urinary system lectures Flashcards
lower urinary tract components, main functions
Ureters, urinary bladder, urethra
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Two main functions:
- urination
- keep pathogens out (incl. vesicoureteral valve)
Bladder distension/rupture - not always mechanical! can also be:
neuroparalytic
urolith predisposing factors
High levels of calculogenic material
Urine pH
Reduced water intake
Cystitis – the defense
- molecules that defend us
Tamm-Horsfall mucoprotein
IgA,IgG
Surface GAGs
Urinary oligosaccharides
Cystitis – the culprits
- for all species
- specific to cows, dogs, and pigs
Ascending - usually rectal flora, cutaneous
Common to all species
> Uropathogenic E. coli
> Proteus vulgaris
> Streptococcus spp.
> Staphylococcus spp.
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Species specific pathogens that specifically target the urinary system:
- Cows: Corynebacterium renale group (C. renale, pilosum, cystiditis)
> C. urealyticum in dogs > “encrusted cystitis” -struvite
- Pigs – Actinobaculum suis
Stromal tumours - what percent of LUT tumors
- progression / character?
- who gets it? prognosis?
- associated with what condition?
- < 20%
- Usually benign
- Fibrosarcs met, leoimyosarcs not so much
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Botyroid rhabdosarcoma
Young animals (<2), big dogs (esp St. Bernards),♀ > ♂2:1
Infiltrates wall – guarded prognosis, can met
Associated with hypertrophic osteopathy in dogs
Bovine enzootic hematuria
- cause
- what it is?
Pteridium aquilinum (bracken fern)
> Hematuria
> Benign and malignant tumors (50 % mixed)
Hydronephrosis - why does this happen?
Capsule is not readily expansile
Intrarenal pressure increases
Lymphatics and veins obstructed
Reduced blood flow, hypoxia
Pressure atrophy
Apoptosis of cells
Juvenile nephropathy
- congenital condition
- type 4 collagen deficity in glomerular basement membrane
> membranoproliferative GN
> tubular disease of unknown cause with tubular atrophy and interstitial fibrosis - uremia in dogs age 4-18 months
renal dysplasias
Abnormal structures
Blind ended collecting ducts
atypical tubular epithelium
primitive ducts
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Inappropriate structures
Immature glomeruli
undifferentiated mesenchyme (cortex or medulla)
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Rarely osseous or cartilaginous metaplasia
Often concurrent ureteral abnormalities so very
predisposed to pyelonephritis ALSO: hypoplasia, aplasia
Renal cysts
3 main mechanisms
Obstructive
Altered tubular basement membrane
Disordered growth of tubular epithelial cells with focal hyperplastic lesions (altered basement membrane, increased tubular secretion)
Polycystic kidney disease
> Autosomal dominant polycystic kidney disease
- who is affected, pathogenesis, causes
– Persian cats, Bull terriers, pigs, lambs
Bilateral, convoluted tubules > expand > renal failure
+/- hepatic and pancreatic cysts
PKD1 (polycystin proteins) mutation in Persians
Polycystin is important for cell-cell and cell-matrix interactions
Medullary necrosis
Why does this happen? possible sequelae?
Not all glomeruli are equal
Cortex is high flow, high demand area
> Very sensitive to hypoxia
> Blood from most glomeruli supplies cortex and veins exit directly
Juxtamedullary glomeruli supply most of blood to medulla – flow maintained
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Medulla is hypoxic environment
Autoregulation of blood flow plus direct protective effect of prostaglandins and nitric oxide maintains medulla
NSAIDS (COX1 inhibitors) inhibit autoregulation and protection.
Can break off and cause obstruction
Acute papillary necrosis causes:
hematuria, proteinuria, casts, and oliguria.
> This leads later to polyuria with poor concentration function
renal Infarcts - how common? how relevant?
Very commonly seen
Far less commonly clinically relevant (kidney wise)
renal neoplasias - what do we see
Rare, metastatic more common than primary
Adenoma – rare – when seen usually horse, cow
Carcinomas – #1 in cows, horse, dogs
Nephroblastomas – #1 chicken, pigs.
Other
Kidneys
3 basic needs
- Adequate inflow – renal perfusion
- Adequate functional mass - GFR
- Adequate outflow – no obstruction
glomerular filter components
Endothelium
50-100μm fenestrations
Anionic coat > slow down the filtration of large anionic proteins
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Basement membrane (endothelial cells + podocytes)
100-300μm thick
Anionic molecules
> also slows down the filtration of anionic proteins
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Epithelium (podocytes)
Anionic coat
Filtration slit – nephrin (Ig- like CAM)
Glomerulonephritis
Types of GN
Membranous (cats)
Proliferative (mesangioproliferative) – older term
Membranoproliferative (dogs, horses, ruminants)
Glomerulosclerotic
what is the most suggestive urinalysis sign of glomerular damage
“Proteinuria, occurring in the absence of urinary tract inflammation, is suggestive of glomerular damage”
Immune complex glomerulonephritis
Pathogenesis
- When does it occur?
- Circulating antigen-antibody immune complexes
- Deposition
Subendothelial
Subepithelial
Intramembranously
> Complement activation
Thought to occur when antigen in slight excess of antibody or even
what type of infections are able to cause immune complex glomerulonephritis?
any infection of low pathogenicity that is able to produce persistent antigenemia has the potential to cause immune-complex disease
Chronic glomerulonephritis
- pathogenesis
Injury to glomerulus affects filter
Proteinuria can damage/activate tubules
> proinfl cytokines, growth factors > interstitial fibrosis
Altered blood flow to cortex causes hypoxia
Cytokines from glomerular lesion affect cortex > fibrosis
FIBROSIS: diffuse, interstitial, > further affects renal function
The end is the same regardless of the beginning
If Ag exposure is reasonably short/can be cleared –
resolution and some repair/clearance of complexes can
occur.
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“Once the glomerular filtration rate has decreased to 30-50 % of normal, progression to end-stage renal failure tends to be inexorable.”
Amyloidosis - what do we see? what causes damage? what we see in various species?
Massive proteinuria without fibrosis
Damage via pressure atrophy caused by amyloid
deposition
Most common in older dogs
Cats, cows – often more medullary so…
Often see thrombosis
> hypercoagulable
Outcomes of massive proteinuria
Thrombosis
Loss of antithrombin III and plasminogen activator
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Nephrotic syndrome
Hypoproteinemia/hypoalbuminemia
Hyperlipidemia
> Liver has generalized increase in protein production including lipoproteins > hyperlipidemia / hypercholesterolemia
Edema
reduced plasma colloid oncotic pressure
Embolic nephritis pathogens
Foals – Actinobacillus equuli
Pigs – Erysipelothrix rhusiopathiae
Cattle – Trueperella (FKA Arcanobacterium) pyogenes
Calves – E. coli
Sheep/Goats – Corynebacterium pseudotuberculosis
PCT
- what do we excrete into the tubule?
- what do we reabsorb?
Excrete:
- creatinine
- antibiotics
- diuretics
- uric acid
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reabsorb:
- NaCL
- K
- H2O
- HCO3-
- glucose
- amino acids
loop of henle - what do we reabsorb?
- NaCl
- H2O
- Mg
- Ca
DCT - what do we reabsorb? what do we excrete??
proximal part:
- reabsorb: NaCl, Ca
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distal part:
- reabsorb: NaCl, H2O
- excrete: K, H, urea
Acute Renal Failure
- how much renal loss?
- causes?
- 75 % loss
1. Acute tubular necrosis (aka ATI, AKI) - Bacteria/Viruses
- Nephrotoxic Drugs
- Toxins (e.g. ethylene glycol)
2. Obstructive nephropathy (uroliths, neoplasia)
3. Renal ischemia > necrosis (vasculitis, vascular obstruction due to bacteria, tumour emboli)
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tubulorrhectic - what does this mean?
Patchy focal tubular necrosis, disruption of basement membranes
> ischemic injury to kidney
Ethylene glycol toxic metabolites, effects
Glycoaldehyde, glyoxylate
Peracutely neurologic
~ 12 hr – respiratory/cardiovascular
1-3 d – renal failure
Hemoglobinuric nephrosis - causes
Hemoglobin and myoglobin
Copper toxicosis in sheep
Immune hemolytic anemia in dogs
Red maple toxicosis in horses
Myoglobinuric disease in horses
Hb not directly toxic (well – maybe), but exacerbates hypoxic/anoxic type diseases
Interstitial nephritis due to lepto - which species are affected? which are more likely multifocal?
Dogs
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More likely to be multifocal:
Calves
Pigs
E. coli in calve kidneys - disease, significance
“white spotted kidney” E. coli
- Suppurative > non-sup.
- Common
- Usually incidental
> Some can die of renal failure
Metabolic/ischemic/toxic disease of the kidney
- effects and lesions
- causes
Acute tubular necrosis
Macroscopic lesions minimal
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Cause
Anoxia, hypoxemia, anemia
Low renal blood flow (dehydration, hypotension)
Toxic
why are PCTs susceptible to toxic damage
PCTs:
increased Metabolic rate Exposure to agents in large vol. of ultrafiltrate
ischemic vs tocic kidney disease lesions
Ischemic
Patchy focal tubular necrosis, disruption of basement membranes
= “tubulorrhectic”
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Toxic
Extensive necrosis, basement membrane preserved
Hairy vetch toxicosis
- what causes it?
Legumes used in pasture
Used in Ontario, US (Midwest)
Toxin in seeds – prussic acid
Immune mediated?
Other systems involved – dermatitis, conjunctivitis, adrenal glands, lymph nodes, myocardium, thyroids
Vesicoureteral valve - involvement in pyelonephritis
Compromised in obstruction, cystitis > increased reflux
Pyelonephritis
- what part of the kidney is most susceptible?
- contributing factors?
medulla is highly susceptible to bacterial infection
- A poor blood supply
- increased interstitial osmolality a/o osmolarity > inhibits neutrophil function
- increased [NH3+] > inhibits complement activation
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- female > male
what bacterial product can inhibit normal ureteral peristalsis?
NB Endotoxin (Gm –ves)
Metastatic mineralization in renal failure
- why?
- who?
- what else?
Calcium phosphorus mismatch > precipitate
pH (alkaline tissues)
Dogs especially subpleural
Also uremic pneumonopathy
Uremic gastropathy - what do we see?
Mineralization > Midzone!
Vasculopathy > mucosal infarction
Ischemia
uremia - what do we see? what are the causes?
Azotemia - elevation of blood urea and creatinine = ↓ glomerular filtration
Renalfailure-acuteorchronic
Death
> hyperkalemia, acidosis, pulmonary edema (uremic pneumonopathy)
Renal and nonrenal lesions
Renal lesions can vary depending on inciting cause
Chronic > fibrosed, mineralized kidney with sclerosed glomeruli, and sometimes areas of hyperplastic and hypertrophic tubules
Uremia – Non-renal lesions
Pulmonary edema
Increased vascular permeability
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Fibrinous pericarditis
Increased vascular permeability
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Ulcerative & hemorrhagic gastritis
Ammonia secretion and vascular necrosis
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Ulcerative and necrotic stomatitis
Ammonia secretion in saliva and vascular necrosis
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Atrial and aortic thrombosis
Endothelial and subendothelial damage
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Pallor due to non-regenerative anemia
Lack of EPO production in the kidney
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Soft-tissue mineralization
Altered Ca-Phos metabolism (stomach, lungs, pleura, kidneys)
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Fibrous osteodystrophy
Altered Ca-Phos metabolism
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Parathyroid hyperplasia
Altered CA-Phos metabolism
Uremic glossitis/ulcerative necrotic stomatitis
- causes
Ammonia
Vasculopathy
Metastatic mineralization causes, outcomes, similar condition in dogs
Calcium phosphorus mismatch > precipitate
pH (alkaline tissues)
Dogs especially subpleural
Also uremic pneumonopathy
