Brainscape's Knowledge GenomeTM

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


See full index

Renal > Glomerulonephritis > Flashcards

Glomerulonephritis Flashcards

1
Q

what makes up the renal parenchyma

A

tubules, interstitium, glomeruli

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

what type of disease is glomerulonephritis

A

glomerular disease

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

what are the two types of glomerulonephritis

A

chronic- 2nd commonest cause of end stage renal failure

acute- important treatable cause of acute renal failure

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

what is glomerulonephritis

A

range of immune mediated diseases of the kidneys affecting the glomeruli (with secondary tubulointerstitial damage)

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

what is the difference between primary and secondary glomerulonephritis

A 
primary= no associated disease (majority idiopathic)
secondary= glomerular involvement is part of systemic disease (e.g. SLE, infections, drugs, malignancies, ANCA, goodpastures, HSP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does damage to endothelial or mesangial cells cause

A

a proliferative lesion

  • red cells in urine
  • aggressive nephritic picture
  • influx of inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does damage to podocytes cause

A

a non proliferative lesion

  • protein in urine
  • dont get dramatic inflammatory response
  • loose ability to retain albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what happens when there is podocyte damage

A

it atrophies
loss of specific barrier function
proteinuria

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

what happens when there is mesangium damage

A

proliferative response
release of Ang.2, chemokines
attract inflammatory cells

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

what causes damage to the glomerular endothelium

A

vasculitis

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

what tests to diagnose GN

A 
blood tests 
urinalysis 
urine microscopy- RBC (dysmorphic), 		RBC  & granular casts, lipiduria
urine protein: creatinine ratio 
kidney biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what types of haematuria will renal presentation cause

A

asymptomatic microscopic

episodes of painless haematuria (wont produce painful haematuria)

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

what are the parameters of proteinuria

A 
Microalbuminuria (30-300mg albuminuria/day)
Asymptomatic proteinuria (< 1 g/day)
Heavy proteinuria (1-3 g/day)
Nephrotic syndrome (> 3 g/day))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

do you do a kidney biopsy for everyone

A

no as risk of bleeding

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

what are red cell casts Pathognomonic of

A

GN with injury to mesangium

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

what are the clinical presentations of GN

A

impaired renal fucntion (AKI, CKD/ ESRD)
hypertension
nephritic/nephrotic syndrome
nephritic-nephrotic syndrome

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

what is nephritic syndrome

A
  • acute renal failure
  • oliguria
  • oedema/ fluid retention (caused by reduce urine output)
  • hypertension
  • active urinary sediment (RBC’s, granular casts)
18
Q

what is nephritic syndrome indicative of

A

proliferative process

affecting endothelial cells

19
Q

what is nephrotic syndrome

A
  • proteinuria >3g/day
  • hypoalbuminaemia
  • oedema
  • hypercholesterolaemia (live working overtime)
  • usually normal renal function (normal creatinine and BP)
20
Q

what is nephrotic syndrome indicative of

A

a non proliferative process affecting podocytes

21
Q

what are the possible complications of nephrotic syndrome

A

infection (loss of opsonising antibodies)
renal vein thrombosis
PE (increased DVT risk)
volume depletion (overaggressive use of diuretics may lead to ARF)
vit d def
subclinical hypothyroidism

22
Q

How does the presentation of GN differ from a non glomerular disease like Interstitial Nephritis?

A

In glomerular disease can have blood or protein in urine

In a interstitial nephritis- should not have blood or protein or urine

23
Q

how do you classify GN

A

aetiology (primary or secondary)

histology (renal biopsy, light microscopy, immunofluorescence, EM)

24
Q

what are the histological classifications of GN

A

proliferative vs non proliferative (proliferation of mesangial cells)

focal/ diffuse (< or > 50% glomeruli affected)

global/ segmental (all or part of glomerulus affected)

crescentic (presence of cresents- epithelial cell extracapillary proliferation- e.g. RPGN in vasculitis)

25
Q

what are the principles of GN treatment

A

reduce degree of proteinuria
induce remission of nephrotic syndrome
preserve longterm renal function

26
Q

what are the non immunosuppressive treatments for GN

A 
Anti-hypertensives (target BP <130/80 - <120/75 if proteinuria)
ACE inhibitors/ ARBs
Diuretics
Statins (hypercholesterolaemia)
? Anticoagulants/ Aspirin/ Antiplatelets
? Omega 3 fatty acids/ Fish oil
27
Q

what are the immunosuppression therapies for GN

A

Drugs
Corticosteroids (Prednisolone po/MethylPred IV)
Azathioprine
Alkylating agents (Cyclophosphamide/ Chlorambucil)
Calcineurin inhibitors (Cyclosporin/Tacrolimus)
Mycophenolate Mofetil (MMF)

Plasmapharesis (TPE-therapeutic plasma exchange)

Antibodies:IV Immunoglobulin
Monoclonal T or B cell Antibodies

28
Q

what is the general treatment for nephrotic patients

A 
Fluid restriction
Salt restriction
Diuretics
ACE Inhibitors/ ARBs 
? Anticoagulation
IV Albumin (only if volume deplete)

IMMUNOSUPPRESSION

29
Q

what is the aim of treatment for nephrotic patients

A 
to induce sustained remission: 
complete remission (proteinuria < 300 mg/day) 
partial  remission (proteinuria < 3g/day)
30
Q

what are the types of non proliferative GN

A

minimal change GN
focal segmental glomerulosclerosis
membrane GN

31
Q

describe minimal change GN

A

damage to podocytes
commonest cause of nephrotic syndrome in children
seen on EM
94% complete remission with oral steroids
doesnt cause progressive renal failure

32
Q

describe focal segmental glomerulosclerosis

A

commonest cause of nephrotic syndrome in adults
primary/ secondary to HIV/herion/obesity/reflux/ nephropathy
segements of glomeruli develop sclerosis
60% response to steroids
50% progress to ESRF

33
Q

describe membranous nephropathy

A

2nd commonest cause of nephrotic syndrome in adults
primary/ secondary (hep b, parasites, CTD- lupus, malignancies, drugs (gold, pencillamine))
renal biopsy- immune complex deposition in BM
thickened glomerular BM
steroids/ alkylating agents/ B cell monoclonal Ab
1/3rd progress to ESRD
1/3rd go into remission
anti PLA2r antibody

34
Q

what are the types of proliferative GN

A

IgA nephropathy
rapdily progressive GN
membranoproliferative GN
post infectious GN

35
Q

describe IgA nephropathy

A

most common GN in adults
proliferative
macroscopic haematuria after resp/GI infection
AKI/CKD
associated with HSP (arthritis, colitis, purpuris skin rash)
renal biopsy- IgA deposits, proliferation
5% ESRF in 10 years

BP control, ACRi, ARBs, fish oil

36
Q

describe rapidly progressing GN

A

cresenteric (glomerular cresents on biopsy)
either ANCA positive or ANCA negative
treatable cause of AKF
rapid deterioration in renal function over weeks/ days
RBCs and granular casts in urine

37
Q

what are the ANCA positive RPGN

A

GPA (vasculitis affecting lungs, kidneys, ect. c-ANCA positive, treat with steroids + cyclophosphamide)

MPA (small vessel vasculitis, p-ANCA +ve, tx with long term steroids)

38
Q

what are the ANCA negative RPGN

A

Goodpasture’s disease-Anti-GBM

Henoch Scholein Purpura HSP/IgA

Systemic Lupus Erythematosus SLE

39
Q

what is the tx for RPGN

A

AIM IS TO CONTROL THE SYSTEMIC AS WELL AS RENAL DISEASE

Immunosuppression
Steroids (IV Methylprednisolone / Oral Prednisolone)
Cytotoxics (Cyclophosphamide/ Mycophenolate/ Azathioprine

Plasmapharesis

40
Q

what is membraneprolifrative GN

A

primary/ secondary (SLE, hep)

usually progresses to ESRF

41
Q

describe post infectious GN

A

occurs weeks after URTI (usually strep pyogenes)
supportive Tx
resolves in 2-4 weeks

42
Q

describe IgA nephropathy

A

most common GN in adults
proliferative
macroscopic haematuria after resp/GI infection
AKI/CKD
associated with HSP (arthritis, colitis, purpuris skin rash)
renal biopsy- IgA deposits, proliferation
5% ESRF in 10 years

BP control, ACRi, ARBs, fish oil

Renal (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions