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Anatomy and Physiology 1 - Essay Example

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A coroner was unable to remove the drug vial clutched in a suicide victim’s hand. This is because of rigor mortis. Rigor mortis is stiffening of the body after death due to disappearance of adenosine triphosphate (ATP) from the muscle. The muscles of the body become rigid…
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Anatomy and Physiology 1
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7 May Anatomy and Physiology 1. A coroner was unable to remove the drug vial clutched in a suicide victim’s hand. This is because of rigor mortis. Rigor mortis is stiffening of the body after death due to disappearance of adenosine triphosphate (ATP) from the muscle. The muscles of the body become rigid and the joints immobile. In order for muscle to contract, energy is needed and ATP is the major source. Muscles need a continuous supply of ATP to contract. The aerobic system, the glycogen-lactic acid system and the phosphagen are metabolic systems responsible for supplying ATP in the muscles.

After death, the consumption of ATP continues but the generation stops. Therefore in the absence of ATP, actin and myosin filaments become permanently complexed and rigor mortis sets in (Raff, 290). After three days, the coroner will be able to remove the drug vial from the hand since there was onset of decomposition. Decomposition is degradation or breakdown of the body (Raff, 290).2. During surgery, anesthetics are administered to patients blocking the action potential generation. These anesthetics target the function of voltage-gated sodium channels.

Local anesthetics work by blocking the entry of sodium ions into their channels therefore preventing transient increase in permeability of the nerve membrane to sodium ions into their channels thereby preventing the transient increase in permeability of the nerve membrane to sodium ions for generating action potential. Binding of both protonated and neural local anesthetic molecules interferes with conformational changes that underlie the process of channel activation. The failure of sodium ion channel permeability to increase slows own the rate of depolarization since an action potential is not propagated.

This interferes with nerve transmission since failure in action potential will cause inability of flow of current from depolarized sites inside surface of the cell membrane to adjacent polarized membrane (Raff, 170).3. People with Alzheimer’s disease are forgetful and with disease progression they become confused and lose their ability to speak. These patients often have diminished acetylcholine transferase activity in their brains. The enzyme that synthesizes acetylcholine by transferring the acetyl group from acetyl-coA to choline.

Acetylcholine is a major neurotransmitter in the nervous system. It is produced in cholinergic neurons from choline and acetyl co enzyme A by action of acetyltransferase. Acetylcholine is stored in vesicles at the presynaptic cell terminal and released after excitation. After acetylcholine is released into the synapse, it is broken down into smaller parts and taken up by the nerves so that it can be reused. Decrease of acetylcholine in the brain is usually caused by destruction of brain cells that make and release acetylcholine (Raff, 207).4. In developing drugs to regulate brain disorders, there may be physiological roadblocks such the blood brain barrier which may hinder the drug.

Drug delivery across the blood brain barrier is a major challenge for developing effective treatments of many central nervous system disorders. The blood brain barrier serves to isolate the brain from various substances in the systemic circulation. The capillaries are lined with specialized endothelium which is impermeable to different substances (Raff, 210). The drugs can be designed to bypass the blood brain barrier to deliver drugs to the brain and spinal cord through delivering the drugs locally.

This can be done by the ophthalmic, nasal and pulmonary drug systems. These drugs are also easier to administer, convenient and are accessible. The drug released from the local source will pass into the tumor tissue by passive diffusion down a concentration gradient (Raff, 210).Works CitedRaff, Hershel. Physiology. Philadelphia: Hanley & Belfus, 2003. Book.

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