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Post Lab Worksheet Question And Answer

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Introduction: Post Lab Worksheet Question And Answer

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Arterial Blood gas (ABG) sampling, is a test often performed in an inpatient setting to assess the acid base status of a patient.

The following are the most important normal values on an ABG:

pH = 7.35 to 7.45

pCO2 = 35 to 45 mmHg

pO2 = 75 to 100 mmHg

HCO3- =22 to 26 mEq/L

Patient A is showing signs of respiratory failure due to prolonged chronic obstructive pulmonary disease.

ABG results were as follows:

pH= 7.3

pCO= 55mmHg

pO2= 60mmHg

A.Review blood gases and pH. What acid- base abnormality would you expect from this information? How did you decide that? 

Chronic obstructive pulmonary disease (COPD) is a leading disease that is highly prevalent. In this condition, the kidney is unable to reabsorb bicarbonate which leads to cause low pH. This condition even increases PCO2, which indicates progression in airflow limitation.

Acid-base normality in COPD leads to respiratory acidosis, thereby disturbing the acid-base balance. Chronic COPD results in the shifting of carbon dioxide from the normal acid-base towards acidic (O’Donnell et al. 2019). Linking with the case scenario, patient A suffers from respiratory failure which is indicated by ABG results. Therefore, acid-base normality in COPD condition has been imbalanced as pCO values are higher 55mmHg than the normal range. It signifies the occurrence of respiratory failure due to COPD condition.

What is the compensatory mechanism and how is this brought about?

Tip: What is the control center and effectors for this acid-base balance and what is the relationship between pCO2 and pH? 

COPD conditions are abnormal conditions of inflammation in the lungs and reversible airflow construction. The compensatory mechanism in respiratory acidosis results in the secondary enchantment of concentration of bicarbonate which is usually characterized by ABG by increasing increased pCO2, lowering pH and increasing compensatory response (bicarbonate levels). Disease in pH response needs the central chemoreceptor to be stimulated with the respiratory centre. This occurs due to an increase in the inspiration rate (Benditt, 2018). The control centre and effectors for acid-base balance can modify ventilation which leads to developing variables for homeostasis to maintain the inner stable environment for breathing. Hence control center and effectors in compensatory mechanism result in changing the blood gas and pH condition. The relationship between pCO2 and pH in physiologic condition, lowering pH leads to enhance PCO2, which prominently involve increasing minute ventilation. In this aspect, the higher resulted ventilation brings more exchanges of gases and PCO2 loss inversely. As per the case scenario, patient A develops a respiratory failure due to prolong COPD, this result in increasing the pCO and decreasing pH. Therefore compensatory mechanisms prove to increase the bicarbonate in the lung resulting in respiratory acidosis.

How can the kidneys contribute to acid base? 100 WORDS

COPD has been evident in lowering the function of the kidney, this result in the occurrence of severe emphysema and has less effect on airflow limitations. Kidney involvement in acid-base has been profoundly tested in lowering the glomerular filtration rate due to COPD conditions (Halpin et al. 2021). The kidney has been notably involved in reabsorbing bicarbonate that is filtered by glomeruli. It is eventually involved in excreting ammonia and titratable acids into urine. As per the case scenario, the patient has an Arterial Blood gas report depicting a reduction in pO2 and increasing the pCO2. It represents the effective contribution of kidneys plays an acid-base balance regulation within the body. Henceforth, acid-base balance regulations with the body is eventually regulated by kidney, therefore, its role in changing in bicarbonate leads to respiratory acidosis.

Describe the enzymes activity involved in chemical digestion; name the substrate (biomolecule) on which they act and the end-products of digestion, where are they secreted from and where do they act? (Any Words)

ENZYME

SUBSTRATE

PRODUCT

SECRETED BY

ACTIVE IN

Lactase

Lactose

Galactose and glucose

intestinal epithelial cells

Gut

Pepsin

Intact protein

Peptones and proteoses

Gastric chief cells

 Stomach

Carboxypeptidase

Protein and peptide substrate

 Peptide bond 

 pancreatic acinar cells

Intestines

Pancreatic Amylase

Starch 

Maltotriose and maltose 

 pancreas

Duodenum

Pancreatic Lipase

Lipid (triglycerides)

Glycerol and fatty acids

pancreas

 Stomach

Reference list

Benditt, J. O. (2018). Pathophysiology of neuromuscular respiratory diseases. Clinics in chest medicine39(2), 297-308. https://www.chestmed.theclinics.com/article/S0272-5231(18)30011-X/abstract

Gadre, S. K., Duggal, A., Mireles-Cabodevila, E., Krishnan, S., Wang, X. F., Zell, K., & Guzman, J. (2018). Acute respiratory failure requiring mechanical ventilation in severe chronic obstructive pulmonary disease (COPD). Medicine97(17). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944543/

Halpin, D. M., Criner, G. J., Papi, A., Singh, D., Anzueto, A., Martinez, F. J., ... & Vogelmeier, C. F. (2021). Global initiative for the diagnosis, management, and prevention of chronic obstructive lung disease. The 2020 GOLD science committee report on COVID-19 and chronic obstructive pulmonary disease. American journal of respiratory and critical care medicine203(1), 24-36. https://www.atsjournals.org/doi/pdf/10.1164/rccm.202009-3533SO

O’Donnell, D. E., James, M. D., Milne, K. M., & Neder, J. A. (2019). The pathophysiology of dyspnea and exercise intolerance in chronic obstructive pulmonary disease. Clinics in chest medicine40(2), 343-366. https://www.chestmed.theclinics.com/article/S0272-5231(19)30007-3/abstract

Staub, L. J., Biscaro, R. R. M., Kaszubowski, E., & Maurici, R. (2019). Lung ultrasound for the emergency diagnosis of pneumonia, acute heart failure, and exacerbations of chronic obstructive pulmonary disease/asthma in adults: a systematic review and meta-analysis. The Journal of emergency medicine56(1), 53-69. https://www.sciencedirect.com/science/article/pii/S0736467918309259

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