please respond to each discussion post with apa references for each minimum 6-8 sentences. Thank you!
- Describe the pathophysiology, clinical manifestations, evaluation, and treatment of two diseases of the posterior pituitary–syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus (DI).
SIADH and DI are two disorders that often get confused, however, they are opposite each other. SIADH is “Soaked Inside” and DI is “Dry Inside”. The one thing these two disorders have in common is the activity of ADH (Schnur, 2021).
The pathophysiology of Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is first caused by abnormally increased secretion of antidiuretic hormone (ADH) for no apparent reason. Other times there is a CNS disorder such as cancer, cardiopulmonary disorders, vascular diseases, and myxedema for the increased secretion of ADH. Medications such as antidepressants, antipsychotics, narcotics, and NSAIDS can also cause SIADH. The unusually high release of ADH will cause water retention, dilutional hyponatremia, and hypo-osmolarity (McCance & Huether 2014).
Clinical manifestations of SIADH include dilutional hyponatremia. Depending on how fast and severe the sodium levels are dropping will determine the extent of clinical manifestations. Increased thirst, dyspnea on exertion, and fatigue can manifest with sodium levels between 140-130 mEq/l. GI upset with vomiting and abdominal cramps are seen with sodium levels of 130-120 mEq/l. Sodium levels below 115 mEq/l will result in severe sometimes irreversible neurological changes (McCance & Huether, 2014).
Evaluation and Treatment need immediate attention once clinical manifestations are present. A diagnosis of SIADH requires urine and serum lab values to be obtained. Serum osmolality of less than 280 mOsm/kg and hyponatremia of less than 135 mEq/l. Urine hyperosmolarity, and urine sodium excretion match sodium intake.
Treatment includes correcting the cause of SIADH. The priority is to correct severe hyponatremia first with 3% hypertonic saline. Hyponatremia needs to be corrected slowly because too quick of a correction can cause an additional neurological problem called central pontine myelinolysis. Fluid restriction of 800-1000ml/day is also implemented. Continued monitoring of urine and serum lab values to monitor the hyponatremia and frequent neurological assessments to detect any neurological changes. Monitoring of vital signs and I & O’s are also included in the treatment plan (McCance & Huether, 2014)
Diabetes Insipidus (DI) is a decrease of ADH resulting in polyuria and polydipsia. Due to insufficient amounts of ADH being produced, there are three forms of DI with neurogenic (hypothalamic), which are the most common. Tumors, lesions, infection, and immunologic disorders disrupt the synthesis, transport, or release of ADH (McCance & Huether, 2014).
Clinical manifestations include polydipsia, and polyuria, with urine output of as much as 8-12L/day. Polydipsia with a continued thirst for cold drinks. Serum laboratory values will show hypernatremia. Urine lab values will be consistent with a low urine specific gravity because of the body’s inability to reabsorb water (McCance & Huether, 2014).
Evaluation and Treatment-It must first be confirmed that the problem is DI and not Diabetes Mellitus. A diagnosis of DI will reveal polydipsia, polyuria, low specific urine gravity, low urine osmolality, hypernatremia, and high serum osmolality. A water deprivation test will also rule out DI if the urine volume decreases with the decrease in water intake. Treatment will include treating the underlying causes and medication administration such as DDAVP (McCance & Huether, 2014)
McCance, K.L. & Huether, S.E. (Eds.). (2014). Pathophysiology: The biologic basis for disease
in adults and children. (7th. ed.). Elsevier Mosby. https://online.vitalsource.com/books/9780323088541
Schnur, M. B. (2021, October 21). Siadh versus di: What’s the difference? NursingCenter. Retrieved November 21, 2022, from https://www.nursingcenter.com/ncblog/october-2021/siadh-vs-di
2nd discussion post
An expansion of the prostate gland is referred to as benign prostatic hypertrophy (BPH), sometimes known as benign prostatic hypertrophy (Ng, 2022). Lower urinary tract symptoms frequently occur as a result of the prostatic tissue pushing down on the urethra when it travels through the prostate. Typically, males 60 years of age and older exhibit this. BPH and enlargement are linked to aging and androgens in the blood. The need to pass urine, a delay in beginning to urinate, and a weaker urine stream are the typical symptoms. Chronic cases result in prolonged urine retention and overflow incontinence (Huether & McCance, 2014).
A medical history, physical examination, and laboratory testing, such as a urinalysis, are used to make the diagnosis. Drugs have been used successfully to treat BPH. Smooth muscle in the bladder and prostate is relaxed using 1-adrenergic blockers (tamsulosin and prazosin). Antiandrogen medications, including finasteride (Proscar), specifically inhibit androgens at the cellular level of the prostate and cause the prostate gland to constrict (Huether & McCance, 2014).
Huether, S., McCance, K. (2014). Pathophysiology: The Biologic Basis for Disease in Adults and Children (7th ed.). Elsevier Health Sciences (US). https://online.vitalsource.com/books/9780323088541
Ng M, Baradhi KM. Benign Prostatic Hyperplasia. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558920/