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Module 6 Week 2 > Patterns Of Disease In Kidney > Flashcards

Patterns Of Disease In Kidney Flashcards

1
Q

Possible portals/routes of entry into urinary tract

A

Haematogenous- blood

Ascending from lower urinary tract

Epidermal (from skin)

Direct injury

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2
Q

Haematogenous entry
-features

A

Localise in large renal vessel, interstitial vessel, glomerular capillary
- can lead to Infarction
– Septic
– Immune-mediated disease
– Can affect glomerulus, tubule and/or interstitium

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3
Q

Ascending from lower urinary tract

A

– Females mainly
– Secondary to gastrointestinal, genital, or epidermal contamination
– Targets tubules and interstitium primarily

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4
Q

Direct injury
-features

A

Substances secreted into glomerular filtrate
-e.g Formation of crystals which damage cells
-affects tubules mainly

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5
Q

Describe the Defence mechanisms of kidney

A

‒ Vasculature: Basement membrane

‒ Glomerulus:
Glomerular basement membrane (GBM; filtration barrier); glomerular
mesangium (phagocytic)

‒ Tubules:
Basement membrane (provides physical
barrier and scaffolding)

‒ Interstitium:
Innate humoral and cell-mediated immune system responses

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6
Q

Patters of disease in kidney are recognised by…

A

Route of infection

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7
Q

Name the main routes of infection

A

– (Developmental)
– Vascular
– Glomerular
– Tubules/Tubulointerstitial – Pelvis/Ascending
– Endstagekidney (everywhere)
– Anylocation

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8
Q

Developmental infection

A
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9
Q

What is fused kidneys

A
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10
Q

What are polycystic kidneys

A
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11
Q

Vascular lesions
-what is this
-what is it caused by

A

-Blood vessels are blocked
-An infarction (inadequate blood supply)

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12
Q

3 types of progression of vascular lesions infarction

A

Acute—>
Subacute—>
Chronic—>

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13
Q

Vascular lesions- what is haemorrhage

A

Any systemic vascular injury (e.g.: septicaemia, vasculitis, DIC)

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14
Q

Glomerular lesions
-3 types

A

• Glomerulonephritis/glomerulonephropathy
• Glomerular amyloidosis
• Glomerulosclerosis

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15
Q

Endpoint of glomerular disease:

A

Protein losing nephrotrophy

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16
Q

What can glomerular disease lead to?

A

Hypoproteinaemia, decreased oncotic pressure, loss of ATIII (hypercoagulability)

Nephrotic syndrome: hypoproteinaemia, proteinuria, ascites, hypercholesterolaemia

17
Q

Glomerulonephritis / Glomerulonephropathy

A

• most common cause for this; Immune-mediated disease
—Most common is immune complex (Ag-Ab) deposition
-May be due to animal having viral or bacterial infections – FeLV, FIP, pyometra, chronic parasitism (dirofilariasis)
-May be autoimmune;
Systemic lupus erythematosus (SLE)
Neoplasia

• Results in continual damage to GBM via podocyte effacement

18
Q

Glomerulonephritis: Lesions
-grossly
-histological

A

usually normal
May see uniform, tan/red “dots” (limited to cortex)
-so not much

Immune deposits are red “dots” along capillary loops
-should see lesions more clearly

19
Q

How would you do a diagnosis of lesions

A

renal biopsy HE, special stains, EM, immunofluorescence

20
Q

Glomerular Amyloidosis
-grossly

A

Can see enlarged, pale or orange, waxy kidneys
Amyloid deposition which expands mesangium

21
Q

What are amyloids

A

– Insoluble fibrillar protein deposited in
extracellular space
– Associated with source of chronic ongoing inflammation
-Most commonly found in glomerular

Occurs in Glomerular Amyloidosis

22
Q

What glomerular disease is shown in this image

A

Put on anki*

23
Q

Glomerulosclerosis

A

• End-stage glomerulus = obsolescent
– Obliteration of capillary loops with increased matrix and fibrous CT
– Nonspecific response to chronic glomerular injury

• Effects on tubules (via dec flow in efferent arterioles)

• Mild, multifocal, segmental GS is COMMON in aged animals

• can lead to End-stage kidney = severe, multifocal to diffuse

24
Q

What is sclerosis

A

= hardening of tissue (usually due to fibrosis)

25
Q

Protein-losing glomerular injury—>

A
26
Q

Name the Tubulointerstitial Diseases

A

• Acute tubular necrosis
– Nephrotoxic vs. ischemic

Oxalate nephrosis

27
Q

Acute Tubular Necrosis:
-caused by…

A

Toxins; e.g antifreeze consumption, ethylene glycol metabolites
Drugs
Plants; oxalate
Bacterial
Metals; lead mercury
Miscellaneous
Vitamin D
Haem/myoglobin

28
Q

Oxalate nephrosis
-grossly

A

Cortex much paler
Haemorrhages

29
Q

Tubulointerstitial lesions
-grossly
-result of…

A

Pitted, irregular surface due to interstitial fibrosis
– Palefoci= result of inflammation (lymphoplasmacytic to mixed) and fibrosis

30
Q

Leptospirosis lesions
-grossly
-Histological

A

pale radiating streaks in cortex and haemorrhagic foci in cortex and medulla

Histology: interstitial inflammation and tubular degeneration

31
Q

Tubulointerstitial: FIP

A

• Systemic disease with
vasculitis (phlebitis)
• Pyogranulomatous to
• lymphoplasmacytic nephritis
Track along vasculature in FIP
• Lesions can look like lymphoma

32
Q

Tubulointerstitial lesions
-histologically

A

• Tubular dilation, attenuation of epithelium
• Casts
• Interstitial fibrosis
• Interstitial inflammation

33
Q

Renal pelvis
-2 types

A

• Hydronephrosis

• Pyelonephritis

34
Q

Hydronephrosis
-what is this
-lateral or bilateral

A

dilation of renal pelvis
– can cause Obstruction of outflow (calculi) of urine

Likely to be bilateral (affect both kidneys)

Clinical significance variable

35
Q

Pyelonephritis
-result of…
-common diseases causing this

A

-As a result of ascending infection in domestic animals

-Impaired vesico-ureteral reflux (2ndary obstruction, cystitis)

-Common:
E. coli Proteus
Klebsiella
Staph, Strep (all species)
C. renale & T. pyogenes
(cattle)

36
Q

Neoplasia
-main ones in kidney

A

• Epithelial:
-Renal carcinoma – most common primary
– Transitional cell carcinoma (from lower urinary tract)
– Nephroblastoma

• Mesenchymal

• Round cell: Lymphoma

37
Q

End stage kidney in uraemia
-hallmark of chronicity is…
-grossly
-histologically

A

• Hallmark of chronicity is FIBROSIS
• Gross: pale, shrunken, pitted, firm
• Histology: increased connective tissue with ectatic/atrophied tubules and sclerotic glomeruli

38
Q

Sequelae / Nonrenal lesions of renal failure
-2 types

A

• Sequelae of acute renal failure
– Death due to elevated serum potassium,
metabolic acidosis, and/or pulmonary oedema
– Recovery

• Sequelae of chronic renal failure:
– Mineralisation of tissues (usually chronic)
Uremic acids
-Lungs, gastric mucosa, intercostal pleura, renal
tubules, left atrium and great vessels
-Elevated Ca x P product
– Uraemia = clinical manifestation of azotaemia
– Uremic ulcers (glossitis, gastritis)

39
Q

Uremic acids cause…

A

Injury to small vessels

Module 6 Week 2 (10 decks)

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