Brainscape's Knowledge GenomeTM

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


See full index

Met3b > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What are the clinical features of nephritic syndrome?

A
  • haematuria + mild proteinuria (<1-1.5g/day)
  • impaired renal function
  • oliguria with signs of salt and water retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the clinical features of nephrotic syndrome?

A
  • proteinuria >3g/day
  • hypoalbuminuria <30g/dL
  • oedema (legs, periorbital etc)
  • foamy/frothy urine
  • symptoms suggestive of occult malignancy (cough, weight loss, night sweats, tarry stools)
  • symptoms suggestive of SLE (rash, photosensitivity, arthralgia)
  • may get xanthelasmata from severe hypercholesterolaemia (>10 mmol/L)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the primary causes of nephrotic syndrome?

A
  1. minimal change disease
  2. focal segmental glomerulosclerosis
  3. membranous glomerulonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the causes of nephritic syndrome?

A
  1. IgA nephropathy
  2. Post-infectious glomerulonephritis
  3. Membranoproliferative glomerulonephritis
  4. Goodpasture’s syndrome (anti-GBM nephropathy)
  5. Vasculitic disorders: GPA, Churg-Strauss
  6. Henoch-Schlonlein purpurn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What immunological investigations should be carried out in AKI where rapidly progressive glomerulonephritis is a possibility?

A
  1. ANCA:
    - cANCA (GPA)
    - pANCA (microscopic polyangitis)
  2. Anti-GBM (Goodpasture’s)
  3. ANA, anti-dsDNA (SLE)
  4. Complement components, C3+C4 (SLE, MCGN associated with Hep C, post-Strep GN, infective endocarditis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What immunological investigations should be carried out in microscopic haematuria?

A
  1. ANCA

2. Anti-GBM

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

What immunological investigations should be carried out in proteinuria?

A
  1. ANA, anti-dsDNA, C3+C4
  2. HBV, HCV, HIV serology if age >40
  3. Serum protein electrophoresis
  4. Urine protein electrophoresis
  5. Serum free light chains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What immunological investigations should be carried out in nephrotic syndrome (± evidence of multi system disease)?

A
  1. ANA, anti-dsDNA, C3+C4 age >40
  2. Serum protein electrophoresis (SPEP)
  3. Urine protein electrophoresis (UPEP)
  4. Serum free light chains (SFLC)
  5. HBV, HCV, HIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What immunological investigations should be carried out in unexplained CKD (particularly old age group)

A
  1. SPEP

2. UPEP

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

What immunological investigations should be carried out in suspected lymphoproliferative disorders?

A
  1. SPEP
  2. UPEP
  3. SFLC
  4. Cryoglobulins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What immunological investigations should be carried out in thrombotic microangiopathy (diarrhoea -ve)?

A
  1. Anti-ADAMTS13
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does oedema occur in nephritic syndrome?

A
  • could be due to hypoalbuminaemia
  • hypoalbuminaemia is not usually severe enough in nephrotic syndrome to cause oedema on its own
  • 2 potential explanations:
    1. Underfill hypothesis:
    (i) low plasma oncotic pressure
    (ii) reduced circulating volume
    (iii) sodium and water retention
    2. Overfill hypothesis:
    (i) proteinuria directly causes increases tubular sodium reabsorption
    (ii) water follows sodium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why does hyperlipidaemia and thrombotic tendencies occur in nephrotic syndrome?

A
  • hyperlipidaemia is caused by increased hepatic lipoprotein synthesis secondary to reduced plasma oncotic pressure
  • thrombotic tendency is caused by increased hepatic synthesis of procoagulant factors, raised platelet aggregation, and raised urinary losses of anticoagulant factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How should minimal change disease be managed?

A
  1. Glucocorticoids → 90% respond to this alone

2. if relapse, 2nd line = calcineurin inhibitor (CNI) → cyclosporin or tacrolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How should focal segmental glomerulosclerosis be managed?

A
  1. Glucocorticoids → should respond in <4 months
  2. Add CNI if necessary
  3. Relapse = CNI (if not already in use) or cyclophosphamide
  4. Furosemide (loop diuretic) → for oedema
  5. ACE-I or ARB → treat proteinuria by reducing HTN
  6. Statin → hyperlipidaemia
  7. Warfarin → Hypercoagulability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How should membranous nephropathy be managed?

A
  1. Glucocorticoids + CNI
  2. Relapse/2nd line = Cyclophosphamide
  3. Furosemide (loop diuretic) → for oedema
  4. ACE-I or ARB → treat proteinuria by reducing HTN
  5. Statin → hyperlipidaemia
  6. Warfarin → Hypercoagulability

Met3b (21 decks)

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