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Year Two - Urinary System > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

What is another term for glomerulonephritis?

A

Intrinsic kidney disease

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2
Q

What is glomerulonephritis?

A

A group of conditions that cause inflammation of or around the glomeruli in the kidney

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3
Q

What is the role of the glomeruli?

A

To remove excess fluid electrolytes and waste from the bloodstream and pass them into urine

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4
Q

What is the glomerulus?

A

A network of capillaries

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5
Q

How does blood enter the glomerulus?

A

Afferent arteriole

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6
Q

What happens as blood passes through the glomerulus?

A

Small molecules are filtered across the glomerular membrane into the Bowman’s space

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7
Q

What molecules are not filtered at the glomerulus? Give an example

A

Molecules which which are too large to filter across the membrane

Albumin

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8
Q

How does unfiltered molecules exit the glomerulus?

A

Efferent arteriole

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9
Q

What are mesanigial cells?

A

They are specialised pericytes within the kidney that make up the mesangium (middle) of the glomerulus

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10
Q

What is the primary function of mesangial cells?

A

To remove trapped residues and aggregated protein from the basement membrane thus keeping the filter free of debris

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11
Q

What is the role of the glomerular filtration barrier?

A

To ensure that large molecules, such as albumin, are unable to escape from the glomerulus into urine

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12
Q

What are the three layers of the glomerular filtration barrier?

A

Endothelium (Inner Layer)

Basal Lamina (Middle Layer)

Podocytes (Outer Layer)

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13
Q

Describe the endothelium that makes up the glomerular filtration barrier

A

It has perforations called fenestrae

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14
Q

What is the function of the endothelium layer of the glomerular filtration barrier?

A

To restrict the filtration of RBC’s

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15
Q

What is the function of the basal lamina layer of the glomerular filtration barrier?

A

To restrict the movement of negatively charged molecules across the basement membrane

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16
Q

Describe the podocyte layer of the glomerular filtration barrier

A

There are foot-like processes projecting from podocytes that interdigitate to form filtration slits

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17
Q

What is the pathophysiological cause of glomerulonephritis?

A

It occurs when there is damage to the glomerular filtration barrier, resulting in the leakage of RBC’s and albumin

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18
Q

What are the five clinical features of glomerulonephritis? Why?

A

Haematuria, which is the presence of blood within urine resulting in pink-coloured urine

Proteinuria, which is the presence of more than 1.5g (150mg) of protein within urine per day, resulting in foamy urine

Hypertension, which is high blood pressure

Oedema, which specifically affects the patient’s face, hands, feet and abdomen

Oliguria, which is the defined as a decreased urine output – specifically less than 0.5ml/kg/hour

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19
Q

What are the three types of haematuria?

A

Visible

Microscopic

Dipstick positive

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20
Q

Why is proteinuria a clinical feature of glomerulonephritis?

A

This is due to the fact that proteins can pass through the triple filtration barrier and into urine

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21
Q

Why is hypertension a clinical feature of glomerulonephritis?

A

This is due to the fact that salt and water are retained within blood

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22
Q

Why is oedema a clinical feature of glomerulonephritis?

A

This is due to the retention of fluid

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23
Q

Why is oliguria a clinical feature of glomerulonephritis?

A

This is due to the retention of fluid

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24
Q

What is nephritic syndrome?

A

A group of clinical features which reflect inflammation of the kidney

It doesn’t represent a specific syndrome or underlying cause

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25
Are there set criteria a patient must met in order to have nephritic syndrome?
No, instead the patient just presents with the clinical features of glomeruloneprhtiis
26
What is a prominent clinical feature of nephritic syndrome?
Proteinuria
27
What is the pathophysiological cause of nephritic syndrome?
It is caused by the invasion of inflammatory cells into the glomerulus These inflammatory cells then attack the triple filtration barrier, resulting in the leakage of RBCs and some albumin.
28
What is a prominent clinical feature of nephrotic syndrome? What is not a prominent clinical feature of nephrotic syndrome?
Haematuria Proteinuria
29
What are the four criteria of nephrotic syndrome?
Peripheral Oedema Proteinuria, which is defined as >3.5g per 24hrs Hypoalbuminemia, which is defined as serum albumin <35g/L Hypercholesterolaemia, which is defined blood cholesterol > 200mg/dl
30
What is the pathophysiological cause of nephrotic syndrome?
It is caused by podocytes and their foot processes separating, thus resulting in leakage of albumin and some RBCs
31
What are the two main classifications of glomerulonephritis?
Proliferative Glomerulonephritis Non-Proliferative Glomerulonephritis
32
What is proliferative glomerulonephritis?
It is characterised by increased cellularity of the glomerulus This is due to the invasion of inflammatory cells
33
What are the four subclassifications of proliferative glomerulonephritis?
IgA nephropathy Membranoproliferative Glomerulonephritis Diffuse Proliferative Glomerulonephritis Crescentic Glomerulonephritis
34
Is proliferative glomerulonephritis nephrotic or nephritic?
Nephritic
35
What is the most common glomeurlonephritis classification?
IgA nephropathy
36
What are another two terms for IgA nephropathy?
Mesangioproliferative glomerulonephritis Berger's disease
37
What is IgA nephropathy?
It is characterised by a mesangial deposition of IgA immune complexes
38
In which patient group does IgA nephropathy tend to present in?
Male patients Between the ages of 20 – 30 years old
39
What are the three risk factors of IgA nephropathy?
Alcoholic cirrhosis Coeliac disease Hence Schonlein purpura
40
How does mesangioproliferative gloumerulonephritis tend to present?
Macroscopic haematuria Following an upper respiratory tract infection
41
How are the two features of IgA nephropathy on histological examination?
Mesangial hypercellularity Positive immunofluorescence for IgA & C3
42
What is the conservative management of IgA nephropathy?
No treatment Follow up to check renal function
43
When do we recommend conservative management of IgA nephropahty?
In cases of isolated haematuria, with no proteinuria and a normal GFR
44
What are the two pharmacological management options of IgA nephropathy?
ACE inhibitors Corticosteroids
45
When are ACE inhibitors used to manage IgA nephropathy?
In cases of persistent proteinuria > 500 - 1000mg/day, with a normal or only slightly reduced GFR
46
When are corticosteroids used to manage IgA nephropathy?
In cases where there is failure to respond to ACE inhibitors or GFR levels are reduced
47
What are the three differences between IgA nephropathy and post-streptococcal glomerulonephritis?
IgA nephropathy = high complement levels, haematuria, onset of features following infection is 1-2 days Post-streptococcal glomerulonephritis = low complement levels, proteinuria, onset of features following infection is 1-2 weeks
48
How do we diagnose mesangioproliferative glomerulonephritis?
The IgA deposits are not filtered into the urine An elevated level of IgA is only identified within blood
49
What is membranoproliferative glomerulonephritis ?
It is characterised by an increased number of cells within the glomerular basement layer of the glomeruli
50
What is another term for diffuse proliferative glomerulonephritis?
Post infectious glomerulonephritis
51
What is diffuse proliferative glomerulonephritis?
A severe form in which proliferative changes occur in more than 50% of the glomeruli
52
In which patient group does diffuse proliferative glomerulonephritis tend to present in?
Younger patients One to three weeks after an infection of the throat or skin, such as tonsilitis or impetigo
53
What organism tends to cause diffuse proliferative glomerulonephritis?
Lancefield group A streptococci
54
Why do infections cause diffuse proliferative glomerulonephritis?
In order to fight the infection, the body produces extra antibodies that can eventually settle in the glomeruli, causing inflammation and thus glomerulonephritis
55
What is crescentic glomerulonephritis?
It is characterised by the formation of glomerular crescents within the glomeruli This crescent is formed as a result of cellular proliferation and macrophage influx within the Bowman’s space
56
What are the two subclassifications of crescentic glomerulonephritis?
ANCA-Associated Glomerulonephritis Anti-GBM Nephritis
57
What is ANCA associated glomerulonephritis?
It is a condition in which ANCA vasculitis of the lungs starts to affect the kidneys
58
How do ANCA antibodies cause ANCA associated glomerulonephritis?
ANCA antibodies are directed against two neutrophilic enzymes – proteinase 3 and myeloperoxidase. Therefore, when inflammation occurs and neutrophils infiltrate the glomerulus, a high production of ANCA antibodies occurs which then causes tissue damage within the kidney.
59
What is another name for anti-GMB nephritis?
Goodpasture’s syndrome
60
What is anti-GMB nephritis?
It is a condition in which anti-GMB antibodies attack the basement membranes of the glomerulus and lung
61
What are the four clinical features of anti-GMB nephritis?
Acute kidney failure Proteinuria Haematuria Haemoptysis
62
What is non-proliferative glomerulonephritis?
It is characterised by the appearance of a normal glomerulus
63
What are the four subclassifications of non-proliferative glomerulonephritis?
Minimal Change Disease Membranous Glomerulonephritis Focal Segmental Glomerulosclerosis Diabetic Nephropathy
64
Is non-proliferative glomerulonephritis nephrotic or nephritic?
Nephrotic
65
What is minimal change disease?
It is characterised by the presence of minimal damage under a light microscopy This damage can only be visualised using an electron microscopy – specifically demonstrating shrunken podocytes and effaced foot processes.
66
In which patient group does minimal change disease tend to affect?
Children
67
What is a clinical feature of minimal change disease?
Oedema
68
What is membranous glomerulonephritis?
It is characterised by IgG deposition within between the basal lamina and podocytes within the glomerular basement membrane This results in a thickened basement membrane, in which new spikes of basal lamina form underneath the podocytes IgG results in the activation of complement 3 (C3), which attacks the basal lamina thus creating gaps within the basement membrane that albumin can leak through
69
What is the most common classification of glomerulonephritis?
Membranous glomerulonephritis
70
What are the causes of membranous glomerulonephritis? Which is most common?
Idiopathic - most common Malignant Rheumatoid disorders Drugs (NSAIDs)
71
How do we diagnose membranous glomerulonephritis?
We can conduct an immunology screen to look for the presence of anti-phospholipid A2 receptors (PLA2R) The IgG deposits are not filtered into the urine. An elevated level of IgG is only identified within blood
72
What is focal segmental glomerulosclerosis?
It is characterised by scarring of less than 50% of glomerulus tissue
73
What subclassification has a high progression risk into end stage kidney disease?
Focal segmental glomerulosclerosis
74
What is diabetic nephropathy?
It is characterised by the deposition of glycated molecules in the basal lamina and mesangial matrix This results in a thickened, leaky glomerular membrane that allows the leakage of albumin and compression of the capillaries supported by the mesangial matrix
75
What are the deposits in diabetic nephropathy called?
Kimmelsteil-Wilson lesions
76
How do we screen diabetic patients for diabetic nephropathy?
Albumin: creatinine ratio U&Es
77
What are the four investigations used to diagnose glomerulonephritis?
Urine sample Blood tests Kidney biopsy Immunology screen
78
What five urine sample results indicate glomerulonephritis?
Haemoglobin, which is elevated WBCs, which is elevated Proteinuria, which is an elevated albumin level > 30mg/g Creatinine, which is elevated > 15900umol over 24hrs Urea, which is elevated > 20g over 24hrs
79
What seven blood test results indicate glomerulonephritis?
Haemoglobin, which is reduced < 130g/L Serum Creatinine, which is elevated >120 umol/L (80, 160 Serum Urea, which is elevated > 7mmol/L Serum Albumin, which is reduced < 35g/L Cholesterol, which is elevated > 5.5mmol/L eGFR, which is elevated > 120mL/min/1.73m2 Compliment Component C3, which is reduced
80
What is a kidney biopsy?
A kidney biopsy involves using a special needle to extract small pieces of kidney tissue for light and electron microscopic examination
81
How are kidney biopsies used to diagnose glomerulonephritis?
It enables classification of glomerulonephritis
82
How is an immunology screen used to diagnose glomerulonephritis?
It identifies the presence of associated antibodies, such as ANCA antibodies and anti-GMB antibodies.
83
How do we conservatively treat glomerulonephritis?
It involves encouraging a low salt diet, as this will improve the patient’s oedema
84
What are the four pharmacological treatments of glomerulonephritis?
Hypertensive Agents Statins Steroids Loop Diuretics
85
What two hypertensive agents are used to treat glomerulonephritis?
ACEI ARBs
86
What two statins are used to treat glomerulonephritis?
Warfarin Heparin
87
What three steroids are used to treat glomerulonephritis?
Prednisolone Cyclophosphamide Azathioprine
88
What are the three complications of glomerulonephritis?
Acute Kidney Failure Chronic Kidney Disease Hypertension
89
How does glomerulonephritis result in acute kidney failure?
This is due to the glomerular damage can result in the rapid accumulation of waste products
90
How does glomerulonephritis result in hypertension?
This is due to the fact that damage to the kidneys results in a build-up of waste products in the bloodstream, which can raise blood pressure

Year Two - Urinary System (15 decks)

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