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NUR 325 PATHO > Pain Patho (Exam 2) > Flashcards

Pain Patho (Exam 2) Flashcards

1
Q

Signs and Symptoms of inflammation are produced by

A

Chemical Mediators

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2
Q

Chemical mediators are present in the _________ and activated by __________

A

Plasma, Tissue Injury

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3
Q

Chemical Mediators that are present in the plasma and activated by tissue injury

A

-Histamine

-Arachidonic acid metabolites (Prostaglandins and Leukotrienes)

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4
Q

Arachidonic acid metabolites

A

-Prostaglandins and Leukotrienes

-Cause the production of our inflammatory mediators

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5
Q

Prostaglandins

A

-Chemical Mediator that promote inflammation, pain, and fever
-Protect stomach lining
-Platelet function

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6
Q

Prostaglandins: Body Effect

A

-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

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7
Q

What neurotransmitters are we focusing on with thinking about pharmacologic treatment of pain and fever?

A

-Prostaglandins

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8
Q

Acute pain

A

-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

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9
Q

Chronic Pain

A

-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

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10
Q

Types of pain: Nociceptive verus Neuropathic

A

Nociceptive (acute) (Outside the CNS)

Neuropathic (Chronic) (within the CNS) (Does not response to pain medication)

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11
Q

Nociceptive pain: Cutaneous/Somatic Pain

Complaints
Location
Examples

A

-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

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12
Q

Nociceptive pain: Visceral pain

Complaints
Location
Examples

A

-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

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13
Q

Two Types of Nociceptive Pain

A

Cutaneous/ Somatic pain

Visceral Pain

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14
Q

Neuropathic Pain

Complaints
Location
Examples

A

-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

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15
Q

Types of pain: Referred

A

-Pain felt at a distance form the actual pathology

-Common in visceral pain

-Heart attack: Neck jaw and shoulder pain

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16
Q

Types of Pain: Phantom

A

-Sensation of pain that originates from an amputated part

-Constant

-Most intense right after the amputation

-Generally resolves overtime

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17
Q

Pain: What is it?

A

Whatever our patient says it is. COMPLEX

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18
Q

Acute pain

A

Protective. Promotes withdrawal from painful stimuli, allows inured parts to heal and teaches avoidance

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19
Q

Neuroanatomy of Pain: Pathways

A

-3 Parts of the nervous system involved in the sensation, perception and response to pain

  1. Afferent Pathways
  2. Interpretive centers
  3. Efferent pathways
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20
Q

Afferent pathways

A

-Begin in the PNS and travels in spinal gates and ends up in our brain

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21
Q

Interpretive Centers

A

Cortical, Sub-cortical, Brain stem, midbrain, and cerebral cortex

Area that interprets sensation from afferent pathways. Brain interpreting sensation as pain

22
Q

Efferent pathways

A

-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

23
Q

Nociception

A

The process of Afferent, Interpretive, and efferent pathways

24
Q

Nociceptors

A

Pain receptors

-Free nerve endings in afferent pathway

-When stimulated they cause nocicpeted pain

25
Q

Nociceptive stimuli

A

Stimuli of certain intensity that cause, or are close to causing tissue injury

Sharp, electric, currents, thermal, pressure, chemical

26
Q

Low intensity stimuli

A

-Nociceptors may not be activated

27
Q

Place with more nociceptors

A

Feel more pain and can body can localize the pain better

28
Q

Neurotransmiters

A

Chemical found throughout brain and spinal cord

-Modulate control related to the TRANSMISSION of pain impulse

29
Q

Neurotransmitter: Types

A

Excitatory or inhibitory

Can enhance or inhibit pain

30
Q

Examples of neurotrhansmitters

A

Over 50

Noreephinephrine, acetycholine, dopamine, serotonin, GABA

31
Q

Endorphins

A

-Natural neruochemicals or endogenous opioids that aid in inability the pain response (inhibitor)

32
Q

Physiology of Pain (4 Phases of Nociception)

A
  1. Transduction
  2. Transmission
  3. Perception
  4. Modulation

Occurs in PNS and CNS

33
Q

Transduction

A

-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

34
Q

Transduction: Two Types of nociceptors

A

A-Delta and C fibers

35
Q

Nociceptors Transduction: A-Delta

A

-Small diameter

-Myelinated (rapid)

-Well localized

36
Q

Nociceptors Transduction: C-Fibers

A

-Small diameters

-Unmyelinated (Slow transmission of pain)

-Poorly localized

37
Q

A delta fiber pain

A

-Sharp, stinging, cutting

-Feel it in well localized area

38
Q

C-fiber pain

A

-We have more of these in muscle, tendons, body organs, skin

-Dual. achy, burning

-Poorly localized

39
Q

Transmission

A

-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

40
Q

Perception

A

-Brain receives these signals and interprets them as painful (Brain figuring out this is painful)

  • Limbic and reticular
41
Q

Factors that influence perception of pain

A

-Attention

-Distraction

-Anxiety

-Fear

-Fatigue

-Previous experiences and expectations

42
Q

Perception: Pain Tolerance

A

-Greatest intensity of pain a person can handle

-Varies greatly over time

43
Q

Perception: Pain threshold

A

-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)

44
Q

What can decrease pain tolerance

A

-Repeated exposure
-Fatigue
-Anger
-Boredom

45
Q

Increase in pain tolerance

A

-Alcohol consumption
-Drug use
-Hypnosis
-Strong faith beliefs

46
Q

Modulation

A

-Synaptic transmission of pain signals is altered
(can be amplified or dampened)
(ENDORPHINS mediate pre-synpatic transmission)

47
Q

Bodies Pain Killers. Things produced within the body to fight pain

A

Endorphins

Bonding to opioid receptors and inhibiting the transmission of pain impulse by closing spinal cord gates

Morphine mimics the effects of endorphins

48
Q

When are endogenous analgesic substances are released when

A

Body experiences pain or prolong exertion

49
Q

Modulation: Gate Control Theory of Pain

A

-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

50
Q

Gate control Illustration

A

-If one can inhibit the nerve impulse BEFORE it reaches the thalamus/cortex, one can decrease the PERCEPTION OF PAIN

NUR 325 PATHO (30 decks)

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