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Urinary System > Glomerular Injury (Nephritic And Nephrotic) > Flashcards

Glomerular Injury (Nephritic And Nephrotic) Flashcards

1
Q

What are 3 classes of Glomerular Disease?

A
  • Hereditary
  • Primary (most common), disease originates from glomerulus
  • Secondary, due to systemic diseases (Diabetes, Bacterial Endocarditis)
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2
Q

What does Glomerular disease result in?

What If this goes on for a long time?

A

Glomerulonephritis, can progress to Chronic Kidney Disease

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3
Q

What 4 glomerular structures are prone to damage?

A
  • Capillary endothelium
  • Glomerular Basement Membrane
  • Mesangial cells (supporting capillaries)
  • Podocytes (on outer surface of capillary)
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4
Q

What 4 things is Nephrotic Syndrome characterised by?

This syndrome is a group of conditions

A
  1. Proteinuria
  2. Hypoalbuminaemia
  3. Oedema
  4. Hyperlipidaemia (Increased hepatic lipoprotein synthesis)

(Usually associated with high cholesterol)

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5
Q

What is the physiological basis for Nephrotic Syndrome?

A

Glomerular basement membrane damage and increased pore size, lead to increased permeability (of glomerular filter) to Albumin

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6
Q

What are 4 methods of management of Nephrotic Syndrome?

A
  • Control BP (ACE Inhibitors)
  • Control Hyperlipidaemia
  • Antigoagulants (if patient is hypercoagulable)
  • Treat underlying cause

(Risk of thrombosis increases if albumin decreases)

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7
Q

List 4 Nephrotic conditions

A
  • Diabetic Nephropathy
  • Minimial Change Disease
  • Membranous Glomerulonephritis
  • Focal Segmental Glomerulosclerosis (FSGS)
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8
Q

What happens in Diabetic Nephropathy

A
  • Excess blood glucose binds to proteins, especially at efferent Arteriole, obstructing blood flow
  • Initially, increased GFR
  • Mesangial cells secrete more structural matrix, thickening the Basement Membrane of Glomerulus
  • Reduced GFR
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9
Q

How do we treat Diabetic Nephropathy?

Leading abuse of end stage renal disease

A
  • Control BP (ACE Inhibitors, Angiotensin receptor blockers)

- Control blood glucose

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10
Q

State 3 characteristics of Minimal Change Disease

A
  • Most common in Children <6
  • No changes under LM (Podocyte effacement under EM)
  • Good prognosis in children, variable in adults
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11
Q

What happens in Membranous Glomerulonephritis?

What percentage of Adult Nephrotic Syndrome cases is due to this?

A
  • Deposition of immune complexes in Sub-epithelial space (Between epithelia and Podocytes)
  • Results In Basement Membrane thickening

40%

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12
Q

Outline the causes of Membranous Glomerulonephritis

A
  • Idiopathic (85%)
  • Can be Primary
  • Can be Secondary (infections/ tumours/ drugs/ systemic illnesses)
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13
Q

How do we treat Membranous Glomerulonephritis?

A
  • Immunosuppressants

- Treat underlying disease

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14
Q

What is Focal Segmental Glomerusclerosis (FSGS)?

How does this appear?

A
  • Podocyte damage leads to protein build up in Glomerulus
  • Leading to Sclerosis
  • Glassy appearance (Hyalinosis)
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15
Q

Outline the causes of Focal Segmental Glomerusclerosis (FSGS)

A
  • Primary: Idiopathic

- Secondary: Sickle cell, HIV, Heroin, Kidney hyperperfusion

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16
Q

Describe the affected structures in Focal Segmental Glomerusclerosis (FSGS)

A
  • Only SOME Glomeruli are affected

- Only PART of the Glomerulus is affected

17
Q

How do we treat Focal Segmental Glomerusclerosis (FSGS)?

What can it lead to if treatment fails?

A
  • Steroids, however results are inconsistent

- Chronic Renal Failure

18
Q

What are the main 3 signs and symptoms of Acute Nephritic Syndrome?

Name 6 others

How do we treat generally?

A
  • Oliguria/ Anuria
  • Hypertension
  • Haematuria (micro or macroscopic)
  • Fluid retention
  • Uraemia
  • Proteinuria
  • Loin pain
  • Headaches
  • General malaise

Steroids

19
Q

List 4 Nephritic Conditions

A
  • IgA Nephropathy/ Berger’s Disease
  • Rapidly Progressive Glomerulonephritis
  • Post streptococcal Glomerulonephritis
  • Goodpasture’s Syndrome
20
Q

IgA Nephropathy/ Berger’s Disease is the most common Primary Glomerular Disease worldwide, causing recurrent haematuria

What happens in it?

A
  • Raised Hypertension and IgA levels, deposited in Mesangium-> Sclerosis of damaged segment
21
Q

How do we treat IgA Nephropathy?

What do 20% of patients go on to develop

A
  • Control BP (anti hypertensives)
  • Steroids

Advanced CKD (Chronic Kidney Disease)

22
Q

What happens in Rapidly Progressive Glomerulonephritis?

A
  • Severe glomerular injury, fibrin leaks out of BM-> Macrophage and epithelial cell proliferation
  • Crescent shape masses form in Glomerulus , reducing glomerular blood supply
  • Loss of renal function within days to weeks
23
Q

How do we treat Rapidly Progressive Glomerulonephritis?

A
  • High dose steroids
  • Immunosuppressants
  • Plasma exchange to remove immune complexes causing this
24
Q

When does Post streptococcal Glomerulonephritis present?

How do we treat?

A
  • 1 to 3 weeks after group A Beta-haemolytic Streptococcal infection of tonsils/ pharynx/ skin

Antibiotics to treat remaining infection

25
Q

Describe the Prognosis of Post streptococcal Glomerulonephritis in children and adults

A

Children: Recover completely

Adults: 40% develop hypertension or renal impairment (60% recover completely)

26
Q

What happens in Goodpasture’s Syndrome?

A
  • Development of antibodies to Type 4 collagen in BM, causing inflammation
  • Leads to rapidly progressive Glomerulonephritis, Acute Renal Failure and Lung Haemorrhage
27
Q

How do we treat Goodpasture’s Syndrome?

Describe the prognosis without treatment

A
  • Plasma exchange to remove antibodies
  • Corticosteroids to remove inflammation

Poor

28
Q

Of Nephrotic Syndrome and Acute Nephritic Syndrome, which can lead to CKD as as long term consequence

A

Both of them

Urinary System (25 decks)

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