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Itt írjon a(z) Hyperaldosteronism_cats-ról/ről

  • Table of Contents:

1.Abstract 2

2.Introduction 2

3.Etiology 4

4.Clinical findings 4

5.Diagnosis 5

Laboratory abnormalities 5

Diagnostic imaging 6

6.Treatment and Prognosis 6

7.Conclusion 7

8.Discussion 7

9.References 8

1. Abstract

Primary hyperaldosteronism is an underdiagnosed syndrome that appears in cats, yet it is probably the most common adrenocortical disease in cats, as in humans. Cats are often presented with systemic arterial hypertension and/or hypokalemia, leading the practitioner to presume chronic kidney disease as the final diagnosis. As the further investigation is ceased, there might be a high number of cats that don’t receive the proper treatment. Following this, general practitioners need to know about this disease, Primary hyperaldosteronism. This essay describes the pathophysiology, clinical presentation, diagnostic approach, proper treatment, and prognosis of this disease. 2. Introduction

Primary hyperaldosteronism also called Conn syndrome, is the adrenocortical disorder that appears in the “zona glomerulosa” of the adrenal glands. Adrenal glands are paired with the pararenal gland, which is responsible for hormone production. Each gland contains 3 main areas in the cortex: zona glomerulosa, zona fasciculata, zona reticularis. While it has only 1 main area in the medulla. Aldosterone is a steroid hormone with strong mineralocorticoid activity secreted by the zona glomerulosa of the adrenal cortex. Recent studies have shown its production can be done by other tissues including the heart, brain, and blood vessels, in which it has both autocrine and paracrine cellular communication. Its function is to maintain the balance of sodium reabsorption in the distal convoluted tubule of the nephron and at the same time to maintain the balanced excretion of potassium and protons. Its classical target is the kidney epithelium, colon, and salivary glands. Aldosterone overpasses the plasma membrane of the tissues and binds to the mineralocorticoid receptor of the cytoplasm. The receptor in this tissue converts cortisol to cortisone, with a little affinity. Under normal physiological conditions water is absorbed back into the extracellular space followed the sodium retention, thereby vascularization is increased in the blood vessels. Secretion of aldosterone is influenced by adrenocorticotropic hormone (ACTH) but regulated primarily by the renin-angiotensin-aldosterone system and the extracellular concentration of potassium as hyperkalemia directly elicits aldosterone release by depolarization, while hypokalemia is inhibited by depolarization of the zona glomerular cells. Depolarization is affected by sodium and potassium balance. Two pathological mechanisms will lead to hypersecretion of aldosterone. In the primary hyperaldosteronism autonomous hypersecretion of aldosterone is done by neoplastic tissue, adrenocortical or nodular hyperplasia of the zona glomerulosa of the adrenal gland. While the so-called secondary hyperaldosteronism is a reduction of arterial blood volume caused by heart failure or kidney disease or hypoproteinemia, which activates the renin-angiotensin-aldosterone system. Both of them are correlated with the suppression of renin activity.

Under pathophysiological conditions of excessive aldosterone secretion, they are related to the increase of sodium and water retention and at the same time the excretion of potassium. This can trigger systematic arterial hypertension because of water retention, and severe hypokalemia because of the potassium loss. In addition to it, metabolic alkalosis happens because of the movement of hydrogen ions intracellularly. In cats, hyperaldosteronism is correlated to adenomas or adenocarcinomas of the adrenal gland.

3. Etiology

Primary Hyperaldosteronism in felines is caused by unilateral and bilateral adrenocortical neoplasia it’s either adenoma or carcinoma and less commonly by the bilateral nodular hyperplasia of the zona glomerulosa. Unilateral carcinoma happens more often than unilateral adenoma. Aldosterone increases potassium and hydrogen secretion and sodium and chloride reabsorption in the Kidney, which leads to expansion of plasma and extracellular fluid volume, increasing sodium retention and decreasing the potassium concentration of the extracellular and eventually intracellular. Cats with primary hyperaldosteronism secrete excessive amounts of aldosterone independent of the RAAS or the potassium concentration in the extracellular space. The increased aldosterone concentration will result in more sodium and water retention and increased renal potassium excretion, which may lead to systemic hypertension and/or hypokalemia.

4. Clinical findings

Commonly, reports show that middle-aged and older cats are predisposed to the PHA(Primary Hyperaldosteronism), and in cases with neoplasia the median age is of 13 years. The main clinical signs are commonly secondary to hypokalaemia and/or systemic arterial hypertension. blob:http://www.wiki.vetphysiol.hu/e66ab215-c90c-47c0-8593-81be9d806391

However, not all cats with PHA present with clinical signs of hypokalaemia or systemic arterial hypertension.

Hypokalemia effect the depolarization of nerve and muscle membranes, because of that cats that have hypokalemia tend to show more neuromuscular signs. While potassium concentration (K+1) <2.5 mmol/l (3.5-5.5 mmol/l being the average potassium level in a feline) is frequently associated with clinical signs, no connection was found between extracellular potassium concentration and clinical signs. Clinical signs of hypokalaemic polymyopathy are Cervical Ventroflexion (Fig 1), in some cases also difficulties in the jumping, and plantigrade stance of the hindlimb can be observed, in severe cases, flaccid paresis, muscle hypotonia, respiratory failure, and respiratory collapse can be seen. Hypokalaemic polymyopathy is mostly observed in cats with adrenal tumors, while less commonly observed in the cases of bilateral adrenal hyperplasia. Occasionally, cats that are diagnosed with PHA initially present ocular signs of systemic arterial hypertension. Cats with idiopathic bilateral adrenal hyperplasia are more often presented with an ocular sign than cats with adrenal neoplasia. Due to retinal detachment and/or intraocular hemorrhage, there is seen the acute onset of blindness. This is in cats that are presented with arterial hypertension. Polydipsia (great thirst) and polyuria (abnormally large amount of urine), urinary incontinence (involuntary urination), polyphagia (excessive hunger), or symptoms that are unspecific such as lethargy, anorexia, weight loss or restlessness are all less common clinical signs. There have been reports of an abdominal mass, palpable or systolic heart murmur, both secondary to arterial hypertension during the initial physical examination of some patients. A big issue is that there are parallel diseases are presented that mimic PHA, especially in cats of older age. These can include chronic kidney disease, hyperthyroidism, and cardiac disease. After these diagnoses are concluded, they hinder the diagnosis of PHA. The clinical signs in cats with these parallel diseases are predominated by PHA and include polyuria, polyphagia (secondary to diabetes mellitus), poor coat condition, thin fragile skin, and a potbellied appearance . For this reason, PHA should be considered a differential diagnosis in any cat with hypokalemia and/or systemic arterial hypertension, especially in cases where the patient doesn’t respond to treatment.

5. Diagnosis Laboratory abnormalities The most common finding on routine laboratory tests is hypokalemia. It’s important to notice that normal potassium levels do not exclude PHA. To a lesser degree elevation in plasma urea, creatinine, and creatinine kinase. Other, although more uncommon, may include hyperglycemia, hypomagnesemia, hypochloremia, hypophosphatemia, and hyperphosphatemia. To differentiate between the primary hyperaldosteronism from the secondary hyperaldosteronism one measures the aldosterone-to-renin ratio (ARR), more specifically the ratio of plasma aldosterone (ng/dL) to plasma renin activity (ng/dL), which is the most sensitive test one can do. 0.3 - 3.8 is the established reference value and given that cats with adrenocortical tumors have increased levels of plasma aldosterone levels, accompanied by decreased plasma renin levels, one can address the likeliness of a tumor being present. When it comes to bilateral hyperplasia, the levels of plasma renin might be slightly increased or within the upper level of the reference values. In the latter case, the concentration of plasma aldosterone should be weighed against potassium concentration, as hypokalemia is a strong inhibitor of its secretion. As plasma aldosterone concentration is in the upper limit of the reference range and the patient is hypokalemic, the likeliness of PHA is high. As the best screening test, ARR has some disadvantages. Approximately 4ml of blood is needed, and this sample must be cooled or frozen immediately after drawing. The test itself is rarely done locally and reference ranges widely vary among the laboratories. Due to changes in a cat’s physiology, several tests may be acquired in some cases. A more inaccurate test for PHA, but with less disadvantage is the urinary: creatinine ratio (UACR). It measures the aldosterone over time and is easily achievable, and it does not need to be frozen. The inaccuracy is caused by its overlapping reference range between a healthy cat and those with PHA. Later, it has been found that basal UACR <7.5 x 10-9 can be used to rule out PHA. The latter is not a recommended practice of definitive diagnosis. Diagnostic imaging An ultrasound of the abdomen can be a very helpful tool to identify adrenal tumors. But since this procedure is based on equipment and depends on the patient and operator, results vary (Combes et al, 2014). It is still a better choice than x-ray since they are rarely seen unless severely enlarged or calcified. In reported cases, all findings were based on ultrasound. The unilateral masses had a diameter in the range of 10-46mm (Harvey and Refsal, 2013). The contralateral masses, although hard to visualize, maybe evident and present a normal appearance. Both adrenals should be visualized to differentiate between unilateral adenoma and bilateral hyperplasia of the zona glomerulosa. The evidence of change is subtle and only shows increased echogenicity, calcification, or thickening of one pole. Note that these latter small changes are observed in healthy cats too. Furthermore, Abdo ultrasound of the abdomen can detect extended invasion of the mass towards the caudal vena cava, or metastasis in other abdominal organs, but is difficult to diagnose and may go unnoticed before surgery. The observations in a report (Lo et al, 2014), metastasis of the vascular system was discovered intraoperatively in 7 of 10 cats with unilateral adrenal adenomas, and only 1 adrenal adenoma was classified as invasive before surgery after the use of computed tomography (CT) and none using ultrasound. Advanced imaging equipment such as magnetic resonance imaging (MRI) and CT are recommended to disclose and evaluate the spread of the tumor, distant metastasis, staging, and planning of the surgery.

6. Treatment and Prognosis

For cats with unilateral disease, surgical removal is the best option, which means the removal of the adrenal gland (adrenalectomy), the surgery above seems to be curative for both adenomas and carcinomas, with the signs of hypertension and hypokalemia resolving alone after the operation. Cats surviving the immediate postoperative period can survive for many years. Removal of the diseased adrenal gland has been shown to normalize RAAS and cure hypokalemia. Hypertension is improved in all patients and cured in up to 82% of the patients. With cats that cannot undergo a medical procedure for example have bilateral adenoma, the disease can be managed with a medical approach, which consists of spironolactone therapy, potassium supplementation, and antihypertensive drugs as needed. Spironolactone is an aldosterone antagonist that binds to the aldosterone receptors in the DCT (distal convoluted tube). Been reported the survival time of cats treated medically for primary hyperaldosteronism is between months to years. 7. Conclusion In this study, we examined the causes of Primary hyperaldosteronism (PHA) in felines. We researched the clinical signs and the etiology of the disease. After examining the chemistry of the blood including potassium, chloride, magnesium, glucose, phosphate, creatinine, urea, and creatinine kinase level of the blood plasma, and concluding the results of abnormalities, we can confirm our diagnosis of Primary hyperaldosteronism by using ultrasound test and for the discloser of the diagnosis magnetic resonance imaging and CT. After the diagnosis is done, there are 2 types of treatments possible: Either surgery, by the removal of the adrenal gland or in the case of a cat who cannot handle the surgery, the medical approach is more recommended which includes supplementary of potassium as well as prescription of spironolactone therapy and antihypertensive drugs.

8. Discussion

Primary hyperaldosteronism (PHA) is the most common adrenocortical disease in cats. This essay aims to aid by providing a more accurate diagnosis for practitioners by describing the clinical findings, diagnosis, and ways of treatment of PHA. Many cats are often being diagnosed with parallel diseases as they arrive at the clinics with systemic arterial hypertension and/or hypokalemia, especially in cats of older age. These can include chronic kidney disease, hyperthyroidism, and cardiac disease. After these diagnoses are concluded, they hinder the diagnosis of PHA. The clinical signs in cats with these parallel diseases are predominated by PHA and include polyuria, polyphagia, poor coat condition, thin fragile skin, and a potbellied appearance. As a result of this false diagnosis, cats might not get the right treatment. The diagnosis of hyperaldosteronism begins with a simple blood test, which can indicate a medical condition of hypokalemia. However, further diagnostic tests are needed. Then, the aldosterone-to-renin ratio (ARR) testing is used to distinguish the primary hyperaldosteronism from the secondary hyperaldosteronism, specifically, the ratio of plasma aldosterone to plasma renin activity is measured. That is the most sensitive test one can do according to our current knowledge. The reference value of 0.3 - 3.8 indicates cats with adrenocortical tumors due to increased levels of plasma aldosterone levels, accompanied by decreased plasma renin levels, which demonstrates a tendency of a tumor to be present in the adrenocortical area. Another test is the ultrasound of the abdomen by which we can detect an extended invasion of mass towards the caudal vena cava, as well as metastasis in other abdominal organs, but the limit in this method is the difficulty to diagnose it and tumor might be unnoticed before surgery. As for neuromuscular signs, hypokalemia affects the depolarization of nerve and muscle membranes, and because of that cats that have hypokalemia are likely to present more neuromuscular signs. While potassium concentration (K+1) <2.5 mmol/l being below the average potassium level in a feline and is frequently associated with clinical signs but no connection was found between extracellular potassium concentration and clinical signs, a fact which indicates a limit in our information. It is more necessary paying attention to the more common hypokalemic polymyopathy in cats with adrenal tumors, as the cases of bilateral adrenal hyperplasia are less commonly observed.

9. References

Bento, D. D., Zahn, F. S., Duarte, L. C., & Machado, L. H. D. A. (2016). Feline primary hyperaldosteronism: an emerging endocrine disease. Ciência Rural, 46, 686-693. Djajadiningrat-Laanen, S. C., Galac, S., & Kooistra, H. (2011). Primary hyperaldosteronism: expanding the diagnostic net. Journal of feline medicine and surgery, 13(9), 641-650. Fernandez, Y., Seth, M., & Murgia, D. (2016). Feline primary hyperaldosteronism: clinical and surgical approach. Companion Animal, 21(3), 146-153. Schulman, R. L. (2010). Feline primary hyperaldosteronism. Veterinary Clinics: Small Animal Practice, 40(2), 353-359.

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