Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IMED3002 > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What are all conditions affecting the glomerulus known as?

A

All conditions affecting the glomerulus are called glomerulonephritis (glomerulopathy too)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the types of kidney diseases?

A

Tubulointerstitial diseases (diseases of tubules and interstitium)

Vascular diseases of the kidneys

Glomerulonephritis (not all inflammatory so some call it gomerulopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is a problem with separating the 3 diseases?

A

Sometimes all 3 compartments are affected and it is hard to tell where it started.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the second most common common cause of chronic renal failure requiring dialysis/renal transplantation?

A

Glomerulonephritis is the second most common cause of chronic renal failure.

(Diabetes is the most common cause of renal failure, hypertension third most common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is azotaemia?

A

Rise in creatinine/serum urea, this takes days or weeks typically. When it becomes symptomatic it is called ureamia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When is chronic renal failure defined as end stage?

A

Chronic renal failure takes place over long time and is defined as end stage when eGFR is less than 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is done to patients with chronic renal failure?

A

The idea is to maintain quality of life using dialysis for as long as possible after end stage renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the symptoms of renal dysfunction?

A

Extensive list of symptoms and signs of renal dysfunction include primarily:

Lethargy

Anorexia

SOB

Peripheral neuropathy

Oedema

The actual symptoms include many more signs and symptoms that are systemic in nature due to systemic nature of kidney function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the prerenal factors that cause renal failure?

A

Factors that interfere with blood flow to kidney (example dehydration causing hypovolemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the renal factors that cause renal failure?

A

Damage to glomeruli, tubular or interstitium, glomerulonephritis, acute tubular necrosis, acute interstitial nephritis, tumor lysis syndrome, drug induced nephrotoxicity, contrast-induced nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the postrenal factors that cause renal failure?

A

Factors that affect urine outflow through obstruction (eg calculi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is nephritic syndrome?

A

Acute renal failure is similar

Azotemia/uraemia

Oliguria

Haematuria (often macroscopic but hard to tell by patients and urine starts to darken but doesn’t look like blood)

Mild to moderate proteinuria

Hypertension

Usually due to glomerulonephritis (until proven otherwise)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Rapidly Progressive Glomerulonephritis (RPGN)?

A

Subset of nephritic syndrome

Rapid rise in serum urea/creatinine

Usually due to crescenteric glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is nephrotic syndrome?

A

Nephrotic range proteinuria (>3.5g/24 hours) and low albumin in blood (caused by increased glomerular capillary permeability)

Hypoalbuminaemia (low serum protein due to losing it to the glomerulus)

Peripheral oedema (due to reduced serum oncotic pressure due to lower protein and albumin in blood causing fluid to be hypotonic to intracellular environment)

hyperlipidaemia (due to increase in hepatic lipid synthesis)

lipiduria

proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the primary cause of nephrotic syndrome?

A

Abnormal increase in permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens when the serum protein and albumin is low during nephrotic syndrome?

A

Liver compensates by producing more lipids causing hyperlipidaemia in response to loss of albumin and increase of water build up in the kidney due to change in oncotic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the mesangial matrix?

A

Mesangial matrix is the scaffold of the glomerulus which holds the capillary loops together.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes the majority of glomerulonephritis syndromes?

A

Immune complex mediated glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can glomerulonephritis be diagnosed?

A

Glomerulonephritis can only be diagnosed via tissue biopsy using 3 diagnostic modalities: light microscopy, immunoflorscence (using fluorescent microscopy), and electron microscopy (extremely high magnification).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the types of glomerulonephritis and what causes them?

A

Primary no identifiable cause (idiopathic)

Secondary can be caused by drugs, infection, autoimmune disease, or malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Who typically gets minimal change disease?

A

Usually in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Who gets membranous nephropathy?

A

Membranous nephropathy is seen in middle aged males.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens in membranous nephropathy? What causes membranous nephropathy and what is the prognosis?

A

Autoantibodies to A2 receptor on the podocytes

Secondary causes: drugs, infections (HepB and syphilis), autoimmune diseases (Thyroiditis) and malignancy

40% spontaneous remission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is focal segmental glomerulosclerosis?

A

Sclerosis means hardening and scarring

Fibrous adhesions to renal capsule

immunofluorescence shows segmental IgM and C3 because IgM has highest molecular heavy weight and this causes it to deposit in area of large amounts of IgM deposited passively NO IMMUNE COMPLEXES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What causes FSGS? What is the prognosis?

A

FSGS can be secondary to other types of glomerular nephritis. It is a sign of progression of glomerularnephritis

1/3rd will survive but the rest go to chronic renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What causes post-infectious GN?

A

Antigen from streptococcal disease in immune complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is IgA nephropathy? What are the clinical signs/symptoms? What factors are thought to precipitate it? What is the prognosis?

A

IgA nephropothy is called berger’s disease and affects young adults

nephritic syndrome (top of list)

Microscopic haemoturia

present with people going through medical screen for private health insurance

sometimes precipitated by URT? (synpharyngitic)

Mesangioproliferative (mesangial cell hyperproliferation)

IgA mesangial on immunofluorescence)

1/3rd resolve 1/3rd stable 1/3rd chronic renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How many Australians have indicators of chronic kidney disease?

A

1.7 million

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What age groups have the highest percentage of people with indicators of chronic kidney disease?

A

40% of people older than 75 years old

20% of all indigenous people older than 18 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does renal disease get grouped?

A

Acute renal failure

Chronic renal failure

Nephritic syndrome (rapidly progressing glomerulonephritis)

Nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is acute renal failure defined as?

A

Rapid rise in serum urea and creatinine over days to weeks

This rise is usually accompanied by oliguria / anuria (drop or cessation of urine production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the prognosses for acute renal failure?

A

Can completely resolve or progress to chronic renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is chronic renal failure and how is it different to acute renal failure?

A

Gradual and progressive rise in serum urea/creatinine over a timespan of months to years. The longer timespan of rise in creatinine and urea is what makes it different.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What lines the inside of the bowman’s capsule?

A

Parietal epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What results from immune-complex formation?

A

Inflammation. These complexes become trapped in the glomerulus due to its convoluted nature and high protein turnover. where the complex turns up is what determined the type of glomerulonephritis?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What happens when immune complex and inflammation occurs in mesangial cells?

A

They hyperproliferate and produce more mesangial matrix.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What happens when immune complexes happen along capillary loops (Subendothelial immune complexes)?

A

The endocapillary starts proliferating endothelial cells creating more layers of endothelial cells which further occludes the capillary loops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What happens when immune complexes occur on the epimembranou portion of the basement membrane?

A

Forms basement membrane spikes which blocks the holes formed by podocytes and more basement membrane is formed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What determines where the immune complex ends up?

A

The molecular weight

The electrical charge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the secondary causes of glomerulonephritis?

A

Drugs

Infections

Autoimmune diseases

Malignancy

41
Q

What are the types of GN diseases?

A

On a spectrum in which the top are most likely to be present with nephritic syndrome and the bottom are most likely to present with nephrotic syndrome:

NEPHRITIC
Post-infectious GN
IgA nephropathy
Mesangiocapillary / membranoproliferative GN
Focal segmental glomerulosclerosis
Membranous nephropathy
Minimal change disease
NEPHROTIC
42
Q

What is the pathgenesis of minimal change disease?

A

Structural abnormality in the podocytes.

43
Q

How is minimal change disease detected?

A

Looks normal on light microscopy and immunofluorescence

Electron microscopy can detect the defect

44
Q

What is the result of the podocytopathy in minimal change disease?

A

Leads to loss of protein leading to nephrotic syndrome

Swollen foot processes

45
Q

What is the treatment for minimal change disease?

A

Highly steroid responsive especially in children

46
Q

What are the secondary causes of minimal change disease?

A

Drugs (especially NSAIDs)

Malignancy (Hodgkin’s lymphoma)

Immunisation

47
Q

What is the prognosis of minimal change disease?

A

Very responsive to steroids and less predictable in adults

48
Q

What causes membranous nephropathy?

A

Immuno complex GN (subepithelial membranous GN)

Glomerular basement membrane is thickened due to depositing of substances around basement membrane

immune complexes will be seen eith IgG and C3 antibodies

49
Q

How can membranous nephropathy be detected?

A

Electron microscopy will show deposits on basement membrane

50
Q

What causes primary membranous nephropathy?

A

Autoantibodies to podocyte phospholipase - A2 receptor

51
Q

What causes secondary membranous nephropathy?

A

Drugs (NSAIDs, Gold, Penicillamine, Captopril)

Infections (Hep B, schistomiasis, syphillis)

Autoimmune disease (SLE, thyoiditis)

Malignancy (Lung, colorectal, melanoma)

52
Q

What is the prognosis for membranous nephropathy?

A

40% spontaneous remission

40% progress to chronic renal failure

53
Q

What is the difference between focal and diffuse glomerular pathology?

A

Focal = less than 50% of all glomeruli are affected

Diffuse = more than 50% of all glomeruli

54
Q

What is the difference between segmental and global glomerular pathology?

A

Segmental = less than 50% of an individual glomerulus

Global is greater than 50% of entire glomerulus

55
Q

What is focal segmental glomerulosclerosis?

A

A focal and segmental nephrotic pathology in the glomerulus where there is collapse of the capillary loops with scarring and fibrous adhesions to the bowman’s capsule

56
Q

How common is Focal Segmental GlomeruloSclerosis?

A

Most common cause of nephrotic syndrome in adults

57
Q

What does immunofluorescence show with FSGS?

A

Segmental IgM and C3

It is not immune-complex mediated and instead is caused by trapping of large molecules in scarred segments

58
Q

What does electron microscopy show with FSGS?

A

Segmental scarring and effacement of podocytic foot processes and no immune-complexes

59
Q

What does FSGS look like under the light microscope?

A

Focal

Segmental

Collapse of the capillary loops with scarring and fibrous adhesions to the bowman’s capsule

60
Q

What are the secondary causes of FSGS?

A

Can be secondary to any other glomerulnoephritis condition.

HIV, sickle-cell anaemia, heroin abuse, obesity

Any cause of nephorn loss (unilateral renal agenesis, renal ablation)

61
Q

What is the prognosis of FSGS?

A

30% recover with steroids

Others progress to chronic renal failure

62
Q

What does post-infectious glomerulonephritis look like on the light microscope?

A

Light microscopy would show too many mesangial endothelial cells and neutrophilic inflammation

63
Q

Is post-infectious glomerulonephritis a nephritic or nephrotic syndrome?

A

Nephritic syndrome

64
Q

What does post-infectious GN look like on electro microscope?

A

Electron microscope shows no spikes

65
Q

What bacteria is associated most often with post-infectious GN?

A

Streptococcus

66
Q

What is the prognosis for post-infectious GN?

A

95% of children recover with conservative treatment

40% of adults progress to renal failure

67
Q

What kind of people get post-infectious GN most often?

A

Children 6 - 10 but can occur to anyone

68
Q

What condition does post-infectious GN usually start as?

A

Pharyngitis or cellulitis

It is immune complex mediated

69
Q

What antigen is associated most often with post-infectious GN?

A

Planted streptococcal pyogenic exotoxin B

70
Q

What does post-infectious GN look like on the light microscope?

A

Diffuse proliferative GN

Mesangial hypercellularity

Endocapillary proliferation

Neutrophilic inflammation

71
Q

What is another name for post-infectious GN?

A

Diffuse proliferative GN

72
Q

What does post-infectious Gn look like on immunoflorescence?

A

Granular, mesangial and capillary loop IgG and C3

73
Q

What does post-infectious Gn look like on electron microscope?

A

Subepithelial “humps” caused by presence of immune-complex deposits

No spikes

74
Q

Why is post-infectious GN never called primary glomerulonephritis?

A

Because it is always secondary to infection

75
Q

What is the prognosis of post-infectious GN?

A

95% of children recover with conservative treatment

40% of adults progress to chronic renal failure

76
Q

What organisms cause post-infectious GN?

A

Group A beta-haemolytic Streptococcus

Non-streptococcal including bacterial, viral, and parastitic streptococcus

77
Q

What is the most common cause of GN?

A

IgA nephropathy or Berger’s disease

78
Q

What is the most common demographic for IgA nephropathy?

A

Young adults

79
Q

What is the cause of IgA nephropathy?

A

Immune-complex mediated GN

80
Q

How is IgA clinically presented?

A

Nephritic syndrome

Microscopic haematuria (blood picked up during tests)

Sometimes precipitated by Upper Respiratory Tract 1nfection (occurs at the same time as a sore throat unlike post-infectious GN)

Often presented while people are screening for health insurance

81
Q

What does a light microscope show with IgA nephropathy?

A

Diffuse mesangial matrix expansion and hypercellularity (it is a mesangioproliferative GN)

82
Q

What is seen on electron microscope and immunoflorescence for IgA nephropathy?

A

Granular mesangial IgA

Mesangial immune-complex deposits

83
Q

What are secondary causes of IgA nephropathy?

A

Drugs

Infectious

Hepatobiliary, GI, rheumatological diseases and malignancy

84
Q

What is the prognosis for IgA nephropathy?

A

33% resolve spontaneously

33% stable

33% progress to secondary FSGS/CRF

85
Q

What is crescentic GN?

A

Pathological correlate to clinical presentation of rapidly progressive GN

It is a nephritic syndrome with rapid and severe rise in serum urea/creatinine

86
Q

Can crescentic GN be an endpoint for diagnosis?

A

No the cause of it must be identified

87
Q

What is the consequence of not treating crescenting GN?

A

It is a medical emergency. Chronic renal failure will occur within weeks to months if not treated.

88
Q

What is the histological hallmark of crescentic GN?

A

Filling and occlusion of bowman’s space by proliferation of epithelial cells.

Due to rupture of capillary loops and bleeding into the bowman’s space so no urine can be produced

89
Q

What are the types of crescentic GN?

A

Type 1 (anti-glomerular basement membrane disease) (20%)

Type 2 (Immune-complex mediated GN) (25%)

Type 3 (Paci-immune GN) (55%)

90
Q

What is antiGBM disease?

A

Autoantibodies for alpha 3 chain of type IV collagen are produced

91
Q

What is pulmonary-renal syndrome / goodpasture syndrome?

A

Autoantibodies may cross-react with Basement Membrane of pulmonary alveolar capillaries and cause a condition known as pulmonary-renal syndrome / goodpasture syndrome

92
Q

What does crescentic GN look like on microscopy?

A

Light microscopy shows crescents with necrosis

Immunoflorescence shows linear capillary loop IgG

Electron microscopy shows no immune complexes because its too small to see (IgG target individual molecules)

93
Q

What is lupus a secondary cause of?

A

Lupus can effectively reproduce all GN types that were discussed.

94
Q

What is Pauci-immune GN?

A

Anti-neutrophil cytoplasmic antibody associated with GN and vasculitis

Autoantibodies are produced against cytoplasmic enzymes in neutrophils

95
Q

What condition is pauci-immune GN associated with?

A

Associated with systemic small vessel vasculitis

96
Q

What is pauci-immune GN also known as?

A

Anti-neutrophil Cytoplasmic antibody associated GN/Vasculitis (ANCA)

97
Q

What is Wegner’s granulomatosis?

A

Triad of necrotising granulomatous inflammation of upper and lower respiratory tract and kidney

98
Q

What is Churg-Strauss syndrome?

A

Similar to WG but with asthma and peripheral eosinophilia

99
Q

What does Pauci-immune GN look like on light microscopy?

A

Crescents and granulomatous inflammation in WG

Eosinophil rich granuloma in CSS

IMED3002 (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions