pain (nyeri).ppt

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  • NYERI:

    Ada gunanya merupakan mekanisme proteksi badan Terjadi akibat kerusakan jaringan, timbul rasa sakit, walau rasang sangat kecil . Kulit iskemia , rasa sakit dan dapat pingsang Rasa sakit : - cepat 0.1 detik - lambat 1 detik sampai 1 menit Cepat : benda tajam, menyengat dan mendadak Listrik, jarum , kulit teriris Terbakar Tidak perlu masuk ke dalam jaringan sampai dalam Mekanik dan termal Lambat: sakit, nausea, sakit kronis, kerusakan jaringan. Mekanik, termal. Dan kimiawi

  • Reseptor sakit: akhiran saraf bebas, tersebar di seluruh permukaan kulitDi jaringan tertentu: di dalam: periosteum, dinding pembuluh darah, permukaan artikulasio.

    Rangsangan dapat: mekanik, termal dan kimiawiKimiawi: disuntikkan dibawah kulit (bradikinin, ion K, dan enzim proteolitik)

    Jika reseptor lebih sensitif, dinamakan hiperalgesia.

    Termal yang menyebabkan nyeri = 45oC , sebanding dengan kerusakan jaringan.

  • Reseptor sakit tidak seperti reseptor yang lain:Adaptasi : sangat kecil/ tidak ada sama sekali, dalam kondisi tertentu eksitasi menjadi bertambah besarRangsang berjalan terus , jaringan rusak.

    Jaringan iskemia , sakit sekali. Aliran darah tersumbat sakit beberapa menit. Metabolisme bertambah merasa makin sakit.

    Sakit akibat akumulasi asam laktat di jaringan

  • Kejang otot merasa sangat sakit, sindroma sakit Reseptor sakit, mekanosensitif (langsung) Rusak pembuluh darah iskemia (tidak langsung)Dual transmisi signal sakit menuju ke SSP:fast, sharp pain pathwayslow ,chronic pathway

  • Dual, cepat jalan dulu, memberitahu sakit, kemudian hindari, beberapa menit sampai otak

    Jalan sampai otak: traktus neospinotalamus untuk fast pain berhenti di brain stem dan talamus Mekanis, termaltraktus paleospinotalamus untuk slow pain

  • Pain Suppression: bervariasi untuk menekan sakit

    Otak sendiri menahannya untuk tidak ke sistem saraf, Dengan mengaktifkan sistem kontrol sakit = sistem analgesia

  • Sistem analgesia terdiri dari 3 komponen:periaqaeductal dan periventrikuler di mesensefalon dan pons ventrikel 3 dan 4 signal dari neuron-neuron dikirim kenukleus rafe magnus di pons bawah medula atas, Diteruskan turun kekornu dorsalis, medula spinalis

  • Rangsang elektrik: dibawa ke periaqaeduct dan nukleus rafe magnusDapat menekan signal sakit (kuat) pada waktu masuk ke dorsal spinal roots

    Periaqaeduct, periventrikuler menekan sakit tidak terlalu kuatNeurotransmitter , supres sakit (sistem analgesia): enkefalin Serotonin Nuklei periventrikuler dan periaqaeduct ke saraf ujung-ujung mensekresikan enkefalin.Juga rafe magnus mensekresikan enkefalin

  • serabut-serabut asal dari nuklei ini dan berakhir di kornu dorsalis medula spinalis mensekresikan serotonin pada ujung-ujungnya

    serotonin secara setempat merangsang sekresi enkefalin

    enkefalin : presinaps inhibisi dan possinaps inhibisiPada serabut-serabut sakit A dan C dengan sinapsnya di kornu dorsalis dengan cara presinaps inhibisi dan blok kanal ion Ca, Ion Ca melepas transmiter di sinaps blok presinaps inhibisi

  • Pemblok dapat kerja di sistem analgesik mulai dengan menit sampai jam

    Sistem analgesi dapat dihambat di permulaan masuk korda spinalis

    Sistem analgesia dapat menghambat transmisi sakit di perjalanan di nuklei retikuler, batang otak, dan talamus

    Sistem opiat otak: endorfin dan enkefalin

  • Irritasi/rusak jaringan menghasilkan bahan-bahan kimia seperti:prostaglandin, kinins, dan ion kalium yang merangsang nociceptor

    Kondisi yang meningkatkan sakit:Jaringan meregang berlebihanKontraksi otot yang berkepanjanganKejang, iskemia (aliran darah kurang)

  • Phantom Limb Sensation:

    Seorang pasein yang telah diamputasi kakinya merasa sensasi seperti gatal, tertekan atau sakit seakan-akan datang datang dari kaki yang sudah diamputasi

    Mengapa?

  • Korteks serebral menerima impuls datang dari bagian proksimal saraf kaki yang telah hilang

    Di otak sendiri ada jaringan neuron-neuron yang menimbulkan sensasi pertahanan tubuh (neuron masih aktif memberikan sensasi palsu)

    Kadang-kadang dirasa sangat sakit, dengan obat-obatan tidak mereda

  • VISCERAL PAIN

  • Referred Pain

    Pain is initiated in area of the visceral organs and referred to an area on the body surface

    Pain may be referred to an area of the body not exactly coincident with the location of the area producing the pain

  • The pain receptors adapt very little and sometimes not at all

    The average person first begins to perceive pain when the skin is heated above 450C

  • Pain receptor are free nerve endings in the skin and other tissues

    They are widespread in the superficial layers of the skin, and internal tissues (periosteum, arterial walls,joint surfaces, and peritoneum)

  • Pain is elevated by noxcious stimuli on nociceptor (a sesory receptor cell sensitive to xoxious stimuli)

  • Pain is important= is mainly a protective mechanisms for the body= occurs whenever any tissues are being damage= causes the individual to react to remove the pain stimulus

  • Referred pain is important in clinical diagnosis, because may visceral ailments cause no clinical signs except referred pain

  • Mechanical of referred pain

    Branches of visceral pain fibers are shown to synapse in the spinal cord on the same order of neuron that receive pain signals from the skin

  • When the visceral pain fibers are stimulated, pain signal from the viscera are then conducted through at least some of the same neurons that conduct pain signals from the skin, and the person has feeling that the sensations originate in the skin itself

  • Ischemia caused by occluding the blood supply to a large area stimulates many diffuse pain fibers at the same time and can result in extreme pain

  • Ischemia causes visceral pain in the same way that it does in other tissues

    Presumebly because of the formation of acidic metabolic end product or tissue degeneration product such as bradykinin, proteolytic enzymes, or others that stimulate the pain nerves

  • Pain threshold:

    The smallest intensity of a painful stimulus at which a person perceives pain.

    All individuals have the same pain threshold

  • Pain tolerance:

    The greatest intensity of painful stimulation that a person is able to tolerate

    Individuals vary in their tolerance to pain

  • Analgesia, dengan cara menghambat sintesis prostaglandin yang merangsang nociceptorsDapat dengan memberikan obat atau zat yang menghambat enzim yang menyebabkan reaksi arakhidonat menjadi prostaglandin (siklooksigenase, indometasin)

  • Headache of Intracranial OriginThe brain tissues themselves are almost totally insensitive to painTherefore, it is likely that much or most of the pain of headache is not caused by damage within the brain itself

  • HEADACHESHeadaches are a type of pain referred to the surface of the head from deep head structuresSome headaches result from pain stimuli arising inside the cranium, but others result from pain arising outside the cranium such as from the nasal sinuses

  • Conversely, tugging on the venous sinuses around the brain, damage or stretching the dura at the base of the brain can cause intense pain that is recognized as headache (trauma, blood vessels of meninges)

  • Headache of Extracranial OriginHeadache resulting from muscle spasmEmotional tension often causes many of the muscles of the head, especially those muscles attached to the scalp and the neck muscle attached to the occiput, to become spastic

  • Headache caused by irritation of nasal and accessory nasal structuresThe mucous membranes of the nose and nasal sinuses are sensitive to pain

  • Irritative processes in widespread areas of the nasal structure often summate and cause headache , --> referred behind the eyesAlso, pain from the lower sinuses such as from the maxillary sinuses, can be felt in the face

  • Headache originate in the eyes or the extra occular spasm of the muscle, the pain is referred to the surface of the head or retro-orbitally.