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Pathology II > Test 1- Urinary > Flashcards

Test 1- Urinary Flashcards

1
Q

Where is the kidney located?

A

Kidneys have retroperitoneal location

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2
Q

How is the renal parenchymais divided?

A

The renal parenchymais divided into: cortex, medulla and pelvis (papilla).

  • Renalpapilla→renal calices → renal pelvis → ureters
  • There are anatomic variations among animal species.
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3
Q
A

Multipyramidal with external lobation. Normal bovine kidney

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4
Q
A

Normal feline kidney

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5
Q
A

Multipyramidal without external lobation. Normal porcine kidney

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6
Q
A

Bovine kidney. Normal peri‐renal fat

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7
Q

Structure and Function of the Kidney

A

STRUCTURE AND FUNCTION

STRUCTURE

  • Gomerulus=Filtering mechanisms
  • Tubules=selective reabsorption

FUNCTIONS

  • 1=regulationoffluidand electrolyte content
  • 2=endocrinesuchas renin and erythropoietin
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8
Q

RENAL APLASIA

A

Defined as absence of development of a kidney, can be unilateral (incidental finding), or bilateral (fatal)

Failure of development of one or both kidneys.

  • Itisararedevelopmental abnormality.
  • Seeninswine,dog (familial tendency in Doberman pinscher and beagle dogs), and cattle.
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9
Q

Renal hypoplasia

A

Renalhypoplasiaisa quantitative defect caused by reduced mass of metanephric blastema.

  • Hypoplastic kidneys appear smaller than normal.
  • Renal hypoplasiahas been described in pigs, foals, dogs (Cocker spaniels), and chickens.
  • Differentialdiagnoses includes renal dysplasia (see next), and differentiation requires histological examination.
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10
Q

Renal Dysplasia

A

Renal Dysplasia is a rare condition very difficult to diagnose grossly.

• Bydefinition,renal dysplasia is an abnormal and asynchronous differentiation (disorganized development) of renal tissues.

Severe bilateral dysplasia may lead to renal failure.

• CasesofRenaldysplasia are difficult to differentiate from other conditions, such as chronic renal disease with diffuse fibrosis.

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11
Q
A

Renal dysplasia

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12
Q
A

Renal hypoplasia

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13
Q

Causes of renal dysplasia:

A

Congenital infections: Feline Panleukopenia, Canine herpesvirus, Bovine virus diarrhea

  • Autosomaldominantin Suffolk sheep
  • HypovitaminosisAinpigs

Renal dysplasia in a calf.

• Intrauterineureteral obstruction in pigs and calves

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14
Q
A

Renal dysplasia in a calf.

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15
Q

RENAL CYSTS

A

Renalcysts area common congenital renal malformation found in pigs, calves and to a lesser extent, in other species.

• Cystsofvariablesizeare typically filled with fluid and lined by flat or cuboidal epithelium.

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16
Q
A

Renal cysts. Porcine

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17
Q
A

Renal cysts can be uniorbilateral,singleormultiple. • Significance:Often it is just an incidental finding.

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18
Q

Polycystic kidneys

A

Grossly,kidneyscontain numerous variably‐sized cysts, in both cortex and medulla.

  • Oncutsurfaceseverely affected kidneys have a “honeycomb“ appearance.
  • Cystsarefilledwith colorless fluid.
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19
Q
A

Polycystic kidneys

Polycystic kidney in a Persian cat. Cut surface.

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20
Q

CAUSES OF POLYCYSTIC KIDNEYS

A

Congenital polycystic kidneys may be inherited as an autosomal dominant condition in pigs and lambs.

• It also occurs as an inherited condition in: – Cairn terrier dogs (in conjunction with cystic

biliary disease)

– Bull terriers

– Collie dogs

– Nubian goats

– Persian cats

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21
Q

CONSEQUENCES OF RENAL CYSTS

A

CONSEQUENCES OF RENAL CYSTS

1) Cysts may grow slowly or remain static.
2) Cysts may increase in size and/or number, causing compressive atrophy.

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22
Q
A

Acquired (non developmental) cysts may develop from obstructed tubules in chronic renal disease
See below: cut surface and close up of chronic renal disease in a dog

ddx for polycystic kidney dx

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23
Q

Ectopic Kidneys

A
  • Definition: Normal kidneys in abnormal locations.
  • Often unilateral.
  • Described in dogs and pigs.
  • Ectopic kidneys are predisposing factors for ureter obstruction and development of hydronephrosis.
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24
Q
A

Ectopic Kidneys

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25
Q

Horseshoe kidney

A

Congenital malformation that results from a fusion of the cranial or caudal poles of the kidneys.

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26
Q
A

Fused kidneys. Bovine.

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27
Q
A

Horseshoe kidney in a cat. Incidental finding at necropsy.

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28
Q

AUTOLYSIS

A

Autolysis is a common post‐mortem finding.

• Kidneysaresoft,friable

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29
Q

What is this post-mortem change?

A

Autolysis

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30
Q
A

Autolysed bovine kidney. Renal infarct is still detectable.

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31
Q
A

PSEUDOMELANOSIS

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32
Q
A

Pseudomelanosis in a kidney

Pigment is staining the surface of the kidney, as demonstrated on the image depicting the cut surface .

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33
Q

Hemoglobin

A
  • Gross features: Dark red to black kidneys.
  • Consequence of severe intravascular hemolysis and hemoglobinuria. Examples:
  • Leptospirosis
  • Bacillary hemoglobinuria • Babesiosis

•Chronic copper poisoning, etc.

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34
Q
A

Hemoglobin

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35
Q
A

Hemoglobinuria secondary to copper poisoning in a sheep.

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36
Q
A

Hemoglobinuria secondary to copper poisoning

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37
Q
A

Hemoglobinuria in a dog (Cut surface) and sheep (histology).

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38
Q

Myoglobin

A
  • Gross findings: dark red to black kidneys and dark red urine.
  • Mechanism: occurs when high levels of myoglobin are filtered into tubules (myoglobinuria).
  • Examples:

Source: Knottenbelt and Pascoe, 2003

  • Rhabdomyolysis in capture myopathy in wild animals
  • Equine paralytic myoglobinuria.
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39
Q
A

Myoglobinuria in a horse.

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40
Q

LIPOFUCSINOSIS

A

Incidental finding in old cattle.

• Grossly, kidneys are dark brown to black.

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41
Q
A

Lipofucsinosis in a bovine

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42
Q
A

Lipofucsinosis in kidney and heart. Bovine tissues

Descriptions:

1) The kidney is normal in size, diffusely dark brown to black.
2) This is the cut surface of the left ventricle and atrium in a bovine heart. The cardiac parenchyma is uniformly dark brown.

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43
Q

BILE PIGMENT

A

In obstructive jaundice or severe liver disease, the kidneys excrete conjugated bilirubin resulting in choluria.

• •

Grossly,the kidneys are yellow‐green.

Evidence of icterus/jaundice is seen in other tissues (mucous membranes, connective tissue).

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44
Q
A

Bile pigment in the renal cortex in a dog with autoimmune hemolytic anemia.

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45
Q

Hyperemia and congestion

A

Bright or dark red kidneys.

• Hyperemia can be physiologic.

Hyperemia and congestion

•Hypostatic congestion is common as a result of prolonged prostration and circulatory failure.

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46
Q
A

Hyperemia and congestion

  • Brightor􏰀dark􏰀red􏰀 kidneys.
  • Hyperemia can􏰀be􏰀 physiologic.
  • Hypostatic􏰀congestion􏰀is􏰀 common􏰀as􏰀a􏰀result􏰀of􏰀 prolonged􏰀prostration􏰀 and􏰀circulatory􏰀failure.
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47
Q

Hemorrhages

A

Hemorrhages are commonly seen in kidneys as a result of vasculitis or vascular necrosis.

• Hemorrhages could be petechial or ecchymotic.

• If the renal capsule is not removed, renal hemorrhages can be easily overlooked.

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48
Q
A

Petechiae(sometimes called turkey egg) in the cortical surface of a pig’s kidney.*

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49
Q

Renal Hemorrhage- what does it affect and how does it look pathologically?

A

Petechial or ecchymotic

  • Glomeruli are preferentially affected.
  • Speckled appearance.
  • Numerous causes:

Examples:

  • Coagulopathies • Viral infections • Septicemia
  • Toxins
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50
Q
A

Cortical hemorrhages. Herpes virus infection in a puppy

THIS IS VERY TYPICAL- NAVLE QUESTION

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51
Q

Causes of renal petechia

A

Extensive vascular injury or platelet consumption leading to disseminated intravascular coagulation (DIC).

• Acquired or congenital clotting defects (Sweet clover‐ coumarin poisoning, vitamin K deficiency, Hemophilia A and B)

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52
Q
A

Petechiae in the cortical surface. Bovine kidney(external lobulation).

white areas- neoplasic process that is interferring with cogulation

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53
Q

Causes of renal petechia and ecchymosis

A

• Viremia:
– Hog cholera leading to

endothelial damage

– African Swine fever leading to platelet destruction

– Canine herpes virus in neonatal puppies.

  • Bacteremia: such as Erysipelas, Streptococcal infections, salmonellosis in pigs.
  • If septicemia is suspected, different tissues such as lung, kidney and liver should be sent for bacteriological examination.
  • Toxins: oak toxicity, endotoxins and enterotoxins.
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54
Q
A

Herpes virus

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55
Q
A

Bacteremia in the kidneys

petechia on the cut surface

histo section- lots of hemmaroage

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56
Q
A

Renal torsion in a deer.

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57
Q
A

Renal torsion in a deer (next to a normal kidney)

one on the right- ishemia- complete cut off of the blood supply

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58
Q

Renal Infarcts

A

Typically triangular (wedge) in shape with the apex pointing towards the medulla.

• Renal infarcts are associated with thrombosis of renal vessels (usually the interlobular artery).

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59
Q
A

The size of the infarct depends on the size of affected vessels.

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60
Q
A

In acute cases, infarcts appear red due to s hemorrhage

pale areas of discoloration the body will think of as non-self

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61
Q
A

Renal infarct in a dog. Capsular and cut surface

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62
Q

What is a common cause of renal infarcts?

A

Valvular endocarditis (left side) is a common cause of renal infarcts

Thrombosis

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63
Q

Chronic Renal Infarcts

A

Prolonged ischemia leads to infarction/ coagulative necrosis.

• The affected area will heal by fibrosis and scar tissue

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64
Q
A

Healed renal infarcts in a cat.

Fibrosis causes retraction of the parenchyma and characteristic depressions on the renal cortex.

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65
Q

Which of these is a chronic and which is an acute infarct?

A

Chronic is on the right

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66
Q

Renal infarcts are most commonly seen in:

A
  • Cattle and pigs with vegetative valvular endocarditis of the left heart.
  • Cats with left atrial thrombosis associated with cardiomyopathy.
  • Dogs with renal amyloidosis due to loss (through the urine) of plasma anticoagulants such as antithrombin III.
  • Endotoxin‐mediated thrombosis due to Gram‐ negative sepsis or endotoxic shock (example: dogs with suppurative prostatitis).
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67
Q
A

Amyloidosis in a cat(remember cats have a lot of vascularness on the surface)

pale, diffuse change

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68
Q

AMYLOIDOSIS

A

Definition: heterogenous group of diseases due to deposition of amyloid in tissues.

  • Kidney is one of the most important targets of this condition.
  • Glomerular amyloidosis is a protein‐losing nephropathy.
  • Deposition of glomerular amyloid impairs its function with resulting marked proteinuria.
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69
Q

TYPES OF AMYLOIDOSIS

A

Primary amyloidosis:

very rare in domestic animals.

due to deposition of amyloid AL,derived from Ig light

chains produced by abnormal plasma cells.

Secondary (reactive) amyloidosis:

most common form in domestic animals.

deposition of amyloid AA that originates from serumα‐

globulin

• associated with chronic antigenic stimulation e.g.chronic inflammation, infection, neoplasia.

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70
Q
A

Staining fresh kidneys with iodine solution reveals many solid black dots which correspond to glomeruli filled with amyloid protein.

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71
Q
A

Kidneys with amyloidosis are enlarged, pale, and have a finely granular surface.

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72
Q
A

RENAL AMYLODOSIS‐ GROSS APPEARANCE

Kidneys are pale, have rounded edges. The cortical surface could be smooth and pale or slightly granular. Cut surface is pale, waxy.

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73
Q
A

Canine kidney. Glomerular and medullary amyloidosis.

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74
Q

RENAL AMYLOIDOSIS: Microscopic Appearance

A
  • Deposition of pink amorphous material in glomeruli (most species) or in medullary interstitium (cats and cattle).
  • Amyloid(pink homogeneous relatively acellular material) is deposited in the mesangial matrix and along the adjacent basement membrane.
  • Special stains such as Congo red (polarizedlight) and Thyoflavine‐T (Fluorescence) are used to microscopically confirm amyloidosis.
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75
Q
A

GLOMERULAR AMYLOIDOSIS‐ HISTOLOGIC AND ULTRASTRUCTURAL APPEARANCE

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76
Q

Glomerular amyloidosis: diagnosis is confirmed with

A

Glomerular amyloidosis: diagnosis is confirmed with congo red stain

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77
Q

FAMILIAL RENAL AMYLOIDOSIS

A
  • Familial renal amyloidosis occurs in Abyssinian cats and Chinese Shar Pei dogs, and it is characterized by medullary deposits of amyloid, with fibrosis and papillary necrosis.
  • Amyloidosis can lead to thrombosis of pulmonary arteries or renal veins due to hypercoagulable state caused by:

– stimulation of production of acute‐phase proteins such as fibrinogen

– simultaneously losing (because of increased glomerular permeability) low‐molecular weight anticoagulants, such as antithrombin III.

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78
Q
A

Renal necrosis and nephrosis(the necrosis of the tubular epithelium)

Papillary necrosis, cut surface. Canine kidney- DIABETES

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79
Q

Bilateral Renal Cortical Necrosis

A
  • Bilateral RenalCortical Necrosis is an acute and severe ischemia of the renal cortex due to vasospasm of cortical vessels.
  • It is an intriguing lesion that has traditionally been associated with endotoxemia.
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80
Q
A

Bilateral Renal Cortical Necrosis

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81
Q
A

Renal cortical necrosis

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82
Q
A

Renal Medullary (Papillary) Necrosis

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83
Q

Renal Medullary (Papillary) Necrosis

A
  • The mechanisms are controversial.
  • Caused by a localized ischemia of the renal medulla.

cortex is extremley pale; there is a ring that separates the healthy from the unhealthy kidney

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84
Q

CAUSES OF MEDULLARY NECROSIS

A

Amyloidosisi n cats

Pyelonephritis

Diabetes mellitus

Urinary obstruction

Use of anti- inflammatory and analgesic drugs such as phenylbutazone,phenacetin,aspirin.

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85
Q
A

Medullary Necrosis

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86
Q
A

Papillary necrosis in a horse due to NSAIDs toxicity

Greenish areas from vaso-constriction

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87
Q
A

Papillary necrosis in a foal NSAID toxicity

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88
Q

ACUTE TUBULAR NECROSIS (NEPHROSIS)

A

Acute necrosis of tubular cells is the primary process of nephrosis.

Renal tubular epithelium (especially proximal tubules) is metabolically very active,thus highly susceptible to ischemia or to toxic damage

Grossly, acute tubular nephrosis is difficult to diagnose.

The kidneys are swollen, the capsular surface is pale and moist, and bulges on cut surface.

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89
Q
A

ACUTE TUBULAR NECROSIS (NEPHROSIS)

Oak toxicity causing tubular necrosis.

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90
Q
A

Oxalate nephrosis, pig. Cut surface

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91
Q

DDx for pale kidneys

A
  • Amyloidosis- Congo Red
  • Acute Nephrosis-Tubular problem
  • Glomerulonephritis- inflammation in the glomeruli and kidney

• Lymphosarcoma-

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92
Q
A

Oxalate nephrosis. Porcine kidney.

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93
Q
A

Lymphosarcoma- Rabbit

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94
Q
A

Diffuse glomerulonephritis Canine

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95
Q
A

Nephrosis􏰁 Cougar

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96
Q

NEPHROSIS: histological appearance

A

• Most cases of nephrosis are acute to peracute with minimal to absent inflammatory cell infiltration.

• Cases of chronic
nephrosis are characterized by fibrosis,tubular loss, architectural disorganization,regeneration and limited inflammatory response.

Histologically, acute tubular nephrosis is characterized by swelling of the tubular epithelium.

The cytoplasm may be vacuolated and the nucleus may be pyknotic,karyolytic or karyorrhectic.

The􏰀tubules􏰀may􏰀be􏰀 hypocellular,􏰀are􏰀often􏰀 dilated􏰀and􏰀contain􏰀 necrotic􏰀cellular􏰀debris􏰀 and􏰀hyalinized casts.􏰀

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97
Q
A

NEPHROSIS: histological appearance

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98
Q
A

Melamine/Cyanuric acid toxicity

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99
Q

Pathogenesis of necrosis of tubular epithelium

A
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100
Q

Tubular Necrosis- Outcome

A

If the basement membrane is intact, regeneration of the proximal convoluted tubules is seen as early as three days after the toxic insult is removed.

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101
Q

CAUSES OF NEPHROSIS

A
  • Ingestion of exogenous substances.
  • Some substances precipitate as crystals in tubules (e.g. ethylene glycol oxalate)
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102
Q
A

Oxalate nephrosis

cut surface will bulge

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103
Q
A

Oxalate nephrosis Ethylene glycol(antifreeze) toxicity

tubular necrosis

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104
Q

Causes of toxic nephrosis

A

Heavy metals:
– Mercury (in herbicides)

– Lead (old paint,batteries) - MOST COMMON; gives intranucleular inclusions

– Cadmium
– Chromium
– Copper

– Phosphorus.

• Carbon tetrachloride, chlorinated hydrocarbon insecticides.

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105
Q
A

lead- toxic nephrosis

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106
Q

Nephrotoxic Plants

A

– Pigweed (Amaranthus retroflexus)

– Oaks (Quercus sp.).

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107
Q
A

Pigweed(Amaranthus retroflexus) causes tubular degeneration and peri-renal edema in pigs and cattle.

Edema is around the kidney

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108
Q

Oak Poisoning

A

Oak poisoning occurs in cattle and horses.

• The pathogenesis of the condition is not completely known but tannins and/ or their metabolites are incriminated.It is proposed that tannic acid binds to endothelial cells causing necrosis of the epithelium.

109
Q
A

Acute tubular necrosis, oak toxicity

110
Q

What is the general routes of infection that bacteria comes into the kidney?

A

General routes of infection:

Hematogenous infection- descending infection- comes in via the lood

Ascending infection- from the urethra

111
Q

Glomerulitis

A

if the glomeruli are the only structure that are infected

112
Q

Glomerulonephritis

A

Glomerulus and parechmya involved

113
Q

Interstitial nephritis

A

inflammatory process in the intersitium

114
Q

Pyelonephritis

A

Ascending Infection- etioloigcal agent that goes up the urinary tract to the kidney

115
Q 
Glomerulitis.
Embolic Nephritis (suppurative glomerulitis)
A

Caused by bacteremia.

Pattern is multifocal suppurative glomerulitis.

Bacterial colonies are seen in glomerular and interstitial capillaries.

116
Q
A

Embolic Nephritis (suppurative glomerulitis)

117
Q
A

Foal kidney, cut surface–

Actinobacillus equuli

118
Q
A

Progression of embolic nephritis

• Chronic renal microabscesses may develop as a result of embolic nephritis.

119
Q

Differential Dx for embolic nephritis

A

You have more neutrophils going into the infected area. Eventually the capsule will be full of bacteria and the capsule then looks like this.

Embolic nephrtisis- can’t be dx grossly

ddx: when all you have is a kidney from an animal and list 3 ddx
Neoplasia
Abscesses
G- multi-focal granulamotosi

120
Q

Glomerulonephritis

A

Glomerulonephritis and glomerulopathies are a heterogenous group of diseases in which the main morphologic change takes place in the glomeruli.

Glomerulonephritis are largely, but not exclusively, associated with immune mediated injury.

121
Q

GLOMERULITIS AND GLOMERULONEPHRITIS

• Pathogenesis:

A

Pathogenesis: two main mechanisms, related to immune mediated processes:

– Deposition of antigen antibody (Ag/Ab) complexes- infectious disease that triggers a response

–Autoantibodies directed against the GBM (antibasement membrane disease)-body develops antibodies against the basement membrane

122
Q

Deposition of antigen antibody (Ag/Ab)complexes

A

Persistent antigens in the blood result in deposition of Antigen Antibody (Ag Ab) complexes in glomerular basement membranes.

Persistent antigen can be viral, bacterial, parasitic, etc.

123
Q

Autoantibodies directed against the glomerular basement membrane

A

Also known as anti basement membrane disease

– formation of auto antibodies against the GBM —> complement fixation–> leukocyte infiltration.

– important in humans (e.g. acute post streptococcal glomerulonephritis), but rare in domestic animals.

124
Q

Gross lesions of Glomerulonephritis

A
  • Acute
  • Subtle changes; kidneys appear swollen and pale.
  • Chronic
  • kidneys are shrunken and granular

Both have diffuse patterns!

125
Q
A

Glomerulonephritis

126
Q

Histopathology of Glomerulonephritis

A

Three morphologic types:

–Membranous glomerulonephritis characterized by thickening of basement membrane

–Proliferative glomerulonephritis characterized by increased cellularity-more cells than normal;

–Membrano proliferative glomerulonephritis, often leads to glomerular sclerosis-That particular glomerulus will dissapear functionally

127
Q
A

Membranous glomerulonephritis

128
Q

Proliferative vs, membranous glomerulonephritis

A

Membranous- thickening of basement membrane( can see on PAS stain); increased eosinophilia within the glomeruli; you use congo red to ddx from amyloid and both present with proteinuria

Proliferative- more cells than normal

129
Q

Membrano proliferative glomerulonephritis versus glomerulosclerosis

130
Q

What is a way to get a definative dx?

131
Q

INTERSTITIAL(TUBULOINTERSTITIAL) NEPHRITIS

A
  • Inflammatory infiltration in the interstitium affects tubular functions such as impaired reabsorption, concentration and/or excretion.
  • Distribution
  • Multifocal
  • Diffuse
132
Q
A

INTERSTITIAL (TUBULO INTERSTITIAL) NEPHRITIS

133
Q
A

Diffuse versus multifocal interstitial nephritis

134
Q
A

Diffuse Interstitial Nephritis

135
Q

Multifocal Interstitial Nephritis

A

Common, usually incidental finding.

May represent a sequel of resolved bacteremia/ septicemia.

Grossly:off white foci randomly scattered throughout the renal cortex and medulla.

Common in young cattle.

It is called “white spotted kidney.”

Presumed to be someresidual lesions of E.coli bacteremia in the first few weeks of life.

136
Q
A

Multifocal Interstitial Nephritis

137
Q
A

It is called “white spotted kidney.

Multifocal Interstitial Nephritis

138
Q
A

WHITE SPOTTED KIDNEY

139
Q

Pathogenesis of Bacterial Interstitial Nephritis

A

Following bacteremia the bacteria localize in the renal interstitial capillaries, migrate through the vascular endothelium, persists in the interstitial spaces, and migrate via the lateral intercellular junctions to reach the tubular lumina.

140
Q

Causes of interstitial nephritis

A

• Dogs
– Leptospira interrogans serovars canicola,

icterohaemorrhagiae, and others
– Infectious canine hepatitis virus, recovery phase – Theileria parva

• Cattle:
– E. coli septicemia (white spotted kidney)

– Leptospira interrogans serovar canicola – Malignant catarrhal fever

141
Q
A

Leptospira- goes in between the tubules

142
Q

Causes of interstitial nephritis

A

• Sheep:
– Sheeppox

• Pigs:
– Leptospira interrogans serovar pomona

– Porcine reproductive and respiratory syndrome – PCV2 (porcine circovirus 2)

• Horses:
– Equine viral arteritis

143
Q

Chronic interstitial nephritis

Gross apperance

A

Gross appearance: –kidneys shrunken,

pale, firm

–capsule firmly adhered to cortex

144
Q
A

Chronic interstitial nephritis

145
Q

PYELONEPHRITIS

A

Definition: Pyelonephritis is inflammation of the renal pelvis and renal parenchyma.

• Unlike other forms of nephritis, the lesions of pyelonephritis are not necessarily symmetrical.

It is commonly seen in pigs, cattle and dogs.

Occasionally seen in cats, horses and other domestic animals.

146
Q
A

Unilateral pyelonephritis in a cat.

147
Q
A

Pyelonephritis in a dog

148
Q

Pathogenesis of pyelonephritis

A

Most often originates from ascending bacterial infection.

•Bacteria ascend ureters (ureteritis) invade the renal pelvis and then move through the renal tubules and reach the renal parenchyma.

149
Q

Pyelonepritis Predisposing factors

A

Urinary obstruction causes stasis of urine and facilitates bacterial growth.

  • Renal medulla is most susceptible to infection.
  • Abnormal vesico ureteral reflux (retrograde flow of urine) normally prevented by the oblique insertion of the ureters into the bladder wall.
  • Frequent sequel to cystitis (females>males).
150
Q

Abnormal vesico ureteral reflux

A

Common in puppies due to short intravesical length of the ureters and less oblique entry through the bladder wall.

Cystitis and ureteritis may interfere with ureteral peristaltic waves and predisposes to vesicoureteral reflux.

151
Q

Pyelonephritis Gross appearance

A

Suppurative exudate in pelvic cavity, partial destruction of medulla,irregular discoloration of cortex.

Marked scarring and fibrosis are often seen.

Evidence of inflammation in ureter and urinary bladder.

152
Q
A

Suppurative pyelonephritis in a dog

153
Q
A

Severe suppurative pyelonephritis

154
Q

Pyelonephritis Microscopic features

Acute and Chronic

A

Acute:Large number of neutrophils and bacteria within the lumen of renal tubules.Necrosis and exfoliation of the tubular epithelium.

• Chronic:white bands of scar tissue extending from cortex to medulla, interstitial fibrosis, loss of tubules and

finally “end stage kidney.“

155
Q
A

Pyelonephritis

156
Q

Granulomatous nephritis

A

• A form of chronic nephritis characterized by predominance of macrophages in the inflammatory infiltrate.Etiology includes:

– Viruses such as corona virus [causing cell mediated immune response] Or FIP

– Fungal organisms

– Bacteria (such as mycobacteria i.e. TB)

– Parasite migration

157
Q
A

Granulomatous nephritis (dry form) Feline infectious peritonitis

Multifocal to coalescing off-white raised nodules (interpreted as granulomas) on the cortical and cut surface.

The raised surfaces are cut off from blood circulation

158
Q

What is the main differential dx for the dry form of FIP?

A

Look at age etc, but HISTOLOGY will give you the final answer.

159
Q
A

Tuberculosis in a bovine

160
Q
A

Granulomatous nephritis due to parasite (ascaris) migration in a dog

161
Q

GRANULOMATOUS NEPHRITIS

A

Halicephalobus gingivalis migration in horses.

Saprophytic nematode – rhabditiform; previously known as (Micronema deletrix, Halicephalobus deletrix)

162
Q
A

GRANULOMATOUS NEPHRITIS

Kidney from a horse

163
Q

Dioctiophyma renale

A

Dioctiophyma renale

  • Also called giant kidney worm.
  • Occurs in mink,dogs,other fish eating mammals.
  • Large nematode (up to 1m long x 1cm in diameter).
  • Nematode resides in renal pelvis.
  • Can be found free in peritoneal cavity
164
Q
A

Dioctiophyma renale

165
Q

Stephanurus dentatus

A

Larvae migrate from intestine to liver (causing hepatitis, phlebitis, abscesses) and then across the peritoneal cavity to the peri renal fat and adjacent tissues

• Cysts often communicate with the renal pelvis

  • seen in pigs, espesically backyyard pigs
166
Q
A

Stephanurus dentatus (pigs)

167
Q
A

Stephanurus dentatus in a pig kidney

168
Q
A

Hydatid cyst. Moose kidney.

This can also affect people.

If you see a cyst in a dog, it’s probably congential

In a pig, cysts can be parasitic(softer feeling) or congential.

169
Q
A

Hydronephrosis in a ferret

kidney is the white bubble on the right

170
Q

Hydronephrosis

A

Definition: abnormal and permanent dilation of the renal pelvis and calyces with progressive atrophy of renal parenchyma.

171
Q
A

Hydronephrosis in a sheep.

172
Q

Cause of hydronephrosis

A

CAUSE: due to an increased pressure following partial or complete obstruction of the urine outflow.

Commonly associated with hydroureter (ureteral dilatation).

These look like water balloons

173
Q
A

Unilateral hydronephrosis

174
Q

Causes of urine outflow obstruction:

A

Congenital malformation of ureter, vesicoureteral junction or urethra.

Calculi (urethral uroliths in dogs and cats, ureteral or pelvis uroliths in cattle and rams).

Iatrogenic (ligation of ureter in lieu of, or with the ovarian stump).

Chronic inflammation.

Neoplasia such as urinary bladder transitional cell carcinomas or rhabdomyosarcomas located in the trigone of the urinary bladder.

Torsion of ureters or bladder.

175
Q
A

Pyelonephritis (notice exudate) and hydronephrosis.

176
Q
A

urolith- green thing on the kidney on the top

178
Q

Hydronephrosis pathogenesis

A

Hydronephrosis can be unilateral or bilateral.

Initially, urine filtrate diffuses to the renal interstitium where it is absorbed by lymphatic vessels.

With time, increased pressure shuts down blood vessels causing papillary necrosis and finally atrophy of renal parenchyma (Pressure ischemia atrophy)

179
Q
A

normal is on the right
abnormal kidney has no parchemya left

180
Q

UROLITHIASIS

A
  • Urolithiasis is the process of formation of solid or semisolid concretions (calculi) anywhere in the urinary collecting system.
  • Calculi are known as uroliths.
  • Uroliths are composed of a wide variety of minerals, often mixed with protein material.
181
Q
A

Multiple smooth calculi are seen within a distended urinary bladder. Canine.

182
Q

UROLITHIASIS- predisposing factors

A
  • Increased urinary concentration of the stones’ constituents (supersaturation).
  • Low urine volume (due to dehydration, low water consumption).
  • Urine pH (e.g., cystine stones form at low pH)

Urinary tract infections (due to the formation of an organic matrix and pH increment).

  • Diets high in phosphate in sheep.
  • High levels of silica of native pastures grazed by cattle.
183
Q
A

UROLITHIASIS

184
Q
A

Uroliths vary in size, shape, consistency

Feline kidney- multifaceted uroliths

185
Q

UROLITHIASIS BY STRUVITES

A
  • Struvites (magnesium, ammonium, phosphate): most common type in dogs, linked to urinary bladder infection.
  • Struvite calculi are seen in feedlot cattle feeding on high grain rations.
  • Formation of calculi of struvite also occurs as a result of bacterial infection of the bladder.
186
Q

UROLITHIASIS

A

Urethral obstruction is common in males.

Clinical signs: dysuria, stranguria, pollakiuria and hematuria.

187
Q
A

UROLITHIASIS

188
Q

UROLITHIASIS Possible consequences

A
  • None, urolith passed in the urine
  • Hydronephrosis if urolith is lodged in ureter
  • Chronic cystitis, or bladder distension and rupture if urolith is lodged in urethra
  • Acute hemorrhagic urethritis
189
Q
A

UROLITHIASIS

190
Q
A

Ruptured bladder (“waterbelly”) due to urethral obstruction

191
Q

Familial Renal Diseases

A
  • Most commonly seen in dogs compared to other species.
  • Origin: may be the result of abnormal structure or abnormal

function.
– Abnormal structure:

Examples:

  • Familial glomerulopathies in Samoyed and Doberman Pinshers
  • Familial renal fibrosis in Norwegian Elkhounds
192
Q

Familial Renal Disease

Abnormal function

A
  • Biochemical defects in renal tubules.
  • Kidneys may appear grossly and microscopically normal Examples:

– Fanconi Syndrome in Basenji dogs
– Primary renal glucosuria in Norwegian Elkhound

193
Q

Renal response to injury

A

Tubular regeneration.

Healing by fibrosis if basement membrane is damaged.

Nephroscleros is if fibrosis is severe.

194
Q

Urinary system defense mechanisms

A

Barrier system

Glomerular mesangial cells (part of monocyte macrophage system)

General immune response

195
Q

Renal response to injury

A

• Degeneration

  • Necrosis
  • Hyperplasia
  • Hypertrophy
  • Atrophy
  • inflammation
  • Regeneration
  • Fibrosis
196
Q
A

Tubular degeneration versus normal

197
Q
A

Renal fibrosis and nephrosclerosis are common sequelae to chronic inflammation.

198
Q
A

End stage kidneyis a term often used to describe􏰀kidneys that are severely affected by chronic inflammation and fibrosis.

199
Q

End-Stage Kidney

A

Severe chronic inflammation and fibrosis efface the normal architecture.

It is not possible to identify the primary insult.

200
Q
A

End-Stage Kidneys

Kidneys are pale, shrunken, and firm

201
Q

Causes of CRF in dogs

202
Q

Causes of CRF in a cat

203
Q

Causes of CRF in LA

204
Q
A

Chronic renal disease Canine. Cut surfaces.

205
Q

Renal disease versus renal failure.

A

•Renal disease is any deviation from normal

renal structure or function.

  • Renal failure is the inability of the kidney to maintain normal function; renal failure requires a loss of at least 70-75% of renal function.
  • The kidney has poor functional and structural correlation.
  • Renal failure requires a loss of at least 70% of kidney function.
206
Q
A

Chronic renal disease, Feline

207
Q

RENAL􏰀FAILURE

A

Glomerular function tends to be disrupted by diseases that alter glomerular structural arrangements such as damage to basement membrane, endothelium, epithelium or mesangium.

Tubular function tends to be disrupted by metabolic insults to the tubular cells (e.g. hypoxia or toxins).

Renal filtration allows elimination of many metabolic waste products. Two of these substances are urea and creatinine.

Urea and creatinine have particular significance since their concentrations in plasma are clinically used to detect a renal malfunction.

208
Q

Biomarkers of renal function

A
  • Ureais produced in the liver from nitrogenous byproducts of the protein metabolism (ammonia).
  • Creatinineis the normal byproduct of phosphocreatine,a substance involved in the contraction of muscle fibers.
  • Blood urea (BUN) and creatinine are filtered and excreted in the urine at a relatively regular rate.
209
Q

Renal disease versus renal failure

A

•Renal disease is any deviation from normal

renal structure or function.

•Renal failure is the inability of the kidney to maintain normal function; renal failure requires a loss of at least 75% of renal function.

210
Q

AZOTEMIA VERSUS UREMIA

A
  • Azotemia is an abnormal elevation of urea and creatinine in the blood without clinical manifestations of renal disease (azotemia is, therefore, a biochemical abnormality mostly due to decreased GFR).
  • Uremia is a clinical syndrome of toxemia due to intravascular accumulation of endogenous toxic waste substances such as urea, creatinine,uric acid, guanidine, phenolic acid, high molecular weight alcohols plus other metabolites.
211
Q

Clinical signs of Uremia

A
  • Vomiting
  • Dehydration or anasarca
  • Polydypsia, anuria, oliguria,poliuria
  • Ammoniacal breath
  • Malaise due to “uremic toxins”
212
Q

NON RENAL LESIONS OF UREMIA

A

NON RENAL LESIONS OF UREMIA

  • Uremic stomatitis / glossitis
  • Hemorrhagic ulcerative gastritis and colitis
  • Endocarditis /mucoarteritis
  • Tissue mineralization
  • Pulmonary edem
213
Q

Uremic Stomatitis /Glossitis

A
  • Occurs in cats and dogs due to fibrinoid arteriolar necrosis and bacterial production of ammonia.
  • Oral bacteria transform urea into ammonia (NH3) which irritates the oral epithelium and causes ulceration of the mucosa.
  • Ulcerative and necrotizing stomatitis is characterized by a brown,foul smelling mucoid material adhered to the eroded and ulcerated lingual and oral mucosa.
  • Thus, clinical exam will reveal halitosis (urine breath).
214
Q
A

Uremic Stomatitis /Glossitis

215
Q
A

Uremic Stomatitis /Glossitis

216
Q

Hemorrhagic ulcerative gastritis

A

Occurs as a result of arteriolar necrosis with

(a) mucosal infarction and (b) mineralization of the gastric glands and submucosal blood vessels.

The ulcerated mucosa may get secondary bacterial invasion.

217
Q
A

Hemorrhagic ulcerative gastritis

218
Q

Uremic gastritis/ colitis

A

• Uremic gastritis is seen in dogs and cats, whereas the colon is affected in horses and cattle.

219
Q
A

Uremic gastritis/ colitis

220
Q

Mucoarteritis/ endocarditis.

A

Thisisanon-inflammatory condition due to deposition of glycosaminoglycans with subsequent fibrinoid degeneration of the subendocardial connective tissue.

Intheheart,uremic mucoarteritis is most common in the left atria and proximal aorta.

Grossly,itconsistsofopaque, light yellow roughened endocardial plaques.

221
Q
A

Mucoarteritis/ endocarditis.

222
Q

Dystrophic and Metastatic Calcification.

A

Deposition of mineral in the walls of the:

– alveolar septa,

– pulmonary arterioles

– Pericardium

– soft tissues

– parietal pleura in the cranial intercostal spaces (“pleural frosting”)

It may be associated to deposition of calcium secondary to cell injury or hypercalcemia, or hyperphosphatemia.

223
Q
A

Dystrophic and Metastatic Calcification

224
Q

Pulmonary edema

A

Pulmonary edema results from damage to the air blood barrier and plasma fluid leaks into the alveoli.

• Pulmonary edema is often the cause of death in uremic animals.

225
Q
A

Pulmonary edema

226
Q
A

Uremic Pneumopathy

  • Gross appearance: Lungs fail to collapse, have rounded edges, would be heavy and moist at cut surfaces.
  • Histologic appearance: eosinophilic material (edema) within alveoli, basophilic material (mineralization) may be present in alveolar walls.
227
Q

NON RENAL LESIONS OF UREMIA

A

Uremic stomatitis /glossitis

  • Hemorrhagic ulcerative gastritis and colitis
  • Endocarditis/mucoarteritis
  • Tissue mineralization
  • Pulmonary edema
  • Secondary hyperparathyroidism
228
Q

Secondary renal hyperparathyroidism

A

One of the many functions of the kidney is to excrete phosphorus.

Abnormal renal function results in excessive retention of phosphorus (hyperphosphatemia)

In order to maintain homeostasis,after retention of phosphorus the body responds by increasing calcium.

Thus, parathyroid glands are activated to compensate and promote reabsorption of calcium from bone.

229
Q
A

Secondary renal hyperparathyroidism

230
Q
A

Thyroid hyperplasia.

secondary renal hyperparathyroidism

231
Q
A

Parathyroid gland hyperplasia (renal hyperparathyroidism)

232
Q

CYSTITIS

A

•Natural antibacterial activity of normal animal urine:

–normal voiding of urine

–low pH

–high osmolality.

233
Q

CYSTITIS- causes

A
  • Bacterial infections: bacteria involved are similar to those causing pyelonephritis.
  • Due to formation and accumulation of uroliths.
  • Exposure to toxic compounds (less common)

–ingestion of blister beetle in alfalfa (cantharidin toxicity in horses)

–Ingestion of bracken fern (enzootic hematuria in cattle);

–treatment with cyclophosphamide (dog, cat)

234
Q
A

Suppurative cystitis in a dog.

235
Q

Braken Fern in Cattle

236
Q

Acute cystitis

A
  • Mucosal hemorrhage and ulceration.
  • Production of exudate (hemorrhagic, fibrinopurulent).
237
Q
A

Acute cystitis

238
Q

Chronic cystitis

A

•Mucous metaplasia of transitional epithelium.

239
Q
A

Multifocal lymphoid hyperplasia, also known as follicular cystitis.

240
Q
A

Formation of mucosal polyps, also known as polypoid cystitis.

241
Q

Cystitis

A

Emphysematous cystitis develops in some dogs and cats with diabetes mellitus.

Glucosuriaprovides a good growth media to bacteria.

242
Q
243
Q

Feline Lower Urinary tract disease/ Feline Urological Syndrome

A

– A common condition of male cats.

– Characterized by obstruction of the urethra by a urethral plug.

– Plug is composed of a mixture of protein, cellular debris and struvite.

-Diet high in magnesium and phosphate.

Alkaline urine pH.

Decreased fluid consumption.

244
Q
A

Feline Lower Urinary tract disease/ Feline Urological Syndrome

245
Q
A

Feline Lower Urinary tract disease/ Feline Urological Syndrome

246
Q

Feline Urological Syndrome- pathogenesis

A
  • Complex and multifactorial.
  • Bladder infection by viruses.
  • Inhibition of urethral growth by early castration
247
Q
A

Feline Urological Syndrome- pathogenesis

248
Q

Feline Urological Syndrome- gross features

A

Bladder is distended.

The mucosa has red discoloration, often diffuse and transmural.

249
Q
A

Feline Urological Syndrome-

250
Q

NEOPLASTIC DISEASES

A
  • Primary tumors of the urinary tract are rare.
  • Bladder tumors are seen more often than renal tumors.
  • Frequency:dogs>cats> other species
251
Q
A

Transitional cell carcinoma- urinary bladder- canine

252
Q

Primary epithelial tumors

A

• Renal adenocarcinoma

-Renal adenocarcinoma

• Renal cystadenocarcinoma

253
Q
A

Renal adenocarcinoma

254
Q
A

RENAL ADENOMA EQUINE

255
Q
A

RENAL CARCINOMA IN A MULE. CUT SURFACE

256
Q
A

RENAL CARCINOMA

257
Q

Primary urinary tumors

A

Nephroblastoma (embryonal nephroma, Wilm`s tumor)

Common in pigs, rats and chickens, also diagnosed in cattle and dogs

259
Q
A

Nephroblastoma

260
Q
A

Transitional cell papilloma in ureter

261
Q

Transitional cell carcinoma

A

Transitional cell carcinoma

•Possible exposure to carcinogens:

–transitional cell carcinoma of bladder in dogs exposed to

insecticide dips;

–enzootic hematuria in cattle ingesting bracken fern (Pteridium spp):

• Multifocal raised nodules or focal thickening (plaques) of the urinary bladder, commonly in the trigone region

262
Q
A

Transitional cell carcinoma

263
Q
A

TRANSITIONAL CELL CARCINOMA IN A DOG

264
Q

Primary mesenchymal tumors

A

leiomyoma/ leiomyosarcoma

fibroma/fibrosarcoma

hemangioma/ hemangiosarcoma

265
Q
A

Embryonal rhabdomyosarcoma in the urinary bladder of a young dog

266
Q
A

Rhabdomyosarcoma. Canine urinary bladder.

267
Q
A

Renal lymphosarcoma in a cat

268
Q
A

Metastatic tumors of the kidney Malignant melanoma

Pathology II (20 decks)

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