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Pages:
1 page/≈275 words
Sources:
2 Sources
Style:
APA
Subject:
Education
Type:
Essay
Language:
English (U.S.)
Document:
MS Word
Date:
Total cost:
$ 3.96
Topic:

week discussion 2

Essay Instructions:
Question 1: Brad ran a 6.2-km race for his cross-country team. The weather was cool, but he started to sweat during the race and continued to sweat for a short time afterward. Evaporation of the sweat from his body then caused him to feel cold. Explain how the autonomic nervous system functioned to control Brad's body temperature during and after the race. (135 words) Question 2: A patient has been exposed to the organophosphate pesticide malathion, which inactivates acetylcholinesterase. Which of the following symptoms would you predict: blurring of vision, excess tear formation, frequent or involuntary urination, pallor (pale skin), muscle twitching, or cramps? Would atropine be an effective drug to treat the symptoms (see Clinical Impact, “Influence of Drugs on the Autonomic Nervous System,” for the action of atropine)? Explain.(135 words)
Essay Sample Content Preview:
Discussion week 2 Name: Institution: Date: The automatic nervous system (ANS) is responsible for maintaining homeostasis in the body through automatic reflexes (Raff, 2003). Human beings typically maintain a core body temperature with balancing occurring because of heat loss or gain. In the process of running, the body generates heat even in cold weather raising the core body temperature. At the initial stages of running, the heat is necessary, but as running continues there is excess heat generated in the body. Sweating is one of the ways through which to cool the body by way of evaporation and cooling of the skin, also characterized with increased blood flow. After running, the thermoreceptors also send signals to the nervous system, leading to vasodilation which lowers the Basal metabolic rate causing heat loss. Ultimately, the thermoreceptors in the skin and hypothalamus maintain the core body temperature. Exposure to Malathion inactivates acetylcholinesterase ...
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