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health homework helper Both personal and family history can influence the risk of developing breast cancer can you buy cialis over the counter in south africa. For example, a woman who has a history of breast cancer has a fivefold increase in risk of developing contralateral breast cancer. Prior histories of cancers involving the uterus and ovary also appear to be associated with an increased risk of developing breast cancer. Breast tissue with atypical changes appears to be a premalignant lesion. Even though family history is often linked to disease risk, the percentage of familial breast cancer, in reality, is quite low (ie, ~10%). Nonetheless, clarification of several key elements related to family history includes findings that. •• a first-degree relative (ie, mother or sister) with breast cancer is associated with a 3-fold increase in risk. •• a first-degree relative diagnosed with breast cancer younger than 45 years is associated with a more than threefold increase in risk. 1317 1318  section 16  |  oncologic disorders extrinsic components table 89–1  risk of developing breast cancer. Seer areas, women, all races, 2008 to 2010 age interval (years) probability (%) of developing invasive breast cancer during the interval 30–40 40–50 50–60 60–70 from birth to death 0. 44 or 1 in 227 1. 45 or 1 in 69 2. 31 or 1 in 43 3. 49 or 1 in 29 12. 15 or 1 in 8 seer, surveillance, epidemiology and end results. Probability derived by devcan 6. 7. 0, june 2013 ( surveillance. Cancer. Gov/devcan). •• multiple first-degree relatives with breast cancer have not been consistently shown to be associated with risk greater than one first-degree relative. •• a second-degree relative with breast cancer is associated with 1. 5-fold increase in risk. •• family members on the paternal side contribute to risk similar to the maternal side. A number of endocrine factors have been linked to an increased risk for breast cancer. Many of the risks relate to the total duration of estrogen exposure. Hence, early menarche (before age 12 years) and late menopause (after age 55 years) are associated with an increased risk of the disease. Support for this association is the finding that bilateral oophorectomy before age 35 years decreases the relative risk of developing breast cancer. Nulliparity and late age at first birth (30 years or older) have been reported to double the lifetime risk of developing breast cancer.

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teacher career essay However, if the sa node fails to generate depolarizations at a can you buy cialis over the counter in south africa rate faster than that of the av node, the av node may take over as the pacemaker. If both the sa node and av node fail to generate depolarizations at a rate more than 30 to 40 per minute, ventricular tissue may take over. Ventricular action potential ventricular action potential is depicted in figure 9–2. Ventricular myocyte resting membrane potential is usually –70 to –90 mv, due to the action of the sodium–potassium adenosine triphosphatase (atpase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane slowly increases to a threshold potential due to a slow influx of sodium into the cell, raising the threshold to –60 to –80 mv. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to enter the cell rapidly. This rapid influx of positive ions creates a vertical upstroke of the action potential, such that r t 1 mv p q +30 + na 140 k+ 4 2+ ca 2 myocardial cell ecg s phase 1. Transient efflux of k+ phase 2. Influx of ca2+ and na+ 0 10 mm 135" 10 mm extracellular fluid overshoot phase 3. Efflux of k+ greater than influx of ca2+ and na+ phase 0. Fast na+ influx tension mv −70 threshold (internal – external potential) = phase 4. Na+ - k+ - pump contraction −90 0 absolute refractory period fast na+-channels are closed steep phase 0 means rapid depolarization relative refractory period 300 ms kmc figure 9–2. The ventricular action potential depicting the flow of specific ions responsible for each phase. The phases of the action potential that correspond to the absolute and relative refractory periods are portrayed, and the relationship between phases of the action potential and the electrocardiogram (ecg) are shown. (ca, calcium. K, potassium. Na, sodium.

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http://projects.csail.mit.edu/courseware/?term=essay-on-online-classes essay on online classes The resulting increase in afterload contributes to an increase in myocardial oxygen demand and opposes the desired increase in sv. In the kidneys, angiotensin ii enhances renal function acutely by raising intraglomerular pressure through constriction of the efferent arterioles. 6 however, the increase in glomerular filtration pressure may be offset by a reduction in renal perfusion secondary to angiotensin ii’s influence over the release of other vasoactive neurohormones such as vasopressin and endothelin-1 (et-1). Angiotensin ii also potentiates the release of aldosterone from the adrenal glands and norepinephrine from adrenergic nerve terminals. Additionally, angiotensin ii induces vascular hypertrophy and remodeling in both cardiac and renal cells. Clinical studies show that blocking the effects of the raas in hf is associated with improved cardiac function and prolonged survival. Thus, angiotensin-converting enzyme (ace) inhibitors and angiotensin receptor blockers (arbs) are the cornerstone of hf treatment. Aldosterone  aldosterone’s contribution to hf pathophysiology is multifaceted. Renally, aldosterone causes sodium and water retention in an attempt to enhance intravascular volume and co. This adaptive mechanism has deleterious consequences because excessive sodium and water retention worsen the already elevated ventricular filling pressures. Aldosterone also contributes to electrolyte abnormalities seen in hf patients. Hypokalemia and hypomagnesemia contribute to the increased risk of arrhythmias. In addition, evidence supports the role of aldosterone as an etiological factor for myocardial fibrosis and cardiac remodeling by causing increased extracellular matrix collagen deposition and cardiac fibrosis. 6 aldosterone potentially contributes to disease progression via sympathetic potentiation and ventricular remodeling. In addition, the combination of these multiple effects is likely responsible for the increased risk of sudden cardiac death attributed to aldosterone. As elevated aldosterone concentrations have been associated with a poorer prognosis in hf, its blockade has become an important therapeutic target for improvement of long-term prognosis. Norepinephrine  norepinephrine is a classic marker for sns activation. It plays an adaptive role in the failing heart by stimulating hr and myocardial contractility to augment co and by producing vasoconstriction to maintain organ perfusion. However, excess levels are directly cardiotoxic. In addition, sympathetic activation increases the risk for arrhythmias, ischemia, and myocyte cell death through increased myocardial workload and accelerated apoptosis. Ventricular hypertrophy and remodeling are also influenced by norepinephrine. 8 plasma norepinephrine concentrations are elevated proportionally to hf severity, with highest levels correlating to the poorest prognosis. Several mechanisms relate to diminished responsiveness to catecholamines (eg, norepinephrine) as cardiac function declines. 6 adrenergic receptor desensitization and downregulation (decreased receptor number and postreceptor responses and signaling) occurs under sustained sympathetic stimulation. The desensitization contributes to further release of norepinephrine. Β-adrenergic blocking agents, although intrinsically negatively inotropic, have become essential therapy for chronic hf. Endothelin  et-1, one of the most potent physiological vasoconstrictors, is an important contributor to hf pathophysiology. 9 et-1 binds to two g-protein coupled receptors, endothelin-a (et-a) and endothelin-b (et-b). Et-a receptors mediate vasoconstriction and are prevalent in vascular smooth muscle and cardiac cells. Et-b receptors are expressed on the endothelium and in vascular smooth muscle, and receptor stimulation mediates vasodilation and endothelin clearance.

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https://graduate.uofk.edu/user/diploma.php?sep=american-government-homework-help american government homework help Levels of et-1 correlate with hf functional class and mortality. Arginine vasopressin  higher vasopressin concentrations are linked to dilutional hyponatremia and a poor prognosis in hf. Vasopressin exerts its effects through vasopressin type 1a (v1a) and vasopressin type 2 (v2) receptors. 5,7 v1a stimulation leads to vasoconstriction, whereas actions on the v2 receptor cause free water retention through aquaporin channels in the collecting duct. Vasopressin increases preload, afterload, and myocardial oxygen demand in the failing heart.

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