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3. Sys Path 2 > urinary system lectures > Flashcards

urinary system lectures Flashcards

1
Q

lower urinary tract components, main functions

A

 Ureters, urinary bladder, urethra
<><><>
Two main functions:
- urination
- keep pathogens out (incl. vesicoureteral valve)

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2
Q

Bladder distension/rupture - not always mechanical! can also be:

A

neuroparalytic

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3
Q

urolith predisposing factors

A

 High levels of calculogenic material
 Urine pH
 Reduced water intake

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4
Q

Cystitis – the defense
- molecules that defend us

A

 Tamm-Horsfall mucoprotein
 IgA,IgG
 Surface GAGs
 Urinary oligosaccharides

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5
Q

Cystitis – the culprits
- for all species
- specific to cows, dogs, and pigs

A

 Ascending - usually rectal flora, cutaneous
 Common to all species
> Uropathogenic E. coli
> Proteus vulgaris
> Streptococcus spp.
> Staphylococcus spp.
<><><><>
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

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6
Q

Stromal tumours - what percent of LUT tumors
- progression / character?
- who gets it? prognosis?
- associated with what condition?

A
  • < 20%
  • Usually benign
  • Fibrosarcs met, leoimyosarcs not so much
    <><><>
    Botyroid rhabdosarcoma
     Young animals (<2), big dogs (esp St. Bernards),♀ > ♂2:1
     Infiltrates wall – guarded prognosis, can met
     Associated with hypertrophic osteopathy in dogs
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7
Q

Bovine enzootic hematuria
- cause
- what it is?

A

 Pteridium aquilinum (bracken fern)
> Hematuria
> Benign and malignant tumors (50 % mixed)

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8
Q

Hydronephrosis - why does this happen?

A

 Capsule is not readily expansile
 Intrarenal pressure increases
 Lymphatics and veins obstructed
 Reduced blood flow, hypoxia
 Pressure atrophy
 Apoptosis of cells

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9
Q

Juvenile nephropathy

A
  • 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
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10
Q

renal dysplasias

A

Abnormal structures
 Blind ended collecting ducts
 atypical tubular epithelium
 primitive ducts
<><>
Inappropriate structures
 Immature glomeruli
 undifferentiated mesenchyme (cortex or medulla)
<><>
 Rarely osseous or cartilaginous metaplasia
 Often concurrent ureteral abnormalities so very
predisposed to pyelonephritis ALSO: hypoplasia, aplasia

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11
Q

Renal cysts
 3 main mechanisms

A

 Obstructive
 Altered tubular basement membrane
 Disordered growth of tubular epithelial cells with focal hyperplastic lesions (altered basement membrane, increased tubular secretion)

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12
Q

Polycystic kidney disease
> Autosomal dominant polycystic kidney disease
- who is affected, pathogenesis, causes

A

– 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

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13
Q

Medullary necrosis
Why does this happen? possible sequelae?

A

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
<><><><>
 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

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14
Q

Acute papillary necrosis causes:

A

hematuria, proteinuria, casts, and oliguria.
> This leads later to polyuria with poor concentration function

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15
Q

renal Infarcts - how common? how relevant?

A

 Very commonly seen
 Far less commonly clinically relevant (kidney wise)

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16
Q

renal neoplasias - what do we see

A

 Rare, metastatic more common than primary
 Adenoma – rare – when seen usually horse, cow
 Carcinomas – #1 in cows, horse, dogs
 Nephroblastomas – #1 chicken, pigs.
 Other

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17
Q

Kidneys
3 basic needs

A
  1. Adequate inflow – renal perfusion
  2. Adequate functional mass - GFR
  3. Adequate outflow – no obstruction
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18
Q

glomerular filter components

A

Endothelium
 50-100μm fenestrations
 Anionic coat > slow down the filtration of large anionic proteins
<><><><>
Basement membrane (endothelial cells + podocytes)
 100-300μm thick
 Anionic molecules
> also slows down the filtration of anionic proteins
<><><><>
Epithelium (podocytes)
 Anionic coat
 Filtration slit – nephrin (Ig- like CAM)

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19
Q

Glomerulonephritis
 Types of GN

A

 Membranous (cats)
 Proliferative (mesangioproliferative) – older term
 Membranoproliferative (dogs, horses, ruminants)
 Glomerulosclerotic

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20
Q

what is the most suggestive urinalysis sign of glomerular damage

A

“Proteinuria, occurring in the absence of urinary tract inflammation, is suggestive of glomerular damage”

21
Q

Immune complex glomerulonephritis
 Pathogenesis
- When does it occur?

A
  • Circulating antigen-antibody immune complexes
  • Deposition
     Subendothelial
     Subepithelial
     Intramembranously
    > Complement activation
     Thought to occur when antigen in slight excess of antibody or even
22
Q

what type of infections are able to cause immune complex glomerulonephritis?

A

any infection of low pathogenicity that is able to produce persistent antigenemia has the potential to cause immune-complex disease

23
Q

Chronic glomerulonephritis
- pathogenesis

A

 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.
<><><><>
“Once the glomerular filtration rate has decreased to 30-50 % of normal, progression to end-stage renal failure tends to be inexorable.”

24
Q

Amyloidosis - what do we see? what causes damage? what we see in various species?

A

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

25
Q

Outcomes of massive proteinuria

A

Thrombosis
 Loss of antithrombin III and plasminogen activator
<><><><>
Nephrotic syndrome
 Hypoproteinemia/hypoalbuminemia
 Hyperlipidemia
> Liver has generalized increase in protein production including lipoproteins > hyperlipidemia / hypercholesterolemia
 Edema
 reduced plasma colloid oncotic pressure

26
Q

Embolic nephritis pathogens

A

 Foals – Actinobacillus equuli
 Pigs – Erysipelothrix rhusiopathiae
 Cattle – Trueperella (FKA Arcanobacterium) pyogenes
 Calves – E. coli
 Sheep/Goats – Corynebacterium pseudotuberculosis

27
Q

PCT
- what do we excrete into the tubule?
- what do we reabsorb?

A

Excrete:
- creatinine
- antibiotics
- diuretics
- uric acid
<><><><><>
reabsorb:
- NaCL
- K
- H2O
- HCO3-
- glucose
- amino acids

28
Q

loop of henle - what do we reabsorb?

A
  • NaCl
  • H2O
  • Mg
  • Ca
29
Q

DCT - what do we reabsorb? what do we excrete??

A

proximal part:
- reabsorb: NaCl, Ca
<><><><>
distal part:
- reabsorb: NaCl, H2O
- excrete: K, H, urea

30
Q

Acute Renal Failure
- how much renal loss?
- causes?

A
  • 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)
    <><><><>
  • increased K+ > cardiotox, met acidosis, pulmonary edema
31
Q

tubulorrhectic - what does this mean?

A

Patchy focal tubular necrosis, disruption of basement membranes
> ischemic injury to kidney

32
Q

Ethylene glycol toxic metabolites, effects

A

 Glycoaldehyde, glyoxylate
 Peracutely neurologic
 ~ 12 hr – respiratory/cardiovascular
 1-3 d – renal failure

33
Q

Hemoglobinuric nephrosis - causes

A

 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

34
Q

Interstitial nephritis due to lepto - which species are affected? which are more likely multifocal?

A

 Dogs
<><><>
More likely to be multifocal:
 Calves
 Pigs

35
Q

E. coli in calve kidneys - disease, significance

A

“white spotted kidney” E. coli
- Suppurative > non-sup.
- Common
- Usually incidental
> Some can die of renal failure

36
Q

Metabolic/ischemic/toxic disease of the kidney
- effects and lesions
- causes

A

 Acute tubular necrosis
 Macroscopic lesions minimal
<><>
 Cause
 Anoxia, hypoxemia, anemia
 Low renal blood flow (dehydration, hypotension)
 Toxic

37
Q

why are PCTs susceptible to toxic damage

A

PCTs:
increased Metabolic rate Exposure to agents in large vol. of ultrafiltrate

38
Q

ischemic vs tocic kidney disease lesions

A

Ischemic
 Patchy focal tubular necrosis, disruption of basement membranes
= “tubulorrhectic”
<><>
Toxic
 Extensive necrosis, basement membrane preserved

39
Q

Hairy vetch toxicosis
- what causes it?

A

 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

40
Q

Vesicoureteral valve - involvement in pyelonephritis

A

Compromised in obstruction, cystitis > increased reflux

41
Q

Pyelonephritis
- what part of the kidney is most susceptible?
- contributing factors?

A

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
<><><><>
- female > male

42
Q

what bacterial product can inhibit normal ureteral peristalsis?

A

NB Endotoxin (Gm –ves)

43
Q

Metastatic mineralization in renal failure
- why?
- who?
- what else?

A

 Calcium phosphorus mismatch > precipitate
 pH (alkaline tissues)
 Dogs especially subpleural
 Also uremic pneumonopathy

44
Q

Uremic gastropathy - what do we see?

A

 Mineralization > Midzone!
 Vasculopathy > mucosal infarction
 Ischemia

45
Q

uremia - what do we see? what are the causes?

A

 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

46
Q

Uremia – Non-renal lesions

A

Pulmonary edema
Increased vascular permeability
<><>
Fibrinous pericarditis
Increased vascular permeability
<><>
Ulcerative & hemorrhagic gastritis
Ammonia secretion and vascular necrosis
<><>
Ulcerative and necrotic stomatitis
Ammonia secretion in saliva and vascular necrosis
<><>
Atrial and aortic thrombosis
Endothelial and subendothelial damage
<><>
Pallor due to non-regenerative anemia
Lack of EPO production in the kidney
<><>
Soft-tissue mineralization
Altered Ca-Phos metabolism (stomach, lungs, pleura, kidneys)
<><>
Fibrous osteodystrophy
Altered Ca-Phos metabolism
<><>
Parathyroid hyperplasia
Altered CA-Phos metabolism

47
Q

Uremic glossitis/ulcerative necrotic stomatitis
- causes

A

 Ammonia
 Vasculopathy

48
Q

Metastatic mineralization causes, outcomes, similar condition in dogs

A

 Calcium phosphorus mismatch > precipitate
 pH (alkaline tissues)
 Dogs especially subpleural
 Also uremic pneumonopathy

3. Sys Path 2 (47 decks)

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