chapter 49 Flashcards
Define pain.
Pain occurs when body tissues are damaged or injured—it’s the body’s warning system, pushing us to react and prevent further harm.
Why does sitting too long cause pain?
Sitting too long causes ischemia (reduced blood flow) under pressure points, leading to skin damage; normally, we shift to relieve pressure, but those without pain sensation may develop serious skin damage like open sores or desquamation (peeling skin).
What is fast pain?
- Fast pain begins within 0.1 seconds,
- feels sharp, pricking, or electric,
- is felt only in the skin, and
- occurs with events like cuts, burns, or electric shocks.
What is slow pain?
- Slow pain starts after 1 second or more,
- builds gradually,
- feels burning, aching, throbbing, or sickening,
- results from deep tissue damage,
- and can occur in skin, muscles, or organs.
What are pain receptors?
Pain receptors are free nerve endings located in the:
1. skin’s outer layers,
2. periosteum,
3. blood vessel walls,
4. joint surfaces, and
5. brain coverings like (the falx and tentorium.)
What causes pain?
Pain is caused by:
1. mechanical stimuli (cutting, pressing, hitting),
2. thermal stimuli (extreme heat or cold),
3. chemical stimuli (body substances like bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, proteolytic enzymes).
What types of stimuli cause fast pain?
Fast pain usually comes from mechanical and thermal stimuli.
What types of stimuli cause slow pain?
Slow pain can result from mechanical, thermal, or chemical stimuli.
What chemicals directly cause pain?
Bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes directly cause pain.
What chemicals increase pain sensitivity without directly causing pain?
Prostaglandins and substance P make pain receptors more sensitive and worsen pain sensations during injury.
Do pain receptors adapt to continuous pain stimulation?
Pain receptors barely adapt to continuous stimulation and may become more sensitive (hyperalgesia) to ensure danger signals persist.
What temperature causes pain from heat?
Pain starts when skin is heated above 45°C.
What determines pain intensity: the amount of damage or speed of damage?
Pain is more related to how fast tissue damage occurs rather than the amount of existing damage.
What are some examples where fast damage causes pain?
Examples include:
1. infection (bacterial damage),
2. ischemia (lack of blood flow), and
3. contusion (bruising).
What chemicals are released by damaged tissue to cause pain?
Damaged tissues release bradykinin, potassium ions, and proteolytic enzymes, which damage or sensitize nerve endings by affecting ion movement.
What causes pain during ischemia?
Ischemia causes pain by producing lactic acid (anaerobic metabolism) and releasing bradykinin and enzymes from dying cells, irritating nerve endings.
How fast does ischemia cause pain in muscles during activity?
Pain from ischemia can begin within 15–20 seconds if muscles are active under blocked blood flow, and 3–4 minutes if muscles are inactive.
How do muscle spasms cause pain?
Muscle spasms cause pain by direct compression of pain-sensitive nerves and by causing ischemia due to reduced blood flow; the need for more oxygen during tight contraction worsens ischemia.
What additional chemicals are released during muscle spasms?
Bradykinin and proteolytic enzymes are released during muscle spasms, increasing pain.
How many pathways carry pain signals to the brain?
Two pathways carry pain signals: one for fast-sharp pain and one for slow-chronic pain.
What are the two types of peripheral fibers for pain transmission?
- Type Aδ fibers (small, fast) carry sharp, stabbing, acute thermal pain at 6–30 m/s,
- while Type C fibers (very small, slow) carry dull, aching, burning pain at 0.5–2 m/s.
What is double pain?
Double pain occurs when an injury causes an immediate sharp pain from Aδ fibers followed by a delayed, dull, aching pain from C fibers.
What is the benefit of fast and slow pain?
Fast pain helps the body react quickly to danger, while slow pain keeps reminding the person to protect and care for the injured area.
Where do pain signals enter the spinal cord?
Pain signals enter the spinal cord through the dorsal roots and reach the dorsal horn.
What are the two main spinal tracts for pain signals?
The neospinothalamic tract (fast pain) and paleospinothalamic tract (slow pain) are the two main pathways for pain signals.
Describe the neospinothalamic tract.
- The neospinothalamic tract carries fast pain signals from Aδ fibers;
- signals enter lamina I (marginal layer),
- synapse with second-order neurons,
- cross the spinal cord through the anterior commissure, and
- ascend the anterolateral columns.
Where do fast pain signals go in the brain?
- Fast pain signals first reach reticular areas of the brainstem,
- then mainly the thalamus (especially ventrobasal complex), and
- finally the somatosensory cortex for perception and localization of pain.
How well can we localize fast pain?
Fast pain can usually be localized quite well, meaning you can tell exactly where it hurts. However, if only pain receptors are activated (not touch receptors), even fast pain might feel like it’s coming from a wider area. When both pain and touch receptors are triggered together, the brain can locate the pain very precisely.
Which chemical sends fast pain messages?
The main neurotransmitter used by Aδ fibers is glutamate. Glutamate works quickly and its effects last only a few milliseconds.
What is the paleospinothalamic tract?
The paleospinothalamic tract is an older pain pathway that
1. carries pain signals from type C fibers (slow, aching pain) and some Aδ fibers.
2. The C fibers enter the spinal cord and end mostly in lamina II and III, known together as the substantia gelatinosa.
3. The signals then pass through short neurons in the spinal cord and reach lamina V.
4. From there, another neuron takes the signal,
5. crosses to the opposite side, and
6. travels upward in the anterolateral pathway, just like in the fast pain pathway.
Which chemicals send slow pain messages?
C fibers release two main chemicals: 1) Glutamate, which acts fast and short like in fast pain; 2) Substance P, which is released slowly and builds up over time, causing longer-lasting, more intense pain. This explains the ‘double pain’ phenomenon: sharp pain first (glutamate), then slow aching pain (substance P).
Where does slow pain signal go in the brain?
Most slow pain signals don’t go straight to the thalamus. Only 10–25% reach the thalamus directly. Most end in lower parts of the brain:
1. The reticular formation (in the medulla, pons, and midbrain)
2. The tectal area (below the superior and inferior colliculi in the midbrain)
3. The periaqueductal gray (area around the brain’s central fluid canal)
These areas handle the emotional aspect of pain. From there, signals continue to the intralaminar and ventrolateral thalamus, hypothalamus, and deeper brain regions.
Why is slow pain hard to localize?
Slow pain is hard to pinpoint because the pathway has many small, widely spread connections, making the brain locate only a general area (e.g., ‘the leg’) instead of an exact spot. This causes chronic pain to feel vague and hard to describe.
What part of the brain feels pain?
Pain awareness mainly depends on lower brain areas like the reticular formation, thalamus, and brainstem. Even without the somatosensory cortex, people can still feel pain. The cortex mainly helps interpret pain type and intensity. Electrical stimulation of the sensory cortex can cause mild pain sensations.
How does pain affect brain arousal?
Pain activates the brain’s arousal system. Slow pain signals to the reticular formation and intralaminar thalamus excite the whole brain, making it hard to sleep during severe pain.
What is a cordotomy?
A cordotomy is a surgery where doctors cut the anterolateral spinal cord on the side opposite the pain, to block pain signals from the lower body and give temporary relief in extreme cases like late-stage cancer. However, pain may return because some fibers cross later in the brain or weaker pathways become more active.
What is the analgesia system?
The analgesia system is a brain and spinal cord network that can block or reduce pain signals, especially during dangerous or overwhelming situations. It explains why people feel pain differently.
What are the three parts of the analgesia system?
The analgesia system includes:
1) Periaqueductal gray and periventricular areas (midbrain and upper pons around the aqueduct of Sylvius and third/fourth ventricles),
2) Raphe magnus nucleus and nucleus reticularis paragigantocellularis (lower pons and upper medulla),
3) Pain inhibitory complex (dorsal horns of the spinal cord).
How does the analgesia system work?
When areas like the periaqueductal gray are stimulated, they send signals to the raphe magnus nucleus. Then, second-order signals travel down the dorsolateral columns of the spinal cord to the dorsal horn, where neurons are activated to block incoming pain signals. This system acts like a ‘gate’ shutting down pain before it reaches the brain.
Can the pain-blocking system be triggered artificially?
Yes, scientists found that electrical stimulation of areas like the periaqueductal gray or raphe magnus can block even very strong pain signals. Other areas like the periventricular nuclei of the hypothalamus and medial forebrain bundle can also activate the system.
Which chemicals are involved in pain blocking?
The main chemicals are enkephalin and serotonin. Neurons from the periventricular and periaqueductal areas release enkephalin. They signal the raphe magnus nucleus, which sends signals down the spinal cord to release serotonin. Serotonin then causes enkephalin release near the pain fibers (Aδ and C fibers), blocking pain through presynaptic and postsynaptic inhibition.
How does enkephalin block pain?
Enkephalin blocks pain by 1) Presynaptic inhibition: preventing the pain signal from reaching the next neuron, and 2) Postsynaptic inhibition: stopping the next neuron from firing even if the pain signal arrives. This blocks pain at the first point of contact in the spinal cord.
How does the analgesia system affect reflexes?
Besides reducing pain sensation, the analgesia system also prevents reflex actions triggered by pain (like pulling away from something hot), helping control both the feeling and the reaction to pain.
What are natural painkillers in the brain?
The brain produces natural morphine-like substances called opioid peptides, which act on opioid receptors in the brain and spinal cord, similar to morphine. These were discovered after finding that tiny morphine injections in areas like the periaqueductal gray caused strong pain relief.
Which are the main natural opioid peptides?
The main natural opioid peptides come from three large proteins: 1) Pro-opiomelanocortin, 2) Proenkephalin, 3) Prodynorphin. Important peptides include β-endorphin, Met-enkephalin, Leu-enkephalin, and dynorphin.
Where are natural painkillers found?
Enkephalins are found in the brainstem and spinal cord, especially in the analgesia system areas. β-endorphin is found in the hypothalamus and pituitary gland. Dynorphin is found in some of the same areas as enkephalins but in smaller amounts.
What happens when the brain’s analgesia system is activated?
Activating the analgesia system, either naturally or through morphine-like drugs, can almost completely block many types of pain, especially pain from peripheral nerves.
What is the mechanism by which touch can reduce pain?
Touch and pressure signals can block pain when large Aβ sensory fibers are activated. These fibers, from tactile receptors sensitive to rubbing, vibration, or light pressure, send signals to the spinal cord that inhibit pain from the same area via lateral inhibition. Rubbing or pressing near an injury helps reduce pain by activating touch fibers that quiet pain signals. Menthol creams, heat rubs, and acupuncture also work by stimulating tactile nerves, reducing pain at the spinal and brain levels.
How is electrical stimulation used to treat pain?
Doctors use electrical stimulation by placing electrodes on the skin or implanting them near the spinal cord to stimulate the dorsal sensory columns. In advanced cases, electrodes are implanted deep into the brain, targeting areas like the intralaminar thalamic nuclei and periaqueductal/periventricular gray. Patients can control the stimulation with a remote device. Relief can last up to 24 hours after just minutes of stimulation.
What is referred pain?
Referred pain is when pain is felt in one part of the body, but the actual problem is somewhere else, especially common with internal organs. For example, a heart attack can cause pain in the left arm, shoulder, or jaw. It is medically important because visceral diseases often present as surface pain.
How does referred pain happen?
In the spinal cord, pain signals from the organs and skin often converge on the same second-order neurons. The brain, more familiar with skin input, misinterprets organ pain as coming from the skin area connected to the same spinal segment. Example: Heart and left arm pain travel through the same pathway, leading the brain to perceive heart pain as arm pain.
What is visceral pain?
Visceral pain comes from internal organs like the heart, lungs, stomach, and intestines. Viscera lack receptors for touch, temperature, or vibration and respond only to pain. It is crucial for diagnosing internal diseases and differs significantly from surface pain.
What are differences between visceral and surface pain?
Localized damage to an organ often causes little or no pain, while widespread damage causes strong pain due to activation of more pain receptors. For example, intestines can be cut during surgery without much pain, but ischemia causes intense visceral pain.
What causes visceral pain?
Visceral pain arises from stimulation of pain nerve endings in large, diffuse areas of internal organs, triggered by ischemia, chemical irritation, muscle spasm, overstretching, or stretching of surrounding tissues. It is usually deep, aching, and persistent, and carried by slow-conducting type C fibers.
How does ischemia cause visceral pain?
Ischemia reduces blood flow, leading to buildup of acidic byproducts and chemicals like bradykinin and proteolytic enzymes, which stimulate pain receptors. It causes pain in organs just like it does in muscles or skin, such as intestinal or heart ischemia.
How does chemical irritation cause visceral pain?
Chemical irritation happens when harmful substances leak from organs and irritate nearby tissues. For example, a perforated gastric ulcer releases gastric acid into the peritoneal cavity, causing severe, widespread pain by activating many pain receptors.
How does a hollow organ spasm cause pain?
Spasms of hollow organs like the gallbladder, ureters, or intestines cause pain by mechanically stretching/squeezing nearby nerves or reducing blood flow leading to ischemia. This pain feels crampy and comes in waves, matching rhythmic movements like peristalsis.
What are common causes of hollow organ spasm pain?
Common causes include appendicitis, gastroenteritis, constipation, menstrual cramps, labor pain, gallbladder disease, and ureteral blockage (kidney stones).
What is overdistention pain?
Pain occurs when an organ is overfilled with gas, fluid, or contents, stretching the organ wall and/or compressing blood vessels, leading to ischemia. While stretching alone can hurt, blood flow reduction often causes stronger pain.
Which internal organ tissues feel little or no pain?
The liver parenchyma and alveoli of the lungs are mostly insensitive to pain. However, surrounding structures like the liver capsule, bile ducts, bronchi, and parietal pleura are highly sensitive.
What is parietal pain caused by internal organ diseases?
When disease spreads to outer linings like the parietal peritoneum, pleura, or pericardium, sharp, well-localized pain occurs because these surfaces connect to spinal nerves, similar to skin.
Why is visceral pain hard to locate?
The brain is less used to interpreting signals from internal organs. Chest and abdominal organ pain reaches the brain via visceral pathways (dull, cramping pain) and parietal pathways (sharp, localized pain), making sensations mixed and vague.
What causes referred pain?
Referred pain occurs because visceral and skin nerves often join the same neurons in the spinal cord, and the brain misinterprets the source based on embryological development, not the organ’s current location.
What are examples of referred pain?
Heart pain is felt in the left chest, shoulder, neck, or arm (C3–T5 segments). Stomach pain is felt in the upper mid-abdomen (T7–T9 segments).
What is the parietal pain pathway?
The parietal pain pathway carries sharp, well-localized pain signals from outer linings of organs via spinal nerves directly to the brain, not through the autonomic system.
What happens during appendicitis?
Early appendicitis causes dull, cramping pain near the belly button via visceral pathways (T10–T11). As inflammation spreads to the parietal peritoneum, sharp, localized pain appears in the lower right abdomen.
What is hyperalgesia?
Hyperalgesia is increased pain sensitivity. Primary hyperalgesia happens at the injury site due to tissue changes (e.g., sunburn). Secondary hyperalgesia occurs in surrounding areas due to spinal cord or brain changes.
What is herpes zoster (shingles)?
Herpes zoster is caused by the varicella-zoster virus infecting a dorsal root ganglion, leading to severe, burning or stabbing pain and a rash in the corresponding dermatome.
What is tic douloureux (trigeminal neuralgia)?
A condition with sudden, intense, stabbing facial pain on one side, triggered by mild stimuli like touch, chewing, or swallowing, affecting the trigeminal nerve. In severe cases, nerve cutting may be necessary.
What is Brown-Séquard syndrome?
Caused by one-sided spinal cord damage, resulting in ipsilateral loss of touch, vibration, and proprioception, and contralateral loss of pain and temperature sensation due to differences in crossing pathways.
What causes headaches?
Headaches can originate inside (intracranial) or outside (extracranial) the skull. Intracranial causes include meningitis, low CSF pressure, and migraines. Extracranial causes include muscle tension, sinus infections, and eye strain.
What are thermal sensations?
Thermal sensations are feelings of heat and cold, detected by three types of nerve endings: cold receptors (more numerous), warmth receptors (fewer and deeper), and pain receptors for extreme temperatures.
Where are cold and warmth receptors located?
Cold receptors are numerous on areas like the lips and fewer on the trunk. Warmth receptors are fewer and located deeper in the skin.
How do we feel temperature changes?
When skin cools, cold receptors send signals to the brain; when heated, warmth receptors send signals. Extreme temperatures activate pain receptors, causing sharp pain.
What is adaptation to temperature?
Adaptation occurs when thermal receptors reduce their response over time after a sudden temperature change, making sensations less intense after initial exposure.
How do thermal receptors detect temperature?
Thermal receptors sense temperature changes through changes in their metabolism, affecting chemical reactions that help perceive cold or warmth.
How does the brain process thermal signals?
Thermal signals travel to the spinal cord, pass through the brainstem and thalamus, and reach the somatosensory cortex where sensations like touch and temperature are interpreted.
How does skin exposure affect temperature sensitivity?
Larger skin exposure to temperature changes makes it easier to detect small changes. Small area exposure may not feel as noticeable.
