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Renal > 05.15 - Kidney, Systemic 1 (Nichols) - PP + Handout > Flashcards

05.15 - Kidney, Systemic 1 (Nichols) - PP + Handout Flashcards

1
Q

What does factor H regulate

A

Complement

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1
Q

Demographic of SLE

A

Black Female of child-bearing age

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2
Q

Small vessel vasculitis causes

A

Focal necrotizing lesions with crescents, active urinary sediment, Rapid progression of kidney failure

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2
Q

AI necrotizing granulomatous vasculitis of respiratory tract and cause of crescentic GN associated with C-ANCA

A

Wegener’s

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3
Q

Small vessel vasculitis involving glomeruli usually causes

A

Pauci-immune Crescentic GN

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3
Q

Causes of Thrombotic Microangiopathy includes ___ in children and ___ in adults

A

Hemolytic Uremic Syndrome, TTP

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3
Q

Sudden onset of irritability, lethargy, weakness, pallor, and oliguria 5-10 days following gastroenteritis

A

HUS

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3
Q

Most common form of Lupus Nephritis

A

Diffuse Proliferative (Class IV) - Severe disease

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3
Q

Thrombotic Microangiopathy of Glomeruli in small children due to Shiga toxin from E Coli infection

A

Hemolytic Uremic Syndrome

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5
Q

Ab’s in Microscopic Polyangiitis

A

P-ANCA (anti-mpo)

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6
Q

What are Classes I, II, and III of Lupus Nephritis

A

Minimal Mesangial (rare), Mesangial Proliferative (15), Focal Proliferative (25)

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8
Q

Effect of Microscopic Polyangiitis on kidneys

A

Glomerulonephritis

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9
Q

First and second most common Classes/Patterns of GN

A

Diffuse Proliferative (50), then Focal Proliferative (25)

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10
Q

Typical patient with TTP

A

Older adult - Subacute onset of malaise, faitigue, petechiae, pallor, confusion, nausea, abdominal pain, weakness

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10
Q

Urine feature present in 100% of patients with SLE

A

Proteinuria

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10
Q

Manifestation of renal involvement of SS

A

Mild renal dysfunction, Proteinuria, HTN; or Scleroderma Renal Crisis

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11
Q

Which arteries show onion skinning in SS of kidneys

A

Interlobar arteries

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12
Q

Histological findings in kidney in scleroderma

A

Onion skinning, Intimal and Medial proliferation, Fibrinoud Necrosis

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12
Q

Which Class of Lupus Nephritis has significantly worse renal survivial rate

A

IV

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13
Q

Immediate consequence of PMN activation by ANCAs

A

Increased contact and adhesion with endothelial cells and vascular structures

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14
Q

Most forms of vasculitis involve on

A

Arteries

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14
Q

How do you differentiate between TMA and DIC

A

PT and PTT are normal in TMA, but prolonged in DIC

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14
Q

There are granular deposits of ___ in ___ locations in most cases of SLE

A

Ig and Complement, Subepithelial, Mesangial, and Subendothelial locations

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15
Q

Typical onset of HUS

A

Sudden irritability, lethargy, weakness, pallor, oliguria; 5-10 days following gastroenteritis

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16
Q

Vascular changes in Scleroderma Renal Crisis associated with poorer outcome

A

Mucoid Intimal thickening and thrombosis

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17
Q

Patients with Wegener’s develop necrotizing granulomatous inflammation in their ____, in addition to ____

A

Nose, Paranasal sinuses, and Lungs, in addition to Crescentic GN

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18
Q

What are Classes IV, V, and VI of Lupus Nephritis

A

Diffuse proliferative (50), Membranous (10), Advanced Sclerosing (?)

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19
Q

HUS + Fever and neurological dysfunction (seizures)

A

TTP

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21
Q

ANCA-associated GN is usually part of

A

syndrome with extra-renal signs and symptoms

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22
Q

For SLE, anti-dsDNA and anti-Sm Ab’s are less ___ than Anti-nuclear, but much more

A

Less sensitive, but more specific

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24
Q

T/F: Pauci-immune GN may be ANCA-negative and can occur w/out extra-renal disease

A

TRUE

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24
Q

Prevalance of anti-nuclear auto-ab’s in normal individuals

A

15%

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26
Q

90% of patients with ANCA-associated Crescentic GN have ___ before they develop symptoms of GN

A

Flu-like symptoms

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26
Q

PR3-ANCA =

A

Wegener’s

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27
Q

Factor H mutation

A

Uncontrolled activation of complement with intravascular thrombosis –> HUS

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27
Q

AI small vessel vasculitis cause of pauci-immune crescentic GN associated with P-ANCA

A

Microscopic Poly

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27
Q

Only approved tx of Lupus by FDA

A

Aspirin, Glucocorticoids, Hydroxychloroquine

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28
Q

Full House Immunofluorescence

A

In SLE, staining of deposits with antisera to all 3 Ig’s, C3, and Cr

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30
Q

When both P-ANCA and C-ANCA are present, call it

30
Q

Finding MHA and Thrombocytopenia with no other explananation besides TTP should prompt

A

Plasmapharesis

31
Q

Clincially, patients with Thrombotic Microangiopathies have what 3 things

A

Microangiopathic Hemolytic Anemia, Thrombocytopenia, Often renal failure

32
Q

Tx of HUS

A

Transfusions, Dialysis, Supportive measures

32
Q

Mortality for HUS

A

4% if treated, poor if not

33
Q

Which class of Lupus Nephritis is severe? Which is nephrotic?

A

IV is severe, 5 is nephrotic

34
Q

What is Onion Skinning? (in context of kidney in SS)

A

Concentric Sclerosing Intimal thickening of interlobar arteries

36
Q

Which is ANCA+: PAN or Microscopic Polyangiitis

A

Microscopic Polyangiitis

37
Q

A ____ event is likely necessary for endothelial injury with ANCA-associated vasculitis

A

Synergistic pro-inflammatory event (like exposure to TNF-alpha)

38
Q

HUS is usually a complication of

A

intestinal infection of Shiga-toxin producing E Coli

39
Q

New onset of accelerated arterial HTN and/or rapidly progressive oliguric renal failure

A

Scleroderma Renal Crisis

40
Q

3 general locations affected by Wegener’s

A

URT, LRT, Kidney

40
Q

Cause of TTP

A

Deficiency of ADAMTS13 - Cleaving protease of vWF

41
Q

Demographic of SS

A

Black women in their 50s

43
Q

Tx of TTP

A

Plasmapharesis

45
Q

Medium vessel arteritis (eg classic PAN) causes

A

renal infarcts and distal glomerular ischemia

46
Q

Most common and characteristic forms of lupus nephritis involve

A

the glomeruli

48
Q

Negative Ab (pauci-immune) is usually in the setting of

A

Crescentic GN

49
Q

T/F: Pauci-immune means no Ab’s

A

False, can still have ANCA’s

50
Q

T/F: Patients with Wegener’s can also have P-ANCA

A

True, or be ANCA negative

52
Q

Which is usually ANCA positive: Medium or Small vessel vasculitis

53
Q

Tx of SLE

A

Steroids, Immunosuppressants: Mycophenolate, Cyclo, MTX, Azathioprine

53
Q

2 main types of Thrombotic Microangiopathies

55
Q

Vasculitis in SLE

A

Acute necrotizing vasculitis of small arteries and arterioles with fibrinoid deposits

57
Q

Extra-renal signs and symptoms in ANCA-associated GN

A

Athralgias, Arthritis, Myalgias, Fatigue

58
Q

Fundamental pathogenesis of Thrombotic Microangiopathy

A

Loss of Thromboresistance by endothelial cells

60
Q

Type of vasculitis caused by Wegener’s

A

Necrotizing

62
Q

Tx of Wegener’s

A

Cyclophosphamide, Steroids, sometimes plasmapharesis

63
Q

What are Hyaline thrombi

A

Misnomer of wire loop deposits that protrude into lumen

64
Q

Microscopic Polyangiitis vs PAN effects on Kidney

A

MP causes GN, whereas PAN causes macroscopic ishcemia and infarction (thrombosis, aneurysm)

65
Q

Tx of Scleroderma Renal Crisis

66
Q

Scleroderma Renal Crisis

A

New onset of accelerated HTN and/or rapidly progressive oliguric renal failure

67
Q

Hemolytic Uremic Syndrome is triad of

A

Microangiopathic Hemolytic Anemia, Thrombocytopenia, AKI

67
Q

Eculizamab is used for

A

Block complement activation (HUS subtype)

68
Q

Systemic Sclerosis is characterized by

A

Fibrosis of CT and Vascular Occlusive Disease

70
Q

Wegener’s causes rapidly progressive

A

Crescentic GN

71
Q

Microangiopathic Hemolytic Anemia, Thrombocytopenia, AKI

A

Hemolytic Uremic Syndrome is triad of

72
Q

3 significant causes of endothelial damage

A

E Coli toxin (auto-Ab’s), Chemo, Radiation

73
Q

Fibrinoid Necrosis and Thrombosis in Scleroderma

75
Q

What has prolonged PT and PTT: TMA or DIC

A

DIC - Consumptive coagulopathy

76
Q

2 features shared between TMA and DIC

A

Thrombocytopenia and Microangiopathic Hemolytic Anemia

77
Q

PR3-ANCA is specific for Granulomatosis w Polyangiitis

78
Q

Primary target in small vessel vasculitis

A

Endothelial cells

79
Q

Effect of PAN on kidneys

A

Not GN - Macroscopic ischemia and infarction

80
Q

Which arteries are affected by intimal and medial proliferatioin scleroderma renal crisis

82
Q

Who is usually affected by HUS

A

Small children under 5 years

84
Q

4 most common inflammatory manifestations of SLE

A

Non-erosive Synovitis (90), Skin lesions (85), Nephritis (50), Cerebritis (50)

85
Q

2 major features of TTP

A

MHA, Thrombocytopenia

86
Q

Thrombotic Microangiopathy must be differentiated from

87
Q

Wire loop lesions are inidicative of

A

Active disease

88
Q

What do ANCA’s do to their targets in granulocytes

A

Activate neutrophils, which then adhere to endothelial cells; Also prevent inactivation of the targeted granulocyte componens (PR3, MPO, etc)

90
Q

Which part of glomerulus is affected in SLE

A

All 3 locations

91
Q

ANCA cause

A

Endothelial Cell injury in Glomeruli and Blood Vessels

92
Q

Segmental Transmural Necrotizing Vasculitis

93
Q

In about 10% of cases, HUS in children is due to

A

Inherited mutation that inactivates Factor H

94
Q

P-ANCA may be positive in up to ___% of patients with Anti-GBM disease

95
Q

5 features of TTP

A

2 major: MHA, Thrombocytopenia; Others: Neurologic dysfunction, renal dysfunction, fever

96
Q

What causes wire loops in SLE

A

Confluent circumferential Subendothelial deposits cause the glomerular capillary walls to be thickened

Renal (31 decks)

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