Russian Call Girls in Pune Tanvi 9907093804 Short 1500 Night 6000 Best call g...
Ā
RELIEVE PAIN AND INFLAMMATION
1. DRUG USED TO TREAT PAIN
AND INFLAMMATION
Dr. Eiman Sumayyah (PT)
DPT, MSPT (Neuro) KMU, CDP (UK), OMPT (UK),
Neuro Rehab Bobath (UK), Cardiac and ICU PT (RMI)
2. CONTENTS
01 Pain Physiology
02 Therapeutic uses of opioid analgesics
03 Classification of non-steroidal anti-
inflammatory drugs on the basis of
mechanism of action
04 Pharmacological management of
rheumatoid and osteoarthritis
05 Patient control analgesia
3. In 1996 the International Association for the
Study of Pain (IASP) defined pain as āan unple
asant sensory and emotional experience asso
ciated with actual or potential tissue damage
, or described in terms of such damageā.
What is pain?
4. Pain Physiology
01
There seem to be two kinds of pain: fundamental āsensoryā pain, t
he intensity of which is a direct function of the intensity of various
pain stimuli, and āpsychologicalā pain
THEORIES:
1. PHYSIOLOGICAL
2. BEHAVIORAL
3. COGNITIVE
5. It acts as a signal, alerting us to potential tissue damage, and leads to a wide range
of actions to prevent or limit further damage.
6. Pain pathways
Nociceptors are receptors in tissues which are activated specifically by painful stimuli.
This ānoxiousā information is transduced by the receptors into an electrical signal and transmitted f
rom the periphery to the central nervous system along axons.
There are two types of nociceptors:
HIGH-THRESHOLD MECHANORECEPTORS (HTM), which respond to mechanical deformation
POLYMODAL NOCICEPTORS (PMN), which respond to a variety of tissue-damaging inputs:
ā¢ hydrogen ions (protons)
ā¢ 5-hydoxytryptamine (5-HT)
ā¢ Cytokines
ā¢ Bradykinin
ā¢ Histamine
ā¢ Prostaglandins
ā¢ leucotrienes.
7. PAIN PATHWAY
The classic nociceptive pathway involves three types of neurons:
ā¢ Primary sensory neurons in the peripheral nervous system, which conduct pai
nful sensations from the periphery to the dorsal root of the spinal cord
ā¢ Secondary sensory neurons in the spinal cord or brainstem, which transmit th
e painful sensation to the thalamus
ā¢ Tertiary sensory neurons, which transmit the painful sensation from the thala
mus to the somatosensory areas of the cerebral cortex.
9. NERVE FIBERS (PAIN)
There are two major classes of nerve fibers associated with the transmission of pain:
1. Unmyelinated C fibers
2. Myelinated A-delta fibers
10. NERVE FIBERS (PAIN)
The C fibers are small and conduct impulses slowly.
They respond to thermal, mechanical, and chemical stimuli and produce the sensation of d
ull, diffuse, aching, burning, and delayed pain.
A-delta fibers, which are myelinated and thus conduct impulses rapidly, respond to mechan
ical (pressure) stimulus and produce the sensation of sharp, localized, fast pain.
13. Sensitization
Sensitization is a neurophysiologic term that describes the increased responsiveness o
f nociceptive neurons (the pain pathways become more sensitive).
This can include a drop in the threshold for activating nociceptors and an increase in th
e frequency of firing for all stimuli (IASP, 2012).
Clinical Markers for Sensitization:
1. Allodynia
2. Hyperalgesia
15. OPOIDS
Analgesic drug and certain rehabilitation have the same goal?
ANALGESICS:
1. OPOIDS
2. NON-OPOIDS
16. OPOIDS (derived from Opium)
A group of naturally occurring, semisynthetic, and synthetic agents that are ch
aracterized by their ability to relieve moderate-to-severe pain.
ā¢ Bind to specific neuronal receptors in CNS
ā¢ Potential ability to produce physical dependency so in many countries classi
fied as controlled drug (due to potential for abuse)
ā¢ MORPHINE: A prototype for other opioids in terms of efficacy and potency
ā¢ Narcotics: (past) due to sedative and stupor/unresponsiveness in high dose
s
ā¢ Now OPOID ANALGESICS
17.
18.
19.
20. SOURCES OF OPOIDS ANALGESICS
Opioid analgesics can be obtained from natural, synthetic, or semisynthetic sources.
Opium contains about 20 biologically active compounds, including morphine and codein.
The most notable of these precursors is thebaine, which can be modified chemically to yield
compounds such as heroin.
21. ENDOGENOUS OPIOID PEPTIDES
AND OPIOID RECEPTORS
Endogenous Opioids
It is now recognized that three distinct families of endogenous opioids exist: the endorphins, enkephalins,
and dynorphins.
The body manufactures and releases these peptides to control pain and inflammation under specific conditi
ons.
Endogenous opioids may also help regulate the immune system, gastrointestinal (GI) function, cardiovascul
ar responses, and many other physiological systems
22. Opioid Receptors
There are at least three primary classes known as mu, kappa, and delta receptors.
A fourth class known as the nociceptin/orphanin FQ peptide (NOP) receptor has also been identified, but the rele
-vance of the receptor remains unclear because no pharmacological agents have yet been identified that speci
fically affect this receptor.
Stimulation of all three classes of opioid receptors causes analgesia.
However, the mu receptors, located in the brain and spinal cord, seem to be the most important in mediating the
analgesic effects of many opioids, including morphine.
Opioids that are used clinically to reduce pain typically have a fairly high affinity for the mu receptors.
23. Stimulation of mu receptors may cause respiratory depression and constipation, and repeated stimulation
of mu opioid receptors has been associated with the cellular changes that may lead to opioid abuse an
d addiction.
Certain opioid drugs stimulate kappa receptors while avoiding or blocking the mu receptors.
These agents are known as mixed agonistāantagonist opioids.
26. CLASSIFICATION OF SPECIFIC AGENTS
Opioid analgesics are classified according to their interaction with opioid receptors.
ā¢ strong agonists,
ā¢ mild-to-moderate agonists,
ā¢ mixed agonistāantagonists,
ā¢ and antagonists
27.
28. STRONG AGONISTS
Strong agonist agents are used to treat severe pain.
These drugs have a high affinity for certain receptors and are believed to interact primarily with mu opioi
d receptors in the CNS.
Best example: Morphine
29. Mild-to-Moderate Agonists
These drugs are still considered agonists that stimulate opioid receptors, but they do not have as high an
affinity or efficacy as the Strong Agonists.
Used for moderate pain.
Best example:
Codeine
30. Mixed AgonistāAntagonists
Mixed agonistāantagonist drugs exhibit some agonist and antagonist like activity at the same time because the d
rugs have the ability to act differently at specific classes of opioid receptors.
For instance, certain drugs in this category (e.g., butorphanol, nalbuphine, pentazocine) cause analgesia because
they bind to and activate kappa receptors; they are kappa receptor agonists.
At the same time, these drugs block or only partially activate mu receptors, thus acting as mu receptor antagonis
ts or partial agonists, respectively.
Have less effects on respiration, lesser addictive, however causes psychotic effects like hallucinations, vivid dream
s etc.
31. Buprenorphine (Buprenex)
A relatively new addition to this category is buprenorphine (Buprenex).
This drug partially activates mu receptors but is an antagonist at kappa receptors.
Because of these selective effects, buprenorphine has been advocated not only as an analgesic, but also
as a treatment for opioid dependence and withdrawal.
32. Antagonists
Antagonists block all opioid receptors, with a particular affinity for the mu variety.
These agents will not produce analgesia but will displace opioid agonists from the opioid receptors and block any fu
rther effects of the agonist molecules.
Consequently, antagonists are used primarily to treat opioid overdoses and addiction.
Naloxone
When administered in emergency situations, this drug can rapidly (within 1 to 2 minutes) and dramatically reverse
the respiratory depression that is usually the cause of death in excessive opioid ingestion.
33. Naltrexone
Commonly used in conjunction with behavioral therapy to maintain an opioid-free state in individuals recoverin
g from opioid addiction.
This drug may also be useful in treating alcohol dependence.
34. CASE STUDY
A 45-year-old woman, was involved in an automobile accident approximately 6 months ago. She received multiple
contusions from the accident, but no major injuries were sutained. Two months later, she began to develop pain i
n the right shoulder. This pain progressively increased, and she was treated for bursitis using anti-inflammatory
drugs.
Her shoulder motion became progressively more limited; however, any movement of her glenohumeral joint caused
rather severe pain.
She was reevaluated and a diagnosis of adhesive capsulitis was made.
The patient was admitted to the hospital, and while she was under general anesthesia, a closed manipulation of the s
houlder was performed. When the patient recovered from the anesthesia, meperidine (Demerol) was prescribed f
or pain relief.
This drug was given orally at a dosage of 75 mg every 4 hours.
Physical therapy was also initiated the afternoon following the closed manipulation. Passive range-of-motion exerci
ses were used to maintain the increased joint mobility achieved during the manipulative procedure.
1. When should the therapist schedule the treatment session so that meperidine is reaching peak effects?
35. 2. What precautions should the therapist use during the initial treatments given the potential side effe
cts of this drug?
36. ANSWER
1. The therapist should try to treat this patient approximately 1 hour following administration
of the drug.
Meperidine typically reaches peak effects 60 minutes after oral administration and has a 2- to 4-hour duration of a
ction.
Scheduling the initial treatment sessions about an hour after administration will take advantage of the drugās peak
effects while still providing adequate analgesic effects for a few hours after the treatment
37. ANSWER
2. Precautions should focus on meperidineās effects on balance, sedation, hypotension, and respiratory
depression.
If possible, the initial session should be scheduled at the patientās bedside because the patient will still be woozy fr
om the combined effects of the anesthesia and the opioid analgesia. If treatment is provided in the physical th
erapy department, it might be best to transport the patient on a stretcher to prevent an episode of dizziness br
ought on directly by the drugās effects on vestibular function or indirectly by orthostatic hypotension.
The therapist should likewise watch for signs of respiratory depression, including decreased respiratory rate, diffic
ult/labored breathing (dyspnea), and bluish color of the skin and mucous membranes (cyanosis).
Ideally, hemoglobin saturation should be monitored continuously with a pulse oximeter, and excessive respiratory
depression should be reported to the medical staff immediately
38. NEXT:
1. Pharmacokinetics of Opoids
2. Pharmacodynamics of Opoids
3. Mechanism of Actions (MOA) of Opoids
4. Clinical Application/Indications
5. Adverse effects
6. Contraindications
7. Concepts of addiction, tolerance, and physical dependence
8. Special Concerns for Rehabilitation Patients
a subjective experience, which cannot be easily measured. Describing pain as an āexperienceā separates pain from ānociceptionā. Nociception is the neural process involving the transduction and transmission of a noxious stimulus to the brain via a pain pathway. Pain is the result of a complex interplay between signalling systems, modulation from higher centres and the unique perception of the individual.
Physiological, cognitive, and behavioral theories of pain each have their own view of the nature of the two kinds of pain. According to physiological theory and cognitive theory, āpsychologicalā pain and āsensoryā pain are both internal processes, with the former influencing the latter as central processes influence peripheral processes. According to behavioral theory, āsensoryā pain is a reflex (a respondent) while āpsychologicalā pain is an instrumental act (an operant). Behavioral theory claims that neither kind of pain is an internal process ā that both are overt behaviors.
These inflammatory mediators bathe the nociceptors, activating and sensitizing them. Prostaglandins and bradykinin sensitize nociceptors to activation by low-intensity stimuli. Histamine and 5-HT cause pain when directly applied to nerve endings. Hydrogen ions and 5-HT act directly on ion channels on the cell membrane, but most of the others bind to membrane receptors and activate second-messenger systems via G proteins.
These substances sensitize (increase the excitability of) nociceptors by creating an āinflammatory soupā environment that enhances pain sensitivity by reducing the threshold of nociceptors activation (Zouikr et al., 2016). Under normal circumstances, peripheral hypersensitivity returns to normal when inflammation subsides or the source of the injury is removed (Kyranou & Puntillo, 2012).
In CENTRAL, nociceptive-specific neurons may progressively increase their response to repeated non-painful stimuli, develop spontaneous activity, and increase the area of the body that is involved with the pain. The hyperalgesia of central sensitization usually develops as part of ongoing pathology (ie, damage to peripheral or central nerve fibers, cancer, rheumatoid arthritis) and is considered maladaptive (Kyranou & Puntillo, 2012).