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Glomerulonephritis Flashcards

1
Q

What is glomerulonephritis?

A

This encompasses a number of conditions which do all of the following:

  • are caused by glomerular pathology
  • present with haema or protein uria, or both
  • are diagnosed with renal biopsy
  • cause CKD
  • can cause kidney failure
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2
Q

How do we name different types of glomerulonephritis?

A

Histological appearance
e.g. membranous glomerulonephritis
Associated systemic condition
e.g. lupus nephritis

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3
Q

What is the difference between nephrosis and nephritis?

A

Nephrosis is more about pathology

Nephritis refers to inflammation

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4
Q

What is the difference in urineanalysis between nephropathy and nephritis?

A

Nephropathy will show proteinuria

Nephritis will show haematuria

That said, both come with both if they progress

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5
Q

Give some examples of nephropathy

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis

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6
Q

Give some examples of nephritis

A 
IgA nephropathy
Lupus nephritis
Small vessel/ANCA vasculitis
Henoch-Scholein Purpura
Post-strep A GN
Anti-GBM disease
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7
Q

Which diseases can cause renal damage?

A 
Diabetic nephropathy
Lupus
Small vessel vasculitis
Strep A
Viral Hep
Amyloid
Myeloma
Vasculitis
HUS
TTP
Atherosclerosis
SCD
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8
Q

How do we investigate for glomerulonephritis?

A 
FBC - HUS, infection
UEs - Raised Cr, CKD, AKI
eGFR
LFTs - raised HepB/C
CRP/ESR
Immunoglobs - IgA nephropathy
Lipids
Antibody tests - ANA, ANCA, ASOT, anti-GBM
Blood serology - Hep B/C/HIV

Urineanalysis - ACR, MC+S
Biopsy

CXR - pulmonary haemorrhage
USS Kidney

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9
Q

What differentials of GN must you consider?

A

Bladder cancer
Renal cancer
Pre or post renal failure
Renal stones

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10
Q

How do we treat GN?

A

BP control

Treat the cause

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11
Q

What is IgA nephropathy?

A

Deposition of IgA in mesangium of kidney. Biopsy required to make diagnosis.

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12
Q

How do we treat IgA nephropathy?

A

ACEi and/or ARB
Corticosteroids (pred 40mg)
Fish oil

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13
Q

What is HSP?

A

Henoch-Schonlein purpura.
Small vessel vasculitis, a variant of IgA nephropathy but with IgA deposits in skin/joints and guts too. Manifests as skin rash in children.

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14
Q

How do we manage HSP?

A

Same as IgA
ACEi/ARB
Steroids
Fish oil

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15
Q

What is post-streptococcal GN?

A

Occurs 2 weeks after a throat or 3-6 after skin infection. Strep antigen deposits in teh glomerulus = immune response.
Diagnose with ASOT, lowered C3 and raised anti-DNAse B.

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16
Q

How do we treat post-strep GN?

A

Antibiotics

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17
Q

What is evidence of a streptococcal infection?

A

Anti strep O titre
Anti DNAse B
Lowered C3 (complement)

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18
Q

What is anti GBM disease?

A

Aka Goodpasture’s disease

Auto antibodies to the type IV collagen in glomerular and alveolar basement membranes

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19
Q

What is the presentation of Goodpasture’s disease?

A

Renal disease, lung disease (pulmonary haemorrhage and so SOB and haemoptysis)

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20
Q

How do we treat anti-GBM disease?

A

Corticosteroids
Plasma exchange
Cyclophosphamide

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21
Q

What is rapidly progressive GN?

A

any aggressive GN that progresses to renal failure over days or weeks.

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22
Q

Which GN can be rapidly progressing?

A

Small vessel vasculitis
Lupus
Anti-GBM

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23
Q

How do we treat rapidly progressing GN?

A

Corticosteroids and cyclophosphamide

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24
Q

Why does blood pressure increase in renal diseases?

A

Inappropriate retention of salt and water

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25
Q

What is the gold standard test for checking protein levels in the urine?

A

24 hour urine collection

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26
Q

What test do we do to check protein levels that is quick and easy?

A

ACr and PCr

27
Q

What is something to bear in mind with ACr or PCr?

A

Can get abnormal values if Cr is too low of high after a protein meal.

28
Q

How do we do ACR or PCR?

A

Do urine dipstick which will only show if albuminuria is over 300mg/24 hours so if that is negative, send urine to the lab.

29
Q

What are the different immunological processes involved in GN?

A

1) Immunoglobulin and complement activation within the glomerulus e.g anti GBM
2) Antigens becoming trapped or deposited in glomeruli e.g. IgA nephropathy
3) Immune complexes becoming trapped.

30
Q

What are the 5 most common clinical signs/syndromes that occur with glomerulonephritis?

A
  1. Isolated haematuria, proteinuria or both.
  2. Nephrotic syndrome
  3. Acute glomerulonephritis (acute nephritic syndrome)
  4. Rapidly progressive GN
  5. CKD and ESRD
31
Q

In direct relation to Bowman’s capsule, what’s the difference between nephrotic and nephritic syndrome?

A

Nephrotic - Podocytes breakdown and protein leaks

Nephritic

32
Q

In direct relation to Bowman’s capsule, what’s the difference between nephrotic and nephritic syndrome?

A

Nephrotic - Podocytes breakdown and protein leaks

Nephritic - immune complex (antibody/antigen) in the capillaries causing an immune response in capillaries.

33
Q

Why do patients become oedematous in Nephrotic GN?

A

loss of protein in the blood means the fluid leaks out

34
Q

What things do we lose/gain in the blood when the podocytes start to fail?

A

Lose albumin
Gain lipids to compensate albumin
Lose ATIII (antithrombin 3) so increases clot chances esp in renal vein.

35
Q

What is antithrombin 3?

A

Important anticoagulant.

36
Q

What things do we lose out of the kidney when immune response on endothelial cells?

A

WBC
RBC
Protein

37
Q

What is in the urine in nephrotic and nephritic syndrome?

A

Nephrotic - albumin, protein

Nephritic - haematuria, WBC, maybe protein, granular cells, low output

38
Q

Why do we get oliguria in nephritic syndrome?

A

The immune response can block the filtration so the kidney can’t filter as much.

39
Q

What is the triad that nephrotic syndrome is characterised by?

A

Proteinuria
Oedema
Hypoalbuminaemia

40
Q

What are the different causes of nephrotic syndrome?

A

Primary:

  • Minimal change disease
  • Focal Segmental Glomerulosclerosis
  • Membranous glomerulonephritis
  • Membranoproliferative glomerulonephrits
Secondary:
Lupus
Hep B,C, HIV, Malaria
NSAIDs
Mercury
Tumours
41
Q

How do we manage nephrotic syndrome?

A

Reduce the oedema
Treat the cause
Reduce the proteinuria
Manage complications

42
Q

What are the complications of nephrotic syndrome?

A

Thromboembolism (low AT3)
Hyperlipidaemia (compensated for albumin)
Infection

43
Q

What is minimal change disease?

A

A disease where there is no change under a microscope but slight change of podocytes under electron microscope.

44
Q

What is FSGS?

A

Focal Segmental Glomerulosclerosis

Scarring of some parts of some glomeruli

45
Q

What is membranous glomerulonephritis?

A

Immune deposits are on basement membrane but then a second membrane is formed on top of that causing it to be bumpy

46
Q

What is membranoproliferative glomerulonephritis?

A

in the name

Same as MG, but the immune deposits are also present in the mesangium

47
Q

What are Kimmelstiel Wilson lesions?

A

They are lesions present in the mesangium in nephrotic syndrome secondary to diabetic nephropathy

48
Q

Which streptococci strain that causes post-strep GN and what are its characteristics?

A

Group A ß-haemolytic streptococci which causes complete haemolysis after the production of streptolysin, and is considered nephritogenic as it carries M-protein virulence factor which dodges host immune defence.

49
Q

Which type of hypersensitivity reaction does group A strep cause?

A

Type III

IgG and IgM

50
Q

How does the strep cause GN?

A

The antigen and antibody complex gets beneath the podocytes and causes an immune reaction, allowing RBCs and proteins to filter through

51
Q

When does PSGN occur and how long does it last for?

A

About 6 weeks after skin infection (impetigo)

1-2 weeks after a throat infection (pharyngitis)

Lasts for a month and runs its course but can sometimes cause renal failure (rapidly progressive GN)

52
Q

What is Anti DNAse B?

A

Antigen against group A streptococcus

53
Q

When does IgA nephropathy present?

A

Usually with haematuria 1 to 3 days after onset of URTI, UTI or gastroenteritis.

54
Q

What is the diagnosing test for IgA nephropathy and how often do we do it?

A

Biopsy

Rarely because isolated microscopic haematuria is not an indication for biopsy

55
Q

What do we do for IgA nephropathy?

A

Monitor with BP, urine and kidney function tests

Treat HTN and proteinuria with ACEi.

56
Q

What counts as acute nephritic syndrome?

A

Post strep GN

IgA GN

57
Q

What is RPGN?

A

Rapid progressive GN

Inflammation of glomeruli which eventually causes crescent shaped cells in bowmans space, leading to renal failure.

58
Q

What can cause RPGN?

A 
Type 1- Anti-GBM GN
Type 2-  IMMUNE COMPLEXES:
Post Strep
Lupus
IgA nephropathy
HSP
Type 3- PAUCI IMMUNE (no antiGBM or immune complexes)
cANCA (wegener granulomatosis)
pANCA
59
Q

How do crescent cells come about?

A

The GBM breaks due to cell mediated immune response and macrophage involvement allowing RBC, proteins, complement, immune cells and fibrins into Bowmans space.
All of these things cause the epithelium of BS to become crescent like, thick and scarred.

60
Q

Why do crescent cells cause things to fuck up?

A

The scarred tissue impairs the GFR so reduced eGFR

61
Q

Who most likely gets RPGN?

A

adults 50-60 years

62
Q

What do we do to treat RPGN?

A

Anticoagulants to reduce fibrin in crescent
Plasmapheresis and immunosuppression
Dialysis
Transplant

63
Q

What tests do we do for a glomerular disease?

A 
FBC - anaemia
Renal profile
Bone profile
Lipids
Coagulation screen
HbA1c
ESR/CRP
Immunology screen (IgA)
Myeloma screen
Hepatitis serology
64
Q

If you get a dipstick with high protein, what do you do with more urine?

A

Send for PCR

Renal (8 decks)

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