pathophysiology for the respiratory alkalosis

The pathophysiology of respiratory alkalosis is the situation in which the acid/base balance is disrupted as a result of alveolar hypertension, resulting in a lower partial pressure arterial carbon dioxide (pCO2). The drop in pCO2 causes a rise in the bicarbonate concentration to pCO2 ratio, which raises the pH level (Kamath, 2017). The decrease in pCO2 (hypocapnia) is generated by a condition in which a strong respiratory stimulus motivates the respiratory system to expel more carbon dioxide than is created in the tissues as a result of the metabolism process (Gennari, 2012). The pathophysiology of the respiratory acidosis is the condition that causes the disturbance in the acid/base balance as a result of alveolar hypertension, which results to the reduced partial pressure arterial carbon dioxide (pCO2). The decreased pCO2 will lead to the increase the bicarbonate concentration to pCO2 ratio, and hence increasing the level of the pH (Kamath, 2017). The reduction in the pCO2 (hypocapnia) is caused by the situation whereby a strong respiratory stimulus cause stimulates the respiratory system to eliminate more carbon dioxide than what is being produced in the tissues following the metabolism process (Gennari, 2012).

The pathophysiology of the respiratory acidosis is the condition that causes the disturbance in the acid/base balance as a result of the alveolar hypoventilation (Donnelly, 2014). The carbon dioxide production process takes place rapidly, and the ventilation failure punctually leads to the increase in the partial pressure of the arterial carbon dioxide (pCO2) whose normal level range is 35-45mmHg (Gennari, 2012). The increase in the pCO2 leads to the decrease in the bicarbonate (HCO3-) to partial pressure of the arterial carbon dioxide (pCO2) ratio, which subsequently leads to the decrease in the pH.

The metabolic alkalosis is the main cause of the bicarbonate levels (HCO-3) in the serum. It takes place in the situation whereby there is a loss of the H+ from the body or gain in the HCO3-. It subsequently leads to the alveolar hypoventilation which is as a result of the rise in the arterial carbon dioxide tension (Kamath, 2017). It can be diagnosed by measuring the serum electrolytes and arterial blood gases.

The metabolic acidosis involves the clinical disturbance of the acid/base balance which leads to an increase in the plasma acidity. The metabolic acidosis consequently occurs in a situation whereby there is an increase in the nonvolatile acid production or loss of the bicarbonate acids from the body which overpowers the mechanism of acid/base homeostasis or in the situation whereby the mechanisms of the acidification are compromised (Donnelly, 2014).

Question 1B

The Chronic Obstructive Pulmonary Disease (COPD) causes the respiratory acidosis and is depicted by the following partially compensated arterial blood gas: pH above 7.45, pCO2 above 45mmHg and HCO3- 20 mEq/L (Gennari, 2012). In the respiratory acidosis, compensation occurs via the intercellular buffering system by increasing the plasma bicarbonate.

The propanidid condition causes the respiratory alkalosis and is depicted by the following partially compensated arterial blood gas: pH above 7.45, pCO2 below 35mmHg, HCO3- 30 mEq/L. In the respiratory alkalosis, compensation occurs via the cellular buffering system by decreasing the concentration of the serum bicarbonate (Kamath, 2017).

The kidney diseases such as the distal renal tubular acidosis and proximal renal tubular acidosis cause the metabolic acidosis and are depicted by the following partially compensated arterial blood gas: pH above 7.45, pCO2 less than 35 mmHg, HCO3- below 22 mEq/L (Kamath, 2017). In the metabolic acidosis, compensation occurs via the hyperventilation system by increasing the partial pressure of the arterial carbon dioxide (pCO2).

The conditions such as high levels of the bicarbonate in the blood and various types of kidney diseases cause metabolic alkalosis and is depicted by the following partially compensated arterial blood gas: pH less than 7.35, pCO2 less than 35 mmHg, HCO3- below 22 mEq/L. In the metabolic alkalosis, compensation occurs via the renal compensation system which leads to the decrease in the HCO3- reabsorption.

Question 1C

The level of the electrolyte is increased in acidosis and on the other hand, the level of the electrolyte is decreased in alkalosis (Kamath, 2017).

Question 1D

The electrolyte is increased in acidosis because there is rapid production of the carbon dioxide, hence increasing the pCO2 levels that leads to the decrease in the bicarbonate (HCO3-) to partial pressure of the arterial carbon dioxide (pCO2) ratio that eventually decreases the pH (Kamath, 2017). The electrolyte is decreased in alkalosis because there is the occurrence of the alveolar hypertension which leads to reduced pCO2 that will enhance the increase in the bicarbonate concentration to pCO2 ratio, and hence increasing the level of the pH (Donnelly, 2014).

Question 2A

The functionality of the liver plays an important role in the determination of the specific disease that may arise, as a result of the failure of the liver to perform a specific function. One of the major functions of the liver involves the synthesis of bile. The failure of the liver to synthesize bile juice pose a lot of danger to the individual (Fernández-Solà, 2013). The failure of the liver to synthesize bile would prevent the digestion and emulsification of the fats in the diet, hence consequently increasing the cholesterol levels, hypercholesterolemia.

The second function of the liver is to act as storage site. If the liver fails to perform the role of storage, it would lead to production of dark urine and whiter stools, which are symptoms of jaundice (Parke, Martin & Bunnapradist, 2015). The third function of the liver is to metabolize the carbohydrates (CHO). This is a very vital food component which is required for the proper functionality of the human body system. Therefore failure of its metabolism would lead to inadequate energy supply in the body and consequently liver cirrhosis. Its break down is important from the production of glucose which is used in for the energy generation during metabolism. This would therefore lead to cellular fatigue, and sometimes heartburns and ulcers (Terziroli et al., 2017).

Question 2B

The pathophysiology of jaundice can be based on the fact that the bilirubin is produced during the process of the breakdown of the hemoglobin in the red blood cells into the unconjugated bilirubin which binds to the albumin which is present in the blood, hence transported to the liver. At this point, it will be taken up through the hepatocytes and conjugated with the glucuronic acid in order to enable it dissolve in water (Parke, Martin & Bunnapradist, 2015). This conjugated bilirubin is thereby excreted in the bile into the duodenum, after that, its metabolism takes place in the intestines to produce urobilinogen that can be eliminated via feces or reabsorbed into the bloodstream.

The pathophysiology of the liver cirrhosis takes place when the growth regulators encourage hepatocellular hyperplasia and the arterial growth. Some of the common growth regulators in this case involve the cytokines and the hepatic growth factors (Terziroli et al., 2017).

The whole process involves two major fundamental processes; hepatic fibrosis and the regeneration of the liver cells. The third pathophysiology involves that of the hypercholesterolemia which is a consequence of abnormal metabolism of fats and lipoproteins (Fernández-Solà, 2013). There are various methods which can be used by the oxidized LDL to reduce the effects of the hypercholesterolemia; induction of the growth factors such as the cytokines, recruitment of the macrophages and monocytes and damage to the endothelium.

Question 2C

The dysfunction of the liver can lead to various abnormal lab values. The first dysfunction of the liver, which is the digestive problem that is caused by the failure to synthesize bile, results in abnormal serum lab value of 25 mg/dL (Fernández-Solà, 2013). The hypercholesterolemia which is as a result of the liver dysfunction results in an abnormal serum lab value of 159 mg/dL. The third liver dysfunction, failure to metabolize carbohydrates and blood sugar problems, result to an abnormal serum lab value of 89 mg/dL of the blood sugar (Parke, Martin & Bunnapradist, 2015).

References

Donnelly M, B. (2014). Metabolic Acidosis with a Raised Anion Gap Associated with High 5-Oxoproline Levels; an Under-Recognized Cause for Metabolic Acidosis in Intensive Care. Journal of Clinical Toxicology, 04(06).

Fernández-Solà, J. (2013). Management of extrahepatic manifestations in alcoholic liver disease. Clinical Liver Disease, 2(2), 89-91.

Gennari, F. (2012). In Reply to ‘Potassium and Metabolic Alkalosis’ and ‘Metabolic Alkalosis due to Hypercalcemia’. American Journal of Kidney Diseases, 59(2), 315-316. http://dx.doi.org/10.1053/j.ajkd.2011.11.029

Kamath, P. (2017). Acute on chronic liver failure. Clinical Liver Disease, 9(4), 86-88.

Parke, C., Martin, P., & Bunnapradist, S. (2015). Renal dysfunction in cirrhosis. Clinical Liver Disease, 5(6), 150-153.

Terziroli Beretta-Piccoli, B., Invernizzi, P., Gershwin, M., & Mainetti, C. (2017). Skin Manifestations Associated with Autoimmune Liver Diseases: a Systematic Review. Clinical Reviews in Allergy & Immunology.