Overview of Respiratory Physiology: Functions Gases and Respiratory System Anatomy

Respiratory System in Health & Disease

The current lecture focused to allow gaining an overview regarding respiratory physiology and involved gases along with their function in the body. For example, respiration occurs in two ways which are cellular respiration also known as internal respiration and pulmonary respiration also known as external respiration. The exchange between oxygen and carbon dioxide occurs leading support respiration. The lecture also introduced the air composition present in the inspired and expired air through respiration and gas laws along with atmospheric partial pressure related to support enhanced respiration. It was also learned from the lecture regarding the way air is conducted into the lungs for supporting enhanced respiration. For example, air from outside enters through the upper airways mainly nasal passage that follows down the pharynx to the trachea and enters the bronchus of the lungs to be delivered to the bronchioles and alveoli so that the oxygen from the air is transferred to the blood and the carbon dioxide is released to be expired out. The lecture presented a detailed overview regarding the anatomy of the respiratory system by explaining the way airways are conducted, the role of each organ of the respiratory system, bone and muscle involvement in respiratory process and others. The lecture helped in determining different types of respiratory disorder and the diseases related to each type.

The lecture was informative in the sense that it helped me to understand different types of respiratory disorder and their level which was previously not known to me. Moreover, it assisted in understanding and developing clarified interpretation of the way each part of the lungs and associated organs of respiratory system works. This is going to help in determining the reason of different symptoms found during respiratory failure and would assist to identify which parts of the respiratory system required to be reviewed to diagnose the problem.

Question: Discuss the key pathophysiological mechanism for respiratory failure

There are various pathophysiological mechanism involved in supporting respiratory failure in individuals out of which hypoventilation mechanism in one of the causes that leads to failure in enhanced respiration. In hypoventilation, the arterial carbon dioxide remains highly elevated (Paco2) and the serum bicarbonate levels are also elevated with an associated reduction in the tension of arterial oxygen (Pao2). The reduced entry of air in the alveoli in the lungs causes the oxygen level to be decreased and carbon dioxide in the blood to be increased (Adler and Janssens, 2019). Hypoxemia is another pathophysiological mechanism that results in respiratory failure. In this process, the oxygen saturation in the blood is decreased to abnormal levels leading the body incapable to absorb required oxygen in the blood (Sasannejad et al., 2019).

In physiology of respiration, the ventilation/ perfusion ratio (V/Q) is implemented for assessing the adequacy and efficiency of the air which is reaching the alveoli (V) and the amount of blood which is reaching the alveoli through capillaries (Q). The V/Q ratio helps in determining the key constituent of blood oxygen and concentration of carbon dioxide in the blood (Spinelli et al., 2020). The disruption in the V/Q ratio leads to hypoxemia formation resulting in respiratory failure as seen in respiratory diseases. The pathological condition where the alveoli in the lungs remains perfused and not ventilated leads to Shunt development. In this condition, there is persistent presence of hypoxemia in spite of the presence of oxygen in 100%. During shunt, the deoxygenated blood seen to pass the alveoli with accepting oxygen and interferes to mix with the oxygenated blood which are flowing through the ventilated alveoli leading to hypoxia which is seen in pulmonary edema (Spinelli et al., 2020).

Article 1: Mogassabi, W., Hassen, S.S., Mahadik, S.A., Mubarak, R.S. and Ibrahim, W.H., 2019. Acute and long-term effects of water pipe smoking on the respiratory system: A narrative review. Ibnosina Journal of Medicine and Biomedical Sciences, 11(4), p.142.

The study is chosen because it focused on determining the acute as well as long-term impact caused by water pipe smoking on the respiratory system. This is important because tobacco is inherently related with hindered functioning of the respiratory system and leads towards its failure and the support understanding to what extent it affects the respiratory health. The study is important because it informed eosinophilic pneumonia along with development of acute carbon monoxide poisoning, enhanced respiratory rate, easy transfer of respiratory infection and acute lung deterioration in seen as side-effects of pipe smoking which results in hindered respiration in people which was not previously known by me.

Article 2: Bai, J.W., Chen, X.X., Liu, S., Yu, L. and Xu, J.F., 2017. Smoking cessation affects the natural history of COPD. International journal of chronic obstructive pulmonary disease, 12, p.3323.

The presence of chronic obstructive pulmonary disorder (COPD) is one of the common respiratory disease faced by individuals which is mainly developed due to increased smoking habit. Thus, this study is chosen because it focus was to determine impact of smoking cessation on the natural history of COPD among individuals. For this purpose, 204 patients are involved. It was led to revealed that increased death due to respiratory failure in COPD was seen among people who are involved in increased smoking time, have lower prevalence of cessation of smoking, late onset of COPD, expressed lower ratio of FEV1/forced vital capacity and expressed lower forced expiratory volume. This results helped me to understand that smoking time may be involved in mortality among COPD patients which would help me to inform people regarding the importance of reducing smoking time.

Article 3: Nasser, M. and Cottin, V., 2018. The respiratory system in autoimmune vascular diseases. Respiration, 96(1), pp.12-2

The study is important because it focused to determine the autoimmune vascular disease impact on the respiratory system which was not known to me. It is revealed that ANCA-associated vasculitis which also includes eosinophilic granulomatosis, granulomatosis and microscopic polyangiitis are seen to negatively affect the respiratory system. The granulomatosis is seen to be related to upper or lower respiratory tract. In 10% of cases of vascular disease, the lung is the one affected respiratory organ. Hypereosinophila and asthma are always raised due to eosinophilic granulomatosis with polyangiitis. The paper is important because it informs the role played by vascular disease in influencing respiratory failure that is usually seen in people.

References

Adler, D. and Janssens, J.P., 2019. The pathophysiology of respiratory failure: control of breathing, respiratory load, and muscle capacity. Respiration, 97(2), pp.93-104.

Sasannejad, C., Ely, E.W. and Lahiri, S., 2019. Long-term cognitive impairment after acute respiratory distress syndrome: a review of clinical impact and pathophysiological mechanisms. Critical care, 23(1), pp.1-12.

Spinelli, E., Mauri, T., Beitler, J.R., Pesenti, A. and Brodie, D., 2020. Respiratory drive in the acute respiratory distress syndrome: pathophysiology, monitoring, and therapeutic interventions. Intensive care medicine, 46(4), pp.606-618.

Mogassabi, W., Hassen, S.S., Mahadik, S.A., Mubarak, R.S. and Ibrahim, W.H., 2019. Acute and long-term effects of water pipe smoking on the respiratory system: A narrative review. Ibnosina Journal of Medicine and Biomedical Sciences, 11(4), p.142

Bai, J.W., Chen, X.X., Liu, S., Yu, L. and Xu, J.F., 2017. Smoking cessation affects the natural history of COPD. International journal of chronic obstructive pulmonary disease, 12, p.3323.

Nasser, M. and Cottin, V., 2018. The respiratory system in autoimmune vascular diseases. Respiration, 96(1), pp.12-28.

Gastrointestinal System in Health & Diseas

The lecture topic in contrast to other provides overview regarding the function and anatomical features present in gastro-intestinal system. For example, gastrointestinal system mentions supporting ingestion, mechanical processing of food, propulsion, biochemical digestion, absorption, secretion and elimination. The lecture introduced the different layers present in the gastrointestinal tract and what they are made of along with their role and functioning. For example, the initial layer of the gastrointestinal tract is known as mucosa which is made up of layer of epithelium, mucosa-associated lymphatic tissue (MALT) and smooth muscles. The MALT supports protection from body pathogens and the smooth muscles in the tract develop folds to increase the surface area for movement of food and other particles. The lecture also informed about the parasympathetic action control by it. For example, the gastrointestinal tract support swallowing reflex and parasympathetic control of saliva. The anatomy of gastrointestinal tract is explained in detail within the lecture by mentioning the organs related with the tract and way they perform their functioning to support the overall role of the gastrointestinal system in the body. For example, the stomach present in the middle of the gastrointestinal tract at the end of the oesophagus acts in supporting churning of food particles to develop chyme from which nutrients are to be later absorbed in the small intestine. The lecture provided overview regarding different fluid present in the gastrointestinal tract and related diseases to be faced due to hindered functioning in different parts of the tract.

The lecture provided enhanced overview regarding different parts of the gastrointestinal tract and system. The additional information accessed from the lecture which was not previously present in me is the overview of the probable diseases and disorder faced in the gastrointestinal tract and in which parts, their clinical representation and brief pathophysiology.

Question: Discussing pathophysiology of Gastroesophageal reflex (GERD)

The presence of some amount of acid reflux is considered normal physiologic GER and the refluxed acid is cleared through peristaltic action of the oesophagus. During the normal function of the lower oesophagal sphincter, the anti-reflux barrier is controlled that protects the oesophagus from facing the acid gastric content. In GERD, the lower oesophagal sphincter is seen to function improperly and disrupts the anti-reflux barrier leading to reach of gastric acid in the abdomen (Tack and Pandolfino, 2018). The protective pathological mechanism for GERD includes the presence of upright posture so that the gravity allows the augmented gastric acid to be emptied from the abdomen, enhanced peristaltic which support acid clearance from the esophagus and presence of saliva in neutral pH that would be near to 6.0 (Tack and Pandolfino, 2018). Different factors contributes for the development of GERD which includes hiatal hernia, LES dysfunction, enhanced transient relaxation of lower esophageal sphincter, ineffective clearance of esophagus, delayed emptying of gastric juice and presence of acid pocket (Menezes and Herbella, 2017). The transient lower oesophagal sphincter (TLESR) is located at the oesophagus distal end which only opens during swallowing. The TLESR opening and closing is supported by nerve-mediated reflexes and is considered in playing effective part in development of GERD in people (Tack and Pandolfino, 2018). The acid pocket may form in the gastrointestinal tract due to poor mixing of the meal with the gastric acid in the stomach for formation of chyme. It usually occurs after the meal due to esophageal refluxate leading to development of GERD (Menezes and Herbella, 2017). The risk factors which leads to acid reflux and development of GERD includes heavy lifting, specific food, exercise, high-fat diet, food that lower the pressure at LES and others (Menezes and Herbella, 2017).

Article 1: Khan, I., Ullah, N., Zha, L., Bai, Y., Khan, A., Zhao, T., Che, T. and Zhang, C., 2019. Alteration of gut microbiota in inflammatory bowel disease (IBD): cause or consequence? IBD treatment targeting the gut microbiome. Pathogens, 8(3), p.126.

The study mentioned that perturbation of gut microbia in patients led to development of IBD but the detailed cause-effect relationship is unable to be understood in the process. The gut bacteria such as Clostridium leptum, Faecalibacterium prausnitzi, Bacteroides spp and others are mentioned to be involved in causing IBD. The treatment available for IBD are use of complementary and alternative medicine (CAM), traditional Chinese herbal medicine and herbal medicine as prebiotics. Thus, the study is important as it helped me to understand what the causes and possible treatment are to be availed for IBD.

Article 2: Fletcher, J., Cooper, S.C., Ghosh, S. and Hewison, M., 2019. The role of vitamin D in inflammatory bowel disease: mechanism to management. Nutrients, 11(5), p.1019.

The study is important because it helped me understand to identify mechanism of impact of vitamin D in treating inflammatory bowel disease (IBD). This is evident as the study explained that vitamin D helps in maintenance of enhanced gastrointestinal barrier integrity along with manages to lower inflammatory responses and surveillance of the gut microbiota. The possible mechanism includes interfacing with the microbiota in the intestine by recognizing intercellular or defensins pathogen recognition protein that contains nucleotide-binding oligomerisation domain followed by T cell homing in the inflammation sites and suppressing inflammatory response from the Th17 and Th1.

Article 3: Guan, Q., 2019. A comprehensive review and update on the pathogenesis of inflammatory bowel disease. Journal of immunology research, 2019. pp.89-100.

The study is important and interesting to me as it helped me to determine the pathophysiology involved in expression of inflammatory bowel disorder (IBD). The is evident as it mentioned Nucleotide-binding oligomerization domain 2 (NOD2) is identified as one of the genetic loci apart from other 29 genetic loci to be genetically responsible in the expression of IBD. The IL23R variants are other genetic factors responsible for expression of the disease. The environmental factors are seen to play key pathophysiological role in development of IBD such as hindered food intake, smoking, psychological stress, appendectomy, impact of certain medication and others.

References

Khan, I., Ullah, N., Zha, L., Bai, Y., Khan, A., Zhao, T., Che, T. and Zhang, C., 2019. Alteration of gut microbiota in inflammatory bowel disease (IBD): cause or consequence? IBD treatment targeting the gut microbiome. Pathogens, 8(3), p.126.

Fletcher, J., Cooper, S.C., Ghosh, S. and Hewison, M., 2019. The role of vitamin D in inflammatory bowel disease: mechanism to management. Nutrients, 11(5), p.1019.

Guan, Q., 2019. A comprehensive review and update on the pathogenesis of inflammatory bowel disease. Journal of immunology research, 2019. pp.89-100.

Tack, J. and Pandolfino, J.E., 2018. Pathophysiology of gastroesophageal reflux disease. Gastroenterology, 154(2), pp.277-288.

Menezes, M.A. and Herbella, F.A., 2017. Pathophysiology of gastroesophageal reflux disease. World journal of surgery, 41(7), pp.1666-1671.

Renal System in Health & Disease

The current lecture provided overview regarding normal renal functioning, parts and structure involved in the process along with pathophysiology of different renal disorder. For example, the lecture mentioned renal system mainly function by excreting different organic wastes such as NH3, bilirubin, drugs and others through urine. It mentioned that renal system function to conserve valuable nutrients like amino acids and glucose and release of them in the urine is considered abnormal. The lecture provided detailed overview regarding the way renal system is inter-related to support different functioning of the body. For example, renal system function to adjust amount of water absorption and re-absorption to maintain enhanced blood volume to blood pressure. The renal disorder discussed in the lecture includes acute and chronic kidney failure, vascular disease of the kidney, glomerular disease, interstitial disease and others. The lecture mentioned the parts mainly affected in renal disorder and how they are affected which leads to development of various diseases. For example, renal blood vessels are damaged due to development of cardiovascular diseases like hypertension and atherosclerosis. The presence of heart ischemia along with toxins and metabolic disorder in the body affects the hindered functioning of the kidney tubules that leads to development of improper waste removal from the body and raises tubular disease.

The lecture is overall a comprehensive overview and acted in line to educate and approve enhanced learned regarding basic condition, functioning and diseases in relation to renal system in the undergraduate degree from the present modules. It has assisted to understand and develop comprehensive view about the need for renal system and way they are inter-related with other parts of the body and their functioning in leading to express diseases.

Key Question: Discussing the pathophysiology of chronic kidney failure

The kidney is the key part of the renal system which supports in removal of waste and extra fluid in the body that otherwise would lead to development of infection and hindered body functioning. The pathophysiology of chronic renal failure occurs in mainly four stages and the first stage includes supporting reduction in excretory function. The breakdown in the excretory system occurs during confrontation of glomeruli by surplus of waste products leading to development of osmotic diuresis which causes reduction in the increased concentration capacity of the kidney. The lower excretory functioning causes accumulation of extraneous and endogenous substances that leads to alteration in the pharmacokinetics and increase concentration of different medication (Porter et al., 2017). The second stage that follows worsening of chronic renal functioning is reduction in the excretory renal function. In this stage, the shortage of erythropoietin caused by gradual failure of the kidney function leads to reduced endocrinal synthesis that causes anemia leading to reduced erythrocyte functioning (Provenzano et al., 2020). The phosphate secretion is lowered, and vitamin D development is reduced (Provenzano et al., 2020).

The third stage of chronic renal failure is developed with drastic reduction in glomerular filtrate leading to the ability of diuresis and fractional sodium secretion for enhanced body functioning to be hindered. The overhydration and hindered electrolyte balance caused by glomerular filtrate reduction lead to development of hypertension, peripheral edema and pulmonary edema. This indicates that the secretion of salt and water is intricately linked and diuretics aids in secretion of water and salt secretion (Nixon et al., 2018). In this stage, hyperkalemia and acidosis may also rise indicating hindered functioning of the renal system (Porter et al., 2017). The fourth stage is toxic renal damage which is explained as “uremic syndrome”. In this stage, the urinary excreted metabolites are present highly in the blood known as azotemia and they lead to visual clinical representation of renal failure on the skin. This is evident as the condition causes pale and dirty complexion on the skin (Provenzano et al., 2020).

Article 1: Jourde-Chiche, N., Fakhouri, F., Dou, L., Bellien, J., Burtey, S., Frimat, M., Jarrot, P.A., Kaplanski, G., Le Quintrec, M., Pernin, V. and Rigothier, C., 2019. Endothelium structure and function in kidney health and disease. Nature Reviews Nephrology, 15(2), pp.87-108.

The study is important because focused to explain the structure and function of endothelium in kidney health and diseases which plays a major part in detecting the disease. According to the study, the endothelium of the small and large vessels in the kidney supports enhanced renal vasculature. These renal endothelia are seen to be protected by the regulators of complement, thrombosis and inflammation, however endothelial injury caused by inflammatory cytokines, immune cells and others or presence of defective factors on the protection of endothelial leads to acute or chronic renal failure. The transition of the endothelial cells towards the mesenchymal phenotype while favoring renal fibrosis development leads to support formation of chronic kidney disease.

Article 2: Moledina, D.G., Wilson, F.P., Pober, J.S., Perazella, M.A., Singh, N., Luciano, R.L., Obeid, W., Lin, H., Kuperman, M., Moeckel, G.W. and Kashgarian, M., 2019. Urine TNF-α and IL-9 for clinical diagnosis of acute interstitial nephritis. JCI insight, 4(10).pp.9-19.

The study is important as challenges are faced in making clinical diagnosis of acute interstitial nephritis (AIN) due to hindered presence of biomarker and need of kidney biopsy. In this context, exploring if detection of TNF-α and IL-9 presence in the urine can support enhanced diagnosis of AIN is breakthrough to develop diagnosis diagnosis of the disease. It was hypothesized that AIN is caused by presence of specific substrate of T cell like the T cell cytokine level which acts as biomarkers for distinguishing AIN from other causes of acute kidney disease. In this purpose, the study enrolled 218 participants and it was revealed that in all the participants with AIN, they expressed high level of TNF-α and IL-9 in urine compared to other who were diagnosed with other cause of acute renal failure.

Article 3: Jefferson, J.A., 2018. Complications of immunosuppression in glomerular disease. Clinical Journal of the American Society of Nephrology, 13(8), pp.1264-1275.

The study focused to mention the complication regarding use of immunosuppression raised due to glomerular disease. It is revealed that use of Cyclophosphamide results in increased risk of cancer, cytopenia and infection, fertility issues and hemorrhagic cystitis. The use of Rituximab leads to rise of hypogammaglobulinemia, late-onset of neutropenia and others. The rise of infectious complication and infusion reaction were mentioned to be common complication faced with use of immunosuppression in glomerular disease. The study is important to me because it helps me to understand the wide effects to be faced with use of immunosuppression in glomerular disease, in turn making me aware of probable actions to be strategized to provide enhanced care delivery to the patient.

References

Porter, C.J., Moppett, I.K., Juurlink, I., Nightingale, J., Moran, C.G. and Devonald, M.A., 2017. Acute and chronic kidney disease in elderly patients with hip fracture: prevalence, risk factors and outcome with development and validation of a risk prediction model for acute kidney injury. BMC nephrology, 18(1), pp.1-11.

Provenzano, M., Chiodini, P., Minutolo, R., Zoccali, C., Bellizzi, V., Conte, G., Locatelli, F., Tripepi, G., Del Vecchio, L., Mallamaci, F. and Di Micco, L., 2020. Reclassification of chronic kidney disease patients for end-stage renal disease risk by proteinuria indexed to estimated glomerular filtration rate: multicentre prospective study in nephrology clinics. Nephrology Dialysis Transplantation, 35(1), pp.138-147.

Nixon, A.C., Bampouras, T.M., Pendleton, N., Woywodt, A., Mitra, S. and Dhaygude, A., 2018. Frailty and chronic kidney disease: current evidence and continuing uncertainties. Clinical kidney journal, 11(2), pp.236-245.

Jourde-Chiche, N., Fakhouri, F., Dou, L., Bellien, J., Burtey, S., Frimat, M., Jarrot, P.A., Kaplanski, G., Le Quintrec, M., Pernin, V. and Rigothier, C., 2019. Endothelium structure and function in kidney health and disease. Nature Reviews Nephrology, 15(2), pp.87-108.

Moledina, D.G., Wilson, F.P., Pober, J.S., Perazella, M.A., Singh, N., Luciano, R.L., Obeid, W., Lin, H., Kuperman, M., Moeckel, G.W. and Kashgarian, M., 2019. Urine TNF-α and IL-9 for clinical diagnosis of acute interstitial nephritis. JCI insight, 4(10).pp.9-19.

Jefferson, J.A., 2018. Complications of immunosuppression in glomerular disease. Clinical Journal of the American Society of Nephrology, 13(8), pp.1264-1275.