Pain and Narcotics

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Pain and Narcotics

مُساهمة من طرف اسراء في الأربعاء أكتوبر 29, 2008 7:53 pm

Pain and Narcotics

محاضرة يبدو أنها للتخدير-غير متأكدة!-

كتبها لنا الأخ: فادي الصناع- جزاه الله خيراً



عدد المساهمات : 694
تاريخ التسجيل : 19/10/2008
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رد: Pain and Narcotics

مُساهمة من طرف اسراء في الأربعاء أكتوبر 29, 2008 7:55 pm

مادة الشيت- بدون الصور-:

Pain and Narcotics

Pain is not only as physical suffering or anxiety, it is human suffering
The policy for JUH that patients should not suffer! (we are the one who only suffer )

*Categories of Pain:

Acute: It is the pain that appears suddenly as headache and may disappear by simple medication. For example, a patient who have headache can be resolved by paracetamols.

Chronic: It is an existing and continuous type of pain.
We have to find the underlying cause of this type of chronic pain and treat it.

Source of Pain:

a. External: The billion nerve endings that are distributed in our skin serve as a guard (Think of burn) and protect us. Also, they try to transfer all normal and abnormal sensations regardless of what they are to our brain to be translated.

b. Internal: The nerve endings are different in quantity (one tenth of the external nerve endings) and quality. These are distributed mainly in our GIT.

If the colon was obstructed due to any reason (tumor, adhesions, infection…) distention will occur and will reach to a maximum limit above which we start feeling of pain in that area.

So, we can conclude that internal sensation depends upon the following 3 factors:

 Tolerance of the nerve ending: The pressure and dilatations will increase up to a limit above which the nerve endings will be stimulated.

 Ischemia beside pressure: For example, thrombosis of the mesenteric artery in an old patient will lead to ischemia that will give certain chemical substances and alarm the nerve endings

 Invasion: invasion of a tumor till it reaches the internal nerves.

To make things clearer we will present our following ideas from this example:

An abscess was present in a certain area, the body will produce prostaglandins, potassium ions and bicarbonate ions at the site of abnormal sensation that serve as alarming factors to the nerves.

The nerves will conduct the message to next stations in 2 ways:

- Through myelinated nerves: conduction here is fast through salutatory conduction across the nodes of Ranvier (exposed area of the nerve)

- Thinner and non-myelinated nerve: slower conduction

This picture is just to refresh your memory.

“Gate-Control Theory”:

The afferent sensory nerves will enter the spinal cord from the dorsal horn. Of course, some of the nerves will reach sooner than the other due to the way of conduction we explained simply above.
And efferent motor nerves will get out of the anterior horn.

What we want to say that at the level of the spinal cord will protect and filtrate the information it receives. The 12 laminae and especially the “Substantia Gelatinosa” will filter the incoming information according to the sharpness duration of the incoming information (alarm).Also, it will block some of the sensations and protects us.

We will give a simple example: by pricking the tip of a finger with a sharp pin or staple we will feel pain for a very short duration because the spinal cord blocked the sensation as the sharpness and duration of the alarm is very short. Protection occurs when we have reflex mechanism as touching a hot iron.

So, some of the main functions of the spinal cord are:
1. Filtration
2. Blocking
3. Reflex-defense mechanism (protection).

Additional information about “Gate-Control Theory”:
Gate control theory asserts that activation of nerves which do not transmit pain signals, called nonnociceptive fibers, can interfere with signals from pain fibers, thereby inhibiting pain.Afferent pain-receptive nerves, those that bring signals to the brain, comprise at least two kinds of fibers - a fast, relatively thick, myelinated "Aδ" fiber that carries messages quickly with intense pain, and a small, unmyelinated, slow "C" fiber that carries the longer-term throbbing and chronic pain. Large-diameter Aβ fibers are nonnociceptive (do not transmit pain stimuli) and inhibit the effects of firing by Aδ and C fibers.
The peripheral nervous system has centers at which pain stimuli can be regulated. Some areas in the dorsal horn of the spinal cord that are involved in receiving pain stimuli from Aδ and C fibers, called laminae, also receive input from Aβ fibers.The nonnociceptive fibers indirectly inhibit the effects of the pain fibers, 'closing a gate' to the transmission of their stimuli.In other parts of the laminae, pain fibers also inhibit the effects of nonnociceptive fibers, 'opening the gate'.
An inhibitory connection may exist with Aβ and C fibers, which may form a synapse on the same projection neuron. The same neurons may also form synapses with an inhibitory interneuron that also synapses on the projection neuron, reducing the chance that the latter will fire and transmit pain stimuli to the brain.The inhibitory interneuron fires spontaneously.The C fiber's synapse would inhibit the inhibitory interneuron, indirectly increasing the projection neuron's chance of firing. The Aβ fiber, on the other hand, forms an excitatory connection with the inhibitory interneuron, thus decreasing the projection neuron's chance of firing (like the C fiber, the Aβ fiber also has an excitatory connection on the projection neuron itself). Thus, depending on the relative rates of firing of C and Aβ fibers, the firing of the nonnociceptive fiber may inhibit the firing of the projection neuron and the transmission of pain stimuli.
The following pictures may make things clearer:

The firing of the projection neuron determines pain.The inhibitory interneuron decreases the chances that the projection neuron will fire.Firing of C fibers inhibits the inhibitory interneuron (indirectly), increasing the chances that the projection neuron will fire.A lightning bolt signifies increased neuron activation, while a crossed-out bolt signifies weakened or reduced activation.

Firing of the Aβ fibers activates the inhibitory interneuron, reducing the chances that the projection neuron will fire, even in the presence of a firing nociceptive fiber.

*Identification of Pain Pathway:

In the past they used to think that for each type of pain there is a selective nerve. But, what is true is our recent “Gate-Control Theory”. Since the discovery of this theory our understanding of the pain pathway has improved dramatically. And what is important that the success rate in treating chronic pain reached up to 85%

Now, let us summarize what we have just said:
We revised the categories and source of pain. Moreover, we said how impulses are conducted across the nerves (myelinated and unmyelinated or more correctly thinly myelinated) till reaching the SC. Also, we discussed the “Gate-Control Theory”

The SC will receive, filter the information and is responsible for some direct reflexes. Other information will be sent to the higher centres (those of high duration). So, part of the nerves from the periphery will decussate across the laminae to the other side to get high up to the medulla oblongata  to thalamus and finally to cortex.
The crossing tract is called the dorsal horn. While there is another part that did not decussate and is called spinothalamic tract (STT).

Some nerves pass through the thalamus because it is the centre of emotion and mood.
Which means that according to our situation or pain will be reflected in our mood. Not only that, the education and experience in the past will determine the degree of mood.

On the other hand, the cortex is responsible for organization, severity & localization of pain and it provides information about the pain (sharp sensation in our burned hand).
The cortex also has its special pharmacy providing endorphins that are 6 times more potent than morphine!!! Endorphins will protect our body for a certain period that differs from one person to another. Soldiers in the war can have a gunshot and still fighting without feeling of a severe pain.

"لما تبرد الضربة بتشعر بالوجع"

O hay hadieh la 3yonak ya Dr.Hamzeh:


We have three stations for the pain impulses that narcotics can act upon:
I. Site of action
II. Spinal Cord (SC)
III. Brain

The type of medication should be given according to the type, severity and duration of pain. We don’t give pethidine for a simple and normal headache.

Our Map of Treatment (These are only example):

I. Peripheral source of pain: prevent the pain sensations from passing to next stations by using non-inflammatory drugs that overcome the prostaglandins, potassium and bicarbonate ions.
II. Spinal Anaesthesia in intrathecal space according to the level can paralyze the limbs in about 5 minutes and I can use that when we have a patient with a broken leg.
III. At level of the brain I can give analgesics in the ventricles in cases of tumor.

According to 1.Site of pain, 2.Severity of pain, 3.Degree of pain and 4.Duration we treat our patients.

What is important in management is the 3 step leader of the WHO:

“Three Step Leaders” States that:
1. All mild pain: paracetamol and non-steroidal

2. Moderate type of pain (appendicitis, cholecystitis, piles, colic pain…) we will have no effect by using paracetamols or nonsteroidal alone. So, we mix mild narcotics as codeine(Tramal) with non-steroidal. OR mild narcotics alone are enough.

3. Severe pain of long duration that we can not control it immediately we give narcotics with or without non-steroidal/codeine(mild narcotics) and sometime cortisone is even given.

Done by: “Fadi Riad Sunna’”

عدد المساهمات : 694
تاريخ التسجيل : 19/10/2008
العمر : 31

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