal arousal and initiation of daytime activity
48
Q

Physiologic Effects of Cortisol:

Synergism with Estrogen in Pregnancy

A
  • Suppress maternal immune system to prevent rejection of fetus (?)
49
Q

What is coping?

A

The process of managing stressful demands and challenges that are appraised as taxing or exceeding the resources of the person.

50
Q

Stress & Coping

A
51
Q

Describe the physiologic and psychological effects of a chronic stress response:

A

The stress response is designed to be an acute self-limited response in which activation of the ANS and the HPA axis is controlled in a negative feedback manner.

As with all negative feedback systems, pathophysiologic changes can occur in the stress response system. Function can be altered in several ways, including when a component of the system fails; when the neural and hormonal connections among the components of the system are dysfunctional; and when the original stimulus for the activation of the system is prolonged or of such magnitude that it overwhelms the ability of the system to respond appropriately. In these cases, the system may become overactive or underactive.

Chronicity and excessive activation of the stress response can result from chronic illnesses as well as contribute to the development of long-term health problems. Chronic activation of the stress response is an important public health issue from both a health and a cost perspective. The stress response is linked to a myriad of health disorders, such as diseases of the cardiovascular, gastrointestinal, immune, and neurologic systems, as well as depression, chronic alcoholism and drug abuse, eating disorders, injuries, and suicide.

Occurrence of the oral disease acute necrotizing gingivitis, in which the normal bacterial flora of the mouth become invasive, is known by dentists to be associated with acute stress, such as final examinations.

Similarly, herpes simplex virus type 1 infection (i.e., cold sores) often develops during periods of inadequate rest, fever, ultraviolet radiation, and emotional distress. The resident herpes virus is kept in check by body defences, probably T lymphocytes, until a stressful event occurs that causes suppression of the immune system.

Psychological stress is associated in a dose– response manner with an increased risk for development of the common cold, and this risk is attributable to increased rates of infection rather than frequency of symptoms after infection. In a study in which participants were infected with the influenza virus, those persons who reported the greatest amount of premorbid stress also reported the most intense influenza symptoms and had a statistically greater production of interleukin-6, a cytokine that acts as a chemotactic agent for immune cells.

Elderly caregivers of a spouse with dementia had a significantly higher score for emotional distress and higher salivary cortisol than matched control subjects. The higher stress was correlated with a decreased immune response to the influenza vaccine.

The experience of stress also has been associated with delays in wound healing.

Hannon, Ruth (2016-01-04). Porth Pathophysiology: Concepts of Altered Health States (Kindle Locations 10022-10038). Wolters Kluwer Law & Business. Kindle Edition.

52
Q

Cite Cannon’s 4 features of homesotasis

A

Constancy in an open system, such as our bodies represent, requires mechanisms that act to maintain this constancy. Cannon based this proposition on insights into the ways by which steady states such as glucose concentrations, body temperature and acid-base balance were regulated.

Steady-state conditions require that any tendency toward change automatically meets with factors that resist change. An increase in blood sugar results in thirst as the body attempts to dilute the concentration of sugar in the extracellular fluid.

The regulating system that determines the homeostatic state consists of a number of cooperating mechanisms acting simultaneously or successively. Blood sugar is regulated by insulin, glucagons, and other hormones that control its release from the liver or its uptake by the tissues.

Homeostasis does not occur by chance, but is the result of organized self-government.

53
Q

Describe the components of a control system

A

Homeostatic control mechanisms have at least three interdependent components:

  1. Receptor,
  2. Integrating center
  3. Effector

The receptor senses environmental stimuli, sending the information to the integrating center.

The integrating center, generally a region of the brain called the hypothalamus, signals an effector (e.g. musclesor an organ) to respond to the stimuli.

54
Q

Function of a negative feedback system

A

A feedback loop in which the output of a system reduces the activity that causes that output.

Negative feedback brings a system back to its level of normal functioning.

Adjustments of blood pressure, metabolism, and body temperature are all negative feedback.

55
Q

Function of a positive feedback system

A

A feedback loop in which the output of a system is increased by the mechanism’s own influence on the system that creates that output.

Positive feedback enhances or accelerates output created by an activated stimulus.

Platelet aggregation and accumulation in response to injury is an example of positive feedback.

56
Q

What is a stressor?

A

Activity/Event/Other Stimulus that causes stress / causes release of stress hormones.

57
Q

Cite two factors that influence the nature of the stress response

A

Is stressor percieved or real?

Percieved stressors –> anticipatory response

Real stressors –> reactive response

58
Q

Contrast Anatomic vs. Physiologic Reserves

A

Physiologic reserve- the ability of body systems to increase their function given the need to adapt.

Many body organs , such as lungs, kidneys, and arenals, are paired to provide anatomic reserve.

Both organs are not needed to ensure the continued existence and maintenance of the internal environment many persons function normally with only one lung or one kidney

59
Q

List at least six factors that influence a person’s adaptive capacity

A

Ability to adapt is influenced by

  • previous learning
  • physologic reserve
  • time
  • genetic endowment
  • age
  • health status and nutrition
  • sleep wake cycles
  • and psychosocial factors
60
Q

Eplain the purpose of adaptation:

A

Adaptation is the ability to respond to challenges of physical or psychological homeostasis and to return to a balanced state.

Hannon, Ruth (2016-01-04). Porth Pathophysiology: Concepts of Altered Health States (Kindle Locations 9869-9870). Wolters Kluwer Law & Business. Kindle Edition.

61
Q

Propose a way by which social support may serve to buffer challenges to adaptation:

A

OXT reduces amygdala and HPA axis reactivity to stressors and as such it is an important mediator of the anxiolytic and stress-protective effects of positive social interaction (‘social buffering’).

Oxytocin also has antistress properties, as has been shown in animal experiments in which elevations in endogenous oxytocin level were associated with reduced HPA activation
levels and reduced anxiety.

Oxytocin in some tissues works in concert with estrogen; these two hormones have a calming effect
during stressful situations.

McCance, Kathryn L.; Huether, Sue E. (2015-06-08). Pathophysiology: The Biologic Basis for Disease in Adults and Children (Pathophysiology the Biologic Basis) (Page 352). Elsevier Health Sciences. Kindle Edition.

62
Q
A
63
Q

Describe the three states characteristic of post-traumatic stress disorder

A

Three different types of post-traumatic stress disorder exist.

  1. If symptoms last less than three months, the condition is considered acute PTSD.
  2. If symptoms last at least three months, the disorder is referred to as chronic PTSD.
  3. If symptoms manifest at least six months following a traumatic event, the disorder is classified delayed-onset PTSD, according to the National Institute of Health (NIH).

The eight criteria required for PTSD diagnosis in adult, adolescents, or children over the age of 6 years:

A. Must include actual or threatened exposure to a traumatic event( s) or stressor( s) (e.g., death). The exposure can be in one or more of the following ways: • Direct • Witnessed • Indirect learning about close friend or relative’s accidental or violent death • Repeated

B. Intrusion or re-experiencing (one required) of events such as: • Intrusive thoughts or memories • Nightmares or dreams • Flashbacks or images • Intense psychological distress or physical reactivity to reminders of events (e.g., birthday)

C. Avoidance (one or both required). Persistent efforts to either: • Avoid thoughts, feelings, or conversations connected with traumatic event • Avoid people, places, or situations that may trigger reminders of the traumatic event

D. Negative alteration in mood or cognition (two or more required). A decline in mood or thought patterns, including: • Memory problems about specific traumatic event • Persistent and exaggerated negative beliefs about oneself or others • Distorted sense of blame about the cause of the event • Persistent negative emotional state • Significant diminished interest or participation in pre-trauma activities • Feeling of detachment or isolation from others • Persistent inability to experience positive emotions

E. Hyperarousal (two or more required). Symptoms worsening after traumatic event such as: • Irritability and increased temper or anger • Self-destructive behaviour • Hypervigilance • Exaggerated startle response • Concentration problems • Sleep disturbances

F. Duration of symptoms (B, C, D, and E) must be more than one month.

G. This disturbance must cause clinically significant distress or impairment in functioning.

H. This disturbance is not due to any other medical conditions or substance use.

Hannon, Ruth (2016-01-04). Porth Pathophysiology: Concepts of Altered Health States (Kindle Locations 10063-10089). Wolters Kluwer Law & Business. Kindle Edition.

64
Q

List five nonpharmacologic methods of treating stress.

A
  1. Relaxation
  2. Guided Imagery
  3. Music Therapy
  4. Massage Therapy
  5. Biofeedbac

Pathophysiology - UT Houston SON Grad School (5 decks)

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