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is characterized by some patterns of inflammation. Theseinflammations are driven through immunoglobin dependent mechanisms(Huether &amp McCance, 2012). Cytokines are of particular interests,as they are the means by which the cytokines perpetuate theinflammation. Some important sources of cytokines are airwayepithelial, which alongside other mediators such as endothelin andnitric oxide, the condition is described. The inflammation leads tobronchoconstriction and plasma exudation (Laureate Education Inc,2012e). This activates neural mechanisms to fight the conditions,such as secretion of mucus. During this process, structural changesare effected, which may result in the increase in size of the airwayand fibrosis. These processes cannot be reversed. At the start of theattack, the normal Pa02, say 100mm Hg, falls to about 40mm Hg. This fall is continuous while the pH continues to rise. Therereaches a point where the lungs are unable to expel carbon dioxide,and at this point, PaC02 beings to rise while pH begins tofall. However, PaO2 continues to fall (McPhee &ampHammer, 2012). As the attack worsens, the abnormal levels of PaC02and pH begin getting back to their normal. In the extreme, thelevels again go beyond their normal values, which become fatal andmay lead to death if intervention is not quick. According to Iannuziet al (2007), many patients with this type of asthma maintain arather stable arterial blood gas tension.


In this case, it involves inflammation of the bronchial mucosa. Thisleads to increased production of mucus, thus blocking the passage ofoxygen into system. The result is increased effort to allow enoughoxygen to pass through. While this happens, there is a confusion ofthe expiration and inspiration processes, as the former starts beforethe end of the latter. The patient’s lungs trap air andhyperinflation results. The right ventricular thus becomes overloadedand there is a significant change in the size of the lungs. The leftventricular becomes overloaded because of three things, acidosis,pulmonary vasoconstriction and hypoxia. This fatal case of asthma iswhat leads to the death of many children who have had a long historyof poorly controlled asthma. The function of arterial blood gas is toprovide objective information on gas change (McPhee &amp Hammer,2012). In the case of acute asthma, normal value of PaCO2is an interpretation of muscle fatigue, due to the increased effortto breath. Terminally sick patients often show mixed respiratory andmetabolic acidosis. Additionally, the increased breathing effortleads to production of excess lactic acid, tissue hypoxia anddehydration.

Impactof genetic factor

Genetic factors are have an influential factor in determining whetherthere is a development of atopy. The genetic linkages in asthma recommon to all allergic diseases. Despite the fact that environmentalfactors have a significant role in determining atopic development ofthe disease, genetic factors have a lager influence on how severe thecase becomes and how the body responds to the inflammation occasionedby the attacks.


In chronic asthma, airway inflammation, bronchialhyper-responsiveness ad airflow obstructions are genetic componentsused in its description (Iannuzzi et al, 2007). While patients ofchronic asthma continue to have a normal lung function, the geneticfactors determine how the patients develop structural changes toadapt the lungs to normal function whilst suffering from the illness.In diagnosing the patients, initiation of allergen sensitivity isobserved in suspected cases (Iannuzzi et al, 2007). This is becausethe inhalation of allergens initiates the exacerbations. At the sametime, Genetic study of the cells reveals expression of high-affinityand low affinity IgE receptors. In addition, a mutation causesichthyoids vulgaris, which is a genetic factor associated withchronic asthma. Treatment can be done by individualized plan,lifestyle modification and inhalers.


Patients with acute asthma have grossly inflamed airways. McPhee &ampHammer (2012) say that their airway is blocked by heavy mucus, whichcontain plasma proteins that have been excreted from the surfaceepithelia cells. The airway is shed in a patchy way, and the airwaylumen contains traces of epithelial cells. The inflammation is oftencharacterized by calor and rubor, together with dolor and tumor.These are respectively caused by vasodilation, activation of thesensory nerves and edema. Due to a genetic mutation, the PAF isimpaired. The PAF is an inflammatory mediator that plays a centralrole in most cases of acute asthma. Additionally, the genetic factorinfluences the synthesis of nitric oxide in the system. Thus,increased levels of this as a manifestation of an inflammatorymechanism. According to McPhee &amp Hammer (2012), increased levelsof NO lead to acute exacerbations of asthma, due to a fall in the ph.Given the inflammation, treatment can be done with inhaledsalbutamol. This helps to relax the muscles and free the airway foroxygen to pass through without struggle. Treatment begins withassessment of severity, after which the doctor administers hypoxemiacorrection, reduction of risk relapse and reversal of airflowobstruction. At the same time, there can be treatment with inhaledipratropium bromide, which acts without affecting the systemnegatively.

Mind maps




Huether, S.E. &amp McCance, K.L. (20120. Understandingpathophysiology (Laureate custom ed.). St. Louis, MO: Mosby.

Iannuzzi, M.c., Rybicki, B.A., &amp Teirstein, A.S. (2007).Sarcoidosis. The New England Journal of Medicine, 357(21),2153-2165.

Laureate Education, Inc. (Executive Producer). 2012e). Mid-coursereview. Baltimore, MD: Author.

McPhee, S.J. &amp Hammer, G.D. (2012). Pathophysiology ofdisease: An introduction to clinical medicine (laureate Education,Inc., custom ed). New York, NY McGraw-Hill Medical.