Pain Patho (Exam 2) Flashcards
Signs and Symptoms of inflammation are produced by
Chemical Mediators
Chemical mediators are present in the _________ and activated by __________
Plasma, Tissue Injury
Chemical Mediators that are present in the plasma and activated by tissue injury
-Histamine
-Arachidonic acid metabolites (Prostaglandins and Leukotrienes)
Arachidonic acid metabolites
-Prostaglandins and Leukotrienes
-Cause the production of our inflammatory mediators
Prostaglandins
-Chemical Mediator that promote inflammation, pain, and fever
-Protect stomach lining
-Platelet function
Prostaglandins: Body Effect
-Protect the lining of the stomach from the effects of acid
-Promote blood clotting by activating platelets
-Affect kidney function—–Dilate blood vessels that lead to the kidneys
What neurotransmitters are we focusing on with thinking about pharmacologic treatment of pain and fever?
-Prostaglandins
Acute pain
-Nociceptive pain
-Normal protective mechanism to tissue injury
-Transient can least seconds to months (no longer than 3)
-Relieved after the chemical mediators stimulating the pain receptors are moved or the area is repaired
-Often stimulates the ANS to produce physical response to pain (Increase HR, BP, diaphoresis, dilated pupils
Chronic Pain
-Last more than 3 months
-Serves no purpose, often seems out of proportion to observable tissue damage
-Can be ongoing or intermittent
-Changes in the PNS and CNS cause dyregulation of noiception and pain modulation
-Dont see vital sign changes but see emontioal and psychosocial issues
Types of pain: Nociceptive verus Neuropathic
Nociceptive (acute) (Outside the CNS)
Neuropathic (Chronic) (within the CNS) (Does not response to pain medication)
Nociceptive pain: Cutaneous/Somatic Pain
Complaints
Location
Examples
-Involves the MS system (Skin, joints, tendons)
-Complaints: Constant and Achy
-Location: Well localized in the skin and subcutaneous tissue.
-Examples: Incision, bone fracture, bony metasteses, joint spinal disease, osteoarthritis, PVR, Chronic stasis ulcers
Nociceptive pain: Visceral pain
Complaints
Location
Examples
-Involves organs. Inflammation sometimes present
Complaints: Cramping, splitting, N/V, Diaphoresis
Location: Internal organs, poorly localized, diffuse, deeps
Examples: Kidney stones, appendicitis, constipation, heart attack
Two Types of Nociceptive Pain
Cutaneous/ Somatic pain
Visceral Pain
Neuropathic Pain
Complaints
Location
Examples
-Involves nerves
-Complaints: Shooting, burning, numb, sharp, motor weakness
-Location: Originates in injury to peripheral nerve. Spinal cord. Brain. Poorly localized
-Examples: Diabetic neuropathy. Tumor related nerve compression, phantom limb pain, central post-stroke pain
Types of pain: Referred
-Pain felt at a distance form the actual pathology
-Common in visceral pain
-Heart attack: Neck jaw and shoulder pain
Types of Pain: Phantom
-Sensation of pain that originates from an amputated part
-Constant
-Most intense right after the amputation
-Generally resolves overtime
Pain: What is it?
Whatever our patient says it is. COMPLEX
Acute pain
Protective. Promotes withdrawal from painful stimuli, allows inured parts to heal and teaches avoidance
Neuroanatomy of Pain: Pathways
-3 Parts of the nervous system involved in the sensation, perception and response to pain
- Afferent Pathways
- Interpretive centers
- Efferent pathways
Afferent pathways
-Begin in the PNS and travels in spinal gates and ends up in our brain
Interpretive Centers
Cortical, Sub-cortical, Brain stem, midbrain, and cerebral cortex
Area that interprets sensation from afferent pathways. Brain interpreting sensation as pain
Efferent pathways
-Pathway that goes back down into the CNS and illicit physical and mental response to pain
-Pull hand away from pain. Don’t walk out broken ankle
-Our response to pain
Nociception
The process of Afferent, Interpretive, and efferent pathways
Nociceptors
Pain receptors
-Free nerve endings in afferent pathway
-When stimulated they cause nocicpeted pain
Nociceptive stimuli
Stimuli of certain intensity that cause, or are close to causing tissue injury
Sharp, electric, currents, thermal, pressure, chemical
Low intensity stimuli
-Nociceptors may not be activated
Place with more nociceptors
Feel more pain and can body can localize the pain better
Neurotransmiters
Chemical found throughout brain and spinal cord
-Modulate control related to the TRANSMISSION of pain impulse
Neurotransmitter: Types
Excitatory or inhibitory
Can enhance or inhibit pain
Examples of neurotrhansmitters
Over 50
Noreephinephrine, acetycholine, dopamine, serotonin, GABA
Endorphins
-Natural neruochemicals or endogenous opioids that aid in inability the pain response (inhibitor)
Physiology of Pain (4 Phases of Nociception)
- Transduction
- Transmission
- Perception
- Modulation
Occurs in PNS and CNS
Transduction
-Painful stimuli converted to action potential at the sensory receptor (Something stimulate nerve receptor and cause electrical impulse to travel along axons to the CNS)
-Substances/chemical mediators released as a result of DIRECT injury and inflammation
-Porstaglandins: When activated they LOWER the PAIN threshold
Transduction: Two Types of nociceptors
A-Delta and C fibers
Nociceptors Transduction: A-Delta
-Small diameter
-Myelinated (rapid)
-Well localized
Nociceptors Transduction: C-Fibers
-Small diameters
-Unmyelinated (Slow transmission of pain)
-Poorly localized
A delta fiber pain
-Sharp, stinging, cutting
-Feel it in well localized area
C-fiber pain
-We have more of these in muscle, tendons, body organs, skin
-Dual. achy, burning
-Poorly localized
Transmission
-Process where action potentials move from peripheral receptors to the Dorsal Horn spinal cord and then the brain
-A-delta and C fibers are responsible for transmission of message
Perception
-Brain receives these signals and interprets them as painful (Brain figuring out this is painful)
- Limbic and reticular
Factors that influence perception of pain
-Attention
-Distraction
-Anxiety
-Fear
-Fatigue
-Previous experiences and expectations
Perception: Pain Tolerance
-Greatest intensity of pain a person can handle
-Varies greatly over time
Perception: Pain threshold
-Lowest intensity of pain a person can recognize
-Perceptual dominance occurs (Intense pain of one location my increase pain threshold in other location) (Pain at one site can mask pain at another site)
What can decrease pain tolerance
-Repeated exposure
-Fatigue
-Anger
-Boredom
Increase in pain tolerance
-Alcohol consumption
-Drug use
-Hypnosis
-Strong faith beliefs
Modulation
-Synaptic transmission of pain signals is altered
(can be amplified or dampened)
(ENDORPHINS mediate pre-synpatic transmission)
Bodies Pain Killers. Things produced within the body to fight pain
Endorphins
Bonding to opioid receptors and inhibiting the transmission of pain impulse by closing spinal cord gates
Morphine mimics the effects of endorphins
When are endogenous analgesic substances are released when
Body experiences pain or prolong exertion
Modulation: Gate Control Theory of Pain
-Theory that if we can block pain before it gets to brain to can stop or lower pain perception
-touch, rubbing skin, massage, distraction, acupuncture, getting active.
-Activate larger nerve fibers thus block small nerve fibers
Gate control Illustration
-If one can inhibit the nerve impulse BEFORE it reaches the thalamus/cortex, one can decrease the PERCEPTION OF PAIN
