Patofisiologi Nyeri  

Oleh:

Dewanto, Georgius

Jenis: Article from Journal - ilmiah nasional - tidak terakreditasi DIKTI - atma jaya
Dalam koleksi: Majalah Kedokteran Damianus vol. 02 no. 03 (Sep. 2003), page 203-212.
Topik: PATOLOGI; Pain; Pathophysiology
Fulltext: D01 v2 n3 p203 kelik2023.pdf (5.08MB)

Ketersediaan

Perpustakaan PKPM Nomor Panggil: M61 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada	Lihat Detail Induk
Perpustakaan FK Nomor Panggil: D01.K Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada	Lihat Detail Induk

Isi artikel

Until the 1960s, pain was considered an inevitable sensory response to tissue damage. There was little room for the affective dimension of this ubiquitous experience, and none whatsoever for the effects of genetic differences, past experience, anxiety or expectation. In recent years, great advances have been made in our understanding of the mechanism that underlie pain and the treatment of people who complain of pain. Pain is probably the most common symptomatic reason to seek medical consultation. All of us have headaches, burns, cuts, and other pains at some time during childhood and adult life. Understanding the plasticity of pain and analgesia exhibited in different pain states may improve therapies for the two major types of pain, neuropathic and inflammatory pain, in which nerve and tissue damage leads to alteration at both peripheral and central levels. At the level of peripheral nerve, drugs that act on particular sodium channels may target only pain-related activity. A new generation of nonsteroidal anti-inflamatory drugs, cyclo-oxygenase 2 inhibitors, that lack gastric actions are available. In the spinal cord, the release of peptides and glutamate causes activation of multiple receptors, particularly, the N-methyl-D-aspartate receptor for glutamate, which, in concert with other spinal system, generates spinal hypersensitivity. Blocking the generation of exitability is one approach, but increasing inhibitions may also provide analgesia. Opioid actions are via presynaptic and post-synaptic inhibitory effects on central and peripheral C fibre terminals, spinal neurons and supraspinal mechanisms. Our knowledge of brain mechanism of pain is still, however, limited. Other new targets have been revealed by molecular biology and animal models of clinical pain, but the possibility of a "magic bullet" is doubtfull.

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