Stress and Pain Flashcards
1
Q
Stress
Definition
A
- the disruption of meanings, understanding, and smooth functioning so that harm, loss, or challenge is experienced, and sorrow, interpretation, or new skill acquisition is required
- stress will affect and is affected by physical, emotional, and/or intellectual functioning
2
Q
Stress
Causes
A
- may experience stress as a result of the threat of something stressful, a planned event (such as a surgery), but most often by unexpected events such as trauma or acute disease processes
- loss of control
- financial concerns
- concerns for others involved in the critical situation
- privacy and personal space become virtually non-existent
- noise
- presence and complexity of technology in the room
- multiple tubes and wires
- physiological changes such as pain, hypotension, hypoxia and tissue injury
3
Q
Consequences of Sustained Stress
Catecholamines
A
- sympathetic nervous system stimulation
- vascular response shunts blood to vital organs
- can lead to problematic cardiac dysrhythmias, mycoardial ischemia or infarction
- hyperventilation
- hyperglycemia
- the metabolic and hormonal changes that accompany the stress response of critical illness results in increased glucogenesis, despite abundantly available insulin
- insulin resistance develops as a result of counter
- immunity is also compromised as polymorphonuclear neutophil function is decreased which leads to increased risk of infection and poor wound healing
- impaired neutrophil activity
- decreased gastric motility
- altered cardiovascular tone
- procoagulant state
- enhanced inflammatory response
- increased fluid retention
- prepares the person in dealing with the stressor
- prolonged HPA axis stimulation leads to an overwhelming stress response and appears to break down the autoregulation mechanism for adrenocorticotropic hormone, ADH, and cortisol
- vascular response shunts blood to vital organs
4
Q
Consequences of Sustained Stress
Mineralcorticoids
A
- primary effect of aldosterone is increased reabsorption of sodium and increased renal excretion of potassium
- excecssive reabsorption of sodium leads to increased extracellular fluid volume and increased blood pressure
5
Q
Consequences of Sustained Stress
Glucocorticoids
A
- the hypothalamus secretes CRF which signals the pituitary to release adrenocorticotrophic hormone which then signals the adrenal cortex to release cortisol
- corisol
- affects the immune system by affecting natural kill cells, macrophage production of cytokines, T cells, and B cells.
- initially produces stress response effects that are similar to the actions of epinephrine, but the duration of epinephrine activity is seconds versus cortisol which is hours
- primary effects are gluconeogenesis, and increase in the rate of amino acid conversion to keto acids and glucose
- affects protein metabolism by increasing the rate of protein synthesis in the liver, but has a catabolic effect in muscle tissue, lymphoid tissue, adipose tissue, skin and bones
- produces a negative nitrogen balance and increasing circulating amino acids
- increased protein catabolism that occurs consequent to increased stress induced cortisol may lead to malnutrition in the critically ill
- promotes gastric secretion
- immunosuppressant by inhibiting the macrophage production of cytokines
- reduces the numbers of nearly all immune response cells
- fibrinogen and platelet productions is increased - DIC risk
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6
Q
Stress and Heart Failure
A
- increased level of circulating norepinephrine
- high norepinephrine cause toxicity, hypertrophy, down-regulation of beta receptors, arrythmias and cell death
- increased aldosterone leads to fluid retention and can worsen heart failure
7
Q
Stress and Sepsis
A
- because sepsis is caused by invasion of pathogenic microorganisms, suppression of immune and inflammatory responses can be devastating, particularly in a patient who is already immunosuppressed.
- immunosuppression occurs in stress, related to cortisol levels, changed receptors on immune cells, altered lympoid organs, and decrease in IL-2 which is necessary for T cell proliferation
8
Q
Stress
Treatment
A
- family involvement
- brings a sense of familiarity to the patient’s environment
- pictures of family faces
- explore with the family coping strategies used previously to help manage stress
- reassurance, teaching, and coaching can then be directed toward encouraging these positive, adaptive responses
- controlling the environment
- try to keep unnecessary noises to a minimal
- reassure patients when alarm rings
- communication
- talk to your patient, orient patient to time, place, and person
- whether your patient is conscious or unconscious, always explain what you are doing to them
- do not discuss your patient’s “over top” of them. Always assume that the patient hears your discussion. Eliminate opportunities for the patient to misinterpret what is being said
- keep the day/night schedule for the patinet by keeping the environment dark at night and natural light during the day
- sedation
- physiological interventions
- manage hypotension, hypoxia, and tissue injury
- glycemic control
- normoglycemia is researched to have a reduction in bloodstream infections, acute renal failure, blood transfusions, and polyneuropathy
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- normoglycemia is researched to have a reduction in bloodstream infections, acute renal failure, blood transfusions, and polyneuropathy
9
Q
Pain
Definition
A
- a complex subjective experience that involves physiological, psychosocial, social, cultural, and spiritual components
- often cited as the greatest stressor
- not simply a pure physiologic response to an injury, but is associated with an emotional response to a sensation
- serves as a protective function by alerting the individual to actual or potential tissue damage, indicating the need for action and self defence
- once pain has served its purpose it may become deleterious - impeding recorvey, prolong hospitalization, and even evolve into chronic pain
10
Q
Neurophysiology of Pain
A
- three components or mechanisms involved in the sensation of pain
- afferent
- includes primary sensory peripheral nerve fibres and their receptive endings in the spinal cord circuitry to process pain information
- central nervous system
- pathways projecting pain to the brain; limbic system, thalamus, cortex, hypothalamus, and pituitary gland integration and modulation of pain
- efferent
- sensations and reaction to pain
- afferent
11
Q
Nociceptive Afferent Fibres
A
- free nerve endings sensitive to high-intensity stimuli that are tissue damaging in nature or could cause tissue damage if sustained
- distal portions of primary afferent fibres that transmit the noxious impulse to the dorsal horn of the spinal cord
- two types
- large, myelinated A-delta fibres with rapid conduction velocity
- activated by high-intensity mechanical stimuli such as a cut or electric shock
- can also be activated by heat
- “fast pain”
- sharp, stinging
- smaller unmyelinated C fibres that conduct impulses more slowly
- aching, burning, throbbing
- more abundant
- higher threshold for stimulation
- large, myelinated A-delta fibres with rapid conduction velocity
- vsiceral pain tends to be more diffuse than cutaneous pain
- occurs because visceral nociceptive fibres enter the spinal cord alongside axons from the skin receptors and the dorsal horn neurons do not consistently distinguish the origin of incoming stimuli
- less responsive to ischemia and distention
- more prominent autonomic component than cutaneous pain because nociceptive input from primary afferent fibres traverses the sympathetic and parasympathetic chains
- nociceptors convert the noxious stimuli into an electric signal that is propagated along the length of the nerve fibre.
- many local anesthetics and anticonvulsants exert their antinociceptive effect by blocking these ion channels in the primary afferent fibres
12
Q
Pain Mediating Substances
A
- bradykinin
- most potent released substance with tissue damage
- acetylcholine
- potassium
- hydrogen
- histamine
- substance P
- direct pain mediator
- causes blood vessels in the area to release substances which irritate nerve endings
- prostaglandins
- leukotrienes
- adenosine triphosphate (ATP)
13
Q
Pain Pathways
A
- Lateral Spinothalamic
- Anterior Spinothalamic
- Spinoreticulothalamic
- all carry sensations from the periphery to the thalamus, communicating with the reticular activating system above the brainstem, and then on to the sensory cortex
- both fast and slow components of the pain response may occur
- ascending afferent information and spinal reflex activity are subject to selection, modulation, and control through the influence of descending inhibitory pathways
- the inhibitory effect of the nerve stimulation is throught to be the result of activation of both the inhibitory interneurons at the level of the spine and the descending inhibitory systems
14
Q
Processing of Pain
A
- interconnections between the thalamus and sensory cortex add precision and discrimination to the sensation of pain
- association areas of the sensory cortex are essential to the preception, or learned meaningfulness, of the pain preception
- the emotional and affective responses to pain are determined by the limbic system
- sensory-discriminitive dimension pertains to discerning location, intensity, and modality (chemical, mechanical, thermal) aspects of nociceptive information
- affective-motivational component relates to the unpleasantness of suffering aspects of pain
- cognitive-evaluative component is releated to the role of memory and past experience in mediating the current perception of pain
15
Q
Responses to Pain (Efferent)
A
- adrenal medulla
- sympathetic nervous system is stimulated with pain perception and/or pain trasmission
- catecholamine release increases with pain intensity
- lead to responses that increase oxygen demand
- effects
- pupil dilation
- increased gluconeogenesis
- increased metabolic rate
- increased heart rate
- increased blood pressure through vasoconstriction
- increased preload
- increased myocardial perfusion
- increased myocardial oxygen consumption
- increased respiratory rate
- bronchial dilation
- decreased gastric motility
- urinary retention
- pituitary gland
- posterior pituitary gland releases vasopressin (ADH)
- sodium and water retention
- anterior pituitary gland secretes adrenocorticotropic hormaon which stimulates the release of aldosterone and cortisol from the adrenal cortex
- gluconeogenesis
- reduced insulin secretion
- mobilization of fat and amino acids
- platelet and fibrinogen production
- decreased release of lymphocytes
- altered immune response
- sodium reabsorption
- potassium secretion
- water retention
- posterior pituitary gland releases vasopressin (ADH)
