TAILIEUCHUNG - Chapter 133. Tetanus (Part 2)

Pathogenesis Contamination of wounds with spores of C. tetani is probably a frequent occurrence. Germination and toxin production, however, take place only in wounds with low oxidation-reduction potential, such as those with devitalized tissue, foreign bodies, or active infection. C. tetani does not itself evoke inflammation, and the portal of entry retains a benign appearance unless coinfection with other organisms is present. Toxin released in the wound binds to peripheral motor neuron terminals, enters the axon, and is transported to the nerve-cell body in the brainstem and spinal cord by retrograde intraneuronal transport. The toxin then migrates across the synapse to. | Chapter 133. Tetanus Part 2 Pathogenesis Contamination of wounds with spores of C. tetani is probably a frequent occurrence. Germination and toxin production however take place only in wounds with low oxidation-reduction potential such as those with devitalized tissue foreign bodies or active infection. C. tetani does not itself evoke inflammation and the portal of entry retains a benign appearance unless coinfection with other organisms is present. Toxin released in the wound binds to peripheral motor neuron terminals enters the axon and is transported to the nerve-cell body in the brainstem and spinal cord by retrograde intraneuronal transport. The toxin then migrates across the synapse to presynaptic terminals where it blocks release of the inhibitory neurotransmitters glycine and Y-aminobutyric acid GABA from vesicles see Fig. 134-1 . The blocking of neurotransmitter release by tetanospasmin a zinc metalloprotease involves cleavage of synaptobrevin a protein essential to proper function of the synaptic vesicle release apparatus. With diminished inhibition the resting firing rate of the amotor neuron increases producing rigidity. With lessened activity of reflexes that limit polysynaptic spread of impulses a glycinergic activity agonists and antagonists may be recruited rather than inhibited with the consequent production of spasms. Toxin may also affect preganglionic sympathetic neurons in the lateral gray matter of the spinal cord and parasympathetic centers. Loss of inhibition of preganglionic sympathetic neurons may produce sympathetic hyperactivity and high circulating catecholamine levels. Tetanospasmin like botulinum toxin may block neurotransmitter release at the neuromuscular junction and produce weakness or paralysis but this effect is clinically evident only in cephalic tetanus. Recovery requires sprouting of new nerve terminals. In local tetanus only the nerves supplying the affected muscles are involved. Generalized tetanus occurs when toxin .

TỪ KHÓA LIÊN QUAN
TAILIEUCHUNG - Chia sẻ tài liệu không giới hạn
Địa chỉ : 444 Hoang Hoa Tham, Hanoi, Viet Nam
Website : tailieuchung.com
Email : tailieuchung20@gmail.com
Tailieuchung.com là thư viện tài liệu trực tuyến, nơi chia sẽ trao đổi hàng triệu tài liệu như luận văn đồ án, sách, giáo trình, đề thi.
Chúng tôi không chịu trách nhiệm liên quan đến các vấn đề bản quyền nội dung tài liệu được thành viên tự nguyện đăng tải lên, nếu phát hiện thấy tài liệu xấu hoặc tài liệu có bản quyền xin hãy email cho chúng tôi.
Đã phát hiện trình chặn quảng cáo AdBlock
Trang web này phụ thuộc vào doanh thu từ số lần hiển thị quảng cáo để tồn tại. Vui lòng tắt trình chặn quảng cáo của bạn hoặc tạm dừng tính năng chặn quảng cáo cho trang web này.