Path Final 03
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Transcript of Path Final 03
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Path-202
URINARY SYSTEM
A+B:27/04 LECTURE 11(Continued) C+D:27/04
11.1. URINARY SYSTEM
The urinary system consists of;i) Two kidneys
ii) Two ureters
iii) Urinary bladder
iv) Urethera
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.
11.2. CONGENITAL ANOMALIES OF KIDNEYS
1. RENAL APLASIA OR AGENESIS
It is the failure of development of one or both kidneys but there may be absent or presence of
ureter also along with. If a single kidney is absent then the respective ureter begins as a blind
pouch.
Unilateral renal aplasia may remain undetected for a longer time.2. RENAL HYPOPLASIA
It indicates the incomplete or partial development of kidney in which there would be a fewer
number of nephrones and calyxes at birth. In bovines, there may be absence or decreased
number of tubules.
3. RENAL DYSPLASIA
It is an abnormality of altered structural organization resulting from abnormal differentiation.
CLASS
LECTURESCOMPILED BY
M. SAJJAD HUSSAIN
A Versatile Look of Class Lectures Path-202 /FINAL 3EFFECTIVE FOR
ALL THE FOUR
SECTIONS (A+B & C+D)
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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 thematrix 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
12.1. CIRCULATORY DISTURBANCES
The circulatory disturbances involve the following;
1) HEMORRHAGES:
The hemorrhages over the kidneys may be classified into three types;
a) Patachial hemorrhages:
The most common type of such hemorrhages is renal cortical hemorrhage. It often appears due
to septicemia, which may occur due to any bacterial infection (like Streptococcus andSalmonella infections).
b) Echymotic hemorrhages
Such type of hemorrhages indicates the multifocal tubular and vascular necrosis. These are
commonly observed in Herpes-virus infection.
c) Large spot/Intrarenal/Subcapsular hemorrhages:
It may be due to
i) Direct traumaii) Renal biopsy
iii) Bleeding disorders
iv) DIC (disseminated intravascular coagulatibility)
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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.
12.2. RENAL INFARCTDefinition: It is the area of coagulative necrosis that results from local ischemia and usually due
to thrombo-embolism and aseptic emboli.
Diagnostic Features:
i) There is ischemic necrosis of local area of kidney.
ii) It may be single or multiple.
iii) Infarct area is wedge shaped
iv) The base of wedge shaped area is towards the cortical regionv) The apex of this area is towards the medulla.
GROSSLY:
1. Renal infarct usually appears red or pale white depending on several factors including;
i) interval after vascular occlusion,
ii) Whether an artery or a vein is occluded.
2. Occlusion of arteries results in infarct that is initially hemorrhagic and slightly swollen.
3. It turned pale to yellow grey within 2-3 days, because of lysis of RBCs and loss of Hb.
4. Pale infarct has a central area of coagulative necrosis and usually surrounded by a zone of
congestion and hemorrhages along with pale margin because of surrounded zone of leukocytes.
5. Infarcts are often wedge-shaped with base against the cortical surface and apex pointing towards
the medulla.
MICROSCOPICALLY:
1. Nephrones and interstitium in central zone of infarct becomes necrotic.
2. Glumeruli tend to be spread along the margin of the necrotic zone.
3. Area is infiltrated initially with the neutrophils, few macrophages and lymphocytes.
4. Capillaries adjacent to the necrotic area are markedly engorged with blood.
5. Healing of infracted area occur by lysis and phagocytosis of necrotic tissue and also
replacement by fibrous connective tissue, leaving a discrete fibrotic scar.
6. Scars arranged from linear to broader fashion depending on the size of acute infarct.
ETIOLOGY/CAUSES
Renal infarct may occur as a result of (due to) theses diseases:
i) Vegetative vulvitis
ii) Embolic obstruction
iii) Strongylus vulgaris
iv) Thrombosis
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v) Renal amyloidosis
12.3. NEPHRITIS
It is the inflammation of the kidney.
FORMS OF NEPHRITISIt may be of various forms/types
i) Glomerular nephritis
ii) Tubular nephritis
iii) Glomerulo-tubular nephritis
iv) Interstitial nephritis
12.4. GLUMERULAR NEPHRITIS
It could be of many types depending upon the duration.
i) Acute ii) Subacute iii) Chronic iv) Diffused or local
12.4.1. ACUTE GLOMERULAR NEPHRITIS
It is an inflammatory condition effecting the glumeruli primarily but secondarily damages the
other part of the nephrone as well as interstitial tissues later.
GROSSLY:
i) Kidney is swollen, capsule dense and somewhat stretched.
ii) When kidney is incised, renal substances bulges and numerous thread like rods corresponding
to petechial hemorrhages into the capsular space.
MICROSCOPICALLY:
1. Acute inflammatory exudate is accumulated in the interstitial tissue and mesengium.
2. There is edema and swelling of endothelium of capillary loop.
3. Mesengium becomes widen and resulting compression of capillaries and great ischemia of
glomerulus.
4. Greatly increased in cellularity of tuft as well as swelling and multiplication of epithelium of
tuft.
5. Later, this epithelium desquamated and cast off into capsular space.
6. Polymorphs leukocytes collect in large number in the glomerular capillaries and in capsular
space which then, passes into the urine.
A+B:29/04 LECTURE 13 C+D:29/04
13.1. SUBACUTE GLOMERULAR NEPHRITIS
GROSSLY:
i) Kidney is considerably large (Large white kidney). The consistency is very soft.
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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 incapsular 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
.
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.
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13.2. CHRONIC GLOMERULAR NEPHRITIS
GROSSLY:
i) Kidney is small and shriveled with surface covered with fine granules entirely.
ii) Renal capsule is so adherent that it is stripped off and portion of cortex may come away with it
(Decortication).
iii) Cut surface of the kidney shows extreme irregularity and atrophy of cortex.
MICROSCOPICALLY:
1. There is a complete loss of renal architecture.
2. Renal parenchyma has been replaced with chief substitutes of fibrous tissues with few
scattered glomeruli.
3. Glomeruli show extensive hyalinization.
4. Due to disappearance of tubules and shrinkage of cortex, there may be large number of
hyaline glomeruli.
5. Glomuruli are atrophic, shrinken, but the capillaries still may give the passage to some
blood.
6. Convulated tubules show an extreme degree of atrophy and only the outline may be
detected under high resolution.
A+B:04/05 LECTURE 14 C+D:04/05
14.1. VIRAL GLOMERULAR NEPHRITIS
The glomerular lesions may occur in certain viral diseases such as:
i) Acute infectious canine hepatitis
ii) Septicemic cytomegalovirus infection
iii) Equine arteritis virus infection
iv) New castle disease (in birds).
LESIONS:
1. The Lesions are mild and result from the viral replication in the capillary endothelium.
2. Viral induced intranuclear inclusions are present in glomerular capillaries & endothelium.
3. Inclusion bodies are usually large, basophilic (magenta color) and either fill the nucleus or
separated from the nuclear membrane by clear hallow.
4. Viral antigen can be demonstrated in the endothelium, epithelium or Mesengial cell
through immunovytochemistry.
14.2. RENAL AMYLOIDOSIS
What isAmyloid:
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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 proteincalled as Serum Amyloid Associated (SAA) protein.
Sometime, Amyloid fibril from either source are deposited in the tissues along withglycoprotein 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.
14.3. INTERSTITIAL NEPHRITISIt is also termed as tubulo-interstitial nephritis.
It is a disease in which the aggregates of inflammatory cells can be present in the renal
interstitium, in various systemic infectious diseases of domestic animals like:
i) In Dog: Leptospira infection, Icterohemorrhagiae and Infectious Canine hepatitis.
ii) In Cattle: E.coli septicemia, Malignanat catarrhal fever (MCF), Theleria parva inf.
iii) In Horse: Equine viral arteritis, Equine Infectious anemia.
iv) In Sheep: Sheep pox infection.14.3.1. FORMS OF INTERSTITIAL NEPHRITIS:
It may be i) Acute ii) Subacute iii) Chronic. Either it may be i) Diffused ii) Focal
In Case ofDiffused Interstitial Nephritis:
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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 theouter 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.
14.4. GRANULOMATOUS NEPHRITIS
It is characterized by the multiple granulomas in the kidneys. It is associated with a variety of
infectious agents i.e. viruses, bacteria, fungi, parasites etc.
i)Viral Infections:
-Faline infectious peritonitis
-Encephaliozoon tuniculi (In case of dog)
ii) Bacterial Infections:
-Mycobacterium tuberculosis
iii) Fungal infections:
-Aspergilosis
iv) Parasitic Infections:
- Toxocara canis
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 ii) Corynebacterium renale iii) Klebsiella
iv) Proteus v) Pseudomonas aureginosa
Pyelitis may be unilateral or bilateral but often it is bilateral.
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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.
15.4. RENAL CALCULUSSYN:Nephrolethiasis.
Stone formation in the kidney is termed as nephrolethiasis.
FORMS OF CALCULUS
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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 isdeposited 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 forpain 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.
15.5. NEOPLASMS OF KIDNEY (Tumors of Kidney)It may be classified into three types:
i) Adenomas tumors.
ii) Carcinomas tumors.
iii) Embryonal tumors.
TUMORS OF URINARY TRACT (Its your assignment).
END OF URINARY SYSTEMCOMPOSED BY
M. SAJJAD HUSSAIN
DVM 4th semester (2007-ag-1638)
PRESENTED BY
M. SAJJAD HUSSAIN
