泌尿系统梗阻、结石双语教案
留学生教学教师备课教案泌尿系统The Urinary System
Chapter 19. The Urinary SystemThe Urinary System: IntroductionThe urinary system consists of the paired kidneys and ureters, the bladder, and the urethra. This system helps maintain homeostasis by a complex combination of processes that involves the following:§Filtration of cellular wastes from blood§Selective reabsorption of water and solutes§Excretion of the wastes and excess water as urine.Urine produced in the kidneys passes through the ureters to the bladder for temporary storage and is then released to the exterior through the urethra. The two kidneys produce about 125 mL of filtrate per minute, of which 124 mL is reabsorbed in these organs and 1 mL is released into the ureters as urine. About 1500 mL of urine is formed every 24 hours. The kidneys also regulate the fluid and electrolyte balance of the body and are the site of production of renin, a protease that participates in the regulation of blood pressure by cleaving circulating angiotensinogen to angiotensin I. Erythropoietin , a glycoprotein that stimulates the production of erythrocytes, is also produced in the kidneys. The steroid prohormone vitamin D, initially produced in skin keratinocytes, is hydroxylated in kidneys to an active form (1,25-dihydroxyvitamin D3 or calcitriol ) involved in regulating calcium balance.KidneysEach kidney has a concave medial border, the hilum—where nerves enter, the ureter exits, and blood and lymph vessels enter and exit—and a convex lateral surface, both covered by a thinfibrous capsule (Figure 19–1). The expanded upper end of the ureter, called the renal pelvis, divides into two or three major calyces. Smaller branches, the minor calyces, arise from each major calyx. The area surrounding the calyces, called the renal sinus, usually contains considerable adipose tissue.Figure 19–1.Kidney.Each kidney is bean-shaped, with a concave hilum where the ureter and the renal artery and veins enter. The ureter divides and subdivides into several major and minor calyces, around which is located the renal sinus containing adipose tissue. Division of the parenchyma into cortex and medulla can also be seen grossly. Attached to each minor calyx is a renal pyramid, a conical region of medulla delimited by extensions of cortex. A renal pyramid with associated cortex constitutes a renal lobe. The cortex and hilum are covered with a fibrous capsule.The kidney has an outer cortex and an inner medulla (Figures 19–1 and 19–2). In humans, the renal medulla consists of 8–15 conical structures called renal pyramids, which are separated bycortical extensions called renal columns. Each medullary pyramid plus the cortical tissue at its base and along its sides constitutes a renal lobe (Figure 19–1).Figure 19–2.Nephrons.Within each renal lobe are hundreds of thousands of nephrons, the function unit of the kidney. Each nephron originates in the cortex, at the renal corpuscle associated with glomerular capillaries. Extending from the corpuscle is the proximal convoluted tubule, then the nephron loop (of Henle) into the medulla and back to the cortex, then the distal convoluted tubule and collecting tubule which merges into a collecting duct for urine transport to the calyx. All nephrons are located completely within the cortex except for their medullary loops. Juxtamedullary nephrons usually have much longer loops than cortical nephrons.Each kidney contains 1–1.4 million functional units called nephrons (Figure 19–2). The major divisions of each nephron are:§Renal corpuscle, an initial dilated portion in the cortex§Proximal convoluted tubule, located primarily in the cortex§Thin and thick limbs of the nephron loop (loop of Henle), which descend into the medulla, then ascend back to the cortex§Distal convoluted tubule§Collecting tubule.Collecting tubules from several nephrons converge into collecting ducts which carry urine to the calyces and the ureter. Cortical nephrons are located almost completely in the cortex while juxtamedullary nephrons close to the medulla have long loops in the medulla (Figure 19–2) Blood CirculationAs expected for an organ specialized to process the blood, the anatomical organization of the kidney vasculature and its associations with nephron components are very important. Blood vessels of the kidney are named according to their precise locations or shapes (Figure 19–3). Figure 19–3.Blood supply to the kidney.A coronal view (left) shows the major blood vessels of the kidney. The microvascular components extending into the cortex and medulla from the interlobular vessels are shown on the right. Pink boxes indicate vessels with arterial blood and blue indicate the venous return. The intervening lavender boxes and vessels are intermediate sites where most reabsorbed material re-enters the blood.Each kidney receives blood from a renal artery, which divides into two or more segmental arteries at the hilum. In the renal sinus these branch further to form the interlobar arteries extending between the renal pyramids toward the corticomedullary junction (Figure 19–3). Here the interlobar arteries branch further to form the arcuate arteries which travel in an arc along this junction at the base of each renal pyramid. Smaller interlobular arteries branch off at right angles from the arcuate arteries and enter the cortex.From the interlobular arteries arise the microvascular afferent arterioles, which supply blood to a tuft of capillaries called the glomerulus, each of which is associated with a renal corpuscle (Figures 19–3 and 19–4). Blood leaves the glomerular capillaries, not via venules, but via the efferent arterioles, which at once branch again to form another capillary network, the peritubular capillaries that nourish cells of the proximal and distal tubules and carry away reabsorbed substances. The efferent arterioles associated with glomeruli near the medulla continue as long, straight vessels directly into the medulla providing nutrients and oxygen there, and then loop back into the cortex as venules. These small medullary vessels and their intervening capillary plexuses comprise the vasa recta (L. recta, straight).Figure 19–4.Microvasculature of the renal cortex.(a): Cortical vasculature is revealed in a section of kidney with the renal artery injected with carmine dye before fixation. Having branched at right angles off the arcuate arteries, small interlobular arteries (I) run straight out through the cortex and give off the afferent arterioles (A) which bring blood to the glomerular capillaries. Each glomerulus (G) contains a loose mass of capillaries with nearly a centimeter in total length. These drain into an efferent arteriole which then branches as a large, diffuse network of peritubular capillaries (PT) throughout the cortex. X125. (b): A section of one glomerulus shows many capillaries and the closely associated cells of the renal corpuscle's internal visceral layer. The thick basement membrane of these glomerular capillaries contains much type IV collagen and is visible around the cut capillaries (arrows). Also shown are the simple squamous external parietal layer of the capsule and the vascular pole where the arterioles enter the corpuscle and the macula densa (arrowhead) is located. X400. PSH.Blood leaves the kidney in veins that follow the same courses as arteries and have the same names (Figure 19–3). The outermost peritubular capillaries and capillaries in the kidney capsule converge into small stellate veins which empty into the interlobular veins.Renal Corpuscles & Blood FiltrationAt the beginning of each nephron is a renal corpuscle, about 200 m in diameter and containing a loose knot of capillaries, the glomerulus, surrounded by a double-walled epithelial capsule called the glomerular (Bowman's) capsule (Figures 19–2 and 19–5). The internal layer (visceral layer) of the capsule closely envelops the glomerular capillaries . The external parietal layer forms the outer surface of the capsule. Between the two capsular layers is the urinary or capsular space, which receives the fluid filtered through the capillary wall and the visceral layer. Each renal corpuscle has a vascular pole, where the afferent arteriole enters and the efferent arteriole leaves, and a urinary or tubular pole, where the proximal convoluted tubule begins (Figure 19–5). After entering the renal corpuscle, the afferent arteriole usually divides and subdivides into the two to five capillaries of the renal glomerulus.Figure 19–5.Renal corpuscles.(a): The renal corpuscle is a small mass of capillaries called the glomerulus housed within a bulbous glomerular capsule. The internal lining of the capsule is composed of complex epithelial cells called podocytes, which cover each capillary, forming filtration slits between interdigitating processes called pedicels. Blood enters and leaves the glomerulus through the afferent and efferent arterioles respectively. (b): The micrograph shows the major histological features of a renal corpuscle. H&E. X300. (c): Filtrate is produced in the corpuscle when blood plasma is forced under pressure across the filtration membrane of the glomerular capillary wall and through the filtration slits between the pedicels of podocyte processes. (d): The SEM shows the distinctive appearance of podocytes and their processes covering glomerular capillaries. X800The parietal layer of a glomerular capsule consists of a simple squamous epithelium supported externally by a basal lamina and a thin layer of reticular fibers. At the tubular pole, this epithelium changes to the simple cuboidal epithelium characteristic of the proximal tubule (Figure 19–5). During embryonic development, the simple epithelium of the parietal layer remains relatively unchanged, whereas the internal or visceral layer is greatly modified. The cells of this layer, the podocytes (Figures 19–5d and 19–6), have a cell body from which arise several primary processes. Each primary process gives rise to numerous secondary (foot) processes or pedicels (L. pedicellus, little foot) that embrace a portion of one glomerular capillary (Figures 19–5d and 19–6). The cell bodies of podocytes do not contact the basement membrane of the capillary, but each pedicel is in direct contact with this structure (Figure 19–6).Figure 19–6.Glomerular filtration barrier.The glomerular filtration barrier consists of three layered components: the fenestrated capillary endothelium, the glomerular basement membrane, and filtration slits between podocyte processes. The major component of the filter is formed by fusion of the basal laminae of a podocyte and a capillary endothelial cell. (a): TEM showing cell bodies of two podocytes (PC) and the series of pedicels on the glomerular basement membrane separated by the filtration slits (arrows). On the other side of the membrane is the thin lining of a capillary (C) endothelial cell, with fenestrations. Together these openings allow filtration of liquid from plasma into the urinary space (US) of Bowman's capsule. X10,000. (b): At higher magnification, both the fenestrations (arrowhead) in the capillary endothelium (E) and the filtration slits (arrows) separating the pedicels (P) are better seen on the two sides of the fused basal laminae (BL). The endothelial fenestrations in glomeruli lack diaphragms, but very thin slit diaphragms cross the space between pedicels and play an important role in filtration. X45,750.The pedicels interdigitate, defining elongated spaces 30–40 nm wide—the filtration slits (Figure 19–6). Spanning adjacent processes (and thus bridging the filtration slits) is a thin semipermeable diaphragm of uniform thickness (Figure 19–6). These slit diaphragms are a highly specialized type of intercellular junction in which the large transmembrane protein nephrin is important both structurally and functionally. Projecting from the cell membrane on each side of the slit, nephrin molecules interact to form a porous structure within the diaphragm.Between the highly fenestrated endothelial cells of the capillaries and the covering podocytes is the thick (~0.1m) glomerular basement membrane (Figure 19–6). This membrane is the mostsubstantial part of the filtration barrier separating the blood in the capillaries from the capsular space. It is formed by the fusion of capillary- and podocyte-produced basal laminae and is maintained by the podocytes. Laminin and fibronectin in this fused basement membrane bind integrins of both the podocyte and endothelial cell membranes. The meshwork of type IV collagen cross-linked in a matrix of negatively charged proteoglycans may help restrict the passage of cationic molecules. Thus, the glomerular basement membrane (GBM) is a selective macromolecular barrier which acts as a physical filter and as a barrier against negatively charged molecules.The initial glomerular filtrate has a chemical composition similar to that of the blood plasma except that it contains very little protein because macromolecules do not readily cross the glomerular filter. Proteins and other particles greater than 10 nm in diameter or exceeding 70 kDa, the approximate molecular mass of albumin, do not readily cross the glomerular barrier.MEDICAL APPLICATIONIn diseases such as diabetes mellitus and glomerulonephritis, the glomerular filter is altered and becomes much more permeable to proteins, with the subsequent release of protein into the urine (proteinuria). Proteinuria is an indicator of many potential kidney disorders.Glomerular capillaries are uniquely situated between two arterioles—afferent and efferent—the muscle of which allows increased hydrostatic pressure in these vessels, favoring movement of plasma across the glomerular filter. The glomerular filtration rate (GFR) is constantly regulated by neural and hormonal inputs affecting the degree of constriction in each of these arterioles. The total glomerular filtration area of an average adult has been estimated at 500 cm2 and the average GFRat 125 mL per minute or 180 liters per day. Because the total amount of circulating plasma averages 3 L, it follows that the kidneys typically filter the entire blood volume 60 times every day. In addition to capillary endothelial cells and podocytes, renal corpuscles also contain mesangial cells (Gr. mesos, in the midst, + angeion, vessel) (Figure 19–7), which resemble pericytes in producing components of an enveloping external lamina. Mesangial cells are difficult to distinguish in routine sections form podocytes, but often stain more darkly. They and their surrounding matrix comprise the mesangium (Figure 19–7), which fills interstices between capillaries that lack podocytes. Functions of the mesangium are many and varied, and include the following:§ Physical support and contraction—the mesangium provides internal structural support to the glomerulus and like pericytes, its cells respond to vasoactive substances to help maintainhydrostatic pressure for the optimal rate of filtration.§ Phagocytosis—mesangial cells phagocytose protein aggregates that adhere to the glomerular filter, including antibody-antigen complexes abundant in many pathological conditions.§ Secretion—the cells synthesize and secrete several cytokines, prostaglandins, and other factors important for immune defense and repair in the glomerulus.Figure 19–7.Mesangium.(a): Diagram showing that mesangial cells in renal corpuscles are located between capillaries and are enveloped by a dense extracellular matrix like that of the basement membrane around the capillaries. (b): The TEM shows one mesangial cell (MC) and the amorphous mesangial matrix (MM) surrounding it. This matrix appears similar and in many places continuous with basement membrane (BM). The matrix helps support capillary loops where podocytes are lacking. Mesangial cells extend processes (arrows) around capillaries which may affect their state of contraction. Some mesangial processes appear to pass between endothelial cells (EC) into the capillary lumen (asterisks) where they may help remove or endocytose adherent protein aggregates. The capillary at the left contains an erythrocyte (E) and a leukocyte (L). Podocytes (P) and their pedicels (PD) open to the urinary space (US) and associate with the capillary surfaces not covered by mesangial cells.Proximal Convoluted TubuleAt the tubular pole of the renal corpuscle, the squamous epithelium of the capsule's parietal layer is continuous with the cuboidal epithelium of the proximal convoluted tubule (Figures 19–8 and 19–9). This very tortuous tubule is longer than the distal convoluted tubule and is therefore more frequently seen in sections of renal cortex. Cells of the proximal tubule reabsorb 60–65% of the water filtered in the renal corpuscle, along with almost all of the nutrients, ions, vitamins, and smallplasma proteins. The water and its solutes are transferred directly across the tubular wall andimmediately taken up by the peritubular capillaries.Figure 19–8.Renal cortex: Proximal and distal convoluted tubules.(a): The micrograph shows the continuity at a renal corpuscle's tubular pole (TP) between the simple cuboidal epithelium of a proximal convoluted tubule (P) and the simple squamous epithelium of the capsule's parietal layer. The urinary space (U) between the parietal layer and the glomerulus (G) drains into the lumen of the proximal tubule. The lumen of the proximal tubules appear filled, due to the long microvilli of the brush border and aggregates of small plasma proteins bound to this structure. By contrast, the lumens of distal convoluted tubules (D) appear empty, lacking a brush border and protein.(b): In another section the abundant peritubular capillaries and draining venules surrounding the proximal and distal convoluted tubules are indicated (arrows). Fibroblastic interstitial cells of the cortex are the source of erythropoietin, the growth factor secreted in response to a prolonged decrease in the local oxygen concentration. Both X400. H&E.Figure 19–9.Convoluted tubules, nephron loops, and collecting ducts.(a): In this diagram major regions of the nephron are distinguished by different colors. (b): A micrograph of the renal cortex allows comparison of the wide, eosinophilic proximal convoluted tubules with the smaller, less well-stained distal convoluted tubules. X160. H&E. (c): Diagram shows the differences in size and in microvilli between the cuboidal cells of proximal and distal tubules. Cells of both tubules have basal membrane invaginations associated with mitochondria. (d): Micrograph shows the simple squamous and cuboidal epithelia of the nephron loop thin limbs and thick limbs respectively, as well as the pale columnar cells of the collecting ducts. X160. Mallory trichrome.The cells of the proximal tubules have acidophilic cytoplasm (Figures 19–8 and 19–9) because of the presence of numerous mitochondria. The cell apex has abundant long microvilli which form a prominent brush border for reabsorption (Figures 19–8, 19–9, and 19–10). Because the cells are large, each transverse section of a proximal tubule typically contains only three to five rounded nuclei. In routine histologic preparations, the brush border may be disorganized and give the lumens a fuzz-filled appearance. Capillaries and other microvascular components are abundant in the sparse surrounding connective tissue (Figure 19–8).Figure 19–10.Ultrastructure of proximal convoluted tubule cells.TEM reveals important features of the cuboidal cells of the proximal convoluted epithelium: the long, dense apical microvilli (MV), the abundant pinocytotic pits and vesicles (V) in the apical regions near lysosomes (L). Small proteins brought into thecells nonspecifically by pinocytosis are degraded in lysosomes and the amino acids released basally. Apical ends of adjacent cells are sealed with zonula occludens, but the basolateral sides are characterized by long invaginating folds of membrane along which many long mitochondria (M) are situated. These folds provide a greatly increased surface area for pumping of ions across the membrane. Water and the small molecules released from the proximal convoluted tubules are taken up immediately by the adjacent peritubular capillaries (C). Between the basement membranes of the tubule and the capillary shown here is an extension of a fibroblast (F). X10,500.Ultrastructurally the apical cytoplasm of these cells has numerous pits and vesicles near the bases of the microvilli, indicating active pinocytosis (Figure 19–10). The pinocytotic vesicles contain small plasma proteins (with a molecular mass less than 70 kDa) that passed through the glomerular filter. The vesicles fuse with lysosomes for proteolysis and amino acids are released to the circulation. The cells also have many long basal membrane invaginations and lateral interdigitations with neighboring cells (Figure 19–10). The Na+/K+-ATPase (sodium pump) responsible for actively transporting sodium ions out of the cells is localized in these basolateral membranes. Long mitochondria are concentrated along the basal invaginations (Figure 19–9), characteristically for cells engaged in active ion transport. Because of the extensive interdigitations of the lateral membranes, discrete limits between cells of the proximal tubule are difficult to see in the light microscope. The proximal convoluted tubules actively reabsorb all the glucose and amino acids in the filtrate and about 85% of the sodium chloride and other ions. This absorption involves the membrane sodium pumps. Water diffuses passively, following the osmotic gradient. When the amount of glucose in the filtrate exceeds the absorbing capacity of the proximal tubule, as in diabetes, urine becomes more abundant and contains glucose.In addition to these activities, cells of the proximal convoluted tubules can also move substances from the peritubular capillaries into the tubular lumen, an active process referred to as tubular secretion. Organic anions such as choline and creatinine and many foreign compounds such as penicillin are excreted in this manner, which allows kidneys to dispose of such substances at ahigher rate than by glomerular filtration alone. The cells of the proximal tubule are also involved in vitamin D hydroxylation.Nephron Loop (of Henle)The proximal convoluted tubule continues as a much shorter proximal straight tubule which enters the medulla and becomes the nephron loop. This is a U-shaped structure with a descending limb and an ascending limb, both composed of simple epithelia, cuboidal near the cortex, but squamous deeper in the medulla (Figure 19–2). In the outer medulla, the straight portion of the proximal tubule, with an outer diameter of about 60 m, narrows abruptly to about 12 m and continues as the nephron loop's thin descending limb. The lumen of this segment of the nephron is wide and the wall consists of squamous epithelial cells whose nuclei protrude slightly into the lumen (Figures 19–9 and 19–11).Figure 19–11.Renal medulla: Nephron loops and collecting ducts.(a): A micrograph of a medullary pyramid cut transversely shows closely packed cross sections of the many nephron loops' thin descending limbs (T) and thick ascending limbs (A), intermingled with parallel vasa recta capillaries (C). All these structures are embedded in the interstitium (I) which contains sparse myofibroblast-like cells in a matrix very rich in hydrophilic hyaluronate. The specialized nature of the interstitial tissue helps maintain the osmolarity gradient established by differential salt and water transport across the wall of the nephron loop which is required to concentrate urine and conserve body water. X400. Mallory trichrome. (b): The TEM reveals the slightly fibrous nature of the interstitium (I) and shows that the simple squamous epithelium of the thin limbs (T) is slightly thicker than that of the nearby vasa recta capillaries (C). X3300.Approximately one seventh of all nephrons are located near the corticomedullary junction and are therefore called juxtamedullary nephrons, which are of prime importance in the mechanism that allows the kidneys to produce concentrated, hypertonic urine. Juxtamedullary nephrons usually have long loops, extending deep into the medulla, with short thick proximal straight segments, long thin descending and ascending limbs, and long thick ascending limbs (Figure 19–2).The nephron loop and surrounding tissue are involved in making urine hypertonic and conserving water; only animals with such loops are capable of concentrating urine and thus conserving body water. Cuboidal cells of the loops' thick ascending limbs actively transport sodium chloride out of the tubule against a concentration gradient into the hyaluronate-rich interstitial connective tissue, making that compartment hyperosmotic. Squamous cells of the loops' thin descending limbs are freely permeable to water but not salts, while the thin ascending limbs are permeable to NaCl but impermeable to water. Flow of the filtrate in opposite directions (countercurrent flow) in the two parallel limbs of nephron loops establishes a gradient of osmolarity in the interstitium of the medullary pyramids and countercurrent blood flow in the loops of the vasa recta help maintain this gradient. The interstitial osmolarity at the pyramid tips is about four times that of the blood. The high interstitial osmolarity draws water passively from the collecting ducts in the medullary pyramids (Figures 19–2 and 19–11), concentrating the urine. Water permeability of these ducts is increased by antidiuretic hormone (ADH), which is released from the pituitary when body water is low. The water thus saved immediately enters the blood in the adjacent capillaries of the vasa recta. The roleof the nephron loop and vasa recta in establishing the conditions for urine concentration is called the countercurrent multiplier effect.Distal Convoluted Tubule& Juxtaglomerular ApparatusThe thick ascending limb of the nephron loop is straight as it enters the cortex, and then becomes tortuous as the distal convoluted tubule (Figure 19–2). The simple cuboidal cells of these tubules differ from those of the proximal convoluted tubules in being smaller and having no brush border (Figure 19–9). Because distal tubule cells are flatter and smaller than those of the proximal tubule, more nuclei are typically seen in sections of distal tubules than in those of proximal tubules (Figure 19–8). Cells of the distal convoluted tubule do have basal membrane invaginations and associated mitochondria similar to those of proximal tubules, indicating their similar ion-transporting function (Figure 19–9). The rate of Na+ absorption and K+ secretion by the sodium pumps is regulated by aldosterone from the adrenal glands and is important for the body's water-salt balance. The distal tubule also secretes H+ and NH4+ into tubular urine, an activity essential for maintenance of the acid-base balance in the blood.The initial, straight part of the distal tubule makes contact with the vascular pole of the renal corpuscle of its parent nephron and forms part of a specialized structure, the juxtaglomerular apparatus (JGA) (Figures 19–9, 19–5, and 19-12). Cells of this structure establish a feedback mechanism that allows autoregulation of renal blood flow and keeps the rate of glomerular filtration relatively constant. At the point of contact with the arterioles, the cells of the distal tubule become columnar and more closely packed, with apical nuclei, basal Golgi complexes, and a more elaborate and varied system of ion channels and transporters. This thickened spot of the distal tubule wall is called the macula densa (Figures 19–5 and 19–12). Adjacent to the macula densa,。
泌尿系梗阻教案
性别及年龄
小儿--先天畸形； 成年人--结石，损伤，肿瘤，结核； 妇女--盆腔疾病； 老年男性--前列腺增生
常见疾病
肾： 结石，肿瘤，炎症，结核
肾盂输尿管连接部狭窄 肾下垂，多囊肾，海绵肾
输尿管：结石最常见。肿瘤，炎症，结核也可；
输尿管囊肿，异位开口， 腔静脉后输尿管， 盆腔肿瘤压迫， 放疗或手术损伤
4、治疗：
1）病因治疗：肾盂成型，碎石、取石。 2）肾造瘘术：暂不能去除病因者； 3）肾切除术：积水严重或肾积脓。
第三节 前列腺增生
前列腺增生（BPH）为老年男性常见 病，50岁以上男性患病率达50%。 一、病因： 性激素平衡失调。
雄激素与前列腺的生长发育密切相关。
二、病理： 尿道周围腺体（移行带）--增生 前列腺腺体（外周带）--癌
二、治疗： 原则：解除病因，恢复排尿。
1、有条件时，及时解除病因，恢复排尿。 如取石，切开狭窄，补钾。
2、麻醉后尿潴留：热敷，针灸，新斯的明 3、导尿; 4、耻骨上膀胱穿刺或造瘘。
1、病史： 老年男性进行性排尿困难，尿频；
2、体检： 肛诊--前列腺增大，中央沟变浅；
3、B超：前列腺大小，残余尿。 4、尿流动力学检查：
五、鉴别诊断
1、膀胱颈挛缩（膀胱颈纤维化） 2、前列腺癌 3、膀胱癌 4、神经原性膀胱 5、尿道狭窄
六、治疗
一、非手术治疗：
减轻尿频： -受体阻滞剂 特拉唑嗪，阿夫唑嗪（桑塔），哈乐（坦索罗新）
经尿道前列腺切除术 TURP 电切 汽化电切 激光（钬）
第四节 急性尿潴留
一、病因： 1、机械性梗阻： 前列腺增生， 尿道损伤， 尿道狭窄， 膀胱尿道结石、肿瘤、异物，血块。
2、动力性梗阻： 神经系统损伤、炎症、肿瘤；
泌尿结石教案
泌尿结石教案教案标题：泌尿结石教案教案目标：1. 了解泌尿结石的定义、成因和分类。
2. 了解泌尿结石的常见症状和并发症。
3. 掌握泌尿结石的预防措施和治疗方法。
4. 培养学生的健康意识和预防结石的能力。
教案步骤：引入：1. 利用图片或视频展示泌尿结石的概念和外观，激发学生的兴趣。
2. 引导学生思考泌尿结石可能对人体健康造成的影响。
知识讲解：3. 介绍泌尿结石的定义、成因和分类，包括钙结石、尿酸结石、草酸盐结石等。
4. 解释泌尿结石的常见症状，如腰背痛、血尿、尿频等，并讨论可能的并发症，如尿路感染、肾功能损害等。
预防措施：5. 引导学生了解泌尿结石的预防措施，如增加饮水量、控制饮食中的盐分和蛋白质摄入、避免长时间憋尿等。
6. 讨论其他预防措施，如定期体检、保持适当的体重、均衡饮食等。
治疗方法：7. 介绍泌尿结石的常见治疗方法，包括药物治疗、体外冲击波碎石术（ESWL）、腹腔镜手术等。
8. 引导学生了解手术治疗的适应症和注意事项。
小结与讨论：9. 对本节课所学内容进行小结，并强调预防泌尿结石的重要性。
10. 鼓励学生提出问题和分享个人经验，进行讨论和交流。
作业：11. 布置作业，要求学生调查泌尿结石的发病率和相关数据，并撰写一份关于预防泌尿结石的小册子或宣传海报。
教学评估：12. 设计一份简单的测验，包括选择题和问答题，以评估学生对泌尿结石知识的掌握程度。
扩展活动：13. 鼓励学生进行更深入的研究，了解泌尿结石的最新治疗方法和研究进展，并组织学生进行相关主题的小组报告。
这个教案旨在通过引入、知识讲解、预防措施、治疗方法等多个步骤，全面介绍泌尿结石的相关知识，并培养学生的健康意识和预防结石的能力。
同时，通过作业和扩展活动，激发学生的学习兴趣和主动性。
外科护理学教案泌尿系梗阻
外科护理学教案泌尿系梗阻教案标题：外科护理学教案-泌尿系梗阻教案目标：1. 了解泌尿系梗阻的定义、病因和分类。
2. 掌握泌尿系梗阻的临床表现和诊断方法。
3. 理解泌尿系梗阻的处理原则和护理措施。
4. 能够正确评估和监测泌尿系梗阻患者的病情变化。
5. 培养学生对泌尿系梗阻护理的专业素养和实践能力。
教学内容：1. 泌尿系梗阻的定义、病因和分类a. 定义：泌尿系梗阻是指尿液在排泄过程中受到阻碍，无法正常流出的病理状态。
b. 病因：结石、肿瘤、前列腺增生等。
c. 分类：上尿路梗阻和下尿路梗阻。
2. 泌尿系梗阻的临床表现和诊断方法a. 临床表现：尿频、尿急、尿痛、排尿困难、血尿等。
b. 诊断方法：尿液分析、尿流率测定、超声检查、尿路造影等。
3. 泌尿系梗阻的处理原则和护理措施a. 处理原则：解除梗阻、保护肾功能、预防感染、缓解症状。
b. 护理措施：- 监测患者生命体征和病情变化。
- 维持水电解质平衡，适当限制液体摄入。
- 给予适当的镇痛和抗感染治疗。
- 协助医生进行解除梗阻的治疗措施，如导尿、造瘘等。
- 提供心理支持和教育患者及家属。
4. 评估和监测泌尿系梗阻患者的病情变化a. 监测尿量、尿液性状和尿路引流情况。
b. 观察患者的疼痛程度和症状改善情况。
c. 定期进行血尿素氮、肌酐等相关检查。
d. 注意观察患者的心理状态和情绪变化。
5. 泌尿系梗阻护理的专业素养和实践能力a. 提高对泌尿系梗阻相关知识的学习和理解。
b. 培养责任心和敬业精神，保证患者的安全和舒适。
c. 加强团队合作和沟通能力，与医疗团队密切配合。
d. 不断学习和更新护理技术，提高护理质量和效果。
教学方法：1. 讲授：通过课堂教学向学生介绍泌尿系梗阻的相关知识。
2. 讨论：组织学生进行小组讨论，分享和交流对泌尿系梗阻护理的理解和经验。
3. 视频演示：展示泌尿系梗阻的相关护理操作和技术要点。
4. 案例分析：以实际病例为基础，引导学生分析和解决泌尿系梗阻护理中的问题。
泌尿系梗阻-教案
泌尿系梗阻-教案第一篇：泌尿系梗阻-教案泌尿系梗阻第一节概述1、泌尿系统从肾小管、肾盏、肾盂、输尿管、膀胱至尿道。
管腔梗阻影响尿液的分泌和排出。
2、泌尿系统保持通常是维持正常肾功能的必要条件。
3、泌尿系统梗阻部位近段尿液淤积，可导致肾功能损害，双侧梗阻，导致肾功能衰竭。
4、尿路梗阻性病变在泌尿外科最常见，而且多继发或并发其他泌尿外科疾病。
5、尿路梗阻导致感染和形成结石，感染和结石又会加重梗阻的程度。
6、梗阻、感染、结石可互为因果关系，在诊断和治疗尿路梗阻性疾病时要特别注意这一点。
7、根据梗阻发生的原因分机械性和动力性（1）机械性梗阻先天性梗阻、后天性梗阻。
（2）动力性梗阻。
根据梗阻发生的部位上尿路梗阻、下尿路梗阻。
病理生理（1）基本病理改变是梗阻以上的尿路扩张，导致肾积水，肾组织缺氧和萎缩。
（2）泌尿系感染，菌血症。
（3）肾功能损害。
第三节良性前列腺增生症（benign prostatic hyperplasia ,BPH）病因（1）年龄和睾丸（2）DHT（3）雌雄激素失调（4）上皮生长因子学说病理前列腺分为三部分1 外周带（5%）2 中央区和3 移行区，中央区和移行区（95%）前列腺组成1 腺体，2 间质平滑肌和纤维组织45%（60%）。
急迫性尿失禁残余尿尿潴留充溢性尿失禁膀胱输尿管梗阻返流肾积水肾功能损害感染结石）临床表现前列腺增生的病程一般分三期1 刺激期尿频为主，2 代偿期排尿困难为主，3 失代偿期残余尿充溢性尿失禁慢性尿潴留肾积水肾功能损害，4 其他症状尿路刺激症、血尿、结石、疝、脱肛、内痔、急性尿潴留。
诊断1、病史和体检2、其他检查（1）尿流率检查，（2）B超检查经腹或经会阴，（3）PSA测定，（4）尿流动力学检查。
治疗1.药物治疗（1）激素相关类药物①促黄体释放激素类似物（LHRH-A）抑那通（Enatone）3.75mg，每月一次皮下注射。
② 5а还原酶抑制剂保列治（Proscar）5mg每日服用。
泌尿系梗阻教案
用于预防和治疗泌尿系统感染，特别是在梗阻合并感染的情 况下。
手术治疗
内窥镜手术
通过尿道或膀胱等自然腔道进行手术，如膀胱镜取石术。
开放手术
对于复杂或严重的泌尿系梗阻，可能需要开放手术来解除梗阻。
其他治疗方法
物理治疗
如体外冲击波碎石，可用于治疗某些 类型的泌尿系结石。
生活方式调整
如饮食调整、增加水分摄入等，有助 于预防泌尿系结石的形成和复发。
分类
泌尿系梗阻可分为上尿路梗阻和下尿 路梗阻，上尿路梗阻主要指肾盂、输 尿管等部位的梗阻，而下尿路梗阻则 主要指膀胱和尿道的梗阻。
病因与病理机制
病因
泌尿系梗阻的病因多种多样，包 括泌尿系统结石、肿瘤、炎症、 损伤以及先天性畸形等。
病理机制
泌尿系梗阻发生时，尿液无法顺 利排出，导致泌尿道压力升高， 肾积水形成，长期梗阻可引起肾 功能损害甚至肾衰竭。
运动康复
适当进行体育锻炼，增强体质 ，促进康复。
定期复查
遵医嘱定期进行复查，评估恢 复情况。
预防复发
加强预防措施，降低泌尿系梗 阻复发的风险。
05
泌尿系梗阻的案例分析
典型案例一
患者情况
患者男性，56岁，因排尿困难、腰痛就诊。 查体显示肾积水、膀胱扩大。
治疗
行尿道前列腺切除术和膀胱结石取出术，术 后恢复良好。
临床表现与诊断
临床表现
泌尿系梗阻的典型表现为腰痛、血尿、排尿困难等，严重时可出现肾绞痛、肾 功能不全等症状。
诊断
泌尿系梗阻的诊断主要依靠病史、体格检查和影像学检查，如B超、尿路造影、 CT等。根据检查结果，医生可判断梗阻部位及病因，为后续治疗提供依据。
03
泌尿系梗阻的治疗
泌尿系梗阻-教案
泌尿系梗阻第一节概述1、泌尿系统从肾小管、肾盏、肾盂、输尿管、膀胱至尿道。
管腔梗阻影响尿液的分泌和排出。
2、泌尿系统保持通常是维持正常肾功能的必要条件。
3、泌尿系统梗阻部位近段尿液淤积，可导致肾功能损害，双侧梗阻，导致肾功能衰竭。
4、尿路梗阻性病变在泌尿外科最常见，而且多继发或并发其他泌尿外科疾病。
5、尿路梗阻导致感染和形成结石，感染和结石又会加重梗阻的程度。
6、梗阻、感染、结石可互为因果关系，在诊断和治疗尿路梗阻性疾病时要特别注意这一点。
7、根据梗阻发生的原因分机械性和动力性（1 ）机械性梗阻先天性梗阻、后天性梗阻。
（2）动力性梗阻。
根据梗阻发生的部位上尿路梗阻、下尿路梗阻。
病理生理（1）基本病理改变是梗阻以上的尿路扩张，导致肾积水，肾组织缺氧和萎缩。
（2）泌尿系感染，菌血症。
（3）肾功能损害。
第三节良性前列腺增生症（benign prostatic hyperplasia ,BPH）病因（1）年龄和睾丸（2）DHT（3）雌雄激素失调（4）上皮生长因子学说病理前列腺分为三部分1 外周带（5%）2 中央区和3 移行区，中央区和移行区（95%）前列腺组成1 腺体，2 间质平滑肌和纤维组织45%（60%）。
急迫性尿失禁残余尿尿潴留充溢性尿失禁膀胱输尿管梗阻返流肾积水肾功能损害感染结石）临床表现前列腺增生的病程一般分三期1 刺激期尿频为主，2 代偿期排尿困难为主，3 失代偿期残余尿充溢性尿失禁慢性尿潴留肾积水肾功能损害，4 其他症状尿路刺激症、血尿、结石、疝、脱肛、内痔、急性尿潴留。
诊断1、病史和体检2、其他检查（1）尿流率检查，（2）B超检查经腹或经会阴，（3）PSA测定，（4）尿流动力学检查。
治疗1.药物治疗（1）激素相关类药物①促黄体释放激素类似物（LHRH-A）抑那通（Enatone）3.75mg，每月一次皮下注射。
②5а还原酶抑制剂保列治（Proscar）5mg每日服用。
（2）а受体阻滞剂①高特灵(Hytrin)： 2mg每晚服用②哈乐(Tamulosin)： 0.2mg每晚服用。
梗阻结石-教案概要2
前列腺增生症的临床表现、诊断和鉴别诊断方法。肾、输尿管结石的临床表现、诊断鉴别诊断、保守治疗、体外冲击波碎石、手术适应症及手术方式。膀胱、尿道结石的临床表现、诊断及手术方式。
教学难点
前列腺增生症的临床表现、诊断。尿石症的病因（成人和小儿结石成因的特点），尿石的成分和性质。肾、输尿管结石治疗方法的选择。
参考资料
吴在德.外科学（第6版）
吴阶平.泌尿外科学
Patrick C. Walsh. CAMPBELL'S UROLOGYPDF-the 8th
辅助教学工具
多媒体（√）模型（）标本（）实物（）录像（）
备注：
编写时间：温州医学院第一临床医学院制
课时分配
梗阻的概述（0.2学时）。前列腺增生症的临床表现（0.3学时）。前列腺增生症的诊断和鉴别诊断方法（0.3学时）。前列腺增生症的处理原则（0.2学时）。尿石症的病因（0.2学时）。尿石的成分和性质（0.1学时）。尿石引起的病理变化（0.1学时）。尿石症的预防（0.2学时）。详细讲解肾、输尿管结石的临床表现、诊断、鉴别诊断（0.5学时）、治疗（0.5学时）。膀胱结石的临床表现、诊断及手术方式（0.2学时）。尿道结石的临床表现、诊断及手术方式（0.2学时）。
外语关键词
Urinary tract obstruction Hydronephrosis Urinary lithiasis
Benign prostatic hyperplasia Renal calculi Ureteral calculi
Vesical calculi Urethral calculi Shock-Wave lithotripsy
教案概要
课程名称：外科学教案编号：
2017泌尿外科实习同学小讲课泌尿系梗阻教案-1
➢ 尿液从肾盂排出受阻，使肾内压力升高、肾盏肾盂扩张、肾实质萎缩，造 成尿液积聚在肾内称为肾积水（hydronephrosis）
➢ 成人肾积水超过1000ml、小儿超过24小时的正常尿量，称为巨大肾 积水
第九页，共45页。
泌尿系梗阻---肾积水临床表现（本科大专掌握，中专熟悉）
泌尿系梗阻---良性前列腺增生病理生理（本科大中专了解）
病理生理
前列腺增生
前列腺尿道
前列腺
受体兴奋
前列腺包膜
尿道面积缩小 尿道长度增加
尿道迂曲
机械性梗阻
膀胱颈 前列腺尿道
张力增加
动力性梗阻
BOO
第二十页，共45页。
泌尿系梗阻---良性前列腺增生病理生理（本科大中专了解）
病理生理
BOO
尿道阻力增加
手术治疗的护理/术前护理 术前准备 协助评估其对手术的耐受力 慢性尿潴留者，应先留置尿管引流尿液，改善肾功能
尿路感染者，应用抗生素控制炎症 术前指导 术后护理
密切观察的意识及生命体征变化 术后6小时无恶心、呕吐，可进流食 膀胱冲洗的护理：注意冲洗速度，保持通畅，准确记录尿量、冲洗量和排出量
膀胱痉挛的护理：安慰病人，采取镇痛措施
临床表现
✓腰部隐痛 ✓腹部包块 ✓发作期症状：患侧腰腹部剧烈绞痛，伴恶心、呕吐，尿量减少，患 侧腰部可扪及肿块 ✓肾脓肿、肾衰竭
✓原发病症状
第十页，共45页。
泌尿系梗阻---肾积水临床表现（本科大专掌握，中专熟悉）
肾积水的影像学改变
第十一页，共45页。
泌尿系梗阻---肾积水处理原则（本科熟悉，大中专了解）
✓ 急性疼痛 与逼尿肌功能不稳定、导尿管刺激、膀胱痉
外科学课件：泌尿系统梗阻Urinary Obstruction(英文)
◆ Ageing: Male elder over 50-years-old are more liable to BPH,
and the incidence increases with the age increased.
section 3 Benign Prostatic Hyperplasia (BPH)
一. Definition:
A series of lower urinary tract symptoms（LUTS) , especially including frequence, urgency, difficulty of urination,and urinary retention, often caused by the enlarged prostate in old men.
Urinary Obstruction
Section 1
outline
一. Clinical character： 1.Etiologies: The urinary system disease itself and the surrounding organs disease. 2.Clinical manifestations: Urine stasis ;dilation of urinary tract above obstruction site. 3.Consequences: hydronephrosis;impairment of renal function;even failure of renal function. 4.Obstruction, infection, stones are always reciprocal causation.
泌尿系梗阻教案
泌尿系梗阻教案教案标题：泌尿系梗阻教案教案目标：1. 了解泌尿系梗阻的定义、病因和常见症状。
2. 掌握泌尿系梗阻的诊断方法和治疗原则。
3. 培养学生对泌尿系梗阻的预防和护理意识。
教案内容：一、导入（5分钟）1. 利用图片或视频展示泌尿系梗阻的病例，引起学生的兴趣。
2. 引导学生回忆泌尿系统的基本结构和功能。
二、知识讲解（15分钟）1. 定义：解释泌尿系梗阻的含义，包括上尿路和下尿路梗阻的区别。
2. 病因：介绍泌尿系梗阻的常见病因，如结石、肿瘤、前列腺增生等。
3. 症状：列举泌尿系梗阻的典型症状，如尿频、尿急、尿痛等。
三、诊断方法（10分钟）1. 临床症状：介绍通过病史询问和体格检查来初步判断泌尿系梗阻的方法。
2. 辅助检查：讲解常用的泌尿系梗阻诊断方法，如尿液分析、超声检查、尿流率测定等。
四、治疗原则（15分钟）1. 保留治疗：介绍通过导尿等方法暂时缓解梗阻症状的治疗原则。
2. 手术治疗：讲解手术治疗泌尿系梗阻的常见方法，如腔镜手术、开放手术等。
五、预防和护理（10分钟）1. 预防措施：指导学生了解预防泌尿系梗阻的方法，如饮食调理、定期体检等。
2. 护理指导：介绍患者术后的护理注意事项，如导尿管护理、饮食调理等。
六、小结与讨论（5分钟）1. 总结本节课的重点内容，确保学生掌握。
2. 提出问题，引导学生思考和讨论，加深对泌尿系梗阻的理解。
七、作业布置（5分钟）1. 要求学生阅读相关文献，进一步了解泌尿系梗阻的病因和治疗方法。
2. 提醒学生做好笔记，为下节课的复习做准备。
教案评估：1. 课堂互动：观察学生在课堂上的提问和回答情况。
2. 练习和作业：检查学生完成的相关练习和作业情况。
3. 小结讨论：评估学生对泌尿系梗阻知识的掌握程度。
教案扩展：1. 邀请专业医生或相关领域专家来进行讲座或座谈，加深学生对泌尿系梗阻的理解。
2. 组织学生进行小组讨论，分析实际病例，分享治疗和护理经验。
3. 带领学生参观医院或诊所，亲身了解泌尿系梗阻的诊断和治疗过程。
泌尿系梗阻双语版2012[2月]——【外科学 精品课件】
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1 梗阻原因因疾病而异
机械的 mechanical —— 动力的dynamic 先天的 congenital —— 后天的 acquired 急性的 internal —— 慢性的 external
2 梗阻原因因人群而异
最常见
老年人————前列腺增生 BPH
成年人————结石 Calculus
小 儿————先天性畸形 congenital malformation
1 多无自觉症状 2 可有原发病的表现
a 腰、腹部包块 积水，肿瘤
b 疼痛
积水---钝痛，结石---肾绞痛
c 感染
尿频、尿急、发烧
d 肾衰
少尿、无尿、浮肿
三 诊断Diagnosis
原则
•确定有无积水 •查部位、病因、程度、有无感染和肾 功能损害
步骤
B超
首选
KUB+IVP 最可靠
术前KUB
1次PNL术后
2次PNL术后
逆行肾盂插管造影
补充诊断，还可治疗
排尿性膀胱尿道造影
下尿路、动力性梗阻 （神经性膀胱 、尿道狭窄）
CT ，MRI 区分积水和肿瘤
逆行插管造影或引流
四 治疗Treatment
解除梗阻，引流尿液
逆插术，肾造瘘术 Nephrostomy
去除病因
肾切除
Nephrectomy 对侧肾功能正常
单侧 无（对侧 可代偿）
一 定义Definition
尿液从肾盂排出受阻，造成 ① 肾内压力升高 ② 肾盏肾盂扩张 ③ 肾实质萎缩
肾积水
肾积水示意图
名词解释
巨大肾积水 原（特）发性肾积水 间歇性肾积水
二临床表现Clinical Findings
尿路结石：泌尿系结石(英文版)
Epidemiology and Etiology
Extrinsic Factors (3) Lifestyle（生活方式）:
• Formation of stones involve 3 conditions – Slow urine flow低尿流量 – supersaturation of urine – Damage 損傷to the lining of the urinary tract – form crystals – Decreased inhibitor substances 低抑制物– that would otherwise prevent supersaturation and crystal formation
Stones are Common …
Long standing stone
• Infection • Obstruction • Metaplasia • (組織化生)
Kidney function
Squamous cell Carcinoma（鱗狀細 胞癌）
Suspense 疑問？
If urinary constituents are similar from each kidney and if there is no evidence of obstruction: • 1、Why do most stones present in a unilateral fashion? • 2、Why don't small stones pass uneventfully down the ureter early in their development? • 3、Why do some people form one large stone and others form multiple small calculi?
医学泌尿系统梗阻概论梗阻感染结石PPT课件
编辑本段现代中医史
上个世纪末,本世纪初，1996年,清华学界 对中医 气本质 ，经络 实质， 阴阳， 五行， 藏象， 中医哲 学观等 都有了 新的全 面整体 创造性 的认识 和解说 。如， 邓宇等 发现的 :气是 流动着 的‘信 息－能 量－物 质’的 混合统 一体； 分形分 维的经 络解剖 结构； 数理阴 阳；中 医分形 集：分 形阴阳 集－阴 阳集的 分形分 维数， 五行分 形集－ 五行集 的分维 数；分 形藏象 五系统 －暨心 系统、 肝系统 、脾系 统、肺 系统、 肾系统 ；中医 三个哲 学观－ 新提出 的第三 哲学观 ：相似 观－分 形论等 。
耻骨上可触及膨隆包块
• 鉴别诊断：
无尿
治疗：
原则：解除梗阻，引流尿液
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1、 病 毒 性 肝 炎：由病毒造成的肝炎按照其病毒系列不同分为甲、乙、丙 、丁、 戊和庚 共六种 类型病 毒性肝 炎。能 引起肝 脏细胞 肿胀， 是世界 上流传 广泛， 危害很 大的传 染病之 一。
我国经济和科学技术日益发展， 学术文 化领域 百家争 鸣，（df高血压 958心 脏病983u6糖尿 病87fr ）特别 是思想 家的革 新精神 ，为中 医学理 论的创 新和突 破性进 展，提 供了有 利的文 化背景 。宋代 陈无择 著《三 因极一 病证方 论》一 书，（45传染 病q566丙肝964jo乙肝 28jgsx甲肝gh）提出 三因学 说；并 产生了 最具盛 名四大 学派， 刘完素 倡导火 热论； 张从正 力倡“ 攻邪论 ”；李 杲提出 “内伤 脾胃， 百病由 生”的 理论； 朱震亨 创造性 地阐明 了相火 的演变 规律。
1908年，才发现病毒也是肝炎的致病因 素之一 。1947年，将 原来的 传染性 肝炎（i nfectious hepatitis）称为甲型肝炎（Hepatitis A, HA）；血清性肝炎（serum hepatitis）称为乙型肝炎（Hepatitis B, HB）。1965年人类首次检测到乙型肝 炎的表 面抗原 。
泌尿系结石教案范文
泌尿系结石教案范文一、教学目标：1.知识目标：了解泌尿系结石的定义、分类、病因、临床表现及诊断方法。
2.能力目标：掌握结石患者的护理措施，包括药物治疗和非药物治疗方法。
3.情感目标：培养学生热爱人生，积极面对困难的态度。
二、教学重点和难点：1.重点：泌尿系结石的分类、临床表现和诊断方法。
2.难点：结石患者的护理措施。
三、教学过程：Step 1 引入知识（5分钟）向学生介绍泌尿系结石的定义和分类，引发学生对这一疾病的兴趣。
Step 2 知识讲解（30分钟）1.通过讲解，向学生介绍泌尿系结石的病因和发生机制。
2.根据结石的成分，向学生介绍常见的结石类型及其特点。
3.通过讲解，向学生介绍泌尿系结石的临床表现和常用的诊断方法。
Step 3 讲解治疗方法（25分钟）1.向学生介绍结石患者的非药物治疗方法，如饮食调理和适当的锻炼。
2.向学生介绍结石患者的药物治疗方法，包括融石治疗和痛经治疗等。
3.讲解结石患者的手术治疗方法及注意事项。
Step 4 案例分析（20分钟）以一名泌尿系结石患者的案例为例，通过分析案例，让学生应用所学知识进行思考和讨论，提出治疗方案和护理措施。
Step 5 小组讨论（15分钟）将学生分成小组，每个小组讨论一个泌尿系结石的相关问题，并将结果汇报给全班。
Step 6 总结归纳（5分钟）对泌尿系结石的相关知识进行概括和总结，并与学生进行互动交流。
四、教学方法：1.讲授法：通过讲解结石的相关知识，帮助学生全面了解这一疾病。
2.案例分析法：通过分析具体案例，让学生应用所学知识，提高解决问题的能力。
3.小组讨论法：通过小组讨论，促进学生间的互动和合作，提高学习的效果。
五、教学资源：1.多媒体教学设备。
2.相关教材和参考书籍。
3.病例资料。
六、教学评估：1.通过案例分析和小组讨论，评估学生对泌尿系结石的理解和应用能力。
2.设计一份试题，测试学生对泌尿系结石的理解情况。
七、教学延伸：1.鼓励学生参加医学活动，如参观医院、实习等，加深对泌尿系结石知识的理解。
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泌尿系统梗阻、结石双语教案医学院教案课程名称外科学授课方式大课讲授任课单位任课教师授课年级授课时间教学主要内容与时间分配泌尿系统梗阻（Urinary Tract Obstruction）（讲述时间50分钟）概论Outline（讲述时间15分钟）一、Etiological factor of obstruction二、Pathologic physiology of obstruction1、返流现象2、血管活性物质的改变3、肾功能改变三、pathology of obstruction1、输尿管梗阻2、下尿路梗阻3、泌尿系梗阻时，影响肾积水的多少和肾功受损害的严重程度的因素四、Urinary tract obstruction and infection五、Treatment principle of urinary tract obstruction1、With normal renal function：应尽快明确梗阻原因。
解除梗阻与治疗病因可同时进行。
若病因和解除梗阻不能同时处理，可先解除梗阻，待病情允许后，再进一步行病因治疗。
2、With abnormal renal function：应立即解除梗阻，治疗合并症，恢复肾功能，以后再针对病因作进一步治疗。
3、With acute obstruction：应早作诊治，根据病情，积极采取措施解除梗阻，以保护肾功，然后进行下一步治疗。
4、The method of remove the obstruction：解除梗阻的方法：导尿术或留置导尿管；耻骨上膀胱穿刺造瘘；肾造瘘或经皮肾穿刺造瘘；经膀胱镜置管做内引流；输尿管皮肤造瘘等肾积水（Hydronephrosis）（讲述时间10分钟）一、Clinical manifestation：临床表现和过程不一致；结石、肿瘤、炎症等引起的肾积水主要表现为原发病的症状和体征，很少出现肾积水的病象；肾积水合并感染时，常表现为原发病症状加重；积水有时呈间歇性发作；双侧肾或孤立肾积水可导致renal failure；近年，肾积水常由超声检查发现。
二、Diagnosis：发病情况，实验室检查，影像学检查，积水肾脏的功能评价。
诊断时需要解决的问题：梗阻病因、梗阻部位、梗阻程度、是否合并感染、肾功能损害情况etiological factor、position、degree、with or without infection、the damages of renal function三、Treatment根据病因、发病急缓、有无感染及肾功损害程度，结合病人年龄和心肺功能情况等综合考虑，包括肾造瘘术nephrostomy、膀胱造瘘cystostomy、双J管置入insert double J、控制感染等control the infection etc。
急性尿潴留（Acute Urinary Retention）（讲述时间5分钟）一、Etiological factor：mechanical obstruction、dynamia obstruction二、Treatment：急性尿潴留的治疗原则是解除病因，恢复排尿。
但有时病因不明，只能先作尿液引流，以后再作处理。
导尿是急性尿潴留时最常用的方法，不能插入导尿管者，可自耻骨上缘穿刺膀胱，抽出尿液，如需长期引流，应行膀胱造瘘术cystostomy。
前列腺增生症（Benign Prostatic Hyperplasia）（讲述时间20分钟）The essential condition of growth of prostate: Age increases and with functional testises一、pathogeny具体机制尚不明确，与上皮和间质细胞的增殖和细胞凋亡的平衡性破坏有关。
双氢睾酮说hypothesis of DHT、雌激素学说hypothesis of ESG、其他学说：前列腺间质—腺上皮细胞的相互作用、生长因子、炎症细胞、神经递质及遗传因素等。
二、pathologyTransitional zone是前列腺增生的起始部位，原占前列腺组织仅5%，其余95%腺体由peripheral zone、central zone组成。
增生组织向外压迫使移形带外的组织形成前列腺的外科包膜。
增生组织向内压迫使前列腺部尿道受压，管腔变窄、变形、尿道延长，阻力增加，引起临床症状。
良性前列腺增生引起排尿梗阻有以下两方面原因：腺体增生和平滑肌的作用(hypertrophy of gland and function of smooth muscle)1、hypertrophy of gland增大的腺体向两侧和向膀胱内突出，造成膀胱出口堵塞。
增生使前列腺段尿道弯曲、伸长，尿道受压变窄。
2、function of smooth muscle前列腺内尤其是围绕膀胱颈的、含有丰富的α肾上腺素能受体的平滑肌，在膀胱逼尿肌收缩时并不松驰，造成梗阻。
增生的平滑肌，在膀胱颈形成环状结构。
前列腺增大不明显。
三、Clinical manifestation尿频、排尿困难、尿潴留与尿失禁以及合并症四、Diagnosis病史及I-PSS、digital rectal examination、B超、尿流率检查rate of flow、前列腺特异性抗原PSA测定、放射性核素肾图radionucleiorenogram、经静脉尿路造影IVU、膀胱尿道镜检查cystourethroscopy五、D ifferential diagnosisbladder neck contracture、prostatic carcinoma、urethral stricture、n eurogenic bladder六、Treatmentobservation、drug treatment、operation、other Treatment methods1、ObservationBPH梗阻症状较轻者无需处理，密切随访2、Drug treatmentαacceptor blocker：non-selectivity→ α1→ α1 A5-αreducase inhibitor：缩小体积，长期用药植物类药：成分复杂，机制不明3、OperationIndication：中/重度BPH患者，下尿路症状已明显影响患者的生活质量者，尤其是药物治疗效果不佳或拒绝接受药物治疗的患者，需手术治疗。
BPH导致反复尿潴留、反复血尿、反复泌尿系感染、膀胱结石、继发性上尿路积水时，需手术治疗。
合并膀胱大憩室，腹股沟疝、严重的痔疮或脱肛时，需手术治疗。
Method：TURP: gold standard; TUIP; open operation of prostatectomy；TUVP, PKRP4、other Treatment methods激光治疗、经尿道微波热疗、经尿道针刺消融术、前列腺尿道网状支架、体外高强度聚焦超声、经尿道球曩高压扩张术summarize：泌尿系统梗阻：概述：Etiological factor、Pathologic physiology、pathology、Treatment principle上尿路梗阻：Clinical manifestation、Diagnosis and Treatment下尿路梗阻：Pathogeny、Pathology、Clinical manifestation、Diagnosis、D ifferential diagnosis and Treatment尿石症（Urolithiasis）（讲述时间50分钟）概论outline（讲述时间10分钟）一、概述sum up：男多女少、南多北少、复发率高、上多下少、机制不明二、尿路结石形成机制forming mechanism of urinary calculus1.形成部位form position：肾和膀胱2.结石成分composition：上尿路―草酸钙结石；下尿路―磷酸镁铵结石3.基本学说basic hypothesis：异质成核、取向附生、基质和晶体抑制物质学说4.结石分类classification：代谢性和感染性结石三、结石成份和性质compositions and properties of calculus1.草酸钙结石calcium oxalate calculus：坚硬、粗糙、不规则、棕褐色2.磷酸钙、磷酸镁铵结石calcium phosphate、magnesium ammonium phosphate calculus：易碎、粗糙、不规则、灰白或黄色3.尿酸结石uric acid calculus：质硬、光滑、多发、黄红棕色，纯尿酸结石X线不显影4.胱氨酸结石cystine calculus：光滑、淡黄棕色、蜡样外观四、结石形成的影响因素Influence factor of urinary calculus forming流行病学因素、尿液因素、泌尿系解剖异常、尿路感染、肾上皮细胞转运钙和草酸异常五、病理生理pathologic physiology形成于肾、膀胱；输尿管结石常停留于生理狭窄处上尿路结石upper urinary tract calculus（讲述时间20分钟）一、clinical manifestationHaematuria、colic pain、少数出现膀胱刺激征、发热、寒颤、少尿或无尿二、diagnosis病史；实验室检查，包括尿常规、尿细菌培养+药敏、血及24小时尿钙、磷、尿酸、甲旁素、肾功能测定；影像学检查，包括KUB、IVU、逆行性尿路造影、B超、CT、同位素检查、输尿管肾镜检查三、differential diagnosis胆囊疾患disease of gallbladder、appendicitis、卵巢囊肿扭转torsion of ovarian cyst、宫外孕ectopic pregnancy、腰椎(肌)疾患等disease of lumbar vertebrae四、Treatment1.保守治疗expectant treatment①indication：结石小于0.6cm、光滑、无梗阻、无感染、纯尿酸或胱氨酸结石、结石远端尿路无狭窄。
②method：多渴水、调节饮食、控制感染、调节尿PH值、治疗肾绞痛2.ESWLcontraindication：结石远端尿路梗阻、妊娠、出血性疾病、严重心脑血管病、安置心脏起博器、Cr ≥265umol/L或患侧肾功能差、急性尿路感染、育龄妇女输尿管下段石、过度肥胖3.endoscopic surgery①输尿管肾镜取石或碎石术ureterorenoscope lithotripsy：输尿管中、下段石，无下尿路梗阻，输尿管细小、狭窄或扭曲者。