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 

 Links to an external site.

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).

References

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/