同學： 以下是同學對醫三期末考題有?惑的地方，已請老師們作解答了喔， 請看！ 第42題： D選項"IVIG"有同學認為應為"VZIg"或"IVIg"。 （ C ）42. 下列敘述關於varicella-zoster virus (VZV)何者為非？ （A）帶狀皰疹為潛伏於神經結的VZV病毒，經活化後 沿著其分佈的神經皮節散佈所造成 （B）診斷確認方法包括有觀察水泡內巨細胞及細胞核包 溶物、血清抗體變化、抗原測定、病毒培養及PCR 等 （C）VZV病毒可通過胎盤，而VZV-IgG病毒抗體則無法 通過胎盤 （D）對於周產期水痘、早產兒治療水痘可使用 IVIG(免疫球蛋白) 張老師回覆 Dear 彩鳳 D選項為Intravenous immunoglobulin (IVIG)沒錯 第40題： 有同學認為B、C、D三選項皆為末期臨床表徵。 （ C ）40. 下列何者不是人類免疫缺乏病毒的初期臨床表徵？ （A）疲倦 （B）全身性淋巴腫大 （C）弓漿蟲（Toxoplasmosis） （D）卡波西氏肉瘤（Kaposi's sarcoma） 許老師回覆 妳好! 本題之關鍵在於希望同學了解機會性感染 (如Taxoplasma)為 AIDS病患晚期臨床表徵之特色， 其他選項（A）疲倦　　 （B）全身性淋巴腫大（D）卡波西氏肉瘤（Kaposi's sarcoma） 雖然在晚期也可能有，但在早期臨床表徵均可能出現，因此答案選C, 只有Taxoplasma不是初期臨床表徵。謝謝! 第6題：有同學認為（D）decreased potassium intake應該也不會 增加腎素分泌。 （ B ）6. 有關腎素 (rennin) 分泌之調控，下列何者不會增加腎素 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題： 有同學認為anti-platelet antibody也可能透過針對 soluble antigen的IgG﹝即Type III Hypersensitivity﹞。 （ B ）27. 血小板抗體 (anti-platelet antibody) 是透過下列何種 反應與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 劉老師回覆 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說的，不是我 (最後一段) --

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