Chronic Kidney Failure and Medications
Chronic kidney failure affects renal drug elimination with those medications that are eliminated by the kidney as a result of the illness process's kidney insufficiency. Mary will continue to take metformin at a lower dose dependent on her creatinine clearance and metformin is excreted by the kidney nearly 90% of the time. The medication would aid in lowering Mary's hepatic glucose intake and increasing the response of her body tissues to insulin. Mary will now continue to take Angiotensin Converting Enzyme Inhibitors (ACEIs) at a dose of 25 milligrams TDS, which lowers her blood pressure to 145/95 mmHg and slows the development of kidney disease. She can also continue on lipid-lowering drugs as it helps to reduce cholesterol biosynthesis, mainly in the liver where it is selectively distributed.
Mary's Edema and Excess Fluid Retention
Mary’s edema is caused by excess fluid retention in the body tissues. Edema is aggravated by high sodium levels in the blood of 180 mmol/liter which retain the water causing swelling and kidney is unable to excrete excess fluid. At the same time increased the accumulated fluid shifts to the interstitial space.
Question 3
Kidney disease produces low renin which breaks down angiotensinogen to angiotensin one converted into angiotensin two by angiotensin converting enzyme. The angiotensin two initiates the production of aldosterone which acts on the renal tubules to increase renal tube absorption of sodium hence the high levels 180mmol/liter (Laake & Bugge, 2010). Mary's hyperkalemia of 6.1 mmol/liters aggravated by impaired glomerular filtration rate.
Question 4
The presence of macro albuminuria shows that the kidney disease is advanced; therefore, Mary is put on captopril to reduce the risk of mortality. Hematuria in urine is due to glomerulonephritis, inflammation, of the filtering system of the kidney.
Question 5
Mary is at risk of developing low serum albumin hence developing coagulation problems and unable to bind action such as sodium and potassium leading to hypernatremia.
Gastroenterology Case
Question 1
Metabolic syndrome entails central obesity, elevated blood pressure, insulin resistance, prothrombotic state. There is an elevated serum alanine aminotransferase which indicates liver damage when one has metabolic syndrome. Mary has a type of chronic liver disease known as portal hypertension because she has ascites, her high blood pressure of 145/95 mmHg.
Question 2
Mary’s chronic liver disease is related to her hematemesis due to portal hypertension hence blockage of the smooth flow of blood caused by dilation of the two esophageal veins at the distal part. Mary develops increase intra-abdominal pressure leading to hematemesis.
Question 3
Persistence of hematemesis in Gertha case is due to the fibrosis of liver tissue due to damage. The fibers block the healthy hepatocytes and hence the collection of blood leading to increased pressure in the affected blood vessels (Gustot & Moreau, 2010). This makes the esophagus dilate, and blood pressure is bursting them making her vomit blood.
Question 4
Mary’s ascites is related to her chronic liver disease in that the damaged liver fails to make a protection known as albumin. Insufficient albumin is unable to keep fluid from leaking out of blood vessels into the peritoneal cavity hence leading to the development of ascites.
References
Gustot, T. & Moreau, R. (2010). ‘Renal failure in cirrhosis’, in Ascites, Hyponatremia and Hepatorenal Syndrome: Progress in Treatment, pp. 112–121. doi: 10.1159/000318992.
Laake, J. H. & Bugge, J. F. (2010). “Acute renal failure in critically ill patients.”, Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række, 130(2), pp. 158–61. doi: 10.4045/tidsskr.10.34549.
