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302 SBM: Metabolic & Renal > Nephrotic & Nephritic syndrome > Flashcards

Nephrotic & Nephritic syndrome Flashcards

1
Q

Compare nephrotic and nephritic syndrome according to:

  • renal function
  • cardinal signs
  • AKI and CKD
A

Nephrotic

  • preserved renal function
  • hypoalbuminemia, proteinuria, oedema
  • No AKI/CKD

Nephritis

  • impaired renal function
  • proteinuria, haematuria, leucosuria
  • can get AKI or progressive CKD
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2
Q

How else can you classify glomerulonephritis?

A
  • By histology: minimal change, crescents, focal vs diffuse, area affected
  • By aetiology: toxin, AI, haematological, infectious
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3
Q

How does glomerulonephritis present?

A
  • systemic, flu like symptoms
  • rash
  • arthralgia
  • swelling
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4
Q

How would you examine a patient you expect to have GN?

A
  • Skin
  • CVS (*oedema)
  • Respiratory
  • Abdominal exam
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5
Q

How does urinalysis of nephritic and nephrotic syndrome compare?

A

Nephrotic
-/+ blood, ++++protein, -/+ leucocytes, no nitrates

Nephritic
++ blood, ++ protein, ++ leucoytes, no nitrates

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6
Q

How do you confirm a diagnosis of GN?

A

Blood tests

  • serum albumin, protein; renal function
  • AI screen in some

Renal biopsy analysis
- light microscopy/immunohistology/electron microscopy

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7
Q

Describe minimal change GN

  • What is it?
  • Histology:
  • Associated risk factors
  • Presentation
  • Treatment
  • Sequalae
A
  • Non proliferative structural abnormality
  • Light microscopy and immunohistoloy clear; podocyte fusion seen on electron microscopy
  • NSAIDs, lithium/gold, allergy, Hodgkins, age (commonest nephrotic syndrome in children)
  • Frothy urine (proteinuria), hypoalbuminaemia, oedema (in face of kids), preserved kidney function
  • Corticosteroids (1st), calcineurin inhibitors (2nd)
  • In adults 50% recurrence
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8
Q

What are the implications of having low serum albumin?

A
  • renders patients intravascularly deplete which leads to significant loss of ability to maintain water in circulation (can be an emergency), oedema
  • loss of oncotic pressure, leads hypercholesterolemia, hypertriglyceridaemia, high LDL
  • thrombotic disease*
  • as well as liver albumin synthesis, lipoprotein synthesis, synthesis fo clotting factors
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9
Q

Describe membranous GN

  • What is it?
  • Pathophysiology
  • Histology:
  • Presentation
  • Treatment
  • Prognosis
A

Nonproliferative structural abnormality. Slowly progressive and mainly effects 30-50

  • Immune complex deposition, resulting in complement activation against glomerular basement membrane proteins–> fluid leakage. BASEMENT MEMBRANE IS THICKENED BUT MESANGIUM IS NOT
  • “spikes” seen on BM =immunoglobulins
  • Nephrotic syndrome, AKI/CKD
  • Treat underlying cause; steroids; calcineurin inhibitors; BP control
  • 1/3 enter remission; 1/3 have chronic membranous GN; 1/3 progress to end-stage renal failure
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10
Q

What are the causes of membranous GN

A

Idiopathic

Autoimmune- SLE, Sjogren’s, Rh Arthritis, Ankolysing spondylitis, post-transplant immunosuppressed

Infection- Heb B, Hep C

Drugs- Mercury, Captopril, gold, penicillamine

Paraneoplastic

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11
Q

Describe focal segmental glomerulosclerosis (FSGS)

  • What is it?
  • Causes
  • Histology:
  • Presentation
  • Treatment
  • Prognosis
A

A non-proliferative structural abnormality

Primary causes: idiopathic
Secondary causes: 
- familial (reoccurs after transplant)
- virus (HIV)
- drugs (heroin, pamidronate)
- obesity, HTN, atheroemboli, sickle cell anaemia
  • Specific segments of certain glomeruli show segmental scarring in addition to foot process fusion
  • Presents as nephrotic syndrome
  • Primarily and familial treated with immunosuppression and BP control
  • Other secondary causes: treat underlying
  • End-stage kidney failure in 50% over the years
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12
Q

Consider mesangial proliferative GN

What is its aetiology?
What is its presentation?

A

Aetiology:

  • Infection: Malaria, typhoid
  • IgA nephropathy

Presentation:

  • haeamaturia (asymptomatic, microscopic)
  • aki/ckd
  • hypertensive crisis
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13
Q

Describe IgA nephropathy

  • What is it?
  • Prevalence
  • Histology:
  • Presentation
  • Treatment
  • Prognosis
A

A mesangial proliferative GN that causes an increase in mesangial cells and matrix

Most common GN in adults worldwide

  • Immunohistology will show IgA deposition in the matrix
  • Presents as nephritis syndrome (macroscopic haematuria) 24-48hrs after a URTI (particularly in kids and young males)
  • Prednisolone
  • 30% progress to end stage kidney disease
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14
Q

Consider diffuse proliferative GN

What is its aetiology?
What is its presentation?
Histology?
Treatment?

A
  • endocarditis
  • post-streptococcal GN
  • Disease usually presents 2 weeks after infection with nephritis syndrome (haematuria), oliguria, oedema, AKI
  • Dominant C3 staining (due to C3 deposition, IgG and IgM)

Treat underlying infection
Supportive management

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15
Q

Describe crescentic GN (Rapid progressive)

  • What is it?
  • Prevalence
  • Treatment
  • Prognosis
A

It is acute nephritic syndrome accompanied by microscopic glomerular crescent formation with progression to renal failure within weeks to months.

  • Uncommon, 10-15% of GN cases, 20-50y/o
  • strict BP control
  • ACEi for proteinuria (>1g/day)
  • Immunosuppression: steroids, cyclophosphamide, azathioprine, mycophenolate mofetil, ritiximab
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16
Q

Describe the aetiology of crescentic GM

A

GBM disease (Good pasteurs if lungs involved as well as kidney): Anti GBM against glomerulus basement membrane antigens

Aggressive IgA nephropathy

ANCA associated vasculitis disorders (autoantibodies against antigens in cytoplasmic granules of neutrophils and monocytes)

  • granulomatosis with polyangiitis (GPA)/Wegener granulomatosis
  • microscopic polyangiitis (MPA) Churg Strauss
17
Q

Describe membranoproliferative/ mesangial capillary GN

  • What is it?
  • Histology
  • Aetiology
  • Presentation
  • Treatment
A

a group of immune-mediated disorders characterised histologically by glomerular basement membrane (GBM) thickening and proliferative changes on light microscopy.

  • primary
  • secondary: endocariditis, viral infections (hep C, malaria), sickle cell anaemia, SLE
  • Presents with AKI/CKD, haematuria, proteinuria
  • strict BP control; ACEi for proteinuria; immunosuppression: steroids, mycophenolate mofetil, CNI, rituximab

302 SBM: Metabolic & Renal (6 decks)

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