Physical pain is divided into nociceptive & neuropathic pain.
Nociceptive pain from direct activation of pain nerve fibers, d/t chemical, inflammatory or
mechanical mediators. Most common type of pain occurs when pain receptors, called
nociceptors, respond to stimuli that are potentially damaging, ( noxious thermal, chemical,
or mechanical stimuli),may occur as a result of trauma, surgery, or inflammation, mostly
described as aching. 2 types of nociceptive pain: Visceral pain (internal organs) caused by
stimulation of deep internal pain receptors, most often in the abdominal cavity, cranium, or
thorax. Visceral pain may vary from local, achy discomfort to more widespread,
intermittent, pain. Menstrual cramps, labor pain, GI infections, bowel disorders, organ
cancers all produce visceral pain. Description of quality & extent of pain often serves as a
strong clue to the cause. Deep somatic pain (skin, muscles, bones, connective tissue)
originates in ligaments, tendons, nerves, blood vessels, & bones. Deep somatic pain is more
diffuse than cutaneous pain & tends to last longer. A fracture or sprain, arthritis, bone
cancer cause deep somatic pain. Arthritis is a type of chronic somatic pain.
Neuropathic pain generated by nervous system, complex, often chronic pain arising when
injury to one or more nerves results in repeated transmission of pain signals even in
absence of painful stimuli. Nerve injury may come from many conditions, poorly controlled
diabetes, tumor, viral infection, some meds, chemo can trigger nerve injuries, may cause
neuropathic pain even after d/c. Described as burning, numbness, itching, pins & needles,
prickling pain. Cutaneous / superficial pain in the skin or subcutaneous tissue. If you’ve
touched a hot object or paper cut, that’s superficial pain. Radiating pain starts at origin
but extends to other locations pain of sore throat may extend to ears. Referred pain occurs
in an area that is distant from original site Pain from heart attack may be experienced
down left arm. Psychogenic pain believed to arise from the mind, pt perceives pain despite
fact no physical cause identified, can be just as severe as pain from a physical cause. Acute
pain has short duration, rapid onset, varies in intensity, last up to 6 mo, mostly associated
w/ injury or surgery. It’s protective in that it indicates potential or actual tissue damage &
may absorb pt’s physical & emotional energy for a short time, helpful for pt to know pain
usually ends as tissues heal. Chronic pain lasts 6 mo. or more, often interferes w/ daily
activities, may have periods of remission & exacerbation, can be progressive even if there’s
no current tissue injury, as in neuropathic pain. May be viewed as insignificant by family &
Dr. & lead to pt w/drawal, depression, anger, frustration, & dependence. Next to
incurability, chronic pain is a feared aspect of contracting cancer or other diseases.
Intractable pain is both chronic & highly resistant to relief.
,Transduction, nociceptors activated by perception of mechanical, thermal, & chemical
stimuli. Damaged tissue prompts release of bradykinin, histamine, & prostaglandins, which
activate nociceptors in surrounding tissues. Bradykinin a vasodilator triggers release of
inflammatory chemicals that cause injured area to become red, swollen, & tender.
Inflammation the most frequent cause of pain. Transmission Peripheral nerves carry pain
message to spinal cord along one of two types of fibers: A-delta fibers: large-diameter
myelinated fibers transmit pain impulses fast from acute, focused mechanical & thermal
stimuli (initial sharp pain when you bump your knee). C fibers: smaller unmyelinated
fibers transmit slow pain impulses, dull, diffuse pain impulses from mechanical, thermal, &
chemical stimuli. If you bump your knee, the lingering ache will be carried by C fibers. At
the spinal cord, impulses ascend to brainstem & thalamus, requires chemicals called
neurotransmitters. Pain Perception involves recognition & definition of pain in frontal
cortex. The brain recognizes & defines a stimulus as pain; the pain threshold: the number
& intensity of stimuli necessary to produce pain, duration & characteristics of pain
produced. Pain Modulation process changes perception of pain by either facilitating or
inhibiting pain signals through the endogenous analgesia system & the gate-control
mechanism. Gate control theory asserts that non-painful input closes the "gates" to
painful input, preventing pain sensation from traveling to CNS. So, stimulation by non-
noxious input is able to suppress pain.
Transduction: activation of nociceptors by stimuli
Transmission: conduction of pain message to spinal cord
Pain Perception: recognizing and defining pain in cortex
Pain Modulation: changing pain perception
Cognitively impaired pts not less sensitive to pain but may fail to interpret sensations as
painful, unable to communicate their pain, or unable to recall pain. Nonverbal pain cues
for cognitively impaired pts: ↓ activity, grimacing, moaning, irritable, frightened
expressions, rapid eye blinking, noisy breathing, profanity, verbally abusive, fidgeting,
disruptive behavior, change in routine, refuse food, mental status changes, ↑confusion,
physiological ↑ BP, RR, pulse. Mechanical stimuli external forces result in pressure or
friction against body, involve stretching of body tissues r/t bleeding & swelling,
compression of tissues caused by force of trauma, surgical incisions, friction or skin
shearing, pressure from mechanical device, cast or brace.
Thermal stimuli exposure to extreme heat or cold touching hot object or earache when
outdoors on a cold day. Chemical stimuli can be internal or external. Lemon juice or any
acidic substance on open area on skin causing sharp, sudden pain is ex. of external
chemical stimuli. Chest pain felt during a heart attack is caused by internal chemical
stimuli
,Physiological (Involuntary) Sympathetic Responses to (Acute Pain) dilated blood vessels to
brain, ↑ alertness, dilated pupils, ↑pulse & force of contraction, ↑RR, ↑ systolic BP, rapid speech,
pallor. Parasympathetic Responses Deep or Prolonged Pain: changeable breathing patterns,
constricted pupils, ↓pulse, ↓ systolic BP, feeling faint, syncope, slow monotonous speech.
Behavioral Responses (Voluntary) agitation, crying, grimacing, guarding area, moaning,
w/drawing from painful stimuli. Psychological (Affective) Responses: anger, anxiety,
depression, exhaustion, fear, hopeless. Endocrine Sx: ongoing pain triggers excessive release of
hormones adrenocorticotropic hormone, cortisol, antidiuretic hormone, growth hormone,
catecholamines, & glucagon. Insulin & testosterone levels ↓. Hormone shifts activate
carbohydrate, protein, & fat catabolism (breakdown); hyperglycemia; & poor glucose use.
Inflammatory process, combined w/ these endocrine & metabolic changes, can result in wt loss,
tachycardia, fever, ↑ RR, & even death. Cardiovascular Sx: ongoing pain leads to hyper-
coagulation, ↑HR, BP cardiac workload & oxygen demand may lead to unstable angina,
intracoronary thrombosis, MI & infarction. Musculoskeletal Sx: ongoing pain causes impaired
muscle function, fatigue, immobility, can prevent pt from doing ADLs & physical therapy.
Respiratory Sx: Pts in pain tend to breathe shallow, limit thoracic & abd. movement in effort to
↓ pain, this is called splinting. Splinting reduces tidal volume (air exchanged w/ each breath) &
↑ inspiratory & expiratory pressures that can lead to pneumonia & atelectasis as well as
underventilation retained carbon dioxide, called respiratory acidosis.
Genitourinary Sx: ongoing pain causes release of excessive amt. of catecholamines,
aldosterone, ADH, cortisol, angiotensin II, & prostaglandins, lead to ↓ urinary output,
urinary retention, fluid overload, hypokalemia, HTN, & ↑ cardiac output. GI Sx: In
response to pain, intestinal secretions & smooth muscle tone ↑. Gastric emptying &
motility ↓. Nociceptor free nerve ending receptor for painful (noxious) stimuli. Protective
role of pain doesn’t let nerve endings adapt to repeated painful stimuli. Repeated
stimulation ↑ their sensitivity to pain. Sensitized nociceptors may continue to transmit pain
message even after stimulus is removed. This hypersensitivity is termed hyperalgesia
(allodynia), where nonpainful stimulus, touch of clothing, can be interpreted as painful.
Bone & muscular pain (includes ligaments, joint capsules, fascia, & tendons) mostly occurs
after stretching, ischemia, or forceful/sustained contractile activity. Injury causes release of
lactic acid that ↑ pain intensity. Pain radiates into surrounding tissues. Tension HA often
d/t tense neck & scalp muscles. Muscle ischemia d/t intermittent claudication (a spasm in
extremities during walking) can result from occlusive vascular disease; pain of coronary
occlusion is also d/t ischemia. Vascular pain may be d/t a pathological condition of vessels
or surrounding tissues, such as mixed vascular & neuropathic complications r/t chronic
, diabetes , migraines, brain tumors, & ↑cranial pressure. Pain d/t inflammation occurs from
infection or trauma & subsequent release of acidic chemicals & distension of tissues.
neuropathic pain from injury to a nerve, malfunction of the neuronal transmission process, or
impaired regulation. Neuralgia, or pathological pain, frequently described as paroxysmal (a
sudden spasm-like pain) occurring along the branches of a nerve.
Three words—pain, hurt, & ache—seem to be used across many cultures to describe pain
Taking a pain hx: Do you have pain now & when did it begin? Where is pain located & how do
you rate it? (Use pain scale.) How would you describe pain, Sharp, Dull, Achy, Burning? How
often do you have pain, is it constant or intermittent & is there a rhythm or pattern? What makes
the pain better or worse? How many days this past wk has pain interfered in your ability to do
what you would like to do or take care of yourself? Does pain wake you up at night, interrupt
your concentration & ↓ your ability to think clearly? Have you experienced this type of pain in
the past? Do you have any other associated symptoms (such as N/V) w/ pain? Does pain prevent
you from participating in pleasurable activities, socializing? Have you used any meds to treat the
pain, were they effective & how often do you take pain relievers? Any alternative treatments?
What past experiences or cultural factors influence the pain?
You need to judge intensity & quality of pain based on pt hx & current environment. Does pt
have an underlying painful condition? What is the likely source of pain? Are there physical signs
that indicate pt has ↑ pain w/ movement?
Comprehensive pain assessment includes pain location & quality, intensity, aggravating &
alleviating factors, timing & duration, pain relief & goals for pain relief. Pt self-report most
reliable indicator of pain, including mild cognitive impairment pts.
Central pain injury to CNS d/t tumors, disease, stroke, or damage to spinal cord, pain can
be severe & constant. Brain masses can involve cerebral cortex & elicit central pain in
opposite side of body. Thalamic pain perception of pain in one half of body following injury
to thalamus.
Back pain usually occurs in cervical or lumbar regions, generally d/t spinal disc injury or
herniation of the nucleus pulposus, the cushioning substance between intervertebral discs.
Sensory & motor nerve damage may occur.
Pain Scales:
The Visual Analog Scale (VAS) is a 10-cm horizontal line w/ “No pain” written on left side
& “Worst pain imaginable” written on right. Simple descriptor scale (SDS) list of
adjectives that describe different levels of pain intensity. Simplest version of this scale uses
the words mild, moderate, & severe. The FACES scale uses simple illustrations of faces to
Nociceptive pain from direct activation of pain nerve fibers, d/t chemical, inflammatory or
mechanical mediators. Most common type of pain occurs when pain receptors, called
nociceptors, respond to stimuli that are potentially damaging, ( noxious thermal, chemical,
or mechanical stimuli),may occur as a result of trauma, surgery, or inflammation, mostly
described as aching. 2 types of nociceptive pain: Visceral pain (internal organs) caused by
stimulation of deep internal pain receptors, most often in the abdominal cavity, cranium, or
thorax. Visceral pain may vary from local, achy discomfort to more widespread,
intermittent, pain. Menstrual cramps, labor pain, GI infections, bowel disorders, organ
cancers all produce visceral pain. Description of quality & extent of pain often serves as a
strong clue to the cause. Deep somatic pain (skin, muscles, bones, connective tissue)
originates in ligaments, tendons, nerves, blood vessels, & bones. Deep somatic pain is more
diffuse than cutaneous pain & tends to last longer. A fracture or sprain, arthritis, bone
cancer cause deep somatic pain. Arthritis is a type of chronic somatic pain.
Neuropathic pain generated by nervous system, complex, often chronic pain arising when
injury to one or more nerves results in repeated transmission of pain signals even in
absence of painful stimuli. Nerve injury may come from many conditions, poorly controlled
diabetes, tumor, viral infection, some meds, chemo can trigger nerve injuries, may cause
neuropathic pain even after d/c. Described as burning, numbness, itching, pins & needles,
prickling pain. Cutaneous / superficial pain in the skin or subcutaneous tissue. If you’ve
touched a hot object or paper cut, that’s superficial pain. Radiating pain starts at origin
but extends to other locations pain of sore throat may extend to ears. Referred pain occurs
in an area that is distant from original site Pain from heart attack may be experienced
down left arm. Psychogenic pain believed to arise from the mind, pt perceives pain despite
fact no physical cause identified, can be just as severe as pain from a physical cause. Acute
pain has short duration, rapid onset, varies in intensity, last up to 6 mo, mostly associated
w/ injury or surgery. It’s protective in that it indicates potential or actual tissue damage &
may absorb pt’s physical & emotional energy for a short time, helpful for pt to know pain
usually ends as tissues heal. Chronic pain lasts 6 mo. or more, often interferes w/ daily
activities, may have periods of remission & exacerbation, can be progressive even if there’s
no current tissue injury, as in neuropathic pain. May be viewed as insignificant by family &
Dr. & lead to pt w/drawal, depression, anger, frustration, & dependence. Next to
incurability, chronic pain is a feared aspect of contracting cancer or other diseases.
Intractable pain is both chronic & highly resistant to relief.
,Transduction, nociceptors activated by perception of mechanical, thermal, & chemical
stimuli. Damaged tissue prompts release of bradykinin, histamine, & prostaglandins, which
activate nociceptors in surrounding tissues. Bradykinin a vasodilator triggers release of
inflammatory chemicals that cause injured area to become red, swollen, & tender.
Inflammation the most frequent cause of pain. Transmission Peripheral nerves carry pain
message to spinal cord along one of two types of fibers: A-delta fibers: large-diameter
myelinated fibers transmit pain impulses fast from acute, focused mechanical & thermal
stimuli (initial sharp pain when you bump your knee). C fibers: smaller unmyelinated
fibers transmit slow pain impulses, dull, diffuse pain impulses from mechanical, thermal, &
chemical stimuli. If you bump your knee, the lingering ache will be carried by C fibers. At
the spinal cord, impulses ascend to brainstem & thalamus, requires chemicals called
neurotransmitters. Pain Perception involves recognition & definition of pain in frontal
cortex. The brain recognizes & defines a stimulus as pain; the pain threshold: the number
& intensity of stimuli necessary to produce pain, duration & characteristics of pain
produced. Pain Modulation process changes perception of pain by either facilitating or
inhibiting pain signals through the endogenous analgesia system & the gate-control
mechanism. Gate control theory asserts that non-painful input closes the "gates" to
painful input, preventing pain sensation from traveling to CNS. So, stimulation by non-
noxious input is able to suppress pain.
Transduction: activation of nociceptors by stimuli
Transmission: conduction of pain message to spinal cord
Pain Perception: recognizing and defining pain in cortex
Pain Modulation: changing pain perception
Cognitively impaired pts not less sensitive to pain but may fail to interpret sensations as
painful, unable to communicate their pain, or unable to recall pain. Nonverbal pain cues
for cognitively impaired pts: ↓ activity, grimacing, moaning, irritable, frightened
expressions, rapid eye blinking, noisy breathing, profanity, verbally abusive, fidgeting,
disruptive behavior, change in routine, refuse food, mental status changes, ↑confusion,
physiological ↑ BP, RR, pulse. Mechanical stimuli external forces result in pressure or
friction against body, involve stretching of body tissues r/t bleeding & swelling,
compression of tissues caused by force of trauma, surgical incisions, friction or skin
shearing, pressure from mechanical device, cast or brace.
Thermal stimuli exposure to extreme heat or cold touching hot object or earache when
outdoors on a cold day. Chemical stimuli can be internal or external. Lemon juice or any
acidic substance on open area on skin causing sharp, sudden pain is ex. of external
chemical stimuli. Chest pain felt during a heart attack is caused by internal chemical
stimuli
,Physiological (Involuntary) Sympathetic Responses to (Acute Pain) dilated blood vessels to
brain, ↑ alertness, dilated pupils, ↑pulse & force of contraction, ↑RR, ↑ systolic BP, rapid speech,
pallor. Parasympathetic Responses Deep or Prolonged Pain: changeable breathing patterns,
constricted pupils, ↓pulse, ↓ systolic BP, feeling faint, syncope, slow monotonous speech.
Behavioral Responses (Voluntary) agitation, crying, grimacing, guarding area, moaning,
w/drawing from painful stimuli. Psychological (Affective) Responses: anger, anxiety,
depression, exhaustion, fear, hopeless. Endocrine Sx: ongoing pain triggers excessive release of
hormones adrenocorticotropic hormone, cortisol, antidiuretic hormone, growth hormone,
catecholamines, & glucagon. Insulin & testosterone levels ↓. Hormone shifts activate
carbohydrate, protein, & fat catabolism (breakdown); hyperglycemia; & poor glucose use.
Inflammatory process, combined w/ these endocrine & metabolic changes, can result in wt loss,
tachycardia, fever, ↑ RR, & even death. Cardiovascular Sx: ongoing pain leads to hyper-
coagulation, ↑HR, BP cardiac workload & oxygen demand may lead to unstable angina,
intracoronary thrombosis, MI & infarction. Musculoskeletal Sx: ongoing pain causes impaired
muscle function, fatigue, immobility, can prevent pt from doing ADLs & physical therapy.
Respiratory Sx: Pts in pain tend to breathe shallow, limit thoracic & abd. movement in effort to
↓ pain, this is called splinting. Splinting reduces tidal volume (air exchanged w/ each breath) &
↑ inspiratory & expiratory pressures that can lead to pneumonia & atelectasis as well as
underventilation retained carbon dioxide, called respiratory acidosis.
Genitourinary Sx: ongoing pain causes release of excessive amt. of catecholamines,
aldosterone, ADH, cortisol, angiotensin II, & prostaglandins, lead to ↓ urinary output,
urinary retention, fluid overload, hypokalemia, HTN, & ↑ cardiac output. GI Sx: In
response to pain, intestinal secretions & smooth muscle tone ↑. Gastric emptying &
motility ↓. Nociceptor free nerve ending receptor for painful (noxious) stimuli. Protective
role of pain doesn’t let nerve endings adapt to repeated painful stimuli. Repeated
stimulation ↑ their sensitivity to pain. Sensitized nociceptors may continue to transmit pain
message even after stimulus is removed. This hypersensitivity is termed hyperalgesia
(allodynia), where nonpainful stimulus, touch of clothing, can be interpreted as painful.
Bone & muscular pain (includes ligaments, joint capsules, fascia, & tendons) mostly occurs
after stretching, ischemia, or forceful/sustained contractile activity. Injury causes release of
lactic acid that ↑ pain intensity. Pain radiates into surrounding tissues. Tension HA often
d/t tense neck & scalp muscles. Muscle ischemia d/t intermittent claudication (a spasm in
extremities during walking) can result from occlusive vascular disease; pain of coronary
occlusion is also d/t ischemia. Vascular pain may be d/t a pathological condition of vessels
or surrounding tissues, such as mixed vascular & neuropathic complications r/t chronic
, diabetes , migraines, brain tumors, & ↑cranial pressure. Pain d/t inflammation occurs from
infection or trauma & subsequent release of acidic chemicals & distension of tissues.
neuropathic pain from injury to a nerve, malfunction of the neuronal transmission process, or
impaired regulation. Neuralgia, or pathological pain, frequently described as paroxysmal (a
sudden spasm-like pain) occurring along the branches of a nerve.
Three words—pain, hurt, & ache—seem to be used across many cultures to describe pain
Taking a pain hx: Do you have pain now & when did it begin? Where is pain located & how do
you rate it? (Use pain scale.) How would you describe pain, Sharp, Dull, Achy, Burning? How
often do you have pain, is it constant or intermittent & is there a rhythm or pattern? What makes
the pain better or worse? How many days this past wk has pain interfered in your ability to do
what you would like to do or take care of yourself? Does pain wake you up at night, interrupt
your concentration & ↓ your ability to think clearly? Have you experienced this type of pain in
the past? Do you have any other associated symptoms (such as N/V) w/ pain? Does pain prevent
you from participating in pleasurable activities, socializing? Have you used any meds to treat the
pain, were they effective & how often do you take pain relievers? Any alternative treatments?
What past experiences or cultural factors influence the pain?
You need to judge intensity & quality of pain based on pt hx & current environment. Does pt
have an underlying painful condition? What is the likely source of pain? Are there physical signs
that indicate pt has ↑ pain w/ movement?
Comprehensive pain assessment includes pain location & quality, intensity, aggravating &
alleviating factors, timing & duration, pain relief & goals for pain relief. Pt self-report most
reliable indicator of pain, including mild cognitive impairment pts.
Central pain injury to CNS d/t tumors, disease, stroke, or damage to spinal cord, pain can
be severe & constant. Brain masses can involve cerebral cortex & elicit central pain in
opposite side of body. Thalamic pain perception of pain in one half of body following injury
to thalamus.
Back pain usually occurs in cervical or lumbar regions, generally d/t spinal disc injury or
herniation of the nucleus pulposus, the cushioning substance between intervertebral discs.
Sensory & motor nerve damage may occur.
Pain Scales:
The Visual Analog Scale (VAS) is a 10-cm horizontal line w/ “No pain” written on left side
& “Worst pain imaginable” written on right. Simple descriptor scale (SDS) list of
adjectives that describe different levels of pain intensity. Simplest version of this scale uses
the words mild, moderate, & severe. The FACES scale uses simple illustrations of faces to
