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Systemic Pathology > Urinary Tract > Flashcards

Urinary Tract Flashcards

1
Q

By what mechanisms does renal dysplasia occur?

A

Genetic or acquired via BVDV or Feline Panleukopenia virus infection.

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2
Q

What are the two types of renal dysplasia?

A

Retention of fetal structures or K9 Progressive juvenile nephropathy which is a collagen defect (fibrosis)

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3
Q

Mutation of a polycystin gene could lead to what clinical and pathologic findings? Gene names? Most commonly affected animals/breeds?

A

Heritable PKD1/PKD2 mutations can lead to polycystic kidney disease. Lots of cysts, disrupt nephrons and kidney function. Persian cats, pigs, cairn terriers and Westies.

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4
Q

What is the pathogenesis of hydronephrosis? What are some causes?

A

Obstruction of urine outflow -> increased renal pelvic pressure -> dilation of renal pelvis -> progressive atrophy -> large “cystic” kidney +/- hydroureters
Developmental anomaly, iatrogenic, displacement, urolithiasis

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5
Q

Explain why are certain proteins excluded from the glomerular filtrate, and what are the roles of protein size and charge?

A

Filtration barrier is made of endothelial cells, basement membrane and podocyte processes. Size barrier (must be small) and charge barrier (negative charge repels negatively charged proteins).

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6
Q

What is the role of the juxtaglomerular apparatus in RAAS signaling and blood pressure/volume?

A
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7
Q

What is the important vessel that serves as a bottleneck where embolisms can happen?

A

Interlobular artery

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8
Q

What molecule maintains vascular dilation in deep medulla?

A

PGE2

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9
Q

What electrolytes/substances are absorbed and excreted along the kidney tubule? Which sections are sensitive to aldosterone/ADH?

A

PCT: Resorb Na+, water, glucose, Ca++ others
LofH: Resorb Na+ and water- ONLY AREA SENSITIVE TO ADH and ALDOSTERONE
DCT: Resorb Na+, EXCRETE K+

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10
Q

What is the role of the juxtaglomerular apparatus in RAAS signaling and blood pressure/volume?

A

JG apparatus drives the RAAS system. Low O2 tension, low blood volume, hypoosmolality cause JG cells to release Renin into circulation. Angiotensin affects vessels to increase BP, ADH affects water balance to conserve water, and Aldosterone affects sodium to increase blood volume. JG also releases erythropoietin.

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11
Q

What are the end results of RAAS signaling and what are the consequences of RAAS system malfunction?

A

Increase in blood supply to brain, heart, kidneys. Too much renin -> Hypertension, too little renin -> dehydration

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12
Q

If the kidney loses function, what happens to acid-base balance?

A

Renal tubules normally resorb HCO3- and secrete H+, so in the absence of kidney function, there is a metabolic acidosis.

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13
Q

What are 2 reasons for death following renal failure?

A

Hyperkalemia (can’t excrete K+ from distal tubule) and acidemia (can’t secrete H+ and resorb Bicarb)

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14
Q

What is the typical gross appearance of acute, subacute, and chronic renal infarcts?

A

ACUTE- red wedge. SUBACUTE- pale wedge with red rim. CHRONIC- sunken, firm, pale wedge. Fibrosis.

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15
Q

How does glomerular disease affect the primary renal functions?

A

Loss of filtration barrier, so proteins escape into the urine.

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16
Q

What are key features of urinalysis, hematology and/or serum biochemistry in animals with glomerular disease?

A

PROTEINURIA is hallmark of glomerular change in absence of LUTI. Clinical presentation is called nephrotic syndrome. Consists of: Proteinuria/Hypoalbuminemia and Hypercholesterolemia/ hyperlipoproteinemia.

17
Q

What is the pathogenesis of embolic glomerulitis? What organisms cause it?

A

Bacteremia (neonates, failure of passive transfer/umbilical sepsis) -> emboli in glomerular capillaries -> small random foci of necrosuppurative inflammation. E. coli!

18
Q

What is nephrotic syndrome? Clinical features? Laboratory features?

A

Clinical consequences of glomerular disease. Proteinuria/Hypoalbuminemia and Hypercholesterolemia/ hyperlipoproteinemia. Clinical features: Generalized edema, Cavitary effusion, Hypercoagulability, DIC, death by renal failure or thrombosis. Lab features: PROTEINURIA, hypoalbuminemia, low anti-thrombin III, hypercholesterolemia. NO AZOTEMIA.

19
Q

What types of renal lesions most commonly result from bacteremia?

A

Embolic lesions

20
Q

What is the typical gross appearance of Glomerulonephritis?

A

Enlarged glomeruli- can see and feel them. Diffuse swelling, wet, bulges on cut section. Pale tan color. Acutely just glomeruli affected. Chronic- tubules affected. Get shrunken, end stage kidneys.

21
Q

What is the typical gross appearance of Renal amyloidosis? Special diagnostic?

A

Normal size to enlarged. Can be glomerular- glomeruli are enlarged. Deposits can be visualized with Lugol’s iodine staining. Diffuse looks orange and waxy. Firm, may bulge on cut section. DRY!

22
Q

Describe the main mechanisms leading to glomerulonephritis in domestic animals.

A

Caused by immune complex deposition in glomeruli, disrupts filtration, induces inflammation and tissue damage. Can be autoimmune. Can be antibodies directed at BM or just get trapped there. In any case, there is a type III hypersensitivity reaction and glomerular damage. Tubule damage follows and ischemic injury due to swelling and impingement on capillaries.

23
Q

What are causes of Infectious glomerulonephritis in dogs? Cats? Horses?

A

Dogs: Pyometra, pyoderma. Cats: Feline leukemia, Feline infectious peritonitis. Horses: Equine infectious anemia, Streptococcus sp. infection. Rare in cattle.

24
Q

What is the key feature of glomerular disease versus tubular disease? Caveats?

A

Glomerular disease = PROTEINURIA. In absence of LUTI. Tubular disease = AZOTEMIA. In absence of pre- or post-renal azotemia.

25
Q

How many nephrons have to be lost to get Azotemia?

A

75% loss

26
Q

What is the most important cause of acute renal failure?

A

Acute tubular injury/necrosis

27
Q

What is the typical gross appearance of acute tubular necrosis?

A

Diffusely pale tan, swollen. Wet, bulge on cut section. Retain normal shape and architecture. Cannot palpate glomeruli- distinguishes from glomerular disease.

28
Q

Compare and contrast nephrosis and nephrotic syndrome.

A

Nephrosis is acute kidney injury aka acute renal tubular necrosis. Nephrotic syndrome is the consequence of renal glomerular disease.

29
Q

Why are proximal tubules more susceptible to damage than distal tubules and collecting ducts?

A

Tubular epithelial cells are most sensitive to hypoxia, especially proximal tubule cells due to blood flow pattern. These are injured first and most severely by ischemic acute kidney injury.

30
Q

What are the 3 mechanisms of acute tubular necrosis? Example of each?

A

Ischemia/hypoxic nephrosis- Thrombosis, shock, sepsis
Toxic nephrosis- Aminoglycosides, Ethylene glycol, heavy metals
Obstructive nephrosis- hemoglobinuric nephrosis: Horses Maple leaf, Dogs, IMHA, OR myoglobinuric nephrosis Horses: Exertional rhabdomyolysis.

31
Q

How do you know if AKI is reversible or not?

A

If tubular BM is intact, possibility for repair. If BM is lost, get loss of tubules, replacement with fibrosis.

32
Q

What is more likely to be irreversible- hypoxic AKI or toxic AKI?

A

Hypoxic is more likely to be irreversible than other types of AKI.

33
Q

What are the 2 mechanisms of AKI in Ethylene glycol toxicity?

A

1- Direct damage by nephrotoxic nephrosis to tubules, cell membrane damage
2- Obstructive nephrosis by calcium oxalate crystals in tubules, physical obstruction

34
Q

What are the 3 clinical features of tubulointerstitial nephritis?

A

Azotemia, Isosthenuria, Dysuria

35
Q

What is the typical gross appearance of tubulointerstitial nephritis?

A

Diffusely swollen, hyperemic, evidence of hemorrhage. Multifocal pale areas possible.

36
Q

Of the causes of tubulointerstitial nephritis, which organisms cause suppurative vs. lymphoplasmacytic vs. granulomatous? What are some viral, protozoal, bacterial, and non-infectious causes?

A

Granulomatous- FIP (Feline), Hairy vetch (Bovine), Mysobacterium, Fungi
Viral: FIP, Canine adenovirus
Fungal
Bacterial: Leptospira, Sepsis in general, Mycobacterium
Non-infectious: Hairy vetch, immune-mediated, allergic

Systemic Pathology (3 decks)

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