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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
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bhsgurlz
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Critical Thinking and Clinical Application Questions #2-5 found on Page 428
Short Answer Essay Question's  #14, 16, 18, 20, 22-25, 27, & 30 found on page 482.

Book: Human Anatomy & Physiology 8th Edition
Authors: E. Marieb, K. Hoehn

Last Edit: Jun 9, 2011 by bhsgurlz LoggedReport this PostReport Abuse

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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

Hello  Grin
I don't have this textbook, but if it's possible to post the actual questions I may be able to help you somewhat.  Waving Hand



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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

Here are the Critical Thinking Questions:

#2: What specific process do anesthetics impair? How does this interfere with nerve transmission?

#3: When admitted to the emergency room, John was holding his right hand, which had a deep puncture hole in its palm. He explained that he had fallen on a nail while exploring a barn. John was given an antitetanus shot to prevent neural complications. Tetanus bacteria fester in deep, dark wounds, but how do they travel in neural tissue?

#4: Rochelle developed multiple sclerosis when she was 27.  After eight years she had lost a good portion of her ability to control her skeletal muscles.  Why did this happen?

#5:  In the Netherlands a young man named Jan was admitted to the emergency room. He and his friends had been to a rave. His friends say he started twitching and having muscle spasms which progressed until he was “stiff as a board.” On examination, staff found a marked increase in muscle tone and hyperreflexia involving facial and limb muscles. In his pocket, he had unmarked dark yellow tablets with dark flecks. Analysis of the tablets showed them to contain a mixture of ecstasy and strychnine. Ecstasy would not cause this clinical picture, but strychnine, which blocks glycine receptors, could. Explain how.



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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

Good suggestion Wink

(2) They block neurotransmitters in the brain, thus blocking impulses out (i.e. muscle movement) and impulses in, sensation of pain. Thus, you are asleep, paralyzed and don't feel a thing. They block neurotransmitter release by altering the flow of sodium ion into neurons, and as I mention, this prevents nerve impulses from being generated, causing the brain to become unconcious.



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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

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(4) Multiple Sclerosis is a very unpredictable disease. It can strike once and then go dormant for years, or it can come on hard, fast, and strong. MS is a very personal disease; it affects everyone who gets it in a different way. There is a range of symptoms that MS causes, but they differ from person to person.

Does Rochelle have a "relapsing" form of MS? If so, did she get on one of the disease-modifying drugs as soon as she was diagnosed? If not, she may have had a "progressive" form of the disease known as "Primary-Progressive" MS, where there are no significant "relapses" or "remissions" but a slow, steady worsening of symptoms with no discernible highs or lows. PPMS is rare, but it's out there. There are a few new drugs which help PPMS; previously, there were no drugs for those with "Progressive" forms of the disease.

If she had a "Relapsing" form of the disease, and did not take any medication, she may have progressed to a "Progressive" form of the disease called "Secondary-Progressive" MS. Current statistics show that 50% of people with RRMS (Relapsing-Remitting MS) who go untreated will progress to SPMS within 10 years. Some earlier, some later, but half of those untreated will be into their progressive stage within 10 years.

The disease-modifying medications hope to extend the length of time before the progressive phase of the disease begins, but there is too little information at this point to say conclusively whether or not they do. Scientists believe that they will, but without empirical evidence to back it up, it's just speculation. The medications do lengthen the time between relapses, reduce their severity, and reduce the amount of active lesions on the brain, but we don't know yet if they delay the onset of the progressive form of the disease.

Nerve damage and spasticity are common in MS. Rochelle may be able to prevent further loss of control by removing saturated fats and dairy products from her diet, and by taking Vitamin D and Fish Oil supplements.

Generally, in MS, the myelin sheaths are destroyed. Loss of this insulating sheath results in
shunting of current and eventual cessation of neurotransmission.



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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

Quote
Rochelle developed multiple sclerosis when she was 27.  After eight years she had lost a good portion of her ability to control her skeletal muscles.  Why did this happen?

Multiple sclerosis affects the electrical signals that are send form the brain to different parts of the body.



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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

2) Local anesthetics such as novocaine and sedatives affect the neural processes usually at the nodes of Ranvier, by reducing the membrane permeability to sodium ions.



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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

3) The bacteria remain in the wound; however, the toxin produced travels via axonal transport to reach the cell body.



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Anatomy & Physiology 1: Human Anatomy & Physiology 8th Edition
Jun 9, 2011

5) Glycine is an inhibitory neurotransmitter that is used to modulate spinal cord transmission. Strychnine blocks glycine receptors in the spinal cord, leading to unregulated stimulation of muscles, and spastic contraction to the point where the muscles cannot relax.



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