搜尋此網誌

2019年11月11日星期一

爸爸生病了

Hypertension can result from a change in cardiac output, a change in peripheral resistance, or both. The medications used for treating hypertension decrease peripheral resistance, blood volume, or the strength and rate of myocardial contraction.

Most of the people with high blood pressure are having primary hypertension, it is due to an unidentified cause. The remaining population have secondary hypertension, high blood pressure related to identified causes, such as renal disease.

Once identified, elevated blood pressure should be monitored at regular intervals, because hypertension is a lifelong condition.

Hypertension often accompanies other risk factors for atherosclerotic heart disease, such as dyslipidemia (abnormal blood fat levels), obesity, diabetes mellitus, metabolic syndrome, and a sedentary lifestyle.

High blood pressure can be viewed in three ways: as a sign, a risk factor for atherosclerotic cardiovascular disease, or a disease. As a sign, nurses and other healthcare professionals use blood pressure to monitor a patient's clinical status.

Prolonged blood pressure elevation eventually damages blood vessels throughout the body, particularly in target organs such as the heart, kidneys, brain, and eyes. The usual consequences of prolonged, uncontrolled hypertension are myocardial infarction, heart failure, renal failure, strokes, and impaired vision.

Although no precise cause can be identified for most cases of hypertension, it is understood that hypertension is a multi-factorial condition. Because hypertension is a sign, it is most likely to have many causes, just as fever has many causes. For hypertension to occur, there must be a change in one or more factors affecting peripheral resistance or cardiac output. In addition, there must also be a problem with the body's control systems that monitor or regulate pressure.

Many factors have been implicated as causes of hypertension:

  • Increased sympathetic nervous system activity related to dysfunction of the autonomic nervous system
  • Increased renal reabsorption of sodium, chloride, and water related to genetic variation in the pathways by which the kidneys handle sodium
  • Increased activity of the renin-angiotensin-aldosterone system, resulting in expansion of extracellular fluid volume and increased systemic vascular resistance
  • Decreased vasodilation of the arterioles related to dysfunction of the vascular endothelium
  • Resistance to insulin reaction, which may be a common factor linking hypertension, type 2 diabetes mellitus, hypertriglyceridemia, obesity, and glucose intolerance
Structural and functional changes in the heart and blood vessels contribute to increases in blood pressure that occur with age. These changes include accumulation of atherosclerotic plaque, fragmentation of arterial elastins, increased collagen deposits, and impaired vasodilation. The result of these changes is a decrease in the elasticity of the major blood vessels. Consequently, the aorta and large arteries are less able to accommodate the volume of blood pumped out by the heart, and the energy that would stretched the vessels instead elevates the systolic blood pressure.

Pathological changes in the kidneys (indicated by increased blood urea nitrogen and serum creatinine levels) may manifest as nocturia.

Smeltzer, S.C., & Bare, B.G. (2008). Brunner & Suddarth's Textbook of Medical-Surgical Nursing. Philadelphia, PA: LWW


Nocturia is a risk factor for morbidity and mortality but is frequently overlooked and underreported by patients and unrecognized by physicians. Epidemiologic studies reported that nocturnal voiding is associated not only with aging and benign prostatic hyperplasia, but also with many other clinical conditions. The majority of epidemiologic studies reported a significant relationship between nocturia and hypertension. However, the cause-and-effect relationship between them has not been established. Some physiopathological changes in hypertension are conducive (促成) to result in nocturia. These include the effects of hypertension on glomerular filtration and tubular transport, resetting of the kidney pressure-natriuresis relationship, atrial stretch and release of atrial natriuretic peptide when congestive heart failure complicates hypertension, and peripheral edema. Another link between hypertension and nocturia is obstructive sleep apnea. Furthermore, some evidence supports the relationship between nondipping behavior of blood pressure and an increased prevalence of nocturia. The use of some classes of antihypertensive agents may result in nocturia. The present review aims to provide a comprehensive evaluation of the epidemiologic evidence and physiopathological links that correlate hypertension and nocturia. Emphasis is placed on the need to take a pro-active attitude to detect and treat this hazardous condition.

Carlos, A. (2013). Nocturia in arterial hypertension: a prevalent, underreported, and sometimes underestimated association. Journal of the American Society of Hypertension, 7(1), 75-84. https://doi.org/10.1016/j.jash.2012.12.004

Natriuresis: excretion of sodium in the urine
A natriuretic peptide is a peptide which induces natriuresis.



For suspected cases of BPH, the doctor may carry out some investigations. These include rectal examination, blood tests, urine tests, ultrasound examination and procedures to obtain tissue samples for laboratory examination to isolate any cancerous cells.

沒有留言:

發佈留言