Nephrotic Syndrome Flashcards

1
Q

What is nephrotic syndrome?

A

Nephrotic syndrome is defined as the presence of proteinuria, hypoalbuminaemia, and peripheral oedema.

V. Rare

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2
Q

To have nephrotic syndrome the patient must have what symptoms

A
  • Hypogammaglobulinemia
  • proteinuria
  • hypoalbunameia
  • Hyperlipidemia
  • Hypercoagubility
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3
Q

Proteinuria would present as

A

frothy urine

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4
Q

Cause of nephrotic syndrome

A

Due to direct sclerosis of podocytes on the glomerulus

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5
Q

Primary aetiology of Nephrotic syndrome

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • membrano proliferative glomerulonephritis
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6
Q

Secondary aetiology of NS

A
  • Diabetes
  • Amyloidosis
  • Infections (Hep B+ C)
  • Drugs, NSAIDs
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7
Q

Pathophysiology of NS

A
  • glomeruli are damaged and become more permeable
  • plasma proteins pass through
  • leads to proteinuria, hypoalbuminemia
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8
Q

Why is there peripheral + preorbital edema in NS?

A

there’s less oncotic pressure in the blood vessels so the fluid leaks out due to hypoalbuminemia

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9
Q

Why would a nephrotic patient present with a hypercoaguble state?

A

patient is also losing antithrombin III proteins which is the body’s anticoagulant.

This means that individuals with nephrotic syndrome are prone to thrombotic and thromboembolic complications

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10
Q

What is else is lost in urine in NS?

A

Immunoglobulins - higher risk of infection
Lipids - urine looks frothy - compensation liver increases lipoprotein synthesis resulting in hyperlipidaemia

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11
Q

Key presentations of NS

A

proteinuria, hypoalbuminaemia, oedema

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12
Q

S + S of NS

A

HT
Proteinura
Frothy urine
Recurrent infections

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13
Q

What is minimal change disease

A

Most common form of nephrotic syndrome characterised by heavy proteinuria, odema, hypoalbuminaemia and hyperlipidaemia affecting children

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14
Q

Investigations for NS

A

Urinalysis
ACR
24hr urine protein
U&Es
LFTS
Lipid profile

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15
Q

Complications of Nephrotic syndrome

A

CVD - hypercholesterolemia + hypertriglyceridemia, CKD
Haem - thrombosis
Infection

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16
Q

Pathophysiology of minimal change disease

A
  • caused by t cells in the blood releasing cytokines - glomerular- permeability factor
  • directly damages foot cells of podocytes making them flatten out (effacement)
  • due to the damage , negatively charged ions such as albumin slip into the nephron
  • albumin goes through but larger proteins like Ig dont - selective proteinuria
17
Q

investigations for Minimal change

A
  • On light microscopy, the glomeruli look completely normal.
  • In some cases, there can be lipids in the proximal tubular cells.
  • Immunofluorescence is negative.
  • The only changes are seen on electron microscopy, where there’s effacement of podocyte foot processes.
18
Q

How would you diagnose nephrotic syndrome

A

EM- effacement of podocyte foot processes

19
Q

Treatment of minimal change disease

A

corticosteroids

20
Q

What is focal segment glomerulosclerosis

A

disease in which scar tissue develops on the glomeruli

21
Q

Aetiology of focal segment glomerulosclerosis

A
  • idiopathic
  • linked to IV Drug users, HIV
  • adults, African + Hispanic
22
Q

Pathophysiology of focal segment glomerulosclerosis

A
  • not clear
  • effacement of podocyte foot processes
  • hyalinosis caused by deposition of lipids and proteins in the glomerulus
23
Q

Investigations for FSG

A
  • On light microscopy, there’s sclerosis and hyalinosis among the glomeruli.
  • FSG is segmental - only a part of the glomeruli is affected - and focal - only some of the glomeruli are affected.
  • Immunofluorescence is often negative, but can sometimes be positive for deposits of C3, C1 or IgM.
24
Q

Management of focal segment glomerulosclerosis

A

-steroids
- ACE-I /ARB

25
Q

What is membranous nephropathy

A

immunologically mediated disease of the glomerular basement membrane

26
Q

What antibody would most likely be present in patients with membranous nephropathy

A

anti- phospholipase A2 receptor antibody

27
Q

Management of membranous nephropathy

A

ACE-i / ARB

28
Q

where is the deposition of immune complexes in membranous nephropathy

A

between podocytes and the glomerular basement

29
Q

Pathophysiology of membranous nephropathy

A

Damage caused by immune complexes called subepithelial deposits (SD)
SD activate complement system - damage podocytes + mesangial cells

30
Q

Key causes of nephrotic syndroem

A

-minimal change disease
- membranous gn
- focal segment glomerulosclerosis
- amyloidosis
- diabetic nephropathy