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Flashcards in Pain Deck (30):

Pain (2)

1. Pain is the most common symptom that brings a patient to a physician's attention.

2. Pain is defined as an unpleasant sensation localized to a part of the body.
*It is often described in terms of a penetrating or tissue-destructive process (e.g., stabbing, burning, twisting, tearing, squeezing) and/or of a bodily or emotional reaction (e.g., terrifying, nauseating, sickening).

3. Pain of moderate or higher intensity is accompanied by anxiety and the urge to escape or terminate the feeling; pain is both a physical sensation and an emotion.
*Has a strong neurological basis


Function of Pain

The function of the pain sensory system is to protect the body and maintain homeostasis by detecting, localizing, and identifying potential or actual tissue-damaging processes.


Acute Pain

1. associated with behavioral arousal and a stress response consisting of increased blood pressure, heart rate, pupil diameter, and plasma cortisol levels.

2. In addition, local muscle contraction (e.g., limb flexion, abdominal wall rigidity) is often present.
*Limb flexion: to withdraw limb from painful stimulation
*Abdominal wall rigidity: bear down when we feel pain


How is Pain sensed?

1. The Primary Afferent Nociceptor

2. Nociception: physical sensing of pain

3. Nociceptor: neuronal cell that senses painful stimulation
*They are afferent nerves, which are types of peripheral nerves (peripheral nerves start off as spinal nerves)


Classifications of Primary Afferent Nerves (3)

1. Diameter,
2. Degree of myelination
3. Conduction velocity


A-beta fibers (4)

1. Have the largest diameter

2. Respond maximally to light touch and/or moving stimuli
*Somatosenosray fibers that convey touch and movement across skin

3. They are present primarily in nerves that innervate the skin

4. The activity of these fibers DOES NOT PRODUCE PAIN


myelinated A-delta fibers (2)

1. Smallest diameter

2. Respond to low intensity painful stimulation


Unmyelinated C-fibers (3)

High intensity painful stimulation


Painful Stimuli (4)

1. Includes noxious stimuli such as: intense heat and cold, intense mechanical

2. Stimuli like a pinch, changes in pH (especially acidity), and application of chemical irritants (both endogenous and exogenous.)

3. Exogenous irritants: things from the outside world

4. Endogenous: inflammatory mediators and some components of intracellular fluid, like potassium is irritating to nerves


C-fibers that project into dorsal horn of spinal cord (2)

1. These are somatosensory

2. Convey painful stimulation from the surface of the skin that we are conscious of


C-fibers that project into the sympathetic ganglia (2)

1. These are visceral afferent, and conveys visceral pain/stimulation
*Ex: if there is death of myocardial tissue that triggers inflammation/pain, the pain will be conveyed through the c-fiber that goes into the sympathetic chain

2. Project into the sympathetic ganglia where the autonomic nerves project into


Sensitization (4)

1. When we injure our body, the area of the wound becomes extremely sensitive and even an area surround the laceration becomes tender
*The lightest tough that would normally not be painful all of a sudden becomes painful
*This process is called sensitization

2. When intense, repeated, or prolonged stimuli are applied to damaged or inflamed tissues.

3. The threshold for activating primary afferent nociceptors is lowered, and the frequency of firing is higher for all stimulus intensities.
*This is process is called sensitization and a variety of inflammatory mediators contribute the process.

4. Designed to stimulate you to protect the wounded area; cover it, shield it, etc. from further injury


Primary Activation Stage of Sensitization (3 steps)

Happens at the site of injury

1st: Cell damage and death at site of injury
*When cells die, their intracellular material becomes acidic, and the acidic material gets released into the extracellular fluid
*Also have release of intracellular potassium

2nd: As a result of inflammation and cell damage → get production of prostaglandins (PG) and bradykinin (BK)

3rd: All of these mediators are increasing the excitability of the nocicpetor nerve ending
*This increased excitability is sensitizing the nerve ending, meaning that even the lightest touch on the area of injury will trigger pain because the pain receptor is already highly excited by the mediators


Secondary Activation Stage of Sensitization (6 steps)

Nerve endings connected to the site of injury convey pain from the surrounding areas of the skin

1st: The pain message comes down from primary location to spinal cord and secondary branches

2nd: It causes a release of substance P (SP) at secondary sites

3rd: Substance P triggers mast cells in the area, and stimulates platelets
*Platelets and mast cells = players in inflammatory response that will release histamine, serotonin, etc.

4th: Histamine and serotonin will increase excitability of the nerve ending, just like acidity, potassium, prostaglandins, and bradykinin did in primary pathway

5th: Result is increased excitability on these nerve endings

6th: Now, not only is the area of the injury sensitive to pain, but now the surrounding area is highly sensitive


Direct Activation

Occurs by intense pressure and consequent cell damage. Cell damage induces lower pH (H+) and leads to release of potassium (K+) and to synthesis of prostaglandins (PG) and bradykinin (BK). Prostaglandins increase the sensitivity of the terminal to bradykinin and other pain-producing substances.


Secondary Activation

Impulses generated in the stimulated terminal propagate not only to the spinal cord but also into other terminal branches where they induce the release of peptides, including substance P (SP). Substance P causes vasodilation and neurogenic edema with further accumulation of bradykinin (BK). Substance P also causes the release of histamine (H) from mast cells and serotonin (5HT) from platelets


Referred Pain

The spatial displacement of pain sensation from the site of the injury that produces it.
*We can think of referred pain as being primary visceral pain from a visceral organ
*Instead of us feeling the pain where the organ is, the pain is felt on the surface of the body


Referred Liver Pain

Right shoulder and upper abdominal quadrant


Referred Cardiac Pain

left chest, shoulder, left arm, can be up into left side of jaw


Referred Colon Pain

middle of abdomen


Referred Small intestine pain

epigastric region of stomach


Mechanism of Referred Pain (3)


1. When we feel pain in a visceral organ, that pain is being conveyed by the c-fibers that ultimately are going to converge onto a spinal nerve

2. The convergence onto the spinal nerve is converging with a somatosensory afferent nerve
*This is including somatosensory nociceptors (a-delta and somatosensory c-fibers)

3. When the visceral pain comes in and moves up to the brain, it is perceived by the brain as coming from the corresponding dermatome for that spinal nerve due to this convergence


Ascending Pain Pathways

Pain that is felt at the surface of the skin is sensed by peripheral nociceptors, and it is conveyed into the spinal cord


6 Steps of Ascending Pain Pathway

1st: Noxious stimuli activate the peripheral ending of the primary afferent nociceptor.

2nd: The message is then transmitted to the spinal cord, where it synapses with cells of origin of the major ascending pain pathway that ultimately go to the brain: the spinothalamic tract.

3rd: It goes from the dorsal horn of the spinal cord then the to the contralateral side and enters the white matter of the spinal cord

4th: Ascends through the spinalthalamic tract, which is the white matter tract that carries affernt fibers up to brain centers

5th: At the midbrain, it terminates at the thalamus, which is a major relay station for a lot of ascending projections

6th: The message is relayed to the contralateral thalamus to the somatosensory cortex and/or broad areas of cerebral cortex such as the anterior cingulate and the frontal insular


Somatosensory Cortex

Pure sensory aspects of pain (location, intensity, and quality)
*this is responsible for the purely sensory aspects of pain, as in our ability to know we feel pain, to localize it, and know the intensity and quality


Broad areas of cerebral cortex such as the anterior cingulate and the frontal insular (3)

1. Affective or unpleasant emotional aspects of pain; suffering

2. These areas are responsible for the unpleasant emotional aspects of pain
3. This is responsible for what we experience as the suffering associated with pain


Pain Modulation

1. The descending pain circulate, which doesn't produce pain but modulates it

2. The descending pathway controls the activity of the afferent cells coming in, meaning the brain has the ability to control the ability of the pain message actually going into the spinal cord and being felt (pain-modulation network)

3. Thought to explain the highly subjective nature of the experience of pain.
*Why pain may not be as intense for one person as another


Pain Modulation Pathway (2)

1. Inputs from frontal cortex and hypothalamus activate cells in the midbrain that ultimately control spinal pain-transmission cells.

2. Descending portions from frontal cortex and hypothalamus that relay to midbrain and down the medulla that ultimately control spinal pain transmitting cells


Psychological Variables of Pain Modulation

Expectation, memory, and fear can modulate (worsen or lessen) the experience of pain.
*Ex: if a women is having a baby and she has a strong belief that the labor and birth is scary and intolerable, then she may have a higher level of pain during labor than a woman who has a different expectation of labor and birth
*These psychological variables can make pain worse or better


Components of Pain Modulation Pathway (3)

1. Each of the components of the pathway also contain opioid receptors and are thought to be the targets of opioid drugs.

2. The analgesic effects of opioid drugs may be working through this pain-modulating network

3. All components also contain endogenous opioid peptides (e.g. enkephalins & β-endorphin) suggesting an endogenous opioid analgesic pathway.
*Our body makes opiods in the form of enkephalins and B-endorphins