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CLASS LECTURES EFFECTIVE FOR ALL THE FOUR SECTIONS (A+B & C+D)
Path-202 / FINAL
URINARY SYSTEM
A+B:27/04 LECTURE 11(Continued) C+D:27/04
11.1.1. STRUCTURES ASSOCIATED WITH A KIDNEY i) Renal capsule ii) Cortex iii) Medulla iv) Calyx v) Renal pyramids vi) Renal crest vii) Renal pelvis viii) Renal artery ix) Renal vein x) Arcuate artery xi) Renal fat. 11.1.2. STRUCTURES ASSOCIATED WITH A NEPHRON i) Efferent vessel ii) Afferent vessel iii) Bowmans capsule iv) Glomerulus v) Bowmans space vi) Proximal convulated tubule vii) Proximal straight tubule viii) Loop of Henley ix) Distal straight tubule x) Distal convulated tubule xi) Collecting duct.
Microscopically: There is persistence of primitive mesenchyma, Interstitial fibrosis, renal cysts and few enlarged hypercellular glumeruli. 4. ECTOPIC KIDNEYS (FUSED KIDNEYS) It is the fusion of cranial or caudal poles of the kidneys during nephrogenesis which result in appearance of one large/Giant kidney with two ureters. 5. POLYCYSTIC KIDNEY In this condition, kidney have many cysts that involved numerous nephrones. Such kidneys can have Swiss Cheese appearance when incised. CYST: Fluid-filled cavity is known as a cyst. As cyst enlarged, it compressed the adjacent parenchyma that ultimately leading to renal failure or impairment of kidneys. As there is an obstruction in the nephrone, then there is increased luminal pressure and a secondary dilatation that results into modifications in the matrix and weakened the tubular basement membrane. It (obstruction) allowing the secular dilatation of tubules. There is focal tubular hyperplasia. Increased intra-tubular pressure causes development of enlarged dilated tubules.
A+B:28/04
LECTURE 12
C+D:28/04
2) CONGESTION: Kidneys are usually dark in color, red, swollen. When cut, there is oozing of blood. Sometime there is unilateral hypostatic congestion in animals and it died on lateral recumbency.
v) Renal amyloidosis
12.3. NEPHRITIS
It is the inflammation of the kidney. FORMS OF NEPHRITIS It may be of various forms/types i) Glomerular nephritis ii) Tubular nephritis iii) Glomerulo-tubular nephritis iv) Interstitial nephritis
A+B:29/04
LECTURE 13
C+D:29/04
ii) Capsule strips easily and exposed surface is smooth and pale while the cut surface show marked swelling and paler of the cortex. iii) Pyramids appear dark, pale due to great accumulation of lipids in cells of convulated tubules. iv) There may be bright yellow streaks & patches in the cortex region due to large deposits of lipids. MICROSCOPICALLY: 1. Glomeruli show an extreme cellularity which is highly characteristic. 2. There is more proliferation of epithelial and endothelial cells of tufts. 3. The epithelial cells proliferation is referred as Extra-capillary glomerular nephritis: 13.1.1. Extra capillary Glomerular Nephritis: i) In this condition (ECGN), epithelium of bowmans capsule proliferate so that large masses of cells occupy the capsular space. ii) The whole circumference of a glomerulus is involved, so cell form a semilunar mass in capsular space which is known as epithelial crescent. iii) RBCs, desquamated epithelium and fibrin mass is present in capsular space in varying amount. iv) During the coarse of time, crescent becomes fibrosed and fused with the tuft which also under hyalinization. 13.1.2. Intra capillary Glomerular Nephritis i) there are few or more cells in capsular space but there is a great proliferation of endothelial cells which give the tuft a highly cellular appearance. ii) Diffused, homogeneous thickening of capillary basement membrane ! also referred as <Membranous glomerular nephritis>. iii) There is remarkable increase in glomerular permeability especially for protein. iv) Tubules show marked degenerative changes such as fatty degeneration, cloudy swelling. v) As tubular degeneration progresses, many of epithelial cells cast off and tubules become atrophic. 13.1.4. CONSEQUENCES OF RENAL DISEASES (Generally) 1. There is a leakage of various low molecular weight protein into the glomerular filterate and subsequently into the urine. 2. Protein rich glomerular filtrate accumulated in the tubular lamina and subsequently appears in the urine. 3. There is a fusion of visceral epithelium and form a structure called podcyte. 4. As a result, there is a thickening of basement membrane and neutrophilic infiltration. 5. There is hypertrophy of endothelium as well as dense granular deposits of immune complex associated with basement membrane.
A+B:04/05
LECTURE 14
C+D:04/05
It is an insoluble, fibril protein with a beta pleated sheath conformation, produced after incomplete proteolysis of several soluble amyloidogenic proteins. Amyloid protein deposits are composed of fragments of serum acute phase reactant protein called as Serum Amyloid Associated (SAA) protein. Sometime, Amyloid fibril from either source are deposited in the tissues along with glycoprotein called Amyloid P-component. 14.2.1. Site of Deposition of Amyloid The Glomerulus is the most common renal site for deposition of Amyloid. 14.2.2. GLOMERULAR AMYLOIDOSIS It is a protein loss nephropathy resulting in marked protein urease and uremia. GROSSLY: i) Kidney is enlarged, pale tan to yellow and have smooth to finally granular capsular surface. ii) Amyloid laden glomeruli can be visible as fined dots on the cut surface. iii) Cortex can have finally granular appearance, but if treated with I2 solution, result in brown staining of glomeruli that become purple when exposed to H2SO4. MICROSCOPICALLY 1. There are Glomerular Amyloid deposits in the mesengium and subendothelial location. 2. The Amyloid is usually acellular and accumulate segmently within a glomerular tuft, thus replaced the normal architecture by eosinophilic, homogenous to slightly fibrilar matrix. 3. Glomeruli enlarged, capillary lumina become obliterated and tuft can appears as a large hypercellular eosinophilic hyaline sphere. 4. Tubulo-basement membrane may become hyalinized and thickened. 5. Renal tubules are markedly dilated and contain proteinous material. 6. Amyloid is conformed with Congo Red (green) stain.
GROSSLY i) Kidney is swollen, and pale in color. ii) Cut surface bulges, there may be grey infiltrate of varying amount and intensities which obscure normally, readily striated cortical architecture. iii) Predominantly, grey foci are present in the cortical surface but sometime, it may occur in the outer medullary region. MICROSCOPICALLY 1. The aggregates of lymphocytes, plasma cells, monocytes and few neutrophils are randomly scattered or intensely localized throughout the interstitium. 2. Degenerated necrotic tubular epithelium (DNTE) is a distinguishable characteristic.
A+B:05/05
LECTURE 15
C+D:05/05
15.1. PYELITIS: inflammation of the pelvis of the kidney. 15.2. PYELONEPHRITIS: Inflammation of the both pelvis and renal parenchyma (kidney
itself). ETIOLOGY: It mostly occur due to: i) ascending infections of the urinary tract ii) Abnormal reflex of urine contaminated with the bacteria (vesico-uretral reflex) Other most common causative agents are: i) E. coli iv) Proteus ii) Corynebacterium renale iii) Klebsiella v) Pseudomonas aureginosa
GROSSLY i) Mucus membrane is inflamed, thickened , reddened, roughened and granular. ii) It is coated with purulent exudate iii) Pelvis and ureter are markedly dilated and present purulent exudate in their lumina. iv) Medullary crests or papillae are ulcerated and necrotic. MICROSCOPICALLY 1. Most common and severe lesions of pyelonephritis are usually in the inner medulla. 2. Transitional epithelium usually necrotic and desquamated. 3. Necrotic debris, fibrin, neutrophils and bacterial colonies can be adherent to denuded area -< seems to have a look of filled exudate.
15.3. HYDRONEPHROSIS
It refers to dilatation of renal pelvis due to obstruction of urine outflow and it increased the pelvis pressure, dilatation of pelvis and progressive renal parenchymal atrophy. ETIOLOGY/CAUSATIVE AGENTS 1) The urine outflow may be stopped due to i) tumor ii) Stone formation, so urine can accumulate in the kidney and cysts formation occur that leads to atrophy of the parenchyma. 2) Congenital absence or malformation of ureter(s). 3) Chronic inflammation of urinary tract that leads to Neoplasia in ureter and urethra. 4) Congenital malposition of kidney(s). GROSSLY i) Dilatation of the pelvis and calyxs ii) Kidney(s) become(s) enlarged with rounded extremitites. iii) Cortex and medulla are progressively thin. iv) Hydronephrotic kidneys are thin walled and contain fluid filled sac. v) Occasionally, such kidney may become contaminated by bacteria and thin walled sac becomes filled with pus instead of urine. Such type of lesion is known as Pyonephritis. MICROSCOPICALLY 1. There is a loss of tubules by degeneration and atrophy followed by condensation of interstitial connective tissue and fibrosis of renal parenchyma. 2. The thin sac is lined by flattened transitional epithelium.
The stone (calculus) may single or multiple. It may presents variable color depending upon the salt deposited. Such as: i) White to grey stone: indicated deposition of oxalalate. ii) Yellow stone: indicates deposition of urate, cystine, xanthene and benzocumorin. ii) Brown stone: indicates deposition of silica, urate and xanthene. 15.4.1. DEVELOPMENT OF CALCULUS Renal calculus consists of nucleus of organic material around which the urinary salt is deposited in several concentric layers which are bound together by colloidal matrix of organic matter. During its passage, calculus excites violent spasmatic contrations which are responsible for pain of the kidney (also named as renal colic). Bacterial colony (known as nidus) is responsible for the salt deposition. It may lodges in the pelvis of the kidney or ureter. ETIOLOGY 1) Less water intake 2) Excessive Salt intake. 3) Any damage to the endothelial lining of the kidney that leads to nidus formation.