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Respiratory System

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Structure and Function of the Respiratory System Case Forty-five-year-old Brad has, ever since the age of 20, been working in the mines in the post of coal cutter. He is happy with his job as he earns a good wage and his father also worked in the very same mine. Akin to several co-workers of his, he suffers from chronic cough. However, Brad has neglected going...

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Structure and Function of the Respiratory System Case Forty-five-year-old Brad has, ever since the age of 20, been working in the mines in the post of coal cutter. He is happy with his job as he earns a good wage and his father also worked in the very same mine. Akin to several co-workers of his, he suffers from chronic cough.

However, Brad has neglected going for yearly health checks as is required for mine workers owing to his fear of being diagnosed with “black lung” (i.e., coal worker pneumoconiosis). This ailment results in fibrosis, lasting dilation of the small airways, and reduced diffusing capability. At more advanced stages of the disease, alveoli, airways and pulmonary capillaries get destroyed. Chronic obstructive pulmonary disease (COPD) COPD has been described as a persistent inflammatory lung ailment which obstructs flow of air from the patient’s lungs.

Disease symptoms include difficulties in breathing, wheezing, coughing, and sputum (or mucus) secretion. COPD results from continuous exposure to particulate material or irritants in gaseous form such as cigarette smoke. Patients are highly vulnerable to contracting lung cancer, heart ailments, and various other health conditions. The biggest contributors to COPD contraction are chronic bronchitis and emphysema. The former is characterized by inflammation of bronchial tube linings (bronchial tubes are responsible for carrying air back and forth from the lungs’ alveoli (air sacs).

Symptoms include coughing and sputum (mucus) generation on an everyday basis. Meanwhile, the latter condition entails destruction of the alveoli situated at the bronchioles’ (tiniest air passages’) end owing to exposure to harmful cigarette smoke as well as other particulate material and gaseous irritants (Mayo Clinic, 2019). Accurate COPD diagnosis is vital as proper management may reduce symptoms (particularly dyspnea) and aggravation intensity and incidence, prolong life, and improve patients’ health status and exercise capacity.

According to GOLD (Global Initiative for Chronic Obstructive Lung Disease), COPD has been defined as a widespread, typically-progressive, avoidable, and curable ailment marked by restricted airflow and linked to intensified chronic inflammatory reaction within the lungs and airways to poisonous gases or particles. Comorbidities and aggravations increase overall disease intensity among individual COPD-diagnosed persons (Angelis et al, 2014).

Mismatch between Ventilation and Perfusion Hypoxemia’s key contributor among COPD-diagnosed persons is V/Q (ventilation/ perfusion) mismatch stemming from a progressive constriction of airflow and the pulmonary capillary bed’s emphysematous breakdown. Researches that employed multiple inert gas elimination method revealed COPD-diagnosed individuals exhibiting a chiefly emphysematous phenotype depict increased badly-perfused lung unit ventilation (or in other words, elevated V/Q ratio), thereby experiencing a larger physiological dead space. On the contrary, those having advanced airway disease display increased likelihood of having a small V/Q ratio, coupled with heterogeneous hypoventilation of the alveoli, significant under-ventilated area perfusion, and resultant physiological shunt.

Whilst V/Q mismatch because of small airway illness and pulmonary emphysema can be measured even among patients having mild COPD, it apparently increases at later stages of the disease. COPD aggravations are often related to gas exchange deterioration and connected hypoxemia.

Predictably, greater V/Q relationship inequality is apparently a key change determinant. Enhanced oxygen consumption by the tissue, with resulting lower mixed oxygen levels in the veins apparently play a role in increasing hypoxemia at the time of exacerbations as well; however, it is, at the very least, counterbalanced partly by a parallel cardiac output growth (Kent, Mitchell & McNicholas, 2014). The V/Q ratio has been gauged with the use of the pulmonary V/Q scan examination.

The test entails two scans: the first measures efficiency of airflow through patient lungs while the other reveals where blood flows within the lungs. It involves injecting the patient with radioactive material which accumulates in parts where there is abnormal blood or air flow. This is subsequently evident within images generated by a special scanner (Healthline Media, 2019).

COPD and Difficulty in Breathing Chronic airway inflammation largely manifested through more goblet cells, mucus fibrosis, gland hyperplasia, airway breakdown on account of alveolar wall damage-caused tethering loss in emphysema and constriction and reduced small airway number plays a pivotal part in COPD pathophysiology. Pulmonary emphysema has been related to enhanced proteolytic enzyme activity (MMP-2, MMP-9, MMP-12, neutrophil elastase, and cathepsin K, L and S) activated because of oxidative stress and inflammation that occur in COPD.

Further, hyper-secretion of mucus linked to increased exacerbation frequency potentially radiates inflammatory lesions around submucosal glands as well as more acute inflammation in a majority of peripheral airways (Angelis er al, 2014). Patients might hear a musical or whistling sound (commonly known as wheezing) whilst exhaling, as air is coerced through smaller or blocked air passages within the lungs. Among COPD patients, it mostly occurs due to airway obstruction by excess mucus. This is accompanied by muscle tightening which aggravates the issue of airway narrowing.

Additionally, wheezing might be a sign of pneumonia or asthma. Some COPD patients might exhibit a condition which encompasses asthma as well as COPD symptoms, labeled ACOS (i.e., Asthma-COPD Overlap Syndrome). Roughly 15-45% of COPD- or asthma- diagnosed adult patients suffer from ACOS (Healthline Media, 2019). COPD and Fick’s Law of Diffusion Gaseous diffusion takes place during net molecular movement from a space where the specific gas exerts higher partial pressure into one where a smaller partial pressure is exerted.

Thus, gas movement via diffusion differs from its movement across conducting airways that takes place through convection or mass movement. In bulk flow, gases move due to total pressure differences, and multiple gases’ molecules move simultaneously along the overall pressure gradient. In the course of diffusion, individual gases move based on their distinct partial pressure (pp) gradients. Transfer of gases in diffusion takes place through random motion of molecules and, hence, depends on temperature as molecular motion increases with increase in temperature.

A gas moves both ways in the course of diffusion; however, the place with greater partial pressure experiences a proportionately larger number of random “departures” owing to a greater molecular concentration per unit volume. Therefore, net gas movement depends on the difference in partial pressure between both spaces.

Under static conditions, diffusion will continue up to the time that there is no difference in partial pressure for any of the gases within both areas; carbon dioxide and oxygen within the lungs constantly enter and exit the alveoli; consequently, no such equilibrium occurs. Oxygen enters the alveoli through bulk flow across conducting airways. During flow of air across conducting airways in the process of inspiration, the bulk flow’s linear velocity reduces upon approaching the alveoli owing to drastic increase in overall area of cross section.

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