What are the pathophysiological findings specifying bronchitis

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Discussion #1

1. What physical findings might be indicative of a patient with emphysema?  The diagnosis is made on patients that usually are long term smokers, and they complaint of dyspnea, cough, and mucus expectoration. Most patients seek medical attention late in the course of their disease, usually ignoring smoldering symptoms that start gradually and progress over the course of years. The cough typically is worse in the morning with finite production of clear-to-white sputum. Dyspnea, emphysema’s most significant symptom, does not generally occur until the sixth decade of life. However, patients with emphysema due to alpha 1 -antitrypsin deficit will exhibit the following characteristics: early presentation (< 45 y), predilection of emphysematous changes in the lung bases, and the panacinar morphological pattern.

Although the sensitivity of the physical evaluation in mild-to-moderate disease is relatively poor, the physical signs are quite sensitive and specific in severe disease. Patients with severe disease may experience tachypnea and dyspnea with mild exertion.

The respiratory rate increases in proportion to disease severity with the use of accessory respiratory muscles and paradoxical contraction of lower intercostal spaces becoming evident during exacerbations.

In end-stage emphysema, cyanosis, elevated jugular venous pressure, atrophy of limb musculature, and peripheral edema due to the development of pulmonary hypertension, right-to-left shunting, and/or right heart failure can easily be observed.

Thoracic examination reveals a 2:1 increase in anterior to posterior diameter (“barrel chest”), diffuse or focal wheezing, diffusely diminished breath sounds, hyperresonance upon percussion, prolonged expiration, and/or hyperinflation on chest radiographs.

2. What is the purpose and interpretations of the pulmonary function test? Pulmonary function tests will test the mechanical function of the lungs, chest wall, and respiratory muscles by measuring the total volume of air exhaled from a full lung (total lung capacity [TLC]) to maximal expiration (residual volume [RV]). This volume, the forced vital capacity (FVC) and the forced expiratory volume in the first second of the forceful exhalation (FEV1), In Emphysema, spirometry may show typical obstructive pattern due to the blockage of the air during expiration. As a result of the air trapping, the spirometry will show decreased in FVC, but less than the FEV 1, and increased FRC and RV.(McCance, & Huether, 2013).

3. What are the pathophysiological findings specifying emphysema? As a result of the cellular apoptosis, and early cellular senescence, the alveolar cells are damaged, and a reduced surface of gas exchanged occurred. The destruction of the alveoli creates bullae, which are large spaces in the lung parenchyma and air spaces adjacent to pleurae(blebs). Both elements bullae, and blebs difficult the air exchange. In addition, areas of the lungs that are bad perfused contributes to worse the hypoxemia during the expiration, which is a passive process. As a result, the air remains trapped in the lungs. (McCance, & Huether, 2013).

4. What are the three functions of the respiratory center located in the brain stem? The respiratory center is in the brainstem, and it controls respiration. Four groups of neurons with specific functions are forming the center; for example, the Dorsal part(DRG) sent impulses to diaphragm and external intercostal muscles to start the inspiration; in addition, they received impulses from the chemoreceptors located on the carotid and aortic centers which are activated in front of variations of the PaCO2, and PaO2.The DRG is inhibited by the pneumotaxic center Located in the medulla, the ventral part(VRG) of the respiratory center contains inspiratory and expiratory neurons, and it is activated when increased ventilatory effort is required. The apneustic center and the pneumostatic centers are structures located in the pons and they modify the depth and rate set by the medullar level. The apneustic center shortens the expiration, prevents inspiratory neurons to switched off, in other words it provokes a long inspiration.The pneumotaxis area shortens the breath, by promoting exhalation and inhibiting inhalation.

5. Please provide a description of  the oxy-hemoglobin dissociation curve. The curve of dissociation of the oxy-hemoglobin  represents the relationship between the oxygen saturation of hemoglobin (Sao2) in the Y axis, and the partial pressure of arterial oxygen (Pao2) in the X axis. Normal Pao2 ranges from 80 to 100 mm Hg. Normal Sao2 measures about 97% but may range from 93% to 97%. The relation id not linear, but an S-shape curve. The most horizontal part of the curve represent that the lungs has been oxygenated at the maximum level , and they achieved high level of PO2 .Dramatic changes in the PO2 in the flat part of the curve will make small changes into the SO2 ; then , the oxygenation status of the patient is better protected at this point .Some conditions can alter the affinity of the Hemoglobin for the oxygen , such as the concentration of Hydrogen-anions (pH), the body temperature, the concentration of DPG or PCO2. A shift the right decreases the affinity of the oxygen for the hemoglobin and leads for an easier relief of the oxygen to the tissues; it happens when temperature rises, in acidosis (low pH), and elevated levels of DPG. In the other hand, alkalosis(high  pH), low temperature and low levels of DPG leads to a shift to the left of the curve ; as a result , the oxygen-Hemoglobin affinity increases, and  less oxygen is released to the tissues but more oxygen is bound to hemoglobin in the lungs; the SaO2 value is higher than normal for a given PaO2 value.((McCance & Huether, 2014)

6. What are the pathophysiological findings specifying bronchitis? Pathophysiological findings in Bronchitis include airways inflammation, with neutrophil and macrophage infiltration, and lymphocyte in the wall of the bronchi, bronchial edema, hyperplasia of the mucus gland and globet cells, thick mucus production, and impaired ciliary activity. Those changes predisposed the patient to have respiratory infections.