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CP3 Medicine > RENAL - PKD, IN, Glomerulonephritis and Nephrotic/Nephritic syndrome > Flashcards

RENAL - PKD, IN, Glomerulonephritis and Nephrotic/Nephritic syndrome Flashcards

1
Q

What 3 ways can diabetes affect the kidneys

A

Direct glomerular damage
Ischaemia due to aa disease
Ascending infection

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2
Q

What is the most common cause of ballotable kidneys

A

PKD

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3
Q

PKD inheritance (2)

A

AD - PKD1 - 85%

AR - PKD2 - 15%

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4
Q

PS PKD (3)

A

HTN
CKD
Abdominal swelling b/c v large kidneys bilaterally

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5
Q

Where can cysts be found in PKD

A

Tubular epithelium - up to 4cm + brown

Also in liver –> portal HTN + fibrosis

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6
Q

What serious condition is PKD associated with

A

Berry aneurysm –> SAH

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7
Q

Mx PKD

A

Same as CKD

+ screen for berry aneurysms

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8
Q

From when does PKD start

A

Birth

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9
Q

What age does PKD usually present

A

From 30s

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10
Q

What are the 2 types of chronic interstitial nephritis

A

Reflux associated chronic interstitial nephritis

Obstructive chronic intersitial nephritis

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11
Q

What is Reflux associated chronic intersitial nephritis due to?

A

Incompetent VU valves

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12
Q

PS reflux associated chronic interstitial nephritis

A

Early adulthood

Deteriorating renal function

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13
Q

What is obstructifve chronic interstitial nephritis due to

A

Recurrent episodes of infection due to anatomical abnormality or a stone

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14
Q

What is glomerulonephritis

A

Inflammation of the glomerulus and can be a cause for both AKI and CKD

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15
Q

What are the 3 layers of the glomerulus

A

Fenestrated capillary epithelium
Basement membrane
Visceral layer - interdigitating podocytes

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16
Q

What are the 2 things causing damage to the glomerulus in glomerulonephritis

A

EIther autoantigens

Or immune complexes

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17
Q

Secondary factors –> auto-antigens (NSAID HSP)

A 
NSAID HSP
Neoplasm
SLE
Amyloid 
Infection 
Diabetes 
HSP
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18
Q

Damage to capillaries in glomerulonephritis (3)

A

Endothellial cell proliferation
Capillary wall necrosis
Glomerulosclerosis –> fenestra + capillaries being. pulled apart

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19
Q

Damage to basement mebrane in glomerlunephritis

A

Thickened membrane 00> structural distortion hence more permeable

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20
Q

Histology - global glomerulonephritis

A

Whole glomerulus is disease

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21
Q

Histology - segmental glomerulonephritis

A

Small patches of 1 glomerulus = damaged

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22
Q

Histology - diffuse glomerulonephritis

A

Affecting >50% glomeruli

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23
Q

Histology - focal glomerulonephritis

A

Affecting <50% glomeruli

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24
Q

How can glomerular disease manifest (6)

A 
AKI 
CKD 
Asymp haematuria 
Nephrotic syndrome 
Nephritic syndrome 
Rapid progressive glomerulonephritis
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25
Q

What is nephrotic syndrome due to?

A

Increased permeability at the glomerulus (b/c inflammation and damage)

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26
Q

Triad - nephrotic syndrome (3)

A

Proteinuria >3days
Hypoalbuminaemia (<30g/L)
Oedema

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27
Q

Why does proteinuria occur in nephrotic syndrome

A

B/c increased glomerular permeability

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28
Q

Appearance urine nephrotic syndrome and why

A

Frothy

B.c mass proteinuria

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29
Q

Is nephrotic syndrome proliferative

A

No

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30
Q

What are the 3 most common 1’ causes of nephrotic syndrome (3)

A

Minimal change nephropathy
Membranoproliferative glomerulonephritis
Focal segment glomerulosclerosis

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31
Q

What is the most common cause of nephrotic syndrome in children

A

Minimal change nephropathy

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32
Q

What is the most common cause of nephrotic syndrome in adults

A

Focal segment glomerulosclerosis

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33
Q

2’ causes of nephrotic syndrome

A 
Drugs 
Neoplasm 
Amyloid 
SLE 
Malaria
HIV
Hepatitis 
NAIDS
Obesity 
Pre-eclampsia
34
Q

Tx nephrotic syndrome (5)

A 
Diuretics
Salt/H2O rstrict 
ACEi (reduce proteinuria) 
Anticoagulation 
Tx cause
35
Q

Tetrad Nephritic syndrome

A

Haematuria + red cell casts
Oliguria
Proteinuria
HTN

36
Q

Is nephritic syndrome proliferative

A

Yes

37
Q

2 most common 1’ causes nephritic syndrome

A

IgA nephropathy

Goodpastures

38
Q

Ix nephrotic/nephritic syndrome

A 
Bloods - FBC, U+E, CRP, culture 
Urine dip - rule out infection 
MCS - Red cells/casts 
Urine protein - creatinine ratio mg/mmol 
Nephritic screen
Renal USS
Renal biopsy
39
Q

Urine protein:creatinine ratio nephrotic syndrome

A

> 300mg/mmol

40
Q

What are the 6 causes of nephritic syndrome

A

IgA nephropathy
Membranoproliferative glomerulonephritis
Post infectious glomerulonephritis
Goodpastures
Microscopic polyangitis
Granulomatosis with polyangiitis (Wegners)

41
Q

Non-Proliferative: Minimal change glomerulonephritis what changes

A

Abnormal podocytes seen on EM

42
Q

Minimal change glomerulonephritis - what is it assoc w/ (3)

A

NSAID use
Allergy
Hodgkin’s lymphoma

43
Q

Tx Minimal change glomerulonephritis (2)

A

PO prednisolone

Cyclophosphamide if relapse

44
Q

Prognosis Minimal change glomerulonephritis

A

99% resolve 4-6w w/ steroid Tx

1% –> ESRD

45
Q

Non-proliferative: MGN (Membranous Glomerulonephritis) changes

A

Thickened BM

46
Q

Cause of MGN

A

80% idiopathic

47
Q

How is MGN diagnosed

A

Biopsy

48
Q

Prognosis MGN

A

⅓ –> chronic MGN
1/3 –> remission
⅓ –> ESRD

49
Q

Mx MGN

A

Alternating steroids + chlorambucil

50
Q

Non-proliferative: Focal segmental glomerulosclerosis changes

A

Segments of glomeruli develop sclerosis

51
Q

Mx focal segmental glomerulosclerosis

A

Steroids in effective

52
Q

What % focal segmental glomerulosclerosis –> ESRD

A

50%

53
Q

Proliferative: IgA nephropathy (Buerger;s disease) - WHO

A

Young men

54
Q

IgA nephropathy - changes

A

IgA deposits in matrix

55
Q

Cause IgA nephropathy

A

Largely unknown

But appears 24-48h after URTI/GI infection

56
Q

Sx IgA nephropathy

A

Macroscopic haematuria

57
Q

Mx IgA nephropathy

A

Supportive

58
Q

Prognosis IgA nephropathy

A

20% –> ESRD 20y

59
Q

What is Membranoproliferative glomerulonephritis + changes

A

Mixed nephrotic and nephritic

Large glomeruli w/ double BM

60
Q

1’ cause Membranoproliferative glomerulonephritis

A

Immune mediated

61
Q

2’ Membranoproliferative glomerulonephritis

A

SLE/ Hep

62
Q

Prognosis Membranoproliferative glomerulonephritis

A

50% ESRD 10y

63
Q

Proliferative: Post-infectious/streptococcal GN changes

A

Diffuse proliferation GN w/ IgG + C3 deposit

64
Q

When does Post-infectious/streptococcal GN PS

A

Weeks after URTI

65
Q

Usual causative agent Post-infectious/streptococcal GN

A

Strep pyogenes

66
Q

Blood results Post-infectious/streptococcal GN

A

Raised AASOT/ anti-DNAase B

Reduced complement levels

67
Q

Mx Post-infectious/streptococcal GN + prognosis

A

SUpportive

Usually resolves in 2-4w

68
Q

Proliferative - Goodpastures - changes

A

ANti-GBM ab = IV collagen on glomerular BM and in lungs

69
Q

PS Goodpastures

A

Haematuria + rapidly progressive GN

+ Pulmonary haemorrhage –> haemoptysis + breathless

70
Q

CXR Goodpastures

A

Pulmonary shadowign

71
Q

Renal Biopsy Goodpastures

A

Linear deposition IgG in BM

72
Q

Mx Goodpastures (3)

A

Plasma exchange
CCS
Cytotoxins

73
Q

What ages get HSP

A

3-15 y/o

74
Q

Sx of HSP (5)

A 
Purpuric rash on extensors 
Polyarthritis 
ABdominal pain
Scrotal/scalp swelling 
GN
75
Q

How is a diagnosis of HSP made?

A

Clincal

+ ve immunofluorescence

76
Q

Granulomatosis w/ polyangitis - which organs affected (3)

A

Kidney
Lungs
+ others

77
Q

Which marker is +ve in granulomatosis w/ polyangiitis

A

C-ANCA

78
Q

Tx of granulomatosis with polyangiitis

A

Steroids

+ Cyclophosphamide

79
Q

What kind of vasculitis is microscopic polyangiitis

A

Small vessel vasculitis

And Rapidly proliferative glomerulonephritis (crescentic)

80
Q

Which marker is +ve in microscopic polyangiitis

A

p-ANCA

81
Q

Tx microscopic polyangiitis (2)

A

LT steroids

+/- cytotoxic agents

CP3 Medicine (29 decks)

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