Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

*Urinary System > Glomerular Disease (Pathology) > Flashcards

Glomerular Disease (Pathology) Flashcards

1
Q

What are podocytes?

A

Podocytes are cells in the Bowman’s capsule in the kidneys that wrap around capillaries of the glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What proteins are filtered by the glomerulus?

A

All that are smaller than albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What structual feature do podocytes have?

A

From outside they have interdigitating ‘fingers’ or foot processes (‘podo’) which clamp on to the capillary loop and stop massive fluxes of proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 3 layers of the filter barrier membrane?

A

Endothelial cell cytoplasm

Basal lamina (connective tissue)

Podocyte (foot process)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are mesangial cells?

A

‘tree-like’ group of cells which support capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does filtrate travel after being filtered from the glomerulus?

A

Goes into Bowman’s space then into proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What 3 substances exit the glomerulus via the efferent arteriole?

A

Blood cells, some fluid and albumin + larger proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is glomerulonephritis? Is it inflammatory or non-inflammatory?

A

Disease of the glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is affected in primary glomerulonephritis?

A

Only affects glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is affected in secondary glomerulonephritis?

A

Other parts of body affected e.g. SLE (lupus) or Wegner’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Glomerulonephritis is sometimes cause by immunoglobulin deposition, but sometimes it isnt, e.g. in…

A

diabetic glomerular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 4 common presentations of glomerulonephritis? (IMPORTANT)

A
  1. Haematuria (blood in urine)
  2. Heavy proteinuria (nephrotic syndrome)
  3. Slowly increasing proteinuria
  4. Acute renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is haematuria diagnosed in a lab test?

A

Dipstick urine - positive for blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

4 causes of haematuria? (IMPORTANT)

A
  • UTI
  • Urinary tract stone
  • Urinary tract tumour
  • Glomerulonephritis (uncommon compared to first three)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What should be done after haematuria is diagnosed?

A
  • Send off urine culture
  • Arrange hosp appointment for USS (to find calculi/tumours)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What to do if urine culture and USS are both normal?

A

Renal biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is important to do before performing biopsy?

A

Clotting screen (risk of bleeding to death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What could be found in a renal biopsy of glomerular pathology in a patient with haematuria (Case 1)? What would the light microscopy show? What would electron microscopy show?

A

Immunoglobulin (of IgA type) and complement component C3 in mesangial area of all glomeruli

LM - Accumulation of pink mesangial matrix; profileration of mesangial cells

EM - deposits of IgA with prominent mesangial cells (and profileration of mesangial cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Aetiology of IgA glomerulonephritis is not entirely known, what could cause it?

A 
Execess antibody (IgA) sometimes present in serum (but this also true of ppl who dont have IgA glomerulonephritis)
IgA is for some reason not removed by the glomerulus and is 'stuck' within the mesangium

Mesangium (not the filter membrane), becomes clogged with antibody

21
Q

What effect does IgA have on the mesangial cells?

A

‘irritates’ mesangial cells and causes them to proliferate and produce more matrix

22
Q

Is it known why IgA nephropathy causes haematuria (RBCs in urine)?

A

Nope

23
Q

What is the usual prognosis of IgA nephropathy?

A

Usually self-limiting i.e. return to normal

24
Q

What happens in a small % of people with IgA nephropathy?

A

Go into chronic renal failure (via continued deposition of matrix) - histology shows completely sclerosed glomerulus

(can be up to 25% - particularly high in Japan)

25
Q

A 50 yr old male presents with 3 weeks of feeling unwell and swollen legs - what to do?

A

Send off biochemistry and haematology tests

26
Q

The man’s serum albumin is low, what next?

A

Dipstick proteinuria

Send into hosp to see nephrologist

27
Q

The nephrologist measures the protein (albumin) in the man’s urine, it shows a v heavy loss, what then is th diagnosis?

A

Nephrotic syndrome (showed that it must be an abnormality of glomerular filter)

28
Q

Check clotting screen of man and then do renal biopsy - what features be seen in this mans histology? (hint - ‘membranous glomerulonephritis’)

A
  • thickened glomerular basement membrane
  • deposits of IgG
  • spikes of new basement membrane matrix material under podocytes - ‘basal lamina spikes’ (to try and surround and remove the deposit)

-

29
Q

In membranous glomerulonephritis (one of most common causes of nephrotic syndrome), IgG deposits itself in the glomerular membrane, is it stuck there?

A

Yep; deposits itself between basal lamina and podocyte but cannot go further and is not filtered into urine as it is too big

30
Q

What does IgG stuck in the membrane activate? How does this cause nephrotic syndrome?

A

Complement (C3) which punches holes in the filter and this now leaky filter allows albumin to be filtered into urine, causing nephrotic syndrome

31
Q

What is the prognosis for membranous glomerulonephritis?

A

1/4 in chronic renal failure within 10 yrs; then progressively more after that

Treatment is not v good at moment

32
Q

Is the underlying cause of IgG production and accumulation in membranous glomerulonephritis known?

A

No, but can sometimes have underlying malignancy

In many patients antigen is phospholipase A2 receptor - unknown why this protein specifically as it is on podocytes which are a v immunologically isolated part of the body - almost never meed inflammatory cells

33
Q

(case 3 - type 1 DM; poor glycaemic control; retinopathy; albumin in urine slowly inreasing over last few yrs, not has heavy protein leakage in urine; renal biopsy done)
Where does matrix deposition in diabetic nephropathy occur?

A

In basal lamina underlying endothelium and in mesangial matrix

34
Q

In diabetic nephropathy, what effect does matrix deposition have on basement membranes?

A

Makes them thickened but leaky

35
Q

What effect does mesangial matrix have on capillaries in diabetic nephropathy?

A

Compresses them

36
Q

Are there any immune complexes in diabetic nephropathy?

A

Nope

37
Q

Describe some histological features of diabetic nephropathy

A
  • thickened capillary wall which is leaking albumin
  • increased mesangial matrix - leading to small, compressed capillary lumens
  • thickened, narrowed arterioles reducing BF to glomerulus
  • adhesions to Bowman’s capsule (glomerulus’ trying to stop massive leakage of albumin into urine)
38
Q

What is a Kimmelsteil-Wilson lesion (‘in established diabetic nephropathy’)?

A

Nodule of mesangial matrix (gross excess of matrix forming nodules)

39
Q

Prognosis for diabetic nephropathy?

A

Inevitable decline if established diabetic nephropathy and continued poor diabetic control

40
Q

Case 4 - female, 50 yr old; unwell 3 wks; cough; serum biochem - creatinine 500)

What is rapidly rising creatinine associated with?

A

Acute renal failure

41
Q

What else should be done in this case?

A

USS to see if renal tract lesion

Check clotting then do renal biopsy

42
Q

What type of glomerulonephritis has cellular proliferation and influx of macrophages (crescent) within Bowmans space?

A

Crescentic glomerulonephritis

43
Q

GIve 4 causes of the crescentic glomerulonephritis pattern of injury

A
  • Granulomatosis with polyangitis (aka Wegners granulomatosis)
  • Microscopic polyarteritis (similar to Wegners)
  • Antiglomerular basement membrane disease
  • Many other forms of glomerulonephritis
44
Q

What is granulomatosis with polyangitis?

A

A form of vasculitis which affects vessels in kidneys, nose and lungs (which is why woman presented with cough)

45
Q

Further test in Wegners is serum test, which might show what?

A

Presence of anti-neutrophil cytoplasmic antibodies (ANCA)

46
Q

What are ANCAs directed against? Are they deposited in the kidney?

A
  • Proteinase 3 and myeloperoxidase, 2 enzymes + primary granules of neutrophils
  • NO
47
Q

How do ANCAs produce damage?

A

Via interactions with primed neutrophils and endothelial cells

(not sure why they form - possibly a form of autoimmunity)

48
Q
A
49
Q

Prognosis for Wegner’s?

A

Fatal - mean survival is 6 months if left untreated

Must be treated v quickly with cycophosphamide chemo - 75% complete remission

*Urinary System (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions