Anatomy and Physiology of the Human Body

Part A

Q 1

a. If I'm being hunted through the forests by a hungry bear, the sympathetic nervous system is the one that gets activated. The sympathetic nervous system is responsible for mobilizing the body's fight or flight response (Esler, 2011). Furthermore, the sympathetic nervous system is responsible for the production of localized changes such as sweating in response to a temperature increase and the relaxation of the body's cardiovascular system (Esler, 2011). If a hungry bear is chasing me, I'll become stressed, and my sympathetic nervous system will be activated, resulting in an immediate widespread response known as the fight-or-flight response, which is characterized by the activation of the sympathetic nervous system. The fight-or-flight response is also characterized by an increase in cardiac output, rise in heart rate, vasodilation of skeletal muscles, pituitary dilation, piloerection, bronchial dilation, as well as gastrointestinal and cutaneous vasoconstriction (Esler, 2011). The overall effect would be to prepare me for the imminent danger posed by the bear.
b.
i. The effect of the sympathetic nervous system on my eyes would be the dilation of the pupils to enhance my vision (Ondicover & Mravec, 2010; Esler, 2011).
ii. The effect of the sympathetic nervous system on my skin would be the stimulation of the sweat glands thereby increasing the rate of sweating on my skin (Esler, 2011).
iii. The effect which the sympathetic nervous system would have on my respiratory system would be the dilation of my lungs’ bronchioles as well as mildly constriction of the blood vessels around the respiratory system to increase the rate of respiration (Ondicover & Mravec, 2010; Esler, 2011).
iv. The effect of the sympathetic nervous system on my skeletal muscles would be increasing the force of muscle contraction as well as increasing the rate of glycogen breakdown (Ondicover & Mravec, 2010).
c. The neurotransmitter family which gets activated in such a situation is the Adrenaline. It consists of norepinephrine, dopamine, and epinephrine (Ondicover & Mravec, 2010; Esler, 2011). The hypothalamic pituitary-adrenal (HPA) system triggers the production of Adrenaline. The hormone then activates the part of the brain known as the amygdala, which triggers an emotional response to a stressful event, which is fear in the case of the bear (Ondicover & Mravec, 2010; Esler, 2011). The HPA system also triggers the production and release of glucocorticoids (steroid hormones), including cortisol or the primary stress hormone. Cortisol plays an essential role in organizing various body systems, including the lungs, heart, metabolism, blood circulation, skin, and the immune system to quickly deal with the bear (Ondicover & Mravec, 2010; Esler, 2011). Additionally, in such a situation, the brain would release neuropeptide S, a type of protein which moderates stress by increasing a sense of anxiety and alertness, and decreasing sleep thus sensitizing me on the urgency to run away from the hungry bear (Ondicover & Mravec, 2010; Esler, 2011).

Q 2

a. If I was at home with the flu, the nervous system which would get engaged is the parasympathetic nervous system. This is because it is the parasympathetic nervous system which controls homeostasis as well as the body's rest and digest responses (Masuda, 2000).
b.
i. The effect of the parasympathetic nervous system on my eyes would be constriction of the pupils and enlargement of the lenses for more light accommodation as well as enhancement of close vision (Masuda, 2000; Ondicova & Mravec, 2010).
ii. The effect of the parasympathetic nervous system on my skin would be stimulating the arrector pili muscles which are connected to hair follicles to contract and create goose bumps on the skin (Masuda, 2000; Ondicova & Mravec, 2010).
iii. The effect which the parasympathetic nervous system would have on my respiratory system would be constricting my lungs' bronchioles to lower the rate of respiration (Masuda, 2000; Ondicova & Mravec, 2010).
iv. The parasympathetic nervous system would cause dilation effect on my skeletal muscles (Ondicova & Mravec, 2010).
c. The neurotransmitter family, which gets activated in such a situation is acetylcholine. When the preganglionic neuron gets stimulated, it releases acetylcholine transmitter at the ganglion, which then acts on the postganglionic neuron’s nicotinic receptors. Acetylcholine then stimulates the receptors of the body’s target organ (Masuda, 2000; Ondicova & Mravec, 2010).

Part B

Q 1

Yes, I would classify Jack as an Alzheimer’s patient. This is because one of the symptoms of Alzheimer disease is that the patient often forgets most recent events without being aware of their problem of forgetfulness or short-term memory (Cummings, 2004; Wood, 2012).

Q 2

Currently, Alzheimer’s disease has no cure. Thus, once Jack starts indicating signs of memory loss, there are no proven treatments which can stop or reverse such a situation (Cummings, 2004; Wood, 2012). However, certain medicines are helpful in easing the symptoms of the disease which I would recommend for Jack. Such medications can slow down the worsening rate of the disease as well as help Jack's brain work better for an extended period (Cummings, 2004; Wood, 2012). Some of such medicines also control the breakdown of acetylcholine chemical in the brain thus boosting the patient’s memory and learning (Cummings, 2004; Wood, 2012). Such medicines include donepezil (Aricept), rivastigmine (Exelon), Memantine, galantamine (Razadyne), and Namzaric (Cummings, 2004; Wood, 2012).
Aricept is recognized by the Food and Drug Administration (FDA) as the only treatment applicable in all the mild, moderate, and severe stages of Alzheimer's disease. Furthermore, it can be taken as a tablet which dissolves in the mouth of the patient or gets swallowed (Cummings, 2004; Wood, 2012). Razadyne is preferable for mild and moderate stages of Alzheimer’s disease and is available as a capsule, tablet, and in liquid forms (Cummings, 2004; Wood, 2012). Exelon is also used for patients with mild to moderate cases of Alzheimer’s and is available in both capsule and liquid forms (Cummings, 2004; Wood, 2012). Memantine is helpful in treating moderate-to-severe conditions of Alzheimer's disease and works by controlling the amount of glutamate, a brain chemical which boosts memory and learning (Cummings, 2004; Wood, 2012). Brain cells of individuals with Alzheimer's disease produce excess glutamate. The role of Namenda is, therefore, to keep the glutamate levels in check thus improving the workability of the brain as well as an individual’s performance in other every-day tasks (Cummings, 2004; Wood, 2012). Namenda can work better when coupled with Exelon, Aricept, or Razadyne. However, the use of Namenda treatment has various side effects, such as dizziness, tiredness, constipation, confusion, and headache (Cummings, 2004; Wood, 2012). Namzaric is a combination of Aricept and Namenda and is it most preferable for patients with moderate to severe Alzheimer's condition (Cummings, 2004; Wood, 2012). Jack can, therefore, use one of the above medicines depending on the doctor's assessment of the level of his Alzheimer's condition.

References

Cummings, J. (2004). Long-Term Treatment for Patients with Alzheimer Disease. Alzheimer Disease & Associated Disorders, 18, S1. http://dx.doi.org/10.1097/01.wad.0000127491.57408.4c
Esler, M. (2011). The sympathetic nervous system through the ages: from Thomas Willis to resistant hypertension. Experimental Physiology, 96(7), 611-622. http://dx.doi.org/10.1113/expphysiol.2011.052332
Masuda, Y. (2000). The role of the Parasympathetic Nervous System and Interaction with the Sympathetic Nervous System in the Early Phase of Hypertension. Journal of Cardiovascular Pharmacology, 36, S61-S64. http://dx.doi.org/10.1097/00005344-200000006-00013
Ondicova, K., & Mravec, B. (2010). Multilevel interactions between the sympathetic and parasympathetic nervous systems: a mini-review. Endocrine Regulations, 44(2), 69-75. http://dx.doi.org/10.4149/endo_2010_02_69
Wood, H. (2012). Alzheimer disease: Prostaglandin E2 signaling is implicated in inflammation early in the Alzheimer disease course. Nature Reviews Neurology. http://dx.doi.org/10.1038/nrneurol.2012.145