Brainscape's Knowledge GenomeTM

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


See full index

RENAL > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

how does nephrotic syndrome arise

A

when the basement membrane in glomerulus becomes highly permeable
- proteinuria >3.5g of protein in 24 hrs = frothy urine
- hypoalbumiaemia < 30g per litre
- peripheral oedema
- hypercholesterolaemia

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

what are complications of nephrotic syndrome

A
  • higher risk of infection
  • VTE
  • progression of cKD
  • HTN
  • hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the most common cause of nephrotic syndrome in children

A

minimal change disease
- usually idiopathic
- treated w steroids

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

what are the most common causes of nephrotic syndrome in adults

A
  • FSGS: idiopathic or secondary to infection, malignancy, drugs
  • membranous nephropathy
  • HSP
  • infection e.g. HIV

  • membranoproliferative GN but more common in nephritic syndrome
  • amyloidosis/myeloma may have nephrotic range proteinuria but not necessarily other features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the features of nephritic syndrome

A
  • haematuria
  • oliguria
  • proteinuria
  • fluid retention
  • AKI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the most common cause of primary GN

A

IgA nephropathy or Berger’s disease

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

how does IgA typically present and what are investigatio findings

A
  • patient in 20s presenting w episodic gross haematuria or directly after URT, GI infection or strenuous infection
  • histology: IgA deposits in glomeruli and mesangial proliferation
  • normal C3,C4
  • asymptomatic microhaematuria w intermittent visible haematuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the treatment of IgA nephropathy

A

supportive therapy
- ACEi/ARB for proteinuria/HTN

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

when does post-strep GN present and who does it commonly affect

A

weeks after Group A B haemolytic strep infection
- 1-2 wks post tonsilitis/pharyngitis
- 3-4 wks post impetigo/cellulitis
- affects children 3-12

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

what are investigation findings of PSGN

A
  • positive anti-strep antibodies (ASO titre)
  • low serum C3
  • biopsy: immune complex deposition IgG, IgM, C3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the treatment of PSGN

A

usually self-limiting but supportive therapy:
- ACEi/ARB for proteinuria/HTN
- low sodium diet
- if ESRF then RRT

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

give 3 examples of small vessel vasculitis aka ANCA associated cellulitis

A
  • granulomatosis w polyagiitis
  • microscopic polyangiitis
  • eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

granulomatosis with polyangiitis (GPA)
- key features
- investigation findings
- treatment

A
  • features: pulmonary and nasopharyngeal involvement e.g. nasal ulcers/polyps
  • investigation: c-ANCA, biopsy shows segmental necrotising GN
  • ✅: immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

microscopic polyangiitis
- key features
- investigation findings
- treatment

A
  • features: usually only mild resp symptoms
  • investigation: p-ANCA (MPO), biopsy shows segmental necrotising GN
  • ✅: immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Churg-Strauss syndrome
- key features
- investigation findings
- treatment

A
  • features: asthma, allergic rhinitis, purpura, peripheral neuropathy
  • investigations: p-ANCA, eosinophilia, focal segmental necrotising GN
  • ✅immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens in Goodpasture syndrome aka anti-GBM disease

A
  • anti-GBM antibodies against type IV collagen attack the glomerulus and pulmonary basement membranes
  • pulmonary haemorrhage + haemoptysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the investigation findings of anti-GBM disease

A
  • anti-GBM antibodies
  • pulmonary infiltrates on CXR
  • biopsy: linear deposition of IgG along basement membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the treatment of Goodpasture’s syndrome

A
  • plasma exchange
  • immunosuppression e.g. cyclosphophamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is thin basement membrane disease due to

A
  • hereditary
  • abnormalities of type IV collagen
20
Q

what are the investigation findings of thin basement membrane disease

A
  • persistent microscopic haematuria - possible visible intermittent haematuria
  • biopsy: diffuse thinning of GBM
21
Q

what is the treatment of thin basement membrane disease

A
  • monitor renal function
  • supportive treatment
22
Q

what is alport syndrome

A

X-linked so usually affects males
- mutation in gene coding for type V collagen
- associated with hearing loss and abnormalities of the eyes
- often leads to ESRF

23
Q

what are the investigation findings of alport syndrome

A
  • persistent microscopic haematuria w intermittent visible haematuria
  • sensorineural hearing loss
  • biopsy: splitting of GBM and alternating thickening and thinning of GBM
  • genetic studies - FHx
24
Q

what is the treatment of alport syndrome

A
  • supportive treatment
  • RRT
  • renal transplant: can lead to Goodpasture’s
25
Q

what are the investigation findings of lupus nephritis

A
  • ANA & anti-dsDNA positive
  • biopsy: 6 different classes of lupus nephritis
26
Q

what is the treatment of lupus nephritis

A
  • supportive therapy
  • immunosuppressive therapy based on classification/presentation
27
Q

what is supportive therapy in the management of GN

A
  • If suspect GN – discuss with Renal team
  • MDT approach depending on underlying diagnosis
  • ACEi/ARB for proteinuria Control BP
  • Salt and water restriction if volume overloaded
  • Diuretics for fluid overload
  • If hypoalbuminaemic <20g/dl then higher risk for VTE – consider therapeutic LMWH
  • Statins for hypercholesterolaemia
28
Q

what is immunosuppressive therapy in the management of GN

A
  • Specific to cause of GN – decided by Renal team (+/- Respiratory / Rheumatology teams if lung or systemic involvement )
  • Oral Corticosteroids, IV pulsed methylprednisolone, Cyclophosphamide, Tacrolimus, Ciclosporin, Rituximab, MMF, Azathioprine
29
Q

what is invasive therapy in the management of GN

A
  • Renal replacement therapy/haemodialysis for those in severe AKI or ESRF
  • Plasma exchange for AAV (with lung involvement), anti-GBM
30
Q

what is one of the main complication of anti-GBM syndrome and what factors increase the risk of this

A

pulmonary haemorrhage
* smoking
* lower respiratory tract infection
* pulmonary oedema
* inhalation of hydrocarbons
* young males

31
Q

what are the causes of membranous nephropathy

5 categories

A
  • idiopathic: due to anti-phospholipase A2 antibodies
  • infections: hepatitis B, malaria, syphilis
  • malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
  • drugs: gold, penicillamine, NSAIDs
  • autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
32
Q

what is the managment of membranous nephropathy (3)

A
  • all pt receive ACEi/ARB: shown to reduce proteinuria and improve prognosis
  • immunosuppression: combination of corticosteroid + another e.g. cyclophosphamide
  • consider anticoagulation for high-risk patients
33
Q

what are the causes of FSGS

A
  • idiopathic
  • secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
  • HIV
  • heroin
  • Alport’s syndrome
  • sickle-cell
34
Q

in what setting is there a high recurrence rate of FSGS

A

renal transplant

35
Q

what does renal biopsy of FSGS show

A
  • focal and segmental sclerosis and hyalinosis on light microscopy
  • effacement of foot processes on electron microsocopy
36
Q

what is the management of FSGS

A

steroids +/- immunosuppression

37
Q

what does RPGN describe

A

a rapid loss of renal function associated with the formation of epithelial crescents in the majority of glomeruli

38
Q

what are 2 main causes of RPGN

A
  • Goodpasture’s syndrome
  • Wegener’s granulomatosis
39
Q

what are the features of RPGN

A
  • those of nephritic syndrome: haematuria + red cell casts, proteinuria, HTN, oliguria
  • features specfic to underlying cause: haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s
40
Q

what are differences between IgA nephropathy and PSGN

A
  • IgA onset develops 1-2 days after URTI vs PSGN develops 1-2 weeks after URTI
  • PSGN associated low complement levels
  • main symptom in PSGN is proteinuria
41
Q

when does Alport’s syndrome usually present and what features may be present

A
  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • lenticonus: protrusion of lens surface into the anterior chamber
  • retinits pigmentosa
42
Q

what is the treatment of proteinuria (2)

A
  1. ACEi or ARBs: 1st line in pt w co-existent HTn + CKD
  2. SGLT-2 inhibitors
43
Q

how do SGLT2 inhibitors help in the management of proteinuria

A
  • mainly act by blocking reabsorption of glucose in PCT which lowers the renal glucose threshold –> glycosuria
  • by blocking the co-transporter, they also reduce Na+ reabsorption –> natriuresis reduces the intravascular volume + BP
  • but also inc delivery of Na+ to the macula densa cells which normalises tubuloglomerular feedback and reduces intraglomerular pressure
44
Q

how does nephrotic syndrome predispose to thrombosis

A

loss of antithrombin III, protein C & S with an associated rise in fibrinogn levels

LMWH

45
Q

how does anti-GBM disease present

A

the disease affects type IV collagen that is found in both the kidneys and the lungs which causes chest symptoms such as haemoptysis, coughing and chest pain

RENAL (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions