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#Phase 2.1: GI > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

1
Q

What are Glomerular Diseases?

A

Group of conditions that damage Renal Glomeruli (site of ultrafiltration)

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2
Q

What can Glomerular diseases cause?

A

AKI / CKD

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3
Q

What are the 2 general clinical manifestations of Glomerular disease?

A

Nephrotic Syndrome

Nephritic Syndrome

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4
Q

What are the Kindey’s uses? (5 things)

A
  1. Waste product excretion
  2. Acid-base balance
  3. Fluid balance
  4. Calcium-phosphate balance
  5. BP control
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5
Q

What does a Bowman’s Capsule involve?

A
  1. Capillaries
  2. Mesanguim (Cells + CT supporting capillaries)
  3. Filtration barrier:
  • Endothelial cell (capillary wall)
  • Basement Membrane (made from Collagen + Glycoproteins)
  • Foot processes of Podocytes
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6
Q

What is the essence of Glomerular disease pathophysiology?

A

Damage to Filtration barrier –> leakage of Protein / Blood

aka Proteinuria / Haematuria

aka The Hallmarks of Glomerular Disease

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7
Q

What are the layers of the Filtration Barrier of the Glomerulus? (3 things)

A
  1. Endothelial cell (capillary wall)
  2. Basement Membrane (made from Collagen + Glycoproteins)
  3. Foot processes of Podocytes (specialised epithelial cells)
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8
Q

What are the different ways Glomerular Diseases are classified? (4 things)

A
  1. Primary vs Secondary
  2. Focal vs Diffuse
  3. Global vs Segmental
  4. Immune vs Non-immune mediated (Pathophysiological Classificiation)
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9
Q

What is the difference between Primary n Secondary Glomerular Diseases?

A

Primary: Glomerular injury bc renal pathology

Secondary: Bc systemic process

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10
Q

What are examples of PRIMARY Glomerular Diseases? (3 things)

A
  1. IgA nephropathy
  2. Minimal change disease
  3. Focal segmental glomerulosclerosis
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11
Q

What are examples of systemic processes causing SECONDARY Glomerular Diseases? (3 things)

A
  1. Vasculitis
  2. Amyloidosis
  3. DM
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12
Q

What is the difference between Focal n Diffuse Glomerular Diseases?

A

Focal: Less than 50% of glomeruli damaged

Diffuse: More than 50% of glomeruli damaged

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13
Q

How can you diagnose between Focal n Diffuse Glomerular diseases?

A

Renal biopsy will tell you

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14
Q

What is the difference between Global n Segmental Glomerular Diseases?

A

Global = More than 50% of each individual glomerulus damaged

Segmental = Less than 50% of each individual glomerulus damaged

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15
Q

What is the Pathophysiology of IMMUNE Mediated Glomerular Disease? (2 types)

A
  1. Deposition / In-situ formation of Immune Complexes (iG collections) –> activate Inflamm response
  2. Circulating iGs come n clart proteins on BM / Endothelial cells –> activate Inflamm response (Vasculitis)
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16
Q

What is the Pathophysiology of NON-IMMUNE Mediated Glomerular Disease? (2 types)

A
  1. Structure / Function of Podocytes clarted –> Macromolecule leak thru
  2. Protein accum –> disrupts glomeruli structure –> Dysfunction (DM / Amyloidosis)
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17
Q

What are the different histopathological changes in Glomerular disease? (3 things)

A
  1. Structural
  2. Proliferative
  3. Crescents
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18
Q

What are the features of STRUCTURAL Histopathological patterns in Glomerular Disease? (2 things)

A
  1. Structural changes in Glomerulus
  2. Sclerosis (scarring of glomerulus)
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19
Q

What are the STRUCTURAL Histopathological patterns in Glomerular Disease associated with?

A

Excess prot loss (Nephrotic Syndrome)

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20
Q

What are the features of PROLIFERATIVE Histopathological patterns in Glomerular Disease?

A

Increase in number of cells in Glomerulus: In Mesanguim / Capillary Wall / Bowman’s Space

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21
Q

What are the PROLIFERATIVE Histopathological patterns in Glomerular Disease associated with? (2 things)

A
  1. Inflamm response bc immune complex deposition
  2. Haematuria +/e Nephritic Syndrome
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22
Q

What are the features of CRESCENTS Histopathological patterns in Glomerular Disease? (2 things)

A
  1. Extra-Capillary lesions in Bowman’s Capsulse
  2. Bc accum of: Immune cells / Epithelial Cells / Fibroblasts / Fibrin
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23
Q

What do the CRESCENTS Histopathological patterns in Glomerular Disease represent?

A

Represent: SEVERE injury –> Glomerular Membrane Rupture

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24
Q

What are the CRESCENTS Histopathological patterns in Glomerular Disease associated with? (2 things)

A
  1. Any Inflamm glomerular diseases
  2. BUT MAINLY: Rapidly Progressive Glomerulonephritis (RPGN)
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25
Q

What are the general manifestations of Glomerular Disease? (4 things)

A
  1. Isolated haematuria (by itself)
  2. Isolated proteinuria (by itself)
  3. Nephrotic Syndrome
  4. Nephritic Syndrome
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26
Q

What are typical causes of Isolated haematuria? (3 things)

A
  1. IgA nephropathy
  2. Alport syndrome
  3. Thin basement membrane disease
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27
Q

What is Nephrotic Syndrome? (3 things)

A

Triad of:

  1. Heavy Proteinuria (3.5+ g / day) (aka Nephrotic Range)
  2. Hypoalbuminaemia (35- g / day)
  3. Peripheral Oedema
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28
Q

What can also accompany the Triad in Nephrotic Syndrome? (4 things)

A
  1. Hyperlipidaemia
  2. Thrombotic disease (venous / arterial clots)
  3. Ascites
  4. Pleural effusions
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29
Q

What are the PRIMARY Glomerular diseases that present w Nephrotic Syndrome? (3 things)

A
  1. Minimal change disease
  2. Focal Segmental Glomerulosclerosis (FSGS)
  3. Membranous Nephropathy
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30
Q

What are the SECONDARY systemic conditions that present w Nephrotic Syndrome? (4 things)

A
  1. DM
  2. Amyloidosis
  3. Lupus
  4. HIV
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31
Q

What is Nephritic Syndrome? (4 things)

A
  1. Haematuria
  2. Variable Proteinuria (can be Nephrotic Range)
  3. Oliguria (AKI)
  4. HTN
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32
Q

What is the term Nephritic Syndrome used interchangeably with?

A

Glomerulonephritis (inflamm of glomerulus)

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33
Q

How does Mild vs Severe Glomerulonephritis present?

A

Mild: Minimal haematuria + proteinuria ONLY

Severe: Nephrtic Syndrome (all 4 parts)

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34
Q

What are main causes of Glomerulonephritis? (3 things)

A
  1. Immune complex deposition
  2. Anti-GBM deposition (Anti Glomerular Basement Bembrane Disease)
  3. Small vessel vasculitis
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35
Q

What are the Glomerular diseases that do the Immune Complex deposition cause of Nephritic Syndrome? (3 things)

A
  1. IgA Nephropathy
  2. Poststreptococcal glomerulonephritis
  3. Lupus (SECONDARY)
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36
Q

What are the Glomerular diseases that do the Small-vessel vasculitis cause of Nephritic Syndrome? (3 things)

A
  1. Eosinophilic Granulomatosis w Polyangiitis
  2. Microscopic Polyangiitis
  3. Polyangiitis w Granulomatosis
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37
Q

What investigations should you do for sus Glomerular Diseases? (5 things)

A
  1. Renal biopsy (GOLD)
  2. Urinary tests
  3. Blood tests
  4. Renal screen
  5. Imaging
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38
Q

What is a Renal Screen? (2 things)

A
  1. Special blood tests
  2. Look for causes of AKI / Glomerular disease
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39
Q

What imaging should you do for sus Glomerular Diseases? (2 things)

A
  1. US
  2. CT KUB (Kindeys + Ureters + Bladder)
40
Q

What is the use of imaging in sus Glomerular Diseases? (2 things)

A
  1. Exclude obst
  2. Look at kidney structure
41
Q

When should you NOT do a Renal Biopsy in sus Glomerular Diseases? (5 things)

A
  1. CI: Uncorrectable Bleeding Diathesis
  2. CI: Uncontrollable severe HTN
  3. CI: Active Renal / Perirenal infection
  4. Diagnosis already confirmed w Serology
  5. Presentation beh stereotypical (e.g Nephrotic Syndrome in kids is probs Minimal Change Disease)
42
Q

What are NEPHRITIC Glomerulonephritis Diseases from Oxf Handbook? (5 things)

A
  1. IgA nephropathy
  2. Henoch–Schönlein purpura (HSP)
  3. Post-Streptococcal Glomerulonephritis
  4. Anti-glomerular basement membrane (anti-GBM) disease
  5. Rapidly Progressive Glomerulonephritis (RPGN)
43
Q

What is IgA Nephropathy?

A
  1. aka Berger’s Disease
  2. Most common cause of Glomerulonephritis
44
Q

What are the CF of IgA Nephropathy? (4 things)

A
  1. Asymptomatic
  2. Nephritic Syndrome
45
Q

What is the classic patient who presents with IgA Nephropathy?

A

Young male w UPRTI

46
Q

What is the Pathophysiology of IgA Nephropathy?

A

Mesangial deposition of IgA immune complexes

(Mesangium: Cells + CT surrounding capillaries)

47
Q

What is the speed of progression of IgA Nephropathy? (2 things)

A
  1. Slow
  2. Progresses to Renal Failure over 30 years
48
Q

How is IgA Nephropathy diagnosed?

What will you see? (2 things)

A

Renal biopsy:

  1. IgA deposition in mesangium
  2. Mesangial proliferation (cah dey usually happen bc immune complex deposition)
49
Q

What are the management options for IgA Nephropathy? (3 things)

A
  1. ACE Inhibitors / Angiotensin Receptor Blockers (ARB)
  • Reduce proteinuria
  • Protect renal function
  1. Corticosteroids (stop immune system from making defective IgA
  2. Fish oil (prevent inflammation –> slows down disease progression)

(Give Corticosteroids / Fish oil if 3-6 months of ACEi/ARB not fixing proteinuria)

50
Q

What is Henoch–Schönlein purpura (HSP)? (2 things)

A
  1. Small vessel vasculitis
  2. Systemic variant of IgA nephropathy
51
Q

Where is IgA depositied in Henoch–Schönlein purpura (HSP)? (4 things)

A
  1. Skin
  2. Joints
  3. Gut
  4. As well as Kidney
52
Q

What are the CF of Henoch–Schönlein purpura (HSP)? (4 things)

A
  1. Nephritis (Haematuria, Proteinuria, Oliguria, HTN) (KIDNEY)
  2. Abd pain (GI bleed) (GUT)
  3. Flitting polyarhritis (one joint gets better –> another gets worse) (JOINTS)
  4. Purple rash on legs (SKIN)
53
Q

How is Henoch–Schönlein purpura (HSP) diagnosed? (2 things)

A
  1. Clinical diagnosis
  2. Confirmed w: Positive Immunofluorescence for IgA (biopsy)

(Renal biopsy same as IgA Nephropathy)

54
Q

What are the management options for Henoch–Schönlein purpura (HSP)?

A

Same as IgA Nephropathy

  1. ACE Inhibitors / Angiotensin Receptor Blockers (ARB)
  • Reduce proteinuria
  • Protect renal function
  1. Corticosteroids (stop immune system from making defective IgA (+ steroids help gut involvement in HSP)
  2. Fish oil (prevent inflammation –> slows down disease progression)
55
Q

What is Post-streptococcal Glomerulonephritis (PSGN)?

A

Complication of Group A Streptococci (GAS) infection (aka bac skin / throat infection)

56
Q

What is the pathophysiology of Post-streptococcal glomerulonephritis? (2 things)

A
  1. Streptococcal antigen deposits in Glomerulus –> Immune complex formation + Inflamm
  2. Proliferation (PSGN is aka Acute Proliferative GN)
57
Q

What are the risk factors for Post-streptococcal glomerulonephritis? (2 things)

58
Q

What are the CF of Post-streptococcal glomerulonephritis? (3 things)

A
  1. Nephritic Syndrome
  2. Generalised oedema
  3. Fever / headache (from GAS infection)
59
Q

Why is a Renal Biopsy rarely needed for Post-streptococcal glomerulonephritis, even though it would give a Definitive diagnosis?

A

Post-streptococcal glomerulonephritis is self-limiting, so wts da point

60
Q

How is a diagnosis of Post-streptococcal glomerulonephritis made (3 things)

A
  1. Serology (anti-DNase B antibody = evidence of GAS infection)
  2. Culture (throat / skin swab = to confirm GAS infection)
  3. Urinalysis (haematuria)
61
Q

What are the management options for Post-streptococcal glomerulonephritis? (2 things)

A
  1. Diuretics (to clear generalised oedema + high BP)
  2. Abx (if evidence of persistent GAS infection)
62
Q

What is Anti-glomerular basement membrane (anti-GBM) disease? 2 things)

A
  1. aka Goodpasture’s Disease
  2. Rare
63
Q

What is the pathophysiology of Anti-glomerular basement membrane (anti-GBM) disease? (2 things)

A
  1. Antibodies attack alpha 3 subunit of type 4 collagen (in BM of kidney glomeruli + lung alveoli)
  2. Auto-reactive T cells also attack alpha 3 subunits –> Crescents (indicate severe damage)
64
Q

What are the CF of Anti-glomerular basement membrane (anti-GBM) disease? (4 things)

A

Renal CF: Nephritic Syndrome + Renal Failure

Lung CF (bc pulmonary haemorrhage)

  1. Haemoptysis
  2. SOB
  3. Cough
65
Q

What indicate poor prognosis of Anti-glomerular basement membrane (anti-GBM) disease? (2 things)

A
  1. Dialysis dependance
  2. Crescents in biopsy
66
Q

How is Anti-glomerular basement membrane (anti-GBM) disease diagnosed? (2 things)

A
  1. Renal biopsy (crescenteric GN)
  2. Bloods: Anti-GBM antibodies
67
Q

What are the management options for Anti-glomerular basement membrane (anti-GBM) disease? (3 things)

A
  1. Plasma exchange (to remove anti-GBM antibody + inflamm mediators)
  2. Corticosteroids
  3. Cyclophosphamide (chemo to suppress immune system)
68
Q

What is Rapidly Progressive Glomerulonephritis?

A

Any aggressive GN that progresses to Renal failure in days / weeks

69
Q

What are the causes of Rapidly Progressive Glomerulonephritis? (5 things)

A
  1. Small vessel vasculitis
  2. Lupus nephritis
  3. Anti-GBM disease
  4. IgA Nephropathy
  5. Membranous GN
70
Q

How is Rapidly Progressive GN diagnosed?

A

Renal biopsy (crescenteric GN: bc breaks in GBM allow inflamm cell influx)

71
Q

What are the management options for Rapidly progressive GN? (4 things)

A
  1. Plasma-exchange (if caused by anti-GBM)
  2. Corticosteroids
  3. Cyclophosphamide (chemo to suppress immune system)
  4. Monoclonal antibodies (if caused by Lupus Nephritis)
72
Q

What are NEPHROTIC Glomerulonephritis Diseases from Oxf Handbook? (4 things)

A
  1. Minimal Change Disease
  2. Focal Segmental Glomerulosclerosis (FSGS)
  3. Membranous Glomerulonephritis
  4. Membranoproliferative Glomerulonephritis
73
Q

What is Minimal Change Disease? (2 things)

A
  1. Most common cause of Nephrotic Syndrome in kids
  2. 25% of Nephrotic Syndrome in adults
74
Q

What is the pathophysiology of Minimal Change Disease? (2 things)

A
  1. Podocytes damaged by T cells + Cytokines
  2. Foot processes of Podocytes damaged –> filtration barrier more permeable to Albumin (explain Hypoalbuminaemia of Nephrotic Syndrome)
75
Q

What are the causes of Minimal Change Disease? (3 things)

A
  1. Idiopathic (mostly)
  2. Drugs: NSAIDs / Lithium / Rifampicin
  3. Haematological Malignancy (usually Hodgkin’s lymphoma)
76
Q

What is good about Minimal Change Disease?

A

It doesn’t progress to Renal Failure

(if you see dat, den sus Focal Segmental Glomerulosclerosis FSGS)

77
Q

What are the CF of Minimal Change Disease?

A

Nephrotic Syndrome (Proteinuria + Hypoalbuminaemia + Peripheral Oedema)

78
Q

How is Minimal Change Disease diagnosed? (2 things)

A

Renal Biopsy:

  1. Electron Microscopy: Shows erasure of Foot processes of Podocytes
  2. Light Micropscopy: Normal (hence the name “Minimal Change Disease”
79
Q

What are the management options for Minimal Change Disease? (2 things)

A
  1. Corticosteroids (80% steroid responsive)
  2. Cyclophosphamide (chemo to suppress immune system) (give if unresponsive to steroids)
80
Q

What is Focal Segmental Glomerulosclerosis (FSGS)? (3 things)

A
  1. Focal: less than 50% of glomeruli damaged
  2. Segmental: less than 50% of each individual glomerulus is damaged
  3. Glomerusclerosis: scarring (–> proteinuria)
81
Q

What are the causes of Focal Segmental Glomerulosclerosis (FSGS)? (6 things)

A
  1. Idiopathic
  2. 2ndary to IgA Nephropathy
  3. HIV
  4. Heroin
  5. Alport’s syndrome
  6. Sickle-cell
82
Q

What are the CF of Focal Segmental Glomerulosclerosis (FSGS)? (5 things)

A
  1. Nephrotic Syndrome (proteinuria / hypoalbuminaemia / peripheral oedema)
  2. Hyperlipidaemia
  3. Haematuria (50%
  4. Swelling around eye (80%)
  5. Facial swelling (60%)
83
Q

How is Focal Segmental Glomerulosclerosis (FSGS) diagnosed? (2 things)

A

Renal biopsy

  1. Light microscopy: Focal Segmental Glomerulosclerosis (literally what u see)
  2. Electron miscroscopy: Erasure of foot processes of Podocytes
84
Q

What is bad about Focal Segmental Glomerulosclerosis? (2 things)

A
  1. Risk of Progressive CKD + Renal Failure
  2. Will recur in 30-50% of Kidney transplants
85
Q

What tells you if Focal Segmental Glomerulosclerosis has a bad prognosis?

A

High proteinuria

86
Q

What are the management options for Focal Segmental Glomerulosclerosis? (4 things)

A
  1. ACE inhibitors / ARB (to reduce BP + proteinuria)
  2. Diuretics (for oedema)
  3. Corticosteroids (only if idiopathic)
  4. Plasma exchange (if recurrence after transplants)
87
Q

What is Membranous Glomerulonephritis? (2 things)

A
  1. Most common GN in adults
  2. 3rd most common cause of End-Stage Renal Failure (ESRF)
88
Q

What are the causes of Membranous GN? (5 things)

A
  1. Idiopathic (bc anti-phospholipase A2 antibodies)
  2. Inf: Hep B / Malaria / Syphilis
  3. Cancer: Lung cancer / Lymphoma / Leukaemia
  4. AI: Lupus / RA / Thyroiditis
  5. Drugs: Gold / Penicillamine / NSAIDs
89
Q

What are the CF of Membranous GN? (4 things)

A
  1. Often asymptomatic
  2. Nephrotic Syndrome (Proteinuria / Hypoalbuminaemia / Peripheral Oedema)
  3. Haematuria (50%
  4. Facial swelling (40%)
90
Q

How is Membranous GN diagnosed? (2 things)

A
  1. Renal biopsy:
  • Light microscopy: Diffuse thickening of GBM (bc subepithelial deposits)
  • Electron Microscopy: Spiky appearance bc thick GBM
  1. Serology: Anti-phospholipase A2 receptor antibody
91
Q

What are the management options for Membranous GN? (3 things)

A
  1. ACE inhibitors / ARB (to reduce BP + proteinuria)
  2. Corticosteroids + Cyclophosphamide (to suppress immune system)
92
Q

What are the 2 types of Membranoproliferative Glomerulonephritis?

A
  1. Immune Complex associated
  2. C3 Glomerulopathy
93
Q

What is the pathophysiology of Immune Complex associated Membranoproliferative GN? (2 things)

A
  1. Subendothelial immune deposits of electron dense material
  2. Caused by: Infection (Hep C) / Cryoglobulinaemia / AI
94
Q

What is the pathophysiology of C3 Glomerulopathy Membranoproliferative GN?

A

Genetic / acquired defect in complement pathway

e.g C3b nephritic factor found in 70%

95
Q

What are the CF of Membranoproliferative GN? (2 things)

A
  1. Nephrotic Syndrome (Proteinuria / Hypoalbuminaemia / Peripheral Oedema)
  2. Nephritic Syndrome (Proteinuria / Haematuria / Oliguria / High BP)
96
Q

How is Membranoproliferative GN diagnosed? (2 things)

A
  1. Renal biopsy:
  • Mesangial cell proliferation (hence da name)
  • Subendothelial deposits
  • BM thickening
  1. Serology: C3 nephrotic factor (distinguishes C3 glomerulopathy from Immune Complex associateD)
97
Q

What are the management options for Membranoproliferative GN? (3 things)

A
  1. ACE inhibitors / ARB (to reduce BP + proteinuria)
  2. Treat underlying cause in Immune Complex associated
  3. Corticosteroids + Cyclophosphamide (to suppress immune system) (if no underlying cause found)

#Phase 2.1: GI (29 decks)

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