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Systemic Pathology > Urinary System > Flashcards

Urinary System Flashcards

1
Q

What are the Major and Minor urinary diseases of Dogs?

A
  • Major:
    • Acute and chronic renal failure
    • Cystitis
    • Urolithiasis
    • Renal infarction
    • Uremia
    • Nephrotic syndrome
    • Toxins: Ethylene glycol
  • Minor:
    • renal neoplasia
    • Toxins: grapes/raisins, melamine
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2
Q

What are the Major and Minor urinary diseases of Cats?

A
  • Major:
    • Acute and Chronic renal failure
    • Lower urinary Tract Disease (FLUTD)
    • Urolithiasis
    • Renal infarction
  • Toxins:
    • Lillies
    • ethylene glycol
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3
Q

What are the Major and Minor urinary diseases of Swine?

A
  • Major:
    • Cystitis
    • Pyelonephritis
  • Minor:
    • Toxins: plants (pigweed)
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4
Q

What are the Major and Minor urinary diseases of Horses?

A
  • Major:
    • Uroperitoneum
    • Patent urachus
  • Mine:
    • acute and chronic renal failure
    • Toxins: NSAIDS, Aminoglycosides, blister beetles/cantharadin
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5
Q

What are the Major and Minor urinary diseases of Cattle?

A
  • Major:
    • Pyelonephritis
    • urolithiasis
    • renal infarction
  • Minor:
    • Cystitis
    • Patent urachus
      • Toxins: plants (Oak, oxalates, Vit D, bracken fern) aminoglycosides
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6
Q

What are the Major and Minor urinary diseases of Sheep/goats

A
  • Major:
    • Urolithiasis; obstruction
    • Toxins: epsilon toxin, enterotoxemia (from C perf type D)
  • Minor:
    • Toxins: plants (oak, oxalates, Vit D)
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7
Q

What are unipyramidal kidneys?

A
  • Bean shaped, one single lobe, single papilla (crest) empties into renal pelvis
  • Carnivores, horses, rodents, small ruminants
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8
Q

What are Multipyramidal/Multilobar kidneys

A
  • Mostly bean shaped, multiple lobes (with external lobe structure) with multiple renal pyramids each drains into calyx which then drains into pelvis
  • Cattle
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9
Q

What type of kidneys do humans/pigs have ?

A
  • Multipyramidal/multilobar kidneys
  • Bean shaped, multiple lobes (no external lobe structure) with multiple renal pyramids, each drains into a calyx which then drains into the pelvis
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10
Q

What is the structure of a nephron?

A
  • Glomerulus (renal corpus)
    • glomerular tuft
    • mesangium
    • filtration barrier
  • Tubules
    • PCT
    • loop of Henle
    • DCT
  • Interstitium
  • Vasculature
  • Collecting ducts
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11
Q

What is the structure of a Renal Corpuscle

A
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12
Q

What makes up the glomerular filtration barrier?

A
  • Fenestrated capillary endothelium
  • Basement membrane (produced by epi and endo cells)
  • Podocytes (visceral epithelium)
  • NB filtration is a function of size and charge
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13
Q

What is the Bowman’s capsule?

A
  • Sac enclosing each glomerulus and forming the uriniferous space (filtrate)
  • Has:
    • Basement membrane
    • Parietal epithelial cells
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14
Q

How does blood flow in the kidney?

A
  • Renal a
  • Interlobar a
  • arcuate a
  • interlobular a
  • glomerular afferent and efferent arterioles
  • vasa recta
  • intralobular v
  • arcuate v
  • interlobar v
  • Renal v
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15
Q

What are the functions of the Kidneys?

A
  • Central organ involved in maintenance of extracellular environment in the body
    • Glomerular filtration
    • Tubular resorption and secretion
      • active and passive
  1. Excretion/elimination of metabolic waste
  2. Acid - Base regulation (reclaim Bicarb from filtrate (PCT)
  3. Salt and water conservation (tubules via ADH - 99% resorbed)
  4. Tubular resorption/secretion (glucose, AA, Ca, P, K resorbed and/or secreted to maintain balance)
  5. Endocrine, metabolism
    1. Vit D ⇢ Ca absroption
    2. REnin-angiotensin-Aldosterone
    3. erythropoietin
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16
Q

What is filtered in Glomerular filtration?

A
  • Size dependent:
    • < 2.5nm (100% passes)
    • > 3.5 nm (0%)
  • Charge dependent:
    • positive & neutrals pass through better than negative
  • GFR is dependent on renal perfusion and # of functional glomeruli
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17
Q

What is essential for normal renal function?

A
  • Adequate blood perfusion (25% of CO)
  • Adequate functional renal tissue
  • Normal elimination of urine
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18
Q

What is Azotemia?

A
  • Increase intravascular nitrogenous waste
    • Pre-renal: due to renal hypoperfusion
    • Renal: failure of the kidney’s filtration function
    • Post-renal: urinary obstruction
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19
Q

What is Uremia?

A
  • Multisystemic syndrome/clinical signs due to renal failure
    • biochemical disturbances (fluid volume, electrolytes, A/B, failure to excrete wastes (uremic toxins) disturbances in endocrine function (PTH)
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20
Q

What is Nephrotic syndrome?

A
  • a clinical syndrome:
    • proteinuria
    • edema
    • ascites
    • pleural effusion
    • hypercholesterolemia
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21
Q

What is renal failure?

A
  • Loss of function
  • Acute
  • Chronic
  • End-stage: ,5% of normal GFR, terminal stages of uremia
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22
Q

What types of damage to the nephron results in renal failure?

A
  • Nephron functions as a unit, damage to one component will affect other components:
    • Glomerular damage due to immune complex deposition, infectious organisms
      • clinical findings: protein leakage, protein-losing nephropathy (PLN)
    • Tubular damage due to infectious organisms, ischemia, nephrotoxic drugs, chemical toxins, or obstruction
      • ischemia, blood-borne/ascending/descending infections, direct damage
    • Interstitial damage due to inflammation, fibrosis, edema
    • Vascular damage due to congestion, thrombosis, infarction
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23
Q

What are the different types of glomerular damage/disease?

A
  • Necrosis, inflammation, membrane thickening
    • immune complex deposition
    • thrombosis / embolization
    • direct viral or bacterial infection of glomerular components
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24
Q

What is the major clinical finding of glomerular disease?

A
  • Protein loss (albumin) and proteinuria, which overwhelms tubular resorptive capacity = PLN
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25
Q

Can nephrons regenerate?

A

No, some compensatory hypertrophy, but no regeneration of whole nephrons

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26
Q

What are the different diseases of the glomeruli?

A
  • Immune-mediated glomerulenophritis
  • Minimal change disease (human children)
  • glomerulosclerosis
  • glomerular amyloidosis
  • acute suppurative (embolic) glomerulitis
  • Viral or chemical glomerulonephritis
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27
Q

What is Immune complex glomerulonephritis (ICGN?)

A
  • Glomerular deposition of immune complexes
    • microscopic and ultrastructural lesions - subtle may see pinpoint cortical spots
  • 2 types:
    • Soluble (most common)
      • persistent infection, prolonged antigenemia
      • Familial are described (Bernese mountain dogs)
    • Auto-immune - directed at GBM itself
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28
Q

What is the general pathogenesis of Immune complex glomerulonephritis?

A
  1. Antigen-antibody (IC) formation in blood
  2. Selective deposition in glomerular capillaries
  3. Stimulation of complement fixation (C3a, C5a….)
  4. Neutrophil chemotaxis
  5. basement membrane damage and inflammation
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29
Q

What diseases can cause Immune-Complex Glomerulonephritis in dogs?

A
  • infectious canine hepatitis
  • chonic hepatitis
  • chronic bacterial diseases
  • Endometritis (pyometra)
  • Pyoderma
  • Prostatitis
  • Dirofilariasis
  • Borreliosis (lyme disease)
  • Systemic lupus erythrematosus
  • Polyarteritis
  • Autoimmune hemolytic anemia
  • Immune-mediated polyarthritis
  • Neoplasia-mastocytoma
  • Hereditary C3 deficiency
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30
Q

What diseases can cause Immune-Complex Glomerulonephritis in cats?

A
  • Feline leukemia virus (FeLV) infection
  • Feline infectious peritonitis (FIP)
  • Feline immunodeficiency virus (FIV)
  • Progressive polyarteritis
  • Neoplasia
  • Progressive membranous glomerulonephritis (GN)
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31
Q

What diseases can cause Immune-Complex Glomerulonephritis in Farm animals?

A
  • Horses:
    • equine infectious anemia
    • streptococcus sp.
  • Cattle:
    • Bovine viral diarrhea
    • Trypanosomiasis
  • Sheep:
    • Hereditary hypocomplementemia in Finnish Landrace lambs
  • Pigs:
    • Hog cholera
    • African swine fever
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32
Q

What are the different patterns of injury ICGN causes in the Glomerular filtration barrier?

A
  • Membranous glomerulonephritis
  • Membranoproliferative glomerulonephritis (Type I)
  • Membranoproliferative glomerulonephritis (Type II)
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33
Q

What does membranous glomerulonephritis look like histologically?

A
  • Extensive loss of foot processes of visceral epithelial cells
  • Flattened visceral epithelial cells
  • Subepithelial deposits (immune complexes)
  • Thickened basement membrane
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34
Q

What is the difference between Membranoproliferative glomerulonephritis Type I and Type II

A
  • Type 1 = subendothelial deposits (immune complexes)
  • Type II = intramembranous deposits (immune complexes)
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35
Q

What affects does glomerular deposition of immune complexes have?

A
  • Deposits of IC can occur at various levels
    • basement membrane
    • subepithelial (podocyte/uriniferous space side)
    • Subendothelial (vascular side)***
  • Inflammatory damage to epithelial cells (podocytes)
    • reaction/loss of podocyte foot processes
    • thickening of the basement membrane
  • Cause is usually not determined (specific antigen)
  • gross lesions are subtle
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36
Q

What gross lesions are common with ICGN?

A
  • enlarged glomeruli are observed as small white foci in the cortex, canine proliferative glomerulopathy
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37
Q

What microscopic/submicroscopic (EM) lesions are common with membranous glomerulopathy

A
  • BM thickening without prominent increased glomerular cellularity
    • leukocytes, endothelia cells, mesangial cells
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38
Q

What microscopic/submicroscopic (EM) lesions are common with membranoproliferative glomerulpathy?

A
  • BM thickening with increased glomerular cellularity
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39
Q

What are the histologic patterns of glomerular lesions?

A
  • focal vs diffuse: <50% vs >50% of glomeruli are affected
  • Segmental vs global: portion or all of glomerular tuft is affected
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40
Q

What is glomerulosclerosis?

A
  • Occurs with chronic glomerular disease
    • Increased fibrous tissue, reduced vessels
    • The vasa recta receive blood from glomerular efferents, so with glomerular injury, there will now be reduced blood flow and oxygen tension in tubules ⇢ tubular epithelial cell dropout and functional loss
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41
Q

What is amyloid

A
  • Amyloid = insoluble fibrillary B-pleated sheet protein
  • AL amyloidosis: primary, light chain immunoglobulins (plasma cell tumors, myelomas)
  • AA amyloidosis: secondary, reactive, associated with chronic inflammatory diseases and serum amyloid A (SAA)
    • hereditary in shar-peis, Abysinnians
42
Q

What affect do amyloid deposits have on the kidney?

A
  • Glomeruli (dog) ⇢ protein loss
  • Medullary interstitium (Cats, Shar-pei) ⇢ incidental or can lead to papillary necrosis
43
Q

What is glomerular amyloidosis?

A
  • Amyloid deposited in mesangium and subendothelial/GBM locations
  • Reduced oxygen to tubules (vasa recta receives blood from glomerular efferents) ⇢ cellular dropout and functional loss
    • Renal medullary necrosis (arrows) occurs with amyloidosis or from other causes
  • In dogs: Enlarged swollen pale (waxy) kidneys
  • Dx: confirm by congo red on fixed tissue
44
Q

What is the difference between descending and ascending bacterial glomerulitis?

A
  • Descending: bacterial embolization of glomeruli
    • bacteria come from hematogenous route
  • Ascending: urinary cystitis + vesicoureteral reflux
    • bacteria come from urinary bladder
45
Q

What happens during bacterial glomerulitis?

A
  • Organisms lodge in glomerular capillaries during bacteremia
  • Gross lesions: multiple raised cortical nodules (<1m)
  • Histo: many bacteria, with neutrophils and debris in glomeruli
46
Q

What are some bacteria that cause bacterial glomerulitis?

A
  • Foals = actinobacillus equuli
  • Piglets = Erysipelothrix rhusiopathiae
  • Small ruminants = Corynebacterium pseudotuberculosis
  • Cattle = Truperella pyogenes, others
47
Q

How is bacterial glomerulitis diagnosed?

A
  • Gross + histo (fixed kidney) + bacterial culture (fresh kidney, spleen, lung, liver)
48
Q

Differential diagnoses for this lesion?

A
  • Pig kidney, hemorrhagic glomerulitis (“renal petechia”)
    • assume glomeruli based on distribution
  • DDx:
    • Hemorrhage
    • endothelial damage
    • bacterial infection of glomeruli
      • septicemia or endotoxemia (Erysipelothrix rhusiopathiae, Salmonella
49
Q

What is Viral/Chemical glomerulitis?

A
  • Caused by direct Viral/chemical insult to glomerulus
    • Due to vascular supply, many systemic viruses ( and some drugs) can affect glomeruli
      • Animals do not usually die from renal lesions
  • Gross lesions: nonspecific swollen kidneys, glomeruli visible as pinpoint red dots in cortex
  • Histo: necrosis, hemorrhage, thrombosis, viral inclusions
50
Q

What is the characteristic finding with renal tubular disease?

A
  • Oliguria or Anuria
    • due to absorption of urine into interstitium or tubular obstruction
51
Q

Can renal tubules regenerate?

A
  • Renal tubular epithelium has great regenerative capacity
52
Q

What diseases affect the renal tubules and interstitium?

A
  • Tubular damage and necrosis
    • Toxic vs ischemic/hypoxic injury
  • Renal pelvis lesions
    • Obstruction/dilation (hydronephrosis)
    • Inflammation (pyelonephritis)
    • necrosis (papillary/medullary crest necrosis)
  • Interstitial inflammation
  • Interstitial fibrosis (end-stage kidney)
53
Q

What is Tubular necrosis?

A
  • single most important cause of acute renal failure
  • Causes:
    • Nephrotoxic injury
    • Ischemic/hypoxic injury
  • Gross lesions - subtle, swollen pale cortex, radial streaking possible
  • Microscopic lesions depend on extend and duration
    • epithelial cell swelling ⇢ cytoplasmic vacuolation ⇢ cytoplasmic hypereosinophilia ⇢ cellular fragmentation/nuclear pyknosis/karyorrhexis ⇢ cells and debris slough into tubular lumens ⇢ morphologic and functional loss
54
Q

What are the mechanisms of tubular injury?

A
  • direct epithelial cell damage (PCTs)
  • reactive metabolites are toxic after resorption (DCT, loops, CDs)
  • indirectly stimulate vasoconstriction ⇢ nephrotoxin-associated ischemia
55
Q

How do nephrotoxins affect renal tubules?

A
  • toxins are filtered into the urine by glomerulus, then toxin or its metabolites are concentrated in tubules
  • Nephrotoxins do NOT usually affect basement membranes, so if toxin is removed ⇢ regeneration and repair can occur quickly, as BM acts as scaffold for epithelium
56
Q

What are common nephrotoxins for domestic animals?

A
  • Heavy metals:
    • mercury
    • lead
    • arsenic
    • cadmium thallium
  • Antibacterial and Antifungal Agens:
    • aminoglycosides
      • Gentamicin
      • Neomycin
      • Kanamycin
      • Streptoycin
      • Tobrmycin
    • Tetracyclines
    • Amphotericin B
  • Growth promoting Agents:
    • Monensin (horses)
  • Nonsteroidal antiinflammatory Drugs:
    • Aspirin
    • Phenylbutazone (horses)
    • Carprofen
    • Flunixin meglumine
    • Ibuprofen
    • Naproxen
  • Food / Contaminants:
    • Grapes/raisins
    • Melamine
    • Cyanuric acid
  • Bacterial /Fungal toxins
    • Clostridium perfringens epsilon toxin (sheep enterotoxemia)
    • Ochratoxin A
    • Citrinin
  • Plants:
    • Pigweed (amaranthus retroflexus) (cattle, pigs)
    • Oaks (quercus sp) (ruminants)
    • Isotropis sp.
    • Yellow weed tree
    • Lilies (cats)
  • Oxalates:
    • Ethylene glycol (dogs, cats)
    • Halogeton
    • Greasewood
    • Rhubarb
    • Sorrel, dock
  • Vit D
    • Supplements
    • Calciferol-containing rodenticides
    • Cestrum diurum
    • Solanum sp.
    • Trisetum sp
57
Q

What are nephrotoxic pigments?

A
  • Hemoglobin and myoglobin
    • increase ischemia-induced damage (additive deleterious effect)
  • Occurs with hemoglobinemia or myoglobinuria once renal threshold is exceeded
    • Any species: intravascular hemolysis / muscle damage
    • Sheep: copper toxicity
    • Cattle: leptospirosis, babesiosis
    • Equine: Red maple toxicity, or exertional rhabdomyolysis
    • Canine: autoimmune hemolytic anemia
  • Gross lesions: diffuse dark discoloration (gun-metal kidneys)
  • Histo: tubular epithelial necrosis, tubular Hb or Mb casts
    • cannot distinguish Hb/Mb grossly or histologically
58
Q

What is happening in this kidney?

A
  • Equine kidney, renal medullary (papillary) necrosis
  • Cause: NSAIDS (phenylbuazone)
    • gross lesion in this specific anatomic locations is key
  • Histo = necoris
  • DX approach: hx of NSAIDS
  • May also find lesions in stomach and colon
59
Q

What is going on in this picture?

A
  • Canine kidney, swollen pale edamatous
  • Gross lesions are non specific
  • Histo: acute tubular necrosis with refractile oxalate crystals
  • Cause: calcium oxalate toxicosis (here, many other causes possible)
  • Dx approach: obtain hx of ethylene glycol exposure (dogs). characteristic histo lesions (formalin fixed tissue); ID of toxin (fresh tissue, mass spec)
60
Q

What is happening in this picture?

A
  • Bovine kidney, pallor, swelling, edema, (all non specific)
  • Cause: Oak bud/tannin toxicity (other causes are grossly indistinguishable)
  • DX approach: consider ddx, investigate exposure to potential toxins, save fresh tissues (as well as stomach/rumen contents, liver) submit tissue fixed for histo, and to direct further ancillary dx testing and toxicology
61
Q

What is happening in this picture?

A
  • Sheep kidney, soft friable kidney.
    • nonspecific, indistinguishable from autolysis
  • Cause: intestinal Clostridium perfringens type D infection
    • lesions in the intestine? - No, its enterotoxemia
    • Epsilon toxin causes tubular necrosis and vascular leakage/edema
  • Dx approach: gross and histo often not helpful (autolysis) so rule OUT other causes of acute death by doing complete necropsy, Culture intestine (C perf) + genotyping +/- toxin ID in intestinal contents
62
Q

What causes ischemic tubular injury

A
  • Causes of reduced renal perfusion:
    • Local or systemic vasoconstriction
    • compromised cardiovascular function
    • Anemia
    • Drugs
  • Mechanisms:
    • Depend on extent and duration of injury, several mechanisms target epithelial cells including sublethal injury, apoptosis or necrosis
    • PCTs are most sensitive to ischemia due to their high metabolic demands and their first line for exposure, but any portions of tubule cn be affected (glomeruli are resistant to ischemia)
63
Q

What affect does ischemia have on renal tubules?

A
  • Usually affects basement membranes, so even if oxygen is restored ⇢ regeneration and repair is slow and distorted because BM is not present to act as scaffolding during regeneration ⇢ less functional tubules or tubular atrophy
64
Q

What occurs following ischemic event?

A
  • Ischemia
    • Many morphologic changes happen in the tubule
    • tubulorrhexis
  • Reperfusion
    • spreading, proliferation
    • repair, regeneration, restoration
      • important histologic lesion indicating previous tubular injury
65
Q

What are the common lesions of the renal pelvis?

A
  • Dilation (hydronephrosis)
  • Necrosis (papillary/medullary)
  • Inflammation (pyelitis, pyelonephritis
66
Q

What causes dilation (hydronephrosis of the renal pelvis?

A
  • Partial or complete obstruction of outflow ⇢ progressive increased pressure
    • Congenital malformation of ureter
    • Accidental ligation of ureter
    • Ureteral or urethral calculi
    • Chronic inflammation
    • Neoplasia
    • Functional disorder (neurogenic)
  • Can be unilateral vs bilateral
67
Q

What are the consequences of renal pelvis dilation (hydronephrosis)?

A
  • Tubules dilate
  • glomeruli probably remain functional
  • blood vessels are compessed/ischemia
68
Q

Why does necrosis of the renal pelvis occur?

A
  • Response of inner medulla to ischemia
    • inner medulla has the poorest blood supply of the kidney
    • Medullary epithelial cells synthesize prostaglandins
  • Primary:
    • NSAIDS most common, usually with dehydration
  • Secondary:
    • Medullary ischemia
      • reduced glomerular flow
      • compression of vasa recta
        • interstitial fibrosis, amyloidosis, inflammation outflow obstruction
69
Q

What are the consequences of renal pelvis necrosis?

A
  • Necrotic tissue sloughs into ureter
    • can cause obstruction or nidus for calculus formation
70
Q

Why does inflammation of the renal pelvis (pyelitis or pyelonephritis) occur?

A
  • Bacterial - extension from the lower urinary tract ascends via ureters
    • lower UTI (uroliths, stagnation, catheterization, incomplete emptying/less dilution
  • Rarely it descends form embolic glomerulitis
  • Medulla- prone to bacterial infection
    • poorest blood supply
    • high osmolality/osmolarity ⇢ inhibits neutrophil function
    • high ammonia ⇢ inhibits complement fixation
71
Q

define pyelitis

A

inflammation of renal pelvis

72
Q

define pyelonephritis

A
  • pyelitis with extension into tubules and parenchyma
  • considered a form of tubulointerstitial nephritis
73
Q

What is tubulointerstitial nephritis?

A
  • usually implies tubular injury leading to interstitial damage and inflammation
  • Causes:
    • bacteria, virus, toxins
      • Canine adenovirus, PRRSV (pigs), EAV (horse)
      • Leptospira may be one one of the few specific causes of true interstitial inflammation, it persists in the interstitial space, and progresses to fibrosis over time
  • Gross Lesions:
    • nonspecific
    • depends on chronicity (swollen / shrunken / firm)
    • capsule adhered firmly
  • DX:
    • gross lesions + histo (formalin)
    • bacterial culture / molecular diagnostics (fresh tissue)
    • Serology
74
Q

What is happening in this picture

A
  • feline kidney, granulomatous interstitial nephritis
  • Gross: firm, white/tan, raised nodules, often tracks along blood vessels (most obvious on cats
  • Histo: neutrophils and macrophages (pyogranulomatous) suggests FIP
  • DX approach:
    • gross + histo (formalin)
    • IHC (FIPv fixed tissue)
    • PCR (fresh)
75
Q

Differential Dx for these lesions?

A
  • renal lymphoma
  • abdominal carcinomatosis
  • granulomatous interstitial nephritis
76
Q

What is Chronic Renal Disease?

A
  • The end result of lost renal functional parenchyma (tubules, glomeruli, interstitium, vessels) with replacement by fibrosis
  • FINAL Common Pathway
  • General Pathogenesis:
    • Primary insult to any component of the nephron
      • loss of nephrons, fibrosis, decreased GFR are all progressive
    • Renal failure (seen clinically a:
      • inability to concentrate Urine
      • Increased metabolic wastes;
      • fluid and electrolyte imbalances.
      • Failure to maintain homeostasis
77
Q

What diseases of the vasculature affect the kidneys?

A
  • hyperemia
    • active, with inflammation
  • congestion
    • passive, with cardiac insufficiency or hypovolemia
    • hypostatic (gravity) observed mostly in the postmortem interval
  • hemorrhage
    • petechia, ecchymoses
      • canine herpes, hog cholera, septicemic salmonellosis, erysipelas, sepsis
  • renal infarction
  • uremia
78
Q

What is an infarction?

A
  • Regions of coagulative necrosis due to localized ischemia, often associated with thromboembolism
    • Endocarditis (bacterial valvular disease)
    • Endarteritis (canine dirofilaria, equine strongyles)
    • Neoplastic cell emboli
    • endotoxemia
79
Q

How do renal infarctions look over time?

A
  1. Acute hemorrhagic renal infarct (0h-2d) - swollen, hemorrhagic
  2. Acute pale renal infarct (2-3d) - swollen, pale center (coagulation necrosis) with a red rim (hyperemia, congestion, hemorrhage, +/- infiltrating leukocytes
  3. Chronic renal infarct (>5-7 d) - pale tan/white, shrunken (fibrosis +/- necrosis
80
Q

What is Uremia?

A
  • Multisystemic clinical syndrome due to renal failure
  • Uremic toins accumulate in the blood
    • small soluble compounds such as urea, phosphate, creatinine
    • medium sized compounds such as FGF, B2 macroglobulin, leptin
    • Protein bound molecules such as phenols, indoles
81
Q

How does Uremia affect various tissues?

A
  • Nonrenal lesions are useful indicators of renal failure
  • endothelial degeneration and necrosis ⇢ vasculitis and infarction
  • Direct caustic injury to epithelium (oral cavity, stomach)
  • Increased erythrocyte fragility; reduced erythropoietin production
  • Altered calcium/phosphorus metabolism (renal secondary hyperparathyroidism)
82
Q

What are renal cysts?

A
  • developmental/juvenile renal disease
  • Primary:
    • Congenital, polycystic disease is a known genetic defect of cilia, an autosomal dominant trait in cats/dogs/pigs/lambs
    • may involve liver, pancreas
  • Secondary:
    • Acquired due to collecting tubule obstruction
    • gross and histo lesions are characteristic
  • Dx approach: gross lesions, histo to characterize
83
Q

What are the primary neoplasms of the kidneys

A
  • Epithelial: renal adenoma, renal carcinoma, transitional cell papilloma/carcinoma
  • Mesenchymal: sarcomas of various sorts
  • Round cells: lymphoma is common
  • embryonal: nephroblastoma (Wilms tumor)
    • young pigs and chickens common
    • common on the spinal cord of other species
84
Q

What is the process for evaluating the Urinary tract? (necropsy)

A
  • Cut kidneys in the sagittal plane
    • evaluate all regions for lesions
  • Remove the Capsule
    • before or after sectioning the kidney
    • should strip easily if Not:
      • poor technique
      • fibrosis
      • interstitial nephritis
      • glomerulonephritis
      • etc
  • Collect samples
    • wedge of renal tissue including capsule, cortex, medulla, crest/papillae
    • gross lesions
  • Evaluate bladder
    • lesions on serosal surface
    • incise examine mucosa
  • Examine distal Urinary tract
    • lesions on serosal surface proximal to distal including prepuce
    • open penile urethra (accessory sex gland, sigmoid flexure, os penis, urethral process, etc)
85
Q

How should collected urinary tract samples be stored? (necropsy)

A
  • for histo:
    • 10% buffered formalin
    • tissue no bigger than 1 cm wide
  • Fresh go to sterile container
    • can be frozen
    • cannot use formalinized tissue
    • cannot go back and get more
86
Q

What is odd but normal in horse and pig urinary tracts?

A
  • Mucus: thick mucus with calcium carbonate crystals
  • Urine appears thick, viscous, yellow, cloudy, possibly foamy
87
Q

How does the lower urinary tract transport urinary waste from the kidney and out the body?

A
  • Ureters:
    • by peristalsis, propel urine from kidneys to urinary bladder via vesico-ureteral valve
  • Urinary bladder:
    • urine storage
    • urine should be clear (except horses)
    • thickness can vary depending on relaxation or contraction
  • Urethra:
    • conduit and valve for urinary bladder
88
Q

What are the mechanisms of urolithiasis?

A
  • Urine concentrations of calculus precursors is high (dietary)
  • unusual metabolism of some substances (uric acid in dalmations)
  • hereditary defects in metabolism (cystine, xanthine)
  • Urine pH affects solute excretion and precipitation
    • acidic = oxalates
    • Alkaline = struvites
  • Reduced water intake, mineral supersaturation
  • bacterial infection (struvites in dogs)
  • obstruction
  • foreign bodies (suture, grass awn)
  • drug metabolites (sulfonamides and tetracyclines
88
Q

What are the mechanisms of urolithiasis?

A
  • Urine concentrations of calculus precursors is high (dietary)
  • unusual metabolism of some substances (uric acid in dalmations)
  • hereditary defects in metabolism (cystine, xanthine)
  • Urine pH affects solute excretion and precipitation
    • acidic = oxalates
    • Alkaline = struvites
  • Reduced water intake, mineral supersaturation
  • bacterial infection (struvites in dogs)
  • obstruction
  • foreign bodies (suture, grass awn)
  • drug metabolites (sulfonamides and tetracyclines
89
Q

What types of uroliths are common in different species?

A
90
Q

What are struvite uroliths?

A
  • magnesium ammonium phosphate
  • white, chalky smooth
  • Cause Infection, alkaline pH
  • common females >> males
91
Q

What are calcium oxalate uroliths?

A
  • hard, heavy, white or yellow
  • various shapes
  • Acidic pH
  • # 1 in dogs (male >> females)
92
Q

What are these?

A
  • silica urolith
  • ruminants >> dogs >> horses
93
Q

What are ammonium biurate nephroliths?

A
  • characteristic green color
  • Cause:
    • from portosystemic shunts (congenital or acquired)
    • Dalmatians due to genetic ammonia/urate metabolism defects
94
Q

Where are common obstruction sites for uroliths?

A
  • Male cattle: ischial arch, proximal sigmoid flexure
  • male rams and wethers: vermiform appendage/urethral process
  • male dogs: base of the os penis
  • male cats: penile urethra, and urethral plugs (struvite sand) often fill the entire urethra
  • Females: Rare, large uroliths in urinary bladder or renal pelvis
95
Q

What is hemorrhagic polypoid cystitis?

A
  • Pathogenesis:
    • chronic urinary bladder stones ⇢ chronic irritation / trauma to surface ⇢ stereotypic response to bladder wall injury ⇢ urothelial damage ⇢ hyperplasia ⇢ polyp formation ⇢ edema ⇢ inflammation ⇢ hemorrhage
96
Q

What is cystitis?

A
  • mostly due to bacterial infection
  • bladder is normally sterile and resistant to infection
    • regular flushing of normal urine flow; acidic pH, IgA, mucin inhibits bacterial colonization, high osmolality, urea
  • Infection more common in females
97
Q

What are the causes and mechanisms of urinary bladder cystitis?

A
  • Common bacteria:
    • hemolytic E coli (all)
    • Corynebacterium renale (cattle)
    • Actinobaculum suis (pigs)
    • enterococus faecalis (cats)
    • Klebsiella sp (horses)
  • MOA:
    • stagnation of urine - obstruction, incomplete voiding, trauma
    • Urinary catheterization, vaginoscopy, urinary incontinence, some medicaitons
    • Urease producing bacteria ⇢ ammonium ⇢ urinary mucosal damage
    • Glucose (diabetes mellitus)
    • chemicals (cyclophosphamide, bracken fern)
98
Q

What are the noninfectious (chemical) causes of cystitis?

A
  • Cyclophosphamide ⇢ acute hemorrhagic sterile cystitis in dogs
  • Cantharadin / blister beetles (Epicauta spp) ⇢ hemorrhagic ulcerative cystitis in horses
  • Bracken fern toxin causes enzootic hematuria and epithelial hyperplasia then transition to neoplasia (cattle)
99
Q

What type of cystitis is common with diabetes mellitus in dogs?

A
  • emphysematous cystitis
    • mucosal gas bubbles, hemorrhage
100
Q

What is ureteral ectopia?

A

ureters empty somewhere other than bladder

101
Q

What is Patent urachus?

A
  • Fetal urachus fails to close, forming a direct channel between the ape of the bladder and the umbilicus
  • Secondary ascending infections are common
  • Most common malformation of the urinary bladder

Systemic Pathology (19 decks)

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