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英国essay代写 诊断和治疗肾小球肾炎

如果我们回顾肾脏的结构,我们发现它是由不同的部分(图1),肾脏的功能单元(图2)和主要的过滤’机械’(图3,I)。

图1:肾脏的结构-肾被肾包膜包围,分为3个部分,髓质,皮质和肾盂。每个肾脏提供氧气的血液,由肾动脉和静脉血经肾静脉去除。一旦肾脏执行他们的过滤机制,他们清空他们的废物产品,从输尿管。

图2:单肾的肾单位是肾功能单位和一百万以上的这些都是在每个肾脏允许它执行其功能的发现。注意它是如何跨越不同的肾脏部分。

图3:肾小球旁器-(我)的肾小球旁器是血液的主要过滤发生在肾单位,肾小球和Bowman胶囊的作用。

(II)的间质细胞存在的肾小球旁器及其在引起炎症肾小球的作用位置的链接过滤部分密切相关。

(iii)足是附近还发现肾小球毛细血管和这些融合在一起,影响肾小球滤过,导致霍奇金病。这种疾病是一种肿胀,由于转移积累的产品,这是没有过滤,所以沉积到身体的其他部分。

If we recall the structure of the kidney, we find that it is made of different sections (Figure 1), the functional unit of the kidney (Figure 2) and the main filtration ‘machinery’ (Figure 3, i).

Figure 1: The structure of the kidney – The kidney is surrounded by the renal capsule and split into 3 sections, the medulla, the cortex and then the renal pelvis. Each kidney is supplied with oxygenated blood, by the renal artery and removes deoxygenated blood via the renal vein. Once the kidneys carry out their filtration mechanism, they empty their waste product, down the ureter.

Taken from web1.stmaryssen-h.schools.nsw.edu.au/SMSHS/ricks%20sites/Biology%20web%20site/HSC_9_2maintaining%20a%20balance/Notes%20for%20point%203/summary%20notes.html

Figure 2: A single nephron – The nephron is the functional unit of the kidney and over a million of these are found within each kidney allowing it to carry out its function. Notice how it spans across the different kidney sections.

Taken from www.uptodate.com/patients/content/image.do

Figure 3: The Juxtaglomerular Apparatus – (i) The juxtaglomerular apparatus is the main filtration of blood occurs in nephrons and this is where the glomerulus and Bowman’s capsule interact.

(ii) The mesengial cells are found closely associated with the filtration part of the juxtaglomerular apparatus and their position links with their role in causing inflammation in glomeruli.

(iii) The Podocytes are also found near glomerular capillaries and these may fuse together and influence the filtration of the glomerulus, causing Hodgkins disease. This disease is a type of swelling due to the diversion of accumulating products, which are not filtered and so deposited to other parts of the body.

Taken from www.siumed.edu/~dking2/crr/images/corp5.jpg.

Glomerulonephritis (GN) is a type of kidney disease; where by filtration of the blood is disrupted. It is mainly associated with the glomeruli in the kidneys, becoming inflamed (NHS Choices 2009) and there can be different types of the disease which may be proliferative or non-proliferative.

这种疾病的主要原因还不清楚,但有许多可能的解释。对于增生性肾小球肾炎中最常见的解释是由于免疫系统的反应,在炎症细胞如血小板和巨噬细胞成为被困在肾小球(考泽1999)。他们在这里传播和积累,启动机制,导致肾小球炎症(考泽1999)。这是为增生性肾小球肾炎中最常见的机制,称为免疫球蛋白A(IgA)肾病(那1987)。这是当IgA蛋白,抗感染,建立在肾小球炎症,因此(书呆子医生2010)。另一种免疫系统反应涉及与抗原的抗体,通过肾小球基底膜形成,也可引发炎症(Watson和罗伊尔1987)。

对于增生性肾小球肾炎中的另一个可能的解释是感染有关,通过对streptoccoci株细菌入侵后(赖安和雷2004),针对皮肤或咽部组织(Watson和罗伊尔1987)。这一结果在感染后肾小球肾炎也可与其他感染如细菌性心内膜炎或HIV相关(梅奥诊所2009)。

The main cause of the disease is not precisely known but, there are many possible explanations. The most common explanation for proliferative GN is due to an immune system response, where inflammatory cells like platelets or macrophages become trapped in the glomeruli (Couser 1999). Here they circulate and accumulate, initiating a mechanism that leads to inflammation of the glomeruli (Couser 1999). This is the mechanism for the most common form of proliferative GN, known as Immunoglobulin A (IgA) nephropathy (D’Amico 1987). This is when IgA proteins, which fight infections, build up within the glomeruli and therefore inflammation (Geeky Medics 2010). Another immune system response involves antibodies interacting with antigens, formed by the glomerular basement membrane, which can also trigger inflammation (Watson and Royle 1987).

Another possible explanation for proliferative GN is infection-related, following invasion by bacteria of the Streptoccoci strain (Ryan and Ray 2004), which targets the skin or pharyngeal tissue (Watson and Royle 1987). This results in post-infectious GN which can also be associated with other infections like bacterial endocarditis or HIV (Mayo Clinic 2009).

In addition, it is also suggested that vasculitic disorders, like Wegeners Granulomatosis can result in crescentic GN (Geeky Medics 2010) (Figure 4).

Figure 4: Crescentic GM – In Wegener’s Granulomatosis, blood vessels become inflamed, having an effect on the filtration rate of the glomerulus and leads to the formation of crescent shaped scars.

Taken from http://uk.ask.com/wiki/Glomerular_crescent

Non-proliferative GN can be idiopathic, such as membranous GN, or may just simply be genetically linked like focal segmental GN (Geeky Medics 2010).

When looking at GN (mainly proliferative) we need to also consider the mesengial cells (Figure 3, ii). GN can be recognised by an increase in the number of mesengial cells and their intracellular contents (Churg 2006). They rapidly multiply, increasing the thickness of this layer and press against the glomerular capillaries (Churg 2006) (Figure 5).

Figure 5: Histology of proliferative GN – As the mesengial cells multiply, they increase in number and compress against the glomerular capillary and contribute towards the glomerulus increasing in circumference. Taken from (Churg 2006).

In some cases, the mesengial cells may even invade the glomerular capillaries and sit in between the filtration part of the nephron, made up of endothelial cells and the basement membrane (Figure 6) (Churg 2006). Hence, the basement membrane appears split, disrupting renal filtration and therefore resulting in a certain type of GN, known as membranoproliferative GN (Hope et al. 1993).

Figure 6: A Normal Glomerular Capillary – Proliferation of the mesengial cells leads to invasion between the epithelial cells and the basement membrane, disrupting glomerular filtration and leading to GN. Taken from www.uncnephropathology.org/jennette/ch1.htm

The glomerular capillaries are also where proteins from the immune system may be trapped between the basement membrane and the epithelial cells, which accumulate and form ‘humps’ in the glomerular capillary walls (Churg 2006), resulting in membranous GN (Hope et al. 1993).

Specifically in crescentic GN, which is infection related, there is an increase in epithelial cells which compress the glomerulus and causes scars, described as ‘crescent shaped’ (Malvinder 2008) (Figure 4).

However there can be milder forms of GN, with the most common being minimal change GN, caused by the fusion of podocytes (Hope et al. 1993) (Figure 3, iii).

When looking at post-infectious GN, we find that it is normally the group A beta-haemolytic streptococcus bacteria which causes infection (Watson and Royle 1987) and brings about acute post-streptococcal GN (APSGN) (Duvuru 2010). The activity of this bacterium is thought to be associated with the accumulation of streptococcal antigens, binding to the immune antibodies, which are then deposited on the glomerulus basement membrane (Field et al. 2010) (Figure 7).

Figure 7: APSGN – (Arrows show where the antigen-antibody complexes have been deposited.) As the antigen is bound to the antibodies, it prevents the antibodies from inflicting a defence mechanism and leads to modification of the glomerular basement membrane (Field et al. 2010).

Taken from www.ndt-educational.org/ferrariomgp.asp

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