INTERNAL MEDICINE Module 1

PAIN 1
Ken Matthew M. Villamin, MD 7/10/2018

ACUTE PAIN CHRONIC PAIN

Outline
o PAIN • Usually occurs in • If related to ongoing
I. Acute vs Chronic
II. Pain Classification response to tissue tissue injury,
a. Nociceptive vs Neuropathic Pain injury presumably caused by
b. Somatic vs Visceral
c. Multifactorial Pain Syndrome • Results from persistent activation of
III. Pain and the Mind activation of peripheral pain fibers
a. Somatic Symptom Disorder
IV. Cognitive Domains Impaired by Pain pain receptors and their • May also result from
a. Attention specific A delta and C ongoing damage to or
b. Memory
c. Concentration sensory nerve fibers dysfunction of the PNS
d. Content of Thought • Frequently associated or CNS
V. Skin Receptors
a. Pain Receptors with anxiety and • Does not involve
b. Wind-up Phenomenon Remodeling hyperactivity of the SNS sympathetic
VI. Substances Involved in the Inflammatory Cascade
VII. Pain Transmission and Modulation (e.g. tachycardia, hyperactivity but may be
VIII. Pharmacologic Analgesia tachypnea, associated with
IX. NSAIDS
X. OPIOID ANALGESICS hypertension, vegetative signs (e.g.
XI. Opioid receptor and Drug interactions diaphoresis, midriasis) fatigue, loss of libido,
XII. Adjuvant Drug Therapy for Pain
XIII. WHO Three- Step Analgesic ladder anorexia, and
The similarity of A delta and dysphoria)
LEGEND C sensory nerve fibers:
 Book Both lack myelination (super Dysphoria - a state of
thin myelin with regards to A
Recordings unease or generalized
delta) and both are thin dissatisfaction with life.
sensory nerve fibers
PAIN
• The most common reason patients seek medical care
• Has both sensory and emotional components
• People vary considerably in their tolerance for pain.

• Pathogenesis vs Pathophysiology
>Pathogenesis basically how a disease or an
abnormality is brought about. It is from the etiology or the
cause.
>In contrast in pathophysiology we talk more about the
symptoms or the manifestations; in this case, how is PAIN
brought about? Symptom oriented ang pathophysiology

 Pain is an unpleasant sensation

localized to a part of the body. It is
often described in terms of a
Review on Nerve Fibers: Batch 2020
penetrating or tissue-destructive
process and/or of a bodily or
emotional reaction. (Harrison’s)

• You can classify the two kinds of pain by time. It can be

classified to Acute or Chronic. If you assign it by numbers,
it is very arbitrary. The differences are very different based
on its characteristics:

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There are two distinct functional categories of axons: Neuropathic Pain – initiated or caused by primary lesion or
➢ Primary afferents with cell bodies in the dorsal root dysfunction in the nervous system
ganglion. ➢ POSTHERPETIC NEURALGIA
➢ Sympathetic postganglionic fibers with cell bodies in
-Associated with herpes zoster or shingles.
the sympathetic ganglion.
Shingles is the reactivation of Chicken Pox
➢ NEUROPATHIC LOW BACK PAIN
Primary Afferent Nociceptor ➢ DISTAL POLYNEUROPATHY -
➢ Primary – first-order neuron -Most common is associated with Diabetes
➢ Afferent – neuron which sends signal Mellitus
from the periphery directed towards the
CNS ➢ CENTRAL POST-STROKE PAIN
➢ Nociceptor – pain receptor ➢ TRIGEMINAL NEURALGIA (or Tic douloureux)
n your peripheral nerve endings, you have -Severe, stabbing pain to one side of the face.
your peripheral nerves. It stems from one or more branches of the
➢ A-beta nerve that supplies sensation to the face, the
➢ A-delta trigeminal
➢ C fibers
➢ CRPS - Complex regional pain syndrome (CRPS)
REMEMBER! -Chronic (lasting greater than six months)
• A-beta (Aβ) fibers – transmit light touch pain condition that most often affects one limb
• A-delta (Aδ) and C fibers – transmit pain (arm, leg, hand, or foot) usually after an injury.
impulses, SOMATIC VS VISCERAL PAIN
both afferent nociceptors
SOMATIC PAIN VISCERAL PAIN
PAIN CLASSIFICATION • Pain receptors are located • If due to obstruction of a
in the skin, subcutaneous hollow organ, pain is
tissues, fascia, other poorly localized, deep, and
PAIN
connective tissues, cramping, and may be
periosteum, endosteum, referred to remote
and joint capsules. cutaneous sites.
Nociceptive Neuropathic
• Stimulation of these ➢ Example is appendicitis:
receptors usually produces Pain begins in the
sharp or dull localized pain. periumbilical area, or
Somatic Visceral Multifactorial • “Burning” pain is not sometimes in the
uncommon if the skin or epigastric area.
subcutaneous tissues are ➢ Pathophysiology of pain
We will go through this one by one:
involved. in appendicitis: the
NOCICEPTIVE VS. NEUROPATHIC PAIN appendix has visceral
Phrase “not uncommon” innervation which extends
means that it is not an to the periumbilical area.
expected finding but it is also ➢ For the first 6 hours of
not surprising. It is not rare or appendicitis it will be
not seldom encountered. It’s painful only in the
right in the middle. periumbilical area, after 6-
8 hours, the somatic
nerves overlying the
appendix will be activated
• If due to injury of organ
capsules or other deep
connective tissues, it may
be more localized and
sharp.
➢ When the appendicitis
Nociceptive Pain – caused by activity in neural pathways in
raptures, the first structure
response to potentially tissue-damaging stimuli
that would be affected is
➢ POSTOPERATIVE PAIN – immediately after an operation
the peritoneum. This time
➢ MECHANICAL LOW BACK PAIN – excessive stretching
the pain will be diffused.
or excessive bending
➢ SPORTS/ EXERCISE INJURIES
➢ SICKLE CELL CRISIS – innervation to a type of anemia
➢ ARTHRITIS
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MULTIFACTORIAL PAIN SYNDROME

• Has a prominent nociceptive component
• May also involve neuropathic pain (due to nerve
damage)
Examples:
Chronic low back pain
Most cancer pain syndromes

PAIN AND THE MIND

• Psychologic factors modulate pain intensity to a highly
variable degree.
• Thoughts and emotions have an important role in the
4 domains impaired by brain
perception of pain.
• Many patients who have chronic pain also have SKIN RECEPTORS
psychologic distress, especially depression and anxiety.
• Because certain syndromes characterized as psychiatric
disorders are defined by SELF-REPORTED PAIN (e.g.
some SOMATIC SYMPTOM DISORDERS), patients with
poorly explained pain are often MISCHARACTERIZED as
having a psychiatric disorder and are thus deprived of
appropriate care.

Pain should be approached both with a somatic perspective as

well as a psychologic one

HYPOCHONDRIAC - Someone who lives in fear of having a

serious illness, despite medical tests never finding anything
wrong, may have somatic symptom disorder, also known as ➢ They usually subserve changes in temperature
illness anxiety disorder. particularly the A-delta.
➢ High pressure as exemplified by your mechanical
SOMATIC SYMPTOM DISORDER receptors
➢ Most remarkable of your pain receptors will be your
polymodal, especially by you C-fibers which would be
activated by your mechanical, thermal or your chemical
stimuli.

4 COGNITIVE DOMAINS IMPAIRED BY PAIN

• For pain, what is important is, for psychologically, there
are four domains which are affected:
➢ Attention
➢ Memory
➢ Concentration
➢ Content of Thought
To just give you a clue as to what one of the questions
in the exam might be. Pag mga gantong mag-isa lang
sa slide.

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PAIN TRANSMISSION AND MODULATION PAIN TRANSMISSION AND MODULATION CONT.

• Pain fibers enter the • The pain signal is modulated at multiple points in both
spinal cord at the segmental and descending pathways by many
DORSAL ROOT neurochemical mediators, including endorphins (e.g.
GANGLIA and enkephalin) and monoamines (e.g. serotonin,
synapse in the dorsal norepinephrine)
horn. o Laughter is the best medicine due to release of
• From there, fibers endorphins
cross to the other side • The mediators interact in poorly understood ways to
and travel up the increase, sustain, shorten, or reduce the perception of and
LATERAL COLUMNS response to pain.
to the THALAMUS and • They mediate the potential benefit of CNS-active drugs
then to the CEREBRAL (e.g. opioids, antidepressants, anticonvulsants, membrane
CORTEX. stabilizers) that interact with specific receptors and
neurochemicals in the treatment of chronic pain.
• Psychologic factors are important modulators.
• They not only affect how patients speak about pain (e.g. in
a stoic, irritable, or complaining way) and how they behave
REMEMBER: in response to it (e.g. whether they grimace), but they also
DORSAL – SENSORY generate neural output that modulates neurotransmission
VENTRAL – MOTOR along pain pathways.
• Psychologic reaction to protracted pain interacts with other
Review of the Lateral Spinothalamic Pathway: CNS factors to induce long-term changes in pain
(doc had us recite this part) perception.

NON-DRUG MEASURES THAT YOU CAN USE TO

CONTROL PAIN
• For Sprain:
o R-Rest
o I-Ice
o C-Compression
o E- Elevate
• Usually acute injury during first 48 hrs. = COLD
COMPRESS
• After 48 hrs. = HOT COMPRESS
• Cold compress- to vasoconstrict and reduce swelling
(primary signs of inflammation)
• Hot compress- to promote circulation
• Ultrasound has also therapeutic properties

PHARMACOLOGIC ANALGESIA
• Acetaminophen (aka Paracetamol)
WIND-UP PHENOMENON AND REMODELING
• Acetylsalicylic Acid / ASA (aka Aspirin)
• Repetitive stimulation (e.g. from a prolonged
• NSAIDS
painful condition) can sensitize neurons in the o Nonselective
dorsal horn of the spinal cord so that a lesser o Selective
peripheral stimulus causes pain • Opioid Analgesic
• Peripheral nerves and nerves at other levels of the
CNS may also be sensitized, producing long- term
synaptic changes in the cortical receptive fields
that maintain exaggerated pain perception

SUBSTANCES INVOLVED IN THE INFLAMMATORY

CASCADE

Vasoactive Peptides Other Mediators

Calcitonin gene-related Prostaglandin E2
protein
Substance P Serotonin
Neurokinin A Bradykinin
Epinephrine

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NSAIDS (Toxicity and Selectivity) OPOID RECEPTORS

Opioid Receptor Effects

Class
Mu1 Euphoria, Supraspinal analgesia,
confusion, dizziness, nausea, low
addiction potential

Mu2 Respiratory depression,

cardiovascular and gastrointestinal
effects, miosis, urinary retention

Delta Spinal analgesia, cardiovascular

depression, decreased brain and
myocardial oxygen demand
Kappa Spinal analgesia, dysphoria,
psychomimetic effects, feedback
inhibition of endorphin system

EXAMPLES OF OPIOID DRUG INTERACTIONS

Drugs Interactions
Sedatives-hypnotics Increased risk of central nervous
• The advent of COX-2 inhibitors causes less GI toxicity system depression, especially
• Even though they have less GI side effects, earlier COX-2 respiratory depression
inhibitors have cardiovascular side effects
• Aspirin is found out to have anti-platelet properties. Tx for Monoamine oxidase Relative contradiction to all opioid
coronary heart disease inhibitors analgesics due to the high incidence
• Most common side effect of NSAID: Gastric irritation -> of hyperpyrexic coma and episodes
Ulceration of hypertension have been
documented
• Acetaminophen, compared to other antipyretics is
ANALGESIC, ANTIPYRETIC BUT NOT ANTI- Antipsychotic Increased incidence of sedation/
INFLAMMATORY. tranquilizers cognitive impairment has variable
effects on respiratory depression
OPOID ANALGESICS
EXAMPLES OF OPIOID DRUG INTERACTIONS

• Morphine- Prototype of all Opioids

• Morphine can also be used in Myocardial Infarction
especially in Pulmonary congestion
• Chronic opioid use results in Respiratory depression and
decrease in consciousness • NSAID toxicity is not only for GI but also can lead to renal
toxicity.
• Tramadol is a weak opioid but is unique because it is safe
for renal toxicity.

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ADJUVANT DRUG THERAPY FOR PAIN NATURE AGAINST “TORTURE”

Drug Examples
Antidepressants Floxac
Anticonvulsants Phenobarbital, phenytoin,
carbamzepine
Anxiolytics Diazepam
Muscle relaxants Myonal
Topical local anesthetics andLidocaine
other agents
Amphetamines Phenylpropanolamine
Phenothiazines Thorazine
Biphosphonates Alendronate
Corticosteroids Prednisone
• Adjuvants- supplement drugs, not drugs that cannot
address pain in their own but has effect in the nervous
system or peripheral receptors that complement those of • Garlic- lower cholesterol levels
main pain medication

References:
o Powerpoint
o Harrison’s Principles of Internal Medicine, 16th edition
o Voice notes
o Batch 2020 Trans

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