Pathophysiology of Acute Renal Failure

Pathophysiology of Acute Renal Failure Intro The following pages will concern the scenario of Georgina Lawson. I will examine the pathophysiology of Acute Renal Failure and then highlight the pharmacological management specific to Mrs Lawsons treatment. I will then concentrate specifically on Mrs Lawsons condition by identifying three signs and symptoms that she displayed upon admission, and discuss how the diagnosis of Acute Renal Failure has been reached. Next there will be a discussion on the tests undertaken at the time of Mrs Lawsons admission, their relevance, results and also the expected findings when the assumption of Acute Renal Failure has already been made. Additional tests that could also been ordered but werent will also be highlighted with their potential benefits shown. In the last part of this paper, I will write about the impact of having a BMI of 50 on the disease of process of T2DM and Acute Renal Failure as well as the pharmacological implications of having such a weight. Part 1 Acute renal failure is a representation of the rapid decline in renal function whereby blood nitrogenous wastes (urea nitrogen, uric acid, and creatinine) accumulate due to a decreased glomerular filtration rate, impairing fluid and electrolyte balances.reference? Filtration of plasma through the glomerular capillaries into the Bowmans space is the initial stage of urine production.reference Large molecules can not easily cross through the glomerular wall during normal production therefore urine is protein free. The capillary filtration pressure is higher in the glomerular than in other capillaries in the body; this increased area of pressure is what allows for the afferent and efferent contraction and relaxation of arterioles to produce high volumes of filtrate. If the glomerular filtration rate is altered the initial stage of urine production does not occur, therefore diminishing the kidneys ability to remove nitrogenous waste from the body (Porth, 2005, p.?). Acute Renal Failure is categorised in 3 areas, prerenal, intrinsic and postrenal. As prerenal characterises the symptoms displayed by Georgina Lawson only that area will be discussed. Possibly intrinsic if going down the line of Glomerulonephritis. 3 Symptoms: BP on admission 160/80 Hypertension is a constant increase of resting systolic blood pressure greater than  140 mm Hg, diastolic blood pressure greater than  90 mm Hg or both.reference Primary hypertension with no known cause is most common where as secondary hypertension with an identified cause is usually due to a renal disorder. referenceUsually, no symptoms develop unless hypertension is severe or long-standing (Bakris G, 2010). Blood flow depends on the rate of heart beats and the volume of blood pumped out with each beat. If rate or volume increases, blood pressure rises, and prolonged hypertension may damage many organsreference. Initially the heart works harder to pump out more blood against higher resistance.reference The heart then requires more oxygen, and is more susceptible to damage, also predisposing arteries and arterioles to damage. Arteriosclerosis results when blood moves through arteries and arterioles at high pressure, damaging the vessel causing white blood cells to be drawn to th e damaged area to form a plaque.reference Prolonged hypertension causes the kidneys to be damaged as the delicate capillaries of the kidney are continually exposed to high blood pressure, they break down, becoming permeable to proteins and other molecules. Tubules can become clogged, decreasing the kidneys ability to make urine. The presence of protein injures capillaries cell wall membranes causing further damage and worsening the situation (Porth, 2005,p.?). Dark, cloudy, odorous urine Protein is present due to damage to capillary cell walls in the kidneys, which allow proteins to pass through pores in the basement membrane during glomerular filtration. Reference Normally red blood cells and plasma proteins do not pass through the glomerulus; therefore urine is a blood and protein-free filtrate. In a healthy person the glomerular filtration barrier will excrete less than 150mg of protein in the urine over a 24hr period (Porth, 2005, p.?). Georgina described to the GP low urine output with burning on passing urine, followed by a fluid increase. On admission urine output is still minimal, concentrated with a strong odour.Why do you think this is happening? Cloudy or murky urine is a sign of infection, which may also have an offensive smell. Reference Murky urine may also be caused by the presence of bacteria, mucus, white blood cells or red blood cells, epithelial cells, fat, or phosphates.reference Osmolality or specific gravity of urine changes with the concentration of solutes, depicting a sliding scale of the hydration status and functionality of the kidneys.reference The ability to concentrate urine is lessened when renal function in impaired, with specific gravity values falling to 1.006- 1.010, while normal values during times of hydration are 1.030- 1.040. What was Georginas result and what does this demonstrate? Pitting Oedema bilaterally Edema is the expansion of the interstitial fluid volume by 2.5-3L which is evident by palpable swelling where?. Edema manifestations associated with Georginas sudden onset of symptoms include; Increased capillary filtration pressure: An increase of extracellular volume is caused by the decrease of sodium and water excretion by the kidneys, increases of capillary volume, pressure and consequent movement of fluid into the tissue space.reference Deceased capillary colloidal osmotic pressure: caused by inadequate production or abnormal loss of plasma proteins, largely albumin, most commonly in the kidney. This is due to the glomerular capillaries becoming permeable to plasma proteins, predominantly albumin, allowing them to be filtered out of the blood and lost through urine.reference Increased capillary permeability; enlargement of capillary pores or integrity of capillary walls are damaged, causing permeability is increased. This allows plasma proteins and other osmotically active particles to move into the interstitial space and increase colloid osmotic pressure, in so doing enabling the accumulation of interstitial fluid. (Porth, 2005, p?) Part 2 Discuss the tests that were ordered for Georgina and explain why they were chosen in regards to your chosen element discussed in part 1. Bloods: Na+: 135 Sodium: 135- 145 K+: 5.5 Potassium: 3.2- 4.3 Cl: 108 Chloride 99 109 Urea: 12.0 3.0- 8.0 Creatinine: 1.5 mg/dl 45- 90 Cholesterol: 6 6, this occurs in the duodenum and small intestine. Highly bound to plasma protein, especially albumin Mainly in the gastrointestinal mucosa and the liver Largely excreted by the kidneys. 2- 4.5hrs 1- 2hrs Medication critique With the fluid overload and lack of urination Goergina is experiencing, aspirin would not have an effect on her current hypertensive. Although some studies have discussed that the vasodilatory effects of aspirin would out weight the negative anti platelet effects on patients with kidney diseases, standard treatments remain that those suffering renal failure and cardiovascular disease should not be routinely prescribed aspirin. Glibenclamide What is the above medication? How does it work? How does it achieve its therapeutic effect? Oral hypoglycaemic Appears to lower the blood glucose acutely in individuals with type 2 diabetes by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells. Therapeutic use? Or indication for use? What about for your patient? It acts with glucose to improved sensitivity of beta cells to physiological glucose stimulus and leads to an insulin secretion in the rhythm of meals. Increased bgls will be lowered by this and help stimulate Georginas pancreas to improve beta cell production What is the therapeutic range for this medication? Side effects? Hypoglycaemia may occur. Gastrointestinal effects such as nausea, vomiting, epigastric fullness and diarrhoea are the most common side effects.    Drug interactions. Drugs which may enhance the hypoglycaemic action should be used with caution. Pharmacokinetics A: D: M: E: HL: P: Nearly completely absorbed (84 +/- 9%) after oral administration. Is extensively bound (99%) to serum proteins. Completely metabolised in the liver. Excreted as metabolites in the bile and urine, approximately 50% by each route. 2-5 hours after oral administration. Peak serum concentration is reached in two to six hours Medication critique In patients with renal insufficiency, depending on the degree of the renal excretion disorder, there is increased elimination of the metabolites via the bile. If Georginas kidney dysfunction is significant she should be continued on this medication. References Metformin What is the above medication? How does it work? How does it achieve its therapeutic effect? Metformin  causes increased peripheral uptake of glucose by increasing effectiveness of available exogenous or endogenous insulin.reference The mode of action of  metformin  may be linked to increased insulin sensitivity. It does not stimulate insulin release but does cause antihyperglycaemic effects when insulin is present. Possible mechanisms of action include inhibition of gluconeogenesis in the liver, delayed glucose absorption in the gastrointestinal tract and increased peripheral uptake of glucose.reference Therapeutic use? Or indication for use? What about for your patient? Metformin  has antiketogenic activity comparable to some extent, to insulin itself.  Metformin  lowers both basal and postprandial blood glucose in diabetic patients but does not cause hypoglycaemia in either diabetic or normal individuals. reference What is the therapeutic range for this medication? 500 mg three times a day is often sufficient to obtain diabetic control, the dose can be increased to 1 g three times daily, which is the maximum recommended daily dose.reference Side effects? Mild gastrointestinal symptoms such as diarrhoea, nausea, vomiting, abdominal pain and loss of appetite are very common, especially during the initial treatment period. These symptoms are generally resolve during continued treatment.reference Drug interactions. Calcium channel blockers may affect glucose control in diabetic patients therefore regular monitoring of glycaemic control is recommended.reference Pharmacokinetics A: D: M: E: HL: P: Oral administration  is absorbed along the entire gastrointestinal mucosa. not bound to plasma proteins. Excreted unchanged in the urine and does not undergo hepatic metabolism. 6hrreference Medication critique In patients with decreased renal function based on measured creatinine clearance, the plasma half-life of  metformin  is prolonged and renal clearance is decreased in proportion to the decrease in creatinine clearance. (Renal failure or renal dysfunction (creatinine clearance