Brainscape's Knowledge GenomeTM

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


See full index

Urology > Lecture 18 Glomerular Disease- Clinical > Flashcards

Lecture 18 Glomerular Disease- Clinical Flashcards

1
Q

Define glomerulonephritis

A

Immune-mediated disorders that affect the glomeruli

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

Name the main features of Glomerulonephritis

A
  • Haematuria (non-visible or visible)
  • Proteinuria (low grade or nephrotic)
  • Hypertension
  • Renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define a Nephritic State

A

• Loss of blood
Active urine sediment: haematuria, dysmorphic RBCs, cellular casts
• Hypertension- salt and water retention and vasoactive hormone release
• Renal impairment
• Inflammation disrupting GBM= haematuria (cola-coloured urine)
• Reduced GFR

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

Define a Nephrotic State

A

Loss of protein
• Oedema
• Increase in hydrostatic pressure in the capillaries
• Nephrotic range proteinuria: >3.5g/day or 350mg/mmol creatinine
• Hypoalbuminemia: serum albumin <35g/L-
• Dyslipidemia

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

Define the term diffuse in terms of pathology

A

> 50% of glomeruli affected

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

Define Focal in term of pathology

A

<50% of glomeruli affected

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

Define global in terms of pathology

A

All glomerulus affected

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

Define segmental in term of pathology

A

Part of the glomerulus affected

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

Name non-proliferative glomerulonephritis

A

Minimal change disease
Membranous nephropathy
FSGS

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

Name proliferative glomerulonephritis

A

Mesangioproliferative GN
Membranoproliferative GN
Diffuse proliferative GN
Crescentic GN

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

Are Nephritic syndrome proliferative or non proliferative

A

Proliferative

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

is IgA nephropathy Nephrotic or nephritic

A

Nephritic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does IgA Nephropathy cause haematuria

A
  • IgA is stuck within the mesanagium and does not get filtered t the urine and it becomes clogged
  • IgA – ‘irritates’ mesangial cells and causes them to proliferate and produce more matrix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is post infectious glomerulonephritis

A
  • Follows 10-21 days after infection typically of throat or skin.
  • Most commonly with Lancefield group A Streptococci.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is post infectious glomerulonephritis treated

A

– Antibiotics for infection, debatable.
– Loop diuretics such as frusemide for oedema (if there is oedema).
– Anti-hypertensives e.g. vasodilator drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name 3 causes of crescentic glomerulonephritis

A 
ANCA-associated
Anti-GBM
IgA vasculitis
POst infection glomerulonephritis
SLE
17
Q

What are the 3 main types of ANCA-asscoaued glomerulonephritis

A
  1. Microscopic polyangiitis.
  2. Granulomatosis with polyangiitis.
  3. Eosinophilic granulomatosis with polyangiitis
18
Q

What is Anti-GBM disease

A

rare crescentic glomerulonephritis

19
Q

What is Good Pasture’s syndrome

A

Nephritis + lung haemorrhage

20
Q

How is anti-GBM treated

A

aggressive immunesuppression: steroid, plasma exchange, and cyclophosphamide.

21
Q

Name 3 causes of Nephrotic syndrome (non-proliferative)

A
  • Minimal change disease
  • Focal and segmental glomerulonephritis
  • Membranous Nephropathy
22
Q

What is the general management of Nephrotic syndrome

A
  • Treat oedema: salt and fluid restriction and loop diuretics.
  • Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
  • Reduce risk of thrombosis: Heparin or Warfarin.
  • Reduce risk of infection e.g. pneumococcal vaccine.
  • Treat dyslipidemia e.g. statins.
23
Q

Minimal change disease is commonly seen in what age group

A

Children

24
Q

What are the clinical features of minimal change disease

A
  • Sudden onset of oedema – days.
  • Complete loss of proteinuria with steroids.
  • Relapse occurs in two thirds of patients.
25
Q

How is minimal change disease treated

A
  • Prednisolone – 1mg/kg for up to 16 weeks.

* Once remission achieved , slow taper over 6 months.

26
Q

If there is an initial relapse in minimal change disease how is that treated

A

• Initial relapse treated with further steroid course.

27
Q

If there are subsequent relapses in minimal change disease how is that treated

A
  • Cyclophosphamide
  • Cyclosporin- immunosuppression (calcineurin inhibitor)
  • Tacrolimus- immunosuppression (calcineurin inhibitor)
  • Mycophenolate mofetil (Anti-proliferative)
  • Rituximab (depleting agent)
28
Q

What is the prognosis for minimal change disease

A
  • Despite relapsing behaviour, prognosis is favourable.
  • Risk of end stage kidney disease is low.
  • Steroids toxicity as multiple exposure.
29
Q

What is focal and segmental Glomerulosclerosis

A
  • Presents with nephrotic syndrome.

* Pathology reveals focal and segmental sclerosis with distinctive patterns

30
Q

What are the distinctive patterns of focal and segmental Glomerulosclerosis

A

• tip lesion, collapsing, cellular, perihilar

31
Q

What is the prognosis of focal and segmental Glomerulosclerosis

A
  • Generally steroid resistant.

* High chance of progression to end stage kidney disease.

32
Q

How is focal and segmental Glomerulosclerosis treated

A
  • Treat oedema: salt and fluid restriction and loop diuretics.
  • Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
  • Reduce risk of thrombosis: Heparin or Warfarin.
  • Reduce risk of infection e.g. pneumococcal vaccine.
  • Treat dyslipidemia e.g. statins.
  • Trail of steroids, positive response , even partial remission, carries better prognosis.
  • Alternative options: cyclosporin, cyclophosphamide, and Rituximab
33
Q

What is membranous nephropathy

A
  • Commonest cause of nephrotic syndrome in adults.
  • 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 IgG activates complement (C3), which punches holes in filter
  • Leaky filter now allows albumin to be filtered into urine  nephrotic syndrome
34
Q

What is the treatment for membranous nephropathy

A
  • Treat oedema: salt and fluid restriction and loop diuretics.
  • Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
  • Reduce risk of thrombosis: Heparin or Warfarin.
  • Reduce risk of infection e.g. pneumococcal vaccine.
  • Treat dyslipidemia e.g. statins.
  • Immunesuppression if symptomatic nephrotic syndrome, rising proteinuria or deteriorating renal function.
  • Cyclophosphamide and steroids (alternate months) for 6 months.
  • Tacrolimus.
  • Rituximab.

Urology (26 decks)

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