M3.1 Flashcards
- are NOT DISEASES but are symptoms of a certain pathologic states
- are body’s response toward a physiologic event and may not always be pathologic
- may lead to discomfort and creates an impact on patient’s health, mental, emotional, psychological, etc.
PAIN and INFLAMMATION
- an UNPLEASANT SENSORY and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
PAIN
- an escessive NOXIOUS STIMULUS giving rise to intense and unpleasant sensation
- pain of recent onset and porbable LIMITED DURATION
- it is usually has an identifiable temporal and causal relationship to injury or disease
ACUTE pain
- are associated with ABERRATIONS of the normal physiological pathway, giing rise to hyperalgesia, allodynia, or spontaneous spasm of pain with no precipitating stimulus
- pain that commonly persists BEYOND THE TIME OF HEALING of an injury and frequently there may not be any clearly identifiable cause
- impacts on emotional health
CHRONIC PAIN
- SEVERE chronic pain produced by NEUROLOGICAL disease affecting the SENSORY pathway
- the pathway itself ang may problema
NEUROPATHIC PAIN
QUALITY OF PAIN
signals tissue injury via an INTACT NERVOUS SYSTEM
NOCICEPTIVE PAIN
QUALITY OF PAIN
NOCICEPTIVE PAIN:
* easy to identify
* muscles, bones
* localized, aching, throbbing
SOMATIC PAIN
QUALITY OF PAIN
NOCICEPTIVE PAIN:
* hard to identify
* internal organs
* vague, diffuse, crampy
VISCERAL PAIN
QUALITY OF PAIN
- signals injury to the NERVOUS PATHWAY ITSELF
- common complication in DIABETES
- burning, shooting, pins & needles, lancinating
NEUROPATHIC PAIN
QUALITY OF PAIN
- PROPORTIONATE tot he stimulation of the nociceptor
- pathologic when chronic
- when acute
* physiologic pain
* serves a protective function
* normal pain - pain in arthritis, chest pain in angina
NOCICEPTIVE PAIN
QUALITY OF PAIN
- DIPROPORTIONATE to the stimulation of nociceptor
- sustained by ABERRANT processes in PNS or CNS
- serves NO protective function
- pathologic pain
- neuralgia, myalgia, cancer pain, neuropathies
NEUROPATHIC PAIN
GENERAL PAIN PATHWAY
brain does NOT have ____
nociceptors
GENERAL PAIN PATHWAY
STIMULATION OF PAIN RECEPTORS (NOCICEPTORS):
pain begins with the ____
activation of nociceptors
specialized receptors that detect HARMFUL STIMULI such as extreme temperatures, mechanical pressure, or chemical irritants
NOCICEPTORS
GENERAL PAIN PATHWAY
- the pain signal is transmitted via ____ from the NOCICEPTOR to the DORSAL HORN of the spinal cord
- this is the ENTRY POINT for sensory information in the CNS
1ST ORDER NEURON
GENERAL PAIN PATHWAY
1ST order neuron
Peripheral nerve (nociceptor) to Dorsal horn
GENERAL PAIN PATHWAY
- the signal then crosses to the OPPOSITE SIDE of the spinal cord and ascends via the SPINOTHALAMIC TRACT to the thalamus
2nd order
GENERAL PAIN PATHWAY
2nd order neuron
Dorsal horn to Thalamus via Spinothalamic tract
a major RELAY CENTER in the brain
thalamus
GENERAL PAIN PATHWAY
in 2nd order neuron, the signal ascends to the thalamus via ____
spinothalamic tract
GENERAL PAIN PATHWAY
- the signal is then sent to the CEREBRAL CORTEX, specifically the SOMATOSENSORY CORTEX, where the brain interprets the pain’s LOCATION, INTENSITY, and QUALITY
3rd order neuron
GENERAL PAIN PATHWAY
3rd order neuron
Thalamus to Cerebral cortex
GENERAL PAIN PATHWAY
where the brain interprets the pain’s location, intensity, and quality
SOMATOSENSORY CORTEX
- thinly
- FAST
- SHARP, localized, IMMEDIATE pain
- provides QUICK AWARENESS; triggers reflex actions
- NEOSPINOTHALAMIC tract (direct, fast pathway)
- a sudden CUT or BURN
MYELINATED FIBERS
(Aδ fibers)
MYELINATED FIBERS
conduction speed
FAST
MYELINATED FIBERS
PAIN type
sharp
localized
immediate
MYELINATED FIBERS
FUNCTION
provides quick awareness
triggers reflex actions
MYELINATED FIBERS
PATHWAY
Neospinothalamic tract
(direct, fast pathway)
MYELINATED FIBERS
example SENSATION
sudden cut or burn
- SLOW
- DULL, ACHING, BURNING or THROBBING pain
- signals PROLONGED pain; encourages rest for recovery
- PALEOSPINOTHALAMIC tract (slower, emotional response pathway)
- persistent SORENESS or aching pain
UNMYELINATED FIBERS
(C fibers)
UNMYELINATED FIBERS
CONDUCTION speed
SLOW
UNMYELINATED FIBERS
PAIN type
dull
aching
burning
throbbing
UNMYELINATED FIBERS
FUNCTION
signals prolonged pain
encourages rest for recovery
UNMYELINATED FIBERS
PATHWAY
PALEOSPINOTHALAMIC tract
(slower, emotional response pathway)
UNMYELINATED FIBERS
example SENSATION
persistent sorness or aching pain
direct, fast pathway
NEOSPINOTHALAMIC TRACT
slower, emotional response pathway
PALEOSPINOTHALAMIC tract
is the transmission of painful stimulus from the SENSORY ORGAN to the BRAIN
ASCENDING PATHWAY
NEUTRALIZE or DIMINISH the transmission of painful stimulus
perceive the pain LESS
DESCENDING INHIBITORY PATHWAYS
(DIP)
PATHWAY
- carries pain signals from the BODY to the BRAIN
- transmits pain stimuli for processing and awareness
- 1st order → 2nd order → 3rd order
- Glutamate, Substance P
- ALERTS the brain to potential or actual tissue damage
- SHARP pain form a cut traveling up the spinothalamic tract
- increases pain perception
ASCENDING PATHWAY
PATHWAY
ASCEDNING PATHWAY:
direction of signal
body to brain
PATHWAY
ASCENEDING PATHWAY:
purpose
transmits pain stimula for processing and awareness
PATHWAY
ASCEDNING PATHWAY:
key neurons involved
123 order neurons
PATHWAY
ASCEDNING PATHWAY:
neurotransmitters
Glutamate, Substance P
(excitatory)
PATHWAY
ASCENDING PATHWAY:
function
alerts the brain
PATHWAY
ASCEDNING PATHWAY:
effect on pain
increases pain perception
PATHWAY
- carries signals from the BRAIN to the BODY
- Modulates or inhibit pain signals to control pain perception
- originates in the brainstem and descends to the dorsal horn
- Endorphins, Enkephalins, Serotnin, Noradrenaline (inhibitory)
- Release of endorphins to reduce pain after injury
- decreases pain perception
DESCENDING PATHWAY
PATHWAY
DESCENDING PATHWAY:
direction of signal
brain to body
PATHWAY
DESCENDING PATHWAY:
purpose
modulate or inhibit pain signals to control pain perception
PATHWAY
DESCENDING PATHWAY:
key neurons involved
originates in the brainstem and descends to the dorsal horn
PATHWAY
DESCENDING PATHWAY:
neurotransmitters
endorphins
enkephalins
serotonin
noradrenaline
PATHWAY
DESCENDING PATHWAY:
function
dampens or suppresses excessive pain signals
PATHWAY
DESCENDING PATHWAY:
effect on pain
decreseas pain perception
MODULATORY MECHANISMS OF NOCICEPTIVE PATHWAY
BK, 5-HT, PGs, etc
pain promoter
MODULATORY MECHANISMS OF NOCICEPTIVE PATHWAY
inhibits NEUROPEPTIDE RELEASE and excitation of transmission of neuron
OPIATES
pain reliever
MODULATORY MECHANISMS OF NOCICEPTIVE PATHWAY
NITRIC OXIDE formation
pain promoter
MODULATORY MECHANISMS OF NOCICEPTIVE PATHWAY
- inhibits DESCENDING inhibitory pathways
- pain promoter
5-HT, NA
A physiologic DEFENSE MECHANISM (an immune response), and is NOT a disease but a symptom signaling tissue injury
INFLAMMATION
INFLAMMATORY RESPONSE
CAPILLARY WIDENING:
key event
vasodilation
INFLAMMATORY RESPONSE
CAPILLARY WIDENING:
effect
INCREASED blood flow
INFLAMMATORY RESPONSE
CAPILLARY WIDENING:
symptom
HEAT
calor
INFLAMMATORY RESPONSE
INCREASED PERMEABILITY:
key event
capillary walls become more porous
INFLAMMATORY RESPONSE
INCREASED PERMEABILITY:
effect
fluid leaks into tissues
INFLAMMATORY RESPONSE
INCREASED PERMEABILITY:
symptom
REDNESS
rubor
INFLAMMATORY RESPONSE
LEUKOCYTE ATTRACTION:
key event
immune cells are recruited
INFLAMMATORY RESPONSE
LEUKOCYTE ATTRACTION:
effect
immune response at the injury site
INFLAMMATORY RESPONSE
LEUKOCYTE ATTRACTION:
symptom
SWELLING
tumor
INFLAMMATORY RESPONSE
EXTRAVASATION:
key event
leukocytes exit blood vessels to attack pathogens
INFLAMMATORY RESPONSE
EXTRAVASATION:
effect
direct immune response at injury
INFLAMMATORY RESPONSE
EXTRAVASATION:
symptom
Tenderness
INFLAMMATORY RESPONSE
SYSTEMIC RESPONSE:
key event
fever and immune cell porliferation
INFLAMMATORY RESPONSE
SYSTEMIC RESPONSE:
effect
enhanced immune cell activation
INFLAMMATORY RESPONSE
SYSTEMIC RESPONSE:
symptom
PAIN
dolor
INFLAMMATORY RESPONSE
loss of function
functio laesa
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
VASOACTIVE AMINES:
key mediators
histamine
serotonin
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
VASCOACTIVE AMINES:
source
mast cells
platelets
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
vasodilation, increased vascular permeability, and itching
vasoactive amines
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
EICOSANOIDS:
key mediators
prostaglandins
leukotrienes
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
EICOSANOIDS:
source
arachidonic acid
metabolism
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
PROSTAGLANDINS cause pain, fever, and vasodilation; LEUKOTRIENES promote bronchoconstriction and inflammation
EICOSANOIDS
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
CYTOKINES:
key mediators
interleukins
TNF-a
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
CYTOKINES:
source
activated immune cells
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
promote fever, pain, and immune cell recruitment
CYTOKINES
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
KININS:
key mediators
bradykinin
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
KININS:
source
plasma proteins
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
strong pain inducer, increases vascular permeability
KININS
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
COMPLEMENT SYSTEM:
key mediators
C3a, C5a
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
COMPLEMENT SYSTEM:
source
plasma
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
promote chemotaxis, mast cell degranulation, and enhance inflammation
COMPLEMENT SYSTEM
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
REACTIVE OXYGEN SPECIES:
key mediators
Superoxide
Hydrogen peroxide
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
REACTIVE OXYGEN SPECIES:
source
activated neutrophils
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
tissue damage, amplifies inflammation
REACTIVE OXYGEN SPECIES
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
NEUROPEPTIDES:
key mediators
Substance P
Calcitonin Gene-related peptide (CGRP)
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
NEUROPEPTIDES:
source
sensory nerve endings
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
enhance pain signaling, vasodilation, and neurogenic inflammation
NEUROPEPTIDES
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
PLATELET-ACTIVATING FACTOR:
key mediators
PAF
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
PLATELET-ACTIVATING FACTOR:
soource
various immune cells
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
promotes platelet aggregation, vasodilation, bronchoconstriction
PLATELET-ACTIVATING FACTOR
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
____ and ____ are crucial in EARLY INFLAMMATION, causing swelling and pain
Histamine & Bradykinin
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
____ amplify pain signals and induce fever
Prostaglandins
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
____ like IL-1 and TNF-a play a central role in SYSTEMIC INFLAMMATION
CYTOKINES
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
____ DIRECTLY stimulates pain pathways
Substance P
CHEMICAL MEDIATORS OF PAIN AND INFLAMMATION
____ enhance immune cell RECRUITMENT and ATTACK PATHOGENS
COMPLEMENT PROTEINS
ARACHIDONIC ACID METABOLISM
inhibits PHOSPHOLIPASE
Corticosteroids
ARACHIDONIC ACID METABOLISM
PHOSPHOLIPASE will turn into
arachidonic acid
ARACHIDONIC ACID METABOLISM
products of ARACHIDONIC ACID
Lipoxygenase
Cyclo-oxygenase
ARACHIDONIC ACID METABOLISM
produces LTA4 (leukotriene)
LIPOXYGENASE
ARACHIDONIC ACID METABOLISM
produces PROSTAGLANDINS (PGH2)
CYCLO-OXYGENASE
ARACHIDONIC ACID METABOLISM
GOOD COX
COX 1
ARACHIDONIC ACID METABOLISM
CORTICOSTEROIDS
NSAID
Celecoxib
Rofecoxib
ARACHIDONIC ACID METABOLISM
inhibits COX1&2
NSAIDS
ARACHIDONIC ACID METABOLISM
inhibits COX2 only
Celecoxib
Rofecoxib
ARACHIDONIC ACID METABOLISM
LTB4
chemotaxis
hyperalgesia
ARACHIDONIC ACID METABOLISM
LTC4, LTD4, LTE4
bronchoconstriction
edema
ARACHIDONIC ACID METABOLISM
inhibits LTC4, LTD4, LTE4
Zafirlukast
Montelukast
effective for ASTHMA
ARACHIDONIC ACID METABOLISM
inhibits LIPOXYGENASE
Zileuton
ARACHIDONIC ACID METABOLISM
PGF2a
uterine contraction
ARACHIDONIC ACID METABOLISM
PGE2
vasodilation
gastric cytoprotection
ARACHIDONIC ACID METABOLISM
TXA2
(thromboxane)
platelet aggregation
ARACHIDONIC ACID METABOLISM
PGI2
(prostacyclin)
inhibits platelet aggregation
vasodilation
gastric cytoprotection
ARACHIDONIC ACID METABOLISM
inhibits THROMBOXANE (TXA2)
Dazoxiben
lead to BLEEDING
ARACHIDONIC ACID METABOLISM
COX that can produce prostanoids with cytoprotection
COX1