Asthma and Treatment Solutions

Discussion Cases
1 Leon
While biological causes for the difference between whites and blacks’ biological mechanisms regarding blood pressure have been speculated as being the cause of higher rates of hypertension among blacks in America, the fact that African Americans as opposed to Africans have higher rates of hypertension suggests that environment has more to do with it than biology (Fuchs, 2011). Environmental factors and daily living habits of African Americans are more than likely the main contributing variables to higher hypertension rates in this population. Environmental factors can include stress and anxiety stemming from racial tension in the U.S. that leads to high blood pressure for blacks in the country. Lifestyle habits can also impact the health of this population: diet and lack of exercise can contribute to hypertension as well (Lindhorst, Alexander, Blignaut & Raynor, 2007). Many diets in America are high in sodium, which can increase blood pressure, and an African American like Leon who likes to consume nachos and hot dogs and undoubtedly other salty foods regularly is bound to have higher blood pressure.
The significance of an elevated systolic pressure, even in the absence of diastolic hypertension, is that it means the patient has a higher risk of suffering from cardiovascular disease. A higher systolic pressure has been associated with hypertrophy in the left ventricle of the heart and a need for more oxygen in the heart muscle, which, if untreated, can lead ultimately to heart failure. So a high systolic pressure is not acceptable even if diastolic hypertension is not present—it is still a troubling sign that needs to be adequately addressed. Other problems that could arise from high systolic pressure include atherosclerosis and a possible aneurysm.
The mechanism of action of the two classes of drugs Leon was prescribed for the management of his hypertension—diuretics and an ACE inhibitor—focus on getting the sodium out of the body and limiting the body’s ability to constrict blood vessels, respectively. The diuretics flush the system by triggering the body’s renal secretion of water and sodium. The ACE inhibitor blocks the body from turning angiotensin I into angiotensin II. As there is less angiotensin II in the body, less aldosterone is released and less vasoconstriction takes place, providing some relief from what would otherwise be the body’s constant hypertensive activity. Thus, the diuretics stimulate the body to release water and sodium, while the ACE inhibitor blocks the body from releasing stimulants that would constrict the blood vessels.
2 Emmanuel
The corticosteroid inhaler uses steroids to reduce swelling of the airways to help the patient breathe better. As Lim et al. (1998) point out, these types of inhalers work well because they “increase interleukin-10 but reduce macrophage inflammatory protein-1 ?, granulocyte-macrophage colony-stimulating factor, and interfere on-? release from alveolar macrophages in asthma” (p. 256). In other words, stimulate anti-inflammatory cytokine while prohibiting pro-inflammatory cytokines.
The action of the corticosteroid inhaler is different from a beta-2 agonist inhalant in that the latter provides short term relief by promoting dilation of the bronchial passage and relaxing the uterine muscle, while releasing insulin into the body. Vasodilation occurs in the muscles and liver of the patient to trigger these latter actions. Inhaled steroids are the recommended course of action for treating asthma, but beta-2 agonists are also helpful for smoothing the airways and helping the patient to gain better control of the breathing process (Erdinc, 2011). It is this type of treatment that Emmanuel most likely would benefit from during an asthma attack so that he does not become panic-stricken over the initial inability to catch his breath while waiting for the steroid to take effect when using the corticosteroid inhaler.
Someone with severe asthma becomes physically fatigued during a prolonged attack because the individual is not getting the oxygen the body needs to maintain proper functions and thus the body is working overtime or twice as hard just to keep up with its routine maintenance jobs while the individual tries to cope with the stress of struggling to breathe. Hypercapnia results, which is what happens when more carbon dioxide is in the blood than should be, and it can cause fatigue and the body to become flush. The body also becomes tense from the stress, and the muscles tighten, causing the individual to expend a great deal of energy over a short duration of time. Once breathing is regained, the body relaxes and a feeling of fatigue can set in—all of which is a natural course of events for someone undergoing a stressful or tense process like trying to regain one’s breath.
The physiological events that occur during an attack are that the airways are narrowed and more mucus is produced, which makes it hard to breathe for the individual. The immune system is activated in the bronchial airways but is actually oversensitive to stimuli, just as an individual who suffers from allergies has a hyper-sensitive reaction to ragweed or pollen in the air during the spring and summer months. For a person with asthma, when the body is triggered by the stimuli the large airways contract and spasm, causing the individual to suffer a loss of breathing control: inflammation occurs, the airways continue to constrict and more mucus builds; the individual has coughing fits as a result and still cannot catch his breath.
The body compensates for an increase in CO2 by attempting to breathe more quickly and expel the CO2 and get more oxygen into the blood. Hypercapnic acidosis can also occur to modulate the effects of inflammation (Vengust, 2012). The effects of hypercapnia on the central nervous system are similar to like a patient is engaged in hypnosis: the elevated CO2 content reduces the person’s threshold for convulsions and cerebral vasolidation. Intracranial pressure can occur and brain swelling can become a problem.
3 Mandy
In Mandy’s case, her low estrogen levels which result from her delayed or absent menstruation cycle (amenorrhea) are causing her to lose bone mineral density. This is the root of her problem of premature osteoporosis. The amenorrhea, moreover, is triggered by her strict diet and exercise routines which are pushing her body to engage in processes that it would not naturally or normally engage in—and as a result, the body’s natural responses to regulating itself are disrupted. The result, as can be seen, is that her bones have lost density and a simple fall has caused her to fracture her foot. The x-rays show that all of her bones are at risk of fracture because of the premature osteoporosis that has set in—all of which can be a common problem for young female athletes who do not take the necessary steps to help their bodies be regulated by compensating for the deficiencies that arise from the strict workout routine and diet that are self-imposed (Jones, Ravnikar, Tulchinsky & Schiff, 1985)
A deficiency in estrogen in women leads to osteoporotic change because estrogen is required for adequate closure of epiphyseal growth plates. For a young female whose bones are still growing, this process is particularly important—but estrogen deficiency can also occur in adult women during menopause. Though the bones are not growing, the lack of estrogen can induce cancellous and cortical bone loss (Vaananen & Harkonen, 1996). Estrogen is necessary because it helps the bone to regulate IL-6 in its marrow cells (Vaananen & Harkonen, 1996). When estrogen is depleted, bone density becomes a problem as these cells are unregulated and bone resorption is increased in the individual as a result.
The general macroscopic differences between osteoporosis and osteomalacia are that when osteoporosis occurs, the bones become brittle and porous, like an old fossilized shell of a spongy sea creature: if dropped, it will shatter into pieces. Osteomalacia, on the other hand, occurs when the bone becomes soft. The difference in mineralization between the two is with regard to the ratio of mineral to organic material in the bone. Osteoporosis occurs when there is too much mineralization with respect to organic material in the bone. Osteomalacia occurs when there is too little mineralization with respect to organic material in the bone. In Mandy’s case, she is suffering from osteoporosis because the estrogen that would normally be produced in her body as a result of a natural menstrual cycle is not being produced, and therefore the mineralization process in her bones is not being regulated. Too much mineralization occurs, which makes the bones brittle—and that is why she suffered a fracture in her foot and why she is now experiencing osteoporosis.

References
Erdinç, M. (2011). Beta-2 agonist discussions in asthma and a review of current
data. Tuberk. Toraks, 59, 205-212.
Fuchs, F. D. (2011). Why do black Americans have higher prevalence of hypertension?:
an enigma still unsolved. Hypertension, 57, 379-380.
Lindhorst, J., Alexander, N., Blignaut, J., & Rayner, B. (2007). Differences in
hypertension between blacks and whites: an overview. Cardiovascular Journal of Africa, 18(4), 241-247.
John, M., Lim, S. A. M., Seybold, J., Jose, P., Robichaud, A., O'CONNOR, B. R. I. A.
N., ... & Fan Chung, K. (1998). Inhaled corticosteroids increase interleukin-10 but reduce macrophage inflammatory protein-1 ?, granulocyte-macrophage colony-stimulating factor, and interferon-? release from alveolar macrophages in asthma. American Journal of Respiratory and Critical Care Medicine, 157(1), 256-262.
Jones, K. P., Ravnikar, V. A., Tulchinsky, D., & Schiff, I. S. A. A. C. (1985).
Comparison of bone density in amenorrheic women due to athletics, weight loss, and premature menopause. Obstetrics and Gynecology, 66(1), 5-8.
Väänänen, H. K., & Härkönen, P. L. (1996). Estrogen and bone
metabolism. Maturitas, 23, S65-S69.
Vengust, M. (2012). Hypercapnic respiratory acidosis: A protective or harmful strategy
for critically ill newborn foals?. Canadian Journal of Veterinary Research, 76(4), 275-280.