Inappropriate Hyponatremia Essay

While at the hospital, the patient, was having excessively slow AV nodal conduction rates that unfortunately haven’t been recognized. He started on the prescribed antihypertensive drug (s). As soon as blood levels climb towards the usual therapeutic range the patient goes into complete heart block. Which of the following drugs most likely provoked this further prolongation of the P-R interval, ultimately leading to the complete heart

Usually angiotensin has an effect on the body to increase blood pressure, increase blood volume and increase pressure in the kidney. As the ACE inhibitor lowers the amount of angiotensin, this causes the blood vessels to become wider and there is an increase in the amount of urine produced by the kidneys. The result of this is the blood pressure goes down, blood volume decreases and decreases pressure in the kidneys. The decrease of angiotensin levels by ACE inhibitors also causes a drop in noradrenalin and aldosterone levels, which helps to reduce blood pressure. Another effect ACE inhibitors have is to increase bradykinin which also causes the blood vessels to widen with a further decrease in blood pressure. Examples of ACE inhibitors include; Lisinopril (Prinivil), Captopril (Capoten) and Enalapril

Aldosterone is the mineralocorticoid steroid which is release from the adrenal gland, situated superior to the kidney. Aldosterone play a major role for the retention of water and sodium in the nephrone (10) in the patient with congestive heart failure, cirrhosis, and nephrotic syndrome (25). The level of the Aldosterone will increase in the patient of heart failure when angiotensin I receptors is activated by Angiotensin II leading to fluid overload (10).

According to J.T.’s labs, high levels of sodium, chloride, magnesium, creatinine and blood urea nitrogen, hemoglobin and hematocrit are indicative of dehydration as well the activation Renin-Angiotensin Aldosterone system. For example, when there is a decreased blood flow to the kidneys due to dehydration leading to electrolyte reabsorption (Mosby’s Diagnostic and Laboratory Test reference, 2014). Furthermore,

Deficient fluid volume happens when there is a significant loss of fluid and electrolytes as with excessive sweating. Dehydration can occur from an insufficient fluid intake, excessive fluid loss, and fluid shifts. The first sign of dehydration is thirst. If the patient would have drunk water when he first became thirsty, him collapsing may not have occurred, and no further treatment may not have been needed. If fluids continue to be lost, the heart pumps faster but is rapid and weak and causes orthostatic hypotension, explaining his pulse being 136 and blood pressure being 88/52. Orthostatic hypotension may have caused him to collapse due to the

Exercise-associated hyponatremia (EAH) is the most reasonable explanation of adverse changes in athletes during the marathon events. Physiologically, EAH is defined as plasma- sodium concentration that is below 135mmol/L. According to the decreasing plasma sodium level and individual, there are diverse symptoms such as nausea, headache, lethargy and restlessness. Although the sodium in sports drink could postpone the beginning of hyponatremia, drinking too much could cause hyponatremia (Rosner and Kirven, 2007). That is, hyponatraemia is influenced by both dilution of body sodium in body water overload and depletion of body sodium in body water losses. A decreased plasma sodium concentration lead to an osmotic gradient between extracellular and intracellular fluid in brain cells, causing water transfer into cells and increasing intracellular volume (Rosner and Kirven, 2007). It triggers problem regarding tissue oedema, neurological and low blood sodium concentration.

All hypertensive drugs lower blood pressure. However, they’re many forms of the drug, all with differing mechanisms of action. Hypertension refers to the constant lingering of blood pressure above the taken normal range of 120/80 mm Hg. Without the proper treatment, hypertension can lead to extreme difficulties such as kidney failure, coronary heart disease or a stroke. Angiotensin converting enzyme (ACE) inhibitors is an antihypertensive drug, which is among the most widely prescribed drug for lowering blood pressure in the United States (Friedman 2004). Angiotensin causes the narrowing of arteries, predominantly in the kidneys. ACE inhibitors assist in producing less angiotensin throughout the body, subjecting the blood vessels to vasodilation,

The symptoms associated with the syndrome are hypoglycemia, encephalopathy, fatty liver, elevated ammonia levels in the blood and elevated liver function enzymes. This lack of mitochondrial metabolism can explain the hypoglycemia due to the body being unable to create ATP. With the lack of ATP production, the body would naturally deplete its glucose stores to gain more energy. The metabolic failure in the liver causes the elevated liver function enzymes, elevated ammonia levels, and over time the fatty liver. The encephalopathy is caused by the increased

Thank you for reading my post and responding. You bring up some good points. I do feel that we would need more information to decide if a potassium sparing diuretic would work for this patient. It would depend on what she is on the diuretic for, if this is the first time that she has been hypokalemic and is the main cause of her hypokalemia because of the diuretic. But if she was switched to a potassium sparing diuretic by the physician then it would be Spironolactone, Triamterene, or Amiloride.

Acidosis can cause the thyroid hormone to be depressed, this could affect the energy metabolism and cell function in the body. (Davies, Carter and Wells, 2004). The main consequence of metabolic alkalosis is decreased ventilation, causing in hypoventilation. Cerebral blood flow is also decreased due to vasoconstriction, this may result in confusion or even seizures.

The efficacy of the treatment can be monitored by observing the blood pressure reading. However, electrolyte disturbance is a common adverse effect of thiazide diuretics as it causes potassium wasting. The frequency of hypokalemia depends on the frequency of administration, dose, diet, and other pharmacologic agents used. During the first two weeks of therapy, electrolytes monitoring is significant. Once a stable state is established, patients are not usually at risk of hypokalemia, unless the dose is increased, extra renal losses of potassium increase, or dietary potassium is reduced. Thiazide diuretics also can cause certain metabolic and endocrine abnormalities such as hypochloremic alkalosis, hypercalcemia and hyponatremia. They can cause photosensitivity and precipitate gout. Hence, it is important to monitor laboratory values periodically in patients on diuretic therapy. The most common drug interactions are pharmacodynamic interactions resulting from potassium depletion caused by the diuretics. Hypokalemia is a risk factor for arrhythmias, and the risk is increased with concomitant therapy with antiarrhythmic agents that prolong the QT interval independently of serum potassium concentration. Therefore, combinations of drugs that can cause hypokalemia such as diuretics, and antiarrhythmic agents require vigilant monitoring of potassium and appropriate replenishment.

Vasopressin (Antidiuretic hormone) also is oxidized by the oxygen released from erythrocytes. Vasopressin plays a role in circulatory homeostasis and serum osmolality. Oxytocin and vasopressin are oxidized with formation of dityrosine [77]. Its oxidation and depletion cause vasodilatory shock - a syndrome with high mortality [78-81]. Low expression levels of Angiotensin II and ACE (angiotensin converting enxyme) are valuable in predicting the mortality of patients

Patients with hypotension usually manifest with lightheadedness, weakness, fatigue, anxiety, vertigo, frank syncope, seizure like episodes, paleness, sweating, abdominal and chest pain, muscle cramps, nausea, vomiting, and dyspnea, although occasionally some patients may be asymptomatic. Vagal symptoms, encompassing yawning, sighing, and hoarseness may be observed before the fall in blood pressure is noticed (3 of 1).

Husband- Semen analysis at least 2- done 4 weeks apart preferably in an infertility center ( examination done by andrologist), Blood sugars

Thiazide diuretics: Chlorothiazide, chlortalidone, hydrochlorothiazide, hydroflurmethazyne, indamapide, methylchlotiazyde, metolazone, polythiazide. The most important side effect of thiazide is hypokalemia, also include metabolic alkalosis,hyponatremia, hypovolemia, hyperglicemia in diabetics, increasing of LDL, azotemia and