What are the signs of organophosphate toxicity? Knowing these signs, what is a possible antidote?
What will be an ideal response?
Organophosphates inhibit acetylcholinesterase, the enzyme that normally breaks down acetylcholine. By inhibiting this enzyme, acetylcholine remains active in the neuromuscular junction. Clinical signs of organophosphate toxicity include excessive salivation, lacrimation, urination, defecation, dyspnea, and emesis.
Antidotes for organophosphate toxicity include agents that reverse the breakdown of acetylcholmesterase or that inhibit
acetylcholine at the neuromuscular junction. One agent that reverses the breakdown of acetylcholinesterase is 2-PAM (pralidoxime chloride). 2-PAM reactivates cholinesterase that has been inactivated by organophosphates. An agent that inhibits acetylcholine is atropine. Both have been used as antidotes for organophosphate toxicity.
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Which correctly describes the heart's apex?
A. Projects slightly anteroinferiorly toward the left side of the body B. Projects slightly anteroinferiorly toward the right side of the body C. Projects slightly posteroinferiorly toward the left side of the body D. Projects slightly posteroinferiorly toward the right side of the body E. Projects slightly posteroinferiorly toward the midline of the body
Receptor sites on the outer surface of the plasma membrane are
a. ATP. b. carbohydrates. c. cyclic AMP. d. DNA. e. proteins.
Achondroplastic dwarfism is a hereditary condition, in which the long bones of the limbs fail to elongate normally because of reduced hyperplasia and hypertrophy of cartilage in the ________.
A. secondary ossification center B. primary ossification center C. epiphyseal plate D. primary bone marrow E. secondary bone marrow
An X-ray determines that Peter fractured the shaft of his humerus. The break is in the _____________ of the bone
A. diaphysis B. epiphyseal line C. articular surface D. epiphysis E. growth plate