Symptoms of Cyanosis - Case Study Example

Question 1: Parameter Prediction pO2( mmHg) Decrease pCO2(mmHg) Increase/ Decrease/ No change pH Decrease Arterial O2 content Decrease Explanation: 1. Decrease in pO2 (mmHg) Some symptoms of cyanosis subject in the preliminary diagnosis which means to get the skin color changed in purple or blue because of getting the oxygen level lower in the blood. The phenomenon is known as deoxy or deoxygenation and an ultimate reduction in HB level as well. Assessment of oxygenation in HB is estimated through PO2. The patient was getting cyanotic because there was up shot from the lowering of arterial PO2 . 2. PCO2(mmHg) Behavior It is the partial pressure of carbon dioxide. Here we have to consider all of the alternatives which are increase, decrease and a neutral effect i.e., no change in the given parameter Increase: The diagnosis of patient’s current situation may lead towards lung disease subject because of preliminary indications. The patient is pointing to the shortage of breath, noisy breaths, labored or difficulty while breathing and crackling rales. The expected lungs disease may be because of incongruity of decreased diffusion capacity with the aeration. All the phenomenon causes hinder in ability to pass away carbon dioxide. In the while, the subject puts its efforts to balance it with oxygen (O2). This usually becomes the reason of increase in PCO2. It has been indicated that the patient is suffering from hyperventilation so it is the cause for PCO2 has been elevated. Decrease: the hyperventilation may cause loss of CO2 because of deprivation of oxygen. It is a sufficient reason for what it is decreased in the given scenario but still depends upon the situation of patient. No change or neutral: if the effect of hyperventilation and diffusion capacity with the aeration in non-diseased area can observed, it will result in normal range of partial pressure of carbon dioxide. 3. Decrease in PH Unlike PCO2, the PH level may be varied according to situation to situation. Cyanotic subject can be observed when the extraordinary occurrence of abridged attention of HB in blood vessels. The overall presence of oxygen hence is lower. Question 2: Parameter Prediction PO2( mmHg) Increase PCO2(mmHg) Increase pH Decrease Arterial O2 content Increase Explanation 1. Increase in PO2 Pulmonary capillary - Alveolar PO2 and PO2 increase induced increases in the incline. Oxygen permeability of the capillaries in the lungs with abnormal lung areas (areas with more growth in the lungs, usually it is possible that it is almost completely saturated HB). This cyanosis, which is confirmed by the absence of HB indicates the presence of high abundance. 2. Increase in PCO2 Decrease in respiratory rate and depth of breathing "ventilation so slow" shows a decrease in alveolar ventilation, alveolar ventilation PCO2 rate is inversely proportional. 3. Decrease in PH Because of inverse relationship, PH will be moving in an inverse manner as PCO2 moves. In this way, PH will be going to reduce. 3. Arterial O2 content Cyanosis is unobservable right now and the skin has been resumed. Thus here is less hbO2 and more hp level. This clearly shows an apparent increase in oxygen content. Question 3: Measurement value High, low, normal Hemoglobin 16 gm/dl High hematocrit 52% High pO2 48 mmHg Low pCO2 90 mmHg High pH 7.35 Low HCO3 (Bicarbonate) 48mM High Question 4: The patient is suffering from the diagnosed problems for either a year or even more than that. It seems to be an older problem because of patient’s test is showing these things. The readings of HB and Hematocrit are showing an elevation. Low PO2 stimulates renal secretion of erythropoietin, which acts on the bone marrow to increase the production of red blood cells. Even if it has not long years to occur, it will take more than a week. It is likely that the patient is a chronic lung disorder for a long time, 7 recently worsened following acute pulmonary infections. Present other changes that have occurred in a much shorter time., Even if it takes several days for the kidneys to increase [HCO3-] in response to respiratory acidosis. Question 5: During the first admission, the patient is an important respiratory control for the effects of low PO2 in the peripheral chemoreceptors. To be placed in an oxygen tent set PO2 enough to remove the incentive for ventilation. Moreover, chronic lung disease, high PCO2, central receptors "adjusted" for the stimulating effect of high PCO2 and ventilation. Only high PCO2 stimulates excessive ventilation. In fact, after the administration of O2, decreased ventilation, PCO2 will still grow (more than 90 mm ​​Hg). At this level of CO2 anesthesia of the central nervous system begins to give, so that instead of increased ventilation. Question No. 6 Question No 7. A nephron is the basic unit of structure and function of a kidney. Each nephron is composed of two components, the vascular structures and the tubules with glomerulus (Mosby’s Medical Dictionary, 2009). These structures act in synchrony to produce concentrated urine (Chmielewski, 2003). The American Heritage Medical Dictionary (2007) defines a nephron as “The functional unit of the kidney, consisting of the renal corpuscle, the proximal and distal convoluted tubules, and the nephronic loop” As mentioned in the Mosby’s Medical Dictionary (2009), there are up to approximately 1.25 million nephrons in each kidney. Question No.8. Glomerular membrane is selectively permeable to the passage of substance across it. Some of the substances that are able to cross it include molecules weighing less than 7000 Daltons, for example water, cat-ions and anions like sodium, potassium, chloride, phosphate, etc. (Holechek, 2003). Moreover, owing to larger size of proteins like myoglobin, they are filtered to a lesser extent. Molecules weighing 70,000 Daltons and more e.g. plasma proteins are unable to cross this barrier. Furthermore, negatively charged substances are restricted from moving across the glomerular membranes. Some other substances filtered are uric acid, creatinine and urea (Holechek, 2003). Glucose is also filtered across glomerular membrane. Glucose is reabsorbed mainly in the tubular portion of the nephron. In the proximal convoluted and straight tubules are present sodium-glucose transporters SGLT2. These are responsible for active glucose reabsorption of almost 90% of the filtered glucose. Question No.9. Mesangial expansion in the diabetic glomeruli, constitute the basic mechanism underlying glycosuria and other nephropathic complications of Diabetes Mellitus (Steffes, Østerby, Chavers, Mauer 1989).With the progression of DM, the renal complications start appearing in the form of expansion of extracellular matrix and thickened basement membranes, both in the glomeruli and the renal tubules (Kanwar et al. 2008). All these changes lead to glomerulo-sclerosis and fibrosis. On the molecular level, hyperglycemia results in the formation of Advanced Glycosylated products (AGEs) and activation of certain molecular pathways which produce reactive oxygen species (ROS). It is these ROS which cause the cellular injury and disruption of renal function (Kanwar et al. 2008). All these mechanisms combined with hyper-filtration can cause diabetic glycosuria, cresenteric glomerular-nephropathy, papillitis, etc. Question No.10. A major complication of Diabetes Mellitus is the development of renal complications, one of which is polyuria. The underlying mechanism behind this condition is the osmotic concentration of urine being produced. Moreover, it has been postulated by Trinder et al. (1994) that “Downregulation of AVP V2 receptors may contribute to the polyuria through diminished V2 receptor-mediated free water retention” Question No.11. Concentration of urine takes place in the kidney due to the counter current mechanism in the renal glomerular system. A concentration gradient exists from the renal cortex to the medulla created by urea. As the urine flows through the renal tubules, exchange of substances takes place between the tubular lumen and the renal interstitium due to this counter current mechanism. Different parts of a glomerulus are involved in dilution and concentration of urine (Schmidt-Nielson, O’Dell, 1961). The system of the ascending and descending limbs of loop of Henle with collecting tubules form a system with the vascular structures surrounding them. Substances are exchanged among them such that the fluid inside the collecting tubules and the descending limb are hyperosmolar while ascending limb forms the diluting portion of a nephron. As a consequence of this, a number of solutes are transported across the tubules thus ultimately forming concentrated urine (Stephenson, 1972). Question No.12.   As a result of cellular injury and hyperglycemia, the filtration capacity of glomeruli is exhausted and beyond a certain concentration, glucose is unable to be absorbed back into the blood. This glucose acts as an osmotic agent and pulls water out into the lumen of tubules. This increases the volume of the urine thus produced and side by side disrupts the concentration gradient that works in concentrating the urine in a normal kidney. Question No.13. According to National Kidney Foundation, 90 - 120 mL/min/1.73 m2 is the range considered normal for the GFR of an adult. Question No.14. ACE inhibitors work on the Juxtaglomerular Apparatus of a nephron. Other parts of a nephron include the various tubules which include proximal tubule (straight, convoluted portions), loop of Henle (ascending and descending limb), distal tubule (straight, convoluted portions) and the collecting tubules.   This patient is started on an ACE inhibitor. She follows up in clinic in 2 weeks, when the following labs are noted: serum creatinine 3.1mg/dL, serum K+(potassium): 5.5mEq/L. This patient has two reasons for hyperkalemia- initiation of her ACE inhibitor as well as possible worsening of her underlying CKD (Chronic Kidney disease). Question No.15. ACE inhibitors work by decreasing the production of Angiotensin 2 and subsequent low levels of Aldosterone. As aldosterone is involved in the excretion of potassium, its lack causes an increases retention of potassium and hence hyperkalemia.   Question No.16. How does addition of an ACE inhibitor change renin, angiotensin I and angiotensin II levels in this patient? ACE inhibitors act on the JG cells and suppress the Renin-Angiotensin system by blocking the conversion of angiotensin 1 to angiotensin 2. As a result, the levels of Renin, angiotensin 2 would fall with an increase in the levels of angiotensin 1.   Question No.17. Aldosterone levels fall further with the administration of ARB, whereas there would be an increase the levels of angiotensin 1 and 2 due to the blockage of angiotensin 2 receptors by ARB. Lab tests obtained during this clinic visit shows pH 7.21, Na+ (sodium) 131mEq/L, HCO3- 12mEq/L, Cl- 115mEq/L. pCO2 28mmHg, pO2 100mmHg on room air. Question No.18.   Metabolic acidosis is the acid base disturbance seen in this patient as shown by the decreased levels of pH, serum HCO3-, Na+. The compensation for this metabolic acidosis is hyperventilation due to the stimulation of the respiratory center in the brain in an attempt to decrease the arterial pCO2. She is admitted for initiation of dialysis. Her admission vitals are temperature 36.80 C, heart rate 94/min, BP 160/50mmHg, respiratory rate 30/min.  Question No.19.  Metabolic acidosis stimulates the peripheral and central chemoreceptors. These trigger the brain which gets stimulated by raised intra-cerebral hydrogen ion concentration. As a result, respiratory system gets activated and brings about hyperventilation in an attempt to decrease the partial pressure of carbon dioxide in the arterial blood. On history, she admits to a pack and a half per day smoking history. Over the next 24 hours, while waiting for dialysis access, her respiratory rate remains high and she complains of feeling poorly. On exam, she is using accessory muscles of respiration and wheezing. An ABG(arterial blood gas) analysis reveals pH 7.16, PCO2 40mmHg, PO2 100mmHg, and HCO3 13mEq/L. Question No.20.   No the patient is not adequately compensated as shown by her lab investigation. This might be due to the effects of cigarette smoking on the pulmonary function. References Hamid, Q., Shannon, J., & Martin, J. (2005). Physiologic basis of respiratory disease. Hamilton: BC Decker, Inc.. Sherwood, L. (2007). Human physiology: from cells to systems (6th ed.). Australia: Thomson/Brooks/Cole. Shields, T. W. (2005). General thoracic surgery (6th ed.). Philadelphia: Lippincott Williams & Wilkins. Starr, C., & McMillan, B. (2010). Human biology (8th ed.). Belmont, CA: Brooks/Cole Cengager Learning. Stellman, J. M. (1998). Encyclopaedia of occupational health and safety. Volume 2(4. ed.). Geneve: International Labour Office/ ILO/ International Labour Organisation. Chang, A. C. (1998). Pediatric cardiac intensive care. Baltimore: Williams & Wilkins. Cameron, P. (2006). Textbook of paediatric emergency medicine. Edinburgh: Churchill Livingstone Elsevier. Chmielewski C (2003) Renal Anatomy And Overview Of Nephron Function Nephrology Nursing Journal: journal of American Nephrology Nursing Association 2003 30(2):185-90 The American Heritage® Medical Dictionary Copyright 2007 Mosby's Medical Dictionary, 8th edition 2009. Holechek M.J. (2003) Glomerular Filtration: An Overview Nephrology Nursing Journal 2003 Vol. 30, No. 3 Marsenic O. (2009) Glucose Control by the Kidney: An Emerging Target in Diabetes American Journal of Kidney Diseases 2009 53: 875-883 Steffes MW, Østerby R, Chavers B, Mauer SM (1989) Mesangial Expansion as a Central Mechanism for Loss of Kidney Function in Diabetic Patients Diabetes September 1989 38: 1077-1081 Kanwar YS, Wada J, Sun L, Xie P, Wallner EI, Chen S, Chug S, Danesh FR (2008) Diabetic Nephropathy: Mechanisms of Renal Disease Progression Exp Biol MedJanuary 2008 233:4-11 doi: 10.3181/0705-MR-134 Trinder D, Phillips PA, Stephenson JM, Risvanis J, Aminian A, Adam W, Cooper, Johnston CI (1972) Vasopressin V1 And V2 Receptors In Diabetes Mellitus Kidney International (1972) 2, 85–94; doi:10.1038/ki.1972.75 Stephenson JL Concentration Of Urine In A Central Core Model Of The Renal Counterflow System Nielson BS, O’Dell R (1961) Structure And Concentrating Mechanism In The Mammalian Kidney AJP - Legacy Content 1961 200:61119-1124 Retrieved from http://www.nlm.nih.gov/medlineplus/ency/article/007305.h Read More