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urinary system > Glomerular Disease Pathology > Flashcards

Glomerular Disease Pathology Flashcards

1
Q

What is glomerulonephritis?

A

Inflammation of the tinu filters in your kidney (glomeruli)

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2
Q

How does blood enter the glomerulus?

A

Via afferent arteriole

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3
Q

What happens once blood enters the glomerulus?

A

Some of it is filtered across glomerular membrane

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4
Q

When blood enters the glomerulus, what happens to large and charge substances?

A

They are not filtered and will stay in plasma

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5
Q

What are the cells called in the Bowman’s capsule that wrap around the capillaries of the glomerulus?

A

Podocytes

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6
Q

What are podocytes observed to have?

A

Interdigitating fingers or foot processes

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7
Q

What can be seen if you took a secrtion through a capillary loop?

A

Filter barrier, which is a membrane composed of endothelial cell cytoplasm, basal lamina and podocyte

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8
Q

What are the 3 parts of the filter barrier?

A

Endothelial cell cytoplasm

Basal lamina

Podocyte

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9
Q

What are mesangial cells?

A

‘Tree like’ group of cells which support capillaries

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10
Q

What happens to filtrate after glomerulus?

A

Goes into Bowman’s space, then into proximal tubule

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11
Q

After the glomerulus, what do blood cells, some fluid and albumin and larger proteins exit via?

A

Efferent arteriole

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12
Q

What are the different kinds of glomerulonephritis?

A

Inflammatory or non-inflammatory

Primary

Secondary

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13
Q

What is primary glomerulus?

A

Only affects glomerulus

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14
Q

What is secondary glomerulus?

A

Affects other parts of the body

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15
Q

What are examples of diseases causing secondary glomerulus?

A

SLE or Wegener’s

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16
Q

What is the aetiology of glomerulonephritis?

A
  • immunoglobulin deposition
  • no immunoglobulin deposition
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17
Q

What are the 4 common presentations of glomerulonephritis?

A
  • Haematuria (blood in urine)
  • Heavy proteinuria (nephrotic syndrome)
  • Slowly increasing proteinuria
  • Acute renal failure
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18
Q

What are different conditions that cause glomerulonephritis?

A

IgA glomerlonephritis

Membranous glomerulonephritis

Diabetic nephropathy

Crescentic glomerulonephritis

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19
Q

What does IgA glomerulonephritis often present with?

A

Often presents with discoloured urine, investigation would be dipstick urine which is positive for blood

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20
Q

What are the main causes of IgA glomerulonephritis?

A
  • Urinary tract infection
  • Urinary tract stone
  • Urinary tract tumour
  • Glomerulonephritis
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21
Q

What investigations are done for IgA glomerulonephritis?

A

Dipstick urine

Urine culture

Ultrasound scan

If all normal, renal biopsy

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22
Q

If all typical investigations are normal for IgA glomerulonephritis, what investigation would be done?

A

Renal biopsy

23
Q

What is immunofluorescence?

A

Method in biology that relies on the use of antibodies chemically labeled with fluorescent dyes to visualize molecules under a light microscope

24
Q

What can be done with urinary biopsy in IgA glomerulonephritis?

A
25
Q

What is seen in a renal biopsy and immunofluorscence for IgA glomerulonephritis?

A
  • Reveals immunoglobulin (of IgA type) and complement component of C3 in mesangial area of all glomeruli
26
Q

What is the aetiology of IgA glomerulonephritis?

A

Aetiology of IgA glomerulonephritis is unknown:

  • Excess antibody (IgA) sometimes present in serum, but this is also true of some people who do not have IgA glomerulonephritis
27
Q

What is the pathogenesis of IgA glomerulonephritis?

A

IgA also does not get filtered into urine, it is “stuck” within the mesangium

This causes mesangium, not the filter membrane to become clogged with antibody – causing red blood cells to escape into urine:

  • IgA irritates mesangial cells and causes them to proliferate and produce more matrix
28
Q

What is the prognosis of IgA glomerulonephritis?

A
  • Usually self-limiting, ie return to normal
  • Small percentage go onto chronic renal failure (via continued deposition of matrix)
29
Q

What is the typical presentation of membranous glomerulonephritis?

A

Could present with feeling unwell and swollen legs

30
Q

What investigations are done for membranous glomerulonephritis?

A
  • Check clotting screen then do renal biopsy
31
Q

What is seen in a dipstick of urine for membranous glomerulonephritis?

A

Proteinuria

32
Q

What is seen in blood biochemistry for membranous glomerulonephritis?

A

Serum albumin low

33
Q

What is the pathogenesis of membranous glomerulonephritis?

A

In membranous glomerulonephritis IgG is stuck in the membrane:

  • IgG deposits itself between basal lamina and podocyte but cannot go further and is not filtered into urine
  • IgG is too big to be filtered into urine, but activates complement (C3) which punches holes in filter
  • This leaky filter now allows albumin to be filtered into urine, causing nephrotic syndrome
34
Q

What does renal biopsy reveal for membranous glomerulonephritis?

A

Thickened glomerular basement membrane

Deposits of IgG

Basal lamina spikes (matrix which tries to surround the deposit)

35
Q

What is deposited on the membrane in membranous glomerulonephritis?

A

IgG

36
Q

What is the prognosis of membranous glomerulonephritis?

A
  • 1/4 will get chronic renal failure within 10 years
37
Q

What is the aetiology of membranous glomerulonephritis?

A
  • Unknown but ca sometimes have underlying malignancy
  • In many patients antigen is phospholipase A2 receptor
38
Q

What investigations are done for diabetic nephropathy?

A

Dipstick urine

Clotting screen

Renal biopsy

39
Q

What can be seen in the biopsy for diabetic nephropathy?

A
40
Q

What is the pathogenesis of diabetic nephropathy?

A
41
Q

What kind of lesion does diabetic nephropathy cause?

A

Diabetic nephropathy causes nodules of mesangial matrix to form, known as Kimmelsteil-Wilson lesion:

  • Is gross excess of mesangial matrix forming nodules
42
Q

What is the prognosis of diabetic nephropathy?

A
  • Inevitable decline if established diabetic nephropathy ad if continued poor diabetic control
43
Q

What is a sign of acute renal failure?

A

Rapidly rising creatinine

44
Q

What are the typical investigations for renal disease?

A

Urine dipstick

Clotting screen

Renal biopsy

45
Q

What is seen in the biopsy for crescentic glomerulonephritis?

A

Early endothelial damage with fibrin deposition

Crush glomerular tuft

Cellular proliferation and influx of macrophages (is the crescent) around glomerular tuft, within Bowman’s space

46
Q

What are some causes for the crescentic glomerulonephritis pattern of injury?

A
  • Granulomatosis with polyangiitis (also known as Wegener’s granulomatosis)
    • Form of vasculitis (inflammation in vessels) which affects vessels in kidneys, nose and lungs
  • Microscopic polyarteritis (a disease very like Wegener)
  • Antiglomerular basement membrane disease
  • Many other forms of glomerulonephritis
47
Q

What is granulomatosis with polyangitis also known as?

A

Wegener’s granulomatosis

48
Q

What is Wegener’s granulomatotis?

A
  • Form of vasculitis (inflammation in vessels) which affects vessels in kidneys, nose and lungs
49
Q

What further tests can be done for Wegener’s?

A
  • Serum test shows presence of anti-neutrophil cytoplasmic antibodies (ANCA)
    • These are not deposited in the kidneys
    • Antibodies directed against proteinase 3 and myeloperoxidase, 2 enzymes in primary granules of neutrophils
    • Antibodies produce tissue damaged via interactions with primed neutrophils and endothelial cells
50
Q

What do serum tests reveal in Wegener’s?

A

Presence of anti-neutrophil cytoplasmic antibodies (ANCA)

51
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies

52
Q

What is ACNA a form of?

A

Autoimmunity

53
Q

What is the prognosis of Wegener’s?

A
  • Fatal (mean survival time is 6 months) if left untreated
  • Cyclophosphamide
    • 75% complete remission

urinary system (29 decks)

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