Primary Hyperaldosteronism Case Study Health And Social Care Essay
Our case study involves a 50-year-old man who has been referred to his primary care physician to be evaluated for weakness and high blood pressure. On the day of his exam the nurse records his blood pressure as 160/110 while in a supine position. This reading indicates that both his systolic and diastolic values are elevated. To further diagnosis the patient, the doctor orders blood to be drawn and for a urine specimen to be collected and both to be sent to the lab for testing. The following results were obtained from the blood: [Na+], 142 mEq/L; [K+], 2.1 mEq/L; [Cl-] 98 mEq/L; and osmolarity, 289 mOsm/L. The urine results were: [Na+], 60 mEq/L (normal); [K+] 55 mEq/L (high); and osmolarity, 520 mOsm/L. The physician determines that our patient has an aldosterone-secreting tumor of the zona glomerulosa of the adrenal gland. This tumor has a caused a condition called primary hyperaldosteronism or Conn’s syndrome. Our case study will discuss the findings from this physical examination, their significance both to the diagnosis and to our patient.
Significance of Each Vital Sign
The patient presents with an elevated blood pressure. Our case study does not include additional vital signs. Elevated blood pressure is an important part of a diagnosis of aldosterone-secreting tumor. The tumor increases the amount of aldosterone in the blood stream, which has a direct affect on sodium and water levels. This condition is called “primary aldosteronism” (John E Hall, 2011, p. 220). “Aldosterone increases the rate of reabsorption of salt and water by the tubules of the kidneys, thereby reducing the loss of these in the urine while at the same time causing an increase in blood volume and extracellur fluid volume. This increase in volume will increase arterial pressure. “There is a sequence of events that cause an increase in blood pressure: increased extracellular fluid volume increases blood volume. Blood volume increases the mean circulatory filling pressure. This pressure increases venous return of blood to the heart. “The increased blood to the heart will increase cardiac output which in turns increases the arterial blood pressure” (John E Hall, 2011, p. 217). Therefore, the arterial blood pressure increases due to sodium and water concentrations. This can become a fatal situation if left untreated.
Reason the Lab Tests Were Ordered
Serum osmolality is used to establish baseline for fluid status. Critical values to be aware of in regards to serum osmolality are values less than 265 mOsm/kg H₂0 and greater than 320 mOsm/kg H₂O. This lab test is ordered to check into the fluid and electrolyte balance and rule out potential issues for patients “with seizures, ascites, hydration status, acid-base balance, and suspected antidiuretic hormone (ADH) abnormalities” (Pagana & Pagana, 1998, p. 314). In healthy adults the expected normal values are 285-295 mOsm/ kg H₂0. Our patient presents with a serum osmolality value of 289 mOsm/L, and is within the accepted normal range, however he is on the low end, which could indicate “over hydration, syndrome of inappropriate antidiuretic hormone secretion (SIADH), or paraneoplastic syndromes associated with carcinoma” (Pagana & Pagana, 1998).
Urine osmolality is used to evaluate fluid and electrolye functions. It looks at the kidney concentrating abilities, and as a tool in evaluating the patient for ADH abnormalities. Normal levels according to Pagana are 50-1400 mOsm/kg H₂O in a random specimen, and for the 12-14 hour fluid restriction, normal value is 850 mOsm/kg H₂0 (Pagana & Pagana, 1998). Urine osmolality is important in evaluating the concentrating ability of the kidney, and is often evaluated along with blood osmolality results (Pagana & Pagana, 1998). The patient presents with the value of 520 mOsm/L, but the type of collection is not indicated. If this is a random specimen the results are within normal range. If this result is from a 12-14 hour fluid restriction, the result is low, and could be indicating “diabetes insipidus, excess fluid intake, renal tubular necrosis, or severe pyelonephritis” (Pagana & Pagana, 1998).
Blood sodium is part of a basic metabolic profile or serum electrolyte panel. This is a marker for fluid and electrolyte baseline. Normal findings are 136-145 mEq/L. Sodium is an important part of serum osmolality. Many factors regulate sodium balance, including aldosterone secretion from the kidney, natriuretic hormone, and ADH. Water and sodium play a close interaction in the balance of the two (Pagana & Pagana, 1998). Our patient presents with a value of 142 mEq/L, and is within normal value range.
Urine sodium is another test to evaluate the fluid and electrolyte balance of the patient from the viewpoint of the kidney. Normal values for urine sodium is 40-220 mEq/L/day or greater than 20 mEq/L in a spot check. This test helps to evaluate sodium loss in the urine in comparison the the sodium level in the blood. In some incidences the sodium level is low in the blood and high in the kidney, and this is indicative of chronic renal failure or Addison’s disease (Pagana & Pagana, 1998). Our patient presents with a normal value of 60 mEq/L.
Blood potassium is also a part of the basic metabolic profile (BMP) or serum electrolyte panel. It is often evaluated as a baseline for patients presenting with cardiac symptoms. Normal values are 3.5-5.0 mEq/L in adults. Our patient is under the critical low value of 2.5mEq/L (Pagana & Pagana, 1998). Serum potassium levels are regulated by many factors including aldosterone, sodium reabsorption, and acid-base balance. Decreased levels of serum potassium could be caused by several factors including; “deficient dietary intake, deficient IV intake, burns, gastrointestinal disorders, diuretics, hyperaldosteronism, Cushing’s syndrome, renal tubular acidosis, licorice ingestion, alkalosis, insulin administration, glucose administration, ascites, renal artery stenosis, cystic fibrosis, trauma, and surgery” (Pagana & Pagana, 1998).
Urine potassium is evaluated to determine electrolyte balance, and is ordered in this case to determine if the patient is excreting potassium through the kidneys. The normal levels are 25-120 mEq/L/day according to Pagana (Pagana & Pagana, 1998). Our patient in the case study has a value of 55mEq/L and is documented as being high. There are many causes for urine potassium being elevated, including: chronic renal failure, renal tubular necrosis, starvation, Cushing’s syndrome, hyperaldosteronism, excessive intake of licorice, alkolosis, and diuretic therapy (Pagana & Pagana, 1998).
Blood chloride is also part of the BMP or serum electrolyte panel. Chloride is used in evaluating the hydration state and acid base balance of the patient. Normal values are 90-110 mEq/L in an adult. Our patient’s value is within normal limits.
Over all the results of the ordered tests, give a picture of the patient’s electrolyte status, and excretion of the electrolytes. This information guides the caregiver to look at the cause for the patient’s symptoms, and determine if they are related to the serum levels or the excretory levels.
Necessity of Laboratory Tests
The physician ordered both a blood chemistry test as well as a urine chemistry test for our case study patient. An elevated blood pressure of 160/110 mm Hg, especially while the patient is in the supine position, is indicative of volume expansion in the extracellular fluid. Volume expansion is a result of increased sodium content in extracellular fluid (Costanzo, 2010). The physician must evaluate the sodium ion concentration in the blood as well as in the urine to determine how the increase in blood pressure is related to a sodium imbalance and the nature of the imbalance. The patient’s complaint of weakness can be a significant sign that the patient is suffering from hypokalemia. According to Hall and Guyton (2011), “When the potassium ion concentration falls below about one-half normal, severe muscle weakness often develops” (p. 926). With the patient’s complaint of weakness during the physician’s assessment, it is necessary to evaluate his potassium ion concentration to determine if indeed his weakness is a symptom of hypokalemia. The evaluation of potassium ion concentration in the patient’s urine is a simple test to allow the physician to determine if the patient’s hypokalemia is related to an increase in potassium secretion leading to an increase in potassium excretion in the urine or if there is another cause for the low potassium ion concentration in the blood.
In our case study, the patient’s serum sodium ion concentration is 142 mEq/L and his urine sodium ion concentration is 60 mEq/L, both values within normal range. However, with such an elevation in blood pressure without a noticeably direct increase in serum sodium ion concentration, it is indicative that the patient’s kidneys are reabsorbing more water with a proportionate increase of sodium content (Costanzo, 2010). This combination of increased sodium content and total body water content explains our patient’s hypertension (Costanzo, 2010).
Our case study patient’s serum potassium ion concentration is 2.1 mEq/L and his urine potassium ion concentration is 55 mEq/L. The serum potassium ion concentration is well below the normal range of 3.5-5.0 mEq/L and the urine potassium ion concentration is high indicating that there is an increase of potassium secretion leading to a decrease in plasma potassium ion concentration and an increase in urine potassium excretion (Costanzo, 2010).
Our patient’s serum chloride ion concentration is 98 mEq and his serum osmolarity is 289 mOsm/L, which are both within their respective normal ranges. His urine osmolarity concentration is 520 mOsm/L, which is also within its normal range.
The laboratory tests, including blood chemistry and urine chemistry, ordered for our case study patient were both necessary not only to obtain baseline values for future follow up testing, but specifically to focus on the patient’s sodium and potassium ion concentrations in both blood and urine specimens to determine their relationship to one another given his presentation of supine hypertension and his complaint of weakness.
What are the physiological principles that explain the patient’s symptoms?
Our patient presents with an elevated systolic and diastolic blood pressure and symptoms of weakness. This is the body’s response to an alteration in electrolyte imbalance caused by the loss of potassium together with increased retention of sodium and hydrogen ion secretion.
“Primary aldosteronism is characterized by over production of aldosterone by the adrenal glands” (Conn, 1955, p. 6). Aldosterone is the principle mineralcorticoid that is secreted by the zona glomerulosa in the adrenal cortex of the adrenal glands. The primary function of aldosterone is the control of intravascular volume (Ganong, 2005).
Aldosterone acts on the distal tubules and collecting ducts of the nephron to initiate the kidney to conserve sodium, secrete potassium, increasing water retention and increasing blood pressure. “Aldosterone binds the mineralcorticoid receptor (MR) and the complex interacts directly with the genomic DNA via a steroid response element (SRE). Transactivation of gene expression leads to transcription of the aldosterone induced proteins SGK (serum and glucocorticoid inducible kinase), Ki-RAS and CHIF (corticosteroid hormone induced factor). These proteins increase the activity of sodium, potassium, and ATPase by increasing pump turnover and recruiting latent ATPase to the basolateral membrane” (Gerhard Malnic, Matthew A. Bailey, Gerhard Giebisch, 2004, p. 484).
The first symptom to present is hypertension and occurs in a majority of patients. “An aldosterone mediated increase in extracellular fluid volume lasting more than 1 to 2 days also leads to an increase in arterial pressure”(Guyton and Hall, 2011, p.925). This condition can exist for as long as aldosterone continues to be secreted in abnormally high amounts. Hypokalemia of < 3.0 meq in blood and elevated potassium levels in urine suggest mineralcorticoid excess. “Muscular weakness is caused by the alteration of the electrical excitability of the muscle and nerve fibers which prevents the transmission of normal muscle potentials" (Guyton and Hall, 2011, p.926). Other patient symptoms of headaches, nocturia and in very rare cases paralysis may occur. “Numbness and tingling in the extremities are related to alkalosis that may lead to tetany" (Tyrell, 2000, p.555). Metabolic alkalosis is a result of decrease in hydrogen ion concentration in extracellular fluid when hydrogen ions are secreted in exchange for sodium ions in the cortical collecting tubules of the kidney (Guyton and Hall, 2011, p.926).
If the treatment was successful, what was the reason?
"Treatment of Conn's syndrome consists of administrations of an aldosterone antagonist such as spironolactone, followed by surgical removal of the aldosterone-secreting tumor" (Constanzo, 2010, p. 422). Aldosterone stimulates the principal cells of the distal tubule and collecting duct to reabsorb sodium, which promotes water reabsorption, and increases the excretion of potassium and hydrogen ion (Huether, 2008). Our patient is placed on spironolactone, which is an aldosterone antagonist, a steroid, and a potassium-sparing diuretic, to block the effects of aldosterone on principal cells. This decreases sodium reabsorption, causing a reduction in extracellular fluid (ECF) volume, and also decreases potassium secretion, allowing the patient's plasma potassium to increase (Constanzo, 2010). The patient's blood pressure will decrease due to the reduction in the ECF volume. Our patient is placed on a sodium-restricted diet, which will also help to decrease blood pressure by decreasing the ECF volume.
Our patient has surgery to remove the adrenal tumor. With the removal of the aldosterone-secreting tumor, aldosterone levels return to normal. Our patient's blood pressure and blood and urine chemistries return to normal. The treatments of spironolactone, sodium restricted diet and surgery were successful for our patient.
If the Treatment was Unsuccessful What was the Reason
The treatment was successful for our patient. The man’s hypertension was treatable by removal of the adrenal tumor. He was given spironalactone and his diet was modified to reduce his sodium, while awaiting surgery. His lab values and vital signs returned to normal.
Our case study involved a 50-year-old man who presented to his physician’s office with hypertension recorded in a supine position, weakness, and electrolyte imbalances indicated in both his blood and urine. It was determined that he had an aldosterone-secreting tumor of the zona glomerulosa of the adrenal gland which had resulted in primary hyperaldosteronism, also known as Conn’s syndrome. Test results were closely examined and a treatment plan was established for our patient. Until surgery could be preformed to remove the tumor he was placed on spironolactone and a sodium-restricted diet to treat his hypertension. Our patient opted to have the tumor removed surgically. The surgery was successful with his blood pressure, blood, and urine chemistries all returning to normal levels.
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