Second pain is also spoken of as pathological pain. Besides, the fast pain is better localized while the

that is why we seek removal of Ihe injurious agent by appropriate measures. For example in leprosy, the pain sensation in the affecled region may be lost, resulting in ignoring of small culs/ sores etc Ultimately, the unattended (untreated) wound may enlarge and lead lo much crippling deformities. In acute abdominal pain, where the exacl cause of pain is yet lo be diagnosed, powerful pain killers should not be given, because this produces only a false sense of well being (as the pain is now absent) withoul elimination of the disease, as a result of which Ihe disease may be masked. However, in some cases, the presence of pain may be counter productive to the mlerest of Ihe patient. The classical example is pain in incurable forms of cancers, where the presence of the pain only adds to Ihe misery of the patient. Receplors and the slimulus Receptors Bare nerve terminals serve as pain receptor. However, other cutaneous receplors, when stimulated excessively, may cause pain. Stimulus. As soon as an acute injury is received, a pain is produced. But long afler the injury is apparently over, the pain may be continued to be felt. [Thus a pain is felt as soon as a hard blow is received, but long after Ihe blow is over, the pain may be continued to be felt]. It is difficult to say whal exactly causes Ihe pain which is produced immediately but the leter pain is almost certainly due to release of some chemicals, liberated by Ihe damaged (damaged due to Ihe injury; blow in this example) lissues; question is, whal are these endogenous chemicals ? A short answer is given below. In Ihe damaged tissues, particularly in the skin, some algogenic (= pain producing) substances are released. These algogenic subslances (AS) come in contact with the pain receptors (bare nerve terminals) ---> pain is produced. Identity of these AS are still controversial. Possible candidates are - (i) a peptide, allied to bradykinin and called 'pain producing peptide', PPS, (ii) bradykmm itself (iii) serotonin (5 HT) (iv) K+ ions (vi) AMP (vi) acetyl cholme; all of them, experimentally, can produce pain. Proslaglandins (PGs) deserve special mention. By Ihemselves, PGs are not very algogenic but they (= the PGs) potentate Ihe algogenic power of serotonin and bradykinin Non opiod analgesics (= pain killers) like (i) NSAIDs as well as (ii) cortisol and related compounds, inhibit the synthesis of PGs and thus relieve pain, for which they are popular in such diseases like rheumatoid arthritis. [NB. 1. NSAID = non steroidal anliinflammatory agent. Example includes, aspirin, ibuprofen etc; chemically Ihey are not sleroids and pharmacologically they are antiin-flammatory, analgesics and anlipyretics. 2. Cortisol and relaled drugs are, on the other hand, steroids]. Characteristics (properties) of pain 1. Threshold and intensity If the intensity of the slimulus is below the threshold (subthreshold), pain is not felt. As the intensity increases more and more, pain is felt more and more according to the Weber-Fechner's law (chap XB1. 1) and the pain sensation spreads, i.e. it begins to be felt in the neighbouring regions also. However, if the mind is distracled, the threshold of pain increases (see chap XB1. 1). Severe excitemenl and emotion can altogether abolish even a severe pain (see, endogenous pain inhibiting system, later this chapter). 2. Adaptation Pain receptors show no adaptation and so the pain continues as long as the receplors continue to be stimulated A s stated already, this is usually beneficial to the subject. 3. Localisation of pain Pain sensation is somewhat poorly localized. However, superficial pain is comparalively betler localized than the deep pain. Visceral pain is usually referred (ie, felt al a place which is other than the area overlying the viscus). 4. Emotional accompaniment Pain sensations are commonly accompanied by emolions. These emotions, as a rule, are unpleasant (recall, touch and other sensations may or may not be accompanied by pleas-ant/unpleasant emotions). 5. Influence of the rate of damage on the intensity of pain If the rale of tissue injury (exlent of damage per unit. time) is high, intensity of pain is also high and vice versa. Therefore, a very slowly growing tissue damaging agent (eg, cancer at early stage), may not produce any pain at all. [Most cancers, in the beginning, are painless]. 6. First (fast) and second (slow) pain After receiving a nociceptive stimulus, two types of nerve fibers are stimulated, viz, and C type of nerve fibers (table 10A.3.1). The fibers are somewhat thick and finely myelinated with a faster rate of conduction, but, C fibers are very thin and non myelmated with a much slower rale of conduction. C type of fibers however outnumber the A fibers. When an injury is received both or any one of the groups of fibers [that is, either A or C may be stimulated (depending on the nalure of the stimulation)], but sensalion due to Ihe stimulation of A fibers are felt earlier whereas that due lo C fibers are felt after a longer interval (because of Ihe slowness of conducting of C fibers). They are called first or fast (due lo A fibers) and second or slow (due to C fibers) pain respectively. Usually, the pain due to C fiber stimulation, is particularly unpleasant and outlasts Ihe period of stimulation. Second pain is also spoken of as pathological pain. Besides, the fast pain is better localized while the slow pain is not. Reactions of pain (i) Behavioral Crying/moaning/whining (in animals). In long standing pain, frustration/ mental irritation /depression can develop. (ii) Muscular Spasm of the skeletal muscles in the affected region (eg. spasm of the muscles around a fraclured bone, abdominal muscular spasm in peritonitis, and so on). Usually speaking, this spasm is beneficial, as it causes immobilisation of the injured part and puts Ihe affected part lo forcible rest (which is essential for healing). However,