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Phase 2 Metabolic > Glomerular Disease > Flashcards

Glomerular Disease Flashcards

1
Q

What is the glomerular filtration barrier composed of?

A
  1. fenestrated glomerular capillary endothelium
  2. glomerular basement membrane
  3. slit membrane between pedicels
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2
Q

What is the function of the mesangium?

A
  • contractile properties

- removal of trapped residues and aggregate protein from the basement membrane

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3
Q
  1. What is glomerular disease?
  2. What is the term given to causes of glomerular disease driven by inflammatory processes?
  3. Name 2 causes of non-inflammatory causes of glomerular disease
A
  1. damage/disease affecting the glomerulus which consequently disrupts filtration, leading to nephritic or nephrotic syndrome
  2. glomerulonephritis
  3. diabetic nephropathy and amyloidosis
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4
Q

Describe what the following terms mean relating to glomerular disease:

  1. diffuse
  2. focal
  3. global
  4. segmental
  5. proliferative
  6. sclerosing
  7. necrotising
  8. primary
  9. secondary
A
  1. all glomeruli are affected
  2. only one/a few glomeruli are affected
  3. whole glomerulus is affected
  4. only part of the glomerulus is affected
  5. increased number of cells within the glomerulus
  6. scarring of the glomerulus
  7. cell death within the glomerulus
  8. glomerular inflammation intrinsic to the kidney
  9. associated with disease extrinsic to the kidney - certain infections, systemic disorders or diabetes
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5
Q

Describe the following mechanisms of glomerular injury, and examples of diseases:

  1. immune complex trapping
  2. in situ antigens
  3. antigen deposition
  4. endothelial cell injury
A
  1. antigen-antibody complexes present in the blood get stuck in the basement membrane, triggering complement activation in the glomerulus
    - e.g. SLE
  2. antigen present in the basement membrane
    - e.g. goodpastures
  3. bacterial antigen becomes implanted in the basement membrane as a result of bacteraemia
    - e.g. post infectious glomerulonephritis
  4. endotoxins activate both classical and alternate complement pathways. leading to endothelial damage
    - e.g. ANCA associated vasculitis; haemolytic uraemic syndrome
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6
Q

name the 5 possible presentations of glomerulonephritis

A
  1. isolated haematuria and/or proteinuria
  2. nephrotic syndrome
  3. nephritic syndrome
  4. AKI
  5. CKD
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7
Q

What are the characteristic hallmarks of NEPHROTIC Syndrome

A
  1. proteinuria (++++; >3.5g in 24 hours)
  2. hypoalbuminaemia
  3. hyperlipidaemia (liver compensates for hypoalbuminaemia which also increases lipid production)
  4. oedema (loss of intravascular oncotic pressure)
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8
Q

Name 4 causes of nephrotic syndrome

A
  1. minimal change disease
  2. focal, segmental, glomerulosclerosis
  3. membranous glomerulonephritis
  4. diabetic nephropathy
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9
Q

How is nephrotic syndrome managed?

A
  1. dietary sodium restriction
  2. thiazide diuretic
  3. albumin infusion
  4. prophylactic anticoagulation
  5. pneumococcal vaccine
  6. statins
  7. ACEi
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10
Q

What are the 4 characteristics of NEPHRITIC syndrome?

A
  1. Haematuria
  2. proteinuria (++)
  3. mild hypertension
  4. oliguria
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11
Q

Name 5 causes of nephritic syndrome

A
  1. IgA nephropathy
  2. post-strep glomerulonephritis
  3. goodpastures syndrome
  4. vasculitis
  5. membranoproliferative glomerulonephritis
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12
Q

does non proliferative glomerulonephritis generally cause nephritic or nephrotic syndrome?

A

Nephrotic syndrome

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13
Q
  1. what is the main investigation for minimal change disease?
  2. in what patients is minimal change disease the most common cause of nephrotic syndrome?
  3. how is minimal change disease managed?
A
  1. renal biopsy - electron microscopy reveals abnormal podocytes
  2. children
  3. supportive care and prednisolone
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14
Q
  1. Name 2 secondary causes of FSGS
  2. how is FSGS managed?
  3. What is the prognosis of FSGS?
A
  1. HIV infection; reflux nephropathy
  2. general management of nephrotic syndrome
  3. poor - 50% progress to ESKD
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15
Q
  1. What is the pathological mechanism underlying membranous glomerulonephritis?
  2. is it a proloferative or non-proliferative glomerulonephritis?
  3. Name 5 causes of membranous glomerulonephritis
  4. What is useful in the management of the disease?
  5. How does prognosis follow the rule of 1/3?
A

1.immune complex deposition within the glomerular basement membrane

  1. non-proliferative
  2. idiopathic; Hep B, SLE, malaria, penicillamine
  3. steroids if the disease begins to progress
  4. 1/3 have chronic membranous glomerulonephritis
    1/3 go into remission
    1/3 progress to ESKD
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16
Q

does proliferative glomerulonephritis generally cause nephritic or nephrotic syndrome?

A

nephritic syndrome

17
Q

What is the most common type of glomerulonephritis in adults?

A

IgA nephropathy

18
Q
  1. What is the main presentation of IgA nephropathy?
  2. When does this symptom occur?
  3. What is the diagnostic investigation?
  4. How is the disease managed?
  5. what is its prognosis?
A
  1. macroscopic haematuria
  2. 24-48 hours following upper respiratory tract infection
  3. renal biopsy (IgA deposits; increased mesangial cells and ECM)
  4. steroids and cyclophosphamide
  5. can be relatively benign or lead to ESKD
19
Q
  1. When does post-streptococcal glomerulonephritis occur?
  2. What is found on renal biopsy?
  3. What is the management and prognosis of the condition?
A
  1. 2-4 weeks after strep pyrogenes infection
  2. proliferation of mesangial cells; neutrophils and monocytes; compression of bowman’s space
  3. supportive treatment; usually resolves within 2-4 weeks
20
Q
  1. What autoantibodies are responsible for goodpastures syndrome
  2. what is the clinical presentation of goodpastures syndrome and why?
  3. How is the disease managed?
  4. What is the disease prognosis?
A
  1. anti-glomerular basement membrane antigens
  2. nephritic syndrome and haemoptysis
    - GMB antigens present in glomeruli and lung alveoli
  3. high dose immunosuppression with IV pred and cyclophosphamide; plasmapheresis to remove autoantibodies
  4. results in CKD
21
Q
  1. What is membranoproliferative glomerulonephritis caused by?
  2. How does it differ from membranous glomerulonephritis?
  3. How is it managed?
A
  1. sub endothelial deposition of immune complexes. Can be primary or secondary to SLE/Hep B/C
  2. mesangium and basement membrane is thickened.
  3. steroids and cytotoxic drugs; treat underlying cause
22
Q
  1. What is Wegener’s Granulomatosis?
  2. What is it caused by?
  3. How is it managed?
A
  1. vasculitis affecting the lungs, kidneys and other organs
  2. c-ANCA antibodies
  3. IV steroids and cyclophosphamide
23
Q
  1. What is microscopic polyangiitis?
  2. What is it caused by?
  3. How is it managed?
A
  1. small vessel vasculitis affecting almost any organ system
  2. p-ANCA antibodies
  3. prednisolone and cyclophosphamide; plasmapheresis to remove antibodies
24
Q
  1. What is Henoch-Schönlein Purpura?

2. Which patient group does this more commonly affect?

A
  1. systemic IgA vasculitis - IgA and complement C3 are deposited in blood vessels
  2. children
25
Q

Name another type of vasculitis that can cause proliferative glomerulonephritis

A

Haemolytic uraemic syndrome

Phase 2 Metabolic (12 decks)

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