同学： 以下是同学对医三期末考题有?惑的地方，已请老师们作解答了喔， 请看！ 第42题： D选项"IVIG"有同学认为应为"VZIg"或"IVIg"。 （ C ）42. 下列叙述关於varicella-zoster virus (VZV)何者为非？ （A）带状疱疹为潜伏於神经结的VZV病毒，经活化後 沿着其分布的神经皮节散布所造成 （B）诊断确认方法包括有观察水泡内巨细胞及细胞核包 溶物、血清抗体变化、抗原测定、病毒培养及PCR 等 （C）VZV病毒可通过胎盘，而VZV-IgG病毒抗体则无法 通过胎盘 （D）对於周产期水痘、早产儿治疗水痘可使用 IVIG(免疫球蛋白) 张老师回覆 Dear 彩凤 D选项为Intravenous immunoglobulin (IVIG)没错 第40题： 有同学认为B、C、D三选项皆为末期临床表徵。 （ C ）40. 下列何者不是人类免疫缺乏病毒的初期临床表徵？ （A）疲倦 （B）全身性淋巴肿大 （C）弓浆虫（Toxoplasmosis） （D）卡波西氏肉瘤（Kaposi's sarcoma） 许老师回覆 你好! 本题之关键在於希望同学了解机会性感染 (如Taxoplasma)为 AIDS病患晚期临床表徵之特色， 其他选项（A）疲倦　　 （B）全身性淋巴肿大（D）卡波西氏肉瘤（Kaposi's sarcoma） 虽然在晚期也可能有，但在早期临床表徵均可能出现，因此答案选C, 只有Taxoplasma不是初期临床表徵。谢谢! 第6题：有同学认为（D）decreased potassium intake应该也不会 增加肾素分泌。 （ B ）6. 有关肾素 (rennin) 分泌之调控，下列何者不会增加肾素 分泌： （A）decreased in afferent arteriolar perfusion pressure （B）increased delivery of filtered sodium to the macula densa （C）sympathetic nervous system increase adenyl cyclase activity （D）decreased potassium intake 第27题： 有同学认为anti-platelet antibody也可能透过针对 soluble antigen的IgG﹝即Type III Hypersensitivity﹞。 （ B ）27. 血小板抗体 (anti-platelet antibody) 是透过下列何种 反应与血小板作用而使病人血小板降低： （A）Type I Hypersensitivity （B）Type II Hypersensitivity （C）Type III Hypersensitivity （D）Type IV Hypersensitivity 刘老师回覆 From Harrison's: The amount of renin released reflects the combined effects of four interdependent factors. The juxtaglomerular cells, which are specialized myoepithelial cells that cuff the afferent arterioles, act as miniature pressure transducers, sensing renal perfusion pressure and corresponding changes in afferent arteriolar perfusion pressures. For example, a reduction in circulating blood volume leads to a corresponding reduction in renal perfusion pressure and afferent arteriolar pressure ( Fig. 321-5). This change is perceived by the juxtaglomerular cells as a decreased stretch exerted on the afferent arteriolar walls, and the juxtaglomerular cells release more renin into the renal circulation. This results in the formation of angiotensin I, which is converted in the kidney and peripherally to angiotensin II by ACE. Angiotensin II influences sodium homeostasis via two major mechanisms: it changes renal blood flow so as to maintain a constant glomerular filtration rate, thereby changing the filtration fraction of sodium, and it stimulates the adrenal cortex to release aldosterone. Increasing plasma levels of aldosterone enhance renal sodium retention and thus result in expansion of the extracellular fluid volume, which, in turn, dampens the stimulus for renin release. In this context, the renin-angiotensin-aldosterone system regulates volume by modifying renal hemodynamics and tubular sodium transport. A second control mechanism for renin release is centered in the macula densa cells, a group of distal convoluted tubular epithelial cells directly opposed to the juxtaglomerular cells. They may function as chemoreceptors, monitoring the sodium (or chloride) load presented to the distal tubule. Under conditions of increased delivery of filtered sodium to the macula densa, a signal is conveyed to decrease juxtaglomerular cell release of renin, thereby modulating the glomerular filtration rate and the filtered load of sodium. The sympathetic nervous system regulates the release of renin in response to assumption of the upright posture. The mechanism is either a direct effect on the juxtaglomerular cell to increase adenyl cyclase activity or an indirect effect on either the juxtaglomerular or the macula densa cells via vasoconstriction of the afferent arteriole. Finally, circulating factors influence renin release. Increased dietary intake of potassium decreases renin release, whereas decreased potassium intake increases it. The significance of these effects is unclear. Angiotensin II exerts negative feedback control on renin release that is independent of alterations in renal blood flow, blood pressure, or aldosterone secretion. Atrial natriuretic peptides also inhibit renin release. Thus, the control of renin release involves both intrarenal (pressor receptor and macula densa) and extrarenal (sympathetic nervous system, potassium, angiotensin, etc.) mechanisms. Steady-state renin levels reflect all these factors, with the intrarenal mechanism predominating. 是textbook说的，不是我 (最後一段) --

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