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Year 3 Pathology > Urinary 1, 2 and 3 > Flashcards

Urinary 1, 2 and 3 Flashcards

1
Q

What should grossly be observes about kidneys at necropsy?

A

Examine shape, position, and size
Contours/adherence of capsule
Cortex is finely radially striated and dark red
Cortex: medula 2:1
R kidney more cranial

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2
Q

How can you distinguish between proximal and distal convoluted tubules in histology?

A

Proximal- cuboidal, bigger- as more metabolically active

Distal- flatter

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3
Q

What is abnormal about this kidney slide?

A

Severe glomerular damage has led to fibrosis

Cannot be replaced- loss of entire nephron

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4
Q

What is the response to injury of the tubular epithelium when

  1. Basement membrane remains intact
  2. Nephrons are lost
  3. Damaged to basement membtane
A
  1. Cells regenerate
  2. Remaining tubules undergo compensatory hypertrophy- but limited capacity and if exceeded causes renal failure
  3. Diffuse ishcaemic necrosis- entire nephron lost
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5
Q

What are the 4 congenital/inherited diseases of kidneys?

A
  1. Ectopic/ fused kidneys- can be functional if blood supply not disrupted
  2. Dysplasia- anomalous differentiation
  3. Familial renal disease- under 2yo, leds to loss of nephrons- fibrosis and proteinuria
  4. Cystic renal disease- single or multiple, blocked tubule, filtrate build up
  5. Aplasia- Fail to form- rare
  6. Hypoplasia- incomplete development
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6
Q
A
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7
Q

What can cause renal haemorrhage?

A

Trauma

Septicaemia- salmonellosis, erysipelas, CSF, canine herpes in pups

DIC

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8
Q

What causes renal infarction?

What does the severity depend on?

A

Coagulative necrosis of renal parenchyma secondary to vascular occlusion by embolus

Severity depends on-
Level of vascular obstruction
Nature of thrombus- septic, neoplastic
Common with endocardial thrombosis

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9
Q

How does renal infarction grossly and histologically appear?

How does a chronic infarct appear?

Bonus question (Coffee if correct)- what are the arteries of the kidneys biggest to smallest?

A

Gross- wedge shaped pale tan, sunken tissue with apex pointing to site of vascular obstruction

Histo- central necrosis and congestion with PCT necrosis at edges, glomeruli often spared

Chronic infarct- replacment of necrotic tissue by fibosis causes contaction and depression of cortical lesion

Arteries- Renal, interlobar, arcuate, interlobar, afferent arterioles, efferent

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10
Q

What is renal papillary necrosis secondary to and what can cause it?

A

Secondary to reduced blood flow, often due to NSAIDs with or without prostolgandin production

Ishaemic necrosis of medulla

Rarely causes progressive renal disease unless large, sloughed sections lodge in ureter and cause blockage

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11
Q

What are the two types of renal cortical ishaemia and what is the difference?

A

Acute tubular necrosis- results from reduced blood flow or toxins- multifocal to diffuse ischaemia, mainly PCT affected

Renal cortical necrosis- gram -ve septicaemia or DIC leads to microthrombi causing multifocal to diffuse necrotising damage- rare

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12
Q

Describe the process of necrosis with Acute tubular necrosis?

A
  • Toxic or ischaemic damage causes PCT loss and tubules fille with cell debris
  • Oligouria (small volume of urine) as cell debris blocks, urine leaks into intersitium
  • Can regenerate if BM intact
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13
Q

What endogenous toxins can cause acute tubular necrosis?

A

Hypoperfused kidneys with Hb-aemia- secondary to Cu tox

Myoglobinaemia

Serum Hb/Mb are increased and pass into filtrate- Houses Leg

Necropsy shows dark red cortices

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14
Q

What are the three types of degenerative renal diseases?

A

Amyloidosis

Hydronephrosis

Hypercalcaemic neuropathy

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15
Q

What is amyloidosis and what causes it?

A

Modified protein deposits as beta-pleated sheets which is proteolysis resistant

Serum amyloid A (amyloid AA)- idiopathic

Imunoglobulin light chain (Amyloid AL)

Some secondary to neoplasia or chronic inflammation

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16
Q

Where can amyloidosis cause deposits?

A

Glomerular deposition- common site
Pressure atrophy of glomerulus- proteinuria to CRF

Medullary deposition- cats, asymptomatic at first, then papillary necrosis due to ischaemia to CRF

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17
Q

Can you identify the following 5 conditions grossly?

A
  1. Acute renal infarct
  2. Cat amyloidosis
  3. Polycystic kidney
  4. Pig with DIC haemorrhage
  5. Dog renal Dysplaysia
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18
Q

Can you identify the conditions from these two slides?

A
  1. Acute tubular necrosis
  2. Renal infarct
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19
Q

What is hydronephrosis and what causes it?

A

Dilation of nephron due to partially obstructed urine flow
Urine pressure build up leading to reduced local medullary blood flow- ischaemie dilation of renal pelvis

In severe cases leads to cortical atrophy leading to urine filled sac in end stage

Caused by slowly developing partial blockages (Congenital abnormalities, ureteral obstruction, LUT inflam, neoplasia, bladder paralysis)

Or

Secondary to infection

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20
Q

What is hypercalcaemic neuropathy?

A

Mineralisation of tubular basement membrane in the epithelium and glomerulus leading to necrosis

Tubular obstruction and loss- renal failure

Secondary to hypercalcaemia
Paraneoplastic, hypervitaminosis D, hyperparathyroidism, hypoadrenocorticism, otesolysis

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21
Q

What stain is used to identify hypercalcaemic neuropathy and what does it show?

A

Von Kossa stain- calcium is highlighted black

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22
Q

What happens when a glomeruli is damaged?

A

Not capable of regeneration but can hypertrophy to extent

Glomerular damage:

  • increases permeability
  • Reduced perfusion of the downstream parts of the tubule
  • Proteinuria (osmotic diuresis)
  • Nephrotic syndrome- hypoproteinaemia/cholesterolaemia- oedema and thrombosis
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23
Q

What is glomerulonephritis and what are the two causes?

A

Indlammation of glomeruli with secondary damage to other parts of the nephron

Caused by:

  • Immune mediated damage
  • Immune complexes deposited in glomeruli
    • Physical action- obstruction to filtration slits
    • Biological acvtivity- type III hypersensitivity
24
Q

What prolonged infections can form immune complexes and therefore glomerulonephritis in dogs, cats, pigs, cattle?

A

Dogs- ICHep, Pyometra, Chronic skin disease, SLE, AIHA, neoplasia

Cats- FeLV, FIP, neoplasia

Pigs- CSF, PRRS, PDNA

Cattle- BVD

Can be acute or chronic

25
Q

What causes post-weaning multisystemic wasting syndrome in pigs?
-mouthful am I right?

What other condition can it lead to?

What does it lead to and where?

A

Caused by porcine circovirus 2

Can lead to PDNS- porcine dermatitis, nephropathy syndrome

Leads to necrogranulomatous hepatitis, interstitial pneumonia and IN inclusion bodies

Liver/Lung/Lymph nodes

26
Q

How does PDNS appear in animals?

How is biochemistry of the animal affected?

A

Causes systemic necrotising vasculitis of skin and kidneys
Kidneys appear enlarged, pale brown with petechial haemorrhages
Multifocal to coalescing erythematous skin lesions, some progressing to necrosis

Raised serum urea, creatinine, gamma globulin levels and proteinuria

27
Q

What is tubulointerstitial nephritis?

A

Disease that caused inflammation that affects tubules and interstitium
damage to one triggers the other

Interstitial inflammation and fibrosis results in tubular atrophy and degeneration with secondary damage to glomeruli and vessels

Tubular damage stimulates inflammation which spills into intersitium

Both lead to chronic renal disease

28
Q

What are the different categories of tubulointerstitial nephritis?

A

Acute interstital nephritis

Supprative intersitial nephritis

Granulomatous interstitial nephritis

29
Q

What can cause acute tubulointerstitial nephritis in dogs, cattle and pigs?

A

Dogs- Leptospires, ICHV

Cattle- MCF, L.hardjo/pomona

Pigs- L.pomona

30
Q

What is the source of canine leptospirosis?

How can it be primary or secondary exposure?

A

Source of infection- Rats

Primary- indirect exposure via contaminated water source, soil food

Secondary- direct via infected urine, bite wounds

31
Q

Describe the development of canine leptospirosis?

In an acute case how do the kidneys appear?

Describe the histology

A
  • Skin abrasions/mm allow entry causing leptospiraemia
  • Localisation in intersitial capillaries
  • Migration to tubular lumen

Kidneys appear swollen and reddened

Histo- leptospiras associate with microvilli of D/PCT cause cause necrosis. Secondary intersitial inflammation with lympocytes, plasma cells and macrophages

32
Q

What happens if a dog survives from canine leptospirosis?

A

Regeneration of tubules is possible

Leptospiras can persist in renal tubules without causing disease but excreted in usine for long periods of time

33
Q

What is the zoonotic form of leptospirosis?

What animal can it affect and what does it cause?

A

L. hardjo

Cattle- causes a transient milk drop

34
Q

What are the diffent causes of supprative interstitial nephritis?

What different organisms can cause it?

A

Pyogenic (cause pus) organisms either haematogenously or ascening up pelvis

E.coli- white spot kidney

Actinobacillus

Erysipelas

Truperalla pyogenes

35
Q

What agents can cause granulomatous interstitial nephritis?

A

Cats- FIP

Mycobacteria- M.Bovis

Fungi- rare

Dogs- systemic encephalitozoan cuniculi

36
Q
  1. What are the alternative names for pyelonephritis?
A
  1. Pyelitis/ Pyonephritis
37
Q
  1. What causes pyelonephritis?
  2. Why is the medulla predisposed?
  3. What agents can cause pyelonephritis
A
  1. Usually ascending LUT infection- Bacteria
    females predisposed, urine stasis, retrograde flow, local trauma
  2. Medulla hypertonicity inbitis neutrophil influx and NH3 inhibitory complement
  3. All species- E.coli, Staphylocci, Strep
    Cattle- Corynebacterium renale
    Foals- actinobacillus equi
38
Q

What parasitic disorders can and how do they affect the kidney?

A

Toxocara canis- Dogs
Migration of ascarid larvae, producing granulomatous nephritis

Dictophyma renale-
Pelvic and peritoneal location
Parenchyma destroyed by pressure atrophy
Zoonotic

39
Q

Why are renal tubules highly susceptible to toxic damage?

Which part of the kidney is particularly susceptible?

What exacerbates damage?

A

High exposure and sensitivity

PCT- high metabolic activity

Shock and dehydration

40
Q

Describe the pathogenesis of renal toxic disease?

A

Leads to acute tubular necrosis

Many toxins alter ion pump in epithelium- reducing Na reabsorption and increased excretions- stimulates RAAS, causing vasoconstriction and ischaemia

Obstruction by cell debrin and intersitial oedema

Impaired glomerular permeability

41
Q

What toxins can cause acute tubular necrosis?

A

Oxalates- Ethylene glycol
Vitamin D compounds
Oak tannins
Myotoxins
Heavy metals
Antibiotics
Endogenous pigments- Hb
Enterotoxaemias- Clostrid perfringens

42
Q

Describe the pathogenesis of ethylene glycol toxicity?

How do kidneys grossly appear?

What can be done to cytology samples for diagnosis?

A
  • Effects CNS
  • Insoluble Ca2+ oxlalate crystals form in PCT- obstruction
  • Metabolic acidosis
  • Azotaemia, hypocalcaemia, hyperkalaemia, renal failure

Grossly appear-red and swollen with white/yellow striated cortex

Polarised light shoes the oxalate crystals

43
Q

What agent causes pulpy kidney disease?

How does it affect lambs and sheep

Where is C. perfringens found and who is most susceptible?

A

Clostridium perfringens D enterotoxaemia

Lambs- Acute, non-contagious disease in lambs- convulsion/sudden death
Older sheep- die after few days of mild GI signs some CNS signs (ataxia)

Found in soil, manure, intestinal commensal in ruminants
All ages- but 3-10 week old fast growers with sudden change in feed

44
Q

How does C. perfringens cause enterotoxaemia?

A
  • Ingest spores which activate in SI, if consumption of undigested starch high (milk) it provides substrate for overgrowth
  • Multiplying bacteria produce inactive protoxin which is activated by trypsin into epsilon toxin
  • Toxin decreases intestinal motility and allows uptake into circulation
  • Systemic circulation causes vascular endothelial degeneration- glucosuria, oedema, haemorrhage
45
Q

What renal neoplasias are common and uncommon?

A

Primary neoplasia uncommon
Epithelial/mesenchymal origin
Metastatic tumours

46
Q

What epithelial neoplasms can form in the kidneys?

A

Adenoma- rare, well circumcised, cortical mass

Adenocarcinoma- most frequent in dogs, cattle, sheep
Large, necrotic, haemorrhagic
Vascular metastasis to lung
May produce erythropoietin- polycythaemia

Transitional cell carcinoma- renal pelvis

47
Q

What mesenchymal neoplasms can originate from the kidney?

A

Lymphosarcoma- cats, cattle, dogs
Primary or secondary
Nodular or diffuse

Haemangiosacrcoma, fibrosarcoma- rare

48
Q

What epithelium makes up the lower urinary tract?

A

Stratified squamous epithelium

49
Q

What congenital disease can affeft the lower urinary tract?

A

Ectopic ureters- ureters terminate somewhere different (more caudal) to bladder
Leads to chronic urinary incompetence and UTI common

Patent urachus- urine from the navel

50
Q

What circulatory diseases can affect the LUT?

A

Haemorrhage- trauma, septicaemia, Viraemia

Infarction- torsion, prolapse

51
Q

What degenerative conditions affect the LUT?

A

Hydroureter/urethra-
Dilation of urter or urethre secondary to partial obstruction
If unilateral distal to bladder, bilateral proximal

Acquires anatomic variatoins-
displacment, torsion, dilation, rupture, herniation

Urolithiasis

52
Q

What can commonly cause bladder rupture, Dilation, Displacement?

A

Rupture-
Ruminants- urethral obstruction
Dogs/Cats- pelvic trauma
Foals- parturition

Dilation- obstructive- can lead to muscle tone loss

Dislacement- abdominal masses, pregnancy

53
Q

What is urolithiasis?

What are its effects?

A

Formation and presence of particles- kidney stones

Effects

  • Partial/complete obstruction
  • Pressure necrosis/ulceration
  • Acute haemorrhagic inflammation with bacterial overgrowth
  • Possible rupture of bladder/urethra
54
Q

What can urolithiasis particles be composed of?

A

Variable mineral content-
Struvite, Calcium carbonate, Silicate, Oxalate

Variable organis content-
Role in formation

55
Q

What are the predisposing factors to urolithiasis?

A

pH- acid (oxalates), alkaline (struvite)

Bacterial infection- urea to NH4++ by bacteria elevates pH

Diet- high phosphorus, oxalate, vit A deficiency

Hereditary

Sex

Species- cats

56
Q

What are the different potential sites of urolithiasis?

A

Renal- pelvic- painful

Ureteral

Cystic- cystitis

Urethral- Os penis dogs, sigmoid flexure

57
Q

What is feline urologic syndrome?

What is it predisposed by?

Describe its pathogenesis?

A

Obstructive urethral urolitheriasis

Predisposed by- neutered males, dry diets, alkalkine urine pH, increased urination intervals

Urethral obstruction to dysuria, haematuria and post renal azotaemia
2nd bacterial infectoin to severe haemorrhagic, transmural cystitis
can lead to rupture or acute renal failure

Year 3 Pathology (21 decks)

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