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Y3 Urinary pathology > Urinary system pathology 1 > Flashcards

Urinary system pathology 1 Flashcards

1
Q

Which species have multilobar renal morphology and which have unilobar?

A 
Multi = cow, pig
Uni = carnivores, small ruminants, horses
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2
Q

Kidney function is what % of cardiac output?

A

30%

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3
Q

What are some of the kidneys function?

A
  • Regulation of electrolytes
  • Conservation of water
  • Excretion of waste products
  • Acid-base regulation
  • Endocrine roles: erythropoietin, vitamin D, renin
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4
Q

What are the functions of the lower urinary tract?

A
  • Transport and storage of urine

- Controlled expulsion

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5
Q

What is the functional unit of the kideny?

A

The nephron

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6
Q

What needs to be observes when looking at a kidney grossly?

A
  • Shape, position, size
  • Contours
  • Adherence of capsule
  • Cortex is finely radially striated + dark red / brown (except cats).
  • Medulla pale brown
  • Ratio of cortex : medulla of ~2:1 to 3:1 in domestic spp
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7
Q

Describe the normal radiographic anatomy of the kidneys

A
  • Dorsal abdomen, retroperitoneal space
  • Right kidney is more cranial
  • Smooth margins, similar size and shape
  • GI tract can hide right kidney
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8
Q

The right kidney lies within which organ?

A

Within the renal fossa of the caudate liver lobe

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9
Q

Which 5 features make up the specialised structures of the kidney?

A
  • Glomerulus
  • PCT
  • LOH
  • DCT
  • CD
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10
Q

Histologically, how can PCT be compare to DCT?

A
  • PCT epithelium is cuboidal and very metabolically active

- The DCT cells are much more flattened and the lumen is larger

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11
Q

What is the response of the glomerulus to injury?

A
  • Severe damage = fibrosis

- Cannot be replaced so loss of the entire nephron

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12
Q

What is the response of tubular epithelium to mild injury?

A
  • Renal tubular epithelium lies on a basement membrane, cells can regenerate if this membrane stays intact
  • Mild to moderate damage
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13
Q

What is the response of tubular epithelium when nephrons are lost?

A

Remaining tubules can undergo compensatory hypertrophy

- limited capacity, which if reached => renal failure

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14
Q

What is the response of tubular epithelium to severe damage?

A
  • Severe damage with disruption to
    b. m. eg. diffuse ischaemic necrosis
  • loss of basement membrane structure so epithelium cant regenerate
  • permanent loss of entire nephron functional unit
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15
Q

Why does damage lead to entire loss of the nephron?

A

Each portion of the nephron is dependant on the others for its function

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16
Q

Give some examples of congenital/inherited kidney diseases

A
  • Ectopic and fused kidneys
  • Dysplasia
  • Familial renal disease
  • Cystic renal disease
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17
Q

Can an animal with ectopic/fused kidneys live normally?

A
  • not a serious defect

- can be fully functional if not obstruction to blood supply or urethral path

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18
Q

What is renal dysplasia?

A

Abnormal development of the organ, its tissue and components

  • can get a dilated ureter (hydroureter)
  • one kidney may be hypertrophied to compensate for the other kidney lacking most of its functional ability
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19
Q

Describe familial renal disease

A
  • occurs in families of animals e.g. cocker spaniels
  • polyuria, polydipsia
  • inflammation of the kidneys
  • excessive tubule dilation
  • eosinophilic
  • proteinuria
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20
Q

Describe cystic renal disease

A
  • Origin blocked tubules => filtrate build up => dilation
  • As the cysts enlarge, pressure increases => pressure atrophy of local renal tissues
  • normal function compromised
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21
Q

How would cystic renal disease appear histologically?

A

Large dilated air cavities (blank white spaces)

- Some may have fluid within them

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22
Q

Polycystic renal disease is heritable in which breed?

A

Persian cats

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23
Q

What are the 4 renal circulatory diseases?

A
  • Haemorrhage
  • Infarction
  • Papillary necrosis
  • Cortical ischaemia
24
Q

How can renal haemorrhage occur - 3 possibilities?

A
  • Trauma e.g. RTA, dog bite
  • Septicaemia e.g. salmonella, herpesvirus
  • Disseminated intravascular coagulation (DIC)
25
Q

How would Salmonella septicaemia with DIC appear grossly on the kidney surface?

A

Disseminated to coalescing dark red/black areas of haemorrhage

26
Q

What is renal infarction?

A

Coagulative necrosis of renal parenchyma secondary to vascular occlusion by an embolus
- A blockage will cause an area of the kidney to be deprived of its blood flow => ischemic necrosis

27
Q

What does the severity of renal infarction depend on?

A
  • Level of vascular obstruction: The smaller the blood vessel the less damage to that section of the kidney
  • Nature of the thrombus
28
Q

In renal infarction, damaged/non-vascularized sections appear how grossly?

A

Wedge shaped pale tan sunken tissue with apex pointing to site of vascular obstruction

29
Q

Describe the branching of the renal blood supply

A

Same for arteries and veins:

  • Renal
  • Interlobar
  • Arcuate
  • Interlobular
  • Afferent arterioles
30
Q

How does a renal infarct appear histologically?

A
  • Congested field: most blood vessels have static blood flow
  • Very little inflammatory component
  • PCT necrosis at edges though glomeruli often spared
31
Q

How does a chronic infarct appear grossly?

A

Replacement of necrotic tissue by fibrosis => contraction and depressed cortical lesion

32
Q

How does an acute infarct become chronic?

A
  • If the animal goes on to survive (only had one infarct, the other kidney is fully functional, etc), you get invasion of the necrotic tissue by macrophages, fibroblasts
  • Fibrous tissue contracts leaving an indented scar
33
Q

What is renal papillary necrosis?

A
  • occurs secondary to reduced blood flow, often due to NSAIDs (horses)
  • decreased blood flow and ischaemic necrosis of the medulla
34
Q

How does renal papillary necrosis appear grossly?

A

Green/grey patches of the renal parenchyma – areas of papillary necrosis – they have to be severe to cause significant disease – these areas slough off and block the ureter

35
Q

What are the two types of cortical ischaemia?

A
  • acute tubular necrosis

- renal cortical necrosis

36
Q

What is the cause of acute tubular necrosis?

A

Results from reduced blood flow (ischaemia) or toxins => multifocal to diffuse ischemia

37
Q

What is the cause of renal cortical necrosis?

A

G-ve septicaemia or DIC => microthrombi => multifocal to diffuse necrotising damage – rare

38
Q

Describe the pathogenesis of acute tubular necrosis

A
  • PCT epithelium loss
  • As cell debris blocks tubules + urine leaks into interstitium.
  • Can regenerate if basement membrane intact
  • If not fibrosis or death
39
Q

Describe the main cause of acute tubular necrosis in sheep

A
  • Copper toxicity

- Tubular epithelial necrosis with cell debris + refractile orange-red granular material (Hb comp) in lumens

40
Q

How does acute tubular necrosis appear histologically?

A
  • eosinophilic material in tubules
  • loss of tubular epithelium
  • loss of cell structure and necrosis
41
Q

How does renal cortical necrosis appear grossly?

A

Gross - Pale/tan areas are affected – necrotising

42
Q

How does renal cortical necrosis appear histologically?

A
  • Tubules lack nuclei within their epithelium
  • Glomeruli still have some nuclei present
  • PCT are all necrotic – no cellular detail
  • Lots of eosinophilic material
43
Q

Give 3 examples of renal degenerative diseases

A
  • Amyloidosis
  • Hydronephrosis
  • Hypercalcaemic nephropathy
44
Q

Describe renal amyloidosis

A
  • Modified protein deposits (serum amyloid A)
  • Some secondary chronic inflammation or neoplasia
  • Deposited in the glomerulus and medulla
45
Q

What are the consequences of amyloidosis deposition in the glomerulus?

A
  • pressure atrophy of the glomerulus

- Proteinuria (hypoproteinaemia) => CRF (“Nephrotic syndrome”)

46
Q

How does a kidney with amyloidosis appear grossly?

A
  • uniform colour change to pale tan
  • waxy/greasy texture
  • diffusely swollen
47
Q

How does renal amyloidosis appear histologically?

A
  • Enlarged glomeruli
  • Protein builds causing a pressure atrophy in the glomerulus
  • Lots of eosinophilic material
48
Q

What is a hydronephrosis?

A

Dilation of the renal pelvis secondary to PARTIAL obstruction of urine flow
- urine pressure build-up => reduces local medullary blood flow => ischaemia => dilation of pelvis

49
Q

What can be seen in severe cases of hydronephrosis?

A
  • Cortical atrophy

- Urine filled sac in end stage

50
Q

Describe the pathogenesis of hydronephrosis

A
  • urine flow is still continuous, despite the partial obstruction, but the pressure builds up over time
  • reduces the flow of blood passing through the renal medulla
  • ischaemic damage occurs
51
Q

Give examples of slowly developing partial blockages that could cause a hydronephrosis

A
  • Congenital urethral abnormality
  • Ureteral obstruction e.g. Calculi (stones)
  • LUT inflammation
  • Downstream neoplasia
  • Bladder paralysis
52
Q

Define pyelonephritis

A

Inflammation of the kidney (specifically of the parenchyma and renal pelvis) as a result of bacterial infection

53
Q

How would Urethral + bladder calculi with obstructive hydronephrosis appear grossly?

A

Dilated renal pelvis with calculi throughout urinary tract but especially in the bladder

54
Q

Hypercalcaemic nephropathy occurs secondary to?

A

Hypercalcaemia

55
Q

Describe hypercalcaemic nephropathy and its pathogenesis

A
  • Mineralisation (deposits of calcium salts) of tubular basement membrane, epithelium + glomeruli => necrosis
  • Destroys the cells it forms upon
  • Tubular obstruction and loss => renal failure
56
Q

How does hypercalcaemic nephropathy appear grossly?

A

Depressed crater like structures multifocally/diffusely distributed over the surface of the kidney

57
Q

How does hypercalcaemic nephropathy appear histologically under different stains?

A
  • Under H & E calcification appears as a purple/black colouration
  • More obvious with a Von kossa stain where calcium is highlighted as black

Y3 Urinary pathology (5 decks)

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