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URI 2 > Urinary pathology > Flashcards

Urinary pathology Flashcards

1
Q

What is in the cortex and medulla?

A
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2
Q

What are the weakness of the kidney/urinary system?

A
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3
Q

Urinary system – Main Portals of Entry/Pathways of Spread?

A

•Haematogenous

•Ascending from ureter (GI, genital tract, dermal contamination)

•Glomerular filtrate (e.g. oxalate crystals, filtered preformed toxins)

•Direct penetration (e.g. heavy metals, drugs with direct toxic action)

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4
Q

Discuss Defense Mechanisms/Barrier systems for the urinary system?

A
  • Barrier system—glomerular basement membrane (GBM)
  • Monocyte-macrophage system—glomerular mesangium
  • Immune system

Innate responses

Humoral responses

Cellular responses

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5
Q

What is Azotemia?

A

= Elevated levels of blood urea and creatinine
(without necessarily any clinical signs of renal disease!)

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6
Q

Discuss pre-renal, renal and post-renal azotemia?

A

1. Pre-renal
Kidney hypoperfusion
(hypovolaemic or cardiogenic shock, thrombosis…)

2. Renal
Damage to renal tissue
(glomeruli, tubules, interstitium, vasculature)

3. Post-renal
Urinary obstruction
(distal to kidneys)

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7
Q

What is Acute renal failure?

A

Rapid onset of oliguria or anuria and azotemia

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8
Q

What are the Common causes of acute renal failure?

A

Common causes:

  • Ischaemia (hypoperfusion)
  • Direct toxic injury to tubules (acute tubular necrosis)
  • Acute glomerulonephritis or tubulointerstitial nephritis
  • Acute urinary obstruction
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9
Q

What is the gross appearance of Acute renal failure?

A

Kidney normal or swollen/pale

Often reversible

May progress to chronic renal failure

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10
Q

What can be seen here?

A

Ethylene glycol intoxication leading to Acute renal failure bright red and shiny medulla is bulging (indicative of presence of oedema)

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11
Q

Discuss Chronic renal failure/disease?

A
  • Prolonged duration of signs of uraemia
  • Progressive renal disease culminating in critical loss of functional nephrons
  • Usually irreversible
  • All renal components are interdependent (limited ways of response to injury). Similar end-result of many chronic renal diseases.
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12
Q

How does CKD progress to end stage?

A
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13
Q

What can be seen here?

A

Chronic kidney disease example of appearance of a kidney in the case of CKD these kidneys are decreased in size irregular surface and can see there are indentations which correspond to areas of fibrosis in the parenchyma

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14
Q

Discuss the Anomaly of development Aplasia/agenesis (kidney, ureters)?

A

Aplasia/agenesis (kidney, ureters)

Unilateral: Asymptomatic if contralateral kidney normal

Bilateral: Inconsistent with postnatal life

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15
Q

Discuss the Anomaly of development of Renal hypoplasia?

A

Renal hypoplasia

Unilateral: Usually asymptomatic

Bilateral: Chronic renal insufficiency

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16
Q

Discuss the Anomaly of development of Renal dysplasia?

A

Renal dysplasia

(Unilateral or bilateral)

  • Disorganised development of renal parenchyma due to anomalous differentiation
  • Chronic renal insufficiency
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17
Q

What are other anomalies of renal development?

A
  • Anomalies of renal position, form, orientation
  • Ectopic ureter, patent urachus, others
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18
Q

What can be seen here?

A

Hypoplasia

Unilateral renal hypoplasia with contralateral renal hypertrophy.

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19
Q

What can be seen here?

A

Agenesis

complete lack of renal tissue. In this case is unilateral.

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20
Q

What can be seen here?

A

Horseshoe kidney (dog)

Fused kidneys – called horseshoe kidneys – may occur in utero, seen in all species. Results from fusion of the cranial or caudal poles of the kidneys. The area of fusion can vary can be so large they share the same pelvis.

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21
Q

Discuss renal dysplasia?

A

Renal dysplasia - disorganised development of renal parenchyma because of anomalous differentiation. Can be unilateral or bilateral.

Usually occurs when there is disruption of the normal development of the collecting duct system.

Usually congenital but in cats, dogs and pigs (have active subcapsular nephrogenic zone at birth), can also be caused by disease in the early neonatal period, until differentiation on of the nephrogenic tissue is completed.

Some cases may be hereditary.

Gross: Small, misshapen, fibrosed, with thick walled cysts and tortuous ureters.

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22
Q

What can be seen here?

A

Ectopic Ureter

Ectopic ureter is the most important ureteral anomaly. Most common in dogs, more frequent in females.

Photo: In the case of this cat, it appears as if the two ureters had joined during development and then enter the urethra as one.

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23
Q

Discuss Renal cysts?

A

One or more grossly visible cystic cavities within the renal parenchyma

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24
Q

Discuss Polycystic kidney disease (PKD)?

A

Occurs in all species; hereditary in: Bull Terrier, Persian cats (autosomal dominant), West Highland White Terriers, Cairn Terrier, Perendale sheep (autosomal recessive)

Consequences:
Highly variable depending on amount of parenchyma effected (from asymptomatic to chronic renal insufficiency)

Cysts can also be acquired (e.g. retention cysts in CKD usually formed due to fibrosis that causes obstruction of tubules)

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25
Q

What can be seen here?

A

Bovine. Cysts effecting different lobes.

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26
Q

What can be seen here?

A

Porcine large cysts effecting cortex and medulla

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27
Q

What can be seen here?

A

Feline multiple cysts can be seen from surface

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28
Q

What can be seen here?

A

Canine multiple cysts thin walled with fluid in centre

Dilation of pelvis

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29
Q

List Non-inflammatory nephropathies/uropathies?

A
  • Renal haemorrhage
  • Renal infarction
  • Acute tubular necrosis
  • Hydronephrosis, hydroureter
  • Amyloidosis
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30
Q

Discuss Renal haemorrhage?

A
  • Usually caused by bacterial infections
  • Bacteraemia (porcine erysipelas, salmonellosis)
  • Viraemia (classical swine fever, African swine fever, canine herpesvirus type 1,…)
  • Other possible causes include: Coagulopathies, vasculitis, trauma
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31
Q

Discuss renal infarction?

A

-Localised coagulative necrosis produced by embolic or thrombotic occlusion of the renal artery or of one of its branches

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32
Q

What causes renal infarctions?

A
  • *Causes:**
  • Thrombotic valvular endocarditis (septic emboli)
  • Systemic vasculitis (immune-mediated, infectious…)
  • Mural cardiac thrombosis (feline cardiomyopathy)
  • Aortic thrombosis (verminous arteritis)

Consequences: Acute renal insufficiency

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33
Q

Where is the common site for renal infarctions?

A

The interlobar artery branches at right angles at the corticomedullary junction to give rise to arcuate arteries that in turn branch to form interlobular arteries that extend into the cortex. Interlobular arteries give rise to smaller branches (intralobular arteries), eventually forming glomerular afferent arterioles that enter the glomerular capillary tuft and then exit at the glomerular vascular pole as efferent arterioles.

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34
Q

How do infarcts appear?

A

Infarcts are usually wedge-shaped in a cross section of kidney, with the base against the cortical surface and the apex pointing toward the medulla, conforming to a zone of cortical parenchyma supplied by the site of the obstruction.

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35
Q

What does an acute haemhorrhage look like?

A

Acute renal infarcts. Initially, renal infarcts are swollen, intensely cyanotic, and congested by the blood that oozes into the vessels from collateral vessels.

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36
Q

What does a chronic haemhorrhage look like?

A

Chronic infarcts are pale, shrunken, and fibrotic, resulting in distortion and depression of the renal contour.

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37
Q

What is Acute tubular necrosis?

A

= Acute necrosis of the epithelium of renal tubules

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38
Q

What are the main causes of acute tubular necrosis?

A

Main causes:
Hypoxia/ischaemia:
Hypotension: hypovolaemic shock, cardiogenic shock, severe dehydration…
Nephrotoxicity:
Lead, aminoglycosides, tetracyclines, monensin, NSAIDs, oak, Ochratoxin A, Vitamin D, ethylene glycol, cisplatin…

-Often exacerbated by haemoglobin when there is haemolysis (haemoglobinuric nephrosis) or myoglobin pigments (myoglobinuric nephrosis)

Consequences:
Acute renal failure or chronic interstitial nephritis (possible chronic renal failure)

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39
Q

What can be seen here?

A

Haemoglobinuric nephrosis

Dark red tinged urine due to haemoglobinuria. Cu toxicity in sheep

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40
Q

What can be seen here?

A

Tubular necrosis due to lead toxicosis, renal cortex, rat – Acid-fast intra-nuclear inclusion bodies present in the proximal convoluted tubular epithelium – diagnositic of lead poisoning.

41
Q

What can be seen here?

A

Papillary (medullary crest) necrosis in a horse. Dark yellow/tan area in the medullary crest.

42
Q

What is Hydronephrosis, hydroureter?

A

= Dilation of renal pelvis or ureter due to obstruction of urine outflow, causing progressive atrophy and dilation

43
Q

What are the causes of Hydronephrosis, hydroureter?

A

-Causes:
Calculi, chronic inflammation, neoplasia, congenital malformations, iatrogenic

-Unilateral or bilateral

-Consequences:
Chronic renal failure

44
Q

What can be seen here?

A

Canine, hydronephrosis, transitional cell carcinoma

45
Q

What can be seen here?

A

Bovine, hydronephrosis

46
Q

What can be seen here?

A

Canine, nephrolithiasis, hydronephrosis

47
Q

What can be seen here?

A

Canine, hydronephrosis, transitioncal cell carcinoma bladder. Mass obstructing outflow leading to hydronephrosis

48
Q

Look at this Revision of the normal glomerulus?

A
49
Q

What is Amyloidosis?

A

= Extracellular deposition of amyloid

  • Kidney is probably the organ most commonly involved
  • Usually glomerular, but medullary location predominates in cats and Shar-Pei dogs

(eosinophilic, homogeneous and proteinaceous material)

50
Q
A
51
Q

What breeds are predisposed to amyloidosis?

A

Predisposed breeds:
Shar-Pei dogs, Abyssinian and Siamese cats

Most common form:
Reactive systemic amyloidosis (caused by accumulation of AA amyloid) – chronic Ag stimulation

Clinically leads to:
Chronic renal insufficiency and proteinuria
(nephrotic syndrome)

52
Q

What can be seen here?

A

Amyloidosis

Papillary necrosis from NSAIDs can be seen too

53
Q

What can be seen here?

A

Amyloidosis

The renal glomerulus contains extracellular deposits of pale homogeneous eosinophilic amyloid. H&E stain.

54
Q

What can be seen here?

A

Congo red stain, polarized light used to confirm amyloidosis.

55
Q

What can be seen here?

A

The amyloid in the glomerulus stains red-orange with Congo red stain.

Congo red stain used to confirm amyloidosis

56
Q

List Inflammatory nephropathies/uropathies?

A
  • Glomerulonephritis
  • Tubulointerstitial nephritis
  • Pyelonephritis
  • Cystitis
57
Q

Discuss Glomerulonephritis (GN)?

A
  • Inflammation of glomeruli with secondary tubulointerstitial and vascular changes (glomerulitis -when inflammation is restricted to glomeruli)
  • Common in domestic animals
  • Damaged glomerular filtration barrier – leading to proteinuria (protein-losing nephropathy)
58
Q

Discuss -Types of glomerulonephritis (based on histological presentation):

A

i. Proliferative (horses)
ii. Membranous (cats)
iii. Membranoproliferative (dogs)

59
Q

What are the causes of GN?

A

Immune-mediated:

  • Deposition of immune complexes
  • Antibodies directed against glomerulus (rare)

Prolonged antigenemia
(persistent infections or other diseases)

-Viral infections
(FeLV, FIV, FIPV, canine adenovirus type 1, EIAV, BVDV, ASFV…)

-Chronic bacterial infections
(pyometra, pyoderma…)

-Chronic parasitism
(dirofilaria, leishmania, trypanosoma, encephalitozoon cuniculi…)

-Neoplasia

60
Q

Look at these different types of GN?

A
61
Q

Discuss Glomerulosclerosis?

A

•Chronic glomerulonephritis evolves to glomerulosclerosis

•Histology:
Shrunken, eosinophilic and hypocellular glomeruli

•Proteinuria, in absence of urinary tract inflammation, is indicative of glomerular damage

62
Q

Look what protein losing nephropathy can lead to?

A
63
Q

What can be seen here?

A

Histo:

  • There are bright pink intratubular casts of protein.
  • Thyroidization, kidney, dog, tubular hyaline casts
  • In dogs, accumulation of protein with a colloid-like appearance in tubules and
  • glomerular capsules dilated from scarring produces a thyroid-like
  • histologic appearance, called “thyroidization”.
64
Q

Discuss Tubulointerstitial nephritis?

A

Diseases involving primarily the interstitium and tubules

65
Q

What are the two portals of entrance for Tubulointerstitial nephritis?

A

Two portals of entrance:

–Haematogenous (descendent)

–Urinary (ascendant)

66
Q

What are the main types of Tubulointerstitial nephritis?

A

Main types:

a. Embolic suppurative (haematogenous)
b. Non-suppurative (haematogenous or ascendant)
c. Pyelonephritis (mostly ascendant)

67
Q

Discuss Embolic suppurative Tubulointerstitial nephritis?

A

Embolic suppurative:

–Bacteria

–Vascular (bacteraemia or septic thromboembolism)

–Multiple small abscesses or fewer large ones

68
Q
A
69
Q

Discuss Non-suppurative interstitial Tubulointerstitial nephritis?

A

-Acute, subacute or chronic (most common in cats and dogs)

‘White-spotted kidney’ of calves – common, largely incidental finding

70
Q

Discuss Chronic Tubulointerstitial nephritis?

A

– Common end-stage of chronic glomerulonephritis, acute tubular necrosis, acute pyelonephritis or acute interstitial nephritis
- Granulomatous
(infection with Aspergillus, Toxocara, Encephalitozoon, Prototheca, mycobacteria, FIPV, PCV2 …)

-Consequences: Chronic renal failure

71
Q

What can be seen here?

A

Granulomatous interstitial nephritis due to FIP

Feline, FIP, granulomatous nephritis. Intertitium expanded by large numbers of inflammatory cells, which will be mostly lymphocytes and histiocytes. Perivascular distribution prominent.

72
Q

What can be seen here?

A

Toxocara interstitial nephritis

Histo: A mature granuloma composed of a central ascarid larva surrounded by epithelioid macrophages and concentrically arranged fibrous connective tissue and inflammatory cells. Inset, Ascarid larva.

73
Q

What can be seen here?

A

Chronic interstitial nephritis

•Irregular surface
(retraction, fibrosis)

  • Small
  • Pale
  • Histologically: Interstitial lymphocytes and plasma cell infiltration, fibrosis, tubular atrophy
74
Q

What is Pyelonephritis:

A

= Inflammation of pelvis and renal parenchyma

75
Q

What is Cystitis:

A

= Inflammation of the urinary bladder
Usually caused by ascending infection

76
Q

What are the risk factors for Pyelonephritis and cystitis?

A

Risk factors:

  • Female gender (short urethras, urethral trauma during pregnancy or parturition)
  • Urine stasis/obstruction

-Others:
Diabetes, hyperestrogenism, congenital malformations (ureteral ectopia, urinary bladder aplasia…)

77
Q

Discuss Causes of pyelonephritis:

A

-Endogenous bacteria of the bowel and skin

Some specific pathogens of the urinary tract

  • Corynebacterium renale (cattle)
  • Actinobaculum suis (swine)

(E coli, staphylococci, streptococci, Enterobacter…)

78
Q

Discuss Causes of cystitis:

A
  • Same bacteria as in pyelonephritis (mostly opportunistic)
  • Viruses: Malignant catarrhal fever, classical swine fever, West Nile
  • Toxins: Bracken fern in bovines (enzootic haematuria), cyclophosphamide treatment in cats and dogs (sterile haemorrhagic cystitis)
79
Q

Look at these images of Pyelonephritis?

A
80
Q

Look at these images of cystitis?

A
81
Q

Discuss Renal neoplasia?

A

-Primary renal tumours are uncommon

  • Most common are renal carcinomas (most common primary renal tumour in dogs, cattle and horses; mostly mature and old animals)
  • typically highly malignant with common metastasis

-Metastatic lymphoma not uncommon in cattle and cats

(< 1% of all neoplasms in domestic animals)

82
Q
A
83
Q

Discuss Neoplasia of the lower urinary system?

A

-Predominantly in the urinary bladder

-Uncommon
(< 1% of all canine neoplasms)

  • Dogs > cats >> other
  • Most common are epithelial tumours, typically urothelial cell carcinoma (formerly called transitional cell carcinoma)

(urinary bladder >> urethra, rare in ureter)

84
Q

What can be seen here?

A

Urothelial cell carcinoma

Appear at trigone of urinary bladder most commonly

About 50% of urothelial cell carcinomas metastasize: usual pattern: regional lymph nodes => lungs.

But peritoneal implantation or retrograde lymphatic spread to the soft tissue and bones of the hindlimbs or vertebrae may occur.

Other types of carcinoma of the lower urinary tract:

  • Squamous cell
  • Adenocarcinoma
  • Undifferentiated carcinoma
85
Q

What is mechanism of these Systemic changes associated to renal failure:

  • Parathyroid hyperplasia
  • Fibrous osteodystrophy
  • Metastatic mineralisation (stomach, lung, pleura, kidneys)
A

Altered calcium/phosphorus metabolism

86
Q

What is mechanism of these Systemic changes associated to renal failure:

Ulcerative and haemorrhagic gastritis and glossitis/stomatitis
(colitis in horses and cattle)

A

Direct urea vascular damage + bacterial production of ammonia from urea in saliva (caustic injury)

87
Q

What is mechanism of these Systemic changes associated to renal failure:

Pulmonary oedema and fibrinous pericarditis?

A

Increased vascular permeability is most likely

88
Q

What is mechanism of these Systemic changes associated to renal failure:

Atrial and vascular thrombosis?

A

Endothelial damage; nephrotic syndrome

89
Q

What is mechanism of these Systemic changes associated to renal failure:

Anaemia?

A

Increased erythrocyte fragility (due to azotaemia) and lack of erythropoietin; +/- gastrointestinal bleed

90
Q

What is mechanism of these Systemic changes associated to renal failure:

Polyuria/polydipsia?

A

Protein-losing nephropathies

Chronic renal failure
(prevents electrolyte and fluid reabsorption)

(osmotic effect)

91
Q

What is mechanism of these Systemic changes associated to renal failure: Hypertension?

A

Reduced renal blood flow

(by compression/obstruction of vessels by fibrosis, inflammation, thrombosis or neoplasia)

92
Q

Nephrotic Syndrome

Damage to glomerular filtration barrier =

A

leakage of various low MW proteins (e.g. albumin) into glomerular filtrate => overload of protein reabsorption capabilities of the PC tubules => protein-rich glomerular filtrate accumulates in tubules => protein in urine

93
Q

Renal diseases that result in proteinuria =

A

-protein-losing nephropathies (one of several causes of severe hypoproteinaemia in animals)

94
Q

Prolonged, severe renal protein loss =

A

-hypoproteinaemia, <plasma> Nephrotic Syndrome</plasma>

95
Q

What is Nephrotic Syndrome characterised by?

A
  • Characterized by generalised oedema, ascites, pleural effusion, and hyperlipidaemia (hypercholesterolemia)
  • There is : proteinuria (albuminuria), hypoproteinaemia (hypoalbuminaemia), hyperlipidaemia, generalised oedema (anasarca)
96
Q

Discuss Nephrotic Syndrome prognosis?

A

-In dogs, worse prognosis compared to patients with only proteinuria

97
Q

What is oedema caused by in nephrotic syndrome?

A

-Oedema – due to decreased plasma colloid osmotic pressure, stimulation of the renin-angiotensin-aldosterone system, and release of antidiuretic hormone (ADH) in response to hypovolaemia

98
Q

What is the Hepatic response to hypoproteinaemia?

A

-generalized increase in production of proteins, including lipoproteins => hyperlipoproteinemia and hypercholesterolemia

URI 2 (44 decks)

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