Path 1 - Urinary 2

drraythe's version from 2015-05-04 16:49

Lecture 3

Question Answer
*What happens if 1 part of the nephron is injured?Injury to 1 part of the nephron results in progressive dmg to other components of the nephron w/ eventual loss of fxn
*Glomerular injury occurs as a result of deposition of? (4)Immune complexes (Type III hypersensitivity)
Bacterial emboli or direct infxns
Proteins (amyloid, fibrin)
*Glomerular injury may also be caused by hyperfiltration, 2 examples of when this happens would be?(1) Prolonged systemic hypertension
(2) ↑ dietary protein (proteinuria can cause dmg when prolonged)
**Chronic Proteinuria can lead to what?Glom. injury
*Glomerular injury also causes dmg in what ways, how?Glomerular injury also interferes w/ the peritubular blood supply resulting in hypoxia w/ tubular atrophy & loss of fxn
*Dmg 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 & Antithrombin III
**What is nephrotic syndrome? Explain how it happens & the CSGlomerular dmg can cause severe proteinuria leading to hypOproteinemia w/ reduced plasma oncotic pressure resulting in ascites, pleural effusion & 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 ↓ oncotic pressure, something else)Loss of Antithrombin III can result in a hypercoagulable state w/ resulting thromboembolic dz
What are some acute responses to injury of the glom?Mesangial hypertrophy & hyperplasia, ↑ 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?Fibrosis which results from chronic glom dmg
*Tubular dmg occurs w/? (6)Bloodborne infxns
Ascending infxns
Infarction / ischemia
Volume overload
Abnormal glomerular filtrate

What are some abnormal glomerular filtrate which can lead to tubular dmg? (2)(1) ↑ protein
(2) ↑ crystalline salts / organic acids (Oxalic acid, Uric acid, Pyruvic acid)
Tubular dmg results in what 4 responses?(1) Atrophy
(2) Degeneration
(3) Regeneration
(4) Necrosis
Tubular atrophy occurs 2° to what conditions?Interstitial fibrosis, compression by space occupying mass, intratubular volume overload due to obstruction & 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 w/ no regeneration
***Is the single most important cause of Acute Renal Failure in animals?ACUTE TUBULAR NECROSIS
*What are the 2 main things which cause Acute Tubular Necrosis?Ischemia or nephrotoxicity
Acute Tubular Necrosis clinically results in what 2 signs & why?Oliguria & Anuria by either:
(1) Leakage of tubular ultrafiltrate from dmgs tubules or
(2) Intratubular obstruction from sloughed necrotic epithelium (cellular casts)
What is going on w/ 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 dmg by what 3 mechanisms?(1) Direct dmg to epithelium
(2) Produce reactive metabolites that dmg the EPIthelium via oxydative injury
(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 w/ 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
Accentuated striations or white streaks may be see.
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 tubule
What part of the nephron is resistant to ischemia & often remains morphologically normal in necrosis?Glomeruli
Lymphofollicular inflammation → What does this look like? What is this a common rxn to?Multinodular lymphocytic rxn to chronic or recurrent inflammation. Most common response to chronic Leptospira infxn
**What does progressive fibrosis lead to?Progressive fibrosis leads to progressive loss of renal fxn
Interstitial Nephritis refers to inflammation of what areas?Interstitium = veins, arteries, lymphatics, nerves, connective tissue, etc
What are some infectious (be specific) causes in Interstitial Nephritis?Canine Ehrlichiosis
Equine Infectious Anemia
When does Interstitial Nephritis lead to renal failure/end-stage kidney?Only severe Interstitial Nephritis will lead to renal failure & end-stage kidney
Tubulointerstitial Nephritis → Acute inflammation is usually 2° to Acute Tubular Necrosis or acute infxn (SUCH AS....)Leptospira, adenoviruses, lentiviruses, herpesviruses
What happens to the kidney w/ chronic inflammation?Chronic inflammation leads to fibrosis, scarring & eventual loss of fxn known as end-stage kidney
Kidney → Vasculature → Infarction → Explain?Localized 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 emboli 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 & glistening mucosa w/ longitudinal folds & transitional epithelium. Longitudinal & circular smooth muscle layers & peritoneal serosa on outside.
What are the 3 main portals of entry (for infxn) (of the lower urinary tract?(1) Ascending infxn (MORE COMMON IN FEMALES)
(2) Direct penetration from lumen (toxins/uroliths dmg mucosa)
(3) Direct penetration from abdomen (cystocentesis)
List 5 defenses of the lower urinary tract(1) Flushing action of urine reduces the risk of ascending infxn
(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 & adaptive immune responses
*Causes of glomerular injury include?Deposition of immune complexes
Bacterial emboli
How does hypercoagubility happen w/ dz of the urinary tract?Glom dmg → protein losing nephropathy → Antithrombin III loss → Hypercoag.
*Renal tubules respond to injury how?W/ atrophy, degeneration, regeneration & necrosis.
Acute Tubular Necrosis is usually caused by what? Which results in what?Ischemia or nephrotoxicity & 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 & metanephric ducts. There is also Adenomatous 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 w/ variable severity & degrees of renal failure. Inherited dz described in Lhasa Apso, Shih Tzu, Golden retriever
~Explain ectopic kidney. Who is it most common in?Abnormal migration of renal tissue during fetal development, the usually described locations is pelvic & inguinal & it usually just involves 1 kidney. It is most common in pigs & dogs
Fused kidneys is aka? Explain itaka horseshoe kidney, during nephrogenesis the L & R kidneys fuse. It creates 1 large kidney but it still has 2 ureters. They usually maintain normal fxn.
How would you describe what a renal cyst looks like?Spherical, thin-walled, distended tubules filled w/ 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 & cattle
How many renal cysts do you usually see? If you see these, what should you think?Usually only 1 or a few & usually incidental finding w/ no clinical significance
How is Polycystic kidneys defined?Defined as many renal cysts affecting numerous nephrons
Who is prone to Polycystic Kidney Dz? How do they get it?Inherited as an autosomal dominant trait in PERSIAN CATS & bull terriers
What is the pathogenesis of polycystic kidney dz? How dangerous is this?Pathogenesis: mutations in 1 or multiple genes (PKD-1 &/or PKD-2) resulting in abnormal tubulogenesis. Renal fxn can be impaired in severe cases where there is significant loss of parenchyma
**Immune-mediated (immune complex) Glomerulonephritis is associated w/caused by? Who does it occur in?Associated w/ persistent infxns or other causes of prolonged antigenemia that enhances the formation of abundant soluble immune complexes in the blood plasma. Deposition of soluble immune complexes w/in glomeruli results in complement fixation, leukocyte infiltration & formation of fibrin thrombi, w/ subsequent glomerular dmg. It occurs most commonly in cats & dogs
What are some gross lesions youd see in Immune-mediated (immune complex) Glomerulonephritis (ICGN)Can be subtle or non-existent, OR may see swollen, enlarged glomeruli as red pin-point foci in the cortex
What are the 3 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 ↑ cellularity of the glomerular tufts caused by proliferation of glomerular endothelial, epithelial & mesangial cells & 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 & fibrosis. Most common form in CATS
How is Membrano-proliferative Glomerulonephritis characterized? Who is this form most common in?Characterized by hypercellularity & thickening of glomerular basement membrane & mesangium. Most common form in DOGS
*What is Glomerulosclerosis? What can it be associated w/? Describe it & what are some results of it?A condition of chronic Glomerulonephritis characterized by fibrosis of the glomerulus. Also associated w/ high blood pressure & unrestricted dietary protein. Glomeruli become shrunken, hyalinized & sclerotic w/ fibrous connective tissue. Glomerular Fibrosis reduced the blood flow to the tubules causing 2° tubular degeneration & atrophy
**Glomerular Amyloidosis is associated w/ what?Typically associated w/ Reactive Systemic Amyloidosis (AA amyloidosis) that occurs w/ chronic inflammatory dzs
**What are the most common site of renal deposition of amyloid? Sp diffs?The glom is the most common site, but Abyssinians typically have predominant medullary interstitial deposition
**Who is genetically predisposed to reactive amyloidosis? What does this mean they are ALSO predisposed to?Abyssinian cats & 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 & have a waxy, smooth, to finely granular capsular surface
What are the microscopic lesions of glom. amyloidosis?Deposition of amyloid protein w/in glomerular tufts diffusely → Congo red stain is specific for amyloid protein

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