Question

In: Anatomy and Physiology

Given the patients acid-base imbalance, discuss the potential risks of prescribing Lisinopril and describe clinical manifestations...

Given the patients acid-base imbalance, discuss the potential risks of prescribing Lisinopril and describe clinical manifestations resulting from that condition.
How does hyperkalcemia occur and its causes

Solutions

Expert Solution

Lisinopril is an inhibitor of ACE or angiotensin converting enzyme. Hence, it will inhibit the conversion of angiotensin I to angiotensin II in lungs. This will inhibit water reabsorption in kidneys. It also inhibits the aldosterone secretion in adrenals which in turn inhibit potassium excretion in kidneys. Thus, Lisinopril induces hyperkalemia due to increase potassium levels.

In patients of acid base imbalance, cause fluctuations in potassium and sodium levels. Increased acidosis is known to cause movement of potassium in exchange for H+ ions to move into extracellular space. Increased alkalosis cause potassium to move into the cells, with H+ ions moving into extracellular space. Thus, acidosis is linked with Hyperkalemia while alkalosis is linked to Hypokalemia.

Hyperkalemia is increased levels of potassium in blood. It is caused by either increased intake of potassium or decreased elimination of potassium by kidneys. Potassium is majorly reabsorbed by the renal proximal tubules by diffusion and the Na+/H+ antiporter. Some reabsorption occurs in thick ascending limb of the Loop of Henle via the Na-K-2Cl cotransporter (NKCC2). The potassium re-enters the filtrate via ROMK channels. A fraction also enters the interstitial fluid. In the distal convoluted tubule, the potassium excretion increases via NCCT and ROMK. Major site of potassium secretion is in collecting duct which occurs in response to aldosterone. This secretion is affected by Lisinopril. Renal insufficiency, low aldosterone levels, Hyperaldosteronism, Pseudohypoaldosteronism (PHA), congenital adrenal hyperplasia (CAH) and constipation can all lead to hyperkalemia.

In patients with acidosis, Lisinopril will increase the hyperkalemia. This will increase the acidosis related problems in the patient. The patient will exhibit visual hallucinations, incoherence, and inarticulate speech. There will be effects on kidney function leading to injury. The person will require hemodialysis to remove the drug form blood. There will be effects on heart function causing slower heartbeats. The pulse will also be chest pain, breathing issues, weakness etc. In case of alkalosis, the hypokalemia will be neutralized with the Lisinopril induced hyperkalemia.

Hyperkalcemia or hypercalcemia is increased amount of calcium in blood. It is mostly caused by increased secretion of parathyroid hormone by parathyroid gland. PTH hormone causes increase breakdown of bone matrix, leading to entry of calcium from bone into blood. Distal tubular reabsorption of calcium in the kidneys is increased by PTH hormone. PTH stimulates the activity of osteoclast, which are bone cells that degrade bone. PTH also increases the absorption of calcium in the intestine. The activity of 1alpha-hydroxylase activity is stimulated by PTH in the proximal tubular cells of intestine. As a result, there is increased production of 1, 25-dihydroxyvitamin D (1,25(OH)2 D3) production. Vitamin D is required by absorption of calcium in the intestine. Hyperparathyroidism, lung diseases, cancer, diuretics and dietary supplements can all increase the levels of calcium in blood.


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