Glomerulonephritis Flashcards

1
Q

what team?

A

WILDCATS

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2
Q

Define Glomerulonephritis

A

immune mediated disease of the kidneys affecting the glomeruli
+ secondary tubulointerstitial damage

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3
Q

Name the 2 different types of mechanisms by which GN occurs

A

Humoral (antibody mediated)

  • Intrinsic/planted antigen
  • deposition of circulating immune complexes
Cell mediated (T-cells)
-cause the release of inflammatory cells, mediators and complement
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4
Q

Describe the structure of the glomerulus?

from internal to external

A

capillary lumen lined with endothelial cells, under that lies the GBM and the mesangial cells at the centre of the capillaries
podocytes are located o the outside of the capillaries (epithelium)
them the bowman’s space

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5
Q

what are the two forces involved in the capillary barrier function?

A

-size and charge (the cm is neg charged)

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6
Q

process behind the development of:

  • proliferative lesion? and presentation?
  • non-proloferative lesion? and presentation?
A

-damage to endothelial or mesangial cells
RBC in urine = haematuria

-damage to podocytes
protienuria (albumin)

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7
Q

investigation and diagnosis in GN

A

Bloods

Examination of the urine:

  • urinalysis for haematuria and proteinuria
  • Urine microscopy (RBC dysmorphia, RBC & granular casts, lipiduria)
  • urine protein /creatinine ratio

-Kidney biopsy

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8
Q

Clinical presentation of Nephritic syndrome? (6)

A
Acute renal failure
Oliguria
Oedema/ fluid retention
Hypertension
active urinary sediment (RBCs/ RBC & granular casts)
Proliferative process
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9
Q

Clinical presentation of Nephrotic syndrome? (6)

A

Proteinuria > 3g/day (albumin)

Hypoalbuminaemia (

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10
Q

Complication of Nephrotic syndrome? (6)

A

infections (due to loss of antibodies)

Renal vein thrombosis

PE

volume depletion (over aggressive use of diuretics,may lead to ARF)

Vit D deficiency

Subclinical hypothyroidism

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11
Q

causes of GN? (4)

A

Idiopathic
Infectious
Drugs
Systemic disease (ANCA assoc vasculitis, lupus, Goodpastures, HSP)

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12
Q

Name the 3 histological investigations done on biopsy?

A

Light microscopy
immunofluorescence
electron microscopy

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13
Q

Histological classification of GN, name the 4 terms used

A

Proliferative/non-proliferative
referring to presence or absence of mesangial cells

Focal/diffuse
50% glomeruli affected

Global/segmental
all part glomerulus affected

Crescenteric
Presence or crescents, epithelial cell extra capillary proliferation e.g. RPGN in vasculitis

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14
Q

Treatment of GN

  • types (2)
  • what these types involve (1=5, 2=3»9)
A

-Non immunosuppressive

Anti-hypertensives (target BP

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15
Q

Principles of treating nephrotic patient

  • general (6)
  • after ^^
  • define sustained remisson in nephrotic syndrome
A
-Fluid/Salt restriction
Diuretics
ACE Inhibitors/ ARBs
? Anticoagulation
IV Albumin (only if volume deplete)
  • immunosuppression
  • Complete= proteinuria
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16
Q

Maine types of GN? (5)

A
Minimal change
FSGS- focal segmental glomerulosclerosis
Membranous
Membranoproliferative
IgA Nephropathy
17
Q

Minimal change nephropathy

  • population
  • biopsy
  • treatment
  • PRF?
  • caused by?
A

-commonest nephrotic syndrome in children

-normal on LM and IF but foot process fusion on EM
non-proliferative

  • oral steroids, 2nd line cyclophosphoamide in resistant/recurrence
  • nope
  • interleukin 13 (IL-13)
18
Q

FSGS

  • population
  • biopsy
  • treatment
  • PRF?
  • caused by (immune component & secondary cause)
A
  • commonest cause of Nephrotic syndrome in adults
  • focal segmental glomerulosclerosis with minimal Ig/complement deposition on IF
  • prolonged steroids
  • yes

-suPAR- up-regulates integrins and causes podocyte effacement
HIV/Heroin use/Obesity/ Reflux nephropathy

19
Q

Membranous nephropathy

  • population
  • biopsy
  • treatment
  • PRF?
  • caused by (immune component & secondary cause)
A
  • 2nd commonest cause of NS in adults
  • subepithelial immune complex deposition in the BM, thickened BM
  • steroids, alkylating agents, B cell monoclonal Ab
  • yes
-Anti PLA2r antibody
infections (hepatitis B/ parasites)
connective tissue diseases (lupus)
malignancies (carcinomas/ lymphoma)
drugs (gold/penicillamine)
20
Q

IgA nephropathy

  • population
  • biopsy
  • treatment
  • PRF?
  • presentation
  • associations
A
  • commonest in world
  • mesangial cell proliferation and expansion and Ig A deposits in the mesangium
  • BP control/ ACE inhibitors & ARBs/ Fish oil
  • yes

-Asymptomatic microhaematuria  +/- non-nephrotic range proteinuria
Macroscopic haematuria after resp/GI infection
AKI/ CKD

-Associated with Henoch-Schonlein Purpura (HSP) (arthritis/colitis/ purpuric skin rash)

21
Q

Rapidly progressive glomerular nephritis

  • presentation
  • associations
  • biopsy
  • blood test and what results indicate?
  • treatment
A
  • AKI + active urinary sediment
  • systemic disease (ANCA pos and ANCA neg)
  • glomerular crescents
  • test for ANCA
    positive: Systemic vasculitis (Wegener’s granulomatosis and microscopic polyangitis)
    negative: Goodpastures disease, HSP, SLE
  • Immunosuppression
    Steroids (IV Methylprednisolone / Oral Prednisolone)
    Cytotoxics (Cyclophosphamide/ Mycophenolate/ Azathioprine
    Monoclonal antibody directed against CD20 receptor of B cells (rituximab).
    Plasmapharesis