Path 1- Urinary 2

kelseyfmeyer's version from 2015-04-16 18:55

Lecture 3

Question Answer
*what happens if one part of the nephron is injured?Injury to one part of the nephron results in progressive damage to other components of the nephron with eventual loss of function
*glomerular injury occurs as a result of deposition of? (4)immune complexes (type III hypersensitivity), thromboemboli, bacterial emboli or direct infections, proteins (amyloid, fibrin)
*glomerular injury may also be caused by hyperfiltration, two examples of when this happens would be?(1) prolonged systemic hypertension (2)*****increased dietary protein (proteinuria can cause damage when prolonged)
**chronic proteinuria can lead to what?glom. injury
*glomerular injury also causes damage in what ways, how?glomerular injury also interferes with the peritubular blood supply resulting in hypoxia with tubular atrophy and loss of function
*damage to glomerular filtration barrier results in leakage of WHAT? what will you see?results in leakage of low molecular weight proteins into the urine (proteinuria). SPECIFICALLY, you will see ALBUMIN and antithrombin III
**what is nephrotic syndrome? explain how it happens and the clinical signsGlomerular damage can cause severe proteinuria leading to hypoproteinemia with reduced plasma oncotic pressure resulting in ascites, pleural effusion, and generalized edema. THIS is nephrotic syndrome.
****nephrotic syndrome is a result of ___ (short answer)protein losing nephropathy
what happens to body weight when there is prolonged proteinuria?weight loss
**how does protein losing nephropathy affect the blood? (NOT edema due to dec oncotic pressure, sthing else)Loss of antithrombin III can result in a hypercoagulable state with resulting thromboembolic disease
what are some acute responses to injury of the glom?mesangial hypertrophy and hyperplasia, increased vascular permeability, infiltration of leukocytes, necrosis
what are some chronic responses to injury of the glom?atrophy, fibrosis (glomerulosclerosis), renal tubules will become secondarily atrophic due to loss of blood supply from efferent glomerular arteriole
glomerulosclerosis is what, that resulted from what?is fibrosis which resulted from chronic glom damage
*Tubular damage occurs with? (6)bloodborne infections, ascending infections, toxins, infarction / ischemia, volume overload, abnormal glomerular filtrate
what are some abnormal glomerular filtrate which can lead to tubular damage? (2)(1) high protein (2) high crystalline salts / organic acids (oxalic acid, uric acid, pyruvic acid)
Tubular damage results in what 4 responses?(1) atropy (2) degeneration (3) regeneration (4) necrosis
tubular atrophy occurs secondary to what conditions?interstitial fibrosis, compression by space occupying mass, intratubular volume overload due to obstruction and backpressure, diminished glomerular perfusion (shock, hypovolemia), reduced oxygen tension (anemia, hypoxemia)
When is regeneration of tubules possible?ONLY POSSIBLE IF tubular basement membrane (TBM) is left intact!!
**which type of injury to the tubules permits regeneration? which does not?toxic injury - TBM is generally preserved which allows for regeneration!!! ischemic injury - TBM is destroyed causing permanent scar with no regeneration
***is the single most important cause of acute renal failure in animals?ACUTE TUBULAR NECROSIS
*what are the two main things which cause acute tubular necrosis?ischemia or nephrotoxicity
acute tubular necrosis clinically results in what two signs, and why?oliguria and anuria by either: (1) leakage of tubular ultrafiltrate from damages tubules or (2) intratubular obstruction from sloughed necrotic epithelium (cellular casts)
what is going on with the chemicals/toxic metabolites in the tubules in order for them to cause nephrotoxic injury?THEY MUST BE CONCENTRATED
**What is nephrotoxin-associated ischemia?Nephrotoxins indirectly stimulate vasoconstriction of the intertubular capillaries causing ischemia
Nephrotoxins cause damage by what three mechanisms?(1) direct damage to epithelium (2) produce reactive metabolites that damage the epithelium (3) indirectly stimulate vasoconstriction of the intertubular capillaries causing ischemia (nephrotoxin-associated ischemia)
**What is nephrosis?a form of acute tubular necrosis that is not caused by inflammation
*What usually CAUSES nephrosis?(a form of acute tubular necrosis that is not caused by inflammation) typically caused by hypoxic injury combined with nephrotoxic injury
What is hemoglobinuric nephrosis?hypoxic injury is exacerbated by hemoglobinuria during a hemolytic crisis
What is myoglobinuric nephrosis?hypoxic injury is exacerbated by myoglobinuria during acute muscle injury
what are the gross lesions of acute tubular necrosis?often difficult to recognize, swollen, pale cortex that bulges on cut surface, and may see accentuated striations or white streaks
Microscopic lesions of acute tubular necrosis?tubular epithelial swelling, vacuolation, hypereosinophilia, pyknosis, karyorrhexis, karyolysis
what part of the nephron is more sensitive to hypoxia due to higher metabolic demands?proximal tubules
what part of the nephron is resistant to ischemia and often remains morphologically normal in necrosis?glomeruli
Lymphofollicular inflammation--> what does this look like? what is this a common rxn to?multinodular lymphocytic reaction to chronic or recurrent inflammation. most common response to chronic Leptospira infection
**What does progressive fibrosis lead to?progressive fibrosis leads to progressive loss of renal function
Interstitial nephritis refers to inflammation of what areas?interstitium= veins, arteries, lymphatics, nerves, connective tissue, etc
what are some infectious causes in interstitial nephritis?canine ehrlichiosis, leptospirosis.....equine infectious anemia
when does interstitial nephritis lead to renal failure/end-stage kidney?only severe interstitial nephritis will lead to renal failure and end-stage kidney
Tubulointerstitial nephritis--> acute inflammation is usually secondary to acute tubular necrosis or acute infection (SUCH AS....)Leptospira, adenoviruses, lentiviruses, herpesviruses
what happens to the kidney with chronic inflammation?chronic inflammation leads to fibrosis, scarring, and eventual loss of function known as end-stage kidney
Kidney-->vasculature-->Infarction--> explain thislocalized areas of coagulative necrosis that result from vascular occlusion (usually thromboembolism, bacterial emboli, or tumor emboli) (results in a well-demarcated, cone-shaped area of coagulative necrosis extending from medulla (apex) to cortex (base))
when does a large emboli occur? when does a small emboi occur?larger emboli → occlusion of arcuate artery (large infarct). smaller emboli (most common) → occlusion of interlobular artery (small infarct)
how do ureters enter bladder? where?obliquely at the bladder trigone
what is the mucosa of the ureters like? muscle? outer covering?smooth and glistening mucosa with longitudinal folds and transitional epithelium. longitudinal and circular smooth muscle layers, and peritoneal serosa on outside.
what are the three main portals of entry (for infection)( of the lower urinary tract?(1) ascending infection (MORE COMMON IN FEMALES) (2) direct penetration from lumen (toxins/uroliths damage mucosa) (3) direct penetration from abdomen (cystocentesis)
list 5 defense of the lower urinary tract(1) Flushing action of urine reduces the risk of ascending infection (2) peristalsis acts to elim bact (3) Slightly acidic urine (pH 6.2-6.5) reduces growth of some bacteria (4) Protective urethral mucus layer reduces bacterial adhesion (5) innate and adaptive immune responses
* Causes of glomerular injury include? deposition of immune complexes, thromboemboli, bacterial emboli, and proteins.
*how does hypercoagubility happen with dz of the urinary tract?glom damage--> protein losing nephropathy--> lose antithrombin III, leads to hypercoag.
*Renal tubules respond to injury how? with atrophy, degeneration, regeneration, and necrosis.
Acute tubular necrosis is usually caused by what? which results in what? ischemia or nephrotoxicity and results in oliguria or anuria.

Lecture 4

Question Answer
what are the 5 developmental anomalies which affect the kidneys?(1) Renal aplasia, hypoplasia, dysplasia (2) Ectopic kidney (3) fused kidneys (4) renal cysts (5) Polycystic kidneys
explain renal dysplasia"asynchronous differentiation of nephrons" (not all developed at same rate into same stages), so there is persistence of primitive mesenchyme and metanephric ducts. There is also adenomatoid tubular epithelium. presence of chondroid or osseous metaplasia
what is Juvenile Progressive Nephropathy? who is it common in?a specific form of renal dysplasia, which occurs with variable severity and degrees of renal failure. inherited disease described in Lhasa Apso, Shih Tzu, Golden retriever
explain exctopic kidney. who is it most common in?abnormal migration of renal tissue during fetal development, the usually described locations is pelvic and inguinal, and it usually just involves one kidney. It is most common in pigs and dogs
fused kidneys is aka? explain itaka horseshoe kideny, during nephrogenesis the L and R kidneys fuse. It creates one large kidney but it still has two ureters. They usually maintain normal function.
How would you describe what a renal cyst looks like?spherical, thin-walled, distended tubules filled with clear watery fluid
renal cysts can be acquired or congenital. How do they occur? Who do they usually occur in?result from tubular obstruction or tubular dysplasia. common in pigs and cattle
how many renal cysts do you usually see? If you see these, what should you think?usually only one or a few, and usually incidental finding with no clinical significance
*how is Polycystic kidneys defined?defined as many renal cysts affecting numerous nephrons
who is prone to Polycystic Kidney Disease? How do they get it?inherited as an autosomal dominant trait in Persian cats and bull terriers
What is the pathogenesis of polycystic kidney disease? How dangerous is this?Pathogenesis: mutations in one or multiple genes (PKD-1 and/or PKD-2) resulting in abnormal tubulogenesis. Renal function can be impaired in severe cases where there is significant loss of parenchyma
**Immune-mediated (immune complex) glomerulonephritis is associated with/caused by? Who does it occur in?associated with persistent infections or other causes of prolonged antigenemia that enhances the formation of abundant soluble immune complexes in the blood plasma. deposition of soluble immune complexes within glomeruli results in complement fixation, leukocyte infiltration, and formation of fibrin thrombi, with subsequent glomerular damage. It occurs most commonly in cats and dogs
list off some Diseases associated with immune complex glomerulonephritis (ICGN)? in DOGS (not in yellow. Read them over tho)infectious canine hepatitis, chronic hepatitis, pyometria, pyoderma, dirofilariasis, SLE, autoimmune hemolytic anemia, etc etc
list off some Diseases associated with immune complex glomerulonephritis (ICGN)? in CATS (not in yellow. Read them over tho)FeLV, FIP, FIV, progressive polyarteritis, neoplasia
list off some Diseases associated with immune complex glomerulonephritis (ICGN)? in HORSES (not in yellow. Read them over tho)Streptococcus sp. infections, equine infectious anemia
list off some Diseases associated with immune complex glomerulonephritis (ICGN)? in CATTLE (not in yellow. Read them over tho)BVD, trypanosomiasis
list off some Diseases associated with immune complex glomerulonephritis (ICGN)? in PIGS (not in yellow. Read them over tho)classical swine fever, African swine fever
what are some gross lesions youd see in Immune-mediated (immune complex) glomerulonephritis (ICGN)can be subtle or non-existant, OR may see swollen, enlarged glomeruli as red pin-point foci in the cortex
what are the three histological forms that Immune-mediated (immune complex) glomerulonephritis can take?Proliferative glomerulonephritis, Membranous glomerulonephritis, Membrano-proliferative glomerulonephritis
how is Proliferative glomerulonephritis characterized? Who is this form most common in?characterized by increased cellularity of the glomerular tufts caused by proliferation of glomerular endothelial, epithelial, and mesangial cells, and an influx of leukocytes (so, lots more cells in the glom than there should be). It is the form most common in horses.
how is Membranous glomerulonephritis characterized? Who is this form most common in?characterized by diffuse glomerular capillary basement membrane thickening due to subepithelial deposition of /immunoglobulin and fibrosis/. most common form in CATS
how is Membrano-proliferative glomerulonephritis characterized? Who is this form most common in?characterized by hypercellularity and thickening of glomerular basement membrane and mesangium. Most common form in DOGS
*What is Glomerulosclerosis? What can it be associated with? describe it, and what are some results of it?a condition of chronic glomerulonephritis characterized by fibrosis of the glomerulus. also associated with high blood pressure and unrestricted dietary protein. Glomeruli become shrunken, hyalinized, and sclerotic with fibrous connective tissue. glomerular fibrosis reduced the blood flow to the tubules causing secondary tubular degeneration and atrophy
**Glomerular amyloidosis is associated with what?typically associated with reactive systemic amyloidosis (AA amyloidosis) that occurs with chronic inflammatory diseases
**what are the most common site of renal deposition of amyloid? sp diffs?the glom is the most common site, but in Abyssinian, they cats typically have predominant medullary interstitial deposition
**who is genetically predisposed to reactive amyloidosis? What does this mean they are ALSO predisposed to?Abyssinian cats and Chinese Shar-Pei dogs are genetically predisposed to reactive amyloidosis--> thus, at risk for Glomerular amyloidosis
what is a common cause of protein losing nephropathy?amyloidosis
What are the gross lesions of glom. amyloidosis?kidneys are enlarged, pale, and have a waxy, smooth, to finely granular capsular surface
what are the microscopic lesions of glom. amyloidosis?deposition of amyloid protein within glomerular tufts diffusely---> Congo red stain is specific for amyloid protein

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